obesity

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Eat Fat But Stay Thin: Mice Can Do It, Maybe Someday We Can Too

Generic lab mice

Generic lab mice

The journal Nature reports that some lab mice have lived out my food fantasy: Even though they ate a heavy, high-fat diet — my particular dream is unlimited Ben & Jerry’s — they did not become obese, because researchers found a novel way to tweak their metabolism.

Sigh. The caveats first: What works in mice might not in humans. It might not be safe. Clinical trials are not on the immediate horizon. This is no reason to stop eating healthy food and exercising.

But we can dream, right? And we can savor the explanations from Dr. Barbara Kahn of Beth Israel Deaconess Medical Center and Harvard Medical School, senior author on the Nature paper. She sums up: “We found an enzyme in fat that appears to be elevated in people with obesity and diabetes. And if we inhibit it in mice, we can increase the amount of energy that the animal burns, and thereby decrease the amount of calories that are stored as fat.”

It’s something like the extra energy you burn when you exercise, she said — except without the exercise.

Dr. Kahn’s team found a gene that, when suppressed, makes metabolism less efficient — which is actually a good thing if you’re trying to avoid obesity.

“Generally, in our lives, we think it’s good to be efficient — and it certainly is good to be efficient in time management,” she said. “But if your metabolism is efficient, it means you need fewer calories to generate the energy that cells need for their basic metabolism, and therefore, if you eat too many calories, you will put on weight. But if the cells are inefficient, they’ll burn up those extra calories and you won’t put on weight.”

So do these findings — centering on an enzyme known as nicotinamide N-methyltransferase or NNMT — indeed hold the promise of some sort of drug to prevent or treat obesity?

“The approach we used in the mice was mainly prevention,” Dr. Kahn said, “but the same idea should work for treatment of obesity. I have to caution, of course: one has to look into all the safety aspects if one considers such a treatment in humans. But all the cellular machinery is there, so it should work.” Continue reading

Obesity: A Disease By Any Other Name

(Photo: Yale Rudd Center for Food Policy and Obesity)

(Photo: Yale Rudd Center for Food Policy and Obesity)

By Melinda J. Watman
Guest contributor

When the American Medical Association declared obesity a disease last year, most of us — advocates who work to help those with obesity — were thrilled.

We saw the new definition’s potential to change how medical professionals regard people with obesity, increase society’s focus on obesity, push insurance companies to cover obesity treatments, reduce social stigma and moderate the anxiety and depression often afflicting those with obesity.

Already, we see some of those hopes being realized. Just last week, the federal government’s Office of Personnel Management issued a ruling that health insurers who cover federal employees may no longer exclude coverage of weight loss drugs on the basis that obesity is a “lifestyle” condition or that obesity treatment is “cosmetic.” This is one more significant step in the recognition and treatment of obesity as a disease.

But nothing is that simple or easy.

The high-fiving was barely over when the first study came out saying “not so fast.” It would seem, according to an article published in the New York Times, no good deed goes unpunished. The article presented a summary of a research paper titled “‘Obesity Is a Disease’: Examining the Self-Regulatory Impact of this Public-Health Message.

Melinda Joy Watman (Courtesy)

Melinda Joy Watman (Courtesy)

The three authors concluded that labeling obesity a disease led their subjects to want to eat more, eat worse and care less about their weight. They suggested that labeling obesity a disease leads to the belief that it is futile to try to manage one’s weight.

Whether one agrees with the study’s findings and conclusions or not, the underlying question of whether obesity should be accepted as a disease is the critical point. The authors certainly question its validity based on the findings that their subjects suffered an “undermining of beneficial self-regulatory processes.”

What is interesting is that if it were any other chronic illness with comparable results, we would not be questioning whether the illness should be classified as a disease. Rather, we would be trying to find better ways to engage, educate, support and treat those patients as we continued to work on new therapeutics to manage the disease.

