IELTS Academic Reading Practice Test 352

In the middle of the nineteenth century, leprosy was still a familiar disease in Norway. Along the wet western coast, and above all in the city of Bergen, hundreds of people lived with the disfiguring condition, and the city's leprosy hospital, known as Lungegårdshospitalet, was one of the largest institutions of its kind in Europe. Medical opinion held that the disease was inherited, or produced by foul air and unhealthy surroundings. Against this background, a young Norwegian doctor, Gerhard Armauer Hansen, began the work that would make his name.

Hansen was born in Bergen in 1841, the son of a merchant. He studied medicine at the university in Christiania, as Oslo was then called, and qualified in 1866. After working elsewhere for a time, he returned to his home city in 1868 to take up a post as assistant physician at the leprosy hospital, where he came under the influence of Daniel Cornelius Danielssen. Danielssen was the leading Norwegian authority on the disease and had co-written a great illustrated treatise on it in 1847, in which he concluded that leprosy was hereditary. Hansen accepted this view at first.

The hereditary explanation was not unreasonable, since leprosy often appeared in several members of the same family. But it sat awkwardly with other observations. The disease clustered in particular districts rather than spreading evenly; it seemed to travel with infected people who moved from one place to another; and it rarely affected those who nursed the sick unless they had been in close contact with them for years. Danielssen's theory also offered patients nothing. If the disease was already in the blood, there was no reason to separate the sick from the healthy.

Hansen began to examine tissue taken from the nodules that give the lepromatous form of the disease its appearance, using the microscopes then available. In 1873 he observed small, rod-shaped bodies in the material, and became convinced that these were living organisms and the true cause of leprosy. He reported the finding to the Bergen Medical Society that year and set out the evidence in a paper published in 1874 in the Norwegian medical journal Norsk Magazin for Lægevidenskaben. The organism is now called Mycobacterium leprae, and it has a strong claim to be the first bacterium shown to cause disease in humans.

The claim was not accepted quickly, and Hansen could not supply the proof that the bacteriologists of the following decade demanded. Mycobacterium leprae has never been grown in artificial culture, and it does not readily infect laboratory animals. Nor could Hansen show that a pure preparation of the organism would produce the disease in a healthy person, an experiment that later became a standard test. His evidence remained circumstantial: the bacteria were found in the tissue of patients, but he could not explain how they passed from one person to another.

Recognition came slowly and was complicated by a dispute over priority. In 1879 Hansen received a visit from Albert Neisser, a young German physician who had recently described the bacterium that causes gonorrhoea. Hansen gave him specimens, and Neisser, who had better equipment and dyes, studied the organisms and published his own account, laying claim to the discovery. Hansen protested that he had described the bacillus six years earlier, and most later historians have accepted his case, though a few have been less generous. The quarrel soured his relations with German science.

Hansen also insisted, against Danielssen, that leprosy must be infectious and that it required long and close contact to pass between people. The idea had practical consequences. If the disease was contagious, separating patients from their families might check its spread, and Hansen became an advocate of measures that removed sufferers from their homes. Norway's system of isolation in leprosy institutions is often attributed to his influence, though historians now argue that better housing, nutrition and hygiene did at least as much to push the disease into retreat.

His commitment could shade into recklessness. In an attempt to demonstrate that leprosy could be transmitted from person to person, Hansen inoculated a patient with material taken from a leprous nodule, an experiment performed without consent and offering no possible benefit to the person concerned. The episode has done lasting damage to his reputation and is still discussed by historians of medical ethics. Hansen nevertheless remained Norway's chief medical officer for leprosy until his death in 1912.

The nineteenth century had no effective cure. Patients were treated with chaulmoogra oil, an unpleasant preparation of doubtful value, and the main benefit of the institutions was shelter. International acceptance of the bacterial cause came at a conference in Berlin in 1897, where delegates from many countries endorsed Hansen's conclusion, but the practical consequences were limited. Segregation remained the principal response until drugs capable of killing the organism were developed in the middle of the twentieth century.

