IELTS Academic Reading Practice Test 332

In 1957 a small German company, Chemie Grünenthal, began selling a new drug called thalidomide. It had been developed as a sedative, and it was marketed as an unusually safe one: even large doses, the company claimed, did not produce the deep unconsciousness associated with the barbiturates then in common use, and no dose had been found that would kill an animal. Sold under names such as Contergan in West Germany and Distaval in Britain, the drug was soon available in dozens of countries. Doctors prescribed it for sleeplessness, and before long also for the nausea of early pregnancy.

The claim rested on laboratory tests. Thalidomide had been given to mice, rats, rabbits and dogs, and none had died from it, remarkable at a time when the lethal dose of most sedatives was easy to establish. Yet the tests had not been designed to reveal subtler kinds of harm. In the late 1950s, regulators in most countries asked only whether a medicine was safe at the doses prescribed; they did not require the manufacturer to show that it actually worked, and they did not insist on experiments with pregnant animals. No such experiments had been carried out.

Between 1958 and 1961 thalidomide was taken by hundreds of thousands of people. It was used not only for insomnia and morning sickness but also as a sedative for children and a remedy for coughs, colds and headaches, and in some countries it could be bought without a prescription. Because it seemed so gentle, doctors were willing to prescribe it to women in the first months of pregnancy, when the fetus is most vulnerable.

The United States came close to approving the drug as well. In 1960 the American company Richardson-Merrell, which held the licence, applied to the Food and Drug Administration for permission to sell it. The application was assigned to Frances Kelsey, a physician and pharmacologist who had joined the agency only a month earlier. Kelsey was troubled by reports from Britain of peripheral neuritis, a painful inflammation of the nerves that could follow long use of the drug, and she was uneasy at how little was known about its effects in pregnancy. She asked for further evidence and repeatedly refused to approve the application. Her caution meant that thalidomide was never marketed in the United States, although a small quantity had been supplied to doctors for trials, and a number of American children were affected.

The link with birth defects emerged in 1961. In West Germany, Widukind Lenz, a paediatrician, was struck by the number of babies born with phocomelia, a rare condition in which the long bones of the arms and legs are missing or shortened, so that the hands and feet seem to attach almost directly to the trunk. He traced the histories of these children to their mothers' use of thalidomide in early pregnancy, and in late November 1961 the drug was withdrawn in Germany; Britain followed within weeks. In Australia, the obstetrician William McBride had noticed a similar cluster in Sydney, and a short letter from him appeared in the medical journal The Lancet in December 1961.

By then the damage had been done. It is estimated that around 10,000 children were born with thalidomide-related disabilities, of whom perhaps half survived infancy; many others died before birth. The injuries were not confined to the limbs. Some children were born deaf or blind, or with damage to the heart, kidneys or digestive tract. The drug crossed the placenta, and its effects depended on timing: the limbs were most at risk between about the twentieth and thirty-sixth day after conception, a window so narrow that a woman might have taken only a handful of tablets.

The consequences for regulation were profound. In the United States, Congress passed the Kefauver–Harris Amendment in 1962, which required manufacturers to prove that a drug was effective as well as safe before it could be sold, and which strengthened the rules on clinical trials and on the reporting of side effects. Britain set up a committee to monitor drug safety in 1963, and the Medicines Act of 1968 created a formal system of licensing. Similar reforms followed in Canada, Australia and much of Europe. Tests on pregnant animals became a standard part of drug development, and the thalidomide case is still cited whenever regulators argue for caution.

Thalidomide itself did not disappear. In 1965 a physician in Israel gave it to a patient with leprosy who was suffering from a painful inflammatory reaction, and found that it relieved the symptoms. The drug was subsequently shown to be useful against that complication, known as erythema nodosum leprosum, and in 1998 the Food and Drug Administration approved it for the purpose. It has since been approved for multiple myeloma, a cancer of the bone marrow. Its use is tightly controlled, with pregnancy testing and other safeguards, precisely because its capacity to damage a fetus has never gone away.

