Although we need only very small quantities, vitamins are no less essential to our health—if we do not get enough vitamin C, for example, we can develop scurvy, a disease from which many sailors died when a lemon would have been enough to save them. To a lesser extent, cognitive disorders, numbness or a persistent state of fatigue can also be signs of a vitamin B deficiency. Moreover, the etymology of the word reveals something of its “vital function”: “vitamin” comes from the Latin “vita,” meaning life.

The B7 engine

Among the many vitamins essential for our body to function properly are the B vitamins, including the famous vitamin B7, also called biotin (sidenote: Biotin Called vitamin B7, or B8 in certain countries. This vitamin plays a key role in the metabolism of carbohydrates, lipids and amino acids. It is also involved in the biosynthesis of other vitamins (B9 and B12). Many foods are good sources of biotin (whole grains, eggs, milk, nuts, etc.). This vitamin is also synthesized by the bacteria in gut flora. Biotin_NIH National Cancer Institut ) . One of our main sources of biotin is food, but that’s not all! The bacteria in gut microbiota also produce it... or not, as the case may be. And this has consequences for our health, especially in the case of obesity.

The vicious circle of obesity

A team of researchers has just shown that the gut bacteria that produce and transport biotin are absent in severely obese patients (BMI (sidenote: Body Mass Index (BMI) Body Mass Index (BMI) assesses the corpulence of an individual by estimating the body fat mass calculated by a ratio between weight ((kg) and height squared (m2). https://www.nhlbi.nih.gov/health/educational/lose_wt/BMI/bmicalc.htm https://www.euro.who.int/en/health-topics/disease-prevention/nutrition/a-healthy-lifestyle/body-mass-index-bmi ) > 35). Their obese host is thus deprived of this additional non-dietary source, despite actually needing more than the average person (vitamin B being necessary for well-balanced adipose tissue). Experiments in animals show that the western diet (sidenote: Western diet Diet rich in processed foods, refined sugar, salt, saturated fats (red meats) and trans fats (pastries) Zinöcker MK, Lindseth IA. The Western Diet-Microbiome-Host Interaction and Its Role in Metabolic Disease. Nutrients. 2018 Mar 17;10(3):365.  ) , well known for promoting obesity, reduces both the quantity of biotin-producing gut bacteria and the circulating levels of this vitamin in serum. Also, paradoxically, the gut inflammation observed in obese patients limits the absorption of biotin supplied by the diet.

In cases of severe obesity, a vicious circle is thus set in motion, since gut dysbiosis is believed to aggravate inflammation (and obesity) as well as tissue biotin deficiency.

Boosting biotin production

How can we break this vicious circle? Weight-loss surgery (bariatric surgery), which improves metabolism and inflammation, stimulates growth of biotin-producing bacteria, resulting in an increase—at least during the first year—in the level of biotin circulating in the body. Another approach involves supplementing with prebiotics (fructo-oligosaccharide type fibers) and biotin. This has been tested in mice fed a high-fat diet, and was found to improve the diversity of gut microbiota and boost bacterial production of biotin and other B vitamins, while limiting weight gain and deterioration of blood sugar levels.

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Recently, research has revealed the involvement of gut microbiota (GM) in the pathogenesis of MS, yet little is still known about its mechanisms.

A novel multiomic approach

For the first time, a research team has investigated interactions between diet, immune system, metabolism and gut microbiota in the development and progression of MS. For this, the researchers adopted a multiomic methodology.

An altered relationship between gut microbiota and the immune system in MS patients

The results were similar to those of previous studies: on the whole, both groups share a similar bacterial community structure. However, MS patients had a lower abundance of bacteria with immunomodulatory properties. Moreover, the microbiota of patients differed depending on the extent of their disability, suggesting a possible link between certain species and disease severity. 

The results of the multiomic analyses also suggest dysfunctional homeostasis of microbiome–immune system interactions, because a disrupted immune cell–microbiome relationship and modification of the blood metabolic profile were observed in the group of MS patients.

Meat consumption: a possible explanation? 

Study of the participants’ food diaries played a key role in this research.

