Endotoxin And Fat Consumption

[Nighteyes]

Ok, so everything seems connected:

man- do I get this feeling often! Maybe everything is, to some degree?

If (and a big if here) there's truth to the whole a1/a2 casein story, then the majority of people consume dairy that contains that type of casein the impairs motility to different degrees.

I have tried switching from drinking a lot of 0.1 % cow milk to using goat whey shakes in water and the latter never causes constipation or sinus issues. The cow milk often does. I am just worried that the whey is too imbalanced somehow. So I add glycine and lysine. really wish I could buy 0,1 % goat or sheep milk.

Any concrete tips for improving antioxidant status as you mention? I would guess lots of fruit?

Thanks for your posts amazoniac. your sense of humor is unique. Do you somehow interact a lot with burtlancast or is it your alias (he is the serious one and amazoniac lets you let loose a bit?)

 

[Mjhl85]

what's 0.1% cow milk? do you mean 1%?

 

[zooma]

what's 0.1% cow milk? do you mean 1%?

More commonly known as skim/skimmed milk

 

[Amazoniac]

man- do I get this feeling often! Maybe everything is, to some degree?



I have tried switching from drinking a lot of 0.1 % cow milk to using goat whey shakes in water and the latter never causes constipation or sinus issues. The cow milk often does. I am just worried that the whey is too imbalanced somehow. So I add glycine and lysine. really wish I could buy 0,1 % goat or sheep milk.

Any concrete tips for improving antioxidant status as you mention? I would guess lots of fruit?

Thanks for your posts amazoniac. your sense of humor is unique. Do you somehow interact a lot with burtlancast or is it your alias (he is the serious one and amazoniac lets you let loose a bit?)

I think that requiring too much antioxidants is a bad sign. One example is bowel tolerance for vit C (the classic article). So I guess that the best way to improve their status is by focusing on less inflammation and better metabolism in general. I guess that not messing things up is an art that I'm still learning; if you try to interpret your cravings, it might give you a clue about what you currently need; because as you know, in excess, they also cause problems.

Endogenous antioxidants are also important; the best way to support that is probably by becoming well-nourished and avoiding wasting resources with unnecessary stressors (like trying to catch burtlan's attention via PMs but being brutally ignored); we're supposed to regulate that naturally when we follow our instincts..

Regarding the last question, pboy disappeared; life gave me lemons, I had to make lemonade with the best available..

 

[Nighteyes]

pboy disappeared; life gave me lemons, I had to make lemonade with the best available..

yeah I thought I made a sighting not too many weeks ago, but the shyness is great in that one.

 

[CarbAppreciator]

Good quote from that last study
"
A 4-h treatment with morphine or milk-derived opioid peptides (1μM) caused a
significant shift toward increased methylation (i.e., promoter hyper-
methylation) in the immediate TSS region. Morphine was most
effective, increasing genome-wide methylation at the TSS peak to 22%
above control levels, followed by bBCM7 and hBCM7, representing
increases of 17% and 10%, respectively, a rank order that mirrors their
inhibition of cysteine uptake."

 

[PakPik]

this might be an insult beyond the capacities of someone in a compromised health state

Good posts, Amazoniac. Basically almost everything under the sun can become an insult to a person with enough compromise/stress to their tissues and organs. Good thing is that if order comes back, the person may regain the ability to process previously problematic food in a proper way and benefit from it -I've been there :) .

I think that requiring too much antioxidants is a bad sign.

in excess, they also cause problems.

Yeah. And supplements won't do much, if they do anything at all -or even cause harm-, if tissues keep deteriorating so out of control. It is key to interfere with the self-amplifying vicious circles of tissue damage, and some people will need more extreme interventions than others, depending on their mileage.

 

[Amazoniac]

People that feel guilty for accidentally slicing in half a larvae that was chilling and feasting inside your food, it was there first;

The Effect of Diet and Exercise on Intestinal Integrity and Microbial Diversity in Mice
"The major findings of these studies indicate that: (1) high-fat diets altered intestinal morphology particularly of the duodenum; (2) exercise protected duodenal morphology in the presence of a high-fat diet; (3) high-fat diets increased intestinal inflammation and exercise reduced it; (4) exercise manifested a unique microbiome independent of diet; (5) exercise reduced blood levels of IL-6, insulin and ghrelin and increased levels of satiety related hormones (Fig 7). We observed that high fat diets accompanied with sedentary behavior increased the width of duodenal villi. We are the first using IHC to substantiate in situ inflammation and loss of intestinal integrity due to high fat diet and sedentary lifestyle in mice. These data correlate with results from others in that animals fed a high-fat diet had a three-fold increase in TG accumulation in intestinal mucosa and an up-regulation of genes for TG synthesis, chylomicron secretion and uptake, oxidation and de novo synthesis of fatty acids [47]. These observations, accompanied with an impaired oral fat tolerance, suggest a reduced rate of intestinal lipid secretion led to increases in mucosal TG accumulation and contributed to the shortening and widening of the villi."
Interesting images, it's worth checking them.

