Delicious; rich in fiber and antioxidants; good for bowel function, the heart, the blood vessels, and bone health; excellent allies for weight loss... In terms of health benefits, prunes get two thumbs up!

Prunes: Their mode of action is still a mystery…

The inclusion of these dried fruits in the diet of postmenopausal women is no exception to the rule. The health benefits of prunes for postmenopausal women, particularly in improving bone health, are well documented, but there are many unknowns surrounding how they work, particularly when it comes to the role of the gut microbiota.

What exactly are the effects of these dried fruits on the gut bacteria during menopause? A team of American researchers has tried to answer this question.

They recruited 143 postmenopausal women aged 55 to 75 and randomly assigned them to 3 different groups:

• one in which they had to eat 4 to 6 prunes per day (50 g),
• another in which they had to eat 10 to 12 prunes per day (100 g)
• and a third in which they did not eat any prunes (control group).

Before and after the experiment, the scientists collected stool samples from the volunteers to analyze and compare the evolution of their microbiota.

More beneficial gut bacteria

They also collected blood and urine samples to measure inflammatory markers (a risk factor for many diseases) and “phenolic metabolites.” 

Phenolic metabolites are beneficial compounds derived from the breakdown of antioxidants (polyphenols). The level of urinary phenolic metabolites reflects the level of activity of the microbiota bacteria that break down polyphenols.

After 12 months of the experiment, the results indicate that women in the “prune” groups show significant changes in their microbiota compared to those in the control group. These changes are different depending on the dose (50 or 100 g). 

In particular, the researchers’ analyses show an enrichment in bacteria of the Lachnospiraceae family, already known for their capacity to maintain the intestinal barrier.

Anti-inflammatory effects mediated by the microbiota

It appears from the study that Lachnospiraceae are able to metabolize prune polyphenols and ferment their fibers to produce short-chain fatty acids (sidenote: Short chain fatty acids (SCFA) Short chain fatty acids (SCFA) are a source of energy (fuel) for an individual’s cells. They interact with the immune system and are involved in communication between the intestine and the brain. Silva YP, Bernardi A, Frozza RL. The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication. Front Endocrinol (Lausanne). 2020;11:25. ) that have anti-inflammatory properties. Calculations show that the presence of some of these bacteria is negatively correlated with inflammatory markers and positively correlated with phenolic metabolites.

According to the researchers, by providing fiber and polyphenols, prunes exert a selection pressure that favors good bacteria in the long term, which could explain their health benefits.

Remember that if you have a sugar craving!

As the prevalence of obesity and associated metabolic disorders increases worldwide, dietary changes are not enough for many patients. Understanding the impact of other environmental factors is crucial to developing alternative treatment strategies. Numerous studies point to a link between dysbiosis of the gut microbiota and the development of obesity, which could at least partly explain the variations from one individual to another in terms of susceptibility to metabolic diseases. However, the molecular mechanisms and the causal link between the bacteria of the gut microbiota, especially their metabolites, and the development of obesity are not fully understood.

High-fat diet and Fusimonas intestini: A synergistic effect on weight gain

It is well accepted that a diet high in fat, especially saturated fat, increases the risk of obesity and its metabolic comorbidities. But we do not know to what extent certain metabolites (such as long-chain fatty acids) produced by the bacteria of the gut microbiota influence the pathogenesis of these conditions. A Japanese team looked at the Lachnospiraceae, a bacterial family in the gut microbiota linked with obesity and type 2 diabetes in previous studies. The team showed that one of the bacterial family’s commensal species, Fusimonas intestini, is significantly more present in cases of obesity and hyperglycemia, in both mice and humans.

To identify a potential causal link between this species and obesity, the researchers compared mice whose gut microbiota was colonized by Escherichia coli and F. intestini or by E. coli alone, fed a normal or high-fat diet. They found a significant increase in body weight and body fat only in those mice fed the high-fat diet and colonized with F. intestini, even in very small amounts. In addition, these mice had elevated levels of plasma cholesterol and of expression of pro-inflammatory TNF-α, lipopolysaccharide-binding proteins, and genes encoding for leptin. By colonizing gnotobiotic mice with F. intestini and 9 species representative of the human microbiota, the researchers found this fat gain. These results suggest that high dietary fat intake and F. intestini act synergistically to change the host metabolism.

