Troubling Meaty 'Estrogen'

Troubling Meaty 'Estrogen'

High temperature cooking can imbue meats with a chemical that acts like a hormone

Women take note. Researchers find that a chemical that forms in overcooked meat, especially charred portions, is a potent mimic of estrogen, the primary female sex hormone. That's anything but appetizing, since studies have linked a higher lifetime cumulative exposure to estrogen in women with an elevated risk of breast cancer.  

HORMONAL HAMBURGER? Depending on the temperature at which this burger was grilled—especially how hot its outer surface got—it may have hosted chemical reactions that created PhIP, a carcinogen that has a potent hormonal alter-ego. It can mimic the biological activity of estrogen, the primary female sex hormone.

Indeed, the new finding offers a "biologically plausible" explanation for why diets rich in red meats might elevate breast-cancer risk, notes Nigel J. Gooderham of Imperial College London.

At the very high temperatures reached during frying and charbroiling, natural constituents of meats can undergo chemical reactions that generate carcinogens known as heterocyclic amines. Because these compounds all have very long, unwieldy chemical monikers, most scientists refer to them by their abbreviations, such as IQ, MeIQ, MeIQx, and PhIP.

Of the nearly two dozen different heterocyclic amines that can form, PhIP dominates. It sometimes accumulates in amounts 10 to 50 times higher than that of any other member of this toxic chemical family, Gooderham says. Moreover, he adds, although heterocyclic amines normally cause liver tumors in exposed animals, PhIP is different: "It causes breast cancer in female rats, prostate cancer in male rats, and colon cancer in both." These are the same cancers that in people are associated with eating a lot of cooked meats.

However, the means by which such foods might induce cancer has remained somewhat elusive. So, building on his team's earlier work, Gooderham decided to probe what the heterocyclic amine did in rat pituitary cells. These cells make prolactin—another female sex hormone—but only when triggered by the presence of estrogen. Prolactin, like estrogen, fuels the growth of many breast cancers.

In their new test-tube study, Gooderham and coauthor Saundra N. Lauber show that upon exposure to PhIP, pituitary cells not only make progesterone, but also secrete it. If these cells do the same thing when they're part of the body, those secretions would circulate to other organs—including the breast.

But "what was startling," Gooderham told Science News Online, is that it took just trace quantities of the heterocyclic amine to spur prolactin production. "PhIP was incredibly potent," he says, able to trigger progesterone production at concentrations comparable to what might be found circulating in the blood of people who had eaten a couple of well-done burgers.

The toxicologist cautions that there's a big gap between observing an effect in isolated cells growing in a test-tube and showing that the same holds true in people.

However, even if PhIP does operate similarly in people, he says that's no reason to give up grilled meat. Certain cooking techniques, such as flipping hamburgers frequently, can limit the formation of heterocyclic amines. Moreover, earlier work by the Imperial College team showed that dining on certain members of the mustard family appear to detoxify much of the PhIP that might have inadvertently been consumed as part of a meal.

The human link

Three recent epidemiological studies support concerns about the consumption of grilled meats.

In the first, Harvard Medical School researchers compared the diets of more than 90,000 premenopausal U.S. nurses. Over a 12-year period, 1,021 of the relatively young women developed invasive breast cancers. The more red meat a woman ate, the higher was her risk of developing invasive breast cancer, Eunyoung Cho and her colleagues reported in the Archives of Internal Medicine last November. The increased risk was restricted, however, only to those types of breast cancers that are fueled by estrogen or progesterone.

Overall, women who ate the most red meat—typically 1.5 servings or more per day—faced nearly double the invasive breast-cancer risk of those eating little red meat each week.

Related findings emerged in the April 10 British Journal of Cancer. There, researchers at the University of Leeds reported data from a long-running study of more than 35,000 women in the United Kingdom who ranged in age from roughly 35 to 70. Regardless of the volunteers' age, Janet E. Cade's team found, those who consumed the most meat had the highest risk of breast cancer.

Shortly thereafter, Susan E. Steck of the University of South Carolina's school of public health and her colleagues linked meat consumption yet again with increased cancer risk, but only in the older segment of the women they investigated. By comparing the diets of 1,500 women with breast cancer to those of 1,550 cancerfree women, the scientists showed that postmenopausal women consuming the most grilled, barbecued, and smoked meats faced the highest breast-cancer risk.

These data support accumulating evidence that a penchant for well-done meats can hike a woman's breast-cancer risk, Steck and her colleagues concluded in the May Epidemiology.

PhIP fighters

Such findings have been percolating out of the epidemiology community for years. Nearly a decade ago, for instance, National Cancer Institute scientists reported finding that women who consistently ate their meat very well done—with a crispy, blackened crust—faced a substantially elevated breast-cancer risk when compared to those who routinely ate rare- or medium-cooked meats.

However, even well-done meats without char can contain heterocyclic amines, chemical analyses by others later showed. The compounds' presence appears to correlate best with how meat is cooked, not merely with how brown its interior ended up.

At high temperatures, the simple sugar glucose, together with creatinine—a muscle-breakdown product, and additional free amino acids, can all interact within beef, chicken, and other meats to form heterocyclic amines. In contrast, low-temperature cooking or a quick searing may generate none of the carcinogens.

Because there's no way to tell visually, by taste, or by smell whether PhIP and its toxic kin lace cooked meat, food chemists have been lobbying commercial and home chefs to reduce the heat they use to cook meats—or to turn meats frequently to keep the surfaces closest to the heat source from getting too hot.

The significance of this was driven home to Gooderham several years ago when just such tactics spoiled an experiment he was launching to test whether Brussels sprouts and broccoli could help detoxify PhIP. "I bought 30 kilograms of prime Aberdeen angus lean beef," he recalls. "Then we ground it up and I gave it to a professional cook to turn into burgers and cook." Professional cooks tend to move meats around quite a bit, he found. The result: His expensive, chef-prepared meat contained almost no PhIP.

In the end, he says, "I sacked the cook, bought another 30 kilos of meat and prepared the burgers myself. It was a costly lesson."

Once restarted, however, that study yielded encouraging data.

One way the body detoxifies and sheds toxic chemicals is to link them to what amounts to a sugar molecule. Consumption of certain members of the mustard (Brassica) family, such as broccoli and Brussels sprouts (both members of the B. oleracea species)—can encourage this process. So Gooderham's team fed 250 grams (roughly half a pound) each of broccoli and Brussels sprouts each day to 20 men for almost 2 weeks. On the 12th day, the men each got a cooked-meat meal containing 4.9 micrograms of PhIP.

Compared to similar trial periods when their diets had been Brassica-free, the volunteers excreted up to 40 percent more PhIP in urine, the researchers reported in Carcinogenesis.

Experimental data suggest that two brews may also help detoxify heterocyclic amines. In test-tube studies, white tea largely prevented DNA damage from the heterocyclic amine IQ (SN: 4/15/00, p. 251), and in mice, extracts of beer tackled MeIQx and Trp-P-2.

The best strategy of all, most toxicologists say, is to prevent formation of heterocyclic amines in the first place. In addition to frequently turning meat on the grill or fry pan, partially cooking meats in a microwave prior to grilling will limit the toxic chemicals' formation. So will mixing in a little potato starch to ground beef before grilling or marinating meats with a heavily sugared oil-and-vinegar sauce. 

Climate Change Pollution Rising—Thanks to Overwhelmed Oceans and Plants

Climate Change Pollution Rising—Thanks to Overwhelmed Oceans and Plants

Carbon dioxide levels in the atmosphere continue to rise thanks to dirtier economies and a weakening in natural systems' ability to remove the greenhouse gas

	WINDS OF CHANGE:  Changed circumpolar winds are interfering with the Southern Ocean's ability to absorb carbon dioxide.

