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The Influence Of Intestinal Bacteria Upon The Thyroid Gland (1923)
- Thread starter Amazoniac
- Start date
I'd like to use this article as the lyric for an opera.
No kidding, this is so completely Ray Peat in every way--except for the mercury & x-ray treatments--that the climax of the plot would have to be that the mixedematous, fermenting gut patient recovers completely, . . .but only after almost dying. Which reminds me of RP's description of morning stress before breakfast where he breaks to say, "if you haven't dropped dead by then" you should eat a couple of eggs & a quart of oj (or something like that).
Of course, Ray Peat would have to sing it.
No kidding, this is so completely Ray Peat in every way--except for the mercury & x-ray treatments--that the climax of the plot would have to be that the mixedematous, fermenting gut patient recovers completely, . . .but only after almost dying. Which reminds me of RP's description of morning stress before breakfast where he breaks to say, "if you haven't dropped dead by then" you should eat a couple of eggs & a quart of oj (or something like that).
Of course, Ray Peat would have to sing it.
OP
Amazoniac
Member
Marco Centanni | Researching the Gates
(both are similar, but each add different details)
↳ Does microbiota composition affect thyroid homeostasis?
↳ "With a little help from my friends" - The role of microbiota in thyroid hormone metabolism and enterohepatic recycling
@Blossom (no pressure for a reply)
(both are similar, but each add different details)
↳ Does microbiota composition affect thyroid homeostasis?
"[..]it has been reported that an avidity of intestinal bacteria for selenium, essential element of selenoproteins (deiodinase, glutathione peroxidase, etc.), is able to reduce the availability of selenium in the host. This, in turn, under selenium shortage, may lower the availability of selenoproteins in the host. Whether, under adequate selenium supply, such a competition has any physiologic role in humans is not known [11]."
"Iodothyronines are metabolized via different interrelated pathways. The most important metabolic pathway of iodothyronines is represented by deiodinating isoenzymes. Deiodinases, asymmetrically distributed in all peripheral tissues, warrant peripheral thyroid homeostasis. Type 2- and 3-deiodinase activities have been detected on rat intestinal wall, being higher in rat fetuses than in adults, possibly because of the inhibition exerted by the resident intestinal microflora [14]. Deiodinase activity was next identified in the human intestine [15], and authors suggested that owing the large surface, its contribution to the whole body triiodothyronine (T3) pool may be relevant."
"Even alternative metabolic pathways may be influenced by intestinal microbiota. In the liver, glucuronoconjugation and sulfoconjugation play a major role in iodothyronine metabolism. Sulfoconjugation increases the rate of deiodination to inactive metabolites, whereas glucuronoconjugation provides a significant amount of conjugated T4 which is secreted into the intestinal lumen through the biliar flow [16]. On this site, bacterial action may deeply affect the enzymatic activity and thus microbiota composition may be involved in a crucial path of thyroid homeostasis. In rats and humans, it has been proven that fecal suspensions hydrolyze significant amounts of iodothyronines conjugates because of the presence of obligate anaerobic intestinal bacteria, normal constituents of intestinal microflora [17]. In fact, most of glucuronidase activity is of bacterial origin [17]. The amount of deconjugated T4, which is the naive form of the hormone, re-enters in the general circulation and contributes to the iodothyronines pool through the hepatoenteric cycle [18]. This mechanism seems to be a limiting factor for thyroid hormones homeostasis in rats [18], while in humans, the exact role of deconjugated thyroxine was never quantitatively ascertained."
"Intestinal bacteria may also specifically bind thyroid hormones and may even compete with albumin in a study in rats [19]. It is intriguing that, using a mathematical model, slow and fast exchanging compartments were identified; the location of the fast compartment has been recognized in liver and kidneys T4 and T3 pools, whereas the slow exchange T4 and T3 pool may be represented by the intestine [20]. The authors conclude that the amount of intestinal exchangeable T3 or T4 in rats is the second reservoir of iodothyronines, just after the thyroid gland [20]. Due to the overwelming role of deiodinases [21] and glucuronidase activities on the iodothyronine economy, the role of resident intestinal bacteria (inhibitor of deiodinase activity and source of glucuronidase activity) may represent an unexplored regulator of human thyroid metabolism. In this view, the dysbiosis might substantially affect thyroid hormone metabolism, but this assumption awaits further evidence."
