IELTS Academic Reading Practice Test 366

When the Second World War ended, tuberculosis remained one of the leading causes of death in Europe. Patients were sent to sanatoria, where treatment consisted of rest, fresh air and good food, sometimes supplemented by surgery that collapsed an affected lung in the hope that it would heal. None of these measures was reliably effective. Some patients recovered and others died, and doctors had no means of knowing in advance which would happen. In Britain, tens of thousands of people died of the disease every year in the 1940s. The bacterium spread through the air, and no vaccine was in general use.

The first drug capable of attacking the bacterium responsible was identified in 1943. Albert Schatz, a graduate student working in the laboratory of the soil microbiologist Selman Waksman at Rutgers University in New Jersey, was studying micro-organisms that live in soil and the substances they produce to inhibit their competitors. From a culture of Streptomyces griseus he isolated a compound that stopped the tubercle bacillus from growing. The substance, named streptomycin, was the first antibiotic shown to be active against tuberculosis. Waksman's laboratory had produced other antibacterial compounds before, but none had proved both effective and safe enough for patients.

Supplies of the new drug were minute. Streptomycin was difficult and expensive to manufacture, and in the late 1940s only small quantities could be produced each month. British hospitals could obtain it, but not enough for every patient who might benefit. Doctors therefore faced an awkward question: with so little of the drug available, how should it be used? Case reports from single hospitals could not answer it, because tuberculosis varied so greatly in its course that no physician could judge a treatment by impression alone, and clinicians across the country pressed for guidance.

In 1946 the Medical Research Council, Britain's main publicly funded body for medical research, set up a committee to test streptomycin properly. Among its members was the medical statistician Austin Bradford Hill. Hill argued that the decision about which patients received the scarce drug should not rest with doctors, whose judgement might be swayed by a patient's apparent chances, but should be made by chance. He prepared a series of sealed envelopes holding allocations derived from a table of random numbers.

Patients were admitted only if they met strict criteria. They had to be young adults with progressive pulmonary tuberculosis confirmed by laboratory tests, and their disease had to be unsuitable for the surgical treatments then in use. Each patient was then matched with the next envelope in the series. Those allocated to treatment received streptomycin for several months in addition to the standard bed rest that every participant received; those in the control group received bed rest alone. Chest X-rays were assessed by clinicians who were not told which group a patient belonged to.

The results, published in the British Medical Journal in 1948, were unambiguous. Six months after entry, four of the 55 patients given streptomycin had died, compared with fourteen of the 52 controls. Fever and weight loss improved in the treated group, and X-rays showed improvement in many of them. The drug was not a cure. In some patients the tubercle bacillus became resistant, and in others treatment had to be stopped because the drug damaged the nerves of the inner ear, producing dizziness and loss of balance. Because the study had been designed in advance, these findings could be reported with a confidence that no earlier series of cases allowed.

The trial is now often described as the first randomised controlled trial in clinical medicine, a claim that historians qualify. Random allocation had been used before, and the Medical Research Council had recently run a trial of patulin, a supposed treatment for the common cold, in which patients were allocated alternately. What made the streptomycin study distinctive was the combination of genuine randomisation, a concurrent control group, clear criteria for entry and a statistical plan agreed before the results were seen. Its influence came less from any single innovation than from the fact that the method was set out in a form others could copy.

Withholding a promising drug from seriously ill patients raised obvious ethical difficulties, and the committee discussed them at length. The shortage resolved the dilemma: since there was never enough streptomycin for everyone, somebody had to decide who would receive it, and a random decision was at least free of favouritism. Had the drug been plentiful, a controlled comparison would have been much harder to defend. The principle that emerged, that an unproven treatment may be tested against no treatment only while genuine uncertainty remains, has been invoked in every debate about trial ethics since.

Streptomycin transformed the treatment of tuberculosis, but it did not remain the standard on its own. Physicians soon learned that giving a single drug encouraged resistance, and from the early 1950s patients received combinations. Credit for the discovery was disputed for decades between Waksman and Schatz, who was little recognised at the time; Waksman received the Nobel Prize in Physiology or Medicine in 1952, and a legal settlement later gave Schatz a share of the royalties. Hill was knighted in 1961, by which time randomisation had become a routine requirement for any claim about a new treatment. Multiple drugs remain the basis of treatment today.

Alcohol is one of the few drugs that most adults in many countries consume regularly, yet the body treats it as a substance to be cleared as quickly as possible. The alcohol in beer, wine and spirits is ethanol, a small molecule that mixes freely with water and passes easily through the membranes of cells. Because of this it needs no digestive enzymes to be absorbed: it slips through the walls of the digestive tract intact and enters the bloodstream, from which it reaches almost every tissue, including the brain. The liver does most of the work of removal.

Absorption begins in the stomach, where a small proportion of the ethanol passes into the blood, but most of it is taken up in the small intestine, which has a far greater surface area. From there it travels in the portal vein directly to the liver, so that the organ meets a concentrated dose before the rest of the body does. This first pass matters: the lining of the stomach contains some alcohol dehydrogenase, the enzyme that starts the breakdown, and the liver removes a fraction of what arrives. The presence of food delays all of this, because a meal slows the rate at which the stomach empties into the intestine.

Inside the liver cells the main route of disposal is a two-step sequence. Alcohol dehydrogenase converts ethanol into acetaldehyde, a compound considerably more toxic than the alcohol itself. A second enzyme, aldehyde dehydrogenase, then converts acetaldehyde into acetate, a harmless substance that other tissues can burn as fuel. Both steps depend on the availability of a molecule called NAD+, and the liver's supplies of it are finite, which is one reason the organ's capacity to process alcohol is limited.

Acetaldehyde is the reason that drinking makes some people flushed, headachy and sick. The enzyme that clears it comes in variants, and one common variant, found in a large proportion of people of East Asian descent, produces a version that works far more slowly. Those who inherit it accumulate acetaldehyde after only a small drink and experience an unpleasant reaction. This is often described as protective, since carriers tend to drink little, but among those who drink heavily despite the symptoms it is associated with a raised risk of cancer of the oesophagus.

When the main enzymes are overwhelmed, a second system takes over. It uses an enzyme known as CYP2E1, which normally handles only a small share of the total but becomes progressively more important as consumption rises. Repeated drinking causes the liver to produce more of it, which helps to explain why heavy drinkers clear alcohol faster than occasional ones. The same system generates free radicals and other reactive molecules that can injure liver cells, and it is one reason that alcohol interacts with a wide range of medicines.

While the liver works, the brain feels the consequences. Ethanol alters the behaviour of nerve cells by binding to proteins on their surface: it increases the effect of GABA, the brain's main inhibitory transmitter, and reduces the action of glutamate, its main excitatory one. The result is a general slowing of activity, which shows itself first in the parts of the brain responsible for judgement and self-control, and later in the cerebellum, which governs balance. Alcohol also prompts the release of dopamine in the reward circuitry, part of the explanation for why drinking can become habitual.

How much alcohol reaches the brain depends on many things besides the number of drinks consumed. Alcohol spreads through the body's water rather than its fat, so a larger person, who has more body water, will reach a lower concentration in the blood than a smaller person drinking the same amount. On average, women have a higher proportion of body fat and lower levels of alcohol dehydrogenase in the stomach lining than men, so the same drink produces a higher blood alcohol concentration. Age, liver size and genetic differences in the enzymes shift the figure further.

Elimination is slow and cannot be hurried. At the concentrations reached by social drinking the enzymes are saturated, so alcohol is removed at a nearly constant rate rather than in proportion to how much is present, roughly a unit an hour for a typical adult, though the figure varies widely between individuals. Nothing that can be eaten, drunk or done in a shower changes that rate. Coffee may make a person feel more alert, but it does not lower the amount of alcohol in the blood.

The consequences of long-term drinking are well documented: fat accumulating in the liver, inflammation and eventually cirrhosis. Acetaldehyde is classified as a carcinogen, and alcohol is recognised as a cause of several cancers. What remains disputed is whether small quantities are harmful. Some studies have found that light drinkers live slightly longer than abstainers, but such comparisons are easily distorted, because people who abstain may do so because they are already ill. Analyses that use genetic variants to separate cause from coincidence have largely failed to confirm a protective effect, and a large global study published in 2018 concluded that the safest level of consumption was none.

