IELTS Academic Reading Practice Test 308

Florence Nightingale was born in 1820 in the Italian city whose name she was given, the younger daughter of a wealthy English family. Her education, at home and on a long tour of Europe, was unusually broad for a young woman of the period. Her father taught her mathematics, a subject rarely offered to girls at the time.

The life expected of her, however, was marriage, and when she announced that she wished to nurse the sick, her mother and elder sister were appalled. Nursing was then regarded as a lowly occupation, close to domestic service. She refused to be dissuaded. In 1851 she trained at a Protestant nursing school in Kaiserswerth, in what is now Germany. Two years later she became superintendent of a small hospital for gentlewomen in Harley Street, London.

War gave her a larger stage. In 1854 Britain, France and the Ottoman Empire were fighting Russia in the Crimea, and the wounded were shipped across the Black Sea to Scutari, now a district of Istanbul. A correspondent for The Times, William Howard Russell, described men lying in filth without blankets or bandages, and his dispatches caused outrage in London. Sidney Herbert, the Secretary at War, wrote to ask whether Nightingale would take a party of nurses to the East. She agreed, and arrived at Scutari on 4 November 1854 with 38 nurses, among them nuns and Anglican sisters.

Nothing had prepared them for what they found. The hospital was a vast stone barracks, hastily converted, and it stood above a sewer that was blocked and overflowing. Wounded men lay on straw in the corridors, two or three to a bed or on the bare floor, and there were few blankets, no laundry machinery and not enough clean water or linen. Rats were seen in the wards. The building had been designed for soldiers in good health, not for the sick. The medical staff, overwhelmed and short of everything, resented the arrival of women who were not under their orders.

Nightingale worked with administrative energy rather than medical skill. Using money subscribed by the British public, she bought food, bedding, shirts and socks, and had boilers installed so that the men's clothes could be washed. She set up a kitchen producing proper meals and a laundry in which sheets were boiled and scrubbed. She wrote letters home for soldiers who could not write. Each night she walked the wards with an oil lamp, the image that gave her the name by which she is still known.

What she could not do was prevent the deaths. The men died in thousands, and the cause was not their wounds. Typhus, cholera and dysentery swept through the crowded wards, and contaminated water and unemptied latrines did more damage than Russian shot. Nightingale did not yet understand this. Her own explanation, set out in letters to London, was that the men had been worn out by the campaign and were dying because they were exhausted and badly fed. She had reached the right building but not the right diagnosis.

Relief came from a different quarter. In March 1855 a sanitary commission sent from Britain inspected the hospital and ordered the sewers to be flushed, the drains repaired and the walls limewashed, and it insisted on better ventilation. Within weeks the death rate collapsed, from more than 40 per cent of those treated to about two per cent. More British soldiers died of disease during the war than were killed in battle, a fact that shaped everything Nightingale did afterwards. The lesson was not lost. The experience turned her into a lifelong campaigner for sanitation, convinced that most of the deaths had been caused by neglect.

She returned to Britain in 1856, worn out by a fever contracted in the Crimea, and for years was too ill to leave her bed. Work continued regardless. She gave evidence to a royal commission on the health of the army and compiled statistics showing how badly soldiers were housed and fed in peacetime. To make the figures intelligible to people who disliked numbers, she developed polar area diagrams, in which the area of each wedge was proportional to a death toll. These made plain that most of the deaths had been preventable. In 1858 she became the first woman elected a fellow of the Royal Statistical Society.

Her influence on nursing itself came through writing and teaching. Notes on Nursing, published in 1859, was addressed not to nurses but to anyone who kept house, and it sold in large numbers. A public appeal launched while she was still in the East had raised the Nightingale Fund. With this money she established a training school at St Thomas's Hospital in London, which opened in 1860. Its pupils were taught to observe, to record and to keep themselves and their wards clean, and they carried these habits into hospitals across Britain and overseas.

She lived until 1910, blind in old age and rarely seen in public, though she continued to advise governments on hospitals and on sanitation in India. She declined a state funeral and was buried, as she had asked, in the family plot at East Wellow in Hampshire. The lamp, the statistics and the training school outlived her, and so did the argument she had begun about whether medicine should concern itself with the conditions in which people fall ill.

