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We Have Happy Pills, Anxiety Drugs, and Therapists Galore: So Why Are We More Stressed and Depressed Than Ever?

More of us than ever are discontented and not experiencing optimum emotional well-being. Why is the vast enterprise of professional mental health unable to help us feel better?

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In 1921, Otto Loewi (1873–1961), a German pharmacologist, demonstrated that nerve cells (neurons) communicate by releasing chemicals. Prior to that time, neuroscientists thought nervous communication was electrical. Among the many important breakthroughs that followed from Loewi’s work were the identification of neurotransmitters and the discovery of receptors on cell surfaces that bind them. Neurotransmitters are chemicals made within the body, stored in tiny sacs clustered within a neuron and released into the synapse, the gap between the neuron and a target cell, which might be another neuron (the postsynaptic neuron) or a muscle or glandular cell. The released molecules then bind to receptors—specialized proteins on the surface membrane of the target cell—causing changes in that cell, making it more or less likely to produce an electrical signal (in the case of a neuron), to contract (in the case of a muscle), or to secrete a hormone (in the case of a glandular cell). Later, the neurotransmitters can separate from their receptors and be taken up by presynaptic cells for reuse or be broken down by enzymes into inactive metabolites. Neuroscientists have now compiled long lists of neurotransmitters, described their actions, and identified many types and subtypes of receptors.

Three of the most studied neurotransmitters are norepinephrine, dopamine, and serotonin, all very relevant to the subject at hand because they influence our moods and emotions. For example, dopamine is involved in what is known as the reward system of the brain; drugs that affect it can alter our experience of pleasure. Cocaine is such a drug. It blocks reuptake of dopamine back into the presynaptic neuron, effectively increasing its action at the synapse to produce an intense pleasurable response. With prolonged use of cocaine, postsynaptic neurons become less responsive to dopamine, leading to depression and dependence on the drug to relieve it. The dopamine hypothesis of schizophrenia attributes psychosis to overactivity of this neurotransmitter. Norepinephrine regulates both reward and arousal. Disturbances in that neurotransmitter system are associated with anxiety disorders. And serotonin affects our moods and sleep.

The most widely used psychiatric drugs today influence the production and effects of these major neurotransmitters. Psychopharmacologists made their first big breakthrough in the 1950s from work with antihistamines, used to quell allergic symptoms. Although antihistamines are best known for blocking the effects of the compound responsible for certain immune responses, they also affect the brain, often making people groggy, sleepy, and depressed. By tinkering with these molecules, chemists produced a new class of psychoactive drugs—the phenothiazines—that blocked dopamine transmission. Thorazine and other phenothiazines were successfully marketed as major tranquilizers and antipsychotics and quickly revolutionized the treatment of schizophrenia. Psychiatrists hailed them as magical compounds that cured psychosis, while critics argued that they simply made psychotic people groggy, sedated, and easier to manage, even as outpatients. Energized by this achievement, psychopharmacologists then turned their attention to depression. Over the past sixty years, they have come up with a number of drugs to treat it.

The efforts of psychopharmacologists give us an opportunity to evaluate the usefulness of the biomedical model in psychiatry. In practice, psychiatric medicine today is synonymous with psychopharmacology. The credo of that field is “There is no twisted thought without a twisted molecule.” (The words of the American neurophysiologist Ralph Gerard, 1900–1974). The biomedical model explains depression as the result of a chemical imbalance in the brain, specifically of neurotransmitters affecting our moods. How well does that explanation enable us to describe, predict, and control depressive illness? In other words, just how effective are the antidepressant drugs that psychopharmacologists have developed, that the big pharmaceutical companies sell such quantities of, and that so many people today take? The answer, I’m afraid, is not very.