IELTS Academic Reading Practice Test 374

At the beginning of the 1930s, psychiatry had almost nothing to offer people with severe mental illness. Patients with schizophrenia or profound depression were kept in large asylums, often for years, and the treatments available were crude and unreliable. Insulin coma therapy, introduced in the early 1930s, involved inducing a coma with injections and then reviving the patient, while other doctors deliberately provoked convulsions with drugs. Neither approach rested on any clear understanding of what had gone wrong in the brain, and both carried serious risks. It was in this climate of desperation that a Portuguese neurologist proposed cutting into the brain itself.

The neurologist was Egas Moniz, who had already had an unusual career. He had been a professor of medicine and, briefly, his country's foreign minister, and in 1927 he had pioneered a technique for photographing the blood vessels of the brain. In 1935, working with the surgeon Pedro Almeida Lima, he began operating on patients whose illness had lasted for years. The procedure, which he named prefrontal leucotomy, involved cutting bundles of nerve fibres running between the prefrontal cortex and deeper structures. Moniz first injected alcohol to destroy the tissue, and then used a wire loop, the leucotome, to sever it.

Moniz published his results in 1936 and reported that a substantial proportion of his patients had improved. The claims rested on short periods of observation and on judgements that were not made blind, and later critics argued that the benefits had been overstated. Nevertheless, the idea travelled fast. Within a few years surgeons in Italy, Britain, the United States and Scandinavia were performing variations of the operation. In the United States the work was taken up in 1936 by Walter Freeman, a neurologist with a flair for publicity, and James Watts, the neurosurgeon who carried out his first operations.

Freeman was not content with an operation that demanded a skilled surgeon and an operating theatre. During the Second World War he learned of an Italian psychiatrist, Amarro Fiamberti, who had reached the frontal lobes through the roof of the eye socket. In 1946 he began using a thin steel instrument, later marketed as an orbitoclast but resembling an ice pick.

He drove it through the thin bone above the eyeball with a hammer and then swept it sideways to sever the fibres. The transorbital lobotomy took only minutes, and Freeman believed that any competent doctor could learn it. He travelled the country performing it in hospitals that had no psychiatrist on the staff.

Such speed had obvious appeal. Hospitals were overcrowded, staff were scarce and long-term care was expensive, so a procedure that might allow a difficult patient to be managed on an open ward seemed attractive. Newspapers reported dramatic recoveries, and relatives of patients, often given little information about the risks, pressed for the operation. Yet the evidence remained weak. No controlled trial was ever carried out, patients were followed for months rather than years, and improvement was usually assessed by the same clinicians who had recommended the surgery.

The damage was considerable. Bleeding and infection sometimes killed patients, and a proportion developed epilepsy or died during or shortly after the operation. Many survivors were left apathetic and passive, without initiative or emotional depth, and some lost the ability to plan. Others were undoubtedly calmer and easier to nurse, and a minority returned to work. The best-known casualty was Rosemary Kennedy, sister of a future American president, who was operated on in 1941 at the age of twenty-three and was left with impaired speech and mobility for the rest of her life.

Official recognition came in 1949, when Moniz received the Nobel Prize in Physiology or Medicine for his discovery of the therapeutic value of leucotomy in certain psychoses. By then he had retired, having been shot in 1939 by a former patient, an injury that left a bullet in his spine and deprived him of the use of one arm. Even at the time the award was questioned, and it has been debated ever since. In 1950 the Soviet Union banned the operation outright, on the grounds that it was mutilating and unscientific.

The decisive change, however, came from pharmacology. In 1952 psychiatrists in Paris reported that a compound developed as an antihistamine, chlorpromazine, calmed patients with psychosis and relieved hallucinations. The drug reached North America and Britain within a few years. For the first time there was a treatment that could be given in tablet form, adjusted in dose and stopped if it did harm. Admissions to mental hospitals in many countries began to fall, the incentive to cut into the brain diminished, and the number of lobotomies declined steeply from the mid-1950s.

Public memory of the operation owes much to Ken Kesey's novel One Flew Over the Cuckoo's Nest, published in 1962, and to the film made from it in 1975. In both, the surgery appears as an instrument of institutional punishment. Historians have since argued that this image obscures a more complicated reality in which desperate doctors, hopeful families and insufficient evidence all played a part. Psychosurgery never disappeared entirely: a small number of operations are still performed for severe obsessive-compulsive disorder, and deep brain stimulation, which uses implanted electrodes rather than a cutting instrument, has been authorised for that condition in the United States since 2009.

