Why Is There So Much Soluble Fibre In Human Breast Milk?

[Amazoniac]

I created a poll because I'm genuinely curious to know if someone already had success with an antibiotic treatment for GI infections..

If you want to know about results of antibiotic treatment for GI infections you need to make it clear in that thread.

This is known in general medicine. No need to sample a small subset of the population (a.k.a. raypeatforum.com). People get GI infections - and infections of all sorts - cleared up using antibiotics...

I agree but I'm interested in people here because they are supposedly doing all aspects of diet right, and when they resort to antibiotics is because they aren't seeing the results they wanted..

 

[Amazoniac]

Another relevant point is that when you are malnourished for a long time, the pancreas starts losing its ability to excrete enzymes, first loses its ability to digest dietary fats. But MCTs don't require that process, in fact they don't even stimulate the formation of chylomicrons (a lipoprotein), they are carried directly to the liver via the portal vein. The problem is that they can carry LPS directly to there in the mean time.
This is another example of a healthy food becoming toxic if the person has poor intestinal health..
And the solution is not to exclude the foods, but work on healing the intestines, even if it requires the use of antibiotics as a last resource..

http://www.parthenon.gr/goldmembers/vip ... knower.php

 

[Giraffe]

I created a poll because I'm genuinely curious to know if someone already had success with an antibiotic treatment for GI infections..

If you want to know about results of antibiotic treatment for GI infections you need to make it clear in that thread.

This is known in general medicine. No need to sample a small subset of the population (a.k.a. raypeatforum.com). People get GI infections - and infections of all sorts - cleared up using antibiotics...

I agree but I'm interested in people here because they are supposedly doing all aspects of diet right, and when they resort to antibiotics is because they aren't seeing the results they wanted..

Amazoniac, in that poll you neither specified the reason for that antibiotic treatment nor did you ask when the treatment took place.You will not get the information you are seeking.

My antibiotic treatments were all before I found Ray Peat's writings. None of the treatments was aimed at solving gut issues. I think that lack of certain nutritions nutrients (and maybe gluten) played an important role in the infections I had, but there are other factors too.

 

[Amazoniac]

I created a poll because I'm genuinely curious to know if someone already had success with an antibiotic treatment for GI infections..

If you want to know about results of antibiotic treatment for GI infections you need to make it clear in that thread.

This is known in general medicine. No need to sample a small subset of the population (a.k.a. raypeatforum.com). People get GI infections - and infections of all sorts - cleared up using antibiotics...

I agree but I'm interested in people here because they are supposedly doing all aspects of diet right, and when they resort to antibiotics is because they aren't seeing the results they wanted..

Amazoniac, in that poll you neither specified the reason for that antibiotic treatment nor did you ask when the treatment took place.You will not get the information you are seeking.

My antibiotic treatments were all before I found Ray Peat's writings. None of the treatments was aimed at solving gut issues. I think that lack of certain nutritions (and maybe gluten) played an important role in the infections I had, but there are other factors too.

It targets microbes hoping to eradicate pathogens and leave the rest for immunity. It doesn't matter if it's on the skin, intestines, lungs; they are all dealing constantly with microbes and healing must take place in between. I should've noted that I was reffering to a recent course though. But I won't edit because we'd lose the votes..

 

[EnoreeG]

@ EnoreeG
Re the Duncan Crow line you quoted:

Of course, many people still posess the character to be followers, but increasingly many are waking up and an increasingly free-thinking majority will use this information to think for themselves. This is for you.

Although I agree with his views about prebiotics, I think it isn't helpful to cast aspertions on contrary views as being a 'follower' mindset. It isn't conducive to constructive discussion. It's a bit like Such_ saying that I ' ... always see things in black and white'. I felt like replying that it actually depends if they're in colour, but thought better of buying into even mild ad hominem.
Somebody with a contrary opinion will always think you are a 'blind' follower, don't you think?

The most useful thing I've ever heard about subscribing to any one guru as your philosophical saviour is the Buddhist adage : 'If you meet the buddha on the road, kill him'. But even that is a bit ultra violent for my blood.

Lots of new, interesting thoughts Stuart, even on this little tangent. It shows how minds see differently! I agree on the casting aspersions, of course, and in a way that's exactly what he did in a soft way. I was actually commenting on the softness with which he did it, as I saw his statement as a social comment with minimal negative impact but with a careful objective, and was actually praising him for doing it, as he seemed to do it as a subtle attempt to give incentive to those who might be at a tipping point toward opening their minds.

Yes, I think there is a tendency for one with a contrary opinion to think of myself as a 'blind' follower. At least that's one attitude they may take. And it's definitely prejudicial, but then it's a "quick protection" for their point of view. Again, I'll reference "Blink" as the best reference on the actual utility of all this "prejudice" which is really "intuition" and is not scientific but it works sometimes to save a lot of time and often to save your life. It's just that when we are dealing with people and must communicate with them in a considerate manner, we must never appear prejudiced. A difficult balance that we must all attempt, to stay friendly in conversation. I think generally, this forum is quite full of people who are good at giving the appearance of consideration of other points of view.

