Migraines May Raise a Woman's Odds of Depression

WEDNESDAY, Feb. 22 (HealthDay News) -- As if the debilitating headaches weren't bad enough, women who get migraines or have had them in the past are at increased risk for depression, a new study suggests.

Migraines are intense, throbbing headaches often accompanied by nausea and sensitivity to light or sound. They are three times more common in women than in men.

The study, by researchers at Brigham and Women's Hospital in Boston, suggests that women with any history of migraines were about 40 percent more likely to develop depression than women without a similar history.

"We believe the most important aspect of our study is that migraine patients and their physicians should keep this potential link in mind," said senior study author Dr. Tobias Kurth, a neuroepidemiologist at Brigham and Women's Hospital.

Kurth noted that doctors who treat patients who have migraines might consider asking some specific questions about depression.

The researchers analyzed data from more than 36,000 participants in the U.S. Women's Health Study who did not have depression and had answered questions about their migraine history. The women, aged 45 or older, were categorized either as having active migraine with aura (visual disturbances such as flashing lights or temporary loss of vision); active migraine without aura; prior history of migraine; or no history of migraine. The women also provided information about any depression diagnoses during the study's follow-up period.

Kurth and his colleagues found that more than 6,400 of the women had current or past migraines, and that during an average 14 years of follow-up, nearly 4,000 developed depression.

Women with any history of migraines were 36 percent more likely to develop depression than women with no history of the headaches, and there was no difference between migraines with aura and migraines without aura. The researchers also found that women with only a past history of migraine had 1.41 times the risk of developing depression.

Although the results suggest a link between migraines and depression, they do not show cause and effect.

Kurth said further research is necessary to determine why migraines might increase the risk of depression. "There is not really an easy answer," he said, adding that future studies might look at whether there is a specific common biological mechanism linking both diseases.

Dr. Richard Lipton, vice chair of neurology at Albert Einstein College of Medicine and director of the Montefiore Headache Center in New York City, applauded the research.

"This is a very strong study because of the cohort design, the large sample and the long-term follow-up," he said.

Lipton noted several study limitations, however. The results don't apply to men or to younger women, he said, and it is possible the number of women with depression was even greater, since the diagnosis was based on self-reporting.

The study is scheduled for presentation at the American Academy of Neurology annual meeting in New Orleans in April. Funding was provided by the U.S. National Heart, Lung and Blood Institute and the National Cancer Institute.

Research presented at medical meetings should be considered preliminary until published in a peer-reviewed medical journal.

More information

To learn more about migraines, visit the National Headache Foundation.

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Mutated Trout Raise New Concerns Over Selenium

Photographs of variously mutated brown trout were relegated to an appendix of a scientific study commissioned by the J. R. Simplot Company, whose mining operations have polluted nearby creeks in southern Idaho. The trout were the offspring of local fish caught in the wild that had been spawned in the laboratory. Some had two heads; others had facial, fin and egg deformities.

Yet the company’s report concluded that it would be safe to allow selenium — a metal byproduct of mining that is toxic to fish and birds — to remain in area creeks at higher levels than are now permitted under regulatory guidelines. The company is seeking a judgment to that effect from the Environmental Protection Agency. After receiving a draft report that ran hundreds of pages, an E.P.A. review described the research as “comprehensive” and seemed open to its findings, which supported the selenium variance for Simplot’s Smoky Canyon mine.

But when other federal scientists and some environmentalists learned of the two-headed brown trout, they raised a ruckus, which resulted in further scientific review that found the company’s research wanting.

Now, several federal agencies, an array of environmental groups and one of the nation’s largest private companies are at odds over selenium contamination from the Idaho phosphate mine, the integrity of the company’s research, and what its effect will be on future regulatory policy.

The implications extend beyond Idaho. Selenium is a pollutant at 200 of the 1,294 locations designated by the federal government as toxic Superfund sites. And even though its effects on wildlife have been known for decades, federal agencies have not been able to agree on what level should be prohibited. The E.P.A. is currently reviewing federal selenium rules.

After hearing about the mutant trout, Senator Barbara Boxer of California, the Democrat who heads the chamber’s Environment and Public Works Committee, asked the federal Fish and Wildlife Service to step in and vet the mining company’s scientific research and conclusions.

The service’s review, released last month, was scathing, describing the study as “biased” and “highly questionable.” Joseph Skorupa, the service’s selenium expert, cited a “lack of valid field controls” and the absence of any analysis of the selenium’s impact on reptiles, birds or the 12 other types of fish in the creeks’ waters. Most troubling, he wrote, was that the researchers systematically undermeasured the rate of serious deformities in baby fish, which were pictured only in an appendix.

