The intestinal tripod is THE keystone of health, the starting point of any nutritional approach. But before you understand the reasons, do you answer yes to many of these questions?
- You suffer from intestinal functional disorders : digestive discomfort, bloating, regular transit disorders (diarrhea, chronic constipation, alternating diarrhea / constipation), colitis, intestinal inflammations?
- You suffer from chronic inflammatory disorders extra-digestive : tendonitis, osteo-articular disorders, chronic muscular pain?
- You have an inflammatory pathology or disorders of the immunity : bronchitis, asthma, otitis, angina, sinusitis or repetitive rhinitis, hay fever, celiac disease, food intolerances, allergies, rheumatoid arthritis, multiple sclerosis, lupus, scleroderma, Crohn’s disease, ulcerative colitis?
- You are athletic and you suffer from digestive disorders with effort and / or rest?
- You suffer from migraines, Meniere’s syndrome, acne, eczema, urticaria, schizophrenia, autism?
Then the following concerns you! For non-followers of scientific explanations, arm yourself (a little) with courage and obstinacy, they really deserve to be read to the end. We are all concerned by the intestinal balance but unfortunately far too little to be aware of the direct effects of it on our health. The rave about the interest of probiotics or the sometimes dogmatic stopping of certain dietary proteins (cow’s milk, gluten) are legion. However, few of them bring a scientific pedagogy to explain the mechanisms. What I will try to do, without any pretension and with all the moderation that such a subject requires.
The essentials to remember
The intestinal balance is based on a “tripod”:
- The intestinal mucosa : representing more than 300m2 of surface, the intestinal mucosa represents a considerable area of exchanges between the external environment and the body. It is the seat of the assimilation of water and nutrients by using specific transporters. Conversely, it ensures the non-passage of pathogens, toxins and dietary proteins into the internal environment . Consisting of intestinal cells, enterocytes, the mucosa is very fragile because of a thickness of about 1/40 th of a millimeter. However, many factors can attack it: insufficient chewing, inadequate nutrition (excess of carbohydrates or dietary proteins), oxidative stress, lack of omega 3 fatty acid intake, taking medication (anti-inflammatories, antibiotics), repeated physical activity (including running associated with dehydration), etc.
The intestinal mucosa is also often called “second brain” because of the presence of some 200 to 600 million neurons and the number of nerve connections between the brain and the intestine.
- The immune system : about 70% of the immune system is derived from the intestine . It is essential for the proper maturation of immune cells, responsible for two complex equilibrium roles: the defense against pathogens and the tolerance of proteins in the body or certain dietary proteins.
- The intestinal flora : composed of more than 100,000 billion bacteria, the intestine hosts 10 times more cells than we have cells in the body. Grouped under the name of intestinal flora, these bacteria play essential roles:
- They limit the implantation of pathogenic agents (viruses, bacteria),
- They contribute to the synthesis of certain vitamins B and K, they participate in the metabolism of cholesterol and bile acids,
- They participate in the regulation of the transit and the digestion of the lactose,
- They participate in the maturation of the immune system by producing immune messengers, the cytokines, necessary for the subtle balance between defense and tolerance.
As soon as one of the elements of the tripod is disturbed, the entire intestinal balance will be altered. Thus, a disturbed intestinal flora or a repeated aggression of the mucosa can cause what is called an ” intestinal hyperpermeability ” “, Causing an abnormal passage of proteins or dietary peptides through the mucosa. Depending on the genetic predisposition and the level of exposure of the body to these antigens, the immune system may react more or less important. Some individuals will tolerate these proteins while others may trigger reactions, either inflammatory or immune type and this very variable. Symptoms may range from localized inflammation of the autoimmune disease. We can for example quotechronic tendinitis, osteo-articular disorders, colitis, intestinal functional disorders, Crohn’s disease, ulcerative colitis, recurrent ENT and bronchial infections (sinusitis, ear infections, bronchitis, etc.), migraine headaches, Meniere, multiple sclerosis, fibromyalgia or rheumatoid arthritis. It is understood that the intestinal hyperpermeability combined with an inappropriate reaction of the immune system is not the only factor that can be the cause of these disorders or diseases. However, their association with functional intestinal disorders (TFI) should be an evocative sign for the health professional specialized in micronutrition.
Certain dietary proteins are particularly involved in this mechanism: they are cow’s milk proteins and gluten present in wheat, rye, barley and oats (and in all derived products). These proteins have the particularity of having a strong antigenic structure, namely that they can generate from the immune system a possible immune and / or inflammatory reaction in a part of the population. It does not mean falling into a dogmatic logic by incriminating milk products based on cow’s milk, or even gluten, all the ills:the exacerbated reaction of these proteins is primarily the result of a set of factors: intestinal inflammation, causing intestinal hyperpermeability in a context of genetic predisposition and / or disturbance of the flora. It is therefore the response to the protein more than the protein that poses a problem. In particular because these proteins were incorporated late in the human diet, while the human genotype was constituted by its current form more than 40 000 years ago. Cow’s milk proteins have been incorporated into the human diet while their nutritional composition is poorly adapted to the human genome,
In practice, if you think you are concerned, the first step will be to approach a health professional micronutrition expert to establish the nutritional program best suited to your situation. The analysis of functional disorders and pathologies will represent the main means of diagnosis, biological tests for antibodies may sometimes be negative despite the existence of hypersensitivity.
In general, the advice will aim to:
- Restore the integrity of the intestinal mucosa:
- Avoid punctually foods that cause intestinal irritation (complete cereal products, legumes, hard-fiber or insufficiently-walled vegetables, cooked fats, etc.) before reintroducing them gradually.
- Take the time to chew well, rebalance the dietary intake of carbohydrates and proteins,
- Hydrate well (1.5 to 2L of water / day),
- Ensure a satisfactory intake of antioxidant nutrients (vegetables, spices, green tea) and omega 3 fatty acids, especially for regular and / or running athletes,
- Use glutamine supplementation and mucosal protective nutrients such as green clay, turmeric, feverfew, antioxidant nutrients and green tea.
- To restore a balance of the intestinal flora thanks to a complementation of quality probiotics: the choice of the bacterial strains, their number, the mode of consumption, the means implemented by the manufacturer to ensure their viability throughout the lifespan of the product and during digestion will be decisive choice criteria.
- Depending on functional disorders and / or existing pathologies, limit or even remove punctures cow milk proteins to replace them with products based on vegetable milk, goat’s milk or ewes. In the most important cases, the eviction of gluten proteins may be justified and will first be accompanied by a micronutrient health professional who can determine the level and duration of eviction.
If you want to know more, enjoy reading!
I. The intestinal ecosystem: everything rests on a tripod
Our digestive balance depends on that of our “tripod” intestinal, consisting of three interdependent pillars: the intestinal mucosa, intestinal flora and intestinal immune system.
1. The intestinal mucosa, 300m2 of exchanges with the external environment
Imagine for a moment that your intestinal mucosa can easily cover a tennis court with its more than 300m2 of surface! Hard to believe ? This is the case. The mucosa represents a fabulous surface of exchanges between the outside world (the light of the intestinal tube) and the internal environment, thanks to the presence of multiple microvilli. These microvilli form a mat of cells, the enterocytes , also called ” brush border ” and covered with mucus forming a film promoting exchanges with bacteria of the intestinal flora. The total exchange area can thus represent up to 600m2 if we consider this brush border. However,this surface is thin and fragile, of the order of 1/40 th of a millimeter, thereby exposing at increased risk of external aggression. We will come back to it.
Some reminders of anatomy: the small intestine weighs about 1.5 kg, measures an average of 6m (4 to 7m) and is broken down into three segments: the duodenum , which starts after the pylorus (the terminal sphincter of the stomach ) and which measures about 25cm. Then appear the jejunum (2.5m) and the ileum (3.5m). The wall of the jejunum is thicker than the ileum and its lumen (the diameter of the intestinal “tube”) is greater. The colon follows the small intestine and is about 1.5 m long, located between the cecum and the rectum: four segments are classically distinguished: ascending colon, transverse colon, descending colon, and sigmoid colon.
