Genetic explanations Essay

Custom Student Mr. Teacher ENG 1001-04 14 June 2016

Genetic explanations

Genetic explanations for the Initiation of addictions

Heritability of addictions such as alcoholism and gambling can be studied through family and twin studies. The presumptions of twin and family studies are that if family members share similar behaviours, then the degree to which the behaviours are caused by genetic factors can be examined. There are two types of twins, identical and non-identical. Identical twins are monozygotic (MZ) as they came from the same egg, and therefore share an identical set of genes. Non-identical twins are dizygotic (DZ) as they come from two different eggs that were fertilised at the same time, and as a result their genes are no more alike than any brother or sister’s. Twins can also differ in the environment that they are brought up in. Some twins may, rarely, be separated at birth and therefore have very different upbringings. If researchers are able to find MZ twins who have been raised apart (i.e. same genes but different environments) then they will be able to distinguish between the influence of genes and environment on a certain behaviour.

If MZ twins who have been raised apart booth show the same behaviour, then the behaviour is probably genetic; but if only one of them has that behaviour then it may well be caused by the environment. The degree to which twins and family members share a behaviour is termed a concordance rate, with 1 (or 100%) being entirely 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 behaviour disorders rather than addiction, and these behaviour disorders may manifest as many antisocial behaviours including alcohol and drug use.

The sensitivity of the dopamine system is one biological explanation for the imitation, maintenance and relapse of addictive behaviours (see below), and so it would make sense for researchers to look for genes that are responsible for causing particularly sensitive or insensitive dopamine systems. One such gene is called 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 person with fewer dopamine receptors is unable 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 behaviour

Genetic inheritance may explains individual differences in addiction Genetic inheritance can, through the diathesis-stress model, explain why some people 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 circumstance – 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 linked to alcoholism (the gene was found to be carried by 48% of severe 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 far more complex than simply claiming that the gene causes addiction.

The dopamine model of addiction

Initiation of addictive behaviour:

Dopamine is released in the mesolimbic dopamine system of the brain, 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 an organism/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 rewarding substance or behaviour persists even in the absence of the substance or behaviour.

Maintenance of addictive behaviour:

Repeated exposure to an addictive behaviour or substance causes reduced 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 leads 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 addict’s behaviour.

Relapse of addictive behaviour:

When 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 location 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

Support for the dopamine model of addiction:

Support for the dopamine model comes from many experimental studies, such as a 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 factors:

An 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. replacing cigarettes with nicotine patches.

Implications from animal research:

Grant et al (1998) found that animals that lost social status 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 individual’s 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 reductionist:

Neurochemical explanations for addiction reduce addictive behaviour to a simple 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 useful to be reductionist.

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