Researchers have long suspected that living in a bad neighborhood can be hazardous to your health—whether because of poor access to health care and a paucity of areas to exercise in and stores that sell healthy food, or some combination of other factors, living in a poor area means you have a disproportionate chance of becoming ill and obese. But how can you tell whether that effect is intrinsic to poverty, or whether it can be reversed if people move into more well-off neighborhoods? With a giant, long-term study that gives families in poor neighborhoods a chance to move to other areas.
The results of such a study, conducted by the US Department of Housing and Urban Development, have now been published, and they show that moving from low-income housing projects to a neighborhood with less than 10% of people living below the poverty line does have a positive effect on health. (more…)
What’s the News: Scientists found that periodic fasting may decrease the risk of coronary artery disease and diabetes, and also causes significant changes in heart-disease risk factors like cholesterol, blood-sugar, and triglyceride levels, which hadn’t been linked to fasting before. “We’ve shown it is not a chance finding. Fasting is not just an indicator for other healthy lifestyles,” says lead researcher Benjamin Horne of the Intermountain Medical Center Heart Institute. “It is actually the fasting that is working to reduce the risk of disease.”
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They’re about three and a half feet tall and their origins are mysterious, but an isolated group of Ecuadorians with a genetic mutation causing dwarfism are making news for another reason: They hardly ever get cancer or diabetes. Medical researchers say the villagers’ genetic protection from these diseases could lead to preventative treatments for the general population–and could therefore increase human longevity.
The villagers’ condition is called Laron syndrome, which is caused by an insensitivity to growth hormone.
Laron syndrome results from a mutation in the gene that codes for growth hormone receptor (GHR), a protein that binds with the human growth hormone and ultimately results in the production of the insulin-like growth factor 1 (IGF1), causing cells to grow and divide. When a person has two of these mutated and non-working genes, they can develop the disease. [LiveScience]
Jaime Guevara-Aguirre, the leader of the study about the Ecuadorians appearing in Science Translational Medicine, has been looking into their condition and extraordinary resistance to age-related diseases for more than two decades, since his serendipitous discovery of the people while riding horseback in Ecuador.
“I discovered the population in 1987,” Dr. Guevara-Aguirre said in an interview from Ecuador. “In 1994, I noticed these patients were not having cancer, compared with their relatives. People told me they are too few people to make any assumption. People said, ‘You have to wait 10 years,’ so I waited. No one believed me until I got to Valter Longo in 2005.” [The New York Times]
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In an attempt to find a cure for type 1 diabetes, researchers are looking to an unlikely source: testicles. In a new study, researchers extracted stem cells drawn from human testes and reprogrammed them to produce insulin. When implanted into diabetic mice, the altered cells brought down the mice’s blood glucose levels, temporarily curing their diabetes.
In type 1 diabetes, the body’s immune system mistakenly destroys the pancreatic beta and alpha cells, which regulate blood glucose levels. Without the insulin created by their beta cells, diabetics experience high glucose levels that cause serious health problems.
Lead researcher G. Ian Gallicano and his colleagues took human spermatogonial stem cells–precursor cells that give rise to sperm–and reverted them to an embryonic state. Then the researchers coaxed them to develop into insulin-producing cells that resemble beta cells. Finally, they injected these pseudo-beta cells into the pancreases of mice with type 1 diabetes.
In a presentation on Sunday at the American Society for Cell Biology annual meeting, Gallicano said the graft was able to produce enough insulin to “cure” the mice of their diabetes for a week, though insulin levels were not high enough to treat humans this way.
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Scientists knew that overweight mothers tend to have more overweight children. But is the same true for fathers? This week in Nature, Margaret Morris and her team demonstrated this effect in male rats, the first time it’s been shown to work in males. The findings are another example of how non-genetic factors, like how much a parent eats, can have a biological impact on offspring.
The researchers put one of their two groups of male rats on a high-fat diet, the other on a normal one. Unsurprisingly, the high-fat rats put on a lot of weight and began to show symptoms of type II diabetes, like insulin resistance and struggles with metabolizing glucose. And then there were their kids:
The real surprise came when Morris’s team went on to examine the obese rats’ female offspring. These too had problems regulating insulin and glucose levels. The healthy fathers, however, had correspondingly healthy daughters. Whether similar defects emerge in sons remains to be seen. [Nature News]
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A new device may one day save those with diabetes from the frequent finger-pricking and cumbersome external monitors required to check glucose levels–by instead keeping tabs from inside their torsos. In a study published online today in Science Translational Medicine, researchers report that an implantable glucose sensor has worked in pigs. Ultimately, clinical trials and FDA approval will determine if the device holds any promise for humans, but researchers say this animal test is an important first step.
