Eat less and exercise more and you will burn off calories and lose weight. I, like most doctors, used to say this regularly to my patients. Experts tell us that the reason we have increased our weight so dramatically in recent years is that we have become more sedentary and are consuming more food. Put another way, people become fat because they eat more calories than they expend. On the face of it, this reasoning seems hard to contest.
Fixating on the basic laws of thermodynamics – energy in must equal energy out – has distracted us from the questions of how and why. We don’t say that someone becomes alcoholic simply because they drink more alcohol than they can metabolise. We are obviously interested in the reasons some people but not others become alcoholic in the first place. Yet we are happy to say that obese people are fat simply because they eat more calories than they use up, without asking why.
The misleading medical calorie dogma
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?
One real-life study exposed some of these fallacies. Forty-two monkeys were fed two different diets with identical calories for six years in controlled conditions. The ingredients were identical except for the fat content: one group had 17 per cent of total calories based on natural vegetable oils; the other had 17 per cent based on artificial and unhealthy trans fats. The diets were designed to keep weight constant, but the trans-fat group gained weight and scored three times the harmful visceral (belly) fat and much worse insulin profiles (meaning that glucose in the blood is not disposed of quickly) compared to the other group.1 This suggests that all calories are not the same. 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.
These formulas are just based on estimated ‘averages’ in a non-average world. Errors have been found that overestimate calories for foods such as almonds by over 30 per cent, and manufacturers are legally allowed error rates of up to 20 per cent on their product labels.2 Many common items, such as processed frozen foods, underestimate calories by up to 70 per cent, and high-fibre products by 30 per cent; and while health claims are scrutinised by regulators, in most countries there is astonishingly little oversight of the accuracy of nutritional labels.
To add to these errors, there is even more uncertainty around the average numbers of calories men and women need each day to replace energy lost. Recent recalculations have increased the gold-standard averages to 2,100 per day for women and 2,600 for men. Many people believe that this is too much – for a start, the guideline figures obviously fail to account for age, height, weight or amounts of activity.
Clearly, the use of calorie counting in diets depends not only on the accuracy of the system, but also on people’s ability to estimate correctly the number of calories in their food. Studies consistently show that only about 1 in 7 people comes close to estimating the number they need. The idea that the source of calories is unimportant can also lead to major imbalances in protein, carbohydrate and fat intakes, noticeably high or low levels of which can have serious health consequences. In America, restaurants and cinemas are now required to provide calorie counts on their menus. The evidence that they will help customers is unclear, although it may force manufacturers to reduce the number of calories in new products.3
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.5 But response to calories also depends on your own physical and genetic make-up and, last but not least, on the microbes in your gut. None of these factors are considered when food is reduced to calories on a food label. 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.
The fatted calf and the 3,600-calorie diet
Jerome was one of twenty-four student volunteers in Quebec who took part in a unique research study in 1988. It was a dream summer job: nearly unlimited free food and accommodation for three months – he would also be paid, and all in the name of science. He had passed the qualifying test, showing he had no family history of obesity or diabetes, and he was of normal height and weight. He, like the other volunteers, was a typical healthy but slightly lazy student who did no regular sport. Once he had signed his consent forms and waivers he found himself prisoner in a specially rented campus dormitory sealed off from the outside world, where for the next 120 days he was to eat, sleep, play video games, read and watch TV. There was twenty-four-hour supervision, and no sport, alcohol or smoking was allowed during the study except for a thirty-minute walk outdoors every day.
Jerome’s first two weeks involved daily weigh-ins, food questionnaires and immersion in a water tank to calculate his body fat. He was similar to the other subjects who were all on the skinny side, weighing only 60 kg (132 lb), with a normal healthy body mass index of 20. He was taken to a dining room where for each meal there was a buffet and a choice of foods. Every bit of food on the plate that he ate was carefully weighed. His baseline intake was calculated over two weeks and found to be 2,600 calories on average. After the run-in period he and the other volunteers were then overfed with an additional 1,000 calories a day for 100 days, under strict conditions so that they couldn’t cheat and pass food to each other. They were given a regular diet of 50 per cent carbs, 35 per cent fats and 15 per cent protein. Jerome was measured and scanned at the beginning and end of the study.
