DNC News


JK Rowling’s Ministry of Magic, and Bisphenol A

Jacob Schor, ND

January 5, 2007

Writers often resort to literary analogies in order to convey their ideas.  Typically these references allude to the classics.  I confess, I still haven’t finished War and Peace.  To best explain the current situation in regard to the chemical Bisphenol A, let me instead reference the work of J.K. Rowlings.  In her Harry Potter books, the Ministry of Magic denies the reappearance of He Who Must Not Be Named, aka, Lord Voldemort, despite all the evidence to the contrary.  For Harry, his friends, professor Dumbledore and certainly, the reader, the truth is obvious and the Ministry’s position of denial seems absurd.  Yet the Ministry’s officials don’t see the world the same way.  This contrariness on part of the ‘authorities’ and reluctance to admit to an obvious threat in these story books is about where we stand today with Bisphenol A. 

Bisphenol A (BPA) is the starting material used to make polycarbonate plastic. This is the hard, clear plastic used in baby bottles, disposable flatware, watercooler bottles, Nalgene bottles, the work bowls of food processors and countless other kitchen and food containers. It is also an essential ingredient of epoxy resins used to line food and beverage cans and to seal cavity-prone teeth.  Any plastic household product that is hard and clear is probably made of polycarbonate and contains bisphenol A.  The public’s assumption has been that polycarbonate is an inert material, a safe, lightweight alternative to glass.

The problem is that Bisphenol A (BPA) in not inert; tiny amounts leach out and end up inside us.  Not just in some of us, but pretty much all of us. The Center for Disease Control data suggests the tissue concentrations of BPA in 95% of the US population are above those shown to cause problems in test animals.

Or at least the experts with the most experience researching BPA think so.  Other experts, the Ministry sort, think BPA is only a problem if you are a mouse.  I’ll come back to this in a moment.

Though BPA has been used in plastic for decades, it is only in the last dozen years that researchers have started to worry about it.  BPA mimics the hormone estrogen and this effect underlies many of its unwanted actions.

This recent chapter in which BPA starts to look menacing starts with Patricia Hunt, a researcher at Case Western Reserve.  Hunt reported in 2003 that BPA injures mouse eggs.  OK, I know mice don’t lay eggs.  Hunt discovered, quite by accident, that BPA damages the eggs inside the ovaries of female mice.

Hunt was researching why some fertilized human eggs have an abnormal number of chromosomes, a condition called aneuploidy. The only factor clearly known at the time to cause this kind of abnormality in humans, was a mother's age. The older the woman, the more likely she will have abnormal chromosomes and give birth to a child with Down's syndrome. Hunt tried to test if hormonal fluctuations were responsible.

Hunt’s first attempt was a failure.  The aneuploidy rates in the ‘control’ mice, that is those not receiving any experimental treatment, fluctuated wildly.

Hunt and her fellow scientists traced the cause of the unexpected data to the cages the mice lived in. They were made of polycarbonate plastic and the BPA was leaching from the cages into the mice.  Hunt and her colleagues were able to duplicate these high aneuploidy rates by housing the mice in polycarbonate cages and housing control mice in BPA free homes.  Aneuploidy rates skyrocketed in mice living in the BPA plastic cages compared with those of the BPA free control mice. As part of the experiment, the Hunt and her team gave mice with drinking water tainted with BPA at concentrations matching those of the accidental cage exposures. The same result occurred, in fact, the more BPA the animals ingested, the higher the aneuploidy incidence. [Hunt 2003]

Hunt took this research a step further, implanting BPA pellets into pregnant mice. The pellets released the same dose used in the earlier experiment. The researchers compared eggs from the female offspring of these pregnant mice with eggs from mice whose mothers had carried a placebo pellet. Up to 40 percent of the eggs from daughters of the exposed mice had abnormal numbers of chromosomes.  Only about 3 percent of the placebo group showed that abnormality. [Susiarjo 2007]

In August 2006, Beverly Rubin from Tufts reported that injecting tiny doses of BPA into pregnant and nursing female mice masculinized the brains of their female offspring. Their theory is that BPA mimics estrogen and affects anatomical development that distinguishes male and female brains.  As a result BPA modifies brain formation in female mouse fetuses and make the lab animals, later in life, display a typically male behavior pattern. [Rubin 2006]   An average person's daily exposure to bisphenol A is similar to the doses given to animals in this study.

BPA also increases insulin resistance.  A 2007 study reports that just four days injecting BPA, changed pancreatic function in mice to the degree they were pre-diabetic. The study authors suggest that this may partially explain the global epidemic of diabetes. [Ropero 2007]

BPA causes epigenetic damage. Epigenetic changes occur when hormones or other chemical agents add or remove methyl groups to genes, changing the way the genes fold and thus changing the way they are expressed.  These changes are preserved and passed to future offspring. Agouti mice are used experimentally to test if chemicals cause epigenetic changes. Agouti mice carry a gene that is particularly vulnerable to epigenetic effects.  If epigenetic changes occur, the offspring, instead of looking like typical lean brown haired Agouti mice, grow into fat blond mice.  Anyone can tell if this kind of molecular genetic damage has occurred just by looking at the mice.

