The Biggest Loser study shows persistence of slower metabolism after 6 years

May 2nd, 2016 No comments »

Gina Kolata of The New York Times has a front-page story on May 2, 2016, covering a study of winners of the TV ‘reality’ show, The Biggest Loser. The study published in the journal Obesity shows that not only is most the lost weight regained, but that the slower metabolic rate, which occurs during active weight loss, persists for up to 6 years in the subjects. This is the process of adaptive thermogenesis which we have discussed on several occasions. What the article does not mention is that most of the weight loss programs used in employer wellness programs are based on The Biggest Loser. In other words, thanks to Obamacare, employees can be penalized for failing at a weight loss program where failure is all but assured.

Where is Your New Year’s Resolution? Or, Where did I put my Adaptive Thermogenesis?

January 17th, 2014 No comments »

It’s mid-January: do you know where your New Year resolution went? You know the one about losing weight.

So maybe you are losing the weight you put on over the holidays? Maybe you are underway with a good weight loss program? Maybe you have already given up? No matter what your status, there is something you should know:

The human body is programmed to defend its weight and, when it senses weight loss, it starts cutting down its energy expenditure…big time!

Let’s talk about energy expenditure or “EE”. About 65-70% of calories burned each day are used to keep the routine body functions going, e.g. pumping blood, working the lungs, kidneys and liver. About 10% are used up in thermogenesis or the digestion of food. The rest, about 20%, is spent by the muscles in physical activity.

As far back as 1987, researchers compared the daily resting metabolic rate (RMR) of obese women who had lost weight and were no longer obese with women who were  never obese. The researchers found that the post-obese women had metabolic rates approximately 15% lower than the never-obese group and they ate less.

So, metabolism in persons who have lost weight and those who are lean may not be the same.

Exercise and the heat value of food are skewed against those with obesity. In one experiment, 10 lean women and 10 women with moderate obesity were measured during periods of eating and exercise. Eating before exercise increased the exercise metabolic rate in lean women by 11% but only by 4% in women with obesity. The thermic effect of food was 2.54 times greater during exercise than at rest for the lean group, but only 1.01 greater for the women with obesity.

In a now classic 1995 paper by Jules Hirsch, Rudy Leibel and Michael Rosenbaum at Columbia University found that when a body loses weight, it adjusts by reducing its energy expenditure. This effect is so strong that an obese person who went from 250 lbs to 200 lbs would have to consume about 30% less than a 200 lbs person who had not lost weight just to maintain the same weight. This extra-reduction in food intake would have to continue indefinitely if the person were to maintain their weight loss.

This process, called by researchers “Adaptive Thermogenesis” can persist after active dieting for up to a year in one study.  In an experiment involving subjects with severe obesity who were on a program of diet restriction and vigorous physical activity, researchers saw dramatic weight loss (over 30%) but a slowing of the resting metabolic rate (RMR) “out of proportion to the decrease in body mass, demonstrating a substantial metabolic adaption.”

Some researchers considered adaptive thermogenesis a major factor in the plateauing one sees in dieters, the increase in hunger and the eventual regain of lost weight. In one study of short-term severe diet and exercise subjects, the ‘metabolic compensation’ was seen as a major contributor to the less-than-expected weight loss. Individuals will have different adaptions to weight loss. In some cases, the effect can be significant. Tremblay et al state, “Indeed, as it is difficult to prescribe food intake that imposes an energy deficit exceeding 700-800 kcal per day to obese individuals, the decrease in energy expenditure in response to weight loss can entirely compensate for this prescribed deficit.”

Others are less sure. They seem to accept adaptive thermogenesis but see measurement problems and questions as to its utility in weight management.

The point is that our bodies contain a defensive mechanism against the disease of obesity. Until we realize that our strategies for prevention and treatment are like a novice chess player going up against a Grand Master. The point is: obesity is a lot tougher than our simplistic policy prescriptions assume.

The quandary of obesity has been expressed by Tremblay Chaput and Doucet in their article “Obesity: a disease or a biological adaption? An Update,“ Additionally, substantial body fat loss can complicate appetite control, decrease energy expenditure to a greater extent than predicted, increase the proneness to hypoglycaemia (low blood sugar) and its related risk towards depressive symptoms, increase the plasma and tissue levels of persistent organic pollutants that promote hormone disruption and metabolic complications, all of which are adaptations that can increase the risk of weight regain. In contrast, body fat gain generally provides the opposite adaptations, emphasizing that obesity may realistically be perceived as an a priori biological adaptation for most individuals. Accordingly, prevention and treatment strategies for obesity should ideally target the main drivers or root causes of body fat gain in order to be able to improve the health of the population.”

