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  What if we alter the type of food available to the population from hunter-gatherer food through farming produce and on to industrialized foods (the Western diet).fn2 What happens to a population exposed to this type of food?

  Figure 2.2 Frequency of underweight, normal-weight and overweight people in farming communities

  Among the UK population, approximately a quarter of adults are now obese; in the US this figure has reached 30–35 per cent; in the Gulf States, among the adult female population we now have obesity rates approaching 50 per cent.5 On average, you could say that populations that are exposed to processed, or canteen-type, food are approximately one third normal weight, one third overweight and one third obese.

  Is the Risk the Same for Everyone?

  Does the change to processed food or a Western diet affect all people in the same way? Are we all at a higher risk of obesity or are some people more susceptible than others? Does the weight set-point of the whole population increase by the same amount or is there a difference in susceptibility between individuals?

  If we are all at the same risk of developing obesity in response to a Western diet, then you would expect everyone in the population to be affected in a similar way. For example, take the population of a village living at the foot of a mountain in Switzerland. If you measure the level of haemoglobin (the blood test for anaemia) in the population, most people (about 90 per cent) will have a haemoglobin level in the normal range of 12–16g/dl. About 5 per cent of people will be anaemic and 5 per cent will have too much haemoglobin, a condition called polycythaemia. Now imagine that the local council have decided to build a big tunnel through the mountain, but unfortunately the small village is in its path. They must relocate the whole village to living accommodation halfway up the mountain – at an altitude of 2,000 metres. After one year, they retest the haemoglobin level of the population and find that now only half of the population has a normal level and no one is anaemic. But half of the population has developed polycythaemia, the condition of too much haemoglobin (Hb). What has happened to the health of the population? Well, the much thinner air halfway up the mountain has caused the population to adapt by increasing the haemoglobin in the blood to compensate – haemoglobin carries oxygen from the lungs to our working organs, so if there is less air you need more Hb. But if you look at the distribution of the level of haemoglobin in the population, it looks the same as when they were living at sea level, it’s just shifted up for everyone. The environmental change to thinner air has affected everyone equally.

  In our population, if all were affected equally by the change in the food environment, then a similar scenario would occur to the Swiss villagers.

  Figure 2.3 shows clearly that the majority of the population would be in the overweight category, with occasional members being of normal weight and a similar small proportion obese. But this is not the case when we look at the current distribution of people’s sizes.6

  Figure 2.3 Change in population size if processed food affects everyone equally. Everyone’s weight would shift upwards equally

  Some Immune, Some Hypersensitive

  Some people, about one third, remain a normal weight and don’t seem to have been affected too much by the environmental change. Another third have gone from normal weight to overweight and have been moderately affected by the change. But that leaves a third of the population who have gone from normal weight to become severely overweight (obese) – all because of the environmental change.

  To make things simpler, we could separate anyone exposed to processed food as falling into one of three categories. These would be:

  Obesity-resistant – still normal weight and able to maintain this weight easily.

  Obesity-vulnerable – normal weight/overweight. Aware that if they consume too much processed food or don’t go to the gym regularly they will gain weight.

  Obesity highly sensitive – overweight/obese – struggle with weight even when trying to watch their calories and exercise.

  Figure 2.4 Actual change in weight of population after the switch to a Western diet. One third of the population is resistant to weight gain, one third is vulnerable to obesity and one third is highly sensitive to obesity

  Free Will, Poor Education or Unlucky Genes?

  The next question to ask when trying to understand obesity is which factors contribute to someone’s sensitivity (or resistance) to developing obesity? Or, to put it another way, what leads someone to develop a higher weight set-point?

  Is obesity a condition that is a person’s free choice, as has been implied by most of the media for years, and supported by many of the scientists (we will consider the reason for this later), or does it come about because of home environment and parenting? Can we blame obesity in children on poor parenting? Or does it run in families, is it genetic? When I lecture medical students on this topic I ask them to rank in order the most to the least important factors in determining whether someone will become obese.

  What would be your ranking of the most to least important factors determining someone’s risk of becoming obese?

  Free will/character

  Home environment/parental influence

  Hereditary predisposition/genetic

  If we were to ask the US population, we would get one overwhelming answer.7 A 2012 poll of over a thousand Americans showed that 61 per cent of them thought that personal choices about eating and exercise were responsible for the obesity epidemic. This is similar to the answers I receive from my medical students – that obesity is controllable by free will (as you would expect when they are only taught Metabology Rule 1) and therefore anyone who suffers from it must, by definition, be weak-willed.

  Identical Twins – Different Homes

  The answer is in fact very different. Jane Wardle was an epidemiologist at University College London and published an eloquent study looking at pairs of identical twins who had been separated at birth and adopted into different homes.8 She looked at over 2,000 pairs of twins and compared their BMIs (a measure of how obese a person is by considering their height and weight). Identical twins as we all know share identical DNA. They have the same eye colour, hair and complexion and are of almost identical heights.

