This month, Dr. Sydney Spiesel discusses the disappointing research on low-fat diets, whether chills cause colds, the newfound benefits of drinking the eggs of pig whipworms (truly), and why saw palmetto won’t help your prostate. (Click here and here for the last two monthly columns.)
Low-fat diets: Don’t give up yet.
State of the science: For many years, doctors were pretty sure that if people ate less fat and more fruits, vegetables, and grains, they would reduce their risk of cancer in general and of breast and colorectal cancer specifically. They believed this about colorectal cancer because in countries in which people on average consumed half the fat that Americans do, the risk of colorectal cancer is a third lower. Immigrants who come to the United States from such countries take on the higher cancer risk of their new home, suggesting that the difference is caused by an environmental factor, like diet, rather than simple genetics. The evidence for reduced risk of breast cancer came from experiments in which low-fat rodent diets decreased the risk of mammary tumors in rats and mice, as well as some (though by no means all) human epidemiological studies.
Just the thought that excess dietary fat might lead to colon or breast cancer generated many plausible hypotheses to explain how it was true. I even thought of some myself. So, I’m as disappointed as anyone about the published results of three studies by the Women’s Health Initiative on whether decreasing dietary fat would decrease the risk of cardiovascular disease, breast cancer, and colon and rectum cancer.
Latest study: The Women’s Health Initiative is an example of Big Science applied to medicine—large, carefully planned studies that attempt to resolve important questions affecting many lives. Begun in 1991 by the National Institutes of Health, the WHI studies on post-menopausal women have included more than 100,000 participants. Many are just now coming to fruition. (The past month also saw publication of a WHI study on calcium supplementation and bone loss; click here for my thoughts on that.)
In the low-fat studies, almost 50,000 post-menopausal women between the ages of 50 and 79 were randomly divided into two groups. One group (40 percent of the participants) underwent behavioral modification to decrease their dietary fat and to increase their intake of fruits, vegetables, and grains. The remaining 60 percent were given written dietary advice but not asked to make changes. Both groups were observed for an average of eight years (by people who didn’t know anything about the group assignments). Researchers took note of actual changes in the diets of both groups and tracked rates of breast, colon, and rectum cancer. They had less success than they hoped at getting the research subjects to change their diets. But as a whole, the intervention group ate less fat than the women in the other group, reducing their contribution of energy from fat by about 10 percent (researchers had hoped for 20 percent). The differences were tracked by diet histories and confirmed by blood tests.
Results: Unfortunately, the lower-fat diet made virtually no difference in the risk for colorectal cancer and only a small change in the risk for developing invasive breast cancer. Extending the study longer may show that this improvement is genuine. Still, the results are disappointing (unless, of course, you’ve got a taste you can’t shake for fatty foods) though we clearly need to be cautious about accepting them. We don’t know whether these results for post-menopausal women also apply to younger people or to men. And we don’t know whether a greater average reduction in dietary fat—perhaps at the level that the researchers originally hoped for—would have led to a significant decrease in cancer risk. For now, though, the WHI results remind us that early, plausible-seeming research doesn’t always hold up when a question is re-examined on a larger scale with a really careful study design.
Cold feet and colds: dashed dreams.
State of the science: Like most people, I take great and perverse pleasure when common wisdom trumps science. So, as you can imagine, I felt a thrill of anticipation when I heard about a study showing that a chill can cause a cold. My grandmother always said so, but medical science insisted otherwise, based on some experiments in which chilled subjects were deliberately infected with cold viruses. So, who was right?
Latest research: In a new study, Claire Johnson and Ronald Eccles of Cardiff (Wales) University’s Common Cold Centre intended to show that chilling the feet sometimes causes symptoms of the common cold. The experiment randomly divided 180 people into two groups. (So far, so good.) Half put their feet in a pot of cold water for 20 minutes, and the other half put their feet in an empty pot for 20 minutes. (Less good, since it would be no secret which group a subject was placed in.) Four or five days later, the participants were mechanically tested by a machine that measured stuffed-up-ness. (Good.)
Results: But the objective measurements were too varied to provide meaningful data and, accordingly, were not considered when the data were analyzed. (Uh-oh.) Instead, the subjects, fully aware of the group to which they had been assigned, kept diaries in which they recorded their subjective sense of whether they were experiencing cold symptoms. (Double uh-oh.) Thousands of experiments have demonstrated just how easily subjects are influenced by expectations when they make subjective judgments. I have little doubt that this study, which claimed to find a connection between chilled feet and cold symptoms, is just one more example. It wouldn’t have helped much, but couldn’t the researchers at least have counted Kleenex?
Pig whipworm: Your bowels will love it.
OK, it’s gross: I don’t know why I’m attracted to the icky (I’m also not sure I want to know). I found pee in the River Po pretty interesting and was quite taken with the dangers of eating camel liver sashimi. I am fascinated by the charms of head lice and have a scholarly interest in the unfortunate side effects of a weight-loss pill. Today I am hot on the trail of a new treatment for inflammatory bowel disease that definitely meets my standard for grossness.
The disease: IBD is the general heading for two severe and serious disorders that cause inflammation of the intestines: Crohn’s disease and ulcerative colitis. Both cause pain and diarrhea as well as weight loss and, in children, poor growth. In the long term, patients with ulcerative colitis are at substantial risk for colon cancer.