The researchers found that MS patients consumed more meat. This consumption was correlated with an increase in the quantity of Th17 cells, involved in the autoimmune process, and of S-adenosyl-L-methionine (SAM), a metabolite produced from methionine (an amino acid enriched in meat) and involved in the activation of Th17 cells. Conversely, MS patients had reduced proportions of B. thetaiotaomicron bacteria, known for being highly capable of digesting polysaccharides.

A new therapeutic approach? 

This data points to pathways of interaction between diet, gut microbiota, immune response and blood metabolome through B. thetaiotaomicron, Th17 and SAM. For the authors, these results suggest that decreasing dietary consumption of meat or methionine could reduce the number of circulating pro-inflammatory Th17 cells in MS patients.

Microplastics (MPs) are now everywhere, including in what we eat and the air we breathe. Does this increased human exposure present a health risk? Although the answer to this question is still largely unknown, researchers suspect a link, in the digestive system, with an increased risk of inflammation, oxidative stress, increased intestinal permeability and microbiota dysbiosis. This is an already long list, to which we may have to add IBDs, such as Crohn’s disease and ulcerative colitis, if we are to believe the results of a study comparing the characteristics of fecal MPs in 52 IBD patients and 50 healthy subjects from 10 Chinese provinces.

Microplastics in stools: Significant differences

First observation: the researchers detected MPs in all stool samples. Most were much smaller than 300 µm and shaped in the form of sheets (1 MP in 2) or fibers (1 MP in 3). 

In contrast, MP concentrations differed according to the person’s state of health. The stools of IBD patients contained:

• 50% more MPs (41.8 pieces/gram of dry fecal matter, vs 28.0 in healthy subjects);
• more very small MPs (<50 μm), whereas those of healthy participants contained MPs measuring 50 to 300 μm;
• a different relative abundance of each type of MP in terms of its chemical nature, among the fifteen or so types found. In the stools of healthy participants, the researchers found mainly PET, a plastic typical of water bottles (22.3%), and to a lesser extent polyamides from textiles (8.9%) and polypropylene typical of food packaging (8.7%).

In IBD participants, PET (34.0%) and polyamides (12.4%) were more abundant, followed closely by the type of PVC found in pipes, PVC floors, etc. (10.3%), and ahead of polypropylene (9.5%).

Bottled water and fast food are suspected

So where do these MPs come from? Based on the answers to their questionnaire, the team showed that the concentration of MPs in stools increased twofold when drinking bottled water (vs boiled tap water). This is because bottled water contains 22 times more MPs, in particular PET, than tap water.

Other factors that went hand in hand with a near twofold increase in fecal MP concentration were consumption of fast food (vs homemade food) and exposure to dust at work or in daily life.

Spring goes hand in hand with... sneezing! Itching, tingling, a runny nose, watery eyes... every year, the arrival of spring and high concentrations of pollen bring hay fever back with a bang. Allergic rhinitis—commonly known as hay fever—and its succession of symptoms plague the lives of 40% of the world’s population (sidenote: Cheng L, Chen J, Fu Q, et al. Chinese Society of Allergy Guidelines for Diagnosis and Treatment of Allergic Rhinitis. Allergy Asthma Immunol Res (2018) 10(4):300–53.  Eifan AO, Durham SR. Pathogenesis of Rhinitis. Clin Exp Allergy (2016) 46 (9):1139–51. ) . This complex condition results from a combination of genetic and environmental factors, including an interaction between a respiratory microbiota imbalance and an abnormal and excessive immune system response. But what are the effects of this dysbiosis? And which microorganisms are involved?

An unbalanced respiratory microbiota

To find out, a Chinese team compared respiratory microbiota in nasal samples taken from 28 people suffering from acute episodes of seasonal allergic rhinitis with those of 15 non-allergic subjects. They found no difference between the two groups in terms of microorganism diversity and abundance, but important disparities in their composition. The bacterial genera Moraxella, Haemophilus, Streptococcus and Flavobacterium, predominant in the respiratory microbiota of healthy individuals, had been replaced in allergic individuals by the genera Klebsiella, Prevotella and Staphylococcus. In total, the researchers identified 10 bacterial genera that were over-represented in the latter.

A disturbed metabolism 

The scientists then applied serum metabolomics, a technique that consists in analyzing the concentration of metabolites (sidenote: Metabolites Small molecules produced during cellular or bacterial metabolism. For example, short-chain fatty acids are metabolites produced by intestinal microbiota during fermentation of non-digestible complex carbohydrates (fibers, etc.). 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.  Lamichhane S, Sen P, Dickens AM, et al An overview of metabolomics data analysis: current tools and future perspectives. Comprehensive analytical chemistry. 2018 ; 82: 387-413 ) in serum. This revealed the presence of 26 different metabolites in allergic people compared to healthy people. They also discovered the presence of 16 altered metabolic pathways, including those of arachidonic acids, already known to produce inflammatory mediators involved in some inflammatory diseases, such as allergic asthma.

Hope for individualized treatments?

The combined results of these two approaches confirm the hypothesis that inflammatory reactions of allergic origin influence the balance of respiratory microbiota. More importantly, they provide important candidate biomarkers of potential use in the diagnosis of allergic rhinitis. The authors therefore suggest continuing this work to refine the identification of different subtypes of allergic rhinitis (seasonal/perennial, intermittent/persistent, mild/moderate/severe), which may pave the way for the development of individualized treatments... and an end to the ordeal of thousands of people.

Unfortunately impedes some attempts to stop smoking: former smokers tend to put on weight. On average an extra 4.5 kg on the scales 6–12 months after the last cigarette. Something that discourages the best intentions. Unless our gut microbiota offers us welcome assistance? In any event, this is what is suggested by a recent study in mice.

^{Sources : OMS (sidenote: https://www.euro.who.int/en/health-topics/disease-prevention/tobacco )}

Smoking cessation: a microbiota that carries weight

As in humans, mice exposed regularly to cigarette smoke tend to gain weight after stopping smoking. After a long series of experiments, the researchers seem to have identified the mechanism potentially in play. Some compounds in tobacco (nicotine?) are thought to be able to reach the digestive system of “smoker” mice after traveling in the blood. They are then thought to modify the composition of the gut microbiota. And in fact, it is enough to transplant the microbiota of smoker mice into non-smoker mice to make them gain weight. Something that designates this microbiota as being partially responsible for the kilos gained.

The mechanisms involved elucidated?

But in practice, how is this possible? It would appear that smoking disrupts the delicate balance between the molecules that promote weight gain and others that restrict it. In smokers, the molecule that promotes weight gain is thought to be produced in greater quantities, whilst the molecule that blocks it becomes increasingly scarce. So why don't they get fat? Because the mechanism is gradual, allowing the body time to adjust by associating every cigarette lit to the necessity to eat less. Except that on stopping smoking, this appetite-suppressant effect of the tobacco disappears immediately, while the imbalance in the microbiota that encourages weight gain lasts much longer. Direct consequence: the scales go into panic mode!

Supporting ex-smokers

said Prof. Evan Elinav who led the research team. While waiting to find out how to repair the microbiota of ex-smokers (diet? microbial therapy, postbiotics?) in order to limit weight gain after quitting smoking, this study makes a “weighty” argument for never smoking your first cigarette, or exposing those around you to passive smoking: protecting the equilibrium of the microbiota.

Fish, coral reefs, shellfish and marine bacteria are not the only casualties of microplastics derived from the degradation of plastic bags. Microplastics are now everywhere: in the air we breathe, in the water we drink, and in the food we eat. No-one can escape them, as shown by a research team who found them in 100% of the stools of patients with IBD and also in those of healthy individuals.

CIBD: stools full of microplastics 

From homo erectus... to homo plasticus! Although we have all unwittingly become consumers of microplastics, it seems that we are not all in the same boat. So, depending on the health of our intestines, our stools do not contain the same number, size or type of plastic particles. This study showed that in people with Inflammatory Bowel Diseases (or IBD) such as Crohn's disease or ulcerative colitis, these microplastics were:

• more numerous (around 42 pieces/gram of dry fecal matter vs. 28 in healthy subjects),
• generally smaller (<50 μm),
• and of different origin, with PET (a plastic typically used in bottles of water), polyamide (derived particularly from synthetic textiles) or PVC (pipes, plastic flooring) being more abundant.

