tag:blogger.com,1999:blog-69869079899469805682024-03-12T15:58:28.853-07:00Random InterestsAnonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.comBlogger49125tag:blogger.com,1999:blog-6986907989946980568.post-4125628912801615112016-01-11T06:23:00.000-08:002016-01-11T06:23:08.035-08:00Food SensitivitiesThis is for my personal use, though it should help anyone in a similar boat.<br />
<br />
Since cutting out dairy and gluten four days ago the heavy breathing that I used to get in the mornings, afternoons and evenings has greatly subsided. However, it seems to have made a bit of a comeback today (Monday 11th January 2016) and yesterday (Sunday 10th January 2016). I also felt very tired earlier in the afternoon which is a symptom I haven't had in a month or so.<br />
<br />
This may be due to a sensitivity to fried foods as I ate chips on Saturday and Sunday night. It may also be totally unrelated to food and just a part of recovering from fatigue. I shall see how I feel tomorrow and whether or not the heavy breathing is present then as today I will only be eating fruits, vegetables, noodles, meat and some herbal and fruit drinks.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-8354640898911245232015-06-13T04:07:00.002-07:002015-08-27T07:11:01.277-07:00Question 5: How might a patient's white blood cell count be affected by a drug that reduces cell division, and how may this person be treated differently to compensate for this effect?<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;">*These posts are from coursework answers for my degree, but the Figures that are referred to in the text didn't scan well and have already been handed in. These long posts would probably not interest most people but if you enjoy quite in-depth reading of scientific problems then this may be for you.</span></u></b><br />
<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;"><br /></span></u></b><b><span style="font-size: 12pt; line-height: 17.1200008392334px;">Question 5: </span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;">If
a patient with an inoperable cancer is treated using a drug that reduces the
rate of cell division, how might the patient’s white blood cell count
change?</span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;"> </span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;">How might the patient’s
environment be modified to compensate for the effects of these changes?</span></b><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;"><br /></span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;">Answer:</span><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;"><br /></span>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">If a drug
that reduces the rate of cell division is given to a cancer patient, one would
expect a decrease in that person’s white blood cell count (Prinjha, and
Tarakhovsky, 2013).This is because not only would the cancer cells have their
rate of cell division stunted, but the immune cells would also. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">A drug which
inhibits cancer cell growth and is given to a patient with an inoperable cancer
is likely to be a form of targeted therapy in regard to cancer treatment. These
drugs are more specialised in choosing cancer cells to exhibit their effects.
Older drugs find it harder to differentiate between healthy and cancerous
cells, and given that their effect usually increases depending on the rate of
cell reproduction (advantageous because cancer cells tend to rapidly
reproduce), these older drugs commonly cause much harm to fast-growing cells
such as the skin and digestive tract. However, targeted therapies still have
substantial side-effects, particularly fatigue, nausea, skin and clotting
problems as well as elevated blood pressure. These forms of drugs, however,
would have less effect upon the white blood cell count than ordinary drugs
(National Cancer Institute, 2014).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Chan, Koh
and Li (2012), state that cancerous cells are most vulnerable during mitosis
and that the use of drugs centred on cell division is therefore of high
importance to cancer treatment. They also state that drugs producing
antimitotic effects tend to be highly specific, but that the body reacts
unpredictably when exposed to them. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">According to
Schmidt (2000 pp. 112-115), the production of thymidylate and dihydrofolate are
of substantial importance in the role of DNA synthesis. Given that cancer is
fundamentally a cellular error causing uncontrolled replication, the inhibition
of DNA synthesis plays a pivotal role in treating cancer. A compound called
5-fluorouridine bears strong similarity to the substrate acted upon by
thymidylate synthase, once it has been phosphorylated by a nucleoside kinase
(the only difference is that this product contains a fluorine where the natural
substrate, dUMP, contains hydrogen). However, once this end-product (called
5-fluorouridine monophosphate) binds with thymidylate synthase, the fluorine
stays bonded to the enzyme, causing it to no longer function. Since the 5-fluorouridine
monophosphate reacts with the enzyme, and the enzyme can no longer function
afterwards, it is called a “suicide substrate”. DNA necessary for cell division
can also be reduced by decreasing the reduction of dihydrofolate to
tetrahydrofolate. When N<sup>5</sup>,N<sup>10</sup>-methylene tetrahydrofolate
donates a methyl group to deoxy-UMP under the supervision of the thymidylate
synthase enzyme, thymidylate (deoxy-TMP) is formed. This reaction is
illustrated in figure 5.1.<o:p></o:p></span></div>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Since the
tetrahydrofolate compound in this reaction is oxidised to dihydrofolate, the
converse of this (reduction of dihydrofolate by dihydrofolate reductase (DHFR)),
will consequently lead indirectly to thymidylate production. Thus, the
inhibition of DHFR will also reduce thymidylate production. Substrates which
are competitive inhibitors of folates are called folate antagonists, where an
antagonist is a substance that binds to a receptor, without producing the
receptor’s activity. Thus, a substance binding to a folate-receptor, may not
produce the same effect as a folate-containing substance binding to it. The <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">antagonists
in this example will attempt to out-compete the folate substrates involved in
activating the DHFR enzymes, thus preventing the chemical reactions leading
initially to the reduction of dihydrofolate to tetrahydrofolate and eventually
to the production of thymidylate, which would increase DNA synthesis and allow
cell division to occur.</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">From Schmidt
(2000, p. 230), information is given about the G1 phase of cell division. This
particular phase is actually a point of non-division, in which various
biochemical reactions take place, but the cell does not actively divide. Many
animal cells can spend years in the G1 phase without dividing, which makes it
highly important in cancer treatment. If the G1 phase could be clearly
understood, then cells could be encouraged to remain within it, not dividing,
and consequently not resulting in cancer formation. An unfortunate consequence
of decreasing cell division non-specifically however, is that all cells in the
body which take in a particular drug that decreases cell division will have
their rate of replication decreased. This makes it more difficult for the body
to combat infections which are not affected by the drugs, given that the body
cells may be subjected to division-inhibition for many weeks or months before
encountering a new infection, its immune cells are likely to be lower in number
and therefore not be as capable of combating the threat.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">If the
number of white blood cells that a patient has, decreases, then that person is
more susceptible to all possible infections as these cells fight them.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Among the
white blood cells or leukocytes, the form most important during consideration
of possible infections is the neutrophil. This is the type of white blood cell
most abundant in plasma, constituting roughly 54-62% of the overall number of
circulating leukocytes (Mescher 2013, p. 235). Neutrophils are relatively small
phagocytic immune cells that are produced in vast quantities every day (roughly
126 billion enter the digestive tract daily, according to Seeley, VanPutte,
Regan and Russo, 2011, p. 791), and are often the first of the immune cells to
reach infected regions in great numbers. Once at an infected site, neutrophils
are responsible for increasing immune cell activity and inflammation at this
area. This is brought about by their release of cytokines which encourage the
proliferation and differentiation of immune cells, and by chemotactic agents,
respectively (Seeley, VanPutte, Regan and Russo, 2011, p. 792).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The test for
abundance of circulating neutrophils is called the absolute neutrophil count
(ANC), and is considered the most important risk factor for both bacterial and
fungal infections, according to Johnston and Spence (eds, 2003, p. 253). The
diagnosis of neutropenia (a deficiency of neutrophils), is stated as an ANC of
less than 500 per millilitre of plasma, or expected to fall to this level
within the next 24 hours of being tested. These writers also state that risk
increases as neutrophil count decreases, and that the rate at which neutrophil
count is decreasing, as well as how long neutropenia has presented, also play a
pivotal role in contracting bacterial and fungal infections. The more rapidly
neutrophil count is falling, and the longer a person has had neutropenia, the
more likelihood there is of becoming infected, and the more severe the
infection is likely to be. Thus, it is highly important to consider
neutropenia, although B-cell and T-cell function is also compromised in cancer
treatment, usually due to chemotherapy, but further exacerbation can occur via
concomitant utilisation of steroids (Johnston and Spence, eds, 2003, p. 246).
These authors also explain that the use of catheters in immunocompromised
cancer patients poses a significant risk of subsequent infection, this is due
to the ease with which microbial colonies can form within the synthetic
catheter, possibly migrating into the host and causing infection. Therefore, it
is of the utmost importance that catheters be monitored and if possible,
sampled, in order to gauge microbial growth.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">There are
many other types of immune cell that are important in the response to
infection. This first section deals with those cells which are an integral part
of the innate immune system, i.e. the branch of the immune system acts in a
non-specific manner:<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Neutrophils
fall into this category but are explained in detail above.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Monocytes
are white blood cells that circulate the body and are enticed by
chemo-attractants to enter damaged tissue and differentiate into macrophages
which are important for consuming toxic substances and cells that may damage
the body, they may also stimulate B-cell and T-cell activity during infection (Seeley,
VanPutte, Regan and Russo, 2011, p. 791). Macrophages are roughly 5 times the
size of monocytes, and have additional lysozymes and mitochondria. They are
larger, longer-lasting, and are capable of engulfing larger particles than
neutrophils, though they appear at the site of infection a little later than
neutrophils. Thus, they are most used in the later stages of infection. Their
large size makes them ideal for engulfing cellular debris, and even whole
neutrophils which have died earlier on during the immune response. Macrophages
may also secrete various substances such as interferons, complement, and
prostaglandins. The roles of interferons and complement are discussed
elsewhere, but prostaglandins have a variety of actions, perhaps most
importantly of which are its function in increasing the permeability of blood
vessels (which can allow immune cells to permeate vascular and reach infected
or damaged tissue, and also in causing vasodilation, again allowing immune
cells to reach a particular site by aiding blood flow to the affected region.
This is shown by Seeley, VanPutte, Regan and Russo, 2011, pp. 789, 792.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Both
basophils (motile) and mast cells (nonmotile) are immune cells that promote
inflammation within tissues through the release of various chemicals, e.g.
leukotrienes and histamine. This inflammatory response can increase blood flow
to the area, signal other leukocytes to arrive on the scene, and encourage the
formation of either a platelet plug or clot to seal off the affected region to
further damage and/or infection. Conversely, eosinophils are motile immune
cells that enter tissues and inhibit the inflammatory response. They do this by
breaking down the substances secreted by the basophil and mast cells.
Therefore, eosinophils are produced in larger quantities during immune
reactions where a large inflammatory response occurs, such as in allergies.
Additionally, eosinophils have the ability to kill some forms of parasites (Seeley,
VanPutte, Regan and Russo, 2011, pp. 791-793).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Finally, NK
(natural killer) cells are important in the attack on cancer cells. NK cells
contain enzymes that can chemically lyse or split tumour cells, preventing the
growth spread of cancer, one of their preferred mechanisms of actions is to
chemically lyse the plasma membrane of harmful cells (Seeley, VanPutte, Regan
and Russo, 2011, p. 791-792).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The adaptive
immune system then, deals with specific and personalised threats to the body. This
branch of the immune system is capable of responding to a specific substance,
called an antigen. These antigens may be produced by the body, for example, a tumour
cell (a self-antigen), or produced by a foreign invader or microbe which has
found its way into the body and may cause harm (a foreign antigen). Within the
umbrella term of adaptive immunity, there are two main categories of immune
response; cell-mediated immunity and antibody-mediated immunity.
Antibody-mediated immunity is brought about by the production of antibodies
(these are released by cells that result from the differentiation of B-cells)
that bind with antigens to form antigen-antibody complexes that inhibit the
actions of harmful cells. On the other hand, cell-mediated immunity arises from
the activity of T-cells, which can destroy whole cells instead of inhibiting
vital components. This is highly useful for infections from viruses, which essentially
‘hijack’ the biochemical reactions of a cell for their own needs (Seeley,
VanPutte, Regan and Russo, 2011, p. 794-806).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The adaptive
immune system almost entirely consists of B-cells and T-cells to combat
infection:<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">B-cells can
be stimulated by antigens on the cell surface membrane of a pathogen and
differentiate to produce either a plasma cell or memory B-cell. The plasma cell
in this scenario would produce antibodies complementary in shape to the harmful
antigen which would inhibit the effectiveness of the pathogen and signal for
its lytic destruction by neutrophils, eosinophils, macrophages or monocytes.
The memory B-cells formed by differentiated of B-cells can promote a rapid and
lasting immune reaction to a specific form of pathogen. If this pathogen were
to enter the body, memory B-cells would mass-produce antibodies that would
inhibit its actions. (Seeley, VanPutte, Regan and Russo, 2011, pp.791, 803).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">There are
many types of T-cells; delayed hypersensitivity T-cells promote inflammation through
the release of cytokines, helper T-cells stimulate the activity of effector
T-cells and B-cells, Suppressor T-cells do the opposite, inhibiting the action
of both T-cells (effector forms) and B-cells, and lastly, memory T-cells are
similar to memory B-cells in their ability to maintain a lasting immunity
towards a particular antigen that has been previously encountered. (Seeley,
VanPutte, Regan and Russo, 2011, p. 791).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Finally,
dendritic cells activate both B-cells and T-cells after recognition of a harmful
antigen (Seeley, VanPutte, Regan and Russo, 2011, p. 791).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Another area
of concern is the mucous membrane throughout the digestive tract. This membrane
can become inflamed and mouth, stomach and other ulcers can result from the use
of both chemotherapy and radiotherapy (depending on where the latter is
targeted to), these ulcers and general damage to the mucous membrane can
facilitate the harbouring of pathogens which can infect the body (Johnston and
Spence, eds, 2003, p. 253). Further to this, though beyond the scope of this
essay, is the effect of the underlying cause or simultaneous condition with
regard to cancer. Chronic lung or liver diseases as well as AIDS, can
independently compromise immune function, which would only be worsened by cancer
treatment.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Care must be
taken to ensure proper health of skin, teeth and the general oral cavity.
Healthy skin and mucous membranes in the oral cavity produce secretions that
prevent bacterial infection. For example, skin secretes oils and has an acidic
pH due to the actions of sebaceous and sweat glands. Saliva in the oral cavity
contains many antimicrobial agents, including the protein lysozyme, which
destroys the cells walls of bacteria. These are some examples of nonspecific
barriers (methods that provide a broad-spectrum of defence not limited to a
single pathogen at a time). See Houghton Mifflin Harcourt (2014). Broken skin,
infected gums and rotting teeth can all harbour bacteria that can lead to an
infection the immunocompromised patient. Antibiotics may be taken to control
overall and in particular, digestive bacteria, lest these should turn
pathological.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">According to
Pack (2001, pp. 210-212), there are three types of barrier preventing
infections to the body. These are the nonspecific barriers, the nonspecific
defences, and the specific defences of the body. Many of the nonspecific
barriers have already been covered, these are; skin, sweat, proteins such as
lysozyme, cilia, digestive juices, and commensals (symbiotic organisms exist in
and on the human body that can compete against harmful microbes). These
barriers prevent the inward movement of harmful substances and microbes into
the body.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
nonspecific defences are responsible for nonspecific removal and destruction of
threats that have found their way into the body. Examples include phagocytes
(white blood cells that engulf and digest pathogens, neutrophils, eosinophils,
macrophages and monocytes are included in this category). Natural killer cells,
are also on the list, as well as interferons and a defensive chemical called
“complement”. Interferons are released by cells that are infected by viruses,
and help the immune system recognise when a viral infection has occurred. Interferon
is also aptly named for its ability to interfere with the production of viruses
(Seeley, VanPutte, Regan and Russo, 2011, p. 789). Complement is a compound
formed by roughly 20 proteins bonded together which attracts phagocytic immune
cells to the site of an infection, as well as lysing cells by its own actions
(Pack, 2001, p. 211).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The immune
system forms the specific defence system against foreign microbes (Pack, 2001,
p. 213). Some of the nonspecific defences such as natural killer cells and
phagocytes are used for specific defence, particularly when an antigen has become
part of an antigen-antibody complex and immune cells are signalled to engulf
it.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">On page 254
(Johnston and Spence, eds, 2003), the authors make known the vices of surgical
removal of the human spleen, which can take place occasionally as part of cancer
treatment. They state that the spleen is necessary for removal of opsonized
pathogens (those bound by antibodies in the preparation of phagocytosis) and
erythrocytes which have been infected with parasites. Surgical removal of the
spleen also reduces the body’s ability to develop immune reactions to
previously unencountered antigens. According to Pack (2001, pp. 204-209), the
spleen is the largest organ in the lymphatic system. It contains two distinct
regions; the white pulp and the red pulp. The white pulp contains many
lymphocytes (T cells and B cells), as well as reticular fibres, whereas the red
pulp contains many venous sinuses that act as a reservoir of red blood cells.
The spleen has several main functions; filtering the blood of pathogens and debris
from dead and aged cells, the destruction of old erythrocytes and subsequent
recycling of organelles and nutrients, acting as a reserve for blood, and
providing a site of T cell and B proliferation (T cells reproduce before
returning to attack non-self cells and B cells produce antibodies and plasma
cells which go on to inactivate harmful antigens. Thus, its removal can have
dangerous consequences.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The above
effects combined produce a patient who is highly susceptible to infection. They
mention several bacteria whose infections are more commonly and severely
present in immunocompromised patients, there are; <i>Streptococcus pnuemoniae, Capnocytophaga canimorsus </i>and<i> Babesia microti </i>(a bacterium that
presents with malaria-like symptoms such as fever, chills, sweating, and head
and body aches information that is elaborated upon by the Centers for Disease
Control and Prevention, 2014a).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Wigglesworth
(2003) gives a lot of information on the use of environment changes for
immunosuppressed patients. If such patients are currently residing in a
hospital then they can be separated from the main hospital population and wads,
usually by keeping them in a single room. Hygiene is of particular importance
to ensure that no pathogens are transferred from care workers to the patient.
Hand-washing is a must in this scenario. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">According to
the University of Utah Health Care (2003), proper hand-washing is the most
important action in the prevention of infectious diseases. The amount of
visitors that a person meets during the day and the foods that they eat must be
monitored to ensure there is little risk of infection. Certain foods are
considered high-risk when it comes to patients with a weakened immune system,
extra care must be taken to avoid these foods. Soft cheeses and anything made
with raw eggs are a hazard for such patients. Therefore, mayonnaise was also be
avoided. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Additionally,
the use of vaccinations before a person is likely to become immunocompromised
can decrease the likelihood of infection. This has been proposed as a strategy
for persons likely to exhibit lower immune function for a number of different
reasons including cancer and HIV (Tolan, et al, 2013).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The Centers
for Disease Control and Prevention recommend that any sign of fever in patients
receiving chemotherapy be treated as an emergency, even if it is the only
symptom (Centers for Disease Control and Prevention, 2014b). Further safety
precautions can be taken to reduce the chance of infection can be taken. One
can avoid sharing any personal items, such as cups or utensils or anything that
requires insertion into the mouth, e.g. toothbrushes. Daily washing should be
done with unscented lotions. Lotions which are scented can damage or dry the
skin, allowing pathogens to colonise or pass through this layer. Meat and eggs
must be cooked thoroughly, raw fruit and vegetables must be washed carefully,
gloves should be worn around pets and for gardening, and care must be taken to
avoid damaging the gums during tooth-brushing (thus a soft toothbrush is highly
recommended), see Centers for Disease Control and Prevention, 2014c. This same
source provides ample knowledge of the warning signs of infection in order to
warn immunocompromised patients. Some of the more noticeable signs are; a fever
of >38<sup>o</sup>C for over one hour, sore throat, burning or other pain
upon urination, shortness of breath, diarrhoea, vomiting and increased
urination. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Finally, the
Centers for Disease Control and Prevention also note that white blood cell
usually drops to its lowest value as a result of chemotherapy around 7 to 12
days after the chemotherapy dose has finished, and from this point the low
count can last for around a week before increasing again. This lowest point is
when most vigilance is required in protecting oneself from infection, as the
immune system will be most weakened and unable to respond adequately (Centers
for Disease Control and Prevention, 2014d).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Question 5 References:<o:p></o:p></span></u></b></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Centres for
Disease Control and Prevention, 2014a. <i>Babesiosis
FAQs</i>, [online] Available at: <</span><a href="http://www.cdc.gov/parasites/babesiosis/gen_info/faqs.html#symptoms"><span style="font-size: 12.0pt; line-height: 107%;">http://www.cdc.gov/parasites/babesiosis/gen_info/faqs.html#symptoms</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 13 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Centres for
Disease Control and Prevention, 2014b.<i>Emergency
Room Personnel</i>, [online] Available at: <</span> <a href="http://www.cdc.gov/cancer/preventinfections/pdf/er_personnel_poster.pdf">http://www.cdc.gov/cancer/preventinfections/pdf/er_personnel_poster.pdf</a>
<span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 13 April 2015]. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Centres for
Disease Control and Prevention, 2014c.</span> <i>How can I prevent an infection?</i><span style="font-size: 12.0pt; line-height: 107%;"> [online] Available at: <</span> <a href="http://www.cdc.gov/cancer/preventinfections/pdf/neutropenia.pdf">http://www.cdc.gov/cancer/preventinfections/pdf/neutropenia.pdf</a>
<span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 13 April
2015]. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Centres for
Disease Control and Prevention, 2014d. <i>Protect:
Know the Signs and Symptoms of Infection, </i>[online] Available at: <</span><a href="http://www.cdc.gov/cancer/preventinfections/symptoms.htm"><span style="font-size: 12.0pt; line-height: 107%;">http://www.cdc.gov/cancer/preventinfections/symptoms.htm</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 13 April 2015]. <o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Chan, K.S.,
Koh, C.G., and Li, H.Y., 2012. <i>Mitosis-targeted
anti-cancer therapies: where they stand.</i> [online] Available at: <</span><a href="http://www.nature.com/cddis/journal/v3/n10/full/cddis2012148a.html"><span style="font-size: 12.0pt; line-height: 107%;">http://www.nature.com/cddis/journal/v3/n10/full/cddis2012148a.html</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 7 April 2015]. <o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Houghton
Mifflin Harcourt 2014. <i>Nonspecific
Barriers,</i> [online] Available at: <</span><a href="http://www.cliffsnotes.com/sciences/anatomy-and-physiology/the-immune-system-and-other-body-defenses/nonspecific-barriers"><span style="font-size: 12.0pt; line-height: 107%;">http://www.cliffsnotes.com/sciences/anatomy-and-physiology/the-immune-system-and-other-body-defenses/nonspecific-barriers</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 7 April 2015]. <o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Johnston,
P.G., and Spence, R.A.J., eds. 2003, <i>Oncologic
Emergencies</i>. United States, New York: Oxford University Press Inc.<o:p></o:p></span></div>
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<span style="font-size: 12.0pt;">Mescher,
A.L., 2013. <i>Junqueira’s Basic Histology
Text & Atlas</i>, 13<sup>th</sup> ed. China: The McGraw-Hill Companies.<o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">National
Cancer Institute, 2014. <i>Targeted Cancer
Therapies</i>, [online] Available at: <</span><a href="http://www.cancer.gov/cancertopics/treatment/types/targeted-therapies/targeted-therapies-fact-sheet"><span style="font-size: 12.0pt; line-height: 107%;">http://www.cancer.gov/cancertopics/treatment/types/targeted-therapies/targeted-therapies-fact-sheet</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 7 April 2015].<o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Pack, P.E.,
2001. <i> Anatomy and Physiology,</i> Hoboken, NJ: Wiley
Publishing, Inc.<o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Prinjha, R.,
and Tarahovsky, A., 2013. <i>Chromatin
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<span style="font-size: 12.0pt; line-height: 107%;">Schmidt, F.,
2000. <i>Biochemistry II, </i>New York, NY:
Wiley Publishing, Inc.<o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Tolan, R.W.,
Brook, I., Windle, M.L., Domachowske, J., Rauch, D., and Steele, R.W. 2013. <i>Infections in the Immunocompromised Host, </i>[online]
Available at: <</span><a href="http://emedicine.medscape.com/article/973120-overview"><span style="font-size: 12.0pt; line-height: 107%;">http://emedicine.medscape.com/article/973120-overview</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 7 April 2015]. <o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">University
of Utah Health Care, 2003. <i>Prevention of
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<span style="font-size: 12.0pt; line-height: 107%;">Wigglesworth,
N., 2003. <i>The use of protective isolation</i>,
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Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com1tag:blogger.com,1999:blog-6986907989946980568.post-4502398884415114682015-06-13T04:02:00.002-07:002015-06-24T04:21:31.899-07:00Question 4: Discuss causes, effects and treatments of atherosclerosis<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;">*These posts are from coursework answers for my degree, but the Figures that are referred to in the text didn't scan well and have already been handed in. These long posts would probably not interest most people but if you enjoy quite in-depth reading of scientific problems then this may be for you.</span></u></b><br />
<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;"><br /></span></u></b>
<b><span style="font-size: 12pt; line-height: 17.1200008392334px;">Question 4: </span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;">Atherosclerosis
in the coronary circulation causes heart disease; discuss the causes of
atherosclerosis and its effect on the cardiovascular system.</span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;"> How are stents used to treat
atherosclerosis?</span></b><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;"><br /></span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;">Answer:</span><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;"><br /></span>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Atherosclerosis
is the build-up of plaque formed primarily by white blood cells and cholesterol
within the innermost membrane of an artery wall, called the tunica intima
(Seeley, VanPutte, Regan and Russo, 2011, p. 725). This accumulation of plaque
is a slow process, often taking years or decades to present with any symptoms,
if at all, to the person suffering from it. It is important to note that
oxidised low-density lipoproteins (ox-LDLs) are considered more atherogenic
than native LDLs. This is agreed upon in many works, for example; Samsioe
(1994), Panza, and Cannon, eds. (1999, pp. 89-92), and Kummerow, (2013). Dr. Kummerow,
in particular, gives much weight to the pathological effects of oxidised
cholesterols, known as oxysterols. He believes that the intake of oxysterols
via fried foods, excess vegetable oils (especially partially hydrogenated
vegetable oils) and cigarette smoking play a far greater role than simple
dietary cholesterol. This will be a part of the original thought later on in
this essay.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Schmidt
(2000, p. 38), explains that as cells take in LDL cholesterol to satisfy their
metabolic requirements, they begin to exhibit fewer cell membrane receptor
sites for LDLs. Therefore, if a high concentration of LDL cholesterol exists in
the bloodstream, then cells will take in as much as they need, down-regulate
their receptor sites, and the remaining cholesterol will be free to circulate
the body. This means that more of the cholesterol will be free to travel the
circulatory system and become deposited in walls of blood vessels, leading to
an increased risk of arterial diseases. The use of receptors on cell surface
membranes in order to take in a specific molecule or nutrient is an example of
receptor-mediated endocytosis (Pack, 2001, pp. 26-27). When this occurs, a
vesicle is formed as the cell membrane folds inwards around the substance being
received. Once the substance is safely inside of the cell, the vesicle can
break-down, releasing, in this case, the LDL.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;"> The resultant problems associated with
atherosclerotic lesions are typically due to the narrowing of blood vessels
(stenosis), this decreases the available size of lumen for blood to travel
through, leading to a reduction in blood supply to tissues (ischemia). There
are many causes of atherosclerosis, these include: Hypercholesterolemia or
dyslipidemia (particularly increased LDL [low-density lipoprotein]
concentrations, but decreased levels of HDL [high-density lipoproteins that
appear to offer a protective effect against plaque build-up] are also a risk factor
[</span><a href="http://circ.ahajournals.org/search?author1=Rafael+Carmena&sortspec=date&submit=Submit"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;">Carmena</span></a><span class="contrib-degrees"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;">,</span></span><span style="color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold;"> </span><a href="http://circ.ahajournals.org/search?author1=Patrick+Duriez&sortspec=date&submit=Submit"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;">Duriez</span></a><span class="contrib-degrees"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;"> and</span></span><span class="apple-converted-space"><span style="color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold;"> </span></span><a href="http://circ.ahajournals.org/search?author1=Jean-Charles+Fruchart&sortspec=date&submit=Submit"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;">Fruchart</span></a><span class="name"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;">, 2004])</span></span><span style="color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold;">. </span><span style="font-size: 12.0pt; line-height: 107%;">Habitual cigarette smoking (</span><span class="name"><span style="border: none windowtext 1.0pt; color: #333333; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Lucida Sans Unicode"; mso-bidi-font-weight: bold; mso-border-alt: none windowtext 0cm; padding: 0cm;">Lin, et al,. 1992) has also been found
as a potential factor in disease progression. Mitchell, et al. (2007, p.345)
show that diabetes, elevated C-reactive protein in serum, growing older, male
gender, genetic faults that produce high levels of cholesterol and family
members who have suffered from atherosclerosis and its related cardiovascular
incidences (more detail further on in this essay), were more likely to get the
disease. Concomitant disorders also include obesity and insulin resistance (as
well as type 2 diabetes), as shown by Hotamisligil (2010).</span></span><span style="font-size: 12.0pt; line-height: 107%;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The above
factors will be touched upon briefly, however a lot of this write-up will be
dedicated to biochemical pathways within the body that both decrease and
contribute to atherosclerosis, and how a down-regulation of antiatherogenic
chemicals can lead to this disease. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Some of the
more microscopic changes that occur to bring about atherosclerosis include but
are not limited to the following: Monocyte and macrophage adhesion to
endothelial cells, platelet aggregation, reduced endothelial nitric oxide
levels, high endothelial permeability increasing the migration of lipoproteins
into the walls of arteries, and increased vascular smooth muscle cell
proliferation, this rapid reproduction rate greatly speeds up the aging process
(Panza, and Cannon, eds., 1999, p. 44).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">One of the
largest factors in the occurrence and progression of atherosclerosis is the
movement of lipoproteins, primarily LDLs, into the arterial wall, where they
can then deposit cholesterol which can become oxidised. HDL is considered
protective in this situation as it bonds to cholesterol and carries it to the
liver. This is one of the main reasons why proportions of varying types of
lipoproteins is an important study in these diseases, in particular, having low
HDL and high LDL is considered a strong factor in the onset of atherosclerosis
(American Heart Association, 2014a). <o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; margin-bottom: 0.0001pt;">
<span style="font-size: 12.0pt;">Mescher (2013, pp.
