Obesity and Diabetes – Is Your Gut in Control?

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.

For a link to this story, click here.

Vaginal or C-section: Does it matter?

Feb. 20, 2015

An infant

In the climax of William Shakespeare’s “Macbeth,” the title character is sword fighting and believes himself invincible because he was given a prophesy that said “no man born of woman shall harm thee.” Yet, that is how he was tricked, for his rival, Macduff, was “from his mother’s womb untimely ripped.” This and other historical references show that cesarean sections have been used for centuries, but today the high success rate has made them more common than ever.

The origin of the term Cesarean is popularly and probably falsely attributed to the birth of Julius Caesar. This is unlikely, since C-sections at this time almost always resulted in the death of the mother, and historical records mention Caesar’s mother later in his life. However, the origin may still be linked to Caesar as a law enacted during Caesar’s reign stated that a dead or dying pregnant woman was to be cut open and the child removed from her womb to save the child. Widespread use of this procedure began after anesthetics and antimicrobial therapies became available in the 20th century.

In 1965, 4.5 percent of America’s babies were delivered via C-section. Today that figure has risen to almost one in three, and is on the rise worldwide as well. There are plenty of medical and nonmedical reasons for this shift from vaginal childbirth. Both come with side effects and consequences, some lasting longer than others. For example, C-sections have been linked to increased rates of diabetes and obesity, although we’re not sure why. In a recent study, birth by C-section lead to epigenetic changes in the child’s DNA.

Epigenetics are changes in our DNA that don’t result from changes in our genetic code. These changes can come from environmental factors, such as smoking, that alter the ability of a gene to be seen or expressed. What we didn’t understand until relatively recently is that epigenetic changes can be transmitted to offspring. So you are the product of your parents’ DNA and the environmental factors that affected your DNA in your lifetime and their lifetime before you were born. Then your DNA and epigenetic information is passed on to new generations. These changes accrue and could affect your children or grandchildren. So the descendants of a smoker may inherit more than their name, but epigenetic changes in DNA as well.

New research suggests certain epigenetic changes in a baby’s DNA called methylation are different depending on the type of birth. When DNA becomes methylated, it changes whether a gene is used to make a protein and this can then alter the properties of specific cells. In this study, researchers compared the DNA methylation patterns in stem cells of 25 vaginally delivered babies and 18 delivered by C-section. Distinct methylation changes were seen in more than 300 different regions of the genome between the two groups. Interestingly, many of these regions are associated with genes that control the immune system. We don’t know how these epigenetic changes affect the immune system and ability to fight disease, and don’t have sufficient information to link these differences to later health issues. But this remains an intriguing possibility and awaits more research.

For a link to this story, click here.

Bear-ly Understanding Diabetes

May 30, 2014

By Medical Discovery News

What can studying grizzly bears reveal about human diabetes?

While they are some of the largest bears on earth, Grizzly bears aren’t usually accused of being fat. Regardless, these animals are helping scientists discover new and better treatments for human obesity and diabetes.

Grizzlies spend the late summers consuming more than 50,000 calories per day. As a comparison, a moderately active 50-year-old human female is recommended 2,300. Grizzlies then hibernate for up to seven months, relying on the pounds of stored fat they accumulated before winter. While hibernating, bears do not eat, urinate, or defecate. 

Scientists wondered if all the weight and fat bears gain results in diabetes like it does in humans. Overweight people face an increased risk of type 2 diabetes, in which the body does not make enough of the hormone insulin or cells do not respond to it. Insulin helps move a type of sugar called glucose from the blood into cells, where it is used for energy and as a precursor for other molecules the body needs. If sugar levels in the blood remain elevated and the body doesn’t have enough insulin, cells are starved for energy, leading to damaged eyes, kidneys, nerves, and hearts. 

Interestingly, Grizzly bears can actually control their insulin responsiveness. When they are the fattest, they are most sensitive to insulin, thereby keeping their blood sugar levels healthy. Soon after going into hibernation, they switch to complete insulin resistance, meaning they develop type 2 diabetes. But unlike humans, their blood sugar levels remain normal. When they awaken in the spring, their insulin responsiveness is restored. Bears do this not so much to regulate their blood sugar levels as to regulate their storage and utilization of fat. So how do bears control their insulin responsiveness? And could it lead to new treatments for type 2 diabetes in humans?

PTEN is a protein that regulates cells’ sensitivity to insulin. Scientists know exactly when Grizzlies increase or decrease PTEN activity, they just don’t know how. People with a PTEN mutation have a metabolism similar to Grizzlies’.  These people have an increased risk of obesity and cancer but a decreased risk of developing type 2 diabetes because they are more sensitive to insulin.

