Addiction is the Product of Brain Reward Deficiency
It is now known that individuals who seek treatment for chemical dependency have an impairment in the reward system of the brain that leads to low levels of the neurotransmitter dopamine which plays a significant role in feelings of pleasure and well-being. The impairment may be due to genetic or evironmental factors. The sense of pleasure and satisfaction produced when adequate dopamine is released into the reward site (nucleus acumbuns) are deficient when the reward system is impaired. Impairment leads to craving and discomfort and other symptoms of what is referred to as Reward Deficiency Syndrome (RDS). When RDS is present, an individual often uses addictive substances or behaviors to relieve the pleasure deficit caused by the impairment. Because the substance or behavior works to bring relief, the individual is likely to continue to use and is in high risk of becoming addicted.
Brain Reward Cascade (BRC)
Evidenced-based medicine has revealed a well-defined interaction of certain neurotransmitters in the reward system of the brain that leads to normal dopamine release. This was first reported by Drs. Kenneth Blum and Gerad Kozlowski in 1989 and has been termed the "Brain Reward Cascade" (BRC). Any impairment, due to either genetics or environment, on this cascade will result in a reduced amount of dopamine released in the brain reward site and in symptoms such as cravings, anxiety, depression, and poor memory.
The following schematic describes the known interaction of the neurotransmitters showing how dopamine is released and regulated. Serotonin (by activating serotonin receptors in the hypothalamus) stimulates the release of enkephalins (opioid peptides). then enkephalins (by activating mu receptors) influence the release of the inhibitory neurotransmitter GABA (gamma-Aminobutyric acid in the Sustania Nigra). In turn, GABA inhibits the release of dopamine (at the Ventral Tegmental Area) via GABA receptors: and the correct amount of dopamine is released at the reward site of the brain to bring about a sense of well_being.
In the schematic, the happy brain (A) is illustrated showing the normal amount of dopamine being released as explained above. However, the schematic also shows the unhappy brain (B). It is noteworthy that GABA is a higher amount and as such significantly reduces the amount of dopamine released. This could be due to, for example, a genetic deficit of serotonin synthesis and/or receptor function (including an increased serotonin transport resulting in not enough serotonin to stimulate the needed endorphins to inhibit GABA). Certainly, other genetic deficits would also lead to less control of GABA. The regulation of dopamine is so important because too little leads to depression and too much leads to schizophrenia. Neurotransmitters of the BRC include at least four known pathways: serotonin, opioid peptides, GABA, and dopamine. Impairments of specific neurotransmitters (serotonin, endorphins, GABA, dopamine) in the BRC can occur via genetics, stress and/or over-consumption of psychoactive substances like alcohol, drugs, nicotine, or glucose. However, due to the known interaction of these brain chemical messengers it is the net dopamine release that translates to well-being.
Reward Deficiency Syndrome can manifest as many different disorders such as Attention Hyperactivity Disorder, Tourette's Syndrome, Obsessive Compulsive Disorder, and numerous personality disorders. SynaptaGenX is effective for any of these disorders and early intervention can prevent addiction.
Copyright © David Miller. All rights reserved.
What is Reward Deficiency Syndrome?