Showing posts with label estrogen. Show all posts
Showing posts with label estrogen. Show all posts

Wednesday, March 5, 2014

Plastics Are Unsafe in Any Form for Foods

We have known for a long time that bisphenol A (BPA) is a dangerous endocrine disruptor, but now we also know it is associated with prostate cancer.  Here is the introduction to the press release of the new study published in PLoS ONE, which is open access.

BPA linked to prostate cancer, study shows

March 4, 2014CINCINNATI—Findings by Cincinnati Cancer Center researchers show that levels of bisphenol A (BPA) in men's urine could be a marker of prostate cancer and that low levels of BPA exposure can cause cellular changes in both non-malignant and malignant prostate cells. 

This research, published in the March 3 edition of PLOS ONE, provides the first evidence that urinary BPA levels may help predict prostate cancer and that disruption of a cell duplication cycle through exposure to low-dose BPA may cause cancer development in the prostate.
BPA, an environmental pollutant with estrogen activity, is used to make hard, clear plastic and is common in many food product containers. It has been linked to neurological defects, diabetes and a number of cancers, including breast and prostate.
Many of us who care about our health have tried to eliminate BPA from our lives and hoped that would be good enough to protect us somewhat. Not so much.

In a new article from Mother Jones, it seems all of those BPA-free plastics have a lot of different, and sometimes even more toxic, endocrine disrupting chemicals. Oh joy!

The Scary New Evidence on BPA-Free Plastics

And the Big Tobacco-style campaign to bury it.


—Mariah Blake | March/April 2014 Issue


Photographs by Evan Kafka

Update (3/3/14): After this story went to press, the US Food and Drug Administration published a paper finding that BPA was safe in low doses. However, the underlying testing was done on a strain of lab rat known as the Charles River Sprague Dawley, which doesn't readily respond to synthetic estrogens, such as BPA. And, due to laboratory contamination, all of the animals—including the control group—were exposed to this chemical. Academic scientists say this raises serious questions about the study's credibility. Stay tuned for more in-depth reporting on the shortcomings of the FDA's most recent study.

EACH NIGHT AT DINNERTIME, a familiar ritual played out in Michael Green's home: He'd slide a stainless steel sippy cup across the table to his two-year-old daughter, Juliette, and she'd howl for the pink plastic one. Often, Green gave in. But he had a nagging feeling. As an environmental-health advocate, he had fought to rid sippy cups and baby bottles of the common plastic additive bisphenol A (BPA), which mimics the hormone estrogen and has been linked to a long list of serious health problems. Juliette's sippy cup was made from a new generation of BPA-free plastics, but Green, who runs the Oakland, California-based Center for Environmental Health, had come across research suggesting some of these contained synthetic estrogens, too.

He pondered these findings as the center prepared for its anniversary celebration in October 2011. That evening, Green, a slight man with scruffy blond hair and pale-blue eyes, took the stage and set Juliette's sippy cups on the podium. He recounted their nightly standoffs. "When she wins…every time I worry about what are the health impacts of the chemicals leaching out of that sippy cup," he said, before listing some of the problems linked to those chemicals—cancer, diabetes, obesity. To help solve the riddle, he said, his organization planned to test BPA-free sippy cups for estrogenlike chemicals.

The center shipped Juliette's plastic cup, along with 17 others purchased from Target, Walmart, and Babies R Us, to CertiChem, a lab in Austin, Texas. More than a quarter—including Juliette's—came back positive for estrogenic activity. These results mirrored the lab's findings in its broader National Institutes of Health-funded research on BPA-free plastics. CertiChem and its founder, George Bittner, who is also a professor of neurobiology at the University of Texas-Austin, had recently coauthored a paper in the NIH journal Environmental Health Perspectives. It reported that "almost all" commercially available plastics that were tested leached synthetic estrogens—even when they weren't exposed to conditions known to unlock potentially harmful chemicals, such as the heat of a microwave, the steam of a dishwasher, or the sun's ultraviolet rays. According to Bittner's research, some BPA-free products actually released synthetic estrogens that were more potent than BPA.

Estrogen plays a key role in everything from bone growth to ovulation to heart function. Too much or too little, particularly in utero or during early childhood, can alter brain and organ development, leading to disease later in life. Elevated estrogen levels generally increase a woman's risk of breast cancer.

