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Sleep is a mystery. Although no one knows exactly why, it’s required for good health. But now, scientists have found a surprisingly clear connection between sleep and a healthy body: the regulation of sugar levels in the blood. The new studies, all online December 7 in Nature Genetics, describe the first genetic link between sleep and type 2 diabetes, a disease marked by high blood sugar levels.
In the
This newfound link between melatonin and type 2 diabetes intrigues sleep researchers like Orfeu Buxton at
The findings fill in some of the molecular details of how sleep can change blood sugar levels. The key, it appears, is a melatonin receptor, a protein on the outside of cells that senses melatonin in the blood and triggers sleep- or wake-related changes in cells.
Human bodies have a clock, an internal rhythm that dictates when to fall asleep and when to get up. Molecular timekeepers, made and degraded every 24 hours, set this daily cycle. When part of the ticking molecular clock goes awry, sleep schedules change.
Disordered sleep can spark a constellation of intertwined pathologies: Studies in humans have shown that depression, obesity, weakened immune system function and even death are all correlated with a lack of shut-eye. Population studies have shown that diabetes rates rise as sleep declines. While these data provide compelling reasons to get eight hours of quality sleep every night, they couldn’t explain how diabetes might be influenced by sleep.
The three new genomic studies show that melatonin, a major regulator of the body’s sleep clock, is closely linked to increased glucose levels and diabetes. Best known for its sleep-inducing properties, melatonin is sold as an over-the-counter, nutritional supplement to aid sleep. Melatonin levels in the body are tied to daylight: When the lights go down, melatonin levels rise and drowsiness soon follows.
The finding identifies melatonin as a “fascinating new target” for diabetes treatments, says endocrinologist Leif Groop of
Two studies, one listing 109 coauthors, analyzed data from earlier studies that had measured blood sugar levels and had collected DNA samples from their participants — the larger study analyzed data from 36,610 people and the other from 2,151 people. All participants were of European descent.
In both studies, comparing the DNA sequences of participants who had high blood sugar levels with the DNA of those who had normal blood sugar levels turned up a surprise. In both studies, MTNR1B, a gene encoding a melatonin receptor, caught researchers’ attention. People with high blood sugar levels, and thus diabetes, were much more likely to have a change in a single DNA base, or letter, within the gene than were those with healthy blood sugar levels.
"The finding that the melatonin receptor has an influence on diabetes was unexpected,” Groop says.
A third paper, which analyzed results from two large studies of over 18,000 participants, took the findings a step further. The researchers showed that the same DNA change in MTNR1B identified in the other two studies — a seemingly innocuous G instead of the more common C — was correlated with high blood sugar levels, low insulin levels and most important, a greater risk of developing type 2 diabetes during the multiyear studies.
The scientists, including Groop, also did experiments that looked at how melatonin might directly interact with insulin-producing cells.
The melatonin receptor was thought to be primarily expressed in the brain — where the body’s master clock resides. Groop and colleagues now show that insulin-producing cells, called beta-cells, in the pancreas of mice, rats and humans, also have the melatonin receptor.
The presence of the melatonin receptor on the insulin-secreting cells makes it more likely that the receptor is directly controlling the output of insulin. When scientists added melatonin to human beta-cells in the lab, insulin production went down. That melatonin and insulin are connected makes sense, because in the dead of night, when melatonin levels are high, the need for insulin should be low. Researchers don’t yet know how melatonin levels are different in sleep-deprived people, and how this difference could lead to decreased insulin production.
The tie between sleep and blood sugar didn’t come as a surprise to some sleep researchers. Buxton says that evidence has accumulated for years on the relationship between sleep and blood sugar levels. “However, such a direct role for melatonin was very surprising,” he says
Researcher James Gangwisch of Columbia University in New York City says the identification of the melatonin receptor as an important regulator of blood sugar “fits well” with earlier studies looking at the effects of poor sleep on blood sugar levels.
A 2007 study found that people who get less than five hours of sleep a night were significantly more likely to have type 2 diabetes. Experiments on sleep in the lab confirm this trend: Healthy young adults who were prevented from entering deep sleep for just three nights couldn’t properly regulate blood sugar levels, a 2008 study shows. What’s more, the subjects became more resistant to insulin during the study, eventually reaching the levels of insulin sensitivity that resemble the insulin resistance of diabetic people.
Sleep-deprived subjects, Gangwisch says, crave starchy, sweet foods and don’t regulate blood sugar well. “We know it’s true, but the question is why.”
“This paper ties those two things together,” says Gonçalo Abecasis of the University of Michigan School of Public Health,
“These findings raise more exciting questions than they answer,” says Buxton. But he cautions that the data on melatonin’s impact on insulin-producing cells in humans is still early. Many more studies are needed before scientists will fully understand how melatonin affects blood sugar levels and type 2 diabetes.
Groop agrees, and points to the need for more basic studies on the melatonin receptor and clinical tests of glucose levels in people who have been given melatonin supplements.
People taking melatonin to aid sleep may be just such a group. Says Abecasis, “I think it would be interesting to track incidences of diabetes in such people.”
Prostate cancer remains the most common malignancy among U.S. men, and internationally it ranks fourth. Though few studies have offered much insight into what triggers this disease, a growing number of researchers have found evidence suggesting that dietary selenium protects men against this cancer.
