Science in Society Archive

The obesity epidemic and how to beat it

This special mini-series tells you the latest on how metabolic interventions can make genes work to slim you down. This series was first published in Science and Society 21

  1. The Obesity Epidemic
  2. How to Survive 40 Days Starvation
  3. How carbohydrates make fats

The Obesity Epidemic

Prof. Peter Saunders punctures some myths about obesity

Over the past two to three decades, there has been an alarming increase in obesity throughout the developed world. In the UK, the proportion of the population who have a body mass index (BMI) greater than 30 has tripled in twenty years and now stands at about one in five. Your BMI is your weight in kilograms divided by the square of your height in metres. If you find it easier to think in Imperial units, someone who is 5’10" tall is considered to be obese if he weighs more than 15 stone, i.e. 210 lbs.

Obesity is also on the increase in other countries, including many in Asia where it has not previously been common. Most alarming of all, it is increasing rapidly in children.

People tend to think about weight chiefly in terms of appearance; but obesity is first and foremost a health issue. Not only is it bad for us to be less fit and have more weight to carry around, obesity is also associated with a significantly increased risk of illnesses such as heart disease and diabetes. In particular, the recent increase in Type 2 diabetes has been so great and so rapid that health experts are describing it, too, as an epidemic. Type 2 diabetes is often called "late onset" diabetes because it has typically been a disease of middle age or beyond, but it is now found in teenagers.

What we don’t know about obesity

As with any health problem, the obvious question to ask is where it comes from. Why do people become obese? Up to a point, that’s easy enough to understand. We need energy to keep our bodies going and to allow us to be active, and we get it from the food we eat. Any energy that we don’t use is stored as fat, which provides a reserve that we draw on when we are using more energy than we are taking in. If we take in more energy (usually measured in calories) than we are using, we gain weight, if we take in less than we are using we lose weight. And if we keep taking in more than we use, then in the end we become obese.

But it’s not as simple as that. If it were, our weight would fluctuate a lot more than it does. The reason it doesn’t is that the body has mechanisms for regulating our weight. It controls the amount of energy we take in by making us feel hungry or sated. It also controls the amount we use by such means as changing our metabolic rate (the "idling speed", so to speak).

On the whole, it does this pretty effectively. According to the US Department of Agriculture, the average American consumed 300 calories per day more in 2000 than in 1985. There’s no reason to suppose that Americans are more active now than they were then, so taking a pound of fat as equivalent to about 3500 calories, Americans should be constantly putting on weight at a rate of about a pound every 12 days. That’s thirty pounds a year, or three hundred pounds a decade. In fact, nobody is gaining weight at anything like that rate, which shows that the body is somehow keeping the balance between input and output quite well, though in many of us not quite well enough.

This also means, by the way, that it is nonsense to say you can lose ten pounds a year just by leaving out your piece of toast and jam in the morning or by jogging for fifteen minutes a day. Both are good for you, and both will probably help you lose weight, but you can’t work out how much just by adding up the calories and dividing by 3500. It’s a lot more complicated than that.

There are many factors involved in regulating body weight and they combine in complicated ways. Heredity matters, but so does our entire life experience from the moment we were conceived – and even before that, because of the influence of our mother’s state of health and what she ate (see "Diet trumping genes", SiS 20).

Physiological systems are also remarkably difficult to manipulate from the outside. Something may work for a short time and then the body somehow senses what is happening and finds a way of countering it, which is why many diets work well but only for a week or two. There may be special interventions that help a few people with specific problems, but we’re not likely to find a magic bullet that works for the rest of us.

What we do know

Fortunately, we can be reasonably sure we know what are the important factors, even if we don’t understand how they operate. It comes from a world-wide scientific experiment that was unintentionally carried out over the second half of the twentieth century. We have masses of data from several different populations in which obesity, and the health problems that it brings, have greatly increased. Unless there has been a significant change in their genetic makeup in the 50 years since the experiment began, and no one has brought forward evidence for this, the increase must be due to changes in the environment and in the way people live.

What changes have there been in these countries? Two obviously stand out. First, their diets have changed. People are eating more and they are eating different foods. And second, they are exercising less. More people are in sedentary occupations; more drive where they used to walk.

It’s fairly obvious why eating more and being less active should lead to obesity, and there is now evidence to suggest why changes in what we eat can also matter. For example, studies have shown that we are sensitive to the amount of food we consume much more than to its energy content. If we eat foods with a relatively high energy content – which includes most snack foods – we tend to take in more energy before we feel sated. The pancreas may also secrete additional insulin to prevent the blood sugar level from rising, and this can make us feel hungry again sooner than we otherwise would.

Researchers have recently been studying a gut hormone called PYY3-36, which seems to be a specific signal to the brain to tell us that we have eaten enough. Foods that we digest quickly produce less of this hormone, which again makes us likely to take in more energy than we used to or than we need.

