IELTS Academic Reading Practice Test 340

Cholera has been feared for centuries, not only because it spreads quickly through contaminated water but because of the speed with which it kills. The bacteria attack the lining of the small intestine, which stops absorbing fluid and pours water and salts into the gut instead. A healthy adult may lose several litres in a day, and an untreated patient can die within hours. In the nineteenth century this dehydration accounted for the overwhelming majority of deaths from the disease, yet physicians could do little beyond offering water that the body was unable to take up.

The first effective response came from a Scottish physician, Thomas Latta, during the cholera epidemic that reached Britain in 1831 and 1832. Working in Leith, near Edinburgh, Latta injected a solution of salt and water into the veins of patients who were close to death, and reported that several of them recovered.

The method worked because it bypassed the intestine altogether, delivering fluid directly into the bloodstream. But intravenous treatment required needles, sterile equipment and a trained hand to administer it, and in villages and refugee camps there was nothing of the kind. For more than a century, therefore, most cholera patients had no access to the one treatment that could save them.

The scientific key to a simpler remedy was found only in the 1960s, in laboratories investigating how the intestine absorbs salt. Robert Crane and his colleagues, working in the United States, established that sodium ions and glucose molecules are taken up across the gut wall by the same molecular mechanism. Sodium was absorbed far faster when glucose was present, and water followed the sodium. The discovery overturned the assumption that an inflamed intestine simply leaked. Even in severe cholera, the cells responsible for this transport continued to function. What a patient needed, therefore, was a drink that supplied sodium and glucose together, and in the right proportions.

Clinical confirmation followed quickly. The cholera hospitals of Dhaka, then in East Pakistan, provided the setting for a trial carried out in 1968 by two young American physicians, David Nalin and Richard Cash. They gave patients a mixture of glucose, sodium chloride, potassium chloride and a source of bicarbonate, and measured how much of it each patient needed to drink in order to replace the fluid being lost. Patients who would otherwise have required intravenous drips for days were rehydrated by mouth with a simple fluid, and the clinicians who saw the results needed little persuading.

The mixture could be made from ingredients available almost anywhere: table salt, sugar, and either bicarbonate of soda or, later, sodium citrate, which keeps better in hot, damp conditions. Its strength, however, had to be precise. Too little salt and the water would not be absorbed at all; too much would draw still more fluid into the gut and make the diarrhoea worse. The standard proportions, later adopted by international agencies, became known as oral rehydration salts.

The treatment's power became apparent in 1971. In that year, the conflict that led to the independence of Bangladesh drove millions of people across the border into refugee camps in eastern India. Cholera broke out in the camps, where there was no prospect of providing intravenous fluid for everyone who needed it. Medical staff and volunteers used oral rehydration on an enormous scale, mixing solutions and teaching families to do the same, and the results helped to convince aid agencies that a treatment which a mother could give at home could alter the course of an epidemic.

In the late 1970s the World Health Organization made oral rehydration salts a central element of a new programme against diarrhoeal disease, and sachets containing the correct mixture began to be distributed in tens of millions. The recipe was simple enough to be taught at a village meeting, and the sachet became one of the most familiar medical products in low-income countries. Governments were encouraged to keep the salts among the basic supplies of rural clinics and to train community health workers in their use. Few interventions in the history of public health have been adopted so widely, so quickly or at such modest cost.

Oral rehydration is not, however, a cure. It replaces what has been lost but does not stop the flow of fluid from the body, so a severely affected patient may need to drink small amounts continuously for hours. Anyone who is vomiting persistently, or is already deeply dehydrated, still needs intravenous treatment, or fluid through a tube passed into the stomach. In the early 2000s the World Health Organization recommended a formulation of lower osmolarity, in which the concentration of glucose and salt was reduced, after trials showed that it shortened the illness and reduced the need for drips. Zinc supplements, recommended from 2004, also shorten each episode.

Diarrhoeal disease nevertheless remains one of the leading infectious causes of death in young children, responsible for hundreds of thousands of deaths a year, most of them preventable. Surveys in several countries have found that many children who become ill never receive the salts at all, and that those who do often receive them too late. The treatment that Nalin and Cash tested has saved millions of lives; the remaining task is one of distribution rather than of science.