As is often the case with obesity, it would appear this line of thinking and research has the potential to further marginalize the problem and those affected by it. This is completely counter to what the AMA policy strives for – the same medically accepted framework to diagnose, treat and support patients as exists with any other chronic illness. Continue reading

Are Antibiotics Partly To Blame For Obesity Epidemic?

(Tobyotter/flickr)

(Tobyotter/flickr)

This morning’s On Point with Tom Ashbrook raised a critical question: might antibiotics be “a scale-tipping X-factor” driving the American obesity epidemic?

Featuring reporter Pagan Kennedy, who just wrote a piece on this topic, “The Fat Drug,” for the New York Times Magazine, and researcher, Dr. Illseung Cho, with the New York University School of Medicine, author of a recent Nature article on antibiotics’ impact on the microbiome, the radio segment explored the possibility that missing microbes in our gut might be party responsible for our growing weight.

Who knew, for instance, that a single course of antibiotics can potentially alter your gut bacteria forever?

Here’s more from Kennedy’s report:

American kids are prescribed on average about one course of antibiotics every year, often for ear and chest infections. Could these intermittent high doses affect our metabolism?

To find out, Dr. Blaser and his colleagues have spent years studying the effects of antibiotics on the growth of baby mice. In one experiment, his lab raised mice on both high-calorie food and antibiotics. “As we all know, our children’s diets have gotten a lot richer in recent decades,” he writes in a book, “Missing Microbes,” due out in April. At the same time, American children often are prescribed antibiotics. What happens when chocolate doughnuts mix with penicillin?

The results of the study were dramatic, particularly in female mice: They gained about twice as much body fat as the control-group mice who ate the same food. “For the female mice, the antibiotic exposure was the switch that converted more of those extra calories in the diet to fat, while the males grew more in terms of both muscle and fat,” Dr. Blaser writes. “The observations are consistent with the idea that the modern high-calorie diet alone is insufficient to explain the obesity epidemic and that antibiotics could be contributing.”

Exporting The Couch Potato Lifestyle (And Obesity) Via TV, Computers, Cars

(Aaron Escobar/Wikimedia Commons)

(Aaron Escobar/Wikimedia Commons)

A new study finds that the luxuries of modern life come at an extremely high cost: a greater chance of becoming obese or developing diabetes.

Researchers report that in lower-income countries, ownership of a household device — including a car, computer or TV — significantly “increased the likelihood of obesity and diabetes.”  Specifically, owning these items was “associated with decreased physical activity and increased sitting, dietary energy intake, body mass index and waist circumference.” Of the three “devices,” owning a TV had the strongest association with the bad health outcomes.

In poorer countries, such big-ticket items are clearly less prevalent than in rich countries, however they are fast becoming more ubiquitous. And so, apparently, are the ills associated with sitting around watching TV, typing on a computer and driving.

Here’s more from the news release:

The spread of obesity and type-2 diabetes could become epidemic in low-income countries, as more individuals are able to own higher priced items such as TVs, computers and cars. The findings of an international study, led by Simon Fraser University health sciences professor Scott Lear, are published today in the Canadian Medical Association Journal.

Lear headed an international research team that analyzed data on more than 150,000 adults from 17 countries, ranging from high and middle income to low-income nations.

Researchers, who questioned participants about ownership as well as physical activity and diet, found a 400 per cent increase in obesity and a 250 per cent increase in diabetes among owners of these items in low-income countries.

The study also showed that owning all three devices was associated with a 31 per cent decrease in physical activity, 21 per cent increase in sitting and a 9 cm increase in waist size compared with those who owned no devices. Continue reading

How Obesity May Lead To Asthma — And Perhaps How To Break That Link

asthma inhaler

This just in from Boston Children’s Hospital: The immune system may play a key role in the asthma that can develop along with obesity — and that new understanding may point to possible ways to stop or treat obesity-related asthma.

