When sports chiropractors first appeared at the Olympic Games in the 1980s, it was alongside individual athletes who had experienced the benefits of chiropractic care in their training and recovery processes at home. Fast forward to Paris 2024, where chiropractic care was available in the polyclinic for all athletes, and the attitude has now evolved to recognize that “every athlete deserves access to sports chiropractic."
B-Vitamin Supplementation in the Prevention of Cancer, Heart Disease and Dementia
In recent years, a number of well-controlled studies have highlighted the importance of optimal B-vitamin status as a means to reduce the risk of heart disease, certain cancers, and inflammatory states; improve detoxification processes; and maintain brain and cognitive function as we age. B vitamins are also essential for the synthesis of red blood cells, normal cell replication, and many more crucial functions. Known for their anti-stress and anti-fatigue properties, a B-50 complex is an important consideration in a health optimization/anti-aging program.
B Vitamins Reduce the Risk of Cervical and Colon Cancer
The nutritional status of certain B vitamins has emerged as an important factor in the risk profile for cervical and colon cancer. Folic acid and vitamin B12 are required to help the body convert a compound called homocysteine to methionine. Once formed, methionine is readily converted to S-adenosylmethionine, which is necessary to form the DNA that makes up our genetic blueprints for life.
If folic acid and/or vitamin B12 status become suboptimal, the amount of S-adenosylmethionine declines. This results in an inability to properly produce DNA as cells replace themselves from one generation to the next. The danger is that genetic errors become more common, and genetic linkages become more fragile (hypomethylated DNA) and prone to breakage with resulting mutations. These alterations to genetic structure provide the foundation for cancerous changes to occur in our genes. It is well-established that our DNA is much more prone to cancerous mutations under conditions of suboptimal intake of folic acid and vitamin B12.
Women in a marginal deficiency state of folic acid are known to be prone to cervical dysplasia and cervical cancer. This is related to the fact that the cells which line the cervix replace themselves every 7-14 days, and therefore, must continuously synthesize DNA. Studies have demonstrated that poor folic acid status can lead to DNA abnormalities, with subsequent development of cervical dysplasia or megaloblastic features of cervical cells (large abnormal cell appearance). With respect to cervical dysplasia (a precancerous condition), folic acid, via its role in DNA synthesis and DNA repair, has been shown to inhibit the ability of the human papillomavirus (HPV) from invading the DNA of surface cervical cells. HPV is strongly associated with cervical cancer; thus, folic acid supplementation is an important step to prevent HPV's invasion into cervical tissue. Women who have experienced multiple sex partners are most prone to infection with HPV, as contact with human semen is the way in which cervical cells are typically exposed to the virus.
Oral contraceptives are also known to increase the rate of cell division of cervical cells, thereby increasing the need for adequate folic acid intake. Studies by Whitehead, et al., and Butterworth, et al., have demonstrated that folic acid supplementation can reverse cervical megaloblastic changes and cervical dysplasia, respectively, in patients using oral contraceptives. In fact, oral contraceptive use is a known risk factor for cervical dysplasia, primarily due to its effect on speeding up cell division rates.
In the study by Butterworth, et al., patients with mild and moderate degrees of cervical dysplasia showed reversal of their condition over a three-month trial period with folic acid supplementation at very high levels (5,000-10,000 mg per day). In both studies, the authors noted a statistically lower mean red blood cell concentration of folic acid in oral contraceptive users compared with nonusers, particularly in patients with cervical dysplasia. Other population studies (epidemiological studies) consistently support the research showing that folic acid plays a protective role in the prevention of cervical dysplasia.
Unfortunately, up to 88% of the population consumes less than 400 mcg per day of folic acid. This is the level that women should ingest to reduce the risk of spinal birth defects in their offspring. As it turns out, the same level of folic acid intake appears to be sufficient to reduce the risk of cervical dysplasia.
With respect to colon cancer, Giovannucci and fellow researchers assessed dietary intake for a one-year period in women enrolled in the Nurses' Health Study, and men enrolled in the Health Professional Follow-up Study, using a semi-quantitative and food frequency questionnaire. Of the 25,474 subjects, 895 developed adenomatous polyps of the left colon or rectum.