After the hundred days on this 3,600-calorie diet and virtually no activity, his weight had increased by 5.5 kg (13 lb). When the researchers looked at all the students’ results they were surprised to see such a wide range of weight gain. Jerome was the second-lowest weight gainer – some of his colleagues had gained an impressive 13 kg (29 lb) in the same time. The only student that had gained virtually the same weight as him over the three months was Vincent, who happened to have been born in the same town, went to the same school and shared all his genes. In fact, he was his identical twin brother. Dr Claude Bouchard, a professor at Laval University, Quebec, and his colleagues had cleverly selected twelve pairs of volunteer twins. They all gained weight to very different extents, but in each case their weight gain was very similar to their twin’s.6 Although all the twins gained total weight and fat mass, some details varied too. Some pairs converted the calories not just into fat, but into additional muscle. They also seemed to gain the fat in the same places as their twin, around the belly or more unhealthily around the intestines and liver – what is called visceral fat.
This classic study, in which the students were overfed like lab rats, might now have trouble getting ethical approval (though we don’t protect actors like Bradley Cooper who gained 40 lb for the film American Sniper and was paid millions of dollars for his role in it). The twins study unequivocally shows that much of how quickly we use energy or store fat and so gain weight is clearly down to our genes. My studies of thousands of twins in the UK and other studies around the world have consistently shown that identical twins – who, as mentioned earlier, are genetic clones – are much more similar to each other in body weight and fat than are fraternal twins, who share only half the same genes. This again shows the importance of genetic factors, which can explain around 70 per cent of the differences between people. Furthermore, we found these similarities extend to other, related, characteristics such as how much muscle or fat you have, and where the fat is stored on the body.7 No one knows what sends signals to our fat cells to expand typically around our stomachs and buttocks, and why we don’t, for instance, have chubby elbows.
Individual habits to do with eating (for instance, whether you are a grazer or a gorger) are not just picked up by watching your family or friends eat well or badly: they also have genetic components. This includes a like or dislike of certain foods, such as salads, savoury snacks, spices and garlic. How often you take regular exercise was also shown by our twin consortium to have a strong genetic component right across the world.8 A combination of novel experimental and cross-national twins studies have shown that people with genes for obesity also have genes that make them less likely to exercise than naturally skinny people, thereby highlighting some of the extra pressures obese people are under when they try to slim. Their genes and bodies conspire against them when they try to burn off calories.
Thrifty genes
For a long time, the best theory to explain why we were rapidly getting fatter was the ‘thrifty gene’ hypothesis of the 1960s.9 The idea was that in the last thirty thousand years or so (that is, in our recent past, since our ancestors left Africa) we survived a number of major events that dramatically reduced populations through illness or starvation, such as mini ice ages or enforced long trips to find food. An example is the Pacific Islanders, who sailed thousands of miles across the ocean to find both food and more hospitable lands. En route many would have perished. The theory goes that those who could best build up their reserves beforehand and then retain their fat on the voyage were more likely to survive (sometimes by eating the skinny ones). That fat protects against starvation is well documented.10 So when the diminished population eventually arrived on their paradise islands, the skinny ones had been weeded out and subsequent generations were highly selected for fat-retaining genes.
This appeared to make sense, because some of the most obese humans on the planet come from the islands of Nauru, Tonga and Samoa, who became fat only recently when their environment changed and they were exposed to an abundance of easy food and little incentive to exercise. The high death rates of transported African slaves en route to the US offer us another example often used to explain the higher risk of obesity in African-Americans today. Any differences in obesity between countries could then be explained by their stage of development from food scarcity to food abundance. So the theory proposes, in fact, that we are all descended from just a few families who supposedly survived famines or climate changes. Many of us have therefore inherited variations of genes that at some point in the past were a great advantage, but now are definitely not.
