Supplements & functional ingredients
into another individual – is an effective treatment for clostridium difficile infection (CDI). It has an efficacy rate of nearly 90% for multiple recurrent CDI. “That is something that we do have a causal relationship for,” Sanders says. “But beyond that, we don’t know.”
Research suggests the gut microbiome can play an important role in our mental health.
obesity and inflammatory bowel disease. What’s often under-reported is the fact that researchers were not able to establish any causal link between the make-up of the gut microbiome and any of these conditions.
As Dr Mary Ellen Sanders, a consultant with three decades of experience in the probiotic field, explains: “The hope was that if we could identify this ideal healthy microbiota, then we could shift people with aberrant microbiota patterns to be healthier. But the excitement about the science got ahead of what the conclusions from it could legitimately be.
“With the gut-brain targets, there’s a clear mechanism and a clear reason to expect that you could manipulate the microbiota and that it would have an effect on the brain, but we simply don’t have rigorous end points in humans yet.”
We don’t know whether those differences in microbiota compositions are caused by the disease or condition or whether changing those microbial patterns will have any effect on it.”
For this reason, she believes that any discussion about the microbiome needs to be approached with some level of understanding of what the limits of the current research are, recognising what we know and what we don’t.
Research challenges
There is one thing we do know at present. A faecal microbial transplant, also known as a stool transplant – whereby faecal bacteria and other microbes from a healthy individual are transferred
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One field of research Sanders finds exciting is the growing body of evidence that the gut microbiome is an important factor in a number of mental health conditions, such as depression and anxiety. In layman’s terms this revelatory yet infantile field is centred around the gut-brain connection. In short, neural pathways in the brain affect the stomach and intestines, and vice versa, which is why people feel nauseous or get “butterflies” when they’re anxious. Research on the enteric nervous system (ENS), essentially two layers of more than 100 million nerve cells lining the gastrointestinal tract, is beginning to show that the ENS can communicate with the brain in complex ways. As a result, studies have suggested that ingesting probiotics – which comprise live microorganisms promoted with claims that they can provide health benefits – can reduce symptoms.
For example, in a 2021 meta-analysis of seven trials, Viktoriya Nikolova, a PhD student and researcher at King’s College London, and colleagues, found that probiotics can significantly reduce depressive symptoms after just eight weeks. The caveat was that the probiotics only worked when combined with an approved antidepressant. A few years earlier in 2018, another meta-analysis also showed that probiotics, when compared with placebo, improve the mood of people with depressive symptoms, without the need for antidepressants. On the anxiety front, there is compelling evidence from animal studies to show that ingesting probiotics can relieve anxiety, although human studies are less convincing. It’s a similar story with schizophrenia. But as Sanders stresses, the difference between an animal model and a human model is huge. “With the gut-brain targets, there’s a clear mechanism and a clear reason to expect that you could manipulate the microbiota and that it would have an effect on the brain, but we simply don’t have rigorous end points [an event or outcome that can be measured objectively to determine whether the intervention is beneficial] in humans yet,” she says. We’re at a similar point in the area of metabolic health. “We want to know whether or not we can administer a probiotic to help control different expressions of metabolic disease such as obesity, high blood pressure, high cholesterol or blood lipids,” Sanders explains. “There are strong mechanistic expectations, but finding the right strain, the right dose, the right subpopulation, where it’s going to be
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