Prior, we discussed similarities between addiction and obesity (See Obesity and Addiction: How They Are Similar). An understanding of addiction theory may offer further insights into potential ways to help people suffering from addictive aspects of overeating.

Addiction Cycle
The cyclical nature of addiction is widely recognized. To facilitate thinking about the possibility of obesity being caused by an addiction-like process, let’s look at the addiction cycle that is widely recognized for substance abuse and substitute food-related words for drug-related terms.

The addiction cycle starts with physical and emotional triggers leading to an urge to use the substance / unhealthy food / amount of food. The urge is characterized by preoccupation with thinking about the food, obtaining the food, anticipating eating it, and craving it. These feelings build until the afflicted person eats the food, sometimes to excess, and experiences pleasure from the experience and temporary relief from the urge. The period of relief is soon replaced by a growing physical urge to eat the food again. The individual may suffer a bad mood, with guilt and/or depression as a consequence of the last unhealthy food eaten or last eating binge. The growing urge to eat unhealthily is then relieved temporarily again.

Imaging studies in animals and humans have shown that different areas of the brain are centers for the three stages of the addiction cycle (Koob & Volkow, 2010):

1. Ventral tegmental area and ventral striatum for binge/intoxication
2. Amygdala for withdrawal/negative affect stage
3. Orbitofrontal cortex-dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula for craving
4. Cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices for interruption of inhibitory control

The brain undergoes physical changes over time in substance use disorders. Interventions that target the cognitive/emotional aspects of addiction need to be powerful enough to counteract these changes.

Therapies aim to interrupt addiction at various points in the cycle. Adjunctive supports might also interrupt progression from encountering a food cue, to experiencing an urge to eat it, to actually eating the food or too much food.

Inhibitory Control
Inhibitory control is an executive function that involves controlling one’s thoughts, attention, and emotions and one’s behaviors in response to them. Inhibitory control is thus important in recovering from addiction. Research has shown that training can improve executive functions across the lifespan (Best et al., 2010; Best et al., 2014). Working memory is an important component of inhibitory control. It involves short-term storage and manipulation (Malenka et al., 2015). Thus, it plays a role in decision-making and is important in changing behavior. The prefrontal cortex is an important part of the brain in executive functioning (Malenka et al., 2015). Engaging the prefrontal cortex exerts control over more automatic responses occurring in other cortical regions, such as the association cortex, and subcortical structures responsible for emotion and motivation, including the amygdala and ventral striatum or nucleus accumbens.

Next, we’ll look at Therapeutic Approaches Commonly Used for Treating Addiction for further insights into possible ways to interrupt addictive aspects of overeating.

References

• Best JR, Miller PH. A developmental perspective on executive function. Child Dev. 2010; 81(6): 1641-1660. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058827/. Accessed, 2/19/2016.
• Best JR, Nagamatsu LS, Liu-Ambrose T. Improvements to executive function during exercise training predict maintenance of physical activity over the following year. Front Hum Neurosci. 2014; 8: 353.
• Koob GF, Volkow ND. Neurocircuitry of addiction. Neuropsychopharmacology. 2010. 35, 217-238. Available at: http://www.nature.com/npp/journal/v35/n1/abs/npp2009110a.html. Accessed 2/23/2016.
• Malenka RC, Nestler EJ, Hyman SE. Chapter 13: Higher Cognitive Function and Behavioral Control. Chapter 14 & 15. In Sydor A, Brown Ry. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.) New York: McGraw-Hill Medical. pp. 313-321. 2015 ISBN 9780071481274.