Multiple sclerosis (MS) is a chronic condition affecting the central nervous system.
Symptoms, including muscle weakness and vision problems, occur when the immune system attacks the outer coating of nerve cells.
Scientists do not know the exact cause of MS but suspect that multiple factors contribute to its occurrence.
Now, a study has found that a toxin from a common gut bacterium may trigger MS in people with a genetic susceptibility.
Multiple sclerosis (MS) is a chronic condition of the nervous system. It most commonly affects young adults between the ages of 20 and 40 and is more often seen in women than men.
In this autoimmune disorder, a person’s immune system attacks the myelin sheathTrusted Source covering the nerve fibers. The damage leaves a scar or lesion, called ‘sclerosis’. These lesions occur most commonly in the central nervous system and lead to a range of symptoms, which may include:
The most common form of MS, relapsing-remitting MS, which causes 85% of cases, is characterized by episodes of new or increasing symptoms, and periods, where symptoms lessen or, disappear.
The exact cause is still unknown, but scientists believe that genetic susceptibility and environmental factors may contribute to the onset of the condition.
“There are many mysteries to MS. Why do some people get MS and others don’t, despite similar or identical genetics? What accounts for the episodic nature of relapses and remissions? How is the central nervous system targeted and why myelin specifically?,” co-senior author Dr. Timothy Vartanian, a professor of neuroscience in the Feil Family Brain and Mind Research Institute at Weill Cornell Medicine, said.
Now, research led by scientists from the Brain and Mind Research Institute at Weill Cornell Medicine has found that epsilon toxin — produced by a bacterium found in the small intestine — may trigger the onset of MS and cause continuing symptoms.
“The development of MS is thought to be due to a combination of genetic and environmental factors. This very elegant study implicates a specific bacterial toxin as an environmental etiologic agent in MS.”
— Dr. Barbara Giesser, neurologist and MS specialist at Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, California, speaking to Medical News Today
The gut microbiota is made up of trillions of microbes that live in your digestive system. Most of the microbes are bacteria, but there are also viruses, fungi, and tiny, single-celled animals called protozoaTrusted Source.
These microbes are generally useful, and indeed vital, to our health. However, problems can occur if the microbiota gets out of balance — known as dysbiosisTrusted Source. StudiesTrusted Source have indicated that changes in the microbiota may contribute to some autoimmune disorders.
“The researchers used novel and sensitive techniques to identify the presence of the bacterium, and then investigated how the toxin produced an MS-like disease in a mouse model.”
— Dr. Barbara Giesser
The researchers took fecal samples from people with MS and healthy controls. They analyzed these samples using polymerase chain reaction (PCR)Trusted Source to detect the gene for producing epsilon toxin (ETX), which is found only in C. perfringens.
They found that 61% of the samples from people with MS contained the ETX gene, compared with only 13% of those from healthy controls. Further to this, they found that the gut microbiota of people with MS was more likely to be colonized by ETX positive C. perfringens than that of age and sex-matched healthy controls.
They next tested the effect of ETX in miceTrusted Source known to be susceptible to developing MS symptoms. Some mice were injected with ETX; others were injected with a different toxin (PTX, which had previously been shown to induce MS-like symptoms).
The mice they injected with ETX developed demyelination in many areas of the CNS, in a similar pattern to that seen in people with MS.
They had twice as many lesions in the cerebellum — the part of the brain responsible for balance and coordination that is commonly affected in MSTrusted Source — as the mice that were given PTX. The ETX mice also had lesions in the white matter bundle of the corpus callosumTrusted Source, which were not seen in the other mice.
“This study builds on the present body of what is known about the gut microbiome in persons with MS. It is known to be different than those of non-MS controls, and has been shown to respond to treatment with some disease-modifying therapies.”
— Dr. Barbara Giesser
C. perfringens produces epsilon toxin only when it is in the rapid growth (exponentialTrusted Source) phase. If ETX is responsible for MS lesions, the researchers suggest, this would explain the episodic nature of the disease, with symptoms reducing when bacteria are not producing the toxin.
They conclude that they have found a strong clinical association between the bacterium, its toxin, and MS. This finding raises the possibility of treatments that target this pathway, as Dr. Giesser told MNT:
“The toxin helps immune cells gain access to the central nervous system. This suggests that treatments targeting the bacterium or the toxin might potentially be useful as disease-modifying therapies.”
However, the researchers note that clinical trials would be needed to test whether this will give rise to potential treatments for MS.
StudiesTrusted Source have suggested that the gut microbiome may be an important factor in the progression of MS. A 2017Trusted Source review of several studies found that diet could be used to modify the gut microbiota and improve the course of MS.
The benefits of maintaining a healthy gut microbiota are increasingly recognizedTrusted Source, and this study adds further evidence that an unbalanced microbiota may contribute to disease development.
As well as potentially reducing the risk of MS, a healthful diet and lifestyle that encourages the growth of beneficial gut bacteria could reduce the risk of developing many health conditions.
Bezzy MS provides meaningful peer connections, empathetic ears, and real-world ideas for living well — inspired by guides and members who truly understand what it’s like living with Multiple Sclerosis.
In a study of mice, researchers show their microbiomes play a role in how much they run and how quickly they grow fatigued
Gut bacteria, more than genetics, impact mice’s motivation to exercise, a recent study suggests.
Microorganisms in the gut, known as the gut microbiome, play an important role in human health. They stimulate the immune system and protect against pathogens. They also impact our sleep, moods and risk for certain diseases, according to the Washington Post’s Gretchen Reynolds.
Now, scientists may be able to add one more thing to that list: The gut microbiome might also affect motivation to exercise, suggests a recent study of mice published in Nature.
“The study shows pretty conclusively that in mice, the desire to exercise is influenced by the microbiome,” Anthony Komaroff, a physician at Harvard University who did not contribute to the study, tells National Geographic’s Sanjay Mishra. It “provides a mechanistic explanation as to how the microbiome could influence the appetite of the animals to exercise.”
Scientists wonder whether humans’ willingness to hit the gym is regulated in a similar way. Mouse studies alone can’t prove that your proclivity for moving or sitting is affected by your microbiome—and people might also be motivated by external factors, such as praise from others—but studying these rodents is a step toward understanding ourselves, scientists say.
This paper isn’t the first to look at exercising mice and their microorganisms. Research published last June in the journal Behavioural Processes found that mice bred specifically to be strong runners ran less when given antibiotics that destroyed their microbiomes, per the Post.
