IELTS Academic Reading Practice Test 397

For centuries, people living in certain mountain valleys were familiar with a disfiguring swelling at the front of the neck. In the Alps, the Himalayas and the Andes it was so common that it was almost regarded as a feature of the landscape, and in parts of England it was known as 'Derbyshire neck'. The swelling is a goitre, an enlarged thyroid gland. The gland sits just below the larynx and produces hormones that control how quickly the body uses energy, so a goitre is often the visible sign that something has gone wrong with the body's supply of a single chemical element, iodine.

The link between goitre and iodine was suspected long before it was understood. Physicians in earlier centuries had noticed that preparations made from burnt sponge or seaweed, both rich in iodine, sometimes reduced the swelling, and in 1811 the element itself was isolated from seaweed ash by a French manufacturer, Bernard Courtois. Eight years later a physician in Geneva, Jean-François Coindet, began treating goitres with iodine solutions and reported considerable success. Iodine appeared to be a remedy; what nobody realised was that a lack of it might be the cause.

The explanation emerged slowly. In 1895 a German chemist, Eugen Baumann, found that the thyroid gland contains iodine in a form found nowhere else in the body, and in 1914 the American researcher Edward Kendall isolated one of the hormones responsible, later named thyroxine. It took another decade to establish the structure of the molecule and to show that it is built around iodine atoms; without a steady supply of the element, the gland simply cannot manufacture its hormones.

The consequences of deficiency are not limited to the neck. In regions where the soil and drinking water contain very little iodine, a pregnant woman who lacks the element may give birth to a child with severe mental and physical impairment, a condition once called cretinism and once common in Alpine communities. In milder cases, children grow up with reduced concentration and learning difficulties. Because iodine is needed by the developing brain before birth and in the first years of life, the World Health Organization describes deficiency as a leading preventable cause of brain damage. Goitre itself is rarely dangerous, but a large one can press on the windpipe and make breathing or swallowing difficult.

In the United States, a surgeon named David Marine set out to show that goitre could be prevented rather than treated. With a colleague, O. P. Kimball, he persuaded the authorities in Akron, Ohio, to allow a trial in the city's schools, in which girls were given small doses of iodine and compared with classmates who were not. The results, published shortly afterwards, were striking: goitre appeared far less often among those who received iodine, and existing swellings shrank. The study is now regarded as a landmark in preventive medicine.

Prevention required a vehicle, and salt provided it. In 1922 iodised salt went on sale in Switzerland, and in 1924 Michigan became the first American state to iodise its salt. Goitre rates in schoolchildren fell sharply within a few years, and Switzerland, which had one of the highest rates in Europe, eventually saw the condition become rare. Salt was chosen because it is consumed in small, fairly constant amounts all year round, is cheap, and is processed in a limited number of places, making supervision straightforward. In humid climates, iodisation is now usually carried out with potassium iodate, which keeps better in storage than the iodide used in drier countries.

Success, however, was uneven. Iodised salt reached the market only where governments or producers took the trouble, and for decades many countries used little or none. Measurement became an issue as well. The iodine content of salt falls during storage and cooking, so a programme has to be checked by testing samples and by measuring iodine in the urine of the people it is meant to protect. Programmes that are not monitored have sometimes faltered.

Two complications deserve attention. The first is that iodine, like many nutrients, can be harmful in excess; sudden large increases in intake have occasionally provoked thyroid disorders, which is why fortification levels are set with care and raised gradually. The second is an awkward overlap with campaigns against salt itself. Health agencies advise people to eat less salt in order to lower blood pressure, yet salt is the single most important source of iodine in many diets. Countries that reduce consumption substantially must therefore watch iodine status and adjust the concentration used.

Today iodised salt is one of the cheapest and most effective public-health measures ever devised, and most households worldwide use it. Yet surveys continue to find regions where intake remains inadequate, particularly in parts of Europe and Africa, and iodine deficiency has not disappeared from rich countries either. The conquest of goitre is thus largely, though not entirely, complete. No single campaign or discovery achieved this; the change came through decades of small technical decisions, and it depends on an unglamorous routine of testing, regulation and quiet adjustment that rarely attracts attention.

