Neurobiology of Binge Eating Disorder – A Synopsis
Food cravings and food addiction are an important component of obesity; however, the idea that food addiction is a behavioural model in obesity is hotly debated. In the context of binge eating behaviours, it is suggested that these behaviours are similar to those observed in patients that experience drug addiction. [Ziauddeen H et al., 2012]
Palatable and energy-dense food and fluids are instead considered the chosen drugs of abuse, which when consumed, activate reward pathways that reinforce a behavioural phenotype.
This phenomenon is akin to substance abuse and is relevant not only to patients with obesity but also to those with binge-eating disorder (BED) or bulimia nervosa.
BINGE EATING DISORDER - HISTORY AND CRITERIA
Binge eating is characterised by recurrent episodes of rapid and excessive food consumption and mainly affects adolescents and younger adults. [Hay P et al.,2017]
BED was introduced into the DSM-V in 2013 as a distinct subset of the eating disorder diagnoses, (e.g. anorexia nervosa and bulimia nervosa). [APA, 2013]
The DSM-V criteria for Binge Eating Disorder
The hypothalamus acts as the main appetite regulatory centre via a range of peptides and pathways to the reward pathways. [Subramaniapillai & McIntyre (2017)]
The hypothalamus plays a central role in orchestrating the bodily response to food and hunger, controlling the release of leptin, ghrelin and orexin.
The two key areas of the hypothalamus that are involved in appetite regulation are the arcuate nucleus (ARC), which reduces appetite and the lateral hypothalamus, which increases appetite.
Behavioural aspects of eating
The mesolimbic reward pathway projects from the ventral tegmental area (VTA) to the nucleus accumbens (NA) in the limbic system. This pathway stimulates pleasure by increasing the release of dopamine.
Food is known to activate the mesolimbic reward system leading to the experience of pleasure which in turn can activate food-seeking behaviours through activation of cognitive processes involved in motivation.
GENETICS OF BINGE EATING DISORDER
BED has a complex and heterogeneous genetic background however it is influenced by both heritability and environmental factors. [Kessler R et al., 2016]
BED has heritability estimates of between 41% to 57%.
Unique environmental factors
- The interplay between genetic susceptibility with environmental components has been shown using data from the Australian Twin Registry. [Wade T et al., 2006]
- Moreover, it has been highlighted that genetically susceptible individuals have a higher risk of developing eating disorders when there is a trigger such as trauma or the encouragement to diet. [Pike K et al., 2006]
NEUROBIOLOGY OF BINGE EATING DISORDER - FUNCTIONAL ASPECTS
Patients with BED exhibit habitual overeating: a Pavlovian conditioning mechanism whereby goal-directed actions become compulsive and stimulus-driven.
The repeated pairing of a reward-associated stimulus with a compulsive seeking behaviour is an important element of habitual responding. [Watson P et al., 2014] , [Voon V et al., 2015]
BED is associated with abnormalities in key cognitive domains – impulsivity and compulsivity, executive function, attention and decision making. These areas mainly involve the prefrontal cortex and the striatum. [Kessler R et al., 2016]
- Impulsivity is premature decision making without forethought or lack of reflection of the consequences of one’s behaviour and the inability to postpone reward with a preference for immediate reinforcement over delayed reinforcements and a failure of motor inhibition.
- Compared to obese and normal weight individuals, patients with BED have increased impulsivity scores in the Barratt BIS-11 and UPPS impulsiveness scales.
- The main brain circuit involved in impulsivity is underpinned by the ventral striatum which is linked to the thalamus, the ventromedial prefrontal cortex and the anterior cingulate cortex
- Obese patients with BED have a higher risk of comorbid mental disorders as well as exhibiting more severe motor and cognitive impulsiveness. [Mobbs O et al., 2011], [Schmidt F et al., 2012]
- Repetitive and persistent actions that are not related to a goal or reward but can persist despite adverse consequences.
- The persistent repetition of binge eating episodes despite obvious adverse consequences is an important component of addiction.
- Compulsivity is mediated by the dorsal striatum, thalamus and the orbitofrontal cortex.
Other cognitive deficits
- Cognitive domains such as executive function and mental flexibility are negatively affected in patients with BED.
- Moreover, obese patients with BED exhibit more severe deficits in these cognitive domains.
Attention and memory biases
- When patients with BED attempt to process information in the presence of food-related cues (e.g. pictures of high caloric foods), there is evidence of cognitive interference with an attentional bias towards food-related cues. [Svaldi J et al., 2014]
- The presence of inattention is a cognitive deficit that prevents patients from focussing when presented with a stimulus.
