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as a greater tendency to contract depression in the face of stress.

It is almost the rule in behavioral genetics for later studies to weaken or complicate early findings. The New Zealand study has raised eyebrows on a number of grounds.

Competing studies had found a less dramatic level of stress immunity in people with the protective variant of the gene. But even if its effect turns out to be less absolute than the Caspi and Moffitt study suggests, 5-HTT would be interesting as an example of one kind of gene that contributes to the heritability of depression. The gene has effects on personality (to the extent that it causes neuroticism) and it leads to depression via vulnerability to psychological stressors, like financial losses or the death of close relations.

The Caspi and Moffit findings, and others like them, point to a particular sort of liability to depression—extreme sensitivity to psychological disruption. This route is one long noted by observers of the disease. As Burton writes in The Anatomy of Melancholy, “ that which is but a flea-biting to one, causeth insufferable torment to another; and which one by his singular moderation and well-imposed carriage can happily overcome, a second is in no whit able to sustain.”

But the heritable part of depression is almost certainly mediated by a variety of mechanisms shaped by a variety of genes—and most likely by different combinations of genes in different people. Kendler’s statistical analysis indicates that there must be genes that influence depression and do not give rise to the neurotic personality style. The primary effects of these (presumed) additional genes is uncertain. Some researchers have suggested that there may be genes for the stability or variability of a cluster of functions that includes both bodily cycles (such as daily and, for women, monthly hormone swings) and mood; people who are less “ stable” physiologically may be more vulnerable emotionally. There may be genes that contribute to the protection of brain neurons. Defects in (or less active forms of) a gene that produces neuronal growth and repair factors, like BDNF, might predict depression. Genes that influence the prevalence of glial cells or the size of the hippocampus might play a role.

But neuroticism is a behavioral marker for some of the genes that predispose to depression. Much of the appeal of behavioral genetics lies in these detailed, seemingly incidental revelations that arise from data gathering. It’s not (as the psychoanalytic theory has it) that your unresolved neurotic conflicts lead to disordered mood; it’s that the genes that make you look conflicted happen also to be genes for depression.

The larger body of Kendler’s work on depression leads to a comprehensive model of how illness develops. The research has points of interest all along the way. To turn to environmental causes: What sort of stressors lead to mood disorder?

In twin studies, geneticists divide events into “ shared” and “ nonshared.” These adjectives sound self-explanatory. Certainly “ shared” does. Much of what twins encounter they encounter together. But “ nonshared” environment is a less intuitive concept.

Some experiences clearly happen to one person uniquely. A brick hits one twin (and not the other) on the head; the resulting brain damage leads to depression. But “ nonshared” is a broader category, one defined by events’ effects. Nonshared environment is any environment that just does influence two people differently, even if, from the outside, it looks as though both have encountered the same experiences and lived in the same milieus.

Religion provides an illustration. Sociologists have studied the effect of childhood environment on religious identification. If both your parents are practicing Catholics, and if in childhood all your peers and neighbors are Catholic, the odds are extremely high that even as adults you and your siblings will identify yourselves as Catholic. That result is reliable and it is independent of what each child brings to the environment in terms of temperamental endowment or early traumata. As regards the factors that affect religious identification, you and your siblings have experienced a shared environment.

But for most outcomes, the effect of experience on thought and behavior is more variable. If we look beyond identification and ask about church attendance, differences emerge. By late adolescence, some of your siblings will be churchgoers, and some will not. Personality factors may play a role. One sibling will be rebellious, another will be anxious in crowds, and a third will be left cold in matters of faith or attachment, while from early life you have been especially eager to please and also especially moved by religious feelings. Even if from the outside the environment looks uniform, for each of you internally it will have been distinct—off-putting to one, inspiring to another, constraining to a third, welcoming to a fourth, simply uninteresting to a fifth, and so on. For churchgoing, as observed in adult life, the seemingly uniform surround of practicing Catholic parents and neighbors will register as nonshared environment, an influence that differed for each child.

The measure for whether an environment is shared, for a given outcome, is whether identical twins respond to it identically—that is, whether they are concordant for the outcome.

In many cases, discordant outcomes point to obvious differences in what the twins encounter. Parents may be accepting of one daughter and rejecting of the other, so that the nuclear family provides nonshared environments. But the same measure picks up the elaboration of subtle differences within the twins. For a host of reasons, from intrauterine incidents to the vagaries of fortune on the playground, by age five, even with a shared pair of 5-HTTs and every other gene, one identical co-twin may be confident and the other insecure. Then, a given level of parental support will be adequate for the first and insufficient for the second. In both the experiential and the statistical sense, the home environment is nonshared. That category applies even if the parents swear up and down that they have treated their children identically.

In Kendler’s large-scale studies, it turns out that virtually all the environment that matters for depression is nonshared.

This result is unexpected. You might think that twins raised by neglectful parents would become vulnerable to depression, while twins raised by attentive and attuned parents would attain protection from mood disorder. Depression would be like religious identification: if you come from an abusive or perhaps a depressive family, you will be depressed. If you come from a supportive or upbeat family, you will avoid depression. Or you might imagine that being raised in poverty, or in a dangerous neighborhood, or in a bleak school