 

Hunger, Prader-Willi Sydrome and differences between the brains of persons at normal weight and with obesity

January 15th, 2014 No comments »

A New York Times report today by Andrew Pollock details the efforts of researchers and drug companies to unravel the mysteries of Prader-Willi Syndrome. Prader-Willi Syndrome is marked by insatiable appetite and obesity. Patients often slow metabolisms, intellectual difficulties and autistic behavior. (For more information see the Prader-Willi Syndrome Association website.) The condition is known to be caused by missing segments on chromosome 15. While Prader-Willi is a genetic disease, it is not necessarily found in families. 70% of cases are due to a deletion in chromosome 15 from the father; deletion from the maternal side is responsible for about 20%.  This is known as genomic imprinting where the gene turns on or off depending on which parent contributes it.

Drug developers Ferring Pharmaceuticals, Rhythm, Arena Pharmaceuticals (which sells Belviq, an FDA approved drug for weight loss) and Zafgen are looking at drugs for the condition. Zafgen is releasing results of a small clinical trial today.

While Prader-Willi is a rare condition and is well-understood regarding its genetic cause, research on the syndrome is helping to open up research on the fundamental aspects of hunger.

One of the great gaps in public and policy-makers understanding of obesity is the role of hunger, driven by powerful networks within our bodies. Hunger is clearly one of the most powerful of human emotional states as it involves existential survival, much like the inability to breathe or drowning. In my experience, many persons with obesity report nearly constant states of hunger which our food-laden environment is almost universally able to slake. But reports from individuals are a poor substitute for research. Now, in the past decade, science has filled in the gaps.

After a meal, appetite is suppressed; after energy expenditure hunger is increased. Those sensations, satiety and hunger, are caused by changes in nutrients and hormones, including PYY, GLP-1, ghrelin, leptin and insulin circulating in the body. In normal physiology, the hypothalamus balances the food intake with the metabolic requirements. This system works, usually, with great precision. This appetite process is called homeostatic. Non-homeostatic food control is driven by sight, smell, taste, habits, emotional and economic influences. The brains areas involved in nonhomeostatic food control include the hippocampus, the amygdala, insula, striatum and orbitofrontal cortex. The two systems are not independent but highly integrated.

Recent research points to understanding that higher food intake in persons with obesity is due, probably in substantial part, to differences in how the brains of  persons with obesity respond to food cues compared to  persons at “normal” weights.

Researchers using techniques such as functional Magnetic Resonance Imaging (fMRI) are mapping the physiological networks of hunger and are understanding  why we get hungry and why maintaining weight loss is so hard. FMRI allows scientists to locate specific areas of the brain which show responses to specific stimuli. Thus they can compare obese and lean subjects in different conditions. (For an explanation of the use of fMRI studies in appetite regulation see this article from de Silva and colleagues and from which this illustration is taken.

Using fMRI, researchers at Emory University have identified areas in the brain identified with taste and the reward system that ‘light up’ when subjects just looked at pictures of appetizing food.  Meanwhile, other researchers, also using fMRI, found different reactions to pictures of high-calorie foods between men and women. When healthy subjects were given injections of ghrelin, fMRI scans showed increased brain activity in response to pictures of food and were correlated with self-reported hunger ratings. (Ghrelin is a peptide hormone that stimulates hunger and food consumption.) Just in October, a study was published showing that images of high fat foods produced stimulation of the brain’s reward network in Hispanic females.

It isn’t only pictures of food which tweak the brain. Subjects with obesity differed from lean subjects in which area of the brain responded to food aromas. The brain areas affected by food aromas are similar to those affected by addictive substances, like alcohol.

In short, individuals prone to weight gain and obesity have altered neuronal responses to food cues in brain regions known to be important in energy intake regulation and these differ from lean person’s responses.

Of great concern is when such differences occur? A study from the University of Kansas Medical Center used fMRI on children and adolescents, ages 10-16, half at a healthy weight and half with obesity. They found the obese group showed greater activation to food pictures both before and after a meal than the healthy weight group. Unlike the healthy weight group, the obese group’s response to food stimuli did not diminish significantly after eating. The authors concluded, “This study provides initial evidence that obesity, even among children, is associated with abnormalities in the neural networks involved in food motivation, and the origins of neural circuitry dysfunction associated with obesity may begin in early life.”

