The obesity epidemic; fat, fact and fiction!
This essay was written by Randip Bains and was first published in the 2002 Mill Hill Essays.
For the first time in history, the world’s total of overweight people equals the total of those who are underfed. Up to 1.2bn people eat more than they need, and as many go hungry each day.
Guardian, March 2000
It is estimated that more than half the British population and two thirds of the American population are overweight or obese. The past twenty years has also seen a dramatic increase in childhood obesity with twice as many American children and three times as many adolescents being overweight now compared with 1980. Obesity is the second leading killer of Americans, beaten only by cigarette smoking. What is the reason for such a dramatic increase in this epidemic?
Consider one of the most severe cases of obesity in Britain, that of Barry Austin. Barry was obsessed with eating, saying that food was his god and he worshipped it. He weighed 318kg at the age of 29 and clearly consumed more food than his body required or was able to burn. Typically, for breakfast Barry would eat four packets of crisps and half a box of biscuits. After lunch, from the chip shop, he ate several plates of beans on toast, fruit-cakes and more crisps. For tea he would have 6 lamb chops, 12 roast potatoes, vegetables and gravy, pie and custard. Finally for supper he had five large hamburgers. This was all washed down with 12 litres of cola each day. Can today’s society really feel sorry for someone like Barry? Is he simply another obesity case who practices two of the deadly sins, greed and gluttony? Or is it something he cannot help and should certainly not be ‘blamed’ for?
Obesity is a disease and it can lead to heart disease, diabetes and an increased risk of cancer. More than a quarter of cancer cases worldwide are related to being overweight, while over three-quarters of sufferers of type II diabetes are also obese. Type II diabetes is the form of diabetes that usually occurs in adults. Sufferers develop a resistance to their own insulin and become unable to regulate the sugar levels in their blood. However, in recent years this previously adult-only disease is being diagnosed increasingly in teenagers and even in children. Some experts insist that it’s not just how much fat you have but where you carry it that affects your risk of developing other diseases. Men and post-menopausal women have an “apple-shaped” distribution of fat, carrying it predominantly inside the abdomen. Pre-menopausal women tend to have a “pear-shaped” distribution, with flab on the thighs and buttocks. “Apples” carry a higher risk of developing heart disease and diabetes than do “pears”.
There is a paradox here. How can nations like America and Britain that are so body-obsessed become so overweight? Over the past 20 years the media, bookshelves and TV programmes have been filled with the notion of healthy eating, pro-carbohydrate, pro-fibre, low fat, no cholesterol, no sugar foods and diets. Supermarket and food chains have participated in this consumer hype and developed so called ‘healthy eating’ options. Many people are devotees of ‘weird and wonderful’ fitness regimes; Yoga, Pilates, Spinning, Body Pump, Tae-Bo, Boxercise, just to name a few. But despite being encouraged to get fitter, the population as a whole has instead got fatter by the year. One simple reason for this is that our lifestyles have changed such that the majority of people live more sedentary lives. The price we pay in all age groups is a sharp increase in obesity.
In our society there is no longer a need to search for food and water. You only have to walk through any town centre and you will be offered an array of inexpensive and convenient fast food restaurants. It is no coincidence that the rapid increase in obesity has accompanied a rapid increase in the number of fast food chains. Dining out is more common and eating food is seen as a means of entertainment, often accompanied by alcohol. With greater variety and more social eating people may tend to gorge more and drink more alcohol leading to larger and unhealthier individuals. Why is this? Have we lost the will to stop eating when food is plentiful? People are busier than ever so they grab whatever is quick and convenient. Unfortunately “quick and convenient” does not necessarily mean “nutritious and healthy”. But this is a poor excuse considering that most supermarket aisles are well-supplied with fresh vegetables and salads that require no washing, no cutting – just eating!
It is thought that the greatest contributory factor to ‘childhood’ obesity is diminished physical activity. Gone are the days when children played outside until dusk and walked to and from school. After-school and holiday activities often consist of playing computer games, watching television and surfing the Internet, but these do not burn off many calories. Television also adds to the temptation: the average American child apparently sees 27,000 food advertisements on television every year!