Altered lipid metabolism and intestinal impermeability

The researchers found that F. intestini produced an abundance of various long-chain fatty acids. On the high-fat diet, the gut microbiota colonized by this bacteria contained twice as much elaidate, a trans fatty acid that is known to increase the risk of cardiovascular disease, obesity and insulin resistance. It also had more saturated fatty acids such as palmitate, stearate and margarate. According to the researchers, the high-fat diet leads to an overexpression of microbial genes involved in lipid production, in particular FadR (Fatty acid metabolism regulator), which regulates fatty acid metabolism. Their blood and tissue analyses suggest that metabolites of F. intestini degrade the intestinal barrier, leading to endotoxemia that promotes the development of obesity.

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Obesity and its accompanying metabolic disorders, such as type 2 diabetes, are taking an increasing toll on public health worldwide. For many sufferers, just correcting the diet is not a good enough solution. Over the past ten years or so, various studies have highlighted the role of the gut microbiota in obesity. It may explain, at least in part, individual differences in vulnerability to obesity and the effects of diets. However, not all the mechanisms involved have been elucidated yet. Researchers are therefore exploring the specific composition and functioning of the microorganisms of the gut microbiota that can influence obesity.

Microbiota bacteria that “make fat”

We all know that a diet that is too rich in fats, especially saturated fats, increases the risk of obesity. But the bacteria of the gut microbiota also produce fatty acids. To what extent and in what way could their metabolism contribute to the development of the condition? To answer this question, a Japanese team from the research institute RIKEN looked at the Lachnospiraceae, a bacterial family in the gut microbiota that has already been linked with obesity and type 2 diabetes in previous studies. The team showed that one of the bacterial family’s species, Fusimonas intestini, is significantly more present in the gut microbiota in individuals with obesity and high blood sugar, in both mice and humans.

To determine whether this bacterium could be a cause of obesity, the researchers compared mice whose gut microbiota was colonized by Fusimonas intestini or not, fed normally or fed a high-fat diet. They found that the “fatty” diet increased body fat gain in the presence of Fusimonas intestini bacteria even in very small amounts.

Hindered metabolic genes and leakage through the intestinal barrier

The researchers found that Fusimonas intestini produced an abundance of various “long-chain” fatty acids. Only under the effect of the high-fat diet, the gut microbiota colonized by this bacteria contained twice as much elaidate, a trans fatty acid (sidenote: Trans fatty acid Trans fatty acids (TFAs) are not synthesized in the human body but are generally consumed in our meals. They come from ruminants (via meat and dairy products) or are of industrial origin. TFAs, especially those of industrial origin, are believed to contribute to cardiovascular disease, obesity and diabetes.
Sarnyai F, Kereszturi É, Szirmai K, Mátyási J, Al-Hag JI, Csizmadia T, Lőw P, Szelényi P, Tamási V, Tibori K, Zámbó V, Tóth B, Csala M. Different Metabolism and Toxicity of TRANS Fatty Acids, Elaidate and Vaccenate Compared to Cis-Oleate in HepG2 Cells. Int J Mol Sci. 2022 Jun 30;23(13):7298. )  known to increase the risk of developing cardiovascular disease, obesity and insulin resistance. Furthermore, the intestinal flora had more saturated fatty acids such as palmitate, which is also implicated in these diseases. The high-fat diet is thought to modify the expression of microbial genes that regulate fatty acid metabolism, thus increasing lipid production. But that’s not all: the metabolites of Fusimonas intestini appear to compromise the integrity of the intestinal barrier, making it more permeable and allowing the passage of harmful molecules. This leads to a phenomenon called endotoxemia (sidenote: Endotoxemia Endotoxemia is a condition characterized by the presence of endotoxins in the blood. Endotoxins are components of the cell walls of certain bacteria. They are released when the bacteria die or multiply. When the gastrointestinal barrier is compromised, endotoxins enter the bloodstream and cause inflammation.
André P, Laugerette F, Féart C. Metabolic Endotoxemia: A Potential Underlying Mechanism of the Relationship between Dietary Fat Intake and Risk for Cognitive Impairments in Humans? Nutrients. 2019 Aug 13;11(8):1887. ) , known to cause inflammation in the body and implicated in the development of obesity and type 2 diabetes.

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Which role may play the microbiota in Covid-19 infection?

