IELTS Academic Reading Practice Test 383

For thousands of years people have eased pain and fever with preparations made from plants containing salicylates, the family of chemicals to which aspirin belongs. Willow leaves appear in records from ancient Mesopotamia, and willow bark features in Egyptian medical texts. The Greek physician Hippocrates, writing in the fifth century BC, is said to have recommended a bitter powder obtained from willow bark for pain and fever. Similar remedies were used in traditional medicine across Europe, Asia and North America, from meadowsweet to the bark of birch trees.

The active ingredient was not identified until the nineteenth century. In 1828 a German pharmacist named Johann Buchner extracted a yellow crystalline substance from willow bark and called it salicin, after the Latin name for the willow. Other chemists improved the method, and salicin was eventually converted into salicylic acid, the compound chiefly responsible for the relief of pain. Salicylic acid worked, but it had serious disadvantages. It irritated the lining of the stomach, and some patients could not tolerate it at all. Chemists therefore began to search for a modified version of the molecule that would keep the benefits while causing less discomfort.

The first person to make such a compound was the French chemist Charles Gerhardt, who in 1853 treated sodium salicylate with acetyl chloride and obtained acetylsalicylic acid. His product was impure and unstable, and he did not pursue it further. Salicin itself remained a crude remedy, and its journey from bark to bedside depended on the new science of organic chemistry. A German chemist produced the same substance a few years later, again without developing it as a medicine, and for the rest of the century acetylsalicylic acid remained in the chemical literature, a curiosity rather than a treatment.

The decisive work was carried out in the laboratories of Bayer, a German company that had begun as a maker of dyes and had recently moved into medicines. In 1897 a young chemist there, Felix Hoffmann, found a reliable way of producing pure acetylsalicylic acid. Accounts of the discovery often mention that his father suffered from rheumatism, and that Hoffmann was looking for a remedy that would ease the condition without damaging the stomach. Tests supervised by the company's pharmacologist, Heinrich Dreser, indicated that the new compound was better tolerated than salicylic acid, and Bayer patented the process.

Bayer put the drug on the market in 1899 under the name Aspirin. The name pointed to the plant world: Spiraea, the genus that includes meadowsweet, had long been a source of salicylates, and the ending was a common one in chemical names. The initial letter has often been explained as standing for acetyl, although the company never gave a definitive account of its choice.

Success was rapid and international. Aspirin was sold as a powder at first, and from the early twentieth century also as a tablet, which was easier to take and to carry. Doctors welcomed a remedy that relieved pain and fever without the drowsiness caused by opiates, and by the 1920s the drug was in use around the world. Its commercial history was less straightforward. After the First World War, Bayer's rights to the name were seized in several Allied countries as part of the peace settlement, and aspirin became a generic word in the United States, Britain and France, where any manufacturer could use it.

For decades no one could explain how the drug worked. That changed in 1971, when John Vane, working at the Royal College of Surgeons in London, showed that aspirin blocks the production of prostaglandins, a group of hormone-like substances that the body makes in response to injury and that generate pain and fever. Vane shared the 1982 Nobel Prize in Physiology or Medicine for the discovery. The finding transformed the understanding of inflammation, and it also explained the drug's side effects, since the same prostaglandins help to protect the lining of the stomach.

A second chapter opened with the heart. In the 1950s a Californian general practitioner, Lawrence Craven, noticed that his patients who took aspirin regularly appeared to have fewer heart attacks, but his reports attracted little attention. The idea was tested properly in the United States in a trial whose results were published in 1988. More than 22,000 male physicians took either aspirin or a dummy tablet every other day, and those given aspirin suffered about 44 per cent fewer first heart attacks. Bleeding, however, was more common among them.

Such findings turned a familiar painkiller into a preventive medicine, prescribed in small daily doses to people who had already had a heart attack or a stroke. The 1980s brought a warning about children as well. Researchers linked aspirin given during a viral illness to Reye's syndrome, a rare but serious condition affecting the liver and the brain, and regulators advised against its use in young children. In 2019 new American guidelines concluded that, for most healthy older adults, the risk of serious internal bleeding outweighed the modest protection aspirin offered against a first heart attack.

