In my last post, I discussed the etiology of addiction through a very biological lens. In this post, I intend on maintaining a similar focus; however, instead of demonstrating how biology effects behavior, my goal is now to demonstrate how ones environment can affect ones biology, which can then, in turn, effect one’s behavior. So without further ado, I will present the findings of Hsu and colleagues (2003). In this study, the researchers were interested in how repeated early life stress would influence the expression of different GABA receptor subunits later on down the road. The GABAergic system is important in the discussion of addiction because it influences the efficacy of one’s stress response and plays a dominating role in the pharmacology of many extremely addictive substances such as alcohol, heroine, morphine, and most other forms of painkillers (Paulsen and Moser, 1998).
With regards to Hsu’s study, the researchers decided to separate groups of rats based upon the experimental manipulation of stress vs. no stress. Separating the infant pup from the mother and handling it vigorously for 30 minutes induced the “stressor” condition. The researchers found that this manipulation led to long-term statistical differences in the types of GABA receptor subunits being expressed. Hsu specifically describes the GABA receptors of the stress condition as being of an “immature phenotype,” suggesting and altered response to stress throughout the entirety of their lifespan.
I understand that the salience of this article with respect to humans and addiction may seem nebulous, but fear not! I have found another article incorporating humans that may help put this altered GABA concept into perspective. In this study by Enoch and colleagues (2010), the researchers where interested in measuring correlational interactions between GABRA2 genotype and childhood trauma as predictors of eventual addiction. As outlined in their study, everyone has a segment of genes and codes for the expression of GABA receptors subtypes. Different possible allelic combinations within this gene have been identified, which contribute to subtle differences in the proportional appearances of these different GABA receptor subtypes. These researchers discovered a statistical “interaction” between the two variables, suggesting that a certain GABRA2 genotype, when combined with an unhealthy dose of childhood stress will lead to an especially high chance of developing an addiction.
While is not a simple pathology, these studies suggest both strongly implicate the GABAergic system DNA strands in the biological etiology of addiction—these studies both show that genes can predict the onset of a pathology; however, environmental effects such as repeated stress can act as an intermediary modulator between genes and behavior. This provides support for what is known as the “diathesis-stress” model of psychology (Grant and Potenza, 2010), which asserts that in the interaction between diathesis (biological vulnerability) and stress (life stressors, traumatic events) serves as the best predictor of pathology’s eventual onset.
Enoch, M.A., Hodgkinson, C.A., Yuan, Q., Shen, P.H., Goldman, D., and Roy, A. (2010). The influence of GABRA2, childhood trauma, and their interaction on alcohol, heroin, and cocaine dependence. Biological Psychiatry, 67, 20-27.
Grant, J.E. and Potenza, M.N. (2010). Drug use disorders among young adults: Evaluation and treatment. Young Adult Mental Health, 10, 448.
Hsu, F.C., Zhang, G.J., Raol, Y.S., Valentino, R.J., Coulter, D.A., and Brooks-Kayal, A.R. (2003). Repeated neonatal handling with maternal separation permanently alters hippocampal GABAA receptors and behavioral stress responses. Developental biology, 100, 12213-12218.
Paulsen, O and Moser EI. (1998). A model of hippocampal memory encoding and retrieval: GABAergic control of synaptic plasticity. Trends Neuroscience, 21, 273-278.
2 thoughts on “The Stress Diathesis Model of Addiction”
Maybe environment doesn’t necessarily have to be the stress in the diathesis-STRESS model… biological diatheses that encounter positive environments or even neutral ones are less vulnerable to developing the disorder. It’s reassuring to think that even if we are biologically at risk (not quite doomed!) from the womb, the environment and people around us can potentially help us avoid the stressful triggers.
I am a huge fan of the diathesis stress model (mainly for schizophrenia, but i can see the applicability of this model to be used very broadly). I think it makes sense that you might have an initial predisposition that makes the individual vulnerable to a later stressor. I also agree with Hannah, in that it may not have to be negative, per se, but could just react to create a negative outcome.