Anyone who has ever taken high doses of cortisone is well aware of the profound effect of glucocorticoids on appearance and body weight.

Not only do patients on high doses of cortisone regularly develop a typical Cushingoid phenotype (with abdominal obesity, moon face and buffalo hump) but patients also develop a ravenous hunger and appetite with an often dramatic increase in food intake.

Given this impact of the glucocorticoid system on ingestive behaviour, it may be reasonable to ask whether genetic differences in this system can perhaps also play a role in eating disorders?

This question was now addressed by Cellini and colleagues from the University of Florence, Italy, in a paper just published online in Psychiatric Genetics.

The authors studied the distribution of various variants of the glucocorticoid receptor gene in 572 Italian patients: 118 patients with anorexia nervosa, 108 patients with bulimia nervosa, 62 patient with binge eating disorder, 177 obese non-binge eating disorder patients, and 107 unrelated, normal, age-matched controls.

While there were no significant relationships between any of the receptor polymorphisms and other eating disorders, there was a significant association between one variant (rs6198) and binge eating disorder.

In addition, irrespective of eating behaviour, individuals with another genetic variant of this receptor (N363S) tended to have higher a BMI.

While it is always wise to treat such findings, especially when they come from a single, relatively small study, with caution, these results are certainly compatible with the notion that the glucocorticoid system (perhaps not unexpectedly) may well play a role in the development of obesity and binge eating disorder (at least in a subset of patients).

Although it is highly unlikely that finding these genetic variants will lead to a genetic diagnostic test anytime soon, people with this problem may find some comfort in the idea that their genetic makeup may well be a factor that determines their susceptibility to this disorder.

Fortunately, binge-eating disorder is highly responsive to treatment, and professional psychological counseling (sometimes in combination with pharmacotherapy) can lead to the resolution of binge-eating behaviours in the vast majority of patients.

AMS
Montreal, Quebec

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Cellini E, Castellini G, Ricca V, Bagnoli S, Tedde A, Rotella CM, Faravelli C, Sorbi S, & Nacmias B (2010). Glucocorticoid receptor gene polymorphisms in Italian patients with eating disorders and obesity. Psychiatric genetics PMID: 20440229

Recent population surveys show that as many as two out of three women will report trying to lose weight in the past year.

Obviously, this answer does not really tell us much about what women are actually doing, as the types of diets and weight loss strategies seem virtually countless - some perhaps healthier than others.

Now a study by Stephanie Lanza and colleagues from Pennsylvania State University, published in the latest issue of OBESITY, suggests that women’s weight loss strategies can be divided into four common strategies and that simple questions can help predict these behaviours.

The study used a statistical method called latent class analysis (LCA) to identify subgroups of individuals who shared similar patterns of weight-control strategies amongst 197 non-Hispanic white women living in central Pennsylvania by analysing their response to 14 commonly used healthy and unhealthy weight-loss strategies.

Four groups were identified:

“No Weight Loss Strategies” (10%): individuals in this group are characterized by a low probability of reporting any weight-control strategy.

“Dietary Guidelines” (26.5%): individuals in this group have a high probability of reporting use of strategies consistent with healthy practices present in current guidelines, such as increased fruits and vegetables intake, increased exercise, decreased fat intake, eliminating certain foods, and reducing calories.

“Guidelines+Macronutrient” (39.4%): individuals in this group, in addition to the healthy practices of the guideline users, also have a high probability of reporting trying a low-carbohydrate diet.

“Guidelines+Macronutrient+Restrictive” (24.2%): individuals in this group report having tried nearly all weight-loss strategies, including both healthy and unhealthy strategies. This is the only subgroup of individuals who were likely to report skipping meals; use of appetite suppressants/liquid diets/diet pills; reducing alcohol consumption; and fasting.

Perhaps not surprisingly, women with weight concerns, the desire to be thinner, and dietary restraint were far more likely (in fact 10 to 30 fold more likely) to be in the “Guidelines+Macronutrient+Restrictive” class than in the “No Weight Loss Strategy” class.

The relationship between disinhibition and behaviour was more complex: disinhibition increased the odds of engaging in any weight-loss strategy when restraint was low; whereas, disinhibition increased the odds of engaging in unhealthy compared to healthy weight-loss strategies when restraint was high.

The authors interpret these findings to suggest that being both highly restrained and disinhibited may be a strong predictor of unhealthy, extreme weight-loss behavior that may ultimately be counterproductive.

As a clinician, I wonder if the identification of these behavioural classes will help better manage patients in these classes or even provide reasonable predictors of attrition and outcomes in clinical weight management programs. My guess is that individuals in the “Guidelines+Macronutrient+Restrictive” will pose a far greater clinical challenge than individuals in any of the other classes.

Clearly, in the same manner that obesity is not a homogeneous disorder, weight control behaviours come in different flavours - something that should perhaps never be forgotten in counseling.