The team also noticed that the greater the quantities of microplastics present in the stools of IBD patients, the more severe was the disease. For all that, this does not necessarily mean that microplastics are responsible for IBD. Other explanations are possible. For example, the disease could cause greater retention of microplastics in the intestines, to such an extent that they are found in greater quantities in the stools. The researchers are still working to determine which is the consequence of the other, microplastics or IBD.

Our diet in the firing line

As for knowing where these tiny pieces of plastic come from, the team points to three sources:

• the consumption of bottled water, which goes hand in hand with a doubling of the quantity of plastic in the stools. This is not surprising, if you consider that bottled water contains 22 times more microplastics (especially PET) than tap water. 
• the consumption of fast food, doubtless due to the plastic packaging;
• and exposure to dust, whether at work or elsewhere in life.

Another reason, if it was needed, to prefer home cooking and inert containers (glass jars): not only is it good for the planet, but good for our bodies too.

An additional 4.5 kg in the 6–12 months following smoking cessation, indeed more than 10kg in one year in 13% of ex-smokers: weight gain represents a major obstacle to giving up cigarettes. A team of researchers used a mouse model to assess the potential role of the gut microbiota in this weight gain.

Tobacco, dysbiosis and weight gain

First observation: rodents regularly exposed to cigarette smoke stayed in shape, even with a high-fat, high-sugar diet. On the other hand, as in humans, smoking cessation led to weight gain, unless the mice were given broad-spectrum antibiotics that depleted their microbiota. In question? Compounds linked to tobacco, such as nicotine, appear to penetrate the digestive system of “smoker” mice, causing long-term changes (after cessation) in the bacterial composition of the gut microbiota. With into the bargain, a metabolism better able to extract energy from foods (fewer calories in their feces).

Transfer of the microbiota of “smoker” or “ex-smoker” mice confirms the role of the gut microbiota: the recipient mice (axenic (sidenote: Germ-free mice mice that have no microbes at all, raised in sterile conditions. ) and never exposed to smoke) gradually gained weight, unless they had previously been given antibiotics (markedly lower weight gain).

Two metabolites at issue

There remained the task of determining which metabolites were involved. Two molecules with opposite effects were isolated from the thousands of bioactive compounds whose levels varied at the time of cessation:

• dimethylglycine (DMG), manufactured by the intestine and liver from dietary choline, which increases weight gain; 
• acetylglycine (ACG) which has the opposite effect. 

Whereas the two antagonistic molecules allowed the “non-smoker” mice to stay in shape, smoking gradually disrupted this equilibrium (increased DMG production and less ACG production). According to the authors, an “anorexic reaction”, leading to reduced food intake is thought to be set up, to avoid calorie overload. The problem: with smoking cessation, this appetite-suppressant effect disappears whilst the obesogenic dysbiosis and the accumulated metabolites are thought to be slow to reverse. Hence the weight gain.

“The diagnosis of endometriosis starts by talking to the patient” 

Dr. Erick Petit

Do we know when endometriosis dates back to?

Erick Petit : Endometriosis has a long and sinuous—if not tumultuous—history. Even though the symptoms have been described for 4,000 years, it was not until the end of the 19th century that it was recognized as an organic disease. Unbelievably, that means it was left undiagnosed for almost 4,000 years. The first clinical description of endometriosis dates back to 1855 BC, concerning an Egyptian woman. The disease was next listed in the Greek body of clinical literature around the year 500 BC.
That was when the symptoms were clearly catalogued and the association was made with menstruation. The disease was subsequently considered to be a condition of the feminine psyche and was consigned to limbo until the Renaissance. Hysterikos being Greek for “uterus,” the physicians of the time had a field day with this so-called illness that they believed had been entirely made up by what they referred to as “hysterical” women. The pain, however, was very real... 

For centuries, women were imprisoned in the belief that pain was inevitable. They were committed to specially created institutions and marginalized. It was only in the 19th century, thanks to the work of Carl von Rokitansky, a Bohemian pathologist working in Vienna, that endometriosis was histologically confirmed for the first time in 1860.¹

Why is the diagnosis of endometriosis so long and complicated? 

