Why We Eat (Too Much)

  In the third house, when the wood shed got damaged the delivery man from the timber merchants helpfully cleared most of the logs and stacked them at the side of the house – out of view of the owner. The owner didn’t know this and, concerned that his supplies are running low, orders extra wood to be delivered. Unfortunately, most of his extra order is ending up stacked against the growing log-mountain out of view.

  The owners of the three houses have very different interpretations of the outside world, and three very different stores of wood. But note that there was no difference in the amount of wood that the first and second houses ordered. House one burned that wood, house two was more frugal and stored it for an icy day. The only house ordering excessive wood was the third one, and this was only because its owner thought that his wood shed was almost empty. He wasn’t aware of his massive stock of logs because they were out of view.

  It’s helpful to remember this analogy when thinking about obesity, the currently misunderstood disease affecting a quarter to a third of our population. Just substitute our hypothalamus (our weight-control centre in the brain) for the houses’ owners, food for the delivery of logs and fat for the store of wood. Switch the delivery man’s strike for a diet and the icy spell for Western food signals. Switch the three houses for people: the first house is a naturally slim person, the second house an overweight person and the third house is a person with leptin resistance (their log store is excessive, but invisible to the owner), causing fully fledged obesity.

  Our old-fashioned understanding of obesity is slowly being challenged. Many scientists are realizing that it is not the quantity of calories that are available in the food supply to a population that will affect obesity levels: natural foods do not make populations fat. No, it is the quality of the food available that causes obesity. If a grain-, oil- and sugar-based diet is fed to any kind of population, whether it be a herd of cows, mice living in a lab or a continent of humans, the same effect will occur: high levels of obesity.

  The traditional understanding of obesity as a lifestyle choice is of great value to many lucrative and powerful industries. The diet industry, the gym industry, the food industry and the pharmaceutical industry all have a vested interest in perpetuating this view. As we’ve explored, the food industry makes the processed foods that cause obesity. Without obesity, the gym and diet industries would not exist (they didn’t 100 years ago), and without obesity many of the highly profitable drugs that the pharma industry sell would not be needed.

  If the mainstream view of obesity was found to be flawed, people would soon realize that Western food products are slowly poisoning them. They would switch to natural foods – no calorie-counting required. But such a huge change is unlikely. It’s hard to imagine a tax on processed foods coming soon, one that would fund a public awareness campaign on healthy eating – rather than the half-baked calorie-counting campaign we see now.fn1 What is needed is a large-scale, professional media assault on the population’s psyche that encourages people to eat natural instead of processed foods, to cook and embrace food culture. This could work – this could be the solution – but not just yet …

  But instead of waiting for this change, you could try and change your own life, and your weight, by following the steps in this book: not guaranteed to result in a 10kg (22lb) weight loss in ten weeks, but maybe 20kg (over 3 stone) or even 30kg (4 stone and 10lb) … over two or three years? And certainly guaranteed to lead to improved long-term health and hopefully happiness. And, as an ultimate bonus, you will never have to buy another new miracle diet book ever again!

  APPENDIX 1

  The Cholesterol Debate

  In the Acknowledgements pages of this book, I could have added a statement: ‘This book would not have been possible without cholesterol.’ But the cholesterol debate is so fundamentally important that I decided to give it its own section, in order to clarify some scientific points for those readers who are interested.

  If the 1960s diet–heart hypothesis, which linked cholesterol with heart disease (see chapter 8), had not existed, if scientists had not convinced governments of their theory, and if the governments had not advised their people to ditch saturated fat – then I don’t think that we would have needed this book. The diet–heart hypothesis, which was supposed to halt the rise in heart disease, led to a chain of events culminating in another public health crisis – obesity.

  We have all been subjected to public health campaigns, and media articles, explaining how saturated fat leads to heart disease – they have been omnipresent for fifty years. Once a critical mass of people, thought to be 10–25 per cent of the population, become true believers in an idea, then the rest of the population will adopt it.1 This is what happened with the diet–heart hypothesis, and this is why our populations now have a fat phobia.

  Most people living in the West (including doctors) will visualize the link between cholesterol and heart disease this way: if you eat food containing saturated fats (like red meat), this will lead to high levels of cholesterol globules in the blood which can somehow clog the blood vessels and cause narrowing of the coronary arteries, and you will risk heart problems. This picture is absolutely ingrained into our society’s psyche. Such thinking is an integral part of everyday life and normal conversations about health. Now, when you see a fatty steak or sausages (lots of fatty offal), you tend to recall this picture – with the greasy fat in the food clogging your blood vessels. We are now very wary of steak, eggs, cheese and whole milk (unless we are French). As the cholesterol message continues to be reinforced (because the number of believers is now so high), red meat and all dairy products – natural foods that have made up a good proportion of our diet for thousands of years – are seen as bad for us.

  Our governments advised us that it would be better for our health if we switched to a diet with less saturated fat and replaced it with grains (plant seeds) and vegetable oil (plant seeds). Food companies also followed the government advice, but had to add more refined wheat and sugar to make the low-fat processed foods more palatable and therefore commercially viable. Our new diet, high in refined carbohydrates, meant that we needed to develop a snacking culture to help us cope with the blood sugar fluctuations between meals.

