You can download a free Brain over Binge pdf to guide you in learning the basics of this alternative approach to recovery, as well as a free Manage Your Mindset After a Binge course track. The Brain over Binge Basics pdf is an easy-to-follow, 30-page eBook that teaches you a simple and practical way to end bulimia and binge eating disorder, and the Manage Your Mindset track is a 10-minute recording you can listen to after a binge, to help you get right back to having success and moving toward a binge-free life. These Brain over Binge resources are yours for free when you sign up below to receive my monthly newsletter, encouraging emails, and updates.
In my darkest days of binge eating, I vowed that if I ever found a way out, I would help others find a way out too, and since my recovery 15 years ago, I have kept that promise to my younger self.
The charts included in The Brain over Binge Recovery Guide are available for download on this page as PDFs. This is especially useful for printing extra copies, and for those who have the Kindle version (Kindle technology does not support adding notes into individual sections of a chart).
Common eating disorders include anorexia nervosa, bulimia nervosa, binge-eating disorder, and avoidant restrictive food intake disorder. Each of these disorders is associated with different but sometimes overlapping symptoms. People exhibiting any combination of these symptoms may have an eating disorder and should be evaluated by a health care provider.
Bulimia nervosa is a condition where people have recurrent episodes of eating unusually large amounts of food and feeling a lack of control over their eating. This binge eating is followed by behaviors that compensate for the overeating to prevent weight gain, such as forced vomiting, excessive use of laxatives or diuretics, fasting, excessive exercise, or a combination of these behaviors. Unlike those with anorexia nervosa, people with bulimia nervosa may maintain a normal weight or be overweight.
Binge-eating disorder is a condition where people lose control of their eating and have reoccurring episodes of eating unusually large amounts of food. Unlike bulimia nervosa, periods of binge eating are not followed by purging, excessive exercise, or fasting. As a result, people with binge-eating disorder are often overweight or obese.
Food craving, decision making, executive function, and impulsivity are regulated by distinguishable, although somewhat overlapping, brain regions and neurocircuitry. For example, a large brain network including the ventral tegmental area, ventral striatum (nucleus accumbens), lateral hypothalamus, orbitofrontal cortex, and amygdala is involved in the excursion of food craving. In contrast, the dorsal striatum, which can be further divided into dorsomedial striatum (caudate) and dorsolateral striatum (putamen), is essential for orchestrating goal-directed and habitual decision making [17, 18]. Furthermore, the prefrontal cortex, especially the lateral prefrontal cortex, is the major neural substrate of executive function. In terms of impulsivity, although its brain structural correlates have not been clarified, it is believed that various regions, including the striatum, prefrontal cortex, hippocampus, anterior cingulate cortex, temporal pole, and insula, are involved .
The neurotransmitter dopamine has attracted growing attention in the field of binge eating due to its widely distributed receptors in the brain regions and neurocircuitry implicated in food craving, decision making, executive function, and impulsivity, as well as its functional associations with these risk factors.
Dopamine is synthesized and released by dopamine neurons located in three main areas in the midbrain: the ventral tegmental area, the substantia nigra, and the retrorubral field . Dopamine neurons in the ventral tegmental area send projections to the ventral striatum (the main brain region relevant to food craving), forming the mesolimbic circuits . The mesolimbic dopaminergic system has traditionally been associated with motivation. In the context of eating behaviors, the hyperactive mesolimbic dopaminergic system leads to an increased incentive salience or craving for food-related rewards, thus contributing to the initiation of food consumption [20,21,22,23]. In addition to sending projections to the ventral striatum, midbrain dopamine neurons in the ventral tegmental area further project to the prefrontal cortex (the main brain region responsible for executive function), via the mesocortical pathway. Dopamine in the prefrontal cortex serves as a neuromodulator that is essential for regulating inhibitory control, working memory, and set-shifting. For example, neuroimaging and pharmacological studies have provided evidence that dopamine agonists increase frontal cerebral blood flow, which is associated with better inhibitory control [24, 25]. Additionally, an inverted-U relationship of dopamine with working memory and set-shifting has been repeatedly reported such that too low or too high extracellular dopamine concentration in the prefrontal cortex can impair working memory and set-shifting [26,27,28]. In contrast, dopamine neurons in the substantia nigra send projections to the dorsal striatum (the key hub for the regulation of goal-directed and habitual decision making), forming the nigrostriatal circuits. Substantial evidence from animal studies has demonstrated that dopamine sensitization in the dorsal striatum accelerates the development of habit formation from previously goal-directed behaviors [29,30,31]. Finally, studies have found that a high magnitude of dopamine release or higher dopamine receptor capability in the striatum predicts higher levels of impulsivity in humans and animals [32, 33]. The major dopaminergic pathways and corresponding risk factors of binge eating are outlined in Fig. 1.
