Individualized Diets for Irritable Bowel Syndrome Beat Placebo
Patients with irritable bowel syndrome who follow individualized diets based on food sensitivity testing experience fewer symptoms, say Yale researchers. Their study is among the first to provide scientific evidence for this medication-free approach to a debilitating condition.
As many as one in five adults meet the criteria for irritable bowel syndrome (IBS), a disorder that can cause chronic abdominal pain, gas, diarrhea, and constipation. Many patients with IBS try diets based on blood tests that claim to identify foods that trigger their symptoms. However, the majority of these food intolerance tests have not been validated by rigorous study, said the researchers.
The Yale team conducted a double-blind, randomized clinical trial of 58 patients with IBS. For each individual, the researchers collected blood samples and used a specific test that measures immune cell activation in response to individual foods. The study participants were then put on individualized diets that either restricted foods consistent with test results or restricted foods inconsistent with test results.
After several weeks on the individualized diets, participants were assessed for IBS symptoms and quality of life. The research team found that while both sets of participants experienced improvement, the individuals on diets consistent with test results fared much better overall and in terms of symptom severity.
“We didn’t expect results like this,” said Ather Ali, first author and assistant professor of pediatrics and of medicine at Yale School of Medicine. “The people who consumed the diet consistent with the test did significantly better than people on the sham diet.”
The two groups of participants reported no notable difference in terms of quality of life. But at four and eight weeks after starting the diets, the restricted diet group achieved significant improvement in symptoms such as abdominal pain and distention (swelling), among others.
The findings lay the groundwork for further study. “If these intriguing results can be replicated in larger and more diverse samples they can provide insight into another way to treat a condition that can often be very frustrating. It can be debilitating and patients are often looking for dietary approaches to it,” said Ali.
Finding A Natural Defense Against Clogged Arteries
In type 2 diabetes, chronic inflammation drives cardiovascular disease, the leading cause of death among people with the condition. Researchers at Joslin Diabetes Center, Boston, now have identified an unexpected natural protective factor that works against this inflammation.
Scientists have long known that in diabetes, high levels of glucose and lipids (cholesterol and triglycerides) trigger white blood cell called monocytes to move into artery walls and evolve into other cells known as macrophages. These cells engulf lipids but then end up stuck on the artery walls, eventually producing atherosclerosis (a narrowing and thickening of the walls).
During this process, the high levels of glucose and lipids also activate multiple forms of a molecule called protein kinase C (PKC), which help these unhelpful macrophages to activate, survive and multiply, thus boosting inflammation.
In experiments with a mouse model of type 2 diabetes, however, the Joslin investigators showed that one form of the PKC molecule called PKC-delta actually defends against this inflammation process, by suppressing the population of macrophages gone wrong.
“The complete surprise to us was that although most forms of PKC make inflammation worse, PKC-delta happens to be the opposite, a natural protective mechanism,” says George King, M.D., Joslin Chief Scientific Officer and corresponding author on a paper describing the work published in the journal Circulation Research.
Follow-up work in cell cultures by King’s lab showed that this defensive role for PKC-delta is triggered by high levels of lipids rather than glucose. That finding suggests that the molecule also may help to prevent inflammation in related metabolic conditions such as obesity and metabolic syndrome.
Additionally, the scientists discovered a mechanism by which PKC-delta inhibits a biological pathway that protects cells from dying.
This early study in animal models suggests that it may eventually be possible to reduce inflammation by activating PKC-delta in human monocytes, says King, who is also a professor of medicine at Harvard Medical School.
However, he points out that activating this molecule will create different effects in different parts of the body.
Work published last year by his lab, for example, suggested the possibility of treating slow-healing wounds by a cell-therapy approach that suppresses PKC-delta production in connective-tissue cells. Other research in the lab of Joslin’s C. Ronald Kahn, M.D., showed that inhibiting PKC-delta in the liver might aid in overcoming insulin resistance, a key contributor to type 2 diabetes and metabolic syndrome.
These varied roles for PKC-delta indicate that for any potential future therapies, “we need to target treatment to specific tissues,” he emphasizes.
King’s latest research also highlights a major continuing theme for Joslin research. “There are protective factors and risk factors for diabetes complications,” he says. “We need to have equal focus on stimulating the protective factors as well as limiting the risk factors.”