E. P. : The gold standard test is still the endovaginal ultrasound (or an MRI for young girls who have never had sexual intercourse, although this technique is less sensitive and less specific), but I remain convinced that medical imaging does not tell us the whole story. The scans must be compared with the clinical data and the patient should be listened to carefully. That is why, in the RESENDO (sidenote: https://www.resendo.fr/ ) network, we use a clinical questionnaire that contains specific questions and gives a better picture of the pain experienced. In nine out of ten cases, the diagnosis of endometriosis is confirmed. We believe that, first and foremost, listening to the patient and having a real conversation is the basis of the diagnosis. Time constraints mean that nobody can spend even 15 minutes talking with a patient anymore. 

Yet asking patients the right questions is exactly how we can establish a reliable diagnosis and treat women who have in some cases been left undiagnosed for a whole decade!² Not enough large-scale epidemiological studies have been conducted to date, but there are tangible signs suggesting that prevalence has been on the rise over recent years. It is commonly said that one in ten women suffers from endometriosis. It is in fact more likely to be one in seven, or even one in five, women of reproductive age.² 

Does a typical profile exist for women affected by endometriosis? What are the consequences?

E. P. : It is a complex pathology involving many factors. So there is no typical profile. I would say that there are as many forms as there are patients. There is no correlation between the anatomical and clinical findings for this disease. Certain women can have very severe endometriosis anatomically speaking, without experiencing too much pain. Conversely, others with only mild endometriosis may suffer from debilitating symptoms. This illness is the number one cause of hypofertility,² which is the second biggest consequence of endometriosis after pain. We have in fact observed a correlation between the extent of the lesions and fertility. But this is not necessarily linked to pain. 

What are the early signs?

E. P. : The disease appears at menarche. This is why a young girl should be carefully observed at this time. Is the level of pain intense? Does she remain bedridden during menses? Non-attendance at school is also a good indication. Early menarche (before the age of 11) and having a mother or sister who also suffers from endometriosis are risk factors. To avoid leaving the condition undiagnosed and starting treatment too late, I have been campaigning for years to raise awareness about endometriosis among girls between the ages of 11 and 13 during their medical appointments. 

In addition, almost 100% of patients suffering from endometriosis are also affected by some form of irritable bowel syndrome. These symptoms in the digestive system can also be a warning sign of the disease, and they are sometimes the only sign. It is therefore crucial to make gastroenterologists more aware of the condition.

How is it treated?

E. P. : The available care is still very inadequate and is mainly based on hormone treatments. The condition requires multidisciplinary care:  

“Certain clinical signs support the hypothesis of a link between the microbiota and endometriosis” 

Vanessa Gouyot

What links between endometriosis and the microbiota do we know of?

Vanessa Gouyot : Although they are increasingly tangible, these links have not yet been confirmed. To date, no scientific study has been able to formally identify the links between endometriosis and the dysbiosis observed within the various microbiota in the human body.³ However, medical practice has highlighted clinical signs⁴ that support the hypothesis.  We therefore now know, from a dietary perspective, that 90% of women affected by endometriosis also suffer from associated digestive disorders (irritable bowel syndrome or poor digestion in particular). At my practice, I see a great many patients who state that they have an imbalanced microbiota, whether it concerns their oral, gastric and/or gut microbiota. One hypothesis seems to be emerging: endometriosis is an inflammatory disease that could be feeding on the “fertile” inflammatory environment in the digestive tract (i.e., the low-grade inflammation in the gut) in order to develop.  

Could the microbiota nevertheless accelerate the diagnosis of the illness?

V. G. : Endometriosis is a chronic inflammatory disease that is complex and often diagnosed late. The pathophysiology of endometriosis has inspired numerous hypotheses but it has not yet been possible to determine which is the most robust. The gut microbiota is a promising line of investigation that is offering new perspectives for research to enhance our understanding of what causes this pathology.⁵ Eventually, what we might consider is not necessarily an assessment of endometriosis via the microbiota, but instead improved diagnosis of digestive inflammation^6,7 through the assessment of the microbiota.  

Endometriosis can only be diagnosed by taking a holistic approach. Today when treating a new patient suffering from endometriosis, we review her whole lifestyle, i.e., her diet, including liquid intake, the quality of the air in her living environment, etc. We even go right back to birth, because we know that the first months of life are pivotal to the formation of the microbiota. When I take their history, I also question my patients about any digestive system disorders existing prior to menarche. Nearly 90% of my patients who suffer from endometriosis were also affected by disorders of the digestive system before menarche, although the statistic should be analyzed objectively. 

