“If an individual is subjected to low temperatures, the brown adipose system is activated, there is an increase in thermogenesis, energy dissipation, improvement in weight and even diabetes. But now, we are almost no longer exposed to the cold”

Paula Freitas, 57 years old, knows a lot about obesity, as she has struggled with its complexity since choosing the specialty of endocrinology, a branch of biology and medicine that deals with the endocrine system and its diseases, often caused by hormonal disorders . She combines her work as an endocrinologist at the Integrated Obesity Responsibility Center of the São João Local Health Unit and as a teacher at the Faculty of Medicine of the University of Porto. And, since February, she assumed the presidency of the Portuguese Society of Endocrinology, Diabetes and Metabolism, a position she will maintain for the next three years.

Portugal was a pioneer in declaring obesity as a disease 20 years ago. But the numbers keep growing. What needs to be done to reverse them?
We need to know the disease better. Most people and healthcare professionals are still not aware of its complexity. Obesity is a chronic, complex, relapsing disease. Today, we know that 70% of weight is genetically programmed. And we also know something else: obesity is a collision between genetic heritage and the environment in which we live. In other words, there are people who, regardless of the environment they are in, will never be obese. Others have a set of genes that make them more likely to have obesity and forms of severe obesity.

Where are we?
We are at a turning point. If a few years ago we had practically no treatment for the disease, today there are very effective drugs. We need people to have access to them.

But, in Portugal, these medicines are not reimbursed.
And we know that obesity is much more prevalent in lower social classes. A study recently came out showing that these drugs reduce mortality by 20 percent. We have to ask to what extent it is immoral and unethical not to treat patients with severe forms of obesity. It is also necessary to provide even better accessibility to surgical treatment.

This, yes, is reimbursed by the National Health Service.
With some limitations, which have to do with waiting lists, but, yes, people have access to surgeries.

Wouldn’t it be better to reimburse the drugs first, to avoid reaching that point, with much more risks for the patient and costs for the State?
You’re right. Probably, if we treated at an earlier stage, some patients would not end up undergoing surgery.

And how is it treated?
To the guidelines that determine how to treat obesity have changed. We are still very focused on diet and exercise as solutions to obesity. They are very important, but treatment must essentially be based on three fundamental pillars: behavioral intervention, pharmacological intervention and surgical intervention.

Do these interventions happen in phases?
Yes, because people may need one of the pillars or more than one throughout their lives.

If it goes well, could they not make it past the first level?
When people are being treated from a psychological perspective, with behavioral intervention, they will comply more correctly with their diet and exercise prescriptions. The ideal would be to have good prevention plans for those who do not yet have the disease. These plans should begin even before people were born, working with women, before they become pregnant.

What would these prevention plans consist of?
Prevention has to do with health literacy, making more information available, teaching people how to make correct food choices and encouraging regular physical exercise.

But this has already been done over the years. It seems that the message is not getting through…
This is why obesity is so complex, as it has to do with our food choices, which are also determined by availability. That is why what the food industry gives us to eat will have an impact on them, which is defined by the agricultural policies themselves. And they are impacted by something else: endocrine disruptors, which are everywhere.

Give us examples.
Pollution from microplastics in the ocean, pesticides, paints, the plastics we use…

Do they increase our predisposition to obesity?
No. Endocrine disruptors are associated with the activation of cells that will become adipocytes, that is, they will increase our number of adipocytes, which are fat cells.

How do we act in this obesogenic environment, which goes far beyond medicine? Do architects have to think about this too?
Also. The architecture of cities has an impact on obesity.

In what way?
For example, if a building has interior stairs, which are unattractive, fewer people use them. The number of equipment a city has for physical exercise and green spaces are also good indicators.

In this aspect, we have improved a lot. Does not agree?
We have improved a lot, but there is also another dimension, which is the global world, where, for example, the impact of advertising is enormous. Often, products are sold with a healthy label, but they are not. Then, there is a whole health literacy route that needs to be worked on.

But do people generally read labels, for example?
In fact, reading labels is essential, and the nutritional traffic light has improved this information, showing what healthy eating is. But then there is another problem: there are many people who have all the knowledge, but when the time comes to choose, they don’t make the right choices.

What is the reason for this phenomenon?
Today, we know that the regulation of appetite and satiety has three levels. The first, which we call homeostatic control, that is, what I need to eat until I feel a certain amount of satiety. This is regulated by hormones, many of which come from the gastrointestinal tract, which act on my central nervous system, telling me when I have to stop eating.

That feeling of satiety…
Then there is another aspect, which is eating for pleasure. It is associated with a different part of the brain: the mesolimbic system. In other words, I may be full, but I continue to eat more than what I need to feel good. Often, I can have a binge: despite eating, I continue to eat because I’m not satisfied. It is an emotional hunger, in which I need to feed myself to combat any adverse event in life. This compulsion is closely associated with stress, anxiety and nervousness.

And there is still a third dimension, related to appetite regulation.
It’s the cognitive aspect. I can decide, at any given moment, what I eat or not eat. Then, psychology must intervene, to give people tools to…

Go shopping?
To make your choices. It is very curious that even children, when asked what is healthier to eat for dessert, a piece of fruit or a sweet, most of them respond that the healthiest is a piece of fruit. In the next question, “what do you eat?”, the child says he eats candy.

Often, we know what is right, but we don’t put it into practice. And that?
It is difficult to achieve in a society where food is available day and night. There is a very funny study that shows that an American can always be eating things with more than four kilocalories. And, therefore, they no longer had those formal meals: breakfast, lunch, snack and dinner. And there are other theories, such as those related to the intestinal microbiota, pollution, light and even the possibility of global warming itself interfering in this process. In winter, we are always in air-conditioned environments, we don’t even activate brown adipose tissue – when it is activated, it causes energy to be consumed.

Does this thermogenesis only activate when we are cold or also when we feel hot?
Only with the cold. Some experiments have proven that, if an individual is subjected to low temperatures, the brown adipose system is activated, there is an increase in thermogenesis, energy dissipation, weight improvement and even diabetes. But now, we are hardly exposed to the cold anymore. We live in a highly obesogenic environment, where there is enormous food availability and a sedentary lifestyle in the way we work and have fun.

Even the school is very sedentary.
This is one of the problems of childhood obesity, combined with the fact that children are exposed to a very large number of hours of screen time. At the beginning of Man’s evolution, we had a lot of activity and ate little. It was a gene, called sparing, that made it possible to survive in an environment of scarcity. The people who had this gene were the ones who survived.

Something that, I imagine, doesn’t work well in the world of abundance.
Anyone who has this gene is currently at an adaptive disadvantage.

What percentage of people have this gene?
That’s one way of saying it. What we know is that there are more than 240 genes that make people more likely to have severe obesity, different types of obesity and different types of metabolic changes.

Can we talk about slow and fast metabolism?
There is a study from the Mayo Clinic [nos EUA] to identify the phenotype of individuals who need to eat more to stay full (so-called emotional hunger) and a group they called slow burn (people who have a slower metabolism, because even when they exercise, their energy expenditure is lower). Probably the big problem is that we are still treating all obesity more or less equally. The future – they, at Mayo, already have scientific work in this direction – will be to give medication according to the individual’s phenotype, even if there are those who may have more than one, making everything more difficult.

Is it possible to speed up metabolism?
Exercise does that. The more muscle mass we have, the more we can accelerate it. There is research for exactly this purpose – a monoclonal antibody to alter metabolism, lose weight and increase muscle mass. But it is still under study.