--
http://www.nature.com/nature/journal/v487/n7405/full/nature11225.html
"Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts."

--
Gut barrier impairment by high-fat diet in mice depends on housing conditions - Müller - 2016 - Molecular Nutrition & Food Research - Wiley Online Library
This one is interesting because we often read that you cannot go wrong with dairy fat because it wouldn't be composed in a way that harmed babies. Howeva, things start to get messy in adults due to so many adversities, like bad gut composition:

"In addition to metabolic endotoxemia, DIO [diet-induced obesity] is often associated with low-grade inflammation [2]. In the present study, concentrations of the pro-inflammatory cytokines/chemokines TNF and MCP-1 were only elevated in the adipose tissue of DIO mice kept in the CV [shitty] facility. LPS is considered to promote adipose tissue inflammation via the TLR4/CD14 pathway accompanied by infiltration of macrophages [29]. The unchanged inflammatory tone that was observed in SPF [a more sterile conditioned] mice agrees with the absence of metabolic endotoxemia."
"Moreover, Stenman et al. defined the HFD-induced alterations of fecal bile acid profiles as the potential cause of intestinal barrier dysfunction, but not obesity per se [16, 37]." (related to the previous link)
"In conclusion, we here demonstrate that alterations of dominant gut bacterial communities and intestinal barrier integrity in mice fed a HFD depend on housing conditions. The changes found are associated with alterations in intestinal levels of secondary bile acids, intestinal permeability, portal LPS levels and an elevated fat tissue inflammatory tone under CV but not SPF conditions."

 

[Amazoniac]

pboy

 

[Kyle M]

I don't know if anyone pointed this out yet but chylomicrons only go from the enterocytes to lymph to circulation, not from the gut to enterocytes. The endotoxin is probably taking a ride complexed with micelles of bile, fatty acids and monoglycerides.

 

[ecstatichamster]

I don't know if anyone pointed this out yet but chylomicrons only go from the enterocytes to lymph to circulation, not from the gut to enterocytes. The endotoxin is probably taking a ride complexed with micelles of bile, fatty acids and monoglycerides.

can you elaborate? I'm not sure I'm connecting the dots and I want to understand your point. Thanks!

As I understand it, in the lining of the small intestine are villae and these used to process fat into chylomicrons which are absorbed and distributed via lymphatic tissue there.

 

[Kyle M]

can you elaborate? I'm not sure I'm connecting the dots and I want to understand your point. Thanks!

As I understand it, in the lining of the small intestine are villae and these used to process fat into chylomicrons which are absorbed and distributed via lymphatic tissue there.

It is my understanding that there are 2 discreet occurrences vis a vis fat absorption and secretion into circulation, getting into the enterocyte and leaving the enterocyte. I've seen studies where labeled dietary fat can be made to stay in the enterocyte, or pushed out, sooner or later depending on the composition of the subsequent meal. So fat getting into enterocytes does not equate to instantaneous secretion into lymph as chylomicrons. The fat gets into the enterocyte emulsified in bile, and that's where the endotoxin gets in. Then, it sticks with the fatty acids and chylomicrons and gets deposited somehow in circulation. So the main way that not eating fat prevents endotoxin from reaching circulation is that bile does not get produced to pull in dietary fatty acids, and the endotoxin, probably because of it's lipid moiety, does not get in effectively. Whether or not the enterocyte secretes chylomicrons using whatever fat is has at that point is secondary to the initial absorption.

 

[Amazoniac]

Members that finish watching Braveheart feeling like a warrior, but then look down and realize that you put your Spongebob pajama on the wrong side;

Diet-induced bacterial immunogens in the gastrointestinal tract of dairy cows: Impacts on immunity and metabolism

“Rumen epithelium has a multilayer structure whose tight junctions are located in the middle layers, stratum grannulosum, and spinosum [20]. Although the external layer of rumen epithelium has no tight junctions, it may have up to 15 cell layers, which can limit the permeability of LPS, a large molecule [21].”