This understanding of obesity has great implications for the prevention and treatment of obesity and for the establishment of effective public policies.

NIH Director Address Gastric Bypass Surgery and Diabetes

July 30th, 2013 No comments »

Francis Collins, director of the National Institutes of Health, has a new blog out on how gastric bypass surgery affects the development of type 2 diabetes.

Reflections on the AMA Decision – Part 2

July 4th, 2013 No comments »

Sugarpova

One of the more curious comments on the AMA decision came from Hank Cardello of the Hudson Institute. Hank (with whom I have broken bread a couple of times) is a former food industry executive who believes that the food industry can basically down-shift the calories in the marketplace, resulting in lower obesity rates. Writing in Forbes Magazine, Why the AMA’s Obesity Ruling is Bad Medicine, Hank appears offended that doctors went off to decide what is a disease without checking first with the food industry. If they had, Hank would have told them how declaring obesity a disease gives health activists and policymaker a “new blunt instrument to use against the food industry.” Those crazy folks will now revive calls for Twinkie taxes, soda cup size bans and restrictions on full-fat pizza. Writes Hank,“These newly ignited brushfires, fanned and fed by social media and zealous lawmakers, could cost the food and restaurant industries enormous time and money to fight. If the activists were to claim that the industries are selling products that worsen a disease called obesity, they would have no choice but to lawyer up and defend themselves. As the decades-long tobacco wars proved, this would only greatly delay getting both parties to come to an equitable agreement.”

Whoa! Hank! Take a breath! Walk around the block.

First, numerous authorities have recognized obesity as a disease. It has been in the International Classification of Diseases for at least 20 years. The Social Security Administration, Food and Drug Administration, National Institutes of Health, Internal Revenue Service have described obesity as a disease for about 10 years or so. So, it isn’t new. If the ‘health activists’ will now ‘use’ it, where have they been? Do you really want to draw a parallel between the food industry and the tobacco industry? I don’t think it is apt and I would think you wouldn’t either.

But Hank presses on predicting (threatening?) that the food industry will now back off creating more healthy foods because they are being demonized “as purveyors of disease.” Well, it didn’t take any time to throw in the towel on the food industry meeting consumer demands for healthier alternatives! That was quick. Was the industry looking for a way out? It certainly feels that way since there is nothing really new in the AMA policy.

But it is next part of Hank’s paper that is embarrassing. It is like being at a party with a friend who starts to say something really unfortunate. You know it is too late to stop them. So, Hank goes on,

“Labeling obesity as a disease also ignores the almost taboo subject of personal responsibility. Describing obesity as purely a disease overlooks the complex role of a person’s psychological profile and attitudes. A study led by Angela Sutin of the National Institutes of Health highlighted that the most disciplined consumers had lower rates of obesity while larger weight gains were linked to personality factors such as impulsiveness, low conscientiousness, and a willingness to take risks. The authors concluded that any obesity solution must address these psychological factors, which general practitioners cannot.”

Well, I guess ‘personal responsibility’ isn’t so taboo after all. Never too late to call obese people damaged in the head. Persons with obesity have been called worse but trying to rope in a researcher from NIH for support was novel.

A few things are wrong with Hank’s description of this paper. First, it appears the study sample had many more ‘normal’ weight participants than the general population (45% to 31%) which might affect the outcomes. Second, Sutin and her co-authors acknowledge the possibility of reverse causation, i.e. that excess weight and the health and stigma attendant thereto can affect personality development. Hank ignores this. Third, while Hank is trying to say these overweight/obese customers can’t control themselves, Sutin points out, “Individuals high on Neuroticism, in particular the impulsiveness facet, and low on Conscientiousness have elevated triglycerides, hypertension, and clinically elevated levels of inflammation, even after controlling for differences in adiposity. Abnormal weight may be one mechanism that partially mediates the relationship between personality and these health outcomes.” (Emphasis added.) Sutin’s paper concludes, “The cognitive, emotional, and behavioral patterns associated with personality traits likely contribute to unhealthy weight and difficulties in weight management. Identifying the personality traits associated with obesity may help to elucidate the role of personality traits in disease progression.” Whoops! Did she just call obesity a disease?

