Tag Archives: depression

50 whys to look for genes: 31. Root causes

Human behaviors, diseases, and treatments obviously all involved actions taken in a social context, but, given that everyone is made up of cells and all of one’s cells operate under instructions from one’s inherited and more or less unchanging genome, looking for genes is a way to look for root causes—causes on which to build our understanding and any corresponding interventions. Continue reading

50 whys to look for genes: 29. Mental illness–Interaction of “genetic risk” with many environmental factors for behavioral traits

Kendler and colleagues examine behavioral traits in relation to a wealth of environmental factors over the life course as well as to the relatedness of the individuals (Kendler and Prescott 2006). In Kendler et al. (2002), for example, data on over 1,900 twins are used to fit the incidence of major depression to an additive model that incorporates many environmental factors and a “genetic risk” factor. This last factor is derived from the incidence of major depression in the co-twin and parents, with adjustments made for the degree of relatedness of the twins (monozygotic versus dizygotic). The model accounts for 52% of the variance in the trait and provides a picture of development that is rich and plausible (see figure below).

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Life course epidemiology

Idea: How do we identify and disentangle the biological and social factors that build on each other over the life course from gestation through to old age?

The references below mostly relate to “life course epidemiology,” that is, fetal and developmental origins of diseases in late life (Barker being generalized by Ben-Shlomo), in some tension with development over the life course (incl. Berney reviewing lifetime accumulation of hazards in relation to health in old age). In contrast to this approach, we have Brown on life course influences on depression (not necessarily in old age).  A pertinent question: In what ways could either side usefully draw methods, data, results from the other?

(This post continues a series laying out a sequence of basic ideas in thinking like epidemiologists, especially epidemiologists who pay attention to possible social influences on the development and unequal distribution of diseases and behaviors in populations [see first post in series and contribute to open-source curriculum http://bit.ly/EpiContribute].)


Barker, D. J. P. (1998). Mothers, Babies, and Health in Later Life. Edinburgh, Churchill Livingstone.
Ben-Shlomo, Y. and D. Kuh (2002). “A life course approach to chronic disease epidemiology: Conceptual models, empirical challenges and interdisciplinary perspectives.” International Journal of Epidemiology 31: 285-293.
Berney, L., D. Blane, et al. (2000). Life course influences on health in old age. Understanding health inequalities. H. Graham. Buckingham [England], Open University Press: 79-95.
Brown, G. W. and T. O. Harris (1978). Sociology and the aetiology of depression; Depression and Loss; A Model of Depression; Summary and conclusions. Social Origins of Depression: a Study of Psychiatric Disorder in Women. New York, Free Press: 3-20; 233-293.
Davey-Smith, G. (2007). “Life-course approaches to inequalities in adult chronic disease risk.” Proceedings of the Nutrition Society 66: 216-236.
Krieger, N., J. T. Chen, et al. (2005b). “Lifetime socioeconomic position and twins’ health: An analysis of 308 pairs of United States women twins.” PLoS Med 2(7): e162.
Kuh, D., Y. Ben-Shlomo, et al. (2003). “Life course epidemiology.” Journal of Epidemiology and Community Health 57: 778-783.
Lynch, J. and G. Davey-Smith (2005). “A Life Course Approach to Chronic Disease Epidemiology.” Annual Review of Public Health 26: 1-35.

Heterogeneous construction, a variant of intersecting processes

Heterogeneous construction is a variant of the idea of intersecting processes, which, in turn, is an attempt to discipline without suppressing the unruliness of complexity.  The concept of heterogeneous construction can be illustrated by reference to the previous post on the Brown and Harris/Bowlby account of class, family, and psychology combining to explain the onset of serious depression.

As stated in the previous post, the factors are not separate contributing causes, like spokes on a wheel, but take their place in the multistranded life course of the individual [i.e., in the intersecting processes].  Each line should be interpreted as one contributing causal link in the construction of the behavior. The lines are dashed, however, to moderate any determinism implied in presenting a smoothed out or averaged schema; the links, while common, do not apply to all women at all times, and are contingent on background conditions not shown in the diagram.

For example, in a society in which women are expected to be the primary caregivers for children (a background condition), the loss of a mother increases the chances of, or is linked to, the child’s lacking consistent, reliable support for at least some period. Given the dominance of men over women and the social ideal of a heterosexual nuclear family, an adolescent girl in a disrupted family or custodial institution would be likely to see a marriage or partnership with a man as a positive alternative, even though early marriages tend to break up more easily. In a society of restricted class mobility, working-class origins tend to lead to working-class adulthood, in which living conditions are more difficult, especially if a woman has children to look after and provide for on her own. In many such ways these family, class, and psychological strands of the woman’s life build on each other. Let us also note that, as an unavoidable side effect, the pathways to an individual’s depression intersect with and influence other phenomena, such as the state’s changing role in providing welfare and custodial institutions, and these other phenomena continue even after the end point, namely, depression, has been arrived at.