Randy Jirtle from Duke University reported in August 2007 that feeding agouti mice BPA during pregnancy and nursing caused epigenetic changes. The BPA dosed mice grew up blond and fat.  Methyl-donating vitamins like folate blocked BPA’s epigenetic effect. [Dolinoy 2007]

Retha Newbold from the National Institute of Environmental Health Sciences (NIEHS) injected newborn female mice with BPA for 5 days.  When fully grown these mice had all sorts of fertility related problems, including ovarian cysts, glands at inappropriate places in the uterine lining, and polyps or other excessive-tissue growths in or on the uterine lining. [Newbold 2007] None of the doses used in this research were excessive; they were actually less than typical human exposure.

At this point there have been hundreds of animal studies published on the effects of BPA, most of them demonstrating that they affect the animals adversely.  The only good thing about BPA is that it may be useful in treating Lupus. [Sawai 2003] It is unproven whether this chemical is having similar effects on humans.

Two years ago the National Institute of Environmental Health Sciences recruited two panels of experts to review the data on BPA. This past fall, both panels issued reports.  Their reports were what started me thinking about Harry Potter. They came up with opposite conclusions. One panel was very worried and the other not at all.

The first group met in Chapel Hill, North Carolina and concluded that this was a big problem and, ‘that BPA exposure in the womb can permanently alter genes of animals, impair the function of organs in ways that persist into adulthood, and trigger brain, behavioral, and reproductive effects, including diminished sperm production. Effects deemed likely included a heightened sensitivity to carcinogens, impaired immunity, and diminished insulin sensitivity.’ [Raloff 2007] [vom Saal 2007] [Keri 2007]

At a meeting in Alexandria, Virginia, the second panel made up of only 12 experts with specialties unconnected to BPA research, concluded that current BPA exposures appear to pose little risk to people.

The Alexandria conclusions were condemned by some groups from the start.

The Environmental Working Group’s response to the panel was they "largely ignore wide ranging scientific research connecting human health risks with exposure to Bisphenol-A (BPA). The panel instead endorsed an error riddled, industry influenced 'report' minimizing the risks that BPA poses to humans."

Another example comes from the Natural Resources Defense Council (NRDC) which said the panel report "dramatically understates the human health risks from real-world exposure to the toxic chemical Bisphenol A (BPA)."

To the contrary, Steven Hentges, Ph.D., of the American Chemistry Council defended the conclusion saying, “The safety of our products is our top priority. The conclusions reported today provide strong reassurance to consumers that they are not at risk from use of products made from bisphenol A. Most importantly, these conclusions are from a very credible, highly qualified group of independent scientists with no conflicts of interest, operating in an open and transparent review process.”

Why such different conclusions?

It probably had something to do with who the ‘experts’ were on the panels. 

The Chapel Hill group was made of researchers who all had experience either conducting studies on BPA or with other pollutants that mimic estrogen. All these scientists knew the good qualities and shortcomings of past experiments in the field.

It is interesting as a side note to me that while the conclusions of the Chapel Hill panel were immediately published in the peer reviewed literature and are easily accessible through the PubMed Search engine at the National Library of Medicine, the Alexandria panel apparently has not published.  Copies of their interim report from April 2007 can be downloaded from the  National Institute of Health Sciences website at:


The 12 members of the Alexandria panel were selected specifically because they had no direct BPA experience and, therefore, no obvious vested interests. 

The Alexandria panel discounted the animal studies that gave BPA by injection rather than orally.  They also pointed out that none of the research is on humans.

Critics and members of the Chapel Hill group have been quick to counter these arguments.  For example, Hunt’s January 2007 study showed little difference in effect between oral and injected pellets.   Nor did Nadal’s work with insulin resistance.  Oral or implanted BPA both triggered insulin resistance.  Even single doses delivered by either method produced measurable effect.

Waiting for human studies is desirable from a scientific point of view but perhaps not wise if we care about public health.  The more serious predicted effects documented in animal studies are in the test animals’ offspring.  To demonstrate such a cause and effect in people will take years of careful study.  At this point, even finding people with BPA levels low enough levels to serve as a control group could be difficult.

A benign explanation between the two groups of experts evaluating BPA is timing.  The Alexandria group seems to have reached their conclusions early last year while the Chapel Hill group was aware of the many new, still to be published studies, that we are aware of presently.

For example, in October 2007, Soto and his colleagues at Tufts University reported that a pregnant rat's exposure to low doses of BPA "resulted in early puberty in female offspring." These rats were more likely to develop abnormal tissues or outright cancer than were unexposed litter mates.  [Soto 2007]

Back in June, Vom Saal reported that genital cells from male mice exposed to low doses of BPA develop extra estrogen and androgen receptors. Other studies tell us these sorts of changes speed prostate cancer growth. [Richter 2007]

These may help explain Gail Prins’ results.  She found that exposure to low doses of BPA in the womb increased the tendency of prostate glands in adult-male offspring to become precancerous upon exposure to extra estrogen. [Prins 2007]  In the June, her team reported that BPA-exposed animals were more likely to develop hormone triggered cancers. BPA exposure reprogrammed the genes in the fetal prostate and increased the risk of cancer development years later.