Estrogenic chemicals found in many common products have been linked to a litany of problems in humans and animals. According to one study, the pesticide atrazine can turn male frogs female. DES, which was once prescribed to prevent miscarriages, caused obesity, rare vaginal tumors, infertility, and testicular growths among those exposed in utero. Scientists have tied BPA to ailments including asthma, cancer, infertility, low sperm count, genital deformity, heart disease, liver problems, and ADHD. "Pick a disease, literally pick a disease," says Frederick vom Saal, a biology professor at the University of Missouri-Columbia who studies BPA.



BPA exploded into the headlines in 2008, when stories about "toxic baby bottles" and "poison" packaging became ubiquitous. Good Morning America issued a "consumer alert." The New York Times urged Congress to ban BPA in baby products. Sen. Dianne Feinstein (D-Calif.) warned in the Huffington Post that "millions of infants are exposed to dangerous chemicals hiding in plain view." Concerned parents purged their pantries of plastic containers, and retailers such as Walmart and Babies R Us started pulling bottles and sippy cups from shelves. Bills banning BPA in infant care items began to crop up in states around the country.

Today many plastic products, from sippy cups and blenders to Tupperware containers, are marketed as BPA-free. But Bittner's findings—some of which have been confirmed by other scientists—suggest that many of these alternatives share the qualities that make BPA so potentially harmful.

Those startling results set off a bitter fight with the $375-billion-a-year plastics industry. The American Chemistry Council, which lobbies for plastics makers and has sought to refute the science linking BPA to health problems, has teamed up with Tennessee-based Eastman Chemical—the maker of Tritan, a widely used plastic marketed as being free of estrogenic activity—in a campaign to discredit Bittner and his research. The company has gone so far as to tell corporate customers that the Environmental Protection Agency (EPA) rejected Bittner's testing methods. (It hasn't.) Eastman also sued CertiChem and its sister company, PlastiPure, to prevent them from publicizing their findings that Tritan is estrogenic, convincing a jury that its product displayed no estrogenic activity. And it launched a PR blitz touting Tritan's safety, targeting the group most vulnerable to synthetic estrogens: families with young children. "It can be difficult for consumers to tell what is really safe," the vice president of Eastman's specialty plastics division, Lucian Boldea, said in one web video, before an image of a pregnant woman flickered across the screen. With Tritan, he added, "consumers can feel confident that the material used in their products is free of estrogenic activity."

Eastman's offensive is just the latest in a wide-ranging industry campaign to cast doubt on the potential dangers of plastics in food containers, packaging, and toys—a campaign that closely resembles the methods Big Tobacco used to stifle scientific evidence about the dangers of smoking. Indeed, in many cases, the plastics and chemical industries have relied on the same scientists and consultants who defended Big Tobacco. These efforts, detailed in internal industry documents revealed during Bittner's legal battle with Eastman, have sown public confusion and stymied US regulation, even as BPA bans have sprung up elsewhere in the world. They have also squelched debate about the safety of plastics more generally. All the while, evidence is mounting that the products so prevalent in our daily lives may be leaching toxic chemicals into our bodies, with consequences affecting not just us, but many generations to come.

THE FIGHT OVER THE SAFETY of plastics traces back to 1987, when Theo Colborn, a 60-year-old grandmother with a recent Ph.D. in zoology, was hired to investigate mysterious health problems in wildlife around the Great Lakes. Working for the Washington, DC-based Conservation Foundation (now part of the World Wildlife Fund), she began collecting research papers. Before long, her tiny office was stacked floor to ceiling with cardboard boxes of studies detailing a bewildering array of maladies—cancer, shrunken sexual organs, plummeting fertility, immune suppression, birds born with crossed beaks and missing eyes. Some species also suffered from a bizarre syndrome that caused seemingly healthy chicks to waste away and die.

While the afflictions and species varied widely, Colborn eventually realized they had two factors in common: The young were hardest hit, and, in one way or another, all of the animals' symptoms were linked to the endocrine system, the network of glands that controls growth, metabolism, and brain function, with hormones as its chemical messengers. The system also plays a key role in fetal development. Colborn suspected that synthetic hormones in pesticides, plastics, and other products acted as "hand-me-down poisons," with parents' exposure causing affliction in their offspring. Initially, her colleagues were skeptical. But Colborn collected data and tissue samples from far-flung wildlife populations and unearthed previously overlooked studies that supported her theory. By 1996, when Colborn copublished her landmark book Our Stolen Future, she had won over many skeptics. Based partly on her research, Congress passed a law that year requiring the EPA to screen some 80,000 chemicals—most of which had never undergone any type of safety testing—for endocrine-disrupting effects and report back by 2000.