Prof. Irina Spacova and Prof. Sarah Lebeer: COVID-19 does not have the same effect on everyone: some of us remain asymptomatic, while others suffer for months or even years from residual symptoms such as fatigue and muscle weakness. In addition to sociodemographic factors such as age, recent studies suggest that individual differences in our microbiota play an important role in determining COVID-19 outcomes. Indeed, our bodies are inhabited by diverse microbial communities in the gastrointestinal tract and the airways where the SARS-CoV-2 infection takes place. Many of the microorganisms (sidenote: Microorganisms Living organisms that are too small to be seen with the naked eye. They include bacteria, viruses, fungi, archaea and protozoa, and are commonly referred to as “microbes”. What is microbiology? Microbiology Society. ) within the microbiota play a protective gatekeeper function against invading pathogens (sidenote: Pathogen A pathogen is a microorganism that causes, or may cause, disease. Pirofski LA, Casadevall A. Q and A: What is a pathogen? A question that begs the point. BMC Biol. 2012 Jan 31;10:6. ) .

Does the virus impact the gut, oral, nasal and lung microbiota in the same way?

I. S. & S. L.: COVID-19 is linked to microbiota disruptions (sometimes also named dysbiosis) of the gut, oral, nasal and lung microbiota, with many studies reporting less diverse microbial communities in infected patients at these major sites of infection and multiplication of the virus. However, not all studies observe the same alterations in microbiota diversity.

We summarize the main overall findings in what follows:

• The nasal passage, the mouth and especially the throat (the ENT microbiota) are two key sites of SARS-CoV-2 infection and multiplication. Patients with confirmed COVID-19 have generally a lower microbial diversity in nasopharyngeal swabs. The microbial community richness also seems to decrease with increasing disease severity ¹. An increased abundance of a specific bacterium, for example bacterial pathogens such as Pseudomonas aeruginosa is also found in the nasal microbiota of hospitalized patients with COVID-19 ². This indicates that SARS-CoV-2-induced inflammation could promote the growth of opportunistic pathogens in the nose, resulting in superinfection. In the mouth, the oral microbiota also seems to be less diverse associated with the severity of the COVID-19 symptoms. Finally, opportunistic fungal pathogens Candida and Aspergillus, as well as bacteria associated with poor oral hygiene and periodontitis, are more abundant in COVID-19 patients ³.

• Severe COVID-19 can result in acute respiratory distress syndrome (ARDS) associated with widespread inflammation in the lungs (pulmonary microbiota), often requiring prolonged mechanical ventilation in hospital settings. There appears to be a significant association between severe COVID-19 requiring mechanical ventilation and a lower microbial community diversity compared to a healthy lung samples ⁴. Furthermore, lung samples from these patients are frequently dominated by single bacterial genera that contain potential pathogens such as Staphylococcus and Enterococcus.

• In the gastrointestinal tract (gut microbiota), COVID-19 is associated with symptoms such as diarrhea and loss of appetite. Therefore, it is not surprising that it has been linked with an intestinal dysbiosis. Notably, Candida and Aspergillus (opportunistic fungal pathogens) appear to also increase in the fecal microbiota of COVID-19 patients ⁵ and potentially beneficial bacteria such as Faecalibacterium prausnitzii to decrease ⁶. A striking research finding was that the composition of gut microbiota at admission might be predictive of long-term complications of COVID-19. At admission compared to long-term COVID-19 at 6 months, a total of 13 bacteria species, including Bifidobacterium longum were negatively correlated with long COVID-19: that means that the more these bacteria are present in your gut, the less risk you will have to develop long term COVID-19, indicating a putative protective role of these species in the recovery from the infection ⁶. Other species such as Atopobium parvulum were positively correlated with symptoms: the more we found this bacteria in your gut, the more you will suffer severe infection. These differences open up possibilities for better monitoring and predicting of long COVID-19 symptoms.

What is the link between the virus, immunity and the microbiota?

I. S. & S. L.: It is still not well understood whether these observed microbiota changes are cause or consequence of the disease. To better understand this, it is also important to take the immune system into account. Effective immune responses need to be generated upon SARS-CoV-2 infection to clear the virus and prevent future reinfections.

Even before the COVID-19 infection takes place, the resident microbiota can serve a protective function by training our immune system, enhancing the barrier function ⁷ or even directly inhibiting adherence or infectivity of the virus ⁸. Conversely, a disrupted gut microbiota can increase susceptibility to viral disease through disrupting the intestinal mucosal barrier function, impaired antiviral responses and increase in pathogen colonization and adhesion ⁹.

