We now know that our diet shapes the composition of our microbiota and, therefore, our health. While many studies have shown good eating habits to have a positive influence on the composition of the gut microbiota, few have explored the relationship between eating habits and salivary microbiota. Since food enters the body via the mouth, does the composition of the salivary microbiota reflect our eating habits and, accordingly, our health status?

Teenagers’ eating behavior under the microscope

To find out, the authors analyzed the salivary microbiota of 842 healthy Finnish teenagers. The teenagers completed a questionnaire aimed at determining their eating habits and were classified according to whether they avoided fruits and vegetables (no FV diet) (42.9%), had healthy meals (45.5%) or junk food (11.6%) and regularly had breakfast (83.1%) and dinner (82.4%).

Show me your salivary microbiota and I will tell you how you eat

Surprisingly, the teenagers’ salivary microbiota remained similar both in terms of diversity and composition whatever their food preferences (no FV diet, healthy meals, or junk food). On the contrary, the regularity of meals did influence diversity. Teenagers with a regular diet had greater microbial diversity than those who skipped meals. Consequently, “irregular eaters” are likely to show reduced diversity, with a diverse microbiota generally considered beneficial to health.

Increase in bacterial content associated with poor eating habits?

The study also showed an abundance of certain bacteria in the saliva of teenagers with a no FV diet and of those skipping meals. The presence of these bacteria in the saliva has previously been associated with oral disease and poor oral hygiene. The authors believe that meal regularity is more important to the composition of the salivary microbiota than diet, and that some salivary bacteria may serve as an indicator of poor eating habits.

Intestinal flora is built up progressively starting at birth. Various elements influence its composition, in particular the nature of the milk the newborn consumes. Breastfed babies have different microbial flora than that of bottle-fed babies. Although breast milk is still recommended by specialists, infant formulas that are enriched with prebiotics and probiotics have particularly favorable nutritional qualities for the intestinal microbiota ecosystem.

Dietary practices shape the composition of microbiota

In adulthood, the qualitative and quantitative composition of microbiota remains reasonably stable. However, it is still affected by the diversity and the nature of our dietary practices: both a lack of food and the latter’s composition can rapidly change the biodiversity of the bacteria. Macronutrients like polysaccharides (sugars), fats, and proteins consumed by the host are partially broken down by intestinal microbiota. Certain dietary fibers, specifically soluble fibers like inulin (found in artichokes and endives in particular) are prebiotics, which stimulate the growth of good bacteria in intestinal flora. As a result, they contribute directly to the stability and good health of the microbiota.

Therefore, it is very probable that changes in dietary habits, if they are long-lasting, play a role in health, opening the door to new treatment possibilities via nutrition.

The Biocodex Microbiota Institute is dedicated to education about human Microbiota for General Public and Healthcare Professionals, it doesn't give any medical advice.

We recommend you to consult a healthcare professional to answer your questions and demands.

What is a prebiotic?

The first “official” definition of prebiotics was suggested back in 1995. Since then, it has evolved based on breakthroughs in our understanding of the role and inner workings of the human microbiota.^1,2

A potted history

Prebiotics were defined for the first time in 1995 by two scientists, Glenn Gibson and Marcel Roberfoid.³ They described them as “a nondigestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon, and thus improves host health”. This definition underwent various iterations until 2016, when an international panel of experts came to a consensus on “a substrate selectively used by host microorganisms that confers health benefits”.⁴ In layman's terms, prebiotics are substances that target specific microorganisms in our microbiota, the beneficial ones, and “feed” them. In doing so, they improve our health. This means that these substrates (foods) are out-of-bounds to the majority of microorganisms in our microbiota,⁵ especially to bacteria that can make us ill, such as certain species of clostridia and E. coli!⁶

