The massive, long-term Diabetes Prevention Program study has now found (twice!) that altering one’s lifestyle in terms of diet and exercise is more effective than a common prescription drug in delaying the onset of the disease. To power this study and its recently published follow-up, dozens of medical centers conducted multiple examinations each year on thousands of patients - 3234 in the first 3-year study, and 2665 in the 10-year follow. It’s impressive - and more clinically useful - to look at the summary data accumulated from this very large population of patients. But what kind of impact does a huge study such as the DPP have on the individual participants?

With help from Margaret Matulik, the DPP program coordinator at the University of Chicago Medical Center, I connected with a couple of the study subjects to hear about the lives behind the data points. Both Katherine Seaberry, 80, and Robert Nolan, 61, are from Chicago, and enrolled in the study in the late 1990’s. Both were also motivated to join the DPP due to their respective families’ experience with diabetes - Nolan’s sister and mother suffered from the disease and died around the age of 60, and Seaberry said her “whole family” has been diagnosed with diabetes.

“It saved me,” Seaberry said of her involvement with the Diabetes Prevention Program. “It’s amazing that I’m the only one in my family that’s not diabetic. If I wasn’t in this study, I think I would be diabetic by now.”

read more

Pharmaceutical companies often make up trade names for new drugs that semi-subliminally evoke their purpose - some of my favorites are Boniva, for osteoporosis, or Ambien, the sleeping pill that sounds like it was named by Brian Eno.  It’s kind of a silly practice, motivated mostly by marketing reasons, because all of these drugs already have names - Ambien’s true name, Zolpidem, is even kind of fun to say. But the fact that these trade names are so widespread suggests they are effective at attracting consumers, so here’s my modest proposal: let’s give simple changes in diet and exercise that improve health a fancy trade name, Lifestyltrin.

This train of thought stems from a study published last week by medical journal The Lancet, in which one of the largest diabetes studies showed (again) that changes in lifestyle are more effective than a leading medication in preventing the disease. Originally published in 2001, the Diabetes Prevention Program (DPP) followed more than 3000 people at risk for diabetes at hospitals across the United States as they underwent either a lifestyle intervention, treatment with anti-diabetic drug metformin, or a placebo treatment. After nearly 3 years of study, the authors reported that lifestyle changes (meaning diet and exercise to reduce weight) reduced diabetes incidence by almost 60%. Metformin also reduced the disease, but only by about 31% - results so strong that the authors stopped the study and began offering both treatments to everyone in their study.

But the study didn’t end, and the medical centers involved continued to monitor as many patients as were willing to stay in contact. All told, 2766 of the original 3234 participants continued to be monitored, allowing the publication last week of a followup study examining how many of these at-risk patients had developed diabetes 10 years after the original study began. What they found was somewhat status quo - after 10 years, the lifestyle group still showed twice the decrease of new diabetes cases than the drug group, 34% vs 18% lower compared to placebo. But that also means there was no difference in the number of new diabetes cases between lifestyle and drug groups in the 7 years between the original study’s end and the followup study’s end, which authors attributed to the mixture of treatments - the group receiving lifestyle interventions was now allowed access to metformin, and vice versa.

read more

Studies of human disease often work from the patient backwards - doctors and scientists take the common symptoms of a particular disorder and use them as clues to figure out what first went awry to spur the disease. For neurological diseases like Parkinson’s or amytrophic lateral sclerosis (aka Lou Gehrig’s Disease), symptoms and brain images have pointed the research at particular parts of the brain, which are then studied in animal models and on the genetic or cellular level. But disease research can also work from the other direction, where a particular cellular process is identified as a potential culprit in the disorder before a patient with that defect is even found.

That’s the case with a paper published this month by a team of University of Chicago researchers studying the cellular mechanisms that underlie diabetes. There are many types of diabetes mellitus, but all can be traced back to the hormone insulin - the body’s signal that cells should soak up sugar from the blood. Most cases of juvenile, or Type 1, diabetes result from the immune system erroneously attacking and killing the Beta-cells of the pancreas, which release insulin. Type 2 diabetes, which often develops in adulthood, results from a reduced sensitivity to insulin and/or a decreased release of the hormone.

