Читать книгу Panic Nation - Stanley Feldman - Страница 16

BY VINCENT MARKS

‘Corpulence in America is regarded, along with narcotic addiction, as something wicked, and I shall not be surprised if soon we have a prohibition against it in the name of national security.’

ASTWOOD, 1962

THE MYTH: Obesity is caused by eating the ‘wrong kinds of food.

THE FACT: Obesity in humans is caused by eating too much.

Obesity has always been with us but, whereas in the past it was the prerogative of the rich, it is now the scourge of the poor. We are told by numerous newspapers articles, life-insurance companies’ publicity material and governmental publications that it has reached ‘epidemic proportions’. It is blamed on ‘junk food’, but the real reason for its increasing incidence is far more complicated.

Currently, obesity is labelled among the commonest causes of death worldwide and not only in the developed and affluent West – but the evidence is not there. The illnesses to which obesity predispose, such as diabetes, coronary heart disease and hypertension, are undoubtedly a major cause of death in the developed world but uncomplicated obesity is rarely so. It is nevertheless an important risk factor that can be theoretically, and in some cases practically, reduced

Obesity develops when energy intake exceeds energy expenditure. It will be maintained until this balance is reversed. The supply of food as well as the type of food is involved from the start. Until recently, food was plentiful only for the rich – the poor often lived at subsistence level, although they frequently performed more manual work over longer periods. Although now looked upon as a hazard to health, the ability to become fat in times when food was not constantly available could have had an important survival value in the past. The ability to get fat was a status symbol in deprived communities and those subject to periodic famines. It is still so in some parts of the world. People who were fat at the start of a famine would have a better chance of surviving than those who were thin.

However, being fat has become a cosmetic problem for the fashion-conscious over the past half-century or so, and it was the social desirability of being thin that produced the huge diet and weight-reduction industry – not the impact of obesity on health. This has now changed – at least in part – as the medical problems attributable to overweight and obesity have become increasing well recognised. Should we worry about getting fat? Yes, because in the long term overweight predisposes us to a variety of illnesses and a shortened life expectancy. Even though some very fat people live their full three score years and ten and more, most do not.

A lot depends on what you call overweight, fat and obese. They are not the same thing, though often loosely used as such, and definitions change. Until about twenty years or so ago the term overweight was applied to those who exceeded a hypothetical ideal weight derived from survival figures obtained by the Metropolitan Life Assurance Company, whose tables adorned most commercial weighing scales found in stations and other public places, but are now long since gone. A new way of expressing fatness that, made for ease of communication in epidemiological studies, became popular in the 1980s. Called the body-mass index, or BMI, it relates weight to height through a formula devised in the nineteenth century by a Belgian epidemiologist, Adolph Quetelet. A person’s BMI is their weight in kilograms divided by the square of their height in metres. Although it has major shortcomings – it says nothing about the proportion of bodyweight that is fat, which is the real test of obesity – the BMI has become the recognised standard of measurement for fatness, although it does not relate to morbidity as well as other indicators, such as waist-to-hip ratio or even just waist measurement.

Most healthy young adults have a BMI of 20–25. Those with a BMI less than 20 are currently classified as underweight and those with a BMI of 25–30 as overweight or plump. A BMI of over 30 is arbitrarily classified as indicating obesity. Insurance company statistics and more recently large epidemiological studies reveal that people with BMIs under 20 or over 30 are poorer life risks than those with BMIs between 20 and 30. As people get older, there is a population shift from the lower to the upper half of this range. Plumpness in late middle and old age – BMIs of 25–30, especially in women – is not the health risk that it is in young and middle-aged adults; indeed it is an advantage for longevity.

Plumpness in childhood, often called ‘puppy fat’ when it occurs in adolescents, is different and has only recently become the subject of intense media attention and public concern. Evidence linking it to adult obesity is conflicting. What is certain, though, is that the real hazard is gross obesity in childhood, which, in spite of what one reads in the media, is unusual and often due to genetic and metabolic defects, an increasingly large number of which are becoming identified.

Childhood obesity is a medical problem from the start, but how to distinguish it from benign, non-progressive plumpness has still to be resolved. Even the criteria for defining obesity in children are unclear. Though weight and height charts still have an important role to play in monitoring children’s development, the BMI is less predictive of future events in them than in adults. Fat – or adipose tissue, to give it its technical name – constitutes a higher proportion of a woman’s bodyweight than a man’s. It is only when fat deposits become abnormally large – which can be difficult to determine, machines that are said to do so notwithstanding – that it becomes appropriate to talk of obesity. There are almost as many types of obesity as there are individuals afflicted by it. However, two main physical types can usually be distinguished.

Gynaecoid obesity, so called because it is more common in women, is associated with increased deposition of fat in and under the skin – especially below the waist – and is relatively benign. Android obesity, on the other hand, is much more malign. It is more common in men and due to massive deposition of fat within the abdominal cavity. It gives rise to what is often, but wrongly, described as a beer belly. People, including women, with this type of truncal obesity have larger waist than hip measurements, and their limbs are often surprisingly thin. They are sometimes described as apples in contrast to the fancifully described pear shape of those with gynaecoid obesity.

