Читать книгу The Way We Eat Now - Би Уилсон - Страница 18

It was 1971 and Dr Chittaranjan Yajnik was a young medical student training at Sassoon General Hospital, Pune, a big city in the west of India. Yajnik was given the task of measuring the body mass index (BMI) of diabetic patients. This should have been a routine job, little more than number crunching. The main challenge was that Yajnik could not afford a calculator, so he laboriously wrote down the patients’ weight in pounds and height in feet in a log table and used his paper notes to calculate in his head the BMI in kilograms per metre squared.⁴

After taking measurements for the first ten patients, Yajnik noticed something was not right about his numbers. His medical textbooks had taught him that type 2 diabetes was a disease mostly suffered by the old and the obese. But the first ten diabetic patients that Yajnik measured in the hospital at Pune were all young and thin, with low BMIs. If his measurements were correct, then the textbook must be wrong, or at least incomplete, in its definition of type 2 diabetes as an offshoot of old age and obesity. Yajnik tried to raise the problem with his medical supervisor but was told that this was no time to be challenging medical orthodoxy – he should just focus on passing his exams.⁵

Yajnik could not put the puzzle of diabetes in India out of his mind. After some years studying Western diabetes in Oxford, England, he returned to Pune as a fully qualified medical researcher, by which point diabetes was on the rise in his home country. In the early 1990s, Yajnik began a study following mothers and their babies in six rural villages near Pune – the Pune Maternal Nutrition Study. The data he started to gather confirmed his hunch that diabetes in India had a very different face from the supposedly classical type 2 diabetes in the textbooks. Yajnik took detailed birth measurements of more than six hundred Indian babies and compared them with a cohort of white Caucasian babies born in Southampton in the UK. Compared to the UK babies, the Indian babies were smaller and lighter. Yet when Yajnik used calipers to measure the thickness of the babies’ skinfolds, he found that the small Pune babies were actually fatter than the Southampton babies – they were surprisingly ‘adipose’, especially around the centre of the body. Yajnik coined the phrase ‘the thin-fat Indian baby’ to describe this phenomenon. Even at birth, these Indian babies had higher rates of pre-diabetes hormones in their bodies than their British equivalents. The babies may have looked thin but their body composition was actually fat.⁶

We speak of conditions such as heart disease and type 2 diabetes as ‘non-communicable diseases’ or NCDs. You can’t catch an NCD from another person in the way that you would catch a common cold by standing next to someone who is sneezing. But what Yajnik discovered is that babies can actually ‘catch’ a predisposition towards diabetes from their mother in the womb, via the diet she eats. The babies of mothers who were undernourished during pregnancy had ‘fat-preserving tendencies’ – passed on as a survival mechanism.⁷

It used to be believed that India’s diabetes epidemic was mainly due to ‘thrifty’ genes, endowed over many generations on populations that suffered from patchy and inadequate food supplies. Thanks to decades of malnourishment, these populations were poorly adapted to eat a rich modern diet. Yajnik’s breakthrough was to show that the time frame of maladaptation was much shorter. He speaks not of a thrifty gene but a ‘thrifty phenotype’: the interaction of genes with the environment over a single generation. Depending on the environment in which it develops, a given gene may give rise to different phenotypes. The ‘thin-fat’ baby represents a mismatch of biological environments. These babies grew inside their malnourished mothers with phenotypes for hunger but – thanks to the huge changes in India’s food supply between the 1970s and the 1990s – found themselves eating an unexpectedly plentiful diet.⁸

When Yajnik first observed the ‘thin-fat’ baby in the 1990s, this was a radically new way of thinking about the interaction of nutrition and health. It took six years for Yajnik to have his first paper on the subject accepted for publication because the mainstream medical establishment was so sceptical of this idea ‘coming from an obscure Indian in an obscure place’, as he puts it. The idea of the ‘thin-fat’ baby only started to gain acceptance when Yajnik published a paper in 2004 revealing that he was a ‘thin-fat’ Indian himself.⁹

This 2004 paper – which he called the ‘The Y-Y paradox’ – included a now-famous photograph of Yajnik side by side with his friend and colleague John Yudkin, a British scientist: two slim middle-aged men in white shirts. The paper explained that Yajnik and Yudkin had near-identical body mass index readings of 22 kg/m². A BMI of anything between 18.5 and 24.9 is considered healthy in the UK: not underweight and not overweight. Yajnik and Yudkin were both well within this healthy range. But X-ray imagery showed that Yajnik – the thin-fat Indian – had more than twice the body fat percentage of his friend. Yudkin’s body fat was 9.1 per cent whereas Yajnik’s, despite his slim appearance, was 21.2 per cent. Further research has confirmed that the adult Indian population in general has lower muscle mass and higher body fat than white Caucasians or African Americans.¹⁰

The story of the thin-fat babies of India is the story of the nutrition transition written on human bodies. Thanks to the new science of epigenetics, we now know that a pregnant woman’s body sends signals to her unborn child about the kind of food environment he or she will be born into. An underweight pregnant woman who eats a scarce diet is signalling to her child that food will always be scarce, which triggers a series of changes in the baby’s body, some hormonal and some physiological. For example, Yajnik found that a lack of vitamin B12 in the mother’s diet resulted in babies who were more likely to be insulin resistant.

