Does food addiction play a role in obesity?

Posted: June 23, 2012 in Policy, Science

Does food addiction exist? Does food addiction relate to obesity? Does drug addiction and food addiction share common traits and thus potentially share common medications? These and others are the questions discussed in a recent perspective titled Obesity and the brain: how convincing is the addiction model?, published in the journal Nature Reviews Neuroscience. 

Dr. Hisham Ziauddeen, lead author of the article and member of Dr. Paul Fletcher’s research team at University of Cambridge, UK, examines the evidence for a link between obesity and food addiction and determines that there is insufficient evidence and shortcomings of the model. As obesity has become a national pandemic, the authors argue that there needs to be increased scrutiny and evaluation prior to researchers making any major clinical or policy related recommendations.

The World Health Organization reports that “Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health…Overweight and obesity are major risk factors for a number of chronic diseases, including diabetes, cardiovascular diseases and cancer.” As of 2008, 200 million men and nearly 300 million women were obese, and in 2010, over 40 million children under the age of five were overweight in 2010. The WHO attributes obesity to an energy imbalance (calories consumed vs. those expended), with an increase in high fat, salt, sugar, processed foods and a decrease in physical activity. Common health problems include cardiovascular diseases, diabetes, musculoskeletal disorders, and some cancers. The cost of obesity in the US is now in the hundreds of billions of dollars a year, mainly due to medical bills, decreased productivity, and disability, and accordingly there is a big push by health officials policy makers for novel ways to address this issue.

The authors write, “In this Perspective article, we describe how the addiction model has been applied to obesity and overeating and critically review each of the five main lines of research that are usually invoked to support this conflation.” The authors first describe opposing views regarding obesity and addiction. The first idea is that foods high in fat, salt, and sugar are similar to addictive substances in that they activate similar pathways within the brain. Thus, food addiction is possible because these addictive type foods “hijack” the brain’s natural reward system in a way similar to drugs of abuse such as alcohol or cocaine. The second idea is that food addiction is a trait seen in a subset or group of obese individuals (such as binge eaters) and instead of being that same as drug addiction just mimics some of the characteristics. The authors then go on to address the five key pieces of evidence in the scientific literature in support of the addiction hypothesis, “first, a clinical overlap between obesity (or, more specifically, BED) and drug addiction; second, evidence of shared vulnerability to both obesity and substance addiction; third, evidence of tolerance, withdrawal and compulsive food-seeking in animal models of overexposure to high-sugar and/or high-fat diets; fourth, evidence of lower levels of striatal dopamine receptors (similar to findings in patients with drug addiction) in obese humans; and fifth, evidence of altered brain responses to food-related stimuli in obese individuals compared with non-obese controls in functional imaging studies. Below, we consider each of these in turn.”

Dealing with hypothesis one, the authors determine that because only some of the clinical traits seen in obesity and drug addiction overlap, there is insufficient evidence for the claim. Dealing with hypothesis two, the authors state, “It is possible, therefore, that there are some shared vulnerabilities between drug addiction and obesity. However, this does not in itself strongly support an argument that the same processes occur in each condition.” The authors seem to dismiss hypothesis three, for which there is considerable evidence, because “the degree to which models of food addiction in animals may extend to human obesity has yet to be explored.”  Likewise, the authors seem to dismiss the fourth and fifth hypotheses because of the complex nature of data from PET and neuroimaging studies, the lack of findings to be replicated, and discrepancies in the literature. “We clearly need more precise behavioural, temporal, metabolic, genetic and cognitive profiling in such investigations.”

The authors conclude that because of the lack of concrete or consistent evidence supporting a link between food addiction and obesity, the level of acceptance of this model is unwarranted. They worry that continued acceptance “will lead to research that is too narrowly focused and, ultimately, misleading…an associated danger that clinical and policy recommendations will be misguided.”

In the current issue of Nature Reviews Neuroscience, a correspondence in response to Ziauddeen et al.’s perpective titled, Tossing the baby out with the bathwater after a brief rinse? The potential downside of dismissing food addiction based on limited data, was published. In the correspondance the authors argue that further research addressing obesity and food addiction is needed before dismissing the model completely. They explain that while not all obese people may be addicted, food addiction may exist in a subset of obese people, and thus if research is halted, this subpopulation may lose out on new prevention and treatment strategies. The authors state, “Obesity is a heterogeneous entity. A failure to recognize and investigate individual differences could hamper the development of improved treatments and policies. Although Ziauddeen et al. note inconsistencies in addiction-related neurobiological findings in obesity, particularly those related to functional MRI, such findings may reflect the heterogeneity of obesity, as the authors indicate.”

To a point I agree with both groups. As with much of neuroscience research, research findings are difficult to replicate and often contradict one another, so a level of caution is required prior to interpretation. Additionally, because of the extremely intricate and complicated nature of the brain, a large amount of reasearch is required prior to interpretation, and thus patience is needed prior to completely dismissing a hypothesis. Too often in scientific endeavors do research groups adopt a ‘I’m right so you must be wrong’ approach to their analysis of the literature and new research findings. I currently study how kappa opioid receptors play a role in stress, mood, and drug addiction, and my research supports a role for serotonin. Dopamine has always been thought of as the major player in the role of kappa in these behaviors, and I have repeatedly heard that its all dopamine, even when there is an increasing amount of data supporting a role for serotonin. People within the field are basically saying ‘my research says it must be dopamine, therefore your research saying serotonin is important must be wrong.’ The reality is that probably both serotonin and dopamine play a role in these complex behaviors. Likewise, obesity is extremely complex, and it is most likely that food addiction plays a role in at least a subset of obese people. The sooner researchers can accept that the brain is more complicated than the one small molecule they study and that the world is more complicated than being able to group all people with a similar disease or illness together, the better scientific research, and thus the human population, will be.

In the correspondence the authors state, “If found to be applicable to a considerable population with obesity, a food-addiction model may not only help clarify findings in obesity but, importantly, could also lead to new interventions for preventing and treating obesity, facilitated by decades of research in substance addiction. If we are to prematurely dismiss such a potentially important model on the basis of limited studies, we could miss important opportunities to improve health worldwide.”


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