From http://www.raysahelian.com/betaine.html :

BETAINE

Betaine is a metabolite of choline, and is also known as trimethylglycine or TMG. Betaine works by donating methyl (CH3) groups. Betaine has the ability to convert homocysteine to methionine.

Unless your major is college was chemistry, chances are you donít remember learning about methyl donors. A methyl donor is simply any substance that can transfer a methyl group, a carbon atom attached to three hydrogen atoms, to another substance. Many important biochemical processes rely on methylation, including the metabolism of lipids, neurotransmitters, and DNA. Scientists suspect that adequate methylation of DNA can prevent the expression of harmful genes, such as cancer genes. Itís quite likely that our bodyís ability to methylate declines with age, potentially contributing to the aging process, and therefore supplementation is an interesting potential in terms of health benefits.


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Trimethylglycine (betaine), 750 mg
Source Naturals
TMG (trimethylglycine), also known as anhydrous betaine, is found in a variety of plant and animal sources and is used in the conversion of homocysteine to methionine. Maintaining normal homocysteine levels is important for the health of the cardiovascular system. Betaine has been shown to help protect the liver and raise S-adenosylmethionine (SAM-e) levels, in animal studies. Betaine is also mentioned as betaine hcl or betaine hydrochloride.


Betaine Research
Betaine lowers homocysteine levels.
Betaine has been found to protect liver cells from toxins.
Betaine is a well tolerated nutrient that leads to a significant biochemical and histological improvement in patients with nonalcoholic steatohepatitis (NASH).

Betaine Research Update
Effects of betaine intake on plasma homocysteine concentrations and consequences for health.
Curr Drug Metab. 2005 Feb;6(1):15-22.
High plasma concentrations of homocysteine may increase risk of cardiovascular disease. Folic acid lowers plasma homocysteine by 25% maximally, because 5-methyltetrahydrofolate is a methyl donor in the remethylation of homocysteine to methionine. Betaine (trimethylglycine) is also a methyl donor in homocysteine remethylation, but effects on homocysteine have been less thoroughly investigated. Betaine in high doses (6 g/d and higher) is used as homocysteine-lowering therapy for people with hyperhomocysteinemia due to inborn errors in the homocysteine metabolism. Betaine intake from foods is estimated at 0.5-2 g/d. Betaine can also be synthesized endogenously from its precursor choline. Studies in healthy volunteers with plasma homocysteine concentrations in the normal range show that betaine supplementation lowers plasma fasting homocysteine dose-dependently to up to 20% for a dose of 6 g/d of betaine. Moreover, betaine acutely reduces the increase in homocysteine after methionine loading by up to 50%, whereas folic acid has no effect. Betaine doses in the range of dietary intake also lower homocysteine. This implies that betaine can be an important food component that attenuates homocysteine rises after meals. If homocysteine plays a causal role in the development of cardiovascular disease, a diet rich in betaine or choline might benefit cardiovascular health through its homocysteine-lowering effects. However betaine and choline may adversely affect serum lipid concentrations, which can of course increase risk of cardiovascular disease. However, whether the potential beneficial health effects of betaine and choline outweigh the possible adverse effects on serum lipids is as yet unclear.

Betaine in human nutrition
American Journal of Clinical Nutrition, Vol. 80, No. 3, 539-549, September 2004
Betaine is distributed widely in animals, plants, and microorganisms, and rich dietary sources include seafood, especially marine invertebrates; wheat germ or bran; and spinach. The principal physiologic role of betaine is as an osmolyte and methyl donor (transmethylation). As an osmolyte, betaine protects cells, proteins, and enzymes from environmental stress (eg, low water, high salinity, or extreme temperature). As a methyl donor, betaine participates in the methionine cycleóprimarily in the human liver and kidneys. Inadequate dietary intake of methyl groups leads to hypomethylation in many important pathways, including 1) disturbed hepatic protein (methionine) metabolism as determined by elevated plasma homocysteine concentrations and decreased S-adenosylmethionine concentrations, and 2) inadequate hepatic fat metabolism, which leads to steatosis (fatty accumulation) and subsequent plasma dyslipidemia. This alteration in liver metabolism may contribute to various diseases, including coronary, cerebral, hepatic, and vascular diseases. Betaine has been shown to protect internal organs, improve vascular risk factors, and enhance performance. Databases of betaine content in food are being developed for correlation with population health studies. The growing body of evidence shows that betaine is an important nutrient for the prevention of chronic disease.


Betaine as a determinant of postmethionine load total plasma homocysteine before and after B-vitamin supplementation.
Arterioscler Thromb Vasc Biol. 2004 Feb;24(2):301-7.
Betaine is a substrate in the betaine-homocysteine methyltransferase reaction, converting homocysteine to methionine. There are only sparse data on plasma betaine as a determinant of the plasma total homocysteine (tHcy) concentration. Ninety patients undergoing coronary angiography were randomized into 4 groups administered oral: (1) folic acid (0.8 mg), vitamin B12 (0.4 mg), and vitamin B6 (40 mg); (2) folic acid and vitamin B12; (3) vitamin B6 alone; or (4) placebo. Nonfasting blood samples were collected at baseline and 3, 14, and 28 days and 3, 6, and 12 months after treatment start. A 4-hour methionine-loading test (0.1 g/kg) was performed at baseline and after 3 months. At baseline, median (interquartile range) plasma betaine was 36.9 micromol/Land was increased by 15% after methionine loading. The postmethionine load (PML) increase in tHcy was inversely related to plasma betaine and even more strongly to PML betaine. After 3 months of intervention, the relation between the PML increase in tHcy and PML betaine was weakened. CONCLUSIONS: Plasma betaine is a strong determinant of the PML increase in tHcy in subjects not supplemented with B-vitamins. betaine hydrochloride.


