Vitamin B6, B12 and folic acid
In many people, homocysteine metabolism is disrupted, allowing homocysteine to accumulate. It is estimated that 9% of the population and approximately 20% of patients with cardiovascular problems suffer from a genetic abnormality, preventing homocysteine from being correctly broken down. These people therefore have significantly elevated levels of homocysteine in the blood. However, of equal importance is that even relative deficiencies of vitamin B6, vitamin B12 and particularly folic acid can significantly increase levels of homocysteine.
Perhaps to an even greater degree than cholesterol, an elevated level of homocysteine seems to be a major risk factor for the development of cardiovascular diseases. There is increasing scientific evidence that homocysteine can damage blood vessel walls, thereby giving rise to plaque formation and decreased blood vessel elasticity, ultimately restricting blood flow. Homocysteine can also stimulate blood platelet coagulation. Over time, this can result in, for example, cardiac infarction or stroke. Other disorders, such as neural tube defects (open spine), mental deterioration in the elderly (dementia) and rheumatoid arthritis, are associated with an elevated level of homocysteine.
Vitamin B6, B12 and folic acid are substances essential to normalising an elevated level of homocysteine.
Additionally, these ingredients can prove their worth in a number of other disorders, including premenstrual syndrome (PMS), where there is often evidence of (relative) vitamin B6 deficiency.
These three B vitamins all play an important role in so-called methylation reactions in the body, an important biochemical process whereby a methyl group (-CH3) is sustained. Folic acid and vitamin B12 supply the methyl groups required for this process. The reformation of methionine from the harmful homocysteine is an important example of a methylation reaction. But well-functioning methylation is also essential for many other important reactions in the body, such as the synthesis of neurotransmitters and DNA synthesis.
- elevated levels of homocysteine (hyperhomocysteinaemia)
- PMS (premenstrual syndrome)
- migraine (certain types)
- Alzheimer’s disease
- the prevention of kidney stones (oxalate)
- anaemia (megaloblastic anaemia)
- development of the embryo (prevention of neural tube defects, e.g. open spine)
For PMS, start to take the aforementioned B vitamins on the 7th day of your cycle and continue to take these until menstruation. Repeat this process every month. When these B vitamins are taken to prevent neural tube defects (open spine), these have to be commenced a minimum of 4 weeks before fertilisation and taken until at least 8 weeks after fertilisation. However, for optimal neuronal development, it is better to take these B vitamins for the entire pregnancy.
- Rimm EB, et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA 1998 Feb 4;279(5):359-64.
- Robinson K et al. Low circulating folate and vitamin B6 concentrations: risk factors for stroke, peripheral vascular disease, and coronary artery disease. European COMAC Group. Circulation 1998 Feb 10;97(5):437-43.
- Nygard O et al. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med 1997 Jul 24;337(4):230-6.
- De Jong SC et al. Normohomocysteinaemia and vitamin-treated hyperhomocysteinaemia are associated with similar risks of cardiovascular events in patients with premature peripheral arterial occlusive disease. A prospective cohort study. J Intern Med 1999;Jul;246(1):87-96.
- Murray MT. Encyclopedia of Nutritional Supplements. Rocklin, CA: Prima Publishing, 1996.