Selective serotonin reuptake inhibitors, better known as SSRIs, are among the most widely prescribed medicines in the world. To understand what they do, it helps to picture the junction between two nerve cells. The sending cell releases serotonin, one of several chemical messengers known as neurotransmitters, into a narrow gap called the synaptic cleft. Some of it binds to receptors on the receiving cell, passing the signal on; the rest is taken back into the sending cell by a transporter protein embedded in its surface, a process known as reuptake. SSRIs attach to that transporter and slow it down, so serotonin remains in the gap for longer and stimulates the receiving cell more strongly.

The idea that depression has a chemical cause emerged almost by accident in the 1950s. A drug developed to treat tuberculosis, iproniazid, was noticed to lift the mood of patients taking it, and it turned out to block an enzyme that breaks down monoamines, a family of neurotransmitters that includes serotonin, noradrenaline and dopamine. In the same period, reserpine, a medicine used for high blood pressure, was found to deplete the same chemicals and was linked in some patients to severe low mood. Both findings pointed to a link between monoamines and mood. A third class of drugs, the tricyclics, prescribed from the late 1950s, blocked the reuptake of serotonin and noradrenaline, and the monoamine hypothesis of depression was born.

The hypothesis was simplified for public consumption into the notion of a chemical imbalance: depression meant too little serotonin in the brain, and an SSRI corrected the deficit. The evidence for this has always been thinner than the slogan implied. In 2022 a systematic review led by Joanna Moncrieff and colleagues at University College London examined the available studies and concluded that there was no consistent evidence that people with depression have lowered serotonin activity. The review was widely reported and widely criticised. Some researchers argued that it could not rule out subtle effects, and that studies of blood, spinal fluid and brain scans are poor substitutes for measuring what happens at synapses deep inside a living brain.

A more stubborn problem is timing. If the drugs worked simply by restoring normal serotonin levels, they should lift mood within hours, since they alter serotonin signalling within hours of the first tablet. In practice, the lifting of mood typically takes several weeks, and the delay is one reason researchers look beyond the synapse itself. Attention has turned to slower adaptations.

The sensitivity of autoreceptors, which sit on the sending neuron and normally restrain its output, gradually falls, so the neuron releases more serotonin. Signalling cascades inside the receiving cell alter the numbers of receptors on its surface, and levels of a protein called brain-derived neurotrophic factor, or BDNF, rise. BDNF supports the growth and survival of neurons, and in rodents it has been linked to the sprouting of new connections in the hippocampus.

How far any of this applies to people is uncertain. Much of the evidence for new neuron growth comes from studies in rodents, and it is difficult to count synapses or measure serotonin release in the brain of a living patient. There is no blood test, scan or questionnaire that reliably predicts who will respond to a particular drug, so treatment still proceeds largely by trial, with the first choice based on the balance of likely benefit and side effects.

Interest in other messenger systems has grown. Ketamine, an anaesthetic used since the 1960s, blocks receptors for glutamate, the brain's main excitatory neurotransmitter; given in a single low dose, it can lift mood within hours in some patients whose depression has resisted other treatment. A nasal spray derived from it was approved for treatment-resistant depression in the United States in 2019. Ketamine's rapid action suggests that the brain's response to stress can be reversed quickly, and that the glutamate system, and the plasticity of connections between neurons, may matter as much as serotonin. It also suggests that severe depression is not one condition but several.

Clinical trials have their own difficulties. Depressive illness fluctuates, and people who seek help in a trial often improve whatever they are given, so the placebo response is unusually large. The largest independent study of treatment, funded in the United States and reported in 2006, found that roughly a third of patients reached remission on their first antidepressant. Others improved only after switching to a different drug or adding a second one. Trials also suggest that the advantage of medication over placebo is greatest in severe depression and small in mild cases, which is why guidelines generally recommend talking therapy first for milder illness.

Genes, meanwhile, have proved less informative than was once hoped. Early claims that a single gene, or a few, would explain depression have not held up. Studies involving hundreds of thousands of people have found hundreds of common genetic variants, each with a tiny effect, and together they account for only part of the risk. Side effects are a further part of the picture: nausea, disturbed sleep, weight change and sexual difficulties are common, and stopping an SSRI abruptly can cause dizziness and other withdrawal symptoms, so doctors usually reduce the dose gradually. Regulators also require a warning that young people may become more anxious or have suicidal thoughts in the early weeks of treatment.