What was so valuable to me that I gained from reading "Blink" was the realization of how difficult it is for a person to change all the associations that have arisen in their brain in order to support a theory they are living by. That it's so much easier to just "think the same" than to reorganize everything. The brain actually "fights" to keep the status quo, it seems. But this should probably be something that people actively practice, so that they get adept at changing points of view, because it is a key to embracing new concepts.

Maybe it should be a game, taught in 3rd grade? "Assume a point of view. Define and defend it. Now assume a contrary point of view. Define and defend it. Now rise above and view both points from a superior position. Now descend and assume a third point of view."

And all this being said, I hope you didn't think I was being negative on the Duncan Crow information by mentioning the quote from him. I certainly didn't want to distract from his piece, as I thought it was quite appropriate to present that information and I gained a lot from it.

 

[Stuart]

@ EnoreeG
I was having a go at playng the devil's advocate in my comment actually. It's difficult to be sure! I actually did a fair bit of high school debating because my parents wanted me to foster my ability to take the opposite point of view. But I was hopeless at it
I've ordered 'Blink' at my local library. Sounds wonderful.

 

[EnoreeG]

@ EnoreeG
I was having a go at playng the devil's advocate in my comment actually. It's difficult to be sure! I actually did a fair bit of high school debating because my parents wanted me to foster my ability to take the opposite point of view. But I was hopeless at it
I've ordered 'Blink' at my local library. Sounds wonderful.

Strange that you should say that about being encouraged. I tend to fall too easily into the "DA" role! Then people totally misunderstand where I'm ACTUALLY coming from. It's very confusing sometimes when people flip from side to side. Oh well, it's a nice exercise, nonetheless.

 

[Suikerbuik]

I haven’t responded in a while. There are statements or personal beliefs in this thread I do not agree with, but will not address, some things are either too simplistic/theoretical or just wrong, but that is probably my frame of reference, and everything one can know is said imo. On other I made a note see posts below.

In general I like the lines of thinking of my friend from the Amazon. Perhaps Stuart is also bringing more nuance to his posts lately – I like that fiber link and will comment on it. Made a word document and copy / paste some posts :)

Combine those health principles with promoting a healthy microbiome, and strict Peatarianism becomes incalculably more powerful IMHO

The question is not if, but how?? Dietary changes, supplemental fiber, or antibiotics?

Saccharin - in fairness, saccharin has been around for over a century, and despite a lot of trying, has never been proven to have any harmful effects whatsoever.

"Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage."

Non-caloric artificial sweeteners (NAS)
http://www.nature.com/nature/journal/v514/n7521/full/nature13793.html

I wonder why they don't use fructose. Isn't it a monosaccjaride? And aren't both mono and di- saccarhides digested in the small intestine ?

An example of a theoretical approach here. Fructose uptake can be impaired by local inflammation but more interestingly also possibly by circulating cytokines:

Isolated fructose malabsorption is rare and is not linked to protein-altering mutations in GLUT5, and the inheritance pattern is unknown (153). As a consequence, there are few studies on GLUT5 expression and function under pathological conditions in the intestine. In general, GLUT5 expression and activity decrease in inflammatory diseases. A patient with Helicobacter pylori infection exhibited a decrease in intestinal GLUT5 expression (87). In rats, 2–8 days after iodoacetamide-induced colitis, GLUT5 protein and mRNA levels decreased in noninflamed small intestine, thereby paralleling the time course of inflammation manifested in the large intestine and suggesting that GLUT5 in noninflamed tissues may be sensitive to inflammation inducers or to inflammatory signals in the blood (77).

Further reading: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652499/

 

[Suikerbuik]

What about phytic acid, etc.

I am not sure about many of these supposed anti-nutrients Such_, there are, roughly estimated, 8.10(6) genes down there, and sure they express phytase. Not trying to make a hard case against it as it still inhibits digestive enzymes and anti-nutrients with those properties can be bothersome (I imagine).

Perhaps I think that anti-nutrients in general are less detrimental than supposed by some internet cults (sure avoiding makes you not even have worry about it). Especially if a proposed mechanisms of action is established in-vitro or in mice models involving the microbiome, as you know, you cannot simply extrapolate their findings, but it is being done.
http://www.ncbi.nlm.nih.gov/pubmed/19053869

http://www.lucastafur.com/2011/10/is-phytate-really-problem.html
(Just merely for references showing the capacity of some species of our microbiome to degrade phytase. The anti-cancer properties are interesting but always counterintuitive and not so much of interest here.)

 

[Suikerbuik]

The more the bacterial bulk, the more the resultant endotoxins,

Also a ‘healthy’ microbiome can consist of prominent species having LPS it’s not really pathogen related. See for example bacteroidetes or prevotella. However, endotoxemia is something that involves more than having those bacteria down there.
http://www.nature.com/news/2011/110420/full/news.2011.249.html

 

[Suikerbuik]

Stuart’s fiber link:

Dysbiosis is an overgrowth of pathogenic bacteria, viruses, yeasts and fungi that produce gas, irritation and toxins in the bowel 24 hours a day as they ferment your food, because they are not being adequately suppressed by the probiotic organisms, especially bifidobacteria strains.

