The Washington Post

January 28, 2009

MONDAY, Jan. 26 (HealthDay News) — Almost half of tested samples of commercial high-fructose corn syrup (HFCS) contained mercury, which was also found in nearly a third of 55 popular brand-name food and beverage products where HFCS is the first- or second-highest labeled ingredient, according to two new U.S. studies.

HFCS has replaced sugar as the sweetener in many beverages and foods such as breads, cereals, breakfast bars, lunch meats, yogurts, soups and condiments. On average, Americans consume about 12 teaspoons per day of HFCS, but teens and other high consumers can take in 80 percent more HFCS than average.

“Mercury is toxic in all its forms. Given how much high-fructose corn syrup is consumed by children, it could be a significant additional source of mercury never before considered. We are calling for immediate changes by industry and the [U.S. Food and Drug Administration] to help stop this avoidable mercury contamination of the food supply,” the Institute for Agriculture and Trade Policy’s Dr. David Wallinga, a co-author of both studies, said in a prepared statement.

In the first study, published in current issue of Environmental Health, researchers found detectable levels of mercury in nine of 20 samples of commercial HFCS.

And in the second study, the Institute for Agriculture and Trade Policy (IATP), a non-profit watchdog group, found that nearly one in three of 55 brand-name foods contained mercury. The chemical was found most commonly in HFCS-containing dairy products, dressings and condiments.

MORE…

Comment from Leslie

Although the article is a year old – it is important to read.  Fructose is a poisons. Fructose with mercury is a poison.  Fructose with mercury and an exposure to aluminum is lethal.  Think of the diet of teenage girls (soda, Gatorade) especially athletes…..tons of Gatorade.  Fructose and the aluminum in Gardasil a part of the deadly cocktail?

Read the complete article and related information at Study Finds High-Fructose Corn Syrup Contains Mercury

Multiple hormones act in concert to regulate blood sugar and food intake. The idea has already led to a new diabetes therapy; will it also yield new strategies for obesity?

The Scientist.com

By Christian Weyer

Stepping on the scale each day and diligently recording their caloric intake and body weight in a little booklet, my patients marked the progress and failures of their dieting efforts. It was the mid-1990s and I was working as a medical fellow in endocrinology and metabolism at the University of Düsseldorf Medical Center in Germany. During the day, we optimized insulin therapy in patients with Type 1 or Type 2 diabetes, using modern tools such as new insulin analogs, glucose meters, and insulin pumps. In the evening, I supervised an outpatient obesity clinic. Our department was internationally renowned as an accredited World Health Organization collaborating center, and patients came from far and wide to seek care for their diabetes, and a variety of obesity-related conditions.

…I was drawn to endocrinology because I was intrigued by the complexity and elegance with which hormonal signaling systems govern whole-body metabolism and many other vital functions. Most hormones have multiple actions that are well coordinated, and naturally integrated with other hormonal systems. It is, in many respects, the equivalent of individual musicians playing together in a philharmonic orchestra producing the most melodic, beautiful symphonies. Some hormones, such as insulin, thyroid hormone, or cortisol, are “major players,” and their deficiency or excess can result in life-threatening metabolic derangements. Others, such as calcitonin, pancreatic polypeptide, or amylin can be viewed as complementary signals that enhance, or “fine-tune,” a tightly regulated metabolic process. In many cases, the central nervous system (CNS) orchestrates and balances these hormonal interactions, serving as the role of conductor….

MORE…

Read the complete article and related information at Hormones in Concert

Hindustan Times

November 9, 2009

Over 100,000 types of cancers are caused by obesity, according to an American study.

Excess body fat makes a person vulnerable to cancer by increasing the amount of hormones like estrogen circulating in the body and disrupting how the body processes insulin, which is linked to higher risk of cancer. It also triggers low-grade inflammation in the body, which is increasingly being found to play a role in cancer.

Researchers from American Institute for Cancer Research suggest that people should maintain a normal body weight and remain physically active throughout life. Weight gain after a cancer diagnosis is also likely to affect the outcome, say researchers.

