IELTS Academic Reading Practice Test 351

When Richard Doll began investigating lung cancer in the late 1940s, he was struck by how quickly the disease had changed status. A physician who had qualified in the 1930s might have seen only a handful of cases in an entire career; by the end of the Second World War, hospital wards in Britain were filling with patients whose lungs were affected by tumours. Nobody could explain the increase, and a range of culprits was proposed. Among them were the tar used to bind road surfaces, the exhaust fumes of a growing number of motor vehicles, industrial pollution and the lingering damage of the influenza pandemic of 1918.

Doll was then working for the Medical Research Council, and his earlier research had concerned gastric ulcers rather than cancer. For the lung cancer investigation he was paired with Austin Bradford Hill, a statistician at the London School of Hygiene and Tropical Medicine. Hill's contribution was as important as Doll's.

He had designed the trial of streptomycin in tuberculosis that was reported in 1948, widely regarded as the first properly randomised clinical trial, and he brought to the new project a rigorous concern with avoiding bias in the gathering of evidence. It was Hill who insisted that the study be planned so that the result could not be produced by the expectations of the researchers themselves.

The pair chose what is now called a case-control design. Working through twenty London hospitals, they identified 709 patients who were being treated for lung cancer and matched each one with a patient of the same sex and age group in the same hospital who was suffering from some other condition. Hospital almoners, the medical social workers of the day, then questioned both groups using an identical form, asking about smoking, occupation and place of residence. This standardisation mattered: had the researchers conducted the interviews themselves, knowing which patients had cancer, they might unconsciously have pressed harder for a smoking history.

The results appeared in the British Medical Journal in September 1950 and were striking. Smoking was common in postwar Britain, but the difference between the two groups was far too large to be dismissed. The great majority of the cancer patients were smokers, and the heaviest smokers were over-represented among them; among the controls, smoking was equally normal but far less intense. A few lifelong non-smokers did develop the disease, which showed that tobacco could not be the only cause. Even so, Doll and Hill had expected road tar to emerge as the culprit, and the strength of the association with tobacco surprised them.

Correlation is not causation, and the authors were careful to say so. A critic could argue that the disease itself altered habits, so that people in the early stages of cancer smoked more; this difficulty is known today as reverse causation. It was also possible that patients remembered their past smoking differently once they had been diagnosed, or that hospital patients with lung cancer were unrepresentative of sufferers in general. None of these explanations could be ruled out by the data already collected. The only way to answer such objections was to begin with healthy people, record their habits and wait.

In October 1951 Doll and Hill sent a questionnaire to every doctor whose name appeared on the British Medical Register, some 59,600 people, and about 40,000 replied. This was the beginning of what became known as the British Doctors Study, a prospective study, meaning that volunteers are observed before illness occurs rather than selected after it. The doctors were followed for decades, with deaths traced through the national registries, so that the researchers could compare the death rates of smokers and non-smokers without relying on anyone's memory.

The early findings, published in 1954, settled the question of direction. Men who smoked died of lung cancer at many times the rate of those who had never smoked, and the risk rose with the number of cigarettes consumed each day — a dose-response relationship of exactly the kind that a causal explanation predicts. Men who had given up the habit had a lower death rate than those who continued, and the longer they had abstained, the lower it fell. The prospective design also disposed of reverse causation, because the smoking had been recorded years before any diagnosis.

Acceptance was nevertheless slow. Tobacco was a major industry, smoking was almost universal among men, and many doctors were reluctant to believe that a habit they shared could be so dangerous. In Britain a report from the Royal College of Physicians in 1962 gave the evidence official weight, and in the United States a report by the Surgeon General followed in 1964, after which advertising restrictions and health warnings spread. The case-control method that Doll and Hill had refined, and the prospective study that confirmed their conclusions, became the template for modern epidemiology.

Doll had smoked himself, and in 1949, while the first study was still in progress, he stopped and never smoked again. He died in 2005 at the age of 92, and his longevity was sometimes invoked, absurdly, by those who wished to deny the danger of tobacco. The more useful legacy is a methodological one: a careful comparison, a standardised interview, a long follow-up and a refusal to overstate what the data could show. Every later study of smoking, and a great many studies of other exposures, has followed the path those two men laid out.