My mission is to enable my patients to understand that the digestive tract is a passage which is permanently under assault. This aggression may alter the digestive system and lead to inflammation. This holistic approach should be accompanied by a multidisciplinary component including family doctors, gynecologists, pain specialists and osteopaths, etc. Every effort should be made to avoid leaving patients undiagnosed. I am convinced that a coordinated and multidisciplinary care pathway is the key to early diagnosis and improved treatment for patients with endometriosis.  

Could the microbiota eventually be used in the search for future treatments?

V. G. : Research into the microbiota8,9is making rapid advances.  It is a source of much hope and should, in the medium term, reduce the time to diagnosis for endometriosis patients suffering from disorders of the digestive system. Probiotics currently represent one of the solutions that can be offered to restore the gut flora and reduce inflammation. The problem is the knowledge deficit regarding their use. 

It should be pointed out that taking probiotics alone is not a cure for intestinal hyperpermeability. It can help, but it does not restore the condition of the gut. Certain patients judge that they do not need them, others take them but not regularly, and others have abandoned their course of priobiotics because they felt that the treatment had no effect. Time must be set aside to explain, reassure, and also adjust treatment according to needs. The objective of probiotic therapy is to give our patients the tools to manage their condition, so that they become more attentive to signals from their body. Helping our patients live a normal life with less symptomatic pain is the ultimate victory for us. 

“Diet plays a major role in relieving a painful digestive system associated with endometriosis”

Dr Laetitia Viaud Poubeau

In the case of endometriosis, can nutrition play a role in restoring balance to the microbiota? 

Laetitia Viaud Poubeau : An anti-inflammatory diet, such as a Mediterranean diet for example, can only be beneficial to the gut microbiota for those suffering from endometriosis. 
This type of diet is rich in vegetables, fruits, pulses and whole grains, but also in Omega-3 fatty acids, which are both prebiotics and anti-inflammatory, and it encourages the development of a flora that is eubiotic, rich in bifidobacteria and lactobacilli.^10-12 

Such nutrition optimizes the synthesis of short-chain fatty acids, such as butyrate, which fuels the microbiota and the cells in the gut.^13,14 
 

There are three benefits:  it promotes a balanced gut microbiota, combats intestinal permeability and thereby reduces the underlying low-grade inflammation.

What foods should be excluded from the diets of endometriosis patients?

L. V.-P. : The “Western diet,”^11,15 which is rich in processed foodstuffs, refined sugar, salt, saturated fats (red meat for example) and trans fat (such as pastries),¹⁶ is detrimental to the balance of microbes in the gut. This type of diet causes gut dysbiosis and low-grade inflammation. Drinks like sodas, fruit syrups, fruit juice and strong alcoholic beverages should also be avoided. 

Studies have also demonstrated the benefits of reducing the intake of gluten^11,17,18 which, by activating zonulin (sidenote: Zonulin Protein involved in the regulation of epithelial and endothelial permeability.
It is secreted by the liver, among other organ tissues, and at the surface of enterocytes in the intestinal mucosa, acting on the tight junctions. Fasano A. Intestinal permeability and its regulation by zonulin: diagnostic and therapeutic implications. Clin Gastroenterol Hepatol. 2012 Oct;10(10):1096-100. ) , opens tight junctions and increases systemic inflammation. 

On the other hand, the consumption of dairy products does not seem to put individuals at a higher risk of developing endometriosis.^19,20 The levels of growth hormones that they contain may, however, be conducive to the relative hyperestrogenism of patients suffering from endometriosis.²¹ Additionally, hypersensitivity to milk proteins maintains low-grade inflammation.¹¹

Attention should also be paid to the impact of additives, endocrine disruptors, antibiotics used in the agri-food industry, pesticides and other chemical pollutants. Many of these are found in our foods and affect the balance of our microbiota. 

What are the consequences of a Western-style diet on the gut microbiota? Is this diet responsible for the gastrointestinal disorders observed in endometriosis? 

