Chapter 8. Why SIBO matters, my experience with SIBO and why I keep SIBO as a pertinent topic in relation to IBD, IBS, Crohn’s, colitis and other gut/immune disorders. Primarily as it is one of the few if not the only associated/highly correlated with not breastfeeding, malnutrition (especially B12 and folate), extremely poor outcomes, auto immunity, seizure activity, infancy/toddlerhood and chronic dysbiosis/inflammation inability to achieve homeostasis as well as the most common immune deficiencies, extreme childhood conditions, e coli and poor sanitation. It is also the only one that has a very similar pathology to SAM regarding bifido and chronic dysbiosis, cascading to serious immune failure, severe malnutrition, increasingly common liver problems etc. In other words the trail of SIBO research also leads to early gut malformation and/or possible external conditions very similar to the hierarchal risk factors and poor outcomes as found in SAM. They are more than just closely correlated but nearly identical so a proper early diagnosis for SIBO is crucial. I would also remind you diagnostics were attempted decades ago, primarily in pediatric settings.
I forgot to mention the excruciating pain and inflammation that I used to describe as feeling like I was being gutted like a fish from morning until night for approx. 27 YEARS until SIBO recipe and natural oral immune therapy healed my gut and restored a healthy microbiome.
And of course I forgot the main component in SIBO recipe (Milk Of Magnesia), a form of magnesium that creates a slow dissolve oxygen (to reduce H2S) while also reducing formation of caustic substances that is chemically similar to a safe wastewater treatment industrial application that doesn’t require other measures to reduce undesired byproducts. Milk of Magnesia low dose pretty much does the same thing and it was by studying industrial applications to reduce dangerous H2S that I knew how SIBO recipe would work and would also be safe. The others I did remember to explain in the video.
Lactose prevents H2S formation (fiber breakdown) as does pantothenic acid and baking soda (alters ph and neutralizes gases or acids), zinc affects electrons. These are the short answers.
Baking soda also affects macrophage activation from pro inflammatory to anti inflammatory.
“Methane is not driven by
the lactulose or the glucose;
it’s driven by the presence of
hydrogen, because hydrogen
gas from fermentation of
other bacteria fuels — “
“It’s (hydrogen sulfide) the
food for the methanogens.“
Dr. Mark Pimentel
What is the role of H2S in
Sulfate reducing bacteria
and methanogens eventually
outcompete all other bacteria
in the small intestine in
patients with SIBO.
Unlike the colon, the small
intestine is not designed for
heavy bacterial colonization…..
Therefore SIBO affects commensal bacteria.
PCR testing not likely as pathogenic/infectious cause pretty much abandoned (aside from e coli as most common aspirate) and gases (gaso transmitters) are a greater determinant factor.
Previous chapters explain the association between e coli (= immune surveillance capability) and endotoxemia resulting in faster progression to immune system failure.
And I forgot. I wanted to add a Peepso demo to the previous video for the writer who asked how it works. I discovered, I did not delete customers but I did delete probably mostly spammers (Spring cleaning); so if you find you can’t log in and you don’t see yourself in community you may have to re-register. Pretty simple.
Final food for thought….
One of the researchers I know of who I believe came up with a very simple urine test for H2S detection (not hard to do; detecting certain metabolites) has basically been forced out of the arena to the best of my knowledge. A short snippet from another gut doctor regarding his test…. “And I was also using another test that at the time was very inexpensive, way back then. It was a urine test developed by (blank)—who focuses on hydrogen sulfide in the context of myalgic encephalomyelitis (another name for that is fibromyalgia)—in Europe”.
Just some of the common reindeer games perpetuated toward an ignorant public as it is extremely easy to detect H2S toxic byproducts in any fluid even after oxygen exposure has dissipated the gas itself.
I’ll let you be the judge of the ‘red herring’ called fibromyalgia until more and more gut doctors began calling it what it is and was…… ‘bullshit syndrome’. When I got charged a couple hundred for that one; I got up and walked out and then went on to expose it and promote the exact same products I do today, unfortunately unbeknownst to me at the time how close I was to the truth and my own eventual healing. Word to the wise, expect to encounter intentional roadblocks that make headlines.
Regarding H2S, oxidative stress, liver failure and other malnutrition syndromes…..
Glycogenolysis is the biochemical breakdown of glycogen to glucose whereas glycogenesis is the opposite, the formation of glycogen from glucose. Glycogenolysis takes place in the cells of muscle, and liver tissues in response to hormonal and neural signals….
H2S has long been regarded as a strong toxin that inhibits mitochondrial respiration. H2S generates a state of oxidative stress. H2S causes blockage of electron transfer within the mitochondria.
Beriberi is characterized in its early stages by dysautonomia, appearing as postural orthostatic tachycardia syndrome (POTS). This well documented modern disease cannot be distinguished from beriberi except by appropriate laboratory testing for thiamine deficiency. Blood thiamine levels are usually normal in the mild to moderate deficiency state.
