Obesity is not only a rising national pandemic, but a global epidemic. According the WHO, children weigh more now than they have ever in the past and more than half of adults are classified as overweight. So, the fundamental question becomes: Can food be classified as an addiction? Research confirms that highly processed and palatable foods, which are essentially unavoidable in present society, are candidates for addictive substances (Frascella et al., 2010). I wanted to examine the similarities between food and drug addictions, which have directed researchers to a possible neurobiological treatment to addiction.

When applying the Koob et al.’s (2009) definition of substance addiction to food, food addiction is a chronically, relapsing disorder characterized by (1) compulsion to seek and ingest the food item, (2) loss of control in eating, a.k.a. binging on food (3) emergence of a negative state (dysphoria, anxiety, irritability) when access to food is prevented. Food addiction appears to be plausible under this definition. Koob et al. (2009) identify the ‘dark side of addiction’ as the decreased function of reward systems, leading to a continual recruitment of anti-reward neurocircuitry. In other words, the distinction between drug abuse and dependence is when the individual no longer takes the substance to get high, but to feel normal. Likewise, food fits into the ‘dark side of addiction’ all too easily because individuals that give into food cravings are not eating to reduce their hunger or maintain homeostasis. Like drugs, these individuals are complying with food, cue and context (perhaps they entered a dining hall or it is lunch time), or stress induced reinstatements (Stewart, 2008).

Increasing evidence from experimental research has revealed the similarities in neural mechanisms that underlie excessive intake of food, particularly sugar, and drug addiction (Frascella et al., 2009). First, both palatable foods and drugs activate dopamine signaling in mesolimbic system, thereby acting as potent reinforcers. Likewise, PET scans reveal similar reductions in striatal dopamine D2 receptors in pathologically obese and drug-addicted, specifically methamphetamine, individuals as compared to control subjects (Frascella et al., 200; Wang et al., 2004). This study correlated the lack of D2 receptor to Body Mass Index (BMI) and discovered that the fewer D2 receptors, the greater the BMI of obese participants.

Secondly, dependence on sugar is now linked to the withdrawal symptoms associated with physical dependence on a different drug of abuse. Avena et al. (2006) found evidence that rats with intermittent, excessive sugar intake showed endogenous opioid dependence. Rats were food deprived for 12 hours and provided excess sugar with their rat chow. The researchers induced withdrawal through deprivation of food or naloxone, an opiate antagonist. The experimenters measured withdrawal symptoms through observations, in vivo microdialysis, elevated plus maze test, and ultrasonic recordings. Their results revealed the similarities in naloxone and food deprivation withdrawal signs. The rats showed behavioral signs, such as teeth chattering, and neurochemical signs, like decreased extracellular dopamine and increased acetocholine in the nucleus accumbens, of opiate withdrawal. This study suggests that, in rats, the overconsumption of sugar results in signs and symptoms of a drug like dependence.

The endocannabinoid system is another region of interest due to its participation in the motivational properties of the reward system (Maldonado et al., 2006). Evidence of cannaboid’s involvement in addiction is provided through clinical trials on a cannabinoid antagonist, pharmaceutically known as rimonabant. This drug blocks the CB1 receptor, which reduces the drug seeking behavior. Tallett et al. (2010) tested the effects of low doses of rimonabant in male rats. The drug did not appear to alter behavioral profiles, such as grooming tended to reduce consumption and the amount of time spent eating. Therefore, the cannaboid CB1 receptor antagonist may combat addictions by suppressing cravings or appetite.

As a result of the current research on rimonabant, pharmaceutical companies are marketing the FDA approved drug as an appetite suppressant. Perhaps a new generation of compounds may be found in the endocannabinoid receptor system.
Just as Gladwell (2010) clarifies, “drinking must precede alcoholism… [but] drinking in not necessarily followed by alcoholism”, obesity is a result of food addiction; however, not all obese individuals are addicted to food. Overall, addiction a difficult pathology to define: Where exactly is the line between compulsion and addiction? Furthermore, food addiction is unique because food is a necessary substance for survival. A food addict cannot simply stop eating; In order to overcome the addiction, he or she must overcome the vicious cycle of withdrawal, or fasting, and binging. In the end, the knowledge gained on both side of the spectrum, drug addiction and non-substance compulsions, will provide beneficial insight to overcoming all types of addiction. Hopefully, the obesity epidemic is high on the list.

References:

In addition to the four articles from class,

Aveno, N.M., Rada P., Moise M., Hoebel B.G. (2006) Sucrose sham feeding on a binge schedule releases nucleus accumbens dopamine repeatedly and eliminates the acetylcholine satiety response. Journal of Neuroscience. 813-8120.

Maldonado, Rafael; Valverde, Olga & Fernando Berrendero (2006). Involvement of the endocannabinoid system in drug addiction. Trends in Neurosciences: 29(4), 225-232.

Tallett A.J., et al. (2010) Effects of acute low-dose combined treatment with rimonabant and sibutramin on appetite and weight gain in rats. Pharmacology Biochem Behavioral: 12 (10)

Wang, Gene-Jack; Volkow, Nora; Thanos, Panayotis & Joanna Fowler (2004). Similarity between obesity and Drug addiction by Neurofunctional Imaging. Journal of Addictive diseases: 23 (3), 39-53.