Hanger Games: The Neurobiology of Food Addiction

Food Addiction as a Major Cause of Obesity

Obesity ranks among the top three causes of preventable illness and death in the United States and, as elsewhere, its prevalence has risen dramatically since the 1980s. More than one-third of American adults currently meet the criteria for obesity. This alarming growth prompted the American Medical Association (AMA) to classify obesity as a disease: a disease that poses a greater risk to your health than smoking cigarettes.

Reasons for the rise are not entirely known and remain keenly debated. Given, however, the overwhelming individual and societal costs associated with it, new models for understanding and treating obesity need to be explored. One such new model (“Food Addiction”) incorporates the view that certain foods, particularly those high in processed sugars and fats, are habit-forming. It follows, then, that some forms of obesity can be effectively treated as a food addiction.

Historically, obesity has been viewed from a purely metabolic perspective, with an emphasis on energy balance. More recently and temporally coinciding with the obesity epidemic, a motivating factor for eating has shifted from sustenance and energy (“eat to live”) to pleasure and hedonism (“live to eat”). More than that, however, certain “comfort” foods have become indispensable to many of us for dealing with uncomfortable and painful emotions, such as anger, fear, sadness, disappointment, and even boredom (“emotional eating”).  When considered thusly, it is easy to see how food could become addicting in vulnerable individuals: we need it to live, it can powerfully provide pleasure and reward, and it can equally powerfully soothe painful emotions. Who among us, for example, is unfamiliar with the “HANGER”– hunger induced anger – phenomenon?

The food addiction framework is supported by a growing body of scientific research demonstrating that the repeated consumption of calorie-rich, energy-dense foods causes changes in the brain’s reward and pleasure circuits that are central to the development and maintenance of both food and drug addictions. For example, many common foods have been compared to such frequently abused substances as alcohol, nicotine, opioids, cocaine, methamphetamine, and marijuana.

Brain Responses to Palatable Foods are Similar to Brain Responses to Common Drugs of Abuse

Drugs of abuse and palatable foods show similarities in terms of how they engage the reward circuitry in animals and humans in several ways:

1. Addictive drugs activate reward regions and learning centers in the brain through dopamine signaling; palatable foods (those high in refined sugars and fats) activate those same pathways.
2. Individuals escalate drug usage to levels of tolerance due to structural alterations in the dopamine system (for example, decreased sensitivity of D2 receptors and increased sensitivity of D1 receptors); repeated intake of palatable foods creates similar changes in brain receptors.
3. Cravings, when trying to quit drug abuse, lead to relapse because of rebound hypersensitivity of reward and attention circuits in response to everyday drug cues; obese and overweight persons demonstrate similar patterns of exaggerated activation when exposed to palatable food cues.
4. Overweight and obese persons display patterns of eating behavior that closely resemble patterns of behavior observed in individuals addicted to drugs.

TAAR1 – Trace Amine-Associated Receptor 1

As mentioned above, converging lines of evidence indicate that compulsive, binge-eating of highly palatable food (food addiction) constitutes a core feature of many forms of obesity. Furthermore, recent scientific research has identified a plausible mechanism underlying food addiction. Enter a newly discovered receptor found in key brain regions – trace amine-associated receptor –  TAAR1.  Since its discovery in 2001, TAAR1 has been investigated as a target to treat numerous seemingly disparate medical conditions, including:

• ADHD
• Schizophrenia
• Bipolar disorder
• Food addictions
• Drug abuse
• Obesity
• Diabetes

TAAR1 promises to be so versatile because it appears to function as a natural dimmer switch maintaining central neurotransmitter activity, especially dopamine activity, within normal physiological parameters. More specifically, TAAR1 powerfully regulates dopamine activity in brain regions associated with drug and food addictions. Activation of TAAR1 has been shown to reduce binging on highly palatable, sugary foods, inhibit junk food associated cues, and block compulsive eating by preventing the exuberant dopamine release in key brain reward centers seen with drugs of abuse and with highly palatable foods.

Based on the strength of such data, researchers and pharmaceutical concerns are furiously working on medications that can safely activate TAAR1.

Fortunately, we need not wait for that utopian day to arrive.  It turns out that the most potent activator of TAAR1 is our own (human) natural trace amine – PEA (phenylethylamine).  Interestingly, many individuals who suffer from ADHD, addictions, and other common psychiatric maladies also suffer from low levels of PEA.

Therapeutic Implications

The mainstream medical approach – often necessary, seldom sufficient – to such a state is to mimic the effects of a brain chemical at its corresponding receptor (a TAAR1 agonist→TAAR1 receptor).

Another approach, usually safer and more sustainable, is to build more of the brain chemical in question (PEA in this case) through lifestyle, diet, exercise, targeted amino acid therapy, or to provide it directly via a supplement, or both. As several of my blogs indicate, I’ve become a big fan of supplementing, where appropriate, with PEA-based nutraceuticals, such as Cogniben and DopaMaxx ES.

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