Most of us have heard the same advice for weight loss throughout our lives: exercise and make sure you’re eating the right foods, in the right amounts. But new scientific research could add a different dimension: the cellular activity in your body affects how much weight you lose, or how your body responds to certain foods.
At the Nestlé Institute of Health Sciences, our team is looking at weight loss on the molecular level: how does your body metabolise food? Why do some people lose weight more easily than others? Why do some people maintain weight loss, while others don’t? And why does weight loss help to prevent diabetes in some people, but not in others?
Why do some people lose weight more easily than others?
These are all important questions to move towards a more personalised way of looking at nutrition and health. Understanding the molecular variations from person to person means that the health community can provide solutions that really work, rather than trying to apply a one-size-fits-all approach.
We’ve been investing in research to help everyone better understand their unique metabolism and nutrition needs, in hopes of finding solutions that are more personalised. Here are three new learnings from our latest scientific research:
The little engines that can
Your cells contain mitochondria: think of these as the engines that power your cells. These mitochondria convert food into energy — and we don’t all have the same number of them. Young people who exercise a lot have hundreds of mitochondria in their cells, while older people or those who are inactive have far fewer and therefore less ‘power’ to produce energy from food.
We at Nestlé led a study in December 2016 together with the University of Lausanne and the École Polytechnique Fédérale de Lausanne in Switzerland to look at the effects of exercise on these cellular engines. We found something fascinating: exercise not only increases the number of mitochondria present in your cells, it also makes the energy-producing proteins that mitochondria contain cluster together. This means that exercise actually changes the process of turning food into energy and makes energy generation more efficient.
Why does this matter? As we look to create personalised nutritional solutions to capture the effects of exercise, we now know that increasing the number of mitochondria wouldn’t be enough. To be more efficient, we would have to help them make their proteins cluster, too — we’re basically trying to throw a mitochondrial party inside a cell and make the guests interact with each other!
A metabolic ‘Master-Switch’
Ok, we know it sounds a little crazy that there could be a real nutritional product that could mimic the effects of exercise. But it’s not as far-fetched as it sounds.
We’ve been researching the effects of an enzyme called AMPK, a kind of metabolic master-switch which helps your muscles turn glucose and fat into energy. AMPK alerts your body when you need more energy, like when you’re exercising. Our research teams have discovered that AMPK can be controlled — meaning there could be a way to work with the enzyme to bring more glucose from blood into muscle and increase the amount of fat turned into energy.
An innovation like this shouldn’t be an exercise replacement. But it could help people with chronic conditions such as obesity or type 2 diabetes who cannot work out regularly, or those recovering from an injury that limits their physical activity. If we can develop a product which boosts the effects of AMPK, it could give someone who goes for a brisk walk the metabolism-boosting effect of a 20-minute run or 40-minute bike ride. It’s a pretty exciting prospect for those struggling with chronic disease.
A different kind of fingerprint
Type 2 diabetes is also a high-potential area of research. For individuals who are pre-diabetic and overweight, losing weight is believed to prevent development of the disease. However, this is not always the case. The research community has never been sure why some people who lose weight successfully prevent the development of type 2 diabetes, while others develop the disease despite weight loss.
We undertook new research along with researchers from universities in Maastricht and Copenhagen that identified certain markers in blood — what we’re starting to think of as a ‘lipid fingerprint’ — that can start to differentiate between pre-diabetic people who are likely to respond to weight loss with better sugar control that may successfully prevent type 2 diabetes.
This fingerprint provides a so-called ‘biomarker’ that allows healthcare professionals to know which patients will or will not respond with better sugar control after weight loss. This can help them in choosing an individual nutritional path best suited to the patient’s situation. In other words, it could change the way we approach diagnosis and treatment for those at risk of developing diabetes.
What does it all mean?
Increasingly, we’re discovering that everyone’s body behaves in different ways. While there are basic approaches that we can all take to better our health, there is also room for discovery and improvement on a more personal level.
Our research is helping us to understand how personalised nutritional products could reshape the way we look at our health. Weight loss is just one part of that puzzle.