Around this time, the University of Missouri's vom Saal, a garrulous biologist who previously worked as a bush pilot in Kenya, began studying the effects of synthetic estrogens on fetal mouse development. The first substance he tested was BPA, a chemical used in clear, hard plastics, particularly the variety known as polycarbonate, to make them more flexible and durable. (It's also found in everyday items, from dental sealants and hospital blood bags to cash register receipts and the lining of tin cans.) Naturally occurring estrogens bind with proteins in the blood, limiting the amount that reaches estrogen receptors. But vom Saal found this wasn't true of BPA, which bypassed the body's natural barrier system and burrowed deep into the cells of laboratory mice.

Vom Saal suspected this would make BPA "a hell of a lot more potent" in small doses. Working with colleagues Susan Nagel and Wade Welshons, a professor of veterinary biology, he began testing the effects of BPA at amounts 25 times lower than the EPA's safety threshold. In the late 1990s, they published two studies finding that male mice whose mothers were exposed to these low doses during pregnancy had enlarged prostates and low sperm counts. Even in microscopic quantities, it seemed, BPA could cause the kinds of dire health problems Colborn had found in wildlife. Before long, other scientists began turning up ailments among animals exposed to minute doses of BPA.

These findings posed a direct threat to plastics and chemical makers, which fought back using tactics the tobacco makers had refined to an art form. By the late 1990s, when tobacco companies agreed to drop deceptive marketing practices under a settlement agreement with 46 states, many of the scientists and consultants on the industry's payroll transitioned seamlessly into defending BPA.

Plastics and chemical interests worked closely with the Weinberg Group, which had run Big Tobacco's White Coat Project—an effort to recruit scientists to create doubt about the health effects of secondhand smoke. Soon Weinberg, which bills itself as a "product defense" firm, was churning out white papers and lobbying regulators. It also underwrote a trade group with its own scientific journal, Regulatory Toxicology and Pharmacology, which published studies finding BPA was safe.

The industry also worked hand in glove with the Harvard Center for Risk Analysis, a think tank affiliated with the university's school of public health that has a history of accepting donations from corporations and then publishing research favorable to their products. In the early 1990s, its founder, John D. Graham—who was later tapped as George W. Bush's regulatory czar—lobbied to quash an EPA finding that secondhand smoke caused lung cancer, while soliciting large contributions from Philip Morris.



In 2001, as studies on BPA stacked up, the American Chemistry Council enlisted the center to convene a panel of scientists to investigate low-dose BPA. The center paid panelists $12,000 to attend three meetings, according to Fast Company. Their final report, released in 2004, drew on just a few industry-favored studies and concluded that the evidence that low-dose BPA exposure harmed human health was "very weak." By this point, roughly 100 studies on low-dose BPA were in circulation. Not a single industry-funded study found it harmful, but 90 percent of those by government-funded scientists discovered dramatic effects, ranging from an increased breast cancer risk to hyperactivity. Four of the 12 panelists later insisted the center scrub their names from the report because of questions about its accuracy.

Chemical interests, meanwhile, forged deep inroads with the Bush administration, allowing them to covertly steer the regulatory process. For decades, the Food and Drug Administration has assured lawmakers and the public that BPA is safe in low doses. But a 2008 investigation by the Milwaukee Journal Sentinel revealed that the agency had relied on industry lobbyists to track and evaluate BPA research, and had based its safety assessment largely on two industry-funded studies—one of which had never been published or peer reviewed.

The panel the EPA appointed to develop guidelines for its congressionally mandated endocrine disruptor screening was also stocked with industry-backed scientists. It included Chris Borgert, a toxicology consultant who had worked closely with Philip Morris to discredit EPA research on secondhand smoke. He later served as the president of the International Society of Regulatory Toxicology and Pharmacology, the Weinberg Group-sponsored outfit, which met in the offices of a plastics lobbyist.

