IELTS Academic Reading Practice Test 326

For most of human history the idea that an adequate diet might nevertheless lack something essential was barely considered. Scurvy, beriberi and rickets were familiar to physicians, but their causes were sought in foul air, in damp climates or in the habits of the sufferer. That a person could eat their fill and still be deficient seemed a contradiction in terms. A substance needed in amounts too small to be weighed had no place in medical thinking.

The first convincing demonstration came from the Royal Navy. In 1747 the naval surgeon James Lind, serving on HMS Salisbury, divided twelve sailors with scurvy into pairs and gave each pair a different remedy: cider, vinegar, elixir of vitriol, seawater, a paste of garlic and mustard, or a daily dose of citrus fruit, in the form of two oranges and a lemon. The pair given the fruit recovered quickly, while the others did not. Lind published a full account of the trial in 1753, yet he never entirely accepted the explanation his own results suggested, and the concentrated lemon preparation he later recommended was probably worthless. Only in 1795, after lobbying by the physician Gilbert Blane, did the Royal Navy begin issuing lemon juice to its sailors.

In the 1890s a comparable puzzle occupied a Dutch physician in the East Indies. Christiaan Eijkman, sent to Java to investigate beriberi, noticed that prisoners and chickens fed on polished rice developed weakness in the limbs, while those given unpolished rice stayed well. Because the illness seemed to spread, Eijkman blamed a toxin or an infection rather than the diet, and he never identified the nutrient in the bran. Even so, his work established that a disease could result from what had been removed from a food.

The idea that foods contain unidentified 'accessory factors' was placed on a firmer footing by Frederick Gowland Hopkins in Cambridge. In 1912 he reported that rats kept on a purified mixture of protein, fat, carbohydrate and salts stopped growing, but grew again when given a small daily quantity of milk. The amount was far too small to supply energy or building material, which suggested that milk contained something the animals could not manufacture for themselves. Some contemporaries remained sceptical, arguing that a diet containing all the known nutrients must be sufficient.

The word was coined by Casimir Funk, a Polish biochemist working in London. In 1912 he isolated a nitrogen-containing substance from rice bran that appeared to prevent beriberi in pigeons and, believing it to belong to a class of compounds called amines and to be essential to life, named it a 'vitamine'. The term was soon applied to every newly discovered factor. It was also altered: in 1920 the biochemist Jack Drummond proposed dropping the final 'e', since not all the substances proved to be amines.

Work in the United States meanwhile established that there was more than one such substance. Between 1913 and 1915 Elmer McCollum and Marguerite Davis, at the University of Wisconsin, found that rats fed on lard failed to thrive unless given butter fat or egg yolk, while a second factor, soluble in water, was present in wheat germ and milk. They labelled the first fat-soluble A and the second water-soluble B, and this use of letters, intended only as a temporary convenience, became the naming system that survives today, with vitamins C, D, E and K added later.

Not every deficiency disease was studied in the laboratory. Pellagra, which caused skin rashes and mental disturbance, had become widespread in the southern states of the United States, and in 1914 the Public Health Service sent Joseph Goldberger to investigate. He noticed that it appeared among people whose diet consisted largely of maize, while staff in institutions where patients were fed differently remained free of it. Goldberger argued that pellagra resulted from a poor diet, and even swallowed material from patients to show that it was not contagious. Yet the belief that it was infectious persisted for years, and he died in 1929 before opinion had turned.

Rickets, a softening of the bones common in crowded industrial cities, was traced to a similar deficiency, though the history is more tangled. In experiments published around 1920, Edward Mellanby showed that dogs kept indoors on a poor diet developed rickets and that cod liver oil prevented it. Because cod liver oil was known to be rich in the newly discovered vitamin A, Mellanby assumed that this was the active ingredient. Elmer McCollum then demonstrated that the oil still cured rickets after its vitamin A had been destroyed, and the substance responsible was designated vitamin D.

Vitamin C was isolated later. In the late 1920s the Hungarian scientist Albert Szent-Gyorgyi obtained small quantities of a reducing substance from animal adrenal glands and from plants, and by 1932 he and Charles Glen King, working separately in Pittsburgh, had isolated the same compound from lemon juice. Ascorbic acid, as it was named, was synthesised in 1933, and by the late 1930s the structures of the principal vitamins had been worked out.