In the more recent study, scientists collected 2.1 million data points on 199 mice, ranging from the rodents’ genetic makeup and gut microbiome composition to their exercise capacity, according to New Scientist’sGrace Wade. The researchers also used antibiotics to either partially or fully remove some of the mice’s microbiomes, per the Scientist’s Katherine Irving.
“It’s an insane amount of data,” Matthew Raymond Olm, a computational microbiologist at Stanford University who did not contribute to the study, tells National Geographic.
After examining all this information, the team found that genetics played only a limited role in the mice’s inclination to exercise. But their gut microbiomes had a greater effect: The mice with diminished microbiomes spent less time exercising on a wheel and grew fatigued more quickly when running on a treadmill. To verify these findings, researcherstransplanted microbiomes from mice that were strong runners into other mice, which made them able to exercise more.
The team then looked for why such a connection between exercise and the microbiome might exist. They found that when they inhibited neurons involved in producing dopamine, a neurotransmitter that helps us feel pleasure, it similarly reduced mice’s ambition to exercise. They also tied these neurons to molecules produced by the microbiome. Blocking any part of this path from the microbiome to dopamine release led the mice to exercise less.
“Surprisingly, the motivation for exercise is not brain-intrinsic but is regulated by the gastrointestinal tract,” Christoph Thaiss, a microbiologist at the University of Pennsylvania and a co-author of the study, tells New Scientist.
“This is the most comprehensive study I have ever seen,” Theodore Garland Jr., an evolutionary physiologist at the University of California, Riverside, who did not participate in the recent research but co-authored last June’s paper, tells the Scientist. “[It’s] pulling together lots of different pieces that we knew before in different contexts or in isolation of other parts in a way that hasn’t been done before.”
Now, the researchers want to look at humans to see if the rodent research holds up in ourselves. If so, it could have implications for treating symptoms of various diseases that might be eased with exercise, reports the Scientist.
“There are many differences between mice and human physiology,” Thaiss tells National Geographic. “But we’re embarking on a human study that will answer this question.”
However, up to halfTrusted Source of patients with cancer do not respond to ICI treatments. A growing number of studiesTrusted Source show that the gut microbiome may play a role in ICI treatment efficacy.
ResearchTrusted Source shows that mice that lack gut microbiota or that are treated with antibiotics respond less to ICI. StudiesTrusted Source also suggest that replacing microbiota via fecal transplants may increase response from ICI.
It remains unclear which gut bacteria are most effective for increasing ICI response and how gut bacteria improve immune response.
Recently, researchers investigated how gut bacteria diversity influences ICI efficacy in a mouse model of melanoma.
They found that ICI treatment causes inflammation in the digestive system, allowing bacteria to leave the intestines and travel to lymph nodes near tumors, where they activate immune cells.
Dr. Anton Bilchik, surgical oncologist and division chair of general surgery at Providence Saint John’s Health Center and chief of medicine and director of the Gastrointestinal and Hepatobiliary Program at Saint John’s Cancer Institute in Santa Monica, CA, not involved in the study, told Medical News Today:
“Since there is a plethora of research studying the impact of the gut microbiome on the immune system this provides a novel explanation as to how immunotherapy may work outside of the intestinal tract. Furthermore, it shows the deleterious effect that antibiotics may have in reducing the efficacy of immunotherapy by neutralizing bacteria within the gastrointestinal tract.”
For the study, the researchers administered ICI therapy to mice with and without melanoma tumors.
They found that ICI treatment increased inflammation in the digestive tract, which allowed certain bacteria to leave the gut and travel to lymph nodes near the tumor, as well as the tumor site. There, the microbes activated a set of immune cells that killed tumor cells.
The researchers also investigated how antibiotic exposure may affect ICI efficacy. To do so, they treated mice with antibiotics, then implanted them with melanoma tumors and treated them with ICI a week later.
They found that antibiotic exposure reduced gut microbiota movement to lymph nodes, and decreased immune cell levels.
Finally, they investigated whether administering different kinds of bacteria could reverse the effect of the antibiotics on ICI efficacy. They found that treatments with Escherichia coli and Enterococcus faecalis improved ICI efficacy.
MNT spoke with Dr. Andrew Koh, associate professor at the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern, senior author of the current study, about the study’s limitations.
A major limitation, noted Dr. Koh, is that they only used one preclinical cancer model, meaning that further tests are needed to know whether the findings may apply to other cancers, too.
“We believe that our findings could apply to other cancers too, but we have not generated data to support that supposition,” he said.
“There are published dataTrusted Source that different human tumors harbor unique or distinct tumor microbiomes — and many of the predominant taxa are bacteria that typically reside in the gut. So our study may provide a mechanistic link or explanation as to how gut microbiota can travel from the gut and seed different types of human tumors,” added Dr. Koh.
Dr. Guilherme Rabinowits, a hematologist and medical oncologist at Miami Cancer Institute, part of Baptist Health South Florida, not involved in the study, also told MNT that “[i]t is very likely that the findings reported in this study apply to other cancer types, since the gut bacteria translocation is unlikely to be tumor-specific.”
“Unfortunately, without proper testing, it is impossible to say for sure,” he noted.
When asked about other limitations of the study, Dr. Bilchik added that it remains to be seen whether the findings translate to humans.
Dr. Lance Uradomo, an interventional gastroenterologist at City of Hope Orange County Lennar Foundation Cancer Center in Irvine, CA, not involved in the study, also told MNT that “the type of therapy applied for testing melanoma can be linked to adverse side effects, such as colitis.”
“Further study is needed before it is understood if microbiome therapy — and the correct application — is truly effective,” he added.
When asked about the study’s implications, Dr. Koh said that the findings beg the question of whether there may be more direct ways to deliver probiotic treatments to patients than via the intestines.
“Perhaps giving live oral precision probiotics — which are fraught with many logistical challenges, such as maintaining stable engraftment in the human gut, which can easily be derailed by exposure to antibiotics or changes in diet — is not the best way to administer gut microbiota-based therapies,” he noted.
To this end, he noted that his lab is currently developing microbiota-derived therapy that can be administered outside the gastrointestinal tract.
“We hope to submit this story by the end of this year. I have filed two patents and formed a startup company, Aumenta Biosciences, which is developing this technology. Aumenta was awarded its first NIH [National Institutes of Health] grant last year to develop this technology,” he commented.
Looking after the multitudes of bacteria, fungi and other microorganisms living in our guts could help us think better and even offer new ways of treating mental health conditions.
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Your gut is a bustling and thriving alien colony. They number in their trillions and include thousands of different species. Many of these microorganisms, including bacteria, archaea and eukarya, were here long before humans, have evolved alongside us and now outnumber our own cells many times over. Indeed, as John Cryan, a professor of anatomy and neuroscience at University College Cork, rather strikingly put it in a TEDx talk: “When you go to the bathroom and shed some of these microbes, just think: you are becoming more human.”