The kidneys are a pair of bean-shaped organs about the size of a fist, lying at the back of the abdomen on either side of the spine, partly protected by the lowest ribs. Each is roughly ten to twelve centimetres long and weighs about 150 grams. Although they are small, they receive between a fifth and a quarter of all the blood the heart pumps. That blood arrives through the renal artery and leaves through the renal vein, while a tube called the ureter carries away the urine. Before it leaves, the urine gathers in a funnel-shaped cavity called the renal pelvis.

That generous blood supply is a clue to the kidney's method. The organ does not merely remove a few waste products; it filters the entire volume of the blood plasma many times a day, and then returns almost all of the water and most of the dissolved substances to the bloodstream, leaving a small concentrated residue of urea and other waste to be carried away as urine. In doing so it holds constant the concentration of sodium, potassium and other ions, the acidity of the blood and its total volume.

The work is done by about a million microscopic units in each kidney, called nephrons. Each begins with a cup, Bowman's capsule, enclosing a knot of capillaries known as the glomerulus. Blood arrives here at high pressure, and water and small molecules are forced through the walls of the capillaries into the cup, while cells and large proteins are held back. The filter is not a simple sieve. Its three layers — the pores of the capillary lining, a basement membrane and the narrow slits between the foot processes of cells called podocytes — also discriminate by electrical charge, so that some molecules of similar size pass more easily than others. The glomeruli lie in the outer region of the kidney, the cortex.

The result is a filtrate produced at a remarkable rate. In a healthy adult the glomeruli together turn out roughly 180 litres of fluid a day, well over a hundred times the volume of urine finally produced, and the rest is reclaimed. Most of this reabsorption happens in the first section of the tubule, which coils away from the capsule. Its cells are densely packed with mitochondria to power the pumping of sodium out of the filtrate, and water follows the sodium by osmosis, together with glucose, amino acids and other useful molecules.

The next section, the loop of Henle, is the part that allows the kidney to produce concentrated urine. It dips down into the inner region of the kidney, the medulla, where the fluid surrounding the tubules becomes progressively saltier. The descending limb of the loop is permeable to water but not to salt, so water leaves it; the ascending limb does the opposite, pumping salt out while water cannot follow. The result is a gradient of salt concentration in the medulla that the collecting ducts later exploit.

Final adjustment takes place in the collecting duct, which passes back through the salty medulla. How much water escapes from it depends on hormones. When the body is short of water, the pituitary gland releases vasopressin, which makes the duct walls more permeable, so water is drawn out and the urine becomes concentrated. Aldosterone, from the adrenal glands, increases the reabsorption of sodium. The kidney also senses for itself: cells in the wall of the tubule detect changes in salt and trigger the release of renin, which sets off a hormonal cascade that raises blood pressure.

Filtration is only one of the kidney's functions. The organ produces erythropoietin, the hormone that instructs the bone marrow to make red blood cells, and it completes the activation of vitamin D, without which calcium cannot be absorbed properly from food. It also regulates acidity by excreting hydrogen ions and returning bicarbonate to the blood. This is why advanced kidney disease damages almost every system in the body: patients become anaemic, their bones weaken and their blood becomes acidic.

Much about the kidney remains uncertain. The number of nephrons in a single kidney varies enormously between individuals, from a few hundred thousand to more than two million, and there is no easy way to count them in a living person. Nephron number falls with age and appears to be fixed before birth. A growing body of evidence links a low number at birth to a higher risk of hypertension and kidney disease in later life, but the reasons are disputed and it is not yet clear whether the association is causal.

Research is now directed at several fronts. Scientists have grown miniature kidneys, or organoids, from stem cells, which allow the development of the organ to be studied in the laboratory. Drugs developed for diabetes, known as SGLT2 inhibitors, have been found to slow the loss of kidney function in people with chronic disease, a discovery that has changed treatment. Roughly one adult in ten has some degree of chronic kidney disease, most of them undiagnosed, so cheaper ways of detecting it early are urgently needed. Transplant waiting lists remain long, and many donated organs are judged unsuitable and discarded.

