Smoking has a significant effect on biotin metabolism. The research also suggests that smoking could lead to biotin deficiency and teratogenesis.
Smoking has a significant effect on biotin metabolism, according to
researchers from the University of Arkansas for
Medical Sciences, USA. The research, published in the October issue of The
American Journal of Clinical Nutrition, also suggests that smoking could
lead to biotin deficiency and teratogenesis.
Biotin is a water-soluble vitamin generally classified in the B-vitamin
complex. The researchers assessed the effect of smoking on the biotin status of
women via a cohort-controlled study. Smoking women (n=8) and nonsmoking control
subjects (n=15) provided 24 hr urine sample; excretion rates of biotin, the
biotin metabolites, and 3-hydroxyisovaleric acid were determined. Increased
urinary excretion of 3-hydroxyisovaleric acid, which reflects a reduced activity
of the biotin-dependent enzyme 3-methylcrotonyl-Co A carboxylase, is a sensitive
indicator of biotin depletion at the tissue level.
The researchers found that the urinary excretion of biotin decreased by 30%
(P=0.04), and the ratios of urinary bisnorbiotin and biotin sulfoxide to biotin
increased significantly, which indicated accelerated catabolism in smokers.
Also, the urinary excretion of 3-hydroxyisovaleric acid was greater in the
smokers than in the control subjects (P=0.04), which indicated biotin depletion
in the smokers at the tissue level.
'Although the degree of biotin deficiency detected in smoking women was
marginal, marginal biotin is of concern. Marginal biotin deficiency is
teratogenic in some animal species,' note the researchers.
'Although care must be taken in applying the results of such small studies to
general recommendations, the results of this study could reasonably be added to
the substantial body of evidence that smoking should be avoided during
pregnancy,' concluded the researchers.
The paper, 'Smoking accelerates biotin catabolism in women,' by W. M. Sealey,
A. M. Teague, S. L. Stratton and D. M. Mock was published in The American
Journal of Clinical Nutrition (2004) 80: 932-935.
The abstract can be read here.
Contact: Donald M Mock, Department of Biochemistry and Molecular Biology,
516, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Email: mockdonaldm@uams.edu