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Obesity

Behavioral Science, Health and Fitness, Obesity, Public Health, Sleep

How insufficient sleep can lead to weight gain

How insufficient sleep can lead to weight gain

SnackNap

I don’t think I’ve ever met a person who hates sleep and can’t wait to get less of it. Yet, even though most people want more sleep and know it’s important for their health, few people get as much shut-eye as they need. If you’re one of the many who needs a bit more motivation to get to bed earlier, a recent BeWell@Stanford article on how sleep can affect your weight may do the trick.

In the Q&A, sleep expert Emmanuel Mignot, MD, PhD, director of the Stanford Center for Sleep Sciences and Medicine, explains why and how insufficient sleep can increase your risk of weight gain:

It is very clear that if you’re not sleeping enough, you’re putting yourself at risk for increasing your weight.  If you sleep less than six hours a night, you’re likely to have a higher BMI (body mass index). Longitudinal data — and the evidence is quite strong — shows that if you sleep more over time, you’ll lower your BMI, which correlates with weight reduction.

In the first centuries of human life on earth, if humans weren’t sleeping they were probably looking for food or fleeing a predator. Not sleeping enough was a sign that we were in danger or that we were under stress. When we are sleep deprived, we feel hungry. Data indicates that if you sleep less, you eat more, and it disrupts your hormones. This problem is magnified in today’s world because food is too available!

Mignot also discusses the top reasons why people sleep so little, the importance of naps, and how being sleep-deprived skews our perception of doing and performing well. “[W]e have to make sure we don’t burn the candle at both ends, Mignot said. “Sleeping brings creativity, productivity and the ability to perform at a higher level.”

The piece is a quick, and informative, read.

Previously: Exploring the history and study of sleep with Stanford’s William Dement“Father of Sleep Medicine” talks with CNN about what happens when we don’t sleep wellStanford doc gives teens a crash course on the dangers of sleep deprivation, Narcoleptic Chihuahua joins Stanford sleep researcher’s family and More evidence linking sleep deprivation and obesity
Photo by Goodiez

Events, Health and Fitness, Nutrition, Obesity, Stanford News, Women's Health

Women’s health expert: When it comes to prevention, diet and exercise are key

Women's health expert: When it comes to prevention, diet and exercise are key

16262076932_96f8309b43_zThis Monday was the sixth annual Stanford Women’s Health Forum, hosted by Stanford’s Women and Sex Differences in Medicine center (WSDM), and I was happy to have been present for the lively talks. The forum focused on prevention, and the keynote, delivered by Marcia Stefanick, PhD, professor of obstetrics and gynecology and WSDM director, highlighted physical activity and weight management as the key preventative actions for women to take.

High blood pressure remains the number one preventable cause of death in women, with physical inactivity and high BMI, both of which contribute to high blood pressure, in third and fourth place. (For the curious readers, smoking comes in second.) Because prevention requires changes in behavior, behavior was what Stefanick focused on. Rather than reinforcing many women’s feelings of embarrassment about their weight, she said, providers should help women feel that they can do something about it.

Healthier behaviors must include diet and exercise. Both fatness and low fitness cause higher mortality; realistic expectations about how to change both should factor into care. Stefanick emphasized that weight loss should be slow: 10 percent of one’s body weight baseline over six months, or one pound per week for moderately overweight people, and no more than two pounds per week. And we need to stop being so sedentary, Stefanick exclaimed. The classic principles of exercise apply – gradually increase the frequency, intensity, and/or duration of exertion. Adults should be getting at least two and a half hours of moderate-intensity aerobic physical activity per week, in addition to doing muscle-strengthening activities at least twice a week, the conference flyer read.

However, citing the problems of eating disorders and older women losing weight without trying, Stefanick stressed that “weight management is a spectrum; there are extremes at both ends.” In describing variations on mesomorphic, endomorphic, and ectomorphic body types, she stated that “we don’t know what the optimal body type is.” It probably varies for each person.

Something I found particularly interesting was Stefanick’s description of gynoid vs android fat distribution patterns (which I learned as “pear” and “apple” body shapes, respectively). Gynoid distribution around the hips, thighs, and butt is more common in women, and includes more subcutaneous fat, while in android distribution, which is more common in men, fat collects around the belly and chest and is actually dispersed among the organs. Such intra-abdominal fat is more damaging to health, as it affects the liver and lipid profile and can cause heart disease, but it’s also much easier to get rid of through exercise (which is one reason men overall have less trouble losing weight than women).