Some things change, some things stay the same: prebiotics today and tomorrow

According to the 1995 definition, only certain compounds from the carbohydrate family would be classed as prebiotics.⁷ The word “substrate”, which has recently been preferred by experts, extends the concept of prebiotics beyond carbohydrates to anything that specifically feeds bacteria in the microbiota and thus improves our health.^8,9 In addition, prebiotics can work in other areas of the body with a microbiota, not just the intestines. They can support the skin, mouth, and vagina.¹⁰ 
Neither the first nor the most recent definition specifies which microorganisms are targeted by prebiotics. Historically, these have been bifidobacteria and lactobacilli, known to be beneficial for our health and also used as probiotics.¹¹ They are still the most commonly tested and used as a target for prebiotics. However, we now know that other microorganisms can metabolize prebiotics and contribute to our good health.¹² Researchers are turning their attention to prebiotics able to stimulate species such as Propionibacterium, Faecalibacterium, Eubacterium, Akkermansia, and Roseburia.^13,14

Requirements for a “prebiotic”

The definition may have been extended,¹⁵ but this doesn’t mean any old product can call itself a prebiotic!

Before a product can be classified as prebiotic, its chemical structure must first be clearly described. Preclinical laboratory studies must then be conducted, followed by clinical trials in humans, to confirm:

• Its resistance to digestive enzymes (e.g., stomach acid and bile) allowing it to reach the target microbiota (e.g., gut microbiota) intact;
• its selectivity and action on the target microorganisms;
• how it affects the microbiota and its measurable health benefits;
• the effective dose with no side effects.^16,17,18

Sources, functions, mechanism of action... Prebiotics

Find out what prebiotics look like, where to find them, and how they target our beneficial microbes.

Time for some chemistry: what are prebiotics? 

Nowadays, most compounds classified as prebiotics belong to the family of complex carbohydrates: oligosaccharides and polysaccharides.^25,26 Oligosaccharides are chains, or polymers, of several simple sugars or monosaccharides (usually between 3 and 10), such as glucose, fructose, and galactose. Polysaccharides contain more than 20;²⁷ However, some of the rarer prebiotics contain only two sugars; these are known as disaccharides.

The main prebiotics are

FOS (including inulin) and GOS are the prebiotics whose effects on the beneficial microbes in our intestinal microbiota and on our health are most scientifically recognized. They are therefore currently the “stars” of the prebiotic world;^32,33 The recommended dose for a prebiotic effect in adults is 5-8 g FOS or GOS per day.³⁴

However, other substances are being tested for their prebiotic potential, such as:

• Other complex carbohydrates (fibers): xylo-oligosaccharides (XOS), isomalto-oligosaccharides (IMO), polydextrose, soybean oligosaccharides (SBOS), beta-glucans, and pectin;
• Starch derivatives, such as polyols: sorbitol, maltitol, etc.;
• Polyunsaturated fatty acids; o Polyphenols: such as cocoa and tea.^35,36,37,38

Where exactly can you find them?

Prebiotics are found naturally in many fruits and vegetables and in breastmilk. They are also added to foods, such as cookies, cereals, drinks, and dairy products, as well as to baby food.⁴¹ Finally, they are available as dietary supplements,⁴² alone or combined with probiotics, vitamins, minerals, or plant extracts, etc.

Natural sources of prebiotics

Many fruits, vegetables, cereals, and other natural foodstuffs contain prebiotics. For example: 

• Artichokes, chicory root, leeks, asparagus (which contain inulin);
• Bananas, garlic, onions, honey, wheat (which contain FOS);
• Soy and oat milk, cashew nuts, lupins, chickpeas, and pistachios (which contain GOS).^43,44

These foods contain small quantities of prebiotics and eating them only occasionally will not have any significant effect on your health.⁴⁵

Our hunter-gatherer ancestors ate lots of foods containing natural prebiotics, consuming up to about 135 g per day. However, this is quite uncommon with our modern Western diets, which usually only provide us with 1-4 g a day in the US, and 3-11 g a day in Europe.⁴⁶

Prebiotics are now manufactured industrially, either isolated from foods rich in prebiotic substances or made synthetically from sugars, such as fructose, lactose, or sucrose.^47,48,49

What are prebiotics for?