Thin-fat babies are graphic evidence of a society in a state of dietary flux, with a shift from starvation to abundance in a generation. These Indian babies were born to mothers who lived and ate not so long ago, but the circumstances of their lives feel like another universe. There was seldom enough food, especially fats and protein, and people had to walk many miles just to get fresh water. When these women became pregnant, their babies’ bodies were metabolically programmed before birth – with their ample deposits of abdominal fat – to survive in circumstances that were harsh and lean. But the babies grew up eating in a very different and more affluent environment: a world of improved buses and electricity and labour-saving farm machinery, of cheap cooking oil and rising incomes. Millions of people in Indian cities – a new and rising middle class – have scooters where once they had only bicycles or feet. Diabetes is the worm in the apple of this new Indian prosperity.

The problems of babies born into a rapidly changing food environment are compounded by the way they are fed during the early years of life. The memory of scarcity still informs the strategies mothers use to feed babies, not just in India but everywhere in the developing world. Many of the thin-fat babies will have been fattened up in their first two years by emergency food aid. In the old India, the most urgent nutrition problem was outright hunger and overfeeding a child seemed to be the last thing anyone should worry about. This hungry India still exists to a shocking extent, with 38 per cent of all children under five so short of food that it will impair their future development, according to the Global Nutrition Report. If the alternative is to starve, rapid weight gain in the first two years of a child’s life can be a miracle. But it’s now known that this rapid growth in children who were previously malnourished may have unintended long-term consequences. Rapid growth is a risk factor for obesity and elevated blood pressure in later childhood and diabetes in adulthood. There is gathering evidence that high intake of protein and vegetable oils during the early years of feeding may result in a higher risk of obesity later in life.¹¹

Given India’s vast population, it is perhaps not so surprising that the country currently has more patients with type 2 diabetes than any other in the world. The more startling fact is that people with diabetes form such a high percentage of that population. Already, in large cities such as Chennai, around two-thirds of the adult population is either diabetic or pre-diabetic.¹²

What can be done to correct the nutritional mismatch suffered by the thin-fat babies? Those working with malnourished babies in developing countries have started to talk of ‘optimal’ nutrition: the kind of childhood diet that will provide all the essential micronutrients and promote growth while minimising excess weight gain. Yajnik and his colleagues are currently working on a project giving a cohort of adolescent girls vitamin supplements which should, in theory, mean that in pregnancy their bodies will send the message to their unborn children that a world of plenty awaits them. The aim of the project is to get the bodies of the mothers to communicate more accurately with their unborn children about what food is like in modern India and thus to reduce the risk to future generations of developing NCDs. Only time will tell if these hopes come to fruition. The epigenetic messages in our bodies cannot be rewritten straight away.

Spare a thought for the grown-up thin-fat babies of the 1980s and 1990s, many of whom are now diabetics living in modern India. Through no fault of their own, these people are stuck while young with a disease they will spend a lifetime trying to manage. Living with type 2 diabetes means living on a diet that is directly at odds with the prevailing food supply. In food markets awash in lavish amounts of refined carbohydrates, they must teach themselves to be sparing with sugar and white rice. They must try to limit their calorie intake in a world that offers them ever-larger portions.

The dilemmas faced by the thin-fat Indian are an extreme version of the problems facing millions of others in the modern world. We are all affected to some degree by a series of biological clashes between the basic instincts of our bodies and the environments in which we live, and taken together, these clashes seem almost designed to make us fat. Every human baby has an inbuilt preference for sweetness, which didn’t matter too much in the days when sugar was a luxury, but which becomes a problem in a world of cheap sweeteners. We also have a natural inclination to conserve energy, which served us well as physically active hunter-gatherers and farmers but doesn’t pan out so well in cities full of cars. Many of the human instincts that evolved to help us survive have now become a liability. Yet another example is the fact that, in human biology, hunger and thirst are two separate mechanisms, which means we can drink almost any amount of sugary drinks without deriving much satisfaction from them.