Why We Eat (Too Much) Page 7

  The Pima have obesity rates of 67 per cent, the second highest rate of obesity in an ethnic group in the world, only behind those from the island of Nauru in the Pacific.14 The rate of diabetes in the Pima is 50 per cent, eight times greater than the US average.

  The African Migration

  To test our thrifty gene theory further, let us look at another migration that caused terrible attrition rates among settlers in a new land. Enslaved people arriving in America from West Africa had to endure a harrowing transatlantic journey. Packed below deck and manacled in chains, they were treated as sub-human by their captors and were exposed to starvation, beatings, and disease due to poor sanitation. The average duration of a trip across the ‘middle passage’ of the Atlantic was two agonizing months. In this time, despite only the young and fit being selected to embark on the journey, 20 per cent of the slaves did not survive.fn3, 15

  Here we see another powerful natural selection operating, this time affecting the population of enslaved people arriving in America. The sea passage selected against those with genes that could not withstand famine and energy-sapping diseases such as dysentery. Just as we had seen with our Polynesian sailors, the sea passage favoured those metabolically strong enough or with enough fat stores to survive it.16 What happened to the population of African Americans, generations later, once they had become exposed to an all-American, Western-type diet? If our theory that obesity is predetermined by inherited genes holds up then they should be at more risk than other ethnic groups living in America (apart from the Pima) whose ancestors had not undergone such attrition. If obesity is not preordained by genetics, then the rates between groups should be similar – because all the ethnic groups in America are equally exposed to Western foods. Look at the statistics below:

  Current Obesity Rates in the USA by Ethnic Grouping17

  All Adults: 35 per cent

  Black: 48 per cent

  Latino: 43 per cent

  White: 33 per cent

  The obesity rate among black women living in America is a scary 57 per cent.

  A sad irony for African Americans is that they were enslaved to increase the agricultural workforce, with many working on sugar plantations. The increased availability of sugar as a commodity and its falling price was a by-product of these plantations. Now the new generation of African Americans, still holding the legacy of their metabolically efficient and strong ancestors – genetically primed with a thrifty gene – are again engaged in a fight, this time against obesity and diabetes, brought about by the legacy of the sugar trade.

  CASE STUDY – ATOMIC TESTING

  ‘Mr Freeman, please!’ my nurse shouted for the next patient to come through to the clinic.

  The room darkened for a moment and I looked up from my notes. Mr Freeman’s large frame and body had blanketed out the light coming through the door frame. He was the biggest man I had seen, 300kg (47 stone), BMI 90kg/m2. He was about forty years old, well dressed in elasticated blue corduroys and a home-knitted jumper, softly spoken and intelligent. As part of the consultation I asked him when he had become obese. He told me he had always been big, even as a young child. He had a voracious appetite. The curious part came when I asked him about his family history. ‘Who else suffers with obesity in the family?’ ‘No one,’ he replied. He came from a family who were all skinny or normal weight. ‘And you are not adopted?’ I asked. ‘No,’ he replied. This staggered me: how could he have reached this tremendous weight without there being a genetic link somewhere. Then he mentioned something as an aside. ‘My father worked on the atom bomb during testing.’ And we had the reason that he was so different from the rest of his family.

  We know that radiation causes increased levels of mutation within a gene. Farmers used to irradiate corn in order to encourage mutations that they wanted to nurture. In Mr Freeman’s case, his father had been exposed to radiation during the atomic testing and this had led to a genetic mutation in the DNA that he had passed on to his son: a mutation causing massive obesity.

  The Bedouin

  Let’s go back to the food court in that shopping mall in Dubai. I had observed that the local population, the Emiratis, had a more severe type of obesity problem than other ethnic groups in the mall who were eating the same types of food. We could consider that the explanation for this is the same as the reason that Pacific Islanders, the Pima tribe and African Americans suffer more than other groups with obesity. Maybe the ancestors of the Emiratis had also been exposed to famines that were so extreme that those with ‘fat genes’ had much more chance of surviving. Maybe they have more of the thrifty gene than other ethnic groups.

  I’m not so sure that this is the whole story for the Emiratis. Yes, we know that they originate from nomadic Bedouin tribes. They still proudly carry their legacy of the desert. The two black bands around the white headdress of the traditional male Emirati were used to secure their camels’ feet at night to stop them wandering away into the desert. We know life was harsh for their ancestors, but many other ethnic groups have been exposed to generations of hardship and struggle. For example, the ice age which covered northern Europe took hold rapidly and lasted for many generations, and yet the obesity rate for Caucasians of European descent who had endured this hardship is half that of the Gulf Arabs.

  Primed for an Oasis Not a Food Court

  An alternative theory is emerging as to why the Gulf Arabs suffer so severely with obesity.18 This theory is gaining acceptance and personally I think it is a more realistic explanation for their current health problems. It has been suggested that the pace of change in their environment is the primary cause for their difficulty in coping with it. Emiratis do not particularly harbour more obese genes than other groups, but their genes have been primed to survive in a harsh environment, without plentiful foods. The theory is based on a new area of scientific research called epigenetics.