Collectively, these microbial legions are known as the “microbiota” – and they play a well-established role in maintaining our physical health, from digestion and metabolism to immunity. They also produce vital compounds the human body is incapable of manufacturing on its own.
But what if they also had a hotline to our minds? In our new book, Are You Thinking Clearly? 29 Reasons You Aren’t And What To Do About It, we explore the dozens of internal and external factors that affect and manipulate the way we think, from genetics, personality and bias to technology, advertising and language. And it turns out the microbes that call our bodies their home can have a surprising amount of control over our brains.
Over the last few decades, researchers have started to uncover curious, compelling – and sometimes controversial – evidence to suggest that the gut microbiota doesn’t just help to keep our brains in prime working order by helping to free up nutrients for it from our food, but may also help to shape our very thoughts and behaviour. Their findings may even potentially bolster how we understand and lead to new treatments for a range of mental health conditions, from depression and anxiety to schizophrenia.
The picture is still very far from complete, but in the wake of the Covid-19 pandemic, which has had a deleterious impact on people’s mental health in many parts of the world, unpicking this puzzle could be more important than ever.
Our guts are a menagerie of different species of bacteria, some of which appear to communicate with our brains
One of the research field’s key origin stories took place in the North American wilderness – and, be warned, it makes for some stomach-churning reading. The year was 1822 and a young trader named Alexis St Martin was loitering outside a trading post on what is now called Mackinac Island, in what is now Michigan, when a musket accidentally went off next to him, firing a shot into his side from less than a yard (91cm) away. His injuries were so bad that part of his lungs, part of his stomach and a good portion of his breakfast that day spilled out through the wound in his left side. Death seemed certain, but an army surgeon named William Beaumont rode to the rescue and saved St Martin’s life, although it took the best part of a year and multiple rounds of surgery.
What Beaumont couldn’t repair, however, was the hole in his patient’s stomach. This persistent fistula would remain a grim and lasting legacy of the accident, but Beaumont wasn’t one to pass up a good opportunity – however unpleasant. Realising that the hole provided a unique window into the human gut, he spent years investigating the intricacies of St Martin’s digestion. Exactly how willing a volunteer St Martin was is open to debate as Beaumont employed him as a servant while conducting research on him – the murky arrangement almost certainly wouldn’t be considered ethical today. Among the findings Beaumont uncovered during his studies of St Martin’s guts, however, included how they were affected by its owner’s emotions, such as anger.
Through this finding, Beaumont, who would go on to be lauded as the “father of gastric physiology“, had hit upon the idea of a “gut-brain axis” – that the gut and the brain aren’t entirely independent of one another but instead interact, with one influencing the other and vice versa. And now we know that the microorganisms within our gut make this process even more complex and remarkable.
“More and more research is revealing that the gut microbiome can influence the brain and behaviour across a variety of different animals,” says Elaine Hsiao, associate professor in integrative biology and physiology, at the University of California, Los Angeles (UCLA).
It’s important to remember that the microbes were here before humans existed, so we have evolved with these ‘friends with benefits’ – John Cryan
How exactly our microbiota might be influencing our mind is a growing, pioneering and still relatively novel field. But there have been advances over the last 20 years or so, particularly in animals. And, slowly, a case is being built to suggest that these microorganisms aren’t just a vital part of our physical selves, but also our mental and emotional selves, too.
“In medicine, we tend to compartmentalise the body,” says Cryan. “So, when we talk about issues with the brain, we tend to think about the neck upwards. But we need to frame things evolutionarily. It’s important to remember that the microbes were here before humans existed, so we have evolved with these ‘friends with benefits’. There has never been a time when the brain existed without the signals coming from the microbes.
“What if these signals are actually really important in determining how we feel, how we behave and how we act? And could we modulate these microbes therapeutically to improve thinking, behaviour and brain health?”
Hsiao is one of the researchers leading the way in this field and her lab at UCLA has explored the part these microorganisms might play in everything from foetal brain development to cognition and neurological conditions such as epilepsy and depression. She has also investigated how these microbes might be influencing our brains and thinking.
Indeed, research suggests our microbes may be communicating with our brains through numerous pathways, from immunity to biochemicals. Another candidate is the vagus nerve, which acts as the superfast “internet connection” between our brain and internal organs, including the gut. The bacteria Lactobacillus rhamnosus JB1, for example, appears to improve the mood of anxious and depressed mice. This beneficial effect is removed, however, when the signals travelling along the vagus nerve are blocked, suggesting it could be being used as a communication pathway by the bacteria.
William Beaumont’s research on the digestive juices of Alexis St Martin gave some of the first hints of the interaction between our guts and brains
Much of the research in this field is conducted in mice (and other small animals). And mice, of course, aren’t humans. But given the mindboggling complexities of establishing causality between microbial signals and changes in human thought and behaviour, animal studies have provided some intriguing insights into the strange interactions between bacteria and brain. Research, for example, shows that “germ-free” rats and mice (those without any microbiota after being reared in sterile conditions) are more prone to anxiousness, and less sociable than those with an intact microbiota. Germ-free mice, and those given antibiotics have also been found to be more hyperactive, prone to risky behaviour and less able to learn or remember. Antibiotics, which can reduce the microbiota in an animal, also reduce shoaling behaviour in zebrafish, while probiotics boost it.
Again, the human brain is vastly more complex than that of a rodent or fish, but they do share some similarities and can offer clues. It makes sense that bacteria, wherever they live, might benefit from helping their hosts to be more sociable and less anxious. By interacting with other people, for example, we help our bacteria spread. And whether or not they’re really pulling our strings, it’s in our microbes’ evolutionary interests to make their environment as conducive to survival as possible.
But do communicative microbes, congregating zebrafish or friendly mice really matter? Hopefully, yes, say the researchers. Ultimately, a better understanding of these processes could lead us towards ground-breaking new treatments for a range of mental health conditions.
Psychobiotics might one day be used to nurture populations of “good” bacteria and treat a variety of mental health conditions
“We’ve coined the term ‘psychobiotics‘ for [microbiota-based] interventions that have a beneficial effect on the human brain,” says Cryan. “And there are more and more of these psychobiotic approaches coming.”
There are caveats, of course. While some strains of bacteria appear to have a positive effect on the human mind, many others don’t and researchers have yet definitively to establish why – and how. Humans are also unfathomably complex, and when it comes to thinking and mental health, there are countless other factors at play, from genetics and personality to the environment around us.
