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Drug addiction is not merely a failure of will or weakness in character, however having this 'brain disease' does not absolve the addict of responsibility for his or her behavior, but it does explain why an addict feels compelled to continue using drugs (Leshner 2001). Environmental cues that surround an individual's initial drug use and development of the addiction, actually become "conditioned" to the drug use and thus are critical to the problem of addiction (Leshner 2001).
Therefore, when those cues are present at a later time, "they elicit anticipation of a drug experience and thus generate tremendous drug craving" (Leshner 2001). This type of cue-induces craving is one of the most frequent causes of drug use relapses, independently of whether drugs are available and even after years of abstinence (Leshner 2001).
In March 2006, it was reported that researchers from Liverpool, England discovered a gene that directly affects the risk of an individual vulnerability of addiction to the Class A drug (James 2006). Researchers tested 700 cocaine users and 850 non-users in Brazil, where use of crack and cocaine is widespread, and found that individuals (some 30%) who had a particular variant of a gene called the Dopamine Transporter were more likely to become dependent on cocaine (James 2006). A small number of participants who had two copies of the DAT gene, one from each parent, were 50% more likely to become addicted (James 2006). Previous research has demonstrated that cocaine weakens the DAT's ability to help control the amount of dopamine in the body, "giving the effect of a drug's high" (James 2006).
According to Professor John Quinn of the University of Liverpool, this research proves that much of an individual's "desire to use, and re-use cocaine depends on their genetic make-up" (James 2006). The findings from this study could help develop drugs to treat cocaine addiction and better understand the effect of other addictive substances, such as tobacco and alcohol (James 2006). "Genes are passed on from our parents, so if your mother and father both had this gene and were cocaine users, then you could be at a high risk of becoming dependent," said Quinn (James 2006).
The study, which was published in the journal of the American Academy of Sciences, has been hailed as one of the most important-ever in understanding addiction.
The study was conducted in collaboration with the Medical Research Council (MRC) Social, Genetic and Developmental Research Center at the Institute of Psychiatry, King's College, London (James 2006).
According to the lead investigator, Dr. Gerome Breen, "This study is the first large-scale search for a genetic variant influencing the risk of developing cocaine addiction or dependence...The target we investigated, DAT, is the single most important in the development of cocaine dependence" (James 2006). This research helps in the understanding of the development of cocaine addiction and could influence the design and use of drugs to treat cocaine addiction in the future (James 2006). Although repeated exposure to cocaine will lead to compulsive use in everyone, for some people the addiction to the drug will manifest more quickly because of a genetic difference (James 2006). Professor Homero Vallada, from the University of Sao Paulo Medical School, noted
It would be our hope that this is the first of many finding showing how genes, as well as environment, contribute to our risk for addiction...and may help predict pharmaceutical drug response to patients and how they might respond to different forms of psychological therapies"
Genetic and common environmental influences contribute to twin associations for substance use, yet twin concordance rates may vary by environmental setting, thus suggesting the presence of genetic-environmental interactions (Eaves 2005). Researchers explored socio-regional moderation of alcohol use in Finland and showed how extra-familial environmental influences can exert potent moderating effects on the expression of genetic and environmental influences on adolescent drinking patterns (Eaves 2005). Results suggest that genetic factors contributed to alcohol use to a greater extent in urban settings compared with rural settings, while common environmental factors assumed greater importance in rural settings (Eaves 2005). "Community level factors, including the proportion of young adults in the regional area, the frequency of migration in and out of a region and the relative amount of money spent on alcohol in an area, were found to moderate influences on alcohol use among drinking adolescents, rather than urban vs. rural residency" (Eaves 2005).
Although the importance of genetic influences on adult alcohol use has been well supported, adolescent samples have only recently been included in the research and highlight the importance of both environmental and genetic influences on teen substance use and abuse (Eaves 2005). According to Lindon Eaves, the next step in behavioral genetic research "is to examine the interplay between genetic and environmental factors (e.g., the modification of genetic risk factors by environmental risk and protective factors)" (Eaves 2005). Eaves writes in the July 01, 2005 issue of the Journal of Studies on Alcohol:
An adoption study by Riggins-Caspers et al. (2003), found zero-order correlations between biological risk as measured by biological parent psychopathology) and indicators of adolescent problem behaviors for the total sample were small to moderate and explained around 6% of the variance, leading to the conclusion that genetic influences on problem behavior were minimal.
Estimating these same correlations separately, however, for the low and moderate environmental risk groups, as measured by adverse factors present in adoptive parents e.g., psychopathology, divorce and legal problems), showed that biological risk explained almost 20% of the variance in adolescent problem behaviors for the moderate environmental risk group, compared with less than 1% for the low environmental risk group. This suggests that genetic influences on adolescent problem behavior played a larger role in the moderate environmental risk group, whereas genetic influences were negligible in the low-risk environment (Eaves 2005).
The same Israeli researchers who, in 1996, discovered a gene linked to impulsiveness and adventurousness, discovered a year later that the same gene slightly increases an individual's risk of becoming addicted to "hard" drugs (Siegel 1997). The researchers tested the blood of 141 men undergoing drug rehabilitation and compared their genetic make-up with those of 110 men with no history of drug abuse, and found that 29% of the addicts had one form of the gene, compared to only 12% in the non-addict group - thus the addicts were more than twice as likely than non-addicts to have the gene (Siegel 1997).
In 2001, Dr. Susan M. Gordon, director of research at the Caron Foundation, noted that heroin addiction is a bio-psycho-social disease, saying "On the biological front, a large body of clinical research points to a genetic vulnerability that some individuals have to drug abuse in general. This means a child can partially inherit a susceptibility to using heroin from a parent" (Heroin 2001). On the psychological level, research indicates that many heroin addicts also suffer from psychiatric disorders, including depression, anti-social personality disorder, and post-traumatic stress disorder (Heroin 2001). Gordon explains that once in the brain, heroin, much as other drugs of abuse, causes the release of dopamine, neurochemical that mediates pleasure and is critical to the normal functioning of the central nervous system. It is believed that heroin's addictive properties are related to a chronic and unnatural increase in dopamine levels (Heroin 2001). Gordon admits that heroin's characteristics and its interactions with the brain are complex, noting "Much still needs to be learned...But we do know addiction produces a variety of neurochemical and molecular changes in the brain that can have long-term negative effects" (Heroin 2001).
In April 2006, Yale School of Medicine researchers reported that they had identified a genetic linkage for dependence on drugs such as heroin, morphine and oxycontin (Large 2006). In a collaborative effort involving investigators at Yale, the University of Connecticut Health Center, McLean Hospital in Boston, the Medical University of South Carolina, and Boston University, and the National Institute on Drug Abuse, the study, based on date obtained from one of the largest family sets of its kind, was lead by Joel Gelernter, professor in the Department of Psychiatry, and included a sample of 393 small families, most with at least two individuals with opioid dependence (Large 2006). Researchers then searched genetic signposts throughout the entire genome in an effort to find markers (within the same family) that would demonstrate that individuals who share the illness also share marker alleles, or gene variants (Large 2006). This information allowed the researchers to identify the location of genes that influence opioid dependence. According to Gelernter, not only did the researchers find evidence of gene linkage for opioid dependence, they "also found strong evidence of linkage in the family groups for the symptom cluster traits characterized by dependence on substances other than opioids, specifically alcohol, cocaine and tobacco" (Large 2006). These findings provide the first basis to identify genes…[continue]
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