There are major flaws in this theory, however. First, it assumes that for most of their lives our ancestors had only just enough food to survive and would rapidly gain weight if faced with a surfeit. But the idea that they were always running out of food and rarely had any excess is probably incorrect. Studies of current and past hunter-gatherers suggest that most of our ancestors generally took in plenty of calories. This makes sense, as humans have also lived in travelling groups of fifty to two hundred who varied widely in size, age and food needs. This meant that if most of the time they had sufficient food to feed the biggest and most needy, the rest must have had food in excess.
The thrifty theory also assumes that protection from starvation was the main explanation for these genes being selected by evolution. But it is more likely that deaths from childhood infections and diarrhoea, as in the developing world today, rather than famine, were the major evolutionary drivers. Increasing body fat whether in children or in adults is not a strong protection against infections.
The other myth is that all our ancestors ran around all the time looking for food, like hyped-up ultra-marathon runners. Although it’s likely that some were keen runners, the same studies of hunter-gatherers suggest they would have been resting or sleeping much of the day and didn’t consume many more calories overall than we do now. Other studies have shown that wild animals brought into captivity and faced with abundant food don’t suddenly become obese. Finally, every population group studied has skinny exceptions to the rule. Even where the ‘normal’ state now is to be obese and diabetic (like the Pacific Islanders or the Gulf States’ populations), there is always at least a third of the population that manages to stay lean, despite being surrounded by an abundance of cheap calorific food or lazy compatriots. Such increasingly rare slim individuals may become the best groups to study.
Drifty genes
These holes in the ‘thrifty gene’ theory led a British biologist, John Speakman, to propose a rival model of obesity, not as well known, called the ‘drifty gene’ hypothesis.11 The idea is that until two million years ago our genes and our mechanisms for retaining body fat were more tightly controlled, and that we would have had a major survival problem if we had been too chubby. Old skeletons of our ancestor the Australopithecus show many signs of having been regularly eaten by hungry predators. Some of these species, such as Dinofelis, a variety of not-so-cuddly 120-kilo sabre-tooth tiger, even specialised in hunting early humans. Being fat meant not only that you couldn’t run as fast and so would be easier prey, but that you would taste better than a stringy marathon runner. These are two very good reasons why those obesity genes in our distant past would be selected against, and our upper fat limit controlled.
Becoming too thin, however, was of course always a disadvantage. Although food was generally plentiful, everyone needed fat reserves for emergencies in the days before fridges and freezers. So at both ends of the thin–fat spectrum our genes masterminded mechanisms to push us back towards the middle road. As we evolved into Homo sapiens with our bigger brains, hunting and weapons skills, we lost our fear of predators but still had occasional threats of famine and changes in climate to contend with. This maintained our tight genetic controls for minimal levels of fat, particularly in the useful storage areas. Many women, in particular, know personally how tough it is to shift those last bits of fat from their bottoms or thighs, despite dieting and months in the gym.
Gradually, though, as our natural predators disappeared so did our need to run away quickly. 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.12 This also makes sense as the genes for leanness overlap with those for increased physical activity.13
Another popular misconception is that in recent decades thin people have become fat. Studies of obesity trends have confirmed that in the last thirty years of global obesity epidemics most lean people have stayed lean; it is the slightly chubby that become obese and the obese that become very obese. 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.14 In the USA, where the epidemic started, the adult figures for obesity have for the first time started to flatten (but not drop).15 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, Americans may be relatively genetically protected compared to Asian populations. Judging by the speed with which they are catching up, and their tendency to lay down visceral belly fat, Asian populations may have even higher upper thresholds, and could keep growing outwards for even longer.
Good taste and supertasters
The ability to taste has been called our nutritional gatekeeper. People who completely lose their sense of taste don’t get fat. We all have up to ten thousand taste buds on our tongues for five main tastes: sweet, bitter, sour, salty, umami (a savoury taste related to monosodium glutamate (MSG)). We may even have a sixth one called kokumi, meaning heartiness. Contrary to the myth, our taste buds are not separated and we can taste the different tastes across the tongue. The buds regenerate every ten days and are controlled by genes influencing their relative sensitivity. The differences in our genes produce the variations in how sensitive we are to certain foods and how much we like bitter or sweet tastes.
