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In part 2 of this Exclusive Interview, Dr. W. Timothy Garvey talks with Diabetes in Control Publisher Steve Freed during the AACE 2018 convention in Boston, MA about the changes in medications to treat obesity as well as the treatment methods.
W. Timothy Garvey, MD, FACE is a professor and Director of the University of Alabama Diabetes Research Center in Birmingham.
Transcript of this video segment:
Freed: If you go back maybe 40 years ago, you’d have diet doctors and you go in and you get speed and it would cause you not to eat as much and maybe clean the house a little bit more effectively. How has it all changed?
Garvey: Well, that’s not an option for long-term therapy, obviously, I mean there are addiction issues and health-related issues there; there’s no long-term safety outcomes for those types of drugs including, for that matter, phentermine and related sympathomimetic means that are approved for short-term treatment of obesity. Usually that’s felt to be three months or less. When those drugs were approved in the 1950s and 1960s, the FDA did not require year-long studies or real rigorous safety-efficacy type studies like they do now. So, we don’t have safety data on phentermine even though it’s the most widely-prescribed drug for obesity at this point, it’s generic. The five that are approved for long-term, chronic therapy are lorcaserin, combination phentermine, topiramate extended release, we have naltrexone extended release, combined with bupropion extended release, liraglutide 3mg which is an injectable, and orlistat.
Freed: So what other changes have you seen in the treatment of obesity as far as maybe the education has changed quite a bit. We know the drugs have changed but where do you see the biggest changes?
Garvey: Well, you know, we’ve made slow progress actually. What we do know more about is the pathophysiology of obesity – the mechanisms that underscore why this is a disease process that involved interactions between satiety hormones that derive from the gastrointestinal tract, how they interact with the satiety center and the hypothalamus, and that’s regulated to create and sustain a higher body weight in people with the disease. Inheriting numbers of susceptibility genes is a part of that, but if you have a lot of susceptibility genes, each conferring a very small relative risk to the disease, but in aggregate, you’re going to have a greater body weight than somebody who doesn’t have those genes at any given environment – there is always an interaction between genes and environment. That is the disease process and the medications that we have act on those satiety centers, and that is why they help patients out – they help them adhere to reduced calorie diet by blunting appetite. That is really the bottom line. And that is all kind of new.