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:

  1. Is BPA really a problem?
  2. Does BPA affect everyone the same way —
    or do genetic variants play a role?

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.

Brief overview:  Bisphenol-A is a component of some plastics (recycling symbol 4 and 7) and is also found on some types of thermal printed cash register receipts.  It is considered to be an endocrine disruptor because of the molecules similarity to estrogen.

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 true 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]

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]

Genetic variant responses to BPA

Oxidative Stress:

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

  • rs5277 – Those with GG have a 3x increase in risk for liver dysfunction with BPA exposure (study on elderly population) [ref]

CAT gene

  • rs769217 – CT has a 4x increased risk of liver dysfunction in the elderly with BPA exposure [ref]

SOD2 gene

  • rs4880– AA has OR=2.59 for liver dysfunction in the elderly with BPA exposure [ref]

Metabolism of BPA:

UGT2B15  metabolizes BPA (through glucuronidation)[ref]; “the polymorphic alleles of UGT2B15 are closely associated with variations in the metabolism and toxicity of BPA.”[ref]

A study looked at the expression of UGT2B15 during the third trimester and in infants (3 – 15 weeks).  UGT2B15 levels varied (by 31 fold) among the group due in part to gender and UGT2B15 polymorphisms. [ref]

rs1902023 (A is the minor allele, also referred to as  253G>T and UGT2B15*2)

  • A allele causes decreased enzyme activity [ref]

rs3100 (G is the minor allele, also referred to as 761T>C)

  • G allele causes decreased enzyme activity [ref]

UGT1A1 – also metabolizes BPA through glucuronidation [ref]

rs34983651 — dbSNP has the insertion (I or AT)  as UGT1A1*28 [ref] but snpedia.com has the deletion (D) as UGT1A1*28

  • lower liver clearance of BPA with UGT1A1*28 (homozygous had much lower liver clearance) [ref]
  • 10x lower glucuronidation in breast tissue for UGT1A1*28 [ref]


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)

  • low activity of the enzyme [ref] [ref]

Caffeine induces the SULT1A1 enzyme (rat study) [ref][ref]


Stopping exposure:  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 which ones make sense for you to focus on, because, realistically, it isn’t possible to cut out all exposure.   Common sources of BPA exposure include:

  • plastic water bottles,
  • plastic food containers (don’t microwave in them!),
  • thermal printed receipts (some, not all)
  • pantyhose [ref]
  • composite dental resins and sealants [ref]
  • food – whether through plastic containers or through the soil [ref]

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.


More to read:


Updated 2/6/17

1 Comment

Thyroid Hormone Levels and Your Genes – · February 21, 2018 at 6:26 pm

[…] receipts) affect thyroid levels.[study] Read more about how genes play a role in your ability to detox BPA and […]

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