Highlights of the North American Association for the Study of Obesity 2005 Annual Scientific Meeting

October 15-19, 2005; Vancouver, British Columbia, Canada

Sachiko T. St. Jeor, PhD, RD; Raymond A. Plodkowski, MD


May 30, 2006

In This Article

Key Lectures and Symposia

The conference was organized into 4 tracks: cell and molecular biology, integrative biology, clinical studies, and population studies.

The theme of energy homeostasis and the role of various hormones produced and/or regulated by adipose tissue acting on the central nervous system were especially interesting. Emphasis was placed on how the quantity and location of adipocytes can signal brain behavior to regulate feeding and target the liver to regulate glucose metabolism. In addition to insulin and leptin, increasing attention is being devoted to the action of adiponectin, as discussed by Rexford S. Ahima, MD, PhD,[12] University of Pennsylvania, Philadelphia, and sex hormones, as presented by Deborah Clegg, PhD,[13] University of Cincinnati, Ohio.

Dr. Ahima outlined the role of adiponectin, a highly complex, large polypeptide produced by the mature adipocyte, as inversely related to glucose and induced by severe (not acute) weight losses in animals. Unlike leptin, adiponectin does not appear to inhibit feeding, and it works on the muscle to enhance glucose uptake and on the liver to blunt gluconeogenesis. A major effect of adiponectin is through thermogenesis by rapidly increasing O2 uptake, as measured by indirect calorimetry.

The potentially beneficial combined effects of adiponectin and leptin were suggested. Apparently, adiponectin does not affect sex hormones. Dr. Clegg presented studies that outlined the differential effects of gonadal steroids in determining fat distribution by differing adiposity signals. Major sex differences in fat deposition and regulation in women are influenced by leptin, which acts on the subcutaneous fat or smaller adipocytes in women and through insulin in the visceral fat or larger adipocytes in men. The phenomenon induced by menopause (decreased estrogen) on increasing fat in the viscera was discussed. The sensitivity of the brain to adiposity signals differs between men and women, and partially explains differences in the regulation of energy expenditure, body weight, and body fat distribution.

Taste as the gatekeeper of food intake was an interesting theme addressed in a series of talks. Robert Margoskee, MD, PhD,[14] Mount Sinai School of Medicine, New York, NY, discussed the role of taste transduction, perception, and regulation by the gut. The physiology of the tongue in conveying 5 primary taste-quality receptors and channels (salty, sour, umami, sweet, and bitter) tells us little about nutrient sensing in the gut and how taste is regulated and controlled. Although these taste transduction molecules do underlie mechanisms of nutrient sensing in the gut, we need to better understand how physiologic effects depend on these taste elements and how the release of enteroendocrine hormones is induced and regulated. An important question to ask is, "what are the specific chemosensory stimuli, and how are appetite and food intake affected?[14]"

David V. Smith, PhD,[15] University of Tennessee, Memphis, discussed the neural processing of taste through the central nervous system, and suggested that how taste information is processed provides information in regard to what may be ingested. In other words, stimuli evoke recognized sensations and may induce particular eating preferences.

Finally, Danielle Reed, PhD,[16] Monell Chemical Senses Center, Philadelphia, Pennsylvania, suggested that people have different perceptions of taste due to specific genotypes. She presented examples of how specific conditions may have genetic influences and may affect preferences for sweet and bitter tastes and create phenotypic behaviors that can predict overall taste and food-intake behaviors.

Other signals emanating from the gastrointestinal tract are complex and affect the regulation of food intake. For example, André Bado, PhD,[17] Institut National de la Santé et de la Recherche Médicale, Paris, France, who is credited with the discovery of gastric leptin, pointed out that gastric leptin has a key role in energy homeostasis and food-intake regulation in controlling meal frequency and meal size. This is effected through a combination of digestive processes in the stomach and intestine, circulating fuels (glucose, free fatty acids, and protein), and fuel stores (fat, muscle, and carbohydrate). Leptin apparently reduces meal size by vagal-dependent mechanisms and can enhance satiation. Cholecystokinin and leptin have synergistic actions to activate vagal afferents and reduce food intake.

A symposium focusing on behavioral strategies brought together 3 speakers. Matthew Clark, PhD,[18] Mayo Clinic, Rochester, Minnesota, discussed the transtheoretical model of behavior change; Delia West, PhD,[19] University of Arkansas, Little Rock, discussed motivational interviewing; and Thomas Wadden, PhD,[20] University of Pennsylvania, Philadelphia, discussed cognitive behavioral treatments.

