Gut Bacteria May Cause ALL Autoimmune Conditions; Antibiotics Can Cure

[Vinero]

A few things I have to add.

First, I think a pretty overlooked subject is that of the ear/nose/mouth/throat microbiome - and their connection to the gut. My gut tells me it's not just the gut, hahah, it seems a lot of endotoxin can be seeded from the sinuses / gums etc. I think that is where things like nasal irrigation / oil pulling / water-picking, can be of great value. In terms of permeability, whatever is living inside your gums right now, most likely is tapped directly in to your bloodstream - I don't think there is a significant barrier there compared to the permeability of the gut.

Secondly, I strongly believe taking antibiotics many times as a child truly screwed up my health long term. I think it is all about low and slow maintenance, and I think antibiotics should be reserved for when one is outright sick, I don't see the point in attacking all bacteria both gram positive and negative, unless one is desperate. Xylitol is awesome stuff for busting bio-films all over the place. I think it really compliments things like the carrot salad. Other 'Low and slow' things I have had success with: activated charcoal, molybdenum (to detox faster / reduce nausea from die-off), vinegar, grapefruit seed extract, castor oil, turpentine, lysine, boron. For maintenance purposes, I prefer downing a little turpentine or gse with castor oil once or twice a week, followed by some activated charcoal.

Thirdly, I have not found a good report on lipopolysaccharide as a whole in commonly available foods. However one can look at reports on E. Coli and other food-borne illnesses as a proxy and get a feel.

Here for instance is a report estimating the sources of various foodborne illness outbreaks:
https://timedotcom.files.wordpress.com/2015/02/ifsac-project-report-508c.pdf

Another of interest:
Table 1 - Attribution of Foodborne Illnesses, Hospitalizations, and Deaths to Food Commodities by using Outbreak Data, United States, 1998–2008 - Volume 19, Number 3—March 2013 - Emerging Infectious Disease journal - CDC

After digging around my take away is the biggest risks stem from: raw vegetables, raw dairy, poultry (easy to undercook) and beef (particularly pre-tenderized, or ground).

I knew there was something wrong with ground beef, as I have gotten endotoxin symptoms after eating a lot of it.
I have pure xylitol powder which I swish around in my mouth for it's anti-bacterial effect. I never swallow it though.

 

[Captain_Coconut]

I knew there was something wrong with ground beef, as I have gotten endotoxin symptoms after eating a lot of it.
I have pure xylitol powder which I swish around in my mouth for it's anti-bacterial effect. I never swallow it though.

This is my very crude understanding. In theory at least, xylitol consumption will increase intestinal butyrate production, which will help to thicken up the intestinal wall (fight against leaky gut), in turn helping to protect against endotoxin. In addition to this, biofilms are broken up because xylitol acts like a sort of trojan horse, sugar hungry microbes eat the xylitol but do not have the ability to properly digest it - so they die off, this breaks up the film and makes it vulnerable to your immune system / or being carried out by activated charcoal for instance. I have taken xylitol off and on, it creates a massive uncomfortable die off reaction if you ramp up too fast, you want to go slow with it, and always compliment it with other gut friendly protocol. For around 10 days I would take xylitol (3 or 4 tsp daily) with my coffee, in addition I was having daily carrot salad, and occasionally having activated charcoal. It definitely fixed up my gut, not to tmi you, but after those 10 days were up, for around a month after I had the healthiest bowel movements of my life.. It did much more for me than carrot salad or charcoal have done alone. YMMV

 

[managing]

Manuka is great, I did think it was interesting that in a study they showed it wasn't necessarily much better than any other honey, including heat processed. And that has been my experience, too. I wonder how much of it just has to do with the quick hit of sugar.

Fructose to be specific. I love that quick rush of wide open and clear breathing . . .

This is my very crude understanding. In theory at least, xylitol consumption will increase intestinal butyrate production, which will help to thicken up the intestinal wall (fight against leaky gut), in turn helping to protect against endotoxin. In addition to this, biofilms are broken up because xylitol acts like a sort of trojan horse, sugar hungry microbes eat the xylitol but do not have the ability to properly digest it - so they die off, this breaks up the film and makes it vulnerable to your immune system / or being carried out by activated charcoal for instance. I have taken xylitol off and on, it creates a massive uncomfortable die off reaction if you ramp up too fast, you want to go slow with it, and always compliment it with other gut friendly protocol. For around 10 days I would take xylitol (3 or 4 tsp daily) with my coffee, in addition I was having daily carrot salad, and occasionally having activated charcoal. It definitely fixed up my gut, not to tmi you, but after those 10 days were up, for around a month after I had the healthiest bowel movements of my life.. It did much more for me than carrot salad or charcoal have done alone. YMMV

Good stuff, thanks.