234-239) shows that the whole blood consists of approximately 1% leukocytes and
platelets combined (white blood cells) which are usually inactive while
circulating the body. Their activity is apparent however, when they are
signalled to sites of infection, inflammation or general damage. Here they will
migrate into tissues and exert (generally) appropriate action. In the case of
atherosclerosis, the prime white blood cell to be considered is the monocyte,
an agranulocytic blood cell that, among many other functions, modulates the
concentrations of LDLs in the arterial wall, it has this capability because it
is a precursor of the macrophage (an immune cell of the mononuclear [one
nucleus] phagocyte system, that engulfs cellular remnants and infectious
agents, among other substances and living matter). Whenever LDLs and
particularly oxidised LDLs are present in the arterial wall, monocytes (a form
of leukocyte) are coaxed into adherence to the endothelial cells by the
presence of a protein, VCAM-1 (vascular cell adhesion molecule 1 or vascular
cell adhesion protein 1, as shown by the National Center for Biotechnology
Information, 2015). </span><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; color: #222222; font-size: 12pt;">Without this protein, the monocyte would
continue its journey around the body without stopping. Instead, the monocyte
will migrate into the endothelium experiencing LDL-induced inflammation and
will differentiate into a macrophage, in order to phagocytise the offending
molecule and carry it aw</span><span style="color: #222222; font-size: 12.0pt; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-GB;">a</span><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; color: #222222; font-size: 12pt;">y.</span><span style="color: #222222; font-size: 12.0pt; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-GB;"><o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; margin-bottom: 0.0001pt;">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">If this
process becomes chronic, i.e. many LDLs are constantly permeating the
endothelium and causing inflammation, then a high concentration of macrophages
will exist within the endothelium in order to try and remove these LDLs. This
accumulation of monocytes is called extravasation (Mescher, 2013, p. 245).
Unfortunately, the presence of so many macrophages and resultant inflammatory
response leads to disproportionate tissue damage within the artery. </span><span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">As the macrophages engulf lipoproteins they begin to change
size and shape, and are termed “foam cells” (Oh, et al., 2012). The change in
appearance is due to the high concentration of lipoproteins within the
macrophages. When this occurs, the atherosclerotic lesion begins to look like a
fatty streak. This point in the progression of atherosclerosis is usually not
severe enough to induce significantly restricted blood flow within the artery
to the point of producing symptoms, but the artery becomes more rigid and
susceptible to damage. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Thus, we can see that endothelial
permeability to low-density lipoproteins is a prime factor in atherosclerosis.
If the endothelium did not allow LDL to move into it, then there would be no
need for macrophages to enter either, possibly preventing atherosclerosis from
even beginning.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">As time goes on, macrophages begin to die
and release chemicals that further exacerbate inflammation, leading to a
greater immune response within the area. This causes more monocytes to be
signalled to the vessel wall and differentiate into macrophages, furthering the
progression of plaque formation. This occurs primarily between the tunica
intima and tunica media (American Heart Association, 2014a). Also over time,
calcium deposits build up due to poor clearance of cellular debris from these
deceased cells. This is because the atherosclerotic plaque proves too great a
physical barrier to facilitate their removal. Further to this, if the
atherosclerotic plaque ruptures, possibly due to the high blood pressure in the
artery and weak structural strength of the plaque, then a clot may form. A clot
is the entrapment of blood cells, fluid and platelets by fibrin (a protein that
encourages clotting). <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Another name for a blood clot is
coagulation, and the proteins involved in its production are called either coagulation
or clotting factors, which are contained in blood plasma. Under ordinary
conditions, these factors remain inactivated, however, when damage occurs to
tissue, such as a weakened blood vessel in our case of atherosclerosis, the
coagulation factors become more active. The initiation of clotting can occur
via an extrinsic or intrinsic pathway, though both link into a later route of
chemical reactions called the common pathway (</span><span style="font-size: 12.0pt; line-height: 107%;">Seeley, VanPutte, Regan and Russo, 2011, pp. 660-661).</span><span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The extrinsic pathway of clotting starts
due to the presence of chemicals that are not contained within the bloodstream.
This could be from the release of thromboplastin (other names for this chemical
are factor III or tissue factor) as a result of tissue damage. If calcium ions
react with thromboplastin, the result is a compound containing factor VII which
can react to activate another chemical called factor X. This is the point where
the common pathway begins at the end of the extrinsic pathway (</span><span style="font-size: 12.0pt; line-height: 107%;">Seeley, VanPutte, Regan and Russo,
2011, p. 661).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
intrinsic pathway starts off differently, with chemicals that are contained
within the blood stream, such as collagen which can be exposed when blood
vessels are injured. Whenever a chemical called plasma factor XII reacts with
this collagen, the factor XII becomes active. Consequently, factor XI is
activated, leading to stimulation of factor IX, which binds with various other
molecules, such as factor VIII, phospholipids contained within platelets, and
positive calcium ions. The result of this is that factor X becomes acitivated,
and this is the point where the common pathway begins, just like at the end of
the extrinsic pathway </span><span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">(</span><span style="font-size: 12.0pt; line-height: 107%;">Seeley, VanPutte, Regan and Russo,
2011, pp. 661-662).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">At the
beginning of the common pathway, prothrombinase is formed by the binding of
factors X and V, along with phospholipids from platelets, and calcium ions.
Prothrombinase is capable of converting a protein dissolved in plasma, called
prothrombin, into thrombin, an enzyme highly important in clot formation. This
enzyme produces a protein called fibrin from fibrinogen (another protein
dissolved in plasma). The fibrin formed is responsible for the entrapment of
platelets, blood cells and fluids that make up a blood clot. Blood clotting is
a relatively rare example of positive feedback in the human body, because its
presence can lead to the production of its own precursors (e.g. factor XI and
prothrombinase). Vitamin K is necessary for clot formation, and its deficiency
can lead to excessive bleeding </span><span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">(</span><span style="font-size: 12.0pt; line-height: 107%;">Seeley, VanPutte, Regan and Russo,
2011, p. 662).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">When a clot is attached to an arterial
wall it is called a thrombus. After a clot has formed and attached itself, it
starts to become denser due to clot retraction. This occurs because platelets,
arranged as extensions to fibrinogen (which are bonded to fibrinogen receptors
on cells of the blood vessel wall), begin to contract through the use of actin
and myosin filaments, effectively pulling on the fibrinogen and drawing the
clot into a more compact structure. This process liberates serum (a fluid
similar to plasma, but which doesn’t contain some clotting factors, as well as
fibrinogen). As a result of this, the injured blood vessel is more tightly
sealed up, allowing it to recover more easily, and reducing the possibility of
infection (</span><span style="font-size: 12.0pt; line-height: 107%;">Seeley,
VanPutte, Regan and Russo, 2011, p. 663).</span><span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Figure 4.1 shows the development of
atherosclerotic plaque and subsequent clot formation. Here we see that the
plaque itself is enough to cause significant narrowing of the blood vessel,
however, due to rupture of plaque, a thrombus has started to form. This
thrombus is further restricting blood flow through the artery and will be
discussed further blow. The diagram also shows that the plaque is developing
between the tunica intima (innermost membrane of the artery, and one that
separates other tissue layers from the lumen) and the tunica media. </span><span style="font-size: 12.0pt; line-height: 107%;">(Seeley, VanPutte, Regan and Russo,
2011, p. 725).</span><span style="background: white; color: #222222; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">A
fundamental chemical involved in atherosclerosis is nitric oxide. A reading of
the literature greatly brought up the antiatherogenic importance of this small,
highly-reactive free radical. Its production is decreased in atherosclerosis
(Panza, and Cannon, eds., 1999, p. 20) and this has a strong effect in the
progression of the disease, as will be elaborated on below. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">It is
important to note before continuing that the following substances either
inhibit nitric oxide (NO) directly, either in production (which occurs via the
nitric oxide synthase enzyme), release or functional effect: <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Endothelin-1,
abbreviated to ET-1. This is a petide composed of 21 amino acids that is
produced in the endothelium, one of its main effects is as a vasoconstrictor.
ET-1 has been shown to be elevated in atherosclerosis and likely contributes to
the disease. Its vasoconstriction effects are roughly a hundred times stronger
than noradrenaline per unit of concentration. Oxidised low-density lipoproteins
increase its release, explaining its increased production during
atherosclerosis. It also attracts monocytes to atherogenic lesions because it
has chemoattractant effects (Panza, and Cannon, eds., 1999, pp. 97-109). <o:p></o:p></span></div>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Angiotensin
II or Ang II is also implicated in the development of atherosclerosis and
reduction of nitric oxide. This is a peptide hormone that also has
vasoconstrictive effects. Its administration has been shown to increase the size
of atherosclerotic lesions in mice deficient in apolipoprotein E (this is a
molecule that breaks down lipoproteins, and without it, mice as well as humans,
have a much greater risk of developing atherosclerosis, <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">Daugherty,
A., Manning, M.W., and Cassis, L.A. 2000).</span><span style="font-size: 12pt; line-height: 107%;">
</span><span style="font-size: 12pt; line-height: 107%;">Nitric oxide also inhibits the effects of Ang II in the vasculature
(Toda, N., Ayajiki, K., and Okamura, T. 2007).</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Asymmetrical
di-methylarginine (ADMA), this is a circulating amino acid that is similar in
structure to L-arginine. As l-arginine is a precursor to nitric oxide, ADMA is
able to interfere with this metabolic pathway, by interacting with its
components, namely the nitric oxide synthase enzyme (NOS). <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">N<sup>G</sup>-monomethyl-L-arginine
(L-NMMA) as well as L-nitroarginine methylester (L-NAME) share a similar
effect, by competing with L-arginine for the active site of the NOS enzyme
(Panza, and Cannon, eds., 1999, p. 165).
This occurs because the production of nitric oxide from L-arginine results from
the oxidation of the terminal containing a guanidine-nitrogen bond, which is
also contained within the inhibitors mentioned above.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Implicated
as well in the down-regulation of various aspects of nitric oxide are many
reactive oxygen species (ROS) including the superoxide anion (O<sub>2</sub><sup>-</sup>)
and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). This is due to the effect
of these species to rapidly and chemically alter nitric oxide. Panza, and
Cannon, eds. (1999, p. 134) show that the reaction between the superoxide anion
and nitric oxide produces the peroxynitrite anion, a relatively stable ion
compared to the particular radicals in this example of its creation. The
peroxynitrite anion loses many of the qualities of nitric oxide, but retains a
small ability to cause vasodilation, unfortunately it is also damaging to cells
and therefore needs to be detoxified (Panza, and Cannon, eds., 1999, p. 23).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
following substances in some way enhance the effect, production or release of
NO:<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Estrogen,
via its effect of up-regulating the eNOS enzyme (Chambliss, K.L., and Shaul,
P.W. 2013). Interestingly, estrogen has also been shown to alter lipid profile
in humans. Specifically, estrogen has been shown to reduce both total and
LDL-cholesterol levels while raising HDL. Evidence is currently gathering which
points towards an additional antiatherosclerotic effect of estrogen, namely in
the inhibition of lipid oxidation, this is based on an overall review of the
literature by Samsioe, 1994. As mentioned above, oxidised lipids are considered
more important in the onset and progression of atherosclerosis.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">L-arginine
is also important (as mentioned above, L-arginine is a precursor for NO). <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
peroxynitrite anion (the actual formation of this anion actually greatly
reduces the effect of NO because it is formed via the reaction of nitric oxide
with the superoxide anion and attenuates the vasodilatory effects of NO,
however, the presence of the peroxynitrite anion itself still contributes to
some of NO’s effects, this information is referenced above in the text about
reactive oxygen species).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
cysteine-containing NO donor SPM-5185, as demonstrated in (Panza, and Cannon, eds.,
1999, p. 22). <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Finally,
antioxidants such as vitamin C (in some trials), and the enzyme superoxide
dismutase (SOD) as shown in (Panza, and Cannon, eds., 1999, p. 135).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">When talking
about nitric oxide in relation to atherosclerosis, the endothelium of arteries
is the primary point of interest. Thus, the notation eNO (for endothelial
nitric oxide) and eNOS (short for endothelial nitric oxide synthase) can be
used interchangeably with NO and NOS for this topic.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">eNO is
highly important in alleviating and preventing atherosclerosis because it first
of all decreases endothelial permeability. As covered previously, when the
endothelium is highly permeable, more low-density lipoproteins are allowed to
pass through it into the arterial wall, and this is what requires macrophage
activity. In decreasing endothelial permeability, the whole onset of
atherosclerosis could be abated. Much of the information regarding nitric oxide
as shown above is available in the works of Panza, and Cannon, (1999) where it
is backed up by hundreds of in-text citations.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The eNO
radical also reduces monocyte adhesion to cells of the endothelium, seemingly
by inhibiting the expression of VCAM-1. This would prevent the influx of
monocytes and subsequent differentiation into macrophages, thus inhibiting foam
cell occurrence. eNO also attenuates platelet aggregability, as shown by Panza,
and Cannon, eds. (1999, pp. 120-122). The cohesion of platelets at the site of
inflammation of endothelium can lead to a thrombosis (a clot attached to a
blood vessel) that starves cells and tissue further down the vessel of oxygen.
If the cells further downstream of the thrombosis are cardiac muscle cells
(myocardium) then the result can range from angina to a heart attack.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">This next
section details the possible adverse effects associated with atherosclerosis.
It is important to note that each issue may occur as both a result of the build
of plaque directly, but also indirectly, as plaque formation can lead to blood
clots that cause and/or exacerbate many cardiovascular incidents. As plaque
builds up between the tunica intima and the lumen there is a possibility of
plaque rupture. This is shown on the atherosclerosis webpage of the American
Heart Association (2014b). The subsequent effect of this is that a stationary
clot (thrombus) in the wall of the affected blood vessel may further reduce the
size of the lumen and ability of blood to through the vessel. This can cause or
contribute to all of the problems shown below, for the same reason as a gradual
build-up of plaque, for it limits the blood flow to areas of the body
downstream from the affected blood vessel.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Alternatively,
the blood clot formed at the rupture site of plaque can dislodge from the
arterial wall and become free-floating. In this case it is called an embolus
and can cause an embolism (a substance that produces obstruction within a blood
vessel). This can cause the same effect as a thrombus, but the embolism can
float around and block a vessel located in the distal systemic circulation (</span><span style="background: white; color: #252525; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Kumar, Abbas, and Fausto, 2004). This is also briefly pointed
out in the work of </span><span style="font-size: 12.0pt; line-height: 107%;">Seeley,
VanPutte, Regan and Russo, 2011, p. 663.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Angina
pectoris usually presents as a pain in the chest, though it may also appear in
the lower jaw, neck and possibly also the left arm or shoulder. It is caused by
anaerobic respiration in the heart. It can arise from atherosclerosis due to
narrowing of blood vessels within the coronary circulation. This causes
restricted blood and oxygen flow to the cardiac muscle. Unable to respire
aerobically but still requiring energy, the cardiac muscle cells must survive
on anaerobic respiration due to hypoxic conditions. Unfortunately, this
respiratory pathway causes a build-up of acidic by-products that raise acidity
(and lower pH) in the affected area. This causes a pain response to be
stimulated. This situation is exacerbated by any process demanding additional
cardiac output, for example physical and mental stress. On the other hand,
relaxation would have the opposite effect by reducing cardiac exertion.
Vasodilation via chemical intervention (nitro-glycerine or free radical NO) or
placement of a stent can increase the blood flow through the affected artery
and improve oxygen of the cardiac muscle as well as improving the removal rate
of acidic by-products of respiration. A clot could also cause this issue as a
result of atherosclerotic plaque rupture. The formation of a clot in a blood
vessel in this situation would further restrict blood flow through the vessel,
provided that the clot doesn’t cause severe obstruction. Angina pectoris is a
relatively minor condition, provided that it is only short-lasting. Normally if
the blood flow is restored, there is only mild permanent damage to cardiac
tissue.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Myocardial
infarction (heart attack), is caused by a more lengthened condition of hypoxia
(or even anoxia). In this circumstance, instead of just pain, the cardiac cells
may die in large numbers in affected areas. Atherosclerosis increases the
possibility of myocardial infarction because the resultant lesions can greatly
reduce the size of the lumen of coronary arteries, thus increasing blood
pressure and possible clot formation (thrombus). This thrombus further narrows
the blood vessel and exacerbates cell hypoxia, perhaps leading to total anoxia
in some areas, depending on severity. This leads to cell death in the cardiac
tissue. The above information on angina pectoris and myocardial infarction can
be found in the work of Seeley, VanPutte, Regan and Russo (2011), p. 686.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Stenosis can
also lead to enlargement of certain regions of the heart, such as the left
ventricle. Because the left ventricle is required to pump blood around the
whole body via the aorta, if there is stenosis in the aorta as a result of
atherosclerotic plaque, then there is increased resistance to the contraction
of the left ventricle. This means that the left ventricle must work harder in
order to overcome the resistance, otherwise the whole body will become affected
by hypoxia due to decreased blood supply. This can lead to hypertrophy of the
left ventricle, an increase in size of the muscles located here. The ventricular
hypertrophy allows the left ventricle to have more contractile force and push
more red blood cells through the stenosed aorta and into the systemic
circulation. It was mentioned in question 2 that the arterial stenosis causes
an increase in ventricular afterload which the left ventricle must overcome
(Jardins, 2008, p. 210). The increased force through the aorta increases
systolic pressure. This information was found from Seeley, VanPutte, Regan and
Russo, 2011, Appendix G, A-34 9 a-f.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">A stent can
be used to treat atherosclerosis. In this case, the stent is typically made of
metal and is transported into the artery which is clogged with atherosclerotic
plaque. This occurs during a procedure called angioplasty in which an empty
balloon is inserted via catheter into the blood vessel which has narrowed. Once
inside the vessel, the balloon is inflated in order to open it up and reduce
stenosis. This occurs because the pressure of the balloon is both able to
forcibly widen the blood vessel and also in squeezing the atherosclerotic
plaque so that it takes up less space within the lumen of the blood vessel. At
this point, if the catheter also contains a stent, as it would in the case of
atherosclerosis, then this stent can hold the vessel open to the extent that
the balloon did. Thus, even when the inflating balloon has left the blood
vessel, it stays open to the same extent via the stent. Therefore, the stent
provides a more long-term ability to reduce stenosis. This has the same effect
as a vasodilator in holding the blood vessel open. So far, only the mechanical
properties of the stent have been touched upon. However, a stent can also
produce pharmacological effects as well. This is achieved by coating the outer
surface of a stent with medication which slowly releases into the arterial wall
and/or blood stream. Stents that have this capacity are called
drug-eluting-stents (DES). Blood which would ordinarily be forced through a
narrower space in the vessel, possibly leading to a blood clot or greatly
increased blood turbulence, is now free to travel through at the normal speed
and pressure. This can decrease the likelihood of cardiovascular incidences,
such as those covered above. Additional
lifestyle measures must also be taken however, as over time the stent itself
can become clogged if the underlying cause of arterial stenosis is not removed.
This process of repeated narrowing of the blood vessels after a measure has
been taken to reduce it is called restenosis. This information is shown clearly
on the stent webpage of the American Heart Association (2014c). Figure 4.2
shows the placement of a stent in the coronary artery. As can be seen from this
diagram, the stent is made of a metal mesh and is pressing against the
atherosclerotic plaque, thus opening up the lumen of this blood vessel. Once
the stent has been placed via the catheter, both it and the guide wire are
removed, leaving the stent to hold the artery open. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">This portion
of the essay is dedicated to thought not seen in work by other sources on
atherosclerosis. Any relation to previous work done by any author on this topic
is purely coincidental. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">It is
possible that some of the development of atherosclerosis is due to increased
ventilation and oxidative stress during mental stress. Granted modern society
has many problems when it comes to eating nutrient-depleted, high-fat foods and
breathing indoor air, but with many economic factors causing significant stress
and subsequent increases in respiration occurring as part of the
fight-or-flight reaction, various bodily changes are likely to occur. For
example, it is possible that prolonged mental stress and resultant
over-breathing reduce the bodily carbon dioxide levels and inhibit the Bohr
Effect, leading to an increased need for erythrocytes and a permanent shifting
towards elevated ventilation. This would also increase the level of oxygen
dissolved in blood plasma, as a result of air pressure within the lung during
inspiration. From this, more oxygen would travel through the bloodstream, and
cause oxidative stress throughout the body. This would exacerbate the
peroxidation of lipoproteins and oxysterol production, thus contributing
towards atherosclerosis. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Another
possible related mechanism for atherosclerosis is mouth-breathing. Because
nitric oxide is also produced within the nose, nose-breathing may also allow
significant quantities of nitric oxide to diffuse into the blood stream, which
may perhaps be unlikely given that it is a highly-reactive free radical, but it
could bind to haemoglobin, as opposed to travelling freely, see Seeley,
VanPutte, Regan and Russo, (2011) p. 653. The aforementioned reaction between
the superoxide anion and nitric oxide would readily result, decreasing the
amount of oxygen available for lipid peroxidation and subsequent atherosclerotic
plaque formation in blood vessels. <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">Research
into the use of cancer cell growth inhibitors brought up the topic of
iron-mediated reactive oxygen species production (Galaris, and Pantopoulos,
2008). This abstract points towards iron accumulation as being a cause of
reactive oxygen species formation with toxic effects. It is possible that this
could further add to lipid peroxidation, with formation of oxidised LDLs
capable of atherogenesis.</span></div>
<div class="MsoNormal">
<span style="font-size: 12pt; line-height: 107%;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Question 4 References:<o:p></o:p></span></u></b></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">American
Heart Association, 2014a. <i>Cholesterol and
CAD</i>. [online] Available at: <</span><a href="http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=chlcad"><span style="font-size: 12.0pt;">http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=chlcad</span></a><span style="font-size: 12.0pt;">> [Accessed 4 April 2015]. <o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">American
Heart Association, 2014b. <i>Atherosclerosis</i>.
[online] Available at:
<http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=athero>
[Accessed 4 April 2015]. <o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">American
Heart Association, 2014c. <i>Stent</i>.