In the spirit of more personalized care, Stefanick also discussed how recommended weight changes during pregnancy should vary according to the person’s prenatal BMI. Someone underweight could gain up to 40 pounds and be healthy, she pointed out, while obese people might actually lose weight during pregnancy for optimal mother-baby health.

Previously: Why it’s critical to study the impact of gender differences on diseases and treatmentsWhen it comes to weight loss, maintaining a diet is more important than diet typeApple- or pear-shaped: Which is better for cancer prevention?A call to advance research on women’s health issues and To meet weight loss goals, start exercise and healthy eating programs at the same time
Photo by Mikaku

NIH, Obesity, Public Health, Research

Capturing the metabolic signature of obesity

Capturing the metabolic signature of obesity

scale_weightWorldwide obesity rates have more than doubled since 1980, and today the majority of the global population live in areas where being overweight kills more people than being underweight, according to data from the World Health Organization. But new research that provides a comprehensive view of the metabolic signature that may correlate with obesity could help scientists develop more effective ways to manage and prevent obesity, and it offer insights into how variability in genes, environment, metabolism and lifestyle affect our health individually.

As reported today on the NIH Director’s Blog:

The new analysis uncovered changes to 29 molecular metabolites, or biomarkers, that correlated with obesity in 1,880 people from the United States. Most of those biomarkers—25 to be exact—also turned up in the urine of obese people from the other side of the Atlantic, offering confirmation that the findings represent a shared metabolic signature of obesity.

Several of the biomarkers are byproducts of what a person eats, which may reflect differences in the diets of obese and non-obese people. For example, urine from obese people was more likely to contain a metabolite that comes from eating red meat, while thinner folks were more likely to have a metabolite indicative of citrus fruit consumption.

However, not all of the biomarkers were directly related to food. Some appeared to stem from widespread changes in kidney function, skeletal muscle, and metabolism that may occur as a person packs on extra pounds. And, intriguingly, nine of the biomarkers significantly associated with obesity weren’t even produced by the human body, but rather by the trillions of microbes that live inside our guts. Those microbial partners play important roles in the breakdown of essential vitamins, amino acids, and protein. In fact, recent research findings suggest that a significant portion of obesity risk may be explained by the activity of gut microbes. This discovery adds to mounting evidence, spurred in recent years by the NIH-funded Human Microbiome Project, for the intricate and essential role of microbes—collectively known as the microbiome—in many aspects of our health.

The piece goes on to say that the findings also “raise the intriguing possibility that people might one day be able to visit their health-care providers, receive a blood or urine test, and leave with precise, individualized information regarding their risk” for obesity and other health issues.

Previously: Childx speaker Matthew Gillman discusses obesity prevention, Discussing how obesity and addiction share common neurochemistry, Stanford team awarded NIH Human Microbiome Project grant and Obesity is a disease – so now what?
Photo by Matthew

Events, Obesity, Pediatrics, Stanford News, Videos

Childx speaker Matthew Gillman discusses obesity prevention

Childx speaker Matthew Gillman discusses obesity prevention

The inaugural Childx conference was held here last month, and video interviews featuring keynote speakers, panelists and moderators are now on the Stanford YouTube channel. To continue the discussion of driving innovation in maternal and child health, we’ll be featuring a selection of the videos this month on Scope.

The prevalence of childhood obesity in the United States has not changed significantly since 2004 and remains at about 17 percent. However, the rate of obesity among preschool children, ages 2 to 5, has dropped from nearly 14 percent to 8.4 percent, according to data from the Centers for Disease Control and Prevention. Matthew Gillman, MD, a professor in the Department of Nutrition at Harvard Medical School, is among the group of researchers working to understand why rates of obesity among younger children have decreased.

In the above video interview from the Childx conference, Gillman discusses two possible reasons why fewer children under the age of five are obese and how this statistic points to potential prenatal underpinnings that influence a child’s risk of obesity. He goes on to explain how researchers previously believed that our health habits in adulthood gave rise to chronic disease, but that studies have shown the risk for these conditions may be determined early in life, even before birth. Watch his full interview to learn more about how fetal development influences our overall health.

