This past week the national media attempted to cover the breaking news story that obesity was linked to the wrong type of bacteria in your stomach. The inability of each station’s supposed health expert to properly explain what the study meant is a testament to the poor training physicians have in actually understanding how the human body functions. As soon as a story isn’t involved with a surgery, diagnostic procedure, or drug to be given they are at a loss.
The widely reported story was based on animal research performed at Emory University School of Medicine. Lead author, Matam Vijay-Kumar, PhD, has been studying a mouse engineered to lack an important gene signal that helps to recognize bacteria propelling themselves around, Toll-like receptor 5 (TLR5). This one change causes the mouse to have an excessive appetite (eating 10% more than normal), develop insulin resistance, have high blood pressure, have elevated levels of cholesterol and triglycerides, develop fatty liver disease, and become 20% heavier than normal mice. In short, the mouse develops the condition known as metabolic syndrome that is an epidemic in America. The mouse also tends to develop ulcerative colitis and Crohn’s disease.
The researchers determined that it is the flora content, or microbiota of the intestinal tract that is the source of the problem. Because the mouse lacks TLR5 the wrong type of bacteria overgrow in the stomach. Interestingly, when the researchers transferred the overgrown bacteria to normal mice they also developed metabolic syndrome abnormalities. This overgrowth of bacteria fueled obesity and it was found that the bacteria actually made the mice have inappropriate food cravings. If food was restricted the mice did not get fat but insulin resistance persisted, which of course leads to type II diabetes.
While there are over a thousand different kinds of bacteria that naturally live within your digestive tract, there are two main classes: Firmicutes and Bacteroidetes. TLR5 mice have abnormal Firmicute populations causing the problem.
“It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods,” says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. “However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism.”
Earlier Research on Firmicutes and Bacteroidetes
The famous mouse that makes no leptin, the ob/ob mouse, eats endlessly and becomes extremely obese. This mouse has a 50% reduction in Bacteroidetes and a proportional increase in Firmicutes. This means that the condition of obesity itself is causing there to be excess numbers of Firmicutes.
Through a variety of experiments with genetically altered mice scientists now believe that excessive populations of the wrong type of Firmicutes activate enzymes that promote the storage of fat in fat cells (adipocytes). This means that what is going on in your gut can have a direct impact on where calories go in your body.
Firmicutes are gram positive bacteria, many of which are friendly and essential to human digestion, such as Lactobacillus. On the other side of the Firmicute coin are Streptococcus, responsible for many infections. Other potential problematic forms of Firmicutes include strains of Clostridium and H. pyloria. H. pyloria is a normal inhabitant in your stomach. When it overgrows it causes ulcers. As an undesirable level of a Firmicute it may also help cause obesity and heart disease. I mention it in particular as it is a common human health problem.
What Does All This Mean to Your Health?
The short answer is plenty. A bit more explaining is required.
Also this past week Chinese researchers released a report on 3.3 million microbial genes obtained from the fecal samples of 124 individuals from Denmark and Spain. The gene set is 150 times larger than the entire human genome. Over 99% of the genes are bacterial, indicating between 1,000 and 1,150 prevalent bacterial species. Each individual has at least 160 species, which are also largely shared. This is the first catalog of organisms found in the human digestive tract.
In this preliminary work the researchers identified gene signals associated with obesity and Crohn’s disease. “Apart from helping you digest, these bacteria may also play a very important role in … diseases like Crohn’s disease, cancer, obesity,” said lead author Jun Wang, executive director of the Beijing Genomics Institute.
Wang and colleagues in China are working on a similar 120-sample study in Chinese hospitals. “There are four groups: obese diabetics, obese non-diabetics, lean diabetics and lean non-diabetics. And we found some interesting bugs related to each type of diabetes,” Wang said.
In other words, gene signals arising from populations of gut bacteria have a direct interaction with human metabolism – a dramatic finding.
Another angle to this problem is that bacteria produce endotoxin from the shedding of their cell wall called lipopolysaccharide (LPS). LPS is commonly studied compound as it reliably induces inflammation. Researchers have found that gut-derived bacterial LPS enters the bloodstream and directly triggers insulin resistance, especially liver-related insulin resistance that is typically accompanies type II diabetes. Furthermore, a chronic high-fat diet for four weeks raises LPS two-three times normal levels. It is also documented in obese women that LPS activates inflammation that sets the stage for metabolic disease.
Of great importance is the fact that LPS is another factor that inhibits leptin from entering your brain correctly. LPS has been shown to cause a rise in blood levels of leptin, meaning that it directly induces leptin resistance. It also raises blood levels of triglycerides, which are the main known cause of leptin resistance at the blood-brain barrier.
It has been demonstrated in overweight and obese children that a lack of friendly flora and an excess number of the Firmicute Staphylococcus aureus are common findings.
Overweight women are known to have imbalanced microbiota with excess numbers of Firmicutes in the Clostridium and Staphylococcus families. This problem is aggravated during pregnancy when the mother’s immune system is down-regulated so as not to reject the fetus, leading to excessive weight gain during pregnancy. Furthermore, the mother’s microbiota pattern is typically passed to the child. Interestingly, women given friendly flora probiotic supplements in the first trimester of pregnancy had less abdominal fat 1 year after pregnancy.
Another study shows that friendly flora can directly communicate to the Firmicute H. pyloi and stop it from producing the toxic LPS that interferes with human metabolism.
Collectively, all of these studies show a clear path from the overgrowth of the wrong digestive bacteria to the creation of leptin-resistant and insulin-resistant obesity which eventually leads to higher risk for type II diabetes and heart disease.
While killing Firmicutes with antibiotics does lessen the metabolic problems of TLR5-lacking mice, that remedy in humans would be of no value as it would encourage regrowth of equally bad if not worse Firmicutes, encourage the overgrowth of another anti-metabolic population – Candida albicans, and make the societal problem of antibiotic resistance and new superbugs even worse than it already is.
Rather, it appears that natural remedies are the front line of defense against this problem. This begins with diets that do not promote imbalanced digestion; i.e., diets too high in fat, refined sugar, alcohol, and junk food. Encouraging the growth of friendly flora with probiotic supplements (acidophilus) and prebiotic supplements (various types of fiber) is another very workable solution.
There are also many natural compounds known to kill inappropriate gram positive bacteria in the digestive tract. Oregano oil, medium chain fatty acids, bovine colostrum, and bovine lactoferrin are but a few examples of nature’s toolbox. These all have significant advantages over antibiotics as they do not breed germ resistance or disturb the good flora. While helping to reduce the surplus population of unwanted bacteria they also reduce any surplus population of Candida albicans – unlike antibiotic drugs that encourage Candida albicans overgrowth.
It has always been important to your health to correct any type of digestive problem – actually solving it and not just covering it over with antacids that further induce the spreading of undesirable bacteria in your stomach by reducing your front line of defense (stomach acid). Now we see that improving your digestive tract can also have a significant impact on your metabolism, weight management, and cardiovascular health.
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