  What would happen to a pair of identical twins if one was brought up in a home with an unhealthy food and play environment (lots of processed convenience foods and not much outdoor play) and the other was brought up in a healthy environment? If the answer to our question was that home environment played an important role in triggering whether someone was going to be resistant to, or sensitive to, developing obesity, then we would expect these twins to have very different weights when they became adults. If the answer was that obesity was mostly inherited, then they would have similar weight when they became adults, despite not growing up knowing each other. If it was free will that determined size, we would then expect that their respective weights as adults would be fairly random and would not correlate with genetics or home environment.

  The results may come as a surprise to many. The study found that there was around a 75 per cent consistency in the level of obesity (BMI) between identical twins when they became adults, despite their lifelong separation. She found that there was only a 10 per cent consistency in BMI as a result of the home environment.

  This study firmly established that the main factor determining whether an individual would be normal weight, overweight or obese was not free will or upbringing but something that could not be changed by the individual – their genes.

  Conclusive – Obesity Risk is Three Quarters Inherited

  For the most part this study also exonerated parents, who had previously been criticized for poor parenting (i.e. they had been blamed for their offspring becoming obese). Only a small, 10 per cent, influence of home environment on obesity levels was found. Therefore if a child becomes obese it is 75 per cent because of their genes and 10 per cent influenced by their parental upbringing and home environment.

  We should also highlight he
re the difference between the ‘home environment’ and the ‘country environment’. If a country has adopted a Western culture, this trumps a healthy-living home environment. If Western culture pervades the home environment, the study indicated that, if you have obese-sensitive genes, even a healthy home environment may not protect you. The results of Jane Wardle’s study of twins have been repeated and confirmed by many separate researchers around the world.9 They certainly fit in with what many of my patients have been telling me for years – ‘It’s in my genes, doctor.’ In this respect they are mostly right, but unfortunately this important research is still not widely known, or quoted.

  Group 3 Humans

  If we go back to our cow analogy, the largest and fattest cows were in Pen 3 and they were exposed to both canteen-type food and had a genetic predisposition to obesity (due to selective breeding). In humans who suffer with obesity we have now unpicked the two main factors involved in predetermining if they will struggle with their weight. These people would be in Group 3 Humans: a combination of the Westernized environment they live in (discussed in later chapters) and a genetic predisposition.

  The genetic predisposition of some humans to become obese does not originate from artificial or unnatural selection, as in our cow analogy, but probably from natural selection. But are all human populations, races and tribes the same, or are some more susceptible to becoming obese – in the context of a Western environment – than others?

  The Dubai Mall Food Court

  I regularly travel to the Gulf to hold clinics for my patients and when I walk around their massive, air-conditioned shopping malls I am struck by how much more prone to obesity the local population of Emiratis seem to be compared to other ethnic groups living there, despite them having equal exposure to Westernized foods. The food courts are dripping with tasty hedonic Western foods from Burger King to Taco Bell to Subway. The mix of people within the food court’s seating areas include Indian, Filipino, Caucasian, African and local Emirati. People from each individual ethnic group seem to be suffering with obesity, but the problem seems to be much more severe and more common in the local Emirati people. Is this backed up by research? A look at the current obesity league table confirms my observations: the Emiratis are near the top.

  The Pacific Islands – the island of Nauru is top with 94 per cent overweight and 71 per cent of those obese (so only 6 per cent normal weight!).

  The Gulf States (including Emiratis) – Qatar and Saudi Arabia are nearing 50 per cent obesity rates in female adults.

  United States – 36 per cent obesity rate in Louisiana, with other states close behind.

  Europe – 55 per cent overweight, 25 per cent obese.

  The Pacific Islanders have stunningly high rates of obesity. It is almost as if they have been perfectly selected to have obese-sensitive genes. How could this be?

  Brave Polynesians

  As I write this, I turn to the globe on my desk, kept there so that I can daydream about the world and what’s happening in it. Why are the Pacific Islanders suffering with such extreme obesity? The origins of the modern human are almost certainly to be found in East Africa, near to present-day Ethiopia. If I turn the globe around to the opposite side of the world to Ethiopia, we come … to the Pacific Islands.

