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NEW YORK (Reuters Health) - An enzyme has been recently identified that is able to degrade gluten in a laboratory simulation of the gastrointestinal tract.

If clinical trials bear out the findings, adding the enzyme to gluten-containing meals "might eliminate gluten toxicity, thus offering patients the possibility of abandoning (occasionally) their strict gluten-free diet," write the authors.

The enzyme, a prolyl endoprotease from Aspergillus niger, was recently shown to efficiently degrade gluten peptides and proteins in laboratory experiments, the authors explain. The enyzme's pH is compatible with that found in the stomach, and it is not broken down by gastric acid in the stomach.

Dr. C. Mitea from Leiden University Medical Center, the Netherlands and associates tested the enzyme in a system designed to closely mimic the human gastrointestinal tract, according to their report, published in the medical journal Gut.

The enzyme accelerated the digestion of glutenins and gliadins that are found in white bread, the authors report. After 90 minutes, the gluten proteins could no longer be detected. Without the enzyme, glutens persisted in the stomach for at least 120 minutes.

Similar results were obtained when a fast food meal was tested instead of white bread alone, the investigators say.

This enzyme treatment also completely abolished T-cell stimulatory activity found in untreated samples, the report indicates.

The results demonstrate that in the time that food is normally in the stomach, the enyzme led to "a complete disappearance of T-cell stimulatory peptides of gliadins and glutenins," the authors conclude.

They believe that this enzyme is a good candidate for clinical trials to see if it can remove all gluten toxicity, the researchers conclude. They add that the enzyme is available on an industrial scale.

SOURCE: Gut, January 2008.

Copyright © 2008 Reuters Limited.

NEW YORK (Reuters Health) - Shedding excess pounds may restore some of the heart's youth, whether the weight loss comes from eating less or exercising more, the results of a small study suggests.

Researchers found that among 25 healthy but overweight middle-aged adults, moderate weight loss appeared to restore some the heart's youthful elasticity -- making it easier for the heart to relax between contractions and refill with blood.

It did not appear to matter whether the weight loss was achieved through diet changes or exercise, the researchers report in the American Journal of Physiology.

"If individuals want to do something that's good for their heart, then my message to them is lose weight by the method they find most tolerable," Dr. Sandor J. Kovacs, the senior researcher on the study, said in a statement.

"They're virtually guaranteed that it will have a salutary effect on their cardiovascular system," said Kovacs, a professor of medicine at Washington University School of Medicine in St. Louis, Missouri.

As people age, their body tissue accumulates collagen fibers, which causes tissue -- including heart muscle and arteries -- to become more stiff. So over time, the heart starts to take a bit longer to relax between contractions and fill back up with blood.

Excess weight, obesity in particular, has been shown to affect the heart's elasticity as well. But while studies suggest that weight loss achieved by diet and exercise improves cardiac function, it hasn't been clear if the same is true if weight loss is accomplished using just one of these strategies.

So Kovacs and his colleagues looked at weight loss and heart function in 25 men and women who were overweight, but not obese. For one year, half of the participants cut their daily calories by about 12 percent, while the rest took up an exercise routine -- doing activities like walking, running or cycling six days per week.

The exercisers did not make diet changes, but burned roughly the same percentage of calories as the diet group cut from their food intake.

In the end, both groups lost a similar amount of weight -- about 12 percent of their original weight. What's more, ultrasound imaging showed that dieters and exercisers also had similar improvements in the heart's ability to relax between contractions.

According to Kovacs, one challenge to getting people to lose weight is that the potential consequences of being overweight -- including diabetes, high blood pressure and heart disease -- are often far off in the future.

"But now we can tell them, lose weight and right away you can have better cardiovascular health," he said.

SOURCE: American Journal of Physiology, online January 10, 2008.

Copyright © 2008 Reuters Limited.

NEW YORK (Reuters Health) - Taking antioxidant supplements won't reduce cancer risk, according to a new analysis of a dozen studies including more than 100,000 patients. In fact, the researchers found, smokers who take beta carotene supplements could be increasing their risk of smoking-related cancer and death.

While antioxidants have been touted for cancer prevention, different antioxidants have different effects, and their effects may also vary depending on the part of the body involved, Dr. Aditya Bardia of the Mayo Clinic in Rochester, Minnesota and colleagues note in their report.

To investigate, the researchers looked at 12 trials that compared antioxidant supplements with placebo on cancer incidence and mortality.

