Introduction to kefir series as well as highlighting some of the differences between artisanal and industrial or commercial kefir. As with other natural substances effects can be dose dependent, degradation or digestion dependent and change their bio active qualities as a result. Storage can also impact some of the beneficial qualities of kefir.
The major products formed during keﬁr fermentation are lactic acid, CO2 and alcohol in the form of ethanol at 0.48%. Despite being called the ‘champagne of milk’ short fermentation periods and moderate to low sugar content will not produce ‘intoxicating’ keﬁr.
If it gets confusing as to how ‘good’ organisms can cause problems see tolerance below, requires galactose for the ability of the immune system to ‘see’ and respond properly. Edited to remove some of the science speak post recording except where dosage was a factor regarding anti inflammatory or immune stimulation (like many nutritional components kefir plays dual roles). Also see checkpoint blockade toxicity a ‘new’ drug induced IBD colitis. IBD can also be caused by systemic targeting via injections.
H2S is a major intoxicant that can have severe impacts on gut, immune and general health. SIBO can begin at birth.
Food for thought, the fastest way to make someone sick…. intoxicate the blood.
For most when starting I recommend using off the shelf and well tolerated friendly organism combinations to avoid potent reactions so artisanal kefir might not be well tolerated for some due to the number and variety of organisms. Similar to a baby who begins with predominately bifido until their microbiome reaches maturity. If artisanal kefir is too ‘potent’ for you switch to a commercial brand.
I also recommend whole foods for the most part. The ability to affect with a single component as compared to the whole without knowing the essential co-factors is slim. Kefir is an essential part of oral natural immune therapy providing many therapeutic effects one of which is macrophage activation.
As with health as with life there is no such thing as salvation by proxy. When you want either it’s there you just have to find it and work to achieve it. As a caring individual be sure you have not crossed the line toward ‘interference’ or sin when it comes to hoping to ‘save’ someone by preventing them from facing the consequence of their own choices. As hard as it is to watch, you aren’t doing them any favors. They are not an animal, infant or invalid that is not capable of changing their situation via prayer or in any other substantial way. In these instances the offending ‘substance’ merely has to be avoided at all cost and/or the person simply has to reach out to the proper authorities for help. I would not be surprised to learn that the other person is facing the results of injection damage as these are new conditions that have arisen in the past year (neurodegenerative effects that are becoming quite severe). I’ve suggested avoiding the current injections and all injections many times due to knowing all known effects as well as knowing all of the unique known effects of this new environmental initial ‘intoxicant’, the immediate effect on red blood cells (loss of hemoglobin and oxygen destroying ability to mitigate the effects of the intoxicant naturally therefore requiring back up detox mechanisms (this exhausts the immune system dependent upon exposure level), unique bilateral pneumonia etc., etc. etc. These can only be described as the fingerprints of known chemical intoxicant culprits as they are so unique and previously unseen in medical literature. I refuse to placate, facilitate or skirt around irrationality and I will not be gaslighted. I do not stand alone in reaching these conclusions but even if I did so be it. The writing is on the wall.
Another crucial point, not breastfeeding would produce SAM (severe acute malnutrition) or SIBO (small intestinal bacterial overgrowth), long before IBD. The majority of the time IBD is the result of a chemical intoxicant damaging the mucosa. The organism factor implicated in Crohn’s the majority of the time is e coli. All are preventable.
Benefits Of Kefir For IBD
What is kefir?
Fermentation of a matrix produces kefir. Milk is the matrix generally used, resulting in a beverage acidic, slightly alcoholic, and with a creamy consistency. It results from milk fermentation by microorganisms that live in symbiosis in kefir grains. Kefir differs from other fermented milk because it is a metabolic result of a diversity of microorganisms. Lactose fermenting and nonfermenting yeast species (Kluyveromyces, Pichia, and Saccharomyces), with a predominance of lactic acid bacteria (Lactobacillus, Lactococcus, Leuconostoc, and Streptococcus), besides acetic acid bacteria make up the grain’s microbiota.