L. V.-P. : Gut dysbiosis caused by a Western diet is conducive to the development of gram-negative bacilli. These bacteria have a lipopolysaccharide (LPS) molecular pattern that causes metabolic endotoxemia and triggers low-grade inflammation via the activation of the TLR4 receptor.^11,22,23 

This induced dysbiosis results in discomfort in the gut, which can range from constipation to diarrhea. We have also observed bloating, intestinal spasms and flatulence that can be odorous to varying degrees, which all add to the discomfort of patients suffering from endometriosis. 

In this case, a diet excluding FODMAPs (Fermentable Oligo- Di- Monosaccharides and Polyols) or a digestive-sparing diet can be introduced during the initial phase of balancing patients’ dietary habits in order to provide rapid relief.²⁴ The digestive-sparing diet is a model that aims to reduce inflammation and help the gut mucosa to heal. It is based on a set of simple dietary and lifestyle rules: excluding raw vegetables and raw fruits; limiting citrus fruits and cruciferous vegetables; cutting out lactose, gluten, and irritant beverages like coffee, strong alcohol and sodas. It can be followed for 4 to 6 weeks, is less restrictive than the FODMAP-free diet and above all does not alter the gut flora balance like the FODMAP-free diet does, which reduces the endoluminal concentration of bifidobacteria.²⁵ 

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BMI 22.07

Our increasingly urban lifestyles mean that our children have less and less contact with nature in their day-to-day surroundings. This has consequences for the microbiota, with the microbiota of children living in rural areas differing from that of children in urban areas. This could partly explain the higher incidence of autoimmune diseases in city children.

Microbiota: nature always wins

This study of the microbial composition of floor surfaces in daycare centers and of children’s gut, salivary, and skin flora showed that greening these spaces had a positive impact on microbial composition. The children’s gut, oral, and skin microbiota saw long-term shifts towards a new equilibrium involving increases in the relative abundance of beneficial bacteria.

Their microbiota also contained fewer potentially pathogenic microorganisms. 

This is important, since we know that a balanced microbiota contributes to the proper functioning of the immune system.

When biodiversity rhymes with immunity 

These effects observed after two years are very promising and potentially form the basis of a strategy for optimizing urban spaces. Reintroducing biodiversity into urban environments could help reduce the quantity of pathogenic microorganisms in cities, which may in turn lower the incidence of diseases linked to microbiota imbalances. However, further studies are needed to confirm any real impact on the incidence of immune-related diseases. In the meantime, feel free to let your children roll around in the grass!

While otitis is common in childhood, it seems to disproportionately affect the children of indigenous peoples (sidenote: Les enfants aborigènes australiens seraient 5 fois plus à risque d’otite sévère de l’oreille moyenne que les enfants australiens non aborigènes. Gunasekera H, Knox S, Morris P et al. The spectrum and management of otitis media in Australian indigenous and nonindigenous children: a national study. Pediatr Infect Dis J. 2007 Aug;26(8):689-92. ) . The problem is that studies seeking to characterize the microorganisms associated with the disease in these populations have so far looked for known otopathogens (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis) or have mainly used culture techniques that do not reveal the presence of microorganisms that are difficult to cultivate.

Moraxella, a marker of previous otitis?

They found a greater relative abundance of Moraxella in children who had previously had an ear infection. This was so even in children who were free of otitis at the time of the analysis and may be due to a lasting remodeling of the nasal microbiota following a previous case of otitis. Moreover, the abundance of Moraxella in the nasal microbiota was negatively correlated with that of Staphylococcus, a bacterial genus found in greater abundance in children with no infectious nasal discharge. In vitro data suggest that certain species of Staphylococcus may inhibit Moraxella, which could explain the negative correlation observed.

A protective duo of microorganisms?

Furthermore, in the children not suffering from an ear condition at the time of the study, a positive correlation was observed between Dolosigranulum and Corynobacterium. This correlation was also found in children with no infectious nasal discharge, leading the authors to consider this co-colonization as potentially protective against pathogens such as S. pneumoniae and guaranteeing the health of the upper respiratory tract and ear.

Towards the identification of new otopathogens

In contrast, Ornithobacterium was found in greater abundance in children with serous otitis than in the children who had never had otitis. It may thus be a new otopathogen. Its presence was correlated with that of two other bacterial genera, Dichelobacter and Helcococcus, whose effects on nasal and ear health have yet to be defined.