IELTS Academic Reading Practice Test 325

By the 1960s, surgeons had learned to open the chest and repair damaged hearts while the patient's blood was circulated and oxygenated by a machine outside the body. Once such operations had become routine, the next ambition was obvious: to remove a failing heart altogether and replace it with a healthy one taken from someone who had died. Several teams in the United States and Europe were working towards this goal. The surgical techniques were largely in place; what no one had solved was how to stop the body rejecting an organ that was not its own. The first operation of the kind was performed not in a wealthy research hospital in America but in Cape Town, South Africa, by a surgeon named Christiaan Barnard.

Barnard was born in 1922 in Beaufort West, a small town in the Karoo, the son of a preacher. He studied medicine at the University of Cape Town, qualified in 1946 and trained as a general surgeon before going to the United States in 1956 for further study. There he worked at the University of Minnesota, where open-heart techniques were being developed, and learned how a heart could be stopped, opened and restarted. Returning to South Africa in 1958, he took charge of the surgical department at Groote Schuur Hospital in Cape Town, where he assembled a team and began experimenting with transplanting hearts in dogs.

The idea was not entirely new. Surgeons had transplanted kidneys between patients since the 1950s, and in 1964 a team in Mississippi had placed the heart of a chimpanzee into a dying man, whose body rejected it within hours. What was new in Cape Town was a heart taken from a human donor, and the organisation that this required: the organ had to be removed and restarted within a few hours, the recipient had to be prepared, and two surgical teams had to work in step.

The patient chosen was Louis Washkansky, a grocer in his fifties who had suffered a heart attack and was now severely disabled by heart failure. His condition was deteriorating, and he and his doctors agreed that an operation offered his only chance. The donor was Denise Darvall, a twenty-five-year-old woman who had been knocked down by a car while crossing a road with her mother and had suffered catastrophic brain injuries. Her heart continued to beat only because a ventilator was breathing for her. Her father gave permission for her organs to be used.

The operation began shortly after midnight on 3 December 1967. While one team opened Washkansky's chest, another removed the donor's heart. The ventilator was switched off, her heart stopped, and only then was the organ taken out. Barnard cut away most of the diseased heart, leaving the back walls of the upper chambers in place, and stitched the donor organ to them. The new heart began to beat, and the surgical team allowed themselves to hope.

For a few days the signs were encouraging. Washkansky woke and spoke to the nurses. But the drugs given to stop his immune system from attacking the foreign organ also left him defenceless against infection, and he developed pneumonia. He died eighteen days after the operation. The first heart transplant patient had survived just long enough to show that the technique was possible, and that the immune system was the real obstacle.

The operation also forced hospitals to confront a question they had avoided. At that time death was generally defined by the heart stopping, and the donor had been kept alive by a machine. Reporters and doctors abroad asked whether it was right to remove an organ from a body whose heart had so recently been beating. Within a few years, medical bodies began to accept that the permanent loss of brain function, rather than the stopping of the heart, was the more meaningful definition of death, a change that transplantation helped to bring about.

Barnard's second patient, Philip Blaiberg, received a new heart in January 1968 and lived for more than eighteen months, a result that did much to silence the sceptics. Within two years, teams around the world were transplanting hearts in growing numbers, but many patients died within weeks, and as the poor results became known the numbers fell sharply, and by the early 1970s only a few centres were still operating. Only in the 1980s, when the drug ciclosporin came into use, did survival improve enough for transplantation to become a standard treatment rather than an experiment.

Barnard went on operating for more than a decade. He had suffered from rheumatoid arthritis since the 1950s, and as it worsened it eventually made surgery impossible, and in 1974 he tried an alternative approach in which a second heart was added beside the patient's own instead of replacing it. He became a celebrity, known as much for his criticism of apartheid and for his turbulent private life as for his medicine, and he spent his later years lecturing and writing. He died in 2001.

Today heart transplantation is an established treatment, performed many thousands of times a year, and the operation of 1967 is remembered as a turning point. It made organ donation a public issue, since every transplant depends on a decision made by a grieving family and on a definition of death that society can accept. That remains true, whatever the technical advances of the decades that followed.

