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
