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Those of us who have
been involved in the study of nutrition for any length of time are aware that
getting one’s body to stimulate its own immune enhancement is far safer than
the offering of isolated substances that supposedly match immune components.
Patients who have
had their asthma under control, but have been taking interferon for the
suppression of hepatitis C, have suffered enough to be hospitalized for the
return of asthma symptoms. Hepatitis C therapy with interferon-alpha can lead
to severe asthma exacerbation in patients with previously mild asthma.
Interferon-alpha therapy has previously been associated with pulmonary
complications, and now we have evidence of asthma exacerbation as well. (Mayo
Clinic Proceedings 1999; 74:367-370)
American Journal of
Clinical Nutrition, Vol. 69, No. 6, 1071-1085, June 1999
© 1999 American
Society for Clinical Nutrition
Isozymes of alcohol
and other dehydrogenases convert ethanol and retinol to their corresponding
aldehydes in vitro. In addition, new pathways of retinol metabolism have been
described in hepatic microsomes that involve, in part, cytochrome P450s, which
can also metabolize various drugs.
In view of these
overlapping metabolic pathways, it is not surprising that multiple interactions
between retinol, ethanol, and other drugs occur. Accordingly, prolonged use of alcohol, drugs, or both, results
not only in decreased dietary intake of retinoids and carotenoids, but also
accelerates the breakdown of retinol through cross-induction of degradative
enzymes.
There is also
competition between ethanol and retinoic acid precursors. Depletion ensues, with associated hepatic
and extrahepatic pathology, including carcinogenesis and contribution to fetal
defects. Correction of deficiency through vitamin A supplementation has been
advocated. It is, however, complicated by the intrinsic hepatotoxicity of
retinol,
which is potentiated by concomitant alcohol
consumption.
By contrast,
ß-carotene, a precursor of vitamin A, was considered innocuous until recently,
when it was found to also interact with ethanol, which interferes with its
conversion to retinol. Furthermore, the combination of ß-carotene with ethanol
results in hepatotoxicity.
Moreover, in smokers
who also consume alcohol, ß-carotene supplementation promotes pulmonary cancer
and, possibly, cardiovascular complications.
Experimentally,
ß-carotene toxicity was exacerbated when administered as part of beadlets. Thus
ethanol, while promoting a deficiency of vitamin A also enhances its toxicity
as well as that of ß-carotene. This narrowing of the therapeutic window for
retinol and ß-carotene must be taken into account
when formulating
treatments aimed at correcting vitamin A deficiency,
especially in drinking
populations.