Imagine your microbiota like a garden, where prebiotics are the “fertilizer” that help beautiful plants grow taller, but not the pesky weeds! So, the whole body benefits.

Just like fertilizer, prebiotics aren't “essential” for feeding the microbes in our microbiota. But they do stimulate the growth and activity of microorganisms that are beneficial for our health. This means they help rebalance our microbiota, especially by increasing the ratio of beneficial bacteria to pathogenic bacteria, allowing the microbiota to correctly perform its role of digestion, absorption of nutrients, supporting our natural defenses, etc.^50,51

During fermentation, prebiotics also help bacteria to produce other substances that help the body and our health.⁵² For example, they increase the production of lactate and the short-chain fatty acids (SCFAs) acetate, propionate, and butyrate, which act in the intestine and travel around the rest of the body in the bloodstream.⁵³ They are a source of energy for the body and play important roles for our health, such as maintaining the integrity of the intestinal barrier, and regulating the metabolism of sugars and fats.⁵⁴

Finally, these SCFAs lower the pH in our colon (making it more acidic), which also has health benefits, such as better absorption of nutrients, and more effective protection against microbes.^55,56

How can prebiotics improve our health?

Prebiotics are a relatively new field of science, and there are fewer clinical studies on their health effects than for probiotics.⁵⁹ However, results suggest that by supporting the growth and metabolism of beneficial bacteria in the microbiota,⁶⁰ prebiotics contribute to several main essential bodily functions, making it better equipped to combat various situations.⁶¹

Dynamic research for uncovering new benefits

Studies are currently under way into other potential health benefits of prebiotics, mainly involving animal models, with promising initial results. For example, prebiotics may help combat the malignant transformation of cells. In fact, their fermentation products, such as butyrate, could provide protection from colorectal cancer. Some prebiotics could also help improve memory and concentration in the elderly, or even slow down cognitive decline in diseases such as Alzheimer’s. Finally, they could lower triglyceride levels in the blood, which would help improve the health of the cardiovascular system. Although there is mounting evidence as to the benefits of prebiotics, much more scientific work is needed before learned societies can release further recommendations as to their use.^85,86

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Psoriasis is a chronic disease alternating between flares and periods of remission, of variable length and intensity.

Epidermis renewing itself too quickly

In the vast majority of cases, psoriasis presents in the form of red patches covered with white scales, located primarily on the elbows, knees, scalp, and lower back. Although it is neither serious nor contagious, this cutaneous condition is, nevertheless, burdensome and has a serious impact on quality of life.

An impoverished intestinal microbiota

The mechanism for the inflammation that characterizes psoriasis is now known: the epidermis is replaced in 4 to 6 days instead of the normal 3 weeks, leading to an accumulation of dead skin and local inflammation. Conversely, the cause remains unknown. Several genetic and environmental risk factors have been identified, but now we need to understand how they interact. We know that stress, certain medications (beta blockers, anti-hypertensives, interferon alpha, etc.) and certain ENT infections increase the likelihood of flares. The role of the intestinal and cutaneous microbiota has also been highlighted. Indeed, an imbalance has been observed in the composition of the cutaneous microbiota in the psoriatic lesions compared to healthy skin, although the disease is not related to any pathogen in particular. For its part, it seems that the intestinal microbiota controls cutaneous inflammation by altering the immune response. The exact molecular mechanisms remain largely unknown. However, it is suspected that overrepresented pro-inflammatory bacteria cause the inflammation.

No cure

At present, no treatment exists to cure psoriasis.
Treatment is based on the application of corticosteroid-based products and vitamin D3 analogues during flares, combined with hydrating creams. Phototherapy is indicated in extended forms, but its use should be limited. Serious forms benefit from other treatments that should be carefully monitored. Research is currently being carried out to evaluate the impact of probiotics on localized cutaneous inflammation and dysbiosis.

Although they affect the face in 95% of cases, acne lesions can be observed on the back, neck, and the front of the thorax. A quarter of adults are affected, particularly women.