-- (bold is his, underlined in mine)

The last part has recently been disproven (Stuart provided links too):

These include absence of Bifidobacterium and differences in microbial composition between the sexes that probably reflect sexual division of labour. http://www.nature.com/ncomms/2014/140415/ncomms4654/full/ncomms4654.html

That graph with bifido’s declining with age is interesting too, however, may be put in another perspective by these 2 Nature articles above. It can also indicate that the gut flora is merely regulated by physique instead of fiber, as I don’t believe that elderly eat less fiber - this is not my observation (might be in the full-text, if someone has access to):
http://nutritionreviews.oxfordjournals.org/content/50/12/438

He refers to articles showing association of dysbiosis to disease. Unfortunately, he does not cite articles showing that a disease phenotype (to some extent) is reversible with fiber - anything that would be supportive to his hypothesis: "because they are not being adequately suppressed by the probiotic organisms, especially bifidobacteria strains.". If the underlined part ia really that simple, why isn’t it shown anywhere?

So for now, I can’t see the value in his findings besides putting emphasis on the fact that pathogen associated species do poor on inulin and are therefore likely not stimulated.

Another quote that could make me wiser maybe??

Recent human experiments conducted by Gibson et al. (1995) at the Dunn Clinical Nutrition Center (UK) demonstrated that a daily intake of 15 grams inulin during 15 days renders Bifidus the numerically predominant species in feces and colon, while stagnating or decreasing numbers of bacteroides, fusobacteria, clostridia and colifoms

There is a review article written by him, but I can’t find that original article, someone?: http://jn.nutrition.org/content/125/6/1401.full.pdf

Interesting table and it might be a reason why carrageenan is associated with all negatives Peat has observed and written about.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC291464/pdf/aem00235-0060.pdf

Edit: changed order and made things, hopfully, more clear.

 

[Suikerbuik]

Continued my research:

FOS and inulin greatly affected the production of short-chain fatty acids in fecal cultures; butyrate was the major fermentation product on inulin, whereas mostly acetate and lactate were produced on FOS.
http://aem.asm.org/content/71/10/6150.full

RESULTS:
Twenty-two patients (mean age 71 years) completed at least 7 days of intervention (mean 12 days). At the end of the intervention, there were no significant differences in the concentrations of bifidobacteria between the groups, after adjusting for baseline values (oligofructose/inulin6.9 + 1.4, placebo 7.8 + 1.3 log10 cells/g dry faeces, P > 0.05), but there were significantly lower concentrations of Faecalibacterium prausnitzii (7.0 + 1.0 vs. 8.4 + 1.3 log10 cells/g, P = 0.01) and Bacteroides-Prevotella (9.1 + 1.0 vs. 9.9 + 0.9 log10 cells/g, P = 0.05) in patients receiving additional oligofructose/inulin. There were no differences in faecal concentrations of any SCFA, secretory IgA, daily faecal score or incidence of diarrhoea between the two groups.
http://www.ncbi.nlm.nih.gov/pubmed/24290345

The species Bifidobacterium longum, Bifidobacterium pseudocatenulatum and Bifidobacterium adolescentis were significantly increased at the end of the treatment in the prebiotic group (p < 0.01) with being B. longum negatively correlated with serum lipopolysaccharide (LPS) endotoxin (p < 0.01). Total SCFA, acetate and propionate, that positively correlated with BMI, fasting insulinemia and homeostasis model assessment (HOMA) (p < 0.05), were significantly lower in prebiotic than in placebo group after the treatment period.
http://www.ncbi.nlm.nih.gov/pubmed/24969566

Overnight fasted healthy subjects (n = 12) were studied for 6 h after consuming 400 mL drinks, containing 80 g high-fructose corn syrup (80HFCS), 56 g HFCS (56HFCS), or 56 g HFCS plus 24 g inulin (Inulin), using a randomized, single-blind, crossover design. A standard lunch was served 4 h after the test drink. Glucose and insulin responses after Inulin did not differ significantly from those after 80HFCS or 56HFCS. Serum acetate, propionate, and butyrate were significantly higher after Inulin than after HFCS drinks from 4-6 h. FFAs fell at a similar rate after all 3 test drinks, but were lower after Inulin than after 56HFCS at 4 h (0.40 +/- 0.06 vs. 0.51 +/- 0.06 mmol*L-1; p < 0.05). Compared with 56HFCS, Inulin significantly increased plasma glucagon-like peptide-1 concentrations at 30 min, and reduced ghrelin at 4.5 h and 6 h.
http://www.ncbi.nlm.nih.gov/pubmed/20130660

Numbers of faecal bifidobacteria and lactobacilli were significantly higher upon VLCI ingestion compared with the placebo. Additionally, levels of Atopobium group significantly increased, while Bacteroides-Prevotella numbers were significantly reduced. No significant changes in faecal SCFA concentrations were observed.
very-long-chain inulin (VLCI)
http://www.ncbi.nlm.nih.gov/pubmed/20591206

