Friday, June 29, 2012

B6 Deficit Tied to CV Disease Risk

By Crystal Phend, Senior Staff Writer, MedPage Today

Low levels of vitamin B6 may play a role in the chronic inflammation that contributes to cardiovascular disease and other common conditions, researchers found.

The top scorers across a panel of inflammatory markers had significantly lower levels of pyridoxal-5-phosphate (PLP) as a plasma marker of vitamin B6 status than the least inflamed individuals in an analysis of the Framingham Offspring cohort study (61 nmol/L versus 80 nmol/L, P0.0001 for trend).

The prevalence of inadequate levels of vitamin B6 marked by PLP under 20 nmol/L roughly doubled across the inflammation tertiles, Lydia Sakakeeny, PhD, of the U.S. Department of Agriculture Human Nutrition Research Center at Tufts University in Boston, and colleagues reported.

“Low vitamin B-6 status, based on plasma concentrations of PLP, has been identified in inflammatory diseases, including cardiovascular disease, rheumatoid arthritis, inflammatory bowel disease, and diabetes,” the group wrote in the July issue of the Journal of Nutrition.

“This study, in combination with past findings, further supports our hypothesis that inflammation is associated with a functional deficiency of vitamin B6,” they added.

The analysis included 2,229 men and women in the 1998-2001 round of examinations in the community-based Framingham Offspring study.

Greater inflammation correlated with lower plasma PLP levels for the primary measure summing scores on standardized values of 13 individual inflammatory markers, including interleukin-6, tumor necrosis factor alpha, and intercellular adhesion molecule-1.

The same was true across various functional groups of inflammation markers.

For both the acute phase reactant markers (C-reactive protein and fibrinogen) and the cytokines (IL-6, TNF factors, and osteoprotegerin), plasma PLP averages went from 76 nmol/L in the lowest inflammatory tertile to 61 nmol/L in the top tertile. Both trends were significant at P0.001.

Likewise for the oxidative stress grouping, plasma PLP averaged 73 nmol/L in the lowest scoring tertile to 63 nmol/L in the highest tertile (P0.0001 for trend).

The selectins — P-selectin and CD40L — tended to follow the same trend but missed statistical significance (P=0.08 for trend).

These multivariate-adjusted associations persisted with additional adjustment for C-reactive protein.

The only marker without a significant correlation to vitamin B6 was serum monocyte chemotactic protein-1 (MCP-1).

High vitamin B6 intake was linked to higher plasma PLP levels, as expected. Yet the most inflamed individuals had significantly lower plasma PLP levels than the least inflamed participants, even after controlling for how much of the water-soluble vitamin people got in their diet.

A sensitivity analysis excluding individuals with preexisting cardiovascular disease or diabetes turned up essentially the same results.

Notably, the same associations with overall inflammation weren’t seen with other B vitamins — plasma folate or vitamin B12, suggesting the link was specific, the researchers noted.

Research into the mechanism for the vitamin B6 link is warranted, they suggested, but “an attractive hypothesis is that the low plasma PLP is a reflection of mobilization of this coenzyme into inflammatory sites.”

The observational findings couldn’t determine causality.

Another limitation was that the population studied had higher average vitamin B6 intake compared with the national population, at 3.1 mg per day from food and supplements versus 1.6 mg in the NHANES study over a similar period.

The largely white population of European ancestry might also have limited generalizability.

The study was supported, in part, by a gift from Pharmavit and by a USDA agreement and a Framingham Heart Study core contract.

The researchers reported having no conflicts of interest to disclose.

Primary source: Journal of Nutrition
Source reference:
Sakakeeny L, et al “Plasma pyridoxal-5-phosphate is inversely associated with systemic markers of inflammation in a population of U.S. adults” J Nutr 2012; DOI:10.3945/​jn.111.153056.

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Crystal Phend

Staff Writer

Crystal Phend joined MedPage Today in 2006 after roaming conference halls for publications including The Medical Post, Oncology Times, Doctor's Guide, and the journal IDrugs. When not covering medical meetings, she writes from Silicon Valley, just south of the San Francisco fog.

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