Prediabetics Have Fewer Gut Bacteria
In the global diabetes epidemic, rates of new cases are rising rapidly. I hope this post will help you avoid becoming one of them. Number of People Diagnosed with Diabetes Millions, by region
Source: IDF Diabetes Atlas, Sixth Edition; Managed Care calculation of percentages using data from The World Factbook, published by the CIA TYPES 1 & 2 DIABETES: AUTOIMMUNE DISEASES
During digestion, most of our food gets broken down into glucose (a form of sugar that’s the body’s main source of fuel), which then passes into the bloodstream. Insulin (a hormone produced by the pancreas) must also be present in the blood for glucose to be able to make it into our cells to nourish them. Type 1 diabetes is known to be a serious autoimmune problem of the metabolism. An autoimmune disorder or disease is a result of chronic inflammation in the body’s immune system, causing it to turn against a part of the body – to attack it as if its cells were dangerous, invading pathogens. In Type 1 diabetes, the immune system attacks and destroys the insulin-producing cells in the pancreas. (WebMD, 2008) Type 2 diabetes is now also largely viewed as the result of a different type of autoimmune reaction: one in which B and T immune cells cause inflammation in the fatty tissue surrounding organs in the body. The inflammation occurs when rapidly growing fat cells outstrip their blood supply and begin to die off. These dying cells spew out their contents, and macrophages (another type of immune cell) are called in to clean up the dead cells. “The resulting onslaught by the immune system inhibits the ability of the remaining fat cells to respond to insulin and causes fatty acids to be shed into the blood. This sets in motion a physiological cascade that leads to fatty liver disease, high cholesterol, high blood pressure and further insulin resistance throughout the body.” (Conger, 2011) TYPE 1 DIABETES
In Type 1 diabetes, which used to be called juvenile diabetes, the immune system mistakenly kills off pancreatic cells that make the blood-sugar-regulating hormone insulin. The body’s immune system attacks and destroys these pancreatic cells so they no longer make enough insulin. Type 1 diabetes accounts for about 10% of diagnosed diabetes in the US. TYPE 2 DIABETES In Type 2 diabetes, the pancreas usually produces enough insulin but the cells in the body have become unable to make effective use of the hormone, a condition called insulin resistance. Insulin production eventually decreases. So, as in Type 1 diabetes, glucose builds up in the blood instead of being properly delivered to the cells in the body where they’re needed for fuel.
Type 2 diabetes is associated with obesity, older age, family history of gestational diabetes, and physical inactivity. About 80% of people with Type 2 diabetes are overweight.
Unfortunately, Type 2 diabetes is also increasingly being seen in younger people, even children and teens. PREDIABETES
A prediabetic condition indicates the amount of glucose in the blood is above normal but not yet high enough to be called diabetes. Prediabetic people are at greater risk of developing Type 2 diabetes, heart disease, and stroke. DIABETES STATISTICS IN THE US
Statistics from the American Diabetes Association Report, 2014 show the magnitude of the problem in the US:
PREVALENCE: In 2012, 29.1 million Americans, or 9.3% of the population, had diabetes. Approximately 1.25 million American children and adults have type 1 diabetes.
UNDIAGNOSED: Of the 29.1 million, 21.0 million were diagnosed and another 8.1 million were undiagnosed.
PREVALENCE IN SENIORS: The percentage of Americans age 65 and older remains high, at 25.9%, or 11.8 million seniors (diagnosed and undiagnosed).
NEW CASES: The incidence of diabetes in 2012 was 1.7 million new diagnoses/year; in 2010 it was 1.9 million.
PREDIABETES: In 2012, 86 million Americans age 20 and older had prediabetes; this is up from 79 million in 2010.
DEATHS: Based on the 69,071 death certificates in which diabetes was listed as the underlying cause of death in 2010, diabetes was the 7th leading cause of death in the United States that year. In 2010, diabetes was also mentioned as a cause of death in a total of 234,051 certificates.
CAUSE OF DEATH UNDER REPORTING
Diabetes may be under reported as a cause of death. Studies have found that only about 35% to 40% of people with diabetes who died had diabetes listed anywhere on the death certificate and only about 10-15% had it listed as the underlying cause of death.
DIABETES IN YOUTH
About 208,000 Americans under age 20 are estimated to have diagnosed diabetes, approximately 0.25% of that population.
In 2008—2009, the annual incidence of diagnosed diabetes in youth was estimated at 18,436 with Type 1 diabetes, 5,089 with Type 2 diabetes.
Some other diabetes statistics showing the seriousness of the problem:
Below are diabetes prevalence data from the US Centers for Disease Control and Prevention. The number of reported cases tripled between 1980 and 2008. The CDC estimates that “the number of Americans with diabetes will range from 1 in 3 to 1 in 5 by 2050.”