May healthy diet or probiotics protect against the virus by modulating the gut microbiota?

I. S. & S. L.: As you can understand, disentangling the complex relationship between the microbiota and COVID-19 is a challenging task, since our microbiota composition and immune functioning are affected by many different factors (health, genetics, lifestyle). However, since diet is an important determinant of the human gut microbiota composition, dietary changes hold some promise against COVID-19. For example, a smartphone-based study with more than 30.000 COVID-19 cases in the UK and the USA has suggested that plant-based foods consumption is linked with lower risk and severity of COVID-19 ¹⁰. An interesting theory has been proposed that eating large quantities of fermented vegetables potentially containing beneficial microorganisms might be helpful in mitigating COVID-19 disease severity ¹¹. This is a plausible approach, considering that gut microbiota modulation with probiotic (sidenote: Probiotics Live microorganisms that, when administered in adequate amounts, confer a health benefit on the host. FAO/OMS, Joint Food and Agriculture Organization of the United Nations/ World Health Organization. Working Group. Report on drafting  guidelines for the evaluation of probiotics in food, 2002. Hill C, Guarner F, Reid G, et al. Expert consensus document. The International Scientific Association for Probiotics and Prebiotics consensus statement on the scope and appropriate use of the term probiotic. Nat Rev Gastroenterol Hepatol. 2014;11(8):506-514. ) bacteria often found in fermented foods may prevent or treat acute respiratory infections based on evidence from clinical research ¹².

A small-scale study administering oral probiotic mix of bacteria in patients infected with SARS-CoV-2 reported a decreased risk for respiratory failure and quicker resolution of diarrhea ¹³.  

Overall, the World Health Organization recommends that COVID-19 patients adhere to a healthy diet with fresh and unprocessed foods every day and less salt and sugar, which could support a balanced gut microbiota and optimal general health. Yet, this is a general true for all of us at all time: if only eating healthy could be this easy!

Discover Prof. Sarah Lebber's interview:

^BMI-23.18

Despite decades of research on endometriosis, the means of providing relief are limited for patients who experience recurring issues despite hormone therapy or surgical removal of lesions. The factors contributing to the development of the disease remain poorly understood. Retrograde menstruation towards the peritoneal cavity, which affects 90% of women, is not eliminated by immune cells in 10% of them. The endometrial tissue is then believed to proliferate under the influence of inflammatory cytokines and growth factors, leading to the formation of ectopic lesions. In addition, a growing number of studies on patients highlights the role of the gut microbiota: could the gut dysbiosis observed and the role of gut metabolites be involved in the pathophysiology and progression of endometriosis?

The gut microbiota: A factor in the progression of endometriosis lesions

To explore the role of the gut microbiota in the progression of endometriosis, researchers have developed a new mouse model of endometriosis in which the gut microbiota is depleted (DM) by antibiotics (sidenote: These mice have less bacteria in their gut microbiota compared to the control mice. ) .The first finding: the depletion of the gut microbiota does not have a harmful effect on the general uterine morphology. However, the growth of endometriosis lesions is reduced in the DM mice compared to endometriosis mouse models whose gut microbiota has not been depleted. Fecal microbiota transplantation (FMT) from these control mice to the DM mice resulted in a resumption of endometriosis lesion growth, whereas another experiment with FMT from healthy mice (without endometriosis, with non-depleted gut microbiota) did not result in this resumption of growth. This confirms that the gut microbiota is essential for the growth of endometriosis lesions.

A bacterial metabolite promotes the survival of endometrial cells

Another finding is that the uterine microbiota is not necessary for lesion growth. Researchers also suppose that the gut microbiota has an impact on the growth of endometriosis lesions through modulation of the peritoneal immune cells. Finally, they identify an intestinal metabolic signature specific to endometriosis. One of the metabolites, quinic acid, promotes the survival of endometrial epithelial cells in vitro, and the growth of lesions in vivo.

Food is not the only thing that influences growth… The gut microbiota also plays an essential role. A research team had previously shown in a mouse model that the gut microbiota may buffer the deleterious effects of chronic malnutrition by limiting the body’s resistance to growth hormone (GH) and elevating circulating levels of growth factor IGF-1. The result is less stunting of growth. The researchers focused on a particular strain of Lactiplantibacillus plantarum because of its ability to promote growth in a model of malnourished fruit flies (Drosophila). This time, the team sought to decipher the underlying mechanisms ¹.