“You can run the device for a year or more with it constantly working, and recording glucose quite satisfactorily. Now, we are focused on getting the human clinical trials going. We hope to begin the first human trial within in a few months,” said [lead author, David Gough.] “If all goes well with the human clinical trials, we anticipate that in several years, this device could be purchased under prescription from a physician,” said Gough.[University of California - San Diego]
As Popular Science reports, the device is “just a bit smaller than a Double-Stuf Oreo”–around 1.5 inches wide and half an inch thick. Gough and colleagues implanted the device in two pigs: one for 222 and and another for 520 days. It works by monitoring oxygen consumed in a chemical reaction with the enzyme glucose oxidase–the amount of oxygen consumed is proportional to the amount of glucose in the user’s blood. Though some already use similar sensors, none have lasted this long.
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We know that skimping on sleep gives many of us heavy eyes and sends us on an early afternoon run for a large coffee (or, for those with an iron stomach who don’t mind ingesting 8,300 percent of our daily value of vitamin B12, an energy drink). But studies out this week outline possibly dire health consequences for depriving ourselves of lengthy slumber.
A small study In the Journal of Clinical Endocrinology and Metabolism says that even a single of night of sleep deprivation can cause the body to show signs of insulin resistance, a warning sign of diabetes. And in the journal Sleep, a long-term study by a different team chillingly suggests that continuously snoozing less than six hours per night can increase your risk for an early death.
First, the insulin study: Esther Donga and colleagues examined nine patients, first after the patients had slept a full eight hours and then again after they’d slept just four. The scientists say that insulin sensitivity was reduced by as much as 25 percent when the patients were sleep deprived.
“Our data indicate that insulin sensitivity is not fixed in healthy (people), but depends on the duration of sleep in the preceding night,” Donga wrote in the study. “In fact it is tempting to speculate that the negative effects of multiple nights of shortened sleep on glucose tolerance can be reproduced, at least in part, by just one sleepless night.” A study by U.S. scientists published last year found that people who slept less than six hours a night were 4.5 times more likely to develop abnormal blood sugar readings in six years compared with those who slept longer [Reuters].
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Here’s a neat dolphin trick that doesn’t involve jumping through hoops. While dolphins sleep overnight (with half their brains and one eye at a time), they begin to show signs of the kind of insulin resistance that marks type 2 diabetes in humans. But when they wake up and have their breakfast, they switch back to their normal state. A research team led by Stephanie Venn-Watson announced the findings at the American Association for the Advancement of Science meeting in San Diego, and said that dolphins’ apparent ability to switch insulin resistance on and off could lead to better understanding of the disease in humans.
Insulin helps people control their levels of blood sugar, and the resistance to it inherent in type 2 diabetes means those levels can get way too high. The dolphins, though, switch on this temporary insulin resistance to their advantage, boosting blood sugar levels overnight. “Bottlenose dolphins have large brains that need sugar,” Dr Venn-Watson explained. Since their diet is very low in sugar, “it works to their advantage to have a condition that keeps blood sugar in the body… to keep the brain well fed” [BBC News].
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Using a bit of biotech wizardry that is becoming increasingly mundane, researchers took skin cells from patients with type 1 diabetes, and turned them first into induced pluripotent stem cells (iPS cells), the rough equivalent to the embryonic stem cells that can develop into any kind of tissue. Then researchers directed the cells to develop into insulin-producing beta cells, the type of cells that are destroyed by the immune system in type 1 diabetes.
Stem cell expert Meri Firpo notes that this technology could one day be used to create pancreatic beta cells for transplant from a person’s own skin cells. That way, there would be no need for immunosuppressive medications. However, because the current technique uses genetic manipulation to change the cell, Firpo said long-term safety issues would have to be addressed. Mouse cells that have been similarly manipulated have developed benign tumors, she said. So, using such cells for transplant is definitely not “a near-term thing,” she stressed [HealthDay News].
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In recent years, antioxidants have been touted as a secret to healthy living: The molecules bind to reactive oxygen compounds called “free radicals” that are known to damage the body’s tissues. The amount of oxidative damage increases with age, and according to one theory of aging it is a major cause of the body’s decline [The New York Times]. But a new study examined the effects of the antioxidant vitamins C and E when combined with an exercise regimen, and found a considerably more complicated story. The researchers found that free radicals may be beneficial in small doses, and may even help protect against diabetes. And mopping them up with antioxidants may do more harm than good [BBC News].
During a workout, the muscles metabolize glucose to create energy, but in the process some free radicals are released. The body has a natural defense mechanism to combat these free radicals, but many researchers had theorized that the body can’t catch all of the harmful compounds, which makes antioxidant supplements sound like a logical solution.
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Blood vessels grown from patients’ own skin cells have been used to make the process of dialysis safer and easier for people with failing kidneys, and researchers say the process may one day be used to custom-produce blood vessels for patients with circulatory problems in their hearts or legs [AP].
Kidney patients need frequent dialysis to filter their blood, and that requires a vessel, or shunt, to connect them to dialysis machines. This can be made from their own vessels. But because dialysis is done so regularly, kidney patients often run out of healthy vessels and need an artificial one, often made out of [Gore-Tex]. Those are prone to infection and inflammation [AP].