Some people can maintain a normal body weight despite overeating. Changes in feeding behaviour do not always correlate with changes in bodyweight: it seems that some of us are predisposed to become obese. Studies of certain populations show that genetic factors certainly can have a role in obesity. Studies of identical twins and of families indicate that as much as 80% of the variation in body weight may be attributable to genetic factors. There are also diseases, caused by changes to a single gene, whose symptoms include obesity but these types of disorders are extremely rare and cannot account for the current ‘epidemic’ in obesity.
Animals and humans eat for a variety of reasons: hunger, time of day, social setting, stress, boredom, palatability/reward, and food availability. Some animals have evolved so that they are able to burn fewer or more calories depending on the circumstances of their life or changes in the weather. For example, the ability to store substantial amounts of energy in the form of fat allows dairy cows to achieve high rates of milk production. Hibernating animals also depend on the ability to reduce their energy expenditure while still maintaining the body processes necessary for life. Some hibernators are able to reduce their metabolic rate by 95%, which causes a drop in body temperature and enables the animal to survive during the winter. Humans possess many of the same genetic adaptations but they remain “dormant” since current lifestyles do not require such responses. The differences in these genes between individuals may explain some of the differences in bodyweight between people who otherwise seem to eat the same and exercise the same amount.
From an evolutionary perspective the ability to store energy when food is plentiful for use in times when food is short would at one time have conferred a survival advantage. Food was not as easily available to our ancestors as it is today. Contemporary humans can therefore be seen as having been selected for genes that favour energy intake and storage and that diminish energy expenditure. However, in modern lifestyles the combination of easy access to highly palatable, inexpensive, larger portions, high calorie foods and a sedentary lifestyle have made the metabolic consequences of these genes detrimental to health. These genes may now have become culprits, making disadvantageous contributions to fat accumulation, obesity, and heart disease.
Over the past 45 years a number of obesity mutations have been described in mice and rats. In the last 10 years research in this field has mushroomed and researchers now have many clues to the role of genetics in obesity. Now that the human genome has been completely described the equivalents of these rodent genes have also been identified in humans. In 1950 a mutant mouse, the obese mouse, was identified. This became the most well-known of obesity models but it was forty years before researchers discovered why it was obese. The defect was the absence of a hormone called leptin (from the Greek leptos meaning thin), resulting in a mouse that ate too much and became obese. When treated with leptin, the mice stopped overeating and lost weight. The discovery of leptin in 1994 and, a year later, the discovery of the site that it targets in the brain, were major breakthroughs in obesity research. Scientists quickly began to conduct numerous experiments to discover how this hormone worked, its role in obesity and its possible use as a target for drugs that might prevent severe obesity in humans.
Leptin is a hormone, produced by fat tissue, which sends information to the brain. A decrease in body fat leads to a decrease in the hormone, which in turn stimulates food intake. Increased body fat leads to increased levels of the hormone, which act to reduce food intake. By this mechanism, weight is maintained within a relatively narrow range. Mutations that block leptin production are associated with massive obesity as in the obese mouse. The obvious next step was to screen obese humans to find out if they had mutations which led to a lack of leptin and overeating as in the mouse. However, when thousands of obese people around the world were tested for leptin, they were found to have much higher levels of the hormone than non-obese people. This is not completely unexpected since obese people have more fat and so will produce more leptin. Why then is this excess of hormone not signalling to their brain to eat less? It seems that the brain’s sensitivity to leptin is variable and that, in general, obese individuals are ‘leptin resistant’. This scenario is superficially similar to people with type II diabetes, where patients become resistant to insulin and although they have high levels of insulin, their bodies are unable to respond well to it. Likewise, in obese people with high leptin, their bodies are unable to respond to the high circulating levels of the hormone. Since its discovery, leptin has been shown to have a role in a number of other body processes as well as the regulation of bodyweight. These include the initiation of puberty, establishment of secondary sexual characteristics, bone formation and a role in the immune system. It is not too surprising that this hormone has a role in both body weight and reproduction; it makes sense to avoid becoming pregnant when there are inadequate nutritional stores to support a growing fetus.