The functions of the intestinal mucosa are essential for the good functioning of the organism: it is in fact primarily the main seat of assimilation of nutrients resulting from digestion and exposure to molecules foreign to the body (bacteria, viruses, food peptides, endotoxins, etc.).
at. The intestinal mucosa, second or first brain?
And yes, our gut is a real brain! A true integrative system consisting of 200 to 600 million efferent, afferent neurons and interneurons, the enteric nervous system has an activity independent of the central nervous system although it comes from the neural crest. Enteric sensory neurons have specific properties: they regulate, for example, the tension and elasticity of the intestinal walls, the chemical composition of the contents of the stomach and intestine, and the level of certain hormones in the blood.
Moreover, many ramifications exist between the central nervous system and the enteric nervous system, as well as the latter is the seat of production of many neuromediators: it is also commonly mentioned that when a nerve connection from the brain to the gut, nine return from the intestine to the brain. The links between nerve functions and intestine are thus narrow and more and more studied.
Source: Thesis F. Voinot.
b. The intestinal lining is an organ of digestion and assimilation of nutrients
Once engulfed, the contents of your plate transits to the stomach to form what is called the “food bolus”: the body will start its digestion in contact with saliva and gastric juice. Recall in passing the importance of chewing well to facilitate the fractionation and contact of food with the enzymes present in saliva (amylases): a good digestion begins already in the mouth! The stomach in turn interferes by mixing the bolus and facilitating digestion with its acidic pH, before gradually ejecting some of its contents to the small intestine by contracting. This is called peristalsis. It is then the turn of enzymes from pancreatic juice discharged into the small intestine and intestinal juice to intervene to break down food macronutrients: these are amylases, saccharases, maltases and lactases (to digest the starch and sugars), lipases (for digesting fats) and proteases (for digesting dietary proteins). Once the work of our infantry digestion realized, the intestinal mucosa will be able to assimilate the different families of nutrients:
- Vitamins and minerals , which have not been digested as such but are released from foods digested by enzymes,
- Fatty acids and monoglycerides from the digestion of fat, which will be used for reconstitution by the body of triglycerides once the intestinal barrier crossed,
- Amino acids and peptides , small protein fragments composed of 2 to 3 amino acids and resulting from the digestion of proteins,
- Monosaccharides from carbohydrate digestion: fructose, glucose and galactose.
The body plays Lego all the time: it breaks to build!In more technical terms, it hydrolyzes – under the action of enzymes – macronutrients from food to allow them to cross the intestinal barrier, to be transported in the blood to the target cells and to serve as constituents or fuels for different molecules of the body: phospholipids (basic structure of cell membranes, including neurons), triglycerides (basic structure of lipids stored mainly in adipose tissue), proteins (enzymes, neuromediators, hormones, peptides, proteins muscle, etc.) and glycogen (a form of carbohydrate storage in the liver and muscle). All this is however only possible thanks to the action concerto of thousands of cellular enzymes using vitamins, minerals and trace elements to ensure their functioning. Like our game of lego, it is enough to miss a piece to make the whole structure unstable …
Keep in mind that:
1) We manufacture our own cells and constituents of our organism from the components of the foods we eat, under the aegis of genetic coding . If we push (a bit) the reasoning, we could say that “we are what we eat “ …
2) The integrity of the intestinal mucosa depends on the assimilation of nutrients, therefore the proper functioning of the body. Transporters of the different nutrients are indeed integrated into the cells of the intestinal mucosa. Water is also absorbed at this level.
c. The intestinal mucosa is a barrier organ
The mucosa is indeed the organ “barrier” between the inner environment of the body and the intestinal lumen. As we have just mentioned, enterocytes are ultra-selective: all is well, it does not let pathogens or their toxins, or proteins or antigenic food peptides, or in insufficient quantity to trigger a reaction . If necessary, these foreign molecules expose themselves to the onslaught of the great guardian of the body: the immune system.
2. The immune system: everything starts in the intestine
The intestine is a key organ functioning of the immune system: it is estimated that 70% of the body’s immune cells originate or are hosted by the intestine .
A subtle balance between defense and tolerance
To fully understand the role of the gut in the maturity of immune cells, let’s go back for a few moments to the basics of how the immune system works. It is based primarily on two properties as essential as the other: that of defending ourselves against pathogenic bacteria or viruses, the “no self,” and that of tolerating the body’s proteins, the “self” , or certain dietary peptides considered harmless to the body. Everything is therefore a question of subtle and complex equilibrium: the two systems, whose roles are however opposite, must indeed be the subject of a fine regulation to coexist together. In more detail, the organization has:
- An immune system involving a family of cells, cytotoxic T lymphocytes or killer cells (CD4 and CD8) . This is to simplify the immune system to “cell-mediated”, or TH1.
- Of an immune system involving another family of cells, B cells. This is the “humoral mediated” immune system, or TH2. In case of intrusion of foreign molecules, so-called antigens , B cells are able to produce and secrete antibodies, also called immunoglobulins (Ig).
There are 5 classes of immunoglobulins: IgA, IgG, IgM, IgD and IgE. The mechanism of protection of the body via the production of immunoglobulins involves another family of cells, able to capture the antigens from the environment, including food, to present them to B cells. Presenters of Antigens (CPA) . These APCs then produce immune messengers, the cytokines . Cytokines are the messengers of information to other cells of immunity. Their role is notably to transform neutral lymphocytes (Th0) into Th1 or Th2 type lymphocytes: thus the nature of the cytokines produced is essential.It is indeed it that directs the specific immune response, either towards a cellular immune response (in the case of viruses or cancer cells for example) or of humoral type (in the case of bacterial infections generally). There are many families of cytokines: interleukins (IL), tumor necrosis factors (TNF), interferons (IFN). Do you still follow?
The immune system also has the ability to preserve the memory of antigens already encountered , in order to act more effectively in case of new intrusion. It is also the principle of the vaccine that inoculate antigens previously dispossessed of their pathogenic nature, to allow the body to react powerfully in case of actual infection. Unfortunately, these vaccines are not always devoid of side effects on the immune system, especially before the age of two years or when the adjuvant used is aluminum. But this is another subject …
In certain cases of autoimmune pathologies, a mutation of the genes at the origin of the synthesis of so-called proteins of the HLA class II system“Gives rise to an overexpression of these. It then follows an abnormal uptake of antigens by the diseased cells. The immune system then reacts exacerbated against these cells, thus causing some “self-destruction” of the cells concerned. Indeed, in a physiological situation, APCs are specific cells of the immune system, which allows other cells of immunity to recognize two major points in their intervention: antigens, which characterize non-self, present on the CPA but also the CPA itself, which characterizes the self. In case of genetic predisposition to an autoimmune disease, it may be that the APCs are no longer immune cells, but colon cells, articular cells or Pancreas cells for example.It will then suffice for a psychological or physiological stress, a vaccine for example, to trigger this autoimmune reaction and the disease that characterizes it.
This situation is encountered, for example, in the case of rheumatoid arthritis, multiple sclerosis or lupus, and is often triggered following a stress that causes a high production of cytokines, interferon gamma, acting directly on immunity.
What is the role of the intestine with respect to immunity?
The intestinal immune system is composed of:
- Several families of immune cells : B cells, T lymphocytes (CD4 and CD8), macrophages and plasma cells responsible for the secretion of immunoglobulin type A (IgAs) disseminated throughout the intestinal mucosa. IgAs are also abundant throughout the body’s mucous membranes: they constitute the first defenders against toxins and infectious agents in direct contact with the mucosal environment. An IgA deficiency can therefore be associated with respiratory or digestive tract infections : here we begin to understand the close link between gut and health. The production of IgA is particularly induced at the time of colonization of the intestine by the intestinal flora in the newborn.
- Lymphoid follicles and Peyer’s patches : Peyer ‘s patches contain particular cells, the M cells, interposed between the enterocytes and having a particularly important role in understanding the appearance of immune dysfunction which we will discuss later. They act as antigen presenting cells (APCs).
