TIME Diet/Nutrition

Soda May Age You as Much as Smoking, Study Says

The link between soda and telomere length

Nobody would mistake sugary soda for a health food, but a new study published in the American Journal of Public Health just found that a daily soda habit can age your immune cells almost two years.

Senior study author Elissa Epel, PhD, professor of psychiatry at University of California San Francisco, wanted to look at the mechanisms behind soda’s storied link to conditions like diabetes, heart attack, obesity, and even higher rates of death. She studied telomeres, the caps at the end of chromosomes in every cell in our body, from white blood cells. Shorter telomeres have been linked to health detriments like shorter lifespans and more stress, cardiovascular disease, diabetes and cancer, the study notes.

Epel and her team analyzed data from 5,309 adults in the National Health and Nutrition Examination Survey (NHANES) from about 14 years ago. They found that people who drank more sugary soda tended to have shorter telomeres. Drinking an 8-ounce daily serving of soda corresponded to 1.9 years of additional aging, and drinking a daily 20-ounce serving was linked to 4.6 more years of aging. The latter, the authors point out, is exactly the same association found between telomere length and smoking.

Only the sugary, bubbly stuff showed this effect. Epel didn’t see any association between telomere length and diet soda intake. “The extremely high dose of sugar that we can put into our body within seconds by drinking sugared beverages is uniquely toxic to metabolism,” she says.

She also didn’t see a significant link between non-carbonated sugary beverages, like fruit juice, which Epel says surprised her. But she thinks the results might be different if the data were more modern. “We think that the jury’s still out on sugared beverages—theoretically they’re just as bad,” she says. “But 14 years ago people were drinking a lot less sugared beverages…they were mostly drinking soda.” At the time of the study, 21% of adults in the study reported consuming 20 ounces or more of sugar-sweetened soda each day, but soda consumption has been on the decline for years.

Telomere length dwindles naturally as we age, but it may not be an irreversible process. Previous research shows that it’s possible to increase telomere length by as much as 10% over 5 years by stressing less and eating a healthy diet—no soda included.

Read next: Here’s How to Stop Teens From Drinking Soda

TIME Obesity

How Jet Lag Can Contribute to Obesity

Woman sleeping in airplane
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Changing your circadian clock messes with your microbes

Working the night shift has long been linked to an increased risk of obesity, heart attack and breast cancer. One 2011 study even showed that shift work lasting a decade or more boosts your risk for type-2 diabetes by 40%. And new study published in the journal Cell looked at why.

Researchers led by Eran Elinav, MD, PhD, senior scientist in the immunology department at the Weizmann Institute of Science in Israel, suspected the gut microbiome, which he calls “the neglected organ,” might be affected by a disrupted circadian rhythm. It wasn’t an obvious choice. Microbes hang out in the dark of our guts, so they’re never directly exposed to light and dark cycles, he says. That’s why it was surprising to find out that the microbiome is very much affected by disruptions to our bodies’ inner clocks.

Elinav started by making mice work the graveyard shift, subjecting them to a state that would be the equivalent of jet lag from an 8-hour time difference in humans. Mice are nocturnal, so in this case, they stayed awake during the day. “We saw that in the presence of jet lag, their microbes were completely messed up,” he says. The bugs changed in composition and function, losing their circadian rhythm and becoming far less efficient at tasks like cell growth, DNA repair and detoxification. Like humans, mice microbes perform housekeeping and repair functions while they sleep, and growth and energy-promoting functions when they’re awake. But in the study’s graph of these functions in jet-lagged mice, the tasks hardly vary throughout the day and are performed at much lower levels.

These mice were also more susceptible to obesity and diabetes, and when Elinav transferred their gut bacteria into sterile, germ-free mice, they also transferred the heightened risk for disease, “proving that it’s actually their microbes driving this susceptibility,” he says.