“An increasing number of studies suggest that regular physical activity improves cancer survival, even among survivors who are overweight or obese,” the Independent quoted AICR researchers as saying.

“Public awareness of the link between obesity and cancer risk is alarmingly low,” said Alice Bender, MS, RD, Nutrition Communications Manager at AICR. We are working towards a day when obesity is right up there with tobacco in the public eye,” Bender added.

The AICR estimates show that excess body fat is linked to 49 per cent of endometrial cancers , 35 per cent of esophageal cancers 28 per cent of pancreatic cancers, 24 per cent of kidney cancers, 21 per cent of gallbladder cancers, 17 per cent of breast cancers and 9 per cent of colorectal cancers.

MORE…

Read the complete article and related information at Obesity can cause cancers, says study

Examiner.com

By Jennifer Gunter
SF Sexual Health Examiner

July 6, 2009

Read the complete article and related information at Obesity and the rise of endometrial cancer in young women

Examiner.com

By Jennifer Gunter
SF Health Examiner

Read the complete article and related information at Obesity and the rise of endometrial cancer in young women

Miller-McCune.com

Lean times make for chubbier teenage girls. That’s the conclusion of a newly published study that suggests the current recession may exacerbate the nation’s obesity problem.

May 5, 2009
By: Tom Jacobs

Fifteen- to 18-year-old females generally gain weight during weak economic periods, according to a report just published in the journal Social Science and Medicine. Researcher Jeremy Arkes of the Naval Postgraduate School in Monterey, Calif., found the opposite is true for young men in that age range: They tend to gain weight when the economy is strong.

Arkes drew his conclusions by analyzing data from the National Longitudinal Survey of Youth, focusing on the years 1997 to 2004. After controlling for other variables known to affect weight (including a range of family characteristics), he compared the body mass index of teens with the unemployment rate in their home states, as averaged over the previous year. (BMI is a calculated using an individual’s weight and height; most health experts consider it a reliable indicator of body fatness.)

He found that “an increase in the state unemployment rate of one percentage point causes the female teenagers in that state to rise 1.8 percentiles in the BMI distribution, on average.” In contrast, “a one-percentage-point increase in the state unemployment rate is estimated to move teenage males down about 2.0 percentiles in the BMI distribution.”

To put it more simply: “For females, a higher unemployment rate leads to a higher probability of being overweight,” while the opposite is true for males in the late teen years.

Arkes has no definitive explanation for these divergent trends, but he strongly suspects the results have a lot to do with what teens do in their spare time. His analysis of 2001 data from the Youth Risk Behavior Suveillance System reveals that “teenage males clearly exercise more than females, especially in activities with exertion (i.e., making one sweat or breathe hard) and to strengthen or tone muscles.

“Thus, with a weaker economy, we may be more likely to see females gain weight than males because males are more likely to exercise in their free time.”

So, for a teenage boy, time spent on a job is often time spent away from the athletic field or swimming pool. His wallet may be getting fatter, but so is he.

Arkes also notes that, according to a study he conducted in 2007, “a weaker economy leads to greater marijuana use,” especially among teenage girls. “The greater marijuana use could cause an increase in food intake and more weight gain, which could contribute to the female weight gain during weaker economic periods,” he speculates.

Never underestimate the cumulative effect of the munchies.

Comment from Leslie

Well, other than the munchies – it is all about hormones – stress and hormone fluctuations; poor diet due to less resources  can certainly add to weight gain too.

Read the complete article and related information at Economic Expansion: Teen Girls Gain Weight During Downturns

Reuters

April 27, 2009

By Anne Harding

NEW YORK (Reuters Health) – Girls are beginning to grow breasts at an earlier age, and starting their periods sooner too, new research from Denmark shows.

The findings back up recent studies that found earlier breast development in American girls over the past several years, but still can’t answer the question of why this might be happening, Dr. Lise Aksglaede of Rigshospitalet in Copenhagen, the lead researcher on the study, told Reuters Health. “At this point, we don’t know what is happening, and that is also what worries us.”