AMS
New York, New York

p.s. Join my new Facebook page for more posts and links on obesity prevention and management

Lanza ST, Savage JS, & Birch LL (2010). Identification and prediction of latent classes of weight-loss strategies among women. Obesity (Silver Spring, Md.), 18 (4), 833-40 PMID: 19696754

Readers of these pages will be quite familiar with my previous posts on food addiction.

A new paper by Paul Johnson and Paul Kenny from the Scripps Research Institute, Jupiter, FL, just released online in Nature Neuroscience, demonstrates that in rats development of obesity is coupled with a progressively worsening deficit in neural reward responses (as seen in cocaine or heroin abuse).

In drug users, this decreased neural reward response is considered crucial in triggering the transition from casual to compulsive drug-taking.

In their experiments, the researchers found compulsive-like feeding behavior in obese but not lean rats, and showed that this compulsive overeating was even resistant to disruption by an aversive conditioned stimulus.

The researchers also found down regulation of dopamine D2 receptors in the striatum (an area of the brain involved in reward behaviours) in a manner similar to what has been reported in humans addicted to drugs.

Genetic knockdown of striatal D2 receptors also rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with access to palatable high-fat food.

Together these data clearly demonstrate that overconsumption of highly palatable foods can trigger addiction-like neuroadaptive responses in brain reward circuits that can drive the development of compulsive overeating.

As I noted in several media interviews on this article yesterday,

“while not all forms of obesity can be reduced to food addiction, anyone dealing with obesity needs to be aware of the possibility that they may be addicted to certain foods and must therefore approach their obesity in the same manner as they would approach any other addiction. Unfortunately, in contrast to substance abuse, food abstinence is not an option“.

I can certainly now see why diet plans for treating food addiction are about as successful as drinking plans are for managing alcoholism.

AMS
Edmonton, Alberta

I have previously noted that the real problem with fast food is not so much the ‘food’ but rather the ‘fast’ - i.e. the fact, that it is designed to be eaten quickly.

I also, earlier this year, blogged about novel approaches like the MandoMeter or the SMART device to help people slow down their eating to better control their weights.

it turns out that the speed of eating may in fact be one of the earliest predictors of obesity, even in 4-year old kids.

Thus, in a study by Robert Berkowitz and colleagues from the University of Pennsylvania, published in the latest issue of OBESITY, rapid eating (higher number of mouthfuls per minute) of a single laboratory testmeal was a remarkably strong predictor of subsequent weight gain in kids.

At 4 years of age, 32 children of overweight mothers and 29 children of normal weight mothers were given a test meal in a controlled laboratory setting. Mouthfuls of food per min at this single meal not only predicted changes in BMI from 4 to 6 years but also changes in sum of skinfolds and total body fat.

As the authors note, rapid eating could well be an innate (genetic?) trait related to food reward and it will be interesting to see if slow eating can be taught and if this would reduce the risk for weight gain. Of course you can always trick your 4-year old into eating slow by providing slow foods that take longer to eat. 

In the meantime, if your 4-year old prefers to play with her food and takes forever to finish, you can at least comfort yourself with the notion that she is probably not in danger of having to worry about excess weight any time soon.

AMS
Toronto, Ontario

Last week, an article in the New York Times with the title “The Obesity-Hunger Paradox“, addressed the issue of food insecurity - or how, not knowing when or where your next meal will come from, can make you overeat - thus promoting obesity.

Interestingly, this month’s issue of OBESITY uses an animal model to illustrate a similar point.

In this study by Xingshenk Li and colleagues from the University of Alabama, one set of mice was first allowed free access to food for six weeks and was then mildly calorie restricted (5%) over three more weeks during which the animals were provided access to food only once a day. In a second experiment mice were either mildly calorie restricted or had free access to food.

Interestingly, one of the big changes in feeding behaviours with calorie restriction was overeating, where the mice ate almost four times the amount of food in a two hour period, than when they had free access to food.

Importantly, despite the overall calorie restriction, the researchers found no change in body weights - rather, the calorie-restricted mice appeared to become fatter, exchanging fat for lean tissue. They also showed a significant reduction in energy expenditure.

The researchers interpret their evidence as supporting the notion that the gorging behaviour in response to food “uncertainity” alters energy partitioning resulting in more effective triglyceride production and fat storage. This altered metabolism may in part be due to the hormonal changes resulting from the “stress” of calorie restriction.

Clearly, these findings should be of interest to those of us who wonder about the long-term effects of caloric restriction, meal skipping, and binge eating.

The study may also explain why chronic (especially intermittent) dieting can be counterproductive and in some individuals paradoxically increase fat stores.

Certainly the study should remind us that any restriction of food intake (whether voluntary or involuntary) can profoundly change our “feeding” behaviour and change the way our bodies handle calories.

The next time you wonder why you or your patients are not losing weight despite restricting calories, remember that there is apparently no end to the tricks our body will come up with to protect its weight.

AMS
Edmonton, Alberta