Ultra-Processed People: Why We Can’t Stop Eating Food That Isn’t Food
Genres: Engineering & Transportation
Book Preface
Every Wednesday afternoon in the laboratory where I used to work, we had an event called journal club. The word ‘club’ makes it sound more fun than it was. The ritual, practised in labs around the world, worked like this: one member of the lab would present a recent publication from the scientific literature that they felt was relevant to our work, and the rest of us would tear it to pieces. If the paper wasn’t of sufficient quality, then the unhappy person who had selected it would also be torn to pieces.
The lab, which is run by Greg Towers, is still based at University College London (UCL), in a converted Victorian hospital built by the same architect who designed the Natural History Museum. It is a beautiful old building, full of mice and leaks. It seemed like an improbable venue for the world-class molecular virology research it produced, when I arrived in 2011 to do a PhD.
At these journal clubs, Greg and the other senior lab members taught me that science is not a list of rules or facts, but a living argument. Greg was more up for the argument about any data point in any paper than anyone I have met before or since. Nothing went unexamined. It was the best scientific training I could have hoped for.
The lab specialty was the ongoing competition between viruses like HIV and the cells they need to infect in order to reproduce. This competition is like a military arms race. All cells have defences against viral attack, and all viruses carry weapons to overcome those defences. As the cells evolve ever more sophisticated defences, so too are the viruses constantly evolving better weapons, which in turn drives the evolution of more cellular defences, and so on.
Most of us studied HIV and its viral cousins for exciting reasons, like the development of new drugs and vaccines, but there was a splinter group within the lab that studied a different type of virus, one that barely seemed like a virus at all. Almost half of the DNA in every cell of your body is made of ancient dead virus genes. Known for a long time as ‘junk’ DNA, this topic seemed to be a scientific backwater until, in October 2014, one of the members of the splinter group presented a paper at journal club from the publication Nature, its title dense with jargon: ‘An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons’.1
I gave the paper a quick skim before the meeting and found it incomprehensible. Out of every ten papers presented at journal club, roughly seven would be demolished, two would stand up and provide useful new information, and one would betray evidence of naked fraud. It wasn’t clear to me which category this paper would fall into.
As we talked through the data, I noticed a shift in the atmosphere. Everyone sat forward as the data made the case that these old, dead viruses found throughout the human genome aren’t dead at all. They have functioning genes, ready to make more viruses. Every cell in the human body is a potential virus factory, but something keeps these viral genes quiet. It turned out that they’re suppressed by other genes in the cell.
The paper was saying that one part of our genome is constantly at war with another part.
The implications of this were immediately obvious to everyone in a lab familiar with the nature of arms races. Whether they involve competition between viruses, neighbourhood disputes, sports teams, political campaigns or global superpowers, all arms races must generate complexity. As insurgency develops, so must counterinsurgency. Intelligence begets counterintelligence, with double and triple agents. It’s the development of ever more sophisticated weapons that drives the evolution of ever more sophisticated defences.
Because the human genome is in an internal arms race, with one piece of DNA at war with another, this means that it must inexorably be driven towards ever greater complexity. Over thousands of generations, as those old ‘dead’ viruses evolve, so the rest of the genome must evolve to keep them quiet.
This arms race within our genes has been going on since the dawn of life, and it may very well be the engine of the evolution of complexity itself. The major difference between the human genome and that of chimpanzees is not in the parts that code for proteins (which are around 96 per cent similar) but in the parts that seem to come from the old, dead viruses.2
The paper transformed my understanding of myself, even if it took me a while to get my head around the idea that, at least in part, I’m an assembly of old viruses at war with my other genes. It may change the way you see yourself, too. You aren’t simply living alongside this arms race between different genes – you’re the product of it, an uneasy coalition of competing genetic elements.
These coalitions and competitions extend beyond our genes. Where ‘you’ end and ‘not you’ begins is far from clear. You’re covered in microbes that keep you alive – they’re a part of you as much as your liver is – but those same microbes can kill you if they get into the wrong area of the body. Our bodies are much more like societies than like mechanical entities, comprising billions of bacteria, viruses and other microbial life forms, but just one primate. They’re full of odd, negotiated compromises and imperfections. Arms races blur boundaries.
I worked in Greg’s lab for six years before going back to being a doctor, but the idea of arms races, the complex systems they create and the boundaries they blur became a key part of the way I think about the world. I continued to do research, but my focus shifted from studying viruses, towards investigating scientific research that was biased or fraudulent. Now I mainly study the food industry and how it affects human health. My laboratory grounding has proved crucial for this: arms races and their effects will come up a lot throughout this book.