Dr. Skorupa wrote that the Simplot report did not provide raw data that would enable him to independently calculate deformity rates. He estimated, however, that the level of selenium that Simplot says causes a 20 percent rate of deformity actually causes a deformity rate of a minimum of 70 percent of all fry. Asked about the wildlife service’s findings, Alan L. Prouty, Simplot’s vice president for environmental and regulatory affairs, declined to comment beyond saying that the agency’s review was “totally outside the regulatory process.”

He added that his company’s research was conducted with the guidance of the E.P.A. and other government agencies.

Senator Boxer said that she was not seeking to take sides on Simplot’s variance request, but that she wanted the government to get the science right because it could effect national standards on selenium.

According to an E.P.A. document provided to The New York Times by the Greater Yellowstone Coalition, a local conservation group that has been battling Simplot over contamination for years, the trout data from the Smoky Canyon study has already been included in a “national criterion document” — a larger database used to help establish those standards.

Selenium is a naturally occurring element that, when disturbed, can be released as a toxic byproduct of human activities like farming, mining and burning coal. The regulation of selenium pollution is, for example, a highly contested issue in mountaintop coal mining in West Virginia and in agriculture in the San Joaquin Valley in California.

The metal can also affect human health, with symptoms including hair and fingernail loss and numbness in fingers and toes. It has been regulated in drinking water since the 1970s.

But the metal is far more dangerous to aquatic egg-bearing animals like fish, birds and reptiles — a fact revealed in the early 1980s when excessive selenium in agricultural runoff resulted in fatal deformities in waterfowl at the Kesterson Reservoir in California, including missing eyes and feet, deformed beaks, legs and wings, and protruding brains.

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Juvenile Idiopathic Arthritis May Raise Kids' Cancer Risk

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Y Chromosome Can Raise Heart Disease Risk by 50 Percent

Image courtesy of iStockphoto/luckyraccoon

Men tend to get coronary artery disease much earlier than do women. For some men, the reason for that might be in part because of their fathers and their father’s father according to a new study, published online Wednesday in The Lancet.

The study analyzed data from 3,233 unrelated white men enrolled in previous U.K. studies. From this information, the researchers took a close look at genetic markers on the Y chromosome, which is passed on from father to son. They found that 15 to 20 percent of the men fell into one of the 13 ancient ancestry branches known as haplogroup I.

Men in this haplogroup, who all showed a common variant on the Y chromosome, were 50 percent more likely to have coronary artery disease than those without it even when age, body mass, cholesterol, high blood pressure, smoking and other risk factors were taken into account. The genetic link is not entirely surprising, given that heart disease has been known to run in families, but the finding adds support to previously observed trends and insights into additional lines of research.

The finding follows well-described geographic distribution of coronary artery disease. Haplogroup I has been traced back to hunter-gatherers who arrived in Europe from the Middle East some 25,000 years ago and who today remain more prevalent in the northern areas of western Europe, where incidence of coronary artery disease is still higher than it is in the south where the haplogroup R1b1b2 is more common.

The genetic variant came with altered patterns of regulation in 19 key pathways all of which were linked to immune and inflammatory responses. These differences might play a role in atherosclerosis, or the hardening of the arteries, noted the researchers, who were led by Fadi Charchar, of Australia’s University of Ballarat. “Dysfunction of immune response is a well established contributor to atherosclerosis and coronary artery disease,” they wrote. Previous research had found other immuno differences in men from this haplotype, such as HIV-positive men in this group taking longer to show an immune response after getting antiretroviral therapy.

The findings do not suggest that heart disease risk for men is entirely or even mostly lodged on the Y chromosome. And the researchers noted that knowing which haplogroup a man is from is unlikely to yield predictions of his individual risk of coronary artery disease. But, as they pointed out, a better understanding of this widespread association “could have important public health implications,” especially in attempts to assess the prevalence of the disease within a population. And further study should help “to decipher complex interplay between human Y chromosome, immunity and cardiovascular disease,” the researchers wrote.

“These findings are exciting,” Virginia Miller of the Mayo Clinic wrote in an associated Lancet essay (Miller was not involved in the new research). The new work also suggests that there could be another side to the genetic equation that is protective, she added.

Follow Scientific American on Twitter @SciAm and @SciamBlogs. Visit ScientificAmerican.com for the latest in science, health and technology news.
© 2012 ScientificAmerican.com. All rights reserved.

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Y Chromosome Can Raise Heart Disease Risk by 50 Percent

y_chromosome_heart_disease Image courtesy of iStockphoto/luckyraccoon

Men tend to get coronary artery disease much earlier than do women. For some men, the reason for that might be in part because of their fathers and their father’s father according to a new study, published online Wednesday in The Lancet.

The study analyzed data from 3,233 unrelated white men enrolled in previous U.K. studies. From this information, the researchers took a close look at genetic markers on the Y chromosome, which is passed on from father to son. They found that 15 to 20 percent of the men fell into one of the 13 ancient ancestry branches known as haplogroup I.