Indeed, a February 2003 paper in the International Journal of Cancer found that among 445 U.S. men, high blood concentrations of selenium appeared to reduce by 30 percent the risk that a man would develop prostate cancer.
Selenium is a constituent of the enzyme glutathione peroxidase, one of the body's more potent antioxidants. Such agents have the ability to quash biologically damaging reactions triggered within the body by any of a host of naturally produced chemicals called oxidants.
Because oxidant damage has been linked with many cancers, some scientists have suspected that any anticancer benefit from selenium probably would trace to its antioxidant contribution.
In fact, however, several new studies suggest that at least one of the nutrient's primary anticancer benefits may be its protection or repair of a suicide switch in genetically damaged cells. It's when the body allows this switch to fail that cancer's runaway growth occurs.
Dogging the problem
David J. Waters of Purdue University and his colleagues were the first to report this discovery in a study of prostate health in elderly beagles. They chose these dogs because, like men, this species spontaneously develops prostate cancer at rates that increase with age.
For 7 months, the scientists supplemented the diets of 38 male dogs�animals physiologically equivalent to 65-year-old men�with either of two dietary supplements: selenomethionine or high-selenium yeast. Another 10 dogs received a similar diet but no extra selenium.
At the end of the trial, the researchers sampled blood from each of the animals and then sacrificed the dogs to examine their prostate glands.
Cancers typically trace to DNA damage, and Waters' team found far less of it in the white blood cells and the prostate tissue of dogs treated with selenium than in the untreated group. For instance, 79 percent of the prostate cells examined from untreated dogs had "extensive DNA damage" compared with just 57 percent of such cells from dogs getting supplemental selenium.
However, Waters and his colleagues report in the Feb. 5 Journal of the National Cancer Institute that the degree of DNA protection bore no relationship to the activity of glutathione peroxidase in those tissues. "In other words," Waters told Science News Online, "[selenium's] beneficial effects cannot be explained by the fact that it was pushing antioxidant enzymes higher."
So how does selenium protect the prostate? It may be by controlling the selective culling of cells with damaged DNA.
Helping cancer cells die
Normally, cells develop, grow old, and then die. Cancer cells, however, don't die naturally. Like Methuselah, they seem immortal and continue to produce endless progeny throughout their long lives.
Cancer cells would pose far less of a problem if the normal suicide switch within them could be reactivated. Such programmed cell death is known as apoptosis. Interestingly, Waters' team found roughly twice the level of apoptosis occurring within the prostate tissue of selenium-supplemented dogs as in untreated beagles. In fact, hot spots of apoptosis appeared in 16 of the 38 treated beagles (42 percent) but just one of the 10 dogs from the untreated group.
The elevated apoptosis in the selenium-treated animals could put a break on the development of prostate malignancies. "The idea here," explains Waters, who also holds a research appointment at the Seattle-based Gerald P. Murphy Cancer Foundation, "is that the cells that are most DNA damaged�and presumably have the highest propensity to turn cancerous�may be selectively purged in the presence of [supplemental] selenium."
The supplementation that conferred this protection was anything but massive. Half the dogs receiving each supplement got a low dose�just 50 percent more than typically occurs in a dog-chow diet and the rest got double the normal dietary selenium supply.
"These are really nontoxic doses," Waters emphasizes. In fact, the lower supplemental dose was roughly equivalent to 200 micrograms per day in men. That's the same amount being administered to some people taking part in a massive, 12-year National Cancer Institute (NCI) nutrition trial. What's more, the forms of selenium tested in the dogs are identical to the forms given to men in earlier trials. In fact, the NCI trial is using selenium methionine.
In the dog trial, the two forms of selenium appeared equally protective, and the low doses were just as good as the high doses.
Why did the Purdue researchers test agents that already have shown their value in people? "Because we want to understand the mechanisms," Waters says, which may point to better doses, the chemical forms that perform best, the ideal timing for supplementation, and whether there will be deleterious interactions between the supplements and drugs or other nutrients in the diet.
Even broccoli may help
John W. Finley and his colleagues at the Agricultural Research Service's Human Nutrition Research Center in Grand Forks, N.D., have been probing a more natural selenium supplement. They aim to deliver anticancer benefits from selenium by enriching the nutrient's concentrations in broccoli (SN: 4/21/01, p. 248: Available to subscribers at http://www.sciencenews.org/20010421/note12.asp).
At the Experimental Biology 2003 meeting in San Diego last week, Finley's group reported data from mice that spontaneously develop precancerous tissue in their digestive tract. Animals downing high concentrations of the novel broccoli developed several anticancer changes�among them, the activation of apoptosis-promoting genes.
In another paper at the same meeting, Aimee L. Taylor and her colleagues at Brigham Young University in Provo, Utah, provided data from test-tube studies of prostate cancer cells treated with high concentrations of selenium. Here, too, the nutrient inhibited a series of genes that can turn off the molecular suicide switch in cancer cells.
Looking for other natural sources of this trace mineral? Try seafood, organ meats such as kidney and liver, and to a lesser extent, other meats. Though some grains can be rich stores of selenium, whether they do depends on the mineral status of the soil in which they're grown.
