SInce the dawn of the 20th century, almost all weight loss guidelines have used calories as a simple measure of how much energy we consume from our food. But according to Giles Yeo, a research scientist at the University of Cambridge who studies the genetics of obesity, there is a problem: Not all calories are created equal. In his new book, Why Calories Don’t CountYeo explains that what really matters is not how many calories a particular food contains, but how that food is digested and absorbed by your body.
Can you explain why you think calorie counting is a flawed approach to weight loss?
There was an American chemist in the 19th century named Wilbur Olin Atwater who calculated the number of calories in different foods, calculating the total energy intake you get from them. But their calculations never took into account the energy our cells need to metabolize food in order to use it. This is important. That’s why, for example, a protein calorie makes you feel fuller than a fat calorie, because protein is more complex to metabolize. For every 100 calories of protein you eat, you only absorb 70.
Therefore, we must consider the type of food we eat, instead of looking only at caloric content. You could try consuming 800 calories a day, but how much energy your body actually absorbs will depend on whether you are eating sugar, celery, or steak.
How could people use this information in a practical way when trying to control your weight?
What really bothers me is when weight loss gurus say things like, “Oh, just replace the candy bar with a banana.” Of course, it is silly to say it, because sometimes life demands a banana and sometimes life demands a bar of chocolate.
But you can make a better practical decision in those situations by considering how the body processes food. It takes a lot longer to digest food items like protein and fiber, so you absorb fewer of those calories, so if you choose a chocolate bar with more nuts or dried fruit, that will make it a better chocolate bar.
Speaking of more nuanced approaches to weight management, recently, the body mass index has been criticized for being an inherently flawed measure of obesity. Is it still appropriate for doctors to use BMI?
I would define an obese person as someone who has too much fat, so it starts to influence their health. But then the question is, how much is too much fat? Your fat cells are like balloons, they get bigger when you gain weight, they shrink when you lose weight. But everyone’s fat cells expand and contract in different amounts, so each person has a different safe capacity to transport fat. It is famous that we East Asians cannot get too high a BMI before increasing our risk of diseases like type 2 diabetes, because we have a lower safe fat-carrying capacity.
BMI is very useful for looking at population trends as it can be measured for free and you only need your height and weight. But on an individual level, this is not useful for predicting health because it does not take into account genetic and ethnic differences in fat capacity. You could be a rugby player, or the same size as a rugby player, and be all fat and yet have the same BMI. That is why I believe that healthcare professionals should look at the whole, rather than just the BMI itself.
FDA semaglutide approval – the first new drug approved for obesity since 2014 – has made headlines this year. Is obesity something we should treat with medication?
I see it as part of the toolkit. Many people consider obesity a lifestyle disease; they perceive that being bigger than another person comes down to choice, when this is not the case. For many people, it is more difficult to say no to food simply because of genetics.
Semaglutide makes your brain think it’s a little fuller than it is, so you eat less, and if someone is having a hard time losing weight, why not use it? I’m not in favor of drugging the entire population, but I think semaglutide should be one of the tools we use, along with lifestyle intervention, exercise, all of those things.
You investigate genetic factors that control susceptibility to obesity. What do these genes do?
We now know that more than 1,000 genes are linked to obesity, and the vast majority of them influence pathways in three different parts of the brain that ultimately influence your eating behavior. One is the fuel sensor of the brain called the hypothalamus, then there is the part of the brain that detects how full you feel, and then there is the hedonic part of the brain that makes eating feel good. All of these regions communicate with each other, and some of these 1,000 genes influence these pathways. A mutation that makes your brain slightly insensitive to how full you are could influence how much you want to eat, making it harder to say no to temptations.
For example, we know that one in 330 people in the UK has mutations in a particular pathway called the leptin-melanocortin pathway, which makes their brain slightly less sensitive to the amount of fat they carry.
We will be able to use our genetic knowledge of obesity to develop new treatments that regulate the appetite?
Yes, there is now a drug called setmelanotide, which targets the leptin-melanocortin pathway. It has just been approved in the US for rare genetic causes of obesity, and the European Medicines Agency should approve it in a few weeks. Over time, it will be tested on a larger population, much like semaglutide, to see if it can trick your brain into thinking you have more fat and therefore end up eating less. This is an example of how understanding the basic biology of obesity, the wiring, the genes involved, can result in compelling and hopefully sustainable ways to approach it.
In his book, he mentions how obesity is not solely genetic, and factors such as socioeconomic status play a key role in determining how those genes are expressed and how much they matter.
The heritability of body weight, the percentage of the trait that depends on your genes, is a range that is between 40 and 70%.
A colleague of mine, Professor Clare Llewellyn from UCL, has a twin cohort called Gemini Study, where he analyzed the role of socioeconomic status on body weight. She has shown that if middle class families are taken, the heritability of their body weight is approximately 40%. But if you go to the households with the lowest socioeconomic class and the highest levels of food insecurity, it suddenly jumps to 70%.
Genetically, there is no difference between the poorest and the richest people: it is an accident of birth. But due to your socioeconomic status, your risk of obesity can go from 40% to 70%. It shows that if we can cure poverty, child poverty in particular, we can reduce the inherited risk of obesity from 70% to 40% without even touching the biology of the system.
The exercise has had a bad reputation for its weight loss powers. Is that really deserved? You run a lot – do you run to keep fit or for other reasons?
By itself, exercise is not effective for weight loss. In principle, it is possible to lose weight through exercise: Tour de France cyclists consume at least 5,000 calories a day and still lose weight during the three weeks of racing. The problem is that most of us mere mortals don’t exercise close enough for this to be effective. However, it is helpful in maintaining weight after weight loss has been achieved. So I stay active on my bike and running, to stay in shape, but also to maintain my weight.
George is Digismak’s reported cum editor with 13 years of experience in Journalism