“Therefore, it seems the ruminal epithelium is impermeable to endotoxin at the physiological state unless the rumen epithelial structure is disrupted to a greater extent. Thus it is likely that LPS translocation occurs mainly in the intestines. Epithelium in the intestines is of a monolayer structure with tight junctions at the apical pole of the cells. In the study of Chin et al. [25] using intestinal epithelial cell lines, an abnormal increase in luminal LPS induced cell apoptosis, disrupted tight junction protein zonula occludens-1, and enhanced epithelial permeability in a dose and time dependent manner by increasing the production of nitric oxide.”

“LPS flowing to the intestines could be detoxified in the duodenum by bile acid [27]. However, since the rumen is an immense LPS source, LPS entering the intestines may not be completely detoxified in the duodenum and may be translocated into circulation across the intestines. In addition, a source of LPS which is translocated into blood circulation may be produced originally in the lower gut. In this case, the LPS production would not be pH dependent, but starch dependent. The bypass starch which reaches the ileum and large intestine may result in a change of microbiota there and thus the release of LPS in a manner described previously for the rumen.”
Humans, just as a reminder, this is on grain-fed ruminants.

“Although studies on diet-induced bacterial immunogens are focused on LPS, it does not mean the inflammation in relation to grain-induced SARA [Sub-Acute Ruminal Acidosis*] is caused solely by LPS. Other immunogenic virulence factors in the digestive tract following feeding a high grain diet may have contributed to the inflammation which has been observed in many studies on grain-induced SARA in dairy cattle.”
*I think it ties back to the previous discussion here, how acidification permeabilizes the membranes of gram-negative bacteria and that in turn releases a massive amount of endotoxin.

“Feeding dairy cows high-grain diets rich in rapidly fermentable carbohydrates will lead to increased yield of volatile fatty acids, especially propionate in the rumen, and its absorption into the bloodstream [44]. The absorption of propionate into blood circulation or its effects on rumen receptors may result in decreased feed intake in cows fed high grain diets [6]. In addition, deceased feed intake with increasing the amount of grain in the diet may be due to enhanced release of endotoxin and other bacterial immunogens in the digestive tract and their translocation into blood. Increased endotoxin concentrations in the bloodstream will lead to release of cytokines such as IL-1, IL-6, and TNF-α due to activation of macrophages [32], and IL-1 and TNF-α can suppress feed intake in different species [45].”

“Cows fed the greatest amount of barley grain (i.e., 45%) had the lowest concentrations of Ca, Fe and Zn in the plasma, whereas the highest concentrations of Ca, Fe and Zn were observed in the plasma of cows fed the 15% grain-based diet.”

“As discussed previously, endotoxin and other bacterial immunogens which are translocated into blood will elicit systemic inflammatory responses. Under the circumstances, nutrients will be directed to support proinflammatory events. The redirection or repartition of nutrient use in addition to a low nutrient supply due to depressed low feed intake will decrease nutrient flow to the mammary gland.”

--
https://actavetscand.biomedcentral....4-S1-S141?site=actavetscand.biomedcentral.com

“On the basis of these findings it can be conjectured that endotoxin-induced gastro- intestinal hypomotility might be of significance in the development of bovine indigestion.”

“The prostaglandins, and especially the PgE's, affect the tonus and motility of the gastrointestinal tract. In goats, systemic administration of these prostaglandins induces, among other effects, hypomotility and diarrhoea (Veenen-daal et al. 1980) and cessation of ruminal contractions (van Miert et al. 1977).”

“During inflammation, the liver acutely (i.e. within few hours) increases the production of acute phase proteins, such as haptoglobin, a1-acid glycoprotein, α1-protease inhibitor, fibrinogen, ceruloplasmin and amyloid A, at the expense of synthesis of for example albumin (Conner et al. 1986, Eckersall & Conner 1988). This shift in protein synthesis is initially mediated by IL-1 and TNF, and then amplified by a second wave of IL-1 and IL-6, synthesized by fibroblasts and endothelial cells (Conner et al. 1989. Dofferhoff et al. 1990. Fey et al. 1994).”

“After tolerance is induced, endotoxin administered in even lethal doses does not elicit detrimental biological responses.”

“It is generally agreed that endotoxins are not contaminants of systemic blood in healthy individuals and that impairment of liver function may result in systemic endotoxemia in otherwise healthy humans (Bjørneboe et al.1972, Prytz et al. 1973). This seems to be the case for ruminants too.”