Such a theory is much harder to test in humans, of course, but Elinav studied two people traveling from the U.S. to Israel, which induced an 8-hour jet lag similar to the mice. He sampled their gut bacteria three times over two weeks, capturing the main stages of jet lag, and found that their microbes indeed changed in composition, and in ways that were startlingly similar. Elinav even transferred the humans’ jet-lagged bugs into germ-free mice. “We could very nicely see that transferring the gut microbes from the point where jet lag was at its highest induced much more obesity and glucose intolerance,” he says.

Thankfully, the gut microbes of the travelers had returned to normal two weeks after their flight, and transferring their bugs into mice no longer led to increased obesity and glucose intolerance. But the implications of the findings are troublesome for frequent travelers and especially shift workers, whose work demands a consistent disruption of circadian rhythms.

TIME diabetes

How Race Affects Diabetes Care—and Leads to Amputations

High Blood Sugar Test
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Black diabetics are much more likely to face amputation

Black type-2 diabetes patients are three times more likely to lose a leg to amputation as non-black patients, finds a new report from the Dartmouth Atlas Project. That’s partly because they’re also far less likely to get preventative care like foot exams, cholesterol testing and blood sugar testing.

Researchers looked at Medicare claims from 2007-2011 from patients diagnosed with diabetes and peripheral arterial disease, a condition in which plaque builds up in the arteries and blocks blood flow, primarily in the legs. They found significant disparities, both racial and regional: black patients and the rural Southeast region of the U.S. both saw elevated amputation rates.

Diabetes-related amputation, a last resort, generally results from wounds on the feet and poor circulation. Foot exams and testing for blood sugar and cholesterol levels can help lower the risk of having to resort to extreme measures. But in 2010, 75% of diagnosed black diabetics received a a blood lipids test, while 82% of non-black patients had the test.

An average of 2.4 leg amputations for every 1,000 Medicare patients with diabetes and peripheral arterial disease happen nationally, but regionally, the situation is much more grim. Mississippi, which currently ties West Virginia for the most obese state, also has some of the highest amputation rates—6.2 per 1,000 patients in the city of Tupelo. It’s not just racial: For every 1,000 black Medicare beneficiaries with diabetes, 14.2 amputations occurred in the Mississippi city of Meridian, but only 2.1 occurred among black patients in San Diego.

“The resources needed to prevent amputation are currently severely misaligned,” says co-author Philip Goodney, MD, director of the Center for the Evaluation of Surgical Care at Dartmouth Hitchcock Medical Center. “While we must look for opportunities to expand education and preventive care for all patients at risk for amputation, it seems clear to us that we can make the greatest gains by focusing on African-American patients in the highest risk regions, typically in the poor rural regions of the Southern United States, where the highest amputation rates remain.”

TIME Research

Stem-Cell Researchers Make Breakthrough in Type 1 Diabetes Treatment

"We are now just one pre-clinical step away from the finish line"

Updated Oct. 13

Researchers have made a major breakthrough in finding a treatment for type 1 diabetes, Harvard University announced Thursday.

For the first time, scientists were able to create insulin-producing beta cells using human embryonic stem cells, at a volume required for cell transplantation and pharmaceutical use. Type 1 is the variety of the metabolic disease that can be inherited and which is likely due to an underlying autoimmune condition in which the body destroys the beta cells that produce insulin, a hormone that regulates glucose and helps the body process sugar. (Unlike type-2 diabetes, there is no way to prevent type-1.)

“We are now just one pre-clinical step away from the finish line,” said Doug Melton, who led the research and who has worked toward finding a cure for diabetes since his son was diagnosed as an infant 23 years ago.

That final step is finding a way to protect the 150 million beta cells needed to for transplant in the treatment of each patient from their immune systems, which automatically attack those cells. Melton is working with other researchers to develop a device for such protection. Tests of a device in mice have so far protected insulin-producing beta cells for several months.