The world may finally acknowledge that global warming is a major environmental hazard. But new research shows that reducing the main greenhouse gas behind it may be even more difficult than previously believed. The reason: the world's oceans and forests, which scientists were counting on to help hold off catastrophic rises in carbon dioxide, are already so full of CO₂ that they are losing their ability to absorb this climate change culprit.

"For every ton of CO₂ emitted [into] the atmosphere, the natural sinks are removing less carbon than before," says biologist Josep "Pep" Canadell, executive director of the Global Carbon Project—an Australia–based research consortium devoted to analyzing the pollution behind global warming. "This trend will continue into the future."

Specifically, oceans and plant growth absorbed only around 540 kilograms per metric ton (1,190 pounds per short ton) of the CO₂ produced in 2006, compared with 600 kilograms per metric ton (1,322 pounds per short ton) in 2000. Coupled with an emissions growth rate of 3.3 percent—triple the growth rate of the 1990s—the atmospheric burden is now rising by nearly two parts per million of CO₂ a year, the fastest growth rate since 1850, the international team of researchers reports in Proceedings of the National Academy of Sciences USA.  

"We have yet to make real progress in turning the world toward decreasing CO₂ emissions," says the study's co-author Chris Field, director of the Carnegie Institution of Washington's Department of Global Ecology in Stanford, Calif. "A greater buildup of CO₂ means more warming."

Atmospheric concentrations of the most ubiquitous greenhouse gas reached 381 parts-per-million in 2006 after emissions of CO₂ from burning fossil fuels rose to 8.4 billion metric tons (1.85 X 10¹³ pounds) per year, according to figures from the United Nations, British Petroleum and the U.S. Geological Survey.

All told, human activity released 9.9 billion metric tons (2.18 X 10¹³ pounds) of carbon in 2006, up from just 8.4 billion metric tons (1.85 X 10¹³ pounds) in 2000. At the same time, poleward shifts of westerly winds in the Southern Ocean reduced the region's ability to suck up CO₂ as have mid-latitude droughts, which slowed the growth rate of forests and plants that capture carbon.

New maritime measurements over the past decade also show that the North Atlantic's ability to absorb CO₂ has been cut in half, according to researchers from the University of East Anglia who were not affiliated with the study by Canadell and his colleagues. "Until now, we thought that the decline in the efficiency of natural sinks was going to happen during the 21st century and more strongly during [its] second half," Canadell says. "If we didn't [include in the assumptions] that this was going to happen [so soon], have we underestimated the decline in the efficiency into the future?"

In addition, this research shows that CO₂ emissions over the past decade were higher than those considered in the most dire scenarios for future climate change, which means that even more drastic actions will be needed to stem global warming. "The longer we wait to reduce emissions," Canadell says, "the harder the cuts that will be required to stabilize atmospheric CO₂ emissions."

Taming Baby Rage: Why Are Some Kids So Angry?

Taming Baby Rage: Why Are Some Kids So Angry?

New research indicates babies are born with violent tendencies that most learn to control

	FAILURE TO UNLEARN:   A Canadian researcher suggests that all children have a tendency to be aggressive as toddlers, but, through socialization, many learn to communicate through different means.

It is not the cartoons that make your kids smack playmates or violently grab their toys but, rather, a lack of social skills, according to new research.

"It's a natural behavior and it's surprising that the idea that children and adolescents learn aggression from the media is still relevant," says Richard Tremblay, a professor of pediatrics, psychiatry and psychology at the University of Montreal, who has spent more than two decades tracking 35,000 Canadian children (from age five months through their 20s) in search of the roots of physical aggression. "Clearly youth were violent before television appeared." 

Tremblay's previous results have suggested that children on average reach a peak of violent behavior (biting, scratching, screaming, hitting…) around 18 months of age. The level of aggression begins to taper between the ages of two and five as they begin to learn other, more sophisticated ways of communicating their needs and wants.

