Today’s sessions of the Obesity Society’s annual scientific meeting covered a lot of ground. I think the most interesting was the session on the relationship of cancer and obesity organized by Ruth Ballard-Barash of the National Cancer Institute and Ted Adams of the University of Utah School of Medicine. Christine Friedenreich, Ph.D. of the Alberta Health Services presented a comprehensive overview of the association between specific cancers and obesity, reviewing the published literature for each cancer. At the end, she proposed that obesity was responsible for about 20% of all cancers. If (in an ideal world) obesity levels could be resolved to normal BMIs, she speculated 1.6 million deaths due to cancer could be saved, 2.2 million new cancer cases could be avoided and we could avoid having 5 million persons living with cancer.
Other key presentations addressed the powerful influence of sleep and circadian rhythms, or the lack thereof, on rising rates of obesity. This led one presenter to suggest that we should have our biggest meals at breakfast and gradually reduce caloric input throughout the day to a light salad at dinner. Rena Wing reported on the 4 year results of the Look Ahead Trial which provided persuasive information for intensive lifestyle counseling over less intensive interventions in reductions in body fat and related metabolic indicators.
Sometimes these meetings morph into abstract, perhaps irrelevant, discussions of minutia among researchers. At other times, you feel you are witnessing an emerging new insight into obesity and its effects. So it was today in a session, Is There Good and Bad Body Fat? chaired by Richard Bergman, editor of Obesity, and including prominent researchers, Tamara Harris, Michael Jensen (who readers may remember from our conference at the 2008 Republican National Convention) and Sam Klein. Their task was to unravel which fat was bad and which was good. Their presentations covered detailed, precise research into these tangled issues. Why are there some obese individuals who were, nevertheless, metabolically normal? Why did bariatric surgery resolve diabetes in some cases but not others? Why does weight loss resolve some metabolic disorders but not others? For many in the audience, these are the cutting edge questions – today – to understand the metabolic sequela of weight gain, insulin resistance, diabetes and cardiovascular disease. The presenters provided exciting new data interspersed with a camaraderie and jocularity which is the realm of highly accomplished and competitive scientists who admire each other’s works but are not going to give them an inch. Bottom line: adipose cell build up in the liver may explain many of the inconsistencies in present views of the obesity-insulin resistance-metabolic disorders axis. But, build up of adipose cell in the liver is hard to measure given today’s technology and bio-statistical resources. On the other hand, there may well be another factor, not yet identified (kind of like dark matter in astrophysics), which modulates the effects of obesity, insulin resistance and metabolic disorders. The large, enthusiastic audience no doubt left with many possible research proposals in mind to unravel this conundrum. Stay tuned, as they say, “we wait with bated breath,” for the next insight.