The Molecular Neurobiology of Twelve Steps Program & Fellowship: Connecting the Dots for Recovery

Abstract

There are some who suggest that alcoholism and drug abuse are not diseases at all and that they are not consequences of a brain disorder as espoused recently by the American Society of Addiction Medicine (ASAM). Some would argue that addicts can quit on their own and moderate their alcohol and drug intake. When they present to a treatment program or enter the 12 Step Program & Fellowship, many addicts finally achieve complete abstinence. However, when controlled drinking fails, there may be successful alternatives that fit particular groups of individuals. In this expert opinion, we attempt to identify personal differences in recovery, by clarifying the molecular neurobiological basis of each step of the 12 Step Program. We explore the impact that the molecular neurobiological basis of the 12 steps can have on Reward Deficiency Syndrome (RDS) despite addiction risk gene polymorphisms. This exploration has already been accomplished in part by Blum and others in a 2013 Springer Neuroscience Brief. The purpose of this expert opinion is to briefly, outline the molecular neurobiological and genetic links, especially as they relate to the role of epigenetic changes that are possible in individuals who regularly attend AA meetings. It begs the question as to whether “12 steps programs and fellowship” does induce neuroplasticity and continued dopamine D2 receptor proliferation despite carrying hypodopaminergic type polymorphisms such as DRD2 A1 allele. “Like-minded” doctors of ASAM are cognizant that patients in treatment without the “psycho-social-spiritual trio,” may not be obtaining the important benefits afforded by adopting 12-step doctrines. Are we better off with coupling medical assisted treatment (MAT) that favors combining dopamine agonist modalities (DAM) as possible histone-deacetylase activators with the 12 steps followed by a program that embraces either one or the other? While there are many unanswered questions, at least we have reached a time when “science meets recovery,” and in doing so, can further redeem joy in recovery.

Lyme and dopaminergic function: Hypothesizing reduced reward deficiency symptomatology by regulating dopamine transmission

“…Fortunately, the addicted brain, specifically DRD2 A1 carriers, favors Neuroadaptagen-Amino-Acid therapy [38] due to an increased sensitivity to promote dopaminergic activity. This occurs as a result of dopamine synthesis: DRD2 A1 allele carriers display augmented striatal activity of L-amino acid decarboxylase.…”

“…In fact, our proposal is extended to the fact that the hospitalization and perhaps mortality due to enhanced relapse of RDS seeking should consider prevention tactics such as the Neuroadaptagen–Amino-Acid therapeutic (KB220), now referred to as the Natural Assisted Treatment™ [38]. …”

The Benefits of Genetic Addiction Risk Score (GARS™) Testing in Substance Use Disorder (SUD)

“…It is well-known that many patients in treatment programs deny that they have a biological problem and are therefore able to control addictions [14]. Through the "war on drugs," the justsay-no campaign, and into the early years of this century, the overarching approach to Substance Use Disorders (SUDs) called for a single outcome (abstinence) and a single methodology (spiritual connection with a higher power) as the remedy for SUDs.…”

Neurogenetics of acute and chronic opiate opioid abstinence treating symptoms and the cause

“…It is noteworthy that over many years, some relevant preclinical models that have attempted to understand relapse to "reward deficiency" (66), emerged and © 1996-2017 have been reviewed in the literature (61,64,65,(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77)(78)(79). In fact, the current FDA-approved MATs favor this approach that, although not optimal, has success in many patients (80)(81)(82).…”