Understanding that Addiction Is a Brain Disorder Offers Help and Hope

We refute the controversial statement that addiction is not a brain disorder. Extensive peer-reviewed studies support the underlying neurobiological and neurogenetic basis of addiction’s “disease model”. In the 70s and 80s, a few clinical scientists suggested that it is possible to use behavioral training to teach controlled drinking. However, this controversial model failed drastically and increased labeling and stigmatization. Additionally, it was unhelpful in the search for treatment. Instead, we assert that addiction is a neuropsychiatric disorder characterized by a recurring desire to continue taking substances despite harmful physical and mental consequences. Work from our laboratory in 1995 supported the Reward Deficiency Syndrome (RDS) concept based on a common neurogenetic mechanism (hypodopaminergia) that underlies all substance and non-substance addictions. Non-substance addictions include behaviors like pathological gambling, internet addiction, and mobile phone addiction. Certain impulsive and compulsive behaviors or the acute intake of psychoactive substances result in heightened dopaminergic activity, while the opposite, hypodopaminergia, occurs following chronic abuse. Patients with Substance Use Disorder (SUD) can have a genetic predisposition compounded by stress or other epigenetic insults that can impact recovery. Relapse will occur post-short-term recovery if dopaminergic dysfunction remains untreated. Addiction, a brain disorder, requires treatment with DNA-directed pro-dopamine regulation and rehabilitation.

Hypothesizing That Pediatric Autoimmune Neuropsychiatric Associated Streptococcal (PANDAS) Causes Rapid Onset of Reward Deficiency Syndrome (RDS) Behaviors and May Require Induction of “Dopamine Homeostasis”

Pediatric autoimmune neuropsychiatric disorders associated with group A streptococcal infections (PANDAS) is a concept that is used to characterize a subset of children with neuropsychiatric symptoms, tic disorders, or obsessive-compulsive disorder (OCD), whose symptoms are exacerbated by group A streptococcal (GAS) infection. PANDAS has been known to cause a sudden onset of reward deficiency syndrome (RDS). RDS includes multiple disorders that are characterized by dopaminergic signaling dysfunction in the brain reward cascade (BRC), which may result in addiction, depression, avoidant behaviors, anxiety, tic disorders, and/or OCD. According to research by Blum et al., the dopamine receptor D2 (DRD2) gene polymorphisms are important prevalent genetic determinants of RDS. The literature demonstrates that infections like Borrelia and Lyme, as well as other infections like group A beta-hemolytic streptococcal (GABHS), can cause an autoimmune reaction and associated antibodies target dopaminergic loci in the mesolimbic region of the brain, which interferes with brain function and potentially causes RDS-like symptoms/behaviors. The treatment of PANDAS remains controversial, especially since there have been limited efficacy studies to date. We propose an innovative potential treatment for PANDAS based on previous clinical trials using a pro-dopamine regulator known as KB220 variants. Our ongoing research suggests that achieving “dopamine homeostasis” by precision-guided DNA testing and pro-dopamine modulation could result in improved therapeutic outcomes.

Nonconscious processing and a novel target for schizophrenia research

Analysis of the pattern of altered cognition observed in schizophrenia provides better insight into neurocognitive deficits. It reveals a potential novel target for schizophrenia research. To understand this target we reviewed the findings of neuroimaging studies on implicit [nonconscious] memory. These studies have consistently reported attenuated activity in the area V3A of the extrastriate cortex during retrieval of studied items. It was suggested that the attenuation limits the pool of information available for further cognitive processing. Therefore, if V3A is functionally damaged, individuals will have access to a larger pool of information for cognitive processing. Since cognitive tasks that are not dependent on attention [attention independent] process a larger pool of information more efficiently, performance in these tasks is likely to improve after V3A is damaged. Conversely, tasks that are dependent on attentional resources are more efficient in processing smaller pool of information. Performance in these tasks therefore is expected to deteriorate if a large pool of information is made available following V3A damage. A review of cognitive performance in schizophrenia suggests that patients perform at above normal level in attention independent priming tasks and perform at subnormal level in attention dependent episodic and working memory tasks. These findings indicate possible impairment of V3A activity. It could therefore be a potentially important unstudied target for schizophrenia research, particularly because a number of investigators have reported that the activity in this area is altered in schizophrenia.