None of this means that everyone responds in the same way. The liver's capacity to break down alcohol is influenced by genes, by habit and by health, and definitions of consumption differ between countries. The practical implication is firm: the rate at which alcohol leaves the body cannot be altered, and the amount that enters it is the only figure easily controlled.

Walk into any shop that sells cigarettes and the packet itself will warn you, in large letters or in a photograph, that smoking kills. Buy a bottle of wine and you will find, at most, a small logo, the volume in millilitres and a figure for alcohol by volume. Yet ethanol is classified by the International Agency for Research on Cancer in the same group of carcinogens as tobacco. Why one carries a warning and the other does not is a question about politics rather than chemistry.

The tobacco experience is the obvious place to start, and it offers a lesson that is more modest than campaigners sometimes suggest. Studies of cigarette warnings have generally found that large, pictorial messages increase knowledge of risk and prompt some smokers to think about quitting. The effect on actual smoking, however, is small, and it fades as people become used to the images. Warnings work best as one element of a wider strategy that includes higher prices, smoke-free workplaces and help for people who want to stop. A label on its own is a cheap intervention with a real but limited reach.

The case for adding warnings to alcohol rests on a simple observation: many people do not know what they are drinking. Surveys in several countries have found widespread ignorance of the link between alcohol and cancer. A warning on the container reaches people at the moment of purchase, costs the state nothing, and cannot be avoided in the way that a health campaign can be switched off. For a product that is legal, widely advertised and socially expected, that combination is attractive.

The objections are not trivial. A cigarette is harmful however it is used; alcohol is not, or at least not in the same way, and a warning that treats a glass of wine as the equivalent of a cigarette will strike many drinkers as absurd. There is also a risk that any warning carrying a number, such as a suggested weekly limit, will be read as permission, so that a figure intended as a ceiling becomes a target. Warnings, moreover, can be absorbed into the background with remarkable speed.

Public health bodies nevertheless regard labelling as one element of a wider package. The World Health Organization has stated that no level of alcohol consumption can be considered safe for health, and has urged governments to require warnings on containers. In Britain the Alcohol Health Alliance, a coalition of medical charities and professional bodies, goes further, arguing that labels should carry not only a health warning but also a list of ingredients and the number of calories.

The trade associations that speak for drinks producers take a different view. They argue that voluntary codes, drawn up and enforced by the industry itself, are a more proportionate response than statutory warnings, and that their members already provide information about units and about drinking during pregnancy. They point out that the great majority of people who drink do so in moderation, and that the heaviest drinkers, whose risk is greatest, are the least likely to be influenced by a label.

Critics of the labelling agenda make a related point from a different direction. Sir Liam Donaldson, when he was England's chief medical officer, argued that the single most powerful instrument available to government was price, and called for a minimum price per unit of alcohol. Professor David Nutt and his colleagues, in an analysis of drug harms, placed alcohol above several illegal substances, and have argued that policy should follow evidence of harm rather than legal status. On this account a label is a gesture; a tax is an intervention.

Both camps must reckon with evidence that has not settled. Whether light drinking carries any benefit has been argued over for decades, and the studies that appeared to show a protective effect on the heart have been criticised for comparing drinkers with people who had given up because they were ill. The conclusion of a large global analysis published in 2018, that the safest amount to drink is none, is not universally accepted. A warning must nevertheless say something true, and a statement that alcohol causes cancer is easier to defend than an assurance that it is safe in moderation.

There are practical questions too. A bottle has little space on it, and the label already carries an ingredients list and a barcode. Graphic images of diseased livers, familiar from cigarette packets, would be hard to justify for a legal product that most people use without harm, and small producers argue that the cost of compliance would fall hardest on them. Where warnings should appear, on the bottle, on the shelf or on a menu, has barely been examined.

My own view is that mandatory warnings on alcohol are justified, but not for the reason usually given. They should not be sold as a way of reducing consumption, since the evidence suggests that they will not do much of that; they should be defended as a matter of information. A person buying a drink is entitled to know that the product causes cancer, how many units it contains and what is in it. Warnings are a modest measure, and become harmful only if they allow governments to claim that they have acted while leaving price, availability and marketing untouched.