Obesogens: Eating tin is how your mother made you fat
Competency # 18 Environmental Toxins
Reference: Grün, F, Blumberg B, Environmental Obesogens: Organotins and Endocrine Disruption via Nuclear Receptor Signaling Endocrinology Vol. 147, No. 6 s50-s55
Obesogens are a new type of chemicals that are being identified as toxins in our environment that affect our fat storage genes. They are labeled as “obesogens” because they may explain part of how we get overweight, when otherwise we would not have. Organotins (organic molecules attached to tin, the metal) have been described as one of the first sets of chemicals that do that. The establishment of a genetic imprint early in life becomes our blueprint for all our lives. That becomes the risks for the risks for the risks, R3.
How do they do that? We are learning that there are events and exposures that can predict our risk for obesity from what we are exposed to during pregnancy. For example, smoking during pregnancy doubles the risk of obesity, compared to smoking after delivery. So, it’s not the smoking environment by itself, but the smoking while your mother is pregnant that matters. And we have found that the chemicals we are talking about work at the nanogram level. As our measuring technology becomes sophisticated enough to measure nanograms, we are able to measure the effects of chemicals that work at that minute level.
Organotin compounds are found in a variety of sources. They are used as stabilizers for paint, for example. TBT, or tetrabutyl–tin is the most talked about example of this class, as it seems to be what lasts in the environment the longest. They are also used as fungicides on crops and in PVC pipe manufacture. They have been found in seafood like clams and oysters, so they are relatively ubiquitous. And they work through a variety of mechanisms.
What they seem to effect are your genes that regulate the set point for your fat storage. Your “thrifty genes” are a set of genes that influences how efficiently you store fat. Organotins seem to be implicated as stimulating the expression of those genes very early in life, and set the table for you for the rest of your life. If your genetic predisposition is set while you are still a fetus, your activated “thrifty” genes make your metabolism more sensitive to weight gain later on in life. The PPAR system is part of how we regulate and differentiate fat tissue. As is the RXR system. Organotins stimulate both in utero. That’s a problem. To quote, “RXR-PPAR has been shown to play a key role in adipocyte differentiation and energy storage and is, therefore, key to the control of whole-body metabolism. PPAR activation increases the expression of genes that promote fatty acid storage and represses genes that induce lipolysis in adipocytes in white adipose tissue.”
Ouch. We live in an industrial world. We presumed that all those chemicals we’ve invented to fight agricultural pests have been tested and found to be safe. Well, they haven’t been. We haven’t had the technology to test to nanogram levels, or the sophisticated science to understand the mechanisms of how our genes work. But this is the cutting edge of science today. The brave new world of understanding how our genes work, and how they get expressed by chemicals at the most subtle of levels is opening up a whole new world. The risks for the risks for the risks. R3.
WWW: What will work for me. This is too early to point fingers and definitively say what is what. But this builds in me a conviction that eating local organic food is probably better. For example, did you know that those perfect apples imported from far away have been sprayed over 40 times. Did you think all that chemical washed off? I’m washing my fruit more often. So should you. And those slightly blemished locally grown apples look suddenly much tastier. They don’t have that tinny taste.