When the system stops, it’s immune cacophony
Why is it important to understand? Simply because it is this mechanism that determines the balance between defense against infectious agents and tolerance to dietary peptides and proteins in the body.
Imagine that cytokines (immune messengers) direct the immune response of the body to a deficit of the so-called “Th1” pathway: then there is insufficient response to viral infections or to cancerous cell developments. This will lead to an overexpression of the so-called “Th2” pathway, which will predispose to food intolerances and allergies. Conversely, imagine that the immune response of the body is oriented towards an excess of the Th1 pathway: the body then potentially faces chronic inflammatory pathologies such as Cröhn’s disease, ulcerative colitis or rheumatoid arthritis. .
Th2 deficiency may be responsible for vulnerability to mucosal infections, due to a lower production of secretory IgA: intestinal infections, gastric infections, infections in the ENT sphere or bronchial.
Everything is a question of message, so of production of cytokines! Now there exists in the intestine a tribe able to modulate the production of these immune messengers: the intestinal flora …
3. Our intestine is populated with 100,000 trillion probiotics
Our gut is populated with about 100,000 billion bacteria, 10 times more than the number of cells that make up our entire body! These bacteria are grouped under the generic term “intestinal flora” or ” probiotics “.
It consists of several families of microflora:
- the dominant flora , mainly lactobacilli and bifidobacteria. Which reminds you certainly some references to dairy products. And yes, yogurts and fermented products are due to the seeding of milk by these bacteria called “lactic”.
- subdominant flora, composed mainly of E. coli and enterococci.
- the so-called flora or fluctuating flora : as the name suggests, it is made up of passage bacteria from the microbial environment. It is often a reflection of infections.
The proportions between different strains of bacteria may vary from one individual to another, particularly depending on the nature of the bacteria that colonized the sterile gut of the newborn at the time of delivery: more than 1000 different species have been listed. The term “ecosystem” is not overused! When all is well, the different species cohabit in a relatively harmonious way between them. Unfortunately, when a pathogen – such as Candida Albicans – settles in the flora of passage, the latter can then change the immune balance. It sows zizanie in this ecosystem.
In case of pregnancy, it will be particularly important to ensure that the expectant mother has a balanced intestinal flora: indeed, the intestinal flora of the baby who will establish in the first hours will be the flora that will naturally tend to remain in the gut throughout his life. This has led some doctors sensitized to the importance of intestinal flora to limit the sanitation of the environment of childbirth to a bare minimum, with a discharge at the key.
What is the intestinal flora for?
In exchange for lodging and cover, the intestinal flora fulfills many roles essential to our health:
- It provides metabolic and nutritional functions : the intestinal flora is at the origin of the production of short chain fatty acids used as fuel by the colon cells (colonocytes). Similarly, it contributes to the metabolism of cholesterol, bile acids and synthesizes vitamins B and K.
- It participates in the regulation of the intestinal transit by stimulating its motricity and its trophicity.
- It has a barrier effect : the bacteria of the intestinal flora, because of their mere presence, oppose the implantation of pathogenic bacteria for the body: circulate, the place is taken! They are also able to manufacture molecules that help maintain the general balance of the flora, the bacteriocins.
- They modulate the immune system : This is one of the most exciting and complex functions of the intestinal flora. Indeed, the bacteria of the flora produce the famous cytokines that we mentioned earlier: depending on the nature of the bacteria present in the intestinal flora, the nature of the secreted cytokines will be different, and consequently the immune response too . This means that a disturbance of the intestinal flora can lead to an imbalance of the immune response. Who believed it?
Lactose and intestinal flora
Physiologically, the human body has an enzyme capable of digesting lactose in the first years of life. However, this lactase activity gradually decreases and disappears physiologically at the age of 6 if the child stops his milk consumption. He is indeed weaned! The maintenance of milk consumption during life will allow, for a part of the population whose proportions vary according to the origins, to have a residual lactase activity allowing them to consume 0 to 50g of lactose per day, the equivalent of more than one liter of milk at best. Conversely, another part of the population naturally loses this ability to digest lactose, even if it maintains its milk consumption. It is estimated that 80% of the world’s population will have difficulty digesting lactose in varying proportions. In France, the prevalence is of the order of 30 to 50%. This notion also explains why a number of people who initially consume milk and stop eating it for a certain period of time are becoming lactose intolerant simply because stopping is at the origin of the resumption of the process. loss of lactase activity.
Lactose intolerance results in intestinal transit disorders (diarrhea or alternating diarrhea / constipation essentially) and digestive discomfort. This is therefore very different from the concept of milk protein intolerance, which will be discussed later.
The intestinal flora naturally has a lactase activity: the use of a supplementation of quality probiotic bacteria in case of intolerance to lactose can contribute to restore a sufficient lactase activity.
II. The essential role of maintaining the balance of the intestinal tripod on health
1. How the mucosa becomes a colander!
Because of its fineness (as a reminder, 1/40 th of a millimeter thick), the intestinal mucosa is subject to many aggression factors, especially at the level of the enterocyte junction zone assuring in theory its selective impermeability .
at. Tell me how you eat, I’ll tell you what is your flora
Diet is one of the main factors that can modulate the development of one flora compared to the other, and indirectly the integrity of the intestinal mucosa.
Intestinal bacteria feed on peptide and carbohydrate food debris, particularly so-called “prebiotic” fibers , the snacks of “probiotics” . The fermentation flora uses carbohydrates as substrate, it is particularly abundant in the right colon and evolves in a rather acid medium. The flora of putrefaction It feeds on protein waste and is abundant in the left colon, in an alkaline environment. All these bacteria will themselves produce metabolites (waste) from the digestion of these nutrients. The fermentation flora produces mainly short chain fatty acids, including butyrate, a real fuel for colon cells (colonocytes). The flora of putrefaction produces essentially basic metabolites, namely amines with evocative names such as putrescine or cadaverine, causing the characteristic smell of stool. However, beyond their potentially “disturbing” effect for those around them, these amines have especially specificity to attack the tight junctions of intestinal cells, thus promoting inflammation of the mucosa, or even hyperpermeability of the intestine .
So, when you do not take the time to chew enough or consume a family of excess nutrients, undigested carbohydrate and / or protein fragments reach the gut and you then serve as a snack at one of the families of flora, thus favoring their growth to the detriment of the other. In general, high users of animal protein or high protein products will tend to develop flora putrefaction and amines toxic to the mucosa that result. High consumers of fiber and carbohydrates, such as athletes during the pasta-party the day before a test for example, will rather develop a fermentation flora causing bloating, gas and intestinal discomfort.Irritable Bowel Syndrome) and consuming large amounts of short-chain carbohydrate-rich foods, grouped together as FODMAP. It’s about :
- Sorbitol, present in chewing gums and sweets without sugar, some fruits (apple, pear, plum, apricot, nectarine, peach, cherry)
- Fructose, abundant in fruits and honey
- Lactose, milk sugar
- Fructo-oligosaccharides (or fructans), present especially in endive, wheat, rye, artichoke, garlic and onion
- Galacto-oligosaccharides (or GOS) derived from pulses
These foods are usually malabsorbed and thus fermented by the intestinal flora, thus accentuating symptoms such as bloating, gas and intestinal discomfort. Reducing the consumption of these foods, especially those containing fructans or GOS, represents a common nutritional strategy to limit these digestive discomforts.
b. Digestive infections
Certain bacterial infections, in particular with Staphylococci and Candida albicans , can generate important cellular and tissue lesions, thus favoring an intestinal hyperpermeability, or even a release of toxins, at the origin of a development of inflammation and inflammation. overload of the liver.
c. You said antibiotics and anti-inflammatories?
Antibiotics, as their name implies, are “anti” “biotic” drugs, literally “against” “life”. Beyond their effect on the target bacteria at the origin of the infection, they transit mainly through the intestine before being absorbed, killing some bacteria of the intestinal flora. It was also common to advise ultralevide in combination with antibiotics in order to protect or restore the intestinal balance. From now on, and we will come back to this later, taking probiotics, which are constitutive bacteria of the intestinal flora and not dead yeasts, represents an optimal solution not only in healing after the action of the antibiotics, but also and especially as a preventive for support long-term immunity.