Those drugs arrived slowly. Dapsone, the first effective treatment, came into use in the late 1940s, but the bacterium developed resistance to it, and treatment remained difficult until the 1980s, when the World Health Organization recommended a combination of medicines known as multidrug therapy. The organism was at last produced in large quantities in the nine-banded armadillo, in which it grows unusually well. Roughly 200,000 new cases are still reported each year, most of them in a small number of countries, and leprosy remains a reminder of how long a discovery can take to become a cure.

The shoulder is the most mobile joint in the human body, and also one of the most frequently injured. It is not a single structure but a group of joints, of which the largest, the glenohumeral joint, connects the upper arm to the trunk. Unlike the hip, a deep socket that holds the thigh bone securely, the shoulder is built for reach: the arm can be lifted overhead, rotated through almost a full circle and swung across the body. That freedom has a price, because the arrangement that allows such movement gives the joint relatively little bony stability, and the shoulder dislocates more often than any other large joint.

Three bones meet at the shoulder. The scapula, or shoulder blade, lies against the back of the ribcage and carries a shallow, pear-shaped cavity called the glenoid. The head of the humerus, the bone of the upper arm, is much larger than the socket, and only about a third of its surface is in contact with the glenoid at any moment. A ring of fibrous cartilage, the labrum, runs around the rim of the socket and deepens it slightly. The clavicle, or collarbone, props the shoulder outwards and is the only bony link between the arm and the rest of the skeleton. The socket faces sideways and slightly forwards, which is why the arm can be swung in so many directions.

Because the socket is shallow, the joint depends on soft tissue. A loose fibrous capsule surrounds it, lined with a membrane that produces synovial fluid, and thickened bands within the capsule form the glenohumeral ligaments. When the arm hangs at the side these structures are slack; they tighten only as the arm is rotated or lifted, which is why the joint moves so freely in the middle of its range and feels firmer towards its limits. The capsule also encloses a slightly negative pressure, and this suction, together with the labrum, resists downward pull on the arm. In a joint with a deeper socket, such as the hip, the same task is done by bone.

The most important active restraint is a group of four muscles known as the rotator cuff. The supraspinatus, infraspinatus, teres minor and subscapularis arise on the scapula and send tendons that merge with the capsule and wrap around the head of the humerus. The supraspinatus begins lifting the arm away from the body, the infraspinatus and teres minor rotate it outwards, and the subscapularis rotates it inwards. Because the tendons blend into the capsule, the cuff works as a dynamic ligament as well as a motor, pulling the ball into the socket whenever the arm moves and giving the joint a stability that the shallow socket cannot provide on its own.

Raising the arm is a partnership between two joints. For the hand to reach above the head, the humerus must rotate within the socket while the scapula rotates upwards on the chest wall, and the two movements are coordinated in a fairly consistent ratio of about two to one. This pattern, known as scapulohumeral rhythm, depends on the trapezius and the serratus anterior, broad muscles that are not part of the cuff but are essential to overhead movement. When the scapula cannot rotate, as happens in some forms of paralysis and in chronic shoulder pain, the arm cannot be lifted fully even if the glenohumeral joint itself is healthy.

Above the head of the humerus lies a bony arch formed by the acromion, a projection of the scapula, and beneath it sits the subacromial bursa, a thin fluid-filled sac that reduces friction between the cuff tendons and the bone. For decades surgeons assumed that pain in this region came from tendons being pinched under the arch, and an operation to widen the space became common. A large British trial published in 2018 compared the operation with a placebo procedure, in which the surgeon made the same incisions but removed no bone. The trial found no meaningful difference in pain or function, which cast doubt on the impingement theory that had justified tens of thousands of operations.

Imaging has produced a further surprise. Scans of people with no shoulder pain frequently reveal partial or complete tears of the cuff tendons, and the proportion rises steadily with age, so that among people in their seventies such findings are commonplace. A scan therefore shows what the shoulder looks like but not necessarily why it hurts. Tears in younger people usually follow a fall or a sudden pull, but in older people they often appear without any injury at all. Other conditions are equally puzzling: in adhesive capsulitis, or frozen shoulder, the capsule contracts and the joint stiffens for a year or more, and although the condition is more common in people with diabetes, its cause is not understood.