Human beings are warm-blooded: whatever the weather, the temperature inside the body stays close to 37°C. This stability is not a luxury. The proteins and membranes inside cells work efficiently only within a narrow band of temperatures, and a rise of a few degrees begins to distort them, while a fall of a few degrees slows the chemical reactions on which every organ depends. The body therefore treats its core temperature as one of the variables that must be defended, and it has an elaborate set of responses for doing so.

The control centre is a region at the base of the brain called the hypothalamus, and in particular a part of it known as the preoptic area. Cells there act as a thermostat. They receive information from two sources: from temperature-sensitive nerve cells in the hypothalamus and spinal cord, which report on conditions deep inside the body, and from receptors in the skin, which report on the surroundings. These receptors respond both to the temperature of the skin and to the rate at which it changes. The hypothalamus compares these signals with an internal reference value, or set point, and when the two differ it triggers responses.

Some of those responses are behavioural, and they are the ones people notice least. Putting on a coat, moving into the shade, drinking a hot drink or curling up under a blanket are all acts of thermoregulation, and in everyday life they do most of the work. Only when behaviour is not enough does the body call on the physiological responses that physiologists study, which fall into two categories: making more heat and losing it faster.

Heat is a by-product of metabolism, and the body can increase production in two ways. The first is shivering, in which muscles contract and relax rapidly without doing any useful work; the energy released appears as heat, and prolonged shivering can raise heat production several-fold. The second is non-shivering thermogenesis, in which specialised fat cells burn fuel to produce heat rather than to do work. This tissue, known as brown adipose tissue because of its colour, is important in newborn babies, who cannot shiver effectively and who lose heat quickly because of their small size.

Losing heat is a matter of physics. Heat leaves the body by radiation and conduction to cooler surroundings, by convection as air moves across the skin, and by the evaporation of sweat. The last of these is the only mechanism that still works when the air is as warm as the body, and it is remarkably powerful: water absorbs a great deal of energy as it turns into vapour. Sweating therefore keeps people cool in hot weather, but only if the sweat can evaporate. In humid conditions the air is already close to saturation, evaporation slows, and the same amount of sweat removes much less heat.

Blood flow is the other adjustable part. In the heat, vessels near the surface of the skin widen, so that warm blood is carried outwards and heat can be lost; the skin reddens and feels warm. In the cold, the same vessels narrow, blood is kept in the core, and the skin becomes pale and cool. Hands and feet are sacrificed first, which is why fingers stiffen long before the core temperature falls.

Fever is not the same as overheating. During an infection, substances released by microbes and by the immune system act on the hypothalamus and raise the set point, so that the body behaves as though it were too cold. Patients feel chilled, shiver and wrap up, and their temperature climbs towards the new target. Drugs such as aspirin and paracetamol lower fever by interfering with the chemical signals that raise the set point. In hyperthermia, by contrast, the set point is unchanged but the body cannot lose heat fast enough, and the temperature rises dangerously.

Failure of the system is dangerous in both directions. In hypothermia the core temperature falls and the responses themselves become weaker, since shivering generates less heat as the body cools, so that a person may stop shivering while still in danger. At the other extreme, heat stroke occurs when the temperature rises so far that the control mechanisms begin to fail, and sweating may stop altogether. Both are medical emergencies.

The system can also be trained. People who move to a hot climate begin to sweat earlier and more profusely than before, and their sweat becomes more dilute, so that less salt is lost. This acclimatisation takes one to two weeks. Adaptation to cold is much less impressive in humans, and consists largely of behavioural adjustment and of tolerating discomfort. Even the changes produced by heat fade within a few weeks if a person returns to a cool climate.

Much remains uncertain. The familiar figure of 37°C comes from a nineteenth-century German physician, Carl Reinhold August Wunderlich, who averaged readings from thousands of patients, and modern measurements suggest that the average healthy temperature is slightly lower. Normal values also vary between individuals and across the day, being lowest in the early morning. Whether adults retain active brown fat was long doubted; imaging studies in the past two decades have shown that many do, though its contribution to daily energy use appears modest and differs greatly between people. Nor is it settled whether fever itself helps patients to recover, which is why advice about treating it has changed more than once.