And your avatar cracks me up every time I see it . . .

 

[Elchapchapchapo]

It is possible, but it is probably limited to...ahem...using the mouth on not so clean "exits". I think you know what I mean

Hahah get it haidut!!!

 

[Tarmander]

This is my very crude understanding. In theory at least, xylitol consumption will increase intestinal butyrate production, which will help to thicken up the intestinal wall (fight against leaky gut), in turn helping to protect against endotoxin. In addition to this, biofilms are broken up because xylitol acts like a sort of trojan horse, sugar hungry microbes eat the xylitol but do not have the ability to properly digest it - so they die off, this breaks up the film and makes it vulnerable to your immune system / or being carried out by activated charcoal for instance. I have taken xylitol off and on, it creates a massive uncomfortable die off reaction if you ramp up too fast, you want to go slow with it, and always compliment it with other gut friendly protocol. For around 10 days I would take xylitol (3 or 4 tsp daily) with my coffee, in addition I was having daily carrot salad, and occasionally having activated charcoal. It definitely fixed up my gut, not to tmi you, but after those 10 days were up, for around a month after I had the healthiest bowel movements of my life.. It did much more for me than carrot salad or charcoal have done alone. YMMV

This is interesting. Care to share more? Care to share where you first started reading about this?

 

[Wagner83]

This is interesting. Care to share more? Care to share where you first started reading about this?

Effects Of Consuming Xylitol On Gut Microbiota And Lipid Metabolism In Mice

I cured a year long sinus infection with xylitol neti-pot irrigation over a month. There was apparently a biofilm up there.

from my leukemia notes re Xylitol

Chew your way to fewer ear and upper respiratory infections
OK, here is a more upbeat and fun little factoid.

Vaccine. 2000 Dec 8;19 Suppl 1:S144-7.

Xylitol in preventing acute otitis media.

Uhari M, Tapiainen T, Kontiokari T.

Department of Paediatrics, University of Oulu, FIN-90220 Oulu, Finland. [email protected]

Xylitol is a polyol sugar alcohol and is referred to as birch sugar, because it can be produced from birch. Natural sources of xylitol include plums, strawberries, raspberries and rowan berries. Xylitol inhibits the growth of Streptococcus pneumoniae and it inhibits the attachment of both pneumococci and Haemophilus influenzae on the nasopharyngeal cells. In two clinical trials xylitol was found efficient to prevent the development of acute otitis media with a daily dose of 8.4-10 g of xylitol given in five divided doses. The efficacy in these 2-3 months follow-up trials was approximately 40% when chewing gum was used and approximately 30% with xylitol syrup. The need to use antimicrobials reduced markedly when using xylitol. In a high-risk group of children with tympanostomy tubes xylitol was ineffective in preventing otitis. Xylitol appears to be an attractive alternative to prevent acute otitis media. A more practical frequency of doses should be found before its use can be widely recommended.

PMID: 11163479

Xylitol is a sugar substitute. You can find it in the forms of lozenges, chewing gum, syrup, nasal spray, mouthwash etc. The abstract above reports on a clinical trial done in Finland, using a large group of high risk pediatric patients. Lo and behold, it reduced the incidence of severe ear infections, to the tune of 40%, when children chewed gum containing xylitol.

Wikipedia has a very nice write-up on this interesting molecule, easily readable, so I won’t belabor the points made there. Basically, xylitol has half the calories of plain table sugar, no after taste and no known toxicity. Here are a few quotes, for those of you lazy enough not to click on the link:

• Xylitol is a “tooth-friendly”, nonfermentable sugar alcohol; dental health benefits in caries prevention; recent research confirms a plaque-reducing effect.
• Bacteria prefer fermentable six-carbon sugars (i.e., normal table sugar), or disaccharides such as sucrose, as opposed to the nonfermentable xylitol, whose antimicrobial properties then “starve” the bacteria, reducing their growth and reproduction.
• Xylitol also inhibits the growth of Streptococcus pneumoniae, as well as the attachment of Haemophilus influenzae on the nasopharyngeal cells. (since strep and flu cells find it harder to attach to the cells of of your nose and throat in the presence of xylitol, there is hope for reduced bronchitis, pneumonia etc. As I have told you on many previous occasions, the single biggest cause of death in CLL patients is lung infections in general, pneumonia in particular).
• Studies have shown xylitol chewing gum can help prevent ear infections.
• Xylitol has been found to increase the activity of neutrophils, the white blood cells involved in fighting many bacteria. This effect seems to be quite broad, acting even in cases such as general sepsis. (but please be aware this is from an animal study. I have not been able to find a similar study in humans).

