Longer sleep times may counteract genetic factors related to weight gain

ScienceDaily (May 1, 2012) — Toss out another old wives' tale: Sleeping too much does not make you fat. Quite the opposite, according to a new study examining sleep and body mass index (BMI) in twins, which found that sleeping more than nine hours a night may actually suppress genetic influences on body weight.

See Also:Health & MedicineObesitySleep Disorder ResearchDiet and Weight LossMind & BrainSleep DisordersInsomniaObstructive Sleep ApneaLiving WellReferenceCircadian rhythm sleep disorderOverweightBody mass indexSleep deprivation

The study looked at 1,088 pairs of twins and found that sleeping less than seven hours a night was associated with both increased BMI and greater genetic influences on BMI. Previous research has shown that genetic influences include things like glucose metabolism, energy use, fatty acid storage and satiety. In this study, the heritability of BMI was twice as high for the short sleepers than for twins who slept longer than nine hours a night.

"The results suggest that shorter sleep provides a more permissive environment for the expression of obesity related genes," said principal investigator Nathaniel Watson, MD, MSc, of the University of Washington. "Or it may be that extended sleep is protective by suppressing expression of obesity genes."

Watson and colleagues determined that for twins sleeping less than seven hours, genetic influences accounted for 70 percent of the differences in BMI, with common environment accounting for just 4 percent and unique environment 26 percent. For twins averaging more than nine hours of sleep, genetic factors were attributed to 32 percent of weight variations, with common environment accounting for 51 percent and unique environment 17 percent.

More research is needed, Watson said, but these preliminary results may suggest that behavioral weight loss measures would be most effective when genetic drivers of body weight are mitigated through sleep extension.

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Research Gets Closer to Genetic Roots of Glaucoma

HealthDay – 16 hrs ago FRIDAY, April 27 (HealthDay News) -- Two genetic variations are linked to a common form of glaucoma, known as primary open-angle glaucoma, according to new research.

Glaucoma affects about 2.2 million people in the United States, the U.S. National Eye Institute said in a news release.

"Loss of vision from glaucoma, a common cause of blindness worldwide, is due to irreversible damage to the optic nerve," noted one expert, Dr. Mark Fromer, an ophthalmologist at Lenox Hill Hospital in New York City. "Glaucoma is usually associated with high eye pressure leading to optic nerve damage. There is also a form of glaucoma with normal pressure."

In the new study, Janey Wiggs, of Harvard Medical School and Massachusetts Eye and Ear Infirmary in Boston, and colleagues analyzed the DNA sequences of more than 6,000 people. Half of them had primary open-angle glaucoma. This form of the disease is typically associated with increased eye pressure, but one-third of these patients had normal-pressure glaucoma.

The study, published online April 26 in PLoS Genetics, found that two genetic variations were linked with primary open-angle glaucoma, including those who have normal-pressure glaucoma.

One variant is in a gene located on chromosome 9. The second variant is in a region of chromosome 8, where it may affect the expression of one or two other genes. These genes may interact with a molecule that regulates cell growth and survival throughout the body, the researchers explained in the news release.

The investigators believe future studies could focus on this molecule as a treatment for various forms of glaucoma.

Fromer concurred. "These results reveal new insights into the genetic pathways of optic nerve disease in glaucoma for the first time and are an important step toward the development of preventative and protective therapies," he said.

More information

The U.S. National Library of Medicine has more about glaucoma.

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Certain Genetic Regions May Be Tied to Osteoporosis

HealthDay – 9 hrs ago SUNDAY, April 15 (HealthDay News) -- A large international group of researchers has identified 32 new genetic regions linked to fractures and osteoporosis.

Variations in these regions could offer protection from, or greater risk for, bone-weakening disease, the investigators reported in a new study published in the April 15 online edition of Nature Genetics.

The study authors added that their findings could lead to the development of new osteoporosis drugs.

"We're learning that the genetic architecture of disease is very complex," one of the study's authors and the methodological leader of the consortium, Dr. John Ioannidis, chief of the Stanford Prevention Research Center, said in a university news release.

The research, which involved 17 studies that compared common genetic variants in more than 100,000 people, pinpointed six regions linked to risk of fractures of the femur (thigh bone) or lower back.

The study authors pointed out, however, that it would still be difficult to predict who is at greater risk for bone disease. People with the highest number of variants associated with decreased bone mineral density were only about one and a half times more likely than people with an average number of variants to have osteoporosis. The risk for fractures was only slightly higher.

Meanwhile, compared to those with the fewest variants, people with the most variants were still just three to four times more likely to have had fractures and lower bone mineral density, the study revealed.

"As a result, the next step of incorporating this information into basic patient care is not clear," Ioannidis concluded. "Each variant conveys a small quantum of risk or benefit. We can't predict exactly who will or won't get a fracture."

The authors noted, however, that by identifying some previously unsuspected pathways involved in bone health, their research could lead to the development of new anti-osteoporosis drugs. But even larger studies are needed to identify all of the genes critical to fighting bone disease, they added.

"We saw many of these regions and genes clustering within specific types of pathways, which suggests certain disease mechanisms. It certainly wouldn't be unexpected to eventually identify many more genetic regions involved in the regulation of osteoporosis and fracture risk," Ioannidis said.

"In reality, there may be 500 or more gene variants regulating osteoporosis. To find all of them, we'll need to study millions of patients. Is this unrealistic? I don't think so. Sooner or later this will be feasible," he added.

More information

The U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases has more about bone-weakening diseases.

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