But diabetes can also have a genetic origin, in some rare cases, when one of the genes involved in the secretion of insulin is disrupted. Previously on the blog, we’ve talked about the story of Lilly Jaffe, whose diabetes was found to be caused by a rare genetic mutation in a protein called a potassium channel, critical for the release of insulin. The mutated potassium channel seen in Lilly’s case interferes with the trigger of insulin release, causing lower amounts of the hormone to circulate through her blood. Thus, Lilly was treated by daily injections of insulin, until doctors at the University of Chicago detected the mutation and prescribed her a drug that directly targeted the potassium channel.

Now researchers at the University of Chicago have found another ion channel that must function properly for the right amount of insulin to be released. Only problem: there’s no patient.

read more

Whether you call it pop, soda, a soft drink or lower-case coke, sugary, carbonated beverages have become a staple of the American diet. And as we all know, the American diet is not exactly the healthiest. So with obesity racking up an estimated $150 billion a year in health care costs - which, as you may have heard, is in the news lately - some researchers have considered whether Coke, Pepsi and their sucrose-packed brethren should be subject so the same type of “sin tax” that has been applied in the past to alcohol and tobacco by some governments.

Here in ScienceLife’s home state of Illinois, carbonated soft drinks (as well as most candy) were recently reclassified from being considered as food to “general merchandise” - a seemingly innocuous change that actually means a sales tax increase from 2.25 percent to 10.25 percent in Chicago. In Illinois, the switch was justified as a way to generate much-needed revenue for state services, but could it also have a direct public health benefit by discouraging people, particularly children and teenagers, from drinking hundreds of calories in soda pop each day?

In this week’s New England Journal of Medicine, seven public health experts assess the best methods of improving public health through taxation of soft drinks. Soda is already taxed in 33 states, according to the article, at an average of 5.2%. But research indicates that those taxes have only marginal effects on soda consumption and obesity. One recent study out of UIC found only “weakly significant” effects of tax rate on the body mass index of children “at risk” of being overweight. In NEJM, the authors immediately state that the current tax rates are too small to have an effect on consumption - after all, a 5% tax on a 75-cent can of Coke is less than 4 cents, hardly enough to get someone to switch to water.

But the authors go on to suggest different methods of taxation that could be more effective in motivating people to change their beverage behavior. Rather than imposing an increased sales tax on all soda purchases, the authors suggest a tax of 1 cent per ounce on beverages with “added caloric sweetener” - your standard sugary Coke or Pepsi, but not your Nutrasweet-infused Diet versions. So a 12 oz. can of soda would set you back 12 cents, and a convenience-store fountain drink behemoth would cost almost a dollar extra, but if you opt for the diet version, no tax. Thus, the authors hope the tax will encourage (or financially push) consumers to make healthier decisions rather than merely opting for cheaper sugary drinks.

read more

Three years ago, University of Chicago Medical Center physicians spotted an unusual genetic mutation in 6-year-old Lilly Jaffe - a finding that meant the girl could switch from painful insulin injections to pills as a means of controlling her Type I diabetes. Last Friday, Illinois Governor Pat Quinn signed a state bill bearing Lilly’s name, which will establish the first mandated statewide diabetes registry in the United States, an effort that researchers hope will help more diabetic children receive the proper treatment for their disease and help decode previously-unknown genetic causes of diabetes.

Illinois House Bill 2481, known unofficially as Lilly’s Law, originated with Rep. Tom Cross (R-Oswego) and passed both houses of the Illinois General Assembly by unanimous vote — no small achievement in the state’s current political climate. The bill establishes a registry of Illinois children diagnosed with neonatal diabetes before the age of 12 months, to be used by clinicians and diabetes researchers. Physicians will now be required to report any such cases to the Illinois Department of Public Health and, if the family agrees, will also report results of lab tests that measure blood sugar control in the diabetic children.

Dr. Louis Philipson, medical director of the Kovler Diabetes Center at the University of Chicago, helped Cross craft the bill along with U. of C. professor of medicine and human genetics Graeme Bell, and Dr. Siri Atma Greeley, instructor in pediatric endocrinology. Philipson said the registry will be beneficial in both the clinic and the laboratory, helping doctors connect children with the most appropriate and least disruptive treatments, while also pointing scientists toward potential new genes that underlie neonatal diabetes.

“There’s a double benefit here,” said Dr. Louis Philipson, medical director of the Kovler Diabetes Center at the University of Chicago. “It will not only help patients, but we can also learn more about the various genes that cause diabetes.” read more