IELTS Academic Reading Practice Test 337

In the first decade of the twentieth century, visitors to parts of the rural American South noticed a pattern of listlessness that appeared to affect whole communities. Children were pale and undersized, labourers in the fields tired after a few hours, and many adults were set down as simply lazy. The soil, warm and damp for much of the year, suited the survival of a parasite, and the habit of going barefoot out of doors gave that parasite an easy route into the human body.

The worm was identified by Charles Wardell Stiles, a zoologist employed by the United States government. Stiles had studied in Europe, where he learned to recognise the eggs of parasitic worms in human waste, and samples from patients in the South contained eggs of a kind not previously reported there. In 1902 he described the worm as a new species, and the following year he placed it in a new genus, giving it the name Necator americanus, from Latin words meaning 'American killer'. The name was inaccurate in one respect, since the worm is now thought to have been carried to the Americas from Africa, but it drew attention to a genuine danger.

An adult hookworm is slender and barely a centimetre long, and it lives attached to the lining of the small intestine, where it feeds on blood. A female worm releases thousands of eggs a day, which pass out of the body in faeces and hatch in warm, moist soil. The larvae survive for weeks in damp shade and enter a new host by penetrating the skin, usually between the toes of a child with no shoes. From there they travel in the blood to the lungs, are coughed up and swallowed, and so reach the intestine, where they mature. A heavy infection causes anaemia, because the worms remove blood and the body loses iron faster than it can replace it.

The South provided almost ideal conditions for this cycle. The soil was often sandy and well drained, farm workers commonly went without shoes, and many rural households had no toilet, so waste was left in woods, fields or shallow holes near the house. Infection was therefore widespread, especially among the poorest families. Stiles argued that the condition was not a moral failing but a disease that could be diagnosed, treated and prevented, a claim that some Southerners took as an insult to their region.

Persuading others took years. Stiles wrote reports and lectured to medical societies, and eventually attracted the interest of John D. Rockefeller, the oil magnate, who was looking for a way to fund work of practical benefit. In 1909 Rockefeller gave one million dollars to establish the Rockefeller Sanitary Commission for the Eradication of Hookworm Disease. The commission began work in the following year under the direction of Wickliffe Rose, a former professor of philosophy, and it operated through state boards of health that were asked to share the cost.

The commission's most visible activity was the travelling dispensary. Where infection was suspected, a team would arrive with microscopes and set up in a school or a courthouse. Local people were invited to bring a small sample of faeces, which was examined on the spot, and anyone found to be infected was treated free of charge. The standard remedy was a dose of thymol, a compound obtained from thyme, followed some hours later by a purge of Epsom salts to carry the paralysed worms out of the body.

Drugs alone could not prevent reinfection while the ground around a house remained contaminated, so the campaign also promoted sanitation. Families were encouraged to build a privy, a small outdoor toilet with a sealed pit, and the commission supplied designs and practical advice. The message was carried by posters, pamphlets, lantern slides and talks in schools, and children were enlisted to pass it on at home. Rose insisted that the aim was not merely to cure individuals but to change habits, and he counted privies as well as patients.

The campaign was energetically reported in newspapers, which popularised the phrase 'the germ of laziness'. Not everyone welcomed it. Some doctors doubted that so small a worm could cause so much ill health, and some politicians resented the suggestion that their communities were backward. Others objected that the work was financed by a northern industrialist. Support from local physicians, teachers and editors gradually overcame this resistance, and the commission's surveys produced the first systematic picture of the disease.

By the time the commission closed in 1914, its programme had been absorbed into the public health work of the Rockefeller Foundation, which later extended similar campaigns to other parts of the world. Hookworm infection fell sharply in the counties that had been surveyed, although it never disappeared entirely, and its decline owed as much to rising incomes, paved roads and piped water as to medicine. The commission's lasting contribution was less the drug it distributed than the principle that a government could survey a population, measure a disease and act on what it found.

