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George Bray Part 2, The Problems and Limitations of Obesity

In part 2 of this Exclusive Interview, George Bray talks with Diabetes in Control Medical Editor Joy Pape about the inequality of obesity and the issues with moving forward in solving the obesity problem.

George A. Bray, MD, MACP, MACE is Professor of Medicine Emeritus at the Louisiana State University Medical Center in New Orleans.


Transcript of this video segment:

Pape: So, obesity is increasing in prevalence as anyone visiting a public place can tell. Can you expand a bit on how bad a problem it is and whether you’re optimistic about the future?

Bray: Oh, I’m always an optimist.

Pape: (Laugh)

Bray: If I weren’t being an optimist, I suppose I would have gone to do something else years ago. Unfortunately, I have not been as successful as my optimism would like to have led me to hope I would be. As I said, it’s a worldwide problem but it doesn’t occur equally in the population. One of the fascinating observations is that you could watch people move from one area to another. And we know that the prevalence of excess weight is higher in some ZIP codes than in other ZIP codes. And where we have information tracking people who move from one to another. If you move from a lower income ZIP code to a higher income ZIP code, you’ll become thinner, so you’ll move to the ZIP code mean, if you like. If you move the other direction, you’re at greater risk for gaining weight. So, there’s clearly a demographic component to weight gain that’s got an income element to it. And we know that the income inequality in this country is directly related to the prevalence of obesity. The people at the lower-ends of the income distribution are at considerably greater risk than people at the upper-ends of this income distribution. So, we need to do something about those sociodemographic features which set the environment in which this disease process can occur, which is not an easy thing to do but it’s clearly important.  

Pape: So, where do you think we have limitations that prevent us from moving forward?

Bray: One of them is that we can’t predict very well who’s going to succeed, that’s a clear limitation. One of the other fascinating things to me is, I mentioned leptin a few minutes ago which was discovered in 1996. It’s a rare defect when you don’t have it. When you don’t have it, you become very fat. We had the opportunity to study a Turkish family who had three individuals with leptin deficiency, who came down to the Pennington Center in Baton Rouge and spent some time living in our unit and they are all very, very overweight individuals. And after completing the studies, we were able to obtain leptin for them on a at-needed basis. And when you treat leptin deficient people with leptin, their weight comes down to normal. They will return to the weight you and I are. And if you take leptin and give it to someone who’s overweight, it doesn’t do that. So, one of the really fascinating questions is what is different about people who never had leptin and get it back, and like the person who gains weight and then loses it acutely? The person who had no leptin and gets leptin will slim down perfectly normally. But if you have leptin from birth onward and you picked up those one to two pounds a year over a decade, you don’t respond to leptin. And understanding the mystery of why that leptin resistance or leptin ineffectiveness is there is clearly a very important question. The other very important question is what is it about some people that keeps them from getting fat? We live in a society where food is equally abundant to everybody. I’ve got the same food supply as you do and anybody else watching this show. So, what is it about those who don’t get overweight versus those that do? Well, we know that a good bit of it is genetic. We also know that among the genetically susceptible people there are some kinds of genes that play a particularly important role. And we’ve been interested clinically in pairs of animal groups, one of which gets fat eating a high fat diet and the other animals don’t at all. I mean, you’d feed them on it and they’ll eat a little bit, and then their weight drops right back to normal. While the others will go right on up just like that. Forty percent of our population has been doing this sort of creeping up all of the time. So, what’s the difference in this? And we’ve explored that over a good many years, like 40 years of my career and finally working with a group in New York, we’ve identified a gene protein complex in the brain areas that are involved with feeding and food regulation that is present in one but not in the other. And when you modify it, you change the responsiveness to the high fat diet to which we seem to be sensitive. So, it looks like we’ve began to get some molecular basis for some of the biology that we’ve been seeing about the susceptibility some people have to a high fat diet which others do not have. So, this is I think an important message that will be of use in trying to develop new medications.

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