So, how reliable is all this good news? Some of you may be aware of a group called the Cochrane Collaboration. This group does an excellent job of looking at clinical trial results and sorting out credible stuff from poorly done studies or results biased by ugly agendas. Well, we are fortunate that they have looked at the Finnish study and in their considered opinion, the results are valid. You can read the full chapter and verse of their findings here. While these studies were done with pediatric patients, I am reasonably convinced that the results are equally valid in the case of adults. Xylitol is quite safe (except to dogs, so please be careful), so the risk is minimal. Like chewing gum? Choose to chew xylitol containing gum. Use a mouthwash? Find a brand that contains xylitol. Frequent bronchial infections during the flu season? There are all kinds of nasal sprays available that contain xylitol.

upper respiratory infections are often the end for those w leukemia......

________________

Could soaking the carrot salad in xylitol be an interesting prospect?

 

[Tarmander]

Effects Of Consuming Xylitol On Gut Microbiota And Lipid Metabolism In Mice

Yeah I found that interesting study. I wonder about it being a soluble fiber. Generally you want to stick with the insoluble ones...

 

[MyUsernameHere]

I've done a course of azithromycine a few days ago prescribed by my doctor. Can't say that I feel any better or even different at all..

 

[Captain_Coconut]

Thank you Wagner83. Yes, I have found that xylitol compliments other natural antiseptic things like carrot salad. Apparently Xylitol consumption if very big in Finland, I would like to see some large studies detailing more than oral health there, most of the studies I find are focused on oral health... Maybe I will dig around for studies focusing on consumption of fruits high in naturally occuring xylitol...

Tarmander, The butyrate claim I have read on various sites... here is a study also, in-vitro though... The effects of polydextrose and xylitol on microbial community and activity in a 4-stage colon simulator. - PubMed - NCBI

Nosing around some more - found this interesting:
Xylitol inhibits carcinogenic acetaldehyde production by Candidaspecies
https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.25844

 

[Tarmander]

I asked Peat about xylitol and he said the following:

