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Abstract
While individual genetic differences contribute to the development of substance dependence, genetic factors are considered one contributor to the complex interplay of physiological, social, cultural and personal factors that are involved.The classical (and popular) view of human genetics is one in which genetic mutation is the direct and usually only cause of a particular illness, for example, the single gene – or Mendelian – disorders such as Huntington’s disease.Single gene diseases are caused by specific mutated gene and the mutation is both necessary and sufficient to cause the illness. Unlike single gene disorders, which are rare and might affect 1 in 10000 people, complex disorders such as substance dependence,are common in the population, often affecting 1 in 100 or more people. Complex disorders are clearly not caused by genes alone, but by the interaction between genes and the environment thus exposure to psychoactive substances could have a much greater effect on somebody who carries a genetic vulnerability to substance dependence than on someone who does not.
Genetic vulnerability or predisposition. to substance dependence is likely to be tied to several distinct genes(or multiple alleles), each producing a small effect which might increase risk of developing substance dependence by 2-3 fold. Any one of the genes on its own will be insufficient to cause dependence but several different genes may all contribute to the vulnerability. It is hypothesized that not everyone who carries a risk gene for substance use or dependent will become dependent and likewise some of those who become dependent will not carry that particular genetic risk factor. It is the combination of the presence of several distinct genes or alleles which may be important, rather than a single gene. These genetic contributions to vulnerability seem likely to be distributed over several distinct regions (loci) on the chromosomes.One overwhelming finding from genetic studies of psychoactive substances is that the heritability (i.e. genetic contribution) of dependence for one substance correlates highly with dependence for other substances. Thus, there may be some common genetic components to substance dependence in general, as well as to dependence for specific psychoactive substances.
Family, twin and adoption studies provide strong evidence for a significant, but not exclusive, genetic contribution to the development of substance use and dependence. Environmental factors, and individual exact experiences, are also of major importance. Family and adoption studies that have focused on general risk for substance use show that substance dependence is a familial trait, which can be attributed to either shared environment or shared genes.
Twin studies consistently show higher monozygotic than dizygotic concordance for substance dependence, indicating a genetic effect. The significant and complex genetic contributions to substance dependence continue to motivate efforts to identify allelic variants that contribute to dependence vulnerability, even if each allelic variant contributes only a modest fraction to the whole problem. Genotypes at loci containing vulnerability alleles could provide improved approaches to treating vulnerable individuals and thus maximize the use of resources for prevention and treatment. Individual and societal suffering could be relieved by better understanding the complex human processes of dependence through careful application of complex genetic approaches.
The two main approaches to estimate genetic and environmental components of phenotypic variance are twin and adoption study. In addition to estimating genetic liability, these studies provide further information about environmental contributions, identifying that which is shared (i.e. that which both twins have in common and which contributes to their similarity) and that which is non-shared (contributing to the relative dissimilarity)