One of the explanations of addiction is the biological approach; this is based on the idea that addiction is caused by genetics. In relation to alcoholism, there is a heritability of alcohol dependency between 50-60% in both men and women (McGue, 1999). There are also similar findings for drug addiction, with Agrawal and Lynskey (2006) suggesting a heritability of between 45-79% for drug abuse. A specific gene associated with addiction is the D2 receptor gene. Noble, Blum, Ritchie, Montgomery and Sheridan (1991) found A1 (a variant of the gene) in more than 2/3 of deceased people with alcoholism compared to 1/5 of people without alcoholism. This is also found with people who smoke; A1 was found in 49% of a group of smokers, whilst in only 26% of the general population (Comings et al., 1996). Those with fewer A1 receptors are also linked to having fewer dopamine receptors, suggesting that people with A1 are more likely to become addicted to drugs which increase dopamine levels.
This approach is supported with various research evidence, such as Noble (1998), who found A1 receptors in 48% of people with alcoholism, 32% of people with less severe alcoholism and in 16% of controls. There is also support shown for the link between D2 receptors and dopamine using Ritalin. Some of a group of volunteers given Ritalin (lifts dopamine levels) loved the way it made feel, whilst others hated it. It was found that those who liked it had fewer D2 receptors than those who hated it; in other words some people are vulnerable to the added rush given by dopamine enhancing drugs (Volkow et al., 2001).
This approach allows us to explain individual differences; why some people develop an addiction and others who experience the same environmental factors do not. Some people are more vulnerable to developing an addiction due to genetic predisposition, which also may explain why some people are more resistant to treatment and more likely to relapse.
However, the biological approach can be criticised for being reductionist, as it reduces complex behaviours down to a relatively simple explanation. Although, this can have advantages, it can also be problematic. The influence of neurotransmitters, such as dopamine, is clearly important, but by reducing the explanation to just genetics and chemicals, it ignores all other factors which can be equally influential, such as social context.
The biological approach is also guilty of extrapolation; it relies heavily on animal research. Research has shown that animals can get addicted to the same drugs as humans, but there are problems when trying to generalise these findings to humans. Hackam and Redelmeier (2006) stated that even high quality animal studies are rarely replicated in human research. However, Banks, Gould, Czoty and Nader (2008) used monkeys to show that cocaine could be substituted with a less addictive drug. Banks stated that the real value of the research was that it replicated findings that were already found in smaller studies using humans.
There is evidence that supports the idea that both genetics and environment are influential in developing an addiction. Grant et al. (1998) showed that dopamine systems can be affected by social interactions; low interactions results in a loss of D2 receptors. A relationship between genetics and the environment is also shown by Volkow, Fowler and Wang (2003), who found that people who grow up in stimulating surroundings are less likely to develop an addiction.
However, in general, there are problems with defining addiction. Griffiths and Larkin (2004) stated that it is important to acknowledge that the meanings of ‘addiction’ in both daily and academic use are contextual and socially constructed. If we argue that it is hypothetically possible to be addicted to anything, then it must be taken into account that many people become addicted to alcohol whilst very few become addicted to gardening.
Agrawal, A., & Lynskey, M. T. (2006). The genetic epidemiology of cannabis use, abuse and dependence. Addiction, 101, 801-812. doi: 10.1111/j.1360-0443.2006.01399.x.
Banks, M. L., Gould, R. W., Czoty, P. W., & Nader, M. A. (2008). Behavioural Pharmacology, 19(4), 365-369. doi: 10.1097/FBP.0b013e32830990b.
Comings, D. E., Ferry, L., Bradshaw-Robinson, S., Burchette, R., Chiu, C., & Muhleman, D. (1996). The dopamine D2 receptor (DRD2) gene: A genetic risk factor in smoking. Pharmacogenetics, 6, 73-79.
Grant, K. A., Shively, C. A., Nader, M. A., Ehrenkaufer, R. L., Line, S. W., Morton, T. E., Gate, H. D., & Mach, R. H. (1998). Effect of social status on striatal dopamine D2 receptor binding characteristics in cynomolgus monkeys assessed with positron emission tomography. Synapse, 29, 80 – 83.
Griffiths, M. D., & Larkin, M. (2004). Conceptualizing addiction: The case for a “complex systems” account. Addiction Research and Theory, 12(2), 99-102. doi: 10.1080/1606635042000193211.
Hackam, D. G., & Redelmeier, D. A. (2006). Translation of research evidence from animals to humans. The Journal of the American Medical Association, 296(14), 1731-1732. doi: 10.1001/jama.296.14.1731.
McGue, M. (1999). Behavioural genetic models of alcoholism and drinking. In: K. E. Leonard, H. T. Blane (Eds.), Psychological Theories of Drinking and Alcoholism (2nd ed.) (pp. 372-421). New York: Guilford Publications.
Noble, E. P. (1998). The D2 dopamine receptor gene: A review of association studies in alcoholism and phenotypes. Alcohol, 16(1), 33-45. doi: 10.1016/S0741-8329(97)00175-4.
Noble, E. P., Blum, K., Ritchie, T., Montgomery, A., & Sheridan, P. J. (1991). Allelic association of the D2 dopamine receptor gene with receptor-binding characteristics in alcoholism or geneism. Archives of General Psychiatry, 48(7), 648-654.
Volkow, N. D., Fowler, J. S., & Wang, G. (2003). The addicted human brain: insights from imaging studies. The Journal of Clinical Investigation, 111(10), 1444-1451. doi: 10.1172/JCI18533.
Volkow, N. D., Wang, G., Fowler, J. S., Logan, J., Gerasimov, M., Maynard, L., Ding, Y., Gatley, S. J., Gifford, A., & Francesch, D. (2001). Therapeutic doses of oral methylphenidate signiﬁcantly increase extracellular dopamine in the human brain. The Journal of Neuroscience, 21, 1-5.