The thyroid is a small gland, weighing roughly twenty-five grams in an adult, that lies at the front of the neck, wrapped around the upper part of the windpipe. It has two lobes, one on each side, joined across the middle by a narrow band of tissue called the isthmus, which gives it the shape of a butterfly or a shield — the word thyroid comes from the Greek for shield. Despite its modest size it is one of the most richly supplied organs in the body, and it is composed of millions of tiny spherical follicles filled with a jelly-like material. Its peculiar talent is that it can capture iodine from the blood and use it to build hormones.

Those hormones are thyroxine, usually written T4 because each molecule carries four atoms of iodine, and triiodothyronine, or T3, which carries three. Both are assembled from the amino acid tyrosine, and in both the iodine atoms are essential: without them the molecule has no biological effect. The hormones act on almost every cell, setting the pace at which the body burns fuel, influencing heart rate and body temperature, and shaping growth and brain development in the young. Because the hormones contain iodine, and because the body cannot make the element itself, a continuous dietary supply is required; the gland has no alternative raw material.

The first step in production is capture. Iodine reaches the gland in the blood as iodide, a form that cannot cross cell membranes freely, and the follicle cells pump it inward with a dedicated protein known as the sodium-iodide symporter. This pump is remarkably powerful, and it can raise the concentration of iodide inside the cell many times above the level in the blood. Once inside, the iodide is oxidised by an enzyme, thyroid peroxidase, and attached to tyrosine units within a large protein called thyroglobulin, which is released into the centre of the follicle. There the modified protein is stored as colloid, and pairs of tyrosine units are linked together to form the finished hormones.

Storage is one of the gland's unusual features. Because the hormones remain attached to thyroglobulin in the colloid, the thyroid holds a reserve sufficient for several weeks of normal demand, a buffer that protects the body against short interruptions in iodine intake. When the hormones are needed, small amounts of colloid are taken back into the cells, the links are broken, and the hormones pass into the bloodstream. The gland secretes mainly thyroxine; much of it is later converted into the more active T3 by enzymes in the liver, kidneys and other tissues, which remove one iodine atom. This conversion allows the body to adjust hormone activity locally, rather than depending entirely on the gland.

Production is controlled by a feedback loop involving two other structures. The hypothalamus, at the base of the brain, releases thyrotropin-releasing hormone, which instructs the pituitary gland to secrete thyroid-stimulating hormone, usually shortened to TSH. TSH travels in the blood to the thyroid, where it accelerates every stage of hormone manufacture. When hormone levels in the blood rise, the hypothalamus and pituitary reduce their output, and production falls; when levels drop, the system speeds up. This loop explains why an enlarged thyroid, or goitre, can appear in someone whose gland is underactive: deprived of hormone, the pituitary drives the gland harder, and constant stimulation makes it grow.

The loop is also the basis of diagnosis and treatment. Because TSH responds so sensitively to the amount of hormone circulating, a blood test for TSH is the standard first step when thyroid disease is suspected. When the gland is overactive, as in Graves' disease, an autoimmune condition in which antibodies imitate TSH, one treatment is radioactive iodine. The gland's appetite for iodine means that a dose of radioactive iodine is taken up almost exclusively by thyroid cells, which are then destroyed; the technique has been used since the 1940s. An underactive gland, as in Hashimoto's disease, is treated with tablets of synthetic thyroxine, taken daily.

Important questions remain. The range of TSH considered normal is still debated, and it shifts with age, so that mild abnormalities are common and their significance uncertain. A single measurement can also vary with the time of day and with illness, which complicates interpretation. A condition known as subclinical hypothyroidism, in which TSH is raised but hormone levels are normal, is often found by chance; whether treating it with tablets does any good is disputed, and trials are underway. Some patients also report persistent tiredness despite normal test results, a pattern that researchers have not yet explained. Researchers are also trying to understand why thyroid function varies between populations, and how much of that variation is due to iodine intake rather than to genetics.

Official guidance sets the daily iodine requirement at about 150 micrograms for adults and 250 micrograms during pregnancy and breastfeeding, when the developing brain depends on the mother's supply. Most people obtain enough from dairy products, seafood, eggs and iodised salt, but intakes vary widely with diet and with the iodine content of local soil. Excess is not harmless: a sudden jump in intake can trigger either overactivity or underactivity, which is why programmes that add iodine to food are introduced gradually. Selenium matters too, because the enzymes that convert thyroxine into T3 depend on it, and some researchers argue that the two nutrients should be considered together. In many countries the iodine status of schoolchildren is now checked every few years, and the results are used to adjust the programme.