[online] Available at: <http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=cstent>
[Accessed 4 April 2015].<o:p></o:p></span></div>
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<br /></div>
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<span style="color: #252525; font-size: 12.0pt; mso-bidi-font-family: Arial;">Carmena, R., Duriez, P., and
Fruchart, J.C., 2004. Atherosclerosis: Evolving Vascular Biology and Clinical
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<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Chambliss,
K.L., and Shaul, P.W., 2013. Estrogen Modulation of Endothelial Nitric Oxide
Synthase. <i>Endocrine Reviews.</i> [online]
Available at: <</span><a href="http://press.endocrine.org/doi/full/10.1210/er.2001-0045"><span style="font-size: 12.0pt; line-height: 107%;">http://press.endocrine.org/doi/full/10.1210/er.2001-0045</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 4 April 2015].<o:p></o:p></span></div>
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<span style="font-size: 12.0pt; line-height: 107%;">Daugherty,
A., Manning, M.W., and Cassis, L.A., 2000. Angiotensin II promotes
atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice. <i>The Journal of Clinical Investigation. </i>[online]
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<div class="MsoNormal">
<span lang="FR" style="font-size: 12.0pt; line-height: 107%; mso-ansi-language: FR;">Galaris, D., and Pantopoulos, K., 2008. </span><span style="font-size: 12.0pt; line-height: 107%;">Oxidative Stress and Iron
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<span style="color: #252525; font-size: 12.0pt; mso-bidi-font-family: Arial;">Hotamisligil, G.S., 2010. Endoplasmic
reticulum stress and atherosclerosis. <i>Nature
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<h1 style="background: white; margin-top: 0cm;">
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<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Kummerow,
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<span style="font-size: 12.0pt;">Mescher,
A.L., 2013. <i>Junqueira’s Basic Histology
Text & Atlas</i>, 13<sup>th</sup> ed. China: The McGraw-Hill Companies.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="color: #252525; font-size: 12.0pt; mso-bidi-font-family: Arial;">Mitchell, R.S., Kumar, V., Abbas,
A.K., and Fausto, N., 2007.<span class="apple-converted-space"> </span><i>Robbins
Basic Pathology: With STUDENT CONSULT Online Access.</i><span class="apple-converted-space"> </span>8<sup>th</sup> ed. Philadelphia:
Saunders.<o:p></o:p></span></div>
<h1 style="background: white; margin-bottom: 6.0pt;">
<span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-hansi-theme-font: minor-latin;">National Centre for
Biotechnology Information, 2015. </span><span class="gn"><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;">VCAM1</span></span><span class="apple-converted-space"><i><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;"> </span></i></span><i><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;">vascular
cell adhesion molecule 1 [<em>Homo sapiens</em><span class="apple-converted-space"> </span>(human)]
</span></i><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;">[online] Available at: <</span><a href="http://www.ncbi.nlm.nih.gov/Structure/biosystems/docs/biosystems_publications.html"><span style="font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;">http://www.ncbi.nlm.nih.gov/Structure/biosystems/docs/biosystems_publications.html</span></a><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;">> [Accessed 4 April 2015].<o:p></o:p></span></h1>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Oh,
J., Riek, A.E., Weng, S., Petty, M., Kim, D., Colonna, M., Cella, M. and
Mizrachi, C.B., 2012. Endoplasmic Reticulum Stress Controls M2 Macrophage
Differentiation and Foam Cell Formation. <i>The
Journal of Biological Chemistry, </i>[online] Available at: <</span><a href="http://www.jbc.org/content/287/15/11629.long"><span style="font-size: 12.0pt;">http://www.jbc.org/content/287/15/11629.long</span></a><span style="font-size: 12.0pt;">> [Accessed 4 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Pack, P.E.,
2001. <i> Anatomy and Physiology,</i> Hoboken, NJ: Wiley
Publishing, Inc.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Panza,
J.A. and Cannon, R.O., eds., 1999. Endothelium, Nitric Oxide, and
Atherosclerosis. Armonk, NY: Futura Publishing Company, Inc.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Samsioe, G.,
1994. Cardioprotection by estrogens: mechanisms of action—the lipids. [online]
Available at: <</span><a href="http://www.ncbi.nlm.nih.gov/pubmed/8199640"><span style="font-size: 12.0pt; line-height: 107%;">http://www.ncbi.nlm.nih.gov/pubmed/8199640</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 4 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Seeley, R.R,
VanPutte, C.L., Regan, J. and Russo, A.F., 2011. <i>Seeley’s Anatomy & Physiology</i>, 9<sup>th</sup> ed. New York, NY:
McGraw-Hill.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Schmidt, F.,
2000. <i>Biochemistry II, </i>New York, NY:
Wiley Publishing, Inc.<o:p></o:p></span></div>
<div class="MsoNormal">
</div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Toda, N.,
Ayajiki, K., and Okamura, T. 2007. Interaction of Endothelial Nitric Oxide and
Angiotensin in the Circulation. <i>Pharmacological
Reviews. </i>[online] Available at: <</span><a href="http://pharmrev.aspetjournals.org/content/59/1/54.abstract"><span style="font-size: 12.0pt; line-height: 107%;">http://pharmrev.aspetjournals.org/content/59/1/54.abstract</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 4 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;"><o:p></o:p></span></div>
Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-34206952813005018052015-06-13T03:59:00.003-07:002015-06-24T04:21:37.373-07:00Question 3: Multiple questions on a patient with chronic lung disease and shortness of breath<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;">*These posts are from coursework answers for my degree, but the Figures that are referred to in the text didn't scan well and have already been handed in. These long posts would probably not interest most people but if you enjoy quite in-depth reading of scientific problems then this may be for you.</span></u></b><br />
<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;"><br /></span></u></b><b><span style="font-size: 12pt; line-height: 17.1200008392334px;">Question 3: </span></b><b><span style="font-size: 12pt; line-height: 115%;">Davy Smith is a 65-year-old male with a 50-year
history of smoking 2 packets of cigarettes a day. Over the past 5 years,
he has become increasingly short of breath. At first, he noticed this only
when exercising, but now he is even short of breath at rest. Over the past
two years, he has had several bouts of lower respiratory tract infection
treated successfully with antibiotics. His shortness of breath hasn't
subsided, and his breathing is assisted by use of his accessory muscles of
respiration. </span><span style="font-size: 12pt; line-height: 115%;">Pulmonary function testing revealed the graph
below:</span></b><b style="font-size: 12pt; line-height: 115%;"><img height="277" src="file:///C:/Users/Admin/AppData/Local/Temp/msohtmlclip1/01/clip_image002.jpg" v:shapes="Picture_x0020_1" width="423" /></b><br />
<div>
<ol start="1" style="margin-top: 0cm;" type="1">
</ol>
<br />
<div class="MsoListParagraphCxSpFirst" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<b style="text-indent: -18pt;"><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Calibri; mso-bidi-theme-font: minor-latin; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin;">a.<span style="font-size: 7pt; font-stretch: normal; line-height: normal;">
</span></span><span style="font-size: 12.0pt; line-height: 115%;">Based
on the graph, fill in the following data:</span></b></div>
<div class="MsoListParagraphCxSpMiddle" style="margin-left: 72.0pt; mso-add-space: auto;">
<span style="font-size: 12.0pt; line-height: 115%;"><b>The tidal volume:
____________ <br />
The inspiratory reserve volume: ______________ <br />
The expiratory reserve volume: _______________ <br />
The forced vital capacity: ______________ <o:p></o:p></b></span></div>
<div class="MsoListParagraphCxSpMiddle" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<!--[if !supportLists]--><b><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Calibri; mso-bidi-theme-font: minor-latin; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin;">b.<span style="font-size: 7pt; font-stretch: normal; line-height: normal;">
</span></span><!--[endif]--><span style="font-size: 12.0pt; line-height: 115%;">Describe
the microscopic changes that are occurring in Davy's lungs. What effect do these
microscopic changes have on Davy’s ability to transfer oxygen and carbon
dioxide in the lungs?<o:p></o:p></span></b></div>
<div class="MsoListParagraphCxSpMiddle" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<!--[if !supportLists]--><b><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Calibri; mso-bidi-theme-font: minor-latin; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin;">c.<span style="font-size: 7pt; font-stretch: normal; line-height: normal;">
</span></span><!--[endif]--><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Arial;">Blood testing showed Davy’s hematocrit to be 59%
(normal = 42-50%). Why was his hematocrit so high?<o:p></o:p></span></b></div>
<div class="MsoNormal" style="margin-left: 36.0pt;">
</div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<!--[if !supportLists]--><b><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Calibri; mso-bidi-theme-font: minor-latin; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin;">d.<span style="font-size: 7pt; font-stretch: normal; line-height: normal;">
</span></span><!--[endif]--><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Arial;">Why is Davy susceptible to lower respiratory tract
infections?</span><span style="font-size: 12.0pt; line-height: 115%;"><o:p></o:p></span></b></div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<b><span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Arial;"><br /></span></b></div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<span style="font-size: 12pt; line-height: 115%;">Answer:</span></div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<span style="font-size: 12pt; line-height: 115%;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Part a:</span></u></b><span style="font-size: 12.0pt; line-height: 107%;"><o:p></o:p></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;"><br /></span></u></b></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Each box on
the graph is roughly 125 cc of volume.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The tidal
volume is the amount of air breathed in during a relax breath. On the graph
this is roughly 4 boxes in height. 4x125
= 500 cc.<o:p></o:p></span></div>
<div class="MsoNormal">
<u><span style="font-size: 12.0pt; line-height: 107%;">Therefore,
the tidal volume is 500 cc in volume.<o:p></o:p></span></u></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
inspiratory reserve volume is the extra air that can be inhaled after a relaxed
inhalation. Thus it is the difference between the height of the forced
inhalation and that of the normal inhalation on the graph. This is
approximately 14 boxes in height. 14x125 = 1750 cc.<o:p></o:p></span></div>
<div class="MsoNormal">
<u><span style="font-size: 12.0pt; line-height: 107%;">Therefore,
the inspiratory reserve volume is 1750 cc in volume.<o:p></o:p></span></u></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
expiratory reserve volume is the extra air that can be exhaled after a relaxed
exhalation. So it is the difference between the height of the forced exhalation
and that of the normal exhalation on the graph. This is approximately 3.5 boxes
in height. 3.5x125= 437.5 cc.<o:p></o:p></span></div>
<div class="MsoNormal">
<u><span style="font-size: 12.0pt; line-height: 107%;">Therefore,
the expiratory reserve volume is 437.5 cc in volume.<o:p></o:p></span></u></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The forced
vital capacity is the total volume of air which can be exhaled after a full
inhalation. This is can calculated as either the difference between the highest
and lowest points of the graph, or by adding up the tidal volume, inspiratory
reserve volume and expiratory reserve volume. This is roughly 21.5 boxes in
height. 21.5x125 = 2687.5 cc<o:p></o:p></span></div>
<div class="MsoNormal">
<u><span style="font-size: 12.0pt; line-height: 107%;">Therefore,
the forced vital capacity is 2687.5 cc in volume.<o:p></o:p></span></u></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">(Bass, 1974
p.7).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The work of
Bass showed how to calculate volumes from a lung function graph, however much
of its other work may be outdated so it was only used for this initial piece of
work. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Part b:<o:p></o:p></span></u></b></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;"><br /></span></u></b></div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
</div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">It is likely
that Mr. Smith is suffering from chronic obstructive pulmonary disease. This is
a chronic lung disease that is usually caused by cigarette smoking. Given that
Mr. Smith has a history of 100 pack-years of cigarette smoking (packets of
cigarettes per day multiplied by years of duration, i.e. 2 packets daily x 50
years = 100 pack-years) this particular pulmonary condition is highly likely. It
encompasses other respiratory diseases such as chronic bronchitis, emphysema
and possibly also chronic obstructive airways disease. The repeated lower
respiratory tract infections also point to this diagnosis so Mr. Smith is
certainly at risk of the disease and he has the decreased lung function test to
match. With regard to the microscopic changes occurring in Davy’s lungs, there
is probably dilation and enlargement of the bronchioles, which is only
partially reversible, i.e. much of the damage at this stage of illness is
likely to be permanent (Mescher, 2013 p. 361). Alveoli are also enlarged in
this condition as shown in Figure 3.1. This is due to the walls separating each
alveolus gradually being destroyed over the years. Alveolar enlargement can
occur because cigarette smoking provokes an inflammatory immune response which
causes the release of various proteases <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">(enzymes
that break-down proteins, in this case these enzymes are mostly elastase and
trypsin, and the immune cells they are most associated with are neutrophils,
however macrophages are also involved in alveolar destruction), in the lungs
from immune cells (Davies and Moore, 2003 pp. 26-28). This can break down the
elastic protein in alveoli (called elastin) and render them inflexible (Seeley,
VanPutte, Regan, and Russo, 2011, pp. 830-862). </span><span style="font-size: 12pt; line-height: 107%;"> </span><span style="font-size: 12pt; line-height: 107%;">In healthy persons the use of these enzymes is
inhibited by a chemical called alpha-1-antitrypsin. This stops the immune
cell-induced damage from continuing. However, in smokers and persons with a
genetic fault causing an alpha-1-antitrypsin deficiency, the damage goes
largely unchecked and pulmonary destruction ensues. In smokers the lack of
alpha-1-antitrypsin activity is attributed to its reaction with free radicals
in cigarette smoke, rendering it ineffective. What can then result from this is
that instead of having very many alveoli, the alveoli can break down their
walls to the extent that they form one larger air sac (Mayo Foundation for
Medical Education and Research, 2015a). This results in a much lowered surface
area for the diffusion of gases both into and out of the lungs which causes
many of the reduced volumes seen on the lung function test (Mayo Foundation for
Medical Education and Research, 2015b). Chronic bronchitis obstructs the larger
airways of the respiratory tract while emphysema causes the same effect in
small airways, as well as air-trapping in the alveoli (The McGraw-Hill
Companies, 2000). The differences between healthy alveoli and those affected by
emphysema are shown in Figure 3.2. Initially, the damage will reduce the amount
of oxygen diffusing into the bloodstream, leading to an increase in
ventilation. This hyperventilation lowers the concentration of carbon dioxide
in the blood, while attempting to compensate for lowered oxygen. Usually, there
is still some decrease in blood oxygen levels despite the hyperventilation. As
the damage progresses however, there comes a point when the respiratory tract
is so compromised that eventually carbon dioxide will accumulate in the
bloodstream because it cannot diffuse out of the lungs at this stage and oxygen
in the blood becomes significantly more decreased as well. The conditions of
elevated carbon dioxide and decreased oxygen in the blood are termed
hypercapnia and hypoxemia respectively (University of Maryland Medical Center,
2013). </span><span style="font-size: 12pt; line-height: 107%;"> </span><span style="font-size: 12pt; line-height: 107%;">The inability to adequately
remove air from the lungs explains the elevated residual volume in Mr. Smith’s
lungs. The use of accessory muscles of respiration helps to create more
pressure in the lungs to expel air during expiration.</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">One
beneficial effect of the elevated level of carbon dioxide in the blood is that
oxygen is unloaded more readily from haemoglobin. This is known as the Bohr
Effect and may occur due to the conversion of carbon dioxide to carbonic acid
with simultaneous release of a hydrogen ion which reduces the blood pH. This
effect is very useful during exercise because the increased carbon dioxide
concentrations in the blood cause subsequent reduction in pH (which also occurs
via other metabolic by-products, e.g. lactic acid) will cause preferential
off-loading of oxygen to cells that are respiring more vigorously. This allows
cells that are under the heaviest workload to receive adequate amounts of
oxygen from haemoglobin (Razani, B., 2014). This means that in the case of Mr.
Smith, his body actually requires less oxygen to reach his erythrocytes, (i.e.
not as high an oxygen saturation in the blood is required) because it is
off-loaded to other cells and tissue within his body more readily. A similar
effect also occurs as the concentration of a substance called 2,
3-Diphosphoglycerate <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">(2,3-DPG)
increases. This is a compound that is formed as a result of anaerobic
glycolysis, therefore its production increases under hypoxic / hypoxemic
conditions. It is important to note that hypoxia and hypoxemia are not
equivalents. Rather, hypoxemia is the state of reduced oxygen content in the
blood stream of arteries (or a pathologically low arterial oxygen tension),
whereas hypoxia is a condition in which too little oxygen is delivered to
tissues. It can therefore be possible, though unlikely, that hypoxemia may
exist in a patient, but compensatory mechanisms may be sufficient to encourage
oxygen dissociation from haemoglobin in order to oxygenate tissues adequately.
The aforementioned 2, 3-DPG however, increases under hypoxic conditions (given
its production occurs under anaerobic conditions), and consequently, increases
tissue oxygenation in a similar way to the Bohr Effect (Jardins, 2008, p.236).</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Figure 3.3
shows the oxygen-haemoglobin dissociation curve. Note that when exercising,
erythrocytes will off-load oxygen more readily to respiring tissue (possibly
due to any number of reasons, for example, increased CO<sub>2</sub> or 2, 3-DPG
production as well as increase in temperature) which explains the point
labelled deoxygenated blood on the graph. At rest, tissues respire more slowly,
and produce less CO<sub>2</sub>, 2, 3-DPG, heat and other metabolic by-products
that encourage the dissociation of oxygen from haemoglobin. The dashed curve to
the right of the continuously drawn curve shows what would happen if any or all
of the following components were increased: CO<sub>2</sub>, 2, 3-DPG, acidity,
and temperature, though more possibilities exist. This produces an effect known
as a “right-shift”, which means that a higher pressure of oxygen is required to
produce the same oxygen saturation percentage compared to normal conditions.
This means that under right-shift conditions, haemoglobin loses oxygen more
readily, and consequently, respiring tissue receives oxygen in greater amounts.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Figure 3.4
shows the diffusion of carbon dioxide and oxygen into and out of an alveolus.
This forms a diagrammatic representation for the equation of Fick’s Law of
diffusion, which is also shown in this figure. Relating this to the case at
hand, the reduced ability to both remove carbon dioxide from and deliver oxygen
to the alveoli in Mr. Smith’s lungs results in a higher partial pressure of
carbon dioxide and lower partial pressure of oxygen in these air sacs. A
consequence of this is that less carbon dioxide will diffuse out of the
bloodstream and into each alveolus, while less oxygen will diffuse from the
atmosphere into the same region. This is because the difference in partial
pressure between the blood stream and alveoli, relating to carbon dioxide, is
smaller for Mr. Smith than a regular person. Similarly, the partial pressure
difference of oxygen between the atmosphere and the diseased alveoli will be
smaller as well. Thus, less carbon dioxide is encouraged to diffuse into the
alveoli and be removed from the lungs in expiration, and less oxygen will diffuse
into the lungs during inspiration (Jardins, 2008, p. 139). This explains why
Mr. Smith is forced to use his accessory muscles of respiration.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The use of
accessory muscles of respiration can improve the delivery of gases both from
the atmosphere to the lungs and vice versa. Firstly, the accessory muscles of
inspiration must be considered. The largest muscles of this category are the
scalenus, sternocleidomastoid, pectoralis major, trapezius, and external
intercostal muscles. Without getting into excessive <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">detail, the
overall function of these muscles is to help decrease the pressure within the
lungs to such a level below atmospheric pressure that gases flow more readily
into the alveoli, diffusing via a pressure and concentration gradient. As the
concentration of any gas increases in a given area, so also does its tension.
Therefore, the fact that Mr. Smith is having difficulty ventilating his lungs,
means that the concentration of oxygen normally extracted from the alveoli into
the blood stream has decreased (therefore, both alveolar partial pressure and
concentration of oxygen have decreased) and Mr. Smith’s blood carbon dioxide
levels have increased (regarding both partial pressure and concentration of
arterial carbon dioxide). Thus, for inspiration, the lower the pressure inside
the lungs, relative to the surrounding atmosphere, the greater the diffusion
gradient for gases moving from the atmosphere into the lungs (and consequently
alveoli). Therefore, the result of using the accessory muscles of inspiration
is to increase oxygen supply to the blood stream. A person who is using their
accessory muscles of inspiration while breathing will be quite noticeable, with
much of their upper chest expanding and elevating during each inhale and some
shrugging occurring also (Jardins, 2008, pp. 54-58). Conversely, the accessory
muscles of expiration will increase the pressure within the lungs, relative to
that of the surrounding atmosphere. This helps compensate for airway
resistance, such as that seen in COPD. The primary accessory muscles of
expiration are the rectus and transversus abdominis muscles, the external and
internal abdominis obliquus muscles and the internal intercostal muscles. The
basic movement of these muscles during expiration is of compression. The
abdomen becomes compressed, and the diaphragm is pushed into the thoracic cage,
increasing the pressure in the lungs well above atmospheric pressure and
causing a diffusion of gases out of the alveoli into the surrounding
environment (Jardins, 2008, pp. 59-61).</span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Part c:</span></u></b><span style="font-size: 12.0pt; line-height: 107%;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Haematocrit
is the proportionate measure of red blood cells compared to the overall blood
volume (Seeley, VanPutte, Regan, and Russo, 2011, p 668).Thus, if Davy’s
haematocrit was 59% then this is the percentage of his blood which was composed
of red blood cells.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Red blood
cells are used strongly in the transfer of various gases both to and from the
lungs, and from and to cells. Therefore, an elevated level of red blood cells
would occur in an individual who had trouble dealing with both the build-up of
gases, and the inadequate diffusion of gases into the blood. In the case of
Davy, he is suffering from both hypoxemia and hypercapnia. Therefore, he will
need additional red blood cells to carry oxygen from his lungs. This sets up a
steeper concentration gradient between the alveoli of the lungs and the
bloodstream, thus allowing more oxygen to diffuse into the blood and be carried
to various cells. Approximately 98.5% of the oxygen in our blood is bonded to
haemoglobin to form oxyhaemoglobin, the remainder is dissolved in plasma
(Seeley, VanPutte, Regan, and Russo, 2011, p 652) and tends to be ignored in
calculations of arterial oxygen content.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">There are
numerous equations for approximating oxygen delivery and content within the
body. Shown below is an equation for oxygen content in arteries (Gutierrez, and
Theodorou, 2009).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">C<sub>a</sub>O<sub>2</sub>,
shorthand for the content or amount of oxygen in the arterial blood, is
calculated by the following equation:<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">C<sub>a</sub>O<sub>2</sub>
~ [Hb](SO<sub>2</sub>)x1.34<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Where ~
means roughly equal to (because here we are neglecting the amount of dissolved
oxygen within plasma [roughly 1.5 to 2%], and instead focusing entirely on
oxygen bonded to haemoglobin), [Hb] is the concentration of haemoglobin in the
blood, and SO<sub>2</sub> is the fractional oxygen saturation of haemoglobin. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Thus, we can
see that the oxygen content of arterial blood is proportional to the
concentration of haemoglobin, and also to the fractional oxygen saturation of
haemoglobin. This means that if either haemoglobin concentration or oxygen
saturation increases while the other remains the same, then oxygen content of
arterial blood will also increase. Also, if C<sub>a</sub>O<sub>2</sub> remains
the same value, then [Hb] and SO<sub>2</sub> are inversely proportional to each
other. This means that as one quantity increases, the other will decrease in
order to achieve the same result for C<sub>a</sub>O<sub>2</sub>. Therefore, if
we assume C<sub>a</sub>O<sub>2</sub> to be an unchanging quantity, then we can
clearly see that if oxygen saturation of haemoglobin decreases, then the
concentration of haemoglobin must increase.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">In the case
of Davy Smith, his ability to extract oxygen from alveoli has greatly
decreased. Even with a normal tidal volume of 500 cc, his blood is still not
receiving an adequate supply of oxygen. This means that in our equation SO<sub>2</sub>
has decreased. Mr Smith’s body will still need to utilise roughly the same
amount of oxygen, provided that compensatory mechanisms are not in place to
reduce overall metabolic rate. Thus, the concentration of haemoglobin (also
known as the haematocrit) will have to increase in order to supply to the same
demand for oxygen content. This particular form of increased erythrocyte
production (i.e. from hypoxic lung disease) is called either secondary
erythrocytosis or secondary polycthemia (Seeley, VanPutte, Regan, and Russo,
2011, p. 669). This means that if Davy Smith was to somehow have his lung
condition cured, then his haematocrit would drop to normal levels. However,
while his condition remains, his kidneys will secrete more erythropoietin in
response to decreased oxygen delivery.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Carbon
dioxide is also a highly important consideration in this situation. As Davy
Smith’s lung function deteriorates, his carbon dioxide levels will continue to
increase. This accumulation of carbon dioxide must be dealt with. The body will
naturally convert much of its extracellular carbon dioxide into bicarbonate
ions (roughly 66% takes this form). Of the remaining 34%, 7% will be dissolved
in plasma and the remaining 27% will bind to haemoglobin. The formed complex is
called the carbaminohemoglobin molecule (Mescher, 2013, p. 236). Thus, elevated
carbon dioxide levels will cause increased erythrocyte concentrations in order
to bond the plasma carbon dioxide and transport it away from cells.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">A more
serious gas in the body that requires an elevated haematocrit level is carbon
monoxide. Carbon monoxide is a poisonous gas found in cigarette smoke among
other sources, especially those involving combustion of carbon-containing
compounds in a region of inadequate oxygen (incomplete combustion) which has a
very high affinity for haemoglobin and bonds to form carboxyhaemoglobin. Once
carboxyhaemoglobin has formed, it is unlikely that the carbon monoxide will
dissociate again in the lifespan of the red blood cell, usually it stays bonded
until the red blood cell is broken down by the body. During this time the
haemoglobin is unable to bind to oxygen or carbon dioxide molecules, or
anything else for that matter. Thus, carbon monoxide essentially disables the
effect of haemoglobin towards other molecules and requires increased red blood
cell concentrations. It has been found that the blood of chronic smokers
contains between 5 and 15% carboxyhaemoglobin. This alone provides a strong
reason for the elevated red blood cell concentration found in Davy Smith
(Seeley, VanPutte, Regan, and Russo, 2011, pp 653-655).<o:p></o:p></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Part d:<o:p></o:p></span></u></b></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Davy is
susceptible to lower respiratory tract infections. This could be due to the act
of smoking tobacco which has been reported to damage cilia in the lungs
(Mueller, 1997). Cilia are microscopic projections that protrude from cells and
sweep away various substances and microbes that can damage the body. When these
are damaged, various toxins and microbes can enter the lower respiratory tract
in greater numbers, requiring a stronger immune system to combat it.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Further to
this, differences in bacterial populations within regions of the respiratory
tract between smokers and non-smokers have been found. The exact location of
these bacterial colonies is unlikely to be of concern, considering that as long
as they are present somewhere in the respiratory tract, they may allow
pathological microbes to travel past them into lower regions, whereas bacterial
populations in healthy non-smokers would have some sort of inhibitory effect.
Brook, and Gober (2005) found that the nasopharyngeal flora of smokers
contained more potential pathogens than non0smokers, as well as fewer
beneficial bacteria which might inhibit their growth and harm. Fujimori, et al.
(1995) also found that healthy smokers had higher levels of Streptococcus
Aureus (S. Aureus) and lower levels of alpha-streptococci (the forms which
inhibit S. Aureus), as compared to healthy non-smokers. Forms of
alpha-streptococci that inhibit another potential pathogen called S. pyogenes
were similar in both healthy smokers and non-smokers. This indicates that
smokers are more susceptible to infections via Streptococcus Aureus.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">A review of
many studies by Arcavi, and Benowitz (2004) revealed some interesting data
about smokers. Several studies that were examined showed decreases of 10-20% in
serum Immunoglobulins IgA, IgG and IgM. These are all vital antibodies that
play a major role in the response against infection. These same authors also
found that specific antibody responses to influenza (both as an unaltered virus
and as vaccine) and <i>Aspergillus fumigatus</i>
were decreased in smokers.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Additionally,
the act of smoking can cause excessive mucus production and due to the impaired
function of the damaged cilia in the respiratory tract, this mucus can build up
without being removed. Mr. Smith likely has a “smoker’s cough”, a heavy cough
which attempts to dislodge and remove this built-up mucus. Unfortunately, this
accumulating mucus in the bronchial tree provides vital nutrients for
pathological microbes that take up residence in the lungs. Thus, Mr. Smith is
more susceptible to lower respiratory tract infections. Antibiotics are likely
only to act as a short-term aid, with recurrent infections being a part of his
life in the long-term (The McGraw-Hill Companies, 2000).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Question 3 References:</span></u></b><span style="font-size: 12.0pt; line-height: 107%;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Arcavi, L.,
and Benowitz, N.L., 2004. <i>Cigarette
Smoking and Infection. </i>[online] Available at: <</span><a href="http://archinte.jamanetwork.com/article.aspx?articleid=217624"><span style="font-size: 12.0pt; line-height: 107%;">http://archinte.jamanetwork.com/article.aspx?articleid=217624</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Bass, B.H.,
1974. <i>Lung Function Tests An
introduction.</i> 4<sup>th</sup> ed. London: H.K. Lewis & Co. Ltd.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Brook, I.,
and Gober, A.E., 2005. <i>Recovery of
potential pathogens and interfering bacteria in the nasopharynx of smokers and
nonsmokers. </i>[online] Available at: <</span><a href="http://www.ncbi.nlm.nih.gov/pubmed/15947322/"><span style="font-size: 12.0pt; line-height: 107%;">http://www.ncbi.nlm.nih.gov/pubmed/15947322/</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Davies,
A., and Moore, C., 2003 <i>The Respiratory
System.</i> Spain: Churchill Livingstone.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Fujimori I.,
Goto R., Kikushima K., Ogino J., Hisamatsu K., Murakami Y., and Yamada T. 1995.
<o:p></o:p></span></div>
<div class="MsoNormal">
<i><span style="font-size: 12.0pt; line-height: 107%;">Isolation of alpha-streptococci with
inhibitory activity against pathogens, in the oral cavity and the effect of
tobacco and gargling on oral flora. </span></i><span style="font-size: 12.0pt; line-height: 107%;">[online] Available at: <</span><a href="http://www.ncbi.nlm.nih.gov/pubmed/7745286/"><span style="font-size: 12.0pt; line-height: 107%;">http://www.ncbi.nlm.nih.gov/pubmed/7745286/</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Gutierrez,
J.A., and Theodorou, A.A, 2009. <i>Oxygen
Delivery and Oxygen Consumption in Pediatric Critical Care</i>, [online]
Available at: <</span><a href="http://www.springer.com/cda/content/document/cda_downloaddocument/9780857299222-c1.pdf?SGWID=0-0-45-1328038-p174130681"><span style="color: #0000cc; font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">http://www.springer.com/cda/content/document/cda_downloaddocument/9780857299222-c1.pdf?SGWID=0-0-45-1328038-p174130681</span></a><span style="font-size: 12.0pt; line-height: 107%;">><i> </i>[Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Jardins,
T.D., 2008. <i>Cardiopulmonary Anatomy &
Physiology Essentials of Respiratory Care, </i>5th ed. Delmar, USA: Nelson
Education, Ltd.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Mayo
Foundation for Medical Education and Research, 2015a. <i>Diseases and Conditions Emphysema</i>. [online] Available at: <</span><a href="http://www.mayoclinic.org/diseases-conditions/emphysema/basics/definition/con-20014218"><span style="font-size: 12.0pt;">http://www.mayoclinic.org/diseases-conditions/emphysema/basics/definition/con-20014218</span></a><span style="font-size: 12.0pt;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Mayo
Foundation for Medical Education and Research, 2015b. <i>Diseases and Conditions Emphysema</i>. [online] Available at: <</span><a href="http://www.mayoclinic.org/diseases-conditions/emphysema/multimedia/emphysema/img-20007614"><span style="font-size: 12.0pt;">http://www.mayoclinic.org/diseases-conditions/emphysema/multimedia/emphysema/img-20007614</span></a><span style="font-size: 12.0pt;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Mescher,
A.L., 2013. <i>Junqueira’s Basic Histology
Text & Atlas</i>, 13<sup>th</sup> ed. China: The McGraw-Hill Companies.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Mueller,
D.M., 1997. <i>Smoking Any Substance Raises
Risk of Lung Infections</i>, [online] Available at: <</span><a href="http://archives.drugabuse.gov/NIDA_Notes/NNVol12N1/Smoking.html"><span style="font-size: 12.0pt; line-height: 107%;">http://archives.drugabuse.gov/NIDA_Notes/NNVol12N1/Smoking.html</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Razani, B.,
2014. <i>Bohr Effect</i>. [online] Available
at: <</span><a href="http://www.pathwaymedicine.org/bohr-effect"><span style="font-size: 12.0pt; line-height: 107%;">http://www.pathwaymedicine.org/bohr-effect</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Seeley, R.R,
VanPutte, C.L., Regan, J. and Russo, A.F., 2011<i>. Seeley’s Anatomy & Physiology</i>, 9<sup>th</sup> ed. New York, USA:
McGraw-Hill.<o:p></o:p></span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The
McGraw-Hill Companies, 2000. <i>Case History
13: Restrictive and Obstructive Lung Disease, </i>[online] Available at: <</span><a href="http://www.mhhe.com/biosci/ap/ap_casestudies/cases/ap_case13.html"><span style="font-size: 12.0pt; line-height: 107%;">http://www.mhhe.com/biosci/ap/ap_casestudies/cases/ap_case13.html</span></a><span style="font-size: 12.0pt; line-height: 107%;">> [Accessed 7 April 2015]. <o:p></o:p></span></div>
<div class="MsoNormal">
</div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">University
of Maryland Medical Center, 2013. <i>Chronic
obstructive pulmonary disease.</i> [online] Available at: <</span><a href="http://umm.edu/health/medical/reports/articles/chronic-obstructive-pulmonary-disease"><span style="font-size: 12.0pt;">http://umm.edu/health/medical/reports/articles/chronic-obstructive-pulmonary-disease</span></a><span style="font-size: 12.0pt;">> [Accessed 6 April 2015].<o:p></o:p></span></div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Arial;"><br /></span></div>
<div class="MsoListParagraphCxSpLast" style="margin-left: 72.0pt; mso-add-space: auto; mso-list: l0 level2 lfo1; text-indent: -18.0pt;">
<span style="font-size: 12.0pt; line-height: 115%; mso-bidi-font-family: Arial;"><br /></span></div>
</div>
Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-18863164619152435202015-06-13T03:42:00.002-07:002015-06-24T04:21:43.090-07:00Question 2: Outline the major functions, histology, location and ultra-structure of cardiac muscle tissue<div class="MsoNormal">
<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;">*These posts are from coursework answers for my degree, but the Figures that are referred to in the text didn't scan well and have already been handed in. These long posts would probably not interest most people but if you enjoy quite in-depth reading of scientific problems then this may be for you.</span></u></b><br />
<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;"><br /></span></u><span style="font-size: 12pt; line-height: 17.1200008392334px;">Question 2: </span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;">Describe
with the aid of diagrams the histology, ultrastructure, location, and function
of cardiac muscle tissue.</span></b><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;"><br /></span>
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 18.3999996185303px;">Answer:</span><br />
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The heart itself is a hollow organ consisting of four chambers, weighing
approximately 250g to 350g. The uppermost chambers are smaller and contribute
little to the forceful expulsion of blood from the heart. These are called the
right and left atria. Below these atria are the ventricles, which are much more
muscular and exert a great deal of pressure upon blood during their
contraction. The right and left atria of the heart are divided by the
interatrial septum, a relatively thin wall of muscle. The ventricles are
separated by a thicker wall of muscle termed the interventricular septum. The
four chambers operate as two individual pumps; the right atrium and ventricle
pump deoxygenated blood to the lungs, while the left atrium and ventricle pump
oxygenated blood to the rest of the bodily tissues. The heart is covered by the
pericardium, a thick wall consisting of two layers, namely, the fibrous
pericardium (outer layer) and the serous pericardium (inner). The serous
pericardium is further sub-divided into three thin layers, the parietal layer,
the pericardial cavity, and the visceral layer. The function of the cavity
between these other two layers is to allow the heart to experience relatively
low friction, so that its efforts of pumping are made more efficient and much
less damage is caused by the repeated rubbing together of the two separated
layers. The visceral layer of the serous pericardium is also known as the
epicardium and forms one of three parts of the heart wall. The other parts are
called the myocardium (muscle cells of the heart) and the endocardium. The
epicardium is frequently thought of as being the outer layer of the heart, with
the other previously mentioned layers being the external protective membranes
enclosing it. The epicardium consists of one sheet of squamous epithelial cells
on top of fragile connective tissue. The
endocardium is the innermost layer of the heart wall, it too is composed of
squamous endothelial cells resting on delicate connective tissue. This is the layer that rests on the surface
of each of the chambers of the heart (Jardins, 2008, pp. 188-193).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The myocardium however, is of great importance for this piece of work.