The metabolism of anti-inflammatories such as corticosteroids or salicylates also leads to an increase in oxidative stress favoring intestinal hyperpermeability.
Taking non-steroidal anti-inflammatory drugs (NSAIDs) is no less harmful. This family of drugs indeed has the property of reducing the production of prostaglandins, the molecules responsible for the control of inflammation: it follows then a decrease of the defenses of the mucous membrane, a spacing of the enterocytes and a slowing of their renewal. But taking NSAIDs becomes commonplace, especially in the sports world, to cope … with digestive disorders. In wanting to treat the consequences (the pain), one aggravates the origin (the hyperpermeability) … Clearly, it is the vicious circle!
d. Ischemia-reperfusion: Did you say “play sports?” “
Here is an explanation that should delight fans of the least physical effort. When you are at rest, in front of the TV or concentrated on your favorite reading, the total blood volume of your body is distributed so as to irrigate all the tissues such as the brain, the muscles and the organs, in particular the digestive system. When you start a physical activity, this distribution will change in order to strongly prioritize the muscular blood supply in order to provide the oxygen and nutrients necessary for the realization of the effort. The flow can thus be multiplied by 20. This mechanism will unfortunately occur at the expense of the digestive organs, causing what is called ” mesenteric ischemia ” Blood flow can drop to 20% of basal rest, especially in young athletes. When the exercise is performed in high heat, the situation is even worse, the blood being diverted to the skin to promote thermoregulation. The consequences of this ischemia are multiple:
- The capacity for digestion and assimilation is strongly altered, especially as the intensity of effort increases: so this is not the best time to feast around a steak fries!
- Oxygenation of the intestinal cells drops sharply, potentially causing tissue necrosis. This situation is also aggravated in sports generating a mechanical shock wave during the stride (running, triathlon, trail, etc.) compared to sports worn (cycling, swimming for example).
- When stopping the effort, the reperfusion of the digestive organs (within a time varying from a few minutes to a few hours) causes a significant blood flow. This blood flow naturally provides oxygen, thus free radicals themselves at the origin of a major oxidative stress. However, unlike most other cells in the body, the enterocyte adapts very little to this increased exposure to free radicals because of the punctual nature of the effort and its short life span. The intestinal mucosa is completely renewed every three weeks.The repetition of these episodes during regular training leads to increased fragility of the intestinal cells and an alteration of the integrity of the tight junctions, resulting in an intestinal hyperpermeability which is all the more frequent as dehydration with exertion is important.
The intestine is not an organ that adapts to the effort. Regular sports practice, because of its effects on the intestinal blood supply, makes the endurance athlete a population “at risk” of increased intestinal permeability. It should be noted that 50 to 70% of endurance athletes evoke suffering from low or high digestive disorders during the effort … The use of a diet to preserve the integrity of the intestinal mucosa is therefore an essential strategy to optimize health and sports performance. This strategy will include:
- Preserving digestive comfort through appropriate food choices and consumption frequency,
- C open the daily needs of antioxidant nutrients through the consumption of plants and spices,
- Hydrate regularly during training and in the recovery phase.
The vicious circle of inflammation
In general, any situation of intestinal inflammation generates a real vicious circle : we have mentioned several factors that can promote intestinal inflammation: pathology, infections, inadequate feeding or inadequate chewing, taking medication, regular sports, etc. However, the resulting intestinal hyperpermeability is itself a source of inflammation, particularly following the passage of bacterial endotoxins that cause a large production of pro-inflammatory cytokines (IL-1 alpha, TNF alpha). .
According to “Defects in Mucosal Immunity Leading to Crohn’s Disease,” Cobrin GM, Abreu MT, Immunological Reviews, 200n5, Vol 206.
In addition, remember that spontaneous dietary intake is at the origin of a risk of increased deficit of omega 3 polyunsaturated fatty acids, precursors of prostaglandins for anti-inflammatory purposes. To which is added food intake often excessive in arachidonic acid (omega 6) pro-inflammatory protaglandin precursor.
The current general food context therefore predisposes to maintain the chronic inflammatory mechanism. In addition, the onset of inflammation is often generated by emotional or physiological stress, such as infection, shock or major oxidative stress.
e. How does one define the existence of intestinal hyperpermeability?
There are specific biological tests to diagnose intestinal hyperpermeability. They consist in measuring the ratio between two sugars absorbed under controlled conditions: one large, unabsorbed in a physiological situation, undigested by the enzymes and lacking a specific intestinal transporter; the other small, able to cross the brush border of the intestine, possessing a specific carrier and also undigested by enzymes. The lactulose / rhamnose or lactulose / mannitol pairs are usually measured by urinary dosage for 5 to 6 hours. If the ratio is high, the result is either intestinal hyperpermeability or less assimilation of micronutrients by the enterocytes. Logically,
In the case of pathological hyperpermeability, certain dietary proteins (in particular gluten-derived gliadin) can also induce a release of a specific protein, zonulin. Beyond its particular name, it is a protein capable of increasing the permeability between the intestinal cells, thus inducing an abnormally large passage of food proteins or endotoxins.
f. When the food becomes the target of the immune system
In normal situations, residual amounts of foreign peptides pass through the intestinal mucosa, without triggering an immune reaction. This background noise can also be seen through the existence of positive responses to food antigens during blood measurements of antibodies without the person showing signs of hypersensitivity or allergy to this protein. Several factors determine the threshold of tolerance of a food protein beyond which it will trigger an immune reaction:
- genetic predisposition,
- the nature and dose of the antigen present,
- the frequency of ingestion,
- the age of the first contact with the antigen.
Tolerance is allowed thanks to the existence of certain bacteria in the flora, in charge of limiting the action of the immune system vis-à-vis dietary peptides. The absence of these bacteria in the flora could also be the cause of certain food intolerances or pathologies such as Crohn’s disease. When this threshold of tolerance is exceeded, appear hypersensitivities. These are exacerbated immune responses against dietary proteins (for our purposes here) and not against infectious agents. We distinguish :
- Allergies : This results in a production of type E immunoglobulin (IgE), a reference biomarker occurring rapidly, of the order of a few seconds to a few minutes after contact with the antigen.
- Food intolerances : the reaction is later and more discreet than in the case of an allergy. The symptoms are less specific and less important. These are often chronic inflammatory reactions and intestinal hyperpermeability that can not be detected by traditional biomarkers. Only certain immunoglobulins, of IgG type, are identified in the most significant cases. Moreover, if intolerances are real, current tests to identify them from IgG are not considered as always reliable. It would appear that the presence of these IgG is more a reflection of repeated exposure to the proteins studied than a relevant means of diagnosing hypersensitivity. This partly explains the difficulty for a healthcare professional to identify a real hypersensitivity based on the existence of functional disorders without relying on specific biological markers. This is especially so since high IgG markers can be demonstrated despite the absence of functional disorders or clinical signs. Without counting on strong interindividual variabilities.
All this highlights:
- On the one hand the doubts and debates about the relevance of prediction protocols for foods containing suspected food proteins .
- On the other hand, there may be a close link between the intestinal secretory flora of cytokines, the integrity of the intestinal mucosa and the existence of inappropriate immune reactions.
III. Are cow’s milk and gluten proteins good or bad
Intestinal hyperpermeability is therefore responsible for the passage of certain dietary proteins in the body causing an exacerbated immune reaction. This mechanism can be involved in many inflammatory and / or immune diseases:
- Autoimmune diseases resulting from genetic mutation (HLA) : rheumatoid arthritis, multiple sclerosis, lupus, scleroderma
- The so-called “fouling” pathologies :
- cutaneous level: acne, eczema, urticaria
- at the digestive level: colitis, Crohn’s disease, ulcerative colitis
- at the bronchial level: bronchitis, asthma
- at the level of the ENT sphere: otitis, angina, sinusitis, rhinitis
- at the level of the tendons and muscles: tendonitis, chronic muscular pain
- at the cerebral level and the inner ear: migraine headaches, Ménière syndrome, schizophrenia, autism.