"Oral thyroxine is considered a low permeability drug from Biopharmaceutics classification system [34] mainly absorbed and possibly reabsorbed from the hepatoenteric cycle into circulation in the upper intestinal tract [19]. The intestinal absorption of thyroxine is linear in the first hour after ingestion [35] and ranges between 62 and 82 % of the ingested dose [19]. The ability to cross the cell membrane is key for the pharmacokinetics of thyroxine. Although thyroid hormones are considered lipophylic molecules, the presence of an alanine side chain is a barrier to the efficient passage through the central part of the double hydrophobic lipid status [34]. Thyroxine, in fact, is taken up by target cells through different mechanisms: (a) by specific transporters; (b) by multispecific transporters (which also transports aromatic amino acids and steroids); and (c) by passive diffusion [36]. However, whether all these mechanisms are operating and what may be their contribution to intestinal thyroxine transport is not well established."
"It is well known, however, that some disorders of the upper intestinal tract are associated to different microbiota profiles [37] and concurrently to an increased need for thyroxine [38–41]. Patients with celiac disease (CD) have fewer lactobacilli and bifidobacteria as compared to controls, and some bacterial species belonging to the genera Lactobacillus and Bifidobacterium may protect epithelial cells from gliadin-dependent damage [37]. Whether an altered microbiota profile is the cause or the consequence of CD in these patients is still unclear. An important role for colonic metabolism of lactose in patients with lactose intolerance (LI) has been also claimed [42]. Despite the absence of studies dealing with the absorption of thyroxine in subjects with different microbiota profile, the T4 malabsorption clearly shown in CD and LI [38, 39] may recognize a different microbiota composition as a pathogenic cofactor. Recently, an intestinal dysbiosis has been shown in hypochlorhydric patients [43]. This is potentially relevant in that an increased need for thyroxine has been described in patients with gastric atrophy [44]. Although the increased T4 dose in these patients is mainly due to the altered biochemical status of the hormone at higher gastric pH, dysbiosis may represent an additional source of thyroxine malabsorption."
"Iodothyronines are metabolized via different interrelated pathways. The most important metabolic pathway of iodothyronines is represented by deiodinating isoenzymes. Deiodinases, asymmetrically distributed in all peripheral tissues, warrant peripheral thyroid homeostasis. Type 2- and 3-deiodinase activities have been detected on rat intestinal wall, being higher in rat fetuses than in adults, possibly because of the inhibition exerted by the resident intestinal microflora [14]. Deiodinase activity was next identified in the human intestine [15], and authors suggested that owing the large surface, its contribution to the whole body triiodothyronine (T3) pool may be relevant."
"Even alternative metabolic pathways may be influenced by intestinal microbiota. In the liver, glucuronoconjugation and sulfoconjugation play a major role in iodothyronine metabolism. Sulfoconjugation increases the rate of deiodination to inactive metabolites, whereas glucuronoconjugation provides a significant amount of conjugated T4 which is secreted into the intestinal lumen through the biliar flow [16]. On this site, bacterial action may deeply affect the enzymatic activity and thus microbiota composition may be involved in a crucial path of thyroid homeostasis. In rats and humans, it has been proven that fecal suspensions hydrolyze significant amounts of iodothyronines conjugates because of the presence of obligate anaerobic intestinal bacteria, normal constituents of intestinal microflora [17]. In fact, most of glucuronidase activity is of bacterial origin [17]. The amount of deconjugated T4, which is the naive form of the hormone, re-enters in the general circulation and contributes to the iodothyronines pool through the hepatoenteric cycle [18]. This mechanism seems to be a limiting factor for thyroid hormones homeostasis in rats [18], while in humans, the exact role of deconjugated thyroxine was never quantitatively ascertained."
"Intestinal bacteria may also specifically bind thyroid hormones and may even compete with albumin in a study in rats [19]. It is intriguing that, using a mathematical model, slow and fast exchanging compartments were identified; the location of the fast compartment has been recognized in liver and kidneys T4 and T3 pools, whereas the slow exchange T4 and T3 pool may be represented by the intestine [20]. The authors conclude that the amount of intestinal exchangeable T3 or T4 in rats is the second reservoir of iodothyronines, just after the thyroid gland [20]. Due to the overwelming role of deiodinases [21] and glucuronidase activities on the iodothyronine economy, the role of resident intestinal bacteria (inhibitor of deiodinase activity and source of glucuronidase activity) may represent an unexplored regulator of human thyroid metabolism. In this view, the dysbiosis might substantially affect thyroid hormone metabolism, but this assumption awaits further evidence."
