Homocysteine Reduction with Vitamin B

Published on June 27, 2013 by Dr. Traj Nibber

Two recent studies from Oxford University have provided major clues about the cause, as well as how to significantly delay the progression of Alzheimer’s disease (AD) in the elderly.

AD is the most common form of dementia, a neurodegenerative disease that progressively worsens in severity with time as it destroys nerve cells. The physiological and social impact of this condition is huge, with an estimated cost of over 200 billion in the US alone. There are 35 million sufferers world-wide, with that number expected to triple by 2050. Unfortunately, neither the cause nor cure has yet been identified. There are several chief culprits, including amyloid beta protein and tau tangles which may be caused by both oxidative damage and/or inflammation, although causation has not yet been proved.

Normal ageing is associated with a slight shrinkage of the brain, approximately half a percent every year. However, that figure doubles that when mild cognitive impairment sets in, and increases to 5 percent in AD patients!

The relationship between cognitive function and B vitamin intake is well known but has never been proven. Additional evidence comes from other diseases like chronic alcoholism, where absorption of B vitamins is greatly reduced with impaired cognitive function.

The initial 2010 study involved 271 patients with early signs of memory impairment and learning skills; both are considered to be signs of mild to moderate AD. In addition to various standard memory tests, the patients underwent total brain scans to “see” what effects the B-vitamins had on the size of the brain. Various scans like Positron Emission Tomography (PET) or MRI are widely used techniques to look at the size of the brain.  A shrinking brain is another sign that closely correlates with AD and is largely due to a loss of brain cells called neurons. Patients given the highest dose of B vitamins were reported to undergo a 50% reduction in the shrinking of the brain compared to those patients taking placebo or “dummy” pills. Another major finding was that the reduction in brain shrinking only occurred in those patients with a high homocysteine level in the brain, but not in those patients that had normal homocysteine levels. The significance here is that homocysteine may be a marker for AD.

Homocysteine is an amino acid that is generally present in our blood in tightly controlled concentrations. However, when excess amounts are produced, the amino acid is prone to oxidation of its free cysteine residues by free radicals from various oxygen and nitrogen species circulating in our blood. Free radicals are generally created by poor diet, toxins, carcinogens and other chemicals, stress and radiation such as UV light. Oxidized homocysteine is highly toxic to many cells including blood vessels; it may cause atherosclerosis or hardening of the arteries, or in the case of the brain, death of neurones. Kilmer McCulley a pathologist in Boston, first reported the link between homocysteine and atherosclerosis in 1969, and was promptly fired by his hospital for daring to make such a link. He was vindicated three decades later for his pains.

One theory for shrinking of the brain is perhaps that as we age our bodies are less able to extract B vitamins from the foods we eat, in part due to a reduced level of acidity in our stomachs, and/or over prescription of anti-ulcer drugs that lower acid levels in the stomach. High acid levels in the stomach are needed to let the various enzymes in the stomach perform optimally.

There has been plenty of research showing that when combined, certain nutrients particularly, vitamin B6, vitamin B12 and folic acid can significantly reduce homocysteine levels. These three nutrients have been found to be helpful in protecting blood vessels by reducing homocysteine levels and thus preventing atherosclerosis.

The Oxford research team revisited the homocysteine-B-vitamin-AD link this year and published even more impressive results. This time the study looked at a part of the brain called the hippocampus that is specifically associated with memory and learning; its atrophy or shrinkage is closely linked to AD. The study looked at 80 mild to moderate AD patients who consumed B-vitamins in daily doses (B6- 20mg, B12- 0.5mg, and folic acid 0.8mg) and compared them to 76 patients who took a placebo for two years. Once again, the researchers confirmed their 2010 findings, but this time there was a 90% reduction in shrinking of the brain that is specifically associated with memory, the hippocampus.

How does Homocysteine fit in with the cause of AD?

A current hypothesis of AD formation is one of two possibilities. The first possibility is that a small molecule called beta amyloid peptide begins to turn into “sticky” plaques, much like the cholesterol plaques that form in our blood vessels which eventually lead to the hardening of the arteries; similarly, these beta amyloid plaques eventually destroy the brain cells. An alternative hypothesis is that fibril like tau proteins begin to form “knots” or tangles that literally end up choking the brain cells causing death. It is not clear which possibility will win the day or for that matter both may be responsible in some manner. Nonetheless, it is now thought that homocysteine encourages the formation of these aggregates of tau fibrils. By lowering the homocysteine levels, it is suggested that fibril formation will be prevented, brain cell death averted and thus cognitive functions preserved.

The Oxford University group have certainly provided more ammunition for the regular intake of B vitamins to prevent and/or delay the onset of the dreaded AD. But which vitamin B formula to take? Not All B vitamins are the same. B vitamins like many other nutrients have to be converted into a more active or readily useable form. Thus folic acid has to be converted into a more active form that the body can use, this being 5-methyl tetrahydrofolate. Similarly, pyridoxal-5-phosphate is the activated form of vitamin B6, and methylcobalamin is a more superior form of B12 than the conventional cyanocobalamin form used in most vitamin formulations. There is much to be said about using these active forms that are used in formulations such as Advanced B Complex.

There are other nutrients that may also play a role in preserving cognition by some different mechanism, for example the Longvida form of curcumin which is a highly bioavailable form that not only reaches much higher concentration levels in the blood, but also in the brain tissues as shown by the recent study conducted at Ohio State University. In this study, participants taking only 80mg of the Longvida form of curcumin found in CurcuViva daily showed high levels of curcumin in the brain, as well amyloid levels were significantly reduced.

Another very exciting natural molecule is Vivimind. Vivimind is naturally extracted from seaweed and has probably the most impressive array of clinical studies of ANY natural product to back up its effectiveness in improving cognition in patients with Alzheimer’s disease. Over sixteen studies have been conducted, ranging from phase I (animal studies), phase II (human dose-response studies), and phase III (full-scale long- term, gold standard, randomised, double-blind, multi centre studies) which are so expensive that few if any natural product make it this far. Vivimind is backed by over two-hundred million dollars and has twelve years of research investment to its credit and in establishing its efficacy.

Vivimind phase III studies also looked at brain scans of the hippocampus. Treatment with Vivimind showed a 68% reduction in the shrinking of the hippocampus, plus a host of other improvements including reduced levels of free radicals, inflammation markers and significantly better cognition scores. Another key finding was that Vivimind works well for the more aggressive form of AD, in patients that have the ApoE4 genes.

The mechanism of Vivimind is different than B-vitamins or CurcuViva in that Vivimind prevents both the formation of beta amyloid peptide and tau fibrils, and in addition speeds up the clearance of amyloid and tau fibrils. Certainly, taking Vivimind, plus a B-vitamin formula like Advanced B Complex, and a curcumin product like CurcuViva would be an excellent combination to take.

You may also be interested in: "The Link Between Alzheimer’s Disease & Vitamin B"

Image by © 2013 gitusik via DollarPhotoClub


Daoud G et al. “Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment” PNAS, 2013; 110:9523-9528

Smith DA et al. “Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: A randomised controlled trail” PLOs ONE, 2010; 5: 1-10

Miller G “Stopping Alzheimer’s before it starts” Science, 2012; 337: 790-792

Di Silvestro R et al “Diverse effects of a low dose supplement of lipidated curcumin in healthy middle aged people. Nutrition Journal 2012, 11:79-85

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    B vitamin really is a super vitamin. I take it with my selenium supplement, and see such good results.