The practical consequences were considerable. Wartime feeding plans, the fortification of flour and margarine, and the free issue of cod liver oil and orange juice to British children in the 1940s all rested on the new knowledge. Yet the science also bred a lasting faith in supplements that has outlived much of the evidence for it: for anyone eating a varied diet, the discovery of vitamins confirmed the value of ordinary food rather than the need for pills.

Stem cells are cells that have not yet acquired a specialist role. Two properties define them. The first is self-renewal: when a stem cell divides, at least one of the daughter cells remains a stem cell, so a pool of them is maintained for years. The second is potency, the capacity to produce cells of other kinds. Together these properties allow stem cells to build tissues during development and to replace cells that are worn out or lost in adult life. The best-established example is the bone marrow, which produces billions of blood cells every day.

Potency is not the same in every stem cell. A fertilised egg and the cells produced in the first few divisions are totipotent: each can form a complete embryo, placenta included. Cells taken from the inner mass of a blastocyst, an early embryo of about five days, are pluripotent and can give rise to any of the body's specialised cells but not to the placenta. Embryonic stem cell lines were first grown from human embryos in 1998, by a team led by James Thomson in Wisconsin. Adult tissues, by contrast, contain multipotent stem cells, whose output is restricted to the cell types of the tissue in which they sit.

The clearest adult example is the bone marrow. In 1961 two Canadian researchers, James Till and Ernest McCulloch, found cells in the marrow of mice that could generate colonies of blood cells in the spleen, the first direct evidence of a self-renewing cell. Similar populations have since been found in the gut lining, where stem cells replace the surface within days, in the skin and in skeletal muscle. Most of these populations are small and hard to grow outside the body, which is one reason that progress with adult cells has been slower than early hopes suggested.

Medicine already relies on stem cells. Bone marrow transplantation, developed largely through the work of E. Donnall Thomas from the late 1950s, is used to treat leukaemia and other disorders of the blood. Because the treatment destroys the patient's own marrow, donor cells are given as an intravenous infusion, and they find their way to the cavities inside the bones. The approach carries serious risks, among them graft-versus-host disease, in which donor immune cells attack the patient's tissues, and it works best when donor and patient are closely matched.

A second route avoids embryos altogether. In 2006 Shinya Yamanaka, working in Kyoto, introduced four genes into ordinary adult mouse cells and found that a small proportion reverted to a pluripotent state; a year later his group did the same with human cells. These induced pluripotent stem cells earned Yamanaka a share of the 2012 Nobel Prize in Physiology or Medicine, with John Gurdon, whose frog experiments in the 1960s had shown that adult nuclei retain the full set of instructions. Because iPS cells can be made from a patient's own tissue, they sidestep both the ethical objections to embryo research and the problem of immune rejection.

Stem cells also allow researchers to grow miniature tissues. In 2009 a group led by Hans Clevers in Utrecht showed that a single stem cell from a mouse gut could be coaxed into forming a hollow structure with the folded surface of an intestine. Brain, kidney and lung organoids followed. Such structures are not organs: they lack blood vessels and nerves, and they are rarely more than a few millimetres across. But they allow diseases to be studied in human tissue and drugs to be tested, and in cystic fibrosis they have been used to predict which medicine will help a particular patient.

Transplanted stem cells have also restored damaged tissue. Sheets of skin grown from a patient's own cells have been used to close burns since the 1980s. In people whose eyes have been injured by chemicals, stem cells taken from the limbus, the rim of the cornea, can be transplanted to repair the surface of the eye. Corneal repair of this kind is now routine in specialist centres. These treatments use the patient's own cells and are well established; many other applications, from heart muscle to spinal cord, remain experimental.

The obstacles are considerable. Pluripotent cells left to themselves will form teratomas, tumours containing fragments of many tissues, so the cells must be converted into the required type with great precision before they are transplanted. The resulting cells must survive, connect to existing tissue and function for years. Manufacturing billions of identical cells under pharmaceutical standards is expensive, and regulators want to know exactly what is being transplanted. Trials also struggle to recruit enough participants, and a treatment that works in a mouse rarely works as well in a person.