^{Sources (sidenote: Malnutrition_World Health Organization_June 2021 )}

Positive effect of Lactiplantibacillus plantarum on chronic malnutrition

For this new experiment, the researchers took newly weaned mice and subjected them to a reduced-protein diet, where daily protein intake was 75% lower than in a standard diet. The mice were separated into two groups, one receiving the bacteria and the other a placebo for 56 days. At the end of the experiment, the mice receiving the bacteria were larger and heavier than the placebo group, even if they did not fully make up for the growth delay caused by malnutrition. The researchers also observed metabolic and hormonal changes in the mice receiving the bacteria, including improved circulating levels and activity of IGF-1 and insulin. These changes were mediated by components of the bacterial cell wall, particularly muramyl dipeptide.

_{Sources (sidenote: Malnutrition_World Health Organization_June 2021 )}

Increased absorption of nutrients

Chronic malnutrition reduces the number of gut stem cells, leading to a reduction in epithelial cells, which also have shorter villi, resulting in a lower absorption of nutrients. Based on their findings, the authors suggest that after the ingestion of Lactiplantibacillus plantarum certain bacterial compounds, including muramyl dipeptide, are released from the bacterial cell wall. The NOD2 receptor in the intestinal wall detects muramyl dipeptide and is stimulated by it, leading to a cascade of cellular signaling that increases intestinal cell proliferation and allows for the maturation of the epithelium, thus improving the absorption of nutrients. This in turn stimulates the activity of the nutrient-sensitive GH/IGF-1/insulin axis, improving postnatal growth among mice.

Three ways to fight malnutrition

These results suggest that, coupled with renutrition, certain strategies may mitigate the stunting caused by malnutrition: 

• probiotic supplements (containing Lactiplantibacillus plantarum)
• postbiotic (sidenote: Postbiotics A preparation of inanimate microorganisms and/or their components that confers a health benefit on the host. Salminen S, Collado MC, Endo A, et al. The International Scientific Association of Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of postbiotics. Nat Rev Gastroenterol Hepatol. 2021 Sep;18(9):649-667. )  supplements (pieces of bacterial cell wall or purified NOD2 ligands). A ray of hope for the 149 million children under the age of five who suffer from malnutrition. ² 

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First, take mice that have just been weaned after 21 days of breastfeeding. Then, give some of them Lactiplantibacillus plantarum, a bacterium known to boost the growth of malnourished fruit flies, and a placebo to the rest. Lastly, observe the growth of the mice, which have been intentionally undernourished for the needs of the study. The mice that did not receive the bacteria develop into very stunted young adults after 56 days, 10% lower in weight and 3%-4% smaller in size than the other mice in the experiment. On the other hand, in the mice that did receive Lactiplantibacillus plantarum, the effects of malnutrition were largely mitigated, even though they developed less than mice fed a normal diet.

^{Sources (sidenote: Malnutrition_World Health Organization_June 2021 )}

Lactiplantibacillus plantarum, a bacterium with superpowers

Still missing from this experiment is the reason for this difference. This study ¹, makes it clear that diet is not the only key factor in the growth of baby mice: bacteria in the gut microbiota also play an essential role. What mechanisms allow this super bacterium to make such a difference in malnourished mice? According to the scientists, once the bacterium is ingested, a compound in its cell wall binds to a specific gut receptor, promoting the maturation of the mouse’s digestive tract. A more mature digestive tract lets young mice benefit more from their food by absorbing nutrients more effectively, partly compensating for malnutrition, and reducing resistance to growth hormone. And that’s how it’s done!

Hope for 149 million malnourished children

Should similar results be discovered in humans, these findings will have major implications.  They suggest that it may be possible, in combination with a renutrition strategy, to mitigate the stunting associated with prolonged malnutrition by treating malnourished children with probiotics containing Lactiplantibacillus plantarum or simply pieces of this bacterium’s cell walls (i.e. postbiotics (sidenote: Postbiotics A preparation of inanimate microorganisms and/or their components that confers a health benefit on the host. Salminen S, Collado MC, Endo A, et al. The International Scientific Association of Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of postbiotics. Nat Rev Gastroenterol Hepatol. 2021 Sep;18(9):649-667. ) ). A ray of hope for the world’s 149 million children under the age of five who suffer from malnutrition ².

