Estimating the number of microbial guests in our gut is challenging; to date, the best guess is that our intestines are host anything up to 40 trillion bacteria, viruses and fungus.
Collectively, these are called the microbiota. To put this in perspective, our bodies consist of roughly 30 trillion cells. So, in a very real sense, we are more bacteria than human and we carry more bacterial DNA than human. Most of our gut bacteria belong to 30 or 40 species, but there can be up to 1,000 different species in there. Bacteria benefit from the warmth and nutrition in our bowels, but they also give back. Recent research infers that loss of regulation of gut bacteria might be an important factor in inflammatory and autoimmune conditions.
The latest and perhaps most remarkable finding is the ability that gut bacteria have to moderate our brain and behaviour. To illustrate this amazing new discovery, let’s take a look at altered behaviour observed and proven in certain animals:
The parasite that causes malaria makes mosquitoes that carry it more attracted to human body odour, and not only that: humans carrying the parasites´ gametocytes (the stage transmissible to mosquitoes) attract about twice as many mosquitoes as non-carriers, so they can find new mosquitoes to use as carriers or vectors to infect new human hosts. These are transient changes in behaviour, meaning that the mosquitoes’ behaviour only changes while carrying the parasite. However, what if there were infections that permanently changed the host’s behaviour? Well, there is at least one that we know of: Toxoplasma gondii, a parasite that infects up to one-third of people around the world, may have the ability to permanently alter a specific brain function in mice, making them losing fear of cats even when the infection has been cleared and parasites are no longer detectable. This is thought to be an evolutionary adaptation to help the parasite complete its life cycle: Toxoplasma can reproduce only in the cat´s gut, and for it to get there, the pathogen’s rodent host must be eaten. The behavioural changes are not limited to mice: in humans, studies have linked Toxoplasma infection with behavioural changes and schizophrenia. People with schizophrenia are more likely than the general population to have been infected with Toxoplasma, and medications used to treat schizophrenia may work in part by inhibiting the pathogen’s replication. However, this association is not completely clear, and there are suggestions that people with schizophrenia might be more prone to pick up the parasite, and not the other way around. More studies are needed to clarify this.
The relationship between intestinal bacterial flora (IBF) and chronic illnesses was suggested by Dr Edward Bach before he developed his Bach Flowers system, about 90 years ago, while he was working as a microbiologist.
Recent studies show that the IBF interacts with the host, whether humans or other animals, through a variety of mechanisms, most importantly through association with the mucosal immune system (the lymph nodes or glands located in the gut lining) and through release of physiologically active substances, such as hormones or neurotransmitters. When imbalance of the IBF occurs, certain disease states arise. This imbalance is referred to as dysbiosis, and has been associated with gastrointestinal disorders including C. difficile infection, irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD) and slow transit constipation (STC). In addition, alteration in the intestinal bacterial flora has been associated with non-gastrointestinal disorders including obesity and metabolic syndrome, neuropsychiatric disorders (mental illness), multiple sclerosis, atherosclerotic cardiovascular disease, autism, fibromyalgia, chronic fatigue syndrome, and idiopathic thrombocytopenic purpura. Significant changes in the composition of intestinal bacterial flora have also been observed in patients with rheumatoid arthritis, psoriatic arthritis, or spondyloarthritis, according to recent research. Indeed, understanding the influence of the IBF on host health has been described as one of the most exciting areas in medicine.
An article published in Scientific American Magazine in 2010 describes a second brain rooted in the abdomen.
The pathways that allow communication between the brain and the gut are physical and chemical, and it is referred to as the gut-brain axis. Although, at first glance, the connections between the gut and brain might seem surprising, we have all experienced it in action. The relationship between stress, anxiety, and a swift bowel movement are no stranger to anyone. This brain in our innards, although it is not the seat of any conscious thoughts or decision-making, in connection with the big one in our skulls, partly determines our mental state and plays key roles in certain diseases, as previously discussed, throughout the body.
