Fat, Fate, and Disease : Why we are losing the war against obesity and chronic disease (13 page)

Quite clearly, governments need to insist that knowledge about healthy eating is included in the school curriculum, and even the preschool curriculum, for data show that nutritional education at an early age can have long-lasting effects. It is irresponsible and inadequate to delegate this job to parents who are often not prepared
to take on this task. In addition, there is increasing evidence that teaching children about good nutrition influences the eating habits of the whole family.

But some politicians insist that the State should not be involved in these matters. They see it rather as sex education used to be viewed—as something personal and private that should be left entirely to parents to impart to their children. The battle for sex education has been won, at least in many developed countries (although some schools still leave it until it is too late). We argue vehemently that in the same way it is totally unrealistic to rely on nutritional information and lifestyle skills being transmitted from parent to child. Many—possibly most—parents do not know the facts, and given the speed of change in nutrition they are not in a position to do anything to change the situation.

Education means genuine knowledge about what food contains, and about what healthy and unhealthy eating are. It is about the energy equation and the consequences of unbalanced diets and the lack of physical exercise. It is also important to avoid all the misinformation that tends to creep into nutritional information, for example overzealous health claims for antioxidants or misleading claims about some food types. Educational information must be accurate. This is similar to the case for genetically modified foods. There may be other reasons, some largely value-laden, why people do not want to eat such foods, but the claims that those opposed to them make regarding their safety are generally unscientific or totally exaggerated.

And then there is the problem of the food label. Many countries now require packaged foods to be labelled. But there is enormous variation in what is required and most of the information is dense, and effectively meaningless. It is expressed in terms that a nutritional scientist, let alone a consumer, can barely understand and so cannot be of much help. We need to provide simple, clear information against the background of the education needed to understand it. Knowing that 100 g of a food contains 12 per cent of the recommended daily
allowance of niacin is meaningless and useless information. What does the recommended daily allowance mean and, in any event, how does 100 g relate to what is being eaten? In any case, there are very few people who need to know how much niacin they are eating.

What we need to know exactly is how much energy is in our food and what form it takes. And we need to know how many calories a day we should eat. We have asked professional people who are not doctors or nutritionists this question and been shocked at the variation in answers we have received—from a few hundred to 5,000 calories a day. If university graduates do not know the answer to this basic question, nutritional literacy is a real problem. In New York, fast food outlets now have to show how many calories are in their hamburgers. Given that fast food is a main source of meals for so many people, this is welcome, but again if we do not know how many calories we should eat each day, does it really help to know if one burger has 550 or 1,550 calories?

If the obese person or family is one target for zealous interventions, another is the food industry itself. It is easy to rail against this industry, but in reality not only does it influence what we want but it also sells us what we want. This is complex because fatty foods tend to be tastier—many taste-evoking substances are dissolved in fat—and in many cases they are cheaper to make and have a longer shelf life. We buy them because we like them, they are cheap, and they keep—we are not being totally exploited here. Mind you, the industry has had its knuckles rapped, justifiably, for making excessive claims about the health benefits of some foods and for fast food advertising targeted at children.

But on the other hand, without the food industry the capacity of the world to support seven billion people—let alone the nine or ten billion people we expect—is doubtful. The food industry is a necessary part of every economy, from the poorest to the richest country.
Food security is an urgent concern for many governments. Supplying food to a hungry world requires the involvement of the private sector. We need their cooperation. We need them to produce healthier foods and to restrict their profit-driven emphasis on producing unhealthy foods. The issue is how much carrot and how much stick we should use. There will be a place for restricting some activities, such as marketing junk food to children—but how do we define junk food? And equally we need the food industry to be our partner in finding a way to produce cheap, healthy food. Getting the balance right requires open minds and a willingness to engage in a partnership rather than a fight.

We urgently need a constructive engagement with that industry to find ways in which they can profit and we can live healthily. Denying this is as illogical as saying that we will not encourage car manufacturers to make safer cars, because when they sell them to us they make a profit from our safety. Safer cars are in our mutual interest.

Earlier in this chapter we stressed that we are all different, in terms of our metabolism, our appetites and tastes, as well as our self-control. Mark can resist the bowl of cashew nuts; Peter cannot. Some people can be fat but not at great risk of diabetes or cardiovascular disease; others seem to be relatively thin but have problems of excess visceral fat and a greatly increased risk of such disease. We need to understand these differences—how much are they due to genetic differences, how much are they population-based, and how much are they due to personal, cultural, and biological factors? For until we do so we cannot appreciate when it is appropriate to tackle the issue of obesity and chronic disease prevention at a population level and when to tackle it on an individual basis. Until then we cannot make real progress—so this is where we need to go next.

Each of us responds differently to living in the modern world. One of the great achievements of Charles Darwin was the recognition that individual variation matters. In what he called natural selection, he described how some variations make an individual more likely to survive and reproduce and others less likely to do so. When such variation was inherited, partly through what we now call genes, those who reproduced most successfully left more descendants, who in turn had more favourable genetic endowments than those who reproduced less successfully. This process gradually changes the population over generations, so that the characteristics of most of its individuals match the environment they inhabit. This is as true for bees and trees as it is for animals, including humans.

