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The growth in popularity
of St. John’s Wort was fueled by a number of published controlled clinical
studies concerning its effectiveness as an antidepressant beginning in
1993. It rapidly became one of the best selling herbs. From 1997–2000,
for example, it was the fifth largest selling herb in the U.S., with retail
sales of about $48 million dollars. The news about herb-drug interactions
triggered a retreat from reliance on this herb, a change that was intensified
when new clinical reports (beginning with one published in JAMA in 2001)
questioned its efficacy for depression. St. John’s Wort sales were cut
in half compared to their peak levels by the year 2002 and by 2003 they
had declined by another 40%. The herb is no longer extensively used, although
it is still available and some consumers remain unaware of its effects
on drug levels. |
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| The mechanism
of herb-drug interaction with St. John’s Wort is clear. (3) The greatest
concern is focused on medications that are substrates on the liver enzyme
CYP3A4; this enzyme degrades many drugs. St. John’s Wort induces production
of the liver enzyme, hence the drugs are degraded faster than usual. This
is the same enzyme that is inhibited by grapefruit juice, which has the
opposite effect of increasing drug levels in the blood. Both St. John’s
Wort and grapefruit juice are among the strongest of the known natural
substances that affect drug levels when consumed at ordinary doses. In
addition to CYP3A4, St. John’s Wort affects phosphorylated glycoprotein
(P-glycoprotein or P-gp), which also metabolizes drugs. Besides Indinavir,
the metabolism of other protease inhibitors are also affected by St. John’s
Wort.
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