When truncal obesity is associated with certain biochemical abnormalities and/or high blood pressure, people with it are said to have the metabolic syndrome, but the usefulness of this term has been questioned. It is the catastrophic rise in prevalence of this truncal obesity, rather than of fatness itself, that is the major cause for concern. Neither type of obesity is an illness in its own right, but each predisposes to the development of incapacity or premature death. Diseases such as sleep apnoea, osteoarthritis of the lower limbs and hypertension are common to both, whereas diabetes and coronary heart disease are much commoner in people with truncal obesity

Like all conditions from which mankind suffers, obesity is the result of the interplay between nature, in the shape of genetic and antenatal factors, and nurture, principally in the shape of the availability of food. While this may seem obvious, it has not always been accepted. As recently as the beginning of the twentieth century, the link between food intake and obesity was appreciated by very few. Anecdotal personal experience suggested that fat people ate no more than thin ones – some of whom seemed to be bottomless pits into which food could be shovelled with seemingly little effect. There is no doubt that this perception is wrong.

Statistically, fat people both expend and consume more calories than thin people, although the overlap between them is enormous. This is mainly due to differences in resting metabolism – the amount of energy required just to keep the body warm – and the levels of physical activity or exercise. It is quite easy to show that quite subtle differences in food intake or energy expenditure could, over a period of many years, produce profound changes in body shape. For example, taking in the energy contained in just one knife-full of butter more than you expend every day would, after a year, theoretically cause a 2-kilogram gain in weight.

This simplistic approach to the causes of obesity belies its complexity. What is truly remarkable is how most people manage to maintain more or less the same weight once they reach adulthood without a conscious effort to control what they eat. It is as if they possessed a ‘bodystat’ analogous to a thermostat in a refrigerator. The mechanics of this bodystat are still being unravelled by biochemists and physiologists throughout the world, and by psychologists, sociologists and epidemiologists in individual communities.

The role of nature – genetics – rather than nurture in the process of getting fat has been known to farmers, veterinarians and experimentalists for over a hundred years, but was only recently established in human beings. This began with studies of the differences in the incidence of obesity in identical and nonidentical twins, where the effect of environment, especially access to food, could be minimised. Even more recent is recognition of the role played by intrauterine and early postnatal nutrition in the development of obesity and the conditions linked with it.

Gross obesity occurs in several very inbred strains of rodent. In one strain the specific gene responsible was given the name ob for obesity. Only mice inheriting a copy of the gene from both parents (ob/ob) develop a condition that led to their depositing so much fat that they weighed 4–5 times as much as their siblings who did not have the gene or had inherited just one copy of it. The fat ones lacked the ability to make a hormone called leptin, which, among its many properties, has the ability to suppress appetite. ob/ob mice eat ravenously until they are so fat they cannot get to their food. Even when fed only as much as their thin siblings, they still put on more weight. Over the past decade or so a similar condition has been recognised in human beings, although it is extremely rare. Another genetic type of obesity in mice causes a condition that resembles ob/ob, but is caused by an inability to respond to, rather than produce, leptin.

The idea that hormones played a part in controlling bodyweight began with the discovery that patients with thyrotoxicosis, caused by an overactive thyroid gland, often develop ravenous appetites yet lose weight. Conversely, those with an underactive thyroid often gain weight, though they very rarely become obese. Investigations into the role of the thyroid gland showed it played no part in the genesis of obesity. Later it was observed that many patients with rare tumours of the pancreas producing too much insulin also became very fat. In these patients with pancreatic tumours, insulinomas, this was because they were incorrectly advised to eat something when they felt symptoms of hypoglycaemia (low blood sugar) coming on rather than because it came naturally to them.

Now that a surgical cure for insulinoma has become simpler and safer, we no longer see the gross obesity we used to associate with this condition. Nevertheless, experience with insulinomas established a role for insulin in the genesis of obesity that has now been confirmed countless times. Paradoxically, voluntarily overeating also leads to increased production of insulin and of reduced sensitivity to some, though not all, of its actions. Which, in real life, is the chicken (overproduction of insulin) and which is the egg (overeating) is probably different from one individual to another.

Although insulin and other glandular products, such as thyroxine, cortisone and oestrogen, have long been known to be associated with obesity, it is only since the discovery of leptin that the part that hormones play in its production has been taken seriously by the scientific fraternity.

Several new hormones, many of them produced in the intestine itself, have been discovered in the past ten years or so that affect the control of appetite and disposition of food within the body after it has been absorbed. Contrary to early expectations, most fat people have more leptin in their blood than normal, so treating them with leptin is unlikely to work except in the infinitesimally small number of people with genuine genetically determined leptin deficiency, for whom it is a ‘miracle drug’, just as cortisone was for patients with Addison’s disease and insulin for Type 1 diabetes.