Bifidobacteria levels were significantly higher on consumption of both the PCS and PPB shots (10.0 (sd 0.24) and 9.8 (sd 0.22) log10 cells/g faeces, respectively) compared with placebo (9.3 (sd 0.42) log10 cells/g faeces) (P < 0.0001). A small though significant increase in Lactobacillus/Enterococcus group was also observed for both the PCS and PPB shots (8.3 (sd 0.49) and 8.3 (sd 0.36) log10 cells/g faeces, respectively) compared with placebo (8.1 (sd 0.37) log10 cells/g faeces) (P = 0.042). Other bacterial groups and faecal SCFA concentrations remained unaffected.
pear-carrot-sea buckthorn (PCS) or plum-pear-beetroot (PPB), containing JA inulin (5 g/d) or the placebo
http://www.ncbi.nlm.nih.gov/pubmed/20187995

The consumption of CH or JA increased counts of bifidobacteria (+1.2 log10 in 21 d) and reduced Bacteroides/Prevotella in number and the Clostridium histolyticum/C. lituseburense group in frequency at the end of intervention (P < 0.05). No changes in concentration of faecal SCFA were observed.
Jerusalem artichoke inulin (JA) or chicory inulin (CH
http://www.ncbi.nlm.nih.gov/pubmed/17445348

So all in all. FOS and other readily fermentable fiber is not so much advised, especially not in the presence of gut dysbiosis. FOS since it seems to enhance lactate and acetate production. Pectin I’d be wary about since it may ferment to methanol. Inulin, however, might be something, but SCFA/ butyrate production is only something they find in-vitro and not in-vivo (using 5g-15g/day). So either it’s not produced or the uptake is nowhere reaching its limit on these doses and we simply can’t detect it.

Also did a search for the relationship between supplemental fiber intake and remission of diseases or disease associated conditions. Generally inulin is associated with modest benefits - if at all, it might offset the diet induced (high fat/ high carb) endotoxemia and it does result in increased bifido counts – with unknown outcome (they expect it to be beneficial).
So it won’t kill you, maybe hurt your wallet - both as expected, but I am just not convinced for the essentiality, at least not as Stuart is. Especially when one is eating vegetables daily I doubt it is going to be something miraculous. Unless doses of 100g are the key :P.

I came across this maybe more promising study as Dr. Gibson was involved in:

RESULTS:
Rifaximin did not affect the overall composition of the gut microbiota, whereas it caused an increase in concentration of Bifidobacterium, Atopobium and Faecalibacterium prausnitzii. A shift in microbial metabolism was observed, as shown by increases in short-chain fatty acids, propanol, decanol, nonanone and aromatic organic compounds, and decreases in ethanol, methanol and glutamate. No genotoxicity or cytotoxicity was attributed to rifaximin, and conversely rifaximin was shown to have a chemopreventive role by protecting against hydrogen peroxide-induced DNA damage.
http://www.ncbi.nlm.nih.gov/pubmed/20852272

Note for Amazoniac, the poll should discriminate between GI disturbances cleared by antibiotics or real infections.

 

[HDD]

Posting this for those who believe Ray Peat is not informed on current microbiome studies. In fact, the host says that the science is justifying what he has been saying.


Raymond Peat, Ph.D.
You are what you Eat
2014, Herb Doctors

Q: (with regard to recent "scientific" findings on the microbiome of a person's body) It's well established that your gut apparently is your second brain, providing more input to your brain than your brain provides to it. And this is why your gut health is largely related in your gut bacteria, including your mental health and emotional well being. There are quite a few journal articles that have come out in 2013 and 2014 about the microbiome and making links...specifically to disease processes and the microbiome, and I know that you advocate several dietary factors that, I think, inadvertently are modulating the microbiome, and I think the science bringing about the explanation of the microbiome is now justifying what you are saying about, for example, indigestible fibers like bamboo shoots, carrots, etc. as being healthful in terms of their modulating the microbial content of the gut, and along with things like Cascara - not just for bowel motility and improving bowel function and wast clearance, but also because the Cascara itself is a cyclic structure quite similar to tetracycline in terms of it being a similar antibiotic in the gut, and how this affects bacterial colonies in a positive way to remove bad bacteria - actually allows normal healthy bacteria to flourish and therefore modulate the gut as an organism.

RP: It's interesting that both Emodin from Cascara and Chinese rhubarb and such and tetracycline and related minocycline and doxycycline - these are anti-inflammatory as well as antiseptic. Emodin and tetracyclines have surprising range of good effects - anti-inflammatory and probably mood improving - minocycline is being found to prevent, possibly improve, dementia, Alzheimer's disease...Emodin has - every year it seems like there are half a dozen functions that are found for Emodin including improving the flora of the intestine.

Q: Emodin - am I right in thinking that Emodin is also present in Aloe Vera.

RP: Yes, in lots of plants. Generally, they're a laxative plant, but it isn't the typical purging kind of a laxative. If the Cascara isn't properly aged, it does have an irritating purging effect, but aging makes it insoluble in water, comparatively, and it loses the irritating inflammatory property and becomes anti-inflammatory and sedative and it actually increases the production of energy while having a nerve calming sedative effect.

