February 22, 2010
By S.L. Baker
Gastroschisis is a birth defect in which the intestines, and sometimes other organs, develop outside the fetal abdomen and poke out through an opening in the abdominal wall. Long considered a rare occurrence, gastroschisis has mysteriously been on the rise over the last three decades. In fact, the incidence of the defect has soared, increasing two to four times in the last 30 years. But why?
Researchers think they’ve found the answer. The culprit behind the suffering of babies born with this condition appears to be the agricultural chemical atrazine. That’s the conclusion of a study just presented at the annual meeting of the Society for Maternal-Fetal Medicine (SMFM) held in Chicago.
Researchers at the University of Washington in Seattle were alerted to a higher than normal number of cases in of the birth defect in babies born in eastern Washington. So they began investigating to see if the increased incidence was due to some kind of environmental exposure in that area.
“Our state has about two times the national average number of cases of gastroschisis,” Dr. Sarah Waller, one of the study’s authors, said in a statement to the media. “The life expectancy for fetuses with this diagnosis is better than 90 percent; however it requires delivery at a tertiary care center with immediate neonatal intervention which often separates families and can cause serious financial and emotional stress.”
The condition can lead to poor function of the bowel after delivery and potential long term feeding problems. Bottom line: babies with this birth defect must undergo the trauma of surgery right after birth. And while most survive, some babies with gastroschisis have significant damage to the bowel due to direct contact between the intestine and amniotic fluid or because the intestine was twisted. These infants may develop a condition known as “short gut” which can lead to stunted growth and a host of feeding and other problems.
For the new study, Dr. Waller and her research team went to work investigating all cases of live born infants with gastroschisis during the period between 1987 and 2006. They matched birth certificates with databases from the U.S. Geological Survey that revealed where agricultural spraying took place and what chemicals were used. It turns out the chemicals atrazine, nitrates, and 2, 4 dichlorophenoxyacetic acid were heavily sprayed in the area.
Of the 805 cases and 3,616 controls in the study, gastroschisis developed far more frequently among babies whose mothers lived less than 25 km from the site of high surface water that was specifically contaminated with one of the chemicals — atrazine. What’s more, the risk of gastroschisis was found to especially rise in babies of women who conceived in the spring, from March through May. Those are the months when use of the chemical is the most prevalent.
The problem with atrazine
According to the Environmental Protection Agency (EPA), atrazine is applied to crops (especially corn, sorghum, and sugarcane) before and after planting to control broadleaf and grassy weeds. It is used most heavily in the Midwest on agricultural crops but it is also applied to residential lawns, particularly in Florida and the Southeast.
Problems linked to atrazine have been in the news previously. Earlier research showed it causes sexual abnormalities in frogs and the chemical has also been linked to prostate cancer in workers at an atrazine manufacturing plant.
So why is it still widely used? Unfortunately, the EPA has done little to address the mounting evidence that atrazine is harmful to humans as well as animals. Last fall the agency announced it was going to start a new assessment of the chemical in 2010 that could take months to years to complete. In the meantime, tons of atrazine will continue to be sprayed on crops and lawns — and mothers and their unborn babies will continue to be exposed to this chemical now linked to a serious and potentially deadly birth defects.
November 12, 2009
by Alice Park
If you have ever fought the battle of the bulge, then you are all too familiar with its key players: diet, exercise and your genes. The less you move (calories out) and the more you eat (calories in), the more fat you gain — an equation that may be heavily influenced by your particular genes. But scientists have long known that these three factors do not adequately explain every case of obesity, and now researchers are discovering increasingly convincing evidence of another important contributor to body weight, one that until recently has been almost completely ignored: the bacteria that live in your gut.
Technically, they’re known as the gut microbiota, a universe of tens of trillions of microbes, which live and thrive in the human intestinal tract and colon and most of which survive without oxygen. These microbes perform an enormous range of vital functions, including helping regulate the calories the body obtains from food and stores as fat. In other words, they may help regulate weight. And a new study published on Nov. 12 in Science Translational Medicine suggests that the particular type and balance of bugs you harbor in your gut may help push your body toward either obesity or leanness and that these microbe populations might even be manipulated to potentially change your weight.
The new study builds on previous research in mice that suggests that heavy bodies may have a different makeup of gut bugs than thin ones. The gut microbiota of obese mice has been shown to have significantly more of one main type of bacteria called Firmicutes and fewer of another kind called Bacteroidetes (both types populate human guts as well); in normal mice, the distribution is the opposite. Jeffrey Gordon at Washington University in St. Louis, Mo., who conducted the previous research, experimented again with mice for the new paper. This time, however, he and his team used human microbiota to colonize mouse guts and then fed the rodents the equivalents of typical human diets to see how their microbes — and their weight — changed.