None of this alters the central point. The kidney is not a filter that wears out so much as a system that keeps the internal environment stable, and that is why its failure is felt everywhere: in the blood, in the bones and in the heart.

Few public-health proposals divide opinion as sharply as the suggestion that advertising of unhealthy food to children should be prohibited. The idea is not new. Sweden and Norway have long restricted television advertising aimed at young children, the Canadian province of Quebec has banned commercial advertising directed at children since 1980, and Chile has gone further, combining restrictions with warning labels on packaged food. Britain has legislated to restrict such advertising on television before 9pm and in paid online advertising. The question is whether measures of this kind do any good.

The case for protecting children rests on two claims. The first is that children are not simply small adults. Research suggests that children younger than about eight seldom recognise that an advertisement is trying to persuade them, and they take its claims at face value. The second is that although children have little money of their own, they influence what their households buy, and habits formed in childhood tend to persist. The volume of such advertising is considerable, and much of it promotes products that nutritionists would place in the least healthy category. If both claims are accepted, the ordinary argument for a free market in advertising, which assumes a consumer able to judge the message, does not apply to them.

There is now a good deal of evidence that advertising changes what children want. A review of experimental studies published in 2016 found that children who were shown food advertisements ate more at a subsequent meal than children who were not, and that the effect was largest for foods high in sugar and fat. Surveys point the same way, though less reliably: children who watch more commercial television tend to request and consume more of the products advertised. What such studies show is a short-term influence on preference and intake, not an effect on body weight over years.

Whether banning advertising reduces obesity is much harder to establish, because the experiment cannot be run in a laboratory. The natural experiments available are few and their results mixed. Quebec's restrictions have been studied repeatedly, and some analyses have found lower spending on fast food in the province than in neighbouring Ontario, while others have found little difference in obesity. Even where a change is detected, it is difficult to separate the effect of an advertising ban from everything else happening at the time, and media markets do not respect provincial borders.

Chile offers the most ambitious test. From 2016 it required black warning labels on packaged foods high in sugar, salt or fat, banned their sale in schools and restricted their advertising to children. Researchers who tracked household purchases reported a fall of about a quarter in purchases of sugary drinks after the law took effect. The difficulty is one of attribution. The law was a package, and its labelling rules, which changed what shoppers saw on every shelf, may have done at least as much as the restrictions on advertising.

Two practical difficulties deserve mention. The first is definition. No government wishes to ban the advertising of cheese, olive oil or breakfast cereal, yet the boundary between healthy and unhealthy food is not always obvious, and the nutrient profiles used to draw it are contested by manufacturers. The second is that much advertising no longer looks like advertising. A cartoon character on a package, a sponsored sporting event or a video by a popular online personality may promote a product without ever making a claim, and rules written for spot advertisements struggle to capture them.

Critics of restriction make three arguments. The first is that responsibility belongs with parents, who are better judges of their own children than any regulator. The second is that a ban would be a modest intervention with a real cost to broadcasters, publishers and small businesses. The third, and the strongest, is that regulation chases advertising around the problem. Television is comparatively easy to control; promotion on social media, inside games and through online personalities is not, and restrictions on broadcasters may simply shift money to channels that nobody has yet learned to police.

None of these arguments is decisive. The parental argument confuses two questions: parents may be responsible for feeding their children, but they cannot filter every message their children see, and the sheer volume of advertising is not something an individual household can control. The enforcement argument is a reason to design regulation carefully, not a reason to abandon it. The cost to industry is real, but modest when set against the costs of diet-related disease.

My own view, then, is that a ban on advertising unhealthy food to children is justified, but that we should be honest about what it can achieve. It is a proportionate restriction, aimed at a group that cannot defend itself, and it will not by itself reverse the rise in childhood obesity. It should be introduced alongside other measures and reviewed, and it must cover the digital world if it is not to be made meaningless within a decade. A ban is worth having, provided nobody pretends that it is sufficient.