TIME diabetes

Here’s Why Women Should Avoid Fried Food Before Pregnancy

Fried chicken
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So much for those burger-and-fries cravings.

A new study published in Diabetologia found that women who eat more fried food before conceiving are at greater risk for developing gestational diabetes—the kind that starts or is first noticed during pregnancy. Researchers looked at diet questionnaires from about 15,000 women enrolled in the Nurses’ Health Study II.

Once they adjusted for BMI, researchers found that women who ate fried food seven or more times a week had an 88% greater risk for gestational diabetes than those who ate fried food less than once a week.

MORE: Mom’s Diabetes Linked To Autism and Developmental Delays

Interestingly, the association was particularly strong with fried foods eaten away from home compared to home-cooked fried food. Restaurants tend to reuse their oil for multiple fryings, a practice that deteriorates oils through oxidation and hydrogenation. “Refrying may produce more of those detrimental chemicals,” says co-author Cuilin Zhang, MD, an investigator at the Eunice Kennedy Shriver National Institute of Child Health and Human Development. Frying also creates inflammatory compounds that may contribute to cell damage and diabetes—which Zhang suspects are related to the fried food.

No one would argue that a chicken nugget is a health food, but that kind of dining may be more hazardous when you’re getting ready to eat for two.

TIME Diet/Nutrition

Grapefruit Juice May Be As Effective as Diabetes Drugs

grapefruit
Chris Turner/Getty Images

A new mice study suggests that grapefruit juice might be just as effective as the type 2 diabetes drug, metformin, at lowering blood glucose. The research, which was funded by the California Grapefruit Growers Cooperative, was published Wednesday in the journal PLOS ONE.

Regarding the funding, study co-author Joseph Napoli, PhD, professor and chair of nutritional sciences and toxicology at the University of California, Berkeley, said this: “I understand the skepticism.” But the funders had nothing to do with the experiment, he says, besides providing some money and grapefruits. “We were very clear in telling them, you’re going to get the data we get,” Napoli says. “We can’t guarantee you’re going to like what you see. It might be nothing.”

What they found was not nothing.

The researchers fed different groups of mice a range of liquids: sweetened diluted grapefruit juice, sweetened water, and water that contained metformin, a diabetes drug. The mice who were fed a high-fat diet typical of the average American and drank the grapefruit juice lost 18% more weight than those drinking sweetened water, and they had a 13-17% drop in blood glucose levels and threefold decrease in insulin levels. (Mice on a low-fat diet had far less dramatic effects.)

But one of the biggest findings was that mice drinking grapefruit juice had glucose-lowering effects that were just as potent as the mice who sipped on metformin. “It was very surprising,” says Napoli.

You might have to drink a lot to get those prescription-level effects, however. The amount of grapefruit juice used in mice equates about four cups a day in people, the study says. But the researchers were so encouraged by the results that they plan to next look at if lower doses have the same impact.

“When someone says a particular food has this magic quality of improving your health all by itself, we mostly take that kind of claim with a grain of salt,” Napoli says. But Napoli, an avid grapefruit juice drinker himself, who says he’s convinced a few colleagues of its health merit, thinks his results show that grapefruits might actually do something special when it comes to diabetes.

TIME diabetes

Type 1 Diabetes Treatment Gets Boost from Stem Cells

Human stem cell derived beta cells
Insulin-making cells grown from stem cells glow green two weeks after they are transplanted into mice (c) Douglas Melton 2014

Scientists started with stem cells and created the first insulin-making cells that respond to changes in glucose

Scientists are closer to a potential stem cell treatment for type 1 diabetes.

In a new article in the journal Cell, Douglas Melton, co-director of the Harvard Stem Cell Institute (and one of the 2009 TIME 100) and his colleagues describe how they made the first set of pancreatic cells that can sense and respond to changing levels of sugar in the blood and churn out the proper amounts of insulin.

