The Diet Myth: The Real Science Behind What We Eat

by Tim Spector

Some people are overweight yet suffer few adverse metabolic consequences, while others are apparently lean with little fat under their skin but have fat around their inner organs, with disastrous consequences for their health. But scientists still don’t understand why this happens.

Some of the popular diets clearly work for many of us in the short term, especially the low-carb, high-protein ones, but longer term it seems to be a different story. The evidence suggests that even with record-breaking dieters, the weight often slowly piles back on.

Since the 1980s the experts have been consistently telling people that eating any amount of fatty foods is bad for us. This campaign has been very effective, and with the help of the food industry has managed to reduce the total amount of fat consumed in many countries. Despite this, rates of obesity and diabetes have increased even faster. We have since discovered that some of the most prolific consumers of fat in the world, the Cretans from southern Greece, are among the healthiest and longest-lived. In order to replace the fat content, the food industry has steadily increased sugar levels in processed foods. This has led to dire warnings of sugar being the arsenic of our times. Yet it turns out to be still more complicated. Cubans, despite eating on average twice the total amount of sugar as Americans, are poorer but far healthier.

(BMI is calculated as your weight in kilograms divided by your height squared in metres).

Our bodies simply seem to adapt to the new reduced calorie intake and do what they are programmed by evolution to do. It appears that the dull monotony of most exclusion diets is overridden by the body’s impulse to hold on to our fat stores. Once someone has been obese for a while, a whole series of biological changes transpire to maintain or increase their fat storage and the brain’s reward mechanisms for food.3 This is why most diets fail.

Yet our bodies contain 100 trillion of them, weighing over four pounds in our guts alone.

Microbes

microbe (by which we mean a living creature seen only by means of a microscope).

Microbes generally get a bad press, but less than a tiny fraction of the millions of species are harmful to us and most, in fact, are crucial to our health.

Until the mid-1990s it was the dogma that most bodily fluids were sterile – that is, contained no microbes. When a team in Madrid claimed to have cultured dozens of microbes from healthy breast milk they were laughed at.1 Now we know that human milk contains hundreds of species, although we still don’t have a clue how they get there. We are no longer sure that any part of our bodies is completely devoid of microbes – even the womb and the eyeball – and they may even travel around our bodies unnoticed.2 When you next go to the toilet, spare a thought for your trillions of microbes. Nearly half the mass you are flushing away are microbes.

Although we are all born microbe-free, this state lasts just a few milliseconds. The process of microbe colonisation is not at all random and has been planned and finely tuned over millions of years. In fact both the microbes and the baby depend on each other for their survival and health. This delicate co-evolution between microbes and man has not left purely to chance the crucial planting of the first microbial seeds in the virgin soil. All mammals, and many other animals studied such as frogs, transmit their own carefully selected microbes to their babies in a process that is at least fifty million years old. This is how evolution has facilitated the leap of microbes from one generation to the next, and how our own unique community of microbes, called our microbiome, is established.

Recent changes in our tiny gut microbes and to the community called our microbiome are likely to be responsible for much of our obesity epidemic, as well as its deadly consequences of diabetes, cancer and heart disease.

Examining the DNA of the microbes in our guts gives us a much better predictor of how fat someone is compared to looking at all of our 20,000 genes. This predictive ability is likely to keep improving as we start to look at viruses and fungi as well. Subtle differences between the types of microbes that we host in our guts explain many of the links between our diets and health, and why the results of food research are so inconsistent between people and populations.

The increasing promotion and use of restrictive diets that depend on just a few ingredients will inevitably lead to a further reduction in microbe diversity and eventually to ill health. Intermittent fasting (such as the Fast Diet or 5:2) may be the exception, as short-term fasting can stimulate friendly microbes, but this is only as long as the other, ‘free eating’, days contain a diverse diet. Fifteen thousand years ago our ancestors regularly ingested around 150 ingredients in a week. Most people nowadays consume fewer than twenty separate food items and many, if not most, of these are artificially refined. Most processed food products come depressingly from just four main ingredients: corn, soy, wheat or meat.

is useful to think of your microbial community as your own garden that you are responsible for. We need to make sure the soil (your intestines) that the plants (your microbes) grow in is healthy, containing plenty of nutrients; and to stop weeds or poisonous plants (toxic or disease microbes) taking over we need to cultivate the widest variety of different plants and seeds possible. I will give you a clue how we do this. Diversity is the key.