“We need many more large-scale human studies to take into account these individual differences,” says Cryan. “And maybe not everyone will respond to a single bacteria in the same way because everyone will have a slightly different baseline microbiota anyway.”
Disclaimers aside, however, more research could bring fresh hope. “The good news is that you can change your microbiota, while there’s not a whole lot you can do to change your genetics – except blame your parents and your grandparents,” Cryan adds. “The fact that you can modify your microbiota potentially gives you agency over your own health outcomes.” Indeed, pro- and prebiotic supplements, simple dietary changes, such as eating more fermented foods and fibre – and even, perhaps, meditation – can help alter our microbiota in ways that benefit our minds.
Philip Burnet, an associate professor in the University of Oxford’s department of psychiatry, notes that many mental health conditions have been associated with changes in the microbiota. Often, this imbalance or “dysbiosis” is characterised by a reduced amount of certain bacteria, particularly those that produce short-chain fatty acids (such as butyrate, which is widely believed to improve brain function) when they break down fibre in the gut.
Indeed, a 2019 study by Mireia Valles-Colomer, a microbiologist at KU Leuven University of Leuven in Belgium at the time, and her colleagues found a correlation between the amount of these butyrate-producing bacteria and wellbeing. Specifically, the researchers noted in the study that: “Butyrate-producing Faecalibacterium and Coprococcus bacteria were consistently associated with higher quality of life indicators. Together with Dialister, Coprococcus spp. were also depleted in depression, even after correcting for the confounding effects of antidepressants.”
Antibiotics can change the shoaling behaviour of Zebrafish
Human studies on the communication between the gut, the brain and the microbiota are still relatively few and far between. And Burnet urges caution: “It is not known whether these altered levels in gut bacteria cause low mood or whether microbial numbers change because people who are depressed might modify their eating habits or eat less.”
Nevertheless, he has been exploring how prebiotics (which encourage bacteria to grow) and probiotics (live bacteria) might one day be used as psychobiotics to nurture populations of “good” bacteria – and treat a variety of mental health conditions.
For example, one 2019 study by Burnet, Rita Baião, a psychologist also at the University of Oxford, and their colleagues uncovered some particularly interesting findings. Although the study was funded by a company that manufactures probiotic bacteria, it used a randomised, double-blind, placebo-controlled trial – considered to be a gold standard study design during which neither participants nor researchers are aware whether they are receiving the treatment or not. The researchers investigated the effect a multispecies probiotic might have on emotional processing and cognition in people with mild to moderate depression. But the study also monitored their mood before and after the experiment using the Patient Health Questionnaire-9 (PHQ-9), which measures depression severity.
The participants, who weren’t taking any other medication, were either given a placebo or a commercially available probiotic – which contained 14 species of bacteria, including Bacillus subtilis, Bifidobacterium bifidum, Bifidobacterium breve and Bifidobacterium infantis for four weeks.
The results were fascinating, not least that the participants on the probiotic experienced a significant subjective improvement in mood compared with the group on placebo, essentially becoming less depressed according to the PHQ-9. Changes in the participants’ levels of anxiety, which were also measured, were not observed.
This was a small (71 participants), brief study and more research is needed to prove causality. But it’s an early indication that “psychobiotics” may one day be a helpful treatment for those with depression – particularly those who are reluctant to seek medical help or take traditional antidepressants, says Burnet. Indeed, psychobiotics won’t replace existing medications – but may eventually provide a helpful adjunct.
“They won’t make everyone happier,” says Burnet, but probiotics could one day complement more established mental health treatments. “Only time will tell whether we will have psychobiotics,” he adds. “But the field is really moving forward… This area of research is dominated by animal studies, however, so we do need more human studies using larger numbers of participants.”
But the potential of psychobiotics has captured imaginations.
Those who had used antibiotics for long periods of time scored lower on cognitive tests such as learning, working memory and attention tasks
“We also attracted a lot of interest from the public,” adds Burnet. “People are extremely interested in maintaining their health and wellbeing with natural supplements and encouraging the growth of good bacteria to support mental health has captured the imagination of the general public. Especially now, when people are more anxious and depressed as a result of the pandemic.”
With Amy Chia-Ching Kao and others, Burnet has also explored the role these microorganisms might play in psychosis – and whether prebiotics (which help to promote the growth of bacteria in the gut) might help people with the condition think more clearly.
Many people are aware that psychosis can cause hallucinations, delusions and a detachment from reality. But people with psychosis also often encounter difficulties with cognitive functions such as attention, memory and problem-solving, which can impact their ability to hold down jobs and relationships. While medication can be used to treat the hallucinations and delusions, improving sufferers’ cognitive impairments has proved more difficult.
A double-blind, placebo-controlled crossover study by Burnet and Chia-Ching Kao, however, suggests a possible way forward. “We found that giving a prebiotic to people with psychosis did improve cognitive function according to the clinical scales,” says Burnet.
At the start of the study, the participants were on medication and free of psychotic symptoms – but were still experiencing the cognitive impairment typical of psychosis. Over 12 weeks, they were given a prebiotic or a placebo while their metabolism, immunity and level of cognitive impairment was measured over time. At the end of the 12 weeks, they were then switched, so both groups had an equal amount of time on the prebiotic and the placebo.
And the effect was small but significant. The prebiotic improved overall cognitive function, particularly attention and problem solving, leading the researchers to conclude that the improvement was sufficient to boost social and mental wellbeing. There was no evidence of the participants’ immunity or metabolism changing so it wasn’t clear how the prebiotic may have triggered this effect. But it’s another small step towards understanding the relationship between our microbiota and our mental health and the potential development of new treatments for disorders that affect our thinking.
There are hints that the gut microbiota may affect cognitive skills more broadly, too. It is well known that antibiotics disrupt the gut microbiota, but do they affect our cognition? One recent study, which monitored the health and wellbeing of 14,542 female nurses for several years while they worked for the NHS in the UK, found that those who had used antibiotics for long periods of time (more than two months) scored lower on cognitive tests such as learning, working memory and attention tasks than those who hadn’t taken such medication. Importantly, the cognition of the women who had taken antibiotics was slightly poorer when they were followed up seven years later. Although this is only a correlation, the researchers think it could be due to antibiotics-induced changes in the gut.
Our gut microbes may even play a role in how sociable we are if research in rodents are to be believed – and we pick up microbes through contact with others
There’s still a very long way to go, though, to understand this properly. This is a fascinating but highly complex field, and research requires funding. The rewards, however, could be profound. “There are only a handful of specific microbes that have been studied so far,” says Hsiao. “Not necessarily because they are the most significant, but because we as scientists have much more to do to really understand the enormous diversity of microbes in the gut and how they function individually and as communities.
