BPA, a chemical found in some plastics, has been linked to a variety of effects on people including obesity, insulin resistance, and epigenetic effects on the fetus. It is everywhere in our food supply. In fact, a CDC report showed that 92% of people have BPA in their urine. [ref]
Two questions come to mind:
I’m diving into the research on the topic, looking past the hyped-up ‘sky is falling’ type of headlines to see if there really is a reason for concern.
Very brief BPA overview:
Bisphenol-A is a component of some plastics (recycling symbol 3, 6, and 7). It is considered to be an endocrine disruptor because of the similarity of the molecules to estrogen. It is now ubiquitous in the environment, and more than 90% of people have detectable levels in their blood.
Recent studies on BPA show:
There are actually a bunch of animal studies that show that BPA can cause weight gain, alter hormone levels, disrupt offspring, etc.[ref] While animal studies are important and have their place, I’m going to focus here on recent human studies from the past couple of months that take into account current levels of exposure.
A study that just came out in the Journal of the Endocrine Society (Sept 2018) looked at the effect of BPA on insulin secretion and glucose levels. The researchers gave an oral dose of BPA at 50 ug/kg body weight, which is the daily limit set by the EPA as being safe daily exposure over a lifetime. They found that this BPA dose increased initial insulin release (oral glucose tolerance) but then showed no statistical difference with the later phase blood glucose response. This is an important study because they used the EPA guidelines for an amount of BPA that was not supposed to elicit a response.[ref] I found it interesting that there was a large variation between individuals in their BPA levels over time after ingestion — individual rates of BPA metabolism varied a lot…
Another recent study looked at BPA and PFOAs in newborns to determine if there was an effect on birth size. First, over 90% of the 6,000+ infants (1,000 were twins) had detectable levels of BPA in their blood, and over 99% had detectable PFOA and PFOS. The study did find that average BPA levels were higher in twins born with lower birth weight, possibly because higher BPA levels also correlated with a greater number being born before 37 weeks of age.[ref] Most remarkable to me is that 90% of the babies were born with BPA in their blood. The study was on infants born between 2008-2010 in NY.
BPA was shown in a recent study (and several previous studies) to reduce sperm motility in men. [ref] Previous studies also showed male adolescent testosterone levels were decreased for those with higher levels of BPA. [ref]
A small study published in Sept 2018 found that children and teens with higher BPA exposure (top third of the group) had a 12x risk of obesity.[ref] This is probably an overestimate of the impact on obesity since the study group was only 138 people. Nonetheless, is one more study in a long line of human studies that show that higher BPA exposure increases weight. [ref] [ref] [ref][ref] [ref][ref]
A study from August 2018 found that BPA at normal exposure levels alters insulin response in a way that is independent of adipogenesis. The study found that it causes a low-level inflammatory response.[ref] This is in line with previous epidemiological studies that tie higher BPA levels to insulin resistance in men, women, and children.[ref][ref][ref]
BPA exposure increases oxidative stress and mitochondrial dysfunction. A study looked at BPA exposure in children with autism found that all children (with and without autism) had an increase in oxidative stress and mitochondrial dysfunction when exposed to BPA.[ref] Another study found increased oxidative stress biomarkers in pregnant women based on BPA exposure. [ref]
COX2 gene: COX2 is an enzyme that acts as part of the body’s inflammatory response
Check your 23andMe results for rs5277 (v.4 only):
(Note that the risk allele is given in the plus orientation here to match with 23andMe data.)
CA/T gene: catalase is an enzyme involved in cellular detoxification
Check your 23andme results for rs769217 (v4, v5):
SOD2 gene: a mitochondrial enzyme that converts superoxide into hydrogen peroxide and oxygen
Check your 23andMe results for rs4880 (v4, v5)
The study results here showed that the more common variant of rs4880 (A/A) was associated with an increased risk of liver dysfunction. This seems contradictory, but a new cell study on vitamin D levels, SOD and BPA helps to clear up the confusion. The study showed that “BPA administration elevated Mn-superoxide dismutase (MnSOD) expression but negatively regulated total SOD activity”. The researchers go on to explain: “Our results suggest that 1,25D3 attenuates BPA-induced decreases in 17β-estradiol and that treatment with 1,25D3 plus BPA regulates granulosa cell mitochondria by elevating mitochondrial biogenesis-related protein levels.” [ref]
Metabolism of BPA:
UG/T2B15 metabolizes BPA (through glucuronidation)[ref]; “the polymorphic alleles of UG/T2B15 are closely associated with variations in the metabolism and toxicity of BPA.”[ref] A study looked at the expression of UG/T2B15 during the third trimester and in infants (3 – 15 weeks). UG/T2B15 levels varied (by 31 fold) among the group due in part to gender and UG/T2B15 polymorphisms. [ref] Another study found that UG/T2B15 metabolizes up to 80% of BPA when concentrations are low, but that another enzyme (UG/T1A9) becomes more important at higher BPA levels.[ref]
Check your 23and Me results for rs1902023 ( v4 only, aka 253G>T and UG/T2B15*2):
UG/T1A: Glucuronidation of BPA through UG/T1A [ref]
Check your 23andMe results for rs34983651 (v4 only):
The BPA that isn’t metabolized through glucuronidation usually gets taken care of through SULT1A1. Mouse studies show that obese livers are less able to sulfate BPA than lean mice. “Taken together these findings establish a profoundly reduced capacity of BPA elimination via sulfonation in obese or diabetic individuals and in those with fatty or cirrhotic livers versus individuals with healthy livers.” [ref]
rs9282861 or i6018900 (T is the minor allele, also known as SULT1A1*2)
This seems like a logical first step, but it can be more difficult than you may first think. Take a look at this list of common exposure routes to BPA and figure out where it makes sense to focus your attention. Realistically, it isn’t possible to cut out all exposure.
Common sources of BPA exposure include:
Sufficient vitamin A:
A recent study on the detoxification of BPA in the liver found that the process depends on the stored retinol (vitamin A) in the liver. If you are a vegetarian and depending on beta-carotene as your source of vitamin A, you may want to check and see if you convert beta-carotene to retinol well.
Sweat it out:
Researchers have found that BPA is eliminated through sweat as well as through urine and feces. [ref] So working up a good sweat through exercise or in a sauna may have the added benefit of helping you eliminate BPA.
Dust your house:
One route of exposure that is especially important in children is through contact with dust. One estimate showed that it contributed to about 10% of BPA exposure.[ref] A good reason to get out a dust rag and take care of all those dust bunnies…
More to read: