Jewish World Review May 31, 2002 / 20 Sivan, 5762




Broccoli kills cancer-causing stomach bug

By Robert A. Wascher, M.D., F.A.C.S.

http://www.NewsAndOpinion.com | 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.

JWR contributor Dr. Robert A. Wascher is a senior research fellow in molecular & surgical oncology at the John Wayne Cancer Institute in Santa Monica, CA. Comment by clicking here.

Up

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02/26/02: The continuing controversy regarding screening mammography
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02/01/02: Antibiotics in livestock feed & human disease; genetic detection of early colon cancer in the stool; genetic analysis of breast cancers may help decide treatment
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01/09/02: Cancer & aging: Two sides of the same coin?
01/04/02: Vitamin a & the risk of hip fracture in postmenopausal women; ovarian cancer risk and oral contraceptives
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© 2002, Dr. Robert A. Wascher