“I’m most excited about the opportunity to uncover new mechanistic understanding of how we and our microbial symbionts can work together to promote health and thwart disease.”
In the meantime, perhaps we should all pay a bit more attention to our microbiota. A Mediterranean diet that’s high in fibre, particularly from vegetables, is likely a good place to start. And fermented foods, such as kimchi and kefir (a fermented milk drink) may also be beneficial. In a small study with 45 participants, for example, Cryan and colleagues showed that those who were put on a diet that included a lot of fibre, prebiotics and fermented food (such as onions, yoghurt, kefir and sauerkraut), reported feeling less stressed than a control group which was on a different diet.
“What I like about fermented foods is that they democratise the science,” says Cryan. “They don’t really cost much and you don’t have to get them from some fancy store. You can do it yourself. In this field, we want to provide mental health solutions to people from all socioeconomic areas.”
The relationship we have with our microbiota is “a bit like a federation”, adds Cryan. “These microbes are our fellow travellers.” We’d do well to remember that – for the sake of both our physical and, quite possibly, mental health.
A diet that is high in either red meat or sugar, or both, increases the growth in the colon of bacteria called Fusobacterium nucleatum that appears to suppress a person’s immunity to increase the growth of cancer cells in the colon. A prospective study of 137,217 adults followed for about 30 years shows that people who ate a lot of red meat and/or sugar were more likely to develop colon cancers that contained bacterium called Fusobacterium nucleatum. People who developed colon cancer and ate a primarily plant-based diet with lots of fiber were more likely to have cancers that did not have that bacterium attached to it (JAMA Oncol, published online January 26, 2017).
Foods You Eat Determine Which Bacteria Grow in Your Gut Your diet determines which types of bacteria live in the first part (right side) of the colon. Bacteria that live in the last part (left side) of your colon receive food that has already been changed by the bacteria that live in the first part of the colon. The food that you eat must be broken down into its basic building blocks before it can be absorbed into your bloodstream. Carbohydrates must be broken down into single sugars, proteins into amino acids and fats into fatty acids. Foods that are not broken down to be absorbed in the small intestines pass along to reach your colon. There, bacteria can break down some of these foods that you could not absorb and use them to supply their energy. Bacteria that cannot break down the food that you eat will not thrive there. That means that bacteria in the right first part of your colon are the ones that grow and thrive on the non-absorbable food that you have eaten. Bacteria in the left (last) part of your colon get food that has already been changed by bacteria in the right (first) part.
The researchers examined healthy and cancerous tissue from 120 people taken during colonoscopies, where small pieces of tissue are removed to look for malignant changes in the inner linings of the colon. They found biofilms in 89 percent of tumors removed from the right colon (the first part), and in only 12 percent of tumors removed from the left side of the colon (the last part). Dense bunches of bacterial biofilms are found on most colon polyps and colon cancers. That means that in the future doctors will be able to check you for developing colon cancer long before it would normally be detected. Most colon cancers develop over five to ten years, and colon cancer is usually a curable disease if it is diagnosed early enough (CA Cancer J Clin, May-Jun 2008;58(3):130-60).
People who have dense biofilm colonies of bacteria in the right (first) part of the colon are five times more likely to have malignant colon cancer and pre-malignant colon polyps, compared to those who have no large biofilm colonies (Proceedings of the National Academy of Sciences, Dec. 16, 2014). The authors used a fluorescent technique to stain biopsy specimens for bacterium. In humans, a bacterial biofilm is a mucilaginous coating that bacteria secrete around themselves to protect them from attack by your immune system so they can live permanently inside your body. Other examples of biofilms include dental plaques in the mouth and the slime that covers stagnant pools or standing water.
How Diet May Cause Colon Cancer Since bacteria in your colon eat the same food that you eat and passes to your colon, what you eat determines which bacteria grow in your colon. Certain bacteria such as Fusobacterium are associated with increased risk for colon cancer as evidenced by studies that show that a low-plant-fiber diet and lots of red meat are associated with the type of bacteria that attach to colon cancer cells. They have also been shown to increase risk for colon cancer by interfering with a person’s immune system that is supposed to seek out and kill cancer cells. Studies show that Fusobacterium increase markedly in the stool after people switch from a high plant diet to one loaded with sugar and red meat.
Survival Rates After Colon Cancer is Diagnosed Right-sided colon cancer is far more likely to kill than left-sided colon cancer. Patients with advanced colon cancer on the right side survived an average of 19 months, compared to patients with tumors on the left side 33 months (PLoS ONE, Dec 6, 2016;11(12):e0167540). Bacteria in your right colon eat the same food that you do. Bacteria in your left colon eat a different diet: what’s left over from what the right-side bacteria ate. People with colon cancer may increase their chances for survival by following a healthful plant-based diet (BMC Cancer, Jan 30, 2017;17:83).
How Sugar May Increase Colon Cancer Risk Many studies have shown that colon cancer is more common in people who are overweight. A new study shows that normal-weight people with markers of high blood sugar called metabolic syndrome are at more than double the risk of developing colon cancer (Cancer Epidemiology, Biomarkers & Prevention, Feb 2017). Markers of metabolic syndrome include: • pinching more than two inches of fat under the skin around the navel • systolic blood pressure over 120 at bedtime • triglycerides over 150, blood sugar over 140 one hour after eating • HDL cholesterol under 40
Link Between Meat and Colon Cancer The World Health Organization (WHO) reported that eating processed meats and meat from mammals increases the risk of colorectal cancer (J Gastroenterol, Dec 2, 2016). Many other studies also show an association between meat and colon cancer (British Medical Bulletin, Dec 23, 2016; J Hum Nutr Diet, Jun 14, 2016; Br Med Bull, Dec 18, 2016). Processing meat increases the risk and some cooking methods increase risk more than others: meats cooked without browning had a lower increased risk while grilled, griddled or barbecued meats had the highest risk (European Journal of Nutrition, Nov 24, 2016). An earlier extensive review of the world’s medical literature showed that eating red meat is associated with a 28-35 percent increased risk for developing colorectal cancer, while eating processed meats is associated with increased risk of 20-49 percent (Rev Esc Enferm USP, Feb 2012;46(1):234-9).
Researchers have proposed many possible mechanisms for the association between colon cancer and eating mammal meat, but there is no agreement at this time (Mol Aspects Med, Oct 2016;51:16-30). Proposed causal factors have included: • TMAO (trimethylamine-N-oxide) • certain bacteria in the colon • high salt intake • saturated fat • environmental pollutants • polycyclic aromatic carcinogens formed from high temperature cooking methods • chemicals such as nitrates added to meats during processing • heme iron • Neu5Gc, a sugar-protein found in mammal meat • possible infectious agents (not yet identified)
The recent research on types of gut bacteria attached to colon cancers suggests that this may be the most likely explanation for the long-observed association between meat and colon cancers. We await further research.