Aspirin remains one of the most widely used medicines in the world and is among the essential medicines listed by the World Health Organization. Its story shows how a remedy known in antiquity became, through chemistry and clinical trials, a drug whose benefits and dangers are both understood in remarkable detail.

Inflammation is the immune system's response to infection, injury or irritation, and it is essential to survival. Without it, a cut finger would never heal and a minor infection could spread unchecked. Doctors have described its outward signs since antiquity: the Roman writer Celsus, in the first century AD, listed redness, heat, swelling and pain, and a fifth sign, loss of function, was added many centuries later. The English word derives from the Latin inflammare, meaning to set on fire, a reference to the heat of an inflamed wound. Acute inflammation is short-lived and usually beneficial, fading once the threat has gone. Chronic inflammation, by contrast, persists for months or years and is now thought to contribute to a wide range of diseases.

The process begins when cells stationed in the tissue detect that something is wrong. Mast cells, which are especially numerous in the skin, the lining of the gut and the airways, release histamine and other chemicals within minutes of an injury. These substances act on the small blood vessels nearby. The vessels widen, so that more blood reaches the area, producing the redness and warmth that Celsus observed. They also become more permeable, allowing fluid and proteins to leak from the blood into the surrounding tissue. The accumulation of fluid is what we call swelling, and the pressure it creates, together with chemicals that sensitise nerve endings, produces pain.

White blood cells are then recruited. Neutrophils, the most abundant type of white cell, normally travel in the bloodstream, but chemicals released at the site of damage attract them to the vessel walls, where they squeeze through the gaps and follow the chemical trail towards the problem, a process called chemotaxis. Once there, they engulf bacteria and debris in a process known as phagocytosis. Neutrophils are short-lived and highly aggressive, and the dead cells that collect at the site are a major component of pus. When an infection is severe, the bone marrow produces them in enormous numbers, which is one reason a serious illness leaves a patient exhausted.

Neutrophils are followed by monocytes, which mature into macrophages when they enter the tissue. Macrophages are larger and longer-lived. They consume dying neutrophils and damaged cells, and they release signalling molecules called cytokines. These coordinate the whole response, calling in further immune cells and instructing the liver to produce certain proteins. They also act on the brain, which is why inflammation is often accompanied by fever, tiredness and a loss of appetite. Some cytokines travel to the hypothalamus, the region that regulates body temperature, and reset it to a higher level, while others make the muscles ache.

For a long time, the end of inflammation was thought to be passive: the response simply faded as the threat disappeared and the chemical signals ran out. Research over the past few decades has changed that picture. Resolution is now recognised as an active process, driven by a family of molecules that the body makes from the same fats as the inflammatory signals themselves. These mediators, which include lipoxins and resolvins, switch off the recruitment of white cells and encourage macrophages to clear away debris, and they promote the repair of tissue. If this switching mechanism fails, inflammation can continue long after the original cause has gone. Aspirin and ibuprofen, which block the production of prostaglandins, ease the symptoms but do nothing to speed resolution.

Chronic inflammation is the price of a system that does not switch off. It may result from a persistent infection, from an autoimmune disease, in which the body's defences turn on its own tissues, or from irritants such as tobacco smoke. Increasingly, however, researchers describe a quieter form, in which low levels of inflammatory activity persist for years without an obvious cause. This has been linked statistically to atherosclerosis, type 2 diabetes, several cancers and some forms of dementia. The associations are consistent across large studies, but they do not on their own prove that inflammation is doing the damage. The risk rises with age, with obesity and with inactivity, which suggests that lifestyle influences this background activity.

How inflammation should be measured remains unsettled. Blood tests for markers such as C-reactive protein are widely used, but they give only a general indication and say nothing about where in the body the activity is occurring. Whether inflammation drives chronic disease or merely accompanies it is also disputed. A large trial reported in 2017 offered some of the strongest evidence so far: an anti-inflammatory drug given to people who had already had a heart attack reduced the number of further cardiac events, but it also increased the risk of serious infection. The result supports the idea that inflammation matters, while showing why suppressing it is not simple. Researchers are now trying to design drugs that imitate the body's own resolving molecules, in the hope of switching inflammation off rather than blocking it altogether. None has yet reached routine use.