Previously: “It’s not just science fiction anymore”: Childx speakers talk stem cell and gene therapy, Global health and precision medicine: Highlights from day two of Stanford’s Childx conference, Innovating for kids’ health: More from first day of Stanford’s Childx and “What we’re really talking about is changing the arc of children’s lives:” Stanford’s Childx kicks off

Autoimmune Disease, Chronic Disease, Health and Fitness, Nutrition, Obesity, Research

Study clarifies link between dieting, exercise and reduced inflammation

Study clarifies link between dieting, exercise and reduced inflammation

4503404991_13da58b6e6_bIf you’ve ever wondered how dieting and exercise reduce inflammation, read on. According to new research, a compound that our bodies crank out when energy supplies are low could be the link between diet and exercise, and reduced swelling in the body.

When diet, fasting and exercise starve the body for calories, the body increases production of a compound called beta hydroxybutyrate (BHB). This compound has long been known as an alternate source of energy; the new research suggests that BHB can also block the inflammatory response.

In their study, published this week in Nature Medicine online (subscription required), a team of scientists co-led by Yun-Hee Youm and Kim Yen Nguyen at the Yale School of Medicine, discovered that the compound BHB reduces swelling in the body by inactivating a group of proteins, called the inflammasome, that drive the inflammatory response.

The research team used human immune cells and mice to explore the effects of BHB in the body. They found that mice given BHB directly, and mice fed a low-carbohydrate diet (that prompted their bodies to synthesize their own BHB), both benefited from reduced inflammation.

These results are noteworthy because a better understanding of the mechanism that links diet, exercise and inflammation could help scientists develop more effective treatments for inflammatory disorders such as Type 2 diabetes, atherosclerosis and Alzheimer’s disease.

Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroesImproving your health using herbs and spices, Exercise may alleviate symptoms of arthritis regardless of weight loss, Study points to inflammation as cause of plaque buildup in heart vessels and Examining the role of exercise in managing and preventing diabetes
Via ScienceDaily
Photo by Dave Nakayama

Chronic Disease, Obesity, Research, Stanford News

Faulty fat cells may help explain how Type 2 diabetes begins

Faulty fat cells may help explain how Type 2 diabetes begins

heavywaterWhy do some obese people develop Type 2 diabetes while others don’t? New evidence suggests the answer may lie just beneath the skin. A study published this month in the Journal of Lipid Research found metabolic anomalies in the subcutaneous fat of a group of people at risk for diabetes. Basically, fat cells under their skin weren’t very good at storing fat.

That’s a problem because fat that doesn’t get stored in these cells must go somewhere, and it often ends up in other organs, such as the liver, muscle, pancreas and heart. In those locations, there is evidence that too much fat causes “lipotoxicity,” in part by interfering with the messages of the sugar-handling hormone insulin.

The new research, a collaboration between Stanford’s Tracey McLaughlin, MD, and her colleagues here and at UC Berkeley and the National Institutes of Health, used a state-of-the-art technique developed by Berkeley’s Marc Hellerstein, MD, PhD, to monitor fat synthesis and storage in the subcutaneous fat cells of 15 people. All of the subjects were overweight or obese. Half were insulin resistant: Although their blood-sugar levels were normal, their bodies responded poorly to their own insulin, a state that precedes full-blown Type 2 diabetes. (Many scientists think that understanding insulin resistance could lead to preventive strategies for Type 2 diabetes.) The other subjects had normal insulin sensitivity.

Each day for four weeks, the subjects drank a few sips of heavy water, a non-radioactive substance labeled with “heavy” hydrogen atoms that have an extra neutron. After four weeks, the scientists took small samples of the subjects’ subcutaneous belly fat and measured how much heavy hydrogen had been incorporated into the cells’ stored fat molecules and their DNA.

The insulin-resistant subjects had less heavy hydrogen in their fat molecules than the insulin-sensitive subjects, suggesting that their subcutaneous fat cells made and stored less fat during the study. The amount of heavy hydrogen in the DNA of the two groups’ fat cells was the same. This means that the insulin-resistant people were making new subcutaneous fat cells at the same rate as the insulin-sensitive people. The bodies of the insulin-resistant people could generate new fat cells under the skin, but the cells didn’t work quite right.