Members of the EPA panel say Borgert seemed determined to sandbag the process. "He was always delaying, always trying to confuse the issue," recalls one participant. And the screening approach the EPA settled on came straight from the industry's playbook. Among other things, the chemicals would be tested on a type of rat known as the Charles River Sprague Dawley—which, oddly, doesn't respond to synthetic hormones like BPA.

How best to test for estrogenic activity would become a key front in the fight over plastic safety. The American Chemistry Council joined forces with an unlikely ally, PETA, to fight large-scale chemical-safety testing on animals. At the same time, Borgert and other industry-funded scientists made the case that the other common method for testing—using cells that respond in the presence of estrogen—did not necessarily tell us how a substance would affect animals or humans. In fact, a massive, ongoing NIH-run study has found that cell-based tests track closely with animal studies, which have accurately predicted the effects of synthetic estrogens, particularly DES and BPA, on humans.

Stanton Glantz, who directs the Center for Tobacco Control Research and Education at the University of California-San Francisco, argues the chemical industry's real aim in challenging specific testing methods is to undermine safety testing altogether. "Like the tobacco companies, they want to set up a standard of proof that is unreachable," he says. "If they set the standard of proof, they've won the fight."

DURING THE HEIGHT of the battle over BPA, vom Saal periodically traveled to Texas and huddled around the dining table with his old friend George Bittner, whose home overlooks a walnut grove on the outskirts of Austin. Bittner, who holds a Ph.D. in neuroscience from Stanford, is quirky and irascible. But he has a brilliant mind for science and an interest in applying it to real-world problems—in his lab at UT-Austin, he had developed a nerve-regeneration technique that had helped crippled rats walk within days. And he had taken a keen interest in vom Saal's research on endocrine disruption. "It struck me as the most important public health issue of our time," Bittner told me when we met at his lab. "These chemicals have been correlated with so many adverse effects in animal studies, and they're so pervasive. The potential implications for human health boggle the mind."

In the late 1990s, Bittner—a squat, ruddy man with thinning red hair and Napoleon Dynamite glasses who had made a tidy sum investing in real estate and commodities—began mulling the idea of launching a private company that worked with manufacturers and public health organizations to test products for endocrine disruptors. He believed this approach could help raise awareness and break the regulatory logjam—while also reaping a profit.

In 2002, armed with a $91,000 grant from the National Institutes of Health, Bittner launched a pair of companies: CertiChem, to test plastics and other products for synthetic estrogens, and PlastiPure, to find or develop nonestrogenic alternatives. Bittner then enlisted Welshons to design a special test using a line of breast cancer cells, which multiply rapidly in the presence of estrogen. It features a robotic arm, which is far more precise than a human hand in handling microscopic material.



But before long Bittner began butting heads with Welshons and vom Saal. Bittner wanted the researchers to sign over the rights to the test Welshons had developed, while they insisted it belonged to the University of Missouri. Eventually, they had a bitter falling out. Welshons and vom Saal filed a complaint with the NIH, alleging that Bittner had misrepresented data from Welshons' lab in a brochure. (Bittner maintains that he merely excluded data from contaminated samples; the institute found no evidence of wrongdoing.) Bittner, meanwhile, enlisted V. Craig Jordan, a pharmacology professor at Georgetown University with an expertise in hormones—he discovered a now-common hormone therapy that blocks the spread of breast cancer—to refine the testing protocol. By 2005, Bittner had opened a commercial lab in a leafy office park in Austin. He managed to attract some big-name clients, including Whole Foods, which hired CertiChem to advise it on endocrine-disrupting chemicals and test some of its products.

At this point, BPA was among the most studied chemicals on the planet. In November 2006, vom Saal and a top official at the National Institute of Environmental Health Sciences convened a group of 38 leading researchers from various disciplines to evaluate the 700-plus existing studies on the subject. The group later issued a "consensus statement" that laid out some chilling conclusions: More than 95 percent of people in developed countries were exposed to levels of BPA that are "within the range" associated with health problems in animals, from cancer and insulin-resistant diabetes to early puberty. The scientists also found that there was "great cause for concern with regard to the potential for similar adverse effects in humans," especially given the steep uptick in these same disorders.