Low dose betaine supplementation leads to immediate and long term lowering of plasma homocysteine in healthy men and women.
Olthof MR. J Nutr. 2003 Dec;133(12):4135-8.
High plasma homocysteine is a risk for cardiovascular disease and can be lowered through supplementation with 6 g/d of betaine. However, dietary intake of betaine is approximately 0.5-2 g/d. Therefore, we investigated whether betaine supplementation in the range of dietary intake lowers plasma homocysteine concentrations in healthy adults. Four groups of 19 healthy subjects ingested three doses of betaine or placebo daily for 6 wk. A methionine loading test was performed during run in, on d 1 of betaine supplementation, and after 2 and 6 wk of betaine supplementation. Fasting plasma homocysteine after 6-wk daily intakes of 1.5, 3 and 6 g of betaine was 12% less than in the placebo group, respectively. Furthermore, the increase in plasma homocysteine after methionine loading on the 1st d of betaine supplementation was 16% less than in the placebo group, respectively, and after 6 wk of supplementation was 23% less, respectively. Thus, doses of betaine in the range of dietary intake reduce fasting and postmethionine loading plasma homocysteine concentrations. A betaine -rich diet might therefore lower cardiovascular disease risk.

Betaine supplementation decreases plasma homocysteine concentrations but does not affect body weight, body composition, or resting energy expenditure in human subjects.
Am J Clin Nutr. 2002 Nov;76(5):961-7.
Betaine (trimethylglycine) is found in several tissues in humans. Betaine is involved in homocysteine metabolism as an alternative methyl donor and is used in the treatment of homocystinuria in humans. In pigs, betaine decreases the amount of adipose tissue. OBJECTIVE: The aim of the study was to examine the effect of betaine supplementation on body weight, body composition, plasma homocysteine concentrations, blood pressure, and serum total and lipoprotein lipids. DESIGN: Forty-two obese, white subjects (14 men, 28 women) treated with a hypoenergetic diet were randomly assigned to a betaine-supplemented group (6 g/d) or a control group given placebo for 12 wk. The intervention period was preceded by a 4-wk run-in period with a euenergetic diet. RESULTS: Body weight, resting energy expenditure, and fat mass decreased significantly in both groups with no significant difference between the groups. Plasma homocysteine concentrations decreased in the betaine group. Diastolic blood pressure decreased without a significant difference between the groups. Serum total and LDL-cholesterol concentrations were higher in the betaine group than in the control group. CONCLUSION: A hypoenergetic diet with betaine supplementation (6 g daily for 12 wk) decreased the plasma homocysteine concentration but did not affect body composition more than a hypoenergetic diet without betaine supplementation did. betaine hci.


An open-label, 24-week pilot study of the methyl donor betaine in Alzheimer disease patients.
Alzheimer Dis Assoc Disord. 2001 Jul-Sep;15(3):162-5.
We investigated the safety and tolerability of betaine in patients with Alzheimer disease (AD). Betaine is an alternative methyl donor, distinct from the folate-and cobalamin-dependent conversion pathway between homocysteine and methionine. Betaine has been used successfully to reduce homocysteine levels in homocystinuria. The rationale for betaine in AD was to decrease serum homocysteine levels and to increase brain methionone and S-adenosylmethionine, both of which might delay disease progression. Hyperhomocysteinemia is a possible risk factor for AD. Eight patients with probable mild AD (7 men; mean age, 69.6 years; mean Mini-Mental State Exam score, 23.7) received oral betaine (3 g twice daily) for 24 weeks. All patients were on donepezil 10 mg/day for at least 3 months before entry and throughout the study. One patient suffered a myocardial infarction and withdrew after 6 weeks. Another patient, who completed the trial, experienced diarrhea and prostatitis. Four of the 7 patients who completed the trial were rated on the Clinician's Global Impression of Change as worse after 24 weeks. On the cognitive portion of the AD Assessment Scale, 2 patients worsened by at least five points over 24 weeks, whereas the others had changes in scores of no more than two points either way. Six of 8 patients tolerated betaine for 24 weeks without difficulty. Several patients worsened over 24 weeks, but as a pilot study without a control group, efficacy measurements cannot be interpreted. The current study provides a basis for pursuing larger controlled trials with betaine in AD. The homocysteine to S-adenosylmethionine pathway is of interest in AD therapeutics.
**** Dr. Sahelian comments: Here's an example of lack of understanding of proper nutrient dosage by researchers. They used 6 grams of betaine a day which can make any condition ,or anyone who is heatlhy, worse off due to overstimulation. Researchers should first take supplements themselves at different dosages before doing a study and wasting everyone's time, money, and coming up with unhelpful data.

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