Mood disorders are common: 300 million people in the world suffer from depression and 60 million have bipolar disorder.These disorders cause mental distress that can often be severe, which can lead to suicide. They are the #1 cause of professional and social disability in the world.

Inappropriate stress response

Each individual has their own vulnerability to depression or bipolar disorder, which is in part genetic.As a result, during unpleasant life events, some people experience an excessive response, with overly elevated secretion of the stress hormones cortisol and adrenaline. This situation can lead to nervous exhaustion and favor the onset of a depressive state. Recent research has also documented the role of intestinal flora (microbiota) in these inappropriate stress responses. Indeed in animals, microbiota participates in the regulation of emotions through communication between the intestine and the brain. In the case of dysbiosis (disruptions in the composition of the microbiota), this regulation is less effective and favors the onset of mood disorders.

A new avenue for treatment

Beyond classic treatments (antidepressants, mood regulators, psychotherapy, etc.), a new avenue is opening: rebalancing the microbiota to influence mood. A recent study also showed that taking probiotics daily, a combination of lactobacilli and bifidobacteria, improved mood and reduced the level of anxiety in healthy subjects.

Anxiety disorders, which include phobias, generalized anxiety disorder, obsessive-compulsive disorder, and post-traumatic stress, are characterized by both physical symptoms (tremors, palpitations, digestive spasms) and mental symptoms (anxious anticipation, hypervigilance, etc.). Fourteen percent of the European population is affected by this illness.

Microbiota activity as a regulator

The gastrointestinal microbiota plays a role in regulating anxiety symptoms related to stress through the microbiota-gut-brain axis. Recent data from humans in good health confirms hypotheses formulated with mice, suggesting that the microbiota influences mood and anxiety.

Stomach-brain paths of interaction

Intestinal microbiota-brain interactions involve the neurological pathway, through the activation of the vagus nerve and the onset of anxious signs (a knot in the stomach), and the blood, through the transportation of molecules from the intestine to the brain. The relevant molecules have several origins: bacterial molecules able to cross the lining of the brain (meninges), molecules secreted by intestinal cells (neuropeptides), and pro- or anti-inflammatory molecules (cytokines) produced by the intestine’s defense system.

New avenues for treatment

Beyond traditional treatment for anxiety disorders (psychotherapy, phytotherapy, anxiolytics, etc.), connections between the gastrointestinal microbiota and the brain are opening new avenues for treatment, such as probiotics, which aim to change the composition of the microbiota. However, the clinical effectiveness of this approach still remains to be proven.

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ASDs include autism, of course, but also Asperger syndrome, Landau-Kleffner syndrome, and PDD-NOS (pervasive developmental disorder not otherwise specified).

Boys affected 4 times as much as girls

Around the world, autism-spectrum disorders affect around one child in 160,2 and affect boys 4 times as often as girls. In spite of the diversity of the disorders, ASDs have characteristics in common: communication problems, alterations in social relationships, limited interests, and behavioral problems.

Indicative signs to watch for

Certain indicative signs should lead to consultations: a child who is indifferent to the sounds around them, who does not point with their finger, who avoids eye contact, who doesn’t react to separations or reunions, whose motor activities are limited and repetitive, etc. Only a specialist can suggest or eliminate an ASD diagnosis and help you tailor treatment.

Causes still unknown

Although the causes of autism-spectrum disorders remain unknown, researchers have closely studied the causes related to genetic or environmental factors. Clinical studies have, furthermore, shown the existence of dysbioses in autistic children,5 associated with a change in metabolic activity in the intestinal microbiota.

No treatment to date

This discovery leads to the idea that correcting imbalances in the digestive ecosystem could improve behavioral anomalies in ASDs and open new therapeutic perspectives. Clinical studies targeting the biological connections between autism and intestinal microbiota are being evaluated. To date, no medication cures autism-spectrum disorders; treatment tailored to the child’s needs can, however, considerably improve their quality of life.

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Parkinson’s disease affects 1% of people over 65 in France, which represents about 100,000 people. The substantia nigra in the brain, the area that controls movement, loses the neurons that produce dopamine. The result is progressive motor symptoms: slowness in movements, muscle rigidity, and tremors. People who have Parkinson’s also face non-motor problems, like sleep problems, depressive episodes, and incapacitating gastrointestinal problems (constipation, bloating, abdominal pain, nausea).

Age is implicated

The primary risk factor is obviously age. Although genetic predispositions have been proven, no single one is sufficient to explain the disease. Environment is also a factor, with pesticides playing a documented role.

Gut-brain communication

Intestinal microbiota participates in communication between the intestine and the brain. Some researchers have hypothesized that chronic intestinal infection by Helicobacter pylori could be the origin of Parkinson’s disease. However, it hasn’t been determined whether the infection triggers the disease or, on the contrary, the disease promotes the infection.
Dysbiosis, meaning a fault in the composition of microbiota, has been highlighted in patients with Parkinson’s disease. They have fewer “anti-inflammatory” bacteria and more “pro-inflammatory” bacteria than healthy people.