Diverse lesions

Acne is a disease of the hair follicles, combining the hair with a sebum-producing gland. This cutaneous condition is characterized by various kinds of lesions, depending on the stage: blackheads and whiteheads are the first stage of acne, then papules and pustules correspond to the inflammatory stage.

The role of the cutaneous microbiota

Genetics, hormones, hygiene…. There are many causes of acne but they all have one thing in common: the involvement of the bacteria Propionibacterium acnes in its development. This germ, naturally present on the skin, multiplies under the effect of excess sebum and leads to an imbalance in the cutaneous microbiota. The skin reacts to this local dysbiosis, creating inflammation.
It is now well-known that chronic skin diseases are often associated with other problems. This is the case for acne, where there is a serious prevalence of stress, anxiety, and depression associated with functional gastrointestinal disorders in people affected. The current hypothesis singles out altered interactions in the “gut-brain-skin” axis, which may cause local and systemic dysbioses and inflammation.

A tailor-made treatment

Acne treatment depends on its severity and its psychological impact. Topical and/or oral treatments (antibiotics or isotretinoin) associated with good hygiene generally give good results. However, with the emergence of antibiotic resistance, the search for a safe and effective alternative has become necessary. For several years, probiotics (local or oral) have been studied for therapeutic purposes. Some have notably shown the benefits of lactobacilli (Lactobacillus acidophilus and Lactobacillus paracasei) on the cutaneous barrier, skin sensitivity, hydration, and the functions of the epidermis.

The number of people affected by lupus is hard to determine. Its worldwide prevalence is estimated to vary between 10 and 150 cases for every 100,000 inhabitants, of whom the majority are women (85%).

When the immune system attacks its own cells

For reasons that remain unknown, the immune system in people afflicted with lupus produces autoantibodies, which cause inflammatory reactions and lesions that can affect all tissues. A whole range of symptoms results from lupus: fatigue, cutaneous eruptions, joint pain, dry eyes, hair loss, thrombosis, fever, pleurisy, and pericarditis. The disease progresses in flares of variable duration and intensity, which alternate with phases of remission. A diagnosis of lupus is confirmed by blood test, and the extent of the damage is measured with imaging examinations.

Predisposing factors but an unknown cause

Although the causes of lupusremain a mystery, several predisposing factors have been identified: estrogen, a genetic disposition, certain medications, UV rays, stress, and certain viruses (Epstein-Barr virus). Research work has also examined the role of the intestinal microbiota. Indeed, an imbalance (dysbiosis) was observed in lupus patients during the remission phase. The microbiota may even be involved in the production of autoantibodies.

Reduce and space out flares

No medication cures lupus. However, combining several molecules (nonsteroidal anti-inflammatories, antimalarials, corticosteroids, immunosuppressants, and monoclonal antibodies, depending on the severity of the disease) eases flares, limits complications, and lengthens the periods of remission. At the same time, less harsh long-term treatments prevent relapses.

If the role of the microbiota is confirmed, modulating it via diet or probiotics could become a promising therapeutic option.

Around 1% of the adult population suffers from rheumatoid arthritis (RA), with women affected more frequently than men.

An autoimmune disease that progresses in flares

RA is an autoimmune disease that develops in flares that cause persistent inflammation in the joints, primarily in the feet and hands. Swelling, pain, and stiffness of the joints are the primary symptoms. Without medical treatment, RA spreads to new joints and progressively deforms or even destroys them.

A genetic predisposition paired with microbiota imbalance

Although there are genes for RA predisposition, they are not enough to cause the disease. They interact with environmental factors, among which the intestinal and buccal microbiota are increasingly being considered. Indeed, patients present microbial imbalances (dysbioses) very similar to those observed in patients affected by inflammatory bowel diseases and which diminish with treatment.

Probiotics as adjuvant therapy

No current treatment cures RA, but there are means of slowing its progression and relieving symptoms: pain medications, control therapy (immunosuppressors or biopharmaceuticals), rehabilitation (physical therapy, ergotherapy, balneotherapy, etc.). Probiotics have recently been used as supplemental therapy, which is considered a promising approach.

