Molecular geneticists are engaged in social work, if we are to believe the Nobel Laureate, James Watson, who is reported to have said: “There is only one science, physics: everything else is social work”.[i]
Of course the sophistication and beauty of molecular genetics research reveals the absurdity of extreme reductionism. The molecular level of analysis of human life is every bit as ‘real’ as a quantum atomic level of analysis. But so are the cellular, psychological and social levels of analysis.
Each of these is just a different ‘take’ on the phenomenon of human life and the scientific virtue of all research is determined not by how ‘low’ a level of analysis a researcher focuses on, but rather the rigour of the methodology, the predictive value of the theory and the replicability of the findings.
By these criteria, social and psychological analyses of disorders of the human mind/brain are every bit as scientifically ‘real’ as a cellular or molecular approach. In fact, when it comes to translational efficacy in developing new models and treatments for disorders of the mind/brain, molecular-cellular approaches have largely failed. Here is what Tom Insel, the director of the US National Institute of Mental Health said in December 2011:
“..there are few validated new molecular targets (like the dopamine receptor) for mental disorders. Moreover, new compounds have been more likely to fail in psychiatry compared to other areas of medicine. Studying the brain and the mind has proven to be much more difficult than the liver and the heart. Most experts feel the science of mental disorders lags behind other areas of medicine. The absence of biomarkers, the lack of valid diagnostic categories, and our limited understanding of the biology of these illnesses make targeted medication development especially difficult for mental disorders.”[ii]
In contrast to this pessimistic finding, very strong social and psychological ‘targets’ – and in some cases associated effective treatments – have emerged across a whole raft of mind/brain disorders.
Here are just a very small number of examples from a pool of hundreds:
- Low socio-economic an immigrant status increases the risk of schizophrenia four fold and this cannot be explained away by ‘drift’ of genetically vulnerable people two lower socio-economic strata. [iii]
- The greatest obstacle to daily life functioning in chronic schizophrenia is impaired cognitive function; the only known effective treatment for this is purely behavioural cognitive remediation training.[iv]
- Low levels of education increase your risk of Alzheimer’s Disease by between 200 and 300% [v]. This cannot be attributed to genetic factors causing both the disease and the educational attainment.[vi]
- Rich social networks eliminate the relationship between Alzheimer’s Disease-related brain pathology on the one hand, and symptoms of the disease on the other.[vii]
- Even in a single-gene disorder such as Huntingdon’s Disease, research on infant mice destined to develop the disease shows enormous effect of environmental enrichment on delaying the emergence of the symptoms, presumably through influencing gene expression.[viii]
Am I saying that we should dispense with all this enormously expensive molecular and cellular research and focus on the social and psychological level of analysis in understanding and treating mind/brain disorders?
No, I am not, though the expenditure is so grossly imbalanced worldwide that we certainly need a significant rebalancing. Furthermore, these are all multi-level disorders and if we are going to find cures, we need multi-level solutions. We will never be able to find an effective treatment for Alzheimer’s Disease, for instance, unless molecular, cellular, brain systems, psychological and social scientists collaborate together on this problem with the mutual respect that can often be absent in many centres.
But there is a solution to this problem: This is for researchers at each level of analysis to try to build links with other levels – psychological with molecular, cellular with systems, social with cellular and so on. We need high scientific rigour at all levels and a mutual respect between every level. Above all, we need to get rid of reductionist delusions that make us believe that ultimately we will explain human behavior in purely molecular or quantum terms. That is a recipe for yet more failure in developing new targets and new treatments for terribly disabling and hitherto uncurable disorders. @ihrobertson
[i] Quoted by Steven Rose in his book Lifelines: Biology Beyond Determinism
[ii] NIMH Director’s Blog Dec 14th 2011; http://www.nimh.nih.gov/about/director/2011/treatment-development...
[iii] Cooper B (2005) Immigration and schizophrenia: the social causation hypothesis revisited. British Journal of Psychiatry 186: 361-363
[iv] Wykes, T., Huddy V, C. Cellard, S. McGurk and P. Czobor (2011). "A Meta-Analysis of Cognitive Remediation for Schizophrenia: Methodology and Effect Sizes." American Journal of Psychiatry 168: 472-485
[v] Stern Y, Gurland B, Tatemichi TK, Tang M, Wilder D and M. R. (1994). "Influence of Education and Occupation on the Incidence of Alzheimer's Disease. ." Journal of the American Medical Association 27: 1004-1010.
[vi] Gatz, M., J. A. Mortimer, L. Fratiglioni, B. Johansson, S. Berg, R. Andel, M. Crowe, A. Fiske, C. A. Reynolds and N. L. Pedersen (2007). "Accounting for the relationship between low education and dementia: A twin study." Physiology & Behavior 92(1-2): 232-237.
[vii] Bennett, D. A., J. A. Schneider, Y. Tang, S. E. Arnold and R. S. Wilson (2006). "The effect of social networks on the relation between Alzheimer's disease pathology and level of cognitive function in old people: a longitudinal cohort study." The Lancet Neurology 5(5): 406-412.
[viii] vanDellen, A., C. Blakemore, R. Deacon and e. al. (2000). "Delaying the onset of Huntington's in mice." Nature 404: 721-722.