“This is an important extension of limited static and nonhuman data supporting the hypothesis that dysfunctional fat storage in subcutaneous adipose tissue contributes to obesity-associated insulin resistance,” the scientists wrote, adding that future identification of the molecules that cause this problem may help researchers develop drugs that could treat insulin resistance and prevent Type 2 diabetes.

Previously: The role of nutrition in diabetes prevention and management, Preventing pre-diabetes from turning into diabetes and The importance of regular exercise in delaying and treating diabetes
Photo by Kim P

Ask Stanford Med, Events, Nutrition, Obesity, Stanford News

Sticky situation: How sugar affects our health

Sticky situation: How sugar affects our health

132244825_dbf0e21d9f_zHere’s a shocking statistic: On average, Americans consume three pounds of sugar each week, or 3,550 pounds in an entire lifetime. This leads some to blame the sweet stuff for the increase of chronic disease in modern society. But simply reducing our sugar intake is easier said than done, in part because identifying foods with added sugars can be tricky.

This Thursday, Alison Ryan, a clinical dietician with Stanford Health Care, will deliver an in-depth talk on sugar and our health as part of a Stanford Health Library lecture series. Those unable to attend can watch the presentation online here.

In the following Q&A, Ryan discusses the controversies surrounding sugar and the role of sugar in our diet, and she offers tips for making sure your consumption doesn’t exceed daily guidelines.

Why does our body need sugar?

Sugar, in the form of dextrose or glucose, is the main fuel or energy source for the cells of the human body. Without glucose, our body has to get creative and rely on other metabolic pathways, like ketosis, to keep our brain and other organs running. There is an optimal range for our blood sugar levels, and our bodies are making constant efforts to keep blood sugar within this range.

Our body can make glucose from any carbohydrate that is consumed, so consuming monosaccharide (glucose and the like) is not biologically required. This is one of the reasons it’s difficult to determine the right amount of sugar that is required for the human body. Do we think of the optimal amount as the amount needed to function at peak level? Or an amount not to go over in order to avoid detrimental effects on our health?

Sugar intake has been on the rise in human diets. Why do you think that is?

At one time, sugar used to be a seldom available food item. It is now ubiquitous and more of a hallmark for highly processed, low nutritional value foods. Now, consider the food industry and the politics of sugar. Soda companies, makers of desserts, cakes, sugary snack foods, the sugar and corn syrup refiners all lobby to keep their products “part of a balanced diet.” The food industry is deeply involved (or at least vocal about) the food and nutrition guidelines in the U.S. Then there’s the reality that sugar tastes good! Most people enjoy the taste of sweet foods and are drawn to consuming them.

What are some of the health risks of consuming too much sugar?

Sugar has been implicated as playing a role in some obvious ways, like obesity, diabetes, and tooth decay; but also in less direct appearing ways such as heart disease, chronic inflammatory conditions, cancer, etc. Often, when we’re consuming foods high in sugar, we’re not consuming foods that are rich in nutrients. These calorie-dense foods displace the nutrient-dense foods. The net effect is higher intake of calories, with concurrent lower intake of vitamins, minerals, phytonutrients, protein, etc.

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Addiction, Obesity, Science, Videos

Discussing how obesity and addiction share common neurochemistry

Discussing how obesity and addiction share common neurochemistry

In a TEDMED talk published last week, renowned neuroscientist Nora Volkow, MD, discusses using insights from her research on drug addiction and brain chemistry to better understand the obesity epidemic.

Volkow, who directs the National Institute on Drug Abuse at the NIH, thought compulsive drug-taking behavior seemed remarkably similar to not being able to control what one eats. And indeed, with the help of PET scans that image living human brains, she found that the brain chemistry behind these two stigmatized problems is very similar.

The problem has to do with fewer dopamine D2 receptors; in her words, that’s “the biochemical signature of a brain where the capacity to control strong urges has been compromised.” She goes on to talk about such things as pleasurable stimuli versus conditioned stimuli, deprivation states, and how modern society could engineer environments that encourage health.