And here’s information from the International Diabetes Federation comparing reported cases of diabetes in 2013 with projected cases by 2035 for countries around the world – an expected increase of 55%.
GUT BACTERIA & DIABETES
Researchers are discovering changes in normal gut bacteria that take place before either Type 1 and Type 2 diabetes turns into a clinical condition. Since we now know that 70-80% of our immune system is located in our GI tract, where digestion takes place, you can see how a serious imbalance in the bacterial make up of the gut microbiome could lead to the development of diabetes in people with a genetic predisposition for it.
“Mounting evidence suggests that the bacteria resident within our GI tract – and the immune response to those bacteria – influence the permeability of the gut mucosa. This idea — which has become to be known as the “leaky gut” hypothesis — proposes that a cycle of dysbiosis, dysregulated immune response, and unintended gut permeability leads to the peripheral host immune system being unbalanced towards a pro-inflammatory response. This in turn is suggested to lead to (some of) the imbalances that are thought to be causative of diabetes and other non-metabolic disorders.” (Moore, 2015) GUT BACTERIA, ANTIBIOTICS & RISK FOR DIABETES
A team of scientists led by Dr Ben Boursi, a Post Doctoral Researcher in Gastroenterology at the University of Pennsylvania in Philadelphia, found people who have taken multiple courses of antibiotics were 37% more likely to develop Type 1 and Type 2 diabetes. The team also found the greater the number of courses of antibiotics, the higher the risk for developing diabetes. Dr Boursi notes, “Our findings are important, not only for understanding how diabetes may develop, but as a warning to reduce unnecessary antibiotic treatments that might do more harm than good.”
Several studies in humans have shown that early childhood exposure to antibiotics is associated with increased risk of obesity in later life – and obesity has long been recognized as risk for developing diabetes. There’s also growing evidence that imbalances in the gut microbiome’s composition contribute to the development of both Type 1 and 2 diabetes. The Boursi team’s future research will focus on identifying the species of gut bacteria necessary to prevent and reverse diabetes, potentially working towards the possibility of transplanting prebiotic and probiotic microbes into the gut as a therapeutic strategy for diabetes. (Arendt, 2015) & (Davenport, 2015) PREDIABETICS HAVE FEWER & LESS DIVERSE GUT BACTERIA
A research team led by Dr Elena Barengolts, an Endocrinologist at the University of Illinois College of Medicine, found irregularities in the composition of the probiotic bacteria in the guts of prediabetic patients: Compared with subjects whose glucose tolerance was good, the prediabetics had fewer and less diverse populations of bacteria living in their gut microbiome. There were 116 participants in the study, all African-American veterans. Their ages ranged from 45 to 70. Their intestinal bacteria were measured by stool samples at the start of the study and again 12 months later. Participants were divided into four groups based on their body’s ability to regulate blood sugar:
Group 1 – Those with stable glucose tolerance (normal)
Group 2 – Those with stable impaired fasting glucose or stable impaired glucose tolerance
Group 3 – Those with worsened glucose tolerance
Group 4 – Those with improved glucose tolerance
The study found that men whose blood sugar control remained normal over the year (Group 1) had higher numbers of beneficial gut bacteria while the men who continued to be prediabetic had fewer beneficial bacteria and higher numbers of harmful bacteria in their guts. Furthermore, the group whose blood sugar management improved over the course of the year (Group 4) had a higher number of a strain of healthy bacteria (Akkermansia) than the group who had maintained normal blood sugar control over the year (Group 1). (Gray, 2015)
At the phylum level, this study found significant differences in the bacterial composition between Groups 1 and 2: Group 2 (people with impaired but stable fasting glucose or glucose tolerance) had higher levels of Bacteroidetes and lower levels of Firmicutes than people in Group 1. The Bacteroidetes/Firmicutes ratio was 1.9 vs 0.9 respectively for Groups 1 and 2 and 1.9 vs 1.1 respectively for Groups 1 and 3. The number of Proteobacteria decreased over the 12-month study period in Groups 2 and 4 compared with Group 1. Proteobacteria are a major phylum of gram-negative bacteria that include a variety of pathogens – such as Escherichia, Salmonella, Vibrio, Helicobacter, and Yersinia. (Wikipedia, 2015)