Aksglaede noted that she and her colleagues have seen an increasing number of girls with precocious puberty, meaning sexual maturation beginning before age eight. To investigate whether this might represent a trend, or simply greater recognition of the problem by parents, they looked at 1,100 girls who were studied in 1991-1993 and 995 examined between 2006-2008. The study participants ranged in age from 5.6 to 20 years old.

While the average age at which breast growth began was 10.88 years for the 1991 group, it was 9.86 for the 2006 group. Age at first menstruation was 13.42 for the 1991 group, and 13.13 for the 2006 group.

Most experts believe that the obesity epidemic may have something to do with earlier puberty in girls, Aksglaede noted, but she and her colleagues found no difference in the prevalence of overweight and obesity between the 1991 and 2006 groups. There also were no differences in levels of several reproductive hormones between the two groups, although the 8- to 10-year-olds tested in 2006 actually had lower estrogen levels than girls of the same age tested in 1991.

Some type of environmental factor, for example chemicals that have estrogen-like effects, may be responsible for the trend, Aksglaede said, but she pointed out that this is extremely difficult to study, given that there are so many different chemicals out there, and that levels girls are exposed to change constantly.

MORE…

Read the complete article and related information at First European evidence for earlier female puberty

The Freeport News

The Grand Bahamas

April 27, 2009

THE TRUTH ABOUT HEALTH

By Angelika Christie

This sounds like a contradiction, especially after I told you about the life preserving and health promoting effects of enough daily sunlight for the production of vitamin D in your body, which is a major cancer protector. When I say that ‘light’ could kill you, I speak of the artificial light we are surrounded with during nighttime.

Are you ‘burning the midnight lamp’ by staying up late, maybe working on your computer? Do you watch TV until late in the night, or even worse, fall asleep with the TV running all night? Is light coming in through your bedroom window during your sleeping hours in the night, or from a light source within your home?

If you answer ‘yes’ to any of these questions, you are compromising your health considerably; you may die earlier. Why is this so? I am glad you ask. You may have heard before that you should sleep in a dark room at night, but did you know exactly why? It makes sense that you just sleep better when it is dark. But that is not the only reason, although part of it. You sleep better in the dark because your brain produces the hormone ‘melatonin’ at night.

Melatonin is a natural hormone made by the pineal gland, a pea size gland which is situated just above the middle of your brain. During the day the production of melatonin is turned off, but as soon as darkness arrives, the gland actively produces melatonin.

Melatonin is the sleep inducing hormone, but it does so much more. The whole day and night rhythm has it’s importance for the proper functioning and recovering of our body systems, and a regular sleep and wake cycle is more important than we used to believe.

You may remember how often I have reminded you about the wisdom of our body; a perfectly functioning system from ancient times. Yes, our bodies were not designed for the 21st Century, not even the 20th Century when artificial light made it’s appearance. By the invention of Thomas Edison’s first ‘light bulb’ in 1882. Today we are ‘polluted’ with constant light throughout the nights, which is a major stress and health hazard that has contributed to many of today’s diseases, especially cancer. You may have heard that people who work night shifts have an increased risk of cancer.

Recent studies confirmed that the development of cancer with fatal outcome is greatly increased for people who do not get a regular good night’s sleep. You may ask what sleep has to do with cancer? In scientific studies (Dr. Russel J. Reiter Ph.D, Dr.h.c.mult is one of the foremost specialists on this subject), it was established that cancer cells stop growing in the night when sufficient melatonin is produced.

These studies were mostly done with breast, prostate, and colon cancer cells. The results were stunning. Of course we always knew that our bodies renew and regenerate during sleep, but we did not know that melatonin actually stops the growth of cancer cells! There are more studies on the way at over 30 Universities worldwide on this subject, but you read it here now so you can take action immediately. For this purpose I attend at least two conferences per year to know about the newest research and discoveries in the field of disease prevention and longevity.

Another misconception is that when we get older we don’t need as much sleep as younger people. You need exactly the same seven to eight hours of good sleep no matter how old you are! It is even more important at a middle and senior age because the threat of cancer and other degenerative diseases grow with age. Night-time is important to repair and rejuvenate, and now you know why.

