Juvenon Health Journal volume 9 number 11 november 2010
By Benjamin V. Treadwell, Ph.D.
Do we need to supplement our diet with vitamins to maintain optimum health? If so, which ones and how much of them? (For more on vitamins, see Juvenon Health Journal, Volume 1, Number 5, “Why Take Vitamin Supplements?”.) Unfortunately, the recommendations we get, from respected and reputed health professionals, are often conflicting.
Perhaps the confusion lies in the shortage of significant clinical studies that definitively demonstrate dosage and benefits. Many of the early studies were flawed due to the lack of knowledge concerning the function(s) of some of the vitamins. Take Vitamin D (actually a hormone), for example.
The vitamin was initially prescribed for rickets, a bone mineral deficiency disease common to children in the 18th century. The minimum daily requirement was calculated for normal bone formation. Over the past several years, however, numerous studies have attributed several additional functions to vitamin D, such as promoting proper function of the immune system and mental health (receptors for the vitamin are present in the brain).
In light of these discoveries, as well as genetic variations and the need for more vitamins as we age, the initial recommended dose is now generally considered too low. In fact, speculation is that, even with supplements, as many as 50-70% of the American population may be vitamin D-deficient to some degree.
Vitamin D is not alone. This issue of the Health Journal focuses on recent findings about another group of vitamins, which seem to indicate we may need much larger doses of vitamin B than previously recommended.
Three Bs for the Brain
If you measured your height today, and it had been a few decades since your last measurement, you would probably find that you’re shrinking. As we age, this is characteristic of more than our height. The organs of the body, including the brain, also become smaller. But there may be good news, at least for the brain. A recent human study has shown long-term positive effects of three B vitamins – B6 (pyridoxine), B9 (folic acid), and B12 (methylcobalamin) – on the age-associated brain shrinkage.
The experiment, performed in the United Kingdom (UK), also established a correlation between B vitamins and improved cognitive ability, as well as lower homocysteine levels. Homocysteine, an amino acid present in variable amounts throughout our bodies, increases in our cells with age. This increase has been linked to overall arterial, cardiovascular and brain health (including mental function).
UK Study Specifics
At the start of the study, all of the subjects were age 70 or older and had been diagnosed with mild, age-related cognitive impairment (minor memory issues not serious enough to interfere with daily routines). Half the group (133) took 20 mg B6, 0.8 mg B9 (folic acid) and 0.5 mg B12 per day, while the other half, the control group, was given a placebo.
Before the study began, blood was drawn from each subject for a number of measurements, most important of which were the existing levels of homocysteine, B6, B9 and B12. In addition, a volumetric MRI was performed to establish a brain-size baseline. All measurements were repeated at the end of the experiment’s two-year duration.
30% Less Age-related Brain Atrophy
Comparisons showed that the vitamin levels increased in the plasma of the subjects taking them as follows: B12 – 100%, B9 – 270%, no change in B6 levels. There was no significant change in the plasma vitamin levels of those taking the placebo. Furthermore, the plasma homocysteine levels decreased by 22.5% in the vitamin group and increased by 7.2% in the controls.
What is most striking is the correlation of this 30% difference in homocysteine levels with a 30% greater loss of brain volume (rate of atrophy) in the placebo group. This would seem to suggest the elevated homocysteine is a causal factor in age-related brain atrophy which can be positively affected by supplementing with a large dose of the B vitamins.
Although this study was not specifically designed to examine the B vitamins’ effects on age-related cognitive impairment, the vitamin B-supplemented group also scored higher in limited testing of mental acuity.
300% Vitamin B Supplementation
Both the vitamin B-supplemented and placebo groups began the UK study with what are, according to many health professionals, normal, healthy plasma levels of the B vitamins. Yet, increasing these levels from 100% to 300% slowed brain atrophy, decreased homocysteine levels and improved mental function.