Few disputes in medicine are as bitter as the argument about whether mental illness is over-diagnosed. In most wealthy countries the number of people diagnosed with, and treated for, a mental disorder has risen substantially over the past three decades. To one group of clinicians this is evidence of an epidemic of mislabelling; to another it is the predictable result of better recognition and of services that are finally reaching people who need them. Both sides, in my view, are describing something real. The difficulty lies in separating two questions that are usually run together: whether more people are being diagnosed, and whether the boundaries of diagnosis have moved outwards.

The most prominent critic is Allen Frances, who chaired the task force that produced the fourth edition of the American Psychiatric Association's Diagnostic and Statistical Manual, or DSM, in 1994. Frances has spent the years since warning that his own field has lowered its thresholds too far. In his account, ordinary sadness after a bereavement, shyness, the forgetfulness of age and the volatility of adolescence have been steadily reclassified as disorders. He points in particular to the decision, in the fifth edition of 2013, to drop the rule that had stopped a recently bereaved person from being diagnosed with depression, and to the influence of drug marketing.

Thomas Insel, who led the National Institute of Mental Health in the United States from 2002 to 2015, approached the problem from a different direction. In his view the weakness of the manual lies less in its thresholds than in its foundations: its categories are defined by clusters of symptoms reported by patients, not by anything that can be measured in the brain, and two people given the same label may share no underlying biology at all. Insel argued that research should be reorganised around measurable processes such as attention, fear and reward, and that a classification built on such findings would eventually replace the symptom-based one.

Jerome Wakefield, a philosopher who teaches social work, has offered a precise account of where the line should fall. A condition, he argues, is a disorder only when two things are true: an internal mechanism is failing to do its job, and the result is harmful to the person. Grief that is proportionate to a loss, however painful, is not a malfunction but a normal response. On this view, diagnosis requires a judgement about context, and the danger of a purely checklist approach is that context disappears.

Others insist that the existing categories, for all their faults, do more good than harm. Among them is Nick Craddock, a professor of psychiatry at Cardiff University, who has argued that diagnoses remain the best guide clinicians have for choosing treatment, and that dismantling them before better ones are available would leave patients worse off. On this view the categories are working summaries, to be refined as evidence accumulates. Precision, these clinicians point out, is not the same as validity: a category can be useful without being fully understood.

The argument looks different from outside wealthy health systems. Vikram Patel, a psychiatrist known for his work in India and for the field of global mental health, has repeatedly warned that the great majority of people with mental illness in low- and middle-income countries receive neither a diagnosis nor any treatment. Where psychiatrists are scarce, the danger is not that ordinary distress will be labelled but that serious illness will be ignored.

Over-diagnosis also has consequences that go beyond the prescription of unnecessary medicine. A label can follow a person for decades, affecting insurance, employment and the way later symptoms are interpreted; clinicians may attribute a physical complaint to a known psychiatric condition and delay the investigations that would have found its cause. Nor is over-diagnosis the same as over-treatment. Prescriptions for antidepressants have risen steeply in many countries, and much of the growth is in long-term use rather than in new cases.

Part of the difficulty is that there is no gold standard against which a diagnosis can be checked. Large surveys can establish how many people meet the criteria for a disorder, but the criteria themselves are what is in dispute. Some studies find that a substantial share of people in treatment do not meet the full criteria for any disorder; others find that many people who plainly need help are never seen at all. Both findings can be true of the same country.

Screening programmes illustrate the point. Questionnaires can identify depression in people who would not otherwise have mentioned it, but reviews of the evidence suggest that screening produces benefit mainly where services exist to offer follow-up treatment. A questionnaire is not a diagnosis, and adding one to a system that cannot treat the people it identifies does little except lengthen waiting lists.

Where does this leave us? Over-diagnosis is real, and it matters most where it displaces something better: a careful conversation, a second appointment, an acknowledgement that distress is sometimes a reasonable response to circumstances. But it is largely a problem of well-resourced systems with plentiful clinicians and attentive marketing, whereas the dominant global problem remains illness that is never recognised at all. The remedy, then, is not fewer diagnoses but better ones, made slowly, reviewed regularly and treated with the seriousness we give to any other illness.