Soil-transmitted worms remain a serious problem elsewhere. The World Health Organization estimates that hundreds of millions of people, many of them children in low-income countries, carry hookworm or related parasites, and deworming tablets are distributed regularly in many schools. But the logic of the campaign of 1910 — find the cases, treat them, and improve the sanitation that lets the worm spread — has changed remarkably little.

The human foot is often described as a single arch, but it contains three. The medial longitudinal arch, which runs along the inner edge from heel to toes, is much the highest and is the one most people mean when they speak of 'the arch'. A lower lateral arch runs along the outer edge, and a transverse arch curves across the middle of the foot from side to side. Together these curves turn twenty-six small bones, linked by ligaments and moved by muscles, into a structure that can absorb the impact of a landing and then stiffen to push the body forward.

The medial arch is built like a bridge. The calcaneus, or heel bone, forms the pier at the back, and the heads of the metatarsals form the pier at the front. At the summit sits the talus, which receives the weight of the leg through the shin bone above it and passes it down and forward. In front of the talus is the navicular, then three cuneiform bones, then the first three metatarsals. Because the talus carries the load and transmits it in two directions, anatomists often call it the keystone of the arch.

A bridge of this kind would collapse without something to hold its ends together, and in the foot that role is played by ligaments and by a broad band of fibrous tissue in the sole. The plantar fascia runs from the heel bone to the base of the toes and is thickest towards the heel. Beneath the head of the talus lies a short, strong ligament, the plantar calcaneonavicular ligament, commonly called the spring ligament. It stops the talus from sinking between the bones on either side of it. These structures are passive: they resist load without contracting.

Active support comes from muscles, most of them in the lower leg. The most important is tibialis posterior, whose tendon passes behind the inner ankle bone and attaches mainly to the navicular. It pulls the arch upward and inward each time the foot takes weight, and if it becomes stretched the arch gradually collapses. Tibialis anterior and the long flexors of the toes assist it. On the outer side, the peroneus longus tendon runs under the foot and helps to hold the transverse arch in shape. Small muscles within the sole, the intrinsic muscles, adjust the curve as the body moves over the foot.

In 1954 the anatomist J. H. Hicks described an elegant mechanism that links the toes to the arch. When the toes bend upwards, as they do at the end of every step, the plantar fascia is wound around the heads of the metatarsals and pulled tight, and the arch rises. Hicks compared the effect to a windlass, the winch used on sailing ships to haul up the anchor, and the name has stuck. The tightened fascia also turns the flexible foot into a rigid lever, so that the muscles of the calf can lift the heel and drive the body forward.

Because the arch flattens when it is loaded and springs back when the load is removed, it can store energy in the manner of a leaf spring. In 1987 a team of British biologists led by R. F. Ker calculated how much energy the structures of the foot could hold and release during running. They concluded that the arch returned a worthwhile fraction of the energy put into it at each step, though they did not claim that this was the foot's principal economy measure. Elastic structures of this kind are common in animals that run and hop, and some researchers have tried to estimate what proportion of the total work of running is saved in this way.

Not every foot has a conspicuous arch. Infants have flat feet, partly because their ligaments are loose and partly because a pad of fat fills the sole. The curve usually becomes visible around the age of five, once the child has been walking for a couple of years. A flexible flat foot, which flattens under load and recovers when the foot is lifted, is common and usually painless. A rigid flat foot, in which the bones themselves are fixed in a flattened position, is rarer and more often a sign of an underlying problem.

Whether the height of the arch matters for injury is surprisingly unclear. Reviews of the evidence have repeatedly found only weak associations between a low arch and the injuries that runners most often suffer. Some studies suggest that both very high and very low arches carry a slightly raised risk. One reason for the uncertainty is that researchers measure the arch in different ways, from footprints, photographs, X-rays or callipers, so findings are hard to compare. Long-term studies that follow large groups of people and measure the arch consistently would help, but such work is expensive and rare.

Modern research has added detail without settling the argument. Pressure sensors placed in shoes record how the load travels across the sole, and magnetic resonance imaging allows the bones and ligaments to be modelled in three dimensions while the foot bears weight. It has also revived an old question about footwear: whether heavily cushioned shoes weaken the foot's own spring, or protect it, remains disputed. Wearable devices that record steps over many months have begun to supply data that a single laboratory visit cannot, although such records come from people who are already interested in their own health.