Researchers started with mice that were specially bred to be germ-free — with no gut microbiota of their own — and to be able to nurture human gut microbiota. Researchers injected the mice with samples of fresh and frozen human feces, the bacteria from which took hold and colonized in the gut of the mice. If that surprises you, it absolutely stunned the researchers. “We were surprised that so much of the diversity present in human microbial communities could be recaptured in mice,” says Gordon, who has been studying gut microbiota for more than five years.
The fact that the human gut flora flourished in the rodents was indeed an experimental coup. Since the mice were genetically engineered to be germ-free, lacking a functioning immune system, the scientists could be certain that any bug colonies that took hold in the mouse guts originated entirely from the human sample, not the mice. Being able to recreate the living human gut environment so faithfully in an animal was a welcome prize.
The main advantage was that Gordon and his team now had the cutting-edge DNA-sequencing capability to scan and analyze all the genes contained in those bacteria. That meant researchers could determine not only which species of bacteria were present and in what proportions, but also which genes these bugs were actively using in different conditions. Before such genomic-analysis technology became available, researchers could study only the gut microbes (animal or human) that could be cultured outside their intestinal home — something that not all of the oxygen-shunning bugs were amenable to — but never the complete microbiota of the gut. “We cannot recapitulate the entire microbial diversity that exists in these complex communities. We simply don’t know how to culture them, so we could miss a lot of diversity,” says Gordon.
That diversity and its impact came into plain view when the researchers started experimenting with the rodents’ diet. When one group of mice was fed a typical Western diet, high in fat and sugars, they tended to gain weight and grow more Firmicutes gut bacteria and fewer Bacteroidetes. In mice given a low-fat plant-based chow, the distribution of the two groups of bugs flipped and the animals remained lean. It’s not clear whether the balance of gut bugs causes weight gain or is a result of it, but the findings suggest that a “gut profile” could potentially serve as a diagnostic tool for identifying who might have a propensity for obesity. If, for instance, your gut environment contains a preponderance of Firmicutes, then your body may be predisposed to digest calories in a way that leads to greater fat storage. In fact, in Gordon’s earlier work with identical twins of different weights, he found that the obese twin tended to have more Firmicutes colonies than the leaner one.
October 26, 2009
By S. L. Baker
It’s not unusual to hear about herbicides having suspected toxic effects or prescription drugs producing side effects. But a new National Institutes of Health (NIH) funded study just published in the Journal of Medicinal Chemistry has found another negative and surprising way common herbicides and fibrate drugs (which are used to lower elevated blood lipids) impact the human body: they block a nutrient-sensing taste receptor on the tongue called T1R3.
So what’s the big deal about this? It turns out there’s emerging evidence these taste receptors are also found in hormone-producing cells in the intestine and pancreas. When working properly, these internal taste receptors in the gut trigger the release of hormones involved in the regulation of normal homeostasis (the ability of the body to maintain internal physiological stability) of glucose as well as energy metabolism. Simply put, screwing up the ability of T1R3 to sense certain nutrients could possibly wreak havoc on the human body in a variety of ways — from playing a role in unhealthy blood sugar levels to causing people to gain weight .
“Compounds that either activate or block T1R3 receptors could have significant metabolic effects, potentially influencing diseases such as obesity, type II diabetes and metabolic syndrome,” said Monell geneticist and study leader Bedrich Mosinger, MD, PhD, in a statement to the media.
For their study, Dr. Mosinger and his research team tested the ability of two classes of chemical compounds to block the T1R3 taste receptor. These compounds were selected because they have strong structural similarities to lactisole, a sweet taste inhibitor that is known to block T1R3. Specifically, the researchers investigated fibrates (a class of drugs often used to lower blood cholesterol, especially triglycerides), and phenoxy herbicides.
Fibrate drugs are sold in the U.S. under several names including gemibrozil (brand name Lopid) and fenobribrate (brand name Tricor). Phenoxy herbicides are chemicals widely used in agricultural fields, on golf courses, rights-of-way and lawns to control broad-leaf weeds. The best known, called 2,4-D, is one of the most extensively used herbicides in the world. According to the Oregon State University Extension Service web site, popular brands of phenoxy herbicides include MCPA, Crossbow, Banvel, Garlon, Weed-B-Gone, and Brush Killer. They are also incorporated into a host of “weed and feed” and brush control products for use on grass.
In laboratory experiments, the researchers found that both classes of compounds were very potent in blocking activation of the human sweet taste receptors. Additional tests showed that this ability of both fibrates and phenoxy herbicides to block T1R3 is specific to humans.
“The metabolic consequences of short and long-term exposures of humans to phenoxy herbicides are unknown. This is because most safety tests were done using animals, which have T1R3 receptors that are insensitive to these compounds,” Dr. Mosinger said in the press statement. “Given the number of compounds used in agriculture, medicine and the food industry that may affect human T1R3 and related receptors, more work is needed to identify the health-related effects of exposure to these compounds.”