This paper was published in 2011. To pull it out, Hank had to skip over 2 of her papers published earlier this year which have produced some dramatic and unexpected findings.

In the first 2013 paper, she and her colleagues found that individuals who rated high on impulsiveness and lacked discipline or low conscientiousness had high circulating levels of leptin, which plays a critical role in regulating body weight, even after controlling for body mass index, waist circumference or inflammatory markers.

Sutin’s second 2013 paper, “I Know Not To, but I Can’t Help It: Weight Gain and Changes In Impulsivity Related Personality Traits,” has much greater implications. In this study, Sutin and colleagues picked up where the 2011 study left off. They looked to see whether weight gain or loss of 10% or more led to personality changes, specifically impulsiveness and deliberation. They found that, compared to participants to stayed weight-stable, those who gained weight became more impulsive. Those who did not gain weight showed a predicted loss in impulsiveness. Then came the surprise. Contrary to their hypothesis, weight gain was also associated with increases in deliberation. That is, with gaining weight, subjects became more thoughtful before acting. This was especially strong among younger participants. The authors considered that, as participants gained weight, they bought into the American stereotypes about persons with obesity. So they saw themselves as more impulsive even as they were increasing in deliberativeness. They had no change in self-discipline. The authors speculate further, “A second possibility is that physiological mechanisms associated with weight gain could contribute to the relation between weight gain and changes in personality. For example, overweight and obese individuals tend to have higher levels of inflammation and chronic inflammation may reduce the ability to effectively regulate emotions and control behavior.”

Sutin et al suggest more research to help identify how considerations of personality traits can enhance interventions. For example, information on healthy lifestyles may be less useful for some than information on emotional aspects of impulsivity.

Finally, Hank concludes that the ‘disease’ label will be a crutch and cause people to stop making lifestyle changes and probably backslide. Why do these pundits make such negative generalizations about 2/3 of the population? Has the food industry decided just to insult its customers? You may want to see what happened with Michael Jefferies, the head of the head of Abercrombie & Fitch who said he did not want fat customers in his store. Donny Deutsch, advertising executive and TV personality, recently called him “disgusting” and “vile.” or University of New Mexico professor Geoffrey Miller who said he did not want students with obesity to apply to his Ph.D. program. He is being investigated by his university.

Oh, if only we would just leave obesity in the hands of the benevolent food industry!

Remember, those are the folks who are re-introducing Twinkie’s to America’s stores.

Twinkies

The same folks who have brought us  tennis superstar Maria Sharapova whole line of candy called, Sugarpova. (Get it?) See picture above.

 

And let’s not forget Sonic’s new 1,700 calorie peanut butter and bacon milk shake.

Sonic" peanut butter and bacon milk shake

Oh, and then there is Safeway’s leadership to shift the costs of health insurance onto overweight and obese employees based on dubious representation of their program and Kroger’s and Safeway’s efforts to derail front of package calorie labeling in supermarkets. Yeah, let’s all follow those guys.

 

Catching Up on Obesity and Neurological Diseases

June 12th, 2013 No comments »

For some time I have been reading papers dealing with the association (or lack thereof) of obesity with neurological disorders, such as Alzheimer’s Disease, autism spectrum disorders, and ADHD. I did not report on them too much, even though I came into the obesity field through my advocacy work in the neurosciences in the 1990s. I just did not ‘get’ the connection.

Now, the veil has been lifted thanks to a talk by Tamas L. Horvath, of Yale University. Dr. Horvath’s talk, at the Research Symposium sponsored by the American Diabetes Association, “Biologic Responses to Weight Loss and Weight Regain,” in Washington DC in April 2013, focused on hunger-producing neurons’ regulation of higher brain functions and longevity.

One slide in particular caught my attention. He was addressing the complexity inherent in satisfying the hunger drive and appetite needs. For example,

-wakefulness is needed. This is controlled by the lateral hypothalamic arousal center. Disorders in wakefulness include narcolepsy and sleep disorders.

– memory of the location of food sources is needed, both long term and short term. This is the role of the brain’s memory and reward systems. Disorders in this realm include dementia, Alzheimer’s disease, mood and addictive disorders.

-decision-making for when and how to acquire and prepare food is required. Related disorders in this sphere include depression and schizophrenia.

-the physical ability to pursue and locate and collect food is needed. Related disorders include Parkinson’s disease and amyotrophic lateral sclerosis (ALS).

-finally, there is food intake itself. Related disorders include obesity, anorexia and diabetes.

