Bisphenol A: Perinatal Exposure and Body Weight

BPA explained ; go more in depth


Bisphenol A: Perinatal Exposure and Body Weight
Chemical structures of BPA, DES and estradiol

Bisphenol A (BPA) is a component of polycarbonate and other plastics including resins that line food and beverage containers. BPA is known to leach from products in contact with food and drink, and is therefore thought to be routinely ingested. In a recent cross sectional study, BPA was detected in urine samples from 92.6% of the US population examined. The potential for BPA to influence body weight is suggested by in vitro studies demonstrating effects of BPA on adipocyte differentiation, lipid accumulation, glucose transport and adiponectin secretion. Data from in vivo studies have revealed dose-dependent and sex dependent effects on body weight in rodents exposed perinatally to BPA. The mechanisms through which perinatal BPA exposure acts to exert persistent effects on body weight and adiposity remain to be determined. Possible targets of BPA action are discussed.

BPA as an estrogen

BPA’s actions as an estrogen may contribute to effects on body weight. Sex-dependent and dose-dependent differences in body weight in response to early postnatal exposure to DES, an estrogenic compound with structural similarities to BPA have been reported. Those studies demonstrated increased body weight at 4 months of age in females exposed to DES (1 μg DES/day) from postnatal days 1 through 5. In contrast, males exposed to DES during that time period demonstrated a decrease in body weight relative to controls at 4 months of age. The administration of another estrogenic compound, the soy isoflavone, genistein to 4 week old male and female mice (in doses of 50–200,000 μg/kg/day for 15 days) also revealed dose and sex-dependent effects on adipose tissue deposition. In this specific paradigm, the males proved to be more sensitive to the effects of genistein showing increased adipose tissue deposition following treatment with nutritional doses of genistein and a significant decrease in fat pads when they were treated with pharmacological doses of the compound. It is intriguing to note that continuous exposure of male mice from conception through adulthood to a high phytoestrogen diet (containing high levels of genistein as well as diadzein) resulted in decreased adiposity, increased energy expenditure, and improved glucose and lipid metabolism. These data further suggest the importance of the dose and the precise timing of exposure to estrogenic compounds as well as the compounds themselves in determining their effects on adiposity and glucose homeostasis.

DES DiEthylStilbestrol Resources

3 thoughts on “Bisphenol A: Perinatal Exposure and Body Weight”

  1. From that paper, “… the lowest-observable-adverse-effect-level (LOAEL) for BPA was determined at 50 mg/kg BW/day”. For a 100 kilogram human being, that translates into a daIly dose of 5 grams (about a teaspoonful) to produce any observable effects! Compare that with DES, where a single dose of 10 micrograms – 10 millionths of a gram – is enough to produce clinically observable estrogenic effects. DES is literally a million times more potent as an estrogen than BPA!

    Those two dimensional representations of the molecules you’ve shown make the structures of BPA and DES look very similar, but in reality their 3 dimensional structures will be completely different.

    DES contains two phenyl groups joined by an ethylene bridge, and molecules containing that particular strucure have the ability to interfere with microtubule synthesis and produce cells with abnormal numbers of chromosomes. These cells can later become cancerous, which is why DES is carcinogenic. Although BPA contains two phenyl groups also, they’re not joined by an ethylene bridge and so BPA is unlikely to be carcinogenic (or if it is, it’ll be through some different mechanism).

    In other words, DES and BPA are two totally different things, and yet there seems to be a major effort underway to conflate the two in the public consciousness. Who’s behind it? My guess is that it’s the pharmaceutical industry, and that they’re trying to make DES and EDCs one and the same as far as the public are concerned. Then, in 20 or 30 years time when most of us are dead, they’ll grandly unmask EDCs as a hoax, and that’ll be that as far as DES is concerned (and probably a few other nasties from the wonder drug years that they’ve swept under the EDCs umbrella as well!).

    Well, maybe I’m being a bit paranoid there, but the fact remains that there’s really no comparing environmental toxins with high dosage medical hormone exposure. They’re two completely different things!

    1. This is so complex. It is my understanding that even though DES and BPA are different in many ways they both work as endocrine disruptors and this is why they’re often compared. I see your point though about the pharmaceutical industry’s motivations. Once again, thanks for sharing your knowledge and expertise about DES.

  2. Just to add to what I was saying, if you look on Wikipedia at the molecular representations for DES and BPA
    you’ll see that they are in fact two completely differently shaped molecules, DES having a flat planar shape quite similar to estradiol whereas BPA is kinked into a V shape and bears no resemblance to estradiol at all!

    Unfortunately, there’s a lot of fake scientific research around that was ghostwritten in the marketing departments of pharmaceutical companies, e.g.Ghost-Written Article at Heart of Pharma Fraud Case and One in Five Medical Journal Articles Include Honorary and Ghost Authors, Study Finds

    Perhaps this paper is one of these phoney ghostwitten articles? It’s basically trying to make out that DES is no more harmful than a widely used, relatively nontoxic industrial chemical that people are exposed to every day without suffering any obvious ill effects. That’s the story the pharmaceutical companies would no doubt like people to hear, but it’s completely untrue and I don’t think we should go along with it!

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