In 1995, Dr. Philipp Scherer discovered adiponectin, a hormone that circulates in the blood after being produced by fat cells. The UT Southwestern professor had essentially won the third leg of the Triple Crown of diabetes research. More than two decades later, he was awarded the 2017 EASD-Novo Nordisk Foundation Diabetes Prize for Excellence (which came with a cash award of close to $1 million) for his research explaining the relationship between body fat and Type 2 diabetes. We talked with him about what his research has taught him about the surprising nature of fat.
What does what you’ve learned say about our society? We are all genetically different. We all cope with this extra caloric load in different ways. Obesity, by itself, is not a negative thing. Many people who are overweight—in some instances morbidly obese—don’t have diabetes. That’s because they have fat tissue that copes very well with that expansion. They don’t need to have a lifestyle change because they don’t have any of the classic criteria we associate with obesity.
So some people can be obese yet healthy? You can go down the checklist. Do they have elevated blood pressure? No. Elevated inflammation? No. Elevated risk for cardiovascular disease? No. Diabetes? No. Kidney disease? No. They are just fine. You could say, “This is an official endorsement for obesity.” No, it isn’t. The percentage of people who can go through life like that is relatively small.
But what this tells us is we have to look at these individuals, whom we refer to as metabolically healthy obese individuals, and we have to learn from them what it is about their fat tissue that helps them preserve normal metabolic parameters in their system. Angry fat talks to other organs. It refuses to perform its functions, to take up these excess calories, and by doing that exerts a lot of negative impact on all these other organs.
Is your goal not to make fat go away, but to figure out a way to make angry fat less angry? Exactly, that’s the bottom line—happier fat. Whether we will ever be able to find a way to control our food intake effectively with a pill still remains to be seen. Eating makes us happy. We have to be wired that way, because we must eat to stay alive. Attempts to intervene with that axis—reward, eating, happiness—have frequently caused depression and not infrequently an increased rate of suicide. It is very complicated to get into that.
Where are we on the timeline of our understanding of these issues? This is basic research still. We are trying to understand the basic mechanisms behind unsolved medical mysteries. That includes how much we eat, when we stop eating, and what we do with the calories once they come in. By definition, the challenges have changed because we’re all hard-wired to eat as much as we can when we can. A couple thousand years ago we didn’t know when the next meal would come along. Now we live in this surplus. We have to learn how to cope with that—and how to build a better fat tissue.
There are surely people who say, “Aren’t we just throwing up our hands and giving up on the idea of ever being a healthy society again?” How do you respond? Some people will argue, “Why are we investing so much in how to cure diabetes and obesity? Wouldn’t it be simpler to take the fork away from those people?” The problem is it doesn’t work that way. We all know that. It takes incredible self-restraint to control your food intake over a prolonged period of time. It’s not about caloric needs. There are so many emotional needs. You’re under pressure. Everybody copes with that a different way.
We can say the brain is complicated—we are trying to understand the wiring—but we are still a long way away from being able to effectively intervene there. In the meantime, we are all eating way too much. Let’s think about what’s happening here and what organ we should think about to minimize the damage. That’s when we have to point to our fat tissue.
This story originally ran in the D Magazine Medical Directory.