This simple schema made a great deal of sense to me. So, with thanks to Dr. Horvath, we will start providing more reports of studies investigating the connections of obesity and these prominent neurological conditions.

For example, Fadel and colleagues are looking at insulin, orexin and leptin, already recognized for regulating food intake, body weight and body composition, for their involvement in addictive behaviors, reproduction and cognitive performance. See, Food for thought: the role of appetitive peptides in age-related cognitive decline.

Vignini et al discuss the association of diabetes mellitus with Alzheimer’s Disease, calling Alzheimer’s Disease “Type 3 Diabetes.” Their paper, “Alzheimer’s disease and diabetes: new insights and unifying therapies” explores common mechanisms and possible remedies for both diseases. Meanwhile, Reitz and colleagues have uncovered variants in the FTO gene (already implicated for obesity) which can be risk factor for Alzheimer’s disease.

 

Gingrich Gets Brain Science Politics Wrong

December 15th, 2011 No comments »

In a Washington Post blog, Gingrich at University of Iowa: ‘I want to talk to you about brain science’ – Election 2012 – The Washington Post, Presidential candidate Newt Gingrich is quoted as saying,  “This (brain science)  is a very big idea in an area that many political leaders won’t attack.” Well, I spent most of the 1990s dealing with neuroscience research funding in Congress and there were many political leaders willing to support (as opposed to “attack”) neuroscience research.

I responded with this comment, “Gingrich has got it all wrong on the politics of neuroscience. In fact, many politicians have embraced it, going back to the 1980s, when the late Congressman Silvio Conte (R-MA), led the efforts on the Appropriations Committee to expand neuroscience research funding, principally at the National Institutes of Health. He also introduced and led enactment by Congress of the Decade of the Brain Resolution which President George Bush (41) signed, declaring the 1990s as “The Decade of the Bran.” There were numerous Congressional briefings and events during the 90s, some sponsored by the Library of Congress, and many by patient and professional groups as well as organizations I was associated with, such as the National Foundation for Brain Research. Congressman Claude Pepper, Senators Pete Domenici, Tom Harkin, Ted Kennedy, and Lowell Weicker were outstanding leaders. Gingrich was not one of them although to be fair he did support expansion of NIH funding overall.”

The blog also had a reference which seemed to indicated that someone was complaining about the lack of action by the FDA to approve anti-obesity drugs. However, the question appeared to pit obesity against neurology. My response, There is a curious reference in the blog, seemingly from a member of the audience, on whether obesity should be stressed over neurology. The question is odd. Obesity is a neuro-endocrine disease and the brain plays a critical, actually the critical, role in regulating body weight. So, one can’t really posit obesity or neurology. This is not to say all treatments have to be neurological. Many, like lap-band or the OTC drug, Alli, do not work on the neurological system.”

As readers have seen, obesity is playing a prominent role in this campaign so far. See Politics. Take the opportunity to comment on news articles such as this one to set the record straight.

Why the weight lost comes back

October 28th, 2011 No comments »

It comes as no surprise that regaining weight after weight loss is common and frustrating to dieters. It also limits choices for policy makers who, in general, had avoided treatment strategies because of the transient nature of weight loss.

It also comes as no surprise that, after weight loss, metabolism of overweight persons slowed down and hormonal changes increased the powerful sensation of hunger. This double whammy makes maintenance of weight loss so challenging.

Now come researchers from Australia who studies a small group (only 50 overweight and obese patients without diabetes) . The group lost about 13.5kg  which led to reductions in levels of leptin, peptide YY, cholesystokinin, insulin and amylin and increases in ghrelin. There was also an increase in subjective appetite.(See Brain and Gut for background.) What is new is that these changes persisted for one year after initial weight loss. They did not revert to the levels recorded before weight loss, probably explaining why so many dieters relapse. See http://www.ncbi.nlm.nih.gov/pubmed/22029981.

Gina Kolata, writing in the New York Times, quotes Dr. Jules Hirsch as saying that researchers may just not know enough about obesity to prescribe solutions yet. “One thing is clear, he said, “A vast effort to persuade the public to change its habits just hasn’t prevented or cured obesity.” “We need more knowledge,” Dr. Hirsch said, “Condemning the public for their uncontrollable hedonism and the food industry for its inequities just doesn’t seem to be turning the tide.” Study Shows Why It’s Hard to Keep Weight Off – NYTimes.com