It is the relatively thick layer of the heart wall that is composed of cardiac
muscle cells. These cardiac muscle cells make up most of the heart and it is
their job to ensure that blood building up in the ventricles are subjected to a
high enough level of pressure to be propelled around both the body and lungs
during contraction of the heart. The heart muscles weave together, producing
characteristic shapes of either bundles or spirals that create a network,
joining all areas of the heart together. The general arrangement of cardiac
muscle is illustrated in figure 2.1. This overall assembly is called the
fibrous skeleton of the heart, and reinforces the structural integrity of the
inner myocardium (Jardins, 2008, p. 192). The force produced by the contraction
or shortening of the myocardial fibres in the ventricles is called the
myocardial contractility. When this
force increases, the condition is called positive ionotropism, with negative
ionotropism being the inverse (Jardins, 2008, pp. 210-211).<o:p></o:p></span></div>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Cardiac muscle tissue is exclusively found within the heart. Its task is
to contract forcibly, ensuring that blood is pumped throughout the body, where
it can deliver nutrients and oxygen to body cells, especially those respiring
at relatively high rates. It differs from skeletal muscle, and shares some
similarity with many smooth muscle types in that it produces its own
contractions, i.e. cardiac muscle tissue is autorhythmic. Cardiac tissue is <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">also not controlled voluntarily. While the average human being can
affect his or her heart rate indirectly by choosing which activities to engage
in, what foods and drinks to consume (caffeine being a strong stimulus for
increasing the heart rate) and by controlling their rate of breathing, the
contractions of the heart are not controlled directly. One cannot decide to
make their heart beat at a certain rate simply by willing it to occur. Cardiac
muscle cells are cylindrical in shape and branch out, forming connections with
one another called intercalated disks. They are typically 100-500 micrometres
in length and 12-20 micrometres in diameter. Their nucleus or nuclei are
centrally located, but most cardiac muscle cells only contain a single nucleus,
with 2 being uncommon. They are striated, and capable of their own spontaneous
contractions without nervous innervation. (Seeley, Vanputte, Regan and Russo,
2011, pp. 275-276). The basic structure of cardiac muscle cells are shown in
figure 2.2. In this diagram the striations are clearly shown.</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Desmosomes are also present within cardiac muscle which helps bind the
cells together. Desmosomes are attachments formed by protein which extend
fibres into the cytoplasms of two adjacent cells, acting as an anchor that
prevents the cells from drifting apart. They are highly useful for bridging
gaps between skeletal or cardiac muscle cells as these types of cell undergo
considerable stresses which would tear them apart if their junctions were weak.
The intercalated disks separating cardiac cells contain gap junctions which
serve the purpose of propagating action potentials, similar to myelin sheaths
which surround nerve cells in the brain. This occurs because gap junctions
contain proteins called connexons which allow small molecules and ions to pass
through them. For this reason, gap junctions are highly useful for the
transmission of electrical impulses (Pack, 2001, pp. 24-25). Both of these
structures and others are shown in figure 2.3. The action potentials are
comparable between both neurons and cardiac muscle cells, except that cardiac
muscle action potentials last longer, followed by a longer period (as compared
to skeletal muscle and nerve cell duration) in which the resting potential
occurs, this may also be described by saying that the cardiac muscle fibres are
in their polarised state (this length of time is called the refractory period),
as shown by Seeley, VanPutte, Regan and Russo (2011), p. 309. While the fibres
of the heart cells are in this resting state, there is an electrical charge
difference between the inside of the cardiac muscle cells and the extracellular
fluid. This difference in charge is called the resting membrane potential or
RMP. This is largely due to the electrolytes potassium, sodium and calcium
(Jardins, 2008, p. 397-398).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Ordinarily, there is close to 40x the concentration of potassium ions
contained within the cardiac cell than outside of it. However, the inside of the cell only contains
about 1/20 the concentration of sodium ions and 1/5 the concentration of calcium
ions compared to the outside of the cell membrane. This large difference in
electrolyte concentrations causes potassium ions to leave the cardiac cell and
sodium ions to enter. However, potassium ions find it very easy to diffuse out
of the cell while sodium ions have more difficulty permeating the membrane. The
result is that roughly 50-75 potassium ion may leave for every sodium ion that
enters. The product of this situation is a relative negativity of the cardiac
cell in relation to its outside environment, due to so many positive ions leaving
the cell. This results in the RMP previously described, giving the cell a
charge of approximately -90 mV (Jardins, 2008, pp. 397-399). </span><br />
<div class="separator" style="clear: both; text-align: center;">
</div>
<span style="font-size: 12pt; line-height: 107%;"><br /></span>
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;"><o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">Normally, the muscle fibres of the cardiac ventricles may be stimulated
to contract between 60 and 100 times per minute (i.e. the resting heart rate).
There are 5 main phases of the action potential in cardiac muscle cells. These
are shown below, and in figure 2.4.</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Phase 0; the early phase, or phase of rapid depolarization is the prompt
for cardiac muscle contraction and begins due to reception of an electrical
impulse propagated from the sinoatrial, or SA node of the heart. This impulse
encourages the mass influx of sodium ions into the cardiac cell through
specific sodium ion channels and results in a net voltage of +30 mV. This
overall event is termed depolarisation. The rise in voltage of the membrane
potential is very rapid, as shown by the steep upward curve in the diagram,
which is labelled with a zero. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Note the label of the threshold value which is at a very low value on
the graph, barely higher than -90 mV. This shows that cardiac muscles cells are
sufficiently excitable to be stimulated for contraction without much influence
from pacemaker cells. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The phases following phase 0 mark specific stages that the cells go
through in order to repolarise and regain their resting membrane potential.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Phase 1; the initial repolarisation, will occur in which potassium ions
leave the cell, lowering its electrical difference to roughly +10 mV. This is a
relatively quick process but continued repolarisation is prevented by the next
phase, this is why the downward movement marked by a one on the diagram is
short-lived.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Phase 2; the plateau state, calcium ions move into the cell, and lower
the outward diffusion of potassium ions, resulting in a slower rate of
repolarisation and consequently prolonged state of stimulation for the cell.
This causes the myocardial cells to contract for a longer period of time than
other cells that operate by a similar mechanism, for example, neurons and
skeletal muscle cells.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Phase 3: the final rapid depolarisation, at point, the diffusion of
calcium ions into the cell stops occurring and the potassium ions once again
flow rapidly out of the cell, causing it to reach an electrical difference of
-90 mV once again with its surrounding environment. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Phase 4: the resting / polarised state. Finally, sodium, potassium and
calcium ion pumps cause all of the ions to return to their normal
concentrations, allowing the cell to once again become stimulated to contract
(Jardins, 2008, pp. 399-400).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The specially adapted pacemaker cells of the heart have the ability to
generate their own action potential without external stimulation.
Parasympathetic and sympathetic stimulation from the nervous system can slow
down or speed up cardiac contractions, but the heart muscles are capable of
contracting by themselves. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Figure 2.5 shows the conductive system of the heart. The electrical
cycle is initiated at the sinoatrial (SA) node, also known as the pacemaker of
the heart, which is located in the right atrium. The impulse produced here is
conducted through both the right and left atria. In the former, it travels
through the anterior, middle, and posterior intermodal tracts, which join at
the atrioventricular (AV) junction. The left atrium receives its electrical
impulses via the <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">Bachmann’s bundle which conducts it from the SA node. Both of these
atria contract at the same time, which pumps blood into their respective
ventricles. At this point, the AV junction transmits the signal along the
bundle of His and into the ventricles. This bundle separates (shown at the
bottom of figure 2.5) into two separate bundle branches which consist of
Purkinje fibres which spread along the apex (base of the heart) and direct
themselves towards the heart’s base. (Jardins, 2008, pp. 402-403).</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The heart is required to pump blood through both the pulmonary and
systemic circulatory systems. Blood is pumped to the lungs via the right
ventricle, and to all other tissues from the left ventricle. The atria are
involved in these contractions, but to a relatively low extent, and thus are
routinely ignored due to consideration of the ventricles. Given the much
greater distance of blood travel that the left ventricle must support, it contains
more cardiac muscle cells and pumps blood at a higher pressure. When the blood
travels around the body, waste products such as carbon dioxide diffuse into the
blood stream, possibly binding to haemoglobin, and are transported ultimately
to the right ventricle of the heart, where they can be taken to the lungs and
breathed out. According to Seeley, VanPutte, Regan and Russo (2011), p. 675,
there are 4 main functions of the heart which are shown below.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Firstly, the generation of blood pressure, which is produced by the
forceful contractions of the cardiac muscle. Without this blood pressure the
blood would either not travel the full distance along blood vessels to the
cells of the body and lungs, or would travel slowly enough to lead to pathology.
This condition is known as circulatory hypoxia and can occur for a few
different reasons, but in this specific case the sluggish movement of blood
through peripheral blood vessels can lead to inadequate unloading of oxygen
molecules in order to oxygenate tissues. These tissue cells will undergo
metabolic reactions at roughly their normal rate, but the slowly moving red
blood cells will have already lost oxygen molecules, causing a reduced oxygen
pressure gradient between them and the respiring cells. Thus, oxygen will be
delivered to the tissue at a reduced rate, resulting in hypoxia (elaborated
upon by Jardins, 2008, p.261).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Secondly, the separation of blood returning from and travelling to, both
the pulmonary and system circulatory systems. This allows deoxygenated blood to
become oxygenated by travelling through the lungs, and then subsequently be
pumped around the body. The result of this is that there is a greater
efficiency in the transport of oxygen and waste products around the body, than
if these two circulations were combined. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Thirdly, blood is kept flowing in its intended direction. This is
achieved by valves present in the heart that prevent the backflow of blood. If
this were not the case then blood could pool inside the heart without reaching
its necessary destination. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Lastly, the heart controls the supply of blood to other cells in the
body as a whole (lungs included). The pressure and frequency of cardiac muscle
cell contraction regulates the amount of blood passing tissue at any given
time. This allows the heart to change condition of blood flow based on how much
oxygen / nutrients are needed by other cells, and how much waste must be
removed from these cells as well. During exercise for example, a person’s
bodily cells would both require more oxygen and nutrients to be delivered to
respiring tissue, as well as needing more carbon dioxide and related metabolic
by-products to be removed at the same time. Such a circumstance calls for a
higher rate and forcefulness of cardiac muscle cell contraction, i.e. an
increase in both frequency and myocardial contractility, with the latter also
known as positive ionotropism. Both of
these factors increase the cardiac output, i.e. the amount of blood that is
pumped by the blood per unit of time. </span><span style="font-size: 22.0pt; line-height: 107%; mso-bidi-font-family: Arial;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The equation for cardiac output (CO) is given below:<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">CO = HR x SV<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Where HR is heart rate and SV is stroke volume. The heart rate is
determined by many factors such as blood pressure and sympathetic and
parasympathetic stimulation of cardiac muscle, whereas stroke volume is mainly
controlled by the following three factors: ventricular preload, ventricular
afterload, and contractility of myocardial cells (Jardins, 2008, p. 209).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">The term ventricular preload describes the extent to which myocardial
fibres stretch before contracting (at the end of diastole). Under normal
circumstances, the greater the stretching, the greater the force of contraction
and resultant cardiac output (Jardins, 2008, p. 209).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Ventricular afterload then, is the force that the ventricles must
overcome in order to pump blood. This is determined by the viscosity and volume
of blood that must be pumped, the resistance of peripheral blood vessels, and
the cross-sectional area of lumen that the blood is pumped into. This
information explains the left ventricular hypertrophy experienced in
atherosclerosis. The systolic pressure of arteries is increased in order to
compensate for a reduced vessel lumen due to the build-up of atherosclerotic
plaque, which means that the left ventricle must work harder in order to
overcome a greater resistive force (ventricular afterload) and pump blood
around the body. The introduction of a stent in an affected artery increases
the size of the lumen, decreasing the resistance experienced by the blood and
reducing the effort of the left ventricle, among other benefits. (Jardins,
2008, pp. 209-210).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Finally, contractility of the myocardium, has been mentioned briefly
above as the force produced by the shortening (or contraction) of muscle fibres
in the ventricles.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Given the chief importance of cardiac function in the body, it is vital
that the heart be able to produce energy from various different sources.
Schmidt (2000, p. 119) explains that the heart is more than capable of breaking
down ketones and fatty acids, even when glucose is adequately present, for its
energy requirements.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">A rough formula for estimating how fast a heart may beat at its maximum
frequency is shown below:<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Maximum heart rate = 220 – age<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;">Thus, we can see that there is a general rule that as one ages, the
maximum frequency of heart rate decreases. While beyond the scope of this
article, the reasons for this are interesting to note briefly. The reasons for
why aging may decrease maximum heart rate are possibly that as age increases,
oxygen supply to heart muscle increases, or that compliance in heart cells
decreases with age, or also, that there is an increase in connective tissue
infiltrating SA and AV junctions, as well as bundle branches (Jardins, 2008,
pp. 387-388).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: Arial;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Question 2 References:</span></u></b><span style="font-size: 12.0pt; line-height: 107%;"><o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Jardins,
T.D., 2008. <i>Cardiopulmonary Anatomy &
Physiology Essentials of Respiratory Care</i> 5<sup>th</sup> ed. USA, NY:
Nelson Education, Ltd.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<span style="font-size: 12.0pt;">Mescher,
A.L., 2013. <i>Junqueira’s Basic Histology
Text & Atlas</i>, 13<sup>th</sup> ed. China: The McGraw-Hill Companies.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 12.5pt; margin-bottom: .0001pt; margin-bottom: 0cm; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Pack, P.E.,
2001. <i> Anatomy and Physiology,</i> Hoboken, NJ: Wiley
Publishing, Inc.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Schmidt, F.,
2000. <i>Biochemistry II, </i>New York, NY:
Wiley Publishing, Inc.<o:p></o:p></span></div>
<div class="MsoNormal">
</div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Seeley, R.R,
VanPutte, C.L., Regan, J. and Russo, A.F., 2011. <i>Seeley’s Anatomy & Physiology</i>, 9<sup>th</sup> ed. New York, NY:
McGraw-Hill.<o:p></o:p></span></div>
Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-32179401374838109112015-06-13T03:35:00.001-07:002015-09-05T13:38:29.396-07:00Question 1: Why is mannitol, a sugar that does not cross the blood-brain barrier, used to treat patients with traumatic brain injury where the brain may swell?<div class="MsoNormal">
<b><u><span style="font-size: 12pt; line-height: 17.1200008392334px;">*These posts are from coursework answers for my degree, but the Figures that are referred to in the text didn't scan well and have already been handed in. These long posts would probably not interest most people but if you enjoy quite in-depth reading of scientific problems then this may be for you.</span></u></b><br />
<b><u><span style="font-size: 12.0pt; line-height: 107%;"><br /></span></u></b>
<b><span style="font-size: 12pt; line-height: 107%;">Question 1: <o:p></o:p></span><span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;">The
brain is protected to some extent by the blood-brain barrier - a membrane
between circulating blood and the brain that keeps certain damaging substances
from reaching the brain tissue. However, the brain is still subject to trauma
that can cause it to swell, much like an ankle swells with a sprain. Because
the cranium (skull) is a cavity of fixed size, brain oedema (swelling) can
rapidly lead to coma and death. Knowing what you do about movement of water
across a membrane, can you explain why mannitol, a type of sugar that does not
cross the blood-brain barrier, is commonly used to treat patients who have
suffered serious head trauma?</span></b><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;"><br /></span>
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;">Answer:</span><br />
<span style="font-family: Calibri, sans-serif; font-size: 12pt; line-height: 115%;"><br /></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">If a patient
has suffered serious head trauma then their brain has already experienced
swelling. Given the physical limitations of swelling due to the cranium’s lack
of flexibility, treatment of the patient must involve the use of substances
which do not further exacerbate the condition of brain oedema. If the swelling
were to be increased, the brain could expand to the point of being pushed
against the skull, leading the brain injury, or death. Thus, in treating a
patient with brain oedema, it is necessary to use a substance which does not
cause any further swelling of the brain. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Mannitol,
being a sugar and therefore a molecule which affects the movement of water into
a cell or membrane, would increase the retention of water by cells which
contain it. This is due to mannitol’s ability to dissolve in water and thus
increase the level of solute contained within the cytoplasm of the cell.
Consequently, the concentration of water molecules within the cell compared to
dissolved solute molecules is decreased. This decreases the pressure of the
solution within the cytoplasm of the cell. As a result of this, water from the
extracellular fluid, will move inward via passive diffusion, or osmosis. This
happens because the pressure of a solution which has more solutes added to it,
decreases. Then, water with less solutes dissolved in it (having a higher level
of pressure), will diffuse into the solution with a higher solute
concentration. This eventually causes the pressures within both solutions to
balance and thus osmosis will conclude. The pressure that would need to be
applied to the solution that has the higher solute concentration (and lower
pressure) in order to prevent the influx of water from a neighbouring solution
of higher pressure, is called the osmotic pressure. Thus, the higher the
concentration of solutes that there are in a solution, then the greater the
osmotic pressure which is required for this solution to not take passively take
in water. There are three main types of solution, as described by their solute
concentrations in relation to either another solution or cell or other entity
placed within them. For the following examples, consider that the respective
solutions are compared to a healthy animal cell which has been placed inside
the solution.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">A hypotonic
solution is one in which there is a low concentration of solutes compared to a
healthy animal cell. The result of this interaction would be that the animal
cell would at least swell up, and at most would actually burst, or lyse apart.
This is shown in Figure 1.1a. In this diagram there are multiple arrows
representing the movement of H<sub>2</sub>O (water), and all of these arrows
are moving into the cell. We can thus consider that the surrounding fluid which
the cell is in has a much higher concentration of water molecules (and lower
solute concentration) than the cell itself. Thus, the cell has a lower pressure
than the surrounding solution and water moves across its membrane until both
internal and external pressures (relative to the cell’s semi-permeable membrane)
equalise. If the surrounding solution is extremely hypotonic then the cell may
take in so much water that it both dies and bursts.<o:p></o:p></span></div>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">An isotonic
solution is one in which the concentrations of water and solutes is equal to
that of a cell placed in the solution. The result of this is that some water
may diffuse out of the cell, but water would also move into the cell at the
same rate. So at any given time there may be a slight difference in
concentration of water and solutes between cell and surrounding solution, but
this produces a pressure gradient that quickly leads to re-<o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">emergence of
the balance in pressure between both solutions (intracellular and extracellular
fluid). This means that the net movement of water is equal in both directions,
i.e. </span><span style="font-size: 12pt; line-height: 107%;"> </span><span style="font-size: 12pt; line-height: 107%;">going into and coming out of the
cell. This is shown in Figure 1.1b, with 1 arrow coming into the cell
representing the movement of water, and another arrow exiting.</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Lastly, a
hypertonic solution is one in which there is a high concentration of solutes
(low concentration of water molecules) in the solution compared to that of the
cell which is here being used as a reference point. As a consequence of this,
water will diffuse out of the cell and into the neighbouring solution. This is
shown in Figure 1.1c, with three arrows of water leaving the cell and none
going back in. Thus, the cell loses a great deal of water and will become
dehydrated. If the extracellular solution is sufficiently high in solutes, then
the animal cell will become desiccated and could die from dehydration. <o:p></o:p></span><br />
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span>
<br />
<div class="separator" style="clear: both; text-align: center;">
</div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhKhD9Ou4PCOdC7Jsv3HmYj0p6wWiUCmXxDGvRfPMrbjo6WU17V0P14IuXvU2Gguioj8XsRMGOXfZ6qi5ayKtzAjrAG7iPCnnN8zih47ZqZ7w48kEHNNz8hvaM2zagi9mjEAx3XTbyo6kpf/s1600/BME104+Q1+pic+1.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhKhD9Ou4PCOdC7Jsv3HmYj0p6wWiUCmXxDGvRfPMrbjo6WU17V0P14IuXvU2Gguioj8XsRMGOXfZ6qi5ayKtzAjrAG7iPCnnN8zih47ZqZ7w48kEHNNz8hvaM2zagi9mjEAx3XTbyo6kpf/s1600/BME104+Q1+pic+1.png" /></a></div>
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span>
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Another way
of describing this is to explain it in terms of concentrations, as opposed to
pressure. If a solution has a high concentration of solute molecules then it by
definition has a low concentration of water molecules. Supposing that the
solution in question is surrounded by a semi-permeable membrane which allows
water molecules to move freely between this and a pure water solution, but
solutes are kept within the aforementioned solution, then a concentration
gradient is set up. Because the first solution has a low concentration of water
molecules and the pure water solution has a high concentration of water
molecules, water will move passively from the pure water solution into the
solution with solutes. This can be explained by saying that water moves down
the concentration gradient. This is passive because movement in this direction
does not require energy, it happens spontaneously. The two different
explanations come together in the end: as the pure water diffuses into the solution
contained solutes, this second solution begins to rise vertically up the
container which it is present in. This increases the pressure of the second
solution. At the same time, the water level decreases in the pure water
solution. Eventually, the solution containing solutes will rise to such an
extent that its overall pressure exerted upon the membrane dividing both
solutions will be sufficient to prevent further diffusion. Thus, the osmotic
pressure has been reached. If we only took into consideration the
concentrations of solutions then the pure water would diffuse freely into the
solution contain solutes ad infinitum. This is because pure water will always
have a higher concentration of water molecules than a solution containing
solutes. This is what would in fact happen if the solution containing solutes
were constantly being drained to reduce its overall pressure. However, because
both solutions are present within a container and the overall pressure between
the two always adds up to the same amount (albeit, with the pressure increasing
on the side with the solution containing solutes and decreasing on the side
containing pure water), then there will always eventually come a point where
the pressures on each side of the membrane will be equivalent and further
diffusion will no longer take place. This situation is illustrated in figures
1.2a and 1.2b.<o:p></o:p></span></div>
<span style="font-family: "Calibri","sans-serif"; font-size: 12.0pt; line-height: 107%; mso-ansi-language: EN-GB; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: Calibri; mso-fareast-language: EN-US; mso-fareast-theme-font: minor-latin; mso-hansi-theme-font: minor-latin;">In a situation where a cell is in a relatively
hypotonic solution, takes in an osmotically active substance (by passive or
active means) and then retains water, there is a gradual accumulation of water
within the cell. The rationale for this being that the cell takes in water via
the above mechanisms previously described, but does not lose as much water </span><span style="font-size: 12pt; line-height: 107%;">because it
has a lower pressure than the surrounding environment, at least temporarily. In
this situation, the water gradually accumulates and thus over time the
difference in pressure between intracellular and extracellular fluids
decreases. This encourages a reduced rate of diffusion over time until
eventually both fluids equalise in pressure/concentration and diffusion rate
can be considered negligible. This is the basis for Fick’s Second Law of
diffusion, represented graphically in Figure 1.3. From this it can be seen that
initially (when Time = 0), the rate of diffusion is at its peak. However, as
time goes on, and water gradually builds up within the cell, the rate of
diffusion decreases. This is due to the difference of pressure or concentration
between internal and external fluids of cell beginning to equalise. At the very
end of the graph, the rate of diffusion is almost zero. The graph is not drawn
to the point where diffusion rate drops to zero because, while this may true in
a hypothetical sense, there will always be some movement of substances between
the cell and its environment, even if the net effect is that there is no
overall difference in concentrations between the two. The point at which there
is no difference in concentrations of substances between two points, and
consequently the concentration gradient has disappeared, is referred to as a
state of equilibrium (Pack, 2001, p. 26).</span>
<br />
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">The term
given to a substance which exerts an effect upon the osmotic gradient or
osmotic pressure of a solution is; osmotically active. Much of the above
information regarding water retention by cells containing mannitol and
subsequent explanations on varying types of solution are widely known from
A-level biology, but elaborated upon in the work of Coan (2008).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">With this in
mind, we turn our attention to animal cells in general. Animal cells are quite
limited in their ability to deal with varying concentrations of solute in a
surrounding fluid. Plant cells are protected by their cell wall which helps
prevent excessive drying out and dangerous water intake. So, a plant cell in a
solution of pure water will swell up to a certain degree, but is unlikely to be
killed by cellular lysis as a result of taking in too much water, provided that
it has a healthy membrane and cell wall, whereas an animal cell almost
certainly would succumb to this. Consequently, the concentration of both water
and solutes in blood and the extracellular fluids surrounding animal cells
inside of a living body is under tight control of various homeostatic
mechanisms. This ensures that the animal cells supplied by these mediums do not
become overwhelmed with either water or solutes and either become excessively
dehydrated, or break down /lyse from over-hydration. This means that the
extracellular fluid or blood surrounding an animal cell provides a strong
indication of the solute and water concentrations of the cell itself.
Therefore, a change in the concentration of a solute or of water in the blood
or extracellular fluid will have a noticeable impact on the cytosol of the cell
which is supported by it (Evans, ed. 2008).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">So we can
see that if mannitol were taken up by the cells of the brain when it was
injected into the blood stream, then these cells would take in the mannitol,
experience an increase in solute concentration and therefore a decrease in
pressure, and this would consequently result in an increase in water retention
from the surrounding fluid. This would occur because the cell’s cytosol would
retain the osmotically active mannitol, resulting in a decrease of cellular
pressure and decrease in overall water concentration. Thus, <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">neighbouring
cells and fluid would then lose water molecules via osmosis, to the cell which
contained more mannitol, provided that all other solutes within the cells in
question remained constant. The fact that other solutes must remain constant in
order for mannitol to have its effect is because the osmotic pressure that we
are considering here is known as a colligative property. A colligative property
is one in which the concentration of both solvent (here, water, the dissolving
agent) and solute are taken into account, but the actual form of both solvent
and solute don’t matter. So, sodium for instance, could exert the same effect
upon the concentration of water molecules as mannitol, thus it must be ensured
that all other osmotically active solutes remain constant, for the effect of
water retention to be caused by mannitol. So, if brain cells took in mannitol
by any means, they would also retain water. This water would be diverted from
other cells in the body with lower solute concentrations and from the blood and
extracellular fluids. The brain cells would increase in size as they gained
this water, and this would worsen the condition of brain oedema. Thus, it is
essential that mannitol not enter the brain cells, or at least not in any
concentration capable of significantly increasing cellular size.</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">This is
where the blood-brain barrier comes in. Because of the potential for brain
damage due to harmful substances entering the brain, a highly specific barrier
called the blood-brain barrier is present and aptly named, for its ability to
regulate the movement of many chemicals between the body’s blood supply and the
brain’s cells. The blood-brain barrier is capable of preventing most harmful
substances from entering the brain, although if a substance is lipid-soluble
then it has a greater chance of getting through. The relatively high
lipid-solubility of alcohol (ethanol) allows it to diffuse into the brain and
explains the rather rapid onset of cognitive impairment when consuming alcoholic
drinks (Seeley, VanPutte, Regan and Russo, 2011, p. 457).<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Regarding
the actual structure of the blood-brain barrier, a simplified diagram is shown
in figure 1.4. It is composed of tightly-knit capillary endothelial cells
(primarily). These are attached to astrocytic foot processes, pericytes and a
basal lamina. Macrophages also occur in this general area to prevent the
movement of harmful materials and life-forms (as well as viruses) into the
brain. The function of the astrocytic foot processes is to maintain the close
proximity of the endothelial cells. This is necessary to ensure that many
substances are incapable of diffusing freely into the brain. If this were
allowed to occur then toxins could enter the brain and damage sensitive tissue.
