http://www.merck.com/mrkshared/mmanual/section1/chapter3/3j.jsp
Thiamine Deficiency And Dependency
The coenzyme thiamine pyrophosphate, the active form of thiamine
(vitamin B1), participates in carbohydrate metabolism through
decarboxylation of -keto acids. Thiamine also acts as coenzyme to the
apoenzyme transketolase in the pentose monophosphate pathway for
glucose. Deficiency causes beriberi with peripheral neurologic,
cerebral, cardiovascular, and GI manifestations.
Etiology
Primary thiamine deficiency is caused by inadequate intake of thiamine,
particularly in people subsisting on highly polished rice. Milling
removes the husk, which contains most of the thiamine, but boiling
before husking disperses the vitamin throughout the grain, thus
preventing its loss.
Secondary thiamine deficiency is caused by increased requirement, as in
hyperthyroidism, pregnancy, lactation, and fever; impaired absorption,
as in prolonged diarrheas; and impaired utilization, as in severe liver
disease. A combination of decreased intake, impaired absorption and
utilization, increased requirements, and possibly an apoenzyme defect
occurs in alcoholism. Frequent, long-term, or highly concentrated
dextrose infusions, coupled with low thiamine intake, may precipitate
thiamine deficiency.
Pathology
The most advanced neural changes occur in the peripheral nerves,
particularly of the legs. The distal segments are characteristically
affected earliest and most severely. Degeneration of the medullary
sheath can occur in all tracts of the spinal cord, especially in the
posterior columns and in the anterior and posterior nerve roots.
Changes also occur in the anterior horn and posterior ganglion cells.
Lesions of hemorrhagic polioencephalitis occur in the brain when
deficiency is severe.
The heart is dilated and enlarged; muscle fibers are swollen,
fragmented, and vacuolized, with interstitial spaces dilated by fluid.
Vasodilation occurs and can result in some edema before frank
high-output heart failure occurs.
Symptoms and Signs
Early deficiency produces fatigue, irritation, poor memory, sleep
disturbances, precordial pain, anorexia, abdominal discomfort, and
constipation.
***
http://www.neuro.wustl.edu/neuromuscular/nother/vitamin.htm
***
http://huntingtondisease.tripod.com/swallowing/id66.html
Vitamin B 12 - deficiency is a common cause of macrocytic anemia and
has been implicated in a spectrum of neuropsychiatric disorders.
peripheral nerve degeneration,mental dysfunction, anorexia, glossitis,
low folate utilization, skin sensitivity, immune suppression
Vitamin C Deficiency - appetite loss, fatigue, bleeding gums, capillary
rupture, immune suppression
Zinc - immune suppression, oxidative stress, poor growth, poor wound
healing, anorexia, abnormal taste and smell,anaemia, skin inflammation,
low plasma zinc levels.
***
http://www.cyber-north.com/vitamins/vitaminb.html
Biotin plays a role in metabolic processes that lead to the formation
of fats and the utilization of carbon dioxide. Biotin deficiency
results in anorexia, nausea, vomiting, inflammation of the tongue,
pallor, depression, and dermatitis.
***
TC
Dusty Bleher said:<[email hidden]> wrote in message
news:[email hidden]...
Quoted message said:Anorexia is a symptom of a B vitamin deficiency. The deficiency leads
Most interesting, TC. Do you by some chance have any links to more info
along that line?
Quoted message said:to anorexia and anorexia in turn leads to more deficiency, etc. Whuch
is why psychiatrists don't have a hope in hell of curing an anorexic
with either medications or with any other of their silly therapies.
Tell me about it! It's the same thing they're doing with T2. Just convince
the fools that they need your "medicine" to live, and then they sit back and
wait for their retirement accounts to fully fund...<damn it!>
DustyB
Quoted message said:
TC
...