"Oral thyroxine is considered a low permeability drug from Biopharmaceutics classification system [34] mainly absorbed and possibly reabsorbed from the hepatoenteric cycle into circulation in the upper intestinal tract [19]. The intestinal absorption of thyroxine is linear in the first hour after ingestion [35] and ranges between 62 and 82 % of the ingested dose [19]. The ability to cross the cell membrane is key for the pharmacokinetics of thyroxine. Although thyroid hormones are considered lipophylic molecules, the presence of an alanine side chain is a barrier to the efficient passage through the central part of the double hydrophobic lipid status [34]. Thyroxine, in fact, is taken up by target cells through different mechanisms: (a) by specific transporters; (b) by multispecific transporters (which also transports aromatic amino acids and steroids); and (c) by passive diffusion [36]. However, whether all these mechanisms are operating and what may be their contribution to intestinal thyroxine transport is not well established."
"It is well known, however, that some disorders of the upper intestinal tract are associated to different microbiota profiles [37] and concurrently to an increased need for thyroxine [38–41]. Patients with celiac disease (CD) have fewer lactobacilli and bifidobacteria as compared to controls, and some bacterial species belonging to the genera Lactobacillus and Bifidobacterium may protect epithelial cells from gliadin-dependent damage [37]. Whether an altered microbiota profile is the cause or the consequence of CD in these patients is still unclear. An important role for colonic metabolism of lactose in patients with lactose intolerance (LI) has been also claimed [42]. Despite the absence of studies dealing with the absorption of thyroxine in subjects with different microbiota profile, the T4 malabsorption clearly shown in CD and LI [38, 39] may recognize a different microbiota composition as a pathogenic cofactor. Recently, an intestinal dysbiosis has been shown in hypochlorhydric patients [43]. This is potentially relevant in that an increased need for thyroxine has been described in patients with gastric atrophy [44]. Although the increased T4 dose in these patients is mainly due to the altered biochemical status of the hormone at higher gastric pH, dysbiosis may represent an additional source of thyroxine malabsorption."
↳ "With a little help from my friends" - The role of microbiota in thyroid hormone metabolism and enterohepatic recycling
"Selenium absorption takes place in the duodenum and at the caecum and may vary depending on its chemical form (Mehdi et al., 2013)."
"It has been estimated that ¼ of total bacteria possesses selenoprotein-encoding genes. Some of these, such as Escherichia Coli, Clostridia and Enterobacteria, are able to colonize the gastrointestinal tract of humans and animals (Hrdina et al., 2009)."
"In a very recent study using an in vitro gastrointestinal digestion procedure model (Lavu et al., 2016), it was proven that selenium not absorbed in the small intestine may be actively taken up in the colon and metabolized by the resident microbes. This represents a real competition for the substrate (selenomethionine being the preferred substrate) which causes a reduction of selenium bioaccessibility, as shown by the reverse effect exerted by the presence of an inactive microbiota (Lavu et al., 2016). This finding is in keeping with a previous one (Hrdina et al., 2009) in which the expression analysis of gastrointestinal selenoprotein isoforms revealed that bacteria may compete with the host, chiefly in the presence of limited selenium supply. This increased selenium uptake by the intestinal bacteria may negatively influence selenoprotein expression in the host (Kasaikina et al., 2011). Furthermore, selenium enrichment in the diet increased the biodiversity of host microbiota, supporting the notion that this micronutrient may also shape intestinal microbial composition (Kasaikina et al., 2011) in a bidirectional fashion, related to the different utilization and toxicity profile of the bacteria."
"Since the early 60s, in vitro studies have shown high affinity binding (T3 > T4) (Roche and Michel, 1960) and uptake (Salvatore et al., 1963) of radioactive iodothyronines in cultured Escherichia coli, a Gram-negative bacterium which is a major component of physiologic intestinal flora. In these cultured bacteria, deiodination, decarboxilation and deamination of iodothyronines have also been detected (Grasbeck et al., 1963; Roche and Michel, 1960; Salvatore et al., 1963)."
"In 1967, Chung and Van Middlesworth showed that bacteria in the intestine of normal rats are able to bind T4. This finding was later confirmed by Di Stefano III et al. (1993) who demonstrated a reversible in vivo binding of radiolabeled T3 and T4 in the feces and caecum contents of normal rats that was abolished or reduced in samples taken from antibiotic treated rats suggesting that the intestine may play a relevant role as a reservoir of an exchanging pool of iodothyronines; a pH-dependent oxidative degradation of T3 and T4 by intestinal flora was also observed."