- allergies : celiac disease
- food hypersensitivities, diagnosed or not by a positive measurement of IgG : intolerance to gluten or cow’s milk protein mainly.
Why these proteins in particular?
To understand its origin, let’s go back again some 10,000 years ago. I invite you to read this article on the acid-base balance as a reminder: http://www.sante-et-nutrition.com/you-suffer-of-endinites-of-fatigue-or-inflammations- chronic-you-want-to-prevent-occurrence dosteoporose-have you-think-a-lequilibre-acid-base /
at. The history of wheat
Since the beginning of agriculture, cereals have undergone many changes in their genetic structure. They are consecutive to:
- the initial selection: choice for example of non-germinating ears,
- the mass selection: consists in resowing the following year only the grains carried by the most beautiful ears,
- hybridization: species crossing is widely used to obtain more productive plants,
- transplantation outside the original medium (soil + climate) exerts a selective pressure on the plants.
Wheat, the most widely grown cereal in the world, appeared around 10,000 years ago between Mesopotamia and Egypt, before undergoing a strong phylogenetic evolution:
- The ancestor of wheat is Triticum monococcum , also known as small spelled . It has 7 pairs of chromosomes. Its hybridization with wild grass, Aegylops speltoides , also composed of 7 pairs of chromosomes, has mostly given a diploid form and in rare cases a tetraploid form with 14 pairs of chromosomes.
- Many recombinations and mutations were responsible for the appearance of the Triticum dicoccum form followed by Triticum durum , a cultivated hard wheat variety consisting of 14 pairs of chromosomes. It is from this hybridization that kamut was born .
- The form Triticum dococcum was subsequently hybridized with the form Aegylops squarrosa , whose fruit is the ancestor of Triticum Aestivum , also called wheat or wheat, namely the wheat that we currently consume: it is a hexaploid form composed of 21 pairs of chromosomes. We are therefore far from the ancestral form of wheat. Barley and rye have 7 pairs of chromosomes but are also diploid, suggesting that they are from common ancestors with wheat. In a simplified way, wheat is genetically very close to barley, a little less rye, a little less oat. These four cereals have the specificity of containing a common protein:gluten. On the other hand, rice, maize and African cereals (millet, sorghum, fonio) are devoid of it and are genetically far removed from wheat.
One of the main hypotheses mentioned, especially by Professor Jean Seignalet, who can undoubtedly be considered as a visionary on this theme, is that gluten would have suffered (as well as corn according to him) too many genetic modifications so that the digestive enzymes and mucins of a part of the human population can be able to recognize it and digest it completely. Gluten, or more precisely prolamins from which it is derived, is composed of two protein structures, glutenins and glyadines: the latter is the least tolerated fraction because of its complex biochemical structure. To this factor would be added, still according to Professor Seignalet,a new modification of the gluten under the effect of the cooking with high temperature (see the article: http://www.sante-et-nutrition.com/corps-de-maillard-succulents-toxiques/ ).
b. And the milk then?
Let’s go back to the history of our Homo Sapiens. For hundreds of thousands of years, the ancestors of Homo sapiens then Homo sapiens itself, drank only one and only milk and this only during the first years of life: breast milk.
The domestication of dairy species began only 9,000 years ago: cow, goat, sheep, donkey, buffalo, camel, yak, mare, etc. Cow farming, whose milk was used primarily to feed calves, dates back 5,000 years in France. It was not until the nineteenth century that breeding turned towards the selection of dairy cows, before experiencing an explosion in the last fifty years since the Second World War. In 2012, the average French consumed 67 liters of cow’s milk and 24 kilograms of cheese. On the other hand, they bought around 700g / year / inhabitant of goat’s milk products and 300g / year / inhabitant of sheep’s milk products. Cow’s milk cheeses accounted for about 90% of the volumes of cheeses bought by households, those of goat’s milk 6,
However, and this is a good sense, the composition of cow’s milk is far from that of human milk for the simple reason that we are genetically two very different species and that the calf has nutritional needs not comparable to those of man. Beyond the differences in carbohydrate and lipid composition, let’s look at proteins. Women’s milk is lower in caseins, betaloglobulin and IgG than cow’s milk. Conversely, it is richer in alphalactalbumin, lysozyme, lactotransferrin (used for the transport of iron and zinc in the intestine) and secretory IgA, which is to be remembered, lining the intestinal mucosa of the young child and opposes the penetration of bacteria and viruses into the blood.
The bovine milk proteins have a primary structure (this is the linear sequence of amino acids constituting the protein) different from that of the woman’s milk: some proteins would resist at least partially according to Pr Seignalet to digestion by enzymes human and intestinal flora, especially in young children. It would follow a passage of these proteins or macropeptides resulting from their partial digestion through the intestinal mucosa, at the origin of a reaction of the immune system whose mechanisms we have previously developed. The passage of proteins is therefore the consequence of hyperpermeability acquired in adults and innate in young children, or at least consecutive intestinal immaturity.
This mechanism, according to Professor Joyeux, is mainly linked to industrial techniques for the preservation of milk. In fact, historically raw milk was boiled slowly in order to exempt it from health risks. However, this technique also made it possible to break the disulfide bonds existing within milk proteins, in particular in caseins, in order to make the proteins more digestible for human enzymes and thus less prone to immune reactions. Conversely, proteins derived from milk or dairy products produced and preserved using the UHT (Ultra High Temperature) method, whose principle is based on a brief passage of milk at very high temperature, do not see their connections. disulfides thus hydrolysed. They would then retain their allergenic or resistant nature to the enzymes of the human digestive tract. Industrial preservation and processing techniques also make sterilized, skimmed milk, an inert food, devoid of living micro-organisms (pathogens, certainly, but not only) and rid of its physiological proportions in micronutrients.
The advent of infant formula has accompanied the decline in breastfeeding in industrialized societies. Attempts to adapt the compositions of these milks to approximate the composition of breast milk also do not allow to reproduce the molecular or evolutionary differences adapted to the development of the newborn:
- colostrum the first five days of the postpartum,
- transitional milk from the 6th to 15 th days,
- then mature milk of the 16 th day to 15 th months.
In summary, we find that these various changes in the modes of production and consumption of food have led to structural changes in food. We also note that anthropological and archaeological studies have revealed that obesity appeared 9,000 years ago with the organization of livestock and agriculture. The observation of the phenomena that have accompanied the evolution of man and the changes in his diet have the merit of allowing us a simple but crucial observation:If we can deduce only by anthropological, archaeological, ethnological, primatological, etc., what our ancestors used to eat during the Paleolithic period, we are quite capable, according to modern food models, of asserting this. they did not eat!
We can also note that the Paleolithic food model was still practiced by man only 500 generations ago, and that it had been done for 1250 generations of hominids before. For some primitive populations, such as Eskimos and Aborigines, such patterns were still applied 5-7 generations ago. Finally very few ethnic groups, barely half a dozen, still practice them today (South America, Bengal, …). These latter models are likely to have disappeared in less than a generation.
The proteins of gluten and cow’s milk are moreover identified as being able to be at the origin of inflammatory reactions. Given their low molecular weight, these proteins may in fact sometimes not generate an immune reaction as we have mentioned previously, but remote effects on small organs, in particular vascularized by capillaries of small diameter.These proteins have structures, called casomorphine and glutomorphine, very similar to certain components of the body and can disrupt the functions of the tissues because of their interactions with receptors located on the cell membranes: the muscles, the ear are particularly affected. internal or neurons. This represents a possible mechanism for the onset of Meniere’s syndrome, certain migraines, autism or schizophrenia. Some dyes, additives (such as glutamate) and preservatives could have similar effects.
