The Science Behind Disordered Eating Drives

Complexities of obesity, intricacies of neurobiology, and dysfunctional eating behaviors appear to intersect at an emerging popular theory of food addiction (Avena et al., 2012; Blumenthal & Gold, 2010). Addiction has been defined as a chronic, relapsing brain disease characterized by compulsive drug seeking and use, despite harmful effects (National Institute on Drug Abuse). Could the palatable nature of food and the pleasure of eating contribute compulsive dietary intake despite negative consequences, like those observed in substance abuse? 

Some investigators suggest addiction-like overeating is a behavior where the brain’s food reward system may be blunted or dysfunctional and possible hedonic deprivation drives food craving, which leads to obesity. Other investigators note inconsistencies in these behaviors, are unable to define cravings (Skinner & Aubin, 2009), and say that labeling such behaviors as addictive is scientifically unfounded and clinically unproven (Umberg et al., 2012; Pandit et al., 2012).  

Binge eating disorder (BED) is often associated with bulimia nervosa (Hudson et al., 2007). Animal models on BED indicate overeating behaviors are often independent of obesity (Cowin et al., 2011), yet appear to be prevalent among obese individuals (de Jong et al., 2012). New evidence indicates the importance of understanding dopaminergic circuits and opioidergic and gamma-aminobutyric acid systems as they relate to BED, especially relative to energy-rich dietary components (Berner et al., 2011). 

Examining the theoretical and neurological evidence suggests many regions of the brain are activated or stimulated in response to visual and sensory food cues (Gearhardt et al., 2011). These neuronal responses, like pleasure and emotional experiences, seem to be linked to dopamine, opioid, serotonin, and acetylcholine systems, which in turn reinforce specific behaviors (Kelley et al., 2005). Some evidence suggests atrophy or dysfunction of these systems or specific regions, particularly the ventral limbic circuit, may contribute to eating disorders (Marsh et al., 2009). For example, animal models and human brain PET imaging suggest eating disorders, such as binge eating, bulimia nervosa, and anorexia nervosa may share common dysfunctional pathways within the brain reward system (Iozzo et al., 2012; Kaye et al., 2010). 

Reward Deficiency Syndrome may be a genetic disorder within neurocircuitry (Blum et al., 2013). Polymorphisms of several genes, such as D2 dopamine receptor gene (DRD2), D4 dopamine receptor gene (DRD4), dopamine transporter gene (DAT1), and at least six other genes that impact neurotransmitters and other brain chemical elements may influence behaviors in response to food cues. For example, dopamine, a neurotransmitter that controls feelings of pleasure, interacts with  compounds such as serotonin and naturally produced opioid-like substances (e.g., endorphins), which may reduce our sense of stress. Upon a reduction of dopamine production and decreased number of receptors, unnatural and natural reward systems are disrupted (Koob et al., 2007). 

There are many neuroadaptive changes associated with peptides, receptor sites, and in the continuum from palatable eating to hedonic overeating and the ensuing eating restraint (pleasure) and relapse (compulsive) feedback loop (Alsiö et al., 2012). In the palatable part of the diet, select regions of the neural network, such as the amygdala and hypothalamus, up-regulate compounds (e.g., mu opioid receptor, glutamate) and down-regulate others (e.g., oxytocin, corticotropinreleasing hormone), respectively. Similarly, upon withdrawal of palatable food, there are additional shifts in other compounds in these and other regions of the brain. 

There are many challenges in attempts to understand the dynamics of hedonic eating above homeostatic need and neurobiology (Allen et al., 2012). Examination of these challenges indicates considerable overlap in neurochemistry and behavior (Albayrak et al., 2012). 

A significant confounding contributor to binge eating, which affects about 5% of the adult population at least once in their lifetime, is physiological and environmental stress (Sinha & Jastreboff, 2013; Mathes et al., 2009). The eating paradox, at least during short periods of stress (84 days), is that among 82% of adults, some increase food intake during periods of stress, whereas others decrease food intake (Stone & Brownell, 1994). 

More recent studies indicate during periods of acute stress, about 30–40% decrease food intake, nearly 20% do not change their dietary pattern, and more than 40% increase intake (Dallman, 2010; Epel et al., 2004). 

Thus one could arguably consider obesity the result of one or more neurological disorders. While public health initiatives focus on energy balance and exercise, there are many neurological explanations and behavioral pathways that contribute to weight gain. These areas demand further research if obesity-reduction interventions are to be successful (DiLeone et al., 2012; Grant et al., 2010).

References cited in this article are available from the author.

Roger Clemens, Dr.P.H., CFS,
Contributing Editor 
Chief Scientific Officer, Horn Company, La Mirada, Calif. 
[email protected]