Written By Dr. Henning Sartor
“All disease begins in the gut.” - Hippocrates
A permanently stable state of health of the intestines and thus of the entire organism can only be achieved with optimal support of the acidifying flora with the aim of: pH 6.0 in the stool.
Health begins in the gut – the root system of the human body. According to the Austrian physician and researcher, Dr. F. X. Mayr (1875 – 1965), the chronic digestive damage, caused by toxicity overload, is what makes a person sick, prematurely old, and unattractive.
Scientific research on the role of microbiome and metabolome are increasingly prevalent as also described by Claude Bernhard around 1870 (Claude Bernard, founder of modern physiology, 1813 – 1878)1 and published by F.X.Mayr’s “intestinal autointoxication”, which was further researched about 100 years ago.
The “silent inflammation” has been recognized as the cause of chronic disease for some time already, but lately is increasingly being supplemented by “silent intoxication”. What is new? It is the differentiation in the evaluation of the milieu in the feces. Some of the putrefactive toxins produced intestinally are strongly alkaline. If there is also a lack of lactic acid and short-chain fatty acids (SCFA) in the intestinal lumen, the result is a stool pH of well over 7. This is chronically common and detectable in most so-called “civilized” worlds. Permanent adjustment of the stool pH to 6.0 is an essential goal of the UPGRADERS™ method.
After cleaning the intestines - the purpose of UPGRADERS™ method is to stabilize the stool environment to a pH of 6.0. If the pH was higher before, which most commonly occurs, the aim is to lower the pH to more acidity. Only very rarely do we initially have a stool pH lower than 6.0. We see this only with severe diarrhea.
This is only possible if you change your diet to include as wide a variety of fermented foods as possible (especially sauerkraut). The optimal gut health is possible only if bacterial toxins are eliminated and are not forming again. Studies show that even the slightest imbalance in the digestive system significantly limits muscular and neurological performance 9.
What does an optimal balance in the digestive system mean?
Balanced Nutrition = Best Food + Best Digestion
The function of the digestive system has to be restored before better nourishment of the organism can take place. As long as the “digestion” is flawed, the body cannot be adequately nourished.
Best Food is the result of selection, quality, quantity and the cooking method and requires:
- Balance within the macronutrients (carbohydrates, fats, proteins)
- Optimal supply of micronutrients (vital substances incl. biophotons, electrons and enzymes, minerals, trace elements)
- Fiber, herbs, and spices that regulate the intestinal environment
- Lowest possible levels of toxins and inhibitors (heavy metals, pesticides, hormones, antibiotics etc.)
- Optimal preparation of meals with emphasis on preservation of vital substances
- Optimal eating habits (eating slowly at specific times)
One of the main causes of reduced performance of all organs is incorrect digestion (= dyspepsia = maldigestion) 2.
100% balanced nutrition (best food + best digestion) = 0% silent autointoxication
Best Digestion means food eaten slowly, in a relaxed state. Food eaten hastily will lead to incomplete digestion and to the following chain reactions:
- Shift of the microbiome (intestinal flora) in fermentation and/or putrefaction or decay processes (=dyspepsia)
- Toxic metabolites produced in the intestines (dyspepsia toxins) paralyze the intestinal muscles
- Slowed passage of the chyme in the small intestine or the stool in the large intestine
- More time for the production of toxic metabolites
- More time for the reabsorption of water from the stool (stool hardening, constipation)
- Increase in the concentration of toxic metabolites (endogenous toxins) in the colon
- Silent auto-intoxication
- Increased diffusion pressure of the toxins into the enterocytes and the surrounding tissue, blood and lymph
- Damage to the intestinal wall cells 2 Malabsorption, carbohydrate intolerance, leaky gut, immunological food intolerance or allergies
- Increased diffusion pressure of the toxins into the enterocytes and the surrounding tissue, blood and lymph
- Damage to muscles, nervous system 3, immune system, vascular system, skin, eyes etc.
- Activation of the immune system and silent inflammation
- Reduced performance of all mitochondria, cells and organs
Before the “silent inflammation” comes the “silent intoxication” (usually)
Many diet guidelines focus on increased protein and reduced levels of carbohydrates. However, large amounts of protein can only be digested if there are enough digestive enzymes available.
Putrefaction and putrefaction processes in the intestines are known to be caused by incomplete digestion of proteins. Even the smallest deficiencies of enzymes lead to incorrect digestion. The most common cause of such enzyme deficits is the lack of saliva in the swallowed food. The oral saliva does contain relevant amounts of proteases. If protein is not optimally chewed and salivated in the mouth, and if it is not sufficiently digested by the acid in the stomach (note: proton pump inhibitors, PPI), the result is an incomplete enzymatic breakdown of the proteins into amino acids. The number of proteases and peptidases available and produced may not be sufficient to cleave 100% of all flooding proteins. Most of the undigested residual proteins or peptides are then not reabsorbed, but further decomposed by the proteolytic bacteria (proteobacteria, H2S-formers, certain clostridia, etc.) in the intestine 4.
This results in metabolites that have cytotoxic properties 5.
The best known and best researched key player is ammonia.
Ammonia induced mitochondrial dysfunction
Evidence of the formation of ammonia and other putrefactive and decomposing toxins in the intestines came about 90 years ago 9.
These endogenous toxins (particularly putrefactive toxins) have been shown to damage the mitochondria in all cells of the body. Our nerve cells are particularly sensitive to this, as they have about 10 times more mitochondria per cell than most other cells in the body. Current studies show the connection between e.g. ammonia from the intestine and an encephalopathy (brain disease), which usually first manifests itself in the sense of general exhaustion (Niknahad et al. 20176). As the intoxication increases, the reduction (degeneration) of all functions of the central nervous system (CNS) takes place: burnout, forgetfulness, memory loss up to dementia (Bobermin et al. 20177; Mahmoudian Dehkordi S et al. 20198), mood swings up to depression, Parkinson’s disease etc.
End products of intestinal putrefaction are: ammonia, skatole, indole, cresol, phenol, cadaverine, …. All of those substances are dose-dependently toxic and carcinogenic 11.
In this context, “hepatic encephalopathy” has best been scientifically researched. Ammonia plays the major role in its pathogenesis 11, 12.
TMA / TMAO
Another group of substances has been increasingly researched in recent years: TMA / TMAO (trimethylamine / trimethylamine-N-oxide, the substance that gives rotting fish its typical smell). Recent research focuses on cardiovascular risk 13.
However, like ammonia, TMAO is a putrefactive toxin produced in the gut by proteolytic bacteria 14.
This toxin also reduces mitochondrial function 15.
The pH in the stool as a decisive regulator
In the context of Alzheimer’s research, it was noticed that certain bile acids are produced in the intestine and damage the brain after reabsorption 8,17.
In particular, ursodeoxycholic acid (UDCA), “unique secondary bile acids (Bas), such as iso-3-oxo-, allo-, 3-oxoallo-, and isoallo-lithocholic acid (LCA)” are considered to be protective against silent inflammation 21.
Cytotoxic bile acids (e.g., deoxycholic acid, DCA) are produced when stool pH rises above 6.5. The enzymes that decide whether neuroprotective or cytotoxic bile acids are produced are (like almost all enzymes) pH-sensitive.
The higher the pH in the stool, the more cytotoxic and the less neuroprotective bile acids are produced.
The relevance of these findings was recently discussed and confirmed in a Nature publication by Sato et al. from 07/29/2021 on microbiome research on centenarians 21.
Other toxic metabolites from the gut include:
Quinolinic acid (from tryptophan), hippuric acid, HPHPA (3-(3-hydroxyphenyl)-3-hydroxypropionic acid), indole-3-acetic acid, indoxyl sulfate, p-cresol sulfate, phenylacetylglutamine, tryptamine...
These have become detectable and measurable in daily practice with unprecedented precision in special laboratories such as BIOVIS. Only ammonia is so unstable that it breaks down on the way to the laboratory and is not detectable in the stool.
