Studies of Trimethylglycine or Betaine
Studies of
TRIMETHYLGLYCINE or BETAINE
GENERAL DESCRIPTION
Trimethylglycine or Betaine (Betaine is also called Betaine but we do not use this name because we can confuse it with Betaine Chloride; this is a strong acidifier that is taken only at mealtimes, and may cause gastric irritation), extracted from sugar beets, is obtained from pure molasses, and separated by chromatography; it is a powerful methylating agent and plays a particularly important role in the process of detoxification of homocysteine (a powerful oxidant and free radical generator), which, as known, is one of the major cause of heart and vascular diseases.
Recent American studies have shown the value and effectiveness of T. as a dietary supplement that can give the following benefits:
- Adjuvant in cardiovascular disease
- Adjuvant in sporting competitions
- Adjuvant in liver diseases
- Adjuvant in baldness
- Adjuvant in depression
- Adjuvant in hepatitis
- Adjuvant in alcohol-induced hepatitis fatty liver
- Adjuvant in chronic general fatigue
- Increasing S-adenosyl-methionine levels
- Conflicting arteriosclerosis
- Decreasing apopletic stroke risk
- Decreasing fat tissue amount
- Improving glucose metabolism
- Improving dry mouth
- Improving homocisteinuria which does not respond to pyridoxine improving use of oxygen
- Improving oxygen utilization
- Reducing triglycerides levels in liver
- Reducing Cholesterol
- Reducing liver lipidosis
- Useful for immune deficiency deficit (immunomodulating)
- Useful for hyperhomocysteinemia
STRUCTURE AND PROPERTIES
From a structural standpoint, T. differs from dimethylglycine in presence of a third methyl group (CH3). T. operates very successfully in methylation or trans-methylation process, which is the process by which methyl groups (CH3) are transferred from one molecule to another; it is a biochemical process essential to life, health and regeneration of body cells. Vitamins, hormones, neurotransmitters, enzymes, nucleic acids (RNA, DNA) and antibodies largely depends on methyl groups transfer to complete their synthesis and function in humans.
There are more than 41 known transmethylation reactions in humans. For example, methyl groups convert homocysteine (toxic amino acid that can cause heart and vascular problems) into amino acid methionine, which is a beneficial amino acid, present in all kind of proteins, of which homocysteine is a normal metabolism byproduct..
Our body uses only small amounts of homocysteine but it is known that if we take some large amount, it become toxic at all.
This is not unusual for a metabolism by-product, in fact, our body has natural mechanisms of detoxification, one of this is methylation.
However, there are some genetic defects that cause a significant increase of homocysteine levels in the blood, which allowed us to discover that homocysteine is the primary cause of heart disease. It was also shown that homocysteine also causes atherosclerosis. The atherosclerosis begins when we have a freeze on nitric oxide production (NO) by endothelial cells. This block is commonly called EDRF [endothelial, derived relaxing factor].
Nitric oxide not only relaxes arteries but also prevents the formation of plaques. High concentrations of homocysteine blocks EDRF thereby starting arteriosclerotic process. Homocysteine irritates muscle cells of arteriesas well , thus causing a proliferation of the arteriosclerotic process.
So we can say that homocysteine is merely a marker of the efficiency of methylation. Methionine ( methylation product of homocysteine) produces high concentrations of SAM (S-adenosyl-methionine), a natural antidepressant and donor of methyl groups.
The increase of SAM is positive, both in prevention and treatment of several metabolic disorders including those caused by serious organic deficit states such as in cancer patients and those caused by alcoholic stress.
It is one of the essential amino acids with an antioxidant activity, it is very important for the functioning of liver because it prevents an abnormal accumulation of fat and the production of antibodies and it can be converted to cystine, in the presence of vitamin B12.
In combination with inositol and B vitamins helps suffering livers. It participates in the formation of carnitine, choline, creatine, adrenaline, etc. interacting with other substances to detoxify body from harmful chemicals and it is included in the supplements as anti-fatigue agent.
If we just take adequate amounts of vitamin B6 a lot of homocysteine we produce would be converted into cistatione, which is an important deactivator of free radicals and is an antioxidant as well. Half of homocysteine is detoxified in this manner, the other half is detoxified through another process called transmethylation. Thus it happens that the 5-methyltetrahydrofolate, which we produce from acid folic, gives its methyl group to homocysteine thus converting it into an essential amino acid: methionine.
Another way in which homocysteine is converted into methionine is by the transfer of a methyl group from T.
DNA of cell nucleus loses methyl groups because of the normal cellular aging. Each molecule of T. gives three methyl groups to DNA and this helps the remethylation process, that is repairing DNA molecules. In general we can say that this program helps to repair cells to slow the aging process. T. reduces homocysteine levels in blood, a molecule that can cause arteriosclerosis, thrombosis and other damage to the body. [T. converts homocysteine to methionine and S-adenosylmethionine (SAME)].
Homocysteine is a sulphured amino acids, osculant of the conversion of methionine to cysteine. The conversion of homocysteine to methionine (remethylation process) or its conversion to cysteine (trans-sulphuration) represents the main metabolic pathways capable of maintaining its intracellular levels within a narrow range. Its controlled release into bloodstream, on the other hand, allows you to measure its plasma concentrations that represent an accurate index of tissue homocysteine status .
Several epidemiological surveys have shown a correlation between clinical vascular origin incidence and homocysteine serum levels (venous thrombosis, embolic events, increased incidence of atherosclerotic diseases): in general we can say that high circulating plasma levels of homocysteine are considered a independent risk factor for vascular disease.
Elevated serum homocysteine levels may depend on several factors, both congenital ones (enzyme deficiencies) or acquired ones. Hyperhomocysteinemia is often correctable with appropriate treatment. By T. there is a double benefit: we donate the methyl group to produce dimethylglycine and homocysteine (Vitamin B15) (Fig. 1).
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