Summary: Gut bacteria affect the behavior of immune cells throughout the body and in the brain, including ones implicated in neurodegenerative disorders such as Alzheimer’s disease. The findings open up the possibility of altering the microbiome to prevent or treat neurodegeneration.
Source: WUSTL
A growing pile of evidence indicates that the tens of trillions of microbes that normally live in our intestines — the so-called gut microbiome — have far-reaching effects on how our bodies function. Members of this microbial community produce vitamins, help us digest food, prevent the overgrowth of harmful bacteria and regulate the immune system, among other benefits.
Now, a new study suggests that the gut microbiome also plays a key role in the health of our brains, according to researchers from Washington University School of Medicine in St. Louis.
The study, in mice, found that gut bacteria — partly by producing compounds such as short chain fatty acids — affect the behavior of immune cells throughout the body, including ones in the brain that can damage brain tissue and exacerbate neurodegeneration in conditions such as Alzheimer’s disease.
The findings, published Jan. 13 in the journal Science, open up the possibility of reshaping the gut microbiome as a way to prevent or treat neurodegeneration.
“We gave young mice antibiotics for just a week, and we saw a permanent change in their gut microbiomes, their immune responses, and how much neurodegeneration related to a protein called tau they experienced with age,” said senior author David M. Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology.
“What’s exciting is that manipulating the gut microbiome could be a way to have an effect on the brain without putting anything directly into the brain.”
Evidence is accumulating that the gut microbiomes in people with Alzheimer’s disease can differ from those of healthy people. But it isn’t clear whether these differences are the cause or the result of the disease — or both — and what effect altering the microbiome might have on the course of the disease.
To determine whether the gut microbiome may be playing a causal role, the researchers altered the gut microbiomes of mice predisposed to develop Alzheimer’s-like brain damage and cognitive impairment.
The mice were genetically modified to express a mutant form of the human brain protein tau, which builds up and causes damage to neurons and atrophy of their brains by 9 months of age.
They also carried a variant of the human APOE gene, a major genetic risk factor for Alzheimer’s. People with one copy of the APOE4 variant are three to four times more likely to develop the disease than people with the more common APOE3variant.
Along with Holtzman, the research team included gut microbiome expert and co-author Jeffrey I. Gordon, MD, the Dr. Robert J. Glaser Distinguished University Professor and director of the Edison Family Center for Genome Sciences & Systems Biology; first author Dong-Oh Seo, PhD, an instructor in neurology; and co-author Sangram S. Sisodia, PhD, a professor of neurobiology at the University of Chicago.
When such genetically modified mice were raised under sterile conditions from birth, they did not acquire gut microbiomes, and their brains showed much less damage at 40 weeks of age than the brains of mice harboring normal mouse microbiomes.
When such mice were raised under normal, nonsterile conditions, they developed normal microbiomes. A course of antibiotics at 2 weeks of age, however, permanently changed the composition of bacteria in their microbiomes. For male mice, it also reduced the amount of brain damage evident at 40 weeks of age.
The protective effects of the microbiome shifts were more pronounced in male mice carrying the APOE3 variant than in those with the high-risk APOE4variant, possibly because the deleterious effects of APOE4canceled out some of the protection, the researchers said. Antibiotic treatment had no significant effect on neurodegeneration in female mice.
“We already know, from studies of brain tumors, normal brain development and related topics, that immune cells in male and female brains respond very differently to stimuli,” Holtzman said.
“So it’s not terribly surprising that when we manipulated the microbiome we saw a sex difference in response, although it is hard to say what exactly this means for men and women living with Alzheimer’s disease and related disorders.”
Further experiments linked three specific short-chain fatty acids — compounds produced by certain types of gut bacteria as products of their metabolism — to neurodegeneration. All three of these fatty acids were scarce in mice with gut microbiomes altered by antibiotic treatment, and undetectable in mice without gut microbiomes.
These short-chain fatty acids appeared to trigger neurodegeneration by activating immune cells in the bloodstream, which in turn somehow activated immune cells in the brain to damage brain tissue. When middle-aged mice without microbiomes were fed the three short-chain fatty acids, their brain immune cells became more reactive, and their brains showed more signs of tau-linked damage.
Evidence is accumulating that the gut microbiomes in people with Alzheimer’s disease can differ from those of healthy people.
“This study may offer important insights into how the microbiome influences tau-mediated neurodegeneration, and suggests therapies that alter gut microbes may affect the onset or progression of neurodegenerative disorders,” said Linda McGavern, PhD, program director at the National Institute of Neurological Disorders and Stroke (NINDS), which provided some of the funding for the study.
The findings suggest a new approach to preventing and treating neurodegenerative diseases by modifying the gut microbiome with antibiotics, probiotics, specialized diets or other means.
“What I want to know is, if you took mice genetically destined to develop neurodegenerative disease, and you manipulated the microbiome just before the animals start showing signs of damage, could you slow or prevent neurodegeneration?” Holtzman asked.
“That would be the equivalent of starting treatment in a person in late middle age who is still cognitively normal but on the verge of developing impairments. If we could start a treatment in these types of genetically sensitized adult animal models before neurodegeneration first becomes apparent, and show that it worked, that could be the kind of thing we could test in people.”
Summary: People with higher levels of the gut bacteria Coprococcus tend to have higher insulin sensitivity, while those with higher levels of Flavonifractor have lower levels of insulin sensitivity. Researchers say specific gut bacteria could play a significant role in the development of Type 2 diabetes.
One type of bacteria found in the gut may contribute to the development of Type 2 diabetes, while another may protect from the disease, according to early results from an ongoing, prospective study led by investigators at Cedars-Sinai.
The study, published in the peer-reviewed journal Diabetes, found people with higher levels of a bacterium called Coprococcus tended to have higher insulin sensitivity, while those whose microbiomes had higher levels of the bacterium Flavonifractor tended to have lower insulin sensitivity.
For years, investigators have sought to understand why people develop diabetes by studying the composition of the microbiome, which is a collection of microorganisms that include fungi, bacteria and viruses that live in the digestive tract.
The microbiome is thought to be affected by medications and diet. Studies have also found that people who don’t process insulin properly have lower levels of a certain type of bacteria that produce a type of fatty acid called butyrate.