Effect of metabolites on stool pH
On the one hand, all of these metabolites have a more or less strong, molecule-specific influence on the ambient pH. On the other hand, the total pH of the stool is also related to the amount of fermenting and glandular acids (such as gastric and bile acids). Ammonia is the most important base and butyric acid is the most relevant acid. The gastric acid is already neutralized by the bicarbonate of the pancreatic juice in the upper small intestine from a pH of approx. 1.5 to 4.0 to 4.5 and therefore plays a subordinate role for the stool pH. Only in the case of gastric acid weakness (e.g. in atrophic gastritis) does the lack of gastric acid have a double negative effect: as a lack of acid itself and via the lack of denaturation (see below) as a promoter of putrefaction dyspepsia.
Acidifying flora protects against putrefactive toxins
Ilja Iljitsch Metschnikow described Lactobacillus bulgaricus and the connection to longevity, the health span, at the beginning of the 20th century. The lactic acid of the acidifying flora became an anti-aging agent.
Actinobacteria and Proteobacteria compete for food in the gut. They try to poison each other. The Actinobacteria (healthy acidification flora) form e.g. lactate and butyrate in order to prevent the proteobacteria from growing via an acidic environment. The latter needs it alkaline. Conversely, the Proteobacteria produce putrefaction toxins, which act as inhibitors for the acidification flora 19.
Actinobacteria mainly metabolize carbohydrates, simple sugars, oligosaccharides, starch, but also pectins, glucans and fructans - i.e. prebiotic roughage from vegetables, grains and cereals.
If you want to increase the number of Actinobacteria and their metabolic activity, you should refrain from insulinogenic sugars and add prebiotic fiber and promote the acidic environment in the intestine. The acidification flora can also be favorably influenced by milieu-stabilizing probiotics. Note: All UPGRADERS™ supplements are designed to bring the ‘milieu’ back to acid-base balance.
The so-called "cross-feeding" takes place between bifidobacteria and lactobacilli that form D-lactate and the butyrate-formers that further process the D-lactate into short-chain fatty acids.
So if you feed the lactate-formers and also add the dextrorotatory lactic acid via fermented vegetables or their juice in the food, you create ideal conditions for homeostasis in the stomach.
Strong energy-forming and anti-inflammatory abilities have been proven especially for the Faecalibacterium Prausnitzii and the butyrate.
- Butyric acid can protect against chronic inflammatory bowel disease (IBD) and colon cancer.
- Crohn's disease patients are also deficient in Faecalibacterium prausnitzii, a butyrate-forming bacterium that secretes substances that have anti-inflammatory effects on gut cells by blocking NF-κB activation and IL-8 production 20.
At what point is fermentation pathological?
Today, fermentation in the gut as the cause of the disease is only considered pathological if the pH in the stool falls well below 5.5.
The consistency of the stool then usually takes on a liquid consistency and smells very sour. This is a rather rare occurrence today compared to the frequency of slow transit constipation.
The therapeutic consequence here would be to greatly reduce the intake of carbohydrates - especially sugar - but without reducing the resistant starch = complex, cross-linked carbohydrates. Fasting or "ketogenic diet = carbohydrate fasting" then leads to a new flora balance and stops the supply of substrate for the fermentation dyspepsia and thus this itself effectively.
Slow Transit Constipation
Most people in the so-called Western way of life show a "slow transit constipation" with a firm consistency and a stool pH of 7 to 9, rarely even higher, due to the serious lack of dietary fiber. Because this putrefaction weakens the mitochondria of the gut wall, about 100 years ago, F.X. Mayr correctly described the "weak small intestine" as a far underestimated problem of mankind.
According to Bodo Kuklinski, most food intolerances are caused by exactly that: weakened enterocytes. He writes: “Lactose, gluten and fructose intolerance are given as causes of unclear abdominal symptoms. These are consequences of mitochondrial cytopathy with secondary vitamin B12 deficiency 22." (Author's note: ... because B12 in the terminal ileum can only be actively reabsorbed in vital, ATP-filled enterocytes.)
Flashback to the Stone Age
During the longest period of human existence, 10 times more fiber from leaves and roots was eaten than nowadays. This led to the profuse formation of Firmicutes and Actinobacteria. Solid stools with a pH above 6.5 were extremely rare in those times. The normal stool consistency of mankind before the beginning of the agricultural age (10,000 years ago) was that of a cow pat in "normal transit".
The diversity of the flora-bacteria (microbiota) in the intestine has been correlated in many scientific works with the overall health of humans in various respects.
Great diversity in the microbiota is achieved
through great diversity in food.
The types of vegetables, herbs and spices are particularly important here. A meal should contain more than 30 different fragments of it, e.g. all the colors of nature.
With this background knowledge, the recommendation to avoid foods in case of intolerances must be reevaluated. Under no circumstances should the long-term recommendation to avoid eating what you do not tolerate during a certain time lead to a monotonous diet with limited diversity. Food that is combined in a variety of ways and eaten slowly reduces the tendency to react with signs of food intolerance as the vitality of the intestines increases under those circumstances.
Vegetables that have been pre-digested enzymatically (fermented) before being eaten and which, without pasteurization, bring along living fermentation bacteria as well as the ferments (enzymes) and the end products, the acids, form an ideal support for the healthy acid environment. These vegetables are not raw, precisely because they are pre-digested, yet they have not - and should not have- been heated.
As the amount of fermented vegetables eaten per day increases, the pH in the stool decreases. The consistency of the stool becomes softer as the portions increase.
"Sauerkraut is the body's chimney sweep" as the saying goes.
If you talk about sauerkraut, the immediate objection is that there is incompatibility because of the histamine it contains. This objection is obsolete as shown by the following considerations:
Fermented foods naturally contain certain amounts of histamine depending on how ripe they are. Histamine is formed during the enzymatic breakdown of the amino acid histidine, which in turn is a component of most proteins. With a high-protein diet and poor digestion (putrefaction dyspepsia), most people already have high histamine levels.
Ammonia as a putrefactive toxin blocks the diamine oxidase DAO and thus the breakdown of histamine.
Histamine intolerance is a putrefactive disease!
However, this ammonia is removed in a (well-managed) UPGRADERS™ 21-day program and the formation of new ones is prevented.
The less putrefaction, the less histamine intolerance!
Therefore, after an UPGRADERS™ program, the DAO as well as the histamine-degrading methylases work better again. This is the ideal time to stimulate the epigenetics to produce DAO and methylases. If there was not too much putrefaction in the intestines, in most cases this has been regulated down by just avoiding foods containing histamine.
After the UPGRADERS™ 21-day program,
the histamine reduction can normalize.
As with muscle training, the degradation capacity is increased with a (carefully) increasing dose of histamine. Ultimately, such histaminosis is treated curatively. The permanent avoidance of histamine is therefore not a solution to the problem.
After the 21-day UPGRADERS™ program, most people only react initially and only to excessive amounts of sauerkraut. A so-called antihistamine training under 0% dyspepsia conditions is expedient here.
The only exceptions are people with rare, genetically determined DAO polymorphisms or severe IgE allergies. However, the latter still benefit in the long term from a correction of the intestinal balance according to the criteria described here.
Diagnostics of maldigestion
- Manual examination of the abdomen is highly recommended (in a clinical setting) - there should be no resistance palpable, but a normal bowel tone under the abdominal wall.
- No sensitivity to pressure (especially in the area of the ileocaecal transition and the radix mesenterii)
- No congestion in the area of the descending colon and sigmoid colon
- No significant accumulation of gas in the colon and certainly not in the small intestine (SIBO)
- Tongue without furrows, coating and edge impressions
- Skin without acne, eczema and edema
- Posture of the spine without protective reactions (especially the iliopsoas muscle on both sides)
- stool frequency 1-2 per day without pressing
- smooth and soft sausage-shaped or blobs-shape stool (Bristol Stool Scale type 4-5) with rounded ends and a smooth surface. It sinks in water because it has no gaseous impurities and has only a slight characteristic odor. A healthy intestine evacuates the stool cleanly, which is why any noticeable soling of the anal region is an indication of damage to the intestinal tract.
The declared goal of UPGRADERS™ method must therefore meet all of these criteria.
Laboratory technology (selection):
- pH in the stool: 6.0 (± 0.2) is a must!
- Water content 82 to 88%
- Fecal calprotectin <17.9 mg/l
- Fecal alpha 1-antitrypsin <10 mg/dl
- Fecal zonulin <30 ng/ml
- Diversity of the intestinal flora >6
- Ratio Actinobacteria / Proteobacteria >2
- Optimum numbers and function of the acidifying flora, especially the butyrate formers
- Sum of straight-chain fatty acids in the stool > 250 mmol/l with a high proportion of butyrate
According to current research results, the special microbiome and metabolome as well as digestive marker analysis mentioned above is suitable for detecting incorrect digestion.
As already mentioned, some of the putrefactive toxins influence the pH value in the stool in the direction of a pH increase (alkaline). A lack of acidifying flora also increases the pH of the stool.
Therefore, measuring the pH value in the stool is both inexpensive and efficient and therefore very useful for follow-up controls.
The usual litmus paper strip, which is otherwise used for determining the urine pH, is also useful for this purpose.
The optimal pH in the stool is 6.0.
The fastest and most thorough therapy for putrefaction dyspepsia (without consulting a specialized doctor) is the UPGRADERS™ Method.
- Eliminating or avoiding any maldigestion is the primary focus of the UPGRADERS™ Method. Optimal abdominal balance is always a "conditio sine qua non".
- According to the current state of research, the relationship between fermentation and putrefaction in the intestine must be reassessed.
- A permanently stable state of health of the intestines and thus of the entire organism can only be achieved with optimal support of the acidifying flora with the aim of: pH 6.0 in the stool.
- The best possible promotion of the acidifying flora requires fermented foods in an individually appropriate dose and variety.
It is our primary target to reach a stool pH of 6.0 in 21 days with the UPGRADERS™ 21-day Gut Health Kit.
- Claude Bernard, Begründer der modernen Physiologie, 1813-1878 zitiert in „Lecon sur les auto-intoxications dans les maladies“ Charles Bouchard 1887
- Simons CC, Schouten LJ, Weijenberg MP, Goldbohm RA, van den Brandt PA. Bowel movement and constipation frequencies and the risk of colorectal cancer among men in the Netherlands Cohort Study on Diet and Cancer. Am J Epidemiol. 2010 Dec 15;172(12):1404-14. doi: 10.1093/aje/kwq307. Epub 2010 Oct 27. PMID: 20980354.
- Ma N, Tian Y, Wu Y, Ma X. Contributions of the Interaction Between Dietary Protein and Gut Microbiota to Intestinal Health. Curr Protein Pept Sci. 2017;18(8):795-808. doi: 10.2174/1389203718666170216153505. PMID: 28215168.
- Zhou ZL, Jia XB, Sun MF, et al. Neuroprotection of Fasting Mimicking Diet on MPTP-Induced Parkinson's Disease Mice via Gut Microbiota and Metabolites. Neurotherapeutics. 2019;16(3):741-760. doi:10.1007/s13311-019-00719-2
- Hayaishi O. My life with tryptophan--never a dull moment. Protein Sci. 1993 Mar;2(3):472-5. doi: 10.1002/pro.5560020320. PMID: 8453383; PMCID: PMC2142392.
- Niknahad H, Jamshidzadeh A, Heidari R, Zarei M, Ommati MM. Ammonia-induced mitochondrial dysfunction and energy metabolism disturbances in isolated brain and liver mitochondria, and the effect of taurine administration: relevance to hepatic encephalopathy treatment. Clin Exp Hepatol. 2017;3(3):141-151. doi:10.5114/ceh.2017.68833
- Bobermin LD, Souza DO, Gonçalves CA, Quincozes-Santos A. Resveratrol prevents ammonia-induced mitochondrial dysfunction and cellular redox imbalance in C6 astroglial cells. Nutr Neurosci. 2018 May;21(4):276-285. doi: 10.1080/1028415X.2017.1284375. Epub 2017 Feb 6. PMID: 28165879.
- MahmoudianDehkordi S, Arnold M, Nho K, Ahmad S, Jia W, Xie G, Louie G, Kueider-Paisley A, Moseley MA, Thompson JW, St John Williams L, Tenenbaum JD, Blach C, Baillie R, Han X, Bhattacharyya S, Toledo JB, Schafferer S, Klein S, Koal T, Risacher SL, Kling MA, Motsinger-Reif A, Rotroff DM, Jack J, Hankemeier T, Bennett DA, De Jager PL, Trojanowski JQ, Shaw LM, Weiner MW, Doraiswamy PM, van Duijn CM, Saykin AJ, Kastenmüller G, Kaddurah-Daouk R; Alzheimer's Disease Neuroimaging Initiative and the Alzheimer Disease Metabolomics Consortium. Altered bile acid profile associates with cognitive impairment in Alzheimer's disease-An emerging role for gut microbiome. Alzheimers Dement. 2019 Jan;15(1):76-92. doi: 10.1016/j.jalz.2018.07.217. Epub 2018 Oct 15. Erratum in: Alzheimers Dement. 2019 Apr;15(4):604. PMID: 30337151; PMCID: PMC6487485.
Itoh et al., Peak blood ammonia and lactate after submaximal, maximal and
supramaximal exercise in sprinters and long-distance runners.
Eur J Appl Physiol Occup Physiol. 1990;60(4):271-6.
- Büngeler, W.: Die experimentelle Erzeugung von Leukämie und Lymphosarkom durch chronische Indolvergiftung der Maus. Frankfurt. Z. Path. 44 (1933), 202
- González-Regueiro JA, Higuera-de la Tijera MF, Moreno-Alcántar R, Torre A. Pathophysiology of hepatic encephalopathy and future treatment options. Rev Gastroenterol Mex. 2019 Apr-Jun;84(2):195-203. English, Spanish. doi: 10.1016/j.rgmx.2019.02.004. Epub 2019 Apr 20. PMID: 31014748.
- Ninan J, Feldman L. Ammonia Levels and Hepatic Encephalopathy in Patients with Known Chronic Liver Disease. J Hosp Med. 2017 Aug;12(8):659-661. doi: 10.12788/jhm.2794. PMID: 28786433.
Mutch et al., Ammonia metabolism in exercise and fatigue: a review.,
Med Sci Sports Exerc. 1983;15(1):41-50.
- Senthong V et al. Trimethylamine N-Oxide and Mortality Risk in Patients With Peripheral Arety Disease. J Am Heart Assoc. 2016; 5:e004237
- Makrecka-Kuka M, Volska K, Antone U, Vilskersts R, Grinberga S, Bandere D, Liepinsh E, Dambrova M. Trimethylamine N-oxide impairs pyruvate and fatty acid oxidation in cardiac mitochondria. Toxicol Lett. 2017 Feb 5;267:32-38. doi: 10.1016/j.toxlet.2016.12.017. Epub 2016 Dec 31. PMID: 28049038.
- Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2019 15, 76-92DOI: (10.1016/j.jalz.2018.07.217)
- Binienda A, Twardowska A, Makaro A, Salaga M. Dietary Carbohydrates and Lipids in the Pathogenesis of Leaky Gut Syndrome: An Overview. Int J Mol Sci. 2020 Nov 8;21(21):8368. doi: 10.3390/ijms21218368. PMID: 33171587; PMCID: PMC7664638.
Lamichhane S, Sen P, Dickens AM, Orešič M, Bertram HC. Gut metabolome meets microbiome: A methodological perspective to understand the relationship between host and microbe. Methods. 2018 Oct 1;149:3-12. doi: 10.1016/j.ymeth.2018.04.029. Epub 2018 Apr 30.
Harry Sokol et al. „Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients”,
PNAS 2008 105:16731-16736
- Sato, Y., Atarashi, K., Plichta, D.R. et al. Novel bile acid biosynthetic pathways are enriched in the microbiome of centenarians. Nature (2021 July 29th). https://doi.org/10.1038/s41586-021-03832-5
- Dr. sc. med. Bodo Kuklinski. „Mitochondrien.“ iBooks 2015, eISBN E-Book 978-3-89901-928-5