The dopamine and opioid systems have been characterised as playing two different functions. The dopamine pathway is associated with the incentive, preparatory aspects of reward, which are experienced as thrill, urgency or craving. In contrast, the opioid system is associated with the satiation and consummatory aspects of reward, such as rest, blissfulness and sedation. (Di Chiara & North, 1992:)
There is evidence that the brain’s endogenous opioid system may play an important role in drug use and misuse. Opiates such as morphine, heroin and codeine act as opiate receptor agonists and readily cause tolerance and dependence. Adaption of opiate receptors occurs quite readily after chronic opiate use, as is seen in the need to use larger amounts to achieve pain relief or euphoria. This vicious circle can lead to addiction. Further, the opiate antagonist naloxone will quickly induce withdrawal symptoms if administered. (Koob 1992:)
Brain neurons containing the neurotransmitter dopamine are involved in emotional responses such as pleasure. The dopamine system connecting the ventral tegmental area and the basal forebrain appears to be critical to the self-administration of psychomotor stimulants (i.e., cocaine and amphetamine) (Koob 1992:).
Dopamine has been implicated in the reinforcing effects of alcohol and cocaine, with their use resulting in the direct stimulation of dopamine and also an indirect increase in dopamine levels (Altman et al., 1996:285). It is also thought that the behavioural rewards of nicotine, and perhaps basis of nicotine dependence, are also linked with the release of dopamine (Benowitz, 1998: Markou et al., 1998:).
Cannabis has been considered an “atypical drug”, in that it did not interact with the brains’ reward system. However, research has revealed that the active component of cannabis, delta-9-tetrahydrocannabinol (THC), produces enhancement of brain-stimulation reward in rats, at (proportional) doses within the range of human use (Gardner 1992:). Studies have also revealed cannabinoid receptors in areas associated with brain reward and that THC increases dopamine levels (Adams and Martin, 1996:) It is these reward systems that addicts have difficulty overcoming.
Subsequent tolerance to the effects of drugs and withdrawal when drug use stops are both the result of neuroadaption (Koob, Caine, Parsons, Markou, & Weiss, 1997:). Animal models have shown that stressful stimuli activate the dopamine reward system, so vulnerability to relapse from abstinence is hypothesised to occur. As a result, drug use continues in an attempt to avoid the symptoms that follow if drug use stops (Koob & Lemoal, 1997:52).
Addiction can be seen as disease. A bacterium infects some people but not all; there are differing degrees of relative immunity. An infectious disease is readily spread by those who catch it so is this comparable to addiction: is it primarily new users who transmit the behaviour to their peers? Or does the disease work on a much more intrinsic level?
Susceptibility depends typically on a complex set of genetic and environmental factors. The strong influence of environmental factors is nowhere more obvious than in nicotine addiction. Forty five years ago a large majority of young Americans began smoking as they entered adolescence, but today only a small minority (around one fifth) become smokers. Of all the people that smoked two thirds go on to quit (Goldstein 2001:102). Obviously genes have not changed in forty five years; the change must have been due to other factors such as education.
The Vietnam experience of some sheds some light on how social acceptance by some (e.g. peer pressure), coupled with easy availability, can influence drug use. Young men were taken from their families and home environment. They were placed in an environment that was alternately terrifying and boring, with cheap heroin readily available, many used the drug and became addicted; some short term and some long term. At the height of the epidemic some 15% of ground troops were using enough to have become dependent on it. Follow up studies showed that, after returning home, most gave up drugs (Goldstein 2001:102).
Family seems to play a big role in the tendencies of siblings to abuse drugs. These tendencies increase with parents’ drug use and attitudes towards drugs (Hawkins, Catalano & Miller 1992:112). The nature of the family relationships also has an affect on the likelihood of adolescents abusing drugs (70). Other factors that will also affect the likelihood of a person developing drug abuse are: socio-cultural background, those who have performed worse in education and those from areas of higher rates of crime (Institute of Medicine, 1996). But these social and environmental reasons go more way to explain the beginnings of drug use rather than the causes of addiction.
Can these social and environmental factors be seen as true causes of addiction or are they more like catalysts? What of those in the above examples that were unable to quit. Is there a predisposition in some that automatically makes them an addict? These issues will be further discussed below.
It seems impossible to look at the causes of addiction without mentioning genetics. Many a study have shown that genetic components have been found to play a part in dependence on many of the most commonly used licit and illicit substances, suggesting that some people are more vulnerable than others to developing drug use problems. Each individual possesses two alleles at each gene, one inherited from each parent. When different alleles of a gene are circulating in a population, the gene is said to be polymorphic, and these different alleles are represented as differences in the base sequence of the DNA coding for the gene product, a protein. So, the first level of genetic variation that can give rise to individual behavioural differences is due to DNA sequence differences. (Crabbe 2002:435)
There are those in the field that would go further to say that genetics is almost the sole cause of addictive behaviour. In a study done on genetic and environmental contributions to alcohol abuse and dependence in a population-based sample of male twins, it was found that genetic factors played a major role in the development of alcoholism. This study also concluded that environmental factors shared by family members appear to have had little influence on the development of alcoholism in males. (Prescott & Kendler1999:40)
There have been a number of approaches to explain addiction and each area of explanation has been supported by some empirical evidence. These different areas remain to be integrated into a more comprehensive model of addiction. Currently the biopsychosocial model of addiction (and causes of addictive behaviour) forms the basis of treatment (Marlatt & VandenBos, 1997) so one would assume that it is the most accepted. In comparison to the disease model it views addiction as a complicated behaviour pattern having sociological, biological, psychological and behavioural components. These include the experience of craving, short term satisfaction at the risk of long term damage, erratic change in psychological and physical states. Addictive behaviour is distinguished from other behaviours by the individual’s pathological, overwhelming involvement in drug use, the desire to continue use and lack of control. It is therefore hard to see it in terms of a habit.
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