Grizzlies have also evolved to the ability to accumulate large amounts of fat only in their adipose tissue, just below the skin so it doesn’t interfere with the rest of their bodies. In humans, on the other hand, fat can accumulate in many places like the liver, in muscles, and around other internal organs, which are all highly unhealthy places to keep fat. Bears can also have elevated levels of cholesterol without the serious consequences of cardiovascular disease.

During hibernation, the Grizzly bears’ kidneys shut down. But despite the high levels of toxins that accumulate in the blood without working kidneys, they don’t die or even suffer from it like a human would. When they wake up, their kidney function is restored with no permanent damage.

After millions of years of evolution, Grizzly bears and other animals have developed solutions for biological challenges humans still face. Studying them is a new approach that has the potential to create treatments for many human conditions.

For a link to this story, click here.

How Much Sugar Is Safe?

Jan. 31, 2014

By Medical Discovery News


Former Mayor Michael Bloomberg of New York City caused a controversy when he tried to ban the sale of sugary drinks more than 16 ounces. Thus the “Big Gulp” rebellion was born and the ban was later overturned by the courts. Yet the rates of diabetes, heart disease, and obesity remain out of control in the U.S.

In the U.S., 24 million people over age 20 have diabetes. Another 78 million have pre-diabetes with blood glucose levels higher than they should be – the start of glucose intolerance.  And down the road, this may lead to life-threatening heart disease (the No. 1 killer of adults), which is also linked to obesity affecting more than 80 million Americans.

Much of the obesity epidemic has been blamed on unhealthy eating and poor nutrition. Refined sugar has been identified as a source of excess calories. According to the U.S. Departments of Agriculture and Health and Human Services, almost 50 percent of sugar in the diets of Americans comes from sugary drinks and sweetened fruit drinks. The debate over just how much sugar is too much in terms of our health was addressed by a recent study and the results are sending shock waves through the medical community. 

In the experiment, one group of mice ate a normal diet and another group ate a diet where one quarter of the calories came from sugar similar to that in high fructose corn syrup. This level of sugar is pretty equal to that consumed naturally by 15 to 25 percent of the U.S. population. This is equivalent to a person consuming three cans of a sugary beverage a day in an otherwise sugar-free diet. Current nutrition guidelines consider this to be at the top of the safe level of sugar for people.

After 26 weeks of a monitored diet, all the mice were released into an experimental natural environment. Over the next 32 weeks, twice as many sugar-fed female mice died compared to the control group. The sugar-fed male mice produced 25 percent fewer offspring and held 26 percent less territory than mice from the control group. Overall, dietary sugar was linked to a shorter life span, limited reproduction, and lowered competitive success. 

Metabolic measurements on the sugar-fed mice showed changes in glucose clearance and increases in cholesterol levels, but these were considered minor. Nevertheless, life outcomes called Organismal Performance Assays were significantly affected. This may represent a new way to gauge important changes in overall life parameters without corresponding physiological changes.

This certainly raises the question of how much sugar is too much, and the debate over the appropriate level of refined sugar for good human nutrition will continue. It will be interesting to watch in the coming months and years to see if these results are substantiated and if they lead to new nutritional guidelines. Who knows – maybe Mayor Bloomberg was right after all!

For a link to this story, click here.

Staving Off Dementia

Nov. 8, 2013

By Medical Discovery News


While American novelist Mark Twain can invariably add his iconic sense of humor to any situation, it is no laughing matter when patients lose their memories and cognitive function to dementia. And for their family members, there is hardly anything harder than caring for a loved one who can no longer remember them or any shared experiences. But lowering a person’s risk of dementia may be as simple as changing their lifestyle.

The incidence of dementia increases with age. As the average age of Americans increase, the number of people with dementia also increases. In 2010, more than 30 million people worldwide had dementia, and this figure is estimated to more than triple by 2050.

Despite the many medical advances over the past 20 years, there are no effective pharmacological therapies for dementia yet. Some drugs are being evaluated and still others are in development, but it could be some time before there is a truly successful treatment for this disease. 

However, studies have uncovered risk factors that can lead to dementia, such as low physical and mental activity, obesity, hypertension, and hyperlipidemia. The good news is that all these risk factors can be controlled by changes in a person’s lifestyle and behavior.

A group of scientists at the Karolinska Institute in Stockholm examined the effects of lifestyle modification on dementia risks. One of the strongest correlations to reducing the risk of dementia is increasing physical activity. Changing from a sedentary lifestyle to one with at least moderate physical activity will also improve cognitive performance. Both aerobic exercise and strength training may delay of the onset of dementia. 

For those with nutritional deficiencies, taking vitamin supplements did help prevent dementia onset, but those with normal levels did not affect their dementia risk by taking supplements. 

Computer games have become a popular way to enhance mental abilities in older people. There are some positive effects of gaming on cognitive performance, but these effects decline with age.  A recent study showed that improvements in language skills and reasoning abilities lasted for a full year after computerized training. While encouraging, more clinical trials are needed to establish the benefits of these activities on cognitive functions and the delay of dementia.