Taste genes probably evolved so that as we travelled and encountered an increasing number of plants we would be better at detecting edible ones containing nutrients, while avoiding those that were toxic. The considerable variations in sensitivity may perhaps have evolved so that whole tribes would not be wiped out by eating the same poisonous fruit. In 1931 a Dupont chemist found out by chance in his lab that 30 per cent of people cannot taste a substance called PROP that 50 per cent of people find bitter and 20 per cent intensely unpleasant. Here was clear proof that our taste experiences are unique.
We probably have hundreds of different taste genes, and more variants are being discovered every year. Most of those found so far belong to two gene families (called TAS1R and TAS2R). There are at least three gene variations for sweet-taste detection (for fruit), over five for umami (as a marker of protein), and at least forty for bitter tastes (toxins). Which gene variants we have influences not only our appreciation or dislike of foods but also our fat, vegetable and sugar intakes. The bitter and sweet receptors are also present in our noses and throats and unexpectedly play a role in signalling to our immune systems when to expect a microbial infection. These taste receptors malfunction when you get abnormal continuous infections, such as sinusitis, that overload the system.16
When it comes to bitter tastes, a small proportion of the population are so-called supertasters. This means they have odd variants of one of the TAS2R genes and they react strongly to the chemical PROP in tiny dilutions. These individuals are very sensitive to strong flavours and tend to be much pickier with their food. The taste genes make supertasters sensitive to subtle differences in many nutritious vegetables, like those of the brassica group that includes cabbage and broccoli, as well as green tea, garlic, chillies and soya. As a result they tend to avoid some of these vegetables, often dislike drinking beer and other alcohol, and find cigarettes too bitter. With their discerning palates, although they miss out on some good foods they are usually healthier and less likely to be fat.17
As food types vary in their calorific content, food preferences in omnivores with plenty of choice can play an important part in determining their energy and weight. In 2007 we performed a twins study combining UK and Finnish twins to explore why some people prefer sugary foods to others. We found that nearly 50 per cent of the differences between people who had a sweet tooth and those who didn’t were due to their genes, and the rest was down to culture and environment.18
Gene variants for greater sweetness sensitivity (TAS1R) are much more common in Europeans than in Africans or Asians, suggesting that Northern Europeans evolved these genes to help them detect new food sources as they moved away from the safety of the equator. The ability to tell by taste whether a new root vegetable was edible and nutritious had clear survival advantages when faced with inconveniences such as an ice age. Unfortunately these same genes do not help us to survive in the aisles of a modern supermarket. Most studies suggest there is only a weak association between having these sweet-tooth genes and increased body fat.19 It used to be thought that you were either a sweet or a savoury person. In children at least, this idea has been dispelled by a recent study showing that the liking for salt and the liking for sweetness go together – and as kids prefer both sugar and salt at higher levels than do adults, they are particularly vulnerable to being exposed early to the modern processed food diet.20
Exercise and willpower
Are we really doing less exercise? We have talked about calories that are simply units of energy produced when foods are burnt as fuel, and calories that are eaten but not burnt off as body fuel are stored as fat. But what is the role of exercise in expending calories? If you are trying to get fit and healthy, exercise works – you don’t need a fancy meta-analysis to prove that. 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 flat-out running or cycling in the form of a short sharp shock is enough to fool your body that it’s getting a good workout.21 The beneficial role of gentle walking is even less clear, but it’s probably still better than doing nothing.
Exercise is not, however, merely a question of willpower. A few years ago we combined the major twin cohorts of Europe and Australia and looked at the exercise habits of nearly 40,000 twin adults. After the age of twenty-one when the influence of parents and family starts to wear off, a liking for participation in leisure exercise several times a week, in every country, was around 70 per cent heritable – that is, highly genetic.22 This shows that exercise is much easier for some people than for others; their bodies and minds find the process more pleasurable than do those others who may feel nauseous even when just watching sports on TV. Clearly, people and their bodies can change, but the starting positions may be very different.
As with recalling meals and diets, smoking and drinking, we have unreliable memories where our exercise habits are concerned, and we tend to exaggerate. One way round this is to use activity monitors, new instruments that correlate your heart rate with movement detected by sensors. These monitors calculate daily activity very accurately and reveal how many of us overestimate it. 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.