For a start, to eat is to compete in an arms race that has lasted billions of years. The world around us has a relatively fixed amount of available energy, and all life is engaged in a competition against other forms of life for that energy. Life has, after all, only two projects: reproduction and extracting energy to fuel that reproduction.
Predators are locked in competition not only with each other to obtain prey, but also of course with the prey itself, which generally wants to hang onto the energy contained in its meat. The ‘prey’ animals also compete for vegetation both with each other and with the plants themselves, which produce toxins, thorns and other defences against being eaten. Plants compete with each other for sun, water and soil. Microbes, bacteria, viruses and fungi constantly assault all the organisms in the ecosystem to extract what energy they can. And no one gets ahead for long in an arms race: wolves may be well adapted for eating deer, but deer are superbly adapted to avoid being eaten by wolves and do, on occasion, kill them.*
We eat, then, as part of a set of interlinking, entangled arms races, competing for energy flowing between life forms. Like all arms races, this competition has generated complexity, and so everything about eating is complex.
Our senses of taste and smell, our immune system, our manual dexterity, our tooth and jaw anatomy, our eyesight: it’s hard to think of any aspect of human biology, physiology or culture that isn’t primarily shaped by our historic need for energy. Over billions of years our bodies have superbly adapted to using a wide range of food.
But over the past 150 years food has become … not food.
We’ve started eating substances constructed from novel molecules and using processes never previously encountered in our evolutionary history, substances that can’t really even be called ‘food’. Our calories increasingly come from modified starches, from invert sugars, hydrolysed protein isolates and seed oils that have been refined, bleached, deodorised, hydrogenated – and interesterified. And these calories have been assembled into concoctions using other molecules that our senses have never been exposed to either: synthetic emulsifiers, low-calorie sweeteners, stabilising gums, humectants, flavour compounds, dyes, colour stabilisers, carbonating agents, firming agents and bulking – and anti-bulking – agents.
These substances entered the diet gradually at first, beginning in the last part of the nineteenth century, but the incursion gained pace from the 1950s onwards, to the point that they now constitute the majority of what people eat in the UK and the USA, and form a significant part of the diet of nearly every society on earth.
And, at the same time as we’ve entered this unfamiliar food environment, we’ve also moved into a new, parallel ecosystem, one with its own arms races that are powered not by the flow of energy, but by the flow of money. This is the new system of industrial food production. In this system we are the prey, the source of the money that powers the system. The competition for that money, which drives increasing complexity and innovation, occurs between an entire ecosystem of constantly evolving corporations, from giant transnational groups to thousands of smaller national companies. And their bait for extracting the money is called ultra-processed food, or UPF. These foods have been put through an evolutionary selection process over many decades, whereby the products that are purchased and eaten in the greatest quantities are the ones that survive best in the market. To achieve this, they have evolved to subvert the systems in the body that regulate weight and many other functions.*
UPF now makes up as much as 60 per cent of the average diet in the UK and the USA.5–7 Many children, including my own, get most of their calories from these substances. UPF is our food culture, the stuff from which we construct our bodies. If you are reading this in Australia, Canada, the UK or the USA, this is your national diet.
UPF has a long, formal scientific definition, but it can be boiled down to this: if it’s wrapped in plastic and has at least one ingredient that you wouldn’t usually find in a standard home kitchen, it’s UPF. Much of it will be familiar to you as ‘junk food’, but there’s plenty of organic, free-range, ‘ethical’ UPF too, which might be sold as healthy, nutritious, environmentally friendly or useful for weight loss (it’s another rule of thumb that almost every food that comes with a health claim on the packet is a UPF).
When we think about food processing, most of us think about the physical things done to food – like frying, extruding, macerating, mechanically recovering and so on. But ultra-processing also includes other, more indirect processes – deceptive marketing, bogus court cases, secret lobbying, fraudulent research – all of which are vital for corporations to extract that money.
The formal UPF definition was first drawn up by a Brazilian team back in 2010, but since then a vast body of data has emerged in support of the hypothesis that UPF damages the human body and increases rates of cancer, metabolic disease and mental illness, that it damages human societies by displacing food cultures and driving inequality, poverty and early death, and that it damages the planet. The food system necessary for its production, and of which it is the necessary product, is the leading cause of declining biodiversity and the second largest contributor to global emissions. UPF is thus causing a synergistic pandemic of climate change, malnutrition and obesity. This last effect is the most studied, and the hardest to talk about, because discussions of food and weight, however well intentioned, make a lot of people feel very bad.*
Much of this book will be about weight because much of the evidence around UPF is related to its effect on weight, but UPF causes suffering in many ways that are independent of effects on weight. UPF doesn’t cause heart disease and strokes and early death simply because it causes obesity. The risks increase with the quantity of UPF consumed irrespective of weight gain. Additionally, people who eat UPF and don’t gain weight have increased risks of dementia and inflammatory bowel disease, but we don’t tend to blame patients for having these problems. So, obesity gets a special mention because it is unique among diet-related diseases – in fact unique among almost all diseases – because doctors blame patients for having it.