At the family and genus levels, Group 2 had fewer Prevotella and a higher Bacteroides/Prevotella ratio than Group 1: 5.6 vs 2.7. Group 2 also had fewer Enterobacteriaceae (a large family of bacteria that includes the pathogens Salmonella, Escherichia coli, Yersinia pestis, Klebsiella and Shigella) and more Ruminococcae and Veillonellaceae. “We speculate that lower abundance of Prevotella may be associated with worsening glycemia, and, conversely, higher abundance of Akkermansia might be associated with improving glycemia, thus corroborating suggestions from previous studies,” the researchers said. Barengolts notes, “Changes in the gut microbiota occur in the early stage of diabetes development. The gut bacteria signature — the composition and abundance — could be a useful tool in assessing a person’s risk for developing obesity and diabetes.” (Ciubotaru et al, 2015) & (Brown, 2015) Other studies are currently underway in Italy and China investigating gut bacterial transplants as a treatment for diabetes. ALTERED GUT BACTERIA PRECEDE TYPE 1 DIABETES IN CHILDREN
A small study followed 33 babies from Finland and Estonia who were at increased genetic risk for developing Type 1 diabetes. Analysis of their stool samples charted changes in the multitude of microorganisms living in their guts. By age three, four of the children developed Type 1 diabetes. Huge alterations in the gut microbes of those four children were seen about a year before onset of the disease. As with the men in the veterans’ study, there was a marked drop in the diversity of the overall microbial community. This drop in gut diversity was accompanied by spikes in inflammation-favoring organisms, gene functions, and serum and stool metabolites. These changes in gut microbial levels did not occur in the at risk children who didn’t progress to Type 1 diabetes. Researcher Dr Aleksandar Kostic, a Postdoctoral Fellow in Computational Biology and Experimental Biology at MIT and Harvard, hopes the study’s results will lead to an early diagnostic test for Type 1 diabetes. (Kostic et al, 2015) & (Norton, 2015) PREVENTING & TREATING DIABETES VIA THE GUT MICROBIOME? Bacteria in the Human Gut
Given what we already know about the gut microbiome’s role in keeping the body in a balanced state so it remains healthy, it makes sense to focus on diet and nutritional supplements for preventing and treating diabetes. For example, we know there is considerable variation among people in the microbes that live in and on us. We also know that an individual’s microbial populations are always changing. The following is from an easy to read summary of changes in the various human microbiomes from birth through old age. It was prepared by the University of Utah’s Genetic Science Learning Center (2015). You might want to take a look at it – it provides useful information along with some delightful drawings: “Before birth, we’re all more or less sterile—we have no microbes. Within a few years, we’re covered in thousands of different species of microbes, and they colonize every millimeter of the body that’s exposed to the outside world. By the time we enter kindergarten, we have vastly different populations living in the different habitats around our bodies. Even as adults and into old age, our microbiota continue to shift. ” … Because so many things affect our bodies’ ecosystems, there is a huge amount of variability in microbial populations even among individuals of the same age. Just like our fingerprints vary, we vary in the microbial species we have as well as their relative abundancies. Our microbes vary with gender, diet, climate, age, occupation, and hygiene. Even differences in our genes influence our microbial populations—indirectly by affecting things like the acidity of the digestive tract, and also more directly through variations in proteins on our cells that communicate with microbes. “Even with all this variability, there are some trends. Microbial populations differ more among body sites than between individuals. For example, the microbes living on the forearms of two different people tend to be more similar than the microbes on the forearm and ear of the same person. And there are certain species of bacteria that will only live in the gut, others that will live only on the teeth, and so on.” GENETICS VS EPIGENETICS
We also know this about autoimmune diseases: DNA IS NOT DESTINY Chronic diseases, especially autoimmune ones, are only 25% determined by genetic inheritance. The other 75% is affected by other factors. It’s a matter of genetics vs epigenetics. You may have a genetic predisposition for diabetes but also have a large say in whether your DNA expresses that predisposition in your body. “We know from twin studies, from identical twin studies, that 25% of autoimmunity is your genetics, and 75% is from the environment. … So that’s an enormous amount that we have control over and can influence.”
Amy Myers, MD. (Sanfilippo, 2015)
If we know that both the composition and abundance of micro-organisms living in our guts change over the course of a lifetime, shouldn’t it be possible to learn how to make deliberate changes to our gut microbiome – changes that prevent diabetes from developing even if we have a genetic predisposition for it?