Xylitol, like ethyl alcohol, shifts cells away from oxidation, and tends to increase reductive stress. It’s a by-product of the pulp and paper industry, so I think it’s susceptible to having traces of industrial chemicals, but even in the purest form it would have risks similar to ethanol.
Biochim Biophys Acta. 1995 Nov 9;1269(2):153-61.
Modulating hypoxia-induced hepatocyte injury by affecting intracellular redox
state.
Khan S(1), O'Brien PJ.
(1)Faculty of Pharmacy, University of Toronto, Ont., Canada.
Hypoxia-induced hepatocyte injury results not only from ATP depletion but also
from reductive stress and oxygen activation. Thus the NADH/NAD+ ratio was
markedly increased in isolated hepatocytes maintained under 95% N2/5% CO2 in
Krebs-Henseleit buffer well before plasma membrane disruption occurred.
Glycolytic nutrients fructose, dihydroxyacetone or glyceraldehyde prevented
cytotoxicity, restored the NADH/NAD+ ratio, and prevented complete ATP depletion.
However, the NADH generating nutrients sorbitol, xylitol, glycerol and
beta-hydroxybutyrate enhanced hypoxic cytotoxicity even though ATP depletion was
not affected. On the other hand, NADH oxidising metabolic intermediates
oxaloacetate or acetoacetate prevented hypoxic cytotoxicity but did not affect
ATP depletion. Restoring the cellular NADH/NAD+ ratio with the artificial
electron acceptors dichlorophenolindophenol and Methylene blue also prevented
hypoxic injury and partly restored ATP levels. Ethanol which further increased
the cellular NADH/NAD+ ratio increased by hypoxia also markedly increased
toxicity whereas acetaldehyde which restored the normal cellular NADH/NAD+ ratio,
prevented toxicity even though hypoxia induced ATP depletion was little affected
by ethanol or acetaldehyde. The viability of hypoxic hepatocytes is therefore
more dependent on the maintenance of normal redox homeostasis than ATP levels.
GSH may buffer these redox changes as hypoxia caused cell injury much sooner with
GSH depleted hepatocytes. Hypoxia also caused an intracellular release of free
iron and cytotoxicity was prevented by desferoxamine. Furthermore, increasing the
cellular NADH/NAD+ ratio markedly increased the intracellular release of iron.
Hypoxia-induced hepatocyte injury was also prevented by oxypurinol, a xanthine
oxidase inhibitor. Polyphenolic antioxidants or the superoxide dismutase mimic,
TEMPO partly prevented cytotoxicity suggesting that reactive oxygen species
contributed to the cytotoxicity. The above results suggests that hypoxia induced
hepatocyte injury results from sustained reductive stress and oxygen activation.
Metabolism. 1996 Nov;45(11):1354-9.
Effect of glucagon on the xylitol-induced increase in the plasma concentration
and urinary excretion of purine bases.
Yamamoto T(1), Moriwaki Y, Takahashi S, Ohata H, Nakano T, Yamakita J, Higashino
K.
(1)Third Department of Internal Medicine, Hyogo College of Medicine, Japan.
To investigate whether glucagon affects the xylitol-induced increase in the
production of purine bases (hypoxanthine, xanthine, and uric acid), the present
study was performed with five healthy subjects. Intravenous administration of 300
mL 10% xylitol increased the plasma concentration and urinary excretion of purine
bases, erythrocyte concentrations of adenosine monophosphate (AMP) and adenosine
diphosphate (ADP), and blood concentrations of glyceraldehyde-3-phosphate (GA3P)
+ dihydroxyacetone phosphate (DHAP), fructose-1,6-bisphosphate (FBP), and lactic
acid; it decreased the blood concentration of pyruvic acid and the plasma
concentration and urinary excretion of inorganic phosphate. However, intravenous
administration of 1 mg glucagon together with xylitol reduced the xylitol-induced
changes in oxypurines, pyruvic acid, GABP + DHAP, and FBP, whereas it promoted
the xylitol-induced increase in the urinary excretion of total purine bases and
did not affect the xylitol-induced increase in the plasma concentration of total
purine bases. In addition, in vitro study demonstrated that sodium pyruvate
prevented the xylitol-induced degradation of adenine nucleotides in erythrocytes.
These results suggested that gluconeogenesis due to glucagon increased the
production of pyruvic acid, accelerated the conversion of NADH to NAD, and
thereby prevented both the xylitol-induced degradation of adenine nucleotides in
organs similar to erythrocytes and the inhibition of xanthine dehydrogenase in
the liver and small intestine, resulting in decreases in the plasma concentration
and urinary excretion of oxypurines. However, it was also suggested that in the
liver storing glycogen, glucagon-induced glycogenolysis accumulated sugar
phosphates, resulting in purine degradation, since the xylitol-induced increase
in the NADH/NAD ratio partially blocked glycolysis at the level of GABP
dehydrogenase. Therefore, administration of glucagon together with xylitol may
synergistically increase purine degradation more than xylitol alone, despite
decreases in the plasma concentration and urinary excretion of oxypurines.
Hepatology. 1998 Nov;28(5):1318-26.
Acute and chronic ethanol increases reactive oxygen species generation and
decreases viability in fresh, isolated rat hepatocytes.
Bailey SM(1), Cunningham CC.
(1)Department of Biochemistry, Wake Forest University School of Medicine,
Winston-Salem, NC, USA.
Although reactive oxygen species (ROS) have been implicated in the etiology of
alcohol-induced liver disease, neither their relative contribution to cell death
nor the cellular mechanisms mediating their formation are known. The purpose of
this study was to test the hypothesis that acute and chronic ethanol exposure
enhances the mitochondrial generation of ROS in fresh, isolated hepatocytes.
Acute ethanol exposure stimulated ROS production, increased the cellular
NADH/NAD+ ratio, and decreased hepatocyte viability slightly, which was prevented
by pretreatment with 4-methylpyrazole (4-MP), an inhibitor of alcohol
dehydrogenase. Similarly, xylitol, an NADH-generating compound, enhanced
hepatocyte ROS production and decreased viability. Incubation with pyruvate, an
NADH-oxidizing compound, and cyanamide, an inhibitor of aldehyde dehydrogenase,
significantly decreased ROS levels in acute ethanol-treated hepatocytes. Chronic
ethanol consumption produced a sixfold increase in hepatocyte ROS production
compared with levels measured in controls. Hepatocytes from ethanol-fed rats were
less viable compared with controls, e.g., viability was 68% +/- 2% (ethanol)
versus 83% +/- 1% (control) after 60 minutes of incubation. Antimycin A increased
ROS production and decreased cell viability; however, the toxic effect of
antimycin A was more pronounced in ethanol-fed hepatocytes. These results suggest
that acute and chronic ethanol exposure exacerbates mitochondrial ROS production,
contributing to cell death.