It’s a critical first step toward a more permanent therapy for type 1 diabetics, who currently have to rely on insulin pumps that infuse insulin when needed or repeated injections of the hormone in order to keep their blood sugar levels under control. Because these patients have pancreatic beta cells that don’t make enough insulin, they need outside sources of the hormone to break down the sugars they eat.

MORE: Stem-Cell Research: The Quest Resumes

Melton started with two types of stem cells: those that come from excess embryos from IVF procedures, and those that can be made from skin or other cells of adults. The latter cells, known as iPS cells, have to be manipulated to erase their developmental history and returned back to an embryonic state. They then can turn into any cell in the body, including the pancreatic beta cells that produce insulin. While the embryonic stem cells from IVF don’t require this step, they aren’t genetically matched to patients, so any beta cells made from them may cause immune reactions when they are transplanted into diabetic patients.

Both techniques, however, produced similar amounts of insulin-making beta cells—something that would have surprised Melton a few years ago. But advances in stem cell technology have made even the iPS cells pretty amenable to reprogramming into beta cells. Melton’s group tested more than 150 different combinations of more than 70 different compounds, including growth factors, hormones and other signaling proteins that direct cells to develop into specific cell types, and narrowed the field down to 11 factors that efficiently turned the stem cells into functioning beta cells.

MORE: Woman Receives First Stem Cell Therapy Using Her Own Skin Cells

The two populations of stem cells churned out hundreds of millions of insulin-making cells, which is the volume of cells that a patient with type 1 diabetes would need to cure them and free them from their dependence on insulin. An average patient, says Melton, would need one or two “large coffee cups” worth of cells’, each containing about 300 million cells. Melton and his team then conducted a series of tests in a lab dish to confirm that the cells were functioning just like normal beta cells by producing more insulin when they were doused with glucose, and less when glucose levels dropped. That was a huge advance over previous efforts to make beta cells from stem cells—those cells could produce insulin, but they didn’t respond to changing levels of glucose and continuously pumped out insulin at will.

Next, the scientists transplanted about five million of the stem cell derived beta cells into healthy mice, and two weeks later, gave them an injection of glucose. About 73% of the mice produced enough insulin to successfully break down the sugar. What’s more, that was similar to the proportion of mice responding to glucose after getting a transplant of beta cells from human cadavers. That was especially encouraging since some type 1 diabetics currently receive such transplants to keep their diabetes under control. “We’ve now shown that we can produce an inexhaustible source of beta cells without having to do to cadavers,” he says.

MORE: First Stem Cells Cloned From Diabetes Patient, Thanks to Egg Donors

Taking the tests even further, the group showed that even mice that were already diabetic showed improved blood sugar levels after receiving a transplant of the stem cell beta cells—in other words, the transplanted cells effectively cured their diabetes. “We showed you can give three sequential challenges of glucose—similar to breakfast, lunch and dinner—and the cells responded properly,” says Melton.

But he acknowledges that as exciting as the advance is, it only solves half the problem for those with type 1 diabetes. The reason their beta cells aren’t able to make enough insulin may be due to the fact that they are attacked by the body’s own immune system for reasons that scientists still don’t understand. So the next step in turning these findings into a potential therapy is to find ways to protect the beta cells from destruction, either by encapsulating them in a mesh-like device similar to a molecular tea bag, or finding ways to genetically modify them to carry ‘don’t attack me’ proteins, the same way that fetal cells do so that an expectant mother’s immune cells don’t attack the growing baby.

MORE: Stem Cell Miracle? New Therapies May Cure Chronic Conditions like Alzheimer’s

“It’s taken me 10 to 15 years to get to this point, and I consider this a major step forward,” says Melton, who began researching ways to treat type 1 diabetes when first his son, then his daughter were diagnosed with the condition more than two decades ago. “But the longer term plan includes finding ways to protect these cells, and we haven’t solved that problem yet.”

TIME Obesity

Are Diabetes Rates Really “Leveling Off”?