Equally exciting as the discovery of leptin is the discovery that there are at least four other hormones, all produced in the intestines or stomach in response to certain foods, that can affect appetite and metabolism of nutrients within the body. Genetically engineered animals rendered insensitive to the hormone called GIP (or gastric inhibitory peptide), for example, do not become obese with overfeeding. This observation supports earlier work, derived from studies in human beings, and suggested that GIP is one of the factors that lead people to become obese and may just be related to the composition of the diet. It also makes GIP an important target for the pharmaceutical industry to develop antagonists to its actions that can be used therapeutically.

Contrary to popular belief, it is extremely difficult to become clinically obese by voluntarily eating excessively. This was established by experiments performed on healthy young volunteer prisoners. These experiments showed that mere access to unlimited supplies of food was not enough for the average person to become obese: something more was required. It clearly has something to do with appetite and the ability to overcome the feeling of satiety that most people experience when they have eaten sufficient for their physical requirements. One of the recently discovered hormones produced in the intestine, called PYY, works on the brain to suppress appetite – so does the even more recently discovered hormone obestatin.

Under experimental conditions, PYY enables obese people to resist the temptation to eat excessively. It is currently being pursued as a potential treatment for obesity. Other gut hormones affecting appetite and the sense of satiety are also known. One of them is called is GLP-1. Like GIP and PYY, it is made and released from the intestine in response to certain foods; like GIP, it is involved with the disposition of the individual constituents of the food within the body, mainly – though not exclusively – through their ability to stimulate the release of insulin. It, or something very like it, is already available commercially for the treatment of Type 2 diabetes. Ghrelin and obestatin, both discovered within the past ten years or so, are produced in the stomach and affect appetite in opposite directions: ghrelin stimulates appetite; obestatin inhibits it.

Just how important the newly discovered hormones are in deciding whether or not you become obese is still uncertain. It’s one thing to discover how a hormone works under research conditions, quite another to apply it in a clinical situation.

We are still a long way from understanding how these new hormones work in human beings under everyday living conditions. Studies on the changes produced in grossly obese patients whose only salvation comes from by bariatric surgery – operations on the stomach that are currently the only effective method of treating this life-threatening condition – will undoubtedly advance our knowledge. So will experiments and clinical trials using pure hormones as they become available, exactly as happened with insulin and diabetes.

While the availability of a plentiful supply of food is a prerequisite for the development of obesity, the relationship is far from being a simple one. Most people with access to alcohol do not become alcoholics; a few, especially those with a genetic predisposition, do. The same is true for food, but whereas it is possible to abstain from alcohol completely – and so achieve a cure of the ill – this option is not available to the obese. Obese patients may find it comparatively simple to stick to a very low-calorie, synthetic, liquid, formula diet and lose weight at just about the maximum theoretical rate – about half a pound or a quarter of a kilo a day – but as soon as they are permitted to replace one of the meals with solid food of their own choosing they stop losing weight and may even gain it.

The idea currently being propagated by single-issue pressure groups is that obesity is due to one particular type of food constituent, whether it be fat, sugar, rapidly absorbed starches or combinations of them – in particular when they are provided in the form of foods such as hamburgers, pizzas, chips, crisps and other energy nibbles. This would be laughable if it were not so misleading. Obesity is a genuine, recognisable medical problem. It will not be resolved by simplistic dogma that is based on unproven opinion rather than on evidence.

The fact that an increase in the incidence of obesity coincided with a rise in the availability of fast or convenience foods is not evidence of their role in its causation. Exactly the same argument could be advanced for the rise in the use of telephones, or – better – central heating. Human beings burn off many more calories to stay alive in a cold environment than when they are warm. It would nevertheless be as foolish to assume that the answer to obesity is to return to the days of cold and damp housing as it is to suggest that banning the sale of energy-dense fast foods, or labelling them as bad for you, will the solve the problem. Decades of dietary advice for the prevention and treatment of obesity based on avoiding first this and then that type of food have all resulted in failure.

Any new way of losing weight is likely to produce an effect lasting a year or two, especially if aided by pharmaceutical appetite suppressants. A small percentage of dieters do manage to sustain their weight loss, but this is achieved not merely by changes in their diet but by altering their whole way of life. Indeed, the few long-term, large-scale interventional studies that have succeeded in reducing the incidence of obesity, and more especially Type 2 diabetes, have relied upon intensive re-education and alterations in lifestyle to incorporate changes in exercise as well as in eating habits. The importance of moderate and regular exercise in achieving weight loss cannot be overemphasised – not because of the calories consumed in doing it but for its general effect upon the metabolism of the body.

Other factors are important also. The way food is eaten, whether as regular meals or ‘on the hoof’, the time of eating, the size of individual portions and what they consist of, as well as the genetic and hormonal factors in the person eating the food, all have a part to play. The old adage that it is better to leave the dining table wanting more than to leave it fully satiated is probably still as good advice as any for those genuinely wanting to avoid obesity.

This may be difficult to achieve in an ‘I want it now’ society, but it might be helped by teaching elementary nutrition and the long-term health risks of obesity at an early age rather than resorting to propaganda based on half-truths and unproven ideas. But for many of the morbidly obese, the ones really at risk, it is only advances in the understanding of the pathology of obesity and its specific and appropriate treatment that offer any genuine hope of sustained benefit.