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Biological Models of AddictionWeb link HYPERLINK "" Disease-Biochemical ModelBiochemistry of the Brain; Neurotransmitters(i) InitiationIn the centre of the brain sits the reward pathway, which is responsible for driving our feelings of motivation, reward and behaviour. Your memory tells you that a particular behaviour will make you feel good; the brain tells the body to initiate the behaviour. Special neurons in the reward pathway release the chemical dopamine (in the Ventral Tegmental Area VTA), which gives you a sense of pleasure (In the Nucleus Accumbens NA). In addition, the reward pathway is responsible for making sure you repeat the behaviour. It does this by connecting to regions of the brain that control memory and behaviour. This increases the likelihood that you will repeat the behaviour. When the reward pathway signals the brain’s motor centre, it strengthens the ‘wiring ‘for behaviours that help you achieve your reward. The Reward Pathway and associated areas of the Brain(ii) MaintenanceAddictive behaviours and addictive substances can induce change in the structure and function of the reward systems neurons that can be shown, using PET scans to last for weeks and months. These changes contribute to tolerance, dependence and craving. Most drugs (such as nicotine which is a psychoactive drug) and activities such as gambling release dopamine into the NA area, prompting incentive to continue and increase the behaviour. The Pre-frontal Cortex, PFC which normally controls decision-making and inhibits risky behaviours is often impaired in addicts, allowing them to choose immediate rewards even in the face of long term negative consequences. Continued over-production of dopamine leads to desensitisation in receptors to compensate. This is known as ‘down-regulation’ and leads to increased desire to engage in the addictive behaviour to return to the same level of ‘dopamine high’ i.e. the subject is becoming tolerant. The addict then engages in the addictive behaviour to avoid withdrawal symptoms and the amount of Dopamine/ drug required to feel pleasure increases Koob & Kreek (2007). (iii) RelapseThe reward pathways also link to other areas of the brain including the memory areas and help make addicts highly sensitive to reminders of past highs, vulnerable to relapse when stressed and unable to control the urge to repeat the addictive behaviour.EvaluationVolkow (2001) gave pps Ritalin, which increases Dopamine levels. A brain scan showed that the pps who enjoyed the Ritalin had less D2 receptors. He concluded that this type of person was vulnerable to Dopamine-enhancing drugs or behaviours. The other pps, who hated it, were thought to have a Dopamine circuitry that was over stimulated.Grant (1998) recorded that monkeys who lost social status also lost D2 receptors. Implied is that humans who have live in poverty & stress are more vulnerable to addiction.Volkow (2003) people who grow up in stimulating environments with healthy social interactions are protected from addiction. They get a natural boost from their everyday lives.2. GeneticsWhen scientists look for "addiction genes," what they are looking for biological differences that may make someone more or less vulnerable to addiction. It may be harder for people with certain genes to stop behaviour once it starts. Or they may experience more severe withdrawal symptoms. Factors that make it harder to become addicted also may be genetic. For example, an individual may feel sick from a drug that makes other people feel good. But someone's genetic make-up will never lead them inevitably to become an addict. Environment makes up a large part of the addiction risk.Scientists will never find just one single addiction gene. Susceptibility to addiction is the result of many interacting genes. Social and environmental factors contribute to this risk of addiction. Like other behavioural diseases, addiction vulnerability is a very complex trait. "Just because you are prone to addiction doesn't mean you're going to become addicted. It just means you've got to be careful." Researchers construct pedigrees of large families with addiction as a first step to understanding the disease. A pedigree can reveal whether or not a trait has a genetic component. That is, whether or not it is passed down from parent to child by way of genes. Using pedigree data, researchers can hunt down genes. They begin by comparing DNA sequences of individuals who have the addictive behaviour with those who do not. They can then narrow down the possibilities to identify a small number of so-called "candidate genes" for addiction.19050176530Twin Studies A US study by K Kendler (2003) found that concordance rates -both twins using, abusing, or being dependent on drugs- were higher for identical than fraternal twins (see chart). For cocaine use, concordance was 54 percent in identical twins and 42 percent in fraternal twins; for abuse, 47 percent in identical twins and 8 percent in fraternal twins; and for dependence, 35 percent in identical twins and zero for fraternal twins.McGue (1992) Minnesota Twin Family Study also found a higher concordance rate of alcohol abuse in MZ twins (77%) compared to DZ twins (54%) suggesting a genetic link to addictive behaviours. Most genes wouldn't have been discovered without the use of animal models, especially mice.The reward pathway functions in much the same way in mice as it does in people. When