Air Date: Week of June 1, 2012

Some researchers, including Bruce Blumberg of the University of California, Irvine, believe chemicals we’re unwittingly exposed to could be making us fat. Blumberg tells host Steve Curwood if the timing is right, chemicals may be instructing stem cells to become fat cells.

Transcript

CURWOOD: From the Jennifer and Ted Stanley Studios in Somerville, Massachusetts, this is Living on Earth. I’m Steve Curwood.

So, why are so many of us getting fat? A majority of Americans are overweight and a third of us are medically obese. Sedentary lifestyles, easy access to calories, inadequate sleep and our genes - they're all factors.

But Bruce Blumberg of the University of California, Irvine, is among a small group of researchers who have found prenatal exposures to common chemicals could be programming us to get fat. Professor Blumberg joins us today, and, Professor, you may have coined a new term. Where did you come up with the word “obesogen”?

BLUMBERG: Well, to be perfectly honest, when we were writing our story about the chemical that we worked on - tributyltin - it seemed absolutely obvious to us that a chemical that makes animals fat should be called an obesogen, and I didn't realize it wasn't a word.

CURWOOD: What is that chemical, by the way?

BLUMBERG: Tributyltin is a chemical that used to be used on ship hulls and it’s used as a fungicide in paints, and it keeps marine life and fungus from growing on various surfaces. We found, accidentally, that tributyltin makes animals fat.

CURWOOD: Now, this tributyltin, this fungicide, is not the only compound that we know can make animals fat, correct?

BLUMBERG: No, there is a variety of chemicals that can make animals fat.

CURWOOD: What might be familiar to us?

BLUMBERG: Well, one of the strongest lines of evidence that there are chemical obesogens is that there are pharmaceutical obseogens. There are drugs, which make people fat. For example, Actos and Avandia are diabetes drugs that improve your insulin sensitivity, but also make you fat. There’s another antipsychotic drug called olanzapine that makes people gain about 10 kilograms a year. Many kinds of antidepressants make people gain weight. And our premise is that if there are drugs that make people fat, why would you expect that a chemical that targets the same pathway in a cell, wouldn't have the same effect?

CURWOOD: So, what are the broader implications of your discoveries?

BLUMBERG: Well, the broader implications are that it isn’t strictly calories in, calories out that is causing people to become fat. We already know that there are a variety of factors. But what our research and the research in other laboratories suggests that prenatal and early life exposure to obesogens can reprogram the metabolism of the individual that’s exposed, so that they use calories differently. Our prenatally exposed mice get fatter on an absolutely normal diet.

CURWOOD: Professor Blumberg, you are finding that exposures to a pesticide are programming animals to be fat throughout their lives. What can you tell us about what’s happening in the body that’s causing this? I mean, do the animals become super hungry?

BLUMBERG: Okay, so as far as we know, there are no big changes in appetite. We’ve seen in our experiments more and larger fat cells. And we’ve seen a population of stem cells that is more predisposed to make more fat cells. That’s with tributyltin.

CURWOOD: And so, what’s happening is that these stem cells are getting instructions from these chemicals to become fat cells and don't become bone or muscle or the other thing.

BLUMBERG: That’s the way it looks. So you’re getting the direct instruction to become a fat cell, but you’re also getting the different kind of instruction that says: this group of you are gonna be more likely to form a fat cell than a bone cell. That doesn’t mean that I can’t override it but in the absence of extra instructions, you’re going to go down the fat pathway.

CURWOOD: So, there’s a two-tiered process here. One is sort of a pre-selection process, sort of nominating cells…chemicals nominate a cell to become a fat cell, and then the chemicals can also then promote that pre-fat cell into a true fat cell.

BLUMBERG: That’s correct.

CURWOOD: I guess one of the most vexing aspects of this is that you’re seeing these effects at levels that are below what the government considers the ‘no effects’ level at the nano-scale. I mean, you really have to listen at a whisper to what’s going on.

BLUMBERG: Yes. So we see effects at very low levels, but as endocrinologists that’s not surprising at all. So, the endocrine hormone systems in your body already work at very, very low levels. So the testosterone receptor and the estrogen receptor and the thyroid hormone receptor work at parts per billion levels of the hormone.

So, it isn’t a big surprise that chemicals have an effect at the same level. That to an endocrinologist is just absolutely expected. To an industry toxicologist who’s used to working at astronomical doses of a chemical, they can’t wrap their minds around the facts that we’re seeing effects at parts per billion. And it’s a difference in training and in world view.

CURWOOD: So, how reversible are these results? Once the animals have had the exposure and developed the fat cells, how can they get rid of them?

BLUMBERG: So, we don’t know of any way to eliminate the number of fat cells. And, in fact, in humans the number of fat cells that you have as an adult is programmed pretty much by the end of puberty. So your body knows how many fat cells it’s supposed to have based on your early life experiences. And your body will defend that number. And when fat cells die, it will replenish just the right number. So, if you have liposuction and remove some of those adult fat cells, they’ll come back. They might not come back in the same place, but your body will replenish that number of cells.

CURWOOD: Does your research mean that if we are being exposed to obesogens and if they are having an effect in humans that, in essence, these effects are irreversible? That no matter how much somebody exercises or eats right, that they’ll never get to lower body weights?

BLUMBERG: No, it doesn’t mean that at all. What it means is that the person who’s been exposed is going to have to work harder. But, I would never, ever say that obesogen exposure dooms you to be fat. What it does is it dooms you to be predisposed. So it dooms you to have a metabolism that tends to store calories more effectively then to burn them. That means that you have to watch what you eat more, you have to exercise more, you have to try harder than someone who has not been exposed.

CURWOOD: Bruce Blumberg is professor in the School of Developmental and Cell Biology in the School of Biological Sciences at the University of California at Irvine. Thank you so much, sir.

BLUMBERG: You’re welcome.

 

Links

Blumberg Lab at UC Irvine

EHP Article on Obesogens

New Study in EHP on Chemicals BPA and BADGE, Fat Cell Differentiation

Michael Skinner Lab at WSU – Effects That Last Generations