Governments have taxed tobacco and alcohol for centuries, and in the past decade several have begun to tax sugary drinks. The idea of applying the same approach to red meat, which campaigners have advocated for some years, has until recently been treated as eccentric. That is changing. A growing number of public health researchers argue that the evidence on processed meat in particular is strong enough to justify a tax. They add that the costs of diet-related disease fall on everyone, not only on those who eat the food. I think they are partly right.

The health case begins with the classification published by the International Agency for Research on Cancer in 2015. The agency placed processed meat — bacon, ham and sausages — in its highest risk group, and classified fresh red meat as probably carcinogenic. Group 1 does not mean that a rasher of bacon is as dangerous as a cigarette; it means that the evidence of a link is considered strong. The agency estimated that a daily portion of 50 grams of processed meat raises the risk of colorectal cancer by about 18 per cent, and that diets high in processed meat are associated with some 34,000 cancer deaths a year worldwide. The agency noted that the risk rises with the amount eaten, and that the case against fresh red meat is weaker and less consistent than the case against processed products.

That is a small risk for an individual and a substantial one for a population, because so many people eat these products. Against this must be set the nutritional value of meat. Red meat is a rich source of iron in a form the body absorbs easily, as well as zinc, vitamin B12 and complete protein. For young children and women of childbearing age, and above all in poorer countries where diets are monotonous, meat does real good. A tax that raised its price could do real harm. A tax designed badly, or set too high, could therefore reduce the quality of some people's diets while claiming to improve it.

Price does change behaviour. Taxes on sugary drinks in Mexico and in Britain have been followed by falls in purchases, and in Britain by the reformulation of many products. The lesson of Denmark is more sobering. The government introduced a tax on saturated fat in 2011 but repealed it in 2012, after complaints from retailers and evidence that shoppers were crossing the border for cheaper food. Food taxes are also regressive: because poorer households spend more of their budget on food, they pay a greater proportion of their income in such taxes.

The regressive objection is serious but not decisive. Diet-related disease is itself concentrated among poorer households, so a policy that reduces it delivers most of its benefit there. The harm can be offset if the revenue is used deliberately: to cut the price of fruit and vegetables, to fund school meals, or simply to raise the incomes of the poorest. Whether governments would in practice do that is a fair question, but it is a question about design, not about whether the tax is justifiable in principle.

Modelling studies go further. Several have estimated the tax rates that would be needed to reflect the health costs of red and processed meat, and have concluded that such taxes would prevent a large number of deaths. These models are useful for showing the scale of the possible effect, but they depend on assumptions that are hard to test. They generally assume, for instance, that consumers respond by buying beans, fish or vegetables. In practice people may switch to cheaper meat, or to cheese and eggs, and no country has yet run a tax on red meat that could show what really happens.

The practical objection is strongest for fresh red meat, which is hard to define and deeply embedded in cooking and culture. Processed meat is a different matter. It is a limited and recognisable category, its health record is the worst, and much of it is eaten in products whose value as food is modest. Meat producers argue, understandably, that a tax would cost jobs, and their lobbying has so far deterred governments from acting.

There is also an environmental argument for eating less meat, since livestock farming occupies a great deal of land and produces greenhouse gases. It would be a mistake to build the case on it. The argument for a tax should rest on health, or it will collapse as soon as someone points out that grazing animals can be raised on land that will grow nothing else. Farming organisations also dispute the health figures, though they rarely dispute the environmental ones.

My conclusion is therefore narrower than that of many campaigners. A modest tax on processed meat is justified: the evidence of harm is consistent and the category is easy to define. The products it covers are not important sources of nutrients that are hard to obtain elsewhere. The revenue should be used to make healthy food cheaper and to protect poor households. A general tax on fresh red meat, by contrast, is not justified at present, and recycling the revenue would not make it so. Meat is not tobacco: advice to eat less of it is sound, but a tax on all of it is not. What is needed is a targeted measure that a government could defend with evidence.