For the survivors, the aftermath has been a long campaign for recognition. Many were told as children that their limbs were the result of a rare genetic accident, and some learned the truth only decades later. In Germany, a foundation was established in the early 1970s to provide payments, and in 2012 the chief executive of Chemie Grünenthal offered an apology to those affected. Groups representing survivors in Britain, Australia, Canada and elsewhere continued for years to seek compensation from the companies that had distributed the drug, and in several countries settlements were eventually reached.

Children grow at the ends of their long bones, in thin layers of cartilage known as growth plates, or epiphyseal plates. The tissue is organised into zones: in the resting zone, small cells act as a reservoir; in the proliferative zone they divide rapidly and line up in columns; and in the hypertrophic zone they enlarge, stop dividing and prepare the matrix for mineralisation. As new cartilage is laid down on the bone side of the plate and old cartilage is replaced by bone, the bone lengthens from within. The plates remain active until late adolescence, when they are finally converted into solid bone and growth stops.

Hormones coordinate this process, and the most important of them is growth hormone, a protein made and stored in the anterior pituitary gland, a pea-sized structure at the base of the brain. Growth hormone is not released steadily. It is secreted in pulses, the largest of which come during deep sleep, and levels also rise after exercise and after a meal rich in protein. The pituitary releases more of the hormone during childhood and adolescence, and production falls again in adulthood, when it helps to maintain muscle and bone rather than to increase height.

Growth hormone acts in two ways. It binds directly to receptors in some tissues, including fat and muscle, but most of its effect on the skeleton is indirect. It stimulates the liver, and to a lesser extent other tissues, to produce insulin-like growth factor 1, usually shortened to IGF-1.

This second hormone travels in the blood to the growth plates, where it encourages cartilage cells to multiply and to produce the proteins that form the scaffolding of bone. Blood levels of IGF-1 are therefore used by doctors as a rough measure of how much growth hormone the body is making. They also fall sharply when a child is malnourished, which is one reason why poor nutrition stunts growth.

Growth hormone does not work alone. Thyroid hormones, produced by the thyroid gland in the neck, are essential for normal development, and a child born with too little of them will grow poorly and may suffer permanent intellectual impairment unless treated early. In many countries newborns are therefore screened for congenital hypothyroidism, and treatment with thyroxine allows most affected children to grow and develop normally. Thyroid hormones appear to act partly by making the growth plates more responsive to growth hormone and IGF-1.

At puberty a further set of hormones takes over. Rising levels of sex hormones — testosterone in boys, oestrogen in girls, though oestrogen is important in both sexes — produce the adolescent growth spurt, during which a child may gain several centimetres in a year. The same hormones eventually close the growth plates, converting cartilage into bone and bringing growth to an end. Girls generally begin their spurt earlier and finish growing sooner than boys, which is one reason why adult men are, on average, taller.

Other hormones can hold growth back. Cortisol, produced by the adrenal glands in response to stress, slows the production of cartilage when present in excess, and children with conditions such as Cushing's syndrome, in which cortisol is chronically high, often stop growing. Long-term treatment with steroid medicines has a similar effect. Severe illness, malnutrition and psychological stress can also suppress the hormonal signals, which is why children who are unwell or badly fed may grow more slowly than their genes would predict.

Genes matter more than anything else. Studies of twins suggest that differences in height within a population are roughly 80 per cent attributable to genetic variation. Yet height is not controlled by a single 'tall' gene. Large studies comparing the DNA of hundreds of thousands of people have identified thousands of common variants, each with a tiny effect, and most of them lie in stretches of DNA that do not code for proteins but appear to regulate when and where genes are switched on. How these variants interact with one another, and with the environment, remains largely unexplained.

Environment nevertheless matters, as the history of the twentieth century shows. Average adult height rose substantially in many countries as nutrition, sanitation and healthcare improved, and in some populations it has since levelled off. The Netherlands, whose young men are now among the tallest in the world, illustrates how quickly such changes can occur: the increase there over the past century and a half is far too rapid to be explained by genes. Childhood infections, especially those that cause diarrhoea, are thought to divert energy from growth, and clean water and vaccination may therefore have contributed to the rise.