Q: Getting on to the wider topic of "You are what you eat," I think probably to bring out some of those things that you mention for many different conditions or processes that can be corrected by various...I mean, you prescribe a lot of dietary advice in terms of modulating the way people's physiology is working and therefore bringing people back to good health in a very natural way with no side effects - it's not a drug-oriented approach. It's very nutritional. I know, obviously, you are very keen on saturated fats as opposed to the poly's and the polyunsaturated fats as being very detrimental to health. Obviously sugar - I know you talk a lot about fruit juices and fructose in particular as an energy promoter. In terms of "You are what you eat," the gut bacteria and the bacteria within the bowel, what do you know from the studies that have been done on mood, for example, and/or autism in children that have shown some definite correlation between gut bacteria and their intestinal flora - and the intestinal flora in populations that are not suffering with autism. And how I think in the future, perhaps, the antibiotics that are very useful - and I know you are an advocate of antibiotics - and know most people unfortunately have a mistaken belief that antibiotics are bad - I think just from the cases where maybe females are getting thrush after using antibiotics, it conjures up this kind of popular myth or popular notion that antibiotics are bad, but actually we know that they are very positive influences on our physiology and especially on our gut for wiping out bad bacteria, but what's your thought about altering the so-called microbiome of the body so that specific bacteria that are known to be detrimental to health can be eradicated and leaving the positive bacteria behind to actually influence the populations within the digestive tract?

RP: About 1990 I read an article from a fertility clinic in which a lot of the women were trying to conceive and the fertilized ovum just wouldn't implant. The doctors thought that it might indicate that there was an infection in the uturus, so they gave all of their patients a course of antibiotics. Besides improving their fertility, a lot of the patients said suddenly that their chronic headaches had disappeared. So they gave them hormone tests to see what was going on, causing both fertility to improve and headaches and other symptoms to disappear - they found that the antibiotics had lowered their cortisol and estrogen production, and increased progesterone in their serum, explaining the increased fertility but a whole range of other symptoms related to stress. Following reading about that, I knew that the estrogen, which is excreted by a healthy liver in the bile...much of it is reabsorbed and stays in the circulation if you have a sluggish intestine. So I suggested that they eat a carrot every day to stimulate the intestine...the carrot will bind the bile and lower the serum estrogen level. That's now a generally accepted that any fiber can slow your absorption of estrogen from the bile. And within 3 or 4 days, these people tested their estrogen, cortisol and progesterone, and it was doing the same thing the synthetic antibiotics had done. Knowing about carrots and that they can get very tiresome if you eat one a day for years, I looked around for other foods that were antiseptic and might have that same effect. And bamboo shoots are something that you don't get too tired of - they don't have much flavor so you can put them in a lot of different foods - and cooking bamboo shoots doesn't destroy the fiber the way a cooked carrot does. So you have to eat raw carrots or cooked bamboo shoots.

Q: Do you know of any other fibers that have that effect?

RP: Mushrooms, I think. Because they grow underground in a very decaying environment, they have to have powerful antibiotics.

Q: You surprised me when you say mushrooms, because I wouldn't have though that would have been naturally one thing you would have said to somebody as something ok to eat...

RP: (laughing) I don't know anything about mushrooms, actually, except that principle - they are antiseptic.They have a high-value protein, and the protein happens to be pretty low in methionine which is the most toxic of the amino acids. Lucine and methionine are the amino acids that most slow your metabolism, so you're getting two of the metabolic stimulants - lowering the estrogen, disinfecting your intestine.

viewtopic.php?f=73&t=5489

 

[EnoreeG]

HDD, to summarize what I think Ray said in your citation, I'd put it something like this:

Ray is in favor of antibiotics for a purpose, but accepts fibrous foods if they function as "antiseptic" foods and reduce the bacterial load, if they at the same time can remove estrogen and other toxins from the gut as they exit the GI tract. Therefore, the fiber Ray favors is the non-fermentable fiber, precisely because that is the kind of fiber that absorbs toxins, but is indigestible by microbes.

This tends to be fibers of the following types, in order of indigestibility: Lignins, Hemicellulose, Chitin, Mucilage. Cellulose is also somewhat indigestible, but is more digestible than those 4. When I say "digestable" I am saying the same thing as "fermentable", the word used mostly in this thread.

Notice that Ray totally side-stepped the idea that the gut functions as a "second brain" and the mention of "studies during 2013 and 2014". No response on that question at all.

These quotes you posted are from a 2014 interview. To me, it seems Ray has not changed his stance on gut microbes from earlier interviews and articles with regard to what other authors are writing in the last 5 years regarding the features of microbes who feast on fermentable fiber. Therefore, from reading the entire transcript and looking at his every comment, it is not possible to know whether he is current on recent studies, because he cited none and didn't respond to any part of the questions that referred to recent findings on the value of what are now known as commensal or beneficial bacteria.

So I am still left in the dark as to whether Ray Peat is, or is not informed on current microbiome studies. The interview leaves me thinking he is an unchanged man regarding the last several years of study, whether he's read any studies or not. It is up to each of us to decide whether this is a positive or a negative. To me, it just leaves a large question mark as to what Ray knows of recent studies.

 

[Suikerbuik]

I second that, EnoreeG! Someone should just ask Peat. Maybe recap this thread to a few 100s words and ask him.

 

[Amazoniac]

53 pages is tantric germophilia..

 

[Such_Saturation]

The thread is akin to a sweaty fever dream.

 

[HDD]

So I am still left in the dark as to whether Ray Peat is, or is not informed on current microbiome studies. The interview leaves me thinking he is an unchanged man regarding the last several years of study, whether he's read any studies or not. It is up to each of us to decide whether this is a positive or a negative. To me, it just leaves a large question mark as to what Ray knows of recent studies.

There is a thread called "20 questions with Ray Peat" from 09/2014 that Dr. Peat has kindly replied to 10 of the questions. If you look at his replies, you will find studies from 2014 along with older studies. There is no doubt in my mind that Dr. Peat is up to date on current research.

From the thread:

2. marcar72 - "Ask him for more insight on what could be the cause of "high anxiety/panic attacks" quite a few of us members have been experiencing lately. Is it RT3 clearing, low serotonin, or maybe a B vitamin deficiency? A thorough answer from him covering all the possible causes in a checklist type answer would be awesome!

Ray Peat - When things are working properly, tissues are activated according to their use in adapting to the environment, and produce CO2 in proportion to their response; CO2 adjusts the blood supply while promoting mitochondrial energy production and regulating energy use. It stimulates normal breathing, while stabilizing (restraining activity of) nerves and other tissues. In the absence of oxygen (or presence of injury that prevents its use), lactate is produced instead of CO2, and displaces CO2 from the system, activating emergency alarm systems, potentially creating vicious circles of hormone changes and inflammation. Intestinal irritation (e.g., undigested food and bacterial toxin) releases large amounts of serotonin. Serotonin (named for its ability to constrict blood vessels) impairs oxygen use and increases lactate production. Hypothyroidism reduces tissues' ability to use oxygen and produce CO2, and slows digestion, increasing a tendency to produce serotonin, which activates stress hormones, etc.
Bag breathing can increase the carbon dioxide in the tissues, helping to reduce lactate production, but stabilizing the metabolic system is the real solution. With high glycogen stores, minor stresses don't tip the system into glycolytic metabolism easily.

===Physiol Behav. 2004 Sep 15;82(2-3):357-68.
Anxiety and aggression associated with the fermentation of carbohydrates in the
hindgut of rats.
Hanstock TL, Clayton EH, Li KM, Mallet PE.
School of Psychology, University of New England, Armidale, NSW 2351, Australia.
Lactic acid accumulation in the caecum and colon resulting from the fermentation
of carbohydrates can lead to deleterious effects in ruminant and monogastric
animals, including humans. In the present study, we examined the behavioural
effects of two types of commonly consumed foods: soluble and fermentable
carbohydrates (FCs). Thirty-six male Wistar rats were fed either a commercial rat
and mouse chow, a soluble carbohydrate (SC)-based diet or an FC-based diet.
Social interaction, anxiety, aggression and locomotor activity were examined by
employing a social interaction test and a light/dark emergence test, while
physical parameters of hindgut fermentation were examined after sacrifice, either
3 or 21 h after feeding. Results showed that anxiety (spending less time in the
light compartment during the light/dark emergence test) and aggression (increased
fighting during the social interaction test) were increased following raised
concentrations of fermentation end products, such as lactic acid and volatile
fatty acids (VFAs) in the caecum of rats. These associations occurred regardless
of dopamine and 5-HT concentrations in the prefrontal cortex (PFC) and provide
evidence supporting a general effect of FCs on behaviour. Possible mechanisms of
action along with similarities between a rat and human model of acidosis are
discussed.

Proc Soc Exp Biol Med. 1986 Dec;183(3):299-310.
Relationship between dietary fiber and cancer: metabolic, physiologic, and
cellular mechanisms.
Jacobs LR.
The relationships between fiber consumption and human cancer rates have been
examined, together with an analysis of the effects of individual dietary fibers
on the experimental induction of large bowel cancer. The human epidemiology
indicates an inverse correlation between high fiber consumption and lower colon
cancer rates. Cereal fiber sources show the most consistent negative correlation.
However, human case-control studies in general fail to confirm any protective
effect due to dietary fiber. Case-control studies indicate that if any source of
dietary fiber is possibly antineoplastic then it is probably vegetables. These
results may mean that purified fibers alone do not inhibit tumor development,
whereas it is likely that some other factors present in vegetables are
antineoplastic. Experiments in laboratory animals, using chemical induction of
large bowel cancer, have in general shown a protective effect with supplements of
*poorly fermentable fibers such as wheat bran or cellulose. *In contrast, a number
of*fermentable fiber supplements including pectin, corn bran, oat bran,**
**undegraded carageenan, agar, psyllium, guar gum, and alfalfa have been shown to**
**enhance tumor development. *Possible mechanisms by which fibers may inhibit colon
tumorigenesis include dilution and adsorption of any carcinogens and/or promoters
contained within the intestinal lumen, the modulation of colonic microbial
metabolic activity, and biological modification of intestinal epithelial cells.
Dietary fibers not only bind carcinogens, bile acids, and other potential toxins
but also essential nutrients, such as minerals, which can inhibit the
carcinogenic process. Fermentation of fibers within the large bowel results in
the production of short chain fatty acids, which in vivo stimulate cell
proliferation, while butyrate appears to be antineoplastic in vitro. Evidence
suggests that if dietary fibers stimulate cell proliferation during the stage of
initiation, then this may lead to tumor enhancement. Fermentation also lowers
luminal pH, which in turn modifies colonic microbial metabolic acidity, and is
associated with increased epithelial cell proliferation and colon carcinogenesis.
Because dietary fibers differ in their physiochemical properties it has been
difficult to identify a single mechanism by which fibers modify colon
carcinogenesis. Clearly, more metabolic and physiological studies are needed to
fully define the mechanisms by which certain fibers inhibit while others enhance
experimental colon carcinogenesis.

Psychiatry Res. 1989 May;28(2):181-91.
Prolactin and sodium lactate-induced panic.
Hollander E1, Liebowitz MR, Cohen B, Gorman JM, Fyer AJ, Papp LA, Klein DF.
Sodium lactate infusions reliably induce panic attacks in panic disorder patients but not in normal controls, but the mechanism underlying this response is unknown. We studied the plasma prolactin response to infusion of 0.5 molar sodium lactate in 38 patients with panic disorder or agoraphobia with panic attacks, and 16 normal controls. As expected, baseline plasma prolactin was significantly higher in female subjects than in male subjects. However, the males who experienced lactate-induced panic had significantly elevated baseline prolactin levels compared to male nonpanickers and controls. Prolactin levels increased in all groups during lactate infusion, which may reflect osmotic effects, but were blunted in the late panickers compared to nonpanickers and controls. The elevated baseline prolactin for male panickers supports a relationship between prolactin and anticipatory anxiety. The blunted prolactin response for late panickers suggests a net diminution, rather than a sensitization, of prolactin response in panic anxiety.

Endocrinol Jpn. 1960 Dec;7:261-70.
The role of serotonin in carbohydrate metabolism. III. The effect of serotonin on
blood lactate level of rats.
UI M, WARASHINA Y, KOBAYASHI B.

Endocrinol Jpn. 1960 Dec;7:271-8.
The role of serotonin in carbohydrate metabolism. IV. Mechanism of serotonin
hyperlactacidemia.
UI M, WARASHINA Y, KOBAYASHI B.

1. Effect of serotonin on blood lactate level of rats were examined.
2. Serotonin, administered intravenously, subcutaneously or intraperitoneally, caused a rise of blood lactate.
3. Effectiveness of serotonin in causing hyperlactacidemia was far more than that of epinephrine if considered on the basis of physiological concentration in circulation.
4. Serotonin had no effect on blood glycolysis both in vivo and in vitro.
5. The possibility that serotonin may act primarily on carbohydrate metabolism in peripheral and/or hepatic tissues are discussed.


J Am Soc Nephrol. 2014 Apr;25(4):657-70.
The gut microbiome, kidney disease, and targeted interventions.
Ramezani A(1), Raj DS.
(1)Division of Renal Diseases and Hypertension, The George Washington University,
Washington DC.
The human gut harbors >100 trillion microbial cells, which influence the
nutrition, metabolism, physiology, and immune function of the host. Here, we
review the quantitative and qualitative changes in gut microbiota of patients
with CKD that lead to disturbance of this symbiotic relationship, how this may
contribute to the progression of CKD, and targeted interventions to re-establish
symbiosis. Endotoxin derived from gut bacteria incites a powerful inflammatory
response in the host organism. Furthermore, protein fermentation by gut
microbiota generates myriad toxic metabolites, including p-cresol and indoxyl
sulfate. Disruption of gut barrier function in CKD allows translocation of
endotoxin and bacterial metabolites to the systemic circulation, which
contributes to uremic toxicity, inflammation, progression of CKD, and associated
cardiovascular disease. Several targeted interventions that aim to re-establish
intestinal symbiosis, neutralize bacterial endotoxins, or adsorb gut-derived
uremic toxins have been developed. Indeed, animal and human studies suggest that
prebiotics and probiotics may have therapeutic roles in maintaining a
metabolically-balanced gut microbiota and reducing progression of CKD and
uremia-associated complications. We propose that further research should focus on
using this highly efficient metabolic machinery to alleviate uremic symptoms.

J Agric Food Chem. 2008 May 28;56(10):3554-60.
Purple carrot (Daucus carota L.) polyacetylenes decrease
lipopolysaccharide-induced expression of inflammatory proteins in macrophage and
endothelial cells.
Metzger BT(1), Barnes DM, Reed JD.
(1)Department of Animal Science, University of WisconsinMadison, 1675 Observatory
Drive, Madison, Wisconsin 53706, USA. [email protected]
Carrots ( Daucus carota L.) contain phytochemicals including carotenoids,
phenolics, polyacetylenes, isocoumarins, and sesquiterpenes. Purple carrots also
contain anthocyanins. The anti-inflammatory activity of extracts and
phytochemicals from purple carrots was investigated by determining attenuation of
the response to lipopolysaccharide (LPS). A bioactive chromatographic fraction
(Sephadex LH-20) reduced LPS inflammatory response. There was a dose-dependent
reduction in nitric oxide production and mRNA of pro-inflammatory cytokines
(IL-6, IL-1beta, TNF-alpha) and iNOS in macrophage cells. Protein secretions of
IL-6 and TNF-alpha were reduced 77 and 66% in porcine aortic endothelial cells
treated with 6.6 and 13.3 microg/mL of the LH-20 fraction, respectively.
Preparative liquid chromatography resulted in a bioactive subfraction enriched in
the polyacetylene compounds falcarindiol, falcarindiol 3-acetate, and falcarinol.
The polyacetylenes were isolated and reduced nitric oxide production in
macrophage cells by as much as 65% without cytotoxicity. These results suggest
that polyacetylenes, not anthocyanins, in purple carrots are responsible for
anti-inflammatory bioactivity.

Bioactives in minimally processed carrots
March 24, 2011
Source: Teagasc
Summary:
Researchers are developing an understanding of how bioactive compounds in vegetables are affected by passage through the food chain. They assessed the impact of Modified Atmosphere Packaging, which is used to preserve ready-to-eat vegetable products such as carrot disks at the point of sale during chill storage.
Researchers at the Teagasc Food Research Centre, Ashtown, as part of the Irish Phytochemical Food Network, are developing an understanding of how bioactive compounds in vegetables are affected by passage through the food chain. They assessed the impact of Modified Atmosphere Packaging, which is used to preserve ready-to-eat vegetable products such as carrot disks at the point of sale during chill storage.
Polyacetylenes are natural products found in certain plants that have been related to a reduction in the risks of developing diseases such as certain types of cancers and other important diseases. Carrots contain relatively high contents of polyacetylenes. Recent studies have focussed on the polyacetylenes from carrots because their bioactive properties could have beneficial health effects.
They can be classified into four groups depending on the impact they have on human health -- anti inflammatory and anti-platelet; anti fungal and anti-viral; anti-bacterial and anti-mycobacterial; and, cytotoxicity and anti-cancer. Falcarinol has emerged as the most active polyacetylene in carrots in terms of cytotoxicity against cancer cell lines.
Researchers at the Teagasc Food Research Centre, Ashtown, as part of the Irish Phytochemical Food Network, are developing an understanding of how bioactive compounds in vegetables are affected by passage through the food chain. They assessed the impact of Modified Atmosphere Packaging, which is used to preserve ready-to-eat vegetable products such as carrot disks at the point of sale during chill storage.
In an article for TResearch, the Teagasc research and innovation magazine, Dr Juan Valverde and colleagues outline the results of their analysis. The results show that Modified Atmosphere Packaging is a useful way to retain polyacetylenes levels in carrots. None of the three major polyacetylenes in carrots showed significant difference from the control.

 

[Stuart]

@HDD
That's really interesting. Thanks for posting that recent update on Dr. Peat's changing perspective on the positive role played by your microbiome in general and fermentable fiber's specific role in promoting beneficial strains of colonic microbiota.
Art Ayers talks a lot about antibiotic properties of various foods too. And you might remember I linked to that article 'Garlic may be your gut's best friend'. Garlic's powerful action against undesirable yeast/fungal overgrowths and pathogenic bacteria while leaving commensal species alone predates modern medicine by millenia.
It's not really surprising is it after all the trouble taken to establish a thriving microbiome in babies. And the anatomical reality of having a huge space ONLY for the proliferation of a healthy mix of bacteria in which the commensals should be in control of the pathogens - the colon ?
But it is indeed heartening to see him keeping up with the latest research !

 

[narouz]

If you are wanting to feed your gas-producing bacteria, I've not struck anything more effective than soup made from jerusalem (f)artichokes. :)

Just curious whether the gas you experienced was from your colon (easy to pass - probably inconvenient - but not bloating type gas in your S.I.) ?
My favourite gut bugs are the gas eating ones. Your colon may be a gas factory , but you'd never know.

TMI, my whole life until starting this fiber/SBO eating experiment my farts smelt exactly like my Father''s Particularly after I'd been eating onions. Familiar, so in a strange way comforting, but unpleasant nevertheless.
About 3 months in, while I was still farting (not SIBO/bloating gas mind you), I gradually became aware that my farts smelt strangely unfamiliar, and increasingly less offensive. Now I just don't fart very often. and when I do, the faint still unfamiliarly inoffensive smell is like an unmistakable signal that all's well.
No idea of the why's and where fors , but it was a really interesting transition.
Jerusalem artichokes have a lot of short chain inulin. Whereas globe artchokes (the above ground ones) have the longest chain inulin you can get (even longer than Orafti HP).
What's been your experience with eating globe artichokes?

Very interesting, Stuart!
Especially about your Dad and those intimate memories, smells, etc

Yes, I've had globe artichokes two suppers in a row, two each night.
Oops, make that three nights in a row!
I forgot the first night I made HDD's/Such's recipe.

Also, taking the FOS and inulin powder.
I misread the labels when I said I was taking about 30grams/day a few days ago.
I was taking about 15g.
Now I am up to about 30g per day with the powders,
and then there's the artichokes.

I don't think I'm bloating any.
But I am farting quite a bit!
Not violently or painfully or anything.
Just a little bit all day.
The smell is not strange or unusual or particularly strong.
Actually, pretty mild.

Ah, how I love writing about my farts.
I hereby decree that that is firmly pro-Peat!
Nothing very dramatic to report about gut activities, sensations, etc.
Nor about things like mood or energy.
Will update!