Tremblay on Wednesday is set to present preliminary study results showing a genetic signature consistent with chronic violent behavior at a meeting of The Royal Society, the U.K.'s academy of science, in London.

"We're looking at to what extent the chronically aggressive individuals show differences in terms of gene expressions compared to those on the normal trajectory," he told ScientificAmerican.com. "The individuals that are chronically aggressive have…more genes that are not expressed." The fact that a gene can be silenced or the level of protein it encodes reduced, he added, "is an indication that the problem is at a very basic level."

When children first begin to poke, prod and even slap, parents, teachers and siblings often react by indicating that those behaviors are inappropriate. But, citing studies done in animals, Tremblay notes that an unfit environment beginning in the womb may affect a child's ability to learn this lesson in the first place. And he plans to extend his genetic studies to include expectant mothers to determine if their behavior during pregnancy is linked to the down tuning of genes that may be associated with chronic aggression.

"In the long studies we've been doing, we've measured a number of characteristics during pregnancy and after birth that are good predictors'' of chronic aggression in children, Tremblay notes. Possible factors that might influence neurobiological development of the fetus, he says, include smoking, drinking, poor nutrition and excessive stress.

Tremblay speculates that genes play a significant role: for instance damaged genes may make it hard for children to acquire language, frustrating them and making them prone to violence, among other means of making themselves heard. "When you don't master language," Tremblay says, "it's hard to get people to understand what you want."

Kate Keenan, an associate professor of psychiatry at the University of Chicago, views this new genetic analysis as the logical next step in Tremblay's long-term exploration into childhood aggression. She believes Tremblay's work may help uncover genetic profiles distinct to chronically aggressive children that may allow researchers to answer questions like, "Can we differentiate [between these kids] even earlier?" [and] "How early can you intervene?" 

Climate change blamed for fading foliage

Climate change blamed for fading foliage

Every fall, Marilyn Krom tries to make a trip to Vermont to see its famously beautiful fall foliage. This year, she noticed something different about the autumn leaves.

"They're duller, not as sparkly, if you know what I mean," Krom, 62, a registered nurse from Eastford, Conn., said during a recent visit. "They're less vivid."

Other "leaf peepers" are noticing, too, and some believe climate change could be the reason.

Forested hillsides usually riotous with reds, oranges and yellows have shown their colors only grudgingly in recent years, with many trees going straight from the dull green of late summer to the rust-brown of late fall with barely a stop at a brighter hue.

"It's nothing like it used to be," said University of Vermont plant biologist Tom Vogelmann, a Vermont native.

He says autumn has become too warm to elicit New England's richest colors.

According to the National Weather Service, temperatures in Burlington have run above the 30-year averages in every September and October for the past four years, save for October 2004, when they were 0.2 degrees below average.

Warming climate affects trees in several ways.

Colors emerge on leaves in the fall, when the green chlorophyll that has dominated all spring and summer breaks down.

The process begins when shorter days signal leaves to form a layer at the base of their stems that cuts off the flow of water and nutrients. But in order to hasten the decline of chlorophyll, cold nights are needed.

In addition, warmer autumns and winters have been friendly to fungi that attack some trees, particularly the red and sugar maples that provide the most dazzling colors.

"The leaves fall off without ever becoming orange or yellow or red. They just go from green to brown," said Barry Rock, a forestry professor at the University of New Hampshire.

He says 2004 was "mediocre, 2005 was terrible, 2006 was pretty bad although it was spotty. This year, we're seeing that same spottiness."

"Leaf peeping" is big business in Vermont, with some 3.4 million visitors spending nearly $364 million in the fall of 2005, according to state estimates.

State tourism officials reject the notion that nature's palette is getting blander. Erica Housekeeper, spokeswoman for the state Department of Tourism and Marketing, said she had heard nothing but positive reports from foresters and visitors alike this year.

The problem is perception, Housekeeper says: Recollections of autumns past become tinged by nostalgia.

"Sometimes, we become our own worst critics," Housekeeper said.

People who rely on autumn tourism in New England are worried.