 

[Captain_Coconut]

I would not argue xylitol should be ingested in large doses on a daily basis without breaks or that it has any superior direct mitochondrial benefit over basic food sugars. I think it shows great benefit in promoting a healthy gut and also in enhancing the efficacy of internal antiseptics. I think it is important to explore potential cheap, effective, and readily available means of limiting endotoxin. For this I think xylitol shows a lot of promise, and that is my own interpretation based from my own experience with xylitol (the results are in the toilet) and from the nutritional literature I have been able to scrape up. I see xylitol as a very useful health supporter for general routine g.i. maintenance, e.g. a 2 or 3 week run every 3 months, to that degree I view it as a relatively harmless supplement.

This is what sparked me on my exploration. And I have to say, one big dose seemed to make a noticeable difference for me as well.
Gut microflora interactions with xylitol in the mouse, rat and man.
https://www.side-effects-site.com/support-files/gut_microflora_interactions_with_xylitol_man.pdf

As for Iron concerns, I think it would take a lot to see any major damage there. Eating large amounts of liver alone is probably more questionable.
Peroral xylitol increases the concentration levels of tissue iron in the rat.
Peroral xylitol increases the concentration levels of tissue iron in the rat. - PubMed - NCBI

 

[Lejeboca]

worried about anti-biotics?....I'll say it again...look into Artemisinin

Wormwood: The Herb Kills Parasites & Cancer Cells!

I've checked this source, @bzmazu , and it actually talks about Artemisia Absinthium as having artemisinin (!?!) However, the only current (and historical) source of artemisinin CNAP - Centre for Novel Agricultural Products - Artemisia Project

is Arthemisia Annua (Sweet Wormwood or Sweet Annie or qinghao) Artemisinin - Wikipedia .

Artemisia Absinthium (Wormwood) and Arthemisia Annua (Sweet Wormwood) are two different, albeit related of course, herbs. And I wouldn't use the former ad libitum (for artemisinin) since it has other, possibly undesirable, effects.

N.B. @lisaferraro , the Dr. Best artemisinin does come from Sweet Wormwood

 

[Tarmander]

I've checked this source, @bzmazu , and it actually talks about Artemisia Absinthium as having artemisinin (!?!) However, the only current (and historical) source of artemisinin CNAP - Centre for Novel Agricultural Products - Artemisia Project

is Arthemisia Annua (Sweet Wormwood or Sweet Annie or qinghao) Artemisinin - Wikipedia .

Artemisia Absinthium (Wormwood) and Arthemisia Annua (Sweet Wormwood) are two different, albeit related of course, herbs. And I wouldn't use the former ad libitum (for artemisinin) since it has other, possibly undesirable, effects.

N.B. @lisaferraro , the Dr. Best artemisinin does come from Sweet Wormwood

I actually was curious about this.

Check out these two products: Uses Carvifolia

https://www.amazon.com/Doctors-Best...F8&qid=1522638415&sr=8-3&keywords=artemisinin

Uses Annua

https://www.amazon.com/Relentless-I...8&qid=1522638415&sr=8-13&keywords=artemisinin

Uses Carvifolia

Is there a difference?

 

[Lejeboca]

I actually was curious about this.

Check out these two products: Uses Carvifolia

https://www.amazon.com/Doctors-Best...F8&qid=1522638415&sr=8-3&keywords=artemisinin

Uses Annua

https://www.amazon.com/Relentless-I...8&qid=1522638415&sr=8-13&keywords=artemisinin

Uses Carvifolia

Is there a difference?