A finding of broad potential impact in a country where one-third of the population is obese and more than 25 million people have asthma. From the Children’s press release on the study just out in the journal Nature Medicine:

A growing body of literature links asthma with obesity, but the reason for the link has been unknown. Both conditions have become more common over the last several decades. The new study, led by Dale Umetsu, MD, PhD, and Hye Young Kim, PhD, of the Division of Allergy and Immunology at Boston Children’s, explored obesity’s effects on the immune system.

The researchers studied mice that were fed a high-fat diet causing them to become obese. Unlike mice fed normal diets, the obese mice developed airway hyper-reactivity or constricted and twitchy airways, the predominant feature of asthma.
In the study, obesity appeared to alter the innate immune system—the body’s first responder to infection—in several ways to cause lung inflammation.

In addition, when IL-1β [a protein linked to inflammation] production was blocked with the drug anakinra (Kineret, Swedish Orphan Biovitrum), used to treat rheumatoid arthritis, the obese mice did not develop asthma.

Continue reading

Recipe For Obesity: Fast-Food Burgers And Sodas, Study Finds

(Wikimedia Commons)

(Wikimedia Commons)

We already know that fast food restaurants are among the culprits in America’s obesity epidemic, but it’s not just where you eat, it’s what. In particular, Boston University has just sent over word of a study that linked specifically fast-food burgers and sodas to obesity in young African-American women. From the press release:

A research team from Boston University’s Slone Epidemiology Center examined the association between consumption of foods from restaurants and risk of becoming obese in a large cohort of young African American women. Their results, published online today in Ethnicity & Disease, provide evidence that frequently eating hamburgers from restaurants is associated with higher risk of obesity. Higher intake of sugar-sweetened soft drinks, which are commonly consumed together with restaurant foods, was also independently associated with obesity risk.

This study was conducted using data from the Black Women’s Health Study, an ongoing investigation of the health of 59,000 African American women that began in 1995. The analysis included younger women, aged 21 to 39 years, because most weight gain occurs before middle age. The women studied were not obese and had no history of cancer or cardiovascular disease at the start of follow-up. Diet was assessed twice (in 1995 and 2001) using validated questionnaires, and information on the participants’ weights was collected every two years from the study’s start until 2011…

The researchers found that women who ate burgers from restaurants at least twice a week were 26 percent more likely to become obese by the end of the study than those who rarely ate burgers, after controlling for many factors including overall diet quality and sugar-sweetened soft drink consumption. In addition, women who drank at least two sugar-sweetened soft drinks per day were 10 percent more likely to become obese than those who drank none, after controlling for overall diet quality and restaurant burger consumption.

The ‘Fat But Fit’ Myth Debunked

On the train to New York for Thanksgiving, we sat next to a family with a very chubby girl. She was about 9, with lovely red hair and a pretty moon-shaped face. But I could see her belly bulging and her chunky arms as she played with her iPad, and I imagined some tough teenage years ahead.

While her mother slept, her dad headed to the cafe car and returned with a box of chocolate chip cookies and peanut M&M’s. “Quiet,” he said, handing the treats to the girl. “Eat them before Mom wakes up.” Then he gave her a Mountain Dew to wash it all down. It was 10 am on Thanksgiving.

“Child abuse,” I thought, but kept my mouth shut.

I imagined the little red-haired girl again today, in light of this headline in MedPage Today “Fat But Fit — Is It Just A Myth?”

Remember the concept of “benign obesity” — the idea that as long as you’re exercising and relatively fit, being a little fat probably won’t hurt you. Well, think again. A new study published in the Annals of Internal Medicine suggests there is no healthy obesity. According to the news report:

Metabolically healthy obese people have a long-term increased risk for death and cardiovascular events compared with their normal-weight counterparts, suggesting there is no such thing as benign obesity, according to a meta-analysis.

(Yale Rudd Center for Food Policy & Obesity)

(Yale Rudd Center for Food Policy & Obesity)

When studies with follow-ups of a decade or more were considered, obese people with no metabolic abnormalities had a 24% increased risk for these events compared with metabolically healthy, normal-weight people (relative risk 1.24; 95% CI 1.02-1.55), reported Caroline K. Kramer, MD, PhD, of Mount Sinai Hospital in Toronto, and colleagues.

