Jean-Pierre Després on the Role of Visceral Fat in Metabolic Syndrome
Special Topic of Metabolic Syndrome Interview, December 2011
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On the other hand, there are individuals like myself, if I ever stop being physically active—say I'm recovering from an injury—I will gain a couple of kilograms, remain in the normal range of BMI, but I'll put on visceral/ectopic fat and the consequence is trouble. I've done CT scans on myself, and this is what happens. When you look at my lab exams, my triglycerides are high, my HDL is low, my blood sugar is drifting up, my blood pressure is going up—I have all the features of the metabolic syndrome, but I'm a skinny guy. And the reason is I'm putting on fat at the wrong place.
It seems like one of your key points is that BMI is not what we should be measuring, or at least not the important variable, when it comes to weight?
Exactly. The problem is that the current guidelines we have to define obesity, and that has been for the last 20 years, look only at BMI. If I can humbly say, this has been my crusade: there's nothing wrong with BMI but we have to go beyond that. Particularly in the overweight range, from BMI 25 to 30, a lot of middle-aged men will be misclassified on their risk if we only use BMI.
Have you demonstrated with intervention trials that reducing visceral obesity reduces metabolic syndrome?
We just did a study with 144 viscerally obese men, and we've reported those results at several meetings over the last year. These gentlemen would come to our lab once a month, to meet a dietitian and an exercise physiologist on a one-to-one basis. The idea was to reshape their lifestyle what you might call a la carte. Let's see what you like, what you want to do, in terms of food and physical activity. Over one year, they lost weight and maintained the weight loss after three years, but more importantly we found a disconnect between the magnitude of weight loss and the loss of visceral fat.
I'll give you an example that's very easy to understand. We found that some of those individuals actually gained some muscle mass and lost some visceral fat. So on the BMI scale, the change was sometimes quite trivial, but they would lose quite a bit of visceral fat. Their triglycerides would go down; their HDL would go up and their glucose tolerance would improve. So the message is that if you're going to pay attention to your cardiometabolic health you should pay attention to how much abdominal fat you have. A simple test is to measure your waist circumference.
Another very important marker that is associated with too much ectopic fat is triglyceride levels. The combination of an elevated waist line and elevated triglycerides is associated with a very high probability—between 75-80%—of having too much fat stored in the wrong place and with features of the metabolic syndrome.
Are all lean people with metabolic syndrome going to turn out to have visceral adiposity, even if their waistlines are relatively small?
They could certainly be an apparently skinny J.P. Després with a lot of ectopic fat—that's exactly my point. What I'm saying is if you have really skinny people—people who don't have ectopic fat—there might be some with metabolic syndrome, but less than 1%. Most, I'm not saying all, but by far most, individuals with the metabolic syndrome have fat stored in the wrong place, irrespective of their BMI. If you want to capture my work in one sentence it would be that.
"I cannot emphasize enough that there's a huge gap between what we know and what we do—we don't apply what we know already in clinical practice and that's the problem."
What are you working on now? What would you say is the most important research you're doing today?
A couple of things. We're interested in the respective contribution of those ectopic fat depots. I'm convinced visceral fat is a very good marker. Whether this is the culprit depot responsible for the complications, I'm still skeptical. So we want to do two things. One is intervention studies. Take viscerally obese individuals; measure all the ectopic fat depots. We want to exercise train them and for a long time—not just for a couple of months but for the long term.
We want to mobilize those ectopic fat depots. What kind of volume of physical activity/exercise do we need? And we want to sort out in a dynamic system, when you intervene, what really matters. Is it the mobilization of liver fat, heart fat, visceral fat, intramuscular fat? That's a big issue right now.
We're also doing studies to try to sort out what is presently a big mess in the literature. Some people will tell you that metabolic syndrome is all about liver fat. Others will say it's all about heart fat, or it's all about visceral fat. I think that the relative contribution of these ectopic fat depots may differ, depending upon the metabolic system involved and the specific complication—heart failure, for instance, arrhythmia, diabetes, coronary heart disease, or hypertension. That should keep me busy for another 25 years.
If you lived in an ideal world and had unlimited research funds, what one experiment would you do now that you can't afford to do in the real world?
It is, again, just to do a large randomized trial to show that with regular support from a dietitian, from a kinesthesiologist, from a behavior expert, that we can reduce cardiovascular disease. We know that we can do that with type 2 diabetes. It's already been shown that if you just lose four kilograms (10 pounds) you can reduce your risk of developing type 2 diabetes by almost 60%. Those are spectacular results.
But now we have to do the same thing and show that we can prevent cardiovascular disease. We need to take patients with abdominal obesity and the features of metabolic syndrome. We need to confirm that they really do have those features, that they have ectopic fat. Then we have to intervene and show that through the mobilization of this ectopic fat we can prevent clinical events.
It's amazing that we went to the moon—you went to the moon in the US—40 years ago, and we still don't have the answer to a very, very simple question: does improving lifestyle habits in sedentary, abdominally obese patients with the features of metabolic syndrome reduce the risk of developing cardiovascular disease or death? We don't have an answer to such a simple question.
Is there anything you'd like to add to what we've discussed?
Yes, that I've been privileged to be working in a very good team; it's a good lab, a good environment with fantastic colleagues. We have tremendous support from our university as well as from our hospital and its research center. From a scientific standpoint, it's been very enjoyable. But I cannot emphasize enough that there's a huge gap between what we know and what we do—we don't apply what we know already in clinical practice and that's the problem.
Jean-Pierre Després, Ph.D.
Research Centre
Institut universitaire de cardiologie et de pneumologie de
Québec
Department of Kinesiology, Faculty of Medicine
Université Laval
Québec, Canada
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JEAN-PIERRE DESPRÉS'S MOST CURRENT MOST-CITED PAPER IN ESSENTIAL SCIENCE INDICATORS:
Després JP, et al., "Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia," N. Engl. J. Med. 353(20): 2121-34, 17 November 2005 with 616 cites. Source: Essential Science Indicators from Clarivate.
KEYWORDS: METABOLIC SYNDROME, ABDOMINAL OBESITY, VISCERAL ADIPOSITY, HEART DISEASE, KINESTHESIOLOGY, ADIPOSE TISSUE, FAT METABOLISM, BMI, MARATHON RUNNERS, LIPOPROTEINS, CHOLESTEROL, WAIST AND HIP CIRCUMFERENCE, CT SCAN, INSULIN RESISTANCE, DYSLIPIDEMIA, INFLAMMATION, LIVER, INSULIN, FREE FATTY ACIDS, TRIGLYCERIDES, VLDL, CYTOKINES, ADIPONECTIN, SUBCUTANEOUS FAT, ECTOPIC FAT.
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