Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Adster, Aug 15, 2012.
Also, when my wife started it wasn't well known that folic acid blocked the process. That was a big breakthrough that probably caused some of the troubles along the way.
Dr. Weil lol. I couldn't find the results of the study mentioned, but I found one that suggests SAMe doesn't raise or lower homocysteine.
Dietary supplement S-adenosyl-L-methionine (AdoMet) effects on plasma homocysteine levels in healthy human subjects: a double-blind, placebo-controlled, randomized clinical trial.
OBJECTIVES: To determine if exogenous S-adenosyl-l-methionine (AdoMet), a commonly used nutritional supplement, increases the level of plasma homocysteine (Hcy), a potential cardiovascular risk factor, in healthy human subjects.
DESIGN: Double-blind, placebo-controlled, randomized clinical trial.
SETTING: Mayo Clinic, Rochester, Minnesota.
SUBJECTS: Fifty-two (52) healthy human volunteers.
INTERVENTION: Subjects received placebo or AdoMet (800 mg per day) for 4 weeks. Hcy levels were measured before and after administration of AdoMet or placebo.
OUTCOME MEASURES: The primary outcome measure was change in Hcy level. Secondary outcome measures included an interim Hcy determination (at 2 weeks) and changes in levels of high-sensitivity C-reactive protein (hsCRP), lipids, and alanine aminotransferase.
RESULTS: There was no statistically significant change in Hcy between groups. Similarly, no statistically significant differences in change in Hcy or hsCRP levels were observed at 2 or 4 weeks. There was a small but statistically significant increase (p < 0.04) in alanine aminotransferase at week 2 and a statistically significant decrease (p < 0.04) in total cholesterol in the AdoMet group compared with the placebo group.
CONCLUSIONS: AdoMet at a daily dose of 800 mg for 4 weeks does not appear to significantly affect Hcy levels in the blood.
Thanks I don't know much about any of this stuff, so I didn't know that.
I'm not sure about that study I posted yesterday which I'm quoting above. According to another study, it seems if methylfolate is added then SAMe is more effective and the first study didn't use methylfolate so we don't really know what the effects of the two are on homocysteine.
The methylation, neurotransmitter, and antioxidant connections between folate and depression.
Depression is common - one-fourth of the US population will have a depressive episode sometime in life. Folate deficiency is also relatively common in depressed people, with approximately one-third of depressed individuals having an outright deficiency. Folate is a water-soluble B-vitamin necessary for the proper biosynthesis of the monoamine neurotransmitters serotonin, epinephrine, and dopamine. The active metabolite of folate, 5-methyltetrahydrofolate (5-MTHF, L-methylfolate), participates in re-methylation of the amino acid metabolite homocysteine, creating methionine. S-adenosylmethionine (SAMe), the downstream metabolite of methionine, is involved in numerous biochemical methyl donation reactions, including reactions forming monoamine neurotransmitters. Without the participation of 5-MTHF in this process, SAMe and neurotransmitter levels decrease in the cerebrospinal fluid, contributing to the disease process of depression. SAMe supplementation was shown to improve depressive symptoms. 5-MTHF also appears to stabilize, enhance production of, or possibly act as a substitute for, tetrahydrobiopterin (BH4), an essential cofactor in monoamine neurotransmitter biosynthesis. There are few intervention studies of folic acid or 5-MTHF as a stand-alone treatment for depression related to folate deficiency; however, the studies that have been conducted are promising. Depressed individuals with low serum folate also tend to not respond well to selective serotonin reuptake inhibitor (SSRI) antidepressant drugs. Correcting the insufficiency by dosing folate along with the SSRI results in a significantly better antidepressant response.
Altern Med Rev. 2008 Sep;13(3):216-26
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