The Atkins diet, in which you are supposed to avoid carbohydrates altogether and the South Beach diet, in which you avoid only those carbohydrates that cause the blood sugar to rise rapidly, are also based on attempts to take advantage of the way that the body reacts differently to different sorts of foods and not just because of the number of calories (see "How carbohydrates make fats", this series).

In both diets, of course, there is the additional factor that people on almost any diet tend to eat less than they did before. And just eating less does seem to be important. A typical French meal includes lots of fat and carbohydrates, yet only about 7% of the French are obese, compared with 22% of Americans. When some American scientists collaborated with a group from the CNRS (the major research agency in France) to investigate this apparent paradox, they eventually concluded that the chief difference between the two countries is simply that portion sizes are much smaller in France.

What can be done

There’s still a long way to go before we understand how our body weight is regulated, but fortunately we don’t have to know that to start combating the obesity epidemic. If it was caused by changes in life style, and the evidence is clear that it was, then the obvious way to tackle it is also by changes in life style. That doesn’t mean trying to go back to where we were 50 years ago, but it does mean taking action.

When, eventually, governments have concluded that smoking has a serious adverse effect on health, they have not banned it outright. Instead, they have made it a general policy to reduce the amount of smoking, and have introduced a number of different measures aimed at achieving that aim. They have restricted advertising, insisted on health warnings, sharply increased the tax on tobacco, and banned smoking in many public places and encouraged other organisations to do the same.

They should do the same in the fight against obesity. It’s not a matter of closing down McDonalds or making Coca Cola a prohibited substance. Instead, the government should take steps to encourage people to adopt a healthier life style, and above all not to make it difficult for those who want to do that for themselves or their children.

For example, they should ban advertisements for food during the times when children are most likely to be watching television (see Box). Schools should provide proper, healthy meals. They should not have vending machines selling soft drinks or snack foods, or get involved in schemes that promote the sale of such foods.

Why Junk Food Adverts Promote Bad Health

A lot of advertising is devoted to pushing the foods that contribute to obesity. In particular, they are heavily advertised on the television and specifically in connection with programmes that children watch, except in the relatively few places (such as Sweden and Quebec) where this is forbidden. This is especially worrying partly because of the great increase in childhood obesity and partly because the food habits we acquire when young tend to persist throughout our lives.

Representatives of the food industry naturally disclaim any responsibility. They argue that it’s parents that decide what their children eat. Advertising, we are assured, has no effect. It may sound odd that they are spending millions of pounds on something that they don’t think helps them make money.

We’ve heard this sort of story before, from the tobacco companies. They insist they should be allowed to keep on advertising cigarettes, because – so they say – the ads do not increase the number of smokers. All they influence is choice among brands. No one is tempted to take up smoking because of tobacco advertisements, but some who are already smokers may move from one brand to another.

That sounds a bit far-fetched, but suppose it were true. It still wouldn’t apply to food advertising because there is important difference between tobacco and food. We don’t all smoke but we do all eat.

The tobacco companies explain that the huge amount each of them spends on advertising is not wasted because it can lead people to prefer their products over the others on offer. But in the case of foods, that’s precisely what we are worried about. We don’t need ads to make us take up eating. The question is about preferences, and if the advertisements can change these – as the tobacco manufacturers claim and as the food manufacturers must also believe or they wouldn’t spend so much money on advertising – then it is wrong to allow ads aimed at making us, and even more so our children, choose foods that are bad for our health.

That’s on the input side. On the output side, we should be encouraging people to walk and to use public transport. A standard recommendation is that people should take about 30 minutes of exercise five times a week. Many of us can do that by walking briskly to and from the bus stop on our way to work instead of getting into the car and driving there. Measures to improve public transport can also be measures to improve health, and that’s before we include the benefits in terms of cleaner air and fewer road accidents. Above all, we should encourage children to walk to school – which also means putting in place measures to make the journey safe.

There have always been obese people, and it may well be that drugs or other special treatments have something to offer them. But the hard scientific data, accumulated through 50 years of over-eating and under-exercising by millions of people, tells us that we can make a major impact on the problem by eating less, exercising more and avoiding the high energy fast foods and junk foods that have been spreading from country to country and bringing obesity with them. Best of all, there are no harmful side effects from eating less and exercising more.

That’s only common sense, but it is also what good science tells us. We mustn’t confuse science simply with "high tech"; they aren’t at all the same thing.

Article first published 12/02/04


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  3. Koeslag, JH, Saunders PT and Terreblanche, E. A reappraisal of the glucose homeostat which comprehensively explains the type II diabetes mellitus – Syndrome X complex. Journal of Physiology 549.2, (2003) 333-346.
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