  Previously we had assumed that the genes we inherited from our mother and father were set in stone. It was thought that they could not be altered. This perception is now changing and it has been proved that selected genes can be switched off (in medical terms this is called methylation because a methyl molecule covers the gene). The switching off of some genes takes place while we are still growing in the womb; we think that it happens in relation to what the growing baby senses in its environment. The whole process is thought to make the baby more adaptable to the environment that it is born into and therefore more likely to survive and thrive. On the whole this is beneficial to the infant as, in most cases, the environment the mother lives in while the baby is busy developing will be the same as the environment the baby is born into and grows up in. In most cases the anticipated future environment is correct, and the epigenetic moulding of offspring in order to optimize them for the future is usually a force for good. However, as with all predictions, they don’t always come true and this is the downside of epigenetics. When a baby is born into an environment quite different from that which was predicted, the baby will struggle to adapt and may develop health problems. I think this may be the case with the Emiratis of the Gulf.

  The Dutch Famine Study

  Let’s look at a famous example of epigenetics when the predicted future environment was wrong. ‘The Dutch famine, 1944–1945, and the reproductive process’ is a research paper that was published in 1975.19 It looked at the Dutch famine and how it affected offspring born to the mothers who had lived through it while they were pregnant.

  To put the famine into historical perspective, it occurred during a freezing winter towards the end of the Second World War, when the German army was retreating through Holland. During this period, the war was very dynamic with many attacks and counter-attacks; it was a critical win-or-lose time. Because of the nature of the fighting, large areas of Holland were isolated for many months. The harsh winter also froze the canals that would have been used to deliver food to remote areas, thus exacerbating the famine. Strict rationing of available food was introduced, with people allowed to c
onsume only 500kcal per day. The affected areas were relatively large and the famine lasted for six months. The population enduring the famine included young women who were pregnant.

  The study was conducted thirty years after the famine and the researchers identified children who had been born to women exposed to the famine. They then compared these offspring to their siblings born before or after the famine. They looked at these two groups and analysed their health as adults. Their findings were surprising. The offspring from starving mothers were, as expected, much smaller than normal when they were born, but once they had reached adulthood they turned out be significantly more obese than their siblings. The type of obesity that the offspring of starving mothers had developed was more dangerous than most – they were more likely to exhibit obesity with fat around the belly rather than on their thighs or buttocks. This type of obesity is seen in men more commonly and it is associated with a higher risk of diabetes and high blood pressure. Not surprisingly, the study also found a higher rate of Type 2 diabetes among the offspring of the starving mothers.

  Betting on a Hungry Future

  Why would this be? How can starvation in the womb lead to a baby having an increased risk of developing obesity and diabetes in their future lives? Let’s look at this from a different angle. What would be the advantage of a baby born to a starving mother having a more robust appetite and gaining weight more easily than normal – or maybe having a more efficient metabolism so that they don’t have to burn as much energy as others? The researchers proved that there was no advantage to these traits; in fact they led to a higher likelihood of disease. But what if the organism (the baby) was somehow being clever and could change the way it behaved without changing its DNA (as its DNA is already set)? Imagine it is behaving like a chameleon and changing in response to its environment. What if the starvation environment that the baby had sensed while in the womb was the same environment that he had experienced while growing up – a perpetual famine or food shortage? If this turned out to be the case, then these traits of increased appetite/food-seeking behaviour and a lower metabolism would confer a significant survival advantage to these offspring. This is a classic example of epigenetic priming of genes to predict a harsh future environment. However, in this case, the prediction was wrong: the future environment was not one of famine but of plentiful food. The bet was a losing one – instead of the epigenetic changes providing a health and survival advantage, their legacy was obesity and diabetes.

  Another terrible famine occurred during the Biafran War (the Nigerian Civil War), between 1967 and 1970. Researchers looked at over 1,300 babies born before, during and after the war. They had similar findings when they compared the health of the offspring born during the war forty years later. Babies born during the famine were more likely to suffer with central obesity, diabetes and high blood pressure.20

  The changes in the expression of obesity genes – those that occur in response to famine – are due to epigenetics. This new understanding of genetic adaptation offers fresh perspectives on the interaction between our bodies and our environment. It also poses new questions about evolutionary processes and who we really are.