Treatment has shifted accordingly. Most guidelines now recommend a period of exercise-based rehabilitation before surgery for all but the largest acute tears, and the evidence suggests that many people with a torn cuff improve without an operation. What remains uncertain is which exercises are best, how long a trial of rehabilitation should last and which patients genuinely benefit from repair. Platelet-rich plasma and injections of stem cells are marketed as ways of encouraging the tendon to heal, but the trials are small and their results inconsistent. The shoulder's great advantage, its mobility, is also the source of most of its troubles.

On a weekday morning in a school hall, a class of ten-year-olds queues to have their height and weight recorded by a nurse. The measurements take a few seconds each, and the children return to their lessons. In England this scene has been repeated every year since 2006 under the National Child Measurement Programme, which covers children in their first year of school, aged four and five, and again at the age of ten or eleven. The programme is unusual in that it measures children in every state school rather than a sample, and it has given England one of the few continuous records of the weight of its children.

The argument for this is straightforward. Childhood obesity is common, and its consequences, from diabetes to joint problems, can last a lifetime. The figures allow local authorities to see where the problem is concentrated and to plan services accordingly, and they reveal trends that no other source can show, since they are measured rather than self-reported, and self-reported weights are notoriously unreliable. The programme also identifies children who are severely underweight, a group that is easily overlooked, and it can prompt a conversation between a school and a family that might otherwise never take place.

Parents, it turns out, are poor judges of their own children's weight. Studies in several countries have found that many parents of overweight children believe their child's weight to be normal, and that parents of very young children are particularly likely to be optimistic. A letter reporting that a child is above the healthy range therefore carries information that the family may not have. In theory it should be a useful nudge, and some parents do indeed respond by seeking advice.

In practice, the letters appear to change very little. Researchers who have followed families after they received feedback have generally found small or undetectable effects on weight, although parents report that they value being told. A letter is a weak intervention. It arrives without explanation, offers no appointment and often points to services that are oversubscribed or that the family cannot reach. The evidence suggests that feedback works only when it is followed by something more substantial, such as a conversation with a health professional and a place on a supported programme.

Against this must be set the risk of harm. Being weighed in front of classmates, or discovering that you are the heaviest child in the year, is a memorable experience, and not a happy one. Teachers report that measurement days provoke anxiety, teasing and questions about diet that no one at school is equipped to answer. Charities that support people with eating disorders warn that focusing attention on weight at an age when children are forming their sense of their own bodies may do damage that outlasts any benefit, and that among vulnerable children such attention can be the beginning of a disordered relationship with food.

Consent is another difficulty. Parents may withdraw their child from the programme, but this is an opt-out rather than an opt-in, so measurement is the default. The results are held in a national dataset, which raises questions about who can see them and how secure they are. Parents whose first language is not English may not understand the letter, and families who move frequently may never receive one at all, which means that the programme's reach is least reliable where the need is greatest.

Then there is the measurement itself. Body mass index, the ratio of weight to the square of height, takes no account of whether the weight is fat or muscle, and a muscular child may be classified as overweight. In children the figure must be compared with growth charts, because the healthy range changes with age and sex, and the thresholds are statistical rather than clinical: they describe where a child sits in relation to a reference population, not whether the child is ill. The measure is useful for describing groups and crude for describing individuals, a distinction that a letter arriving on a family's doormat is unlikely to make clear.

None of this means the programme should be abandoned, only that it should be redesigned. Measurements should always be taken privately, as official guidance already requires, out of sight of other children. Results could be accompanied by an offer of support rather than a bare statistic, and the wording of letters could be tested as carefully as the wording of any other public health message. The data could be linked to other services, so that a family that wants help can find it quickly, and the programme could be evaluated honestly, including for its unintended consequences.

My own view is that universal measurement is justified, but for reasons that have little to do with the individual child. Its strongest claim is that it gives a country a reliable picture of how its children are growing, which no other method provides, and that picture is the foundation of any sensible policy. As a way of helping individual children, weighing them achieves almost nothing on its own. Keep the measurements, then, but stop pretending that a number in an envelope is a public health intervention; it is a survey, and surveys change nothing unless somebody acts on them.