Francis Bacon, who was a philosopher in the 16th century, said that, “Some books are to be tasted, others swallowed, and some few to be chewed and digested.” The same principle can apply to the written word of the present. If we took everything we read in magazines or over the internet as gospel, conflicting words and ideas would create such confusion that the truth would be more elusive than it has been for decades. While we are able to identify and to reject half-truths in the spoken word, we tend to give them credence if they appear in print. Such is the case with news and reports about the human body and its health and maintenance, and the things we can do and take to guarantee them.
Reports from Fox, Reuters and Medline, among other news services, have said that B-vitamins can boost memory. Seeing that headline is all some folks need to draw a hasty conclusion, hoping that their loved ones with Alzheimer’s or some other neurological irregularity will be cured. At best, such a conclusion might be drawn following a syllogistic approach, a form of reasoning that relies on major and minor premises: if this causes this, and if that causes that, then this causes that. Whether or not this is true depends on acceptance of the phrases, “some of the time” and “all of the time.” Let’s see if we can make sense of the original proposition, that B-vitamins can boost memory.
The study cited by the news services was conducted by Dr. Janine Walker, a mental health researcher from the Australian National University, who reported in the American Journal of Clinical Nutrition that long-term supplementation with folic acid and vitamin B12 promotes improvement in cognitive functioning. (Walker, 2012) What the headline doesn’t tell us is that the study lasted two years, and that physical exercise was part of the protocol. You have to read the small print, which means the details of the study need to be chewed and digested. The confounding factors and specific provisions must be considered.
Homocysteine (Hcy) is such a factor--and a provision if it’s measureable. Homocysteine is a homologue of the amino acid, cysteine, differing by an additional methylene group (CH2). It’s best known as a marker for inflammation associated with increased risk of cardiovascular disease. Whether or not lowering homocysteine will also lower CVD risk is still under examination, but it has been accepted that raised Hcy is associated with poor cognitive performance in the general population, not only in the elderly. Increases in serum folic acid levels are accompanied by decreases in Hcy levels. (Durga, 2007) But this doesn’t mean that cognitive function will automatically improve. It takes time, another factor to be weighed. After three years of folic acid supplementation, Durga and his Dutch colleagues learned that the molecule, did, in fact, improve specific domains of cognitive function, particularly those that decline with age. What we are not told is that folic acid (vitamin B9) works best in the company of vitamins B12 and B6, where its role as a promoter of brain function can be fully realized.
If there is a pin to be put into this balloon, it comes courtesy of the Cochrane Database and its systematic reviews of primary research in health care and health policy. One of its 2008 reviews examined the effects of folic acid on demented people and their cognitive shortcomings, only to announce that no consistent evidence supports the use of folic acid—with or without vitamin B12—to effect improvement. They are carefully deliberate to add, however, that long-term use of folic acid (also known as folate in foods) does appear to improve the cognitive function of those individuals with elevated homocysteine levels. (Malouf, 2008) Do you see the factor? Long-term use.
Many elderly present with movement disorders to some degree. Swedish investigators looked at a population of community-dwelling septuagenarians who suffered both movement and cognitive disadvantages, treating them with vitamins B9, B6, and B12. More than 60% of the men and almost 50% of the women had high Hcy levels and high methylmalonic acid (MMA) concentrations, the latter indicating B12 deficiency. Vitamin therapy lowered both markers, but failed to mitigate both the movement and cognitive deficits. This does not mean the therapy is useless, though. The report allows that dosage could have been too low to prove effective, or that the physical and mental declines could have become irreversible. (Lewerin, 2005) If such decline is recognized at all, could it / should it have been identified years—or even decades—sooner? With all illness and debility, isn’t that ounce of prevention worth lots more than the pounds of cure? To be considered also is that stores of nutrients decline sharply with age. For how long were they deficient? How about the form of the nutrient? Methylcobalamin is the much preferred form of vitamin B12, but the Swedish study used cyanocobalamin, a form that is unnatural to plants and animals. And, it contains an “insignificant” amount of cyanide that still must be eliminated from the body. Isn’t the mere four months duration of this study too little time to come to a righteous conclusion? The factor? Time.
“Over the short or medium term,” announces a Glasgow paper, cognitions did not improve with the vitamin cocktail. This study population, older than sixty-five and comparatively small at 185 participants, suffered ischemic vascular disease, that which decreases blood supply to an organ by constricting a blood vessel. Since all ischemia is not the same for all people, that condition might just confound the matter. This study lasted three months to one year. Here is a senior population with constrictive vascular disease, probably taking one or more medications, whose compliance is not monitored, with unknown dietary habits and unmentioned polypharmacy, and possibly experiencing other health issues. (MacDonald, 2005). Are we expected to accept the conclusion without question?
In ameliorative protocols where the patient is ambulatory, exercise is warranted, either as an isolated or as a supportive element. (Wen, 2010) (Harkcom, 1085) (Kirkcaldy, 1990) Nonetheless, the administration of selected B-vitamins has an effect on the factors that interfere with brain function and memory, if only because they can mitigate the adverse effects of inflammation. Homocysteine is a documented CVD factor that is related to both vascular dementia and Alzheimer’s disease. (Stabler, 2003) It appears that the attenuation of Hcy with folic acid, vitamin B6 and vitamin B12, accompanied by a modicum of exercise, and conducted over a reasonable period of time, can yield the desired result in cognitive change. IF homocysteine is related to cognitive decline, and IF a B-vitamin cocktail reduces homocysteine, THEN the cocktail may be able to reverse faulty cognition (in certain circumstances). Because these supplements are water-soluble, toxicity is of little concern regardless of the elevated dosage required.
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