  Can the epigenetic changes that have occurred in one generation of babies be passed on to the next generation? Can the priming of your grandmother’s genes when she was developing in the womb – in response to the environment of the time – be passed on to your mother and then on to you? While these questions are still being investigated, there is a suggestion that some epigenetic traits from previous generations do survive for up to four subsequent generations.21

  Darwin, Lamarck and the Giraffe

  When Charles Darwin published On the Origin of Species in 1859, the research it contained was ground-breaking, based on his exhaustive work examining and observing animal species and fossils. The subsequent discovery of the structure of DNA by Francis Crick and James Watson in the early 1950s confirmed the mechanisms of evolution, with natural selection and genetic mutation driving it. Darwin’s theory is now accepted as the ultimate explanation of our origins. However, recently something has been troubling researchers in this field. They have worked out how long it would take animals and humans to evolve using Darwin’s theory and the numbers don’t add up. There is not enough time for us to have evolved by simple natural selection or rare genetic mutations. This is where epigenetics may offer us a fascinating alternative theory of evolution that was discredited many years ago.

  We know from epigenetic studies that changes to genes, in response to the environment (let’s call them ‘epi-mutations’), occur 100,000 times more frequently than the simple, old-fashioned genetic mutations of Darwin. Can these epi-mutations affect and drive evolution? There is some evidence that, yes, the gene can be permanently altered by a process called genetic assimilation.22 If this was the case, then epigenetically driven inheritance would solve the problem of there being insufficient time for Darwin’s evolutionary processes to explain our pace of adaptation to the world around us.

  The field of epigenetics is new, only a few years old, but it is already challenging traditional theories about how we interact with our environment. Let us spare a thought for a scientist who suggested an epigenetic type of inheritance over 200 years ago.

  The Original Theory of Evolution

  Jean-Baptiste Lamarck was a French naturalist who proposed an evolutionary theory fifty years before Darwin. His idea was that animals evolved in direct response to their environment, and not, as Darwin later suggested, as a side effect to natural selection. His famous example was that giraffes had been able to evolve a long neck because their direct descendants had spent much of their life stretching their necks to eat leaves and fruit from tall trees.

  Because his was the first theory of evolution to be published, Lamarck faced the full onslaught of vicious criticism from the all-powerful Catholic Church for having the temerity to question creationism. His ideas were criticized and discredited by contemporary academics and he was ridiculed in later life when he should have been respected. Unlike Darwin, whom he pre-empted and who became one of the most famous scientists to have lived, Lamarck died in poverty and obscurity in 1829. His theory, like his reputation, is now being resurrected … by epigenetics.

  A new and developing way of understanding evolution is to accept both Darwin’s and Lamarck’s theories together. Neo-Darwinism and neo-Lamarckism can underpin our understanding of how we adapt to and evolve to suit our changing environment. With this in mind, let’s return to the Dubai food court to reconsider how this impacts on obesity.

  Epigenes and the Desert

  How can epigenetics explain the Emirati population’s problem with obesity? Did the Emiratis’ genes make the wrong bet on the future? Let’s look at how the environment in the Gulf has changed so rapidly.

  Oil was discovered in Abu Dhabi in the 1960s. At this time, the country was made up of several disparate nomadic tribes and pearl-fishing was the mainstay of the economy. By 1970 the UAE was producing 2 million barrels of oil per day (currently it produces 3 million). The founding rulers of both Abu Dhabi and Dubai decided to invest most of the proceeds from oil sales in infrastructure. Massive building projects including housing, hotels, schools, roads and hospitals were started. This ‘development’ of their traditional Bedouin way of life into a ‘Western’ lifestyle took only one generation. From enduring baking summers, living in tents, travelling by camel and eating traditional Arabic food, to living in cool air-conditioned apartments, driving Lexus cars and consuming tasty, hedonic, processed foods – all within thirty years.

  In America and Europe this transition from the traditional rural way of life to our modern city-based lifestyle took several generations, the changes for each generation being much more gradual in comparison. For Emiratis, the sudden change in their way of life may be what has left their epigenes unprepared. If your genes have been primed to survive in a harsh environment which changes abruptly within a generation to a modern urban one, you will
be metabolically unsuited to the environment you were born into. Emiratis probably harbour epigenetic changes that would help them survive the harsh desert environment and nomadic lifestyle, yet leave them metabolically unsuited to the food courts they now encounter. This is the reason that many of them fall into obesity. But what of the next generation?

  Eating for Two

  We have learned that if your mother was starving or undernourished while she was carrying you, then your genes will be turbocharged (by epigenetic changes) to give you a survival edge. If your environment does not turn out to be as predicted, then your hyper-efficient metabolism is going to give you big problems when you hit the food courts. As a result, your genes will preordain you to become obese.

  However, it is not just under-nutrition in the womb that causes genes to change and favour obesity in the Western environment. There is now compelling research showing that maternal over-nutrition when pregnant can lead to the development of what is referred to as obesogenic traits in their offspring (obesogenic is a relatively new word used to describe things that can cause obesity). Scientists have confirmed this apparent risk in mice. They found that when pregnant mice were over-fed with canteen-type food, their offspring exhibited increased appetite and aggressive food-seeking behaviour, and then became obese, in comparison to offspring of mice that were fed normally.23