This has been shown in research done by Noble et Al in which a gene DRD2 responsible for the D2 dopamine receptor, to severe alcoholism. It was found that the A1 variant of this gene was present in more than two-thirds of deceased alcoholics. Although this research does not look at smoking behaviour, it suggests that this gene plays a role in the addictive behaviour and can also be generalised to smoking behaviour. There has also been additional evidence to support the biological model as an explanation for smoking addiction. Research has been done by Silverstein et al in which it was found that biological factors may influence a person’s first positive or negative experience with their first cigarette.
This drugs effects are similar to but more rapid than those of amphetamines. Additionally the effects of cocaine are short-lived, which may help explain why this drug is especially addictive both psychologically and physiologically. Dopamine transporters are responsible for removing dopamine molecules from the synaptic cleft after they have done their job. Cocaine blocks thee transporters, leaving dopamine trapped in the synaptic cleft. As a result, dopamine binds again and again to the receptors overstimulation the cell.
Neurotransmitters are known to have an impact on behaviour such as high levels of nor adrenaline and dopamine are seen when a depressed mood is evident e.g. schizophrenia has been associated with an excess of activity in the neurotransmitter dopamine. Whereas serotonin is thought to cause high anxiety levels when there is too much available. Neurotransmitters in the right balance do not cause ill effects but the biological approach suggests it is when there is an imbalance that behaviour and mental health is affected. E.g.
Anti depressants such as MAOI’s which increase the available amount of nor adrenaline in the brain, were found to be effective for elevating the symptoms of depression. So when noradrenalin is increased in the brain, symptoms of depression get better, suggests that it is chemicals that are the root cause of depression. This idea is also found in the results of taking reserpine, a drug used to treat high blood pressure. Depression is a unwanted side effect of this drug, as this drug acts by lowering levels of nor adrenaline. So again strongly suggests that low activity noradrenaline, is a factor contributing to the cause of depression.
First, he points that not all addictions are chemical substances and there are many activities that can be addictive to people. These activities do not alter the brain in such a way to be able to say the addiction has changed the brain so much it is diseased. In addition, the American Society of Addiction Medicine declared addiction to be a brain disease based on findings that addictions effect
This suggest that depression must be passed on through genes if there is a high concordance rate between twins which share the same genetic makeup both having depression. However, biological factors such as the amine hypothesis states that if amines such as serotonin and noradrenalin become unbalanced, they can lead to depression. PET scans support this idea as they show that low levels of serotonin are present in people that are depressed. Other supporting evidence is that drugs such as MAOI’s, which work by increasing the available amount of noradrenalin in the brain, were found to be effective in alleviating the symptoms of depression. A problem with this is that it doesn’t state whether it is cause or effect.
Date: march 21st,2012 The press releases make casual claims from data that is only correlation, for example, they make a claim that nicotine boosts levels of cortisol which is a stress hormone. The press also claims that increased level of cortisol can result into weird hallucinations. However, this is a complete misrepresentation of what the Durham University researchers found. The researches found that cortisol role is to translate the experience of the experience of psycho-social stressors to psychosis. The misconception is that caffeine directly leads to increase in stress levels because cortisol is involved.
Psych 213 Dr. Les White April 9, 2012 Major points the article covers or raises “The Addicted Brain,” by Nestler and Malenka discussed the brain’s memory of addiction which results from repeated use and subsequently abuse of drugs and alcohol. While very technical and scientific in its detailing of the processes, it was also very insightful in spelling out the brains rewarding of the pleasure that results from drugs of abuse (DOA). It seems that we have known for quite a while why someone feels good when they use DOA, but the article points out that new research is just beginning to understand some of the resulting long term changes in the brain. Even though the pleasurable effects of using a particular drug aren’t as strong as they
“Discuss one or more explanation of addiction (8+16)” The biological explanation state that addiction is caused by the A1 variant, people with A1 variant of DRD2 gene have less dopamine receptors on the pleasure centres of the brain. Therefore, they will want to compensate and take more of the drug to release more dopamine and seek pleasure. This shows that addicts have less dopamine receptors and to increase the levels they take drugs and become addicts because of the pleasure. However, a weakness of the biological explanation is individual differences; genetic explanations shows how people get addicted and not others in the same environment this is down to the pre disposition of the gene which makes them vulnerable this shows why some people resist to the treatment. Showing that addiction varies on people because it depends on how vulnerable they are to addiction and biological approaches are dependent on the gene.
Critical Point 3: There is a flaw with one of the key pieces of evidence to support the dopamine hypothesis. The drugs used to treat schizophrenia by blocking the dopamine receptors can actually increases it as neurons struggle to compensate for the sudden deficiency. Haracz, in a review of post-mortem studies of schizophrenics, found that most of those studied who showed elevated dopamine levels had received antipsychotic drugs shortly before death, unlike post-mortem of schizophrenics who hadn’t received medication these results showed that these individuals had normal levels of dopamine. Therefore, this evidence weakens the support for the dopamine