"I don't have a sense that the colors are off, but the timing is definitely off," said Scott Cowger, owner and innkeeper at the Maple Hill Farm Bed & Breakfast Inn at Hallowell, Maine.

"Some trees are just starting to change now," Cowger said Thursday. "It used to be, religiously, it was the second week of October when they were at their peak. I would tell my guests to come the second week if you want to see the peak colors. But it's definitely the third or fourth week at this point."

People in Northampton, Mass., are still waiting on fall color. If foliage-viewing is the goal, "I wouldn't send anybody down this way yet," Autumn Inn desk clerk Mary Pelis said this past week.

"The way things are going, the foliage season is the one sure thing for us," said Amie Emmons, innkeeper at the West Mountain Inn, in Arlington, Vt. "We book out two years in advance. It's very concerning if you think the business could start to be affected."

The colors of fall are seen on trees that frame the First Congregational Church in...

 

Cave Speak: Did Neandertals Talk?

Cave Speak: Did Neandertals Talk?

Discovery of the human variant of the FOXP2 gene in Neandertals suggests they may have had language skills

	PREHISTORIC PRATTLERS:  New study finds Neandertals had human gene for speech

German researchers have discovered Neandertals apparently had the human variant of a gene that is linked to speech and language. A team of scientists, primarily from the Max Planck Institute for Evolutionary Anthropology in Leipzig, made the discovery during efforts to reconstruct a full genome of the extinct hominid.

The findings push back the estimated timing of the FOXP2 gene's selective sweep (rapid spread of a gene mutation due to the survival advantage it conferred) from 200,000 to 350,000 years ago, when the common ancestor of Neandertals and humans roamed the earth.

"From the point of this gene, there is no reason to think that Neandertals did not have language as we do," says Planck Institute geneticist Johannes Krause, a co-author of the study published in Current Biology. "However, many other as yet unknown genes are involved in language, so in the future these will have to be found and looked at in Neandertals."

 

The human version of the FOXP2 (short for fork-head box P2) differs from that of the chimp (the closest living relative of humans) in two places along the genetic code, causing differences in two amino acids in the protein coded by the gene. FOXP2 was first tied to language in 2001, when a mutation in it was shown to affect a person's ability to speak.

To determine which version of FOXP2 Neandertals carried, the research team extracted DNA from a well-preserved fossil found in the El Sidrón Cave in northern Spain. This marks the first time a particular gene was sequenced from a Neandertal's nuclear DNA. Although DNA taken from the cellular mitochondria (energy centers) is typically easier to access, fossils are often contaminated by human contact.

The team took steps to ensure they were sequencing Neandertal DNA and not modern human residues. Among them: sequencing specific parts of the Y chromosome and comparing them with those of modern human DNA. The samples were distinct, indicating that they were dealing with an authentic specimen.

When the sequencing was complete, the Neandertal FOXP2 showed the same two mutations that the human gene carries (compared with the chimp version). The group did not find any genetic evidence of interbreeding between humans and Neandertals, leading them to conclude this incarnation of the gene must have propagated and spread prior to the genetic split of the two hominid species more than 300,000 years ago.

Simon Fisher, a molecular neuroscientist at the University of Oxford in England, says the new work shows a better method for dating the evolution of certain genes, as opposed to inferring from changes throughout human evolution. He was more cautious about its link to Neandertal's speaking ability. "We do not think of FOXP2 as 'the speech gene,'" he says. "It is instead just one piece of a complicated puzzle, which likely involves many different factors. … The FOXP2 gene has been around for a very long time, found in similar form in distantly related vertebrate species, and it may be important not only for brain development and function but also in other tissues."

Krause says the Planck team will continue to cobble together the Neandertal genome and chart the evolution of other genes by comparing Homo sapiens with Neandertal DNA. Some other candidates include ASPM, which is tied to microcephaly (a condition when the head is disproportionately smaller than the body), and MC1R, implicated in skin pigmentation.