Vitamin D is unusual among the substances the body needs, because it is not strictly a vitamin at all. Vitamins are defined as compounds that must be obtained from the diet, yet the human body can manufacture vitamin D itself, provided that the skin receives enough sunlight of the right kind. Only when exposure is inadequate does the nutrient become essential in the dietary sense. This double identity helps to explain why deficiency occurs in sunny countries as well as northern cities, and why the medical literature on vitamin D so often appears to contradict itself.

The synthesis begins in the lower layers of the epidermis, where a form of cholesterol called 7-dehydrocholesterol is waiting. When ultraviolet B radiation, the shorter-wavelength part of the ultraviolet spectrum, penetrates the skin, it supplies enough energy to break a bond in the molecule and convert it into cholecalciferol, or vitamin D3, the same substance found in oily fish and egg yolks. A second form, vitamin D2, is made by exposing a compound in yeast and fungi to ultraviolet light; both forms work, though the body handles them slightly differently.

Cholecalciferol travels in the blood to the liver, where an enzyme adds a hydroxyl group to produce 25-hydroxyvitamin D, also called calcidiol. This is the main circulating form, and it is what a blood test measures when vitamin D status is assessed; its concentration reflects what has been absorbed over the previous weeks. A second hydroxylation, carried out in the kidney, produces 1,25-dihydroxyvitamin D, or calcitriol, the active hormone. Calcitriol acts on the lining of the intestine, increasing the absorption of calcium and phosphate, and it signals to bone, muscle and the immune system as well.

Skin colour is central to the story. Melanin, the pigment that darkens skin and protects it from ultraviolet radiation, absorbs part of the incoming UVB before it can reach the cholesterol precursor. The more melanin a person has, the longer the exposure needed to make a given quantity of vitamin D, so people with deeply pigmented skin living at high latitudes may run a greater risk of deficiency in winter. Some researchers argue that a trade-off between protecting folate from ultraviolet damage and allowing vitamin D synthesis helps to explain the distribution of skin colour, though this remains a hypothesis.

Sunlight is not a reliable year-round resource. The angle at which the sun's rays enter the atmosphere determines how much UVB reaches the ground, and in winter at latitudes above roughly 35 degrees little useful UVB arrives. In Britain this means that almost no vitamin D is made in the skin between October and March. Indoor work, clothing that covers most of the body and the use of sunscreen all reduce synthesis further. A high protection factor will certainly reduce production during deliberate sunbathing; in ordinary daily life, however, studies suggest that the effect is modest.

When synthesis falls short, the consequences are best documented in bone. Severe deficiency in children causes rickets, in which the growing skeleton fails to mineralise properly; in adults the equivalent condition is osteomalacia, with bone pain and muscle weakness. Rickets was once so common in the industrial cities of northern Europe that it was regarded as an inevitable disease of childhood, and it declined only when cod liver oil was given to infants and when cleaner air allowed more ultraviolet light to reach the streets. In the past two decades cases have reappeared in some high-income countries, particularly among children with dark skin.

Beyond bone, the picture becomes much murkier. Vitamin D receptors are found in many tissues, and low blood levels have been associated with respiratory infections, autoimmune conditions, several cancers and cardiovascular disease. Such associations are difficult to interpret, because people with low vitamin D are often ill, elderly, overweight or inactive, and these factors might explain the outcome. The proper test is a randomised trial, and here the results have been disappointing. A large American trial reported in 2018, which followed more than 25,000 adults for several years, found that taking vitamin D did not reduce the incidence of cancer or of cardiovascular events.

Other trials have produced more encouraging signals in narrower areas. An analysis of individual patient data from twenty-five trials, published in 2017, concluded that supplementation reduced the risk of acute respiratory infection, but chiefly in people whose vitamin D levels were severely low; in those with adequate levels the benefit was negligible. This pattern, a benefit concentrated in the deficient, recurs throughout the literature and helps to explain why confident claims about vitamin D and everything from depression to athletic performance have not been borne out.

There is also a genuine risk at the other extreme. Vitamin D is fat-soluble and is stored rather than excreted promptly, so very large doses taken over long periods can raise the level of calcium in the blood, causing nausea, kidney stones and, rarely, more serious damage. Sunlight, by contrast, cannot produce an overdose, because with prolonged exposure the excess is converted into inactive by-products. Experts still disagree about the concentration of calcidiol that counts as sufficient, partly because the evidence for benefits above the amount needed to prevent rickets is thin, and official advice therefore differs from one country to another.

