Vitamin B6 deficiency associated with inflammation

BOSTON, MASSACHUSETTS. Systemic inflammation and oxidative stress have both been implicated in atrial fibrillation. The recent findings, by Dr. Jian Shen and colleagues at Tufts University, that a vitamin B6 deficiency is associated with an increase in the inflammatory marker C-reactive protein (CRP) and with a common marker of oxidative stress, are thus of interest to afibbers.

The study involved 1205 adults of Puerto Rican descent (aged 45 to 75 years) living in Massachusetts. The researchers measured plasma levels of pyridoxal-5í-phosphate (PLP), the main metabolite of vitamin B6, and urinary levels of 8-hydroxydeoxyguanosine (8-OHdG), an indicator of oxidative stress. Participants were allocated to one of four quartiles depending on their plasma PLP level Ė quartile 1 was 5.5 to 28.3 nmol/L, quartile 2 was 28.4 to 42.4 nmol/L, quartile 3 was 42.5 to 65.2 nmol/L, and quartile 4 was 65.3 to 737 nmol/L. A clear correlation between PLP quartile and CRP level was observed, with quartile 1 members having an average CRP level of 4.7 mg/L (0.4 mg/dL) as compared to a level of 2.5 mg/L (0.25 mg/dL) found among those in quartile 4.

Urinary 8-OHdG level was also significantly associated with PLP level, with members of quartile 1 having a concentration of 124 ng/mg creatinine as compared to 108 ng/mg creatinine in quartile 4. Participants in the highest quartile of PLP also had lower fasting glucose and HbA1c (glycated hemoglobin) levels than did those in the lower quartiles. Higher PLP levels were associated with higher intakes of vitamin B6, folate, vitamin B12, vitamins C and E, and a higher intake of vegetables. Finally, the presence of chronic conditions such as metabolic syndrome, obesity, and type 2 diabetes was strongly associated with lower PLP concentrations.

Shen, J, et al. Association of vitamin B-6 status with inflammation, oxidative stress, and chronic inflammatory conditions. American Journal of Clinical Nutrition, Vol. 91, February 2010, pp. 337-42

Editorís comment: It is becoming increasingly clear that having an adequate level of plasma PLP is of significant importance to afibbers. This study shows a strong correlation between low PLP level and increased inflammation and oxidative stress. Another study discussed later on in this issue reveals a correlation between low PLP levels and the risk of heart attack. Perhaps most important, several studies have found a strong correlation between low PLP levels and the risk of ischemic stroke and transient ischemic attacks (TIAs). Researchers at Harvard Medical School compared PLP levels in stroke patients and matched controls and found that study participants with a plasma level of PLP of more than 80 nanomol/L had a 90% lower risk of stroke and transient ischemic attacks (TIAs) than did participants with a level below 20 nanomol/L. The risk decrease was independent of the presence of other risk factors such as hypertension, diabetes, and atrial fibrillation[1].

The 90% relative reduction in stroke risk among people with high PLP levels is very significant and compares extremely favourably with the oft-quoted relative risk reduction afforded by warfarin (64%) and aspirin (25%). Clearly, ensuring adequate blood levels of PLP is a must for all afibbers. Vitamin B6 is converted to its active metabolite PLP in the liver and there is some evidence that the liver can only handle about 50 mg of vitamin B6 at a time. Experiments have shown that the plasma concentration of PLP does not increase further if 100 mg rather than 50 mg of pyridoxine are ingested at any one time. So it is assumed that the conversion to PLP is limited by the liverís conversion capacity[2]. Other experiments have shown that supplementing (orally) with 40 mg of vitamin B6 will increase average plasma concentration from about 23 nmol/L (range: 18-37 nmol/L) to about 230 nmol/L within 3 days of beginning supplementation. No further increases were observed with 40 mg/day supplementation for a 12-week period[3].

The 230 nmol/L concentration achieved is well above the 80 nmol/L concentration associated with the 90% reduction in stroke risk observed by the Harvard researchers. So 40-50 mg/day would seem to be sufficient for stroke protection and is considered entirely safe.

  1. Kelly, PJ, et al. Low vitamin B6 but not homocysteine is associated with increased risk of stroke and transient ischemic attack in the era of folic acid grain fortification. Stroke, Vol. 34, June 2003, pp. e51-e54
  2. Khaw, KT and Woodhouse, P. Interrelation of vitamin C, infection, haemostatic factors, and cardiovascular disease. British Medical Journal, Vol. 310, June 17, 1995, pp. 1559-63
  3. Zempleni, J. Pharmacokinetics of vitamin B6 supplements in humans. Journal of the American College of Nutrition, Vol. 14, 1995, pp. 579-86