Anyone who buys a loaf of bread, a bag of flour or a bottle of cooking oil in most of the world is now buying food that has been deliberately altered. Vitamins and minerals have been added by the manufacturer, sometimes by law, in amounts too small to taste but large enough to prevent disease. Fortification is so ordinary that it is rarely noticed. It is also, I would argue, one of the most successful interventions in the history of public health. What is far less obvious is whether the law should require it.

The case in favour begins with evidence. Iodine added to salt has almost eliminated goitre wherever it has been properly used, and folic acid added to flour reduces the number of babies born with neural tube defects, malformations of the spine and brain that develop before birth. Such programmes cost a few pence per person per year. Vitamins are already delivered in many countries through foods that most people eat daily, and the practical argument is hard to resist: fortification reaches people without requiring them to change their behaviour, visit a clinic or remember to take anything.

Folic acid illustrates both the strength and the subtlety of the case. The neural tube closes within the first month after conception, often before a woman knows she is pregnant, so supplements begun once pregnancy is confirmed come too late. Because that timing cannot be controlled in practice, the United States required manufacturers to add folic acid to enriched grain from 1998, and dozens of countries, including Chile from 2000, have followed. Rates of neural tube defects fell substantially where the fortified flour was widely eaten. The lesson is that the timing of a nutrient's effect determines which method of delivery is rational.

Other nutrients show what is possible. Finland began adding vitamin D to milk and fat spreads in 2003, and average levels in the population rose. Where iron deficiency is widespread, flour, rice and condiments have been fortified with iron, with encouraging results in some places. These examples share a feature: the food chosen is processed in a few places and eaten regularly by most of the population.

The objections deserve a fair hearing. The strongest is that fortification medicates a population without its consent: people who have not asked for a nutrient receive it anyway and cannot easily avoid it. Critics point out that anyone who wishes to obtain folic acid from a supplement, or to avoid it altogether, cannot tell from the loaf which flour was used unless labelling is unusually detailed. There is also a suspicion that compulsory fortification flatters governments, allowing them to claim that they have improved nutrition while doing little about the cost of an adequate diet.

These objections are real but not, to my mind, decisive. The intervention is small, the risk to the individual is negligible when the dose is set sensibly, and the labelling argument is a case for better information rather than for abandoning the policy. More importantly, the alternative the critics prefer — voluntary supplements — has been tried, and it does not reach the people who need it most. Supplement use is highest among the educated and the health-conscious, and lowest among the poor, whose diets are the poorest. A policy that depends on individual initiative will tend to widen the very inequality it claims to respect.

Yet the cheerful version of the story omits real difficulties. Fortification reaches those who eat the fortified food, and not everyone does: families who grow their own vegetables, buy unpackaged staples or eat little bread may receive nothing. Higher-dose products, meanwhile, are not risk-free. Large intakes of folic acid can correct the anaemia caused by vitamin B12 deficiency while the underlying nerve damage continues, which is one reason why official bodies set an upper limit for adults of one milligram a day. Doses that are safe for most of the population may also be too high for a subgroup, such as older people with poor kidney function.

Nor is the evidence always as clean as advocates suggest. When several changes happen at once — fortification, improved diagnosis, shifting diets — it is difficult to attribute a decline in disease to a single one. Some questions, such as whether long-term exposure to the synthetic form of folate has effects that natural folate does not, remain open and require research rather than assertion. A mandate, once introduced, is politically difficult to withdraw, which places a special obligation on governments to monitor and to revise.

Where does that leave the question? I would defend compulsory fortification in three circumstances: when the deficiency is widespread and its consequences serious; when a single widely consumed food provides an efficient vehicle; and when the dose can be justified by good evidence and set well below any level of concern. I would not defend the indiscriminate addition of vitamins to every product marketed as a food, which often looks more like advertising than medicine. Fortified staples are public infrastructure, like clean water, and should be maintained with the same attention and reviewed with the same honesty. Mandatory fortification is not mass medication, but it is not a substitute for decent incomes and good diets either.