For the first time in several decades, we’re starting to see a slowing of new diabetes diagnoses, suggests new data published in JAMA.

The study authors examined data collected from more than 600,000 adults between ages 20-79 from 1980 to 2012—part of the Centers for Disease Control and Prevention (CDC)’s National Health Interview Survey. A broad view paints a grim picture: From 1990 to 2008, the prevalence of diabetes as well as new cases of the disease both doubled. But from 2008-2012, those rates of change leveled off. So while people are still being diagnosed with diabetes, the rate of growth is decelerating.

“It’s encouraging that we may be seeing this slowing and plateauing,” says Ann Albright, PhD, RD, director of the division of diabetes translation at the CDC and one of the study’s authors. The study cites a slowing of rates of obesity—one of the biggest contributors to type 2 diabetes, found one study—as a partial explanation for the results. Black and Hispanic adults, however, have continued to see a rise in new diabetes cases, and prevalence also grew among people with a high school education or less. These disparities, Albright says, could get worse.

“This data is telling us that we are doing some things right,” Albright says, which is especially important given that the population is aging, and baby boomers are hitting peak years for diabetes. Driving down diabetes prevalence is great, but the best way to get there is to curb new cases—not to have people in the diabetes pool die off early, she adds.

“[This study] is important to note, but it doesn’t mean we have this licked and we’re all done,” she says. “We still have a lot of work to do.”

TIME Diet/Nutrition

Artificial Sweeteners Aren’t the Answer to Obesity: Here’s Why

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Artificial sweeteners may be contributing to the very health problems they were supposed to prevent, say researchers Tetra Images—Getty Images/Tetra images RF

They’re supposed to be the sweet alternative to high-calorie, diabetes-causing sugar. But the latest science shows that artificial sweeteners may actually set us up for obesity and diabetes

Aspartame, saccharin, sucralose—sugar alternatives go by many names, but share an almost irresistible promise: all the sweetness of sugar without the calories, weight gain and increased risk of diabetes that comes with uncontrolled amounts of sugar in the blood.

But studies on artificial sweeteners and weight loss—as well as research about whether sugar substitutes helped people avoid metabolic disorders like diabetes—have been mixed. And in a paper published Wednesday in Nature, Dr. Eran Elinav from the Weitzmann Institute of Science in Israel found that the sugar stand-ins actually contribute to changes in the way the body breaks down glucose. How? Fake sugars aren’t digested and therefore pass directly to the intestines, impacting the millions of invisible bacteria that live in our gut. And when he and his colleagues gave seven people who didn’t normally use artificial sweeteners the sugar substitutes for seven days, about half of the people showed higher blood glucose levels after just four days.

MORE: 5 Steps to Quitting Artificial Sweeteners

“What our comprehensive genetic profiling of the microbiome pointed to is that exposure to artificial sweeteners directly impacts the microbes,” Elinav says. “We found that the artificial sweeteners we think of as beneficial and that we use as treatment or preventive measures against obesity and its complications are contributing to the same epidemics they are aimed to prevent.”

In the intestines, gut microbes are hard at work, pulling out some nutrients from food that are helpful in stopping tumor growth, for example, and squirreling away others to store as energy for later use. But while artificial sweeteners aren’t absorbed by our own cells, they may be absorbed by our bacteria—and when that happens, things appear to go haywire.

Higher amounts of the sweetener substitutes, Elinav and his team found, can change the makeup of these bacterial communities. And that in turn can change how those bugs behave, leading to weight gain and poorer glucose breakdown. These alterations in intestinal bacteria were the same as those in a group of 400 people who reported using artificial sweeteners—and those changes were the same in mice as well.