Thus, the vast majority of substances entering the brain must enter via active
mechanisms, e.g. active uptake or any other route requiring energy in which the
substance is selected for its necessity (or shape and therefore ability to bind
to carrier or channel proteins on the surface of the endothelial cells) instead
of traversing the blood-brain barrier without restriction. If the cells of the
blood-brain barrier were to drift apart or decrease in size due to strong
dehydration, then diffusion of more substances into the brain would be a
possibility (</span><span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Times New Roman";">Vries, et al., 1997).</span><span style="font-size: 12.0pt; line-height: 107%;"> <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">With this in
mind, the effects of mannitol on the alleviation of intracranial pressure
following a serious brain injury can be due to one of the following main
mechanisms. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Firstly, the
mannitol can be used to encourage osmosis within the cells of the blood-brain
barrier. If the cells of the blood-brain barrier come into contact with a
hypertonic solution <o:p></o:p></span><span style="font-size: 12pt; line-height: 107%;">then they
will lose water and shrivel up, i.e. their size will decrease. This could occur
by having a high concentration of mannitol in the blood circulating the entire
body, or by injecting mannitol into the bloodstream at an area close to the
blood-brain barrier. Consequently, water from other areas of the brain and also
from the blood, once the blood has had a chance to travel to the kidneys and
other bodily areas where the mannitol content will be reduced and overall
tonicity will be reduced, will act to move water back into the cells of the
blood-brain barrier which have been affected by the mannitol, via the process
of osmosis. Neglecting the blood, this effect will mean that water moving from
other regions of the brain towards the blood-brain barrier will reduce the
water content of the other cells of the brain. This will reduce the size of the
brain cells via dehydration and thus reduce the swelling that the brain is
suffering from, therefore intracranial pressure will be reduced by
mannitol-induced osmosis (Shawkat, Westwood, and Mortimer, 2012).</span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Secondly,
mannitol could help to alleviate brain swelling indirectly by reducing the size
of the cells of the blood-brain barrier and their ability to form a cohesive
barrier against substances in the blood.<sup> </sup>Once this has occurred,
more substances will be able to enter the brain by diffusion. This allows
effective drugs to be administered to the patient and travel to their brain. If
the blood-brain barrier were functioning normally then these drugs would not
reach their site of intended action.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">It is highly
likely that both of the above mechanisms are in play to a large extent and thus
are both responsible for the reduction of brain swelling.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Figure 1.4
shows the blood-brain barrier. In this diagram the small shaded circles are
molecules of mannitol. This figure shows the mechanism of action of mannitol where
it is taken up by cells of the blood-brain barrier. This then encourages water
retention by these cells from various sources, but most importantly, from the
other brain cells. This is one of the ways in which intracranial pressure may
be reduced. Since the blood-stream surrounding the blood-brain barrier is
hypertonic and containing much mannitol, if the cells of the blood-brain
barrier fill with mannitol and then water via osmosis, some of this water may
diffuse into the blood-stream, setting up a relatively constant diffusion
gradient that allows water to move passively from the cells of the brain, into
the blood-brain barrier cells and then into the surrounding blood. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Therefore,
in returning to the original question, mannitol is commonly used to treat
patients who have suffered serious head trauma because it does not cross the
brain-blood barrier and thus provides a way of intervening against brain
swelling, without contributing to it via osmosis. If mannitol crossed the
blood-brain barrier then its administration would worsen brain oedema. However,
because it doesn’t cross the blood-brain barrier, it is able to either draw
water away from the rest of the brain, or to simply open up this barrier and
allow a greater diffusion and utilisation of drugs into and within the brain.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">However,
there is controversy over the effectiveness of mannitol as a standard treatment
for brain oedema in general (Kaufmann, and Cardoso, 1992) and when compared to
hypertonic saline solution (Cochrane, 2013). Kaufman and Cardoso even claim
that mannitol can increase intracranial pressure (however, this is to be taken
with a grain of salt as the study was conducted on cats, not humans) and is
consequently harmful to the brain in cases of head injuries. If this is the
case for humans as well then the administration of mannitol could very well be
dangerous. If mannitol produced this effect then it may simply be a question of
both dosage and frequency of administration. It is possible that if multiple
doses of mannitol are given that their effect could stack upon each other. This
would happen if mannitol caused a shrinkage that lasted for a long time after
the mannitol concentration had been reduced in the blood stream. This would
allow some osmotically active substances to diffuse into the brain, potentially
even mannitol itself. Then, if mannitol were again administered to the patient,
before the blood-brain barrier had a time to undo its shrinkage, this could
further induce decrease in size of the cells. Even more substances could diffuse
freely into the brain and some of these substances could cause water retention
to neural tissue. Thus, mannitol could reduce intracranial pressure in the
short-term, by reducing water content in the brain and allowing
pressure-reducing drugs the opportunity to diffuse into the brain cells, but
excessive use could trigger the opposite effect by letting too many osmotically
active substances enter the brain where they could then encourage water
retention and subsequent swelling. This would certainly exacerbate the
condition of brain oedema and potentially lead to coma and/or death.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;"><br /></span></div>
<div class="MsoNormal">
<b><u><span style="font-size: 12.0pt; line-height: 107%;">Question 1 References:</span></u></b><span class="MsoHyperlink"><span style="color: windowtext; font-size: 12pt; line-height: 107%;"><o:p></o:p></span></span></div>
<h1 style="background: white; line-height: 18.0pt; margin-bottom: 7.5pt; margin-left: 0cm; margin-right: 0cm; margin-top: 0cm;">
<span class="MsoHyperlink"><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-hansi-theme-font: minor-latin;">Coan, M., 2008. </span></span><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Helvetica; mso-hansi-theme-font: minor-latin;">Osmoles,
osmolality and osmotic pressure: Clarifying the puzzle of solution
concentration. [online] Available at: <</span><a href="https://www.researchgate.net/publication/23308894_Osmoles_osmolality_and_osmotic_pressure_Clarifying_the_puzzle_of_solution_concentration"><span style="font-family: "Calibri","sans-serif"; font-size: 12.0pt; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Helvetica; mso-hansi-theme-font: minor-latin;">https://www.researchgate.net/publication/23308894_Osmoles_osmolality_and_osmotic_pressure_Clarifying_the_puzzle_of_solution_concentration</span></a><span style="color: windowtext; font-family: "Calibri","sans-serif"; font-size: 12.0pt; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Helvetica; mso-hansi-theme-font: minor-latin;">> [Accessed 6 April 2015].<o:p></o:p></span></h1>
<h1 style="background: white; line-height: 13.5pt; margin-bottom: 4.5pt; margin-left: 0cm; margin-right: 0cm; margin-top: 4.5pt;">
<span style="font-family: Calibri, sans-serif; font-size: 12pt;">Cochrane, 2013.<i>Mannitol for acute traumatic brain injury</i>,
[online] Available at: <</span><a href="http://www.cochrane.org/CD001049/INJ_mannitol-for-acute-traumatic-brain-injury"><span style="font-family: "Calibri","sans-serif"; font-size: 12.0pt; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: Arial; mso-hansi-theme-font: minor-latin;">http://www.cochrane.org/CD001049/INJ_mannitol-for-acute-traumatic-brain-injury</span></a><span style="font-family: Calibri, sans-serif; font-size: 12pt;">> [6 April 2015 2015].<o:p></o:p></span></h1>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Evans, H.E.,
ed. 2008. <i>Osmotic and Ionic Regulation:
Cells and Animals. </i>Boca Raton, FL: CRC Press.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Kaufmann,
A.M., and Cardoso, E.R., 1992. Aggravation of vasogenic cerebral edema by
multiple-dose mannitol. <i>Journal of
Neurosurgery, </i>77(4), pp. 584-8.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Pack, P.E.,
2001. <i> Anatomy and Physiology,</i> Hoboken, NJ: Wiley
Publishing, Inc.<o:p></o:p></span></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%;">Seeley, R.R,
VanPutte, C.L., Regan, J. and Russo, A.F., 2011. <i>Seeley’s Anatomy & Physiology</i>, 9<sup>th</sup> ed. New York, NY:
McGraw-Hill.<o:p></o:p></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; margin-left: 0cm; margin-right: 3.0pt; margin-top: 0cm; mso-line-height-alt: 8.4pt; vertical-align: baseline;">
<span style="font-size: 12.0pt; mso-bidi-font-family: "Times New Roman";">Shawkat,
H., Westwood, M., and Mortimer, A., 2012. Mannitol: a review of its clinical
uses. <i>Continuing Education in
Anaesthesia, Critical Care & Pain. </i>[online] Available at: <</span><a href="http://www.ceaccp.oxfordjournals.org/content/early/2012/01/12/bjaceaccp.mkr063.full"><span style="color: windowtext; font-size: 12.0pt; mso-bidi-font-family: "Times New Roman";">http://www.ceaccp.oxfordjournals.org/content/early/2012/01/12/bjaceaccp.mkr063.full</span></a><span class="MsoHyperlink"><span style="color: windowtext; font-size: 12.0pt; mso-bidi-font-family: "Times New Roman";">> <o:p></o:p></span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; margin-left: 0cm; margin-right: 3.0pt; margin-top: 0cm; mso-line-height-alt: 8.4pt; vertical-align: baseline;">
<br /></div>
<div class="MsoNormal">
</div>
<div class="MsoNormal">
<span style="font-size: 12.0pt; line-height: 107%; mso-bidi-font-family: "Times New Roman";">Vries, H.E., Kuiper, J., de Boer, A.G., Van Berkel, T.J.C.,
and Breimer, D.D., 1997 The Blood-Brain Barrier in Neuroinflammatory Diseases<i>. Pharmacological Reviews,</i> 49 (2): pp.
143-156.<o:p></o:p></span></div>
Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-33920758881910855722015-06-10T08:21:00.001-07:002015-06-10T08:21:22.409-07:00New content on the wayOver the next several days to a week I will be adding information regarding the following items:<br />
<br />
Mannitol's use in treating brain injury<br />
<br />
The heart and its functions<br />
<br />
Lung disease<br />
<br />
Atherosclerosis<br />
<br />
Cancer treatmentAnonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-80302702642691497542014-12-31T12:32:00.000-08:002013-06-05T05:20:43.447-07:00AboutThe purpose of this blog is to allow me to freely learn about anything that I enjoy while at the same time providing some sort of benefit to the lives of all who visit. If you come across anything on this blog that you found in some way helpful to your life then kindly leave a comment expressing this view.<br />
I am not a medical professional, therefore the views that I express on this blog are through my own personal<br />
research. If you come across information that you believe to be beneficial here, I advise that you confirm it with<br />
a qualified medical professional.<br />
Feel free to contact me privately at: andyhamiltonus1@gmail.com to ask questions, point out spelling or other<br />
mistakes or request that I look into something for you. Thanks for visiting :)Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-68093211499726941142014-05-17T13:04:00.000-07:002014-05-17T13:04:09.004-07:00High-Intensity Interval Training and fat loss - my thoughtsHigh intensity interval training is an increasingly popular form of training that involves short bursts of very high intensity cardiovascular activity followed by very slow and relatively long rest intervals. The idea is that using this rather extreme yet short type of training will cause the body to gain similar cardiovascular benefits as to those gained from long relatively slow runs.<br />
<br />
However, this type of training is something that shouldn't be undertaken lightly, especially for those who are just starting to train. While using a bike or other form of low / zero impact machine will have the benefit of reducing the amount of force exerted on the joints which can be problematic to those who are running, high intensity interval training will always place a large amount of stress on the heart. Therefore, it is a bad idea to undertake it if obese or suffering from any heart conditions.<br />
<br />
To be entirely honest, HIIT or HIT really wouldn't be my thing personally. If I were ever in a situation where I was trying to lose weight, I would eat more vegetables (they leave you feeling fuller with less caloric consumption) and drink plenty of water (in the times of excess food intake we now find ourselves in, it is very easy to be dehydrated and not even realise it. Chronic dehydrated can manifest itself as a desire to eat more food, perhaps a useful adaptation to have when all food used to be very high in water, but with all the junk food around these days, this is more likely to be a problem than a treatment.) I would also eat my food very slowly as sometimes we can bolt our food down and this means our body doesn't have time to tell us we're full before a whole dinner is inside our stomachs.<br />
<br />
So really, while it mightn't mean much coming from a perpetually skinny teenager, my advice for weight loss wouldn't be to <u style="font-weight: bold;">try </u> to eat less, it would just be to drink more water, eat more vegetables, and eat slowly. The best way to eat for maximal absorption is to put one mouthful of food in our mouths, then chew this down to a watery paste before eating anything else.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-35687923818119133412014-05-17T12:58:00.001-07:002014-05-17T12:58:03.158-07:00The Subconscious MindOne of the things that I have been studying while taking a break from this blog is the subconscious mind. This is the part of the brain that is not under our conscious control. This means that we have little to no say in what is occurring. Things like our heart rate, blood pressure, and salivation would all be examples of functions that are carried out subconsciously. However, we can influence these things consciously and indirectly. Heart rate and blood pressure would be both increase if we listened to stimulating music for example, and if for whatever reason we wished to salivate, we could think about our favourite food when we are feeling hungry. But the actual process of increasing or decreasing these parameters is done by the subconscious, though we can place the necessary stimulus in our environment or ourselves in close enough proximity to the stimulus, or even imagine it within the confines of our own minds, and it will affect the subconscious' functioning.<br />
<br />
Breathing is a good example of a function that is carried out by both the subconscious and conscious mind. If I were to tell you to start consciously controlling your breath, you could do it immediately and control each one as you pleased, yet it could just as easily keep on going without your slightest thought, if you were consciously absorbed in another activity.<br />
<br />
Where this gets interesting for me however, is in our thoughts, feelings and emotions. If we are involved in a daydream about some past or future event (we cannot daydream of the present moment in front of us), then our subconscious mind takes over and replays existing beliefs and 'recordings' to any stimulus we presently encounter. What this means is that if you are an angry individual but do not wish to be so, then if you daydream of some other past or future event while doing housework or gardening etcetera, then you will probably get annoyed or upset if you drop something or for whatever reason if something you are doing "doesn't work out". This is because your subconscious is operating under the belief that if something goes wrong, then it should produce a response based on anger in that circumstance. The more present (conscious) that you are, the less your subconscious mind will take over the show. There are stories that I cannot verify the validity of regarding yogis or advanced meditators who are able to control otherwise unconscious / subconscious bodily functions, such as the passge of water through the digestive tract (they can move a column of water from left to right along their intestines) or control their heart beat to some extent or 'decide' whether to react to a loud noise instead of instinctively jumping in fright. Such people are also much more composed and much less likely to react subconsciously to any given situation. This is because they have trained themselves through many meditative practises to be fully present. I imagine that this would then allow their brain to re-wire itself in such a way as to give more power to the conscious mind, and less to the subconscious mind. If the aforementioned angry person were to be more like these people, then upon something going wrong, he would feel less angry, get over it much more easily and it would take more extreme circumstances to produce any such effect upon him.<br />
<br />
The difficulty is in remaining conscious. I believe that each individual would like to be happy and feel fulfilled all the time and not engage in self-sabotaging acts. The question is; why is this not the case then if it is what everybody wants?<br />
<br />
The trick is in the recordings I touched on above. The subconscious mind is estimated to be around 1 to 2 million times more powerful than the subconscious mind, which means it has much more oomph at its disposal. Any ordinary individual trying to experience positivity consciously while within an adverse circumstance has as much chance of remaining fully conscious as a wheelbarrow has of out-racing a Ferrari, if that wheelbarrow is being pulled by a dead cow... uphill. That's a little bit of an exaggeration, but my point remains, it isn't easy. I will cover this topic more fully in a later post though.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-71231324188270706042014-05-17T12:39:00.002-07:002014-05-17T12:39:58.946-07:00Buteyko Update (May 2014)So I haven't written in this blog for a while, but I have remembered it, for the one or two of you that view it each month.<br />
<br />
I stuck with the principles of Buteyko breathing but forewent the breathing exercises. This means I continued to breathe through my nose at all times when awake and tried to sleep on my left side at night. I alsodid a lot of walking in these past few months and my CP is now around 22-25 seconds during the day (the length of time that I can comfortably hold my breath without any involuntary physical movement, for example, like stomach tensing inward or unconscious swallowing / throat movements). I have noticed that I usually feel more awake, have a better memory, and my extremities are much warmer these days.<br />
<br />
I used to have very cold hands and feet, whenever the air was even slightly cold my hands would turn purple and get these orange-highlighter-type blotches all over them, it was kinda freaky, especially since it happened due to the slightest provocation. It wasn't like it had to be a cold day for this to happen at all, really just any sensation of cold would do it. Now, even when I do feel significantly cold, my hands will actually appear as though they belong to a human being, which I find rather comforting to be honest. My feet are still purple nearly all the time, but it is a much lighter shade, and I am confident that if I keep looking after my body and adhering to the principles of Buteyko breathing, that they too will improve.<br />
<br />
The results I have had from this experiment could happen a lot faster, i.e. within a week or 2 if the person doing so was of a more healthy frame of health to begin with and also practised more diligently than I. I retained the unconscious training in the sense that I would automatically breathe through my nose and into my stomach and would immediately correct any mouth or chest breathing while I was awake. I feel that this is a beneficial practice to have in life because it stops one from falling to the lowest depths of breathing disorders. The worst thing you could do is constantly breathe in your mouth and into your chest, causing jaw joint dysfunction and unnecessary oxidative stress upon the respiratory system, not to mention the entire body which becomes fatigued by being forced to participate in such an inefficient exercise for many thousands of repetitions daily. It is such a small change to make just to get into the way of carrying out breathing in a more healthy manner, yet it can bring about very large differences.<br />
<br />
I think that for me, I really need to be drinking more water, I notice now that I am almost always dehydrated and this will certainly affect the rate at which I breathe (more dehydrated = more minute ventilation (the amount of air breathed in and out per minute)). The smaller the amount of air you can tolerate breathing in each minute, the less effort breathing takes up for your body and less damage is done to your lungs and related tissue by the act of breathing in oxygen, which in itself is quite a damaging gas, albeit essential for life.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-23460136388672073692013-10-23T03:12:00.000-07:002013-10-23T03:12:06.599-07:00Alkaline waterI came across a lot of debate with regards to alkaline water. I will try to give you the most important parts here though, in order that you may sift through the most vital pieces of information and not be lost in a maelstrom of sales' pitches and exaggerations.<br />
<br />
There are 2 types of alkaline water that I was able to discern. The first is that which is artificially ionised from a metallic electrode, such as titanium. This increases the amount of electrons that are in the water and consequently gives it a negative voltage. The second form of alkaline water is that which is alkaline due to the presence of mineral ions that have an alkalising effect in the body, for example, magnesium and calcium.<br />
<br />
Artificially ionised water can cost up to several thousand dollars to make as the device used to electrically charge the water is very expensive, and there is a filter too. However, this form of water has been linked to pathological changes in heart muscle tissue in rats.<br />
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<a href="http://www.ncbi.nlm.nih.gov/pubmed/9198011">http://www.ncbi.nlm.nih.gov/pubmed/9198011</a><br />
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While most humans would have to lose more than a few pounds and grow a lot more hair for this study to be completely relevant to them, it is still worthy of note as rats and humans have similar metabolic pathways within their bodies.<br />
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The above study was the reason why I didn't buy artificially ionised water.<br />
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I did, however, buy an alkaline water filter (a 2 litre jug) which filters out some chemicals normally present in tap water and then allows the water to collect in the jug where alkaline minerals such as calcium and magnesium as mentioned above, are free to diffuse into the water. Both types of alkalinisation will usually cause the tap water to reach a high pH of 8 to 11. However, I felt that the presence of minerals instead of artificial ionisation was something that the human body would be more used to in an evolutionary sense, and thus it would be better to do things the more natural way.<br />
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Again, there is a lot of debate as to the effectiveness of alkaline water. Some claim that it helps give all the benefits of an alkaline diet, all the theories of which would be too much to go into in this post but some say it is a significant aid in improving cellular oxygenation and therefore can prevent or treat pretty much every disease of civilisation and cancer too. However, this has not been proven scientifically.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-61708811005862080892013-06-16T12:52:00.002-07:002013-08-15T01:32:17.264-07:00VacuolesVacuoles are used to contain harmful materials, waste products, and small molecules. They also maintain pressure and an acidic pH within the cell. While most, if not all of plant cells have at least one vacuole, not all animal cells have one. In animal cells which contain vacuoles, they aid the processes of exocytosis and endocytosis among others and play a critical role in a process known as autophagy.<br />
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Autophagy, ('self-eating) is a catabolic process in which cell parts that are no longer functioning correctly or are simply no longer necessary are broken down. This occurs by first isolating the targeted components / organelles and then fusing lysosomes to them. Lysosomes are organelles that contain acid hydrolase enzymes. This process is especially beneficial during periods of starvation in which the cell may digest its own components for survival.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-80728961716414227652013-06-16T12:52:00.000-07:002013-06-16T12:52:02.242-07:00Muscle contractionsThere are 3 main types of muscle contraction, these are concentric, eccentric and isometric.<br />
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Concentric contractions occur when the muscle involved is shortened in order to overcome a resistance placed on it, for example, the biceps shorten when lifting a dumbbell in a bicep curl.<br />
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Eccentric contractions are the opposite, they occur when the muscle involved lengthens in order to lower an object or resistance placed upon it, for example, lowering the dumbbell at the end of a bicep curl causes the biceps to lengthen.<br />
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Isometric contractions occur when the length of the muscle remains constant and the resistance is not moved through space, for example, holding, without moving, an object.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-51626686134982647172013-06-05T04:43:00.001-07:002013-06-05T04:43:27.205-07:00Parasympathetic Nervous System - brief overview<br />
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<span style="text-align: center;">Generally involved in the rest and digest response, or other activities that occur when the body is resting.</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">Preganglionic neurons are usually long, postganglionic neurons are usually short, this is because the preganglionic neurons must travel from the brain and spinal cord to a ganglion that is next to or inside of an organ. The postganglionic neurons which communicate with the organ are therefore very short in comparison.</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">Both types of neurons typically use acetylcholine as their neurotransmitter but can also utilise neuropeptides.</span></div>
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<br /></div>
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<span style="text-align: center;">Examples of sympathetic stimulation:</span></div>
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<br /></div>
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<span style="text-align: center;">- Iris (eye muscle): pupil constriction</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Salivary glands: saliva production increased</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Oral / Nasal Mucosa: mucus production increased</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Heart: heart rate and force decreased</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Lungs: bronchial muscles contracted</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Stomach: peristalsis increased and gastric juice secreted as well as an increase in motility</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Small intestine: motility increased</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Large intestine: secretions and motility increased</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Liver: No change</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Kidneys: increased urine secretion</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Adrenal medulla: No change</span></div>
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<span style="text-align: center;"><br /></span></div>
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<span style="text-align: center;">- Bladder: wall contracted, sphincter relaxed</span></div>
Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-48442292467810647422013-06-02T12:31:00.004-07:002013-06-02T12:31:42.120-07:00CortisolMuch is made these days of reducing the level of cortisol within our bodies as if this hormone is some sort of foul demon which seeks to kill us by all means possible. However, cortisol is actually essential to our survival and without it we wouldn't be able to function adequately, actions such as walking would become next to impossible. Cortisol is known most popularly as a major stress hormone, in other words, a hormone which is released whenever we become stressed. This stress can be either emotional (due to an argument or even simply imagining an argument) or physical (because of a strenuous weightlifting workout or a long run). In all of these cases, cortisol is mobilised in order to provide us with the energy to deal with the present circumstance or in anticipation of a circumstance which requires exertion. It provides this energy by suppressing the immune system, increasing blood sugar levels and increasing the metabolism of fats, proteins and carbohydrates, among other activities. The importance of this is that cortisol essentially breaks us down in order to provide the energy that we 'need' or, that our bodies believe we need. This can result in muscle breakdown. The reason that cortisol is so feared these days is because most people are chronically stressed which results in chronically elevated levels of this hormone. This means that most people exist in a state of higher catabolic activity than they should. The result of this is that it is harder to gain muscle mass and there is a fear of raising cortisol even further. Cortisol also inhibits the effects of insulin and testosterone. Insulin is very important for exercise as it brings essential substances such as amino acids back into the muscle tissue in order to bring about reparations. Testosterone is also vitally important for muscle growth and repair and this is why there is such a large emphasis placed on raising testosterone in order to improve muscle gains.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-35746097805557630262013-06-02T12:31:00.002-07:002013-06-02T12:31:14.567-07:00Raising Testosterone NaturallyZinc<br />
Zinc prevents the conversion of testosterone into estrogen. It also aids both sperm count and health. However, zinc will probably only have a noticeable effect on your testosterone levels if you are currently deficient in it, though I feel that it is still worth mentioning.<br />
Lose body fat<br />
Body fat, also know as adipose tissue, is a large storage container for aromatase. Aromatase is an enzyme that converts androgens (hormones largely involved in male characteristics, such as testosterone) into estrogen. Therefore, losing body fat increases testosterone levels while reducing estrogen levels. However, trying to lose excess body fat by extreme dieting is also detrimental to testosterone levels. The trick is to lose weight slowly, this is why many personal trainers will tell you to only lose a few pounds per week at most, as this is healthier for your body.<br />
Avoid plastics<br />
Plastics contain synthetic estrogens called xenoestrogens which again lower your testosterone while increasing your estrogen levels. For this reason it is better to drink from stainless steel bottles if you can.<br />
Testosterone-increasing exercise<br />
Short durations of high intensity exercise have been shown to increase testosterone levels. However, aerobic exercise for moderate to long durations have been shown to have either no effect or to have a detrimental effect on testosterone. Apparently the best exercises for raising testosterone are compound exercises of which you can only perform 5 repetitions for 5 sets.<br />
Relaxation<br />
When we are stressed our bodies release cortisol which is a hormone that inhibits the actions of testosterone. This is a particularly common problem in modern culture as our lives are very stressful, also, having constant worries has a strong impact on both our ability to fall asleep and our sleep quality, both of which have a dramatic effect on our testosterone levels. Sleeping for around 8 hours per day is recommended in order to reduce our cortisol levels and keep our testosterone high. Practising deep breathing exercises is also beneficial for reducing cortisol.<br />
Cut down on sugar and alcohol<br />
The consumption of both of these can lead to large reductions in testosterone. They are both large problems in most peoples' lives as sugar is in many foods and a lot of people drink alcohol. Some studies indicate that drinking heavily can keep testosterone levels low for a few days if not a week. This is particularly detrimental to those of us who drink heavily each weekend.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com5tag:blogger.com,1999:blog-6986907989946980568.post-19754958022184331062013-06-02T12:30:00.003-07:002013-06-02T12:30:42.753-07:00Buteyko; my thoughts and reading through forum postsI came across the Buteyko method online and thought I would try it out to see if the bold claims about its ability to treat many diseases (I believe its practitioners say that it can treat around 150) had any merit. The Buteyko method is a breathing technique in which people breathe through their noses and into the lower portion of their lungs. They then try to reduce their minute ventilation (the amount of air that they breathe in and out every minute). The belief being that this will allow carbon dioxide to accumulate and that for those of us in developed countries, this will greatly improve our health. It is thought that due to our modern diets, lack of exercise, and poor postures, that we don't breathe correctly. More specifically, these aspects of our daily life cause us to breathe using our mouths and to take air into the upper portion of our lungs. I have much more information on this in the "Everything I Know: Breathing" post but I don't agree entirely with Buteyko breathing. The practitioners of Buteyko breathing swear by the idea that if we continuously try to reduce our breathing rate and allow carbon dioxide to accumulate then this will cause the respiratory centre of our brain to adjust itself so that higher concentrations of carbon dioxide in the blood will become tolerable. They say that the level of carbon dioxide in the blood that we have adapted to is a useful indicator of the oxygenation of our cells. They measure the relative oxygenation of cells through a short breath-holding technique called the "Control Pause". This entails holding your breath while paying attention to any involuntary movement of your body. Once any involuntary movement occurs, you record how long you were able to hold your breath for and you begin to breathe normally again. The length of time that you could hold your breath for during the control pause is thought to be both an indication of cellular oxygenation and also the pressure of carbon dioxide that your body is able to tolerate. While this may very well be true, I have read that in Buteyko practitioners who were tested, the higher their control pause, the lower their carbon dioxide levels were (there was only a very slight reduction in carbon dioxide levels but it still goes against the belief of the practitioners). However, this was only one test and can't be considered conclusive. That being said, I do not personally believe that the Buteyko method increases carbon dioxide levels to the extent that its practitioners believe, but I think that the method is still beneficial. I wouldn't be quick to put aside the belief that because of this test the Buteyko method doesn't work. I feel that the Buteyko method has implications in combating stress, believed to be a major cause of disease.<br />
<br />
Reading forum posts on Buteyko Breathing<br />
<br />
So today I went through a lot of forums where people talked about Buteyko... all in all I found 1 negative report, 2 reports of no change, and 33 positive reports.<br />
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Bad news first then, the negative report was about a person who had gone to learn about the Buteyko method and had a panic attack due to the breath holding. In some medical studies that I can't locate but do exist, I swear, there has been a link shown between panic disorder and increased sensitivity to CO2 induced breathlessness. I assume that in persons with this heightened sensitivity that breath holding may produce the panic attack that occurred in the negative report I'm referring to. For these people it would probably be best to not do any serious breath holding (maximum pauses or straining hard on the control pause), and they may also find it better to just do nasal breathing, control pauses seem to be solely for the purpose of measuring progress so they don't have to be done regularly as part of the training exercises.<br />
