Tuesday, September 16, 2014

Is Food Addiction Better Described As Eating Addiction?

sharma-obesity-addiction-typesThe term “food addiction” has found its way into both the scientific and popular literature.

Now, a thoughtful paper by Johannes Hebebrand and colleagues, published in Neuroscience & Biobehavioral Reviews, argues that there is in fact little evidence for addiction to “food” per se (as you would see in addiction to a specific substance) and that therefore, it may be better to describe the addiction-like overconsumption of food as a behavioural addiction, in this case, an addiction to eating.

Eating is intrinsically rewarding and reinforcing, and food consumption is well-known to activate the reward system in the brain; this applies particularly in the physiological state of hunger. It is easy to see that the rewarding properties of food and their activation of the reward pathway might lead intuitively to the idea that food substances may have addictive properties. However, just because eating behavior engages these reward systems, it does not necessarily follow that specific nutrients (substances) are able to evoke a substance addiction. Instead, the complex activation of the reward system as the initial step of the process ending in addiction can be viewed as being dependent on eating (subjectively) palatable foods irrespective of their nutritional/chemical composition.”

Per se, foods are nutritionally complex and there is hardly any evidence to suggest that under normal physiological circumstances humans crave specific foods in order to ingest a specific ‘substance’. Instead, the diet of subjects who overeat typically contains a broad range of different, subjectively palatable foods. It can be argued that access to a diversity of foods, especially a diverse range of palatable foods, may be a pre-requisite for the development of addictive-like eating behavior.”

There is currently no evidence that single nutritional substances can elicit a Substance Use Disorder in humans according to DSM 5 criteria. In light of the lack of clinical studies that have aimed to detect addictions to specific nutrients, it cannot as yet be ruled out that a predisposed subgroup does indeed develop such a substance based addiction, which in theory may be substantially weaker than in the case of addictions based on well-known exogenous substances such as alcohol, cannabis, nicotine or opiates. The fact, that clinical case studies do not abound on an addiction like intake of specific nutrients or even specific foods, would suggest that such cases are rare, if they exist at all. Alternatively, the addiction is so weak that it is not adequately perceived and reported as such. This leads to the question as to the boundaries between excessive consumption and the beginning of a true addiction.”

Thus,

“…there is very little evidence to indicate that humans can develop a “Glucose/Sucrose/Fructose Use Disorder” as a diagnosis within the DSM-5 category Substance Use Disorders. We do, however, view both rodent and human data as consistent with the existence of addictive eating behavior. The novel DSM-5 (APA, 2013) currently does not allow the classification of an “Overeating Disorder” or an “Addictive Eating Disorder” within the diagnostic category Substance-Related and Addictive Disorders; indeed, the current knowledge of addictive eating behaviors does not warrant such a diagnosis. However, efforts should be made to operationalize the diagnostic criteria for such a disorder and to test its reliability and validity. It needs to be determined if such a disorder can occur distinct from other mental disorders.”

Overall I believe that reframing the perceived loss of control over food intake often reported by my patients as a “behavioural” rather than a “substance” addiction may be helpful in approaching this rather complex topic and may well open the path to novel therapeutic approaches more consistent with our current understanding of behavioural addictions.

@DrSharma
Vienna, Austria

ResearchBlogging.orgHebebrand J, Albayrak O, Adan R, Antel J, Dieguez C, de Jong J, Leng G, Menzies J, Mercer JG, Murphy M, van der Plasse G, & Dickson SL (2014). “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior. Neuroscience and biobehavioral reviews PMID: 25205078

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Wednesday, September 3, 2014

Can Targeting Estrogen Receptors Alleviate Binge Eating Disorder?

sharma-obesity-mouse-eatingBinge eating disorder, a loss of control of food intake accompanied by dysphoric mood alterations, is more common in women than in men and may account for as much as 40% of severe obesity seen at bariatric centres.

Strangely enough, a new study by Xuehong Cao and colleagues from Baylor College of Medicine, Houston, Texas, published in the Journal of Clinical Investigation, shows that targeting estrogen receptors in the serotonergic neurons of brain centres involved in appetite regulation may alleviate this behaviour, at least in mice.

Previous observations in humans that women with binge eating often suffer from menstrual irregularity, presumably due to impaired functions of ovarian hormones (e.g. estrogens) and that circulating 17β-estradiol levels are inversely associated with binge eating, prompted these investigators to study the role of estrogen in binge eating behaviours in ovarectomised mice.

While estrogen administration resulted in markedly reduced binge eating behaviour in these mice, this effect was absent in genetically modified mice that lacked the estrogen receptor-α (ERα) in the dorsal raphe nuclei (DRN), an area particularly rich in serotonin (5-HT) neurons known to be important in appetite regulation (and sleep).

