Addicted to palatable foods: comparing the neurobiology of Bulimia Nervosa to that of drug addiction

Abstract

Rationale: Bulimia Nervosa (BN) is highly comorbid with substance abuse and shares common phenotypic and genetic predispositions with drug addiction. Although treatments for the two disorders are similar, controversy remains about whether BN should be classified as addiction. Objectives: Here we review the animal and human literature with the goal of assessing whether BN and drug addiction share a common neurobiology. Results: Similar neurobiological features are present following administration of drugs and bingeing on palatable food, especially sugar. Specifically, both disorders involve increases in extracellular dopamine (DA), D1 binding, D3 mRNA, and ΔFosB in the nucleus accumbens (NAc). Animal models of BN reveal increases in ventral tegmental area (VTA) DA and enzymes involved in DA synthesis that resemble changes observed after exposure to addictive drugs. Additionally, alterations in the expression of glutamate receptors and prefrontal cortex activity present in human BN or following sugar bingeing in animals are comparable to the effects of addictive drugs. The two disorders differ in regards to alterations in NAc D2 binding, VTA DAT mRNA expression, and the efficacy of drugs targeting glutamate to treat these disorders. Conclusions: Although additional empirical studies are necessary, the synthesis of the two bodies of research presented here suggests that BN shares many neurobiological features with drug addiction. While few FDA-approved options currently exist for the treatment of drug addiction, pharmacotherapies developed in the future which target the glutamate, DA, and opioid systems may be beneficial for the treatment of both BN and drug addiction.

Food Addiction and Bulimia Nervosa

“…This finding is in line with the study by Speranza et al (2012) as it clearly demonstrates that eating behaviour in individuals with BN is highly comparable with substance use in SUDs and that bulimic behaviour may itself be described as an addicted behaviour. These findings based on selfreported behaviour are complemented by recent examinations of neurobiological processes that show similarities between BN and substance dependence as well (Hadad & Knackstedt, 2014).…”

“…Techniques such as motivational interviewing or acceptance-oriented imagery to cope with urges may be adapted from SUD treatments to enhance motivation to change and dealing with food cravings (Davis & Carter, 2014). Finally, pharmacotherapy targeting opioid and dopaminergic neurotransmitter systems have been shown to be effective in SUD treatments and may also be helpful in reducing binge eating (Davis & Carter, 2014;Hadad & Knackstedt, 2014). For example, a recent animal study showed that an aldehyde dehydrogenase inhibitor, which has been shown to reduce alcohol and cocaine intake in rats, selectively attenuated binge eating of palatable foods and dopamine release in sugar-bingeing rats (Bocarsly et al, 2014).…”

Pilot clinical observations between food and drug seeking derived from fifty cases attending an eating disorder clinic

“…Many theories supported by scientific neurochemical and genetic studies offer sound evidence that food addiction and psychoactive drug addiction are similar (Hadad & Knackstedt, 2014) in spite of arguments to counter this notion (Ziauddeen & Fletcher, 2013). Genetic and epigenetic impairments of the brain reward circuitry, which cause hypodopaminergic functioning, define RDS (Blum et al., 2011).…”

A Lack of Clinical Effect of High‐frequency rTMS to Dorsolateral Prefrontal Cortex on Bulimic Symptoms: A Randomised, Double‐blind Trial

“…A growing body of data suggests that high-frequency stimulation of the left dorsolateral prefrontal cortex (DLPFC) decreases craving in smoking, alcoholism and cocaine addiction (for review, see Grall-Bronnec et al, 2015;Jansen et al, 2013). BN individuals display aberrant patterns of prefrontal cortex activity during a wide range of experimental task, and BN are assumed to have an addictive component (for review, see Hadad & Knackstedt, 2014). There are also evidences that food craving is associated with DLPFC activity (Kekic et al, 2014), and previous study found that the capacity for self-control depends on DLPFC activity levels (Hare, Camerer, & Rangel, 2009) Thus, it is possible that rTMS of the DLPFC could reduce overeating behaviours by reducing food cravings and by improving cognitive control.…”