Some questions remain open. Researchers still do not fully understand how the growth plates finally close, or why some children who are ill for a period subsequently grow faster than expected and recover lost height. Nor can the height of a child be predicted with much accuracy from the parents' height alone. What is clear is that growth is a sensitive indicator of health: a child who falls behind the expected curve is often signalling a problem that has nothing to do with the bones themselves. Synthetic growth hormone, produced by genetic engineering since the mid-1980s, can now correct a genuine deficiency, though its benefit for healthy children who are simply shorter than their peers is small and disputed.

In most of the United Kingdom, a prescription costs the patient nothing. In England, it does not. Since the National Health Service began in 1948, charges for medicines have been introduced, abolished and reintroduced, and a patient in England now pays a fixed sum for each item dispensed, unless they belong to one of the exempt groups. The other three nations have abandoned the charge altogether: Wales in 2007, Northern Ireland in 2010 and Scotland in 2011. This divergence is rarely discussed at general elections, yet it raises a basic question about the funding of any health service: should the sick pay for their medicine at the moment they need it?

Charges were first imposed in 1952, when the government of the day was looking for money to pay for rearmament. A flat fee of one shilling per prescription was introduced, and although it was unpopular it survived until the Labour government abolished it in 1965. Three years later it returned, as part of an attempt to restrain public spending, and it has remained ever since, rising broadly in line with prices. The history is a reminder that the charge was never designed as a principle. It was a revenue-raising device, adopted and dropped according to the financial pressures of the moment. For most of its life the sum involved has been small, but its symbolic importance has always been greater than its value.

The present system of exemptions is a patchwork. Children, older people, pregnant women and new mothers, and people with certain long-term conditions receive their medicines free, as do those on low incomes. The list of qualifying conditions is long but inconsistent. A person with diabetes or epilepsy pays nothing; a person with asthma, which can also be life-threatening, pays for every inhaler. The result is that the charge falls most heavily on people of working age with chronic illnesses that are not on the list, and on those whose incomes are just above the threshold for help. Two patients with equally serious conditions may therefore face very different bills.

Critics of charging point to evidence that even modest fees deter people from taking medicines they need. Surveys in several countries have found that patients who are charged for prescriptions are more likely to skip doses, to delay filling a prescription or to take less than the amount prescribed, and that the effect is strongest among those on low incomes and those with several chronic conditions. The pattern is not confined to Britain: studies in the United States and Canada, where patients also pay part of the cost of their medicines, have reported similar findings. The sums involved may look small to a healthy person, but for someone collecting four or five items a month the total is not trivial. Doctors report that patients sometimes ask which of their medicines they can most safely go without.

Against this, defenders of the charge argue that it raises money for the NHS and discourages unnecessary demand. The revenue is indeed real, but it is small in the context of the service as a whole, amounting to a fraction of one per cent of its budget, and the cost of collecting it is not negligible. Staff time, printing, checks on exemption and the administration of prepayment certificates all consume part of what is raised. Prepayment certificates, which allow patients who need many items to pay a fixed annual amount, soften the effect for some, but they must be bought in advance and take-up is far from universal. The charge is also regressive: a larger share of the money comes from a minority of patients, many of them with long-term conditions, which is hardly the definition of a fair tax.

The stronger argument for charging is that free medicines may be wasted. A patient who pays nothing has no reason to think twice about ordering a cream or a painkiller that can be bought cheaply from a pharmacy, and unused medicines are a substantial expense. Some doctors would like to see charges retained for items of low clinical value while removing them for everything else. Yet the evidence that charges reduce waste is thin, and the value of a medicine cannot be judged by its price: a cheap tablet that prevents a stroke is worth far more than an expensive one that does little. Waste is better addressed by reviewing prescriptions than by taxing illness.

The founding principle of the NHS was that care should be free at the point of use, financed by general taxation and provided according to need rather than ability to pay. Prescription charges are an exception to that principle, and exceptions have a way of spreading: once it is accepted that patients should contribute towards some parts of their care, it becomes easier to argue that they should contribute towards others. My own view is that the charge should go. The revenue it raises is modest, the cost of collecting it is real, and the deterrent effect falls on the people whose health depends most on regular medication. Removing it would not by itself solve the problems of the NHS, but the money could be found by reallocating a small part of the budget, and the principle that illness should not be a source of financial worry is worth defending.