Over time, compulsive overeating or bingeing usually leads to weight gain. The most common type of food that bingers turn to during binges is “junk food,” or food that is high in empty calories, carbohydrates, fat and sugar. During a typical binge, the average person can consume as many as many as 2,000 to 3,000 calories. This frequent consumption of massive amounts of calories inevitably leads to weight gain.

Thank you for your reply, it’s brilliant. Do you have any supporting paper for what you’ve created?

Please check

Thank you very much

My answer is from the neuro-biological point of view but I also think that the psychological aspects are as important.

The key aspect of these disorders is that they are enduring, relatively immutable conditions that represent a baseline substrate of impaired addictedness, of deficiencies, or distortions that limit the capacity to adapt successfully to stress. That means that the genetic factors in their relationship with the environment can modulate the relationship between the stress effects on the person’s health. But genes do not code a specific psychiatric disorder, nor any symptom, but they do code for proteins and epigenetic regulators responsible for this information processing in brain circuits. So the vulnerability is genetic. The effects of the enviroment (like the stress) affects the neurotrophines levels. Therefore, the neurotrophines that are involved in different mental problems (Ex: major depressive episode association with eating symptoms ). An association between MDE and polymorphism of the brain derived neurotrophic factor (BDNF) gene was also reported. The family of neurotrophins contains four proteins: nerve growth factor (NGFB), brain-derived neurotrophic factor (BDNF) and neurotrophins 3 and 4/5 (NTF3 and NTF4/5) and they play important roles in proliferation, differentiation and maintenance of neurons in the central and peripheral nervous system. An association between Eating Disorders(ED) and polymorphism of the BDNF gene was reported. The Val66Met polymorphism (rs6265) of the BDNF gene is proved to be associated with binge eating dissorder or anorexia.

Evidence show that the sympathetic nervous system, the Hypothalamo-Pituitary-Adreno-medullary (HPA) axis and the inflammatory response system form a major chain reaction released by the immune complex. The interaction established among these systems and the central autonomic network which includes both prefrontal and limbic cerebral structures form an internal regulation system through which the brain controls visceromotor, neuroendocrine, and behavioral responses that are critical for adaptability and health, thus explaining the diversity of psychosomatic symptoms starting with a slight nausea sensation and ending with severe insomnia. The serotonin transporter (5-HTT), encoded by the SLC6A4 gene, may also have an important role in eating disorders. The promoter region contains a functional insertion/deletion polymorphism with two common alleles that have been designated the short (*S) and long (*L) alleles. Meta-analysis showed that the *S allele could represent a moderate but significant risk factor that increases the vulnerability for ED.

Because 5-HT is decreased just like in depression, ED are treated using antidepressants, serotonin reuptake inhibitors being the most frequently prescribed. High doses of SSRIs are usually prescribed in eating disorders. Information about genetic variations of cytochrome P450 could facilitate pharmacotherapy by preventing the administration of high doses in poor metabolizers and identify rapid metabolizes who may require higher doses for efficacy.

So in conclusion, there are several genes with an essential role in the regulation of eating behavior and could be involved in the etiology. The stress factors can act on these genes via 3 ways (HPA axis activation, inflammation and kynurenin pathway) and the person affected cand develop simptoms. Kynurenin patway can be involved in depression/ anxiety/ obesity and also in ED. Clinically, ED can be treated using antidepressants (SSRIs) considering genetic alterations in the serotonin receptor and psychotherapy (CBT, CARe model,...).

PS: Prof. S. Stahl had a nice lecture on this topic with nice slides and my only hope is that my comment here is clear enought to help you on this topic.

Thanks for your very helpful response.

Very interesting