 

[ecstatichamster]

Thanks @Kyle M

 

[Amazoniac]

Members that don't travel alone and mapless every weekend to Paris to do a session of Buteyko's breathing exercises inside the catacombs;
burtlan;

http://ajpgi.physiology.org/content/286/4/G558

"Peptide YY (PYY), a distal gut peptide released in response to a fatty meal, slows intestinal transit when administered intravenously (47). In addition to this slowing effect on intestinal transit, PYY is considered an inhibitory peptide, because it suppresses gastrin-stimulated acid secretion (1, 42), pancreatic exocrine secretion (1, 40), CCK release (41), and gastric emptying (47). These inhibitory effects of exogenous PYY suggest that it may be responsible for the ileal brake (49), a response that suppresses the digestive activities of the upper gastrointestinal tract when nutrients such as fat reach the distal gut. Immunoneutralization studies (38) confirmed that PYY is a key mediator of the slowing of intestinal transit by the fat-induced ileal brake."

"We also showed that delivering ondansetron (a 5-H3 receptor antagonist) (32) or naloxone (a nonspecific opioid receptor antagonist) (59) into the proximal but not distal intestinal segment reversed the fat-induced ileal brake to localize the serotonergic (32) and opioid (59) pathways involved in the fat-induced ileal brake response to the efferent limb of the slowing reflex."

"Because the slowing of intestinal transit by fat was reversed by ondansetron in conscious dogs (32) and rats (8, 9), we further hypothesized that intestinal transit may be slowed by luminal 5-HT in the whole animal."

"In a fistulated dog model, we found that the slowing of intestinal transit by PYY was reversed by ondansetron (a 5-HT3 receptor antagonist) and by naloxone (a nonspecific opioid receptor antagonist) when either of these agents were delivered luminally into the small intestine. However, these antagonists reversed the slowing of transit by PYY only when they were delivered into the proximal half of the small intestine in which transit was measured. This compartment-specific effect suggests that the serotonergic and opioid pathways involved in the slowing of intestinal transit by PYY are located on the efferent limb of the slowing reflex response."

"Previously, we reported in the same model that slowing of intestinal transit by fat in the distal gut as the fat-induced ileal brake depended on the release of PYY (38). In addition, we found that a serotonergic pathway (32) and an opioid pathway (59) located on the efferent limb of this slowing response were required."

"The compartment-specific effect is the strongest evidence that ondansetron or naloxone worked locally and not systematically, because identical amounts of each antagonist were delivered into each segment, but these agents only reversed the ileal brake when delivered into the efferent but not afferent limb of the slowing reflex. This finding simply cannot be explained by a postabsorptive systemic effect."

"The inhibitory action of PYY on intestinal transit is then similar to the effect of this peptide on pancreatic secretion, which is also known to be dependent on a neural pathway located on the efferent limb (43)."

"This slowing effect of 5-HT in whole animals contrasts with the triggering of peristalsis (accelerates transit) by 5-HT in in vitro models (10, 25, 48). A comparison of the different effects of 5-HT in the in vitro models vs. that in whole animals would suggest that the slowing of intestinal transit by luminal 5-HT may depend on extrinsic nerves that participate in long, intestinointestinal reflexes. These nerves would be present in the whole animals but absent in in vitro models."

Cited: www.gastrojournal.org/article/S0016-5085(08)81111-0/

 

[Amazoniac]

Just a few quotes from this:
Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity - Hersoug - 2015 - Obesity Reviews - Wiley Online Library

"It is primarily the lipid A part, which is responsible for its highly toxic and immunomodulatory property of LPS (40). It has been estimated that the human gut contains around 1g of LPS (41)."

"Low levels of bile acids in the gut are associated with bacterial overgrowth and inflammation. The resulting invasion of pathogenic species of bacteria in the proximal small intestine may induce injury to absorptive cells, exacerbate local inflammation, cause villus blunting and alter intestinal permeability (57)."

"Intestinal alkaline phosphatase (IAP) can detoxify LPS by removing the two phosphate groups on the carbohydrate backbone (64). It has recently been shown that IAP is highly expressed on the brush-border of epithelial cells, and it is secreted into the lumen where it co-localizes with intracellular lipids (65). This may function in an adaptive mechanism to sustain potentially toxic effects of Gram-negative bacteria normally found in the small intestine. IAP’s ability to detoxify LPS is also documented by observations that it protects against development of sepsis during acute inflammation and chronic inflammatory conditions such as inflammatory bowel disease (66). It has been shown that IAP knock-out (KO) mice display of metabolic syndrome such as obesity, endotoxemia, elevated blood glucose, glucose intolerance and hyperinsulinemia (67). Oral supplementation of IAP prevents and reverses these conditions in KO mice and as well in models of HFD-induced metabolic syndrome (67)."