At the same time, a new body of research was finding that BPA altered animals' genes in ways that caused disease. For instance, it could switch off a gene that suppresses tumor growth, allowing cancer to spread. These genetic changes were passed down across generations. "A poison kills you," vom Saal explains. "A chemical like BPA reprograms your cells and ends up causing a disease in your grandchild that kills him."

Scientists were also uncovering links between endocrine-disrupting chemicals known as phthalates and health problems, including genital abnormalities and infertility in humans. These chemical additives were commonly found in soft, pliable plastics, such as those used in pacifiers and baby bottle nipples. In 2008, Congress passed a law banning six types of phthalates in children's products. As concerns about BPA hit the mainstream, Congress also launched an investigation into the industry's efforts to manipulate science and regulation, and a number of states proposed BPA bans.

In 2009, the BPA Joint Trade Association—which included the American Chemistry Council, Coca-Cola, and Del Monte, among others—gathered at the Cosmos Club, a members-only retreat in Washington, DC's Dupont Circle. According to meeting minutes leaked to the Milwaukee Journal Sentinel, the group explored messaging strategies, "including using fear tactics (e.g., 'Do you want to have access to baby food anymore?')." The "'holy grail' spokesperson," attendees agreed, was a "pregnant young mother who would be willing to speak around the country about the benefits of BPA."

Even as the industry crafted defensive talking points, some companies began offering BPA-free alternatives. But they often didn't bother testing them for other potentially toxic compounds or synthetic hormones. Nor did they have to: Under US law, chemicals are presumed safe until proven otherwise, and companies are rarely required to collect or disclose chemical-safety data. Michael Green, the Center for Environmental Health director who worried about his daughter's sippy cup, says this results in a "toxic shell game": Corporations that come under pressure to root out toxins often replace them with untested chemicals, which sometimes turn out to be just as hazardous. "It's an unplanned science experiment we're doing on our families," Green told me when I visited him at his Bay Area home, where Juliette, now 5, was padding around in a pink princess costume.

One of the most popular BPA-free options, especially among companies catering to families and health-conscious consumers, was Tritan, a clear, sturdy, heat-resistant plastic that Eastman rolled out in 2007. (Eastman also produces the chemical that sullied the drinking water of 300,000 West Virginians in January.) A company founded by alternative medicine guru Dr. Andrew Weil launched a line of Weil Baby bottles made from Tritan, which it touted as "revolutionary" and "ultra-safe" material. Thermos began churning out Tritan sippy cups, decorated with Barbie and Batman. With more and more consumers demanding BPA-free products, Nalgene, CamelBack, Evenflo, Cuisinart, Tupperware, Rubbermaid, and many other companies also worked Tritan into their production lines.



Eastman, a $7 billion company that was spun off from Eastman Kodak in the 1990s, assured its corporate customers that it had done extensive safety testing on Tritan. But its methods were questionable. According to internal Eastman documents, in 2008 Eastman signed a two-year contract with Sciences International, another product defense firm that had played a key role in the tobacco industry's scientific misinformation campaign. On Sciences' advice, Eastman then commissioned a study that used computer modeling to predict whether a substance contains synthetic estrogens, based on its chemical structure. The model suggested that one of Tritan's ingredients—triphenyl phosphate, or TPP—was more estrogenic than BPA.

Eastman, which never disclosed these findings to its customers, later commissioned another study, this one involving breast cancer cells. Again, the initial results appeared positive for estrogenic activity. In an email to colleagues, Eastman's senior toxicologist, James Deyo, called this an "oh shit moment."
Read the whole article.

Wednesday, September 25, 2013

Mark McManus's 10 Reasons We Should Eat More Broccoli

broccoli

Mark McManus (of MuscleHack) gives 10 excellent reasons to make broccoli a more consistent part of out diets. Because I am dedicated to your health, especially the male readers, I am going to give you 2 additional reasons to eat more broccoli.

11. Cruciferous vegetables, including cabbage, broccoli, Brussels sprouts, and cauliflower all contain diindolylmethane (or DIM), a plant indole that helps the body metabolize estrogens (eliminate them, especially estrodial and 16-hydroxy estrogens) more efficiently. Consumption of cruciferous vegetables has been associated with risk reduction for several estrogen-related cancers, including prostate cancer.

12. Broccoli contains other chemicals, glucosinolates, including glucoraphanin, that are known anti-cancer nutrients. Researchers have also found that those who consumed glucoraphanin-rich vegetable showed signs of an improved metabolism

And now on to the article.