Of course, like almost everything, melatonin de-clines as we age. This is the reason why older people have trouble falling and staying asleep during the night. It will help to completely darken the room, and, if you have to get up during the night for a bathroom visit, try to do so in the darkness or with very dim light.

As soon as you switch on the light, your melatonin drops to almost non- existence; even a few seconds of light signals the body that it is daytime. Your retina signals to the brain to stop the production of melatonin and produce stimulating hormones like cortisol.

Obesity is also related to a lack of sleep. Sleep apnea, a common occurrence in obese people, has risen over 500 percent, and is a major problem throughout the western world.

What can you do? Make sure you sleep in a dark room, not somewhat dark, but pitch dark. If you are over 35 years old and have problems falling asleep or staying asleep, you may want to consult a health care professional to discuss supplementing melatonin. I recommend to almost everybody over the age of 40 to start with small amounts (1-3 mg) of melatonin, not only as a non-addictive, natural sleeping aid, but also because melatonin is a very powerful antioxidant and disease prevention hormone.

Don’t allow ‘light’ in the night to kill you!

Dr. Angelika Christie is the managing director of Radiant Health Center. You can contact her at 352-1010 or email radianthealth1@mac.com

Read the complete article and related information at Is ‘light’ killing you?

Crossfitnewton Blog

NEW YORK (Reuters Health) – Data from the Women’s Health Initiative Observational Study show that higher than normal insulin levels are an independent risk factor for breast cancer.

Study investigators, led by Dr. Marc J. Gunter at Albert Einstein College of Medicine in the Bronx, New York, examined the association between breast cancer and blood parameters at study entry in 835 women who later developed breast cancer and 816 who did not. All of the women were postmenopausal and none were diabetic at baseline.

In the Journal of the National Cancer Institute, the researchers report a positive association between insulin levels and breast cancer risk, with women with the highest levels of insulin having a 46 percent greater risk than women with the lowest levels.

The association between insulin and breast cancer risk varied depending on whether or not the women took hormone therapy. Upon further analysis, insulin level was linked with breast cancer risk only in those who did not use hormones.

For women who did not use hormones, those with a body mass index of 30 (obese) compared with those with a BMI between 18 and 25 (normal weight), had a two-fold greater risk of breast cancer. Adjusting for insulin levels attenuated this association, however.

Fasting levels of estrogen were also linked with 59 percent higher risk among women with the highest versus the lowest estrogen levels.

Given that high levels of insulin and estrogen raise the risk for postmenopausal breast cancer — and largely account for the link between obesity and breast cancer — efforts to bring down fasting insulin or circulating estrogen levels “through weight loss or increased physical activity or via pharmacologic approaches” might be indicated, the researchers conclude.

Read the complete article and related information at High insulin levels may increase breast cancer risk

Our Stolen Future

While Bisphenol A was first synthesized in 1891, the first evidence of its estrogenicity came from experiments in the 1930′s feeding BPA to ovariectomised rats (Dodds and Lawson 1936, 1938).

Another compound invented during that era, diethylstilbestrol, turned out to be more powerful as an estrogen, so bisphenol A was shelved… until polymer chemists discovered that it could be polymerized to form polycarbonate plastic. Unfortunately, the ester bond that links BPA monomers to one another to form a polymer is not stable and hence the polymer decays with time, releasing BPA into materials with which it comes into contact, for example food or water.

Bisphenol A is now deeply imbedded in the products of modern consumer society, not just as the building block for polycarbonate plastic (from which it then leaches as the plastic ages) but also in the manufacture of epoxy resins and other plastics, including polysulfone, alkylphenolic, polyalylate, polyester-styrene, and certain polyester resins.

Its uses don’t end with the making of plastic. Bisphenol A has been used as an inert ingredient in pesticides (although in the US this has apparently been halted), as a fungicide, antioxidant, flame retardant, rubber chemical, and polyvinyl chloride stabilizer.

These uses create a myriad of exposures for people. Bisphenol A-based polycarbonate is used as a plastic coating for children’s teeth to prevent cavities, as a coating in metal cans to prevent the metal from contact with food contents, as the plastic in food containers, refrigerator shelving, baby bottles, water bottles, returnable containers for juice, milk and water, micro-wave ovenware and eating utensils.