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The 2 reports of no change came from people who had either multiple sclerosis or chronic fatigue. They both basically concluded that the treatment was not helpful for their conditions, though I'm unsure as to how long or intensely they tried the method.<br />
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Of the 33 positive reports, 19 were from asthmatics and 14 were anxiety related. Of the asthma sufferers, 7 reports indicated that the persons no longer needed / used inhalers and/or that they considered themselves cured/fixed. The remaining 12 said that the method was in some way helpful. Of the anxiety reports, 4 persons have/had social anxiety, 2 had adrenal fatigue, 1 had panic disorder and agoraphobia, 1 report was quoting a psychologist (Dr Meuret PhD) who advocated reduced breathing in anxiety disorders (though not specifically Buteyko) and the remaining reports were from persons suffering from unspecified anxiety complaints. Of the sufferers, around half said it helped and the other half said it was a huge help / was a massive help or words to that effect anyway.<br />
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Sources: google searched "Buteyko forum" and went through the first 10 pages.<br />
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For both anxiety and asthma it is said (by some Buteyko practitioners) that once the control pause reaches 30 seconds the vast majority of symptoms are alleviated, with seemingly full recovery occurring at a CP of 40 seconds. This is still a long way off the 60 second control pause recommended for optimal health. I'm still not sure if this method lives up to its own theory but as I've said before... it definitely seems to be doing something beneficial.<br />
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By the way, I get most of my Buteyko information online at: http://www.normalbreathing.com/Articles-warm-hands-feet.php#.US48FqKSJ0E if you'd like to check it out.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com1tag:blogger.com,1999:blog-6986907989946980568.post-90805149494958637102013-06-02T12:30:00.000-07:002013-06-02T12:30:06.834-07:00Muscle fibersThere are 3 types of muscle fibers:<br />
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Type 1 fibers; these are slow oxidative (slow twitch) muscle fibers that contain large amounts of myoglobin, this gives these muscle fibers their characteristic red colour. These muscle fibers are capable of carrying out aerobic exercise for hours on end, they are highly fatigue resistant.<br />
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Type IIa fibers; these are also red. They are used for long-duration anaerobic exertion typically lasting up to 30 minutes.<br />
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Type IIx fibers; these are white and are used for short-duration anaerobic exercise, typically lasting up to 5 minutes.<br />
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Type 1 fibers<br />
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These are slow twitch (also known as slow oxidative) muscle fibres that are red in colour due to their large volume of myoglobin, they contain many mitochondria and produce low power contractions. Due to their relatively high level of mitochondria and relatively low power output, these muscle fibres are specialised for low intensity endurance exertion. They are capable of maintaining their power output for hours of exercise. This type of muscle fibres is commonly found in muscles that are used very often during the day, like our postural muscles for example. They are linked to large numbers of blood vessels which supply them with a large volume of oxygen, among many other essential molecules and nutrients. The reason that so much oxygen is needed is because type I fibres split ATP by an aerobic mechanism (hence the name slow oxidative fibre). Without an adequate oxygen supply, these fibres would be unable to produce energy. Endurance runners rely heavily on these muscle fibres as they are highly resistant to fatigue.<br />
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Type IIa fibers<br />
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These are fast twitch muscle fibers, though they are the slowest of the fast twitch fibers. They contract at around 5 times the speed of slow twitch fibers. They produce energy through oxidative processes just like the type I fibers, though they have less mitochondria and have a higher power output. They are also red due to a high myoglobin content. They contain many blood vessels to supply this oxygen need and are consequently resistant to fatigue, though not as much as the type I fibers. In many ways they can be considered to possess a mixture of both type I and type IIb muscle fiber characteristics. Their main storage fuels are glycogen and creatine phosphate. However, these muscle fibers are uncommon in humans, but through training it is possible to convert type IIb fibers into type IIa fibers. Training of any kind causes type IIa fibers to be formed in the body, due to their increased efficiency at generating energy.<br />
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Type IIx fibers<br />
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These are typically referred to as type IIb fibers as they were once indistinguishable and many people recognise them as being different. Type IIx fibers are present in humans the IIb fibers are present in other animals. The IIX muscle fibers are white due to a low myoglobin content and produce energy anaerobically, therefore they contain few blood vessels and few mitochondria. THeir main storage fuel is creatine phosphate though they also contain glycogen. They are extremely fast twitch and are also known as fast glycolytic fibers. A consequence of their high power output is that they fatigue rapidly and are also inefficient in producing energy. Whenever a person trains, these fibers are converted into IIa fibers, no matter what type of training is undergone. This is because the IIA fibers are more energy efficient and the human body favours efficiency over power. For this reason, even though these fibers are most useful in sprinters, the people with the higher type IIb fiber content in their muscles are those who do barely any exercise at all.<br />
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Myoglobin<br />
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Myoglobin is an intracellular oxygen storage protein that is found in both cardiac and skeletal muscle tissue, it is the protein that is responsible for the red colouration of these muscles. It has a capacity for one oxygen molecule (O2), equivalent to two oxygen atoms. It is rare to find myoglobin in the blood stream of humans and this is typically an indicator of muscular damage. As myoglobin has a high affinity for oxygen, it is used by muscles in times of oxygen deprivation. This is because the myoglobin binds to oxygen when there are low concentrations of oxygen and only dissociates when these concentrations become very low. This means that only when there is extremely little oxygen contained within the muscles, will the myoglobin release the oxygen bound to it. Consequently, myoglobin is very beneficial during intense exercise and breath-holding.<br />
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Haemoglobin<br />
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This is an oxygen transport protein that is primarily found in red blood cells. When it is bound to oxygen molecules it has 2 forms. The first form is a tense (T) form and the second is a relaxed (R) form. The tense form is the one which is most likely to give up its oxygen to surrounding cells. The form of haemoglobin when bound to oxygen (called oxyhaemoglobin) is dependent upon the environment in which the protein finds itself. An environment contained a high concentration of carbon dioxide, low concentration of oxygen and low pH favours the tense form and conversely a low concentration of carbon dioxide, high concentration of oxygen and high pH favours the relaxed form. The tense form of oxyhaemoglobin has a lower affinity for oxygen and so releases it much more readily. This is of great benefit for the body when red blood cells pass by respiring tissue. As the tissue is using up all of the surrounding oxygen, releasing carbon dioxide, and this carbon dioxide subsequently forms carbonic acid (which lowers the pH), it follows that the oxyhaemoglobin is much more likely to dissociate from its oxygen molecules and therefore supply the tissue with oxygen and allow it to continue exerting itself for longer periods of time.<br />
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Bohr Effect<br />
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The essence of the Bohr effect is that as pH decreases and the concentration of carbon dioxide increases, the affinity of haemoglobin for oxygen decreases, under such conditions oxyhaemoglobin dissociates from its oxygen more readily. Respiring tissue releases elevated levels of carbon dioxide which are converted by carbonic anhydrase (an enzyme present in red blood cells) into carbonic acid. This acid lowers the pH of the blood. These effects compound each other to improve the oxygenation of respiring tissue. When we breathe out too much carbon dioxide, either through rapid or too-high volume-per-minute breathing, we deplete our bodies of carbon dioxide and this means that the haemoglobin in our blood remains attached to its oxygen and system-wide hypoxia may result. This happens most often when we are stressed and is most noticeable due to its associated light-headedness.<br />
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Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-29591665571858125042013-06-02T12:29:00.002-07:002013-06-02T12:29:24.479-07:00Everything I Know: BreathingIf you can't be bothered reading everything below, here's the stuff that helps you: breathe through your nose all the time and make sure you're breathing into the lower portion of your lungs. Remember that the slower you breathe the more carbon dioxide builds up and that carbon dioxide is not a waste gas, it is very useful within your body but needs to be maintained at a certain level (not causing discomfort unless you are deliberately trying to adapt to different carbon dioxide levels, such as in Buteyko breathing).<br />
<br />
How to Breathe efficiently<br />
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This will help you specifically in dealing with stress but it has many applications and should be done constantly. The instruction to breathe in for 4 seconds and out for much longer is specifically an anti-stress tool. If you did this all the time you would more than likely become very tired, however, it is worth bearing in mind and cultivating it as a skill.<br />
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Close your mouth and press your tongue against the back of your two front teeth, breathe entirely through your nose. Make sure that you are breathing into the lower portion of your lungs. To check that you are doing this correctly, place the palm of your left hand on your belly button and your right hand on your chest. As you breathe in, notice which hand moves most. Ideally, your left hand should be pushed out by your inhale and your right hand should barely move, if at all. This should be how you should be breathing in all circumstances, apart from real danger (being chased by a lion for example). If you have a panic attack, probably the fastest way to stop the panic is by changing to this style of breathing. To get the best anti-stress results from breathing you should aim to breathe in for around 4 seconds and then breathe out for as long as is comfortable. In general, inhalations stimulate the sympathetic nervous system while exhalations stimulate the parasympathetic nervous system. Therefore, if your exhalations are longer than your inhalations you will feel much calmer. If you practise this you can get to a point where you will breathe in for 4 seconds and out for over 20 seconds. As you do this you'll notice that all of the muscles in your body become naturally inclined to relax.<br />
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Diaphragmatic breathing:<br />
<br />
It is important to breathe into the diaphragm as this is where the highest proportion of blood vessels are within the lungs. It has been shown that the upper 7% of your lungs will only take in 4 ml of oxygen per minute whereas the lower 13% of your lungs will take in around 60 ml per minute. Also, using diaphragmatic breathing requires so much less energy to perform that it requires less than 5% of total oxygen intake. If you are over-breathing the energy requirement goes up massively, when volunteers were told to hyperventilate on purpose they used up 30% of their oxygen intake just to breathe in this way. So by breathing into the diaphragm, you not only take up a significantly larger volume of oxygen into your blood, but you also reduce the amount of oxygen (and energy) that you waste in performing the breathing itself.<br />
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Nasal breathing:<br />
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The nose is the narrowest place in the respiratory tract, it creates a bottleneck that results in airflow being restricted before it travels into the lungs. Compared to the mouth, it requires 1.5 times the amount of energy to pull the same volume of air through the nose.<br />
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Within the nasal cavity are bony projections called turbinates They heat and humidify air that is drawn through the nose and into the lungs. This reduces the damage that air causes to the lungs. The nose is also useful in breathing because it filters the air that is drawn into it. This takes place because there are many small hairs on the inside of the nose. This means that we take in less bacteria every time we breathe and consequently, our immune systems are less likely to become overworked. It is estimated that when these particles are caught in the nose hairs and/or mucus within the nose, that they are removed from the body within 15 minutes. However, if they travelled to the lungs they would take a few months to remove. Every time you breathe through your mouth you send these particles to your lungs and increase your chance of having a lung infection.<br />
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It is said that while breathing through your nose, if you are breathing through the right nostril you will be more inclined towards energetic pursuits, or those involving aggression. Conversely, breathing through the left nostril is associated with feelings of calm and introspection. Over the course of a day, the airflow between the nostrils will change of its own accord. You may wake up, for example, breathing through the left nostril and by midday realise that there is more air coming out of your right nostril.<br />
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In a study in which volunteers were subjected to a stress test, with some participants breathing through their mouth and the others through their nose, those who breathed nasally experienced brain wave activity that indicated greater relaxation.<br />
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Nitric oxide is also present in the nose and the slowing of air as it enter the nasal cavity allows nitric oxide to mix with the incoming air. This causes nitric oxide to be taken into the lungs where it dilates the blood vessels (bronchodilation). This allows significantly more oxygen to be taken in by these blood vessels and is very beneficial to the overall health of the organism.<br />
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Breathing through the nose is also beneficial in that it forces our breathing to slow down and as a result, our bodies follow suit. This helps us to reduce stress and think more clearly.<br />
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<br />
Nitric Oxide:<br />
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Nitric oxide (NO) is secreted into the nasal passages and is inhaled through the nose. It is effective in dilating blood vessels and also aids the lungs in the uptake of oxygen. it is produced in the walls of blood vessels and is required for the optimum functioning of every organ in the body.<br />
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Due to its vasodilatory effects, NO is useful in reducing blood pressure, increasing blood flow and treating heart-related diseases (cardiovascular diseases). This is also a reason why it is used in viagra.<br />
<br />
In the cardiovascular system, NO reduces artery-clogging plaque from forming. In the immune system, it helps fight off infections and cancer cells. In the nervous system it helps brain cells communicate properly.<br />
<br />
Its benefits include:<br />
<br />
- Vasodilation / increased blood flow to tissue / reduced blood pressure<br />
- Protecting the heart during heart attacks<br />
- Boosting brain power / cognitive functioning<br />
- Regulating digestion / relaxes the smooth muscles in the gastrointestinal tract<br />
- Improving the immune system<br />
- Re-building muscles after exercise<br />
- Improved sexual functioning<br />
- Aiding the liver and pancreas work more efficiently<br />
<br />
It is produced during exercise and regulates contractility of cardiac muscle, as well as reducing heart rate.<br />
<br />
However, as with all things in the body, nitric oxide must be produced in moderate amounts as it is a free radical, capable of damaging both pathogens and healthy cells alike.<br />
<br />
<br />
<br />
Carbon dioxide:<br />
<br />
Carbon dioxide is commonly referred to as a 'waste gas' from respiration. I feel that this is highly disrespectful to carbon dioxide. Your body requires a delicate balance of carbon dioxide, generally within 35 and 45 mmHg (millimetres of mercury at sea level, a pressure measurement) within the blood. If you breathe too quickly you approach the lower end of this scale and feel dizzy and if you breathe too slowly you approach the upper end of this scale and feel breathless. Most people need around 40 mmHg or above, to function normally. Below this your cells aren't getting adequate oxygen. The reason for this is illustrated by the Bohr effect. Without going into too much detail, the essence of this is that your blood cells offload their oxygen (this is desirable) around cells that are producing more carbon dioxide. Hence, if you breathe too rapidly you deplete your body of carbon dioxide and the blood cells continue to carry oxygen around the body without giving it to cells and tissues that require it. The result of hyperventilation is an impaired ability to think, among many other signs. This is primarily because the brain is suffering from oxygen deprivation (even though you are breathing rapidly and getting a lot of oxygen into the body), because your level of carbon dioxide is inadequate.<br />
<br />
<br />
Role of CO2 in oxygen transport<br />
<br />
Cells that are respiring more actively than others will release a lot more carbon dioxide into their external environment. This causes the dilation of blood vessels and subsequently means that more blood is able to come near tissue that has a higher metabolic rate. When the red blood cells that are carrying oxygen come into contact with this carbon dioxide they are more likely to release their oxygen. It also means that more glucose can be given to these same tissues.<br />
When carbon dioxide increases in the blood it is converted into carbonic acid, causing a drop in the pH of the blood. This increase in acidity is what primarily results in oxygen being deposited by the red blood cells. Conversely, lower levels of carbon dioxide cause less carbonic acid to form and so less oxygen is dissociated from haemoglobin into the respiring tissue.<br />
Thus, when we hyperventilate, we remove carbon dioxide from our bodies before it has the chance to form carbonic acid. The result is widespread hypoxia. Despite taking in much larger volumes of oxygen, this oxygen is not effectively utilised by the body. Also, this loss of carbon dioxide causes our blood vessels to constrict which means that their pressure is increased and red blood cells travel faster through them, further reducing their capability to give up oxygen. The result of this loss of acidity is called alkalosis, a reduction of hydrogen ions. This actually causes increased excitation of cells, e.g. neurons in the brain, and increases their oxygen demand. This can be considered a compensatory response in order to increase the carbon dioxide concentration within the body. However, it is worth noting that by overbreathing due to stress (over-excitability), you actually cause increased excitation and therefore increased stress over the long-term.<br />
The effects of hypocapnia-induced hypoxia are compounded by hypoglycaemia. Due to the constriction of blood vessels mentioned earlier, the blood cells cannot adequately transport glucose to respiring tissue either. The effects of both of these deficits is particularly noticeable in the brain. People who routinely hyperventilate will feel drained, more anxious, more irritable, are more likely to suffer from insomnia and feelings of low-self esteem, vulnerability, being overwhelmed and panic. Fortunately, this particular problem is easily remedied by correct breathing.<br />
<br />
Here is a study showing that taping the mouth can increase the end-tidal carbon dioxide in humans. This suggests that there is a higher concentration of carbon dioxide within the blood as well:<br />
<br />
http://www.sciencedirect.com/science/article/pii/S0031940606001921<br />
<br />
<br />
In order to understand why correct breathing doesn't come naturally to many of us we need to consider the type of lifestyle that we all live. It is primarily one of emotionally suppression and stress, both of which cause us to tense our stomach muscles and breathe into our chest. This is a manifestation of the body's fight or flight response. I think a more illustrative way of thinking of the fight or flight responses are to consider them as being a response to Anticipated Exertion. This way it becomes easier to understand why our bodies react in the way that they do. For example, if we were to undergo physical activity then our cells would greatly increase their carbon dioxide production. If our body anticipates that we will undergo physical activity then it naturally begins to breathe in a way that causes this carbon dioxide to be expelled. The problem occurs when our stressors are imaginary and we stay still. This causes us to lose carbon dioxide without producing more of it. The result is hyperventilation and strangely, increased stress.<br />
<br />
Slow breathing<br />
<br />
Through looking at various biofeedback techniques related to breathing (such as breathing while connected to blood pressure and heart rate monitors) I have come up with the following information:<br />
<br />
For most people, breathing at 10 or under breaths per minute will activate the parasympathetic nervous system (a branch of the nervous system which calms us down and lets us enter a state of rest and repair). Brain waves are affected too, it has been shown via biofeedback that slow, diaphragmatic breathing increases alpha waves in the brain which are associated with a relaxed yet alert state of mind.<br />
<br />
This form of breathing also stimulates the vagus nerve which in turn inhibits inflammation, suggesting that correct breathing reduces inflammation and that improper breathing may exacerbate it. This is significant as inflammatory disease include arthritis, colitis, ischemia, and heart attacks. Negative thinking can also trigger inflammation which may progress to depression. Therefore, breathing exercises which reduce stress and inflammation could be useful in combating depression.<br />
<br />
Slow, diaphragmatic breathing also increases heart-rate variability, if you are stressed your heart rate will remain inside a strict boundary of around 10 beats per minute. For example, it may vary between 75 and 85 beats per minute. If you breathe more slowly this variability increases, a sign of relaxation. In some studies it has been shown that breathing 5 to 7 times per minute can increase heart-rate variability up to 35 beats per minute. This means that your heart rate may go up to 95 bpm while inhaling and drop down to 60 bpm while exhaling. Generally, the larger the heart-rate variability, the greater the effects of relaxation from the exercises.<br />
<br />
It can also dampen pain perception too, in a study where both healthy individuals and those suffering from fibromyalgia were subjected to heat pulses on their hands, it was found that a reduced breathing rate was effective in reducing pain perception for all of the healthy volunteers, although only some of the fibromyalgia sufferers. Both groups were given the heat pulses when first breathing at a normal respiratory rate, and then following this, they breathed at 50% of the previous rate. The participants which had fibromyalgia only reported a decrease in pain perception if they also felt positive affect. Positive affect refers to an elevation in their mood, for example, feeling more happy / content / relaxed.<br />
<br />
<br />
Hyperventilation<br />
<br />
Hyperventilation and overbreathing essentially mean the same thing though hyperventilation is used more in medical and clinical diagnoses. They refer to a state of breathing that is faster or deeper or both in comparison to necessity. Breathing faster and deeper in response to exercise is not hyperventilation as the body is producing more CO2 and so the increased oxygen intake and CO2 removal is necessary. A measure of hyperventilation is 'minute ventilation' and refers to the volume of air that is breathed either in or out during a one minute period.<br />
<br />
Overbreathing refers to the excessive removal of carbon dioxide leading to hypocapnia (lack of CO2). This can occur through chest breathing or diaphragmatic breathing. While diaphragmatic breathing is generally considered as the healthy option for breathing mechanics, it is not immune to the same detrimental effects of chest breathing.<br />
<br />
When we are exercising, stressed or in some way aroused we are more likely to breathe using our chest. This is important because the way in which we breathe is highly influential towards our mood, digestion and the function of our brain and nervous system. When we are stressed but not increasing our physical movement (through exercise), we breathe using our chests in more rapid, shallow breaths. This causes more oxygen to be taken into the body, but this can only be absorbed if carbon dioxide levels are adequate. This is an anticipatory response; because our bodies are programmed to believe that if we are stressed it is because of some sort of danger or other motivation to bring about physical movement (which would increase oxygen demand in respiring tissue and consequently cause more carbon dioxide to be given out by those tissues) this means that we will automatically begin taking in more oxygen. However, this can paradoxically lead to hypoxia, the deficiency of oxygen. Our blood cells release oxygen much more readily into tissue that has higher metabolic activity (and therefore releasing more carbon dioxide). If we take in more oxygen but our cells are not respiring to an extent that creates adequate carbon dioxide to be released, then this oxygen binds to red blood cells and doesn't let go. No matter how much oxygen you have in your blood, if it doesn't want to leave your blood cells and enter your tissue, it is not beneficial and can even be harmful to you.<br />
<br />
<br />
Chronic hyperventilation<br />
<br />
When chronic hyperventilation occurs the body has a number of responses. Red blood cell production increases in an effort to distribute more oxygen to the capillaries. This causes the blood to thicken and consequently the heart must beat faster in order to pump this extra blood around the body. This increased strain causes physical and mental stress within you, leading to chronic low levels of anxiety. This anxiety causes your oxygen demand to further increase and your breathing to become faster and shallower. This leads to the further removal of CO2 which further diminishes your ability to absorb the oxygen which you now need more than ever. This is a major cause of stress and leads to many disruptions in general life contentment, mood and health as will be covered later. Your brain itself takes in around 20% of your total oxygen intake. When oxygen availability to the whole body drops due to inappropriate breathing, your brain experiences this and the many detrimental effects just like the rest of the body. This can lead to a decrease in serotonin and increase in cortisol (stress hormone), which causes the cycle to continue and worsen. This effect on the brain is particular noticeable to the hippocampus (a primary memory area of the brain) which is sensitive to both oxygen deprivation and higher cortisol levels.<br />
<br />
Thoracic breathing is generally believed to stem from emotional suppression. In our Western culture it is usually encouraged that we act as though stressful situations don't bother us. This can cause us to either hold our breath or breathe irregularly which contributes to the effect created by the situation itself.<br />
<br />
Diaphragmatic is considered to be more healthy because many small blood vessels which are instrumental in carrying oxygen to blood, reside here. With thoracic breathing these blood vessels never receive a full share of oxygenated air. This can result in shortness of breath and anxious feelings.<br />
<br />
Breathing is perhaps the most important homeostatic mechanism in the human body and its purpose is to ensure adequate cellular oxygenation. The average human breathes between 12-20 breaths per minute, equating to 17,280 to 28,800 times per day, so if the incorrect mechanism is repeated over and over again each day it is easy to see that it will have repercussions. Thankfully, the ability of humans to take voluntary control of breathing means that we can correct our breathing mechanisms if they are causing problems with our health.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-88356944088259461732013-06-02T12:27:00.002-07:002013-06-02T12:27:29.238-07:00Everything I Know: MagnesiumHow this post benefits you: If you have a magnesium deficiency or are under a lot of stress you may find it beneficial to take a magnesium supplement or consume more magnesium-rich food. From my research the best magnesium supplements are; magnesium chloride (spray and applied to skin), magnesium sulphate (Epsom salt bath), and magnesium glycinate (oral ingestion).<br />
<br />
Under normal circumstances, in a healthy individual, there is more magnesium contained within the cells than calcium. The stress response causes this to change. Magnesium leaves the cells and calcium enters. Unfortunately for modern times, the stress response is triggered by psychological stress as well as physical stress. This means that each time a person worries about the bills or anything that provokes stress, their bodies are excreting magnesium. The significance of this is that magnesium is needed to down-regulate the stress response and its removal from the body causes hypersensitivity to stress. The same also occurs when magnesium intake is either low or inadequate in relation to calcium intake. Our ancestors grew up in a time when magnesium-rich foods were plentiful, with excess magnesium having to be excreted, and calcium having to be stored. Nowadays, however, the opposite is true. The problem is that our bodies haven't changed to storing magnesium and excreting excess calcium efficiently. The result for many people is a deficiency of magnesium and also a possible build-up of calcium. This makes us much more reactive to stress and lowers the threshold for which the stress response occurs. Therefore, it is of great importance that those suffering from anxiety and depression, and every other ailment that would benefit from this, replenish their magnesium stores in order to increase this threshold and subsequently alleviate their anxiety. However, as discussed above, the stress response removes magnesium from the body and so those under heavy stress must consume more magnesium than is given in the RDA (400 mg per day) although many sources say that this is too low and that the true number should be at least 800 mg per day for healthy individuals.<br />
<br />
I actually had magnesium citrate supplements in my room for about half a year but never got round to taking them because I didn't know how good they were. Recently I somehow realised that they are very good for getting to sleep and have been taking them (450 mg of magnesium citrate per day) for a few days now, it definitely helps. Magnesium has many uses in the body, and a deficiency in magnesium is detrimental to our health, despite this, an estimated 68% of american adults don't consume the minimum RDA (recommended daily allowance) of elemental magnesium per day (around 400 mg per day). According to the national institute of health, magnesium citrate contains 16% of elemental magnesium by mass, meaning that my 450 mg dose contains 72 mg of elemental magnesium, however, magnesium is also obtained from various food sources such as many vegetables.<br />
<br />
I'll attempt to list some of the ailments that magnesium treats but there are really far too many to get them all:<br />
<br />
- Anxiety<br />
- Chronic fatigue<br />
- Stress<br />
- Depression<br />
- High blood pressure<br />
- Atherosclerosis<br />
- Inflammation<br />
- Arthritis<br />
- Osteoporosis<br />
- Muscle twitches and tics<br />
- ADHD<br />
- some people with autism<br />
- PMS<br />
- type 2 diabetes<br />
- Fibromyalgia (in a test using magnesium malic acid)<br />
- Insomnia (it is a sedative)<br />
- And perhaps HIV (some studies have shown that 30-65% of HIV sufferers are magnesium deficient).<br />
<br />
Stress causes magnesium to be removed from cells and be excreted from the body. However, it is not enough to simply bombard your body with magnesium in the hopes of fixing these and other ailments because magnesium interacts intimately with calcium. For this reason some recommend to take a 1:1 calcium to magnesium ratio. Calcium generally causes muscular contraction while magnesium inhibits contraction and is therefore a potent relaxer of both body and mind. These minerals compete for absorption (I have heard this claim but have found no evidence for it) so if you take too much of one, the absorption of the other is inhibited and both are necessary for healthy functioning.<br />
<br />
Finland used to have the highest recorded incidence of heart attacks in middle-aged men out of any other country in the world until they increased magnesium intake using magnesium salt substitutes. It is estimated that before this measure was put in place, their calcium to magnesium ratio was 4:1. Now their death rate from heart-related issues is ranked 10th in the world.<br />
<br />
Magnesium is a cofactor for over 300 enzymes and so is very useful in many different reactions which may help to explain why its deficiency can cause so many diseases.<br />
<br />
If you're reading this; magnesium is not just some random element that sort-of helps you, it's a huge deal.<br />
<br />
Magnesium and depression:<br />
<br />
http://www.ncbi.nlm.nih.gov/pubmed/16542786 - "Case histories are presented showing rapid recovery (less than 7 days) from major depression using 125-300 mg of magnesium (as glycinate and taurinate) with each meal and at bedtime."<br />
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http://www.ncbi.nlm.nih.gov/pubmed/19944540 - "we further hypothesize that magnesium treatment will be found beneficial for nearly all depressives"<br />
<br />
<br />
So, obviously I had to read through forum posts on magnesium supplementation to see if this is beneficial to people that have used it. There have been numerous studies, I'll do research into them at a later stage but the vast majority of them are positive, off the top of my head that is. Without further ado, the information I collected from forums:<br />
<br />
There were a total of 60 'reports' (I googled "magnesium forum" and clicked on everything and went through all the pages of each forum thread and did this for the first 10 pages of google search results).<br />
<br />
There were 9 negative reports, 6 reports showing insignificant change and 45 positive (showing significant positive change) reports.<br />
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As I wasn't searching for any particular magnesium supplement there is an assortment of results.<br />
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In the 9 negative reports the breakdown of supplementation went as follows:<br />
<br />
- 4 unspecified (single magnesium source)<br />
- 2 magnesium aspartate<br />
- 1 magnesium oxide<br />
- 1 magnesium malate<br />
- 1 person used many magnesium supplements with negative effects each time<br />
<br />
In the 6 insignificant reports:<br />
<br />
- 3 magnesium oxide<br />
- 2 magnesium citrate<br />
- 1 magnesium taurate<br />
<br />
In the 45 positive reports:<br />
<br />
- 16 unspecified<br />
- 8 magnesium oil (magnesium chloride)<br />
- 5 magnesium citrate<br />
- 6 magnesium glycinate<br />
- 2 magnesium taurate<br />
- 3 magnesium malate<br />
- 3 magnesium threonate<br />
- 1 Epsom salts (magnesium sulphate)<br />
and<br />
- 1 brand product that combined magnesium aspartate, citrate and orotate. The person who used this had social anxiety and said it had "done wonders for my anxiety. It's practically gone."<br />
<br />
Magnesium chloride<br />
<br />
<br />