Overall, the researchers found, antioxidant supplements didn't reduce the risk of cancer. When they looked separately at beta carotene, they found the nutrient actually increased cancer risk by 10 percent among smokers. There was also a trend toward a greater risk of dying from cancer with beta carotene supplementation.

Selenium supplements reduced cancer risk by 23 percent among men, the researchers found, but had no effect on women. While vitamin E had no anti-cancer effect overall, Bardia and colleagues did find that supplementation with the nutrient was tied to a 13 percent lower prostate cancer risk.

A large study looking at vitamin E supplementation for prostate cancer is currently underway, the researchers note. While future studies of beta carotene and vitamin E for cancer prevention are "very unlikely" to show effectiveness, they add, such studies of selenium "could be warranted."

SOURCE: Mayo Clinic Proceedings, January 2008.

Copyright © 2008 Reuters Limited.

LONDON (Reuters) - Natural levels of a man's testosterone do not affect his prostate cancer risk as some had thought, a finding that should spur scientists to rethink their approach to the disease, researchers said on Tuesday.

Nearly two dozen studies have examined a potential link between testosterone and prostate cancer risk but so far results have been inconclusive, said Andrew Roddam, an epidemiologist at the University of Oxford who led the study.

In the Journal of the National Cancer Institute, Roddam and colleagues said they found no such relationship after collecting worldwide data on hormone levels of 3,886 men who eventually developed prostate cancer and 6,438 men who did not.

Prostate cancer, which usually occurs in older men, is the second most common cause of cancer death among men after lung cancer. The prostate is a walnut-sized gland that makes fluid for semen.

"We looked at blood samples of men before they had cancer and men who didn't develop cancer to see if their hormone levels were different," Roddam said in a telephone interview.

"When you compare these two groups there is no substantial relationship between hormone levels and their risk of developing the disease."

Testosterone is the primary "male" hormone that helps maintain muscle mass and strength, fat distribution, bone mass, sperm production, sex drive and potency. Women have testosterone too, but at lower levels.

The hormone's role in men's health is controversial, with the relationship between men's natural testosterone levels and overall health not well understood, researchers say.

The reason scientists had believed it played a role in raising prostate cancer risk was because testosterone makes a tumor grow, and which is why some treatments seek to block the hormone.

A study last year also showed that higher naturally occurring levels of testosterone appeared to protect men from fatal heart attacks or strokes and death from several causes.

The latest findings, however, should prod researchers to shift the focus of their research into new risk factors for the disease, Paul Godley and colleagues at the University of North Carolina at Chapel Hill said in a commentary.

"The study obliges the scientific community to move past a seductive, clinically relevant, and biologically plausible hypothesis and get on with the difficult task of exploring, analyzing, and characterizing modifiable risk factors for prostate cancer," they wrote.

Copyright © 2008 Reuters Limited.

NEW YORK (Reuters Health) - Pot smokers may experience pathological changes in their lungs decades earlier than such changes usually occur in cigarette smokers, a small study of 10 patients shows.

The patients' average age was 41 years and they reported smoking marijuana regularly for at least 1 year. The main feature in all patients was air pockets in the lungs known as bullae, which are typically seen in people with emphysema that develops after many years of cigarette smoking.

About 15 percent of cigarette smokers will develop emphysema by age 65, but less is known about the effects of marijuana on the lungs, Dr. Su W. Hii of Monash University in Victoria, Australia and colleagues note. Because pot smokers typically inhale hot smoke forcefully and hold it in their lungs for as long as possible, the researchers add, it's possible that they may be doing more damage to their lung tissue.

To investigate, Hii and colleagues evaluated 10 marijuana smokers who sought treatment for respiratory symptoms. Four had difficulty breathing, four had collapsed lungs, and two had lung infections. The findings are published in the journal Respirology.

CT scans identified bullae in all of the patients, with nine having severe bullous disease. Seven subjects were in-patients with acute respiratory disorders and one patient had a long history of asthma.

However, five of the patients had normal lung function and the other four had only mildly reduced lung function. Chest X-rays were normal in four patients.

It is estimated that up to 2 percent of the U.S. population are regular marijuana smokers, the researchers note. They therefore call for further study to determine how common such lung disease is among marijuana smokers and to compare pot-related lung damage to the harmful effects of tobacco.

SOURCE: Respirology, January 2008.

Copyright © 2008 Reuters Limited.