Other exposures result from BPA’s use in “films, sheets, and laminations; reinforced pipes; floorings; watermain filters; enamels and vanishes; adhesives; artificial teeth; nail polish; compact discs; electric insulators; and as parts of automobiles, certain machines, tools, electrical appliances, and office automation instruments” (Takahashi and Oishi 2000).

BPA contamination is also widespread in the environment. For example, BPA can be measured in rivers and estuaries at concentrations that range from under 5 to over 1900 nanograms/liter. Sediment loading can also be significant, with levels ranging from under 5 to over 100 µg/kg (ppb) BPA is quite persistent as under normal conditions in the environment it does not readily degrade (Rippen 1999).

What this all means is that most of your life you are within arm’s length or closer to bisphenol A. No wonder the debate over its toxicity is so intense.

 Some important recent studies of bisphenol A:

Experiments with rats demonstrate that low level exposure to bisphenol A during fetal growth causes breast cancer in adults. At all levels tested down to 2.5 parts per billion, BPA induced formation of aberrant cell growth patterns associated in rodents and people with breast cancer. Levels only 5 times higher than EPA’s current safe level caused carcinoma in situ. Using these results to set safety standards would radically reduce use of BPA in plastics and resins. 

In utero exposure to BPA causes long-term effects on mammary tissue development in rats, increasing risks to cancer, and also increases sensitivity to a chemical known to cause breast cancer. The study strengthens support for a link between increasing rates of breast cancer in recent decades and increasing exposure to estrogenic chemicals like BPA. It also indicates that human epidemiological studies that fail to incorporate developmental exposures can’t be trusted to identify cancer-causing agents. More…

Perinatal exposure to extremely low levels of bisphenol A causes precancerous prostate lesions in rats. These lesions, called prostatic intraepithelial neoplasia, or PIN, are cancerous and are considered to be a precursor of metastatic prostate cancer in humans. One hundred percent of rats exposed perinatally and then, during adulthood, treated with estradiol and testosterone to create hormonal conditions analogous to thos of an ageing man, developed high-grade PIN. The effect appears to result from the failure in exposed animals of a gene to become hypermethylated as the rats aged. More…

Experiments with mice reveal that chronic adult exposure to bisphenol A causes insulin resistance. Insulin resistance in people leads to Type II diabetes and congestive heart failure, and is part of the modern epidemic of ‘metabolic syndrome.’ The exposure levels used were within the range that people experience regularly. More…

In a small prospective study, researchers in Japan report that bisphenol A levels are higher in women with a history of repeated spontaneous miscarriages. This research was based on proof that BPA causes meiotic aneuploidy in mice. Meiotic aneuploidy is the commonest cause of miscarriage in people. The researchers also followed the pregnancies of the women to completion, and found evidence of aneuploidy in several of the miscarried fetuses. More…

Bisphenol A and the birth control pharmaceutical ethinylestradiol cause adverse effects in prostate development in mice at levels to which millions of Americans are exposed each year. The results implicate these compounds in human prostate diseases, including prostate cancer. The research also shows the futility of predicting the developmental consequences of low-dose exposures based on high-dose experiments. More…

A flood of new information about bisphenol A revealing both widespread human exposure and effects at extremely low doses sparks a call for a new risk assessment of the ubiquitous compound. Bisphenol A, the basic building block of polycarbonate plastic, alters development of the reproductive tract, the immune system, increases prostate tumor proliferation, changes brain chemistry and structure and affects an array of behaviors, including hyperactivity. Of 11 studies of the compound’s effects at low doses, none funded by industry reported impacts. In contrast, 94 out of 104 government-funded studies found effects. This summary includes audio files of an international teleconference about bisphenol A. More…

Several ‘weakly’ estrogenic compounds including bisphenol A and endosulfan are as powerful as estrogen at increasing calcium influx into cells and stimulating prolactin secretion. The effects are mediated by a cell membrane surface receptor instead of nuclear hormone receptors, the focus of most studies to date. Changes in calcium and prolactin occur at extremely low doses, well within the range of human exposures. Wozniak, AL, NN Bulayeva and CS Watson. 2005. Xenoestrogens at Picomolar to Nanomolar Concentrations Trigger Membrane Estrogen Receptor-alpha-Mediated Ca++ Fluxes and Prolactin Release in GH3/B6 Pituitary Tumor Cells. Environmental Health Perspectives, in press.