Controlling progression and testing

Treatment focuses on limiting the motor symptoms of the disease (tremors, rigidity, etc.) through the use of dopamine precursors. These treatments don’t prevent the progression of the disease, and complications reappear after 5 to 10 years of treatment. Currently, the primary goal is to detect the disease as early as possible and slow down neural degeneration. Manipulating microbiota is one option currently being studied.

Alzheimer's disease, which affects more than 35 million people around the world, is associated with memory loss, language and comprehension problems, attention and concentration problems, apraxia (loss of dexterity), and, in some cases, agnosia (problems recognizing objects or faces). Added to these cognitive symptoms, which worsen over time, are behavioral symptoms such as anxiety, apathy, irritability, sleep problems, disinhibition, and agitation.

Causes still unknown

Several genetic and environmental risk factors have been identified for the disease: hypertension, hypercholesterolemia, smoking, sedentary lifestyle, unbalanced diet, and lack of cognitive stimulation, among others. Lesions in the brain are also a well-known component of the disease, particularly the accumulation of amyloid beta plaques and neuron degeneration. However, the causes of the disease have yet to be clearly determined.

The hypothesis of intestinal microbiota

Researchers are considering whether the intestinal microbiota is involved in Alzheimer’s disease: certain proteins (amyloid peptides) produced by “negative” bacteria in the intestinal flora may favor the development of the disease. Conversely, “beneficial” bacteria may play a protective role, by slowing the formation of amyloid plaques.

Break the therapeutic deadlock

Intestinal microbiota could represent a new avenue for therapeutic research, as no current curative therapy exists for Alzheimer’s disease. Only a few medications lessen symptoms, and their effectiveness is very limited. Some researchers are, therefore, considering carrying out future work on the disease via the microbiota, through dietary changes or by ingesting probiotics.

Prostatitis affects around 10% of men. Symptoms, like in cystitis in women, include a burning sensation when urinating and the frequent need to urinate. Other symptoms may be present, such as pelvic, perianal, or rectal pain, and fever, which requires emergency treatment.

Acute prostatitis: an infectious origin?

The main bacteria responsible, Escherichia coli or other enterobacteria, come from the intestinal microbiota. Escherichia coli bacteria are implicated in 80% of cases of acute prostatitis. The infection most often starts in the urethra, which is the tube coming from the bladder. Sexually transmitted bacteria, like chlamydia or gonococci, can also cause prostatitis.

Urinary microbiota involved in chronic forms

In the case of chronic prostatitis, the origin is less clear; the bacteria are less frequently isolated. Recent studies suggest that an alteration in the urinary microbiota could play a role in the appearance of chronic prostatitis. In fact, we had long believed that urine was sterile, which is not the case. There is such a thing as the urinary microbiota. Furthermore, there is a difference in the composition of the urinary microbiota between patients with chronic prostatitis and that of healthy men. Modification of the urinary microbiota via antibiotic treatment may be the cause of chronic forms.

Antibiotic treatment

Treatment of acute prostatitis is based on the prescription of antibiotics and sometimes requires hospitalization in the event of serious symptoms. Treating chronic prostatitis remains more complicated. Probiotic options are still at a very preliminary stage.

An estimated 105,000 people have been diagnosed with CF across 94 countries. France was the first country to introduce systematic testing at birth.

Alteration in the CFTR protein involved

Cystic fibrosis is caused by a change in the CFTR protein (Cystic fibrosis transmembrane conductance regulator), resulting from a mutation in its gene. The normal CFTR protein regulates exchanges of water and mineral salts across cell membranes. When it is defective, it leads to an increase in the viscosity of the mucus, causing it to accumulate in the respiratory and digestive tracts. This accumulation provides a foundation for bacterial infections in the respiratory tract and can eventually lead to respiratory failure. On the digestive side, cystic fibrosis leads to pancreatic insufficiency that affects digestion, the absorption of nutrients, growth, and presents with alternating diarrhea and constipation.

Imbalance in the microbiota

An imbalance in the intestinal microbiota may be associated with respiratory symptoms of cystic fibrosis. This dysbiosis, observed before the onset of the first signs, may be aggravated by the disease and accompanying antibiotic treatments. It contributes to undernutrition, growth delays, and, more generally, to digestive and respiratory complications in these patients.

Reducing symptoms

Treatment for these patients is given in specialist centers; its specific goal is to clear out the bronchi using bronchial decongestants and bronchodilators, combined with sessions of respiratory rehabilitation. Every three to four months, preventative antibiotic treatment is prescribed. Digestive problems are treated with a hypercaloric diet, supplemented with pancreatic extracts and vitamins.

In the future, new therapeutic strategies that aim to have an impact on the microbiota during the first weeks of life through nursing or the use of probiotics could delay the onset of respiratory damage, reinforce these patients’ immune systems, and, as a result, reduce the morbidity and mortality associated with cystic fibrosis.

Winter diseases, which are most often viral, sometimes have clinical signs very similar to the flu (Influenza virus), which is why they’re called influenza-like illnesses or flu-like symptoms.

Flu-like symptoms, often confused with flu

Flu-like symptoms include some or all of the following symptoms: fever < 38.5 C, chills, cough, fatigue, muscle ache, sore throat, headaches, runny nose, etc. Only blood tests can confirm infection with the influenza virus.