In synthesis, and this is essential, it is not a question of dogmatizing cow’s milk proteins or gluten, let alone the entire population. The possible origin of functional disorders and inflammatory chronic diseases, even autoimmune, is multifactorial and interdependent. Indeed :
1) The immune response to these proteins is the result of an intestinal hyperpermeability and / or a disturbance of the intestinal flora, the details of which we have detailed : inadequate feeding, poor chewing, mode of delivery, intake of antibiotics or nonsteroidal anti-inflammatory drugs, intensive sports practice associated with dehydration, oxidative stress due to lack of antioxidant nutrients, deficiency of omega 3 polyunsaturated fatty acids favoring the perpetuation of inflammation, etc.
Remember also that the liver and small intestine are two closely related organs through what is called the enterohepatic cycle. Any dysfunction of one of them generates an increased solicitation of the second. Thus, a lifestyle that is a source of xenobiotics (pesticides, alcohol, coffee, tobacco, pollutants, medicines, contraceptive pills, etc.) can potentially hinder the proper functioning of this cycle, just like intestinal hyperpermeability. increases hepatic work. A frequent consequence of this disturbance is also a deficiency of tryptophan, the amino acid precursor of serotonin, neuromediator at the origin of appeasement, well-being and sleep preparation.Chronic constipation indeed promotes the synthesis of indican from dietary tryptophan by the bacteria of the intestinal flora. An increased consumption of vitamin B3 by the liver also generates a deviation of tryptophan to synthesize this vitamin. Here again, we can see the interrelationship between diet, the digestive system and health.
2) The immune response to the presence of a protein is very variable from one individual to another. It depends in particular on:
- genetic predisposition,
- the nature and dose of the antigen present,
- the frequency of ingestion,
- the age of the first contact with the antigen.
It is therefore caricatural, even false, to try to incriminate all the evils with proteins of gluten or cow’s milk. One of the experts in pediatric nutrition, Loran Cordain, is particularly concerned about a 40,000-year-old human genotype maladaptation to the ingestion of these proteins in people with an unfavorable phenotype. .
3) Eviction of cow’s milk protein or gluten in people with the mentioned disorders may improve the symptoms. However, if no attempt to restore the intestinal balance is undertaken, the origin of this exacerbated reaction of the immune system or inflammation will not be treated. On the contrary, their subsequent reintroduction may cause an exacerbated reaction against these proteins or against proteins from other foods initially devoid of any antigenic character in the person (soya, egg, corn for example).
4) Cow’s milk proteins have been introduced into the human diet while their composition is significantly different from breast milk. They are also consumed throughout life in a nonphysiological manner, in large quantities, and as a result of industrial processes . The same reasoning can be applied to proteins derived from other animal milks, with the difference that their consumption is spontaneously less important and that their nutritional composition, in particular the nature of the proteins, is different. The levels of hormones and growth factors contained in these milks are moreover adapted to the growth of the animal concerned by the line of the species producing milk, and alone.
5) Gluten proteins, in particular from wheat, have undergone numerous genetic evolutions, much faster than those of man, having resulted in a profound modification of their structure, thus favoring their antigenicity in people with unfavorable phenotype. We do not have any evidence today that ancestral wheat proteins were perfectly digested by enzymes and tolerated by the human body, but the massive consumption of wheat associated with these modifications leads us to the observation that they can actually trigger an inflammatory or immune reaction – verified or not by a measurement of antibodies – in part of the population according to the factors mentioned and in a context of intestinal hyperpermeability. In the same way as for animal milk proteins,
IV. The solutions !
We have seen throughout these theoretical notions how the immune response to certain dietary proteins is individual, multifactorial and interdependent. Any nutritional strategy aimed at reducing or eliminating functional, inflammatory and immune disorders in relation to a disruption of the intestinal tripod therefore needs to be adapted accordingly. Here are, in order of priority, the practical advice to optimize your intestinal comfort and your health.
1) Do you have interest in your gut?
This is the keystone, the starting point of any nutritional approach. If you answer yes to many of these questions:
- You suffer from functional disorders intestinal : digestive discomfort, bloating, transit disorders (diarrhea, chronic constipation, alternating diarrhea / constipation), colitis, intestinal inflammation?
- You suffer from chronic inflammatory disorders extra-digestive : tendonitis, osteo-articular disorders, chronic muscular pain?
- You have an inflammatory pathology or disorders of immunity : rheumatoid arthritis, multiple sclerosis, lupus, scleroderma, Crohn’s disease, ulcerative colitis, bronchitis, asthma, otitis, tonsillitis, sinusitis or rhinitis, Hay fever, diseases celiac, food intolerances, allergies?
- Are you a sportsman and you suffer from digestive disorders with effort and / or rest?
- Do you suffer from migraines, Meniere’s syndrome, schizophrenia, autism, acne, eczema, urticaria?
Then the following concerns you!
2) Take care of your intestinal mucosa
We spoke of the importance of having an intact intestinal mucosa, playing its role as a selective filter by maintaining a selective permeability. In case of hyperpermeability, manifested by the signs mentioned above, use a diet to preserve the integrity of the mucosa:
- In the event of intestinal inflammations, limit for a few days to a few weeks potentially irritating foods : complete grain products, legumes, cooked fats, hard fibers (cabbages, onions, peppers, tomatoes, cucumbers, etc.), insufficiently walled vegetables. Before reintroducing them gradually.
- Limit foods under heavy baking.
- Prefer the consumption of fruits at a distance from meals if you are sensitive at the intestinal level.
- Drink enough : minimum 1.5 to 2L of water a day: water, tea, infusions.
- Choose a diet rich in antioxidants : fresh fruits and vegetables, spices, herbs, green tea.
- Make sure to satisfy your intake of omega 3 fatty acids : http://www.sante-et-nutrition.com/fiche-pratique-nutrition-sportive-les-lipides/
- Take the time to chew your food : “chew your drinks and drink your food”. 20min per meal without devoting to another activity (reading, TV) is a MINIMUM.
- Avoid any excess (“excess” does not mean “suppression”) of foods rich in carbohydrates or in contrast to foods rich in animal protein.
- If necessary, use a nutritional complex to support the restoration of the intestinal mucosa : there are products available on the Glutamine- based market in particular. It is the preferred nutrient of intestinal cells and immune cells. Vegetable extracts can be associated with it: green tea, feverfew, turmeric, green clay, wild garlic, nutrients and vitamins antioxidants, even fibers with prebiotic action (fructo-oligo-saccharides, inulin, galactofructose): attention however to these if you suffer from bloating because of their effect, positive but sometimes uncomfortable, namely the production of gas by the bacteria of the intestinal flora.
3) Balance your intestinal flora
The use of supplementation probiotic bacteria can restore the balance of the intestinal flora punctually. Indeed, the flora settles in the first hours of life following childbirth depending on the nature of the direct environmental flora (anal flora and vaginal mother, delivery environment) and will always tend to return to its own balance, especially at the level of the dominant flora. High delivery (caesarean section) is a risk factor in this sense, as the child’s bowel is not in direct contact with the mother’s flora. The use of supplementation in family atopic sites is in all cases an optimal approach during the last trimester of pregnancy.
The choice of probiotic bacteria is based on:
- the nature of the bacteria present: indeed, some bacteria have capacities to produce immune messengers (cytokines) variable. Depending on the nature of the existing immune or inflammatory disorders, the choice of bacteria may be different.
- the number of bacteria ingested. This is particularly important since it determines the implantation quality of the bacteria in the intestine: according to the products available on the market, the quantities of bacteria present in the capsule can vary from a few hundred million to several tens of billions. Depending on the indications, amounts of 10 to 40 billion seem optimal, in all cases of living bacteria and not dead yeasts (as may be the case with ultralevure). The quality of a probiotic also depends on its ability to maintain optimum viability throughout the life of the product: the choice of medium used in the capsule or tablet, the temperature variations, the industrial process used, the choice of packaging (pillbox or blister), the method of preservation,
- The number of bacteria arriving in the intestine : the bacteria are composed of proteins, their ingestion must be done in the morning 10 to 15 minutes before breakfast, fasting to avoid the action of digestive proteases. In addition, the choice of bacteria by the manufacturer must consider the notion of “gastro-resistance” to ensure optimal passage of the largest number of bacteria through the digestive tract.
