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Affective (AFF-ect-iv) disorders are disturbances of mood and emotion. Depression is the most common, affect­ing about 8-10% of people (when fre­quencies in different countries are aver­aged). Depression is far worse than a sad mood. In its most severe form, depression is disabling: people cannot function.

Typical symptoms of depression are hopelessness, inability to take initiative, and "frozen emotions." Movement and goal-directed activity is reduced; social contact may be cut off. The present moment seems joyless if not unbearable; the future seems bleak.

Multiple forms of evidence including brain scanning show a reduced level of activity in the dopamine circuits of the brain during depression. This is accompanied by reduced sensitivity to reinforcing stimuli and less motivation to pursue previously valued activities.

What are symptoms of depression?

Sufferers of depression include great people of history such as Darwin and Churchill. They unanimously report great psychological pain associated with depression. Adults who have exper­ienced one episode of depression have a 50% chance of another episode.

Major depression runs in families. Close relatives of a person who experiences the disorder are nearly three times more likely to become depressed themselves.

Twin studies show a heritability index of 37% for depression, which is actually lower than many other disorders. "Candidate gene studies provide little convincing support for the involvement of any candidate gene" in major depression (Flint and Kendler, 2014).

What are possible reasons that twice as many women as men report depression?

The reported incidence of depression is twice as high among women as it is among men. Various explanations for this gender gap have been offered over the years, all speculative.

Men are often more reluctant than women to seek treatment, so fewer episodes of depression in men are diagnosed. Men may self-medicate with alcohol, making alcoholism a mask for depression.

Women are are more likely to exper­ience helplessness and victimization in male-dominated cultures, raising stress levels and causing more depression. In all cultures, depression is most common in women of childbearing age (Weissman and Olfson, 1995).

One of the most important findings in recent years is that depression is accompanied by neuron loss in the prefrontal cortex and hippocampus. The hippocampus is one of the few brain regions that grows new neurons in adulthood.

In depression, neurogenesis (generation of new neurons or new branches on existing neurons) is reduced. Ketamine, an NDMA receptor antagonist, produces rapid antidepressant action (within two hours) even in people with treatment-resistant depression. Ketamine also rapidly increases spine synapses in the prefrontal cortex (Durman, 2014).

Patients tend to relapse into depression an average of 18 days after ketamine treatment (Murrough et al., 2013). However, the existence of a drug providing rapid relief for previously untreatable depression is exciting to researchers and clinicians.

Depression can be triggered by many factors. Depression is common after stroke. One study (Ayerbe, Ayis, Wolfe and Rudd, 2013) found in a study of 13,558 references that about 29% of stroke victims experienced depression that remained stable up to 10 years.

We discussed one likely example of depression after stroke. Elizabeth Kubler-Ross, the expert on death and dying, became morose and pessimistic after having a serious stroke several years before her death.

Some women experience depression after a childbirth (post-partum depression). This could be triggered by hormonal changes accompanying pregnancy and childbirth, or to the stressfulness of the events, or both.

True post-partum depression is different from the "baby blues"–a feeling of letdown–which about three-quarters of women experience in weeks after delivery. True post-partum depression affects 10% to 20% of women giving birth and can last for months.

What is post-partum depression?

Psychiatrists have found that post-partum depression is more common when a baby is "difficult" or a woman feels unloved (Vandershaf, 1987). Those factors are likely to raise the levels of stress or feelings of hopeless­ness that correlate with onset of depression.

Princess Diana suffered post-partum depression after one of her two sons was born. She went public with her story, to the applause of British mental health professionals, who said it helped other women talk about their experi­ences.

What is SAD and how can it be cured?

Seasonal affective disorder (SAD) occurs when people fall into a depression during winter months (Hellman, 1982). One theory is that this is caused by lack of sunlight, triggering lower levels of the hormone melatonin. Another theory is that winter may be accompanied by pro-inflammatory cytokines like interleukin, which can produce lower levels of serotonin.