A calorie is a calorie – this is the central tautological dogma of traditional diet and nutritional advice. At a basic level this statement is correct. A calorie is defined as the amount of energy liberated when a standard unit of dried food is burnt off. The phrase means that regardless of the food type the calorie comes from (protein, fat or carbs), the energy needed to extract it and the energy produced will be identical. This has been the basis of calorie-counting for decades. It forms the basis of our food labels which many people use to make nutritional choices. But what if this lab-based approach has been misleading us into thinking we understand nutrition and diets?

Two thousand fast-food calories will have very different energy consequences from 2,000 calories made up of whole grains, fruits and vegetables.

For too long we have taken the accuracy of our food labels for granted, but the formulas behind them are over a hundred years old. They depend on burning the foods and applying calculations to account for different rates of digestion and absorption. The formulas disregard the effects of how old food is and also the different effects of cooking, which can dictate how much is absorbed as well as the speed glucose can rise in the blood. Also, people with longer large intestines can extract more calories from food than those with short ones, and some studies have shown differences of up to 50 centimetres between populations.

manufacturers are legally allowed error rates of up to 20 per cent on their product labels.

How the body produces energy from food varies enormously depending on the source of the food, how much you chew it, how easy it is to digest and what else you eat with it. One study even showed that eating white rice with chopsticks rather than a spoon significantly reduced the speed at which the blood glucose rose and triggered insulin (called its glycaemic index (GI)).4 Many experts believe that this GI score for food is crucial to regulate weight, although the few controlled clinical studies performed in humans have so far failed to show any difference in weight or heart risk factors when high- and low-GI diets are compared directly.

So a calorie may indeed be a calorie, but in the real world inside our intestines they are definitely not equal in the effects they have.

Consequently, over the last million years or so the genetic controls over the upper threshold of body fat have become more relaxed. While some people might by chance have kept these genes, in others the gene effect has weakened and the threshold has drifted upwards. This means that some of us will keep increasing our fat levels up to this raised variable threshold, and others – around a third of the population – will stay lean even if surrounded by food.13 This also makes sense as the genes for leanness overlap with those for increased physical activity.14

There does seem to be a higher threshold or upper limit for most people: most, once they reach a certain weight, and regardless of the extra quantities they then eat, cannot get much fatter.

Surveys of twenty-five countries carried out between 1999 and 2009 show that some (but not all) Western countries may be finally starting to hit this upper fat threshold: there appears to be a flattening of the obesity curves, particularly in children and adolescents.15 In the USA, where the epidemic started, the adult figures for obesity have for the first time started to flatten (but not drop).16 However, for obvious reasons this is not widely advertised – having only a third of the population staying clinically obese is hardly a success story. Paradoxically,

Even the experts and the nutritionists can agree that regular exercise improves your heart and muscles and increases your lifespan. They don’t yet agree on how much exercise you need, but the range is somewhere between 90 minutes and six hours per week of moderate activity, enough to work up a sweat. Others disagree with that, suggesting just a few minutes a day of flatout running or cycling in the form of a short sharp shock is enough to fool your body that it’s getting a good workout.22 The beneficial role of gentle walking is even less clear, but it’s probably still better than doing nothing.

They also show the enormous variation between individuals and how some people move about and fidget even at rest, which also expends energy. Some studies have suggested that a tendency to fidget is a useful protection against obesity. Some fidgeting genes have been found in mice which are also active in the human brain, resulting in some restless people expending up to 300 calories per day more than a restful person.

The reason why millions of us don’t lose weight exercising is that our bodies compensate. The body is programmed to stop us losing weight via fat and we have to expend five times more energy to get rid of fat than muscle.

