Cecilia Lindgren, obesity expert: ‘An excess of 100 calories a day is enough to gain 4.5 kilos a year’

The director of the Big Data Institute at Oxford University sheds light on the genetic roots of surplus weight and combats ‘the misconception that obese people overeat’

Cecilia Lindgren Obesidad
Cecilia Lindgren, director of the Big Data Institute at Oxford University (UK).Universidad de Oxford
Manuel Ansede

Geneticist Cecilia Lindgren says that every time she gives a talk on obesity, someone in the audience raises their hand to suggest that the solution is easy: eat less. This individual will typically add a derogatory remark about how fat people are simply lazy and lack the willpower to not gorge on junk food. Lindgren, director of the Big Data Institute at the University of Oxford, UK, scoffs at this idea. Her team has identified a multitude of genetic variants associated with a greater predisposition to store fat in different parts of the body. Added to other environmental factors, these genes can determine the appearance of “love handles” or a “beer belly,” explains Lindgren, who was born in Gothenburg, Sweden. The 48-year-old geneticist traveled to Reykjavík, Iceland, on May 19 to give a talk at the headquarters of the local company deCODE Genetics, which EL PAÍS attended at the invitation of the parent company, the American pharmaceutical Amgen.

Question. You insist that obesity is not the result of a lack of will.

Answer. It is not.

P. It's not a choice either.

A. No. I don’t think anyone would choose to be obese. Genetic studies tell us that obesity is regulated by feelings of satiety and hunger, and we live in an environment with a caloric surplus. If you are hungry and don’t fill up when you eat, you are going to eat a little more all the time. There is a misconception that obese people just sit back and gorge themselves. There are always photos of very large people eating five McDonald’s hamburgers, but the truth is that if you eat an excess of about 100 calories a day, you will gain 4.5 kilos in a year. It doesn’t sound like much, but if you do that every year, you suddenly are going to become really large.

Q. How many genetic variants are associated with obesity?

A. Currently we know about 3,000.

Q. So there is no such thing as an obesity gene.

A. No, there is not just one. Stephen O’Rahilly, from the University of Cambridge, has investigated diseases caused by one or two serious mutations in a gene, diseases in which patients cannot stop eating. It is called hyperphagia and is due to the disruption of the neuroendocrine regulation of satiety and hunger. And this is what we have seen in common variants, although not in such a brutal way. In my team we found two genetic variants that have 6,400 carriers roughly in the UK, and each variant gives between seven and 10 kilograms excess body weight in an adult.

Q. It's a lot.

A. We are talking about a great effect on many people. You’re not a victim to your DNA, that’s really important. You’re born with the predisposition. But it is really important for these people to get that information and knowledge about why they struggle to maintain body weight.

We found two genetic variants and each variant gives between seven and 10 kilograms excess body weight in an adult

Q. In your field you talk about the obesogenic environment. What is that exactly?

A. An obesogenic environment is one in which there is food everywhere and at all times. It’s unhealthy food and it’s always close at hand, which means if you’re hungry, you just eat more. In the 1960s there was alcohol and tobacco on the tables in the rooms. Today we would never do that, because we know it is wrong. In the 2000s there were nacho chips and bagels on the tables. Now people are more conscientious about this and there is more fruit and mineral water. But people are starting to understand that you don’t have to have food everywhere and at all times.

Q. Is eating 500 calories of bananas the same as eating 500 calories of ice cream?

A. There is a great scientist in Cambridge, Giles Yeo, who has written a book called Why Calories Don’t Count. I don’t believe that fully, but you’re right that if you put 500 calories of bananas on one plate and 500 calories of ice cream on another plate, the bananas would weigh about five times as much as the ice cream. If you eat all those bananas, you’re going to be full for a much longer time. If you eat 500 calories of ice cream, you’ll be hungry again an hour later, because it is very high in calories, but it does not fill you up. In food, the weight, the amount of fiber, the consistency also matter...