Proponents of the melatonin theory suggest that SAD can be reduced by spending several hours a day under bright lamps with natural light frequencies. This simulates the effects of a longer day.

SAD is common only in the northern latitudes where the sun does not shine brightly during the winter. In countries like Finland, which historically had one of the highest rates of depression, light rooms are now a fixture of many houses, along with traditional saunas.

Historically, depression was often treated with electroconvulsive seizures (ECS) commonly termed "shock therapy." Nobody knew why this worked, but in the aftermath of seizures, depressed people sometimes felt better. Doctors in the 20th Century used electric shocks to induce seizures as treatment for depression when other approaches failed.

Full seizures are frightening to watch. In the early days of ECS, several assis­tants might be required to hold down a patient after ECS was administered, until muscle contractions stopped.

With time, doctors discovered they could eliminate both the large-scale seizures and discomfort for patients by pre-medicating them. This confined seizure activity to brain tissue where it had its effect.

By that time, ECS had a terrible reputation, from which it still has not fully recovered. Movie images (e.g. from One Flew Over the Cuckoo's Nest) portrayed it as similar to torture, as unwilling patients were wrestled to a treatment table and forced to have seizures. Modern ECS treatments are nothing like that.

Scientists now have a better under­standing of how ECS works. Like the most successful antidepressant drugs, ECS increases neurogenesis (nerve sprouting) in the region of the hippo­campus. This, in turn, helps to inhibit circuits that overreact to stress (Schloesser et al, 2015).

Two of the most promising non-pharma­ceutical approaches to treating depres­sion are cognitive behavior therapy (CBT) and behavior activation (BA). Controlled studies have shown they are both about equally successful, and both can be combined with pharma­ceutical approaches.

We will discuss cognitive-behavioral therapy more in the Therapies chapter. Its use for treatment of depression is well-known and widely associated with Aaron Beck of the University of Penn­sylvania. Briefly, CBT concentrates on three approaches:

–behavioral strategies for how people act in situations that might trigger depression

–cognitive strategies to change how people think about (and respond to) specific trigger situations

–cognitive strategies designed to change the enduring beliefs that people have about themselves and their future

Activity therapies, advocated by Ferster (1973) are more purely behavioral. They are aimed at re-introducing pleasurable tasks and interactions with others, trying to arrange positive situa­tions in place of depression and inaction.

Convergent evidence shows dopamine is involved in depression (and the bipolar disorder) just as it is involved with psychosis. Dopamine is the transmitter associated with pleasure, reinforcement, and movement.

When dopamine pathways are impaired, the result is a reward processing dysfunction. People are less likely to enjoy things. They have less approach motivation and more avoidance. They are less sensitive to rewards (Whitton, Treadway, and Pizzagalli, 2015).

This helps explain why therapies that encourage movement and emotionally positive events can help depressed people. A survey of 25 high quality studies also showed that any level of physical activity, including walking two hours per week, was highly effective in preventing future depression (Mammen and Faulkner, 2013).

The other major transmitter system involved with depression is serotonin. The central 5-HT [serotonin] system regulates emotion and response to stress, among other things.

Evidence implicates stress and inflammation, which are often linked, in the genesis of depression. Exposure to chronic, unpredictable stress induces depressive-like symptoms, including anhedonia (joylessness).

Stress increased inflammation in the nervous system. Multiple studies have indicated that inflammation plays a role in depression (e.g. Berk et al., 2013).

Slavich and Irwin (2014) integrated those observations. They proposed that social threat and adversity activate components of the immune system called proinflammatory cytokines.

This inflammation is responsible for the profound changes of behavior in depression, including sad mood, fatigue, lack of movement, and withdrawal from social contact. These changes were "critical for survival during times of actual physical threat and injury" so animals could crawl off to a private place and heal.

"However, this response can also be activated by modern-day social, symbolic, or imagined threats," causing depression. This explains, the authors said, why inflammation (a response to injury) is associated with depression.

