Peating Means You Have To Replace EVERYTHING

TheBeard

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The more I read and hear about health, the more I understand how everything is deeply interconnected, to the point where you can't keep track of all interactions unless you are Georgi Dinkov or Peat himself.
It is just inhumanely complex.

For example:

Antibiotics alter bile composition. Not directly, but some bacteria are responsible for producing enzymes that will turn primarily bile acids into secondary bile acids.

If we follow Peat's recommendation to keep a relatively sterile gut in order to limit the harm of endotoxins, how are we supposed to have our bile system work efficiently. We have to supplement bile?
Same goes for stomach acid: it isn't properly produced without the right bacteria and enough bile signaling.

Same goes for androgens: their production by the Leydig cells is dependent on other bacteria:
The Gut Microbiota and Developmental Programming of the Testis in Mice

Sounds to me like once you pull the trigger on a few supplements or medication, you are doomed to replace everything else as the natural cycle is broken.

Help I guess?
 

mrchibbs

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I think any talk of a "natural cycle" is sort of a strawman argument, because we're virtually living in a mass experiment with the fundamental transformations of modern environments. If we were living in a natural setting with exposure to daylight, social relationships, unaldurated foods, no EMF etc. we wouldn't need to implement these interventions like cyproheptadine, thyroid cascara, exogenous vitamin D etc.

I don't think we're doomed to replace everything. I think we have to be constantly trying to improve our immediate environment, and using adaptogens like aspirin, red light and yes, antibiotics as crutches to compensate for the inaquacies of our surroundings.
 

TheBeard

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I think any talk of a "natural cycle" is sort of a strawman argument, because we're virtually living in a mass experiment with the fundamental transformations of modern environments. If we were living in a natural setting with exposure to daylight, social relationships, unaldurated foods, no EMF etc. we wouldn't need to implement these interventions like cyproheptadine, thyroid cascara, exogenous vitamin D etc.

I don't think we're doomed to replace everything. I think we have to be constantly trying to improve our immediate environment, and using adaptogens like aspirin, red light and yes, antibiotics as crutches to compensate for the inaquacies of our surroundings.

I'm not against replacing, I know nature is far behind us at that point and it's a no return point.

I'm happy replacing what I know needs replacement.

However it seems we are triggering an endless cascade we don't even know about, and we don't master how many parameters we need to replace.

In my case it caused long lasting depression for 4 years before I figured I had SIBO and bile deficiency.
I'm wondering what else I'll find out a few years from now...
 

opson123

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I agree with TheBeard. It's difficult to get things right. Instead of the desired balanced loop you get an endless flow leading to nowhere. You can initially feel like you're going in the right direction, but if your last and first variable never connect, you'll never reach a state of balance.
 

ursidae

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yeah it’s a wild goose chase where you have to put a patch on top of a patch on top of a patch and if you’re really competent you can shift the symptoms in the direction that you find most acceptable, like maybe having a little bit of a stutter or needing a thick pair of glasses

I think your best bet at real recovery is placing yourself in a perfect environment, only giving your body its own constituents to work with, and maybe it will reorganise and rebalance
 
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Tarmander

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If you come to a place where you are replacing everything, you are in the same rabbit hole as mainstream medicine, i.e cut out and replace. We can see the results of long term allopathic medicine

Peat's advice about the microbiome is simplistic

He treats all bacteria as having endotoxin

Firmicutes are not gram negative and have no endotoxin. If you skew your ratio of firmicutes to bacteroidetes towards firmicutes, you can have both healthy gut bacteria as well as low endotoxin.
 

TheBeard

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Peat's advice about the microbiome is simplistic

He treats all bacteria as having endotoxin

Which makes the consequences of sterilizing the gut anything but simple, as exposed in my first post of this thread.
 

kaybb

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If you come to a place where you are replacing everything, you are in the same rabbit hole as mainstream medicine, i.e cut out and replace. We can see the results of long term allopathic medicine

Peat's advice about the microbiome is simplistic

He treats all bacteria as having endotoxin

Firmicutes are not gram negative and have no endotoxin. If you skew your ratio of firmicutes to bacteroidetes towards firmicutes, you can have both healthy gut bacteria as well as low endotoxin.
How would we go about the skewing ratio to firmecutes?
 

yerrag

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If you come to a place where you are replacing everything, you are in the same rabbit hole as mainstream medicine, i.e cut out and replace. We can see the results of long term allopathic medicine
We're getting there.
 

