Fwd: DNC News: Harry Potter and Bisphenol A

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denvernaturopathic <denvernaturopathic@...> wrote:

JK Rowling’s Ministry of Magic, and Bisphenol A

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 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 publics' 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

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 Downs 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, 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 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 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 a 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 andria, Virginia, the second panel made up of only 12 people

with specialties unconnected to BPA research, concluded that current BPA

exposures appear to pose little risk to people.

The andria 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. "

The Natural Resources Defense Council (NRDC said the panel report " dramatically

understates the human health risks from real-world exposure to the toxic

chemical Bisphenol A (BPA). "

To the contrary, Hentges, 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 andria 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:

http://cerhr.niehs.nih.gov/chemicals/bisphenol/bisphenol-mtg.html

The 12 members of the andria panel were selected specifically because they

had no direct BPA experience and, therefore, no obvious vested interests.

The andria 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 andria 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

the threat 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 MD, in

which he expressed concern about clear plastic. According to Dr. ,

laboratories performing research culturing breast cancer cells had discarded all

their plastic Petri dishes and replaced them with glass Petri dishes. Apparently

breast cancer cells grew 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 strictly avoid 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

http://denvernaturopathic.com/news/informing.html

References

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

August 2007

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.

Hunt PA et al. Bisphenol a exposure causes meiotic aneuploidy in the female

mouse. Curr Biol. 2003 Apr 1;13(7):546-53.

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

bisphenol A.

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

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.

New Scientist magazine, 20 January 2007, page 4

Prins GS, et al. Developmental estrogen exposures predispose to prostate

carcinogenesis with aging. Reprod Toxicol. 2007 Apr-May;23(3):374-82.

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

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

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.

Ropero AB et al. Bisphenol-A disruption of the endocrine pancreas and blood

glucose homeostasis. Int J Androl. 2007 Oct 30

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

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.

Soto AM, et al. 30 Neoplasia as development gone awry: the role of endocrine

disruptors. Int J Androl. 2007 Oct

Susiarjo M et al.Bisphenol A exposure in utero disrupts early oogenesis in the

mouse. PLoS Genet. 2007 Jan 12;3(1):e5.

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

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