IELTS Academic Reading Practice Test 311

For centuries, students of medicine learned anatomy from the writings of Galen, who was born in Pergamon and practised in Rome during the second century AD. Galen's authority was immense, and it survived the collapse of the Roman Empire, the rise of Islam and the foundation of the first universities. His anatomical conclusions, however, rested largely on the dissection of animals rather than of people. Galen had cut open Barbary macaques, pigs, dogs and goats, and where the structure of these creatures differed from the human body, he assumed that the human body followed the animal model.

One consequence was a catalogue of errors that passed into medical teaching. Galen described a network of blood vessels at the base of the brain, the rete mirabile, which he believed cooled the vital spirit; the network exists in sheep and cattle but not in humans. He stated that the human liver had five lobes and that the lower jaw was formed of two bones. Because he had studied animals whose breastbone was built differently from ours, his account of the sternum was also wrong. Such mistakes were not trivial: for more than a thousand years, physicians who repeated them in lectures had no reason to doubt them and no reliable means of checking.

The man who undermined this tradition was born in Brussels in 1514, the son of a court apothecary. Andreas Vesalius studied at the University of Louvain and then in Paris, where he learned anatomy from the French physicians Jacobus Sylvius and Guinter of Andernach. Both were devoted followers of Galen, and the Paris faculty regarded a public dissection as an exceptional event. The supply of cadavers for teaching was scarce, and the professor who gave the lecture commonly sat in a high chair, reading aloud from a Latin text while an assistant, standing far below, pointed out the parts.

Vesalius came to regard this arrangement as absurd. In 1537 he moved to Padua, where he took a medical degree and was appointed professor of surgery and anatomy almost at once. There he changed the practice of dissection. Instead of reading while a servant did the cutting, he performed the work himself, invited students to handle the organs, and was willing to repeat a dissection when the first attempt had left a question unanswered. The city's authorities allowed him access to executed criminals, and he obtained bodies by less formal means when he had to.

Looking for himself produced results. In 1538 he published a set of anatomical drawings for students, and he soon demonstrated that the human jaw is a single bone, contradicting Galen directly. In the same year a judge in Padua permitted him to dissect the body of a criminal executed in the town, and Vesalius used the opportunity to trace the vessels and organs in detail. He also examined the text of Galen critically rather than reverently, and he noticed that several of its descriptions matched the anatomy of animals rather than that of people.

The fruit of this work was De humani corporis fabrica, On the Fabric of the Human Body, printed in Basel in 1543 by Johannes Oporinus when Vesalius was twenty-eight. It was a large and costly book, containing more than two hundred woodcut illustrations, and the quality of its printing and design set it apart from earlier anatomical texts. The illustrations are usually attributed to Jan Stefan van Kalkar, a Flemish artist who had been a pupil of Titian, though the attribution has been questioned. The book was also remarkable for its honesty: Vesalius recorded what he had seen and admitted when he could not explain why a structure existed.

The Fabrica did not immediately replace Galen. Vesalius was attacked by his own former teacher Sylvius, who defended the ancient texts with considerable bitterness and argued that the human body had altered since antiquity. Some anatomists observed that the book still contained Galenic ideas, particularly about the blood, which Vesalius, like Galen, believed to be manufactured in the liver. William Harvey's account of the circulation of the blood would not appear for more than sixty years, and Vesalius had no way of describing it.

Nevertheless the Fabrica established a method as much as a set of facts. Vesalius's insistence that the dissection itself, rather than the text read aloud, was the source of authority changed what students expected of a teacher. Within a generation, professors at Padua were producing their own observations and correcting him. Gabriel Falloppio, who held the chair of anatomy there from 1551, described structures that Vesalius had missed, including the tubes that now bear his name, and showed that some of Vesalius's own claims were mistaken.

In 1543 Vesalius left Padua to become physician to the Holy Roman Emperor, Charles V, and later served his son, Philip II of Spain. He continued to practise anatomy but published little. In 1564 he set out on a pilgrimage to Jerusalem, and on the voyage home he died, aged forty-nine, on the island of Zakynthos.