We tested our twins with an acti-heart activity device. They wore this trendy type of wristwatch for a week as it recorded their pulse and their activity. The results proved what we already knew – that there is a clear 70 per cent genetic component in self-reported sports. But, more surprisingly, the genetic component of actual energy expenditure was below 50 per cent for most measures, and around 30 per cent for the act of ‘sitting around’. This means that environment is slightly more important than genes in your real energy expenditure.23
Some studies, rather than focusing on exercise, have looked at sitting on your bottom as a risk factor. Regardless of how much exercise you do (or claim to do), the hours you spend watching TV or sitting in a car are independently a risk factor for heart disease and mortality. Large observational studies in the UK and the US have shown that for every two hours of TV viewing per day your risk of heart disease and diabetes increases by 20 per cent, even after accounting for other risk factors.
My father didn’t watch much TV but he spent his life avoiding exercise. He was brought up at a time when many people thought that exercise was bad for you. He was naturally very skinny and my grandmother made huge efforts to build him up. He would jokingly say to us as kids, ‘I used to be a nine-stone weakling, now in middle age I’m a twelve-stone weakling!’ He loathed parents’ school sports days and usually found an excuse not to participate. He couldn’t run as he had flat feet, couldn’t skate, ski or ride a bike as he had no balance, and couldn’t swim as he had heavy bones. He claimed to be descended from a long line of Jewish non-sportsmen and women.
We tend to forget just how recent is the latest craze for fitness and sports. In the 1980s joggers in strange pyjama-like outfits were seen as weirdos and treated with derision. The New York marathon began in 1970 with 137 runners and the London marathon started modestly in 1981 – to date, over 850,000 joggers have crossed the finish line. In the early twenty-first century the number of adults who do some kind of gym or sporting activity is large and growing. In 2014, 13 per cent of adults in the UK were members of a gym or exercise facility and many more trained outdoors in parks or took part in team sports. And more than a third of British over-fifties do some regular gardening.
The UK gym business is worth nearly £3 billion a year and the US has over fifty-one million gym members, the business having grown nearly twentyfold since the 1970s; and there is a similar picture in most countries. But if we are actually exercising more, shouldn’t we be getting thinner, not fatter? – unless most of us just go to the gym to watch TV, sit about in the jacuzzi and drink smoothies – a good way to get fatter without guilt?
Can it be true, as we are often told, that despite all this leisure activity we really are much more sedentary than we were thirty or forty years ago? Our jobs may have become less manual thanks to labour-saving devices, but our leisure time is more likely to incorporate exercise. However, if work-related exercise used to be important in preventing obesity, why are manual workers, who expend more calories in their jobs, consistently more obese than office workers? Part of the problem is that accurate calorie-expenditure data is hard to collect and compare over the decades, leaving us with very few hard facts to rely on.
One long-term study of housewives living in Minnesota has shown that life has got easier for many of them. They observed major shifts in the amount of energy they expended daily on household chores as compared to sedentary behaviour such as watching TV. Compared to 1965, fifty years later they now apparently expend 200 calories fewer per day.24 However, more detailed and representative survey data collected from the Netherlands between 1981 and 2004 shows that while over time body fat has increased significantly, leisure exercise levels, which might have been expected to have diminished, have actually slightly increased.25 Another review of several studies in the US and Europe since the 1980s found that, in contrast to popular perception, there was no overall difference in total daily energy expenditure including working time, and physical activity has not declined.26
Exercise and other physical activity are consistently linked with the strength of bones and muscles, which in turn has been associated with changes in the rates of osteoporotic fractures – especially hip fractures, which affect one in three women. In the 1980s a couple of colleagues and I examined the changing rates of hip fracture in the US and the UK over forty years for which we had accurate data. What we saw was that, adjusting for age and demographic changes, US fracture rates increased dramatically until the mid-1960s, then tailed off. In the UK they also increased after 1950, then plateaued in the 1980s; and according to my colleagues doing further analysis they have not increased further since.27 The results were a surprise to us then, but they now fit with the evidence that, contrary to the received wisdom, our overall level of exercise hasn’t changed much since the 1970s in the US or since the 1980s in the UK.