Mark Goodarzi, MD, Ph.D., the director of the Endocrine Genetics Laboratory at Cedars-Sinai, is leading an ongoing study that is following and observing people at risk for diabetes to learn whether those with lower levels of these bacteria develop the disease.
“The big question we’re hoping to address is: Did the microbiome differences cause the diabetes, or did the diabetes cause the microbiome differences?” said Goodarzi, who is the senior author of the study and principal investigator of the multicenter study called Microbiome and Insulin Longitudinal Evaluation Study (MILES).
Investigators involved in MILES have been collecting information from participating Black and non-Hispanic white adults between 40 and 80 years of age since 2018. An earlier cohort study from the MILES trial found that birth by cesarean section is associated with a higher risk for developing prediabetes and diabetes.
For the most recent study to come out of this ongoing trial, investigators analyzed data from 352 people without known diabetes who were recruited from the Wake Forest Baptist Health System in Winston-Salem, North Carolina.
Study participants were asked to attend three clinic visits and collect stool samples prior to the visits. Investigators analyzed data collected at the first visit. They conducted genetic sequencing on the stool samples, for example, to study the participants’ microbiomes, and specifically look for bacteria that earlier studies have found to be associated with insulin resistance.
Each participant also filled out a diet questionnaire and took an oral glucose tolerance test, which was used to determine ability to process glucose.
Investigators found 28 people had oral glucose tolerance results that met the criteria for diabetes. They also found that 135 people had prediabetes, a condition in which a person’s blood-sugar levels are higher than normal but not high enough to meet the definition of diabetes.
The research team analyzed associations between 36 butyrate-producing bacteria found in the stool samples and a person’s ability to maintain normal levels of insulin. They controlled for factors that could also contribute to a person’s diabetes risk, such as age, sex, body mass index and race. Coprococcus and related bacteria formed a network of bacteria with beneficial effects on insulin sensitivity.
Despite being a producer of butyrate, Flavonifractor was associated with insulin resistance; prior work by others have found higher levels of Flavonifractor in the stool of people with diabetes.
The microbiome is thought to be affected by medications and diet. Image is in the public domain
Investigators are continuing to study samples from patients who participated in this study to learn how insulin production and the composition of the microbiome change over time. They also plan to study how diet may affect the bacterial balance of the microbiome.
Goodarzi emphasized, however, that it is too early to know how people can change their microbiome to reduce their diabetes risk.
“As far as the idea of taking probiotics, that would really be somewhat experimental,” said Goodarzi, who is also the Eris M. Field Chair in Diabetes Research at Cedars-Sinai.
Abstract
Butyrate-Producing Bacteria and Insulin Homeostasis: The Microbiome and Insulin Longitudinal Evaluation Study (MILES)
Gut microbiome studies have documented depletion of butyrate-producing taxa in type 2 diabetes. We analyzed associations between butyrate-producing taxa and detailed measures of insulin homeostasis, whose dysfunction underlies diabetes in 224 non-Hispanic Whites and 129 African Americans, all of whom completed an oral glucose tolerance test. Stool microbiome was assessed by whole-metagenome shotgun sequencing with taxonomic profiling.
We examined associations among 36 butyrate-producing taxa (n = 7 genera and 29 species) and insulin sensitivity, insulin secretion, disposition index, insulin clearance, and prevalence of dysglycemia (prediabetes plus diabetes, 46% of cohort), adjusting for age, sex, BMI, and race.
The genus Coprococcus was associated with higher insulin sensitivity (β = 0.14; P = 0.002) and disposition index (β = 0.12; P = 0.012) and a lower rate of dysglycemia (odds ratio [OR] 0.91; 95% CI 0.85–0.97; P = 0.0025).
In contrast, Flavonifractor was associated with lower insulin sensitivity (β = −0.13; P = 0.004) and disposition index (β = −0.11; P = 0.04) and higher prevalence of dysglycemia (OR 1.22; 95% CI 1.08–1.38; P = 0.0013). Species-level analyses found 10 bacteria associated with beneficial directions of effects and two bacteria with adverse associations on insulin homeostasis and dysglycemia.
Although most butyrate producers analyzed appear to be metabolically beneficial, this is not the case for all such bacteria, suggesting that microbiome-directed therapeutic measures to prevent or treat diabetes should be targeted to specific butyrate-producing taxa rather than all butyrate producers.
Has a high-fat meal ever left you feeling bloated and sluggish? It turns out that a heavier fat diet may keep the many bacteria that live in your digestive system from doing their best, too.
New research found that when people boosted their fat intake to 40 percent of their daily diet for six months, the number of “good” gut bacteria decreased while “unhelpful” bacteria amounts increased.
“The [study] result showed that a high-fat diet is linked to unfavorable changes in the type and numbers of gut bacteria — collectively known as the microbiome,” said the study’s senior author, Duo Li. He is chief professor of nutrition at the Institute of Nutrition and Health at Qingdao University in Qingdao, China.
In addition to changing the make-up of the microbiome, the study authors also noted an increase in inflammatory triggers in the body. These changes may contribute to the development of metabolic disorders, such as diabetes and heart disease, the researchers noted.
Nutritionist Samantha Heller, from NYU Langone Health in New York City, said bacteria living in the digestive system appear to have broad-ranging impacts on human health, and that they “eat what we eat.”
“Research suggests that they thrive on plant fibers — such as those found in fruits and vegetables, legumes, nuts and grains — and that the typical Western diet, which is rich in fat, red and processed meats, cheese, sweets, refined grains and fast-fried junk foods, in a sense, poisons them,” she explained.
In China, where the study was done, a traditional diet has been low in fat and high in carbohydrates. That, however, has been shifting to a diet higher in fat and lower in carbohydrates. At the same time, the rates of obesity and type 2 diabetes have also been rising, the study authors said.
To see if changes occur in the gut microbiome when people transition from a low-fat diet to a higher-fat diet, the researchers recruited about 200 young people, who weren’t obese, for the study. Their average age was about 23 years old.
Li said their average fat intake before the start of the study was about 31 percent.
The study volunteers were randomly placed into one of three groups for six months. One group ate a diet comprised of 20 percent fat, another ate 30 percent of their daily calories from fat, while the third had a 40 percent fat diet.
The researchers altered carbohydrate intake — things like rice and wheat flour — to make up for the changes in fat intake. The amount of fiber and protein in the diets stayed essentially the same.
All three groups had weight loss, but the lowest-fat group lost the most weight and had the greatest reductions in waist circumference, total cholesterol and bad cholesterol. The low-fat diet group also had an increase in gut bacteria that have been linked to lower cholesterol levels.