Water makes up roughly 60 per cent of the weight of an adult human body, and the concentration of the salts dissolved in it is held within remarkably narrow limits. Intake comes from drink, from food and, in small quantities, from the breakdown of food in the cells; losses occur through urine, sweat, breath and faeces. Because every cell depends on the movement of water across its membrane, even a modest disturbance of the balance can produce symptoms within hours. Of all the substances involved, the one the body watches most closely is sodium, the dominant ion in the fluid that surrounds the cells.

Sodium and its partner ions determine how much water stays inside cells and how much remains outside. Water passes freely across cell membranes but dissolved particles do not, so water moves by osmosis towards the compartment where their concentration is higher. In a healthy adult the concentration of sodium in the blood is kept at about 140 millimoles per litre. When it falls, water drifts into the cells and they swell; when it rises, cells lose water and shrink. Swelling is especially dangerous in the brain, which is enclosed in a rigid skull, and a rapid fall in sodium can cause headache, confusion and, in extreme cases, seizures. Doctors refer to a low concentration of sodium in the blood as hyponatraemia.

The first line of defence is a hormone. Specialised neurons in the hypothalamus, deep in the brain, detect a rise in the concentration of the blood; an increase of only a few per cent is enough to make them fire. They signal the posterior pituitary gland to release antidiuretic hormone, also called vasopressin, into the bloodstream. When the hormone reaches the kidney it causes tiny channels called aquaporins to be inserted into the walls of the collecting ducts, so that far more water is drawn back into the body and the urine becomes concentrated and small in volume. A fall in concentration has the opposite effect, and large amounts of dilute urine are produced.

Hormones act within minutes, but they cannot make a person drink. That is the job of thirst, which is generated in a different part of the brain and is a far slower and less reliable signal. Thirst is influenced by dryness of the mouth and throat as well as by the concentration of the blood, and it is easily ignored by someone who is absorbed in work. The sense of thirst also weakens with age, which is one reason why dehydration is common among frail older people.

The kidneys, which filter around 180 litres of fluid a day and return almost all of it to the blood, work with a second system that responds to pressure rather than concentration. When blood pressure or the sodium reaching the kidney falls, specialised cells release an enzyme called renin. This sets off a chain of reactions that produces angiotensin II. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, and aldosterone in turn makes the kidney reabsorb more sodium and excrete more potassium. Angiotensin II narrows blood vessels and also acts on the brain to stimulate thirst, so pressure and concentration are regulated together.

Working in the opposite direction is atrial natriuretic peptide, a hormone released by muscle cells in the atria of the heart when they are stretched by a large volume of returning blood. It relaxes blood vessels and increases the excretion of sodium, and therefore of water, in the urine. The two systems are in constant dialogue, which is why blood volume and blood concentration can each be corrected without disturbing the other.

Ordinary life tests this machinery most severely during exercise in the heat. Human sweat is a dilute salt solution, containing far less sodium than blood does, so a sweating athlete loses proportionally more water than salt. The result is a rise in the concentration of the blood and an urgent sense of thirst. Drinking plain water in large quantities, however, can overshoot: several cases of dilutional hyponatraemia have been described in marathon runners and in military recruits who drank far beyond their losses, some of them fatally. Advice to athletes has changed accordingly and now warns against drinking more than thirst demands.

How much salt people should eat is still contested. Public health bodies in many countries recommend upper limits, on the grounds that high intakes raise blood pressure and with it the risk of stroke. Yet the response to salt varies greatly between individuals, and some people appear to regulate their blood pressure with little difficulty whatever they eat. Measuring how much salt a person actually consumes is also harder than it sounds, because most of it is hidden in processed food and because the amount in a single urine sample is a poor guide to habitual intake. Research on the brain's own sodium sensors is at an early stage.

Failure of the system produces distinctive illnesses. In diabetes insipidus, the pituitary releases too little antidiuretic hormone, and the patient passes many litres of pale urine a day, becoming thirsty and dehydrated unless the hormone is replaced. The condition is unrelated to the more familiar diabetes mellitus, in which the problem lies with insulin and sugar rather than with water. What the study of such disorders makes clear is how much the body invests in keeping its internal sea constant, and how many separate mechanisms must agree before it can do so.