Does exercise really help you lose weight?
The standard advice from dieticians and gym instructors is that if you burn off around an extra 3,500 calories through exercising you will burn off a pound of fat. The ‘go for the burn’ motto certainly helps motivate gym junkies. But the energy expenditure of most people’s weekly sweaty gym-class workout equates only, sadly, to the reward of a large doughnut afterwards.
To compensate for the hours on end I have spent sitting unhealthily on my bottom writing this book, I have also been trying to train for a triathlon. I thought this would mean expending some serious calories. While on sabbatical in Barcelona I enjoyed the luxury of being able to swim around a mile in the sea every day and cycle forty to sixty miles in the surrounding hills at weekends. I walked for about thirty minutes a day and ran occasionally (in between some annoying injuries). I estimated with the help of my GPS sports watch that I was expending an extra 3,500 calories per week on average, and I wasn’t aware of eating more than usual. In ten weeks I lost barely 1 kg (about 2 lb), far from the impressive 10 lb I should have lost if the mythical fat-calorie formula were correct – which it clearly is not.28
My experience, though anecdotal and unreliable, is not unique. In one study, 12,000 regular runners who subscribed to the US Runner’s World magazine were followed over many years and the number of miles they ran per week was tracked to their weight each year. Although there was found to be a correlation between distance running and leanness, nearly everyone – however far they ran – still slowly got fatter each year. The authors suggested that if you added an extra four to six kilometres a week to your run every year you might, if lucky, stay the same weight, but you’d eventually need to be running sixty-plus miles a week.29
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.30 It may convert some of the fat to muscle – but that doesn’t show up on the scales. As children we were told to go outside and play so as to work up an appetite, and this was also for another reason. It made us hungrier the next day too and slowed the body and its metabolism down in subtle ways. Careful exercise studies, in which sedentary volunteers exercised intensively for six months, found they lost only 1.5 kg in weight as opposed to the 4.5 kg expected. Their hunger and food intake did increase, but only by 100 calories a day, which wasn’t enough to explain the failure to lose weight.31 Many other exercise studies show that energy expenditure when at rest stays low or that it drops by up to 30 per cent with more exercise. This reduction is mainly due to a drop in metabolic rate or in subconscious movements like fidgeting, which also expends calories.
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.32 33
Fit or fat?
So is it worth exercising if it doesn’t help you reduce weight? There is an interesting debate going on about whether it is better to be thin and sedentary or fat and fit. 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. A study following up over 300,000 Europeans found that doing no exercise whatsoever carried twice the risk of early death as obesity. Just doing twenty minutes per week brisk walking for a totally sedentary person (which is over one in five Europeans) would reduce their risk of premature death by a quarter.34 So it is very important to get the right overall balance for health even if you are overweight. The exception to the rule is the risk of diabetes, where being thinner consistently reduces your risk, even if you are unfit and do no exercise.35 36
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.
Our microbes are born to run
Our microbes certainly play a part in how exercise can reduce our risk of disease and early death, but the mechanism is currently poorly understood. Exercise stimulates the immune system in beneficial ways, then the immune system in turn sends chemical signals to the microbes in our guts.37 But it could also work the other way round, as exercise alone can also influence the gut microbiota composition directly.
One experiment was done on gym rats (real ones). Healthy rats love to run, and when divided into those with a running-wheel in their cage and those without, the runners, who averaged 3.5 km per day, produced twice the rate of the beneficial short-chain fatty acid butyrate in their guts compared with the sedentary rats.
