Addiction disorders are substance-related disorders. DSM-IV divides them into two groups: substance use disorders and substance-induced disorders. The former comprises substance dependence and substance abuse; the latter, a wide variety of pathologies clustered symptomatically around substance intoxication and withdrawal.
The biological basis of personality disorders is difficult to disentangle. With substance-related disorders on the other hand it is much easier to parse and psychological factors are less important. I will review substance abuse as an example. Substance abuse is defined at DSM-IV as “a maladaptive pattern of substance use leading to clinically significant impairment or distress.” It has a cognitive psychological component based upon the routinization of behavior (e.g. “reaching for a cigarette”). There also is a social psychological component based on environmental availability and affordances (e.g. social settings, conditioning based on family history of dependence). DSM-IV emphasizes lack of functionality in social contexts as an important diagnostic element for addiction disorders as opposed to subjective psychological distress. However by far and away a biological model is more explanatory. As one study observes a personality-based approach to substance abuse has led only to “confusing debates” about the nature of addiction as a biobehavioral disorder instead of a brain disease (LeMoal, 2009).
Heritability. Individuals with a family history (FH+) of substance abuse are more likely to develop a substance abuse disorder than those without such history (FH–). A recent fMRI study showed FH+ individuals had increased activation in the left dorsal anterior cingulated cortex and left caudate nucleus, a key brain decision-making system (Acheson et al., 2009). Twins v. adoption studies show a large extent of shared genetic vulnerability. Genomewide and candidate gene association studies amplify these findings and show common haplotypes in genes that make polygenic contributions to vulnerability to developing dependence (Uhl et al., 2009; Li & Burmeister, 2009).
Neurochemistry. Numerous studies establish the sensitivity of dopamine reward pathways is the most important biological factor for substance abuse. The substance induces a phasic dopamine release within the striatum that does not undergo habituation. Over time the natural function of the mesolimbic dopamine system is impaired as shown by a decrease in the availability of striatal dopamine 2 (D2) receptors (Fehr et al., 2008). DA pathways in the brain in turn connect structures such as the nucleus accumbens, the amygdala and the orbitofrontal cortex. They regulate the anticipation of forthcoming reward as well as the pleasure subsequently experienced from DA-activating behaviors. It follows that individual differences in reward sensitivity strongly affect propensity for substance abuse.
Brain defects or injury. Traumatic brain injury (TBI) dramatically increases risk for substance abuse. A recent study of military personnel suffering from TBI as a result of the war in Afghanistan and Iraq showed they were unusually vulnerable to addiction to opiate analgesics compared to other pain patients (Bjork & Grant, 2009).
Infections, prenatal damage, nutrition, toxins. In utero exposure to substances are common risk factors that have been associated with ADHD. Molecular studies also have shown an association between ADHD and DNA polymorphisms in dopamine pathway-related genes (Neuman et al., 2009).
In conclusion as is generally the case with apparent divergence between biological and psychological models an approach based on dual vulnerability to behavioral disorder and psychopathological comorbidities most likely best accounts for the data. One of the interesting issues in substance abuse studies is the direction of causal association – what causes what. The biological argument is that hypo-dopaminergic functioning (a “reward deficiency syndrome”) is the risk factor. The substance increases brain DA levels, boosts the DA system and increases hedonic capacity. The psychological argument on the other hand is that hypersensitivity to reward increases risk for addictive behavior because of enhanced motivation to approach potentially pleasurable activities. Heightened reward sensitivity thereby becomes associated with intake of the stimulus (Davis et al., 2007).
Acheson, A., Robinson, J., Glahn, D., Lovallo, W. & Fox, P. (2009). “Differential activation of the anterior cingulated cortex and caudate nucleus in persons with a family history of alcoholism during a gambling simulation.” Drug and Alcohol Dependency, 100(1-2), 17 – 23.
Bjork, J. & Grant, S. (2009). “Does traumatic brain injury increase risk for substance abuse?” J. Neurotrauma, Feb. 9 (Epub ahead of print).
Davis, C., Levitan, R., Kaplan, A., Carter, J., Reid, C., Curtis, C., Patte, K., Hwang, R. & Kennedy, J. (2007). “Reward sensitivity and the D2 dopamine receptor gene.” Progress in Neuro-Psychopharmacology and Biological Psychiatry, 32(3), 620 – 628.
Fehr, C. et al. (2008). “Association of Low Striatal Dopamine D2 Receptor Availability with Nicotine Dependence Similar to that Seen with Other Drugs of Abuse.” Am. J. Psychiatry, 165, 507 – 514.
LeMoal, M. (2009). “Drug Abuse: Vulnerability and Transition to Addiction.” Pharmacopsychiatry, 42(1), S42 – S55.
Li, M. & Burmeister, M. (2009). “New insights into the genetics of addiction.” Nature Reviews – Genetics, 10, 225 – 231.
Neuman, R., Lobos, E., Reich, W., Henderson, C., Sun, L. & Todd, R. (2009). “Prenatal Smoking Exposure and Dopaminergic Genotypes Interact to Cause a Severe ADHD Subtype.” Biological Psychiatry, 61(12), 1320 – 1328.
Uhl, G., Drgon, T., Johnson, C. & Qing-Rong, L. (2009). “Addiction Genetics and Pleiotropic Effects of Common Haplotypes that Make Polygenic Contributions to Vulnerability to Substance Dependence.” J. Neurogenetics, 1 – 11.