The Miracle Pill

by Peter Walker

  All this can be hugely excluding. Even lower-cost, mass-market gyms, some of which have made admirable attempts to reach out to a broader market, can remain intimidating environments to many. Smith Maguire is highly sceptical about gyms of any sort making real inroads into overall inactivity levels. ‘The commercial fitness industry itself is a product of that draining away of everyday activity. Markets rely on problems,’ she says. ‘I’m deeply suspicious of any health promotion strategy that rests on individuals making specific choices, because those choices are not individually theirs to make.’

  Numerous governments have bought into the illusion that urging people to exercise in their spare time can make up for reduced activity in everyday life. The UK is something of a poster child for this approach. Recent decades have seen minimal investment in areas such as infrastructure for safer walking and cycling. But at the same time, the amount of public money put into elite sport has grown vastly. At the 1996 Atlanta Olympics, the UK squad, assembled on a total budget of about £5 million, came thirty-eighth in the medal table. This prompted an outpouring of national angst, followed by an inflow of money from National Lottery funds. By the Sydney Olympics four years later, the UK team’s budget was nearly £59 million. For Rio in 2016, with the UK now second in the medals tally, this had reached £274 million.28 Coincidentally, the Rio budget is almost exactly the same as annual government spending on Public Health England,29 which is not only tasked with promoting more activity, but also leads on efforts in areas including tobacco and alcohol, as well as, of course, infectious diseases like coronavirus. This is all about to change, after the government announced it will replace PHE with a new organisation focused on infectious illnesses, with the preventative health work hived off elsewhere, possibly to local government.

  Those millions spent on Olympic medals might have brought a few weeks of national cheer, but there is minimal evidence they boosted overall activity levels, whether in sport or elsewhere. Statistics from Sport England, the same body responsible for handing out the Olympic money, show that the proportion of people who say they never take part in any sport – about 55 per cent of the population – has stayed more or less static for a decade.30

  A particularly telling example is cycling. After British cyclists won dozens of gold medals over a succession of Olympics, and then took a series of Tour de France titles, there was much talk of a boom in cycling numbers. And for a period there was a rise in bike sales, and an increase in cycle commuter numbers in a handful of places. But if you look at the detailed statistics, any impression of real change evaporates. Government figures show that from 2002 to 2018, the average number of bike trips per person per year stayed largely flat, declining marginally from an already minuscule eighteen to seventeen. The average number of miles ridden did rise a bit, which was perhaps the one impact of all the new racing cyclists – they tended to go for slightly longer rides.31

  Another problem with sport is that its benefits are not felt evenly. People from disadvantaged socio-economic groups have long been less likely to participate in physical activity overall, and this effect is magnified with exercise. The most recent UK data shows that while 51 per cent of people in the top social grades as defined in government statistics take part in at least some sport, for those in the most deprived groups this drops to 35 per cent.32

  Prompted by decades of government messaging, many people try exercise and then find that an initial burst of enthusiasm gradually evaporates. Insiders from the fitness industry will happily tell you that a significant part of the business model of most gyms are the clients known as ‘sleepers’ – those who take out a membership but then rarely, if ever, attend. There are varying statistics for absentee members, but one seemingly rigorous 2017 UK poll suggested that 11 per cent of people had not removed their gym cards from their wallets once in the past year.33

  There is deep concern among many public health professionals that the focus on sport rather than more regular movement allows governments to pretend they are tackling inactivity, and ignore the wider problems. Dr Adrian Davies, whom we heard from in the last chapter, is particularly scathing about what he calls the ‘Eton playing fields mindset’, saying: ‘There’s nothing wrong with sport, but if you look at the fitness levels of the whole population, we need to do routine, moderate physical activity before you start to ask people to engage in vigorous activity.’34

  Additionally, the glaring contrast between Harvey Spevak’s small minority of toned, have-it-all, twice-a-day gym-goers and the four-in-ten Britons who barely exert their bodies at all is fertile ground for shame and stigma, particularly when excess weight is involved. Such judgements are deeply unfair.

  This is one of the most vital messages I would hope people take from this book: labelling someone who is inactive as lazy and ignorant, or to condemn yourself in those terms, is to utterly miss the point. This is a process which has played out across whole populations, and over decades. This is not an individual story, or a failure of willpower. It is much, much bigger than that.

  Next steps:

  Think about your routine, and how and when you are physical. Is it just through exercise – and if so, can it be hard to find the time? Then think about how you might be able to incorporate any sort of exertion into everyday life – everything from climbing one flight of stairs to parking 200 metres further away than normal – instead.

  I. What is generally called a calorie is officially a ‘kilocalorie’, which is the amount of energy needed to raise the temperature of a litre of water by one degree Centigrade while at sea level. But as ‘calorie’ is so widely adopted, I’ll use it when discussing energy intake and expenditure.