All metabolically unhealthy people had a similar elevated risk for the events compared with metabolically healthy, normal-weight study participants, they wrote in the Annals of Internal Medicine, specifically an RR of 3.14 for normal weight (95% CI 2.36-3.93), 2.70 for overweight (95% CI 2.08-3.30), and 2.65 for obese (95% CI 2.18-3.12).

“Our results do not support this concept of ‘benign obesity’ and demonstrate that there is no ‘healthy’ pattern of obesity,” Kramer and colleagues wrote. “Even within the same category of metabolic status (healthy or unhealthy) we show that certain cardiovascular risk factors (blood pressure, waist circumference, low high-density lipoprotein cholesterol level, insulin resistance) progressively increase from normal weight to overweight to obese.”

Doctor’s Orders: Get Outdoors

“So Melody, as we finish our check-up today, I have one more thing to tell you about,” Dr. Karen Sadler said as she pulled her stool closer to the examination table where 8-year-old Melody Salhudin sat, legs dangling over the edge.

You know, you come here when you’re sick and need medicine, but you know you also come to the pediatrician so we can help you stay healthy. And part of staying healthy is being active,” Dr. Salder explained as she reached for a glossy brochure and a special prescription pad. On it, she wrote a prescription for Melody to get outside and exercise.

Melody Salhudin hits the swings during a break from her walk (Martha Bebinger/WBUR)

Melody Salhudin hits the swings during a break from her walk (Martha Bebinger/WBUR)

It’s part of a program called Outdoors RX  – a partnership between the Appalachian Mountain Club and Massachusetts General Hospital. It’s funded by three foundations for one year, with a budget of $200,000. The two venerable organizations are testing the idea of having doctors write prescriptions for outdoor exercise in two communities with high rates of childhood obesity, Waltham and Framingham.

Melody, a quick study, got the point. “To help people stay strong and healthy and to make sure they get up and get their body like grooving and moving,” Melody said, giggling and twisting her hips.

The Appalachian Mountain Club isn’t known for Melody’s style of moving and grooving.

“Originally we thought of hiking or biking,” and other more traditional AMC activities, said Pam Hess, who runs Outdoors RX. But Hess soon realized that many kids in these communities are not used to, or even comfortable, spending time outdoors. Continue reading

Girls And Early Puberty: Is It More Than Just Obesity?

An important new study of young girls has determined that childhood obesity is most likely the key driver behind the disturbing, and now widely acknowledged, phenomenon of girls starting puberty at a younger age.

The study, published in the journal Pediatrics, tracked the breast development (thelarche) of girls ages 6-8 in three geographic regions of the U.S. — San Francisco, Cincinnati and New York City.

According to the report, “girls with greater BMI reached breast stage 2 [development] at younger ages.” Ethnicity, too, was an important factor: The “median age at onset of breast stage 2 was 8.8, 9.3, 9.7, and 9.7 years for African American, Hispanic, white non-Hispanic, and Asian participants, respectively,” researchers report. The bottom line:

We observed the onset of thelarche at younger ages than previously documented, with important differences associated with race/ethnicity and BMI, confirming and extending patterns seen previously. These findings are consistent with temporal changes in BMI.

In an accompanying editorial, “The Enigmatic Pursuit of Puberty in Girls,” Marcia. E. Herman-Giddens, of the Gillings School of Global Public Health at the University of North Carolina, Chapel Hill, raises an important question, that is, what else, beyond obesity, might be to blame? “Extensive interacting variables are known to be associated with earlier development in addition to weight and genetics,” she writes, noting a long list of possibilites, including “certain intrauterine conditions and exposures, preschool high-meat diets, dairy products, low fiber intake, isoflavones, high-stress families, absent fathers, certain endocrine disruptors, the microbiome as it influences weight, epigenetics, light exposure, hormone-laced hair products, insulin resistance, activity level, geographical location, and others.”