Try designing an epidemiological study to expose these sorts of relationships.  To get even a hint whether Prins’ data on prostate cancer can be applied to humans, you would have to determine the exposure to BPA for men with current prostate cancer back while they were still in their mothers’ wombs.  Or in regard to Hunt’s data, as New Scientist asked in January 2007,  “How can you prove a chemical is toxic when its effects won't show up until the daughters of the people exposed to it try to have children themselves?” [New Scientist 2004]

See why this reminds of the Ministry of Magic?  The people who know most about this problem are the ones most worried.  Those who know relatively little or, perhaps have something to lose, appear to be in denial.  For example, The American Chemistry Council, a chemical-industry calmly issued a statement in October that previous evaluations "support the conclusion that BPA is not a risk to human health at the extremely low levels to which consumers might be exposed." 

Most of the studies mentioned have used tiny doses of BPA in their test animals, often measured in nanograms or micrograms per kilogram body weight per day. The researchers on the Chapel Hill group, “suggest that BPA concentrations in human tissue are consistent with an exposure level of 0.5 milligrams per kilogram of body weight per day ….”   People are exposed to BPA at doses hundreds of times higher than these test animals.

Given my reading of this information, it seems prudent that we not wait until the scientists and government regulatory agencies reach their final conclusion.  It makes sense that we do our best to avoid Bisphenol A now.  Those most at risk to be negatively affected are pregnant women, or women who will soon be pregnant, and infants. 

Never ever store hot food or liquids in polycarbonate.  Do not heat food in polycarbonate containers.  Probably the worst thing anyone could do is heat infant formula in plastic  baby bottles.  In the long run we do not want any food to touch BPA, but once you start looking around your kitchen you will realize how difficult this may be to do.

Just about everything we eat and drink has contacted polycarbonate somewhere on along its way to our mouth.  My Cuisinart’s mixing bowl is clearly polycarbonate. Our fancy new refrigerator may have a stainless steel exterior but the food drawers and shelves are clear hard plastic no doubt containing you know what.

As I write this I think back many years to a lecture by Jonathan Wright MD, in which he expressed concern about clear plastic.  According to Dr. Wright, laboratories performing research culturing of breast cancer cells had discarded all their plastic Petri dishes and replaced them with glass Petri dishes.  Apparently breast cancer cells grow much faster in the plastic dishes and this was throwing off the data.  I never could find a reference to this anecdote but in hindsight, he was describing a similar phenomenon to what Hunt reported.  With this in mind, it makes sense to avoid especially BPA if you have any sort of estrogen or hormone sensitive cancer. 

Prior Newsletter on this issue:

Information: Induction of Genetic Expression

December 5, 2005



Hunt PA et al. Bisphenol a exposure causes meiotic aneuploidy in the female mouse. Curr Biol. 2003 Apr 1;13(7):546-53.

Susiarjo M et al.Bisphenol A exposure in utero disrupts early oogenesis in the mouse. PLoS Genet. 2007 Jan 12;3(1):e5.

Rubin BS et al. Evidence of altered brain sexual differentiation in mice exposed perinatally to low, environmentally relevant levels of bisphenol A. Endocrinology. 2006 Aug;147(8):3681-91

Ropero AB et al. Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis. Int J Androl. 2007 Oct 30

Dolinoy DC et al. Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13056-61.

Newbold RR, et al. Long-term adverse effects of neonatal exposure to bisphenol A on the murine female reproductive tract. Reprod Toxicol. 2007 Aug-Sep;24(2):253-8.

Sawai C, et al. Effect of bisphenol A on murine immune function: modulation of interferon-gamma, IgG2a, and disease symptoms in NZB X NZW F1 mice.

 Environ Health Perspect. 2003 Dec;111(16):1883-7.

Raloff J. Clearly Concerning: Do common plastics and resins carry risks?

Science News. Sept. 29, 2007; Vol. 172, No. 13 , p. 202

vom Saal FS  et al. Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure.

 Reprod Toxicol. 2007 Aug-Sep;24(2):131-8   


Keri RA  et al. An evaluation of evidence for the carcinogenic activity of bisphenol A.

Reprod Toxicol. 2007 Aug-Sep;24(2):240-52.

Susiarjo M, et al. Bisphenol A exposure in utero disrupts early oogenesis in the mouse.  PLoS Genet. 2007 Jan 12;3(1):e5.

Soto AM, et al. 30     Neoplasia as development gone awry: the role of endocrine disruptors. Int J Androl. 2007 Oct

Richter CA, et al. Estradiol and bisphenol a stimulate androgen receptor and estrogen receptor gene expression in fetal mouse prostate mesenchyme cells.

Environ Health Perspect. 2007 Jun;115(6):902-8.


Prins GS, et al. Developmental estrogen exposures predispose to prostate carcinogenesis with aging. Reprod Toxicol. 2007 Apr-May;23(3):374-82.



New Scientist magazine, 20 January 2007, page 4

Barras C. Plastics chemical is harmful, says expert panel.  New Scientist. 11 August 2007

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