It was interesting to note how these concepts interface with and build on one another. The 4 components of the transtheoretical model are stages of change, processes of change, decisional balance, and self-efficacy.[21] By adding motivational interviewing to this model, patients can be more effectively directed toward change, resulting in significantly greater weight loss with directional client-centered counseling. Counselors are trained to use techniques, such as reflective listening, eliciting "change talk," and using summary statements and the 5 principles of motivational interviewing (expressing empathy, developing discrepancy, avoiding argumentation, rolling with resistance, and supporting self-efficacy). Eating self-efficacy and exercise self-efficacy can be easily assessed and can guide individual treatment plans.[22,23]

Cognitive behavioral treatment, however, is still recognized as the foundation of behavior therapy. Analyzing the antecedents, behaviors, and consequences (ABC) model and understanding behaviors according to who, where, what, and how they occur are essential in developing effective interventions. Cognitive behavioral treatment enhanced by motivational interviewing and the basics of the transtheoretical model has proven to be most effective in the treatment of obesity.

The physical activity literature was presented by the leading expert in this area, Steven N. Blair, PED,[24] The Cooper Institute, Dallas, Texas, who reiterated the importance of increasing physical activity at any level. Low cardiorespiratory fitness was emphasized as a major predictor of chronic disease and decreased longevity in essentially all subgroups of the population. Musculoskeletal strength and fitness was also revisited and emphasized to delay mortality.

The US Department of Agriculture (USDA) My Pyramid Food Guidance System was discussed by Patricia Britten, PhD, USDA Center for Nutrition, Policy, and Promotion, Alexandria, Virginia; and Catherine Champagne, PhD, RD, Louisiana State University, Baton Rouge, Louisiana.[25] On the basis of the dietary guidelines, recommendations with regard to how to achieve different caloric levels are outlined with the various basic food groups and recommendations for physical activity. The inclusion of "discretionary calories" at each calorie level allows choices from added oils, fats, sugar, and/or alcohol in the diet. This food guidance system has new implications for messages to the public. The system emphasizes nutrient-rich food choices from the basic food groups, and the concept of nutrient density for choices that count as discretionary calories.

A newer area of discussion was the role of sleep deprivation in obesity.[26] It was no surprise that 9 studies (6 longitudinal and 3 cross-sectional) provided evidence that children who sleep < 10 hours/day were at higher risk for obesity, and those who slept < 8 hours were approximately 3 times more likely to become obese. Data suggested that adults who averaged < 7 hours sleep/night were more overweight.

This track emphasized public health, epidemiology, and population genetics. An important update on deaths attributable to obesity was presented by Katherine Flegal, PhD,[27] US Centers for Disease Control and Prevention, Hyattsville, Maryland. The health consequences of the obesity epidemic were not a new concept to conference attendees, but the struggle to understand its causes and how to address treatment and prevention issues remains critical. A new way to look at weight as a risk factor was presented, in consideration of weight as a physiologic variable. Weight should be considered a complex outcome that cannot be reduced to zero, such as a toxic substance, or eliminated as some behaviors, such as smoking. It is important to note that the association of weight with mortality differs for different causes of death. In some cases, a higher weight may be associated with improved survival in some circumstances.

The improved treatment outcomes for obesity should also be reflected in greater economic benefits and health outcomes for employers. William Dietz, MD, PhD,[28] US Centers for Disease Control and Prevention, Atlanta, Georgia, asked what the effects of obesity on productivity are, and what strategies show the greatest promise for improvements. Additionally, questions about the cost of childhood-onset obesity should be studied further.

Overall, the future for the prevention and treatment of obesity looks promising, and significant progress is being made in understanding the contributions of specific food items, such as sweetened beverages, without displacement of other foods or calories, as discussed in a debate between Barry Popkin, PhD, University of North Carolina, Chapel Hill, and Richard Forshee, PhD, Center for Food and Nutrition Policy, Alexandria, Virginia.[29] This debate focused on whether there is sufficient scientific evidence to recommend limiting or omitting sweetened beverages because of the consequence of increased weight. Dr. Popkin pointed out that a calorie is not a calorie and that beverages add significantly to overall intake, especially because beverages are not satiating and do not affect the rest of the dietary intake at the same meal. He recommended no caloric sweetened beverages and no more than 10% of energy from beverages overall. Dr. Forshee, on the other hand, debated that to focus on one food item, such as caloric beverages, would be a poor use of limited resources, and we may reduce credibility if it is later found that that there is no major impact on reducing overall weight. He pointed out that the diet is complex and the total diet (not 1 food) should be considered. Both speakers made good points, and the main consideration was targeted toward how best to make population changes. Understanding eating patterns, food choices, and trends will certainly help us develop meaningful strategies to help populations at risk.


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