Obesity and Diabetes – Is Your Gut in Control?

August 28, 2015 by

Aug. 21, 2015

By Medical Discovery News

Your body is like a forest, providing a home to microscopic flora and fauna. In fact, your body is home to up to 100 times more microbes than your own cells, which make up your microbiome. While we provide them residence, these microbes help us out by providing a first line of defense against disease trying to invade our bodies, even breaking down food during digestion and producing vitamins. Now, the microbes that live in the digestive tract are helping us understand diabetes better.

According to the Human Microbiome Project sponsored by the National Institutes of Health, the microbiome plays a huge role in human health. When the microbiome is altered or imbalanced, it can cause conditions like obesity, irritable bowel syndrome, skin disease, urogenital infection, allergy, and can even affect emotion and behavior.

Recently, scientists from Israel discovered another surprising effect of the microbiome while investigating the use of artificial sweeteners in relation to glucose intolerance and diabetes. Artificial sweeteners such as saccharin, sucralose, and aspartame are commonly used in weight loss strategies because they do not add calories while still satisfying sweet cravings. However, artificial sweeteners are not always effective in managing weight and glucose, and scientists at the Weizmann Institute of Science may have figured out why.

Through experimentation they observed that adding artificial sweeteners to the diets of mice caused significant metabolic changes, including increasing blood sugar levels more than mice fed regular sugar. It didn’t matter whether the mouse was obese or at a normal weight, they all reacted the same. Dietary changes can alter the populations of bacteria in our guts, so the study addressed whether those changes affected blood glucose levels as well. After being treated with saccharin for nine days, the populations of gut bacteria in the mice shifted dramatically and corresponded with an increase in their glycemic index. Specifically, the bacterial group Bacteroidetes increased while the group Clostridiales decreased. These changes in bacterial populations is associated with obesity in mice and people.

When they administered antibiotics to reverse this and return the bacterial populations to a healthy state, it also countered the effects of saccharin, returning glucose levels to normal. To take it a step further, researchers took feces from saccharin-consuming mice showing glucose intolerance and transplanted them into other mice that had never consumed saccharin. Remarkably, those mice started showing signs of glucose intolerance.

In a study of 400 people, those who consumed artificial sweeteners had a gut microbiome that was vastly different from those who did not. They had a group of people consume high levels of artificial sweeteners for seven days, and like the rats their glucose levels increased and their microbiomes changed.

Overall, these studies show that artificial sweeteners may induce glucose intolerance instead of preventing it due to the intimate connection between the bacteria that live in our digestive systems and our metabolic state. In the future, expect to see diagnostic and therapeutic procedures that utilize our microbial friends.

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Bring on the Milk

June 22, 2014 by

June 20, 2014

By Medical Discovery News

Milk

Drinking milk might seem perfectly natural, but it’s actually anything but. Humans are the only species who retain the ability to digest milk after childhood, or at least some of us do. Up to half of adults worldwide don’t have the ability to break down lactose, the main sugar in milk, because their bodies stop producing the enzyme lactase after the age of five.

About 65-75 percent of the population has some degree of lactose intolerance, the most common cause for digestive issues with dairy. Lactase breaks down lactose into simpler forms of sugar that can be absorbed by the bloodstream. Without this enzyme, lactose is fermented by bacteria, causing symptoms like abdominal pain, bloating, flatulence, nausea, and diarrhea 30 minutes to two hours after eating. Populations that have long relied on unfermented milk have the lowest rate of lactose intolerance – only five percent among the Swiss.

Humans’ ability to drink milk actually began as a genetic mutation, like the superheroes of X-Men comics. According to the leading theory, 7,800 years ago humans began to move northward. Since the sun is not out as long in northern latitudes, they could not absorb enough vitamin D from sunlight and needed another source to thrive. Milk is high in vitamin D, which aids in calcium absorption. Humans adapted to this change in their diets and developed a variant of the lactase gene that allowed them to continue synthesizing the enzyme throughout their lifetimes. Since humans with the gene variant had the advantage of consuming more vitamin D, they were successful in passing that gene on to future generations.

But new research suggests that this theory is either wrong or other factors were involved. Scientists in northeastern Spain discovered well-preserved skeletons of people who lived 5,000 years ago. DNA testing revealed that none of these eight skeletons carried the genetic mutation for lactase production. Further testing also showed that these ancient humans are indeed related to modern Spaniards. Next, computer simulations determined that over 5,000 years, chance alone would not have allowed one-third their descendants to digest milk. Strong selection for this trait would have been necessary.

These scientists developed a theory that early farmers began eating fermented dairy products such as cheeses, which have lower levels of lactose. But when food was scarce, they ran out of fermented dairy products and began to consume unfermented milk as a food source. Then, those who acquired the mutated gene for lactose production would have thrived. Those without the mutation would have suffered from diarrhea, making their situation worse, perhaps even life-threatening if they were already starving.

While the need for vitamin D from milk may have been a factor in the spread of lactase persistence, these new findings show that other factors may have also been a part of the selection process that drove this mutation into the population. Now if we could only figure out a way to turn on lactase genes again during adulthood, everyone with lactose intolerance could enjoy a pain-free ice cream cone.

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