These results seem to strongly support B12 and folic acid (B9) supplementation at considerably higher than current recommended levels, at least for those with mild, age-associated cognitive impairment. In general, humankind is living longer which means many will reach an age where higher doses of specific vitamins, like the Bs, may help us realize better health and improve our quality of life. Further and broader research is certainly indicated.
A group of investigators, from the University of Oxford, UK and the University of Oslo, Norway, recently authored “Homocysteine-lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: a Randomized Controlled Trial.” The report, published in Public Library of Science One, details a study of the effects of specific B-vitamins on cognition and brain health in older human subjects.
Motivated by numerous reports that implicated homocysteine, an amino acid metabolite, in the development of age-related brain atrophy, the research team set out to determine whether vitamins B6, B9 and B12, known to lower plasma homocysteine levels, would positively affect patients diagnosed with age-related mild cognitive impairment.
The experiment included 266 patients age 70 or older, half in a treatment group taking 20 mg B6, 0.8 mg B9 (folic acid) and 0.5 mg B12 per day, and half in a placebo group. Before the study began, each patient’s blood was analyzed for homocysteine levels and their brains were scanned with an MRI to measure volume. The same measurements were repeated at the end of the two-year study.
The results were impressive, clearly demonstrating a B-vitamin-related decrease in homocysteine levels in the treatment group – 30% lower relative to the placebo group – and a corresponding decrease in the rate of atrophy of the brain, up to 53% less. (The authors also mention a correlation between the rate of atrophy and cognition in the treatment group: those with greater brain atrophy scored lower on a cognition test.)
For brain health in patients with mild, age-related cognitive disorders, the results seem to indicate significant benefits from supplements of the three B-vitamins. Since no safety issues were found, the investigators concluded that high doses of B vitamins can be used to reduce the rate of atrophy of the brain in elderly people with MCI, even those with B-vitamin baseline levels considered to be in the normal range.
The team also speculated that high doses of folic acid, vitamins B6 and B12 might slow the conversion from MCI to Alzheimer’s disease or other forms of dementia. The researchers suggest that clinical trials are warranted to determine whether there is any validity to their hypothesis.
Read abstract here.
This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.
Dr.Treadwell answers your questions.
question: As a layman (financial analysis), I find fascinating what appear to be the two main theories of aging: oxidative damage and the Hayflick limit.
Major question that springs immediately is length of the interval between clippings of the 52 Hayflick “coupons”? Assume it must be variable, depending largely on degree and speed of oxidative damage, itself a function of variable lifestyles and genes? Juvenon, presumably, by ongoing maintenance and repair of mitochondrial machinery, would work to extend the Hayflick intervals, as well as postpone the onset of senescence after the last Hayflick coupon has been spent?
Collateral question is what happens immediately after each “mitosis” in the Hayflick sequence? Surely both “new” cells do not survive? One, perhaps, is loaded with oxidative gunk and is killed off (“apoptosis”)? While the other is “clean” and functions right on through to the end of the next Hayflick interval? – J
answer: As you know, J, Dr. Leonard Hayflick demonstrated that normal cells are not immortal. He theorized that cell division processes have a specific counting mechanism and showed that they are “limited” to 40-60 divisions before growth stops.
The Hayflick limit is actually determined by the length of the telomere, the end of the chromosome. It provides a binding site for the cell-replicating enzyme, DNA polymerase. Because the telomere wears away with every cell division, it eventually (30-50 divisions) becomes too short for the replicating enzyme to function, as it has no receptor on which to bind.
The speed at which the cell divisions occur and reach their limit is, as you suggest, influenced by genetics as well as lifestyle and consequential oxidative damage. By enhancing anti-oxidative protection and supporting mitochondrial efficiency, the Juvenon cellular health formula may help prevent some of the cellular damage, or at least slow it down.
Regarding your question about the mitosis process, during cell division, the two daughter cells share the damaged cellular components from the parent cell. So, both are impaired.
Benjamin V. Treadwell, Ph.D., is a former Harvard Medical School associate professor.