For the new study, published in The Lancet, researchers took small snips of skin from the backs of ten patients’ hands and extracted two cell types — fibroblasts from the skin which provide the structural backbone of the vein, and endothelial cells to form the lining of the vein [Reuters]. In the lab, those cells were grown into sheets of tissue that were then rolled into tubes measuring about six inches long, which then fused at the seams. Those tubes were essentially new blood vessels. The whole process took between six to nine months.
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Stem cell transplants may free type I diabetics of the need for insulin injections, according to a small study in which 20 of 23 patients became insulin-free for up to four years. The study, published in the Journal of the American Medical Association, involved injecting people with stem cells made from their bone marrow cells [Reuters]. Twelve of the patients went for an average of 31 months with no insulin injections. Eight other study participants experienced “transient” insulin independence, meaning they had to start taking insulin again at lower levels [U.S. News and World Report].
The treatment was designed for patients newly diagnosed with type 1 diabetes, a condition that usually develops in childhood and occurs when the immune system goes haywire and starts attacking itself, destroying insulin-producing cells in the pancreas needed to control blood sugar [Reuters]. These beta cells are produced in a part of the pancreas called the islets of Langerhans. In the study, the stem cells were first frozen. The patients were next given a large dose of drugs to knock down their immune systems. The stem cells were then thawed and re-injected back into their bloodstream over about 15 minutes [Australian Broadcasting Corporation]. Over the following days, months, and years, researchers measured their patients’ levels of C-peptides, molecules that indicate how well the body is producing insulin. They found that the stem cell transplants resulted in higher C-peptide levels, indicating healthy beta cells.
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Brown fat—the “good” kind of fat—is often thought of as baby fat, but new research has found that it exists in adults and may play a role in regulating metabolism and staving off type 2 diabetes. White fat, or “bad fat,” stores energy, but also clogs arteries and accumulates as visible body fat. Brown adipose tissue burns calories for heat, but until now has been thought to exist only in childhood, disappearing as the body became more muscular. Now, three new studies published in The New England Journal of Medicine not only found adults still had brown fat, but that slim adults had more of it than fatter ones [BBC]. The researchers are now seeking a way to activate brown fat to improve both weight control and glucose metabolism, which would help prevent obesity and diabetes.
The studies found that brown fat stores decrease as people age, and that thinner people with normal blood glucose levels have more brown fat. However, it isn’t yet clear whether increased brown fat is a cause or a result of being thin. Brown fat was also more active during colder weather, when it plays a key role in burning energy to produce heat [AFP]. For now the only safe way known to activate brown fat is to stay chilly, right at the verge of shivering, for prolonged periods. That reproduces the conditions that led to the evolution of brown fat—namely, life-threatening cold in babies and small furry animals that can’t put on clothes to keep themselves warm [Los Angeles Times].
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It may be old news that people who work the night shift tend to have higher rates of certain medical conditions. But researchers say they have established a direct link between an abnormal sleep cycle and altered hormone levels, which can disrupt metabolism and increase the risk of heart disease, diabetes, and obesity. As soon as their circadian rhythms became separated from a day-night cycle, test subjects’ levels of key metabolic hormones went haywire—the most compelling evidence yet that shift work isn’t just an inconvenience, but an occupational hazard [Wired News].
The study, published in the Proceedings of the National Academy of Sciences, maps a clear path from work-sleep cycles to metabolic disregulation to disease [Wired News]. Scientists cannot yet explain the exact connection between metabolism and the circadian rhythm, the roughly 24-hour cycle that biological and behavioral processes are based on. But they believe the trigger to be a decrease in the hormone leptin, which the body uses to regulate appetite, that results when the circadian rhythm is disrupted.
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Spikes in blood sugar levels seem to be linked to memory problems, and may be a major factor in the normal memory and cognitive problems that crop up as people age, according to a new study. People’s ability to regulate blood sugar begins to deteriorate by their third or fourth decade and continues to decline, so older people are more prone to these sugar spikes. “This would suggest that anything to improve regulation of blood glucose would potentially be a way to ameliorate age-related memory decline,” said senior study author Dr. Scott Small…. The findings may also help explain why people who exercise don’t have as many cognitive problems as they age: Exercise helps stabilize blood glucose levels [HealthDay News].
The findings have important implications for the increasing number of overweight children who are at risk of diabetes, commented neuroscientist Bruce McEwen. “When we think about diabetes, we think about heart disease and all the consequences for the rest of the body, but we usually don’t think about the brain,” he said. “This is something we’ve got to be really worried about. We need to think about their ultimate risks not only for cardiovascular disease and metabolic disorders, but also about their cognitive skills, and whether they will be able to keep up with the demands of education and a fast-paced complex society. That’s the part that scares the heck out of me” [The New York Times].
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