Regular consumption of kefir has been associated to the reduction of severity of inflammatory bowel disease, antihypertensive effect, anticarcinogenic effect, increased insulin sensitivity, improved lipid profile, therapeutic effects on osteoporosis, and neurodegenerative disease. The positive health effects have been related to the antioxidant capacity and modulation of the intestinal microbiota by the kefir drink. Bioactive compounds present in kefir, produced by microorganisms during fermentation and storage of beverage, have been attributed to these benefits; kefiran, exopolysaccharides, bioactive peptides, and organic acids are the bioactive compounds commonly implicated with the therapeutic potential of kefir. There is still a need for study of the bioactive compounds present in the kefir to distinguish them according to their therapeutic potential for each disease.
The possible difference in the functional potential between artisanal and industrial kefir is controversial in the literature. The use of kefir grains results in artisanal kefir, while previously selected starter culture of bacteria and yeast species leads to commercial or industrial kefir. Some studies have reported artisanal kefir with greater therapeutic potential due to its greater microbiological diversity, while other studies have found no significant difference between both. A meta-analysis could be helpful to elucidate the inconsistencies observed between studies. More microbiota characterization from artisanal and industrial kefir is necessary. Kefir grain’s microorganisms can present the ability to
produce bioactive compounds during the fermentation and storage of kefir beverages. Consistently, from 48 strains isolated from Russian kefir grains, ten species of Lactobacillus sp. were recognized with probiotic potential. Some yeast strains, such as Saccharomyces cerevisiae KU200284, present
double importance: a starter culture and a probiotic. In Korean kefir, the acetic acid bacterial strain Acetobacter fabarum DH1801 had viability as a functional starter with food preservative mechanisms and the potential as a probiotic agent. In addition, the species of LAB has a fundamental role in the formation of exopolysaccharide (EPS), which is a significant bioactive compound in kefir. In
this scenario, the Lactobacillus kefiranofaciens is considered the main piece in the formation of kefir grains since its genes demonstrate a great capacity to produce exopolysaccharides (such as kefiran) which make up the structure of the kefir grain. Similarly, Lactococcus lactis ssp. cremoris was found to be capable of producing conjugated linoleic acid (CLA), a bioactive compound, from milk fat.
Kefir And IBD
Inflammatory bowel disease (IBD) Are a heterogeneous group of chronic, multifactorial, relapsing inflammatory diseases of the gastro-intestinal tract. Common clinical signs observed in IBD patients are chronic diarrhea, vomiting and weight loss associated to histopathological evidence of inflammation in various portions of GI tract. In humans, Crohn’s disease (CD) and ulcerative colitis (UC) are the principal types of IBD. There are several acceptable research models to study IBD some of which were used to help demonstrate the following.
Chemical and pathogen assault modeling for colitis in vitro and in vivo used for assessing the benefits of kefir and its bioactive components and compounds
Bioactive compounds from kefir exerted an anti- or proinflammatory impact depending on the IBD model’s presence or absence of inflammatory insult. Thus, they exerted an inhibitory effect in inflammatory diseases’ models, while they had an immunostimulatory effect for models without inflammatory insult. The predominantly studied inflammatory disease model was that of acute colitis, both in vitro and in vivo. For colitis, mainly EPS (exopolysaccarides) and extracellular vesicles, but also lactate have been described to have an anti-inflammatory role against a variety of acute inflammatory insults: DSS (dextran sulfate sodium), TNFα, FliC (flagellin), IL-1β, and TNBS (2,4,6-trinitrobenzene sulfonic acid). For chronic colitis, extracellular vesicles presented an anti-inflammatory effect against piroxicam. Kefiran, in turn, had an inhibitory effect on cotton-induced granuloma in rats. The L. kefirgranum, L. kefir, L. kefiranofaciens, and L. paracasei species were responsible for producing these bioactive compounds. Therefore, the Lactobacillus genus seems relevant for making anti-inflammatory compounds in the kefir. Galactose and glucose, and to a lesser extent, mannose, arabinose, and rhamnose, were the significant precursors of the polysaccharide component of the bioactive compounds. Extracellular vesicles from L. kefir granum reduced the gene expression of proinflammatory cytokines by 58, 64, and 67%, respectively, in Caco-2 cells for DSS-induced acute colitis model. Extracellular vesicles also inhibited TNFα-induced colitis. They reduced the expression and secretion of IL-8 by 65 and 96%, respectively, in the Caco2 cell line. Extracellular vesicles were just as effective as budesonide, a glucocorticoid steroid commonly used to treat Crohn’s disease (inflammatory bowel disease). Still, treatment of Caco-2 cells with extracellular vesicles showed a longer intervention time than treatments with EPS or lactate. In addition, the effect observed with preincubation of cells with EPS or lactate indicates the potential of these compounds as preventive agents of intestinal inflammation. In mice, oral administration of extracellular vesicles could mitigate acute and chronic colitis, corroborating the previous findings in vitro. For DSS-induced acute colitis, both high and low dosages of vesicles prevented weight loss in mice by up to 16% and reduced damage to colon tissue by up to 63%. However, only the highest dosage (3 mg/kg bw) reduced colon atrophy by 29.6%. Similarly, only the highest dosage mitigated colon atrophy by 14.3% for chronic colitis aggravated by piroxicam. Nevertheless, both dosages reduced colon histological damage by up to 85%.
In contrast to acute colitis, ingestion of extracellular vesicles was ineffective in preventing weight loss in chronic colitis. Therefore, due to the broader effects obtained the high dosage seemed more effective for chronic and acute colitis treatment. Vesicles’ administration against TNBS induced acute colitis also effectively prevented the mouse weight loss by up to 12.5%. Moreover, the administration reduced rectal bleeding and diarrheal condition severity by 75 and 91%, respectively.
Damage to colon tissue, in turn, was decreased by up to 85%. Therapy with vesicles from Lactobacillus of kefir was more effective than the prednisolone drug in preventing weight loss, the severity of rectal bleeding, and diarrheal conditions well as in mitigating colon damage. Prednisolone is an anti-inflammatory steroid used to treat inflammation in colitis and Crohn’s disease; however, it does not prevent recurrence of the disease, in addition to having several side effects. Therefore, treatment with bioactive compounds from kefir would be promising both for effectiveness and reduced side effects. Suspensions of EPS-producer Lactobacillus paracasei inhibited by up to 55% the induction of the proinflammatory promoter in Caco-2 cells for flagellin-induced acute colitis model. Lactobacillus paracasei strain showed more dramatic anti-inflammatory potential than the other tested strains, which indicates that the functional potential of the EPS is strain-dependent. Similarly, lactate inhibited by 78, 80, and 42% the promoter induction by flagellin, IL-1β, and TNFα, respectively, in Caco-2 cells. Inline, human intestinal epithelial cells express the lactate receptor. Still, lactate solution and supernatant from kefir with corresponding lactate concentration showed similar inhibitory effects on Caco-2 cells, indicating that the kefir matrix does not reduce the impact of this bioactive compound. In vivo, oral administration of kefiran-rich kefir supernatant was responsible for reducing the weight of cotton-induced abdominal granulomas by 44% in rats. Kefir was as effective as dexamethasone in reducing these granulomas. Dexamethasone is a corticosteroid medication used as a primary option in the treatment of granulomas. This evidence reinforces the anti-inflammatory potential of bioactive compounds from kefir. Therefore, in general, bioactive agents inhibited the expression of proinflammatory cytokines and the activation of the CCL20 promoter for in vitro inflammatory models with Caco-2 cells. In in vivo colitis models, bioactive compounds reduced weight loss, atrophy, and colon histological damage. The compounds displayed anti-inflammatory action mechanisms by inhibiting the NF-κB pathway in the Caco2 cells and the colon mucosa due to the expression of the IκBα inhibitor. In addition, bioactive agents promoted the integrity of the intestinal barrier. Additional anti-inflammatory mechanisms proposed for EPS were nitric oxide radical scavenging ability and inhibition of hyaluronidase activity in cell-free in vitro systems. Hydrolysis of the extracellular matrix by hyaluronidase releases compounds, like hyaluronan, throughout inflammatory pathologies. For extracellular vesicles, blocking myeloperoxidase activation in the mouse
plasma has also been reported. Oxidative stress in inflammatory bowel disease activates inflammatory cells, such as neutrophils, whose myeloperoxidase catalyzes the production of reactive oxygen species. In this scenario, extracellular vesicles were as effective as the prednisolone drug in inhibiting myeloperoxidase. Bioactive compounds from kefir play a decisive anti-inflammatory role. However, EPS, including kefiran, can also have the opposite effect, acting as immunostimulants, in cases where there is no inflammatory insult; this role was also corroborated in an in vivo model. Their precursors in milk were glucose and galactose. In a minority way, bioactive peptides have also been reported as immunostimulants. The Lactobacillus genus was relevant to produce these immunostimulants, especially the L. helveticus, L. pentosus, and L. kefiranofaciens species.
For EPS, although the intervention time has been similar for both a pro- and anti-inflammatory effect assay, the EPS concentration employed was dramatically higher; in vitro, the concentration for immuno-stimulating varied from 50 to 5000 μg/mL, while for inhibition, it reached the maximum of 100 μg/mL. In vivo, 100 mg/kg bw was administered orally for immunostimulating, while to inhibit the immune response, the concentration ranged from 0.03 to 3 mg/kg bw. This fact suggests that the concentration of EPS is a significant factor in determining the role that it will play on the immune system. In line, EPS has been reported to stimulate or inhibit the secretion of TNFα, IL-10, and IL-6 by in vitro murine macrophages, depending on the concentration tested. Thus, it appears that EPS can act by different cell signaling pathways, according to its concentration. In vitro, the immunostimulatory role of EPS and bioactive peptides has been demonstrated in the macrophage’s cell line and primary culture, in addition to human peripheral blood mononuclear cells EPS stimulated proliferation, phagocytosis, phosphatase activity, IL-6 secretion, and NO production by macrophage cells. In the concentration range of 100 to 200 μg/mL, they stimulated the secretion of TNFα, IL-1β, and IL-10. EPSs were as efficient as lipopolysaccharides in promoting cell proliferation, phagocytosis, and cytokine secretion by macrophages. Kefiran at 1000 to 5000μg/mL increased IL-6 secretion, and concentrations from 2000 to 4000μg/mL stimulated cell proliferation of human PBMC culture by up to 200% after 24 hr. Bioactive peptide from L. kefiranofaciens, turn on, improved secretion of TNFα, IL-1β, IL-6, and IL-12 by 1000, 700, 1300, and 3000% by murine peritoneal macrophage culture. However, peptides from different microbial strains showed differences in immuno-stimulatory capacity, suggesting that the functional potential of the peptide is strain-dependent. In addition, bioactive peptide acted via the TLR2 receptor; Toll-like receptor 2 enables macrophages to recognize microbial ligands, thereby promoting inflammation. Consistently, oral administration of kefiran (100mg/kg bw) to healthy mice for up to 7 days enhanced IgA, IL-10, IL-6, and IL-12 in the mucosa of the small intestine, as well as IL-4 and IL-12 in the fluid of the small intestine. In serum, kefiran
increased IL-4, IL-6, IL-10, and IFN. However, broader immunostimulation occurred in the large intestine, increasing IgA, IgG, IL-4, IL-10, IL-6, INF, and TNF content. The most
evident stimulatory activity in the large intestine has been attributed to the kefiran fermentation by intestinal microbiota. Therefore, it appears that bioactivity may vary according to the biochemical transformations that these molecules undergo throughout the digestive process.
Finally, it is essential to highlight that immune stimulation can be interesting for a better prognosis of infectious conditions and stimulating immunoglobulin production after vaccination. Thus, the concentration and environmental context (presence or absence of inflammatory insult) are relevant factors to be considered according to the purpose of administering the bioactive compound. Analysis results corroborated the benefits of kefir bioactive compounds on immune modulation since the findings indicated that treatments had significant immune-modulatory activity compared to control.