If exercise alone does not lead to significant weight loss, when people have successfully lost weight in three to six months through diet, can exercise work to keep it off? The short answer is no. In a recent meta-analysis of seven studies exploring exercise alone or exercise plus diet versus diet alone, exercise failed dramatically to have any effect over placebo or control interventions. Nearly everyone regained weight, and without dietary restriction exercise had little influence.

The studies are pretty consistent: being fat yet fit is definitely better than being thin and unfit for heart disease and for overall mortality. The major risk factors for heart disease associated with being unfit – smoking and not eating vegetables – outweigh the risk of excess body fat.

My father was not fat and didn’t smoke but he was very unfit and had a fatal heart attack at the age of fifty-seven; so there is a lesson there, even though some people (like my father) will find it tougher than others to overcome their anti-sports genes. Exercise is overall a pretty good investment in time for most people – around 270 hours of annual exercise adds around three years to your lifespan and delays the onset of many diseases.

The bottom line, however, is that although exercise is not of much benefit for your weight or for burning fat (unless you are a professional athlete), it is good for you, your heart and your longevity. And since it also makes your microbes healthier and more diverse, it is a good thing.

For those of you who genetically or culturally can’t stand the thought of physical exercise there may be another way to burn calories – thinking hard. Our brain uses 20–25 per cent of our daily energy resources – which is more than any other animal.

The discovery of cooking and the ability to obtain calories easily are now seen as the major event that triggered our brain enlargement, leading to the emergence of modern humans and our subsequent dominance of the planet. Our large brains are greedy and consume about 300 calories a day, even when we aren’t using them much. This is roughly equivalent to the energy of a weak light-bulb, and we can’t turn it off – the energy we use up when we are asleep is nearly the same.

When lipids are joined to proteins they are called lipoproteins, and are much more useful and interesting than total cholesterol. They can now be measured accurately in the blood as high-density or low-density lipoproteins, called HDL and LDL respectively, and they transport cholesterol around. The low-density lipoproteins are the bad guys, allowing small drops of lipids to get caught in the blood vessel walls, which leads to a build-up of plaque and heart disease or stroke. If your liver produces a lot of HDL, the good guys, most of your lipids are transported safely to their target and disposed of without any collateral damage. When lipids are made up of short chains of fatty acids they are generally liquid (oils), and when in longer chains they are solid at room temperature (fats).

Increasingly, the ratio of two transporters of cholesterol around the body, HDL and LDL, is used as a marker of risk, although we cannot yet measure LDL directly. A much better marker of the amount of high-risk lipids in your system is another small cholesterol transporter protein called ApoB, which deposits cholesterol in the wrong places and opens channels in the vessels allowing the lipid to form the plaque that causes the damage. It is not, as previously believed, the total amount of circulating cholesterol that is important but where the cholesterol localises, and this varies widely. Most cardiologists use this more accurate blood test to assess risk, but it is more expensive to test and underused because of our obsession with total cholesterol.1

Fat is a key macronutrient in our diet and comes in many forms. Total fat is often the first thing you read on a food label, but it is pretty unhelpful as it could be either very good or very bad for you, depending on the type. Most foods contain a mixture of many different types of fats: the commonest are saturated fats, monounsaturated fats, polyunsaturated fats and trans fats. Within each of these categories there are many subtypes – for example, there are at least twenty-four types of saturated fat, usually lumped together on the label. Scientists have long thought we knew which combination of fats was good and which was bad for us, but the fact is that we don’t really.

There is still a lack of good evidence for or against coconut oil’s effects on health, notwithstanding its increasing hype and commercial promotion. This is mainly because it is unclear whether this particular type of saturated fat, medium-chain triglycerides, is beneficial or harmful. Many of the promotional web-sites claim there is a wealth of research on coconut, but most that I found were unscientific and some were plainly bogus. Some celebrity chefs now promote the health properties of coconut oil over olive oil, which is a worrying trend and totally lacking in evidence.

Trans fats (also called hydrogenated fats) are the worst kind, and as they are totally artificial come only from processed or fried foods.

