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American Journal of Clinical Nutrition, Vol. 80, No. 5, 1448-1449, November 2004
© 2004 American Society for Clinical Nutrition

LETTERS TO THE EDITOR

Vitamin B-6 status and coronary artery disease

Robert D Reynolds and James E Leklem

Department of Human Nutrition
University of Illinois at Chicago
Chicago, IL 60612
E-mail: reynolds{at}uic.edu
Department of Nutrition and Food Management
Oregon State University
Corvallis, OR 97331
E-mail: j.leklem{at}comcast.net

Dear Sir:

We found the recent article by Friso et al (1) potentially intriguing. An association between vitamin B-6 status and coronary artery disease (CAD) in humans has been discussed for decades, but to date there has been no satisfactory biochemical explanation for this association (see, for example, reference 2). In their study, Friso et al stated " ... we excluded subjects with conditions known to influence B-vitamin metabolism ..."; however, they included smokers and nonsmokers in both their CAD-free subjects and their CAD patients (see Table 1 in their article). Although they further stated that they performed multivariate logistic regression analyses that controlled for smoking and other indexes, such a regression analysis does not preclude an increasing percentage of smokers in each of the successive quartiles of pyridoxal-5'-phosphate (PLP) concentrations (see Figure 1 in their article). Because smoking is a well-documented determinant of PLP concentrations (3-6), we would have anticipated that the PLP data would also have been stratified by smoking load or that the incidence of smokers and nonsmokers would have been reported for each quartile in Figure 1. These data should be fairly easy for the authors to check.

In addition, more information on the intake of vitamin B-6 from the diet and from supplements needs to be provided. Moreover, because of the inverse association between circulating PLP concentrations and the activity of plasma alkaline phosphatase, the activity of alkaline phosphatase needs to be provided for both groups of subjects. After these analyses, if the associations of PLP with C-reactive protein and fibrinogen continue to hold up, then a functional role for vitamin B-6 in the prevention of CAD may finally be at hand.

REFERENCES

  1. Friso S, Girelli D, Martinelli N, et al. Low plasma vitamin B-6 concentrations and modulation of coronary artery disease risk. Am J Clin Nutr 2004;79:992-8.[Abstract/Free Full Text]
  2. Willett WC. Does low vitamin B-6 intake increase the risk of coronary heart disease? In: Reynolds RD, Leklem JE, eds. Vitamin B-6: its role in health and disease. New York: Alan R Liss, 1985:337-46.
  3. Manore MM, Vaughan LA, Carroll SS, Leklem JE. Plasma pyridoxal 5'-phosphate concentration and dietary vitamin B-6 intake in free-living, low-income elderly people. Am J Clin Nutr 1989;50:339-45.[Abstract/Free Full Text]
  4. Vermaak WJ, Ubbink JB, Barnard HC, Potgieter GM, van Jaarsveld H, Groenewald AJ. Vitamin B-6 nutrition status and cigarette smoking. Am J Clin Nutr 1990;51:1058-61.[Abstract/Free Full Text]
  5. Pessah-Rasmussen H, Jerntorp P, Stavenow L, et al. Eighty-year-old men without cardiovascular disease in the community of Malmo. Part II. Smoking characteristics and ultrasound findings, with special reference to glutathione transferase and pyridoxal-5-phosphate. J Intern Med 1990;228:17-22.[Medline]
  6. Serfontein WJ, Ubbink JB, De Villiers LS, Becker PJ. Depressed plasma pyridoxal-5'-phosphate levels in tobacco-smoking men. Atherosclerosis 1986;59:341-6.[Medline]




This Article
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