  These alterations to our diet – the addition of high levels of omega-6 from vegetable oils, and the elevated insulin from sugar and snacking – led to the metabolic changes in our cells (insulin and leptin resistance) that encourage weight gain (chapters 9 and 10). These changes would not have occurred without the diet–heart hypothesis and the demonization of saturated fats.

  The idea that saturated fat causes heart disease is now just as ingrained in us as the knowledge that smoking causes lung cancer. However, unlike the irrefutable science linking smoking and cancer, the diet–heart hypothesis was based on evidence that has subsequently been discredited. Ancel Keys’ original study, linking the saturated-fat intake of a population to their rates of heart disease, was biased by the selection of only the countries that fitted the hypothesis (for example, France and Germany, which consumed high levels of fat but didn’t have high rates of heart disease, were excluded).2 Confounding factors – such as the knowledge that sugar intake was also high in countries with high saturated-fat intake – were ignored. Most recently it has come to light that scientists were paid large sums of money by the sugar industry to deflect the dietary blame for heart disease away from sugar and onto fats.3 Accordingly the influential review published by these scientists shifted the emphasis of their findings for the diet–heart hypothesis to be accepted universally as fact.

  So the reliability of this hypothesis has started to be questioned. There is increasing evidence that saturated fats from fresh foods (like red meat and dairy products) are not strongly associated with heart disease.4 Unfortunately this message, from recent research, hasn’t yet got through to policy-makers. As we have learned in this book, top researchers and scientists, and influential doctors, have vested interests. If an important public health m
essage that they have been promoting for years is disproved, then their reputations will be discredited and the funding for their labs may dry up. This is the reason there is so much inertia about changing public health advice: too many people have their reputations and livelihoods tied up in the diet–heart hypothesis.

  Let’s look at up-to-date evidence to unpick the diet–heart hypothesis and see where we currently stand. Is it OK to eat saturated fat or not?

  When the diet–heart hypothesis was gaining traction, the only relevant blood test available was to measure total cholesterol levels. We now know that it is not the total amount of cholesterol in the blood that is important in calculating the risk of heart disease, but the vehicle that carries the cholesterol within the blood. Cholesterol is a fat and so cannot dissolve in blood (think of balsamic vinegar and olive oil – they don’t mix). When travelling in the blood, it needs to find its way inside water-friendly carriages. These carriages are called LDL and HDL (meaning low density lipoprotein and high density lipoprotein). The LDL can be either type A (small and tight particles) or type B (large and fluffy).

  The Morning Commute

  Think of cholesterol molecules, travelling in the blood, as being similar to people trying to get from home to work. Let’s imagine that for their daily commute they must choose a vehicle to travel in. Some people take a big, hollow red bus (driven safely, by a trained bus driver) and others take tightly packed mini-vans (driven recklessly by freelance drivers). Think of the risk of heart disease as being analogous to the risk of traffic accidents. Immediately you can see that if everyone travelled in safe red buses there would be very few accidents, but when more and more people take mini-vans the accident rate goes up. It is not particularly the number of people travelling that affects the number of traffic accidents, but the type of transport that they choose. The risk for heart disease works in the same way: it is not the total amount of cholesterol travelling in the blood that is important, but the type of transportation. If cholesterol takes more LDL type B transport (red buses), the risk of heart disease is not increased; but if cholesterol travels using LDL type A transport (reckless mini-vans) the risk of heart disease does increase. The total amount of cholesterol in the blood is only significant in people who have hereditary high cholesterol levels. This condition affects 1 in 500 people and leads to heart disease very early in life (in their thirties or forties). It was this hereditary condition that tricked researchers into thinking that cholesterol levels in everyone were an important factor in heart disease risk.

  I want to introduce our third vehicle now. Interspersed with the buses and mini-vans on our commuters’ roads are police patrol cars. As we know, as soon as a police car is around, even the most reckless driver will behave for a while. In our analogy, the police patrols represent the effect of HDL on our cardiac risk. The more police cars on the road, the less the chance of accidents occurring: the more HDL in the blood, the less the risk of heart disease. Police patrol car numbers are the most important variable affecting accident rate: when their numbers drop, accidents rise dramatically. In the same way, healthy HDL levels confer much more protection against heart disease than any other factor.

  The next question should be: what determines the type of transport that cholesterol uses? If the original diet–heart hypothesis was correct – that saturated fats cause heart disease – then we could conclude that increased consumption of these fats causes cholesterol to use LDL type A cholesterol (mini-vans) as their preferred mode of transport. But when the hypothesis was originally formulated, the type of vehicle that cholesterol travelled in was not known – only the total amount of blood cholesterol could be measured. We know from these early studies that a high dietary cholesterol intake does indeed increase total blood cholesterol slightly (the number of morning commuters in our analogy) and therefore that more cholesterol-carrying vehicles will be needed. But here is the catch – the higher-cholesterol traffic from saturated fat does not increase the ratio of LDL type A vehicles (mini-vans) compared to LDL type B vehicles (buses). The total number of LDL (buses and mini-vans combined) increases, but the proportion of good type B (buses) is increased and bad type A (mini-vans) is actually decreased. After eating saturated fat, the level of ‘good’ HDL cholesterol (police patrol cars) also increases, protecting against heart disease. This evidence would suggest that consuming saturated fats does not cause heart disease – and that the diet–heart hypothesis is wrong.