His death ended his career but not the influence of his book. The Fabrica was reprinted and abridged, and anatomists went on using its plates for centuries. Historians often describe it as a turning point, though it is fairer to see it as the beginning of a long argument. The book made it possible to prove Galen wrong about a bone or a vessel, and that possibility, once demonstrated, could not be withdrawn.

Skin is the body's largest organ and its main barrier against infection. It is also constantly being damaged, by cuts, burns, pressure and surgery, and unlike most tissues it repairs itself by producing a scar rather than by regenerating the original structure. The difference matters, because a scar is strong but it is not skin. Repair is not a single event but a series of overlapping stages, described separately below; in a real wound they shade into one another.

A cut sets off the first stage within seconds. The walls of damaged blood vessels narrow, and small cell fragments called platelets adhere to the exposed collagen fibres beneath the torn lining. Platelets are not merely plugs: they change shape, clump together and release chemical messengers that attract more platelets and trigger the coagulation cascade, a chain of reactions in which proteins circulating in the blood are activated one after another. The end product is fibrin, a tough, thread-like protein that forms a mesh across the wound and traps red blood cells inside it. Plug and mesh together make the clot that seals the breach.

Once bleeding is controlled, the site is dominated by immune cells. Signals released there make nearby vessels more permeable, so that fluid and white cells can leave the circulation. Neutrophils, the most numerous white cells, arrive first and engulf bacteria and debris. Within a day or two they are followed by monocytes, which mature into macrophages. Macrophages matter most in this phase: they consume dead tissue and spent neutrophils, and they release further signals that prepare the next stage. Redness, warmth, swelling and pain all follow from these changes in blood flow and vessel permeability.

Rebuilding begins while the clean-up continues. Fibroblasts, normally sparse in the skin, migrate into the wound and manufacture collagen, the protein that gives skin its tensile strength. They need oxygen and nutrients, and new capillaries sprout from existing vessels, a process called angiogenesis, to supply them. The result is granulation tissue, a pink granular material that fills the gap. In larger wounds, specialised fibroblasts called myofibroblasts then contract, drawing the edges together and reducing the area that must be covered; this is useful in a cut on the forearm but can restrict movement if it happens in the skin over a joint.

The outer layer, the epidermis, is restored by a different mechanism. Keratinocytes migrate from the wound edges and from the lining of hair follicles deeper in the skin, spreading across the raw surface until they meet cells arriving from the other side. Contact with another keratinocyte signals them to stop moving, and they then divide to rebuild the normal layered structure. The migration is quick: in a small abrasion the epidermis may be continuous again within days. A wound that removes only the epidermis therefore heals without a scar, because the framework beneath it is intact.

The final stage lasts for months or years. Collagen laid down early in repair is thin and disorganised; over time it is broken down and replaced by thicker fibres aligned along the lines of stress and joined by strong cross-links. The tissue's water content falls and the scar becomes paler and flatter. Even so, the result is imperfect. A healed wound rarely recovers more than about 80 per cent of the strength of uninjured skin, and scar tissue has no hair follicles or sweat glands, which is why a large scar does not sweat.

Sometimes repair does not follow this course. In diabetes, poor circulation and impaired immune function can delay healing, and a minor injury may become a chronic ulcer that persists for months. Infection prolongs inflammation and destroys newly formed tissue. In some people, particularly those with dark skin, the balance between collagen production and breakdown is disturbed: excess collagen produces a raised, thickened scar, called hypertrophic if it stays within the original wound and a keloid if it spreads beyond it. Where the cause of injury persists, as in repeated damage to the liver, the same process produces fibrosis, in which scar tissue replaces working cells.

Many questions remain. Researchers do not fully understand why some people scar heavily and others barely at all, or why wounds in the unborn heal with no scar, a capacity lost soon after birth. Macrophages, once treated as a single kind of cell, are now known to take several forms, some of which appear to promote repair and others to drive scarring, and this has become an active field of research. Trials of biological and cell-based treatments are under way, but no treatment has been shown to make a mature scar disappear, and much of what is sold as scar therapy rests on weak evidence. The most reliable advice remains unglamorous: keep a fresh wound clean and moist, and protect a healing scar from the sun.