Magnesium chloride (MgCl2) is considered by many experts to be one of the best, if not the best magnesium supplement. It is totally ionized at a pH range of around 2 to 7.4 which means that it is very well absorbed. There are three methods for absorption, oral, injection and transdermal (through the skin). While injections of magnesium chloride are typically only given by doctors to those suffering from moderate to severe hypomagnesemia, the other two methods are much more common. When taken orally, the magnesium chloride will aid the production of hydrochloric acid which in turn helps to absorb even more of the magnesium. However, higher doses taken orally increase the probability of causing diarrhoea and this reduces the length of time that the supplement spends within the gastrointestinal tract, thus reducing its absorption. Magnesium tends to stay in the intestines for around 12 hours, this would be massively decreased if diarrhoea were induced, causing drastic impairment to its assimilation. Typical side effects of oral magnesium supplementation may occur with oral magnesium chloride; difficulty breathing, muscular weakness, hypo-tension etc. but this is less common with the transdermal method of absorption. Topical application of magnesium chloride also has a higher absorption rate. The magnesium is fully ionized at the skin's pH of around 4.5 to 6. This improves its absorption greatly. This method also bypasses the problem of diarrhoea.<br />
<br />
http://www.ancient-minerals.com/magnesium-chloride/<br />
<br />
http://www.ancient-minerals.com/transdermal-magnesium/#studies<br />
<br />
Magnesium chloride is also a powerful stimulant of the immune system and studies have shown that when its levels in the blood are elevated, phagocytosis (ingestion of microbes by phagocytes (an immune cell)) is greatly increased, by up to 333%.<br />
<br />
Press ctrl+f and type in: 333 percent http://www.mgwater.com/rod04.shtml<br />
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I found 8 reports on forums of people using magnesium chloride, all of them were positive. The first had had ligament pain in their foot for 1.5 years which is now gone,and they have noticed much faster exercise recovery. Another used it for restless legs and said it "reduced/removed" these feelings. Someone else said it removed their depression. One woman gives it to her husband when he suffers from panic attacks, and it "works within minutes". A chronic migraine sufferer experienced significantly reduced symptoms. Another uses it to help back pain. One more person said it has a noticeable calming effect and the last person said it gives "much relief", referring to their anxiety.<br />
<br />
Based on this research I would say that magnesium chloride is the most effective magnesium supplement, especially when absorbed through the skin instead of ingested orally, 7 of these people said they used magnesium oil which I take to mean that it was applied topically as otherwise it would be a magnesium chloride tablet or pill.<br />
<br />
Magnesium sulphate<br />
<br />
<br />
Magnesium sulphate (MgSO4) is the form of magnesium that people are referring to when they mention Epsom salts. This is an additive to bath water and seems to be best absorbed through the skin in these baths as opposed to being ingested orally or taken in by injection. While soaking in Epsom salts has few complications, the other two methods have some rather common side effects. When magnesium sulphate is taken orally or injected the following symptoms can arise; difficulty breathing (as magnesium sulphate is a respiratory depressant, this means that it can cause shallow breathing or shortness of breath), extreme muscular weakness (some people have difficulty standing or walking), flushing, hypotension (in some people the blood pressure can become so low that the person suffers from light-headedness or even fainting). Therefore, soaking this salt would be my personal preference for its intake. Typically, people will use around 10 grams of Epsom salts for every litre of bath water. For a standard bath of around 60 litres of water, this would require around 500 g to 600 g of Epsom salts. This form of bath can be used to treat epilepsy, magnesium deficiency, anxiety, depression, inflammation, pain, migraines, pre-eclampsia and toxicity. The sulphates within the salt can remove toxins and impurities from the body and allow them to dissolve in the bath. For this reason it is suggested that people bathe for around 10 minutes to avoid reabsorbing these toxins. An added benefit for baths in general is to induce vasodilation and improve blood flow to the extremities and vital organs.<br />
<br />
The following link is to a study testing the effects of magnesium sulphate bathing over the course of 7 days.<br />
<br />
http://george-eby-research.com/html/absorption_of_magnesium_sulfate.pdf<br />
<br />
I only found one person that used Epsom salts as their magnesium supplement (positive report) but they said that they felt significantly relaxed afterwords.<br />
<br />
Magnesium Threonate<br />
<br />
Magnesium threonate (Mg(C4H7O5)2), this compound was developed at the Massachusetts Institute of Technology (MIT) and is available as the product "Magtein". This is believed to be the only magnesium compound that readily crosses the blood-brain barrier and hence improves magnesium concentration within the brain. This has been shown in rats to improve both short and long-term memory. After 24 days of magnesium threonate supplementation it was shown that rats had approximately 15% extra magnesium in their brains compared to the start of the trial. One of its creators, Dr Liu, says that he and his friends have been using Magtein and have increased the level of magnesium in their bodies by 50%. As of now, around 100,000 people in the US are currently taking this supplement. I have little more to say about it however as there are a lack of human trials. This considered though, it does seem to be beneficial and if you would like to learn more about it here are two websites:<br />
<br />
http://www.nature.com/news/testing-magnesium-s-brain-boosting-effects-1.11665<br />
<br />
http://www.magtein.com/<br />
<br />
I found 3 reports for magnesium threonate, all of which were positive.<br />
<br />
The first person said that during the first week of supplementation they experienced euphoria and after this week the euphoria decreased but they still had an elevated mood and increased mental alertness. They also noticed much more vivid and frequent dreaming. The second person noticed similar effects: elevated mood, more dreams, better sleep and also reduced fibromyalgia-related pain.The last person effectively used the supplement to stop cramping.<br />
<br />
Magnesium Glycinate<br />
<br />
Magnesium glycinate (C4H8MgN2O4) is considered to be a useful combination. It is magnesium bonded to the amino acid glycine. This particular chelate is believed to have a very high bioavailability (some sources place it at 5 times the bioavailability of magnesium oxide), also it apparently has less of an effect upon the digestive system. Some magnesium supplements like magnesium oxide and citrate can cause constipation or diarrhoea whereas glycinate is less likely to cause these upsets. While magnesium would normally passively diffuse (a relatively slow process requiring no energy usage), binding it to glycine in this way allows intestinal cells to actively take in the chelate (a faster process but which requires energy expenditure). This means that more of the magnesium is absorbed. Glycine is also an inhibitory neurotransmitter under most circumstances but it also functions as a co-agonist (works with another chemical to bind to a cellular receptor and trigger a response from the affected cell) along with glutamate (a highly stimulating neurotransmitter) to activate certain types of NMDA receptors which are excitatory. Therefore, while moderate doses can cause relaxation (around 3,000 mg is suggested by Wikipedia to improve sleep quality), extremely high doses can cause hyper-excitability by activating this receptor. The level of glycine required for this would be huge however, and very unlikely to occur unless intentional. In rats a dosage of around 4,000 mg is usually fatal, it would be significantly larger for a fully grown human though. Glycine may also help to remove mercury from the body.<br />
<br />
I found 6 positive reports for magnesium glycinate supplementation.<br />
<br />
The first said it improved mood and the other five said it caused significant relaxation.<br />
<br />
Magnesium Taurate<br />
<br />
<br />
Magnesium Taurate (C4H12N2O6S2Mg) is another chelated form of magnesium supplement. It is a complex of magnesium and taurine. Taurine may have anxiolytic (anxiety-splitting) properties but there are mixed results on this. In contrast to magnesium, whose concetrations fall when a person is under stress, taurine concentration actually increases (possible evidence for anxiogenic effects). However, taurine has been know to cause cells to retain potassium and magnesium while regulating sodium and calcium intake (possible evidence for anxiolytic effects). It could be that taurine increases simply to reduce the effects of stress but so far this is just speculation. Anyway, here are the positive studies that I found:<br />
<br />
www.karger.com/Article/FullText/107687<br />
<br />
www.ncbi.nlm.nih.gov/pubmed/16540157<br />
<br />
These show specific anti-anxiety improvements while the following study shows a possible suppression of the sympathetic nervous system due to taurine's effects. An overactive sympathetic nervous system could lead to irritability, and increased susceptibility, severity, and duration of anxiety and anger.<br />
<br />
www.ncbi.nlm.nih.gov/pubmed/8915402<br />
<br />
This next study shows that taurine has some anti-anxiety properties in mice but it seems limited, this study only lasted for 7 days though:<br />
<br />
www.ncbi.nlm.nih.gov/pubmed/15240184<br />
<br />
However, when taurine intake method was assessed it was found that chronic oral supplementation may be anxiogenic (cause anxiety), whereas acute injections where anxiolytic:<br />
<br />
http://www.researchgate.net/publication/232283013_Effects_of_taurine_on_anxiety-like_and_locomotor_behavior_of_mice<br />
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Taurine also has many other uses, it can cause weight loss, lowering of cholesterol, prevention of oxidative stress caused by exercise, preventing congestive heart failure, and is used by some as a dietary supplement in the treatment of epilepsy.<br />
<br />
I found 2 positive and 1 insignificant self-report of magnesium taurate supplementation.<br />
<br />
In the insignificant report the person used magnesium taurate for 5 days but felt no different.<br />
<br />
In the positive reports, one person used it for 2 days and had noticeable reductions in depression and anxiety and reported feeling much more relaxed. The other said it noticeably relieved stress.<br />
<br />
Magnesium Citrate<br />
<br />
<br />
Magnesium citrate (C6H6MgO7) is magnesium attached to citric acid. This is a highly bioavailable type of magnesium supplement, one that allows your body to absorb relatively high quantities of magnesium. The magesium content in magnesium citrate varies from 11-16% and is at least 55% soluble (this is its solubility in water, but increases as pH is reduced, as it would be in the stomach), which greatly increases its absorption, though I came across so many different percentages of absorption that I am unsure which to believe. Citric acid is found in fruits like lemons and oranges, and is alkaline (has a pH above 7). Citric acid has many benefits: it functions as an anti-oxidant, removes excess calcium, prevents kidney stones (due to calcium removal and alkaline properties). However, side effects of citric acid supplementation include nausea, diarrhoea and abdominal pain and it may interact with drugs such as amphetamines or tetracyclines.<br />
<br />
On forums I found 2 insignificant and 5 positive self-reports of magnesium citrate supplementation.<br />
<br />
Of the insignificant reports, one person noticed slightly improved insomnia and the other noticed no change.<br />
<br />
In the positive reports; one person took 500mg of magnesium citrate each day for a week and said "I haven't felt this good in years." Another took it and noticed a significant increase in energy levels. Reduced fatigue, more restful sleep and better ability to cope with stress was noticed with another user. The last 2 used the supplement successfully for cramps.<br />
<br />
Magnesium Malate<br />
<br />
A study showing the beneficial effects of magnesium citrate on exercise tolerance in patients with coronary artery disease:<br />
http://www.ncbi.nlm.nih.gov/pubmed/12615252<br />
<br />
Another studying showing efficacious treatment of fibromyalgia with magnesium citrate, particularly in reducing self-reported depression:<br />
<br />
http://www.ncbi.nlm.nih.gov/pubmed/22271372<br />
<br />
<br />
Magnesium malate (C4H4MgO5) this is magnesium attached to malic acid. Malic acid is a compound that occurs naturally in fruits like apples and has no known serious side effects. It may cause cramping or bloating of the digestive tract but this is rare and not dangerous. For this reason it is considered to be a safe supplement to use. It has been particularly beneficial to those suffering from fibromyalgia and chronic fatigue syndrome. This is probably because malic acid is an essentital component in the Krebs cycle, a cycle which is necessary for the production of ATP and consequently energy in the body. Patients with fibromyalgia seem to benefit from both malic acid and magnesium alone and moreso when these are combined. Magnesium malate also binds to aluminium which is a toxic metal. Aluminium has been linked to memory loss, dementia and Alzheimer's.<br />
<br />
I found 1 negative report on malate and 3 positive.<br />
<br />
The person who reported negative effects said that magnesium malate caused heart palpitations.<br />
<br />
Of the positive reports, one had more relaxed muscles, found it easier to sleep and had less muscular pain. Another had diabetes and used it successfully to stop cramping. The last person used a high dose (1,200mg per day) for 6 months and claimed that it "got rid of fibromyalgic aches and pains, relaxed muscles and aided sleep."<br />
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There have been a few studies on fibromyalgia and magnesium malate (I couldn't find any studies on anything but fibromyalgia) but none have been proved conclusively, however, there does seem to enough evidence for its effectiveness in comparison to the risk (minimal and infrequent) to suggest that supplementation is worth trying.<br />
Source: http://informahealthcare.com/doi/abs/10.3109/13590849208997961<br />
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Magnesium Aspartate<br />
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Magnesium aspartate (C8H12MgN2O8), is believed to be a poor choice of magnesium supplement. This is because while magnesium is a relaxant of nerve cells, aspartate is actually an excitatory neurotransmitter (stimulates the firing of nerve cells). In large doses aspartate is toxic to neurons in that it can cause them to fire until they injure and/or kill themselves. In fact, magnesium and aspartate can be considered to have opposing effects. For this reason it is important that people are aware of aspartates effects, especially those who are magnesium deficient. People who fit this category are much more likely to be affected by aspartate, for example, those suffering from anxiety, depression, any kind of pain, any form of fatigue, or other ailment caused by chronic excitation.<br />
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I found 2 negative reports on magnesium aspartate:<br />
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In both of the negative reports the persons involved said that the supplement had caused depression, though one said it also alleviated their anxiety.<br />
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A study involving supplementation of magnesium aspartate showed no benefit to high blood pressure. This may be due to either magnesium not having an effect ton the patients or the aspartate's effects cancelling out the benefits of magnesium. However, it is difficult to tell, the only thing to take away is that magnesium aspartate did not help blood pressure in this study.<br />
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1416881/<br />
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In another study where magnesium aspartate was given to pregnant mothers, it was shown that this supplement was beneficial in reducing premature birth rates and improving birth weight. Disease was also reduced and side effects either didn't occur or weren't serious in the participants.<br />
Source: http://www.ncbi.nlm.nih.gov/pubmed/3063587<br />
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Magnesium Oxide<br />
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Magnesium oxide (MgO) has been shown to have a very low bio-availability, in one study this value was shown to be as low as 4%. This means that only 4% of the magnesium is absorbed by the living system, in this case, our bodies. Despite its 60% magnesium content by mass, inexpensive cost, and high availability on our planet, magnesium oxide is so poorly absorbed by the gastrointestinal tract that its main use is to act as a laxative.<br />
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This may help to explain the 4 results (1 negative and 3 insignificant) that I found with magnesium oxide.<br />
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In the negative report, magnesium oxide caused diarrhoea and no positive change.<br />
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In the insignificant reports it produced; a slight reduction of social anxiety, no noticeable effects, and no benefit.<br />
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There was a study in which 44 volunteers (8-14 year old healthy girls) with elemental magnesium intake of under 220mg per day participated in a study investigating magnesium's effect on hip bone and spinal lumbar mineral content. Magnesium oxide pills were taken twice per day (each pill containing 150mg of elemental magnesium) over the course of 12 months. 23 volunteers received placebo and 21 received the magnesium oxide. From results taken both during and at the end of the study it was determined that those receiving the magnesium oxide had slightly raised spinal lumbar bone mineral content. They also had significantly elevated bone mineral content in their hips.<br />
Source: 91/12/4866<br />
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Another study showing the beneficial effects of 9mg of magnesium oxide per kilogram of body weight (675mg of magnesium oxide for a 75kg person) on migraine sufferers presented evidence that magnesium oxide slightly reduces frequency of migraine attacks and significantly reduces the severity of them.<br />
Source: Headache. 2003 Jun:43(6):601-10Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-11470456749511453962013-06-02T12:23:00.002-07:002013-06-02T12:23:41.691-07:00Everything I Know: AnxietyWelcome to this post containing everything I know about anxiety. The reason that I have made this post is because when I was researching the Buteyko breathing and magnesium topics covered elsewhere on this blog, I came across many anxiety forums. It seemed that many of the people that were using both Buteyko and magnesium also had anxiety of some form. By going through these forums I came across a wealth of information. Eventually it got to the point where I would be looking up a particular magnesium supplement and I would find that the people on these forums were asking each other questions about other natural methods and treatments for anxiety that I had already come across and knew a fair amount about. Once I realised this I started to go to Youtube videos where people were talking about their anxiety and how it was affecting their lives, and I would try to tell them various things that I had picked up from the forums. However, no one ever responded. I eventually became so frustrated at the lack of response that I just stopped trying and decided to make this post instead. Here you will find everything I ever came across with regard to anxiety, with all of the medical studies I could find, with details of how people on forums responded to them and their relative safety and efficacy. If you try anything that I talk about here please comment below to tell me if it helped, made your condition worse, or had no effect. Also bear in mind that everybody is different, and something that worked for somebody else may not necessarily work for you.<br />
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- Breathing in general: breathe through your nose at all times and into your belly. Breathing slowly allows carbon dioxide to accumulate which is calming. Breathe only as slow as is comfortable, but still as slow as you can. When feeling stressed make a conscious effort to extend your exhales, many people find stress-relief from breathing in for 4 seconds and breathing out as slowly as possible until there is an air hunger. You will probably feel a lot less anxious if you breathe in for 4 seconds and out for, say 10 seconds. Remember: 1) always breathe through your nose and 2) always breathe into your abdominal area.<br />
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- Buteyko breathing: this goes back to the time that I went through Buteyko forums to see if there were enough anecdotal reports to justify myself trying it as an experiment. What I found was that out of the 33 positive reports that I gathered, 14 of these were anxiety-related. You can find all the information you need about Buteyko breathing on the internet but caution is advised if you attempt this without a practitioner. Breathing is a very important part of living, and its easy to underestimate its importance and cause damage by trying to carry out this breathing method alone. I also advise never doing a maximum control pause (this has caused panic attacks in some people) and remember that the function of a normal control pause is for measurement and helping beginners get used to air hunger, it is not a necessary tool for adapting to this technique. I would rate Buteyko breathing as 4 out of 5. There was one negative report on Buteyko breathing in which a person said breath holding caused a panic attack. This is why I have made it clear that the maximum control pause and even the ordinary control pause aren't necessary. The others all said that Buteyko helped them, with some stating that this technique was a huge help in dealing with severe anxiety. I recommend this once you have done a little research on the importance of breathing. It has minimal chance of causing harm as long as you listen to your body. In my opinion you should only ever create a slight level of air hunger in order to adapt to this technique. Also, I do not believe that the theory behind this method is correct, i.e. that it raises carbon dioxide levels to the extent that its practitioners believe. My opinion is that it raises carbon dioxide significantly, but only to the extent that occurs when switching from mouth breathing to nose breathing. However, I stand by this method completely in saying that it is effective for both anxiety and asthma, though I presently don't know why.<br />
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For the following supplements, if you are considering taking them, make sure you do your own research into the side effects. There were too many for me to list each one's potential adverse effects. Make sure that if there is a potential danger to these supplements that you confirm with a medical professional that they are, in fact, safe. Take special care if you are pregnant. I have also added my own rating based upon the studies and anecdotes that I came across for each one, this is almost entirely subjective but I feel that it would help you in deciding which things to try, considering there are so many listed below.<br />
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Vitamin D: Came across a few people that used vitamin D to cure panic disorder, I didn't know this was possible. Safe doses are 3,000 to 4,000 IUs. I once came across a story from a scientist giving a lecture on vitamin D supplementation who said that vitamin D intoxication is hard to do, he spoke of a man who used a supplement where the manufacturers had forgotten to dilute the vitamin D. Once he had tested the supplement he found that the man had taken around 1,000,000 IUs of vitamin D per day. Source: http://www.youtube.com/watch?v=Cq1t9WqOD-0 (about 39:30 into this video_<br />
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- Niacinamide/Nicotinamide/Nicotinic acid amide: these terms all refer to the same thing, an amide version of the B vitamin niacin. Niacinamide differs from niacin in that supplementation with the former vitamin does not cause a flushing reaction. Some people notice profound lessening of anxiety immediately with niacinamide, others do not. Some sources say that it could take up to a month to feel the therapeutic benefits of niacinamide (I found that if people took a dose of 500 mg and it had no effect, they would take a higher dose of around 2 grams and if that didn't work, they would stop supplementing with niacinamide altogether). I am not sure if everyone with anxiety would benefit from niacinamide. If you are considering this supplement please check with a doctor beforehand and make sure that your liver is healthy. Niacinamide does not typically cause side effects in moderate doses; around 500 mg to 1,500 mg per day but it is better to check this with a medical health professional just in case. I rate niacinamide as being 4 out of 5. While it is unknown whether it is beneficial for everyone, those who had no alleviation of their symptoms didn't take it longer than around a week. Other people had complete removal of moderate to severe anxiety within this same timeframe. Tolerance seems to build slowly, over months.<br />
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- Tea: green (try decaffeinated as caffeine is a major contributor to anxiety), the theanine in green tea is a known anxiolytic (anxiety-splitting) agent. Alternatively, skip the tea and supplement with theanine alone. Other beneficial teas include; chamomile, valerian, and Linden, though I'm sure there are more.<br />
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- Chamomile: Based on what I've seen on chamomile it does seem to be an effective agent in reducing anxiety. However, take care if you have asthma, are pregnant, or are allergic to plants in the daisy family. Apart from this, chamomile is described as being one of the safest herbs to take. Low doses typically help anxiety while higher doses help you get to sleep. I rate Chamomile as being 2 out of 5. It is beneficial for mild and perhaps moderate anxiety but a tolerance does build up quite quickly to it (within a week or 2) and high doses can cause diarrhoea.<br />
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- Valerian: this is a herb that is generally regarded as being safe to use. Some say it has helped their anxiety though it doesn't seem to have much effect in treating severe anxiety. Fresh roots seem to have the greatest effect. I rate Valerian as being 3 out of 5. If you wish to try this, make sure you get fresh roots. Tolerance can build up within a couple of weeks.<br />
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- Theanine: this has effects as a neurotransmitter and while it is calming, it has a similar shape to an excitatory neurotransmitter; glutamate. However, theanine has a weak affinity for glutamate receptors in neurons, so it doesn't cause excitability in moderate doses. There is scientific evidence to show that theanine can reduce anticipatory anxiety and also stress when performing tasks while improving focus and helping patients with ADHD sleep. It seems that the only form of theanine supplementation that is effective is called "suntheanine". This appears to be effective in reducing anxiety for most, but not all people, though a moderate tolerance to it is quickly induced. This supplement may cause headaches. I rate this as being 2 out of 5. Despite having numerous studies supporting its beneficial effects, this supplement induces a rather rapid tolerance (within 1 or 2 weeks), may cause headaches, and its best effect is more to increase concentration than to alleviate anxiety. It may be a useful additive that could be taken a few times per week but isn't overly effective by itself.<br />
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- Omega-3: based on medical studies and forum reports where people supplemented with omega-3; I think that this would be a worthwhile supplement for anxiety and also depression. Everyone that I came across (and also in the studies) used around 3 grams of omega-3 supplements per day to alleviate depression and anxiety. Below this, mental health wasn't improved. I rate this as being 3 out of 5. This is mostly for its lack of side effects. This could be a relatively safe additive and I at least haven't heard of any tolerance being built up.<br />
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- Magnesium: there was a study in which mice were deprived of magnesium from their diets and showed both depression and anxiety-like symptoms. I'll include this study at a later stage, right now I'm just firing out everything I know that could possibly help. Also, when I went through many forum posts on magnesium I found that probably around half of the people were using magnesium supplements for either relaxation or anxiety-related reasons. I rate magnesium as being 3 out of 5 for anxiety, although it could be a lot better than I realise. Studies have shown that when we are anxious we excrete extra magnesium as well as phosphorus. Therefore, those suffering from anxiety must consume more magnesium than an otherwise healthy individual.<br />
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- Glycine: this is an amino acid that also acts as an inhibitory neurotransmitter. Inhibitory neurotransmitters decrease the activity of neurons and can reduce anxiety. Glycine also acts as a co-agonist along with glutamate for NMDA receptors. Therefore, while moderate dosages of glycine can have a calming effect, too much can cause increased anxiety.<br />
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- Magnesium Glycinate: I felt that this was important enough to have its own section. Combining magnesium and glycine in this way allows the magnesium to be better absorbed within the body. It also provides anxiolytic properties from each component for added efficacy.<br />
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- Dairy products: if you have anxiety, cut down on these and see if it makes a difference, they contain high levels of calcium, a mineral that doubles as an excitatory neurotransmitter. If you have an excess of excitatory neurotransmitters, you can end up feeling anxiety for no reason. The chances are that you already gain enough calcium from your diet to avoid the necessity of supplementation, for those of you that are considering, or are already taking, calcium supplements.<br />
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- GABA: this is an amino acid that is also the most important inhibitory neurotransmitter within mammals. Increasing the level of GABA within the central nervous system can increase the amount of alpha waves that the brain produces. This causes a person to feel more relaxed yet alert. GABA's role as an inhibitory neurotransmitter is of critical importance to anxiety disorders. By increasing the amount of GABA, you decrease the amount of anxiety in people. Two of the main GABA supplements that I came across are called Phenibut and Picamilon. I personally consider these to be unsafe but I may be wrong. I suggest that if you consider GABA supplementation to be of possible benefit, then you should research both of these supplements rigorously and then speak to a medical professional about their safety. Make sure that if you do take them that you know their effects on the drugs that you may also be taking in conjunction with them. I noticed with Phenibut especially that anecdotal reports claim you can become tolerant to this if you use it more than 2-3 times per day and can experience withdrawal symptoms if you use it every day for only one week. Withdrawal symptoms can include severe anxiety and this supplement should be taken with caution. I rate GABA supplements as being 2 out of 5. They seem highly effective, but I am wary of their side effects and addictive nature. I wouldn't recommend these though they certainly do reduce anxiety.<br />
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- Kava-kava: this is made from the roots of a plant and is well known for its relaxing qualities. It can relieve anxiety, reduce pain, and help with sleeplessness. It seems to be used by a lot of people with anxiety who say it has noticeable relaxing effects. However, caution should be taken when using this drug as it may cause liver damage. For this reason it shouldn't be used in conjunction with alcohol. It also shouldn't be used with many prescription medications as it could adversely interact with these as well. From what I've seen and heard, the kava root powder or paste appear to be the best forms, taking these after consuming oily foods may improve their effectiveness. I found mixed results for people supplementing with kava, it seems to be a case of finding a very good source, though this is very difficult considering it was banned quite recently and manufacturers might take a while to invest into it again. I rate kava as 3 out of 5, just make sure that you buy it from a well-known company and check the reviews of the product to make sure that it is effective. Also, tolerance to this can build quickly so it shouldn't be taken everyday of the week.<br />
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- St. John's Wort: this is a herbal remedy that has been used for both depression and anxiety. In some studies it has been shown to be just as effective as prescription medication and more than placebos for people suffering from depression. However, care should be taken when combining St. John's Wort with SSRIs (selective serotonin re-uptake inhibitors) or serotonin-boosting medication as serotonin toxicity may result. The Mayoclinic considers St John's Wort to have "strong scientific evidence" for use in treating mild to moderate depressive disorders. However, it also states that there is unclear scientific evidence for its application for anxiety disorders. I rate St. John's Wort as 1 out of 5 for anxiety, there was no clear evidence, scientific or anecdotal, of its benefit for anxiety disorders. It may work however, but this is just my opinion.<br />
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- Passionflower: this is another herb that is considered to be quite safe. It seems to be of benefit to many people with anxiety and this is backed by scientific research although more studies are needed for proof. I recommend trying this once you are aware of the side effects and possible drug interactions. I rate passionflower as 3.5 out of 5. This is because some people used it to successfully reduce severe anxiety and it has a relatively low chance of side effects. Again, care should be taken to avoid building up a tolerance.<br />
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- Alcohol: I would suggest cutting down on alcohol if you have elevated anxiety. Using alcohol as a coping mechanism can lead to a dependency and alcohol addiction in itself is a major cause of anxiety. Also, even if you aren't taking it to such a huge extent, the hangovers can wear you out and this will definitely increase your anxiety.<br />
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- High glycemic foods (sugars): These can cause huge blood sugar spikes which can make your mind race and wander and isn't desirable for those suffering from anxiety. Also, the inevitable sugar crash can leave you feeling drained and lethargic.<br />
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Correct Breathing: (This breathing section is an extract from "Everything I Know: Breathing", and is covered more fully on that page.)<br />
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Close your mouth and press your tongue against the back of your two front teeth, breathe entirely through your nose. Make sure that you are breathing into the lower portion of your lungs. To check that you are doing this correctly, place the palm of your left hand on your belly button and your right hand on your chest. As you breathe in, notice which hand moves most. Ideally, your left hand should be pushed out by your inhale and your right hand should barely move, if at all. This should be how you should be breathing in all circumstances, apart from real danger (being chased by a lion for example). If you have a panic attack, probably the fastest way to stop the panic is by changing to this style of breathing. To get the best anti-stress results from breathing you should aim to breathe in for around 4 seconds and then breathe out for as long as is comfortable. In general, inhalations stimulate the sympathetic nervous system while exhalations stimulate the parasympathetic nervous system. Therefore, if your exhalations are longer than your inhalations you will feel much calmer. If you practise this you can get to a point where you will breathe in for 4 seconds and out for over 20 seconds. As you do this you'll notice that all of the muscles in your body become naturally inclined to relax.<br />
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Diaphragmatic breathing:<br />
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It is important to breathe into the diaphragm as this is where the highest proportion of blood vessels are within the lungs. It has been shown that the upper 7% of your lungs will only take in 4 ml of oxygen per minute whereas the lower 13% of your lungs will take in around 60 ml per minute. Also, using diaphragmatic breathing requires so much less energy to perform that it requires less than 5% of total oxygen intake. If you are over-breathing the energy requirement goes up massively, when volunteers were told to hyperventilate on purpose they used up 30% of their oxygen intake just to breathe in this way. So by breathing into the diaphragm, you not only take up a significantly larger volume of oxygen into your blood, but you also reduce the amount of oxygen (and energy) that you waste in performing the breathing itself.<br />
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Nasal breathing:<br />
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The nose is the narrowest place in the respiratory tract, it creates a bottleneck that results in airflow being restricted before it travels into the lungs. Compared to the mouth, it requires 1.5 times the amount of energy to pull the same volume of air through the nose.<br />