An overburdened immune system

Intestinal immune defenses protect you from attacks by pathogenic agents like bacteria and viruses. However, in winter, the immune system is attacked more often. We spend more time confined, and rooms are less well-aired. As a result, more circulating microbes are transmitted (exhaled air, coughs, sneezing).

Probiotic therapy being studied

The viral nature of winter respiratory infections immediately excludes the use of antibiotics. Treatment is symptomatic: acetaminophen, together with hydration and rest, is the basis of the medical prescription.
The use of probiotics has also been proven to be effective in clinical studies on winter respiratory diseases. The daily use of probiotics for several months reduced fever, runny nose, and coughing. It also led to a reduction in the prescription of antibiotics and the number of sick days.

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Up to 70% of patients with Crohn’s disease undergo a bowel resection, two-thirds of whom experience a relapse requiring a further operation. The role of the microbiota associated with the intestinal mucosa in the recurrence of Crohn’s disease is well known, but there are currently few data on the luminal environment following bowel resection. A research team carried out a large randomized longitudinal prospective study on 130 patients with Crohn’s disease following surgery with the purpose to investigate the link between the intestinal microbiota and the risk of recurrence.

Enterobacteriaceae and risk of recurrence

An endoscopy was performed 6 months after surgery in two-thirds of the patients, and a colonoscopy at 18 months in all patients, in order to detect recurrence of the disease. Stool samples were taken two weeks before surgery and 6, 12 and 18 months after surgery in order to analyze the intestinal microbiota via sequencing of the 16S rRNA gene. According to the results, abundance of Enterobacteriaceae prior to surgery and 6 months after surgery is associated with an increased risk of recurrence of the disease at 18 months, whereas an increase in bacteria belonging to the Lachnospiraceae family is associated to a reduced risk. The results also showed that while the relative abundance of these bacteria families is important, increased species diversity within a family also contributes to the risk of recurrence.

An environment conducive to relapse

Following surgery, the intestinal environment is altered (exposure to oxygen, change in pH, antibiotics, etc.), leading to a decrease in Lachnospiraceae (obligate anaerobes), some species of which produce butyrate. This decrease is thought to modify the availability and metabolism of butyrate within the colonocytes, leading to a metabolic switch and an increase in oxygen, which, according to the researchers, is responsible for the proliferation of Enterobacteriaceae (facultative anaerobes). Integrating these new data with those on the changes observed in the intestinal mucosa following surgery (sidenote: De Cruz P, Kamm MA, Hamilton AL, et al. Crohn’s disease management after intestinal resection: a randomised trial. The Lancet. 2015;385(9976):1406–1417 )  should provide a full understanding of the disease.

Although Covid-19 primarily affects the lungs, physicians and researchers have quickly focused on the role of the gut microbiota in the disease, particularly since intestinal symptoms (vomiting, nausea, diarrhea) appear to be more common in severe cases, with three meta-analyses involving around 4,000-10,000 patients reporting a prevalence of 10% to 17.6%. The infection triggers an inflammatory bowel reaction, evidenced by high fecal levels of a specific biomarker, calprotectin.

The virus is present in the digestive system

SARS-CoV-2 infects cells mainly by binding to the ACE2 (sidenote: Angiotensin-converting enzyme 2 )  receptor, which is involved in the homeostasis of the renin-angiotensin-aldosterone system, crucial to the pathophysiology of all organs. ACE2 is strongly expressed in lung tissue, hence the vulnerability of this organ, but it is also expressed in the heart, liver, and intestines. The digestive system may therefore be a gateway for the virus via contaminated food. Fecal-oral transmission may follow. Actually, viral RNA is present in the stool of half of Covid-19 patients, even when the virus is absent from the respiratory tract. In addition, the virus appears capable of replicating in the gut.

Potential mechanisms

Several mechanisms may be involved in the gastrointestinal disorders observed:

• Weakening of the intestinal barrier due to local inflammation or virus replication.

• Deregulation of ACE2, whose deficiency increases gut’s susceptibility to inflammation. SARS-CoV-2 reduces the expression of ACE2 in the lungs and is likely to do so in the gut also.

• Alteration in the composition and functions of the microbiota as a result of hypoxia caused by Covid-19.

• Involvement of gut-brain axis. The enteric nervous system may be affected either via direct viral infection or through an immune response (sidenote: For example, inflammatory cytokines ) , intensifying diarrhea and potentially stimulating the vagus nerve to provoke vomiting.

Dysbiosis of the gut microbiota

An ACE2 deficiency has been shown to alter the composition of the intestinal microbiota in mice, and Covid-19 patients develop an intestinal dysbiosis, with a loss of bacterial diversity and abundance. This dysbiosis has significant consequences: the gut microbiota can remotely stimulate the host’s response to respiratory viral infections; conversely, the dysbiosis can worsen the outcome of the disease, with reduced presence of commensal bacteria favoring the over-representation of pathogenic bacteria. Therefore, the role of the gut microbiota in Covid-19 infections remains to be determined, with the microbiota potentially constituting a biomarker of disease severity or offering therapeutic strategies.