The implications of this for understanding modern humans are important. Evolution is generally a gradual process. Real change in what makes us what we are by this process takes many generations.
But only a few generations have passed since a big change in our world took place with the industrial revolution. And there have been surprisingly few generations since we invented agriculture and started settling in villages and then in larger towns and cities. Most of human evolution had already happened in Africa. When we look at our history in this way we can readily understand that our biology is largely designed by evolution for a very different world from the one we inhabit today.

But Darwin recognized that the ‘survival of the fittest’ was not the only way in which genetic variation could influence a population. Many animals also choose their mates. The choice in many species is made by a female, who decides which male she prefers. This is common in birds, and it is often said that this is why male birds evolved with some particularly attractive characteristics—at least to female birds. These might be the colour of their feathers (males tend to be the more colourful sex), how they sing (only male songbirds sing), how they make a bower, a particular kind of courtship dance, or the length of their feathers (think of peacocks). In many mammals the males fight or compete for mating rights with the female. So the gorilla defends his harem until he is displaced by another male; the elk fights with other male elk for dominance of the herd; the bull elephant seal spends much of his time on the beach fighting off other males. Darwin called this kind of process sexual selection.

Both natural and sexual selection are based on variation in our genes—in other words it was not what made us all the same that was important, but what made each of us different. We each have about 21,000 different genes and every cell in our body has the same set. Genes are made of DNA and it is the DNA that forms our chromosomes.

But although all humans basically have the same repertoire of genes, we may vary in the number of copies of these genes we have and in their detailed structure. Each gene contains thousands of connected molecules of DNA, subunits called nucleotides. It is the
sequence of these nucleotides that creates the particular gene and provides the genetic instructions which make our bodies work. Genes operate by instructing cells to make proteins such as enzymes, hormones, and the structural components that hold our body together. But these nucleotide sequences can have subtle variations between individuals, and that variation is reflected in the way we each have a slightly different genetic repertoire. It turns out that there is actually an extraordinary amount of subtle variation between individuals.

Each chromosome is made up of a long chain of DNA which thus comprises about 1,000 genes. But each gene on a chromosome is separated by sections of DNA which are not active genes. Indeed most of the DNA on a chromosome is not part of any gene. This used to be called ‘junk’ DNA but one of the most exciting developments in molecular biology has been the discovery that this DNA functions to control the switches which instruct the genes when to be turned on and off. Much of the variation in DNA structure lies in these control regions, which leads to even more subtle variation in gene function between individuals.

So do genes explain why we respond differently to living in a world of plenty? In the early 1960s the geneticist James Neel was pondering the question of why the Pima Indians living in Arizona, whom we introduced in the last chapter, showed such a high level of diabetes. Many young adults were clearly insulin-resistant (the technical way of describing the condition when insulin does not work properly in tissues such as our muscles), a condition that is the forerunner of diabetes. Some Pima had even developed diabetes in their thirties. Neel wondered whether the Pima had a genetic predisposition to the disease, and if so, why it occurred in this population in particular, rather than in others. When he thought about the history of these native American people, living for centuries on subsistence agriculture in their tribal homeland, he wondered if their evolutionary history might have contributed to the phenomenon.

Could it be, Neel wondered, that over the course of many generations this particular isolated population had undergone natural selection and become well adapted to their harsh nutritional conditions? If so, might it be that genes which conferred an advantage under these conditions had been selected? He called such possible genes ‘thrifty’ and suggested that they might be genes which conferred a level of insulin resistance in the body. After all, if insulin does not work as well as it should, metabolically active tissues such as skeletal muscle take up less glucose. This means that the body runs on less of this fuel, a bit like a car engine set to run on a leaner rather than a richer mixture of fuel and air. Indeed the Pima Indians were lean or at least had been lean under their traditional way of life.

But then many Pima changed their way of life, particularly in Arizona. This change came in the form of soft drinks and hamburgers and fries, which were widely available along with ice cream, doughnuts, and chocolate chip cookies, as well as alcohol. The Pima also took up sedentary jobs and drastically reduced the amount of manual work they undertook. So the people whose metabolism was set to run on a lean setting were now at very high risk. Here they were, with insulin not working properly, saturating their bodies with sugar and fat from their diet. Needless to say, the calories which could not now be used by muscle were stored as fat. Neel believed that all this was due to the Pima having a different genetic repertoire. His argument seemed highly plausible and was extremely influential. Perhaps these Indians had provided us with a vital clue—if the genes that caused them to have diabetes could be found, then we might know why many of us also get diabetes. This spawned a generation of medical research activity to find the thrifty genes.

But problems were soon found with the story. There was no dispute that thrifty metabolism might lead to metabolic problems, including obesity, diabetes, and cardiovascular disease, in a rich environment—but could the genes be found? A lot of studies looked for gene variations
to explain the findings but the data were rather unconvincing. Only a small amount of disease risk could be explained by the gene differences found. And when it was pointed out that those Pima Indians still living in Mexico had a much lower incidence of diabetes although they were genetically very similar to the Arizonan Pima, the genetic explanation seemed harder to sustain. Indeed the Mexican Pima had an incidence of diabetes very similar to other ethnic groups living near them, but who were very different genetically, suggesting that there was no added genetic risk. It appeared that environment, far more than genes, was influencing the occurrence of diabetes in the Arizonan Pima.

This example concerns a rather specific group of people living in a particular part of the world. What about the general population of a country like the UK or the USA? There is large variation in obesity levels and the risk of getting diabetes, so if genetic explanations were responsible, we would also expect there to be large differences in genetic make-up.