10 Top Reasons You Need Broccoli In Your Diet

by Mark McManus on September 18, 2013 updated September 18, 2013

Want to get healthy or even lose weight? Broccoli needs to be included in your diet.

Here’s 10 reasons why broccoli is good for you!

(1) Broccoli is the king of low carb vegetables – 1.1 grams of net carbohydrate per 100g! (after fiber subtracted) Sometimes I fill my plate up with broccoli and drench it in melted butter or cheese.

(2) A chemical in vegetables such as broccoli, cauliflower and cabbage can boost DNA repair in cells and may stop them becoming cancerous

(3) Eating steamed broccoli reduces the risk of a heart attack by boosting the body’s ability to fight off cell damage, researchers have found.

(4) Did you know broccoli contains more vitamin C than an orange? (ounce for ounce) Vitamin C is great for your hair, skin, teeth, fighting infections and keeping red blood cells healthy.

(5) Did you know broccoli contains as much calcium as a glass of milk? (ounce for ounce) Calcium helps to keep you heart beating regularly and promotes sleep.

(6) Broccoli is also a good source of folate. Folate is necessary for the production and maintenance of new cells.

(7) Broccoli is also a good source of iron. Iron is an essential component of haemoglobin and, therefore, iron is required for normal blood formation and oxygen transport around the body.

(8) Broccoli is also a great source of fiber.

(9) Broccoli is also a good source of potassium. Potassium plays an important role in the physical fluid system of humans and it assists nerve functions.

(10) Broccoli is also a good source of vitamin K. Vitamin K is known to be needed to coagulate blood and to maintain proper bone density. It also plays a key role in proper development of the fetus.

If you’re gonna eat low-carb, broccoli should be a regular feature in your diet. Whether you’re focused on gaining muscle or losing fat, broccoli will greatly assist you in your goal.

Thursday, November 17, 2011

Is the oral contraceptive pill fueling prostate cancer?

People who know better - i.e., cancer researchers who are working at the molecular level and not at the macro level of patient care - have been arguing for years that estrogen exposure (either endogenous or exogenous) is a greater risk factor for prostate cancer than testosterone, which is often still blamed.

In fact, one of the front-line approaches to prostate cancer, despite the evidence that estrogen is the fuel for many cancers (including prostate cancer), is androgen depletion therapy (which has side effects like gynecomastia, diabetes, depression, bone loss, and heart disease, to name a few).

But now there is new evidence that exposure to the chemicals in oral contraceptives may seriously increase the risk for prostate cancer.

This is only a correlation study -  they have not shown cause and effect. And they indicate it's not so much exposure to the chemicals during intercourse (which would be a good reason to switch to a different form of birth control, like vasectomy), but that these chemicals are in the drinking water.

Is oral contraceptive pill fueling prostate cancer?

oral contraceptive pill  
The Pill became publicly available in the 1960s and remains a popular choice of contraceptive

Scientists say research is needed to ascertain if oral contraceptive pill use could be fuelling rising prostate cancer rates.

A Canadian team told the British Medical Journal they had found a possible link.

But experts stress this is not proof that one causes the other and it might be a fluke finding. The researchers believe estrogen by-products in the urine of pill-users may be entering food and drinking water.

The hormone is known to feed the growth of certain cancers.

The latest investigation looked at data from 2007 for individual nations and continents worldwide to see if there was any link.

The researchers found a significant association between contraceptive pill use in the population as a whole with both the number of new cases of, and deaths from, prostate cancer.

This link was irrespective of the nation's wealth, suggesting it might not be down to better disease detection in more affluent countries that also tend to have higher rates of oral contraceptive use.

And it was strongest in Europe.

Additionally, they found no link between prostate cancer and other forms of contraception, like the coil, suggesting it is not something that is sexually transmitted or associated with intercourse itself.

Drs David Margel and Neil Fleshner, from Toronto University, fear that contamination of the food chain with hormones originating from the pill are the likely culprit.

They stress that their work merely suggests a link and is not proof.

"It must be considered hypothesis generating and thought-provoking," they say in their BMJ Open report.

They said more investigations are needed and recommend close monitoring of environmental levels of oral contraceptive by-products or endocrine disruptive compounds (EDCs).