Men in this haplogroup, who all showed a common variant on the Y chromosome, were 50 percent more likely to have coronary artery disease than those without it even when age, body mass, cholesterol, high blood pressure, smoking and other risk factors were taken into account. The genetic link is not entirely surprising, given that heart disease has been known to run in families, but the finding adds support to previously observed trends and insights into additional lines of research.

The finding follows well-described geographic distribution of coronary artery disease. Haplogroup I has been traced back to hunter-gatherers who arrived in Europe from the Middle East some 25,000 years ago and who today remain more prevalent in the northern areas of western Europe, where incidence of coronary artery disease is still higher than it is in the south where the haplogroup R1b1b2 is more common.

The genetic variant came with altered patterns of regulation in 19 key pathways all of which were linked to immune and inflammatory responses. These differences might play a role in atherosclerosis, or the hardening of the arteries, noted the researchers, who were led by Fadi Charchar, of Australia’s University of Ballarat. “Dysfunction of immune response is a well established contributor to atherosclerosis and coronary artery disease,” they wrote. Previous research had found other immuno differences in men from this haplotype, such as HIV-positive men in this group taking longer to show an immune response after getting antiretroviral therapy.

The findings do not suggest that heart disease risk for men is entirely or even mostly lodged on the Y chromosome. And the researchers noted that knowing which haplogroup a man is from is unlikely to yield predictions of his individual risk of coronary artery disease. But, as they pointed out, a better understanding of this widespread association “could have important public health implications,” especially in attempts to assess the prevalence of the disease within a population. And further study should help “to decipher complex interplay between human Y chromosome, immunity and cardiovascular disease,” the researchers wrote.

“These findings are exciting,” Virginia Miller of the Mayo Clinic wrote in an associated Lancet essay (Miller was not involved in the new research). The new work also suggests that there could be another side to the genetic equation that is protective, she added.

Follow Scientific American on Twitter @SciAm and @SciamBlogs. Visit ScientificAmerican.com for the latest in science, health and technology news.
© 2012 ScientificAmerican.com. All rights reserved.

View the original article here

Y Chromosome Can Raise Heart Disease Risk by 50 Percent

y_chromosome_heart_disease Image courtesy of iStockphoto/luckyraccoon

Men tend to get coronary artery disease much earlier than do women. For some men, the reason for that might be in part because of their fathers and their father’s father according to a new study, published online Wednesday in The Lancet.

The study analyzed data from 3,233 unrelated white men enrolled in previous U.K. studies. From this information, the researchers took a close look at genetic markers on the Y chromosome, which is passed on from father to son. They found that 15 to 20 percent of the men fell into one of the 13 ancient ancestry branches known as haplogroup I.

Men in this haplogroup, who all showed a common variant on the Y chromosome, were 50 percent more likely to have coronary artery disease than those without it even when age, body mass, cholesterol, high blood pressure, smoking and other risk factors were taken into account. The genetic link is not entirely surprising, given that heart disease has been known to run in families, but the finding adds support to previously observed trends and insights into additional lines of research.

The finding follows well-described geographic distribution of coronary artery disease. Haplogroup I has been traced back to hunter-gatherers who arrived in Europe from the Middle East some 25,000 years ago and who today remain more prevalent in the northern areas of western Europe, where incidence of coronary artery disease is still higher than it is in the south where the haplogroup R1b1b2 is more common.

The genetic variant came with altered patterns of regulation in 19 key pathways all of which were linked to immune and inflammatory responses. These differences might play a role in atherosclerosis, or the hardening of the arteries, noted the researchers, who were led by Fadi Charchar, of Australia’s University of Ballarat. “Dysfunction of immune response is a well established contributor to atherosclerosis and coronary artery disease,” they wrote. Previous research had found other immuno differences in men from this haplotype, such as HIV-positive men in this group taking longer to show an immune response after getting antiretroviral therapy.

The findings do not suggest that heart disease risk for men is entirely or even mostly lodged on the Y chromosome. And the researchers noted that knowing which haplogroup a man is from is unlikely to yield predictions of his individual risk of coronary artery disease. But, as they pointed out, a better understanding of this widespread association “could have important public health implications,” especially in attempts to assess the prevalence of the disease within a population. And further study should help “to decipher complex interplay between human Y chromosome, immunity and cardiovascular disease,” the researchers wrote.

“These findings are exciting,” Virginia Miller of the Mayo Clinic wrote in an associated Lancet essay (Miller was not involved in the new research). The new work also suggests that there could be another side to the genetic equation that is protective, she added.

Follow Scientific American on Twitter @SciAm and @SciamBlogs. Visit ScientificAmerican.com for the latest in science, health and technology news.
© 2012 ScientificAmerican.com. All rights reserved.

View the original article here