According to this article, a significant amount of our emotions are probably influenced by the nerves in our gut. Irritable bowel syndrome could perhaps be regarded as a “mental illness” of the second brain, the one located in the gut. Evidence supports that the microbiota is significantly altered in patients with IBS when compared with normal patients. Microbial diversity is decreased in IBS, with diminished amounts of Lactobacilli and Bifidobacteria, while aerobes (bacteria that thrive when oxygen is present) and mucosal bacteria are more abundant than in the normal gut. Studies have also shown specific alterations of the IBF in patients with constipation-predominant IBS and Slow Transit Constipation. In the gut of patients with constipation-predominant IBS, sulphate producing bacteria are increased, and lactate producing bacteria are decreased. Interestingly, IBS may develop following infection or treatment with broad spectrum antibiotics, supporting the assertion that altered IBF may impact the development of the disorder. One solution could be fecal microbiota transplant (FMT). FMT, also known as a stool transplant, is the process of transplantation of fecal bacteria from a healthy individual into a recipient. The evidence for microbial manipulation and FMT for IBS and STC is promising and there are multiple studies underway, including randomized controlled trials, evaluating its efficacy.
What about if human cognitive development was also influenced or even regulated by the composition of the Intestinal Bacterial Flora?
At birth the human brain is highly under-developed and the gut is generally regarded as entirely sterile. However, it is worth noting that there is an increasing body of evidence challenging the sterile-womb paradigm and that transmission of certain microbes already occurs in the uterus. Nonetheless, passage through the birth canal exposes the baby to the mother’s microbiota. Initial colonization is dictated by the mother’s microbes and the hospital environment. This colonization plays a fundamental role in brain development in the early post-natal weeks. The subsequent microbial composition of the neonatal gut is influenced by a number of factors including antibiotic use, diet, mode of delivery, environmental factors, and the maternal microbiota. Vaginally delivered infants are colonized by the faecal and vaginal bacteria of the mother, whereas infants delivered by caesarean section (CS) are colonized by other bacteria from environmental sources including health-care workers, air, medical equipment and other newborns. Please note that full-term, vaginally delivered, breastfed, non-antibiotic treated infants are optimal for the development of “healthy” neonatal microbiota.
Post-natal gut microbial colonization occurs in parallel with cognitive development. There is increasing evidence to support the view that the evolving cognitive activity is critically dependent on the microbiota and its metabolic activity. There are even studies in the elderly whose results tempt to speculate that a changing microbiota in the elderly also acts as a modulator of inflammatory processes in the brain, which underlie many age-associated neurological diseases, including dementia and especially Alzheimer’s disease. Resilience to environmental stress also seems to be heavily influenced by the composition of the intestinal microbial composition.
An article published in 2008 concludes that early childhood use of antibiotics is associated with an increased risk of developing asthma and allergic disorders in children who are predisposed to allergic immune responses, for example, children whose parents suffer with allergic disorders such as asthma or hay fever. These findings support recent immunological understanding of the maturation of the immune system. Whether it is due to alteration of the microbiota by the use of antibiotics remains unclear, but it can be postulated as a cause.
In conclusion, having presented the importance of gut microorganisms in cognitive development from the moment of birth, and the role they may play in the development of chronic and autoimmune illness, it follows that indiscriminate treatment with antibiotics might cause the changes in this microbiota needed to trigger the start of the illness. Soon, antibiotics won’t be seen as harmless treatments that can be used just in case, or without a definitive diagnosis that justifies its use. Soon, I hope, antibiotics will be considered critical drugs that can do more harm than good when used inappropriately, and will be only used after a careful risk assessment. What’s more, I hope than even sooner, we start looking at the microorganisms in our guts like part of us, and our willingness to have antibiotics is replaced by the consideration that it might be killing the bacteria that is keeping us sane and healthy.
To find out how you can achieve optimal gut health through balanced nutrition, fasting and mental wellness, please visit my webpage for more information, getting in touch, or to make an appointment. Until then, stay well.