Few public health measures provoke argument as immediately as a tax on sugary drinks. Supporters present it as a cheap, targeted instrument for reducing consumption of the one category of food most closely linked to obesity and tooth decay. Opponents call it a nanny-state levy that punishes ordinary shoppers, fails to change behaviour and quietly fills government coffers. Both descriptions contain some truth, which is why the argument is worth examining rather than dismissing.

The case for acting at all is strong. Sugar-sweetened beverages are, almost uniquely among foods, a source of what nutritionists call empty calories: they deliver energy without protein, fibre or micronutrients, and they appear to satisfy hunger poorly. The sugar they contain also reaches the liver quickly. Systematic reviews have linked regular consumption of these drinks to weight gain, type 2 diabetes and tooth decay, and the World Health Organization has recommended that intake be reduced, particularly among children. Where consumption is high, a small reduction across a whole population may achieve more than intensive treatment offered to a few individuals.

Dozens of countries and cities have now introduced such taxes, and the evidence from the earliest schemes is reasonably consistent. Mexico imposed a tax of one peso per litre in January 2014; studies of household purchasing data reported falls in purchases of taxed drinks of around six per cent in the first year, with larger falls among poorer households. Berkeley, in California, adopted a small municipal tax in 2015, and researchers there reported reductions in consumption. A pattern emerges: prices rise somewhat, purchases fall modestly, and the effect is concentrated where intake was highest.

The most instructive example may be the United Kingdom, which announced a levy in 2016 and brought it into force in April 2018, with two bands set by sugar content. The design was deliberately intended to encourage reformulation, and it worked. Many manufacturers cut the sugar in their drinks to bring them below the thresholds, and the average sugar content of the affected drinks fell substantially before a penny of tax had been collected. Revenue has therefore been lower than originally forecast. The levy changed what companies put in bottles more than it changed what shoppers paid, and the widespread job losses predicted by parts of the industry did not occur.

The objections deserve a hearing. The first concerns fairness. A tax on drinks takes a larger share of income from poor households than from rich ones, and if it does not change behaviour it simply leaves poor families worse off. Yet those same households are at the greatest risk of the diseases in question, and the taxes studied so far appear to reduce purchases most among them. Whether that counts as a fair exchange depends on what is done with the money. Where revenue has been spent on child health programmes, or on making drinking water available in schools, the case for the tax is much stronger than where it has vanished into general taxation.

The second objection is substitution. Anyone who wants a sweet drink can buy fruit juice, which is often exempt and may contain as much sugar, or can spend the money on confectionery instead. Studies have found substitution of this kind, but the effects are small. That is an argument for designing a tax broadly, and for combining it with other measures rather than relying on price alone.

The third objection is that the evidence on health outcomes is thin. It is one thing to show that people buy fewer sugary drinks, and another to show that they lose weight or develop less diabetes years later. Because these taxes are recent, the effect on obesity rates remains contested. Yet the standard of proof that critics demand here is stricter than the one applied to almost any other measure in public health, and waiting for certainty of that kind would mean waiting a very long time.

What, then, should be concluded? A tax on sugary drinks is not a solution to obesity, and anyone who presents it as one is overselling a modest tool. It does not teach anyone to cook, does not make streets safe to walk in and does nothing about the price of fresh food. But it does appear to reduce purchases of the products most strongly implicated in diet-related disease, at low cost and without damaging employment.

My own position is that such a tax is justified, provided it is well designed: levied on a clear measure of sugar, extended to cover drinks currently exempt, and with the revenue visibly directed towards children's health. To reject it because it does not solve everything is to demand that a single instrument carry a burden belonging to an entire policy. The objection to the levy is not that it does harm, but that it does less than its most enthusiastic advocates claim.