Perry Staltic

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If you come to a place where you are replacing everything, you are in the same rabbit hole as mainstream medicine, i.e cut out and replace. We can see the results of long term allopathic medicine

Peat's advice about the microbiome is simplistic

He treats all bacteria as having endotoxin

Firmicutes are not gram negative and have no endotoxin. If you skew your ratio of firmicutes to bacteroidetes towards firmicutes, you can have both healthy gut bacteria as well as low endotoxin.

Some firmicutes produce only L-lactate, which the body can easily metabolize. It seems sensible to skew the ratio away from bacteria that produce D-lactate, which the body cannot metabolize very well, by encouraging bacteria that produce only L-lactate.
 
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milkboi

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Some firmicutes produce only L-lactate, which the body can easily metabolize. It seems sensible to skew the ratio away from bacteria that produce D-lactate, which the body cannot metabolize very well, by encouraging bacteria that produce only L-lactate.

You seen good results doing that?
 

Perry Staltic

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You seen good results doing that?

I've had very good results with bacillus coagulens which produces > 99% optically pure L-lactate. It supposedly populates the small intestine and helps metabolize carbs there (haven't verified that), which means those carbs wouldn't be fermented in the large intestine via D-lactate producing bacteria.

I am getting ready to experiment with lactobacillus bulgaricus and streotococcus thermopolis (used as yogurt starter) because I read they produce only L-lactate, but I have since read conflicting info about bulgaricus. However, this study, though it deals with short bowel syndrome, suggests that the D/L ratio is more relevant than the respective isoform quantities.

Two patients, belonging to the LA [lactate accumulative] group and who particularly accumulated faecal D-lactate, were at risk of D-encephalopathic reactions. Furthermore, all patients of the NLA [non-lactate accumulator] group and those accumulating preferentially L isoform in the LA group had never developed D-acidosis. The D/L faecal lactate ratio seems to be the most relevant index for a higher D- encephalopathy risk, rather than D- and L-lactate faecal concentrations per se.


And this study seems to indicate that streptococcus thermopolis out-competes lactobacillus bulgaricus.

S. thermophilus specifically produced L-lactate, while L. bulgaricus produced only D-lactate, both in vitro and in vivo. S. thermophilus showed competitive and growth advantage over L. bulgaricus in vitro as well as in vivo in the GIT of germ-free rats and, accordingly, L-lactate was the main lactate isomer produced.

 
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Perry Staltic

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L. rhamnosus is another.

Lactic acid comes in two stereoisomers, d-lactic acid and l-lactic acid, and different strains of lactobacilli create these lactic acid isomers in idiosyncratic ratios. No strain creates 100% of one isomer alone but there is wide vari-ability in ratio of d- versus l-forms across the lactobacilli. L. rhamnosus species notably creates l-lactic acid almost exclusively, but does form a minority in d-lactic acid form (94.2 and 5.8%), whereas other species have the opposite pattern [8]

 

milkboi

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I've had very good results with bacillus coagulens which produces > 99% optically pure L-lactate. It supposedly populates the small intestine and helps metabolize carbs there (haven't verified that), which means those carbs wouldn't be fermented in the large intestine via D-lactate producing bacteria.

I am getting ready to experiment with lactobacillus bulgaricus and streotococcus thermopolis (used as yogurt starter) because I read they produce only L-lactate, but I have since read conflicting info about bulgaricus. However, this study, though it deals with short bowel syndrome, suggests that the D/L ratio is more relevant than the respective isoform quantities.




And this study seems to indicate that streptococcus thermopolis out-competes lactobacillus bulgaricus.




Cool, thank you
 

Tarmander

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How would we go about the skewing ratio to firmecutes?
check out Jason Hawrelak. I interviewed him not too long ago and he has some good tips like Inulin FOS.

Some firmicutes produce only L-lactate, which the body can easily metabolize. It seems sensible to skew the ratio away from bacteria that produce D-lactate, which the body cannot metabolize very well, by encouraging bacteria that produce only L-lactate.
that sounds good. I dont know which bacteria do which though, do you?
 

Perry Staltic

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that sounds good. I dont know which bacteria do which though, do you?

These are the ones I know about (so far) that produce mostly L-lactate and what I will be experimenting with. I haven't researched all of their L-lactate percents yet.

Bacillus coagulens (> 99% L-lactate)
Bacillus subtilis (~95%)
Streptococcus thermophilus (99%)
Lactobcillus rhamnosus
Bifidobacterium longum
Bifidobacterium bifidum
Bifidobacterium lactis
Bifidobacterium breve
Bifidobacterium infantis
 
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