Bisphenol A at extremely low levels causes changes in brain structure and behavior in rats. The locus coeruleus is believed to be a key brain center for anxiety and fear. Normally this is larger in females than in males. Rats exposed to BPA at levels beneath the current ‘safe’ exposure level established by the US EPA show a reversal in sex dimorphism, with males’ LC larger than females.’ . Kubo, K, O Arai, M Omura, R Wantanabe, R Ogata, and S Aou. 2003. Low dose effects of bisphenol A on sexual differentiation of the brain and behavior in rats. Neuroscience Research 45: 345-356.

Exposures to 1/5th the level considered safe are sufficient to alter maternal behavior in mice, including reductions in time spent nursing, increases in time resting away from offspring, and increases in time spent out of the nest. Palanza, P, KL Howdeshell, S Parmigiani and FS vom Saal. 2002. Exposure to a low dose of bisphenol A during fetal life or in adulthood alters maternal behavior in mice. Environmental Health Perspectives 110 (suppl 3): 415-422.

An accident in the lab, followed by careful analysis and a series of experiments, reveals that bisphenol A causes aneuploidy in mice at low levels of exposure. Because aneuploidy in humans causes spontaneous miscarriages and some 10-20% of all birth defects, including Down Syndrome, this implicates bisphenol A in a broad range of human developmental errors. Hunt, PA, KE Koehler, M Susiarjo, CA Hodges, A Ilagan, RC Voigt, S Thomas, BF Thomas and TJ Hassold. 2003. Bisphenol A exposure causes meiotic aneuploidy in the female mouse. Current Biology 13: 546-553.

Experiments by researchers at the University of Missouri raise the possibility of widespread contamination of laboratory experiments by bisphenol A. Their results demonstrate that at room temperature significant amounts of this estrogenic substance leach into water from old polycarbonate animal cages. This inadvertent contamination could interfere with experiments designed to test the safety of estrogenic chemicals, and lead to false negatives and conflicting results. Howdeshell, KA, PH Peterman, BM Judy, JA Taylor, CE Orazio, RL Ruhlen, FS vom Saal, and WV Welshons 2003. Bisphenol A is released from used polycarbonate animal cages into water at room temperature. Environmental Health Perspectives doi:10.1289/ehp.5993.

An analysis of the biochemical mechanisms of endocrine disruption suggests why industry has been unable to replicate crucial low-dose impacts of bisphenol A on prostate development. Welshons, WV, KA Thayer, BM Judy, JA Taylor, EM Curran and FS vom Saal. 2003. Large effects from small exposures. I. Mechanisms for endocrine disrupting chemicals with estrogenic activity. Environmental Health Perspectives doi:10.1289/ehp.5494

Using new analytical methods, a team of German scientists measured bisphenol A in the blood of pregnant women, in umbilical blood at birth and in placental tissue. All samples examined contained BPA, at levels within the range shown to alter development. Thus widespread exposure to BPA at levels of concern is no longer a hypothetical issue. It is occurring. Schönfelder, G, W Wittfoht, H Hopp, CE Talsness, M Paul and I Chahoud. 2002. Parent Bisphenol A Accumulation in the Human Maternal-Fetal-Placental Unit. Environmental Health Perspectives 110:A703-A707.

At extremely low levels, BPA promotes fat cell (adipocyte) differentiation and accumulation of lipids in a cell culture line used as a model for adipocyte formation. These two steps, differentiation and accumulation, are crucial in the development of human obesity. Hence this result opens up a whole new chapter in efforts to understand the origins of the world-wide obesity epidemic. Masuno, H, T Kidani, K Sekiya, K Sakayama, T Shiosaka, H Yamamoto and K Honda. 2002. Bisphenol A in combination with insulin can accelerate the conversion of 3T3-L1 fibroblasts to adipocytes. Journal of Lipid Research 3:676-684.

