TY - CHAP
T1 - Dying to Lose Weight
T2 - Genetic Addiction Obesity Risk Assessment (GORA) Panel Embracing Precision Obesity Management (POM)
AU - Blum, Kenneth
AU - Gold, Mark S.
AU - Bowirrat, Abdalla
AU - Elman, Igor
AU - Makale, Milan T.
AU - Bagchi, Debasis
AU - Braverman, Eric R.
AU - Dennen, Catherine A.
AU - Thanos, Panayotis K.
AU - Hanna, Colin
AU - Kai-Uwe-Lewandowski,
AU - Sharafshah, Alireza
AU - Badgaiyan, Rajendra D.
N1 - Publisher Copyright:
© 2025 Taylor & Francis Group, LLC.
PY - 2024/1/1
Y1 - 2024/1/1
N2 - The now well-characterized obesity epidemic is a primary public global health concern. Previously, we were aware of the catastrophic clinical outcome in the late 1990s of the weight-loss pharmaceutical (Phentermine) induction of premature deaths. This book chapter aims to trace the neurochemical mechanisms of unwanted eating disorders and target specific loci, ascertained by understanding reward mechanisms and the function of the brain reward cascade (BRC). Changes in brain functional connectivity based on neurobiological mechanisms related to various polymorphic genes are antecedents to overeating, binging (e.g., bulimia), and undereating (e.g., anorexia nervosa). This approach embraces the induction of “dopamine homeostasis.” It is now well accepted that dopaminergic function at the ventral tegmental area (VTA) and the release of dopamine at the nucleus accumbens (NAc) varies, and low dopamine function is associated with high Body Mass Index (BMI). There are many genetic risk alleles having both central and peripheral functions that lead to unwanted obesity as a generalized phenotype. The inventors are cognizant of the heuristic value of the development for commercial use of an objective genetic assessment tool for both consumer and clinical professionals to identify a predilection for obesity-related sequalae. The non-pharmacological intervention proposed herein a newly developed anti-obesity restoration model (AORM) utilizing a cluster of efficacious therapeutic modalities preferably guided by DNA polymorphisms. These include but are not limited to: optogenetic stimulation, yoga, medication, diet, exercise, fitness coaches, nutrition programs initiated early in recovery, and gentle dopaminergic agonistic therapy. Initially, the consumer obtains results from a simple non-invasive saliva or cheek cell test referred to as a genetic addiction obesity risk assessment (GORA) panel to determine genetic risk severity and identify polymorphic targets for either pharmaceutical or nutraceutical interventions like glutaminergic–dopaminergic restoration. The preferred putative involves various neuro-nutrient formulations (KB220 research name) matched precisely to the deficient neurotransmitter systems identified by an individual’s genetic profile. Known genetic reward mechanisms involving neurotransmission pharmacology promote the long-term development of “dopamine homeostasis” to treat and prevent relapse to eating disorders. This novel therapy now is “precision obesity management (POM).”.
AB - The now well-characterized obesity epidemic is a primary public global health concern. Previously, we were aware of the catastrophic clinical outcome in the late 1990s of the weight-loss pharmaceutical (Phentermine) induction of premature deaths. This book chapter aims to trace the neurochemical mechanisms of unwanted eating disorders and target specific loci, ascertained by understanding reward mechanisms and the function of the brain reward cascade (BRC). Changes in brain functional connectivity based on neurobiological mechanisms related to various polymorphic genes are antecedents to overeating, binging (e.g., bulimia), and undereating (e.g., anorexia nervosa). This approach embraces the induction of “dopamine homeostasis.” It is now well accepted that dopaminergic function at the ventral tegmental area (VTA) and the release of dopamine at the nucleus accumbens (NAc) varies, and low dopamine function is associated with high Body Mass Index (BMI). There are many genetic risk alleles having both central and peripheral functions that lead to unwanted obesity as a generalized phenotype. The inventors are cognizant of the heuristic value of the development for commercial use of an objective genetic assessment tool for both consumer and clinical professionals to identify a predilection for obesity-related sequalae. The non-pharmacological intervention proposed herein a newly developed anti-obesity restoration model (AORM) utilizing a cluster of efficacious therapeutic modalities preferably guided by DNA polymorphisms. These include but are not limited to: optogenetic stimulation, yoga, medication, diet, exercise, fitness coaches, nutrition programs initiated early in recovery, and gentle dopaminergic agonistic therapy. Initially, the consumer obtains results from a simple non-invasive saliva or cheek cell test referred to as a genetic addiction obesity risk assessment (GORA) panel to determine genetic risk severity and identify polymorphic targets for either pharmaceutical or nutraceutical interventions like glutaminergic–dopaminergic restoration. The preferred putative involves various neuro-nutrient formulations (KB220 research name) matched precisely to the deficient neurotransmitter systems identified by an individual’s genetic profile. Known genetic reward mechanisms involving neurotransmission pharmacology promote the long-term development of “dopamine homeostasis” to treat and prevent relapse to eating disorders. This novel therapy now is “precision obesity management (POM).”.
UR - http://www.scopus.com/inward/record.url?scp=85216051501&partnerID=8YFLogxK
U2 - 10.1201/9781003361473-13
DO - 10.1201/9781003361473-13
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AN - SCOPUS:85216051501
SN - 9781032421681
SP - 169
EP - 187
BT - Body Recomposition
ER -