written by Sarah Howard
Coordinator of the Diabetes and Obesity Spectrum Working Group
Over the past 4 days there have been two IOM workshop meetings on obesity; here’s a brief update.
The first was last Thursday/Friday on developmental exposures and obesity (mostly nutrition), and the second was Monday/Tuesday on the environment and obesity (at NIEHS). The slides and presentations of these workshops will be posted online. I would recommend these talks, they were all very informative.
Exposures to a wide variety of environmental factors—from chemicals to lack of sleep to microbiome to inflammation to viruses to antibiotics to nutrition to famine to maternal BMI to hormones to paternal factors to beta cell hypersecretion to artificial sweeteners to fructose—are linked to a higher (or sometimes lower) risk of obesity later in life, especially if exposure occurs during development (or possibly during other vulnerable periods, such as puberty). Obesogens may make it harder to lose weight and easier to gain weight, increasing our susceptibility to obesity.
There was some agreement that it is not obesity per se that is the problem, but metabolic dysfunction and the resulting diseases from that (like diabetes, metabolic syndrome, NAFLD, etc.) (one clinician says she uses the word “malnutrition” with her patients instead of “obesity”). A provocative talk by Sarah Richardson (Harvard) noted that how we present the science (specifically on epigenetics and obesity, in early life) can lead to people blaming the mothers for obesity in children. To combat this, she suggested noting both maternal and paternal effects, focusing on societal and not individual changes, and conveying complexity. And, not showing “headless fat people” (all body types should be considered OK).
There was a lot of discussion on epigenetics, but it is not yet clear if these various environmental factors are causing the epigenetic changes that lead to gene expression and affect health; it could be that the metabolic dysfunction is causing the epigenetic changes, or both. Also, can epigenetics modify the effects of environmental exposures? We don’t know.
Specific talks focused on various chemicals and the risk of obesity; I will not go into specific findings here (many are unpublished), but suggest taking a look at the talks when they are online (see links below).
One alarming tidbit: Sheela Sathyanarayana (University of Washington) did a dietary intervention study that gave catered food to families to try to reduce their phthalate levels, as compared to giving them advice on how to do that at an individual level. Well, the families who ate the catered food (organic, etc.) had a huge *increase* in phthalate levels—it turns out the organic ground coriander was 30% phthalate by weight! This is a great example of how individuals can’t control their intake of chemicals, and not for lack of trying.
Links to workshop info and videos
Examining a Developmental Approach to Childhood Obesity: The Fetal and Early Childhood Years
The Interplay between Environmental Exposures and Obesity
To see videos from the talks, see the “videos” link at the top right of the page. The first link has posted videos already, and the second will soon.
If anyone has other impressions of the meetings, please post! At least 600 people registered for the 2nd meeting online, so that is good to hear.