Junk Foods Trigger Food Addiction in Obesity?

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

Is Obesity an Addiction?

Regular readers of these pages are well aware of the close link between addictions and some forms of overeating. This topic is now nicely addressed in a commentary by Valerie Taylor (McMaster, Hamilton), Claire Curtis and Caroline Davis (both York University, in this week’s edition of CMAJ. As they discuss, “The concept of food addiction, which more accurately may reflect addiction to specific components of food, can be described in much the same way as other addictive behaviours. Both food and drugs induce tolerance over time, whereby increasing amounts are needed to reach and maintain intoxication or satiety. In addition, withdrawal symptoms, such as distress and dysphoria, often occur upon discontinuation of the drug or during dieting. There is also a high incidence of relapse with both types of behaviour.“ To further support their arguments, they cite the many imaging studies showing that specific areas of the reward or mesolimbic system, such as the caudate nucleus, the hippocampus and the insula, are activated both by drugs and by food. Thus, the easy accessibility of highly palatable foods together with our innate preferences for such foods, can increase the likelihood that vulnerable people will “misuse” food, in much the same way that addicts misuse other drugs to blunt negative emotional states, such as depression, anxiety, loneliness, boredom, anger orinterpersonal conflict. While the concept of addiction should not negate the role of free will and personal choice, it does provide a rationale for the including addiction screens as a routine part of assessment for obesity. It may also help explain the success of lifestyle programs that incorporate pharmacotherapy or behavioural strategies specifically designed to address the addictive component of this illness. Thus, as pointed out by Taylor and colleagues, there is not only considerable overlap among the medications shown to interfere with food and drug abuse in animal models, but the many behavioural interventions developed for managing addictions (motivational interviewing, cognitive behavioural therapy and 12-step programs), are increasingly recognised as also being helpful in managing obesity. Health professionals and decision makers charged with tackling the obesity epidemic would do well to familiarise themselves with the science of addictions and utilize learnings from addiction management in their counseling of patients presenting with excess weight. AMS Edmonton, Alberta

Addiction Gene Linked to Common Obesity

Hedonic hyperphagia (overeating controlled by reward rather than need for calories) often underlies excess caloric intake. As the reward centres that regulate drug and other forms of addiction are the same that are stimulated by highly palatable foods, it is not surprising that genes associated with substance and other addictions may also be linked with obesity. This assumption finds new support in a study published this month in PLoS Genetics by Nancy Heard-Costa from Boston University School of Medicine on behalf of the CHARGE (Cohorts for Heart and Aging Research in Genome Epidemiology) consortium . The researchers performed genetic analyses on more than 30,000 subjects participating in 8 large cohort studies, including the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES- Reykjavik Study), the Atherosclerosis Risk in Communities Study (ARIC), the Cardiovascular Health Study (CHS), the European Special Population Network consortium (EUROSPAN), the Family Heart Study, the Framingham Heart Study, Old Order Amish (OOA), and the Rotterdam Study (RS). Genetic loci studied included those identified in previous studies as well as new candidate loci for abdominal fat deposition. In addition to confirming significant associations with the previously reported FTO and MC4R genes, the researchers found a novel locus in the NRXN3 gene associated with waist circumference, BMI and obesity. NRNX3 has previously been associated with addiction (alcohol dependence, cocaine addiction, and illegal substance abuse) and is part of a family of central nervous adhesion molecules, which are highly expressed in sub-cortical regions of the brain in involved with learning and reward training. Although the odds ratio for obesity per copy of the implicated G Allele was only 1.13, this small effect at a population level can be substantial. More importantly, this finding clearly supports the notion that some individuals may be more susceptible to obesity because of an increased genetic predisposition to reward-seeking behaviours, that obviously include seeking out highly-palatable (addictive) foods. Punitive approaches to drug addictions have not worked – neither will punitive approaches to obesity resulting from hedonic overeating. AMS Edmonton, Alberta

Food Cravings, Mood, and Nicotine Addiction

Smoking cessation is one of the most common risk factors for weight gain and there is little doubt that in some people food activates exactly the same hedonic pathways as does nicotine and other drugs – this is why for some people, food is very much an addiction. In fact, previous studies have shown that people who abstain from smoking, not only tend to give in to food cravings more often, but as cravings for cigarettes become more intensified, so do cravings for starchy carbohydrates and fats. These food are also well know to improve dysphoric moods (anxiety, depression, and irritability) that typically accompany nicotine withdrawal. A new study published this month in OBESITY further illustrates these striking similiarities in food cravings and mood states between obese women and women who smoke tobacco. In this study, Yanina Pepino and colleagues form the Monell Chemical Senses Center, Philadelphia, PA, USA, assessed food cravings in 229 women who differed in smoking history (i.e., never smoker, former smoker, and current smoker) and body weight (i.e., normal weight, overweight, and obese). Each subject completed the Food Craving Inventory (FCI), which measures cravings for sweets, high fats, carbohydrates/starches, and fast-food fats, and the Profile of Mood States (POMS), which measures psychological distress. Both smoking and obesity were found to be independently associated with specific food cravings and mood states (particularly depression and anger). Current smokers clearly craved high fats more frequently than former and never smokers. They also craved starches more frequently and felt more depressed and angry than never smokers, but not former smokers. From these findings the authors conclude that while cravings for starchy foods and poor mood may be characteristic of women who are likely to smoke, more frequent cravings for fat among smokers is related to smoking per se. Similarly, obese women craved high fats more frequently than nonobese women and depression symptoms were intensified with increasing body weights. The overlapping neuroendocrine alterations associated with obesity and smoking and the remarkable similarities in food cravings and mood states between women who smoke and women who are obese suggest that common biological mechanisms modulate cravings for fat in these women. Unfortunately, while smoking can be addressed by “smoking cessation” programs it is highly unlikely that we will be able to address the obesity epidemic with “eating cessation” programs. Nevertheless, the recognition that smoking and food cravings interact with mood and involve the same… Read More »

Does High-Glycemic Index Promote Food Addiction?

Yesterday, I was widely quoted in national media on the issue of food addiction. The background for this was an interview done by CanWest’s Sharon Kirkey regarding a recent paper by Simon Thronley and colleagues from Auckland, New Zealand, published in Medical Hypothesis. The basic tenor of their article is that food consumption shows many similarities to features of other addictive behaviours, such as automaticity and loss of control. They hypothesize that Glycemic Index (GI) is perhaps the key element of food that predicts its addictive potential. They quote reports of a withdrawal syndrome from high glycemic food abstinence and argue that both empirical and clinical studies support an addictive component of eating behaviour, with similar neurotransmitters and neural pathways triggered by food consumption, as with addictive drugs. Specifically, they argue that the short time to peak arterial concentration of glucose (similar to the short time to peak concentrations of nicotine in smokers) associated with high GI-foods, essentially ‘spikes’ the addictive potential of palatable foods – thereby making them more addictive than low-GI foods. The authors suggest that subtle changes in the preparation and manufacturing of commonly consumed food items and/or reducing glycemic index through regulatory channels, may help break a cycle of [food-] addiction and draw large public health benefits. While I much like their concept, and certainly buy into the fact that some folks demonstrate features akin to food addiction, this is certainly not a universal thruth that applies to all people with excess weight – in fact, I know a couple of normal weight people, who probably have “sweet addiction” as well. Nevertheless, I do think that this paper should once again remind us of the important mental health component to ingestive behaviour and certainly explains why for some people kicking doughnuts and chocolate is apparently as hard as kicking alochol or cocaine. AMS Edmonton, Alberta.