Chronic stress also reduces serotonin transmission, which decreases hippocampal inhibition of stress circuits (involving the hypothalamic-pituitary-adrenal or HPA axis). Anti-depressive medications, when effective, reverse these effects (Mahara, Bambicoc, Mechawara, and Nobregac, 2014).

The best-known anti-depressive medications, such as Prozac, are selective serotonin re-uptake inhibitors (SSRIs). SSRIs allow serotonin to accumulate at synapses by slowing down the re-uptake of the chemical after it is released into the synaptic gap.

When first introduced, Prozac and similar anti-depressants brought relief to some people for the first time. This led to books like Prozac Nation (1994), a memoir by Elizabeth Wurtzel in which she traced her experiences with depression from age 11 through college and the relief she experienced from Prozac.

Anti-depressants helped many people and are among the most-prescribed drugs. They can easily be combined with cognitive and behavioral therapies.

Several large-scale outcome studies (e.g. Cuijpers et al, 2014) indicate that antidepressant medication plus psychotherapy is significantly more effective than either approach by itself. Medications can create an immediate change, in some cases, while psycho­therapy works on longer-term adjust­ments of attitudes and behavior.


Ayerbe, L., Ayis, S., Wolfe, C. D. A., & Rudd, A. G. (2013) Natural history, predictors and outcomes of depression after stroke: systematic review and meta-analysis. The British Journal of Psychiatry Jan 2013, 202, 14-21. doi:10.1192/bjp.bp.111.107664 .

Berk, M. [and 10 others] (2013) So depression is an inflammatory disease, but where does the inflammation come from? BMC Medicine, 11 Retrieved from: . doi:10.1186/1741-7015-11-200 .

Cuijpers, P., Sijbrandij, M., Koole, S. L., Andersson, G., Beekman, A. T., & Reynolds, C. F. (2014) Adding psychotherapy to antidepressant medication in depression and anxiety disorders: a meta-analysis. World Psychiatry, 13, 56-67. doi:10.1002/wps.20089 .

Durman, R. S. (2014) Pathophysiology of depression and innovative treatments: remodeling glutamatergic synaptic connections. Dialogues in Clinical Neuroscience, 16, 11-17.

Ferster, C. B. (1973) A functional analysis of depression. American Psychologist, 28, 857-870.

Flint, J. & Kendler, K. S. (2014) The genetics of major depression. Neuron, 81, 484-503. .

Hellman, H. (1982, April). Guiding light. Psychology Today, pp.22-28.

Mahara, I., Bambicoc, F. R., Mechawara, N., & Nobregac, J. N. (2014) Stress, serotonin, and hippocampal neurogenesis in relation to depression and antidepressant effects. Neuroscience and Biobehavioral Reviews, 38, 173-192.

Mammen, G., Faulkner, G. (2013) Physical activity and the prevention of depression: A systematic review of prospective studies. American Journal of Preventative Medicine, 45, 649-657.

Murround, J. W. [and 9 others] (2013) Rapid and longer-term antidepressant effects of repeated ketamine infusions in treatment-resistant major depression. Biological Psychiatry, 74, 250-256.

Schloesser, R. J. [and 9 others] (2015). Antidepressant-like effects of electroconvulsive seizaures require adult neurogenesis in a neuroendocrine model of depressoin. Brain Stimulation, 8, 862-867.

Slavich, G. M. & Irwin, M. T. (2014) Psychological Bulletin, 140, 774-815.

Vandershaf, S. (1987, April). New-baby blues. Psychology Today, p.18.

Weissman M. M. & Olfson M. Depression in women: implications for health care research. Science, 269, 799-801

Whitton, A. E., Treadway, M. T., & Pizzagalli, D. A. (2015) Current Opinions in Psychiatry, 28, 7-12. doi:10.1097/YCO.0000000000000122

Wurtzel, E. (1994) Prozac Nation. Boston: Houghton-Mifflin.

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