I must admit that I don't know Artemisia Carvifolia. Looking around now: Apparently it is being genetically modified to increase its artimisinin content several-fold from its wild-plant form for the cheapness of production:

Genetic Transformation of Artemisia carvifolia Buch with rol Genes Enhances Artemisinin Accumulation :
The potent antimalarial drug artemisinin has a high cost, since its only viable source to date is Artemisia annua (0.01–0.8% DW). There is therefore an urgent need to design new strategies to increase its production or to find alternative sources. In the current study. Artemisia carvifolia Buch was selected with the aim of detecting artemisinin and then enhancing the production of the target compound and its derivatives. These metabolites were determined by LC-MS in the shoots of A. carvifolia wild type plants at the following concentrations: artemisinin (8μg/g), artesunate (2.24μg/g), dihydroartemisinin (13.6μg/g) and artemether (12.8μg/g). Genetic transformation of A. carvifolia was carried out with Agrobacterium tumefaciens GV3101 harboring the rol B and rol C genes. Artemisinin content increased 3-7-fold in transgenics bearing the rol B gene, and 2.3-6-fold in those with the rol C gene. A similar pattern was observed for artemisinin analogues.

I also found a very detailed information on the concentration of artemisinin in Annua in Distribution of Artemisinin in Artemisia annua , which concludes

Artemisinin is a sesquiterpene lactone which is produced both in vivo and differentiated in vitro cultures, by Artemisia annua and is equally distributed throughout the plant. Artemisinin appears to be sequestered in glandular trichomes which occur in stems, leaves, and inflorescences. The association of peak artemisinin with flowering is related to the abundance of glandular trichomes in the inflorescence, particularly florets and receptacle. In vitro studies indicate that the biosynthesis of artemisinin is enhanced by the presence of roots. Artemisia annua is unlikely to be produced economically by chemical synthesis or by in vitro production, thus A. annua is a potential new antimalarial crop for temperate areas.

N.B. The price difference on the products to which @Tarmander has shown the Amazon links ($.28 vs $.18 for Annua vs Carvifolia) supports the "cheap production" argument above

 

[lollipop]

N.B. @lisaferraro , the Dr. Best artemisinin does come from Sweet Wormwood

Yeah, I also made sure when deciding which brand. Thank you for your above research and addition into this conversation about Artemisinin @Lejeboca.

 

[haidut]

I asked Peat about xylitol and he said the following:

Xylitol, like ethyl alcohol, shifts cells away from oxidation, and tends to increase reductive stress. It’s a by-product of the pulp and paper industry, so I think it’s susceptible to having traces of industrial chemicals, but even in the purest form it would have risks similar to ethanol.
Biochim Biophys Acta. 1995 Nov 9;1269(2):153-61.
Modulating hypoxia-induced hepatocyte injury by affecting intracellular redox
state.
Khan S(1), O'Brien PJ.
(1)Faculty of Pharmacy, University of Toronto, Ont., Canada.
Hypoxia-induced hepatocyte injury results not only from ATP depletion but also
from reductive stress and oxygen activation. Thus the NADH/NAD+ ratio was
markedly increased in isolated hepatocytes maintained under 95% N2/5% CO2 in
Krebs-Henseleit buffer well before plasma membrane disruption occurred.
Glycolytic nutrients fructose, dihydroxyacetone or glyceraldehyde prevented
cytotoxicity, restored the NADH/NAD+ ratio, and prevented complete ATP depletion.
However, the NADH generating nutrients sorbitol, xylitol, glycerol and
beta-hydroxybutyrate enhanced hypoxic cytotoxicity even though ATP depletion was
not affected. On the other hand, NADH oxidising metabolic intermediates
oxaloacetate or acetoacetate prevented hypoxic cytotoxicity but did not affect
ATP depletion. Restoring the cellular NADH/NAD+ ratio with the artificial
electron acceptors dichlorophenolindophenol and Methylene blue also prevented
hypoxic injury and partly restored ATP levels. Ethanol which further increased
the cellular NADH/NAD+ ratio increased by hypoxia also markedly increased
toxicity whereas acetaldehyde which restored the normal cellular NADH/NAD+ ratio,
prevented toxicity even though hypoxia induced ATP depletion was little affected
by ethanol or acetaldehyde. The viability of hypoxic hepatocytes is therefore
more dependent on the maintenance of normal redox homeostasis than ATP levels.
GSH may buffer these redox changes as hypoxia caused cell injury much sooner with
GSH depleted hepatocytes. Hypoxia also caused an intracellular release of free
iron and cytotoxicity was prevented by desferoxamine. Furthermore, increasing the
cellular NADH/NAD+ ratio markedly increased the intracellular release of iron.
Hypoxia-induced hepatocyte injury was also prevented by oxypurinol, a xanthine
oxidase inhibitor. Polyphenolic antioxidants or the superoxide dismutase mimic,
TEMPO partly prevented cytotoxicity suggesting that reactive oxygen species
contributed to the cytotoxicity. The above results suggests that hypoxia induced
hepatocyte injury results from sustained reductive stress and oxygen activation.
Metabolism. 1996 Nov;45(11):1354-9.
Effect of glucagon on the xylitol-induced increase in the plasma concentration
and urinary excretion of purine bases.
Yamamoto T(1), Moriwaki Y, Takahashi S, Ohata H, Nakano T, Yamakita J, Higashino
K.
(1)Third Department of Internal Medicine, Hyogo College of Medicine, Japan.
To investigate whether glucagon affects the xylitol-induced increase in the
production of purine bases (hypoxanthine, xanthine, and uric acid), the present
study was performed with five healthy subjects. Intravenous administration of 300
mL 10% xylitol increased the plasma concentration and urinary excretion of purine
bases, erythrocyte concentrations of adenosine monophosphate (AMP) and adenosine
diphosphate (ADP), and blood concentrations of glyceraldehyde-3-phosphate (GA3P)
+ dihydroxyacetone phosphate (DHAP), fructose-1,6-bisphosphate (FBP), and lactic
acid; it decreased the blood concentration of pyruvic acid and the plasma
concentration and urinary excretion of inorganic phosphate. However, intravenous
administration of 1 mg glucagon together with xylitol reduced the xylitol-induced
changes in oxypurines, pyruvic acid, GABP + DHAP, and FBP, whereas it promoted
the xylitol-induced increase in the urinary excretion of total purine bases and
did not affect the xylitol-induced increase in the plasma concentration of total
purine bases. In addition, in vitro study demonstrated that sodium pyruvate
prevented the xylitol-induced degradation of adenine nucleotides in erythrocytes.
These results suggested that gluconeogenesis due to glucagon increased the
production of pyruvic acid, accelerated the conversion of NADH to NAD, and
thereby prevented both the xylitol-induced degradation of adenine nucleotides in
organs similar to erythrocytes and the inhibition of xanthine dehydrogenase in
the liver and small intestine, resulting in decreases in the plasma concentration
and urinary excretion of oxypurines. However, it was also suggested that in the
liver storing glycogen, glucagon-induced glycogenolysis accumulated sugar
phosphates, resulting in purine degradation, since the xylitol-induced increase
in the NADH/NAD ratio partially blocked glycolysis at the level of GABP
dehydrogenase. Therefore, administration of glucagon together with xylitol may
synergistically increase purine degradation more than xylitol alone, despite
decreases in the plasma concentration and urinary excretion of oxypurines.
Hepatology. 1998 Nov;28(5):1318-26.
Acute and chronic ethanol increases reactive oxygen species generation and
decreases viability in fresh, isolated rat hepatocytes.
Bailey SM(1), Cunningham CC.
(1)Department of Biochemistry, Wake Forest University School of Medicine,
Winston-Salem, NC, USA.
Although reactive oxygen species (ROS) have been implicated in the etiology of
alcohol-induced liver disease, neither their relative contribution to cell death
nor the cellular mechanisms mediating their formation are known. The purpose of
this study was to test the hypothesis that acute and chronic ethanol exposure
enhances the mitochondrial generation of ROS in fresh, isolated hepatocytes.
Acute ethanol exposure stimulated ROS production, increased the cellular
NADH/NAD+ ratio, and decreased hepatocyte viability slightly, which was prevented
by pretreatment with 4-methylpyrazole (4-MP), an inhibitor of alcohol
dehydrogenase. Similarly, xylitol, an NADH-generating compound, enhanced
hepatocyte ROS production and decreased viability. Incubation with pyruvate, an
NADH-oxidizing compound, and cyanamide, an inhibitor of aldehyde dehydrogenase,
significantly decreased ROS levels in acute ethanol-treated hepatocytes. Chronic
ethanol consumption produced a sixfold increase in hepatocyte ROS production
compared with levels measured in controls. Hepatocytes from ethanol-fed rats were
less viable compared with controls, e.g., viability was 68% +/- 2% (ethanol)
versus 83% +/- 1% (control) after 60 minutes of incubation. Antimycin A increased
ROS production and decreased cell viability; however, the toxic effect of
antimycin A was more pronounced in ethanol-fed hepatocytes. These results suggest
that acute and chronic ethanol exposure exacerbates mitochondrial ROS production,
contributing to cell death.