- BED has also been shown to be associated with risk-taking during probabilistic-reward tasks.
- In particular, obese BED patients have a reduced preference for both delayed rewards (impatience) or a probabilistic reward (risk aversion). [Manwaring J et al., 2013]
- This trait has also been observed in patients with a history of either alcohol or drug abuse behaviours. [Voon V et al., 2015]
In binge eating disorder there seems to be a ventral to dorsal migration and BED is maintained by compulsive behaviour that is underpinned by the dorsal pathway.[Kessler R et al., 2016]
The impulsivity to food or drug initially leads to pleasure and satisfaction.
With chronic substance use, compulsivity may develop as an individual’s drive moves from seeking pleasure to seeking relief from the distressing symptoms of withdrawal and the anticipation of obtaining the drug/food.
This occurs due to a cascade of neural adaptation and neuroplasticity that engage the habit system by which the impulsive act becomes a compulsive act—this is the same mechanism for the pathogenesis of addiction.
NEUROBIOLOGY OF BINGE EATING DISORDER - STRUCTURAL ASPECTS
Brain structure and function has been studied using neurophysiological and neuroimaging techniques, which together have revealed increased synaptic activity in specific brain regions.
For example, EEG recordings have been used to show that obese women with BED have dysfunctional information processing when viewing pictures of high caloric foods. [Svaldi J et al., 2010]
Moreover, patients with BED exhibit increases in regional blood flow in cerebral blood flow when responding to food stimuli. [Karhunen L et al., 2000]
Striatum and insular cortex
These are the brain regions associated with BED-related reward sensitivity and impulsivity.
Brain mapping studies of the ventral striatum have been able to accurately distinguish BED patients from patients with bulimia nervosa, and obese patients that were with and without BED. [Weygandt M et al.,2012]
Increased impulsivity is correlated with decreased ventral striatal and ventral midbrain dopamine D2 receptor levels.
- This brain region is associated with the inhibitory control over behaviour, and therefore dysfunction in cortico-striatal circuits relate to higher attentional impulsiveness and incentive salience. [Volkow N et al., 2013]
- The prefrontal cortex acts as a top-down mechanism to suppress the bottom-up mechanism, i.e., impulsivity coming from the ventral striatum and compulsivity coming from the dorsal striatum.
- Conceptually, this is posited as hyper-responsiveness in the ‘GO’ system and impairment in the ‘STOP’ system. [Koob G and Volkow N, 2016]
Direct and indirect striatonigral pathways
- It is hypothesised that binge eating reflects an imbalance between the direct striatonigral pathway (D1 receptors) and the indirect striatopallidal pathway (D2 receptors).
- The hypofunction of the indirect pathway is evidenced by the reduced D2-like receptor level and may mediate the compulsive eating behaviours in binge eating disorder.
Overall, the research suggests that the brain reward systems mediate reward motivation and incentive salience, which are essential in modulating ingestive behaviours and appetite regulation.
The transition to binge eating pathology and behaviours occur from a ventrally underpinned reward-related food consumption to a dorsal striatal underpinned compulsive mode of food consumption. This involves:
- Decreased cortical inhibition of impulsive pathways.
- Decreased reward sensitivity related to decreased striatal dopamine release.
- Imbalance in the function of indirect versus direct striatonigral pathways.
Two key pathways posited to be involved in BED are dopaminergic and opioid pathways. [Davis C et al., 2009]
- Polymorphisms related to dopamine neurotransmission in the mesocorticolimbic brain pathway are more commonly found in BED patients compared to healthy controls.
- These have been linked to increased D2-like receptor density as well as increased dopamine signalling, which both serve to increase appetitive motivation.
- In binge eating disorder it is likely that the dopamine neurons stop responding to the primary reinforcer and then start responding to the conditioned stimulus, i.e., the sight of the refrigerator or the smell of food.
- Dopamine is also responsible for motivation and the procurement of food or substances.
- The endogenous opioid system is a dominant pathway in regulating reward processes, particularly for substances such as alcohol and heroin.
- Although this is only a hypothesis as there is yet to be any definitive link between a gain-of-function polymorphism in opioid signalling and binge-eating.
BED is characterised by pathological food consumption that is associated with dysfunctional neural mechanisms in the brain’s reward systems.
Food consumption is inherently rewarding and pleasurable; however, pathologies in brain reward functioning can lead to neural sensitisation changes that increase incentive salience and the development of an eating disorder such as BED.
Learn more on the diagnosis and management of BED.