The duration of the supplementation may vary from 1 to 3 months depending on the situation. In any case, a cure of 1 month twice a year will maintain the balance of intestinal flora in the long term. Some people also find optimal intestinal comfort through taking every 3 to 4 days long.
Depending on your intestinal sensitivity, also think of regularly eating lacto-fermented products that naturally have probiotic properties : sauerkraut, kefir, sprouted bread, natural leavened bread, etc.
4) Choose your dairy products
We have discussed at length the potential effect of certain dietary proteins on immune and inflammatory reactions. We have also emphasized that the value of their eviction varies from person to person according to their genetic predisposition and symptoms. If you feel concerned, choose milk products (milk, yoghurt, dairy desserts) based on vegetable milk: soy, rice, almond, oatmeal. Depending on the importance of the disorders, the eviction will concern or not all animal dairy products.In general, progressivity in eviction is often the solution to identify tolerated or non-tolerated foods: the maintenance of dairy products (milk, yogurts, cheeses, milk desserts) based on goat’s milk and ewes , will represent a compromise for many.
Cow’s milk protein may be present in many compound foods and not just in milk, yogurts and cheese. We can cite cream desserts, fresh cream and all products containing it, some biscuits, pastries, pastries but also dishes, meats, breaded preparations, spreads, etc. The hunt for the term ” milk proteins ” on the labels can therefore begin! The use of raw milk products may also be an appropriate solution (eg faisselle). In most cases, the maintenance of butter consumption remains possible, this food being primarily composed of milk fat and therefore low in protein.
This choice of eviction can only be made in my opinion in parallel with a strategy to restore the integrity of the intestinal mucosa and the balance of the intestinal flora given the close interrelations between the various elements of the intestinal tripod . In an ad hoc and selective way at first to see the evolution or not of the symptoms motivating the total eviction of milk proteins of bovine origin. A duration of one to three months often makes it possible to evaluate the interest of the continuation of the eviction regime or not.
5) Eviction of gluten: an implicit approach
As with cow’s milk proteins, the elimination of gluten from the diet requires special attention in the choice of food. Indeed, gluten is present … everywhere!
Wanting to remove gluten from its diet today is the obstacle course:
- Soft wheat is therefore used to make bread and flour for the making of biscuits, pastries, pastries, rusks, breakfast cereals, pizza dough, pie and all the multiple derived products that contain it.
- Durum wheat is used to make pasta, semolina and by-products.
- Gluten is present in three other cereals: rye, oats, barley. The mnemonic means to retain them is also SABO (Rye Oat Wheat Barley).
- Gluten is added as a technological aid in many foods: in bread (see below), but also in cold cuts such as ham or salami, in breaded products, fried, sauces, soups industrial, etc. In short, you will understand, in most industrial products or compounds.
A nutritional orientation aimed at reducing or even eliminating gluten from food is therefore aimed at stopping, first and foremost, the consumption of industrial products and learning to read labels well. Gluten is indeed sometimes where we do not expect, especially because of its use for coating food. In short, gluten is OMNIPRESENT.
Moreover, and fortunately, there are many alternatives of cereal products to meet the nutritional needs and maintain a balanced diet source of pleasure and variety: rice, quinoa, millet, buckwheat, soybeans, legumes, potatoes, corn , soy, etc. In the same way, the supermarket shelves with gluten-free products are constantly growing: we can now find many good products such as gluten-free bread (which you can also do yourself with the help of bread), biscuits, buckwheat crackers ( Bread of Flowers ), rice cakes (even if they have a high glycemic index due to extrusion) See the following article:http://www.sante-et-nutrition.com/sucres-lents-sucres-rapides-est-ce-aussi-simple-dans-lassiette-optimiser-son-bien-etre-et-son-poids-grace- a-lindex-glycemic / ), etc. The use of cereals products based on small spelled or even kamut for the least sensitive people, can also represent an alternative to products made from soft wheat or durum wheat.
The level of eviction of gluten will depend primarily on the importance of food intolerance, functional disorders or pathologies suspected to be consecutive intestinal hyperpermeability associated with an exacerbated reaction of the immune system. An optimal approach will be to approach a health professional specialized in Micronutrition to determine the level of evictions, their duration and the nature of the proteins involved.
The e bread and gluten
When you make bread, one of the key principles of its manufacture is precisely the presence of gluten. In fact, when you knead the dough, you moisturize the wheat flour rich in gluten to allow the elastic mesh thus created to trap the bubbles of carbon dioxide produced by the added yeasts. The bread then swells quietly, before being fed to inflate even more under the effect of heat and form a brown crust (full of Maillard compounds!) Ensuring the stability of the bread. Your crumb is then elastic and hydrated, the regular cells. Here is a beautiful bread ready to consume. In order to meet ever-increasing yield constraints, gluten is also added to a number of wheat flours intended for the industrial production of bread. For information,
6) Sports practice and integrity of the intestinal tripod
We have regularly highlighted the effects of regular physical activity on the intestinal tripod. The advice discussed throughout the article is therefore particularly valid if you are an athlete subject to digestive disorders in the effort and / or rest associated with functional or immune disorders. Indeed, just like all performance factors, digestive comfort is prepared daily. The consequences of disturbances of the intestinal flora and / or intestinal hyperpermeability are largely underestimated within sports platoons. Here are the main tips:
- Apply all or some of the previous tips
- Hydrate regularly during the training and in the recovery phase (on average 500ml / hour of effort). Make a habit of drinking in training to adapt the digestive system to receive a liquid during an effort. During the practice, prefer isotonic or hypotonic drinks, taking care to dilute them more in case of strong heat to avoid a too concentrated supply of carbohydrates and other nutrients. Prioritize the liquid intake to the solid after the effort for 30 to 60min in order to preserve the intestinal comfort. The presence of Glutamine and BCAA in exercise drinks and recovery is an important point: indeed, BCAAs are closely related to that of Glutamine. Any increased need for BCAA will result in metabolic deviation of glutamine, to the detriment of intestinal cells and immune cells.
- Beware of coffee consumption before exercise: it stimulates gastric secretion and speeds up transit.
- In case of competition: use a diet that preserves digestive comfort and digestion time (see article: http://www.sante-et-nutrition.com/programme-alimentaire-pour-une-course-dendurance/ ) . Above all, definitely abandon the nutritional strategy to gorse on carbohydrates the days before the race and energy gels or products of effort too concentrated in carbohydrates during the race. These are the main factors causing digestive disorders in the effort.
In conclusion, let us recall how much the balance of the intestinal tripod (flora, mucous membrane, immune system) is essential to the maintenance of an optimal state of health. It is all too often underestimated, especially in cases of chronic inflammatory disorders (colitis, Crohn’s disease, tendinitis, osteo-articular disorders), pathologies of immunity (repetitive infections, allergies, intolerances, autoimmune diseases). ) or functional (fibromyalgia, skin disorders, migraines, Ménière syndrome, etc.). Gold from the health of our gut depends our general health : including our reaction to the ingestion of dietary protein, especially cow’s milk or gluten. Because it is more the reaction to the food than the food itself that is problematic.This reaction is above all multifactorial and individual: dogmatism does not allow to keep a critical and objective mind on the interest of a specific protocol. The nuance is de rigueur, especially in a subject as complex as the immunity and the intestinal ecosystem. We are just beginning to understand some of their mechanisms. Nevertheless, considering the common sense and the evolution of our genetic capital for 40,000 years, it is clear that we are immersed in a plethora of structurally modified food in the space of a few decades: it would be illusory to refute that they can not be responsible for health effects when the genetic terrain lends itself to them or when the physiological stressors multiply.
A ntico A, Pagani M, Vescovi PP, Bonadonna P, Senna G. Food-specific IgG4 lack diagnosis in adult patients with chronic urticaria and other suspected allergy skin symptoms. Int. Arch. Allergy Immunol., 2011, 155 (1), 52-6.