  Humans migrated from Africa and over many thousands of years inhabited all areas of the planet. Generations of tribes explored the Middle East, travelled through Asia and on to China. It is thought that Pacific Islanders originate from people living in what is now Taiwan and the Philippines. These people mastered the sea and finally discovered the pristine Pacific Islands. But here is a clue as to why Pacific Islanders are the biggest people in the world. The Islands are one of the last places on Earth to be inhabited by humans, probably around 1000 BC.10 The distances involved in travelling by sea to these islands are phenomenal – thousands of miles. The Polynesian sailors would have followed the flight of migrating birds and used the stars to navigate. They probably gazed at the horizon for days and weeks on end looking for clues to nearby land – seabirds and turtles, twigs or coconut driftwood, or the distant build-up of cloud formations around an island. These journeys were the ancient equivalent of a moon landing, long and arduous and at the mercy of the unpredictable elements. Not surprisingly, many of the crew and passengers did not survive the journey, as described here in the collection edited by J. Terrell, Von Den Steinen’s Marquesan Myths: ‘The voyage was so long; food and water ran out. One hundred of the paddlers died; forty men remained. The voyagers finally reached Fitinui, then Aotona.’11

  You can imagine the hardship and risk involved for those people to safely reach the Pacific Islands. Quite often only those people who were ‘strong enough’ to withstand the starvation of a long trip survived to live in these islands. There was therefore automatically a huge selection bias for anyone settled there. Those people who had enough fat reserves before the journey, or those with metabolisms that could shut down in the face of starvation, had a much better chance of surviving the long journey. The sailors and passengers who did not have this insurance perished and did not have the opportunity to pass their genes on to the next generation.

  The massive selection bias of people with good fat reserves, or efficient metabolisms, surviving to colonize this distant part of the world is almost as extreme as the selective breeding of the cows in Pen 3 by farmers (see pages 35–6). In addition, once settled, these people were at the mercy of severe famines affecting their small isolated islands – migration to unaffected areas would have proved much more difficult than for those living in large continents. These famines again reselected for survival those people that had built up adequate fat reserves to keep them going.

  Hidden Obesity Genes

  The Pacific Islanders offer us a unique insight into how genetic selection can, in this case, favour survival of the fittest.12 But for most of the history of the islands, from the early settlers to colonization by Europeans, the population was not overweight, because they had always consumed fresh natural foods. They were well nourished and able to withstand minor food shortages quite well, but there wasn’t an obesity problem. It was not until the recent introduction of a Western-type diet into the islands that the time-bomb in the population’s genetic make-up was unleashed. The Pacific Islanders offer us a great example of Group 3 Humans – those exposed to high-calorie processed foods and genetically primed to gain weight.

  Reproductive Fitness and the Thrifty Gene

  The selection of genes that thrive and survive in times of famine and starvation was first described by the geneticist James Neel in 1962.13 The phenomenon became known as the thrifty gene hypothesis and it gives us an eloquent explanation for why some ethnic groups suffer with obesity more than others in the same environment.

  The thrifty gene hypothesis is based on the theory that people who have an efficient metabolism, or excess fat reserves, can survive periods of famine better than those without. The assumption is that during every famine a certain number of people die, thus thinning out the population, and that the next generation will therefore have hardier genes. The theory offers an explanation for the variations in obesity in different genetic groups, but the mechanism of developing the thrifty gene is actually different to that described by Neel. It seems quite a harsh assumption that swathes of the population were regularly wiped out by famine. There would have been frequent hardship and food shortages, but this stopped short of large numbers of deaths from starvation. A more likely scenario for the development of thrifty genes is that food shortages affected the fertility of the population. If you were a woman with thriftier genes, maybe storing more energy, or fat, than others, you would remain fertile for much longer during a food shortage. Those women without adequate energy reserves would become infertile or lose their baby during pregnancy. The thrifty gene is passed on to the next generation not by physical survival of famine but by the greater fertility of those with more efficient metabolisms in times of hardship. This is known as t
he reproductive fitness hypothesis.

  Don’t Cross the Border!

  A prime example of the reproductive fitness hypothesis is the Native American Pima tribe. It is thought that this tribe has, over the generations, developed an extreme thrifty gene profile for its population. This has come through many documented, and probably many more undocumented, periods of extreme hardship. A number of the Pima Americans still live in Mexico and lead a healthy, outdoor life, farming and fishing. They have not taken on a Western way of life. These Native Americans do not show any signs of suffering from obesity; despite possessing the thrifty gene they are not exposed to the environmental obesity trigger.

  Most of the Pima did not settle in Mexico and now live in the Gila River Indian Community in Arizona, USA. Despite the Pima having their own reservation, much of their traditional way of living has been eroded and replaced by the all-American lifestyle. Their thrifty genes, which would help them survive if America was plunged into a long famine, are unfortunately totally unsuitable for the plentiful, highly processed, hedonic food environment that they find themselves in. Because of the legacy of their past, their thrifty genes now make them the fattest and most unhealthy ethnic group in America. Going back to our cow analogy, they are another example of Group 3 Humans, both genetically selected and environmentally primed to have high weight set-points.