Many factors influence kefir production to either increase or decrease its potential. Fermentation conditions, substrates, ph, denaturing of proteins, temperature, storage conditions the addition of raw milk vs. pasteurized or heat treated milk, the addition or subtraction of various probiotics and yeasts and the effects of freeze drying are among the many of the factors that influence the final kefir product. However, all kefir products have shown significant potential in preventing, modulating and alleviating a myriad of conditions whether kefir is produced from grains or a starter culture. There are no two kefir grain formulations that are exactly alike, making kefir a very localized product with exponentially increasing research outcomes and applications.
The most important tips in realizing increased benefit of kefir are to always choose whole fat mammal milk products. Whole fat mammal milk improves and prevents diabetes and helps obese subjects lose more weight than low fat versions. Whole fat mammal milk fermented dairy products increase energy and endurance. Whole fat mammal milk fermented food products are often hard to find. Whole fat dairy products contain fats very similar in make up and proportion to the healthy person, animal and healthy human breast milk. Storage time leads to changes in fatty acid compositions in milk, so that stocked milk can have higher anti-carcinogenic potential due to the high amount of oleic acid.
Kefir Benefits For IBD
- Alleviates pro inflammatory assault better than steroids
- Reduces intestinal damage and granulomas
- Increases IgA
- Reduces diarrhea
- Reduces bleeding
- Reduces atrophy
- Prevents IBD
- Increases macrophage activation
- Immune modulatory
The natural precursor of ‘gut and immune disorders’ is a dysfunctional autophagic or phagocytic system associated with SAM (severe acute malnutrition) resulting in hundreds if not thousands of chronic ‘conditions’ that worsen over time. See about page for more info and some short lists of these chronic conditions (can eventually impact any and all bodily systems). In the elderly or immune compromised this can occur as ‘senescence’ of the immune system or ‘tolerance’ (an altered immune response, usually over inflammatory). This condition can begin at birth. The immune system includes the ability to detox. The ’cause’ of these conditions is not diet. They can begin or be made worse by acquired immune deficiency syndromes. Natural oral immune therapy ‘resets’ the gut as close to nature as possible as it occurs at birth and helps restore nutrition, tolerance and homeostasis as well as providing anti oxidant protection.
Colostrum and other friendly organisms provide signals to the immune system by inducing tolerance to food and noninvasive antigens, thus avoiding the onset of an abnormal immune response while promoting its maturation and an adequate immune response against pathogens at the same time.
In the absence of A, B, or C (see hierarchy of risk factors in alternavita critical info) it must be D, follow the known intoxicant.
Alternavita: All you need to know (critical info in a nutshell)..... by focusing exclusively on these foundational health and immune development issues up to 90% of chronic conditions can be eliminated.
WHO STATEMENTS: 2017 Millennium Goal
- food (security)
- and water security (sanitation)
are major protective factors against malnutrition and critical factors in the maturation of healthy gut microbiota, characterized by a transient bifidobacterial bloom before a global rise in anaerobes. Early depletion in gut Bifidobacterium longum, a typical maternal probiotic, known to inhibit pathogens, represents the first step in gut microbiota alteration associated with severe acute malnutrition (SAM). Later, the absence of the Healthy Mature Anaerobic Gut Microbiota (HMAGM) leads to deficient energy harvest, vitamin biosynthesis and immune protection, and is associated with diarrhea, malabsorption and systemic invasion by microbial pathogens. A therapeutic diet and infection treatment may be unable to restore bifidobacteria and HMAGM.
Researchers found that malnourished children’s microbiota failed to follow the healthy pattern they identified in healthy children. The microbiota of malnourished children is immature, lagging in development behind that of their healthy peers. Supplementing these children’s meals with widely used therapeutic foods that increase calories and nutrient density reduces deaths from malnutrition, but it does not fix their persistent microbiota immaturity.
“Perhaps more insidious than slowing growth is malnutrition’s effect on less visible aspects of health, including impaired brain development and dysfunctional immunity, which follow these children throughout their lives”.
The Father of The Microbiome
Dr. Jeffrey Gordon
SIBO can cause severe malabsorption, serious malnutrition and immune deficiency syndromes in children (non breastfed) and adults.
Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
The WHO recommends that immunization or treatment be orally administered due to economic, logistical and security reasons. Furthermore, this route offers important advantages over systemic administration, such as reducing side effects, as the molecules are administered locally and have the ability to stimulate the GALT immune responses (Levine and Dougan, 1998; Neutra and Kozlowski, 2006; Bermúdez-Humarán et al., 2011).
For ANY infectious or parasitic disease to start, it is ALWAYS a requisite that the host suffer IMMUNODEFICIENCY. At the same time, infectious and parasitic diseases themselves cause additional IMMUNE SUPPRESSION and more MALNUTRITION. This immune suppression is SECONDARY to the accumulation of free radicals, especially oxidizing species, that occurs during and after infectious and parasitic diseases.
Clinical Aspects of Immunology and Biochem J.
Current IBD Research 2016
Currently available treatments for IBD, which target the systemic immune system, induce immunosuppression, thereby exposing the patient to the risk of infections and malignancy. The interplay between the gut and the systemic immune system determines the final effect on target organs, including the bowel mucosa. Inflammatory bowel diseases (IBD) are associated with an altered systemic immune response leading to inflammation-mediated damage to the gut and other organs.
Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel
Most importantly, the immune modulatory agents used today for IBD do not achieve remission in many patients.
Not all IBD patients benefit from currently available drugs. Young people with IBD do not want to be on long-term drug therapy. Oral immune therapy, while not yet studied in large cohorts of patients, may provide an answer to this unmet need.
Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel
Tolerance is the ability of the immune system to ‘see’ and respond appropriately. Without galactose (a necessary sugar) the immune system can not 'see'. Your immune system would not be able to function without galactose Your body wouldn’t know which cells are
“good” and what cells are “bad.” Your body wouldn’t know who the invaders were and which ones should be attacked by antibodies. As you will learn the importance of these ‘sugars’ in gut microbiota health is a rapidly expanding field of research, only recently
discovered, including HMO's (human milk oligosaccharides).
Why galactose? Milk sugar aka lactose has been shown to be very beneficial for the human body though unlike sucrose, lactose is made up of glucose and galactose. There is no fructose in lactose. It is a healthy disaccharide sugar. Galactose is known as the “brain sugar” and supports brain development of babies and children. Galactose helps triggers long-term memory formation. Galactose has been shown to inhibit tumor growth and stop its spread, particularly to the liver. This beneficial sugar can also enhance wound healing, decrease inflammation, enhances cellular communication, and increases calcium absorption.
What does immune ‘tolerance’ mean in simple language?
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. The Th1 cytokine profile is vital for clearance of certain organisms and ancillary immune activity, and a limiting effect on this cytokine profile may result in reduced chances for overcoming infections especially intra-cellular organisms residing within macrophages. Effective clearance will depend on appropriate macrophage activation (which occurs through IFN≥ release by Th1 and NK cells) and production of nitric oxide. If this pathway is disrupted IFN≥ secretion is blocked, impairing macrophage activation. Persistent blockade of these inhibitory receptors has lead to the breakdown in immune self tolerance, thereby increasing susceptibility to autoimmune or auto-inflammatory side effects, including rash, colitis, hepatitis and endocrinopathies. Many drugs may cause checkpoint blockade toxicity including pharmaceutical drugs termed ‘immuno therapy’ by pharmaceutical companies, these include Mab drugs and cancer treatments. Checkpoint Inhibitor–Induced Colitis: A New Type of Inflammatory Bowel Disease? Madeline Bertha, MD MS, corresponding author1 Emanuelle Bellaguara, MD, Timothy Kuzel, MD, and Stephen Hanauer, MD ACG Case Rep J. 2017; 4: e112. Published online 2017 Oct 11. doi: 10.14309/crj.2017.112 PMCID: PMC5636906 PMID: 29043290
Mammal milk is required for enhanced phagocytosis as shown by research, especially in the elderly. Whole fat mammal milk can actually restore phagocytosis in senescent cells in the elderly. Phagocytosis, by which immune cells ‘eat’ bacteria or infected cells, is one of the mechanisms that help to resist infections. Lactic acid bacteria strains like acidophilus also increases phagocytosis.