In the last few decades, it has become increasingly clear on the theoretical side that addiction is in fact either largely or wholly a physiological disorder.
Researchers have learned that in a few cases, a small number of genetic variations may be enough to provide an individual with a "predisposition" or "vulnerability" to addiction.
It is also becoming clearer that a larger number of milder genetic variations may conspire together to create the same effect.
Commonly abused substances themselves alter the function of the brain's normal pleasure response system, apparently as a result of the brain's adaptation to the substance.
In fact, regardless of cause, the mere usage of certain chemicals (for example cocaine, alcohol, nicotine and morphine) is linked with changes in the brain's functioning and the associated craving for those substances.
The result seems to be a grouping of very similar biochemical neuronal conditions which adversely impact the brain's pleasure responses.
The term "Reward Deficiency Syndrome" (RDS) has been coined to describe these disorders.
Estimates of the number of individuals that display RDS range as high as one third of the population.
U.
S.
Pat.
No.
6,132,724, issued on Oct.
17, 2000 to Blum and entitled "Allelic Polygene Diagnosis of Reward Deficiency Syndrome and Treatment" provides a great deal of background material on RDS and the probable genetic causes thereof.
The brain's neurotransmitter chemicals, receptor cells for those chemicals, and related systems regulating production and maintenance of the appropriate level of these neurotransmitters are at the center of this reward deficiency syndrome.
For example, serotonin and dopamine have been implicated in this process: alterations in the metabolic cycle of these substances is part and parcel of substance abuse behavior and recovery therefrom.
Dopamine levels may be reduced by substance abuse, and dopamine reception by the neurons may be reduced by substance abuse, thus forming one component of the craving for the substance.
It is also possible that the individuals addicted to the substances in question had poor dopamine reception prior to the abuse behavior, and that the poor reception was part of the reason that the individual succumbed to the disease.
More specifically it is known that dopamine release can be induced by application of precursor amino-acids, thus assisting in reduction of craving.
In addition to dopamine and serotonin, GABA and the opioid peptides are also believed to play a complex role in the reward process.
For example, GABA may regulate dopamine release.
Studies in rats and mice having a susceptibility to the abuse alcohol show low levels of serotonin and dopamine and increased levels of GABA and opioid peptides.
One example of a patent for a medication which acts on the dopamine levels in the brain is U.
S.
Pat.
No.
6,057,368, issued to Dewey et al on May 2, 2000 for "Treatment of Addiction and Addiction-Related Behavior.
" The medication taught by the '368 patent uses gamma vinyl GABA as an agent, and is not untypical of modern developments in treatment.