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.
The unchangeability of the inherited genes—the root causes—says nothing about the most effective, economical, or otherwise socially desirable intervention (or combinations of interventions) to pursue. To illustrated this for my students, I use the following stylized example.
A body of research, initiated by the British sociologists Brown and Harris in the 1960s, has interpreted the social origins of mental illnesses. Let me sketch their explanation of acute depression in working-class women in London (Brown and Harris 1978, 1989). I will also work in the extensions of their findings made by Bowlby, a psychologist who focused on the long term effects of different patterns of attachment of infants and young children to their mothers (Bowlby 1988).
Four factors are identified by Brown and Harris as disproportionately true of women with severe depression: a severe, adverse event in the year prior to the onset of depression; the lack of a supportive partner; persistently difficult living conditions; and the loss of, or prolonged separation from, the mother when the woman was a child (under the age of eleven). Bowlby interprets this last factor in terms of his and others’ observations of secure versus anxious attachment of infants and young children to caregivers. In a situation of secure attachment the caregiver, usually the mother, is, in the child’s early years, “readily available, sensitive to her child’s signals, and lovingly responsive when [the child] seeks protection and/or comfort and/or assistance” (Bowlby 1988, p. 167). The child more boldly explores the world, confident that support when needed will be available from others. Anxious attachment, on the other hand, corresponds to inconsistency in, or lack of, supportive responses. The child is anxious in its explorations of the world, which can, in turn, evoke erratic responses from caregivers, and the subsequent attempt by the child to get by without the support of others.
The top three strands of the figure above (class, family, psychology) combine the observations above to explain the onset of serious depression. The factors are not separate contributing causes, like spokes on a wheel, but take their place in the multistranded life course of the individual. Each line should be interpreted as one contributing causal link in the development of the behavior. The lines are dashed, however, to moderate any implied determinism; 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.
Suppose now, quite hypothetically, that certain genes, expressed in the body’s chemistry, predispose a child to being more anxious 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) renders the child more susceptible to the biochemical shifts that are associated with depression. (This hypothetical situation is depicted in the bottom strand of the figure.) 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 interventions 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 the incidence of severe depression for working-class women, the unchangeability of the hypothetical inherited genes says nothing about the most effective, economical, or otherwise socially desirable intervention (or combinations of interventions) to pursue.
Bowlby, J. (1988). A Secure Base. New York: Basic Books.
Brown, G. W. and T. Harris (1978). Social Origins of Depression. New York: The Free Press.
Brown, G. W. and T. O. Harris, Eds. (1989). Life Events and Illness. New York: Guilford Press.
(Introduction to this series of posts)