Sat, Apr-29-23, 23:54
Why are some of us more addicted to junk food than others?
Why are some of us more addicted to junk food than others?
High-calorie, ultra-processed food has taken over our diets. But why are some of us more addicted to it than others, and how much is really down to your family tree?
Chris van Tulleken
You’re a participant in an experiment you didn’t volunteer for. New substances are being tested on all of us all the time. 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? 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”.
These ultra-processed foods (UPFs) are edible substances reconstructed from whole food that’s been reduced to its basic molecular constituents. These are modified and re-assembled into food-like shapes and textures, then heavily salted, sweetened, coloured and flavoured.
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.
These substances entered the diet gradually at first, beginning in the last part of the 19th 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 US, and form a significant part of the diet of nearly every society on Earth.
But what impact are they having on our health? For the past 30 years, under the close scrutiny of policymakers, scientists, doctors, and parents, obesity has grown at a staggering rate. During this period, 14 government strategies containing 689 wide-ranging policies have been published in England, but among children leaving primary school rates of obesity have increased by more than 700 per cent, and rates of severe obesity by 1,600 per cent. So how much of this is down to a UPF diet and how much is it down to other factors like willpower and genes?
I partnered with colleagues at University College London Hospital (UCLH) to take part in a study. 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 US eat.
I was about halfway through the second month of this experiment when I had lunch with Rachel Batterham, a friend and colleague at University College London Hospital where she is a professor of obesity, diabetes and endocrinology. I was half-listening to her talk about genetics and half-wondering if I knew her well enough to ask to finish the food on her plate. I’d pressed her earlier on where we should eat, but it was clear that she simply didn’t care. Even though I know that genetics influences how much we think about food, I still find indifference to food hard to understand. I plan dinner at breakfast. When I’m at a wedding, my whole focus is the canapés.
I was feeling unusually blunt when I asked Rachel if she thought that the fact that she is slimmer than me and her patients was because she can exert more power over her desire to eat. She dismissed the idea: “Some of my patients have lost your entire body weight many times over.” She was right that such weight loss takes incredible willpower. But could Rachel have even more willpower than them?
She rejected that idea too. “I exert no willpower not eating a biscuit,” she explained. “I might be able to imagine it would be nice, but I basically don’t want it.” She continued to pick at the food on her plate. “Food simply doesn’t motivate me. It’s just my genetics.”
As my month of eating UPF went on, I continued to speak to the world’s leading experts on food, nutrition, eating and academia. The more I spoke to experts, the more disgusted I became. Meals took on a uniformity. I was never hungry, but never satisfied. Suddenly there was nothing I wanted more than fresh vegetables.
Almost everyone living with obesity will have genes that drive it. There are two broad kinds of genetic obesity. There are rare defects in single genes, which lead to cases in which weight gain is essentially unavoidable no matter the environment. But the vast majority of people who live with obesity have many minor genetic differences compared with people with lower body mass index (BMI); mostly in the genes that work in the brain and that affect eating behaviour such as the speed at which people eat and the foods they choose.
The fact that genes can affect eating behaviour creates confusion because it seems counter-intuitive — it feels, after all, like we make conscious choices, amenable to the exertion of will. However, that is not the case. The difference between people with the same genes and differing weights is the environment they live in, not their willpower.
My twin, Xand, is seven minutes older, but he has also been up to 20kg heavier than me, the biggest weight difference of any pair of twins studied in the UK. We share a genetic code, meaning we have identical genes, and I know — because I did a test with Giles Yeo, a respected Cambridge geneticist — that we both have many of the major genetic risk factors for obesity. If you are a food-obsessed person, then you probably have these genes too, regardless of your weight.
Xand only began to gain weight in a serious way when he moved to the US. He got a scholarship to an American university to do a master’s degree. Around the same time he found out that he was going to have a child with someone he didn’t know well, in a way that was totally unplanned. It could not now be a happier situation but at the time it was stressful.
Xand also lived in Boston in a food swamp. You may have heard of food deserts — places where shops sell only UPFs. In the UK, more than three million people don’t have a shop selling raw ingredients within 15 minutes of their homes by public transport. With food swamps, fresh food may be available, but it’s submerged in a swamp of fast-food outlets selling heavily processed food.
We know that stress from any source, but especially the chronic stress of poverty, has dramatic impacts on those hormones that regulate appetite, increasing the drive to eat. The exact mechanisms aren’t clear, but when you’re stressed you secrete more of the hormone cortisol, this seems to drive increased intake of calorie-dense UPF through effects on many of those hormones involved in the energy intake regulation system. Cortisol may also lead to fat accumulation around organs, known as visceral fat. Chronic stress in low-income settings combined with the availability of UPF creates a double jeopardy.
The 20kg weight difference between Xand and me was not an exertion of will on my part. Put either of us in a food swamp and stress us out and we’ll gain weight. But Xand didn’t feel like his genes were to blame. Rather, he felt like a failure every day. He said the same thing that many people who live with obesity say, that he was eating “because of his emotions” and this is superficially true. But the fact that some people solve emotional problems with food — that’s genetic.
Clare Llewellyn, an associate professor at University College London, made a remarkable discovery about how the same genes behave very differently in different environments, which helps to explain this difference between Xand and me. She studies the heritability of obesity using twins and leads the Gemini twin study, one of the largest twin studies ever set up. Most of what we know about the varying influence of nature and nurture on obesity has been worked out in similar twin studies. They have shown that body-fat percentage is highly heritable — up to 90 per cent. But, depending on the group you study, heritability can also be as low as 30 per cent. What’s going on?
In a 2018 study of 925 twin pairs, Llewellyn and her colleagues found that in families with secure incomes and high levels of food security, the heritability of their body weight was around the 40 per cent mark. But in households with the lowest incomes and the highest levels of food insecurity it jumped to over 80 per cent. Being born into a lower-income household can double the risk of obesity. So, by alleviating (or more properly “curing”) poverty, especially childhood poverty, we could cut the risk of obesity in half without any other intervention.
We know that low-income households tend to eat more UPF: it’s cheap, it’s quick to prepare, children generally eat it readily and it lasts for a long time. It’s also regularly the only food that’s available and affordable. Almost a million people in the UK lack a fridge, almost 2 million people have no cooker, and almost 3 million lack a freezer. The price of energy is now so high that, even if people own the equipment, many can’t afford to run it. This makes UPF indispensable, and it will mean that if, like me, these people have genetic risk factors for weight gain, then those genes will be allowed to exert their effects. Llewellyn’s findings rightly shift much of the blame on to the more proximate cause of obesity: poverty.
Ultra-Processed People: Why Do We All Eat Stuff That Isn’t Food … and Why Can’t We Stop? by Chris van Tulleken