Watelet J. Gastrointestinal disorders. Science & Sports, 2011, 26, 111-115.
Beyer K, Teuber SS. Food allergy diagnoses: scientific and unproven procedures. Curr. Opin. Allergy Clin. Immunol., 2005, 5 (3), 261-6.
Bouchama A, Parhar R & Coll. Endotoxemia and relapse of tumor necrosis factor and interleukin 1 alpha in acute heatstroke. J. Appl. Physiol., 1991, 70 (6), 2640-4.
Bounous G. Acute Necrosis of the intestinal mucosa. Gastroenterol., 1982, 82, 1457-67
Brouns F, Beckers E. Is gut an athletic organ? Sports Med., 1993, 15 (4), 242-57.
M. Deer Microecology intestinal. Encyclical. Med. Chir. Intestinal Stomach, 1991, 9000 B20, 8.
Cloarec D, Gouilloud S & Coll. Lactase deficiency and symptoms of lactose intolerance in a healthy adult population in western France. Gastroenterol. Clin. Biol., 1991, 15: 588-93.
Cordain L, 2001: The Paleo Diet.
Cordain L, 2012: The Paleo Diet for Athletes.
Derebdeby MJ, Valenzuela S. Meniere’s syndrome and allergy. Otolarylog. Clin. North. Amer., 1991, 25: 213-24.
Egger J, Carter CM & Coll. Is migraine a food allergy? A double-blind controlled oligoantigenic diet treatment. Lancet, 1983, 2: 865-9.
Fried AJ, Bonilla FA. Pathogenesis, diagnosis and management of primary antibody deficiency and infections. Clin. Microbiol. Rev., 2009, 22 (3), 396-414.
Beaugerie L and Thiéfain G. Bowel complications related to NSAIDs, Gastroenterol. Clin. Biol., 2004, 28, C62-C72.
Thiéfain G and Beaugerie L. Toxicity of NSAIDs in the small intestine, colon and rectum, Rheumatism Review, 2005, 72, 601-611.
Jackson PG. Intestinal Permeability in patients with eczema and food allergy. Lancet, 1981, 1, 1285-6.
Kajander K, Hatakka K & Coll. A probiotic mixture alleviates symptoms in irritable bowel syndrome patients: a controllet 6-month intervention. Alimentary Pharmcology and Therapeutics, 2005, 22, 5, 387-394.
Karjalainen J, Martin JM, Knip M. and Coll. A bovine albumin peptide has a possible trigger of insulin dependent diabetes mellitus. N.Engl.J.Med., 1992, 327, 302-307.
Lambert, G & Boylan M. Effect of aspirin and ibuprofen on gastrointestinal permeability during exercise. Int. J. Sports Med. 2007, (28).
KM Lammers, Brigidi P & Coll ,. Immunomodulatory effects of probiotics bacteria: Il_1 and IL-10 response inhuman periperal blood mononuclear cells. FEMS Immunol. Med. Microbiol., 2003, 22, 38 (2): 165-72.
Macpherson AJ, Harris NL. Interactions between intestinal commensal bacteria and the imune system. Nat. Rev. Immunol., 2004, 4 (6), 478-85.
Madsen KL, Malfair D & Coll. Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora. Flammable. Bowel Dis., 1999, 5, 262-70.
Madsen K, Cornish A & Coll. Probiotic bacteria murine and human enhancement intestinal epithelial barrier function. Gastroenterology, 2001, 116: 1107-14.
Hammer PR, De Vrese M & Coll. Protection from gastrointestinal diseases with use of probiotics. Am. J. Clin. Nutr., 2001, 73 (Suppl.), 430S-436S.
Matysiak-Budnik T, Mura IC, Arcos-FajardoM et al. Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease. J. Exp. Med., 2008, 205 (1): 143-54.
Moreau MC. Intestinal flora, probiotics, and effects on the intestinal immune response to IgA., Arch. Pediatr., 2000, 7 (Suppl.2).
Moreau MC & al. Influence of intestinal resident microflora on the development and functions of the gut-associated lymphoid tissue. Microb. Ecology Health Dis., 2001, 13.
O’Farrelly C, Marten D & Coll. Association between villous atrophy in rheumatoid arthritis and rheumatoid factor and gliadin-specific IgG. Lancet, 1988, 8, 819-22.
Paganew R & Coll. Intestinal permeability in patients with chronic urticaria-angiodema with and without arthralgia. Anne Allergy, 1991, 66 (2).
Petrof EO, Kojima K & Coll. Probiotics inhibits nuclear factor-kappa B and induce heat shock proteins by colonizing epithelial cells through proteosome inhibition. Gastroenterol. Motil., 2004, 22 (6), 626.
Rehrer NJ, Smets A & Coll. Effect of exercise on portal vein blood flow in man. Med. Sci. Sports Exerc., 2001, 33: 1533-7.
Ring J, Brockow K & Coll. Adverse reactions to foods. J. Chromat. B. Biomed. Sci. Appl., 2001, 25: 3-10.
Nieman DC & Coll. Ibuprofen use, endotoxemia, inflammation and plasma cytokines during ultramarathon competition. Brain, behavior and immunity, 2006, 20, 578-584.
Ryan AJ, Chang RT & Coll, Gastrointestinal permeability following aspirin intake and prolonged running? Med. Sci. Sport Exerc., 1996, 28: 698-705.
Salminen & Coll, Functional food science and gastrointestinal physiology and function. Brit. J. Nutr., 1998, 80.
Sekirov I, Russel SL & Coll. Gut Microbiota in health and disease. Physiol. Rev. 2010, 90: 859-904.
Thaiss CA, Levy M. & al. The interplay between the innate immune system and the microbiota, Curr. Opin. Immunol., 2014, 26, 41-48.
Ubeda C & Pamer EG Antibiotics, Microbiota and Immune Defense, Trends in Immunol., 2012, 33, 459-466.
TM Brands, Cryan JF et al., Gut microbiota modulation and implications for host health: dietary strategies to influence the gut-brain axis. Innovative Food Science and Emerging Technol., 2013.
Salzman NH Microbiota-immune system interaction: an uneasy alliance. Curr. Opin. Microbiol., 2011, 14, 99-105.
Indiro F., Di Mauro A & al, Microbiota in healthy term infant. Early Human Development, 2013, 89S4, S15-S17.
Forsythe P. Gut microbes as modulators of the neuroimmunoendocrine system. PharmaNutrition, 2013, 1, 115-122.
Koboziev I., Reinoso Webb C., et al., Role of the enteric microbiota in intestinal homeostasis and inflammation. Free Radical Biol. & Med., 2014, 68, 122-133.
Bengmark S. Gut microbiota, immune development and function. Pharmacol. Res., 2013, 69, 87-113.
Xu X., Xu P. et al. Gut microbiota, host health and polysaccharides. Biotechnol. Advances, 2013, 31, 318-337.
Belkaid Y., Bouladoux N & Hard TW, Effector and memory T cell responses to commensal bacteria, 2013, 34, 6, 299-306.
Seignalet J 2004. The feeding or 3 e Medicine, 5th edition. Ed. François-Xavier de Guilbert.
Schnyder B, Pichler WJ. Food intolerances and food allergy. Schweiz. Med. Woch., 1999, 19: 928-33.
Tampli CP, Caucheteux C & Coll. Probiotics in inflammatory bowel disease: a critical review. Res. Clin. Gastroenterol. 2003, 17 (5), 805-20.
Viljanen EC, Kuitunem M & Coll. Probiotic effects on faecal inflammatory markers and on faecal IgA in food allergic atopic eczema, dermatitis syndrome infants. Pediatr. Allergy Immunol. 2005, 16, 65-71.
Pando Kelly J. & Hourihane J. Dietary Intervention in Eczema, Paediatrics and Child Health, 2011, 21, 406-410.
Wishmeyer PE, Kahama M & Coll. Glutamine induces heat shock and protects against endotoxin shock in the rat. J. Appl. Physiol., 2001, 90, 2403-10.