Volkow ends on a sociological note, challenging the moralizing idea that addiction and obesity indicate a failure to self-regulate:

Dismissal of addiction and obesity as just problems of self-control ignores the fact that for us to be able to exert self-control would require the proper function of the areas in our brains that regulate our behaviors… It’s like driving a car without brakes. No matter how much you want to stop, you will not be able to do it.

Previously: How eating motivated by pleasure affects the brain’s reward system and my fuel obesity; The brain’s control tower for pleasure; New tools from NIDA help diagnose and treat drug abuse

Nutrition, Obesity, Research, Stanford News

New insulin-decreasing hormone discovered, named for goddess of starvation

New insulin-decreasing hormone discovered, named for goddess of starvation

530468355_133d4da701_zLimos, the Greek goddess of starvation, must have relied on limostatin, the eponymous hormone recently discovered by Stanford researchers, to survive hunger.

She was clearly not well fed. As Ovid writes: “Her hair was coarse, her face sallow, her eyes sunken, her lips crusted and white; her throat scaly with scurf. Her parchment skin revealed the bowels within…”

Limostatin slashed her insulin levels, keeping nutrients in her blood so they could be used. Without limostatin, humans develop diabetes-like symptoms such as low blood sugar and a tendency toward obesity.

From our press release describing the Stanford work:

The researchers first discovered limostatin in fruit flies but then quickly identified a protein with a similar function in humans.

“Starvation or famine is an ancient, ever-present specter faced by all living organisms,” said Seung Kim, MD, PhD, professor of developmental biology. “The ways to deal with it metabolically are likely to be ancient and conserved. This research clearly connects the dots between flies and humans, and identifies a new potential way to regulate insulin output in humans.”

The researchers discovered limostatin by following a series of “biological breadcrumbs:”

Kim and his colleagues withheld food from their laboratory fruit flies for 24-28 hours and looked to see which genes were highly expressed during this time. They narrowed the list to those genes that encoded proteins resembling hormones, which are special signaling molecules that circulate throughout the body to affect the function of distant cells. They observed that one of these, limostatin, caused characteristics of insulin deficiency when overexpressed in flies…

Once the researchers had identified the receptor for limostatin in fruit flies, they looked to see if it resembled any human protein. A trail of biological breadcrumbs led them to the receptor for a protein called Neuromedin U. The protein is produced in the brain, and controls a variety of physiological responses including smooth muscle contraction, blood pressure control, appetite and hormone function in humans.

Based on their experiments in fruit flies, Kim and his colleagues expected that Neuromedin U might also be important in insulin regulation. They found that the protein is also expressed in the stomach and intestines, and the Neuromedin U receptor is found on insulin-producing beta cells in the pancreas. Neuromedin U and its receptor appeared to neatly connect nutrient sensing in the gut with insulin-producing cells elsewhere in the body.

Previously: Tiny fruit flies as powerful diabetes model, Beta cell development explored by Stanford researchers and Correspondence on the discovery of insulin
Photo by William Murphy

Biomed Bites, Cancer, Obesity, Research, Stanford News

Stanford researcher tackles tricky problem: How does a cell become a fat cell?

Stanford researcher tackles tricky problem: How does a cell become a fat cell?

Here’s this week’s Biomed Bites. Check each Thursday to meet more of Stanford’s most innovative biomedical researchers.

Mary Teruel had no intention of becoming a biology professor — after all, she was in a PhD program for aeronautical engineering. But the more she learned about cells, the more fascinated she became.

“I became very interested in the challenging problem of trying to understand the complex network in cells and trying to see if you could apply some of the principles from engineering to understand theses processes and make an insight into human disease,” Teruel says in the video above.

Teruel’s drive to investigate cells led her into her current role as an assistant professor of chemical and systems biology, where she’s striving to unravel a puzzle that underlies the obesity crisis in America: How do cells called pre-adipocytes (or pre-fat cells) become adipocytes (or adipocytes)?

By learning more about cell differentiation, Teruel’s research can also shed light on processes — and potential treatments — involved in cancer.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Previously: Secrets of fat cells discovered, Fed Up: A documentary looks for answers about childhood obesity and How physicians address obesity may affect patients’ success in losing weight

Stanford Medicine Resources: