Morphology of stomach
You are familiar with the anatomy of stomach and it’s morphological location in the abdomen. It has lower and upper curving, cardiac and pyloric parts, and fundus in the center. You are also aware of its ligaments and links to other body parts, the branch that supplies it with blood and its drainage system. From histological standpoint, it has mucous membranes, muscular part and serosa. Mucous membranes is uneven and cryptographic with secretory and parietal cells that excrete HCI and mucus. Muscle layer is strong with smooth muscles, thus allowing powerful contractions. Serosa covers an entire organ, protecting it from exterior and separating from other organs
Below you can find the basics of physiology as a reminder.
Stomach receives food and its normal capacity is circa 450g.
There is almost no resorption. Exceptions include alcohol (direct resorption) and certain drugs, such as aspirin, ibuprofen etc. Digestion includes moistening, mixing and initiating stage of dissolving large protein structures. Only 10-15% of sugar and fat is being digested. Hence, stomach is important for commencing dissolution of large protein structures. The most important for humans are collagen and casein structures, i.e. animal proteins. Bowels (pancreas) process proteins from vegetables rather than stomach. After stomach processes large protein structures, it releases them to the lower parts of digestive tract.
How does release work?
Tissue hormone named gastrin receives the information on incoming protein, more precisely the cells synthesizing this hormone. These cells are mostly concentrated in pyloric-fundus part of stomach. Gastrin then stimulates production of histamine in the cells of stomach tissue. Parietal cells of stomach’s glandular tissue are thus affected, causing them to produce and excrete HCI. As concentration of HCI is growing, transformation of other glandular enzyme, pepsinogen, into pepsin is stimulated and increased. This transformation (pepsinogen-pepsin activation) takes place when amount of HCI is sufficient, i.e. at the pH level between 2 and 3. It is slower at the pH level 4, while at 5 and up there is no production of pepsin and hence protein structures are not dissolved further. Instead, decomposition process begins. Pepsin begins digestion by decomposing large protein structures that are already mentioned.
As long as there are interconnected reactions in stomach that are described above and HCI concentration is at the necessary level, duodenum prevents food to pass into stomach. This is because stomach operates in alkali environment rather than acidic, as we expect excretion pancreas enzymes. In an acidic environment, HCI decomposes pancreas enzymes and suppresses their excretion.
As pepsin decomposes large protein structures and they decrease in number, the production, excretion and amount of HCI also decreases. In other words, stimulation and excretion of gastrin reduces and the process now goes in the opposite way. Stomach acid decreases, particularly in pyloric part that becomes neutral to mildly alkali. Pyloric part of duodenum registers this change and slowly opens for passage of stomach content. Stomach contracts and gradually displaces its content towards duodenum. Depending on what and when have we taken food, this entire process lasts for 3-4 hours.
It should be noted that the above-said implies that one should not eat often and in large quantities, nor should one add new quantities of food in short time intervals. We should sit and eat, and not intake any food once we are done. By doing so, we disturb the process described above. This is the most common mistake that inevitably leads towards food digestion disorder related to link between stomach and duodenum, thus creating conditions for infection or activation of Helicobacter pylori. Thus, this is a more serious mistake than eating unhealthy. Such mistakes lead towards non-infective gastritis and disorders reflected on lower parts of bowel tract.
Non-processed large protein structures pass from stomach to small intestines that have no mechanisms for their digestion, thus causing them to fully decay once they are in colon. This is compensated for a short amount of time by saprophytic bacteria.
Another important aspect of the process described above is the proper activation of B12 vitamin, however this is not a topic of this text.
Back to stomach and HP.
Helicobacter pylori infection has several theories.
One theory states that Helicobacter pylori is saprophyte living in stomach in an appropriate and controlled environment, mostly in its cardiac part. Its role is to provoke stomach constantly in order to excrete mucus, which in return has shielding effect on its membranes by protecting it from its own HCI. My interpretation is that this may be true; however there are many people who do not have this bacteria in their stomach. Despite this, scientists, that discovered HP and received Nobel Prize for doing so, claim that Helicobacter pylori should always be at least 15% present in stomach since people having it in that amount rarely suffer from cardia cancer (percentage increases with patients that went through HP eradication) and allergic diseases. I am not convinced that one can rely on this, although they claim it is a proven fact. Logical, isn’t it?
