There are more than 100 trillion microbes that are part of the ecology of the human body, and most have remained largely unstudied. It is now known that changes to the ecology of body organs, in particular the gastrointestinal tract, contribute to a variety of diseases, including autoimmune disorders and obesity.
In 2012 the Human Microbiome Project was established to detail the diversity of microbial communities in the human body. Most microbes live in the gut and perform vital functions for health and survival—digesting food, producing anti-inflammatory chemicals, and modulating the immune system’s responses to toxic chemicals and other microbes that enter the gut via the foods we eat. The gut ecosystem is unique to each individual and is constantly changing due to the health of our immune system, the types of microbes present, the toxic chemicals entering the gut through our foods, our genetic makeup, our digestive enzymes, the amount of exercise we do, our sleep patterns and the emotional tension we hold.
Scientists are now realising that our bodies are composed of complex ecosystems colonized by numerous collaborating and/or competing types of microbes. Maintaining health is really about maintaining the stability of the ecology within the different ecosystems of our bodies.
One of the questions central to microbiome research has focused on the reasons why people in modern society, who are relatively free of infectious diseases, are so prone to inflammatory, autoimmune and allergic diseases that have their origins in the gut. Scientists are now beginning to understand that the immune system is the ‘farmer’ of the gastrointestinal tract and when it loses its efficiency, the ecology of the microbial communities in the gut is likely to breakdown.
The huge microbial variation from person to person, has forced scientists to redefine how the immune system interacts with the gut ecosystems. Up until a few years ago, scientists were suggesting that there was a ‘standard’ array of human-adapted microbes in the gut that promoted long-term health. But now they suggest that long-term health is predominantly governed by the interactions between the immune system, the microbes that live in the gut, and the constantly changing chemical environments of the gut due to the foods we eat.
Dr Harry Sokol, a gastroenterologist at Saint Antoine Hospital in Paris, found a link between changes in bowel flora and Crohn’s disease, a chronic inflammatory disorder of the gut. Most inflammatory bowel diseases are linked to disruption by particular plant defence chemicals on the gut ecosystem when changes to immune system communication reduce the ability to farm the ecosystem of the gut. When Dr Sokol did a comparative DNA analysis of diseased sections of intestine surgically removed from patients compared to healthy patients, he noted that the population of one common type of clostridial bacterium was significantly depleted. Rather than ‘bad’ microbes prompting disease, he considered that poor farming by the immune system caused the loss of particular types of microbes, which then reduced the ability of the immune system to modulate its response to particular food chemicals coming into the gut. This was the cause of localised inflammation. When Dr Sokol transferred the types of bacteria that had been reduced/lost, back into the gut of mice, he found their presence, in general, reduced intestinal inflammation. Mixing these types of bacteria with human immune cells in a test tube also reduced inflammation. It appears that certain bacteria are necessary to assist modulation of the immune system.
Dr Kenya Honda, a microbiologist at Keio University in Tokyo, also uncovered a connection between the presence of clostridial microbes and reduced immune inflammatory responses in the gut. To study the effects of gut microbes on animal health, scientists decades ago developed the germ-free mouse—an animal without any gut microbes. These rodents, delivered by caesarean section and raised in sterile plastic bubbles, can exist only in laboratories. Dr Honda noted they had a general lack of the types of immune T-cells that regulate the intensity of inflammatory responses, and without these, inflammatory diseases such as colitis could be easily induced through diet changes. By inserting human-adapted clostridial strains of bacteria, obtained from a healthy lab member, into the gut of mice with induced colitis, he found he could boost the presence of regulatory T-cells and stop the colitis.
There appears to be three ways to stop inflammatory diseases. One is to restore the immune system to normal health. A second is to manipulate the presence of clostridial bacteria in the gut. And a third is to remove the particular foods with toxins which disrupt the ecology of the gut and reduce these types of bacteria.
When we use antibiotics we broadly alter the gut flora by destroying countless numbers of gut bacteria. A number of studies have now found a small but significant correlation between the early-life use of antibiotics and the later development of inflammatory disorders, including asthma, inflammatory bowel disease, childhood obesity, and more recently, colorectal cancer. One explanation for this association might be that sickly people (with damaged or inefficient immune systems) take more antibiotics. Antibiotics are not the cause, in other words, but the result of a pre-existing immune inefficiency.
Dr Honda’s studies suggest that antibiotics may deplete the very bacteria that modulate the immune system, and this leaves it prone to overreacting to the presence of specific food chemicals. Dr Brett Finlay, a microbiologist at the University of British Columbia, has explored this possibility. His studies have demonstrated that early-life vancomycin treatment of mice increases the animals’ risk of developing asthma later in life. He also found that the depletion of clostridial bacteria resulted in a depletion of T-suppressor cells, which then resulted in gut inflammation to food toxins and this is somehow linked to asthma.
Dr Cathryn Nagler, an immunologist at the University of Chicago, destroyed clostridial bacteria in the gut of laboratory mice, using antibiotics and then fed the animals peanut butter. Without those particular microbes and the depletion of T-suppressor cells, the peanut butter caused a rodent version of a food allergy. She was able to prevent the allergy by reintroducing types of clostridial bacteria.
A number of studies over the years have also linked living in moderately less sanitary environments during childhood with a lower risk of inflammatory bowel disease in adulthood. For example, a 2014 study from Aarhus University in Denmark found that among northern Europeans growing up on farms and interacting with livestock, the risk of contracting inflammatory bowel disease later in life halved. Thus exposure to nature as children appears to influence both the immune system and the ecology of the gastrointestinal tract, despite the array of genes we carry.
Does transplanting types of bacteria in the gut through probiotics or through physical insertion into the bowel, benefit the recipient? That viability has been scientifically tested. For example, several years ago Dr Max Nieuwdorp, a gastroenterologist at the Academic Medical Centre in Amsterdam, transplanted microbes from lean donors to patients recently diagnosed with metabolic syndrome, a cluster of symptoms that often predicts Type-2 diabetes. The recipients recorded improvements in insulin sensitivity with the enrichment of their microbiota, including clostridial species. Six months after the transplant however, all the patients had relapsed, metabolic improvements had faded and their microbes had reverted to their original states.
Modifying the ‘diseased’ ecosystem by installing a population of specific microbes will not necessarily overcome a health problem. A damaged immune system simply farms the new community in the image of the old food chemical environment. This helps explain why faecal transplants, which are able to stop bacteria-induced diarrhoea, have so far failed to treat inflammatory bowel disease. The bacteria-induced diarrhoea is caused by a single opportunist, while the latter is driven by a poorly farmed gut ecosystem and eating the ‘wrong’ foods for the individual.
Thus for long-term health with longevity, rather than transplanting bacteria populations which will have difficulty surviving in the long-term, an individual with gut inflammation should either change their diet as they age (to maintain the dominance of certain desirable microbes in the gut environments) or they should improve the efficiency of their immune system so that it can ‘farm’ for optimal gut environments, or undertake a combination of both.
Bill Giles holds workshops on immune ecology and behaviour which can give you tools to achieve optimal health as you age.