Those on the higher-fat fare had an increase in a different type of gut bug — one that’s been linked to higher cholesterol levels. Their diet was also associated with “significant” changes in long chain fatty acid metabolism, producing higher levels of chemicals that are thought to trigger inflammation.
Li said the findings may be relevant in developed countries where fat intake is high, but that further research needs to be done to see if similar changes occur in different populations.
“We suggest that fat intake for a general healthy population should not be more than 30 percent of total energy — at least in Asian populations,” Li said, and added that most fat should come from healthy fats, such as soybean, peanut or olive oil.
Nutritionist Heller said it’s important not to “interpret the findings of this study to suggest that dietary fat is unhealthy. We need to eat fats to be healthy, unsaturated fats in particular.”
But, she added, you can have too much of a good thing. “Fad diets rich in animal fats — such as ‘Keto’ or ‘Paleo’ — over time, are likely to be deleterious to the gut microbiome and subsequently increase the risk of inflammation and chronic diseases,” Heller said.
To keep your microbiome happy and healthy, Heller recommended eating more vegetables, legumes, fruits, grains and nuts, while avoiding processed meats, limiting red meat and cheese, and balancing your intake of fats, carbohydrates and protein.
The more we find out about the bacteria that live in our gut, the more we’re coming to realise how these microbiota could have an impact on every facet of our lives – and not just our physical health and well-being, but our thoughts and emotions too.
A new study has identified associations between two kinds of gut microbiota and how they affect people’s emotional responses, and the researchers say it’s the first evidence of behavioural differences related to microbial composition in healthy humans.
Now, a team led by gastroenterologist Kirsten Tillisch at UCLA has shown that the same kind of associations appear to be affecting human emotional reactions.
The researchers took faecal samples from 40 healthy women between the ages of 18 and 55. When the samples were analysed, the participants were divided into two groups based on their microbiota composition.
One of the groups showed a greater abundance of a bacterium genus called Bacteroides, while the other group demonstrated more clusters of a genus called Prevotella.
Next, the team scanned the brains of the participants via functional magnetic resonance imaging, while showing them images designed to provoke a positive, negative, or neutral emotional response.
What the researchers found was that the group with greater abundance of Bacteroidesin their gut bacteria showed greater thickness of the grey matter in the frontal cortexand insula – brain regions which process complex information – and also a larger volume of the hippocampus, which is involved with memory.
In contrast, the women with higher levels of Prevotella demonstrated lower volume in these areas, and demonstrated greater connections between emotional, attentional and sensory brain regions.
When shown the negative images, the Prevotella participants showed lower activity in the hippocampus – but reported higher levels of anxiety, distress and irritability after looking at the photos.
According to the researchers, this could be because the hippocampus helps us to regulate our emotions, and so with less hippocampal volume – which is possibly related somehow to the makeup of our gut microbiota – negative imagery may pack a greater emotional wallop.
“Reduced hippocampal engagement to negative imagery may be associated with increased emotional arousal,” the authors write in their paper.
“Such changes have been suggested to result in less specificity of encoding the contextual details of incoming stimuli, a deficit seen in the setting of several psychiatric disorders, including depression, post traumatic stress disorder, and borderline personality disorder. While the subjects in this study were healthy, it is possible that the patterns which emerge from the microbial clustering represent vulnerability factors.”
It’s important to bear in mind that the sample studied here was very small – a point the researchers freely admit in their paper, acknowledging that further research with larger numbers of participants will be needed before we can really understand what’s going on here.
But it’s clear that there’s something going on between the organisms in our gut and the thoughts and feelings we experience, and the sooner we delve into this, the sooner we’ll comprehend just how emotionally powerful our ‘second brain‘ really is.
A new study has shown that people with chronic fatigue syndrome have abnormal levels of specific gut bacteria – providing even more evidence that the condition isn’t “just in a person’s head“.
For decades, millions of people have reported experiencing symptoms now associated with a condition called chronic fatigue syndrome – a debilitating disease that causes brain fog, severe pain, and exhaustion so extreme, patients can’t go about their daily lives, and sometimes can’t even get out of bed. But a physical cause has been elusive, leaving many feeling that their condition isn’t being taken seriously.
It was only in 2015 that the US Institute of Medicine detailed a comprehensive way to diagnose chronic fatigue syndrome/myalgic encephalomyelitis (ME/CFS), and earlier this year, scientists linked the condition to faulty cell receptors in immune cells for the first time – which explains why the side effects can be so varied and hard to pin down.
But there are still no effective treatments for the disease, and no cure – some commonly prescribed treatments for the condition have been cognitive behavioural therapy and exercise, neither of which have any evidence to support they work, and could actually be doing more harm than good.
Now, new research has shown that patients with ME/CFS have abnormal levels of specific gut bacteria – and those levels change depending on the severity and type of symptoms they have.
“Individuals with ME/CFS have a distinct mix of gut bacteria and related metabolic disturbances that may influence the severity of their disease,” said one of the researchers, Dorottya Nagy-Szakal from Columbia University’s Mailman School of Public Health.
“By identifying the specific bacteria involved, we are one step closer to more accurate diagnosis and targeted therapies,” added lead researcher Ian Lipkin.
The study adds to research from last year, which showed that up to 80 percent of patients with ME/CFS could be accurately diagnosed by looking at their gut bacteria.
And it’s also known that up to 90 percent of ME/CFS patients have irritable bowel syndrome (IBS), so the latest research began to untangle the specific gut bacteria changes associated with each condition.
The team followed 50 ME/CFS patients and 50 healthy controls, who had been carefully matched. They tested the number of bacterial species in faecal samples, and looked at the immune molecules in their blood.
They found that seven distinct intestinal bacterial species were strongly associated with ME/CFS, so much so that an elevated presence of all of them could predict a diagnosis.
The strains were:
Faecalibacterium
Roseburia
Dorea
Coprococcus
Clostridium
Ruminococcus
Coprobacillus
There were also specific changes seen in the gut bacteria of those who had chronic fatigue syndrome with IBS, and those who didn’t have IBS.
Interestingly, when the team measured bacterial metabolic pathways – the ways that bacteria break down food and send signals to the brain – there were clear differences between the healthy controls and the ME/CFS group.
There were also measurable differences depending on the severity of a patient’s symptoms, which suggests that are different subtypes of ME/CFS that could be identified.
While this study involved only a small sample size, with further verification, this could be the first step towards coming up with targeted ways to not only diagnose the debilitating disease, but also treat it.
“Our analysis suggests that we may be able to subtype patients with ME/CFS by analysing their fecal microbiome,” said one of the team, Brent L. Williams.
“Subtyping may provide clues to understanding differences in manifestations of disease.”
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