  2 The Miracle Pill: Small Doses Have Big Impacts

  Dr Richard Mackenzie knows more than most people about the ways activity can affect the human body. He has worked with elite cyclists, and in the laboratory where the former marathon world record holder Paula Radcliffe had her fitness tested. His current research examines how a lack of movement can make people intolerant to insulin, and thus develop type 2 diabetes, one of the most prevalent, destructive and medically costly chronic conditions of the modern era. A lot of his work involves using isotopes, adapted elements which can be easily traced through the body to try to see the effects of activity at a cellular level.

  But sitting in the student café at Roehampton University in southwest London, a noisy, airy space with decidedly un-London views onto playing fields and then the green expanse of Richmond Park in the distance, Mackenzie is cheerfully honest about how much he has so far discovered about these biological fundamentals. ‘Almost nothing,’ he laughs. ‘Unless you’re a grant-awarding body, and I’ll tell you a very different story.’ The science is, he says, ‘very challenging – even the whole-body level isn’t really understood’.

  Mackenzie is perhaps being unduly modest, given the potential future benefits of his research. One strand examines how certain proteins might act as what he calls ‘a negative feedback loop’ to push people into type 2 diabetes. This is the lifestyle-related variant of diabetes, distinct from type 1, which is a lifelong autoimmune condition. Type 2 diabetes begins when the tissues in someone’s body stop responding properly to insulin, the hormone central to the maintenance of healthy blood sugar levels, putting them into what is called pre-diabetes. Mackenzie’s efforts focus on how some people with pre-diabetes then move to the full-blown condition, with the ensuing regime of medication and possible serious complications, and others do not. He has recruited a test group of pre-diabetic people with the hope of observing various protein interactions which then cause one or the other outcome. The eventual aim, which Mackenzie concedes is ‘a long way off’, could be some form of bespoke treatment based around the metabolic profile of individual patients.

  Other studies led by Mackenzie examine how activity reverses the diabetic starting point. This involves taking a volunteer and infusing them with higher-than-usual levels of insulin to mimic the effects of pre-diabetes, balanced
with a careful counter-dose of glucose to make sure they don’t slip into a diabetic coma. ‘You might laugh,’ Mackenzie says as he explains this to me. ‘But we do make sure no one is harmed.’

  Once this artificial pre-diabetic state is induced, the subject starts exercising, and Mackenzie and his team observe the way activity improves their body’s ability to process glucose. I ask him how long it takes – a few hours, perhaps a day? He replies with a smile: ‘You can see the effects begin within seconds. It’s that quick. The subjects can become pre-diabetic, if you like, and then revert to healthy before they leave the lab.’

  It is not only the timescale which is exaggeratedly tiny – so is the range of movement needed to have a metabolic effect. Mackenzie explains: ‘As we’re infusing the insulin, even modest things like giggling, using muscles that allow you to laugh, mean that we have to infuse more glucose because those muscles are responding very well to the insulin. And it always works. There are very, very few people that exercise won’t help.’

  Cutting-edge studies about the cellular process of glucose intolerance might seem a bit distanced from this book’s story of everyday activity. But they illustrate one of the most astonishing aspects of physical movement: for all the harm caused by its absence, more or less the very moment you start to use your body again, it feels the benefits.

  For decades, the conventional wisdom was that for activity to have much of a health-restoring effect it had to be at least reasonably vigorous and fairly regular. These ideas are now being rapidly rethought, in part due to the advent of sophisticated electronic activity trackers, like the one I borrowed, which have helped researchers to properly measure limited amounts of low-level movement and follow the health outcomes.

  Another emerging consensus dispenses with the assumption that activity has to last a certain period of time, arguing that even the briefest bursts can be beneficial. This is the new, and hopeful, world of inactivity advice. Yes, if you can reach well-known targets like 10,000 steps a day or 150 minutes of activity a week, that’s great. But in terms of both amount and intensity, just about anything is better than nothing at all.

  Making yourself younger

  So why does the human body respond so well to movement – and, in turn, so badly to prolonged periods of immobility? Let’s start with a slightly oblique approach. How do we even know for certain that, as humans, we are intended to be active? This question is tackled in one of the best, and heaviest, of the many activity physiology textbooks I acquired for my research. At the start of the first chapter of the breezeblock-size Physical Activity and Health, it is posed by Professor Claude Bouchard, a venerable and now largely retired US activity expert who led the book’s equally heavyweight editorial team.

  Bouchard’s answer comes in three parts, and I was immediately struck by its elegance. First of all, he says, the body is clearly well adapted to exertion, given that healthy adults are able to increase their resting metabolic rate ten-fold or more, and maintain this state for a considerable period of time. Secondly, he notes in a convincing if somewhat circular answer, we know the body is meant to move on a daily basis because of the range and extent of ill-health that follows if it does not. Finally – and here I slightly précis Bouchard’s more sober academic style – while we modern humans have created an environment in which we can, if we choose, permanently lounge amid a sedentary haze of car travel, home-delivered food and social interaction via a pocket-sized screen, our early ancestors were clearly dependent for survival on regular physical exertion, meaning it is demonstrably inherent to our evolution.1

  In the same way as this book is not intended to be a step-by-step guide to better health, it is definitely not a physiology textbook. But for me to explain why regular physical movement is so fundamental to human wellbeing I need to outline a few principles about how it affects the body, and what happens when it is not there.