Suppose now, quite hypothetically, that certain genes, expressed in the body’s chemistry, increase a child’s susceptibility to anxiousness in attachment compared to other children, even those within the same family.  Suppose also that this inborn biochemistry, or the subsequent biochemical changes corresponding to the anxiety, rendered the child more susceptible to the biochemical shifts that are associated with depression.  It is conceivable that early genetic or biochemical diagnosis followed by lifelong treatment with prophylactic antidepressants could reduce the chances of onset of severe depression. This might be true without any other action to ameliorate the effects of loss of mother, working-class living conditions, and so on.  There are, however, many other readily conceivable engagements to reduce the chances of onset of depression, for example, counseling adolescent girls with low self-esteem, quickly acting to ensure a reliable caregiver when a mother dies or is hospitalized, making custodial institutions or foster care arrangements more humane, increasing the availability of contraceptives for adolescents, increasing state support for single mothers, and so on.  If the goal is reduction in depression for working-class women, the unchangeability of the hypothetical inherited genes says nothing about the most effective, economical, or otherwise socially desirable engagement—or combinations of engagements—to pursue.  Notice also that many of these engagements have their downstream effect on depression via pathways that cross between the different strands.  For example, if self-esteem counseling were somewhat effective then fewer unwanted pregnancies and unsupportive partnerships might be initiated; both effects could, in turn, reduce the incidence of single parenthood and difficult living conditions.

These sequences of multiple causes, building on each other over the individual’s life history, permit a number of conclusions about the nature-nurture debate:

1.  Neither the unchangeability of genes nor the reliability of some gene- or biochemistry-based intervention, such as the hypothetical prophylactic antidepressants, would prove that the genes are the most significant cause of the acute depression that has been occurring in the absence of such treatment.

2.  Critics of genetic explanations could dismiss the attribution of an individual’s behavior to genes (or 50% or 80% to genes) as a technically meaningless partitioning of causes without placing themselves at the other pole from genetic determination.[i] That is, they would not have to make the counterclaim that the environment determines behavior or that, if the right environment were found, any desired behavior could be elicited. The Brown-Harris-Bowlby (BHB) account addresses malleability or immalleability of behavioral outcomes without ruling out genetic contributions.

3.  Similarly, critics would not need to rest their case on demonstrations that behavioral genetics has been or still is methodologically flawed (Lewontin et al. 1984), on textual deconstructions of the categories and rhetoric employed (Lewontin 1979), or on attributions of political bias to the supporters of behavioral geneticists. These are all interesting, but, in light of the BHB account of the behavior, not necessary for a conceptual critique of genetic determinism.

Over and above these conclusions, the BHB account of the origins of acute depression in working-class women also displays the following features that I associate with the idea that something is “heterogeneously constructed,” or an outcome of “intersecting processes.”

a) Without any superintending constructor or outcome-directed agent,

b) many heterogeneous components are linked together, which implies that

c) the outcome has multiple contributing causes, and thus

d) there are multiple points of intervention or engagement that could modify the course of development. In short,

e) causality and agency are distributed, not localized. Moreover,

f) construction is a process, that is, the components are linked over time,

g) building on what has already been constructed, so that

h) it is not the components, but the components in linkage that constitute the causes. Points c) and f–h) together ensure that

i) it is difficult to partition relative importance or responsibility for an outcome among the different types of cause (e.g., 80% genetic vs. 20% environmental). Generally,

j) there are alternative routes to the same end, and

k) construction is “polypotent” (Sclove 1995), that is, things involved in one construction process are implicated in many others. Engaging in a construction process, even in very focused interventions, will have side effects. Finally, points f) and k) mean that

l) construction never stops; completed outcomes are less end points than snapshots taken of ongoing, intersecting processes.

I am aware that there may be objections to the case I have chosen to make the preceeding points.  In discussing depression among working class women, rather than in other groups, I could be seen as perpetuating a male, professional class perspective.  However, the politics of the case can be viewed quite differently.  Although depressed working class women are the focus, the intersecting processes account brings a range of other agents into the picture.  While the account does not identify ways to cure the women studied, other girls and women that follow them might seek support from, or find themselves supported by—to pick up on the potential engagements mentioned earlier—counsellors, hospital social workers, people reforming custodial institutions, family planning workers, social policy makers, and so on.  Moreover, these agents can view their engagement as linked with others, not as a solution on its own.  For example, when women’s movement activists create women’s refuges as a step away from living in unsupportive households, this makes it possible for therapists who specialize in the psychological dynamics of the woman in her family to consider referring women to refuges as a critical disruption to the family’s dynamic.  The politics of highlighting different kinds of causes and their interlinkages can be seen as promoting such exchange among the distributed set of agents and contributing to the potential re-formation of the social worlds intersecting around the development of any given focal individual or outcome.

Extracted from Taylor, P.J., “Distributed agency within intersecting ecological, social, and scientific processes,” pp. 313-332 in S. Oyama, P. Griffiths and R. Gray (Eds.), Cycles of Contingency: Developmental Systems and Evolution.  Cambridge, MA: MIT Press, 2001.

[i] The nonpartitionability of different kinds of biological and social causes, given the interdependence of their effects, is demonstrated well by Lewontin (1974), when he argues that statistical partitioning of effects (“analysis of variance”) does not constitute an analysis of causes. Of course, partitioning of biological and social causes does have ideological meaning (Lewontin et al. 1984).


Lewontin, R. C. (1979). Sociobiology as an adaptationist program. Behavioral Science, 24, 5-14.

Lewontin, R. C., Rose, S., & Kamin, L. J. (1984). Not in our genes: Biology, ideology and human nature. New York: Pantheon.

Sclove, R. (1995). Democracy and technology. New York: Guilford.