"INF-γ, TNF-α, IL-lβ, IL-4 and IL-6 induce intestinal barrier defects by increasing the paracellular permeability, whereas IL-10 is suggested to have a role in protecting the intestinal barrier (39)."

"..lipid absorption occurs in the proximal segment of the small intestine (105). On the contrary, the bacteria concentrations are highest in the distal intestine. This is not necessarily a contradiction because the amount of LPS in the gut is measured in grams and the amount transferred after a high fat meal is measured in micrograms, and we must assume that LPS is not in shortage."

"The principal organ for CM[chylomicron]-remnants clearance seems to be the liver, but animal studies using radioactively labelled TGs and cholesteryl oleate show a profound heterogeneity with estimations ranging from 20% to 88%, depending on the experimental system and type of lipid (112). Therefore other tissues (e.g. AT [adipose tissue]) than the liver may also take part in the removal of CM-remnants; especially large-size CMs may be too large to enter through the fenestrated hepatic sinusoidal endothelium to reach the hepatic CM-remnant receptors (113)."
"Sensing of high lipid content in the diet leads to increased size of CMs, but not in an increase in their number, suggesting that the ApoB48 lipidation capacity adapts to the lipid content of the diet (101,102)."
"Both the incorporation of lipids and LPS into CMs might be an active process regulated by the lipid content in the gut. It is possible that the incorporation of LPS into CMs from the transcellular route could be due to the dual receptor properties of SR-BI and CD36 as FA translocases and LPS receptor, although TLR4 and MD 2 also participate in the absorption of LPS."
"This further implies that LPS could be an important determinant of the CM size because of possibly regulated internalization of LPS by the SR-BI, CD36, TLR4 and MD-2 receptors, where it is transported to the Golgi apparatus prior to the assembly of CMs."

"The importance of the gut microbiome for weight control has been clearly demonstrated in studies on germ-free mice that do not develop obesity when fed a high-fat and sugar-rich diet, whereas they increase rates of weight gain when experimentally colonized with bacteria from the cecum of wild-type mice (117,118)."

"It is worth noting that ~90% of LPS is associated with lipoproteins in human plasma; 60% is bound to HDL (128,129) and the rest is bound to LBP and soluble CD14 (sCD14)."

"In situations of infections and sepsis, adipocytes may function as sinks for clearing excess LPS from the circulation. In situations of sepsis it has already been established that infusion of HDL attenuated the severity of symptoms (104,143,144)."

"CMs in the circulation can attach to the vascular endothelium by interaction with the enzyme lipoprotein lipase (LPL). LPL has been identified in AT, cardiac and skeletal muscles, pancreatic islets and macrophages (106)."

"The liver plays a crucial role in maintaining whole body glucose metabolism, and it seems that LPS also impairs this function. Animal models of periodontitis have indicated that LPS from periodontal pathogens is causally related to glucose intolerance and insulin resistance (164)."

 

[EIRE24]

Just a few quotes from this:
Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity - Hersoug - 2015 - Obesity Reviews - Wiley Online Library

"It is primarily the lipid A part, which is responsible for its highly toxic and immunomodulatory property of LPS (40). It has been estimated that the human gut contains around 1g of LPS (41)."

"Low levels of bile acids in the gut are associated with bacterial overgrowth and inflammation. The resulting invasion of pathogenic species of bacteria in the proximal small intestine may induce injury to absorptive cells, exacerbate local inflammation, cause villus blunting and alter intestinal permeability (57)."

"Intestinal alkaline phosphatase (IAP) can detoxify LPS by removing the two phosphate groups on the carbohydrate backbone (64). It has recently been shown that IAP is highly expressed on the brush-border of epithelial cells, and it is secreted into the lumen where it co-localizes with intracellular lipids (65). This may function in an adaptive mechanism to sustain potentially toxic effects of Gram-negative bacteria normally found in the small intestine. IAP’s ability to detoxify LPS is also documented by observations that it protects against development of sepsis during acute inflammation and chronic inflammatory conditions such as inflammatory bowel disease (66). It has been shown that IAP knock-out (KO) mice display of metabolic syndrome such as obesity, endotoxemia, elevated blood glucose, glucose intolerance and hyperinsulinemia (67). Oral supplementation of IAP prevents and reverses these conditions in KO mice and as well in models of HFD-induced metabolic syndrome (67)."