A major finding of the study was that high folic acid intake was protective against colorectal cancer. Women in the top 20% intake level of folic acid demonstrated a 34% decreased risk of colorectal cancer, compared with women in the bottom 20% intake level of folic acid. For men, a 37% reduction in risk was observed for the highest 20% intake of folic acid versus the lowest 20% intake group. Users of multiple vitamins demonstrated the greatest reduction in the risk of colorectal cancer in this study. Much of this protective effect was shown to be due to folic acid. These findings are consistent with other epidemiological evidence indicating that folic acid reduces the risk of colorectal cancers. It is important to keep in mind that colon cancer is the second leading cause of cancer death in North America.
B Vitamins in the Prevention of Cardiovascular Disease
In regards to the role of B vitamins in the prevention of heart disease and stoke, in the mid-to-late 1960s, several researchers first identified that high blood levels of homocysteine are associated with premature narrowing of arteries, leading to heart attacks and related heart disease. Homocysteine is thought to increase the risk for heart disease through direct toxic effects to the cells that line our blood vessels. It increases the tendency for blood platelet cells to clump together in the bloodstream, thus obstructing blood flow. It also stimulates muscle fibers beneath the blood vessels to grow into the artery, further impairing the flow of blood. A high blood level of homocysteine is now considered to be a significant risk factor for stroke, heart attack, and reduced blood flow to fingers, toes and peripheral body parts.
Homocysteine is formed routinely by the cells of our body during the course of normal metabolism. Fortunately, our bodies can eliminate homocysteine by converting it into other important amino acids such as methionine, cystathionine, serine, and cysteine. However, in order to convert homocysteine into these desirable, nontoxic amino acids, our bodies require an adequate intake of the B vitamins - folic acid, B6 and B12. A number of recent studies have shown that individuals with high blood levels of homocysteine can reduce levels by supplementing their diet with folic acid, vitamin B6 and/or vitamin B12. Presently, elevated blood levels of homocysteine are considered to be responsible for approximately 10% of all heart attacks each year in the United States.
Reporting in the Journal of the American Medical Association (February 1988), Rimm and fellow researchers demonstrated that women who supplemented their diet with a multiple vitamin had a 24% lower risk of nonfatal and fatal heart attacks. During the 14-year follow-up, they documented 658 incident cases of nonfatal heart attacks and 281 cases of fatal heart attacks among the 80,082 women enrolled in the Nurses' Health Study. After controlling for well-known risk factors for heart disease, the researchers showed that high intake levels of folic acid (696 mcg/day) were associated with a 31% lower risk for heart disease episodes, compared with lower folic acid intake levels (158 mcg/day). For vitamin B6, there was a 33% lower risk for heart disease episodes in subjects ingesting 4.6 mg/day, compared with subjects ingesting 1.1 mg/day. Individuals with high intakes of both folic acid and vitamin B6 experienced a 45% reduced risk for fatal and nonfatal heart attacks.
A major conclusion of this study is that intake of folic acid and vitamin B6 above the current recommended dietary allowance may be required to prevent heart disease. Each 100 mcg/day increase in folic acid was associated with a 5.8% lower risk of heart disease. It is estimated that 88%-90% of the population has dietary folic acid intakes below 400 mcg/day. Findings from the Health Professional Follow-up Study (involving male health practitioners) also demonstrated that high folic acid intake was associated with a significant reduction in heart disease risk. Thus, for both men and women, high levels of folic acid intake are strongly linked to the prevention of heart disease.
The current recommended dietary allowance for folic acid is 180 mcg/day for nonpregnant women. The average dietary intake in the United States among women is approximately 225 mcg/day. The overall evidence suggests that this level of intake is insufficient to minimize the risk of neural tube defects (e.g., spina bifida), and possibly heart disease. As such, many experts are urging that the recommended dietary allowance (RDA) be reset to the earlier level of 400 mcg/day.
Obtaining 400-700 mcg/day of folic acid is exceeding difficult to do without supplementation. The potential for this one simple intervention (a folic acid supplement) to prevent life-threatening problems is staggering, when you weigh all the evidence.
B Vitamins Help Preserve Memory and Cognitive Function
Deterioration of mental capacities has long been considered an aspect of the normal aging process. In recent years, however, the emerging scientific evidence has demonstrated that certain natural health products and supplements are effective in their ability to prevent, reverse, or even better manage cognitive impairment problems in older individuals. The Boston Veterans Affairs Normative Aging Study is one of many studies investigating the influence of nutrition on various aspects of age-related disorders.