TO AVOID OR REVERSE INSULIN RESISTANCE
These are Dr Robert Mercola’s suggestions for turning insulin resistance around (Mercola, 8/23/2015) & (Mercola, 8/27/2015): AVOID SUGAR
EAT REAL FOODS INSTEAD OF PROCESSED ONES
Almost all so-called foods that come in a bottle, can, jar, bag, or box have had sugars added to them, usually in the form of high fructose corn syrup. EAT FRESH FRUIT INSTEAD OF PURCHASED FRUIT JUICES
Commercial fruit juices are loaded with added sugar. AVOID “DIET” FOODS AND DRINKS
They promote insulin resistance and other health problems. “The artificial sweeteners saccharin, sucralose, and aspartame decrease function in pathways associated with the transport of sugar in your body, and can induce both gut dysbiosis and glucose intolerance. Research also shows that artificial sweeteners promote diabetes and weight gain by disrupting your gut microbiome. Sucralose (Splenda) was found to reduce beneficial gut bacteria by as much as 50 percent!” AVOID GRAINS, ESPECIALLY WHEAT, BARLEY, OATS & RYE
Grains turn into sugar in your body, sharply raising your glucose and insulin levels, and contribute to insulin resistance. Many grains also contain gluten, which triggers inflammation in the intestines, leading to a state of chronic inflammation in the body and autoimmune diseases. Consuming a lot of refined grains (and even whole grains) is also highly inflammatory for another reason: Humans are designed to eat a diet containing a ratio of 1 or 2 parts of Omega-6 essential fatty acids to every 1 part of Omega-3. This ratio is what we get when we eat real, unprocessed, highly nutritious foods – non-GMO veggies, fruits, nuts, seeds, and pastured animals. Our typical diet now has come to contain 10 to 20 parts Omega-6 to every part Omega-3 – producing a highly inflammatory state in the body. (Kratka, 2011) “Grains are almost single-handedly responsible for the removal of omega-3 fatty acids in the modern diet…. There have been over 2000 studies done on omega-3 and for good reason: the omega-3s in our diet (or the lack their of) have massive implications on our health. It all boils down to ratios: the ratio of omega-3 to omega-6 fatty acids in your diet is so crucial, it goes down to the cellular level.” (Kratka, 2011) Better alternatives to grains are non-GMO almond meal, coconut flour, buckwheat groats, and sweet potatoes. They are much gentler on your blood sugar than grains. Mercola points out that even these healthier alternatives will hamper your body’s ability to heal if you’re already insulin resistant. “Once the clinical signs of insulin resistance have resolved, you can relax your carb restriction.” In addition to the Omega-3s in my diet, I take Standard Process Tuna Omega-3 Oil (1 2X/day). FOCUS ON HEALTHY FATS
Eat fewer saturated and trans fats (unhealthy) and more mono and poly unsaturated fats (healthy). Examples of healthy fats include avocado, butter made from raw grass-fed organic milk, cheese, raw dairy, organic pastured eggs, raw nuts, grass-fed meats, and coconut oil.
Due to the high percentage of nutrient-poor foods, refined carbohydrates, bad fats, and refined sugars in the Standard American Diet (SAD), along with consumption of multiple OTC and prescription pharmaceuticals, we are far from getting the optimal ratio of 1:1 for Omega-6s (inflammatory) and Omega-3s (anti-inflammatory). The ratio in our modern Western diet is often as high as 20:1, creating excessive, chronic inflammation in the body – and chronic inflammation is a precursor to many diseases.
GET ENOUGH VITAMIN D3 Having a sufficient blood level of Vitamin D is essential for maintaining good health and preventing a wide range of autoimmune and neurological diseases: Type 1 and 2 diabetes, asthma, allergies, cancer, Alzheimer’s, MS, susceptibility to infection (including viral respiratory infections) among them.
Vitamin D3 is vitally important for healthy immune functioning – and most of us are seriously D3 deficient. Unless we work mostly naked outdoors in a sunny climate without slathering our skin with sunscreen, we can benefit greatly from adding a high quality D3 supplement to our daily diets. Some good sources of Vitamin D3 are: Exposure of the skin to sunshine (without sunscreen), salmon, tuna, mackerel, sardines, cod liver oil, egg yolks, cheeses, butter, shiitake and button mushrooms, sunflower seeds and sprouts, and high quality supplements.
Guidelines for the Recommended Daily Allowance (RDA) of vitamin D were updated by the Institute of Medicine (IOM) in 2010 and are currently set by age: For those 1-70 years of age, 600 IU daily; for those 71 years and older, 800 IU daily; and for pregnant and lactating women, 600 IU daily. This is thought by many as far too low. Due to a mathematical error, the IOM’s widely cited RDA’s for Vitamin D underestimate the body’s need for it by a factor of 10. The IOM recommends a Vitamin D serum level of 20 ng/ml but we should actually aim for a blood level of 40 ng/ml, supplementing with whatever amount is necessary to reach and maintain that level. (Mercola, 5/10/2015) See The Real RDA for Vitamin D Is 10 Times Higher Than Currently Recommended for information on how the RDA for Vitamin D should be correctly calculated and how to get an adequate amount of it.