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Health Briefs
May
30, 2002
by Robert A. Wascher, M.D., F.A.C.S.
BROCCOLI KILLS CANCER-CAUSING STOMACH
BUG
Broccoli, along with cauliflower,
Brussels sprouts and cabbage, is a member of the so-called cruciferous
vegetable group. Several previous studies have found apparent anti-cancer
substances in these relatively unpopular vegetables. The current issue
of the Proceedings of the National Academy of Science, however, elevates
the lowly broccoli to an even more impressive pedestal with the finding
that broccoli contains a potent antibiotic against a nasty bug that has
been firmly linked to stomach cancer. Helicobacter pylori (H. pylori)
is a stubborn bacterium that is now thought to cause most cases of stomach
and duodenal ulcers, and is also believed to significantly increase the
risk of developing stomach cancer. H. pylori has proven itself a very
formidable pathologic foe, and is very difficult to eradicate in humans.
Sulforaphane, a chemical present in broccoli, and in especially high concentrations
in young broccoli sprouts, effectively killed 90% of H. pylori bacteria,
including those bacteria that were known to be resistant to standard antibiotic
regimens. Moreover, this same study revealed that sulforaphane also appears
to protect mice from developing stomach tumors after exposure to the carcinogen
benzo-[a]-pyrene (a potent inducer of stomach cancer in mice, and a byproduct
of cooking or grilling meat at high temperatures). These results, taken
together, suggest a potentially important role for broccoli-derived sulforaphane
in the prevention and treatment of H. pylori stomach infections and, possibly,
for the prevention of at least some stomach cancers as well. If these
results hold up following human studies, this finding could be a major
breakthrough in disease prevention.
NEW BIOLOGICAL INSIGHTS INTO OBESITY &
WEIGHT LOSS
I have previously reported on the
disappointing results of research into the hormone leptin. Leptin was originally
linked to obesity in mice, but attempts at manipulating leptin levels in
the blood of humans have not proved to be clinically useful. This week’s
New England Journal of Medicine presents new research on another hormone
that has been linked to obesity in the past. Ghrelin is a hormone that
appears to stimulate appetite and feeding in both mice and humans, and is
produced primarily in the stomach. In an intriguing study, blood levels
of ghrelin were measured in 13 obese volunteers, both before and after they
embarked on a weight loss program. Five of these 13 patients were also
matched up against 5 additional obese patients undergoing partial removal
of the stomach as treatment for their obesity (the surgery patients also
had their ghrelin levels measured before and after surgery). In the dieting
patients, successful weight loss was accompanied by significantly increased
levels of ghrelin in the blood compared to their pre-diet levels. In comparison,
the patients who underwent partial removal of their stomachs also lost a
significant amount of weight, however their blood levels of ghrelin were
actually significantly decreased following postsurgical weight loss. The
authors noted that ghrelin blood levels appear to rise prior to meals, and
drop after eating. They hypothesize that ghrelin may stimulate appetite
and feeding in obese patients with intact stomachs, and that the levels
of ghrelin in the blood are stimulated by dieting and weight loss. This
may explain the well-known tendency of most dieters to eventually regain
most or all of the weight that they have lost by dieting. It appears that
partial removal of the stomach reduces ghrelin blood levels, and may play
a role in the more durable weight loss seen in patients who have undergone
surgical treatment for morbid obesity. More investigation into the physiologic
effects of ghrelin needs to be undertaken, and other factors that might
modulate ghrelin secretion (such as exercise, diet, smoking, and various
medications) should also be explored. A note of caution: the disappointing
outcome of leptin research in humans following heavily hyped results in
rodent studies should serve as a cautionary tale when interpreting the results
of this new study.
ANTI-INFLAMMATORY DRUGS AND THE RISK
OF HEART ATTACK
Following recent studies that suggested an increased risk of heart attack
among people taking the COX-2-specific inhibitors Vioxx and Celebrex,
particularly when compared to people who were taking the nonspecific anti-inflammatory
drug naproxen, much confusion has abounded. The association of COX-2
specific inhibitors with an apparent increase in the incidence of heart
attack is thought to arise from their lack of inhibition of the COX-1
enzyme. The COX-1 enzyme affects the blood’s clotting system, and the
platelets in particular, in ways that can increase the likelihood of a
blood clot being formed within a coronary artery that has already been
narrowed by cholesterol plaque formation. Thus, it is not thought that
Vioxx or Celebrex actively cause an increased risk of heart attack. Rather,
it is their lack of heart-protective COX-1 enzyme inhibition that probably
accounts for the increased incidence of heart attacks when compared to
nonspecific anti-inflammatory drugs like naproxen and aspirin, and which
inhibit both COX-1 and COX-2.
Two studies in the current Annals of Internal
Medicine looked specifically at the effects of naproxen (Naprosyn) and
other so-called “nonsteroidal anti-inflammatory drugs” (NSAIDs) on the
incidence of heart attack (aspirin, which is also a nonspecific NSAID,
and is known to reduce the risk of heart attack, was not evaluated in
these studies) . Both studies retrospectively reviewed patient databases
to identify patients who were taking anti-inflammatory drugs and those
who were not. Patients in each category were then matched according to
age, gender, race, cardiac risk factors, other medication use, and underlying
health problems. When the two groups of patients were compared and analyzed,
only the use of naproxen appeared to significantly reduce the incidence
of heart attack. In the first study, there was a 16% reduction in the
risk of heart attack among patients who had taken naproxen within the
previous 6 months, while the second study found a 17% reduction in heart
attack with naproxen use. The authors theorize that naproxen probably
protects the heart better than other nonspecific NSAIDs because its anti-clotting
effects are known to be more powerful than most of the other NSAIDs.
Please remember, however, that the use of NSAIDs can be associated with
bleeding in the gastrointestinal tract and kidney injury in some people.
NSAIDs can also thin the blood so that it does not clot normally (even
NSAIDs other than naproxen), which can be a serious problem in patients
who are taking other medications or dietary supplements that also thin
the blood. If you are contemplating adding aspirin or naproxen to your
list of medications, please see your primary care physician first to help
you evaluate both the risks and benefits of NSAID therapy in your particular
case.
Dr. Robert A. Wascher
Dr. Robert A. Wascher is
a senior research fellow in molecular & surgical oncology at the John Wayne
Cancer Institute in Santa Monica, CA
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