In March of 1996, Drs. Riggs and associates published results from this study in The American Journal of Clinical Nutrition. Their findings indicated that older individuals with low blood concentrations of vitamin B12, vitamin B6, and the B vitamin folic acid had the poorest scores of brain function, measured by a battery of cognitive tests.
In previous studies, clinical deficiencies of B vitamins have been implicated in brain-related disorders, including reversible dementia (vitamin B12 and possibly folate), depression (folate), and electrophysiological dysfunction, including convulsions (vitamin B6). In healthy older adults, blood levels of B vitamins usually considered to be in the normal range were associated with poorer scores on tests of delayed recall, abstract reasoning, and selective attention. There is also good evidence that deficiencies of vitamin B12, folic acid, and vitamin B6 increase with age and are common in older adults. Thus, there is growing support for the premise that optimal B-vitamin status can prevent, slow or reverse the deterioration in memory and other mental capacities important to quality-of-life issues in older individuals.
The Normative Aging Study involved 70 male subjects, ages 54-81. The results of this study revealed that blood levels of vitamin B12 and folic acid appear to be related to cognitive performance in a different manner than vitamin B6 blood levels. Low blood levels of vitamin B12 and folic acid were associated with deficits in spatial copying. Higher blood levels of vitamin B6 were associated with better performance on two tests of memory. Another interesting finding was that nearly one half of the subjects in this study had low blood levels of vitamin B6 (<30 umol/L).
This study is extremely important because B vitamins are known to participate in brain chemistry and physiology. Vitamins B12 and folic acid are required as coenzymes in the synthesis of the neurotransmitters serotonin and catecholamines (adrenaline, norepinephrine). They are also required for the production of S-adenosylmethionine, which has known antidepressant properties. Vitamin B12 deficiency may also result in de-insulation of nerve fibers (demyelination), which produces a constellation of neurological symptoms. Vitamin B6 is a cofactor in the production of other neurotransmitters, including dopamine, norepinephrine, serotonin, GABA, and taurine.
Additionally, higher blood levels of homocysteine often result from subnormal intakes of folic acid, vitamin B12 and vitamin B6. High blood levels of homocysteine are associated with increased risk of cardiovascular, cerebrovascular (narrowed arteries in the brain), and peripheral vascular disease (narrowed blood vessels in the arms, hands, legs and feet).
Narrowed arteries in the brain (cerebrovascular disease) have been shown to be associated with decrements in psychomotor speed and on tests measuring fluid and visual abilities. Such cognitive dysfunction, therefore, may stem from high levels of homocysteine. As previously stated, vitamins B6, B12 and especially folic acid are key nutrients that prevent and reverse high blood levels of homocysteine.
In the Normative Aging Study, subjects with high levels of homocysteine performed, on average, like patients with mild Alzheimer's disease. They also exhibited difficulty in copying the most complex spatial figures. For example, few subjects in the highest 25 percent range of homocysteine concentrations completed the cube (22%) and tapered box (17%) correctly. By comparison, these figures are mastered by 50% of schoolchildren by age 13. Subjects with the lowest blood homocysteine levels demonstrated the best results on these tests.
The body of evidence continues to support the contention that B-vitamin nutritional status is crucial to the development and preservation of mental capacities throughout our lifetime. The sad reality is that many middle-age and elderly members of society have poor dietary intake and nutritional status of various B vitamins (vitamin B6, folic acid, etc.). For this reason, I continue to emphasize the multitude of benefits available from the daily use of a well-formulated multivitamin/mineral supplement that contains a B50 complex.