Modern medicine offers procedures that some of the people asked to provide them find profoundly wrong. Abortion is the most discussed example, but assisted dying where it is legal, contraception, fertility treatment and, in some settings, vaccination have all prompted refusals. The law has generally made room for such scruples: in the United Kingdom, the Abortion Act of 1967 included a clause releasing staff from any duty to take part in treatment to which they had a conscientious objection, except where it was necessary to save a woman's life. Professional codes in many other countries say something similar. The argument, then, is not about whether objection should exist, but about how far it should reach and who should pay for it.

The case for protection rests on moral integrity. To force a person to do what they believe to be seriously wrong is not a trivial imposition: it can damage them as surely as a physical injury, and it treats their deepest convictions as an inconvenience to be managed. Conscientious objection has a long and respectable history, from the exemption of pacifists from military service to the protection of journalists who refuse to reveal their sources. A profession that admits only those willing to perform every legal procedure narrows the range of moral experience within it, and it is not obvious that patients gain from a narrower profession. It is also worth asking who would be left if objectors were excluded, since the people most willing to work in poor and remote places often hold convictions that regulators find awkward.

The difficulty begins when the definition of involvement expands. There is an obvious difference between performing an operation and cleaning the instruments afterwards, yet claims of complicity have been extended to booking appointments, typing letters, dispensing medicines, discussing options with a patient and, in some accounts, telling a patient where help might be found. Each extension is defended as a matter of principle, and each transfers more work to colleagues who may already be hard pressed. There is a kind of inflation at work here, in which every new claim of complicity must be honoured because the previous one was. Where objectors are numerous, the cumulative effect is that a service becomes slow, unpredictable or quietly unavailable, and those who suffer are usually the patients with the least ability to travel elsewhere.

The sharpest version of this problem appears in small communities. A hospital may depend on a handful of general practitioners, a single pharmacist or one duty anaesthetist; if that person declines to be involved, the service may not exist within a hundred miles. Even where it survives, delay matters. A woman whose referral must wait an extra fortnight, or who must travel to another region, is seen later and faces a more difficult procedure than she would otherwise have done. Protecting one person's conscience is a genuine good, but it is not the only good at stake, and the patient's interest is usually the weightier of the two, since it concerns health rather than principle.

This is why regulators have preferred conditions to prohibitions. One Canadian regulator required objecting doctors to arrange what was called an effective referral, that is, to ensure that a colleague willing to help actually took over the patient's care, rather than simply declining and leaving the patient to find someone else. Objectors challenged the policy in the courts, arguing that arranging a referral made them complicit in the very act they condemned. The courts disagreed. The distinction between performing an act and pointing towards someone who will perform it is not always comfortable, but it is the only one on which a workable system can rest. Objectors may reasonably be asked to accept it, together with a duty to declare their position early. The requirement protects the objector as much as the patient, since it makes clear that the patient's progress does not depend on a change of heart.

Not every refusal deserves the name of conscience. An objection that rests on who the patient is — on their sex, their religion, their sexual orientation or their immigration status — is not a judgement about an act but prejudice about a person, and it has no claim on our respect. Nor should any health worker be free to withhold information, mislead a patient or obstruct a lawful service by delay. A genuine objection concerns what the objector would do, not what others may do, and it is entirely compatible with making sure that the patient is treated well and promptly by somebody else. Institutions need care too: a publicly funded hospital that imposes a single ethical view on a whole population is in a different position from an individual with a personal conviction.

My own view is that the case for some form of protection is unanswerable, and that a blanket ban would be both unjust and unworkable. But protection must be conditional. It should apply to the act itself rather than to every task connected with it; it should never delay care in an emergency; it should be declared in advance rather than invoked at the bedside; and it should carry with it a positive duty to see that the patient is passed safely into other hands. Above all, the cost of accommodation should fall on the system, through better planning of rotas and staffing, and not on the patient who happens to live in the wrong place.