Diet, sedentism, and microbiota to blame

In 2012, coronary artery disease caused 7.4 million deaths according to the WHO. It is most often a complication of atherosclerosis. It is the progressive depositing of fats on the walls of the coronary arteries--the arteries that supply blood to the heart muscle. These deposits gradually form an atheromatous plaque, which narrows the diameter of the arteries and reduces blood flow. Atherosclerosis is a result of various factors, including unbalanced diet and a lack of physical activity.

The severity of coronary artery disease depends on the extent of the area deprived of oxygen and the degree of arterial narrowing. There is, therefore, a distinction between angina, myocardial infarction, and sudden death.

Heart and microbiota: a connection?

Coronary artery disease may also be linked to the nature of the microbiota. Certain intestinal bacteria produce TMA (trimethylamine), a substance which, when oxidized in the liver, favors the formation of clots capable of clogging the smallest arteries, such as the coronary arteries that supply the heart.

Revascularizing the heart muscle

In the acute phase (myocardial infarction), the goal of treatment is to unblock the affected artery in order to supply oxygen to the heart muscle. In terms of prevention, the involvement of the intestinal microbiota in the development of coronary artery disease means several therapeutic applications can be envisaged: enrichment of the intestinal flora with non-TMA-producing bacteria via probiotics, the elimination of TMA-producing bacteria, or more radically, the transplantation of a low-TMA-producing fecal microbiota.

Atheromatous plaques, or lipid plaques consisting of cholesterol in particular, are very common; all adults have them. Their thickening can obstruct blood flow, meaning organs are no longer sufficiently supplied, which can lead to pain and changes in heart rate. A local inflammatory reaction can lead to plaque rupture. When plaques become unstable and break off, the results are dramatic: this is the cause of 80% of cases of sudden death. Plaque rupture can also cause myocardial infarction or stroke. Although there seems to be a genetic predisposition, risk factors have been identified: an excess of cholesterol and smoking.

Bacteria and diet in question

Intestinal microbiota may contribute to plaque vulnerability, and therefore to rupture. Some bacteria, as well as the components that they produce, could cause an inflammatory reaction that could eventually lead to atheromatous plaque rupture. Dysbiosis, an imbalance in the composition of the microbiota, might also increase the risk of atherosclerosis in cases of high lipid diets. Bacteria appear to play an important role, because it has even been shown that infections are risk factors for atherosclerosis--gum infections (periodontitis) in particular.

From prevention to probiotics

Prevention is crucial: diet, weight loss, stopping smoking, etc. However, some medications can have a beneficial effect in high-risk people with atherosclerosis. Studies are being conducted to find out if diet or probiotics could reduce the risk of atherosclerosis. The Mediterranean diet is also very beneficial. A new era of therapy could directly target the intestine in order to control the development of atheromatous plaques.

Schizophrenia affects around 0.7% of the world’s population. This psychiatric disease is characterized by delirium and hallucinations, social isolation, and psychological disruption. Onset is most often in adolescence or young adulthood, between ages 15 and 25.

The gut-brain axis involved?

Schizophrenia is very often accompanied by gastrointestinal disorders. In fact the likelihood of experiencing psychiatric diseases such as schizophrenia may be related to chronic intestinal inflammation involving the immune system. The origin may be an imbalance in the intestinal microbiota (intestinal flora) that favors this inflammation. Disruptions in the microbiota have been found in schizophrenic patients, associated with an increase in intestinal permeability (bacteria and other substances that pass into the blood stream through the intestinal wall). These studies seem to indicate a key role played by the gut-brain axis in the development of the disease.

Acting on the composition of the microbiota

With these results, prevention and treatment options emerge: one of them being rebalancing the microbiota to reduce chronic inflammation. Studies have shown that the administration of probiotics can have anti-inflammatory properties by affecting the immune reaction, although to date, no treatment of this type has demonstrated its effectiveness on schizophrenia.