Eggs are packed with cholesterol, and many people stopped eating them decades ago because of erroneous advice to avoid cholesterol at any cost. Cholesterol is a complex lipid that is part of virtually every cell in our bodies: 80 per cent of it is synthesised naturally inside us and only around 20 per cent is eaten as food. As well as providing the protective and nourishing lining to the walls of our cells, cholesterol is a key ingredient of many vitamins and important hormones. It is only thanks to the unfortunate combination of there being an easy blood test for it and a rotten PR campaign that cholesterol has acquired such an ill-deserved reputation.

Unpasteurised hard cheese, when given with antibiotics, has been found to speed up recovery times and reduce bacterial resistance compared to sterile industrial cheeses. It was postulated that the cheese microbes may be helping maintain the greater diversity of microbes in our guts.

The cheese group didn’t increase blood lipid levels or cholesterol at all, whereas the butter group did, showing that not all saturated fat is the same.

Far from being a risk for heart disease, full-fat cheese (but not butter), despite the saturated-fat content, now shows not only no harmful effects but a consistent protective effect on heart disease and mortality.10 So although we can’t depend on the reliability of these observational epidemiological studies, which have misled us in the past, we now have a reasonable hypothesis that the regular eating of traditional cheeses could actually prevent some heart and other health problems, owing to the extra microbes. Highly processed cheese or boiled or grilled cheese contains few viable microbes and doesn’t have the same benefits. Other products like milk and fermented products containing microbes may also offer some advantages, as we shall see.

Mosquitoes in particular seem very sensitive, and different species will avoid some bacterial odours and make a beeline for others, explaining why some people appear immune to insect bites.

Traditional Greek yoghurt also contains the most saturated fat, often 14 grams per pot, and it also has plenty of vitamin B12, folic acid and calcium. Basically, the more traditional and natural the mix, the more the amount of saturated fat. The popular low- or zero-fat yoghurts obviously contain the least, but these use either artificial sweeteners or several spoonfuls of sugar or its equivalent in concentrated sweet fruit to compensate for the lack of flavour, and usually contain fewer vitamins and nutrients.

sugar stops bacteria growing.

The overall conclusion here is that for most of us saturated fat is not the villain to be avoided at all costs. The saturated fat many people eat in products like cheese and yoghurt is not, as we have so often been told, unhealthy, but likely to be beneficial. This is provided the food is ‘real’ and contains living microbes, and is not over-processed or full of other unwanted chemicals and sweeteners.

These sprinting chickens contain less total fat and the lowest proportion of saturated fat – two-thirds of their fat is unsaturated – compared to a roughly equal proportion of unsaturated and saturated fats in beef, pork and lamb.

fact, there is no good data to show that cooking with olive oil is actually harmful or has different properties for health than when consumed cold.

Olive oil comes in three main types: expensive high-quality extra virgin olive oil, which has less than 0.8 per cent acidity, indicating its freshness and quality, plus a strong, sometimes slightly bitter taste. This comes from the rapid first pressing of the olive – which is performed at cold temperatures and marketed as ‘cold-pressed’. Virgin olive oil is a grade lower, possessing higher acidity and still some taste; then finally there’s regular olive oil. This last is made industrially by refining the leftovers and is cheap and normally tasteless, but may be given some flavour by mixing with a small amount of extra virgin oil. We now know there are huge differences between the health properties of the types, and most of the Italian and Greek oil produced now is extra virgin. Good-quality extra virgin olive oil contains the greatest amounts of the chemicals known as polyphenols, which have special properties and probably account for much of its health benefits.

The low-grade oils used in spreads and processed foods probably have no ...

The Mediterranean diet has many current variants but for this discussion I refer to it as the traditional dietary pattern found in the olive-growing areas of Greece and southern Italy in the late 1950s and early 1960s. The main characteristics of this diet are a high consumption of whole grains, legumes, other vegetables, nuts and fruits; a relatively high fat consumption (up to 40 per cent of total energy intake), mostly from mono-unsaturated fatty acids (MUFA, providing up to 20 per cent of energy) mainly from olive oil; moderate to high fish consumption; poultry and dairy products (usually as yoghurt or cheese) consumed in moderate amounts; low consumption of red meats, processed meats and other meat products; and moderate alcohol intake, usually in the form of red wine with meals.