The researchers also showed that a conjugate that combines GLP-1 and estrogen into one molecule is far more effective in reducing binge eating behaviour than GLP-1 alone (again, this effect was much reduced in ERα KO mice) suggesting that such a conjugate may be used to specifically target GLP-1 receptor neurons, thereby perhaps avoiding any potential adverse effects of estrogen administration.

Obviously, there is a long way from such initial observations in mice to safe and effective treatments in humans.

Nevertheless, these observations should open a new field of interest in finding more effective pharmacological treatments for binge eating disorders or perhaps even more “common-garden-variety” obesity in humans.

@DrSharma
Gambach, Germany

ResearchBlogging.orgCao X, Xu P, Oyola MG, Xia Y, Yan X, Saito K, Zou F, Wang C, Yang Y, Hinton A Jr, Yan C, Ding H, Zhu L, Yu L, Yang B, Feng Y, Clegg DJ, Khan S, DiMarchi R, Mani SK, Tong Q, & Xu Y (2014). Estrogens stimulate serotonin neurons to inhibit binge-like eating in mice. The Journal of clinical investigation PMID: 25157819

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Monday, September 1, 2014

Guest Post: Emotional Distress And Weight Gain

Erik Hemmiingsson, PhD, Obesity Research Centre, Karolinska Institute, Stockholm, Sweden

Erik Hemmiingsson, PhD, Obesity Research Centre, Karolinska Institute, Stockholm, Sweden

Today’s guest post comes from Erik Hemmingsson, PhD,  a Group Leader at the Obesity Center, Department of Medicine, Karolinska Institute, Stockholm, Sweden. His group studies the role of psychological and emotional distress in weight gain and obesity by mapping life events that influence stress, metabolism and body weight. Erik has a PhD in Exercise and Health Sciences from the University of Bristol (2004) and a PhD in Medicine from Karolinska Institutet.

I work as a researcher in a specialized obesity treatment center at a university hospital in Sweden. My job is to develop new and more effective treatment and prevention methods so that we can hopefully confine obesity to the history books some day.

For many years I mostly did studies on behaviour therapy combined with low energy diets. Since this did not result in any major breakthroughs, I decided to try something a little different.

I had been aware of that many of our patients had experienced difficult childhoods. There were so many sad stories, but I didn’t fancy doing any research on the topic, it was too painful. But then my attitude gradually started to change about a year ago. It was clear that our current treatment methods were woefully ineffective, but I also became more receptive to all those troublesome stories from the patients. Enough was enough, it was time act. So, like Neo in the Matrix movies, I decided to take the red pill, and delve deeper into the very uncomfortable subject of childhood abuse and adult obesity.

I searched the literature and quickly saw that there were more than enough studies for a systematic review and meta-analysis. I enlisted the help of Dr Kari Johansson and Dr Signy Reynisdottir, and got to work.

What we found very much confirmed all those clinical observations, i.e. there was a very robust association between childhood abuse and adult obesity. The association was also very consistent across difference types of abuse, with an increased risk of about 30-40%. There was also a dose-response association, i.e. the more abuse, the greater the risk of obesity.

While this study confirmed something very important, it was also clear that not everyone who suffers childhood abuse develops obesity, or that all obese individuals have suffered childhood abuse, or the effects would have been even more pronounced. But for me, the study proved that stressful childhood experiences can easily manifest as obesity many years later. This led me even deeper down the rabbit hole. I wanted to know why.

I decided to try and piece together different ideas about how obesity develops in relation to stressful life events. This resulted in a new conceptual causal model consisting of six different developmental stages. Like many diseases, obesity development is more likely when there is socioeconomic disadvantage (applies mainly to Europe and North America). Socioeconomic disadvantage can very easily trigger a chain of events that include adult distress, a disharmonious family environment, offspring distress, psychological and emotional overload, and finally disruption of homeostasis through such mechanisms as maladaptive coping responses, stress, mental health problems, reduced metabolism, appetite up-regulation and inflammation.

Much more research is needed to validate the model, but if there is some truth to this theory, which the childhood abuse meta-analysis clearly suggests that there is, then my hope is that we can use this information to develop more effective treatment and prevention methods.

My other hope is that some of the truly horrendous stigma, shame and discrimination that the obese experience can gradually be alleviated, since there is clearly a lot more to obesity etiology than the commonly held preconception that obese individuals are merely lazy and overindulgent.

After having done all this work on obesity etiology, I would say that my top-3 reasons we have an obesity epidemic (in no particular order) are socioeconomic inequality, the junk food invasion, and psychological and emotional distress patterns (usually established at an early age). And when you combine all three you have the perfect storm for weight gain.

You can find more information at my blog at www.holisticobesity.com

Erik Hemmingsson,
Stockholm, Sweden

References:

Hemmingsson E, Johansson K, Reynisdottir S. Effects of childhood abuse on adult obesity: a systematic review and meta-analysis. Obesity Reviews (epub 15 August 2014).