In fact, let me back up a moment on obesity. We’re still figuring out the language for this discussion. The word is rightly offensive to many people and calling obesity a disease is stigmatising. Many people don’t live with obesity as a disease but as an identity. For others it’s just a way of being, and an increasingly normal way of being at that. Weight gain is not inevitably associated with increased risk of health problems and the risk of death is in fact lower for many people who live with overweight than for those who live at a ‘healthy’ weight. Nonetheless, I will sometimes use the word obesity, and I will sometimes frame it as a disease, because diseases get funding for research and treatment, and sometimes the disease label reduces stigma: a disease is not a lifestyle or a choice, and the word can help to shift the burden of responsibility away from the affected person.
This is important because every discussion of weight gain, whether in the press or in our own heads, is suppurating with blame, which is always directed at the people who live with it. The idea that they are to blame has survived scientific and moral scrutiny because it is simplistic to the point of transparency. It’s based on there being some failure of willpower – a failure to move more or to eat less. This idea doesn’t stand up to scrutiny, as I will show repeatedly. For example, since 1960, the US National Health surveys have recorded an accurate picture of the nation’s weight. They show that – in white, Black and Hispanic men and women of all ages – there was a dramatic increase in obesity, beginning in the 1970s.8 The idea that there has been a simultaneous collapse in personal responsibility in both men and women across age and ethnic groups is not plausible. If you’re living with obesity, it isn’t due to a lack of willpower; it isn’t your fault.
In fact, we’re a lot less responsible for our weight than a skier is for breaking their leg, a footballer for injuring their knee, or a bat scientist for getting a fungal lung infection from working in caves. Diet-related diseases come from the collision of some ancient genes with a new food ecosystem that is engineered to drive excess consumption and that we currently seem unable, or perhaps unwilling, to improve.
For the past thirty years, under the close scrutiny of policymakers, scientists, doctors and parents, obesity has grown at a staggering rate. During this period, fourteen government strategies containing 689 wide-ranging policies have been published in England,9 but among children leaving primary school rates of obesity have increased by more than 700 per cent, and rates of severe obesity by 1600 per cent.10
Children in the UK and the USA, countries with the highest rates of UPF consumption, aren’t just heavier than their peers in nearly all other high-income western countries, they’re shorter too.11,12 This stunting goes hand in hand with obesity around the world, suggesting that it is a form of malnutrition rather than a disorder of excess.
By the time those children reach adulthood they will have been joined by so many of their peers that the proportion of the population that lives with obesity will rise to one in three. The chances of an adult living with severe obesity being able to achieve and maintain a healthy body weight without specialist help are less than one in a thousand. Severe obesity is thus, for the majority of those affected, an incurable condition without drugs or surgery. Overweight now affects more than a quarter of children and half the adult population.13
Policies in the UK and almost every other country have failed to solve obesity because they don’t frame it as a commerciogenic disease – that is, a disease caused by the marketing and consumption of addictive substances. Comparisons to drugs and cigarettes risk yet more stigma, but I will make them with due care in the pages that follow. Like all diet-related disease, obesity has deeper causes than UPF, including genetic vulnerability, poverty, injustice, inequality, trauma, fatigue and stress. Just as smoking is the number one cause of lung cancer, poverty is the main cause of smoking. Smoking rates in the UK are four times higher among the most disadvantaged than among the wealthiest, and half the difference in death rates between rich and poor in the UK is explained by smoking.14
Like cigarettes, UPF is a collection of substances through which these deeper societal problems harm the body. It is a tangible way in which these injustices are manifested, mediating trauma and poverty and allowing the expression of genes that might otherwise remain hidden. Fix poverty and you prevent a lot of both lung cancer and obesity. That’s another book though.
This is a book about the systems that provide our food and tell us what we should eat. I want to prompt you to imagine a world structured in a different way, a world that would offer everyone more opportunity and choice. So, there are no proposals to tax things or ban them – only a demand to improve information about UPF, and access to real food.
This is not a weight-loss book because first, no one has yet devised a method that helps people safely and sustainably lose weight, and second, I don’t accept that you should lose weight. I don’t have a ‘correct’ body and I don’t have an opinion about what one would look like. I don’t have an opinion on the food you should eat; that’s up to you. I make choices that are not ‘healthy’ the whole time, whether it’s dangerous sports or eating junk. But I feel strongly that to make choices we all need accurate information about the possible risks of our food, and that we should be less exposed to aggressive, often misleading marketing.