  To begin with the utter basics, energy is expended every time we move. I’m currently sitting down to write this chapter. Yes, this is not ideal for long periods, as we’ll see later in the book. In a few minutes I plan to get up and make a cup of tea. When I do that, a much more significant selection of my skeletal muscles than are now being used to sit and type will spring, or in some cases creak, into action. Skeletal muscle is the biggest mass of tissue in the human body, comprising more than 600 individual muscles. It’s also the only type of muscle we control consciously. The others are cardiac muscle, which, as the name suggests, is found in the heart, and smooth muscle, located mainly in organs like the stomach and intestine.

  When I get up from the chair and march the six or seven paces from my desk to the compact kitchen of my temporary writing flat, my muscles will be powered by a molecule called adenosine triphosphate, or ATP. This is not a storage for energy, like carbohydrates. ATP is often described as the ‘currency unit’ of energy transfer. Specifically, ATP provides the energy for myosin, a motor protein, to bind to actin, another protein, pulling the actin in, thus shortening muscle fibres. For my imminent mission to the kitchen, these will principally be in my legs, the location of some of the biggest muscles in the body, where the ATP will be converted into adenosine diphosphate (ADP) or adenosine monophosphate (AMP). While I stand waiting for the kettle to boil, my ATP will be replenished by aerobic respiration, using inhaled oxygen.

  But if, hypothetically, I interrupted the tea making to dash out of the front door and run up and down the short if fairly steep hill outside until I was completely out of breath, the ATP would be replaced using the different, notably more short-term, chemical process of anaerobic respiration. This also produces lactate, which is in itself not a problem for the body, but also tends to increase acidity, and in turn the burning feeling known only too well to even recreational athletes, which would before long make my legs ache, and prompt me to come to a wheezing halt. The muscle-aching substance is traditionally known as ‘lactic acid’, but these days scientists like to distinguish between the lactate, which is generally benign, and the acidity, which is not.

  That’s the mechanics, or rather the chemistry and biology. So why is a habitually immobile life, or at least one mainly devoid of moderate exertion, so bad for you? One of the apparent main factors comes back to ATP. It is produced by mitochondria, a sub-part of individual cells that is generally described as their ‘engine unit’. Mitochondria tend to work less well as we age, but this also happens with prolonged inactivity.

  Sluggish mitochondria are bad health news for all sorts of reasons. They are particularly important in the heart, due to the constant energy expended there. Numerous studies have linked poorly functioning mitochondria to all sorts of cardiovascular diseases, including furred arteries, high blood pressure and heart attacks. Mitochondrial dysfunction is also seen as increasing the risk of type 2 diabetes, and is implicated in the cellular mutations that can lead to cancer.

  The good news is how rapidly this process can seemingly be reversed through movement. One 2017 US study put groups of volunteers through various twelve-week exercise regimes. Half the participants were young, under thirty, and the others were aged between sixty-five and eighty. At the end of the process, the younger group had increased their mitochondrial capacity by no less than 49 per cent. For the older participants, the gain was an even more impressive 69 per cent.2

  If such results lead you to think that physical activity can slow the ageing process, you’re perhaps more correct than you realised. Other studies have examined its effect on telomeres, tiny sequences of molecules that effectively act as a cap on chromosomes, shielding them. Elizabeth Blackburn, an Australian scientist who won a Nobel Prize for her work on telomeres, describes them elegantly by saying that if you think of your chromosomes as shoelaces, telomeres are ‘the little protective tips at the end’.3 If telomeres wear down, this can cause cell malfunction and all sorts of diseases associated with ageing. The shortening of telomeres happens with age anyway, but also because of lifestyle factors including a poor diet, lack of sleep
and, particularly, inactive living.

  One particularly striking recent study examined telomere length in nearly 6,000 Americans of various ages and activity levels. It found that the most active people were on average nine years younger by telomere length than those who were completely sedentary.4 Nine years. It’s a repeated refrain of this book, but just imagine the universal acclaim if you could package that effect into a tablet.

  Zooming out a little from this cellular focus, another reason physical activity is so vital is because of the role skeletal muscle plays in human health. It has only been established fairly recently that, rather than being what you might call a neutral force in the body, skeletal muscle is part of the endocrine system, the hormone-producing function associated mainly with glands like the pituitary and thyroid. Muscles secrete not just hormones, but also cytokines, a type of amino acid chain which helps regulate the body’s immune response, and which can prompt inflammation. Studies have shown that a lack of regular movement can unbalance these substances, and assist what one paper called the ‘vicious circle’ of muscle wastage, extra fat, and then the development of all sorts of diseases.

  Any accumulation of fat – or, to use its posh name, adipose tissue – in itself also brings complications, because fat is also now known to be part of the endocrine system, and has a role in the secretion and synthesis of various hormones, some affecting sensitivity to insulin, and thus linked to type 2 diabetes.