Sucrose and trehalose are the only two non-reducing sugars that Peat recommends consistently, and I think the fact they are non-reducing is a big reason why. Both glucose and fructose, individually, are reducing sugars and this is why he probably does not recommend even fructose on its own despite writing a lot about its benefits.

 

[Vinero]

If the theory behind this study is correct, then the way in which autoimmune diseases are commonly treated make no sense.
Most autoimmune diseases are treated by silencing an overactive immune system with cortisol based drugs (prednisone, dexamethasone, cortisone etc.).
This "treats" or decreases the symptoms, but when the immunosupressive drug is removed the symptoms return.
Thus nothing has been cured in this way.
What makes the problem worse is that suppressing the immune system is exactly the wrong thing to do if autoimmune diseases are ultimately caused by gut bacteria.
Using cortisol based drugs, the suppressed immune system can't get rid of the bacteria, and also the cortisol inhibits healing of the gut barrier which defends against gut bacteria.
These two points will worsen the existing condition.
If the bacteria which produce endotoxin are the problem, then using an antibiotic is much more effective then suppressing the immune system with corticol based drugs.
Supressing the immune system allows the bacteria to grow inside the body, worsening the disease.

 

[haidut]

If the theory behind this study is correct, then the way in which autoimmune diseases are commonly treated make no sense.
Most autoimmune diseases are treated by silencing an overactive immune system with cortisol based drugs (prednisone, dexamethasone, cortisone etc.).
This "treats" or decreases the symptoms, but when the immunosupressive drug is removed the symptoms return.
Thus nothing has been cured in this way.
What makes the problem worse is that suppressing the immune system is exactly the wrong thing to do if autoimmune diseases are ultimately caused by gut bacteria.
Using cortisol based drugs, the suppressed immune system can't get rid of the bacteria, and also the cortisol inhibits healing of the gut barrier which defends against gut bacteria.
These two points will worsen the existing condition.
I think using antibiotics to get rid of the bacteria, and improving gut health is the best option to cure the root cause of all autoimmune diseases. This supports the immune system instead of supressing it (which also leads to cancer by the way).

I think you immediately see why mainstream medicine considers autoimmune conditions "incurable". They have been using glucocorticoids on those conditions for almost 100 years and generations of doctors have been raised/educated to think that glucocorticoids are indispensable in these conditions, even if only for acute flares. However, even sporadic use of those glucocorticoids both suppresses the immune system and increases gut permeability enough to ensure that the pathogen remains active for as long as the person is alive.
So, these conditions are effectively incurable...as long as this line of "therapy" is maintained. I really hope this travesty is due to stupidity and not by design. Because if it turns out somebody high up there knew and purposefully steered the course in this direction just to create "incurable" conditions (to ensure lifetime revenue stream) then I am afraid many doctors will face brutal repercussions from the public once the truth becomes more widely known. Even though they may be just unwitting participants in a corrupt system.
Now, since you mentioned cancer - assume cancer is no different and involves endotoxin or even bacteria of some kind (Pancreatic Cancer Driven By Bacteria/endotoxin; Antibiotics Can Prevent/treat). Considering that chemotherapy and radiation are undisputed and publicly acknowledged highly effective immunosuppressants, you see how cancer becomes another "incurable" condition due to stupidity (or maybe by design??). Oh, and btw they do use glucocorticoids on cancer patients most of the time as well.
Immune Decline (Not Genetics) Causes Cancer And It Can Be Easily Fixed

And the solution for many could be quite simple - simply keep the immune system up by keeping estrogen/cortisol down.
Reducing Estrogen Synthesis Regenerates Thymus Destroyed By Aging

 

[yerrag]

Both glucose and fructose, individually, are reducing sugars and this is why he probably does not recommend even fructose on its own despite writing a lot about its benefits.

Do you have references on Ray regarding not recommending fructose? Very interested in knowing why.

 

[greengr]

worried about anti-biotics?....I'll say it again...look into Artemisinin

Wormwood: The Herb Kills Parasites & Cancer Cells!

I've tried it, and it had some strange effects. Made me very fatigued and dehydrated, maybe because it might cause anemia? But it seemed to work.
Is azithromycin acceptable to treat autoimmune disease bacteria?
A bit worried about minocycline because of it links with lupus.