References
B-Vitamins and Cancer
- Butterworth CE Jr., Hatch KD, Gore H, Mueller H, Krumdieck CL. Improvement in cervical dysplasia associated with folic acid therapy in users of oral contraception. Am J Clin Nutr 1982;35:73-82
- Butterworth CE Jr., Hatch KD, Macaluso M, et al. Folate deficiency in cervical dysplasia. JAMA 1992;267:528-33
- Cravo ML, Mason JB, Dayal Y, et al. Folate deficiency enhances the development of colonic neoplasia in dimethylhydrazine-treated rats. Cancer Res 1992;52:5002-5006
- Feinberg AP, Gehrke CW, Kuo KC, et al. Reduced genomic 5-methylcytosine content in human colonic neoplasia. Cancer Res 1988;48:1159-1161
- Feinberg AP, Vogelstein B. Hypomethylation distinguishes genes of some human cancers from their normal counterparts. Nature 1983;301:89-92
- Freudenheim JL, Graham S, Marshall JR, et al. Folate intake and carcinogenesis of the colon and rectum, IntJ Epidemiol 1991;20:368-374
- Giovannucci, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma. J. Natl Cancer Inst. 1993;85(11):875-83
- Goelez SE, Vogelstein B, Hamilton SR, et al. Hypomethylation of DNA from benign and malignant human colon neoplasms. Science 1985;228:187-190
- Hoffman RM. Altered methionine metabolism, DNA methylation and oncogene expression in carcinogenesis. Biochim Biophys Acta 1984;738:49-87
- Lashner BA, Heidenreich PA, Su GL, et al. Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. A case-control study, Gastroenteral 1989; 97:255-259
- Nyce J, Weinhouse S, Magee PN. 5-Methylcytosine depletion during tumor development: An extension of the miscoding concept, Br J Cancer 1983;48:463-475
- Sauberlich HE. Evaluation of folate nutrition in population groups. In: Folic Acid Metabolism in Health and Disease (Picciano MF, Stokstad ELR, Gregory JF, eds). New York: Wiley-Liss, 1990;211-235
- Shivapurkar N. Poirer LA. Tissue levels of S-adenosylmethionine and S-adenosylhomocysteine in rats fed methyl-deficient diets for one to five weeks. Carcinogenesis 1983;4:1052-1057
- Wainfan E, Dizik M, Stender M, et al. Rapid appearance of hypomethylated DNA in livers of rats fed cancer-promoting, methyl-deficient diets. Cancer Res 1989;49:4094-4097
- Wainfan E, Poirier LA: Methyl groups in carcinogenesis: Effects of DNA methylation and gene expression. Cancer Res 1992;52:2071s-2077
- Whitehead N, Reyner F, Lindenbaum J. Megaloblastic changes in the cervical epithelium: association with oral contraceptive therapy and reversal with folic acid. JAMA 1973;226:1421-4
- Willet W. The search for the causes of breast and colon cancer. Nature 1989;338:398,394
- Winkelstein W Jr. Smoking and cervical cancer - current status: a review. Am J Epidemiol 1990;131:945-57;(discussion:958-60)
- Rimm E.B. et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA 1998;279;5:359-64
- McCull KS. Vascular pathology of homocysteinemia; implications for pathogenesis of arteriosclerosis. Am J Pathol, 1969;56:111-128
- Mudd SH, FinkelsteinJD, Irreverre F, Laster L. Homocysteinuria: an enzymatic defect. Science. 1964;143:1443-1445.
- Brattstrom L, Israelsson B, Norrving B, et al. Impaired homocysteine metabolism in early-onset cerebral and peripheral occlusive arterial disease: effects of pyridoxine and folic acid treatment. Atherosclerosis. 1990;81:51-60
- Morrison HI, Schaubel D, Desmeules M, Wigle DT. Serus folate and risk of fatal coronary heart disease. JAMA. 1996;275:1983-1896
- Chasan-Taber L, Selhub J, Roseberg IH, et al. A prospective study of folate and vitamin B6 and risk of myocardial infarction in US physicians. J Coll Nutr. 1996;15:136-143
- Giovannucci E, Stampfer MJ, Colditz GA, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma J Natl Cancer Inst. 1993;85:875-884
- Selhub J, Jacques PF, Wilson PWF, Rush D, Roseberg IH. Vitamin status and intake as primary determinanats of homocysteinemia in an elderly population. JAMA, 1993;270:2693-2698
- Nygard O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997;337:230-236
- Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Willett WC. Dietary folate, vitamin B6, and vitamin B12 intake and risk of CHD among a large population of men. Circulation. 1996;93:625. Abstract
- Tsai JC, Perrella MA, Yoshizumi M, et al. Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis. Proc Natl Acad Sci USA. 1994;91:6369-6373
- Stamler JS, Osborne JA, Jaraki O, et al. Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen. J Clin Invest. 1993;91:308-318
- Tawakol A, Omland T, Gerhard M, Wu JT, Creager MA. Hyper homocysteinemia is associated with impaired endothelium-dependent vasodilation in humans. Circulation. 1997;95:1119-1121
- Pancharuniti N, Lewis CA, Sauberlich HE, et al. Plasma homocysteine, folate, and vitamin B12 concentrations and risk for early-onset coronary artery disease. Am J Clin Nutr. 1994;59:940-948
- Bendich A. Folic and prevention of neural tube birth defects: critical assessment of FDA proposals to increase folic acid intakes. J Nutr Educ. 1994; 26:294-299
- Abou-Saleh MT, Coppen A. The biology of folate in depression: implications for nutritional hypotheses of the psychoses. J Psychiatr Res 1986;20:91-101
- Berg S. Psychological functioning in 70-and 75-year old people. Acta Psychiatr Scand 1980;Suppl 288:1-47
- Bohnen N, Jolles J, Degenaar CP. Lower blood levels of vitamin B12 are related to decreased performance of healthy subjects in the Stroop Color-Word Test. Neurosci Res Commun 1992;11:53-6
- Botwinick J, Storandt M. Memory, Related Functions and Age. Springfield, IL: Charles C Thomas, 1974
- Dakshinamurti K, Paulose CS, Siow YL. Neurobiology of pyridoxine. In: Reynolds RD, Leklem JE, eds. Vitamin B6: Its Role in Health and Disease. New York: Alan R Liss, Inc, 1985;99-121.
- Goodwin JS, Goodwin JM, Garry PJ. Association between nutritional status and cognitive functioning in a healthy elderly population. JAMA 1983;249:2917-21
- Hertzog C, Schaie KW, Gribbin K. Cardiovasular disease and changes in intellectual functioning from middle to old age. J Gerontol 1978;33:872-83
- Jacques PJ, Riggs KM. B vitamins as risk factors for age-related diseases. In: Rosenberg IH, ed. Nutritional Assessment of Elderly Populations. Measure and Function. New York: Raven Press, 1995.
- Joosten E, van den Berg A, Riezler R, et al. Metabolic evidence that deficiencies of vitamin B12 (cobalamin), folate, and vitamin B6 occur commonly in elderly people. Am J Clin Nutr 1993;58:468-76
- Leklem JE. Vitamin B6. A status report. J Nutr 1990;120:1503-7. 1987;83(suppl 5A):104-6
- Levitt AJ, Joffe RT. Folate, vitamin B12, and life course of depressive illness. Biol Psychiatry 1989;25:867-72
- Lindenbaum J, Rosenberg IH, Wilson PWF, Stabler SP, Allen RH. Prevalence of cobalamin deficiency in the Framingham elderly population. Am J Clin Nutr 1994;60:2-11
- Martin DC. B12 and folate deficiency dementia. Clin Geriatr Med 1988;4:841-52
- Riggs K, et al. Relations of vitamin B12, Vitamin B6, Folate, and homocysteine to cognitive performance in the Normative Aging Study. Am. J. Clin. Nutr. 1996; 63:306-14
- Rinn WE. Mental decline in normal aging: A review. J Geriatr Psychiatry Neurol 1988;1:144-58
- Sauberlich HE. Relationship of vitamin B6, vitamin B12, and folate to neurological and neuropsychiatric disorders. In: Bendich A, Butterworth CE Jr, eds. Micronutrients in Health and in Disease Prevention. New York: Marcel Dekker, Inc 1991:187-218.
- Selhub J, Jacques PJ, Wilson PWF, Rush D, Rosenberg IH. Vitamin status and intake as primary determinants of homocysteinemia in the elderly. JAMA 1993;270:2693-8.
- Shane B, Stokstad ELR, Vitamin B12 folate interrelationships. Annu Rev Nutr 1985;5:115-41
- Spieth W. Slowness of task performance and cardiovascular disease. In: Welford AT, Birren JE, eds. Behavior, Aging and the Nervous System. Springfield, IL: Charles C Thomas, 1965:366-400
James Meschino, DC, MS
Toronto, Ontario
Canada
www.renaisante.com