Dr Kate Holmes, of The Prostate Cancer Charity, agreed that more research was warranted.

"While this study raises some interesting questions about the presence of EDCs in the environment, it does not contribute to our overall understanding of the development of prostate cancer."

Jessica Harris, of Cancer Research UK, said uncertainty about the disease remained. "Comparing the rates of two apparently unrelated issues across countries is a notoriously unreliable way of establishing whether they are truly linked, because so many things vary between different countries that it's impossible to say whether one thing is causing the other.

"It has been difficult to identify factors that affect the risk of prostate cancer, but we know that men are at higher risk as they get older, or if they have a strong family history of breast or prostate cancer. The disease is also more common in black men than white or Asian men."

Tuesday, October 6, 2009

The making of the male brain (estrogen required)

Testosterone is THE male hormone, but we wouldn't be men without a little estrogen. Well, OK, these are mice and it may not be the same for humans, but it's interesting.

Hmmm . . . seems like we might see this as a metaphor for psychology, as well, that we might be masculine, but we also need some feminine to be whole, mature men.

The making of the male brain (estrogen required)

It's often said that overly macho males suffer from "too much testosterone." But a new study in mice reveals how estrogen might share in that blame.

The report in the October 2nd issue of Cell, a Cell Press publication, reveals how early estrogen exposure "masculinizes" the brain circuitry, predisposing boys to be boys as it were. That early event is specifically critical in producing male mice that will pick fights with other males and that dutifully mark their territories with urine.

"It's been known for decades that estrogen may play a role in making males behave like males," said Nirao Shah of the University of California, San Francisco. "What we do here is to provide insight into the logic of how estrogen regulates that behavior."

The basis for differences between the sexes in such behaviors, they show, may reside in the neurons that are equipped with an enzyme, called aromatase, that converts testosterone into estrogen. The masculine brain has more of those testosterone-converting neurons in certain regions. The researchers now show that these neurons establish a unique neural circuitry in males, and that this difference in wiring depends on estrogen.

The researchers found that female mice exposed to estrogen as pups get wired to behave as "tomboys" of a sort. Their aromatase neurons now look like what is seen in the male brain, and the female mice take on aggressive and territorial behaviors typically reserved for males.

But if estrogen, the female hormone, establishes male behavior patterns, why don't girls act like boys? Shah explains that the ovaries normally don't pump out any hormone that early in life, but males do see a surge in testosterone at a young age, at least some of which gets converted by aromatase to estrogen.

The findings indicate that adult gonadal hormones are not the entire story when it comes to determining masculine versus feminine behavior, Shah said. "Rather than the gonadal hormones telling the adult brain what do to, the brain interprets signals based on its prior history," he said. Thus, female mice exposed to estrogen as pups respond to estrogen as adults by switching on the aggressive and territorial behaviors typically observed in males.

As for whether differences in early estrogen exposure or in the resulting brain circuitry can account for variation among males in stereotypically male behavior remains to be seen, Shah says.

"About eighty percent of male mice will fight with other males routinely, but there is always a fraction that fight poorly or not much at all," he said, a difference that may be explained by some combination of social experience along with early developmental events that wire the brain differently.

Testosterone itself isn't off the hook yet, however. Shah's team suspects it is also likely to have direct effects. As evidence of that, Shah notes that female mice whose brains are masculinized by exposure to estrogen in early development do fight, but they tend to fight with less intensity than males. But when these females have their ovaries -- their adulthood source of estrogen -- removed and are treated with male levels of testosterone, their will to fight goes up. "It suggests testosterone acts on its own receptor to increase the intensity of male-like fighting," Shah said.

###

The researchers include Melody V. Wu, University of California, San Francisco, San Francisco, CA; Devanand S. Manoli, University of California, San Francisco, San Francisco, CA; Eleanor J. Fraser, University of California, San Francisco, San Francisco, CA; Jennifer K. Coats, University of California, San Francisco, San Francisco, CA; Jessica Tollkuhn, University of California, San Francisco, San Francisco, CA; Shin-Ichiro Honda, Fujita Health University, Toyoake, Aichi, Japan; Nobuhiro Harada, Fujita Health University, Toyoake, Aichi, Japan; and Nirao M. Shah, University of California, San Francisco, San Francisco, CA.