MORE: Why Your Brain Isn’t Fooled By Sugar Stand-Ins

In the mouse studies, Elinav’s team found that the artificial sweeteners pushed one particular group of bacteria, Bacteroides, to thrive, while inhibiting growth of another, Clostridiales. Bacteroides are the microbial equivalent of hoarders, hungrily pulling energy out of food and squirreling it away as fat. The end result of a Bacteroides-heavy gut is a physically heavy gut as well. In studies by other research groups, its dominance, and the resulting drop in diversity of other microbes, is typical of obese people compared to normal weight individuals.

MORE: 7 Not-So-Sweet Lessons About Sugar

The metabolic consequences were also dramatic in both the mice and people studied. In the mouse experiments, animals who were fed the same dose of saccharin that the U.S. Food and Drug Administration considers safe for daily use showed a drop in their ability to break down glucose. When he gave those mice antibiotics, their ability to break down glucose returned to normal, suggesting that wiping out the abnormal balance of bacteria could return the animals back to a healthier state.

And to confirm that the changing microbial communities were indeed responsible for the glucose changes, he also transplanted fecal samples from the people using artificial sweeteners into mice whose own guts had been wiped clean. These mice then developed the same abnormalities in glucose breakdown that the human donors and the mice who were fed saccharin did—even though they never actually ate artificial sweeteners. Simply harboring the microbes that had been exposed to the sweeteners was enough to disturb their glucose metabolism.

MORE: Can Sugar Substitutes Make You Fat?

The good news is that as easily as the gut microbiome can shift toward an unhealthy state, it can just as easily be brought back into line with the proper balance of bacterial communities. The best way to do that isn’t clear yet, but, says Eran Segal, a co-author of the study and a professor of computer science and applied mathematics at the Weitzmann Insttitute, “We believe that the situation today at the very least needs to be re-examined. We were able to induce glucose intolerance in a few days in some individuals, so this massive, unsupervised and unregulated use [of artificial sweeteners] should at the very least be reassessed and perhaps re-examined in additional studies.”

Elinav, for one, isn’t waiting. Based on his findings, he’s stopped adding artificial sweeteners to his coffee.

 

TIME diabetes

Why Inflammation Matters for Diabetics

Anti-inflammatory medications might someday be used to lower the risk of certain kinds of disease among diabetics, found a new study presented at the American Heart Association’s High Blood Pressure Research Scientific Sessions 2014.

In the laboratory, the researchers studied cultured cells from a human aorta, the blood vessel that comes out of the heart and goes to the rest of the body. They put the cells in a high-glucose environment—similar to a what happens inside a diabetic body—and found that without inflammation present, sugar didn’t enter the cells. And even when glucose was forced into the cells, the cells weren’t damaged.

But inflammation changes everything. When researchers added an inflammatory protein called interleukin-1—a common marker for inflammation in the body, whether you are diabetic or not—the cell did metabolize the glucose, which kicked off a cycle of inflammation. Those effects were blocked once the researchers gave the cells a certain type of anti-inflammatory drug.

“What [the study authors] said was, you need the inflammation in order for the glucose to do the damage to the cells,” explained Mary Ann Bauman, MD, a primary care internist at INTEGRIS Health in Oklahoma City and a spokesperson for the American Heart Association. (Dr. Bauman was not an author on the study.) “That could be one of the reasons why in a diabetic, if we can get them to exercise and lose weight, they will have less damage to their blood vessels.”

In diabetes care, doctors and patients often focus on reducing blood sugar levels, and though this preliminary research occurred only in cells, it shows how inflammation might play a role, Dr. Bauman said.

That means that controlling blood sugar isn’t always enough to avoid the cardiovascular disease that sometimes stems from diabetes, and anti-inflammatory drugs may one day be able to help, said study author Carlos Sánchez-Ferrer, professor of pharmacology at the Universidad Autónoma de Madrid in Spain, in a press release. Lifestyle changes can help, too. “We need to reduce the inflammatory environment associated with diabetes,” Sánchez-Ferrer said. “Changes in lifestyle, such as physical exercise and weight reduction, are important not only because they reduce blood sugar but because they reduce inflammation.”

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