Another theory is that HP is not a regular stomach inhabitant, but that we get infected orally. HP then develops once there are conditions in the stomach for its development. This could be the case, but how would one explain frequent Helicobacter pylori re-infections, particularly shortly after thorough treatment and its complete eradication. It is possible that a certain amount manages to survive and redevelops, under condition that there are no other regulatory factors of stomach’s regular physiology. This implies same mistakes, bad habits and inadequate food consumption/diet.
Third theory recently read states that Helicobacter pylori passes gastric barrier and inhabits jejunum (part of small intestine), thus disrupting stomach’s environment and making it alkali. Helicobacter pylori climbs upwards, mostly by regurgitation and inhabits stomach.
There are several other theories that are not proven, such as Helicobacter pylori coming from oral cavity by way of mutation of certain bacteria (i.e. actinomices), or mutation of campylobacter jejuni once it arrives in stomach.
Another interesting theory that peaks my interest despite lacking scientific verification is that candida creates appropriate environment for Helicobacter pylori development and vice versa. It is fact that food implies candida intake, however this is not the only fungus entering the organism in this way.
How does Helicobacter pylori function inside stomach?
Let us now see how does Helicobacter pylori develop and what does it cause. These processes are very complex; however I will make an attempt at simplifying them.
Helicobacter pylori lives in alkaline environment, and due to its built it squeezes into stomach mucous where pH levels are alkaline. It looks like auger, and has long cells on one end that help it propel. They rotate like an auger – by rotating, they rotate an entire body, or cell in this case – thus allowing it to squeeze into mucous. Similar to spermatozoids that has an auxiliary part on its tale that allows it to twiddle the whip but does not allow its head to rotate, Helicobacter pylori has small cilia on its side by which it hooks onto the stomach’s wall. Once it is hooked to the stomach wall’s cryptic cells, its metabolic products begin to destroy these cells, developing inflammatory symptoms. It conducts the destruction of host’s cells. This releases prostaglandins, cytokines, leucine, interleucine and other inflammation products. These products enter the circulation and transfers throughout the organism. As a defensive mechanism, organism reacts with a histamine reaction and we receive the image of strong gastritis (more on this later). Helicobacter pylori then enters the phase of its intensive proliferation. On the other hand, it produces another enzyme called urease, which is ejected in the exterior environment. i.e. lumen of the stomach. This enzyme decomposes nitrogen compounds from food, ie. urea from nitrite and nitrate to ammonia NH3 and carbon dioxide CO2. Hence, now we have high levels of histamine, NH3, CO2 and inflammatory products
What these products do in our body? After resorption, CO2 enters our circulation and finds its path to lungs when we breath it out (this phenomenon is used in diagnosing infectious Helicobacter pylori – so called breath test). CO2 disrupts acid-base blood status. NH3 partly resorbs, additionally disrupts acid-base blood status and metabolizes in our liver. On the side note, urea in liver stems from ammonia and carbon dioxide consequentially leading to excessive levels of urea (uric acid in organism) and acidity of organism. Other parts of NH3 passes further through digestive tract. This part, however, neutralizes HCI by increasing stomach acidity thus creating convenient conditions for Helicobacter pylori proliferation. In such way, Helicobacter pylori creates a convenient environment for its own development.
Initial defensive mechanism of our organism is increased production of HCL due to recognizing its deficit on the one hand, and on the other due to being provoked by high levels of histamine. HCL piles up in lumen, stomach’s central part. We recognize this moment as hyperchlorhydria. This is often when we feel the symptom called heartburn, ie. returning the content once again through esophagus toward oral cavity. This happens because duodenum recognizes excessive levels of HCI and prevents it from passing through. Cardia opens up and content goes back towards esophagus. Irritated by HCI, our organism produces larger quantities of mucus, which only makes more convenient conditions for Helicobacter pylori. Eventually, we enter the GERD syndrome.
Authors remark: Person experiencing these problems starts therapy with h2 blockers, “ranisan” or receives from his/her physician h1 or h2 blockers, inhibits histamine/HCI excretion, thus only enabling HP’s further development. This eventually leads to hyperchlorhydria and issues related to food digestion in stomach.
Gaseous CO2 increases the stomach volume causing the bloated feeling, frequent belching and similar. Gas can eventually cause anatomic movement of stomach enabling easier emptying toward esophagus and worsening GERD symptoms. All that is mentioned leads towards the stomach atony in the final stages, while hiatus hernia may also occur as a consequence. If one adds diet naturally rich with histamine, we may see how the circle closes.