Few medical labels have provoked as much argument as the word 'disease'. When the American Medical Association resolved in 2013 that obesity should be recognised as one, the decision was reported around the world and was welcomed by some doctors and deplored by others. The World Health Organization had already described obesity as a global epidemic and had given it a place in its international classification of diseases. The argument is often dismissed as a quarrel about words. It is not, because the label determines what treatment patients can obtain, how research is funded and, above all, how obese people are regarded by doctors and by themselves. I believe the classification is right, but only if it is made honestly, and with attention to what it leaves out.

The case for the label begins with biology. Body weight is regulated by a system in the brain that defends fat stores with considerable determination. When a person loses weight, whether by dieting or through illness, the body responds as though it were starving: appetite increases, the sense of fullness weakens and energy expenditure falls slightly. The hormones that carry these messages, including leptin and ghrelin, have been mapped in detail. Whatever the original cause of the weight gain, the body of an obese person is not neutral. Losing weight and keeping it off is a physiological struggle, and most people who lose a great deal regain much of it within a few years.

A second argument concerns care. If obesity is regarded simply as a consequence of poor choices, patients may be blamed rather than treated, and clinicians may feel that there is little they can offer. A formal classification encourages health systems to pay for structured programmes, and it encourages research funders and pharmaceutical companies to invest.

The objections are serious. The measure on which the classification rests is the body mass index, devised in the nineteenth century by the Belgian mathematician Adolphe Quetelet as a way of describing populations rather than individuals. It is a ratio of weight to the square of height, and it cannot distinguish muscle from fat, nor fat around the organs from fat under the skin. More fundamentally, obesity is not one condition. A minority of obese people have normal blood pressure, blood sugar and cholesterol, and their risk is lower than that of others of the same weight. The group is unstable, however, and many of its members become higher-risk over time.

Critics also fear the effects of labelling. To tell someone who feels well that they have a disease is to create a patient, with all the anxiety and dependence that follows. Some argue that the language of disease removes responsibility from individuals and can produce a kind of fatalism, in which people conclude that nothing they do will matter. There is some evidence for this worry, though it cuts both ways: research on weight stigma suggests that being blamed for one's condition is itself associated with poorer health and with avoiding medical care.

The strongest objection, however, is not about individuals at all. The environments in which people live have changed enormously in a few decades: energy-dense food is cheap and heavily advertised, cars have replaced walking, and many neighbourhoods offer nowhere pleasant to be active. If obesity is a disease, the argument runs, governments can present it as a problem of individual patients rather than of the conditions they live in. They can then avoid regulating the food industry or redesigning cities. The objection has force, but it proves too much. A condition can be both a disease of individuals and the product of an environment, as lung cancer is.

What, then, would a defensible classification look like? It would define obesity by its effects on health rather than by a single number. It would treat it as a chronic condition that relapses, like asthma, rather than as a failure of will that ends when the weight is lost. Treatment would include behavioural support, medication for some patients and surgery for a smaller number; none of these is a cure, and all require long-term follow-up. Crucially, the definition would have to include the prevention of obesity as part of the disease, not as an alternative to treating it. That is an odd thing to write into a classification, but it is the only way to keep the environmental argument inside.

The problem of stigma deserves the last word. Blaming patients is not only unkind but ineffective: people who feel judged tend to avoid the very services that might help them. Yet explaining that a condition has a physiological basis is not the same as telling patients that their efforts are pointless. Clinicians who treat obesity well do both: they acknowledge the biology and they ask the patient what is worth attempting. The label can support that conversation, or it can close it down.

My conclusion is therefore that obesity should be classified as a disease. The biology is real, the relapse is real, and patients deserve care rather than blame. But a classification is a tool, not a solution. It earns its place only if it brings better treatment and stronger prevention together, and if those who use it resist the temptation to treat a social problem as a matter for individuals alone.