Q. As the rich kids get thinner, the poor kids get fatter. Is the gap in childhood obesity growing?

A. It’s different in different countries. The reason I’m concerned about childhood obesity is because if you are obese as a child, as an adult it’s unlikely that you will be able to break the cycle and become slim. And there is discrimination against overweight and obese people: 24% of healthcare workers think that obese people are less deserving of treatment for various conditions. And 24% of teachers believe that obese children are dumber, so they give them poorer grades, no matter their performance.

Twenty-four percent of teachers believe obese children are dumber, so they give them poorer grades

Q. You have said that body mass index plays an important role in socioeconomic status.

A. Yes, there is a strong correlation between socioeconomic status and body mass index for a range of reasons. Poor children are more likely to be obese. Poor people often struggle with access to the right food. It is very expensive to buy cereals, fruits and vegetables, compared to buying high-calorie food.

Q. If you have a low income, you are more likely to be obese. And if you’re obese, you’re more likely to be low-income.

A. I would be careful about a causation and say instead that there is a correlation, not that one variable is the cause of the other.

Q. A study with 120,000 participants in the United Kingdom, published in 2016, stated that overweight people, especially women, are at a disadvantage; and that tall people, especially men, have an advantage.

A. Yes, but it is a correlation, it does not imply that one variable is the cause of the other.

Q. You defend that obesity is “a brain condition.”

A. It is a condition that is largely regulated through the brain.

Q. It's in our brains and in our pockets, because it also depends on whether you have more or less money.

A. Yes, the question is what dictates that this be so. Obviously, if you’re rich, you can go to a fancy gym and you can afford to buy all kinds of healthy foods, so it’s going to be easier to be healthier. And education also plays a role, whether children have parents who talk to them about the importance of taking care of their health.

Q. You have stated that 10% of the population is not at risk of serious obesity.

A. People with a high predisposition to obesity, with all the genetic variants, could weigh about 20 kilos more than another person of the same age, sex and height. But there are other people who are lucky in that lottery and are not at risk of obesity: they have a predisposition not to be hungry.

Q. With all this genetic information about obesity, is it possible to develop effective drugs? Or is it impossible with 3,000 genetic variants involved?

A. I am excited because there is one drug on the market now that helps people lose up to 15% of their body weight [semaglutide, related to the GLP-1 gene] and there is another drug called setmelanotide which is targeted to a pathway regulating hunger and satiety that Stephen O’Rahilly and I found in common types of obesity and in conditions caused by single-gene mutations. This drug is going to be extremely important. There is research by Karine Clément [an obesity expert at La Sorbonne in Paris] and other French colleagues where they followed people who lost between 12% and 15% of body weight in a few weeks with this drug. So we will get to the point where we have drugs although not every drug will not work for every person, but we need more drugs for different scenarios. The obesity field is far behind other areas where there are better treatments, but it’s really showing you the effect it can have to take a tablet. It doesn’t mean that we should then go and eat chips and say ‘Hey, I don’t have to worry about it anymore!’ because it will only modify so much. But it does mean that if you take a tablet, you can control it and get help, which is amazing.

It is important that obesity is treated as a disease, so that people take it seriously

Q. What is the role of the food industry in the obesity epidemic? Do you think it's like the tobacco industry?

A. I believe that food consumed in the right way and right amount and at the right time is not dangerous. Tobacco, on the other hand, is dangerous even if you smoke moderately. I believe that the food industry must play a role in the discussion [in the fight against the obesity epidemic], especially when it comes to declaring its ingredients. Many governments are working to make labels simpler so that people can understand what foods are healthy. So it’s a societal interplay.

Q. Is obesity a disease?

A. According to the World Health Organization (WHO), yes it is. I think it is important that it be treated as a disease, so that people take it seriously, because it is affecting people and also the economy.

Q. In Spain it emerged in 2018 that Coca-Cola had paid €8 million to medical and scientific associations. What do you think about the food industry putting money into science?

A. We have talked about this in my institute and it is a very difficult question. External companies should not fund research and have a say in the outcome. No company can pay me to say that their product is great, because that’s advertising, not science. If they want to fund my research and I find that their product has a harmful effect, I should be able to publish it. I should also post it if I don’t see any effect or even if it has a positive effect of course. Science has to be critical and free.

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