Butyrate is a small fatty substance produced by our gut microbes that has many beneficial effects on the immune system, and exercise stimulates microbes to produce more of it.38 Having the right kind of gut microbes may also make you run faster or swim further, possibly owing to the microbes’ antioxidant properties. Antioxidants are important chemicals that prevent the release of substances called free radicals from cells – substances that cause a series of chain reactions shortening the life of the cell. So antioxidants are considered healthy chemicals, and are contained in many foods and produced by microbes. Perhaps altering your microbes will become the latest doping trend in the Olympics – although only elite long-distance swimming mice have been caught cheating so far.39
In the American Gut Project and our twin study, which are both cross-sectional observational studies, the strongest factor found to date affecting the richness of the gut microbes in over three thousand people was the amount of exercise they reported performing. However, in this kind of study it is hard to separate this from other associated factors, such as healthy eating. The best human data so far comes from a unique study showing the growing interest in microbes in the elite-sports nutrition world. Many elite sportsmen and women are now having their microbes profiled and their diets modified by their nutritionists.
In one study the stools of elite athletes of the national Irish rugby squad were sampled during their intensive pre-season training.40 Forty of these beefy men had a mean weight of 101 kg and a BMI of 29 – showing, incidentally, that about 40 per cent of them were technically obese and the rest overweight (but you probably wouldn’t want to tell them that yourself). In reality, you would be hard pushed to find any body fat on them (they had average levels of 16 per cent, which is very low). This emphasises how unreliable BMI is, and its weakness in measuring obesity in populations where waist–hip ratios or even belt size may be more effective measures. The researchers tried to find a comparable group, but of course it proved impossible. They found twenty-three men of the same age and BMI from Cork, but their extra BMI came mainly from fat (33 per cent), not muscle. So as an extra comparison they found another group of skinny local men.
The results showed clear differences: gut microbiota diversity was significantly higher in the athletes compared with both the other groups. The rugby players who consumed more calories also had healthier inflammatory and metabolic markers and greater numbers of most microbes. Microbiota-diversity measures positively correlated with the higher protein intake and markers for extreme exercise. By picking such an extreme elite group, the study couldn’t really separate the effects of exercise from those of diet, but suggested that both diet and exercise were driving the changes in microbial diversity. 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.
Brain food
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. Monkeys, for example, have much smaller and more economical brains relative to body size than us because they couldn’t afford the luxury of such a gas-guzzling limousine. Apes would have to be eating for over twenty hours a day to get enough energy to feed a brain of our relative size. About two million years ago we made an evolutionary step change whereby our brains grew and our intestines shrank by a third – particularly our colons, which are now proportionally much smaller. The reason for this was cooking.
The simple idea of using fire to change the composition of plants and meat transformed us into modern humans. Suddenly, by using heat to break down the complex starches of root vegetables and leaves we could extract the energy and nutrients in a fraction of the time that it took before. We no longer needed to spend most of the day chewing food like cows do, and could risk going further afield and hunting. This also meant that we no longer needed to run our elaborate combustion engines – our very long large intestines – which were designed to give plenty of time to digest tough plants. Unlike apes we no longer depended on the energy (like short-chain fatty acids) released from food fermented by our microbes.
Reducing the size of our intestines enabled us to invest more energy and calories elsewhere – most obviously in our brains. 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.
This supply of energy comes in mainly as glucose, and even when we are fasting or asleep the brain ensures it gets over half the body’s supply of circulating glucose and so never goes hungry. Our brains are the greediest organ and use a fifth of our total resting energy despite constituting only 2 per cent of our body weight.41 Just running our bodies at total rest costs us around 1,300 calories a day. The good news is that it is quite easy to expend energy. For example, just watching TV for an hour uses 60 calories; reading this chapter will expend over 80, and even more if you are on the chubby side or are finding the whole experience stressful.
We have seen how relying on counting calories to lose weight is often misleading and that trying to lose weight by exercise alone is futile. However, until we come up with a better system, calories are here to stay, and they give us at least a rough guide to the overall energy content of foods. The rest of the details on food labels show us the other macronutrient components of food that the industry and the government have agreed we can see. They were introduced so we could judge for ourselves which products are healthy and which we should be wary of. But just how reliable are the accompanying health messages that many of us have taken for granted?
I will continue to use the format of the classic food label – somewhat ironically, as these labels are over-simplistic and reductionist as well as misleading. All nutrients – by which I mean the tiny components of food that are critical for all the bodily processes – are important, and form a part of virtually all useful foods, which are complex mixtures of the different food groups.