Friday, May 17, 2019

Genetic explanations Essay

transmitted explanations for the Initiation of dependencesHeritability of habituations such as alcoholism and gambling merchant ship be studied through family and geminate studies. The presumptions of twin and family studies argon that if family members share similar doingss, then the degree to which the conducts are caused by hereditary factors grass be examined. There are two types of twins, identical and non-identical. Identical twins are monozygotic (MZ) as they came from the equal egg, and therefore share an identical set of genes. Non-identical twins are dizygotic (DZ) as they uprise from two dissentent eggs that were fertilised at the same time, and as a result their genes are no more alike than any brother or sisters. Twins nates also differ in the surround that they are brought up in. Some twins may, rarely, be separated at give up and therefore realize very different upbringings. If researchers are able to find MZ twins who have been raised apart (i.e. same gen es but different environments) then they will be able to distinguish in the midst of the influence of genes and environment on a certain demeanour.If MZ twins who have been raised apart stand show the same deportment, then the doings is probably inherited but if only one of them has that conduct then it may well be caused by the environment. The degree to which twins and family members share a doings is termed a concordance rate, with 1 (or 100%) being altogether genetic, and 0 (or 0%) being entirely environmental. McGue (1999) found a concordance rate of 50-60% for alcohol addiction, and Agrawal & Lynskey (2006) found a concordance rate of 45-79% for addiction to illicit drugs. This means that just over half of the factors that cause addiction to alcohol are genetic in origin, as are half to three-quarters of the factors causing addiction to illegal drugs. A problem with this conclusion, however, is that the genetic link may be for conduct disorders rather than addiction, and these behaviour disorders may manifest as umteen antisocial behaviours including alcohol and drug use.The predisposition of the dopamine system is one biological explanation for the imitation, alimentation and relapse of habit-forming behaviours (see below), and so it would make sense for researchers to look for genes that are responsible for causing in particular sensitive or insensitive dopamine systems. One such gene is c everyed the DRD2 gene (or dopamine receptor density 2 gene). The DRD2 gene codes for the number of dopamine receptors available in the mesolimbic dopamine system.A somebody with fewer dopamine receptors isunable to feel the effect of dopamine as well as someone with a higher number of dopamine receptors, and so needs higher levels of dopamine to produce the same effect as a person with more dopamine receptors. People with the DRD2 A1 variant of the gene have fewer dopamine receptors, and also seem more vulnerable to addictions. Evaluation for genetic explanations of addictive behaviourGenetic inheritance may let offs exclusive differences in addiction Genetic inheritance can, through the diathesis- vehemence model, explain why some multitude become addicted whereas others in the same environmental situation do not. The diathesis-stress model is the idea that a genetic vulnerability may manifest in the right precondition e.g. if a person who is susceptible to becoming addicted, due to their genetic inheritance, is suffering from some form of stress or boredom due to environmental factors, then they may partake in an addictive activity. however this is a very deterministic view of human behaviour that ignores environmental factors, as not all people with the A1 variant of the DDR2 gene become addicted even if they partake in a potentially addictive activity.Inconsistent research findings linking specific genes to addictions Noble (1998) found support for the DRD2 A1 gene being associate to alcoholism (the gene was found to be carried by 48% of pixilated alcoholics, 32% of less severe alcoholics, and 16% of non-alcoholic controls), but many other studies have failed to find such a link. Specific genes are linked to other disorders as well as addiction The DDR2 A1 gene is also common in people with autism and Tourettes, as well as in people with addictions. Autism and Tourettes sufferers are not pleasure seekers and do not tend to suffer from addictions, and so the link between the A1 variant of the DDR2 gene and addictions is unclear and faraway more complex than simply claiming that the gene causes addiction.The dopamine model of addictionInitiation of addictive behaviourDopamine is poked in the mesolimbic dopamine system of the head teacher, to signal reward and pleasure. If a behaviour causes dopamine release then the brain knows to do it again e.g. eating, drinking, keeping warm, having sex these are adaptive behaviours in evolutionary terms as they help anorganism/species to survive in its environment. Unfortunately other non-adaptive behaviours (i.e. behaviours that do not necessarily aid survival) can release huge amounts of dopamine (e.g. gambling and drug taking). Certain chemicals (e.g. amphetamines, alcohol, cocaine) can directly cause huge amounts of dopamine to be released. The effect of this dopamine release is to tell the brain that the behaviour is desirable and that it should seek to DO IT AGAIN And according to incentive sensitisation theory, desire for the honor substance or behaviour persists even in the absence of the substance or behaviour.Maintenance of addictive behaviourRepeated exposure to an addictive behaviour or substance causes trim back sensitivity to the dopamine release through a process known as down regulation. This means that more of the behaviour is needed to cause the same pleasurable psychological effect in the mesolimbic dopamine system. Stopping the behaviour altogether creates a state of disequilibrium in the dopamine system, and deals to withdrawal symptoms that can only be reduced by repeating the (now learned) behaviour. This disequilibrium, an increased need for dopamine stimulation, and the unpleasant withdrawal symptoms it causes now drive behaviour so that it is no longer pleasure (positive reinforcement), but the need to reduce withdrawal symptoms (negative reinforcement) that drives the addicts behaviour.Relapse of addictive behaviourWhen an addict finally manages to stop engaging in a behaviour or taking a substance, they are at risk of relapse. According to the dopamine model, relapse can be explained by addiction causing permanent brain changes that lead to lasting memories of the substance or behaviour. Environmental reminders of the addiction (e.g. being in a pub, watching horse racing, returning to a mending where drugs were taken, being under stress) can release small amounts of dopamine, which in turn lead to the addicted person desiring a greater dopamine reward that can only be obtained by re-engaging in the addictive behaviour Evaluation for the dopamine model of addiction certify for the dopamine model of addictionSupport for the dopamine model comes from many experimental studies, such asa study into the effects of ritaline (Volkow, 2001). Volkow gave a drug called ritalin to healthy volunteers and correlate their subjective experience of the drug with the density of dopamine receptors in their mesolimbic dopamine systems. Those that reported pleasurable feelings with ritalin had fewer dopamine receptors than those that hated its effects. This supports the theory that some people are more vulnerable to the effect of dopamine-releasing drugs than others.Neurochemical explanations ignore social factorsAn important point to note is that neurochemical explanations for addiction (e.g. the dopamine model) ignore social and environmental factors that may also contribute to addictive behaviour. However, they can lead to effective treatments for addictions, e.g. replacin g cigarettes with nicotine patches.Implications from animal researchGrant et al (1998) found that animals that lost social location also lost dopamine receptors, and offers therefore a possible explanation for social-class based addictions (e.g smoking in lower socio-economic groups). However, animal studies may not be generalisable to human addictive behaviour. Inevitability of dopamine sensitivity leading to addiction The dopamine model suggests that reduced dopamine sensitivity, as caused by fewer dopamine receptors, inevitably leads to addictive behaviour. However, there is likely to be a complex interaction between an individuals specific environment and whether or not dopamine sensitivity leads to addiction. A stimulating environment may provide enough dopamine reward to protect people from addiction, whereas a dull or boring environment may not (Volkow, 2003).Neurochemical explanations are reductionistNeurochemical explanations for addiction reduce addictive behaviour to a s imple variance in the structure of the dopamine system, and so ignore social and cognitive factors that can influence addictions. However they can lead to effective treatments, so in this case it is utilitarian to be reductionist.

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