  What other factors could change the cholesterol traffic in our bloodstream? Let’s expand our analogy further. Let’s say commuters have to walk to a bus stop to catch a bus, but that the crowded mini-van will come to their doorstep. If there is a torrential rainstorm, commuters are less likely to risk being soaked and therefore mini-bus traffic increases, leading to more accidents. In dietary terms, the rainstorm is produced by a different type of fat to cholesterol – known as trans-fats. As we have learned (see chapter 8), trans-fats are present in many processed foods, including cakes, biscuits and processed meats, and are also produced when vegetable oils are heated to a high temperature. Some of the earlier studies linking saturated fats to heart disease failed to take into account the effect of trans-fats on cholesterol commuter traffic, reinforcing the belief that saturated fats were dangerous.5

  What about a snowstorm? Again, commuters will take the more convenient mini-vans rather than risk slipping over on the walk to the bus stop. The roads will be treacherous and again accidents will increase. For our cholesterol particles, the dietary equivalent to a snowstorm occurs when we take in – you guessed it – sugar.6

  How about if the sun comes out (if you are reading this in a sunny country, bear in mind that a sunny day is a rare event in the UK)? Commuters want to enjoy their walk to the bus stop and avoid those sweaty, crowded mini-vans. In addition, there are more police cars cruising the streets (as they are less likely to call in sick on a sunny day). The result? Safe travel and no accidents. We can reproduce these idyllic cholesterol travel conditions within our bloodstream by something that costs nothing – exercise.7

  So, to sum up, there are various dietary and lifestyle factors that influence the mode of transport that cholesterol takes and therefore affect the risk of heart disease. The most dangerous factors are sugar and the trans-fats in processed foods (snow and stormy conditions in our analogy). On the other hand, recent studies have suggested that saturated fats from natural foods are not a significant risk and, as we already know, exercise (our sunny day) is cardio-protective.

  Good Cop …

  Over the last ten years the growing acceptance that total cholesterol is not a dependable risk factor for heart disease has led to new additions to our everyday vocabulary: good cholesterol and bad cholesterol. ‘Good cholesterol’ is HDL (police patrol cars), while ‘bad cholesterol’ is still used to describe both types of LDL – type A and type B. This means that both our dangerous mini-vans and safe red buses are lumped together and described as bad. This has confounded the analysis of dietary risk, particularly of saturated fats, and muddied the research waters. It is almost as if some scientists are searching for vehicles through a thick fog. Why is this thick fog obscuring the truth about something so important to public health? Personally I am not sure, but suspect that vested interests of top scientific research institutions may play a part. We know that the direction of research is still, unfortunately, under the influence of the companies providing the funding for research labs. Scientists now must disclose their funding, but this still does not influence the direction of research that they take – it just makes it easier to find out whether there may be bias involved.

  The biggest selling class of drugs in the world are the statins. According to a recent Informational Medical Statistics (IMS) report, revenues from cholesterol-lowering medications, including statins, reached $35 billion in 2010. These drugs have been shown to reduce total cholesterol levels in the blood by blocking some of its production in the liver. As well as reducing total cholesterol levels, sta
tins also decrease the risk of heart problems in some patients. But many researchers now doubt that the effect of statins on heart disease is related to cholesterol: there is increasing evidence that they work to reduce inflammation in the cardiac blood vessels. If this is the case, then why does the American Heart Association (AHA), a body of experts that the rest of the world looks to for guidance, still support the diet–heart hypothesis and insist that LDL cholesterol (both types) is the most important marker of cardiac risk? And insist on a diet low in saturated fats? In fact, their recent guidelines have recommended lowering the threshold of blood cholesterol level appropriate for statin treatment,8 guidelines based on a meta-analysis (summary of all previous studies) that excluded the important body of research on LDL subtypes.9 It is as if this research does not exist and suggests a degree of bias. Many doctors around the world look to these guidelines in order to decide whether to prescribe statins, and if the diet–heart hypothesis remains valid then statins will remain bestsellers.

  A particular saturated fat that has raised concern is palmitic acid. A report by the World Health Organization10 has suggested that there is convincing evidence that the consumption of this type of fat can lead to heart disease. Palmitic acid is present in all types of meat and also in dairy products – but in small quantities. The pure form of palmitic acid is made by simply heating up palm oil to an extremely high temperature – this can be done on an open fire and it constitutes the main cooking oil that is used in African villages. Palm oil, when added to food, gives a nice texture and taste, and comes at a cheap price. As a result, large amounts are found in processed foods. It is, I believe, from these foods that the association of palmitic acid with heart disease arises – and not from the small quantities present in natural fats such as red meat, cheese and milk.