researchers discover a gene in mice that plays a role in addiction, they can then identify the counterpart gene in humans by comparing DNA sequences eg mice bred without the serotonin receptor gene Htr1b are more attracted to Cocaine and alcohol. Mice with low levels of Neuropeptide Y, drink more alcohol, whereas those with higher levels tend to abstainThe A1 allele of the Dopamine receptor gene DRD2 is more common in people addicted to alcohol or Cocaine.Noble et al (1991) found there was an A1 variant allele on the DRD2 gene in more than 2/3 of deceased alcoholics, whereas only 1/5 of deceased non-alcoholics. People who inherit the A1 variant appeared to have fewer Dopamine receptors in the pleasure centre of the brain, hence Noble et al referred to the DRD2 gene as the ‘reward gene’. Other research failed to find a link between alcoholism and the DRD2 gene or only found a weak positive correlation.Blum et al (1991) found children of alcoholics had an increased chance of showing the A1 variant. Caine et al (2007) found that mice engineered without the D1 receptor for Dopamine do not self administer Cocaine when given a chance to do so. Normal mice in comparison will keep returning for more as they find it highly addictive just as humans do. Comings et al. (1996). 222 non-Hispanic Caucasian pathological gamblers in the US participated in the study. The results suggested that genetic variants at the DRD2 gene play a role in pathological gambling, and support the concept that variants of this gene are a risk factor for impulsive and addictive ings, et al (1996) 48.7% of a group of 312 non-Hispanic Caucasians who smoked at least one pack per day, had unsuccessfully attempted to stop smoking, and were free of alcohol or other drug dependence, carried the A1 allele of the DRD2 gene. This was significantly greater than the 25.9% prevalence in 714 non-Hispanic Caucasian controls. The results suggest the DRD2 gene is one of a multifactorial set of risk factors associated with smoking. ?Comings also found a link between the A1 variant and disorders such as Tourette’s and Autism. It is difficult therefore to accept Noble’s DRD2 label of ‘reward gene’ when these disorders are not especially linked with pleasure seeking.Initiation, Maintenance & RelapseIndividual differences in behaviour, when faced with smoking or gambling opportunities, are readily explained by genetic predisposition or vulnerability. In order for the predisposition to be triggered, there is usually a stressor. This is known as the ‘Diathesis-Stress Model’. Evaluation Reductionist: As with all attempts to explain human behaviour in biological terms, social factors etc, tend to overlooked or ignored. In other words, explaining addiction by reference to brain structure and function implies that once these have been identified addiction has been fully explained but the same brain activity can be triggered when addicts are not directly involved in their addictive behaviour. This suggests that psychological factors such as conditioned responses and cognitive processes are also involved. Nature;These theories cannot explain why addiction is only present in some MZ twins (predisposition), despite being in the same environment. Neurochemical explanations neglect nurture factors like social situations and social context. eg. Drug taking in Vietnam was high, but most soldiers stopped when back in their US home environment. DRD2 has been linked to alcoholics in 42 % of cases but why not 100%? Explanations should therefore be both nature and nurture. Susceptibility to addiction is the result of many interacting genes. Social and environmental factors contribute to this risk of addiction. (Diathesis –Stress Model). Psychology as a science and methodological problems: Overall, the biological approach has substantial empirical support. There is considerable evidence to support the role of various brain structures and pathways in addictive behaviour. Generally, it uses a very scientific in approach for example; laboratory experiments are mainly used so cause and effect, can be determined. But some of the studies have used post mortem studies of human addicts so causality cannot be certain (real time neural activity cannot be measured and it is not known which way around the cause and effect relationship are, did the drug addiction cause brain abnormalities or brain abnormalities cause drug addiction? ). PET scans are much more scientific and most research now uses scans. Only drug addicts can be used as pps to study drug addiction as it is unethical to give drugs to others, hence there is bias in the choice of participants.Animal studies are also used extensively but are subject to all the usual ethical issues as well as difficulties in interpreting the behaviour of animals that cannot tell you what they are feeling. Moreover, are animals absolutely comparable to humans; some drugs have very different effects on different animals, e.g. Guinea Pigs are allergic to Penicillin and cats are hyper active on Morphine? Most of the research on addiction genes have used family studies and correlated the concordance rates between relatives. This type of research is not scientific. It does not show cause and effect and is non experimental. Genes and environmental influences cannot be separated plus there are many confounding variables. Neurotransmitters have complex effects and these are not fully understood ................
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