In most countries it is illegal to sell cigarettes to anyone below a fixed age, usually 18 or 21. A different proposal has been gaining support among public health specialists. Rather than fixing a minimum age for ever, the law would raise it by one year every year, so that a person born after a particular date would never reach the age at which tobacco could legally be bought. Someone who is 30 today might buy cigarettes for the rest of their life; someone who is 12 today never could. The idea is known as the smoke-free generation, or the tobacco endgame.

The case for it rests on a peculiar feature of the habit. Smoking is not a taste that most people acquire in middle age; it is overwhelmingly a behaviour of adolescence and early adulthood, when the brain is especially responsive to nicotine and when the influence of friends is strongest. A person who reaches the age of 25 without smoking is very unlikely ever to start. Policies that make it harder for teenagers to buy cigarettes therefore attack the point at which almost all smokers are recruited, rather than the point at which most of the harm has already been done.

Practical politics has begun to catch up. In 2020 the town of Brookline, near Boston, became the first place in the world to adopt a rolling age limit, banning the sale of tobacco to anyone born after 1 January 2000. New Zealand passed national legislation in 2022 that would have excluded anyone born after 1 January 2009, but the law was repealed by a later government in 2024. In Britain a Tobacco and Vapes Bill was introduced in 2024 with a similar birth-date mechanism. Fixed increases have been more common: the United States raised its federal minimum age to 21 in 2019, and Singapore did the same in 2021.

The advantages claimed for a rolling limit are considerable. It does not criminalise existing smokers or force anyone to quit; a 50-year-old who has smoked since the age of 16 can continue to buy cigarettes. It phases the habit out gradually, giving retailers and the tobacco industry years to adjust. It is simple to enforce, because a shopkeeper needs only to check a date of birth. And it removes one of the routes by which teenagers obtain cigarettes: at present an 18-year-old can legally buy tobacco and pass it to a 15-year-old, and a rolling limit eventually eliminates that supply.

The most serious objection is not medical but moral. Under a rolling limit, two adults who differ in age by a single year will be treated differently for the rest of their lives, because one was born just before the cut-off date and the other just after. A 45-year-old who has never smoked will be forbidden to buy a product that a 47-year-old may buy freely, and no amount of time will remove the distinction. Critics argue that this is a form of discrimination that no other consumer product imposes, and that a parliament which can prohibit sales to a whole generation can later prohibit them to everyone. Defenders reply that the restriction applies only to the point of purchase, not to possession or use.

Practical objections are also raised. A ban that creates a black market, it is argued, would be worse than the regulated sale it replaced: high tobacco taxes in several countries have been followed by large-scale smuggling, and an age-based prohibition could have similar effects. Enforcement is another difficulty. Much of the tobacco smoked by teenagers is thought to be obtained from older friends and family rather than from shops, so restricting retail sale may achieve less than its advocates hope.

Evidence on the policy's effect is, by its nature, thin. No country has operated a rolling age limit for long enough to observe its consequences, and New Zealand's repeal removed the most promising opportunity for a natural experiment. Supporters rely instead on modelling. Such models depend on assumptions about how many young people would turn to illicit supplies and how many would simply give up, and on how quickly the tobacco industry would shrink. They are plausible projections, not demonstrations.

What the policy cannot do on its own is help the millions who already smoke. A smoke-free generation would be cruel and ineffective if it were introduced instead of, rather than alongside, well-funded services that help people to stop: advice, medication and support by text message have all been shown to work. Nor can the policy ignore the changing market. In many countries cigarette smoking among teenagers is falling while vaping is rising, and a law that closes the door on one nicotine product while leaving another open invites young people to walk through the second.

My own view is that the rolling age limit is a good idea, though not a sufficient one. The equality objection deserves respect, but it loses much of its force once we accept that the state already treats cigarettes differently from other goods, and that the freedom being restricted is the freedom to become addicted. The policy is most defensible as one instrument among several — alongside taxation, smoke-free places and help for existing smokers — and it should be designed so that its effects can be measured and, if necessary, reversed. The evidence is promising rather than conclusive; that is a reason for caution, not for inaction.