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Within the nasal cavity are bony projections called turbinates They heat and humidify air that is drawn through the nose and into the lungs. This reduces the damage that air causes to the lungs. The nose is also useful in breathing because it filters the air that is drawn into it. This takes place because there are many small hairs on the inside of the nose. This means that we take in less bacteria every time we breathe and consequently, our immune systems are less likely to become overworked. It is estimated that when these particles are caught in the nose hairs and/or mucus within the nose, that they are removed from the body within 15 minutes. However, if they travelled to the lungs they would take a few months to remove. Every time you breathe through your mouth you send these particles to your lungs and increase your chance of having a lung infection.<br />
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It is said that while breathing through your nose, if you are breathing through the right nostril you will be more inclined towards energetic pursuits, or those involving aggression. Conversely, breathing through the left nostril is associated with feelings of calm and introspection. Over the course of a day, the airflow between the nostrils will change of its own accord. You may wake up, for example, breathing through the left nostril and by midday realise that there is more air coming out of your right nostril.<br />
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In a study in which volunteers were subjected to a stress test, with some participants breathing through their mouth and the others through their nose, those who breathed nasally experienced brain wave activity that indicated greater relaxation.<br />
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Nitric oxide is also present in the nose and the slowing of air as it enter the nasal cavity allows nitric oxide to mix with the incoming air. This causes nitric oxide to be taken into the lungs where it dilates the blood vessels (bronchodilation). This allows significantly more oxygen to be taken in by these blood vessels and is very beneficial to the overall health of the organism.<br />
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Breathing through the nose is also beneficial in that it forces our breathing to slow down and as a result, our bodies follow suit. This helps us to reduce stress and think more clearly.<br />
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Carbon dioxide:<br />
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Carbon dioxide is commonly referred to as a 'waste gas' from respiration. I feel that this is highly disrespectful to carbon dioxide. Your body requires a delicate balance of carbon dioxide, generally within 35 and 45 mmHg (millimetres of mercury at sea level, a pressure measurement) within the blood. If you breathe too quickly you approach the lower end of this scale and feel dizzy and if you breathe too slowly you approach the upper end of this scale and feel breathless. You need around 40 mmHg or above, if you have adapted to higher pressures of carbon dioxide, to function normally. Below this your cells aren't getting adequate oxygen. The reason for this is illustrated by the Bohr effect. Without going into too much detail, the essence of this is that your blood cells offload their oxygen (this is desirable) around cells that are producing more carbon dioxide. Hence, if you breathe too rapidly you deplete your body of carbon dioxide and the blood cells continue to carry oxygen around the body without giving it to cells and tissues that require it. The result of hyperventilation is an impaired ability to think, among many other signs. This is primarily because the brain is suffering from oxygen deprivation (even though you are breathing rapidly and getting a lot of oxygen into the body), because your level of carbon dioxide is inadequate.<br />
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In order to understand why correct breathing doesn't come naturally to many of us we need to consider the type of lifestyle that we all live. It is primarily one of emotionally suppression and stress, both of which cause us to tense our stomach muscles and breathe into our chest. This is a manifestation of the body's fight or flight response. I think a more illustrative way of thinking of the fight or flight responses are to consider them as being a response to Anticipated Exertion. This way it becomes easier to understand why our bodies react in the way that they do. For example, if we were to undergo physical activity then our cells would greatly increase their carbon dioxide production. If our body anticipates that we will undergo physical activity then it naturally begins to breathe in a way that causes this carbon dioxide to be expelled. The problem occurs when our stressors are imaginary and we stay still. This causes us to lose carbon dioxide without producing more of it. The result is hyperventilation and strangely, increased stress.<br />
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Passionflower<br />
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Passionflower is a herb that is commonly used as an alternative treatment for anxiety. It is believed that its anxiolytic properties stem (no pun intended) from its ability to increase GABA within the brain. It is typically used in conjunction with other herbs, for example, Valerian root. While passionflower is generally considered safe, it may cause nausea, vomiting, drowsiness, rapid heart rate and sluggishness. It may also cause liver failure in rare cases.<br />
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Very few people said that passionflower had no effect on them and this may be due to where they bought it from, though maybe even the best source doesn't work for everyone. Many people used passionflower successfully to treat even severe anxiety and cure mild anxiety.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/11679026 - in a study of 36 people diagnosed with generalised anxiety, a passionflower extract was compared against oxazepam. Both approaches showed similar improvements but passionflower took longer to take effect yet caused less impairment of job performance.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/21294203 - passionflower may improve sleep quality, a 41 person study.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/12244887 - a review of studies on passionflower implying it has proven sedative and perhaps anxiolytic effects.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/11679027 - 65 opiates addicts received either clonidine plus passiflora extract in a tablet or clonidine plus placebo in a tablet. Both treatments were equally effective in treating the physical effects of withdrawal but the addition of passiflora extract showed a marked improvement in treatment of the mental symptoms.<br />
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Valerian<br />
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Valerian is a herb that may have anxiolytic effects. There are many types of Valerian but the one considered to be the most effective is Valeriana officinalis. Typical dosages for Valerian range from around 250 mg to 600 mg per day. The calming effects of Valerian are thought to arise from this herb's ability to increase the amount of GABA within the brain. A tolerance can be built up to this herb (you begin to require ever higher dosages to gain the same beneficial effects) so it is recommended that you don't take it for more than a few weeks without a break. It is considered generally safe within the recommended dosage, however it may adversely react with or exacerbate the effects of medications and alcohol.<br />
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According to anecdotes, the best results come with fresh Valerian roots and consequently a lot of company forms of Valerian which aren't fresh, seem ineffective. The general consensus on Valerian supplementation is that it can cause a small to moderate reduction in anxiety, but seems ineffective in cases of extreme anxiety.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/17054208 - a randomised control trial involving 36 participants with generalised anxiety disorder, those taking Valerian had no significant decrease in anxiety compared to placebo.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/20042323 - a study on mice: Valerian extract and valerenic acid caused a significant reduction in anxiety-related behaviour compared to an ethanol control group.<br />
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GABA<br />
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*From what I've seen regarding Phenibut and Picamilon, I would be very cautious with both of them. Picamilon seems to me to be the safer alternative, though studies are lacking. I'm afraid I wouldn't recommend either of these but if you feel that it would be beneficial then please do a lot of your own research first and then check with a medical professional. It may be that I came across some negative anecdotal reports at the start of reading into these supplements and this put me off them completely.<br />
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GABA is considered to be the most important inhibitory neurotransmitter in mammals. For this reason it is considered to be fundamentally important in the treatment of anxiety disorders. Most if not all of the supplements that I have currently looked into have had some connection with GABA receptors. There are 2 main oral supplements utilising the effects of GABA: Phenibut and Picamilon. Both of these were made with the purpose of passing through the blood-brain barrier.It is believed that GABA has difficulty in doing this by itself (I have not seen proof of this) and this is necessary for inhibition of neuronal excitation, therefore supplementation of a GABA form that can enter the brain is important.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/16971751 - this is a review of 2 studies involving a total of 21 study subjects. In the first study it was found that GABA administration caused a change in brain activity, by increasing the alpha waves produced by the participants. This occurred within an hour of the administration. People producing more alpha brain waves experience a more relaxed and alert state of mind. In the second study it was found that those who took GABA instead of a placebo had significantly higher immunoglobin A while facing a phobia (they crossed a bridge and were afraid of heights). The significance of this is that when we are afraid our immune systems decrease in activity. The fact that GABA maintained a higher level of immunoglobin A in these participants shows that their immune systems were less affected by the situation and strongly implies that the GABA induced relaxation. Together, these studies provide evidence that GABA is beneficial against anxiety, though in total only 21 participants have been tested.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/12467378 - an abstract pointing out that glutamate is the main excitatory and GABA is the main inihibitory neurotransmitter within the brain.<br />
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- Phenibut<br />
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Phenibut is a chemical that mimics the effects of GABA. According to anecdotal reports from users, it seems that tolerance to phenibut is easily attained and withdrawal effects can occur even if you have only been taking the supplement for about a week. The withdrawal symptoms seem pretty horrific, with one of the worst symptoms being extreme anxiety. For this reason many people use phenibut about twice per week. Phenibut may also increase the effects of sedative drugs and alcohol and ideally shouldn't been taken in conjunction with these. There also seems to be the possibility of liver damage and probably many other side effects that haven't yet been discovered. I couldn't find human studies on this drug and for that reason I would be wary of trying it.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/11830761 - phenibut is used in Russia for a variety of ailments, particularly in relation to stress, e.g. anxiety, depression, PTSD etc.<br />
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- Picamilon<br />
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Picamilon is a chemical that is formed from the combination of GABA and niacin. It crosses the blood-brain barrier and is subsequently hydrolysed to GABA and niacin. Apart from the potential anxiolytic effects of GABA, the niacin can also act as a vasodilator. This means that picamilon could also be beneficial for migraines. Anecdotal reports claim that this supplement is quite safe, and may relieve headaches. As far as anxiolytic effects go, the results are mixed. Some people report significant benefit and others very little.<br />
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Niacinamide<br />
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Niacinamide and nicotinamide and nicotinic acid amide are three names used for the same compound, an amide of nicotinic acid, also known as niacin. Nicotinamide is a B vitamin with potential anxiolytic effects. It is not to be confused with niacin, as this molecule can cause a flushing reaction in which a person's face, neck, chest, and maybe even whole body turns red and becomes warmer. Nicotinamide rarely causes this same reaction and is the preferred form used for anxiety treatment. I have seen people on forums taking around 500 mg to 2,000 mg per day. Some of these people have noticed an instant effect whereby their extreme anxiety is practically eliminated, and others notice no effect whatsoever. According to a few websites it can take up to a month for the therapeutic benefits of niacinamide to be felt. I am unsure if this is a beneficial treatment for everyone with anxiety. Dosages of 500 mg to 3,000 mg may be be safe though some people take up to 6,000 mg from what I've seen. I don't know what side effects would occur from such high doses and recommend that if you are considering taking niacinamide that you check with a doctor beforehand. Side effects are considered uncommon with this supplement but could occur at higher doses, for example, liver damage.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/7913840 - nicotinamide has anxiolytic effects and reduces fights in conflict situations.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/6101294 - nicotinamide might interact with the benzodiazepine receptors in the brain. Others believe that nicotinamide has a weak affinity for this receptor but may bring about anxiolytic effects in a different way to benzodiazepine.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/6125374 - a possible alternative mechanism whereby molecules like nicotinamide may cause anxiolytic effects, by acting on receptor sites associated with benzodiazepine receptors as opposed to acting on the benzodiazepine receptors themselves.<br />
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Chamomile<br />
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From what I've seen on chamomile, and based on its relative safety, I would suggest chamomile as being beneficial for most people with anxiety. It is by no means a cure but it should help. Just make sure that you aren't allergic to it or have any health conditions that may be adversely affected.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/19593179 - 28 patients with mild to moderate generalised anxiety disorder took Matricaria recutita (chamomile) extract for 8 weeks. A "significantly greater reduction in mean total HAM-A" (subjective anxiety rating) was observed.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/16628544 - this review states that animal studies show some anxiolytic effects of chamomile, though human studies testing chamomile tea are non-existent.<br />
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There have been surprisingly few human studies on chamomile but I've seen loads of people take it and no one has mentioned side effects. The vast majority of people report noticeable calming and find it easier to get to sleep when taking chamomile tea. This is also considered to be one of the safest herbs that you can take, although care is advised for pregnant women as it may increase the risk of miscarriage and there can be allergic reactions to it. It may also exacerbate asthmatic symptoms. There will be a trial ending in June 2014 that will last 38 weeks, to determine the long-term effects of chamomile. This will give an indication of what sort of tolerance is built up to chamomile.<br />
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Kava-kava<br />
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Searching through the forums on this one was utterly confusing. There were so many forms of kava and added to the fact that there are so many companies and qualities of each individual source, I cannot say for sure which kava form is the most effective. However, it seems like the kava root powder or kava paste are among the best and for best results some people suggest taking oily foods or supplements beforehand as these forms are oil-soluble and this aids absorption. I can't comment on the effectiveness though, so many people had tried each form of kava with wildly different results.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/12076477 - A review of 7 trials involving kava was made. Kava was found to have significant effects in reducing anxiety and with only mild, adverse reactions to the extract.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/12535473 - A review of 11 trials found the same results; significant reduction of anxiety and only mild adverse effects.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/23348842 - a 6 week study showing no adverse effects due to kava.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/1930344 - 29 patients with anxiety syndrome took kava extract (WS 1490), 300 mg per day, and found it caused significant reduction in anxiety after only 1 week of treatment. No adverse events occurred due to the drug.<br />
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There were many more studies done on kava, all of the ones that I came across pointed to the same conclusion, that kava causes statistically significant reductions in anxiety with only mild adverse effects. The potential problem with kava is that it may cause liver toxicity in rare cases. It is unsure at this stage whether the liver toxicity was caused by the kava alone, or in combination with other medications, drugs, or viruses etc. It may also be that the form of kava used by these people was unsafe or impure. It seems that the toxicity of the kava plant may be avoided by using the rhizomes. The stem and leaves apparently contain much more toxic substances. This would explain why locals who use kava experience much fewer and less severe side effects through using only the rhizomes, whereas when the drug was imported, it contained extracts taken from the stem, leaves and rhizomes combined.<br />
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Omega-3<br />
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Summary: based on what I've seen on forums, people seem to benefit most from 3 to 4 grams of omega-3 supplementation per day. These people notice benefits with regard to anxiety and depression and it also keeps their skin healthier. I am unsure what the long-term effects of this level of supplementation are.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/23051591 - 935 women were asked to give a detailed description of their diets. Those with the highest intake of DHA had a calculated 50% reduced chance of having an anxiety disorder. This study suggested a linear link between DHA intake and anxiety and as this was a very large trial it can't be easily discarded.<br />
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191260/ - 68 medical students were sorted into either a placebo or omega-3 supplement group. Those who received 2.5 grams of omega-3s (containing around 2 grams of EPA and 350 mg of DHA) per day had statistically significant reductions in anxiety.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/17110827 - 24 substance abusers were splint into a placebo or test group. 13 supplemented with 3 grams of omega-3 PUFAs (polyunsaturated fatty acids). Those receiving the omega-3 capsules had a progressive decrease in anxiety as the trial went on (it lasted 3 months). 6 of these supplementers were then followed for an additional 3 months and were found to maintain a significantly decreased level of anxiety.<br />
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2275606/ - 22 substance abusers were split into a placebo or test group, the test group supplemented with 3 grams of omega-3 PUFAs daily, this lowered both their anxiety and anger levels. A higher plasma EPA correlated with decreased anxiety and higher DHA correlated with decreased anger.<br />
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I think probably the main problem with omega-3 consumption is that after going through the forums, everyone is taking around 1 gram per day. Upon further looking, everyone that I came across that noticed no benefit either didn't state their dosage or said they were taking up to around 1.2 grams of omega-3 per day. Everyone that said they were taking 3 or 4 grams had noticed significantly reduced anxiety.<br />
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Theanine<br />
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Summary: theanine seems to work for some people, the best source appears to be 'suntheanine', though some people still notice no benefits with this supplement. For those who do notice the benefits, a tolerance appears to be quickly induced, diminishing the effect within a couple of weeks. It's best effect seems to be in improving concentration as opposed to anything else. The only conclusive side effect that I came across was headaches.<br />
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These are all the studies that I could find which tested theanine's anxiolytic effects.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/15378679 - some reduction in anticipatory anxiety but no effect during stressful situation (extremely small study, practically meaningless).<br />
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http://www.ncbi.nlm.nih.gov/pubmed/16930802 - theanine prevented heart rate increase in stressful situation (extremely small study, practically meaningless).<br />
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http://www.ncbi.nlm.nih.gov/pubmed/16759779 - no signs of toxicity or other adverse effects in mice given 4000 mg per kilogram of bodyweight over 13 weeks. This suggests that humans supplementing with theanine would be incredibly unlikely to suffer any adverse effects.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/22214254 - theanine significantly improved sleep for patients with ADHD. No significant adverse effects. This was a moderately sized trial and was placebo-controlled (2 groups undertook the experiment, one group took the substance to be tested and the other took a placebo) and was double-blind (neither the volunteers nor the people in charge were aware of who received the substance under test or the placebo).<br />
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http://www.ncbi.nlm.nih.gov/pubmed/22819553 - theanine administration caused increased nitric oxide production in blood vessels leading to vasodilation of blood vessels. This improves blood flow and reduces blood pressure. This would be beneficial to people suffering from hypertension.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/22707502 - theanine reduces adrenal hypertrophy in male mice housed with other males. It also reduced stress, depression and blocked the negative effects of caffeine. This suggests that drinking green tea may not cause the usual nervousness associated with caffeine intake as this would be counteracted by the theanine found within green tea.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/23395732 - multiple beneficial effects of theanine on mice that were trapped (causing restraint-induced stress), this shows theanine can reverse some cognitive impairment in mice that have undergone stress, and most likely in humans as well.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/23107346 - multiple benefits to theanine administration in human participants with a tendency toward high-stress responses while performing a mental task.<br />
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I also looked over a few forums and saw mixed results, I'd say around half of the people using theanine experienced reductions in anxiety while the rest noticed no change. Also, most of the people that used it said that they quickly developed a tolerance to it (usually within a couple of weeks). However, a lot of people said that the only good quality form of theanine was something called suntheanine, and I'm sure that most of the people on these forums hadn't used this particular form. The people who did use this form usually said it was effective.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-51437399396409819602013-06-02T12:22:00.005-07:002013-06-02T12:22:39.466-07:00SugarStimulates receptors in the brain that are also activated by drugs such as heroin and morphine. This is how sugar can act as an antidepressant and why it is also addictive. In a study conducted by the Mayo Clinic it was found that people with the highest carbohydrate intake were 1.9 times more likely to suffer from cognitive impairment than those who consumed the least carbohydrates. 940 Participants from the age of 70 to 89 provided information on their dietary habits for a year and had no cognitive impairment beyond normal age-related decline when the study began. After four years 200 of these people had begun to show mild cognitive decline. Individuals that had a specifically high sugar intake had a 150% risk of cognitive impairment compared to those with the lowest sugar intake. Those with the highest fat and protein intakes had 42% and 21% reduced risks (respectively) of cognitive impairment after this time period.<br />
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http://www.newswise.com/articles/view/594916/?sc=rsmn<br />
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Overconsumption of sugar leads to an increased risk of obesity, type 2 diabetes, heart disease, high blood pressure, hormonal imbalance (particularly oestrogen and testosterone, though there are others), infertility, arthritis, osteoporosis, dementia, Alzheimer's, depression and many more. Sugars tend to have very high glycemic indices. A high glycemic index means that the substance being described is metabolised rapidly by the body and causes a large, rapid increase in blood sugar levels. Foods with a low glycemic index still contribute to raised blood sugar levels but they cause changes that are longer lasting and much more gradual, i.e. there is an increase in blood sugar, but not a 'spike'. These increases in blood sugar levels stimulate the production and secretion of insulin. Insulin is a hormone that transports the sugar into cells where they are metabolised to create ATP.<br />
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In a study on two groups of rats who each received water containing fructose but only one group received omega-3 fatty acids it was shown that fructose has detrimental effects upon the rat brain (rats have similar metabolic functioning to humans) and that omega-3 fatty acids were neuroprotective (they protected the rat brain from these effects). The rats that didn't receive omega-3 had a decline in synaptic activity, their neurons "had trouble signalling each other, disrupting the rats' ability to think clearly and recall effectively". These same rats also had insulin resistance which may be connected this cognitive decline.<br />
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http://www.medicalnewstoday.com/releases/245469.php<br />
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Cancer cells rapidly metabolise glucose, they have an extremely high number of insulin receptors through which glucose enters their cell surface membrane. Breast cancer cells, for example, have around 17 times the insulin receptors of normal cells.<br />
It is also estimated that around a teaspoon of sugar per day can dramatically increase your levels of inflammation.<br />
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Sugar ingestion also causes an increase in body fat as this sugar is converted to fats for storage. It also raises bad cholesterol and paradoxically stimulates appetite. In another study two groups of rats were either fed normal rat food or processed food from the supermarket. Those fed the normal rat diet put on weight slowly and stopped eating when full. The rats fed the supermarket food ballooned in size in a matter of days and ate a lot more. This is thought to occur by the suppression of leptin, a hormone that, when produced, communicates to the brain that the body has eaten enough. A knock-out mouse without the leptin gene will simply keep on eating and become very overweight.<br />
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Fructose is a particularly unhealthy sugar, it is 7 times more likely to form Advanced Glycation End-Products (AGEs) than glucose. Elevated levels of AGEs are signs of many diseases, for example, diabetes and degenerative eye disease. Also, fructose does not suppress ghrelin, a hormone that makes us feel hungry, therefore a high fructose diet keeps us hungry. Chronic fructose exposure alone is enough to cause metabolic syndrome, an umbrella term encompassing obesity, type 2 diabetes, lipid problems, hypertension, and cardiovascular disease. Fructose consumption is also detrimental to liver function as only the liver can metabolise fructose. Also, approximately 30% of fructose is stored as fat.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-66644822673612365462013-06-02T12:22:00.002-07:002013-06-02T12:22:09.201-07:00Vitamin AVitamin A doesn't seem to be overly important in that we, in the developed world, appear to be getting enough of it from our diets. However, its still interesting to read about. According to Wikipedia: the term vitamin A refers to a group of unsaturated nutritional hydrocarbons. This includes retinol, retinal and retinoic acid and several pro-vitamin A carotinoids of which beta-carotene is the most important. If you have ever heard the old saying "carrots let you see in the dark", then you're about to find out how this could be true. The beta-carotene mentioned above is present in carrots and when ingested by humans, is converted into vitamin A, an umbrella term specifically encompassing retinal in this respect. The significance of this conversion to retinal with relation to low light vision is that retinal is needed by the eye, specifically the retina, to produce rhodopsin, a light-absorbing molecule. Retinol is essentially the storage form of vitamin A that can be converted reversibly to retinal. The conversion to retinoic acid however, is irreversible and this compound is used for growth and cellular differentiation, it is not used in the retina.<br />
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The uses of vitamin A as a whole are the following:<br />
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- Growth and development<br />
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- Immune system maintenance<br />
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- Good vision<br />
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- Gene transcription<br />
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- Embryonic development and reproduction<br />
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- Bone metabolism<br />
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- Healthy skin<br />
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- Antioxidant properties<br />
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- Development of blood cells<br />
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- Tissue repair and replacing intestinal lining, this effect can allow vitamin A to prevent intestinal disorders such as irritable bowel syndrome<br />
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Signs of a vitamin A deficiency are:<br />
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- Blindness<br />
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- Stunted growth<br />
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- Immune system disorders<br />
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- Respiratory infections<br />
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The best food sources of vitamin A: are liver, chillis, sweet potatoes, sweet carrots and green vegetables.<br />
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According to the World Health Organisation, around 250,000 to 500,000 children become blind due to vitamin A deficiency and around 50% of these children die within a year of this happening.<br />
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http://www.who.int/nutrition/topics/vad/en/Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0tag:blogger.com,1999:blog-6986907989946980568.post-23923088314626953842013-06-02T12:21:00.001-07:002013-06-02T12:21:34.229-07:00Vitamin DVitamin D is a hormone; a chemical substance produced in the body which has a specific regulatory effect on the activity of certain cells or a certain organ or organs. It has various uses within the body:<br />
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- It is needed for the absorption and metabolism of calcium and phosphorus, among many other functions, these minerals are necessary for bone health (higher vitamin D levels are associated with greater bone density).<br />
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- It regulates the immune system and therefore is beneficial in treating viruses and infections etc.<br />
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- It may reduce the risk of multiple sclerosis (I don't know whether or not it treats it though): http://www.telegraph.co.uk/health/healthnews/8444739/Health-benefits-of-vitamin-D.html the figure of 80% seems very high but could be true.<br />
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- Reduces cognitive impairment and age-related decline, for example poorer memory or even dementia or Alzheimer's disease.<br />
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- Some people take it to reduce the severity of asthma attacks. So it seems to have efficacy in treating this disease.<br />
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- It reduces the risk of rheumatoid arthritis in women.<br />
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- Many studies have shown that it has a powerful role in reducing incidence of cancer, especially colon cancer: http://www.reuters.com/article/2011/09/01/us-vitamind-idUSTRE78063U20110901 and<br />
http://jnci.oxfordjournals.org/content/98/7/428.full.pdf<br />
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- It also increases the recovery rate from tuberculosis.<br />
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- Finally, it may prevent heart attacks and increase longevity.<br />
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Various uses of vitamin D<br />
http://www.medicalnewstoday.com/articles/161618.php<br />
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According to doctor Oz, dietary supplementation of 2,000 to 3,000 IU of vitamin D is completely safe and nowhere near the levels which could cause toxicity. This is supported by evidence suggesting that you can make around 10,000 IU of vitamin D by exposing yourself to direct sunlight for 10 to 15 minutes. Vitamin D is made when exposed to UVB rays from the sun, and consequently using a sun lotion which blocks these rays will compromise your natural ability to produce vitamin D. This reduces total body vitamin D. However, serum (this is essentially blood plasma) vitamin D levels can be reduced by being overweight. This is because vitamin D is fat soluble. In a study comparing individuals who were of normal weight and those who were obese it was found that when both groups were exposed to the same level of ultraviolet radiation, the obese participants had a 55% lower serum level of vitamin D.<br />
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Typically, a healthy level of vitamin D is shown by a serum level of more than 30ng/ml, but many experts say that this is still too low and a level of around 60 to 80ng/ml is more appropriate. Some doctors place the safe upper limit at 100 ng/ml but life guards who spend a lot of their time on sunny beaches tend to have serum levels at around 125ng/ml with no signs of toxicity. In fact, serum levels of 200ng/ml may even be safe, but not many people reach this level. For average individuals; every 100 IU of vitamin D that is ingested results in a rise of 1ng/ml of serum vitamin D (this is measured by checking the levels of 25(OH)D). Also, regardless of race, vitamin D serum levels predict bone density (remember its effects on calcium and phosphorus). This is important because people of darker skin are more resistant to UVB rays and hence create lower amounts of vitamin D per amount of ultraviolet radiation. This means that these same people, when living in countries which have fewer hours of sunlight, actually have a very high chance of being vitamin D deficient. In a Boston study it was found that those who tanned once per week in a tanning bed had much higher levels of serum vitamin D (an average of ~48ng/ml) than those who didn't tan (~17-18ng/ml). The people who tanned also had noticeably increased bone density compared to those who didn't.<br />
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I can't tell which is more important, D2 or D3, there are conflicting reports, most people tend to think that D3 is more beneficial but I am unsure why and tests on rats (they metabolise many substances in a similar way to humans) indicate that D2 is better for them.Anonymoushttp://www.blogger.com/profile/10731414560002447317noreply@blogger.com0