Is feeling bad good? The evolutionary benefits of depression
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Contemporary botanists and zoologists regularly examine how evolution affects their field; but among psychiatrists, the role
of evolution in major depression remains a controversial topic. Why? Some argue that evolution is too all-encompassing for
us to understand how a specific entity like depression evolved. Others claim that because severe depression would, if anything,
lower an individual's chances of survival, evolutionary theory cannot explain its origin. Still others argue that evolutionary
psychiatry does not generate testable predictions. But there is general agreement that the study of psychological functioning,
neurotransmitters and hormones should take precedence over the study of evolutionary factors in psychiatry. However, most
psychiatrists are unaware of the numerous studies by psychologist Dr. Paul Gilbert and psychiatrists Dr. Michael McGuire and
Dr. Robert Levitan that have used an evolutionary framework to provide a clearer understanding of the interaction among psychological
factors, genes, neurotransmitters and hormonal changes. Here I review two theories that attempt to explain why depressive
disorders have not been weeded out by natural selection.
Social competition model of depression
The social competition model of depression was first proposed by psychiatrist John Price in a 1967 article in the Lancet, where he drew on observations of long-tailed macaques to note the similarity between depressed individuals and monkeys who
lost in hierarchical encounters and were forced into a subordinate social role. Price proposed that depression, anxiety and
irritability in both monkeys and humans are the emotional concomitants of behaviours designed to maintain a subordinate social
role -- to maintain the stability of the dominance hierarchy. We subsequently used the term involuntary subordinate strategy
(IDS) to refer to a genetically pre-programmed strategy that is triggered by the recognition that defeat in social competition
is inevitable.
The IDS has three functions: First, it leads to a sense of inadequacy, which reduces the individual's motivation to continue
the struggle and inhibits aggression and escalating behaviours directed toward a rival or superior. Second, the IDS contributes
to submission, or flight, which brings the struggle to an end. Finally, the IDS signals no threat to the rival, which causes
the latter to give up further struggle. Many clinical depressions demonstrate evidence of strategies designed to terminate
hierarchical conflict. For example, depressed individuals tend to feel inferior and defeated, behave submissively and desire
escape, but feel trapped.
Attachment theory and depression
Many mammalian infants react to separation from their caregivers with stereotypic emotion/behavioural changes such as the
stages of protest, despair demobilization and detachment, as described by John Bowlby in 1969. These sequences are part of
a repertoire for coping with major separation events. In the protest stage, vocalizations of anger and distress make the mother
aware of the child's needs. If successful, the reunion settles the child. However, if unsuccessful, the child's continued
protests could betray the child's vulnerability to a predator. Hence, the demobilization/despair phase may have evolved to
keep the child from drawing attention from predators.
Our ability to elicit and form supportive and caring relationships has a major influence on our social success and status.
In fact, as my colleagues Paul Gilbert and Gary Hasey and I argue in a 2002 article in the Journal of Affective Disorders, attachment and social rank systems have a complementary relationship. For this reason, the social rank theory and attachment
theory models of depression are not as different as they appear. Too much anger can impede the grieving process and also prevent
acceptance of competitive loss. This generates an increasingly powerful IDS, which may manifest as pathological mourning or
depression.
Understanding evolutionary function can be helpful in positively reframing negative symptoms by drawing attention to the original
useful function. Various cognitive and behavioural strategies can be used to avoid unnecessary triggering of the IDS or to
terminate it. When clients describe symptoms of mild or moderate depression, as in the following two case studies, it may
be helpful to look for underlying feelings of anger that may prevent acceptance or effective problem-solving. If anger is
present, one can explore at whom it is directed and whether the IDS plays a role. The evolutionary perspective sees the function
of negative mood as being to redirect our energies into more productive activities.
Case study 1
Jane was a bright, attractive 16-year-old who complained about feelings of inferiority. Her mother was an anxious, controlling
woman. Jane felt a lot of anger toward her mother, which she did not express, because she was afraid to challenge her. Her
feelings of inferiority were attributed to her IDS. I told Jane that her feelings of inferiority were the price she paid for
her decision to be a dutiful daughter and to avoid fighting with her mother. Jane then decided that learning to be more assertive
with her mother would enable her to be more assertive with others.
Case study 2
Muriel was a 55-year-old depressed woman who felt she was going crazy. She was a senior executive who had been let go after
a change in the administration. She said she would fight to the bitter end to keep her job, although it became apparent there
was no hope of succeeding. Because Muriel felt victimized, she felt she had to right the wrong that had been done her and
she became engaged in a struggle she felt she could not win. As a result, her IDS was triggered and she became depressed.
I advised Muriel to accept the loss of her job but to fight for a better severance package, which she did, with some success.
Consequently, her IDS was turned off and her symptoms cleared.
Dr. Leon Sloman is an honorary consultant in psychiatry at the Centre for Addiction and Mental Health and an associate professor in the Department
of Psychiatry at the University of Toronto.
Centre for Addiction