Examples of Dysfunction in Beriberi
The calf muscle often cramps with physical exercise. There is loss of the deep tendon reflexes in the legs. There is diminished visual acuity. Part of the eye is known as the papilla and pallor occurs in its lateral half. If this is detected by an eye doctor and the patient has neurological symptoms, a diagnosis of multiple sclerosis would certainly be entertained.
Optic neuritis is common in beriberi. Loss of sensation is greater on the front of the body, follows no specific nerve distribution and is indistinct.
Foot and wrist drop, loss of sensation to vibration and stumbling on walking are all examples of symptoms that would be most likely ascribed to other causes.
Breathlessness with or without exertion would probably be ascribed to congestive heart failure of unknown cause or perhaps associated with high blood pressure.
The symptoms of this disease can be precipitated for the first time when some form of stress is applied to the body. This can be a simple infection such as a cold, a mild head injury, exposure to sunlight or even an inoculation.
Is Thiamine Deficiency Common in America?
It is extremely common. There is good reason for it because sugar ingestion is so extreme and ubiquitous within the population as a whole. Ingestion of sugar is causing widespread beriberi, masking as psychosomatic disease and dysautonomia. The symptoms and physical findings vary according to the stage of the disease. For example, a low or a high acid in the stomach can occur at different times as the effects of the disease advance. Both are associated with gastroesophageal reflux and heartburn, suggesting that the acid content is only part of the picture.
A low blood sugar can cause the symptoms of hypoglycemia, a relatively common condition. A high blood sugar can be mistaken for diabetes, both seen in varying stages of the disease.
It is extremely easy to detect thiamine deficiency by doing a test on red blood cells.
The lower part of the human brain that controls the autonomic nervous system is exquisitely sensitive to thiamine deficiency. It produces the same effect as a mild deprivation of oxygen. Because this is dangerous and life-threatening, the control mechanisms become much more reactive, often firing the fight-or-flight reflex that in the modern world is diagnosed as panic attacks. Oxidative stress (a deficiency or an excess of oxygen affecting cells, particularly those of the lower brain) is occurring in children and adults. It is responsible for many common conditions, including jaundice in the newborn, sudden infancy death, recurrent ear infections, tonsillitis, sinusitis, asthma, attention deficit disorder (ADD), hyperactivity, and even autism. Each of these conditions has been reported in the medical literature as related to oxidative stress. So many different diseases occurring from the same common cause is offensive to the present medical model. This model regards each of these phenomena as a separate disease entity with a specific cause for each.
Without the correct balance of glucose, oxygen and thiamine, the mitochondria (the engines of the cell) that are responsible for producing the energy of cellular function, cannot realize their potential. Because the lower brain computes our adaptation, it can be said that people with this kind of dysautonomia are maladapted to the environment. For example they cannot adjust to outside temperature, shivering and going blue when it is hot and sweating when it is cold.
So, yes, beriberi and thiamine deficiency have re-emerged. We have forgotten history and appear doomed to repeat it. It is high time that the situation should be addressed more clearly by the medical profession.
SIBO, IBS and Constipation Unrecognized Thiamine Deficiency?
Malnutrition Induced Malnutrition
Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals. Thiamine is notoriously missed by doctors and nutritionists. To summarize, B1 is necessary in the gut for:
- Stomach acid secretion and gastric emptying
- Pancreatic digestive enzyme secretion
- Intestinal brush border enzymes
- Intestinal contractions and motility
- Vagal nerve function
40 million people are intoxicated on any given day in America and the CV19 lockdown hasn’t helped…..
A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol–induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke–Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.
Approximately 80 to 90 percent of alcoholics with WE develop Korsakoff’s psychosis, a chronic neuropsychiatric syndrome characterized by behavioral abnormalities and memory impairments (Victor et al. 1989). Although these patients have problems remembering old information (i.e., retrograde amnesia), it is the disturbance in acquisition of new information (i.e., anterograde amnesia) that is most striking. For example, these patients can engage in a detailed discussion of events in their lives but cannot remember ever having had that conversation an hour later. Because of these characteristic memory deficits, Korsakoff’s psychosis also is called alcohol amnestic disorder. It is still somewhat controversial, however, whether Korsakoff’s psychosis always is preceded by WE or whether it develops in fits and starts, without an overt episode of WE.
Although WKS in developed countries occurs most commonly among alcoholics, other groups of patients are also at risk of developing the disease. For example, all people who are malnourished (e.g., because they have AIDS or are undergoing cancer chemotherapy) or who have a metabolic disease leading to impaired thiamine absorption (i.e., uptake) or utilization can develop thiamine deficiency. Patients with severe kidney disease who are undergoing regular dialysis are also prone to encephalopathy, and a substantial portion of them have been found to suffer from thiamine deficiency (Hung et al. 2001). Finally, patients who receive intravenous infusions of carbohydrates (e.g., the sugar dextrose) may experience episodes of thiamine deficiency, particularly if they are already at risk of receiving inadequate levels of this nutrient because they are alcoholics, as thiamine is used in the metabolism of those carbohydrates (see Ferguson et al. 1997).
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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.