"The explanation of these seminal observations became evident when the presence of deiodinase was detected in several of the rat's tissues, including the intestinal wall (Galton et al., 1991). These enzymatic activities have also been shown in the intestinal content of adult rats being inhibited by the resident microflora (Nguyen et al., 1993). In fact, they proved that both 5-D and 5'-D activities exist in adult rat intestinal contents possibly of cellular origin. In fact, the maximal deiodinase activity was found in frozed/defrosted samples, a step designed to rupture any cells in the media. Their activity was reduced or eliminated by the presence of normal intestinal bacteria. The authors postulated that the observed inhibition might be attributed to bacterial binding of T3 and T4. The presence of type 2 deiodinase (D2) activity has also been described in human intestinal wall (Sabatino et al., 2000)."
"Despite this strong evidence, the metabolic pathways more sensitive to the composition of intestinal microbiota, seem to be those involving phase II hepatic detoxication reactions. These include conjugation reactions encompassing either the esterification of the phenolic hydroxyl group with sulphuric acid or the etherification with glucuronic acid (Visser, 1996). These reactions increase the water solubility of iodothyronines, on the one hand enabling their biliary and renal clearance (Visser, 1996) and on the other reducing their intestinal absorption. T4 and rT3 are preferentially glucurono-conjugated whereas T3 may be equally glucurono-conjugated and sulphated (de Herder et al., 1985). Sulphoconjugation facilitates type 1 deiodination (D1) but not type 2 and 3 (D3) and, in patients with D1 and selenium deficiency or chronic diseases, sulphated iodothyronines may constitute a reservoir of active hormones (Wu et al., 2005). In rats but not in humans, drugs and toxins inducing glucuronidation have been shown to cause goitre and reduced concentrations of T4 and T3 as well as higher serum TSH levels (Wu et al., 2005)."
"It has been shown that diluted human fecal suspension is able to hydrolyze almost all these substrates, due to the presence of bacteria, chiefly obliged anaerobia, such as the Peptococcus productus, one of the major residents of normal human intestinal flora (de Herder et al., 1985). This bacterium has been proven highly active since an amount as small as [3 * 10^7]/ml hydrolyzed as much as 50% of sulphated iodothyronines in 24 h (de Herder et al., 1985). In rats and human intestinal content, a beta-glucuronidase activity has even been shown (de Herder et al., 1986)."
"The presence of glucuronidase and sulphatase activities in fecal content suggested the existence of enterohepatic circulation for iodothyronines. Rutgers et al. (1989) suggested that, in rats, the presence of intestinal microbiota may allow the reabsorption of native triiodothyronine following the hydrolysis of conjugated forms of the hormone. The fraction of reabsorbed hormone that escapes from liver extraction may be detected again in the systemic circulation."
"In humans, a recycling mechanism has been described for steroids hormones, biliary acids and vitamins, while the existence of an enterohepatic circulation of thyroid hormones is not supported by direct proof."
"So far, the role of microbiota seems to be a further regulator of thyroid homeostasis in that it may act directly through its metabolic enzymes as well as by modulating the chemical bioavailability of iodothyronines for reabsorption in the blood (Fig. 1) [No (Wagner, 2018).]. However, the possible effect of the variations in microbiota composition on iodothyronines homeostasis is a reasonable assumption but needs further evidence for being quantified."
"Some of the most common gastrointestinal disorders feature an increased need for oral thyroxine and microflora alterations at the same time. Despite the lack of direct proof regarding the role of microbial composition in the malabsorption of oral thyroxine, an increased need for thyroxine has been noted in patients with untreated celiac disease or lactose intolerance (Virili et al., 2012; Cellini et al., 2014). Interestingly, in children with celiac disease, the ratio between the possibly harmful Gram-negative bacteria (i.e. E. coli and Bacteroides-Prevotella) and lactobacilli and/or bifidobacteria was significantly higher than in controls (de Sousa Moraes et al., 2014). Microbial composition also seems to be changed by the ingestion of lactose in adult patients with hypolactasia (Whalqvist, 2015). Moreover, even in gastric disorders with impaired acid secretion, including H. Pylori infection, the need for oral thyroxine increased (Centanni, 2013; Lahner et al., 2014). Indeed, an intestinal dysbiosis has also been reported in hypochlorhydric patients (Walker and Talley, 2014) and in patients treated with proton pump inhibitors (PPI) (Freedberg et al., 2015)."
"Notably, despite the lack of general consensus, H. pylori infection seems to modify local and distant microbial populations (Kienesberger et al., 2016) and to enhance the expression of Pglycoprotein (P-gp) in the upper GI tract. P-gp, expressed on the luminal surface of the intestinal epithelium, (Omar et al., 2012) is thought to be a mediator of cellular thyroid hormone efflux (Mitchell et al., 2005). Overall, beside the reduction of the small intestine surface and/or the impaired gastric acid secretion in patients with gastric disorders, intestinal dysbiosis may represent an additional cause of thyroxine malabsorption."
"It has been estimated that ¼ of total bacteria possesses selenoprotein-encoding genes. Some of these, such as Escherichia Coli, Clostridia and Enterobacteria, are able to colonize the gastrointestinal tract of humans and animals (Hrdina et al., 2009)."
"In a very recent study using an in vitro gastrointestinal digestion procedure model (Lavu et al., 2016), it was proven that selenium not absorbed in the small intestine may be actively taken up in the colon and metabolized by the resident microbes. This represents a real competition for the substrate (selenomethionine being the preferred substrate) which causes a reduction of selenium bioaccessibility, as shown by the reverse effect exerted by the presence of an inactive microbiota (Lavu et al., 2016). This finding is in keeping with a previous one (Hrdina et al., 2009) in which the expression analysis of gastrointestinal selenoprotein isoforms revealed that bacteria may compete with the host, chiefly in the presence of limited selenium supply. This increased selenium uptake by the intestinal bacteria may negatively influence selenoprotein expression in the host (Kasaikina et al., 2011). Furthermore, selenium enrichment in the diet increased the biodiversity of host microbiota, supporting the notion that this micronutrient may also shape intestinal microbial composition (Kasaikina et al., 2011) in a bidirectional fashion, related to the different utilization and toxicity profile of the bacteria."
"Since the early 60s, in vitro studies have shown high affinity binding (T3 > T4) (Roche and Michel, 1960) and uptake (Salvatore et al., 1963) of radioactive iodothyronines in cultured Escherichia coli, a Gram-negative bacterium which is a major component of physiologic intestinal flora. In these cultured bacteria, deiodination, decarboxilation and deamination of iodothyronines have also been detected (Grasbeck et al., 1963; Roche and Michel, 1960; Salvatore et al., 1963)."
"In 1967, Chung and Van Middlesworth showed that bacteria in the intestine of normal rats are able to bind T4. This finding was later confirmed by Di Stefano III et al. (1993) who demonstrated a reversible in vivo binding of radiolabeled T3 and T4 in the feces and caecum contents of normal rats that was abolished or reduced in samples taken from antibiotic treated rats suggesting that the intestine may play a relevant role as a reservoir of an exchanging pool of iodothyronines; a pH-dependent oxidative degradation of T3 and T4 by intestinal flora was also observed."
"The explanation of these seminal observations became evident when the presence of deiodinase was detected in several of the rat's tissues, including the intestinal wall (Galton et al., 1991). These enzymatic activities have also been shown in the intestinal content of adult rats being inhibited by the resident microflora (Nguyen et al., 1993). In fact, they proved that both 5-D and 5'-D activities exist in adult rat intestinal contents possibly of cellular origin. In fact, the maximal deiodinase activity was found in frozed/defrosted samples, a step designed to rupture any cells in the media. Their activity was reduced or eliminated by the presence of normal intestinal bacteria. The authors postulated that the observed inhibition might be attributed to bacterial binding of T3 and T4. The presence of type 2 deiodinase (D2) activity has also been described in human intestinal wall (Sabatino et al., 2000)."
"Despite this strong evidence, the metabolic pathways more sensitive to the composition of intestinal microbiota, seem to be those involving phase II hepatic detoxication reactions. These include conjugation reactions encompassing either the esterification of the phenolic hydroxyl group with sulphuric acid or the etherification with glucuronic acid (Visser, 1996). These reactions increase the water solubility of iodothyronines, on the one hand enabling their biliary and renal clearance (Visser, 1996) and on the other reducing their intestinal absorption. T4 and rT3 are preferentially glucurono-conjugated whereas T3 may be equally glucurono-conjugated and sulphated (de Herder et al., 1985). Sulphoconjugation facilitates type 1 deiodination (D1) but not type 2 and 3 (D3) and, in patients with D1 and selenium deficiency or chronic diseases, sulphated iodothyronines may constitute a reservoir of active hormones (Wu et al., 2005). In rats but not in humans, drugs and toxins inducing glucuronidation have been shown to cause goitre and reduced concentrations of T4 and T3 as well as higher serum TSH levels (Wu et al., 2005)."
"It has been shown that diluted human fecal suspension is able to hydrolyze almost all these substrates, due to the presence of bacteria, chiefly obliged anaerobia, such as the Peptococcus productus, one of the major residents of normal human intestinal flora (de Herder et al., 1985). This bacterium has been proven highly active since an amount as small as [3 * 10^7]/ml hydrolyzed as much as 50% of sulphated iodothyronines in 24 h (de Herder et al., 1985). In rats and human intestinal content, a beta-glucuronidase activity has even been shown (de Herder et al., 1986)."
"The presence of glucuronidase and sulphatase activities in fecal content suggested the existence of enterohepatic circulation for iodothyronines. Rutgers et al. (1989) suggested that, in rats, the presence of intestinal microbiota may allow the reabsorption of native triiodothyronine following the hydrolysis of conjugated forms of the hormone. The fraction of reabsorbed hormone that escapes from liver extraction may be detected again in the systemic circulation."
"In humans, a recycling mechanism has been described for steroids hormones, biliary acids and vitamins, while the existence of an enterohepatic circulation of thyroid hormones is not supported by direct proof."
"So far, the role of microbiota seems to be a further regulator of thyroid homeostasis in that it may act directly through its metabolic enzymes as well as by modulating the chemical bioavailability of iodothyronines for reabsorption in the blood (Fig. 1) [No (Wagner, 2018).]. However, the possible effect of the variations in microbiota composition on iodothyronines homeostasis is a reasonable assumption but needs further evidence for being quantified."
"Some of the most common gastrointestinal disorders feature an increased need for oral thyroxine and microflora alterations at the same time. Despite the lack of direct proof regarding the role of microbial composition in the malabsorption of oral thyroxine, an increased need for thyroxine has been noted in patients with untreated celiac disease or lactose intolerance (Virili et al., 2012; Cellini et al., 2014). Interestingly, in children with celiac disease, the ratio between the possibly harmful Gram-negative bacteria (i.e. E. coli and Bacteroides-Prevotella) and lactobacilli and/or bifidobacteria was significantly higher than in controls (de Sousa Moraes et al., 2014). Microbial composition also seems to be changed by the ingestion of lactose in adult patients with hypolactasia (Whalqvist, 2015). Moreover, even in gastric disorders with impaired acid secretion, including H. Pylori infection, the need for oral thyroxine increased (Centanni, 2013; Lahner et al., 2014). Indeed, an intestinal dysbiosis has also been reported in hypochlorhydric patients (Walker and Talley, 2014) and in patients treated with proton pump inhibitors (PPI) (Freedberg et al., 2015)."
"Notably, despite the lack of general consensus, H. pylori infection seems to modify local and distant microbial populations (Kienesberger et al., 2016) and to enhance the expression of Pglycoprotein (P-gp) in the upper GI tract. P-gp, expressed on the luminal surface of the intestinal epithelium, (Omar et al., 2012) is thought to be a mediator of cellular thyroid hormone efflux (Mitchell et al., 2005). Overall, beside the reduction of the small intestine surface and/or the impaired gastric acid secretion in patients with gastric disorders, intestinal dysbiosis may represent an additional cause of thyroxine malabsorption."
@Blossom (no pressure for a reply)
@Amazoniac true to form, excellent info connecting many dots highlighting the importance in securing adequate thyroxine for our cells instead of those philphering bugs. Constant tug of war for resources. Thus thyroid replacement is first order of priority in all gut disorders/dysfunction + booting out freeloaders.
I have witnessed TSH come down in individuals just with the introduction of carrot salad and charcoal.
I have witnessed TSH come down in individuals just with the introduction of carrot salad and charcoal.
Can someone elaborate on this "near-death experience," curing hypothyroidism?
Thanks so much for yet another informative post. It’s amazing that all of this was known nearly 100 years ago and yet so little of the information is used for helping people today. It’s as if it has been forgotten.
@Blossom, this was a time before Rockafeller's rule and monopolistic control of the medical and research industries. As modern scientists we were discouraged in looking further than the last 5 years. We were indoctrinated to believe current knowledge was advanced knowledge, only learning decades after venturing down rabbit holes and dead ends that much of the modern knowledge had been corrupted by greed and power.
How many gut fixing gurus are out there promising to fix your gut; yet the problem persists and is reaching epidemic proportions? Orthodox medicine's solution is restrictive diets, elimination diets etc; a healthy gut should be able to cope with whatever you throw at it without ending up in the hospital emergency department.
The latest recommendations in Australia to prevent the increasing allergy rates is to introduce nuts and other highly allergic foods after 4 months of age. Australia has the highest rate of allergic conditions. When my children were in primary school, every third child had an asthma pump and the nut allergies were just starting to escalate; now through the roof along with kiwi fruits - so it is not just gluten. It was thought at the time the nut allergy was due to increasing switch to vegan diets and babies being sensitised via mother's diet in utero.
I have lived >30 yrs in a suburb inhabited by generations of militant greenies and hippies - individuals with all sorts of wild imaginings, so it is of no surprise the children and grandchildren suffer such high rates of allergies. It has always intrigued me why many of these radical personalities in the community suffered and eventually died from asthma attacks. A prominent university lecturer in my street died from cancer at a young age and her mother from pancreatic cancer. The lecturer was a Ayurvedic practitioner and even though she was younger than me, was never a picture of robust health. As a prominent researcher in alternative health, she had access to all the knowledge but somehow was misguided. Yet, I was targeted by these radicals for having strange ideas about the foods I fed my family and our way of life and values. I was labelled an environmental vandal due to my fecundity.
Ray may not have all the answers but he is an excellent historian and researcher who has opened our minds to the complexity of the human organism. The complexity is simplified when we consider the basic needs of our cells.
Even if tolerance is increased, many of these allergenic foods are not ideal when there are superior options.
How many gut fixing gurus are out there promising to fix your gut; yet the problem persists and is reaching epidemic proportions? Orthodox medicine's solution is restrictive diets, elimination diets etc; a healthy gut should be able to cope with whatever you throw at it without ending up in the hospital emergency department.
The latest recommendations in Australia to prevent the increasing allergy rates is to introduce nuts and other highly allergic foods after 4 months of age. Australia has the highest rate of allergic conditions. When my children were in primary school, every third child had an asthma pump and the nut allergies were just starting to escalate; now through the roof along with kiwi fruits - so it is not just gluten. It was thought at the time the nut allergy was due to increasing switch to vegan diets and babies being sensitised via mother's diet in utero.
I have lived >30 yrs in a suburb inhabited by generations of militant greenies and hippies - individuals with all sorts of wild imaginings, so it is of no surprise the children and grandchildren suffer such high rates of allergies. It has always intrigued me why many of these radical personalities in the community suffered and eventually died from asthma attacks. A prominent university lecturer in my street died from cancer at a young age and her mother from pancreatic cancer. The lecturer was a Ayurvedic practitioner and even though she was younger than me, was never a picture of robust health. As a prominent researcher in alternative health, she had access to all the knowledge but somehow was misguided. Yet, I was targeted by these radicals for having strange ideas about the foods I fed my family and our way of life and values. I was labelled an environmental vandal due to my fecundity.
Ray may not have all the answers but he is an excellent historian and researcher who has opened our minds to the complexity of the human organism. The complexity is simplified when we consider the basic needs of our cells.
Even if tolerance is increased, many of these allergenic foods are not ideal when there are superior options.
Last edited:
Hello @rebuke
I didn’t take the article’s author or RP as saying that a near death experience cures hypothyroidism. More like, if you compensate stress, then a stable period follows an unstable period.
In the article it made me laugh when the author said that if the treatment of a thyroxine goiter by removal didn’t prove fatal, then the patient could live to be perfectly healthy.
As you show me (thank you) RP is saying something different. I took him to be saying that few people understand how risky to the physiology it is to be in a fasted state all night. Or, maybe it’s not that different. It would be as if to say, “ A good night’s sleep is health-promoting, but darkness & fasting are as physiologically stressful as it gets in a typical day. So eat breakfast. And have enough fruit/oj.”
I didn’t take these to be near death experiences like you have when you think you’ve just avoided an accident. I take RP to be working extra hard to get his readers to take physiological stresses seriously.
I didn’t take the article’s author or RP as saying that a near death experience cures hypothyroidism. More like, if you compensate stress, then a stable period follows an unstable period.
In the article it made me laugh when the author said that if the treatment of a thyroxine goiter by removal didn’t prove fatal, then the patient could live to be perfectly healthy.