A small-scale study  of eight adults with obesity (but without a diagnosed eating disorder) used electroretinography to estimate brain dopamine activity after oral food stimuli. The authors found that the cone electroretinography response significantly increased to food stimuli, and the increased response was positively associated with binge eating symptoms.
Frank et al.  used fMRI to examine the brain activity in 20 females with BN and 23 healthy controls in a temporal difference model during which participants learned to associate three unconditioned taste stimuli to a paired conditioned visual stimulus. In healthy subjects, it is expected that dopamine levels will increase in response to unexpected unconditioned stimuli, and dopamine levels will decrease if the conditioned stimuli are followed by an omission of the unconditioned stimuli. Results showed that BN individuals had a blunted BOLD response (a proxy of dopamine function) to both unexpected unconditioned stimuli and omission of unconditioned stimuli in several brain areas (e.g., ventral putamen, orbitofrontal cortex) compared to controls. Furthermore, the reduced response was significantly correlated to binge/purge frequency.
In an RCT  with 26 overweight and obese participants who reported binge eating behaviors, the participants were given either a dopamine D3 receptor antagonist or placebo and were exposed to high-fat and general food images. However, fMRI results showed that brain activation (e.g., ventral striatum, caudate, putamen) to food images was not modulated by the D3 receptor antagonist. Additionally, the D3 receptor antagonist had no effect on self-reported eating behaviors.
Another reason that can possibly explain the inconsistency is that this review included two distinct types of eating disorders: BED and BN. Although both BED and BN are marked by binge eating symptoms, BN additionally requires using compensatory behaviors after binge episodes (e.g., vomiting, using laxatives). Notably, the few studies that have compared the etiology and neural underpinnings of BED and BN revealed that despite a large magnitude of overlap , differences exist in the severity of dopamine-related risk factors. For example, patients with BED have been shown to have higher reward sensitivity and less intense top-down control to inhibit the increased food craving than those with BN [91, 92], suggesting the possibility that dopamine may function differently in BED and BN. In this review, among the eight studies that reported an altered dopaminergic state in the BED population, one half of the studies supported the hyperdopaminergic state and the other half supported a hypodopaminergic state but with a stronger level of evidence from RCTs. A more consistent trend was observed in the BN population with nine out of ten studies supporting a hypodopaminergic state, suggesting that dopamine may be downregulated in this specific eating disorder. Future studies may benefit from directly comparing the dopamine function among BED, BN, and preferably purging-only groups to better understand how dopamine contributes to binge-related eating disorders.
Among studies included in this review, although not all of them reported the stage or severity of binge eating, the two studies [59, 78] conducted among community-based adults who were completely or partially free of diagnosed binge eating supported a positive association between dopamine activity and binge eating symptoms. In contrast, eight studies [47, 49, 52, 57, 61, 79,80,81, 93] that included participants with moderate-to-severe binge eating or participants with a long illness duration (three being RCTs) supported a hypodopaminergic state in binge eaters. Plus, the three studies that documented a desensitized dopamine system in remitted BN patients [53, 76, 77] provided further evidence of a hypodopaminergic state in the late stages of binge eating. These results suggest that dopamine elevations may contribute to the initiation of binge eating, but a downregulation may occur after repeated bingeing, which