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Author Topic:   SAMe
BLONDBLDR
Amateur Bodybuilder
(Total posts: 17)
posted July 04, 2000 07:55 AM     Click Here to See the Profile for BLONDBLDR   Click Here to Email BLONDBLDR     Edit/Delete Message
does anyone have any info on SAMe. the new so called wonder drug. suoopsed to help realease more seretonin so moods are elevated. especially around pms times. some people have tried for depression instead of prozac. i know i myself have some real mood swings before period. any info?

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Artemis
Amateur Bodybuilder
(Total posts: 49)
posted July 04, 2000 11:09 AM     Click Here to See the Profile for Artemis   Click Here to Email Artemis     Edit/Delete Message
I had some references regarding SAMe and liver preservation. Supposedly it helps to clear and/or prevent cholestatic jaundice as caused by 17aa oral contraceptives or AAS.
Too bad the stuff is so pricy.

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MS
Pro Bodybuilder
(Total posts: 435)
posted July 04, 2000 03:19 PM     Click Here to See the Profile for MS   Click Here to Email MS     Edit/Delete Message
Wow. Lots of questions on neurotransmitters lately. In most cases ther is not yet any 'black and white' answers to whether a supplement will definitely help a particular individual. The best way to answer the question is to try it and see if it helps. SAMe, as Artemis said, is looking good for treatment of cholestasis, and may help some people with depression where other serotonergic anti-depressants fail. Here's a n abstract to contemplate.

Although one of the first biological treatments of a major psychiatric disorder was
the dietary treatment of pellagra, the use of diet and dietary components in the
study of psychopathology has not aroused much interest. This article reviews
three areas in which the dietary approach has provided interesting information.
The tryptophan depletion strategy uses a mixture of amino acids devoid of
tryptophan to lower brain tryptophan in order to study the symptoms that can be
elicited. One effect of tryptophan depletion is a lowering of mood, the magnitude
of which seems to depend on the baseline state of the subject. Therefore,
recovered depressed patients often undergo an acute relapse, while normal
subjects show more moderate changes of mood. Totally euthymic subjects show
no lowering of mood, but subjects with high normal depression scale scores or
subjects with a family history of depression show a moderate lowering of mood.
These data indicate that low serotonin levels alone cannot cause depression.
However, serotonin does have a direct effect on mood, and low levels of
serotonin contribute to the etiology of depression in some depressed patients.
Folic acid deficiency causes a lowering of brain serotonin in rats, and of
cerebrospinal fluid 5-hydroxyindoleacetic acid in humans. There is a high
incidence of folate deficiency in depression, and there are indications in the
literature that some depressed patients who are folate deficient respond to folate
administration. Folate deficiency is known to lower levels of
S-adenosylmethionine, and S-adenosylmethionine is an antidepressant that raises
brain serotonin levels. These data suggest that low levels of serotonin in some
depressed patients may be a secondary consequence of low levels of
S-adenosylmethionine. They also suggest that the dietary intake and
psychopharmacological action of methionine, the precursor of
S-adenosylmethionine, should be studied in patients with depression. Normal
meals have definite effects on mood and performance in humans. The composition
of the meal, in terms of protein and carbohydrate content, can influence these
behaviors. Because protein and carbohydrate meals can influence brain serotonin
in rats, these effects in humans have usually been interpreted in terms of altered
serotonin functioning. However, the current balance of evidence is against the
involvement of serotonin in the acute effects of protein and carbohydrate meals in
humans. The underlying mechanisms involved are unknown, but there are a
variety of possibilities.

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The Mad Scientist

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