How it works: The mechanism that leads to IBD is not well understood. But it has long been suspected that IBD damages the bowel wall as a result of an aberrant and overactive immune response—one in which activated immune cells release toxic materials that hurt nearby cells. The same kind of “autoimmune” damage is most likely the underlying cause of other diseases in which cells of the immune system destroy normal tissue cells—multiple sclerosis, for instance, and Type 1 diabetes. The cells responsible for this kind of damage are called Th1 cells.
The diseases we typically think of as “allergic” diseases, by contrast—asthma, for instance, or food allergies, or eczema—are activated by materials released by a related immune cell, the Th2 cell. Fascinating to immunologists is our state of Th1-Th2 balance. If the Th1 cells are intentionally stimulated, then the Th2 cells become less active, and vice versa—activated Th2 cells tone down Th1 cells, which is exactly what helps relieve IBD.
The icky part: An audacious and creative scientist at the University of Iowa, Dr. Joel Weinstock, asked this question: What if the bowel of a patient with IBD was stimulated to increase the Th2 immune response and reduce the activity of the Th1 cells damaging the bowel wall? Hmmm—how to do it? Intestinal parasite worms cause the desired Th2 response, but infection with human parasitic worms causes lots and lots of trouble. Parasites, however, tend to be faithful to their species of origin, so what about the worms of a different species? Weinstock and his group decided to feed IBD sufferers a drink containing the eggs of the pig whipworm, a swine parasite known not to survive long in humans.
Results: In a test of seven patients, four of whom had Crohn’s disease and three of whom who had ulcerative colitis, the whipworm-egg treatment resulted in the complete remission of symptoms for six. The seventh patient’s condition was improved. This remarkable effect was better than would be expected from any combination of medications. But it was temporary. Patients needed repeat doses of the whipworm-egg drink every three weeks to maintain the improvement. Four patients who were given such repeat treatments continued to do well for the duration of the 28-week experiment.
Caveat: I suspect that the IBD story will turn out to be more complex than these preliminary results indicate. I hope so, because even if the results of this small study are replicated, drinking pig whipworm eggs will be a hard sell with my patients.
The saw palmetto: Not your prostate’s salvation.
The problem: The prostate is a pesky little gland. It sits at the base of the male bladder and surrounds the urethra. Its function is to produce most of the fluid that suspends, supports, and nourishes sperm as they are about to be launched into the world. As men age, and as the prostate is stimulated by hormones that derive from testosterone, it bulks up and begins to impede the free flow of urine, a condition called “benign prostatic hypertrophy” or BPH.
The usual options: Several methods of treatment or prevention are available, all of which can cause undesirable side effects. Drugs can relax the smooth muscle associated with the prostate. Other medications can block the testosterone derivative that induces the prostate to become larger. Internally directed microwave energy can shrink the prostate. Or there’s surgery that enlarges the interior diameter of the urethra by cutting into it from within (think clearing sewer pipes by cutting away intruding tree roots).
The magic bullet? As you can imagine, many men pine for alternatives. One popular treatment, perceived as safe and effective, is to eat the fruit (or an extract made from the fruit) of the saw palmetto, a plant that grows in the southern United States.
Saw palmetto isn’t a drug. It’s a “dietary supplement” or “nutriceutical.” Products in this category must be composed of materials somehow related to foods (like vitamins, minerals, amino acids, or herbs) and may not be labeled as a specific treatment or prevention method. Their safety and composition are the responsibility of the manufacturer— not the FDA. This means there is no guarantee that the bottle even contains what the label says.
Latest research: Are these products safe and do they have any value? Probably most of them are reasonably safe, though a few other dietary supplements have caused significant harm. Efficacy is another question—about which we have new data. Dr. Stephen Bent, of the Osher Center for Integrative Medicine, and a number of his colleagues investigated the value of saw palmetto by randomly assigning 225 men with BPH to two groups. One group received capsules of saw palmetto extract. The other group got identical-looking placebo capsules. Neither the subjects nor the researchers knew which group was which.
Results: After a year of treatment, there were no significant differences between the two groups in subjective or objective measurements of BPH symptoms (or side effects). Sadly, saw palmetto treatment doesn’t seem to stunt prostate overgrowth or prevent the problems it causes.
Bonus research: Another new study, by Dr. Daniel Clegg (of the University of Utah School of Medicine) and colleagues, studied the effect of glucosamine and chondroitin sulfate, common dietary-supplement treatments for arthritis. Glucosamine is derived from the shells of marine animals; chondroitin sulfate is made from shark cartilage. The study treated 952 osteoarthritis patients with one or both, comparing improvement in knee pain with 631 patients given either a placebo or one of the standard prescription drugs used to treat this condition. As usual in a well-conducted study, neither subjects nor investigators knew who received what.
Results: After 24 weeks, the researchers did not show a significant decrease in knee pain overall among subjects who took glucosamine and chondroitin sulfate. But the study included an intriguing finding: The dietary supplements did seem to relieve a small subset of patients with moderate or severe pain, though it had no effect in patients with mild pain. Some—though not all—earlier studies have also reported positive results. What to make of this? Maybe not much. But I can’t get out of my mind an elderly cat that belongs to one of my wife’s doctors and gets a daily dose of glucosamine plus chondroitin sulfate: The cat can’t get out of bed in the morning without it.