Last September, the National Football League struck a deal with Frito-Lay that allowed the company to produce limited-edition bags of Tostitos tortilla chips, with each package bearing the logo of one of 19 featured NFL teams. Several months earlier, Major League Baseball announced that Nathan’s Famous would be its first-ever official hot dog. Now the first-ever comprehensive analysis of such food and beverage sponsorships by major sports organizations shows just how pervasive these deals are. The confusing messages they send about physical fitness and healthy eating habits can’t be helping our national problem with obesity [1].
Among the 10 sports organizations that young viewers watch most, from the NFL to Little League, the NIH-funded research team identified dozens of sponsors and hundreds of associated advertisements promoting food and beverage products. The vast majority of those ads touted unhealthy items, including chips, candies, sodas, and other foods high in fat, sodium, or sugar, and low in nutritional value.
Those findings are especially concerning in light of the latest figures from the National Health and Nutrition Examination Survey (NHANES), co-supported by NIH [2], It shows that, despite long-standing public health efforts to curb the obesity epidemic, more than 18 percent of young people in America remain obese. Among adults, the picture is even more discouraging: nearly 40 percent of American adults were obese in 2015-2016, up from about 34 percent in 2007-2008.
Caption: Mouse neurons (purple), with their nuclei (blue) and primary cilia (green). Credit: Yi Wang, Vaisse Lab, UCSF
Obesity involves the complex interplay of diet, lifestyle, genetics, and even the bacteria living in the gut. But there are other less-appreciated factors that are likely involved, and a new NIH-supported study suggests one that you probably never would have imagined: antenna-like sensory projections on brain cells.
The study in mice, published in the journal Nature Genetics [1], suggests these neuronal projections, called primary cilia, are a key part of a known “hunger circuit,” which receives signals from other parts of the body to control appetite. The researchers add important evidence in mouse studies showing that changes in the primary cilia can produce a short circuit, impairing the brain’s ability to regulate appetite and leading to overeating and obesity.
The struggle to maintain a healthy weight is a lifelong challenge for many of us. In fact, the average American packs on an extra 30 pounds from early adulthood to age 50. What’s responsible for this tendency toward middle-age spread? For most of us, too many calories and too little exercise definitely play a role. But now comes word that another reason may lie in a strong—and previously unknown—biochemical mechanism related to the normal aging process.
An NIH-led team recently discovered that the normal process of aging causes levels of an enzyme called DNA-PK to rise in animals as they approach middle age. While the enzyme is known for its role in DNA repair, their studies show it also slows down metabolism, making it more difficult to burn fat. To see if reducing DNA-PK levels might rev up the metabolism, the researchers turned to middle-aged mice. They found that a drug-like compound that blocked DNA-PK activity cut weight gain in the mice by a whopping 40 percent!
For the one in three American adults who are obese, recommendations to lose substantial amounts of weight through a combination of diet and exercise can seem daunting and, at times, hopeless. But a new study should come as encouraging news for all those struggling to lose the extra pounds: even a modest goal of 5 percent weight loss delivers considerable health benefits.
In the NIH-funded study, people with obesity who lost just 5 percent of their body weight—about 12 pounds on average—showed improvements in several risk factors for type 2 diabetes and heart disease. They also showed metabolic improvements in many parts of the body, including the liver, pancreas, muscle, and fat tissue. While people who lost additional weight enjoyed further improvements in their health, the findings reported in the journal Cell Metabolism show that sometimes it really does pay to start small [1].
Credit: Adapted from Elliott, P et al., Sci Transl Med. 2015 Apr 29;7(285)
As obesity has risen in the United States and all around the world, so too have many other obesity-related health conditions: diabetes, heart disease, stroke, cancer, and maybe even Alzheimer’s disease. But how exactly do those extra pounds lead to such widespread trouble, and how might we go about developing better ways to prevent or alleviate this very serious health threat?
In a new study in Science Translational Medicine [1], researchers performed sophisticated analyses of the molecules excreted in human urine to produce one of the most comprehensive pictures yet of the metabolic signature that appears to correlate with obesity. This work provides a fascinating preview of things to come as researchers from metabolomics, microbiomics, and a wide variety of other fields strive to develop more precise approaches to managing and preventing disease.
Caption: A stylized image of the MC4R-expressing neurons (in red) within the brain’s PVH, which is the “heart of hunger” Credit: Michael Krashes, NIDDK, NIH
If you’ve ever skipped meals for a whole day or gone on a strict, low-calorie diet, you know just how powerful the feeling of hunger can be. Your stomach may growl and rumble, but, ultimately, it’s your brain that signals when to start eating—and when to stop. So, learning more about the brain’s complex role in controlling appetite is crucial to efforts to develop better ways of helping the millions of Americans afflicted with obesity [1].
Thanks to recent technological advances that make it possible to study the brain’s complex circuitry in real-time, a team of NIH-funded researchers recently made some important progress in understanding the neural basis for appetite. In a study published in the journal Nature Neuroscience, the researchers used a variety of innovative techniques to control activity in the brains of living mice, and identified one particular circuit that appears to switch hunger off and on [2].
Drinking the occasional sugar-sweetened beverage, be it soda, an energy drink, sweetened water, or fruit punch, isn’t going to make you fat. But it’s now clear that many children and adults are at risk for gaining weight if they consume too much of these products.
I want to share new research from three recent papers in the New England Journal of Medicine (NEJM) because, together, they provide some of the most compelling evidence of the role of sugary drinks in childhood obesity, which affects nearly one-fifth of young people between the ages of 6 and 19.
In the first study [1], researchers randomly assigned 641 normal-weight school children between the ages of 4 and 12 to one of two groups. The first group received an 8 oz sugary drink each day; the second received the artificially sweetened version. After 18 months, it was clear that the kids consuming the sugary drink had gained about 2.25 pounds more weight, compared with the kids drinking the zero calorie drinks. They also packed on more fat.
These snapshots reveal a very disturbing trend: the rise in obesity in the US from 1985 to 2010. Today one third of adults in the US are obese, another third are overweight.
Because obesity has risen to epidemic levels—causing devastating and costly health problems, reducing life expectancy, and provoking stigma and discrimination—the NIH has established the NIH Obesity Research Task Force to accelerate progress in obesity research. For example, why are some individuals more susceptible to obesity? Can knowledge of biology and behavior be leveraged to develop better intervention strategies? What strategies work? For whom? Can these approaches be scaled up?