In cell culture experiments, BPA at very low (nanomolar levels) stimulates androgen-independent proliferation of prostate cancer cells. This finding is especially important because when prostate tumors become androgen-independent they no longer respond to one of the key therapies for prostate cancer. Wetherill, YB, CE Petre, KR Monk, A Puga, and KE Knudsen. 2002. The Xenoestrogen Bisphenol A Induces Inappropriate Androgen Receptor Activation and Mitogenesis in Prostatic Adenocarcinoma Cells. Molecular Cancer Therapeutics 1: 515–524.

BPA causes changes in rat ventral prostate cells that appear similar to events that make nascent prostate tumors in humans more potent: Ramos, JG, J Varayoud, C Sonnenschein, AM Soto, M Muñoz de Toro and EH Luque. 2001. Prenatal Exposure to Low Doses of Bisphenol A Alters the Periductal Stroma and Glandular Cell Function in the Rat Ventral Prostate. Biology of Reproduction 65: 1271–1277.

BPA induces changes in mouse mammary tissue that resemble early stages mouse and human of breast cancer: Markey, CM, EH Luque, M Muñoz de Toro, C Sonnenschein and AM Soto. 2001. In Utero Exposure to Bisphenol A Alters the Development and Tissue Organization of the Mouse Mammary Gland. Biology of Reproduction 65: 1215–1223.

BPA lowers sperm count in adult rats even at extremely low levels: Sakaue, M, S Ohsako, R Ishimura, S Kurosawa, M Kurohmaru, Y Hayashi, Y Aoki, J Yonemoto and C Tohyama. 2001. Bisphenol-A Affects Spermatogenesis in the Adult Rat Even at a Low Dose. Journal of Occupational Health 43:185 -190.

BPA at extremely low levels creates superfemale snails. Oehlmann, J, U Schulte-Oehlmann, M Tillmann and B Markert. 2000. Effects of endocrine disruptors on Prosobranch snails (Mollusca: Gastropoda) in the laboratory. Part I: Bisphenol A and Octylphenol as xenoestrogens. Ecotoxicology 9:383-397.

BPA is rapidly transfered to the fetus after maternal uptake: Takahashi, O and S Oishi. 2000. Disposition of Orally Administered 2,2-Bis(4-hydroxyphenyl) propane (Bisphenol A) in Pregnant Rats and the Placental Transfer to Fetuses. Environmental Health Perspectives 108:931-935.

An independently funded, academic laboratory can verify controversial BPA results, even though industry can’t: Gupta, Chhanda. 2000. Reproductive malformation of the male offspring following maternal exposure to estrogenic chemicals. Proceedings of the Society for Experimental Biology and Medicine 224:61-68.

Metabolic differences between rats and humans probably mean that humans are more sensitive to BPA than are rats: Elsby, R, JL Maggs, J Ashby and BK Park. 2001. Comparison of the modulatory effects of human and rat liver microsomal metabolism on the estrogenicity of bisphenol A: implications for extrapolation to humans. Journal of Pharmacology and Experimental Therapeutics 297-103-113.

A confirmation of BPA low dose effects, and demonstration that the effects include impacts on estrous cyclicity and plasma LH levels: Rubin, BS, MK Murray, DA Damassa, JC King and AM Soto. 2001. Perinatal Exposure to Low Doses of Bisphenol A Affects Body Weight, Patterns of Estrous Cyclicity, and Plasma LH Levels. Environmental Health Perspectives 109: 675-680.

BPA speeds the pace of sexual development in mice, and causes mice to be obese: Howdeshell, K, AK Hotchkiss, KA Thayer, JG Vandenbergh and FS vom Saal. 1999. Plastic bisphenol A speeds growth and puberty. Nature 401: 762-764.

Leslie’s Comments

Using natural progesterone helps to balance the estrogen dominance so prevalent in our lives. See Dr. Judi Gerstung’s book on hormone balancing at http://www.estrogenissues.com

Read the complete article and related information at Our Stolen Future – BPA Bisphenol A Levels in Plastic