The ancient physicians and philosophers were fond of saying “You are what you eat” or there were the prophetic words of Hippocrates “Let food be thy medicine”. These statements were held to be fundamental truths. Even though they had little idea about gut microbiota, they did appreciate that the gut was the foundation of overall health.
Every individual gut holds a startling secret, namely the macrocosm holds the microcosm. Both the large and small intestines contain the most complex and concentrated ecosystem found anywhere on the planet. There are estimated to be trillions of little microbes that easily outnumber normal host cells by a factor of ten, housed in the most crowded conditions possible, and which are constantly evolving and surviving the most inhospitable environmental conditions known. These bugs may seem to be free-loaders, content on living off the host (us) in a parasitic relationship, but this is far from the truth. These microscopic organisms perform a myriad of functions that our cells cannot perform, such as breaking down indigestible foods, detoxifying carcinogens, synthesizing important vitamins and other co-factors and supporting our immune system among other things.
Approximately two decades ago, researchers began to appreciate the importance of the interaction between the microbiota, the sum total of all the microbes in our digestive tract, and the nutrients or foods we consume. They quickly realised that it was a two way-street; not only does the food impact the microbes, but equally the microbes impact the food as well. A major breakthrough occurred in 2004 when Jeffery Gordon and colleagues at Washington University School of Medicine reported that there was a link between obesity and gut microbiota.See recent Advances magazine article on Gut Health. They showed that the microbial population was different in fat and thin mice, the implications were huge. Were the different microbial populations causing some animals to be obese and others to be lean? More importantly, what would happen if the bacteria from obese mice were transferred to thin mice and vice-versa?
Gordon’s group wrote a second research paper explaining that when the bacteria were transferred from obese mice to thin mice, these mice also became fat! Other researchers, namely Professor Cani in Belgium, discussed in a series of papers that when animals were fed high fat diets, there were corresponding changes in their gut microflora. Bad bacteria increased, which then caused the intestinal barrier to become more “leaky” and thus spewing out some of the toxins from the “bad” bacteria into the general circulation. This caused inflammation, which in turn caused a host of complications such as metabolic syndrome; this syndrome consists of a cluster of diseases including high blood pressure, cholesterol deposits, obesity and diabetes.
The effects of the microbial influence on weight have also been proven in humans. Professor Liping Zhao from Shanghai’s Jiao Tong University was having a weight problem; his waistline was getting bigger and bigger by the year. After reading Gordon’s papers, he took up the research and decided to change his diet by replacing fatty foods with traditional Chinese foods such as bitter melon and other fermented foods to influence his gut microbiota in a favourable way. To his surprise, he found he dramatically lost weight and, being a microbiologist, he found his gut microbiota also changed for the better. The composition of his microbiota was different when he had lost weight compared to when he was obese. This aroused his curiosity and compelled him to check which microbes were responsible for the weight loss effect.
The first paper published in 2012 showed that when experimental rat diets were changed from normal chow to one containing a high fat diet, there was a change in about eighty microbes. When the diet was changed back to normal chow, these microbes then greatly reduced in number. This was the first discovery indicating if one changes their diet the bacteria can also be changed. Zhao next wanted to replicate the effects he found on himself to larger group in patients. His study on ninety patients for 90 days confirmed what he had found on himself. Changing to a favourable diet increased the beneficial bacteria.
But Zhao wanted to narrow down the list of eighty “bad” bacteria to a smaller number. A more recent paper published this year showed even more interesting results. Zhao was able to isolate single “bad” bacteria from a highly obese patient (weight 385 lb.) with severe high blood pressure, diabetes and high cholesterol. When this bacterium was eliminated by the same diet used by Zhao on himself, the person lost over 113 pounds in twenty three weeks and had their metabolic system completely restored to normalcy!
Zhao went even further; he then gave the “bad” bacteria from the obese patient to rodents and found that these mice quickly became obese as well. They also had all the accompanying metabolic syndrome symptoms of high blood pressure, diabetes, cholesterol etc.
In part 2 we continue Zhao’s research and how he was able to reverse the microbiota to a more favourable composition using a well known herb.
Fei, N and Zhao L “An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice” ISME, 2013;7:880-884
Cani, D et-al “Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat –induced obesity and diabetes in mice” Diabetes, 2008; 57: 1470-1481
Backhed F et-al “The gut microbiota as an environmental factor that regulates fat storage” Proc Natl Acad Sci Usa, 2004; 101:15718-15723
Backhed F et-al “Mechanisms underlying the resistance to diet induced obesity and insulin resistance in germ-free mice” Proc Natl Acad Sci USA, 2007; 104: 979-984
Zhang C et-al ‘Structural resilience of the gut microbiota in adult mice under high-fat dietary perturbations” ISME, 2012; 6: 1848-1857
Zhang, C et-al “ Interactions between gut microbiota, host genetics and diet relevant to development of metabolic syndrome” ISME, 2010; 4: 232-241