Preventive Medicine Column
Dr. David L. Katz
Two new studies, published on-line last week in JAMA Pediatrics, may have us fired up yet again about the genetic variation to blame for obesity. But then again, is that really the problem?
One of the studies examined variation in food and satiety responses, which we may summarize as appetite, in roughly 400 pairs of 3-month-old twins in the U.K., and tracked growth and development over time. There are always lots of important details in biomedical research, but the perhaps predictable punch line was this: the babies with the heartier appetites gained more weight.
The second study was directed at the same basic issue, but went a bit deeper. Investigators again examined the association between appetite and weight gain in a group of over 2000 twin children in the U.K., but this team included an assessment of genes associated with variation in satiety responses, essentially how much eating it takes to feel full. Once again, more appetite meant more weight gain. But this time, more genes for more appetite was identified as the real culprit.
Finally, an accompanying editorial noted the importance of this kind of genetic research because the obesigenic environment “does not affect all children equally.”
That is undeniably true. It is equally true that the sinking of the Titanic did not affect all passengers equally. More generally, falling into water does not affect all human beings equally. Some of us know how to swim, and some do not. Some of us can hold our breath longer than others.
And while there is, I am quite confident, genetic variability we could find and associate with variation in how long we can hold our breath, I am not sure how illuminating that would truly be about the risk of drowning.
Human beings are vulnerable to drowning because we don’t have gills, and the reason absolutely resides in our genes. We have Homo sapien genes that include the recipe for lungs, and exclude the recipe for gills. In contrast, blue fin tuna and guppy genes reliably include the recipe for gills and exclude the recipe for lungs. Blue fin tuna and guppies have just the kind of trouble out of water that we are prone to have in it. We don’t have gills because we aren’t fish- and fish don’t have lungs because they aren’t people. And in both cases, the reason we aren’t them and they aren’t us resides in our respective genes.
Given that, if we approached drowning like obesity, we would go looking for those genes. We would, readily, find the divergences between human and guppy genes. And we might, I suppose, declare that a genetic basis for drowning had been identified. And once genes were indicted for drowning, we could head off down the path of drug development or genetic engineering to deal with the problem.
I am not refuting the value in these new studies. The editorialist very appropriately notes that early identification of genetic vulnerability to weight gain might allow for very early implementation of prevention strategies, so that obesity does not develop in the first place.
I like that- but do we really need maps of our kids’ genomes to take such action? We have pandemic childhood obesity right now-meaning legions of kids around the world are vulnerable to weight gain, whatever their genes. And yet, we routinely feed them junk. We routinely jettison physical activity from their daily routines. We peddle to them foods willfully designed to be irresistible if not addictive, and to maximize the number of calories it takes to feel full. Can we really justify the lunacy of a culture that studies genes looking for variation in satiety responses, while engineering foods to undermine satiety responses?
Yes, our genetic vulnerability to obesity is variable- much, I bet, like our genetic vulnerability to drowning. But I don’t think that invites a genetic study of the drowning victims of the Titanic. I think the bigger issue was the obvious one: the ship went down.
We are all in the same boat, and it’s sinking, too- as evidenced by a global rise in bariatric surgery for ever younger children. The genes underlying vulnerability to obesity in all their variation were there a generation or two or twenty ago, too- when childhood obesity was rare. Those same genes are there now that it is rampant. Knowledge of them may be put to good use, but not if it distracts us from the sinking ship. What has changed is not within our children, but all around them. And we don’t need to wait for a genetic map of each child to fix it.
Human beings don’t have gills, and there are genes to blame. But the right response looks like swimming lessons, and lifeguards, and fences around pools- not studying genes while pushing kids into the surf. Not a new pill to fix an age-old part of who we are that was never really broken.
Dr. David L. Katz