^{Sources (sidenote: Malnutrition_World Health Organization_June 2021 )}

Chronic fatigue syndrome, also known as myalgic encephalomyelitis (ME/CFS), is characterized by symptoms such as exhaustion, post-exertional malaise, memory problems, pain, gastrointestinal disturbances, immune abnormalities, and sleep disorders. Even though it affects between 0.4% and 2.5% of the world’s population, mainly adult women aged between 20 and 40 years, this debilitating chronic disease remains poorly understood. However, scientists are studying the role of gut-brain communications ¹ in the disease and in particular the involvement of the gut microbiota. By focusing on changes in the microbiota, two recent studies published in the journal Cell Host & Microbe ^2,3 have sought to better understand the disease and identify potential biomarkers.

The potential role of butyrate-producing bacteria

In the first study, metagenomic and metabolomic analyses were performed on fecal samples collected from 106 patients and 91 healthy controls living in 5 US states. The study highlights a major gut dysbiosis in CFS patients, with differences between the two groups in terms of gut microbiome diversity, abundance, functional biological pathways, and interactions. Specifically, Faecalibacterium prausnitzii and Eubacterium rectale, two beneficial butyrate-producing bacteria, were depleted in those suffering from chronic fatigue. Further analyses confirmed a lower synthesis of bacterial butyrate in the CFS patients. Moreover, the more F. prausnitzii was depleted, the more severe the fatigue.

Short-term patients vs. long-term patients

The second study, also US-based, included 149 patients and 79 healthy controls, and further distinguished two groups among the patients: 75 patients who had been ill for less than 4 years and 74 patients who had been ill for more than 10 years. Here again, the researchers found a major gut dysbiosis, especially in the short-term patients, with depleted levels of F. prausnitzii. The gut microbiota composition of the long-term patients was closer to that of the healthy controls (with some notable differences in terms of low abundance species and heterogeneity), suggesting a return to relative homeostasis.

On the other hand, these long-term patients presented more severe clinical symptoms and a more greatly altered metabolism than the other patients, including at immune system level. The researchers thus suggest that chronic fatigue may begin with a loss of beneficial bacteria, particularly those that produce butyrate, which then leads to metabolic changes in the host. In some individuals, these modifications may lead to irreversible metabolic and phenotypic changes and thus to an altered state of health over the long term.

One of the collateral effects of Covid – or more precisely of long Covid – has been to bring an illness presenting similar symptoms, chronic fatigue syndrome (also known as myalgic encephalomyelitis), back under the spotlight.

This chronic disease mainly affects women aged between 20 and 40, and its symptoms include debilitating fatigue, post-exertional malaise, memory problems, gastrointestinal disturbances, immune abnormalities, and sleep disorders. Two studies published in the journal Cell Host & Microbe explore this mysterious disease, and more particularly its links to the gut microbiota.

Depleted microbiota observed in chronic fatigue syndrome

Both studies showed depleted levels of a gut bacterium called Faecalibacterium prausnitzii in CFS patients. Moreover, the more F. prausnitzii was depleted, the more severe the fatigue. But that’s not all. This bacterium is known to produce a short-chain fatty acid (SCFA) (sidenote: Short chain fatty acids (SCFA) Short chain fatty acids (SCFA) are a source of energy (fuel) for an individual’s cells. They interact with the immune system and are involved in communication between the intestine and the brain. Silva YP, Bernardi A, Frozza RL. The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication. Front Endocrinol (Lausanne). 2020;11:25. )  called butyrate, which is beneficial to our health. Butyrate protects our gut barrier and modulates the immune system, and far from staying confined in the digestive system, it also enters the bloodstream, where it provides further benefits.

Disrupted immune system

The second study appears to show that this SCFA may determine the long-term clinical course of the disease. In patients who have suffered from CFS for more than ten years, the gut microbiota seems to return to balance over time (although some differences persist compared to healthy people). But long-term patients had more severe symptoms and their immune system seemed more disturbed than that of patients who had suffered from the disease for less than four years. According to the researchers, initial disturbances of the gut microbiota and a decrease in butyrate may, in some people, lead to irreversible changes across the whole body, which in turn lead to an altered state of health over the long term. ²

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