Uncertainty also surrounds the clinics that advertise stem cell injections for conditions such as autism, multiple sclerosis and spinal injury. Such treatments are usually unproven, and some have caused harm. Professional bodies and regulators in several countries have issued warnings, and a handful of clinics have been closed. Meanwhile, questions that once seemed settled are open again: how much plasticity adult stem cells really show, and whether a cell's history leaves traces that limit what it can safely become.

Few areas of medicine raise such awkward questions about public money as fertility treatment. In vitro fertilisation, once experimental, has become routine, and millions of children have been born after treatment. The debate is often conducted as though the answer were obvious. Yet provision through the state-funded health service varies enormously from one district to another, while a single private cycle may cost several thousand pounds. Whether the state should pay at all, and if so for whom, is a question that arouses strong feelings on every side.

The strongest argument for public funding is that infertility is a disease. The World Health Organization defines it as a disorder of the reproductive system and estimates that roughly one in six adults experiences it at some point, which makes it far from rare. Unlike cosmetic surgery, treatment follows a diagnosis: a blocked tube, failing ovaries, poor sperm quality. Patient organisations maintain that the distress it causes is comparable to that of other chronic conditions, and that a health service which treats depression and severe pain has no principled reason to refuse this.

Against this, health economists observe that resources are finite and that every pound spent on one service is unavailable to another. Judged by cost per live birth, fertility treatment compares poorly with, say, hip replacement or the treatment of high blood pressure, and the sums are large because success is uncertain: many cycles produce no child. It would be foolish to pretend that money is unlimited, or that fertility treatment should be exempt from the comparisons that every other service faces. Supporters reply that the quality-adjusted life year, the measure economists usually prefer, was designed for conditions that damage an existing life and fits badly the arrival of a new one.

Age raises a sharper difficulty. Success rates decline steeply, from roughly one live birth in three per cycle for the youngest patients to a small fraction of that for women in their early forties. Clinicians who run fertility services therefore defend age limits, arguing that they rest on evidence about what medicine can achieve rather than on judgments about who deserves to be a parent, and that treating patients who have almost no chance wastes money and exposes them to risk. The line is nevertheless harsh at the margin, since a woman of 41 is biologically much like one of 39. Such limits seem to me defensible, provided they are drawn on the basis of outcome rather than prejudice.

A third argument concerns responsibility. In some areas, commissioners and commentators have proposed that patients should give up smoking or lose weight before treatment is funded. Smoking and obesity do reduce the chance of success and increase the risks of pregnancy, and it would be strange for a service not to mention them. But I am not persuaded that they should become conditions of treatment. Where a treatment is safe and effective, attaching conditions to it looks less like clinical judgement than like a way of reducing the bill, and the burden falls on those least able to bear it.

Critics of public funding raise deeper objections. Some hold that the state should not use scarce money to create a child when so many children wait to be adopted, or that a child conceived in this way may be harmed; others believe the money belongs with the sickest patients. None of these objections is frivolous. Those who study the safety of treatment make a narrower point: the principal risk in fertility medicine is multiple pregnancy, since twins and triplets are far more likely to be born early, and the policy of transferring a single embryo has done more for safety than any other recent change.

The most serious problem, however, is administrative rather than philosophical. In England, decisions about which treatments local areas would fund were for years taken separately, with the result that identical patients in neighbouring districts received different answers. A woman might be offered three cycles in one place and none ten miles away. When a treatment is rationed by address, the principle that the health service provides care according to need rather than income or postcode is quietly abandoned, and those who can pay simply go privately.

My own view is that a limited programme of state-funded treatment is justified and that the arguments against it are weaker than they appear. Infertility is a recognised disorder with effective treatment, the distress it causes is real, and a service that treats the consequences of smoking and heavy drinking can hardly refuse to treat a disorder that is no one's fault. But the programme should be limited: a small number of cycles, which is what national guidance recommends, is defensible, and age limits based on evidence are acceptable if applied uniformly.

What matters most is that the rules be explicit and national. Eligibility should rest on a diagnosis, an age range supported by the evidence and a fixed number of cycles, and it should not depend on the budget of a local board or the depth of a patient's savings. Rationing is unavoidable; arbitrary rationing is not. The question, in the end, is not whether a child has a price, but whether a decent system can admit that it must ration what it cannot buy for everyone.