Dopaminergic and other genes related to reward induced overeating, Bulimia, Anorexia Nervosa, and Binge eating

ABSTRACT

Introduction

Eating Disorders and Obesity are a primary global public health concern.

Areas Covered

This article aims to trace the neurochemical mechanisms of unwanted eating disorders and target specific loci, within the Brain Reward Cascade (BRC) for therapeutic interventions. Changes due to BRC polymorphisms in functional connectivity and neurotransmission can manifest as overeating, Bulimia Nervosa, and Anorexia Nervosa, and other related eating disorders.

Expert opinion

Variations in dopamine function within the Ventral Tegmental Area (VTA), Nucleus Accumbens (NAc), and Ventral Striatum of individuals result in different outcomes related to maladaptive eating behaviors. The goal is to reduce maladaptive eating behaviors by implementing novel strategies that induce Dopamine Homeostasis within the BRC. Clinicians determine genetic risk severity and identify polymorphic targets for either pharmaceutical or nutraceutical interventions. Precision neuro-nutrient formulations of KB220 (Research ID Code) matched precisely to deficient neurotransmitter systems may promote the long-term development of ‘dopamine homeostasis’ to treat and prevent overeating, Bulimia, and Anorexia Nervosa.

KEYWORDS:

• Eating disorders
• overeating
• binging
• Bulimia Nervosa
• undereating
• Anorexia Nervosa
• neurogenetics
• Genetic Addiction Risk Severity (GARS)
• dopamine homeostasis
• polymorphic genetic antecedents
• hypodopaminergia

Article highlights

• According to the National Center for Health Statistics, age-adjusted trends in Obesity stand at 42;4 percent obesity with a 9.2 prevalence of severely obese (2018).

• Human and animal genetic studies support the impulsive nature of individuals possessing mesolimbic reward gene variants that result in dopamine and an array of other reward gene deficits.

• Neurobiological mechanisms of various polymorphic genes change brain function and are trait antecedents to overeating, binging (e.g. Bulimia Nervosa), and undereating (e.g. Anorexia Nervosa).

• Volkow et al. suggested that DA increases can override homeostatic control mechanisms in the brains of vulnerable individuals.

• The goal to treat and prevent unwanted eating behaviors requires the induction of dopamine homeostasis.

• Pro dopamine interventions such as exercise and precision addiction management with glutaminergic-dopaminergic optimization complex, rTMS, among other modalities, can counteract hypodopaminergia by epigenetically targeting reward deficits.

• The suggestion is that clinicians genetically diagnose each patient to determine risk stratification and identify polymorphic targets for either pharmaceutical or nutraceutical interventions.

Additional information

Funding

K Blum and M Gondre-Lewis (Howard University) are recipients of R41 MD012318/Md/NIMHD NIH HHS/United States.