In Britain, a shopper can drop a packet of paracetamol into a basket beside the groceries, while in some other countries the same drug may be bought only in a pharmacy, and in a few it requires a doctor's prescription. British law recognises three categories of medicine: those available only on prescription, those that a pharmacist may sell after a brief conversation with the customer, and those on the general sales list, which any shop may stock. Painkillers appear in all three. Where the most familiar of them should be sold is not a trivial question.

Paracetamol is a good place to begin, because its dangers are unusual. It is among the most common causes of acute liver failure in Britain, and the damage is done not by the drug itself but by a breakdown product that the liver produces when its normal pathways are overwhelmed. In 1998, legislation restricted the size of packs that could be sold: a general-sale packet was limited to 16 tablets and a pharmacy packet to 32. Similar limits exist in many other countries. Deaths from paracetamol poisoning fell in the years that followed, and the change is often cited as a public-health success.

The fall in deaths is real, but the lesson drawn from it is often the wrong one. The measure that accompanied it was a limit on quantity, not a change in the kind of shop allowed to sell the drug, and the restrictions applied to pharmacies as well as to supermarkets. Those who argue that all painkillers should be kept behind a counter therefore cannot claim this evidence as their own. What it shows is narrower: that reducing the number of tablets available in a single purchase reduces the harm that can be done in a moment of despair.

Nor is paracetamol the only concern. Regular use of non-steroidal anti-inflammatory drugs such as ibuprofen carries its own hazards, including bleeding in the stomach and, at high doses over long periods, an increased risk of heart and kidney problems. These drugs can also interact with medicines taken for other conditions, and for people with asthma some of them may worsen the symptoms. A packet sold from a shelf, with nothing but a label to guide the buyer, offers no opportunity to catch such problems before they occur.

This is the strongest argument for pharmacy-only sale. A pharmacist, unlike a shelf-stacker, is trained to ask about other medicines and about conditions such as asthma or stomach ulcers. That conversation takes less than a minute, but it can prevent a hospital admission. Pharmacists also see the same customers repeatedly, and they are well placed to notice when someone is buying painkillers far more often than a minor headache would explain. In principle, at least, the counter is a checkpoint that a supermarket aisle is not. Anyone who has bought painkillers in several pharmacies will know that the conversation is not always as thorough as this description implies.

Against this must be set the practical costs. Pharmacies close in the evening and at weekends, and for people living in the countryside the nearest one may be many miles away. A rule intended to protect the public would, in practice, leave some of them without any painkiller at all on a Sunday night. A packet bought in a pharmacy typically costs several times what a supermarket charges, and the difference falls hardest on those least able to pay it. Supermarkets can keep prices low because selling a packet takes no more time than selling a loaf of bread.

Australia offers a recent test case, though of a narrower kind. In 2018 it moved products containing codeine, a mild opioid included in many combination painkillers, to prescription-only status. Sales of these products fell sharply, and several studies have since reported reductions in codeine-related harm. Yet the change was not costless: some patients with chronic pain found it harder to obtain relief, the extra consultations added to the workload of general practitioners, and pharmacists were left to explain the new rules to customers who had relied on the old ones. Restriction had done good, but it had also displaced a burden rather than removing it.

What, then, should be done? The sensible answer is not a single rule for every painkiller but a graded one. Small packs of paracetamol and ibuprofen, which carry a low risk when used as directed, should remain on open sale, subject to strict limits on quantity and clear warnings on the label. Larger packs, combination products containing codeine, and medicines whose overdose is especially dangerous should be sold only where a pharmacist is present. If that is to mean anything, pharmacists need time to talk, and time has to be paid for. A blanket ban, by contrast, would impose real costs on people with a headache and a bus fare to spare.

Those who want every painkiller behind a counter are asking the right question but offering too blunt an answer. Regulation should follow risk rather than habit. A policy that keeps cheap pain relief within reach of everyone, while placing the more dangerous products where advice is available, would reduce harm more effectively than a rule that treats a packet of paracetamol as though it were a controlled drug.