Consequences listed so far are still benign. We are all aware what this infection may turn into – micro ulcer at the beginning, ulcer later on, and eventually carcinoma, lymphoma, and further spreading on other organs. These are proven facts. An entire book can be written on the formation mechanisms of these diseases. In a nutshell, mucous membrane of stomach wall are irritated by HP toxins induced lesions, which is recognized by our defensive mechanism. Our tissue macrophages, neutrophils and other body soldiers know they can not enter stomach lumen because they will be decimated by their own HCI. This is why they come near the center of infection and fire out radicals in an effort to destroy HP. Hence, they sacrifice their own tissue in order to defend from an enemy. Discomposure products are now increasing thus inflaming our anti bodies in an effort to neutralize them. This fierce combat leads to ulcer, unless it is treated properly. On the other hand, pepsin additionally ruins its own tissue because it treats exposed muscle structures in the same way it treats the steak we just ate. Hence, ulcer creation with HP infection does not follow conventional mechanism taught in school: consequence of HCL’s effect on stomach tissue. Further complications are evident. Stomach pain and excessive food consumption are characteristic for the part when lesions occur and tissue destruction begins. Pain temporary disappears when one gets stuffed with food.
Blood test on anti-bodies is unreliable for several reasons. Firstly, it is too late, and secondly, anti-body concentration remains long after infection is over (6-12 weeks) because our organism needs time to calm down. At that time, it is too susceptive by many products of the infection.
In my opinion, the best method for diagnosing HP infection is breath test with unreactive C13 reagent, so that it could be harmlessly repeated several times.
These complex mechanism could not be described in a shorter manner, but I hope that things are clear.
One should not say much about Gastrolact after everything that was said, having in mind that solutions impose themselves. If one is familiar with processes described above, its composition becomes clear and logical. It also becomes clear why treatment with lb. Reuteri does not result in success.
It is crucial to eliminate Helicobacter pylori, while at the same time keeping it alive at appropriate quantities. Gastrolact achieves this regardless of which Helicobacter pylori infection theories is correct since it collects Helicobacter pylori and eliminates it throughout an entire digestive tract, from mouth to anus.
Another essential work performed by Gastrolact is neutralization of histamine gained from food and inflammatory histamine, whose mechanism and metabolism is another different story that is not a topic of this text (according to which we developed our product “DigestFood”).
Thirdly, one should secure that lb. reuteri gets enough traction with Helicobacter pylori by blending enough of it, along with the “carriers” and other ingredients.
Equally important features of Gastrolact include:
- neutralization of HCI,
- development of saprophyte microflora,
- Immunity improvement and reparation of damaged tissue,
- Preventing further Helicobacter pylori proliferation by eliminating its convenient environment,
- Neutralization of NH3 and CO2,
- Allowing quick subjective feeling of improvement and symptom alleviation,
- Removing main symptoms such as weakness, chronic tiredness, depression, anxiety etc. (this is a result of damaged B12 vitamin activation and its resorption inability) by combining B6 vitamin and folic acid until conditions for B12 resorption are re-established.
- All these factors have been taken into consideration while preparing and testing Gastrolact. However, crucial question was how to technologically create a product that would enable regular and even hookup of lb. reuteri that would later in vivo secure the contact and elimination of HP from an entire digestive tract. Our tak also included packaging, dissolubility, tolerable taste, dosage and time of consumption. We believe me managed to achieve all that is listed.
Gastrolact is designed on basic principles of ayurvedic phytotherapy dravja gune and naturopathy, and also on the knowledge of modern science.
Packaging includes 14-doze pouches, dissoluble in 150ml of water. Product has no additives, aromas, emulsifiers and similar supplements.
Heartburn, bloated belly, intestine gases, flatus, diarea, stomach pains, black stool, nausea, vomiting, numbness, overconsumption of food, rosacea, anemia, apathy, anxiety, chronic tiredness, depression, sinusitis, headache and similar symptoms.
It is present across the globe, regardless of nations, continents or race. However, it dominates among Chinese people while Balkan countries also lead the way along with inhabitants of South and North America.
Generally, there is no region where presence is below 50% – at least according to the data I was able to survey.
It is my sincere hope that we managed to point on this growing problem of today’s human race and the ways in which we live today.
Author: Jovan Lemic