Hemmingsson E. A new model of the role of psychological and emotional distress in promoting obesity: conceptual review with implications for treatment and prevention. Obesity Reviews 2014, 15:769-779.

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Thursday, August 28, 2014

Call For Abstracts: Canadian Obesity Summit, Toronto, April 28-May 2, 2015

COS2015 toronto callBuilding on the resounding success of Kananaskis, Montreal and Vancouver, the biennial Canadian Obesity Summit is now setting its sights on Toronto.

If you have a professional interest in obesity, it’s your #1 destination for learning, sharing and networking with experts from across Canada around the world.

In 2015, the Canadian Obesity Network (CON-RCO) and the Canadian Association of Bariatric Physicians and Surgeons (CABPS) are combining resources to hold their scientific meetings under one roof.

The 4th Canadian Obesity Summit (#COS2015) will provide the latest information on obesity research, prevention and management to scientists, health care practitioners, policy makers, partner organizations and industry stakeholders working to reduce the social, mental and physical burden of obesity on Canadians.

The COS 2015 program will include plenary presentations, original scientific oral and poster presentations, interactive workshops and a large exhibit hall. Most importantly, COS 2015 will provide ample opportunity for networking and knowledge exchange for anyone with a professional interest in this field.

Abstract submission is now open – click here

Key Dates

  • Abstract submission deadline: October 23, 2014
  • Notification of abstract review: January 8, 2014
  • Early registration deadline: March 5, 2015

For exhibitor and sponsorship information – click here

To join the Canadian Obesity Network – click here

I look forward to seeing you in Toronto next year!

@DrSharma
Montreal, QC

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Tuesday, August 26, 2014

Does Facebook Use Promote Eating Disorders?

facebook_button_eu3gSocial media are not just a means of sharing your life with the world – they also open your life to praise (likes and positive comments) or criticism.

Thus, it is easy to see how avid use of such platforms (especially those with ample picture posts) can potentially promote body image and weight obsessions in those who may not be quite confident and happy about their appearance.

That this may not just be an interesting theory is suggested by two studies by Annalise Mabe and colleagues from Florida State University, published in the International Journal of Eating Disorders.

In the first study 960 female college students completed an Eating Attitudes Test that included Dieting and Bulimia/Food Preoccupation subscales with items such as “I eat diet foods” and “I give too much time and thought to food.”

Duration of Facebook use was assessed with the question “How much time do you spend on Facebook per week?” with options ranging from 0 to >7 hours (average used tended to be just over 2 hours per week).

This study found a small but statistically significant positive relationship between the duration of Facebook use and disordered eating.

In the second study, 84 women, who had participated in the first study and endorsed Facebook use on a weekly basis were randomization to either spending 20 mins on their facebook account or finding information about the ocelot on Wikipedia and YouTube.

Participants with greater disordered eating scores endorsed greater importance of receiving comments on their status, and greater importance of receiving “likes” on their status. Those with greater eating pathology reported untagging photos of themselves more often and endorsed comparing their photos to their female friends’ photos more often.

Participants in the control group demonstrated a greater decline in weight/shape preoccupation than did participants who spent 20 min on Facebook. Furthermore post hoc comparisons supported a significant decrease in weight/shape preoccupation in controls.

Facebook use resulted in a preoccupation with weight and shape compared to an internet control condition despite several multivariate adjustments.

As the authors discuss, their finding,

“indicates that typical Facebook use may contribute to maintenance of weight/shape concerns and state anxiety, both of which are established eating disorder risk factors.”

In terms of practical implications of these findings, the authors suggest that,

“Facebook could be targeted as a maintenance factor in prevention programs. For example, interventions could address the implications of appearance-focused comments such as “you look so thin” or “I wish I had your abs,” in perpetuating the thin ideal on Facebook, much as “fat talk” perpetuates this ideal in everyday conversations. An adaption of the “Fat Talk Free” campaign as well as adaptations of media literacy programs could encourage girls and women in the responsible use of social media sites.”

Clearly, this appears to me as a rather fertile area for further research.

I’d certainly be interested in hearing about your experience with facebook and any effects it may have had on your body image or eating behaviours.

@DrSharma
Edmonton, AB

ResearchBlogging.orgMabe AG, Forney KJ, & Keel PK (2014). Do you “like” my photo? Facebook use maintains eating disorder risk. The International journal of eating disorders, 47 (5), 516-23 PMID: 25035882

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In The News

Diabetics in most need of bariatric surgery, university study finds

Oct. 18, 2013 – Ottawa Citizen: "Encouraging more men to consider bariatric surgery is also important, since it's the best treatment and can stop diabetic patients from needing insulin, said Dr. Arya Sharma, chair in obesity research and management at the University of Alberta." Read article

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