For now, the best advice to delay or prevent dementia is to engage in physical exercise and maintain a healthy weight and nutrition.

For a link to this story, click here.

Weight Loss Microbe

Oct. 4, 2013

By Medical Discovery News

John Donne said, “No man is an island.” Scientists would agree – man is more like a forest. And just like the flora and fauna that call the forest home, each human body houses tons of other species in the form of microbes. In fact, most people have 10 times more microbes in and on them than their own cells! These microscopic organisms live on skin, within the gastrointestinal tract, and inside mouths, helping the human body function and keeping it healthy. Now, new research shows that a certain microbe has huge influence on a person’s weight.

Science is just beginning to understand how the relationship between microbes and human cells, tissues, and organs contributes to good health. The key here is mutualism – the cooperation that benefits both the microbes and the human.

Disruption of the relationship of a person’s microbiome can lead to problems. For example, oral antibiotics can upset the microbiome in the gut, resulting in the discomfort some people experience while taking them. While antibiotics are made to be effective against specific types of bacteria, they also disrupt the normal population of bacteria in the intestinal tract. The types and amount of necessary bacteria here are altered. This results in major changes to the interaction between bacteria and cells lining the gut, much to a person’s dismay and inconvenience.

A recent study shows that a bacterium in the intestines appears to control diet-mediated obesity.  Akkermansia muciniphila is a common resident of the human gut, living in the layer of mucus that coats the surface of the intestinal tract. In a healthy person, this bacterium can be 3-5 percent of all the bacteria present – that’s a lot. The amount of Akkermansia muciniphila in a person’s intestinal tract is highly correlated with their weight. That is, people with low numbers of Akkermansia muciniphila are more likely to be obese and have type II diabetes, and those with high numbers are more likely to have a healthy weight.

To figure out this connection, researchers used mice that were fed either a normal diet or a high fat diet and monitored the number of different bacteria in their guts. As expected, mice fed the high fat diet became obese, but their levels of Akkermansia muciniphila were 100 times lower than mice fed the normal diet. Furthermore, when the obese mice on the high fat diet were also given this bacterium, they lost weight and lowered the incidence of diabetes.

This has some remarkable implications and possibilities for future therapies. This interplay between bacterial populations and the host can prevent some major human health issues, like obesity or diabetes. Perhaps Akkermansia muciniphila will soon be an ingredient in probiotics and yogurts and start a new weight-loss trend.

For a link to this story, click here.

Thinking with your Stomach

May 31, 2013

By Medical Discovery News

“The way to a man’s heart is through his stomach.” New research might amend this common proverb to “the way to a man’s brain is through his stomach.” An article in the “New Scientist” argues that the enteric nervous system (ENS), found in the tissues of the gastrointestinal (GI) tract, functions as a second brain of sorts.

Spanning the mouth to anus, the GI system is approximately 30 feet long and can be divided into the upper (esophagus, stomach, and duodenum) and lower (large and small intestine) tracts. This is where digestion occurs, providing metabolic functions and energy to the body. With this complex role, it is not hard to imagine why it needs its own nervous system.

Like the brain, the ENS consists of different types of neurons as well as glial cells, which provide support and protection for the neurons. The human ENS contains upward of 500 million neurons and an equal number of glial cells, more than all of those in a rodent’s brain. However, the human brain contains 90 billion neurons. The ENS communicates with the brain to control unconscious or autonomic processes, like peristalsis, the wave-like motions that push food through the GI tract. 

To accomplish this, the ENS produces hormones and neurotransmitters much like the brain. In fact, the ENS produces as much dopamine (which triggers feelings of reward and pleasure) as the brain and most of the serotonin (which controls mood, appetite, and sleep) within the body.

So, if the ENS truly acts as a second brain, then the GI system can affect a person’s moods and sense of wellbeing. The ENS causes this by transmitting signals to the brain through the vagus nerve. This makes sense, since people typically feel good after enjoying a meal. For example, when rich foods are digested they release fatty acids. The gut detects this, prompting the ENS to send certain signals to the brain. According to brain imaging studies, the brain then releases pleasurable sensations, altering a person’s mood. So it’s no wonder that people crave rich, fatty foods!

On the other hand, people usually eat differently when stressed. Stress can lead to the production of a GI hormone called ghrelin, which causes feelings of hunger and leads to a reduction of anxiety and depression. In experiments, mice subjected to stress sought out fatty foods, which elevated the production of ghrelin. The link between chronic stress and obesity is then a no-brainer.

The main function of the ENS is to monitor the digestion of food and identify threats in what is eaten, such as toxins or infections. So, perhaps listening to the stomach when it comes to choosing meals isn’t all bad. After all, that’s the second brain at work.