If obesity is a disease, is labelling it that way the cure?

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When the American Medical Association formally recognised obesity as a disease in June 2013, plenty of public health officials were thrilled for the increases in research, treatment, and prevention funding that would presumably arise as a result. But were people right to herald the labelling of obesity as a “disease” as something positive for public health? Or could this label have unintended negative consequences that could actually backfire?

Psychologists Crystal Hoyt, Jeni Burnette, and Lisa Auster-Gussman of the University of Richmond and the University of Minnesota were concerned that labelling obesity as a “disease,” a tactic that reduces perceptions of controllability, might have the unintended side effect of demotivating behaviours with the intended goal of losing weight. To examine whether or not this concern held any water, they conducted a series of studies that would determine if exposure to “obesity-is-a-disease” public-health messages negatively impacted nutritional choices. Participants in the experimental group always read a New York Times article detailing the AMA’s recent decision to categorise obesity as a disease, noting the benefits and drawbacks of this reclassification. Control group participants either read a message on “standard tips and tools” for managing weight loss or a message comprised from two pieces about how obesity should not be considered a disease.

After being exposed to these messages about obesity, the subjects were then shown a menu of possible sandwich options, and told to order one of the options from the list: The Italian (980 calories), Smoked Turkey Breast (360 calories), Roast Beef and Cheddar (700 calories), BLT (634 calories) or Vegetable Delight (230 calories).

The good news is that the AMA is right to celebrate the benefits that it has already touted; labelling obesity as a disease, in the experimental group, did lead obese participants to report higher levels of self-esteem and body satisfaction.

The bad news, however, is that this decision might have serious consequences for the public health goal of actually reducing the obesity rate. In both studies, obese participants opted for sandwiches with significantly more calories when they received the “obesity-is-a-disease” message than when they received either the standard information-based message or the “obesity-isn’t-a-disease” message.

Unfortunately, it is the very thing that makes the “disease” message desirable that also makes it a curse. Yes, treating obesity like a disease can help reduce stigma, increase body satisfaction, and aid self-esteem. Yet it is precisely these things that can undermine actual goal pursuit – in both studies, lower levels of weight-related concern and higher levels of body satisfaction actually predicted higher calorie preferences in obese participants (though the messages had no effect on the lunch preferences for the average weight individuals).

Intuitively, this makes sense. If you’re satisfied with yourself, what motivation is there to pursue any goals that involve personal change? This fits into a long history of literature on goal pursuit, which states that emotions and perceived discrepancies between “actual” and “ideal” or “ought” selves are the driving forces underlying motivation and goal pursuit. It’s not particularly hard to see why the labelling of obesity as a “disease,” which decreases perceptions of controllability or stigma, would increase obese individuals’ levels of body satisfaction – and it’s not particularly surprising to see why that could manifest in poorer nutritional choices.

However, as the authors note in their conclusions, it is critically important that research does not stop here. Body acceptance is an important societal movement, and the “thin ideal” has important and meaningful negative consequences as well. It would similarly be dangerous to suggest that we should ignore the importance of reducing stigma and increasing self-esteem, especially given (a) prior research showing that stigma reduction can actually help with goal engagement and (b) our societal focus on reducing bullying. After all, it is important not to be cruel.

Yet if the ultimate goal is actually to aid in public health efforts by incentivising good nutrition, we may not get there by comparing obesity to cancer.

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SOURCE:

BPS Research Digest by guest host Melanie Tannenbaum [https://twitter.com/melanietbaum], UIUC Social Psych PhD Candidate and Scientific American Blogger [http://blogs.scientificamerican.com/psysociety/].(8.6.14)

Hoyt CL, Burnette JL, & Auster-Gussman L (2014). "Obesity is a disease": examining the self-regulatory impact of this public-health message. Psychological science, 25 (4), 997-1002 PMID: 24463553

Fat-boosting gene mystery 'solved'

By James GallagherHealth and science reporter, BBC News

Why some people find fatty foods irresistible could be hidden in their genes.

The mystery of a genetic flaw which greatly increases the risk of obesity in one in six people has been solved by an international group of scientists.

A version of an obesity gene, called FTO, had been linked to a bigger belly, but the reason why was uncertain.

A study, published in The Journal of Clinical Investigation, showed it made fatty foods more tempting and altered levels of the hunger hormone, ghrelin.

Obesity experts said drugs targeting ghrelin might reduce weight gain.

There is a strong family link with obesity, and a person's genetic code is thought to play a major role in the risk of them becoming overweight.

People have two copies of the FTO gene - one from each parent - and each copy comes in a high and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be70% more likely to become obese than those with low-risk genes.

But no-one knew why.

Hormonal

A team, led by researchers at University College London, tested two groups of men. All were a normal weight, but one group had the high-risk FTO genes and the other was low risk.

The first tests looked at levels of the hormone ghrelin either side of a meal in 10 men from each group.

Levels of the hormone, which makes people hungry, did not fall as far in the high-risk patients after the meal. Their ghrelin levels also began to climb more quickly.

In separate tests, a series of brain scans after a meal showed further differences between the two groups. Men with the high-risk genes found pictures of high-fat foods more appealing than the low-risk men.

Dr Rachel Batterham, the head of the centre for obesity research at University College London, told the BBC News website: "Their brain is set up to be particularly interested in anything to do with high-calorie food."

She said they were "biologically programmed to eat more".

Help?

Dr Batterham said understanding how FTO affected the odds of becoming overweight would help patients.

She said exercise such as cycling was an excellent way to lower ghrelin levels and there was a significant amount of research from pharmaceutical companies working on the hormone.

She added: "Also protein meals do lower ghrelin more, so anything that suppresses ghrelin is more likely to be effective in FTO patients."

The FTO mutations were probably life-saving at one point in human history when piling on the pounds in the summer would help people survive the winter.

Commenting on the findings, Prof Steve Bloom, from Imperial College London, said: "We know the tendency to overeat in a society with too much food and no need for exercise is inherited.

"Slowly we are discovering the factors which make us overweight and this study, encompassing not only demonstration of a higher level of hunger hormone, ghrelin, but also changes in the brain associated with ghrelin's action, is an important step forward."

The study was funded by the Rosetrees Trust and the Medical Research Council.

SOURCE:

BBC NEWS:http://www.bbc.co.uk/news/health-23312712 (accessed 16/07/13)