So, you’ll find almost no advice in these pages about how to live your life or how to feed your children. Partly it’s none of my business, but mainly I think advice is a bit pointless. What we eat is determined by the food around us, its price and how it’s marketed – this is what needs to change.
But I do have one suggestion about how you read this book. If you feel like you might want to quit UPF – don’t. Eat along.
Let me explain. You’re a participant in an experiment you didn’t volunteer for. New substances are being tested on all of us all the time to see which of them are best at extracting money. Can a synthetic emulsifier be used instead of an egg? Can a seed oil replace a dairy fat? Can a bit of ethyl methylphenylglycidate be chucked in instead of a strawberry? By buying UPF, we’re continuously driving its evolution. We take the risk in this experiment while the benefits are handed to the owners of the companies producing UPF and the results are largely concealed from us – apart from the effects on our health.
My proposal is that, for the duration of reading this book, you continue the experiment of eating UPF, but that you do it for you, not for the corporations that make it. I can tell you about UPF, but the stuff itself will be your greatest teacher. Only by eating it will you understand its true nature. I know this because I did the experiment myself.
In the course of researching the impact of UPF, I partnered with colleagues at University College London Hospital (UCLH). I was the first patient in this study. The idea was to get data from me that would help us get funding for a much larger study (one we’re now undertaking). The idea was simple: I would quit UPF for a month, then be weighed and measured in every possible way. Then, the next month I would eat a diet where 80 per cent of my calories came from UPF – the same diet that around one in five people in the UK and the USA eat.
I didn’t deliberately overeat during that second month, I just ate as I normally do, which is whenever I feel like it and whatever food is available. As I ate, I spoke to the world’s leading experts on food, nutrition, eating and ultra-processing from academia, agriculture and, most importantly, the food industry itself.
This diet of UPF should have been enjoyable, as I was eating food that I typically deny myself. But something odd happened. The more I spoke to experts, the more disgusted by the food I became. I was reminded of Allen Carr’s best-selling book, The Easy Way to Stop Smoking. The book is unusual in the self-help genre in that it has actually been studied and the intervention it recommends is pretty good. The idea is that you keep smoking while you read about how bad smoking is. Eventually, the cigarettes begin to seem disgusting.
So, give in – allow yourself to experience UPF’s full horror. I’m not urging you to binge or to overeat, but simply to stop resisting UPF. I did it for four weeks – if you feel like trying this then do it for as long as it takes to finish the book. There is an ethical question about encouraging you to do this, but I’m comfortable with it. First of all, you’re already being encouraged to eat UPF all day long. Second, if you are typical, you’re already eating around 60 per cent of your calories from UPF, so increasing that to 80 per cent for a month probably won’t make a big difference.
As you read this book, I hope you’ll also read the lists of ingredients on the back of the packets of food that you eat. You’ll find many more substances than I am able to unpack individually in these pages, but by the end I hope you’ll have begun to understand how everything from the marketing campaign to the strange lack of satisfaction you feel after eating is driving ill health. And you may see that many of the problems in your life that you’ve been putting down to getting older, or having children or work stress, are caused by the food you eat.
I can’t promise that the UPF will become bizarre and disgusting as you read, but you may find that it does, and if you are able to give it up, the evidence suggests that this will be good for your body, your brain and the planet. It’s happened to a number of people involved in the process of making this book, and the podcast that came before it, and I’d love to know if it happens to you.
Contents
Introduction
PART ONE
WAIT, I’M EATING WHAT?
1. Why is there bacterial slime in my ice cream? The invention of UPF
2. I’d rather have five bowls of Coco Pops: the discovery of UPF
3. Sure, ‘ultra-processed food’ sounds bad, but is it really a problem?
4. (I can’t believe it’s not) coal butter: the ultimate UPF
PART TWO
BUT CAN’T I JUST CONTROL WHAT I EAT?
5. The three ages of eating
6. How our bodies really manage calories
7. Why it isn’t about sugar …
8. … or about exercise
9. … or about willpower
10. How UPF hacks our brains
PART THREE
OH, SO THIS IS WHY I’M ANXIOUS AND MY BELLY ACHES!
11. UPF is pre-chewed
12. UPF smells funny
13. UPF tastes odd
14. Additive anxiety
PART FOUR
BUT I ALREADY PAID FOR THIS!
15. Dysregulatory bodies
16. UPF destroys traditional diets
17. The true cost of Pringles
PART FIVE
WHAT THE HELL AM I SUPPOSED TO DO THEN?
18. UPF is designed to be overconsumed
19. What we could ask governments to do
20. What to do if you want to stop eating UPF
Acknowledgements
Notes
Index
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