Research Reveals Increasing Waistlines
American women, on average, can pinch an extra 11/2 inches of flesh around their middles, and men just under an extra inch, proof that many continue to lose in the Battle of the Bulge. The average waist size increased from 37.6 inches to 38.8 inches, according to a survey conducted by the Centers for Disease Control and Prevention (CDC) that documented Americans between 1999 and 2012.
While the recession may have shrunk the economy, Americans’ waist sizes continued to balloon during this period.
“These results, while not surprising, are quite concerning,” says Jessica Bartfield, MD, of the Loyola Center for Metabolic Surgery & Bariatric Care at Loyola University Health System. “Increase in waist size usually suggests much higher health risk. Obesity rates are by no means stabilizing if 54% of Americans are abdominally obese compared to 35% of Americans with obesity defined by the body mass index. Adults with abdominal obesity are at a similar if not increased disease risk as those classified as obese by BMI.”
According to the new study published in JAMA, 46% of Americans were abdominally obese in 1999 and that number grew to 54% in 2012. Data on almost 33,000 men and women aged 20 and older were compiled by the National Health and Nutrition Examination Survey.
“This study provides a very important message that health is not just defined by weight or BMI,” Bartfield says. “Many other factors, such as waist circumference, need to be considered.”
More than one-third of US adults are obese, according to the CDC.
“Hispanics tend to be at higher risk for weight gain around the waist which leads to higher rates of insulin resistance, metabolic syndrome, and type 2 diabetes,” says Bartfield, who cares for clinically obese patients in the Chicago area.
More than one-half of all Americans are overweight, and more than 15 million people suffer from severe obesity.
— Source: Loyola University Health System
Study Reveals Artificial Sweeteners May Induce Metabolic Changes
Artificial sweeteners—promoted as aids to weight loss and diabetes prevention—could hasten the development of glucose intolerance and metabolic disease by changing the composition and function of the gut microbiota—the substantial population of bacteria residing in our intestines. These findings, the results of experiments in mice and humans, were published in Nature.
Eran Elinav, MD, of the Weizmann Institute of Science’s department of immunology, who led this research together with Eran Segal, a professor in the department of computer science and applied mathematics, says that the widespread use of artificial sweeteners in drinks and food, among other things, may be contributing to the obesity and diabetes epidemic that’s sweeping much of the world.
For years, researchers have been puzzling over the fact that noncaloric artificial sweeteners do not seem to assist in weight loss, with some studies suggesting that they may even have an opposite effect. Graduate student Jotham Suez in Elinav’s lab, led the study and collaborated with lab member Gili Zilberman-Shapira and graduate students Tal Korem and David Zeevi in Segal’s lab to discover that artificial sweeteners, even though they don’t contain sugar, nonetheless have a direct effect on the body’s ability to utilize glucose. Glucose intolerance, generally thought to occur when the body can’t cope with large amounts of sugar in the diet, is the first step on the path to metabolic syndrome and adult-onset diabetes.
The scientists gave mice water laced with the three most commonly used artificial sweeteners, in amounts equivalent to those permitted by the FDA. These mice developed glucose intolerance, as compared with mice that drank water or even sugar water. Repeating the experiment with different types of mice and different doses of the artificial sweeteners produced the same results: These substances were somehow inducing glucose intolerance.
Next, the researchers investigated a hypothesis that the gut microbiota are involved in this phenomenon. They thought the bacteria might do this by reacting to new substances like artificial sweeteners, which the body itself may not recognize as “food.” Indeed, artificial sweeteners aren’t absorbed in the gastrointestinal tract, but in passing through they encounter trillions of the bacteria in the gut microbiota.
The researchers treated mice with antibiotics to eradicate many of their gut bacteria; this resulted in a full reversal of the artificial sweeteners’ effects on glucose metabolism. Next, they transferred the microbiota from mice that consumed artificial sweeteners to sterile mice, resulting in a complete transmission of the glucose intolerance into the recipient mice. This, in itself, was conclusive proof that changes to the gut bacteria are directly responsible for the harmful effects to their host’s metabolism. The group even found that incubating the microbiota outside the body, together with artificial sweeteners, was sufficient to induce glucose intolerance in the sterile mice. A detailed characterization of the microbiota in these mice revealed profound changes to their bacterial populations, including new microbial functions that are known to infer a propensity to obesity, diabetes, and complications of these problems in both mice and humans.
Does the human microbiome function in the same way? Elinav and Segal had a means to test this as well. As a first step, they looked at data collected from their Personalized Nutrition Project (www.personalnutrition.org), the largest human trial to date to look at the connection between nutrition and microbiota. They uncovered a significant association between self-reported consumption of artificial sweeteners, personal configurations of gut bacteria, and the propensity for glucose intolerance. They next conducted a controlled experiment, asking a group of volunteers, who didn’t generally eat or drink artificially sweetened foods, to consume them for one week and then undergo tests of their glucose levels and gut microbiota compositions.
The findings showed that many—but not all—of the volunteers had begun to develop glucose intolerance after just one week of artificial sweetener consumption. The composition of their gut microbiota explained the difference: The researchers discovered two different populations of human gut bacteria—one that induced glucose intolerance when exposed to the sweeteners and one that had no effect either way. Elinav believes that certain bacteria in the guts of those who developed glucose intolerance reacted to the chemical sweeteners by secreting substances that provoked an inflammatory response similar to sugar overdose, promoting changes in the body’s ability to utilize sugar.
“The results of our experiments highlight the importance of personalized medicine and nutrition to our overall health,” Segal says. “We believe that an integrated analysis of individualized ‘Big Data’ from our genome, microbiome, and dietary habits could transform our ability to understand how foods and nutritional supplements affect a person’s health and risk of disease.”
According to Elinav, “Our relationship with our own individual mix of gut bacteria is a huge factor in determining how the food we eat affects us. Especially intriguing is the link between use of artificial sweeteners—through the bacteria in our guts—to a tendency to develop the very disorders they were designed to prevent; this calls for reassessment of today’s massive, unsupervised consumption of these substances.”
— Source: Weizmann Institute of Science