(Yves Hanoulle/flickr)

(Yves Hanoulle/flickr)

Indeed, the study’s conclusions, as in so much of research, aren’t completely satisfying, particularly for any mother who has surreptitiously surveyed her daughter’s elementary school and seen breasts clearly budding on second, third and fourth grade girls, who happen not to be obese.

I know, I know, my little scan around the playground means pretty much nothing when it comes to figuring out what’s going on in the population. But it certainly seems like there may be more to this trend than simply the spike in obesity — though that clearly plays a role. (Also, is it still merely a “trend” when it’s on the cover of The New York Times Magazine?)

I asked Diane E. J. Stafford, MD, with the Division of Endocrinology at Children’s Hospital Boston for her initial take on the Pediatrics study and editorial. Here’s are seven (lightly edited) points she made, via email:

1. This supports the previous studies that imply that the “normal” age for puberty may be younger than had been previously documented. It is more helpful in that it was a prospective longitudinal study so it followed the same children over time rather than extrapolating from a cross-sectional study.

2. It is very interesting and, in my opinion, not surprising that those with an increased BMI may be more likely to progress to puberty earlier. I think we have all felt that this was likely be associated. However, “the data support, but do not establish, causality.” This is an important caveat and one that will not likely be brought out in the general conversation about this study.

3. There are very likely to be many influences on the timing of puberty, but most of them cannot be easily measured on a population basis, if at all. The assumption of this and other population based studies is that the various other influences (like genetics) are spread evenly throughout the population and “come out in the wash”, making obesity the “largest driver” on a population basis. A reasonable conclusion for a large population, but not for an individual. Continue reading

Anti-Fat Bias At Work: Should It Be Banned By Law?

Will The Supremes Kill The Health Law?

Dr. W. Scott Butsch, an obesity medicine specialist at Massachusetts General Hospital, keeps hearing deeply disturbing stories from patients who have lost lots of weight.

They tell him that within a few months of slimming down, they find themselves suddenly enjoying new recognition and promotions at work. Which is wonderful — until it hits them that their newfound success suggests that they were being discriminated against when they were heavier.

“They come to this moment where they’re excited that so many things have been positive in their life over the past several months,” Dr. Butsch said. “And then they realize that they have been almost cheated, throughout their business relationship, and it puts a bad taste in their mouth about how they’ve been treated.”

Their weight stemmed from what medical science increasingly understands as a disease, not a character flaw.

A growing body of research bears out those accounts of weight-based bias. Forty-three percent of overweight and obese people say they’ve experienced bias against them by their bosses, one study found. Another calculated that severely obese white women tend to earn 24 percent less than their normal-weight co-workers.

Dr. Butsch saw injustice compounded. His patients had been judged based on their weight, and their weight stemmed from what medical science increasingly understands as a disease, not a character flaw. He felt compelled to speak out: Earlier this year, he testified on behalf of a bill in the Massachusetts Legislature that would ban workplace discrimination based on weight.

Obesity specialist Dr. W. Scott Butsch (courtesy)

Obesity specialist Dr. W. Scott Butsch (courtesy)

It was a somewhat quixotic move. The bill had been proposed every session for the last 15 years, and never gone anywhere.

But this year is different. Last month, the weight discrimination bill sailed through the committee that considered it, gaining easy approval in a 7-to-1 vote.

What changed?

“I think the key to this shift was research,” said Rep. Byron Rushing, the Democrat and now House majority whip who has sponsored the bill for the last 15 years. “It was having academics who’ve been working in the field of obesity, having testimony from a medical doctor. To be able to say that in recent studies of discrimination against women, that a higher number of women report seeing discrimination based on their body shape than you have of women being discriminated against because of race. Those kinds of studies are giving people pause.”

Dr. Butsch notes that there’s also a far bigger scientific shift under way: from the old medical concept of obesity as a failure of willpower to the new understanding that it is a disease — a chronic and complex disease.
Continue reading