Angelo Tremblay on the Environmental Risk Factors for Obesity

Special Topic Interview, August 2010

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Angelo TremblaySW: How did that clinical trial come about and what did you find?

After the publication of the Jacqmain et al. paper, we had a collaboration with Wyeth Consumer Health Care. They agreed to sponsor a clinical trial in which obese woman were subjected to a 15-week weight-reducing program, supplemented either by a placebo or a Caltrate (calcium plus vitamin D) supplement.

What we showed, and what we published in 2007, was that the benefits of the weight-reducing program on blood lipids were significantly accentuated by the calcium plus vitamin D supplementation. We also saw, in agreement with our 2003 paper, that those subjects reporting an intake of less than 600 milligrams of calcium a day had much greater weight loss with the Caltrate supplementation than with the placebo—5.8 kilograms verses 1.4 kilograms. And much of this difference in weight loss and in fat loss was explained by variations in energy intake.

That clinical observation provided support to the idea of a calcium-specific appetite control mechanism that was described in 2001 by Michael Tordorf of the Monell Institute in Philadelphia. This is where we have been over the last decade. There's been some controversy, but so far our results have consistently supported Zemel's hypothesis.

SW: Your third-most-cited paper is also on short sleep duration. How did this idea come about and what have you found?

Once again, the story is not particularly new. When we were screening the literature, we found an epidemiological observation published in the early 1990s in the International Journal of Obesity that documented the relationship between short sleep duration and obesity. It gained credibility in 2004 when Eve Van Cauter and her group in Chicago published a paper maintaining that reduced sleep duration increased the concentration of plasma ghrelin, which in turn is known to increase food intake.

The opposite observation was seen for leptin. Sleep restriction decreased the plasma concentration of leptin and, not surprisingly, hunger levels increased. If you increase the concentration of an orexigenic hormone and decrease the concentration of an anorectic hormone, the expectation is that the subjects will naturally feel more hunger and this is exactly what they observed.

"...one major contribution of the Quebec Family Study has been its extensive documentation of environmental and genetic markers that predict the risk of obesity and the establishment, to some extent, of a hierarchy of their importance."

After we read this work, we analyzed the data from the Quebec En Forme Project—there is no English translation for this—and of the Quebec Family Study and we found greater fat mass level in short-duration sleepers. We also found that in both men and women of the Quebec Family Study, plasma leptin concentration in the short sleepers is significantly lower than what is predicted by their fat mass itself.

We later demonstrated that the risk of hypoglycemia is increased in short sleepers, and also in long-duration sleepers. We published this paper in Diabetologia in 2007 (Chaput JP, et al., "Association of sleep duration with type 2 diabetes and impaired glucose tolerance," 50: 2298-304, 2007) and, more recently, we published a paper in Sleep Medicine (Chaput JP, et al., "Sleep duration as a risk factor for the development of type 2 diabetes or impaired glucose tolerance: Analyses of the Quebec Family Study," 10: 919-24, 2009), reporting that short sleep duration increases the risk of developing glucose intolerance and/or diabetes over time, again using data of Quebec Family Study.

SW: What are you focusing on now in your research?

We're focusing now on mental work, on demanding cognitive effort and its impact on energy intake and some related hormones and substrate regulation. We published several papers on this work so far, although they haven't collected many citations yet.

We did have a tremendous journalistic impact with a paper we published in Psychosomatic Medicine in 2008 (Chaput JP, et al., "Glycemic instability and spontaneous energy intake: Association with knowledge-based work," 70: 797-804, 2008), but so far the scientific impact is not there. What we found is that demanding cognitive effort increases food intake and increases cortisolemia as well as glycemic instability, including the risk of mild hypoglycemia.

SW: Is this conclusion based solely on observational studies or are there clinical trial data as well?

We've done two short-term studies here at Laval University. The subjects were female students, and in each case the main finding was reproduced. We don't have long-term studies, but the short-term studies are quite convincing.

The idea is that mental work has the opposite effect of physical exercise on energy balance and energy intake. When you perform vigorous physical activity, you remain temporarily in negative energy balance even after you eat. When you perform vigorous mental activity—working on a computer in our studies—you end up in positive energy balance. You consume more calories than you expended doing the work.

Now we're working on laboratory studies that will help us better understand this effect. We're also trying to develop a concept of related cerebral aerobic fitness; the idea is that ultimately globalization might be more tolerable for those who are brilliant, those who have excellent cognitive capacities and so for whom mental work will be less demanding, with less damaging consequences on appetite control and energy intake.

This is all preliminary; we haven't done a lot of work on this yet, but it's become the main preoccupation of our laboratory.

Angelo Tremblay, MSc, Ph.D.
Department of Social and Preventive Medicine
Laval University
Quebec, Canada

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KEYWORDS: OBESITY, QUEBEC FAMILY STUDY, EPIDEMIOLOGY, GENETICS, PHENOTYPES, SUBPOPULATION, ENVIRONMENTAL FACTORS, SHORT SLEEP DURATION, DIETARY RESTRAINT, DIETARY DISINHIBITION, LOW CALCIUM INTAKE, LOW PHYSICAL ACTIVITY, LOW VITAMIN INTAKE, HIGH-FAT DIET, HIGH ALCOHOL CONSUMPTION, RISK PREDICTORS, DAIRY PRODUCTS, BLOOD LIPIDS, BODY FAT, WAIST CIRCUMFERENCE, QUEBEC EN FORME PROJECT, LEPTIN, HYPOGLYCEMIA, DIABETES, COGNITION, ENERGY INTAKE, HORMONE REGULATION.

Citing URL: http://sciencewatch.com//ana/st/obesity2/10augObes2Trem/

 
 

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