As you show me (thank you) RP is saying something different. I took him to be saying that few people understand how risky to the physiology it is to be in a fasted state all night. Or, maybe it’s not that different. It would be as if to say, “ A good night’s sleep is health-promoting, but darkness & fasting are as physiologically stressful as it gets in a typical day. So eat breakfast. And have enough fruit/oj.”
I didn’t take these to be near death experiences like you have when you think you’ve just avoided an accident. I take RP to be working extra hard to get his readers to take physiological stresses seriously.
OP
Amazoniac
Member
Thanks to Jorgito's product CamphoSal, I came across this:
- Certain Fundamental Principles relating to the Activity of Bacteria in the intestinal Tract. Their Relation to Therapeutics
- Certain Fundamental Principles relating to the Activity of Bacteria in the intestinal Tract. Their Relation to Therapeutics
OP
Amazoniac
Member
The fraction of lactose that's not absorbed should be primed to have a protective function (let's say that something bad happens to the fetus and suddenly lactose digestion is impaired).
It can't be assumed that lactose in isolation is going to affect the person the same way as when it's consumed in milk. People's diets aren't composed exclusively of milk, other factors may set a problematic ground, increasing the chances of dampening or losing such protective function, lactose may even become an aggravator.
I think that ingesting a relatively large dose of purified lactose early in the day along with venom D and K2 deserves a try, in particular from people who are dealing with chronic constipation or pathogenic microbes. Honey, propolis, organic acids (butter's fartic acid?) or edible fruit skins can be valuable additions, but the meal has to remain simple to avoid weakening the effect. It's an alternative to these (that I prefer):
- Butyric Acid From Fiber And Starch
Adapting to lactose separately from milk may be one option for those whose current attempts are being overwhelming.
The boosting of killcium absorption is another aspect that can be explored.
Note: hospitalization is on you.
- Lactulose, rifaximin or branched chain amino acids for hepatic encephalopathy: what is the evidence?
It can't be assumed that lactose in isolation is going to affect the person the same way as when it's consumed in milk. People's diets aren't composed exclusively of milk, other factors may set a problematic ground, increasing the chances of dampening or losing such protective function, lactose may even become an aggravator.
I think that ingesting a relatively large dose of purified lactose early in the day along with venom D and K2 deserves a try, in particular from people who are dealing with chronic constipation or pathogenic microbes. Honey, propolis, organic acids (butter's fartic acid?) or edible fruit skins can be valuable additions, but the meal has to remain simple to avoid weakening the effect. It's an alternative to these (that I prefer):
- Butyric Acid From Fiber And Starch
Adapting to lactose separately from milk may be one option for those whose current attempts are being overwhelming.
The boosting of killcium absorption is another aspect that can be explored.
Note: hospitalization is on you.
T
TheBeard
Guest
@Amazoniac what is your overall stance on gut bacteria after all the reading you've done and all the connections you've made:
1) always useful?
2) useful in a particular context?
3) always harmful, better sterilize the gut?
1) always useful?
2) useful in a particular context?
3) always harmful, better sterilize the gut?
OP
Amazoniac
Member
- Lactose intolerance | Muscle and Strength
- Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment
I think that lactose powder on its own can be problematic, but if it's combined with some honey (will thicken it) to dress a fruit salad, it should be safer.
The effect from lactose has to predominate.
- Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment
I think that lactose powder on its own can be problematic, but if it's combined with some honey (will thicken it) to dress a fruit salad, it should be safer.
The effect from lactose has to predominate.
My response is predictable. Killing our neurons sounds risky.
OP
Amazoniac
Member
- Bovine milk oligosaccharides decrease gut permeability and improve inflammation and microbial dysbiosis in diet-induced obese mice
"Bovine milk is a source of oligosaccharides that resemble human milk oligosaccharides (HMO), though with different structures and a much lower concentration than human milk (Chichlowski et al., 2011). The majority of the molecules are more simple in structure compared with those found in human milk (Zivkovic and Barile, 2011). New methods for separation and concentration of bovine milk oligosaccharides (BMO) from bovine milk industrial streams such as whey permeate are now available. Because whey permeate is a byproduct in the production of whey protein concentrate and is readily available, it is an attractive source of oligosaccharides for potential application in human nutrition (Zivkovic and Barile, 2011; Barile and Rastall, 2013)."
Peatful
Member
- Joined
- Dec 8, 2016
- Messages
- 3,582
Thx for posting this
EMF Mitigation - Flush Niacin - Big 5 Minerals
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