Anorexia nervosa is one of the most disabling and lethal of psychiatric disorders but it is also, like obesity, an eating disorder. The two disorders show evidence of both genetic and social causes, they can both cause depression and they can lead to death. Studies of identical twins suffering from anorexia have shown that both twins are affected similarly and indicate that genes contribute to a predisposition that is triggered when individuals are exposed to certain environments. Anorexia is characterised by prominent behavioural, psychological and physiological disturbances, including increased physical activity, depression, obsessional preoccupation with food, reductions in heart rate, blood pressure and metabolic rate and decreases in the production of oestrogen (or in males, testosterone). Patients with anorexia have larger amounts of leptin in their brain compared with the amount of leptin in the blood. Since leptin works in the brain to decrease food intake these patients appear to have a stronger signal to stop eating.
Once exclusively hailed as the ‘fat hormone’, leptin has more to it than initially meets the eye. A small number of people have been found to have mutations in their leptin gene or the gene for its receptor, resulting in an absence of the hormone or a malfunction in the way in which it signals to the brain. The first of these cases was discovered by a team of researchers in Cambridge. The patient was a female who at the age of 8 years weighed 86kg and was uncontrollably consuming vast amounts of food. Her desire to eat was so strong that her parents had to lock the kitchen at night to prevent overnight binge eating, including the consumption of still-frozen fish fingers. It was found that she had a complete absence of leptin, caused by a mutation in the leptin gene. Shortly after this discovery she was treated with leptin, which resulted in a significant decrease in the amount of food she desired and ate, and her weight decreased significantly.
The target receptors for leptin lie in an important region in the brain called the hypothalamus, an area which is of much interest to obesity researchers. The suggestion that the hypothalamus plays a role in feeding behaviour was originally based upon studies of brain-damaged patients in the early 1900’s. Injury to one particular area of the hypothalamus produced overeating and obesity, while injury to another part caused undereating and weight loss. It seems that there are ‘satiety’ and ‘feeding’ centres in the brain. There are many other substances that affect feeding behaviour. They are found in the gastrointestinal system and particularly in the region of the brain called the hypothalamus. When activated, these substances have effects on how much and how little we eat and how full or hungry we feel. The discoveries made with leptin have stimulated much research into the mechanism of action of these substances but there is still much to be learned. What seems to be clear is that there is not a single cause of obesity.
Treatments for obesity are under development. Pharmaceutical companies are investigating the functions of the substances involved in feeding behaviour as potential drug targets. Other treatments for obesity include behaviour therapy aimed at modifying eating-related activities, exercise to increase caloric expenditure, and diets to lower calorie and fat intake. Eating less and exercising more leads to losing weight but with willpower alone it can be hard to eat less and some people find it difficult to exercise! For these reasons the concept of taking a pill that will shed the pounds without major life-style changes is much more appealing. Surprisingly, so is the more drastic direct approach of surgery. Nowadays, you can have your jaws wired to restrict the entry of solid foods, your stomach stapled to reduce its capacity to hold food, gastro-intestinal bypasses to prevent absorption of food, and of course the surgical vacuuming of fat from under the skin – liposuction. However, these treatments can cause complications and not all are successful in achieving the desired effects.
A treatment for obesity in the form of a pill is one of the most sought after drugs in the western world. Biotech companies are investing large amounts of money hoping to be the first to find a ‘cure’ for obesity. Previously many anti-obesity drugs have caused serious side effects and consequently have been withdrawn from use. Obesity drugs generally fall into one of four categories. Appetite suppressants that slow down food intake, those that prevent the absorption of fat, enhancers of energy expenditure, and stimulators of fat breakdown. All of these have down-sides, but there are a lot more risks with uncontrollable obesity than with taking the drugs! Furthermore, although these drugs may work in the short term, it is the long-term maintenance of weight loss that obese people find difficult to achieve.
There is no clear answer why some of us are ‘predisposed’ to becoming obese, likewise there is no clear answer for why many of us are predisposed to becoming diabetic or developing cancer, though progress is being made in all these areas. We may be destined to become obese even from the moment we begin to develop in our mother’s womb. Evidence from studies of human populations subjected to undernutrition in fetal development, suggests that early fetal exposure increases the risk of adult obesity, whereas exposure in later gestation may programme obesity resistance. If this is true, does it really matter what life-style we choose to lead, what we choose to eat and how much of it we choose to consume? We may be destined to become obese irrespective of what we do!