"INF-γ, TNF-α, IL-lβ, IL-4 and IL-6 induce intestinal barrier defects by increasing the paracellular permeability, whereas IL-10 is suggested to have a role in protecting the intestinal barrier (39)."

"..lipid absorption occurs in the proximal segment of the small intestine (105). On the contrary, the bacteria concentrations are highest in the distal intestine. This is not necessarily a contradiction because the amount of LPS in the gut is measured in grams and the amount transferred after a high fat meal is measured in micrograms, and we must assume that LPS is not in shortage."

"The principal organ for CM[chylomicron]-remnants clearance seems to be the liver, but animal studies using radioactively labelled TGs and cholesteryl oleate show a profound heterogeneity with estimations ranging from 20% to 88%, depending on the experimental system and type of lipid (112). Therefore other tissues (e.g. AT [adipose tissue]) than the liver may also take part in the removal of CM-remnants; especially large-size CMs may be too large to enter through the fenestrated hepatic sinusoidal endothelium to reach the hepatic CM-remnant receptors (113)."
"Sensing of high lipid content in the diet leads to increased size of CMs, but not in an increase in their number, suggesting that the ApoB48 lipidation capacity adapts to the lipid content of the diet (101,102)."
"Both the incorporation of lipids and LPS into CMs might be an active process regulated by the lipid content in the gut. It is possible that the incorporation of LPS into CMs from the transcellular route could be due to the dual receptor properties of SR-BI and CD36 as FA translocases and LPS receptor, although TLR4 and MD 2 also participate in the absorption of LPS."
"This further implies that LPS could be an important determinant of the CM size because of possibly regulated internalization of LPS by the SR-BI, CD36, TLR4 and MD-2 receptors, where it is transported to the Golgi apparatus prior to the assembly of CMs."

"The importance of the gut microbiome for weight control has been clearly demonstrated in studies on germ-free mice that do not develop obesity when fed a high-fat and sugar-rich diet, whereas they increase rates of weight gain when experimentally colonized with bacteria from the cecum of wild-type mice (117,118)."

"It is worth noting that ~90% of LPS is associated with lipoproteins in human plasma; 60% is bound to HDL (128,129) and the rest is bound to LBP and soluble CD14 (sCD14)."

"In situations of infections and sepsis, adipocytes may function as sinks for clearing excess LPS from the circulation. In situations of sepsis it has already been established that infusion of HDL attenuated the severity of symptoms (104,143,144)."

"CMs in the circulation can attach to the vascular endothelium by interaction with the enzyme lipoprotein lipase (LPL). LPL has been identified in AT, cardiac and skeletal muscles, pancreatic islets and macrophages (106)."

"The liver plays a crucial role in maintaining whole body glucose metabolism, and it seems that LPS also impairs this function. Animal models of periodontitis have indicated that LPS from periodontal pathogens is causally related to glucose intolerance and insulin resistance (164)."

Would Ox bile be a good sub for insufficient bile production?

 

[Amazoniac]

Would Ox bile be a good sub for insufficient bile production?

@lindsay

 

[milk_lover]

what happened to @tyw ? He is not active anymore!

 

[tyw]

what happened to @tyw ? He is not active anymore!

Busy . Mainly with software and Chinese Medicine . I don't like posting short snippets, and therefore have not been posting much.

Still have been reading some stuff though. Most recently, and potentially relevant to this thread, is this stupidly long and detailed article about DNA methylation -- Aging, health and disease – view from the DNA Methylome | AGINGSCIENCES™ – Anti-Aging Firewalls™

I have not finished reading the article, but did find the relation between CpG-mediated DNA Methylation and Toll-like Receptor 9 (TLR9) to be interesting.

This hints at "pathogens disrupting the cell cycle". Some references:

- Toll-like receptor 9 mediates CpG-DNA signaling. - PubMed - NCBI
- Structural basis of CpG and inhibitory DNA recognition by Toll-like receptor 9. - PubMed - NCBI
- Toll-like receptor 9, CpG DNA and innate immunity. - PubMed - NCBI

The relevance to this thread is that the same bacterial that produce endotoxin, may also affect TLR9. (NOTE: endotoxin itself is probably only mostly active at TLR4)

.....