Bad Doctor Experience, Give Up On Doctors? Not Sure What To Do (not Clickbait)

[Kyle M]

@Kyle M
What do you think about (ψm)-Driven K⁺-Enrichment Theory?

Tbh I'm mostly familiar with the AI hypothesis as it pertains to cellular proteins, not mitochondrial membranes. Didn't Ling also contend that the "proton gradient" was artifactual? It would make more sense that the working mitochondrial proteins adsorbed potassium than did the membrane, to my way of thinking. These measurements are so crude any way there's no way of knowing whether it's the membrane or the proteins or something else pulling in potassium the way they do it, half of the conclusions are surmise.

 

[kayumochi]

I had a doctor in Japan and another in the USA not be able to diagnosis a simple hernia in my groin. Later, I mentioned it to a medical resident and he knew what the lump was in a second ...

 

[Travis]

The mitochondrial membrane potential attracts cations so predictably that techniques have been created to measure it this way:

Logan, Angela, et al. "Assessing the mitochondrial membrane potential in cells and in vivo using targeted click chemistry and mass spectrometry." Cell metabolism 23.2 (2016): 379-385.

A change in one millivolt can easily be detected this way. Potassium has the highest migration velocity in capillary electrophoresis, so it it would be expected to be attracted to the mitochondrial membrane the quickest.

And trypan blue has a net negative charge . . .

Gilbert Ling never explained adequately how a live cell would have more affinity for potassium than a dead cell. I think you need the mitochondrial electron transport chain to account for this effect. After cell death sodium and potassium both equilibrate.

 

[yerrag]

I was too lazy, and also didn't have a shot glass. I have a small tumbler now so tonight I'll throw in some copper speaker wire (which was sold to me as full copper, not just coated) into some white vinegar. That's will work right? I promise this time I'll put it in the spec lol

I'd have to check that thread again as I think I had vinegar and hydrogen peroxide together as a mixture, heated it, and dropped the copper in afterwards. This made for a faster reaction into copper acetate.

 

[Kyle M]

The mitochondrial membrane potential attracts cations so predictably that techniques have been created to measure it this way:

Logan, Angela, et al. "Assessing the mitochondrial membrane potential in cells and in vivo using targeted click chemistry and mass spectrometry." Cell metabolism 23.2 (2016): 379-385.

Ok, but proteins (most have a net negative charge) also attract cations. There is no way at that scale to accurately measure what is pulling in the cations. I don't care what the authors of any paper say, I work in that kind of stuff and a lot of it is wishful thinking about what the techniques are capable of.

I am open to an argument proving their techniques are measuring this or that, but what you have shown me so far is only a suggestion that it's the mitochondrial membrane, not total proof

Gilbert Ling never explained adequately how a live cell would have more affinity for potassium than a dead cell. I think you need the mitochondrial electron transport chain to account for this effect. After cell death sodium and potassium both equilibrate.

It's a gradual process as proteins begin to unfold and lose their ability to adsorb cations from lack of ATP and CO2. Without those, the structure of the proteins starts to collapse and the cell becomes, in death, the salt solution that biologists think it always is. Isn't that adequate? He never said ATP wasn't produced by energy harvesting in the mitochondria, only that the ATPase spinny wheel that runs by funneling protons isn't how it happens.

 

[Kyle M]

I'd have to check that thread again as I think I had vinegar and hydrogen peroxide together as a mixture, heated it, and dropped the copper in afterwards. This made for a faster reaction into copper acetate.

I'm in no rush

 

[Travis]

I don't care what the authors of any paper say,

Had you actually read the paper Kyle? Do you even know what the authors "say"?

 

[Travis]

It's a gradual process as proteins begin to unfold and lose their ability to adsorb cations from lack of ATP and CO2. Without those, the structure of the proteins starts to collapse and the cell becomes, in death, the salt solution that biologists think it always is.

This takes time, and the graphs don't correspond: Below are three measures of 'cell death:' The one on the left indicates the results of a dye that can only be activated by the proteolytic capase. In the middle, we have trypan blue determining cell death. The graph on the right is a result of a dye that binds only to disrupted phosphotidylserine. Notice the ordinate on the rightmost graph: it doesn't even reach 25% after one day.

So it would seem that dye-uptake proceeds both apoptosis and any significant nonenzymatic degradation (implied by rightmost graph.)

Expression of Trx2 Increases the Mitochondrial Membrane Potential—To elucidate whether changes in the mitochondrial membrane potential (Δψm) could be the reason for increased lethality of HEK-Trx2 cells due to rotenone treatment, we measured the membrane potential using the JC-1 (Molecular Probes) fluorescent marker. JC-1 is a cationic fluorescent dye (green color as monomer) that accumulates in mitochondria in a potential-dependent manner. Its accumulation in mitochondria leads to high concentrations of the dye and the subsequent formation of red fluorescent aggregates. Upon loss of the mitochondrial membrane potential no accumulation of the dye will occur, leading to a shift from red to green. Hence, at high Δψm there is a low level of green fluorescence and a high red fluorescence. This allows the Δψm measurement by determination of red- relative to green-emitted light. The higher the ratio of the red- to green-emitted light the higher the Δψm. ―Damdimopoulos

I don't care what the authors of any paper say, ―Kyle

Ying, Howard S., Frank J. Gottron, and Dennis W. Choi. "Assessment of cell viability in primary neuronal cultures." Current protocols in neuroscience (2001): 7-18.
https://www.essenbioscience.com/med...IncuCyte_Caspase3-7_Reagents_44404704_PDS.pdf
https://www.essenbioscience.com/med...Cyte_Annexin_V_Reagents_for_Apoptosis_PDS.pdf
Damdimopoulos, Anastasios E., et al. "Human mitochondrial thioredoxin involvement in mitochondrial membrane potential and cell death." Journal of Biological Chemistry 277.36 (2002): 33249-33257.

 

[Xisca]

All it is for me is bloating when consuming carbohydrate, and increased gut irritation from spicy foods

Are you sure it is SIBO then? Why don't you just suppress those guilty foods?

 

[Owen B]

Your doctor has his hands tied behind his back; you can show him evidence until the cows come home; if the medical orthodoxy doesn't allow a treatment, he won't prescribe it, because he's risking his medical licence.

So, use orthodox medicine for the tests and alternative medicine for the cure.

Learn to make the best of both worlds.

I think that's a good plan - MDs for tests and alt med and forums for the rest. And it's unfortunately true; they get their backs up immediately if I bring up evidence. Try even using the word "energy" in a MD's office. I understand their hands are tied.

The endocrinologist i just went to was out and out patronizing. I took a chance. And I got a priggish control freak.

My plan now is to try and concentrate on the way I come across to the doctor emotionally and socially. It's very hard to keep my tongue. I don't want to put the emphasis on him/her. I think that was my problem in the past in some cases. i want to be able to present my situation as clearly as possible, what my needs are, that I'm looking for someone to work with on a one to one basis while at the same time respecting the doctor's position. "You catch more flies with honey than vinegar."

What do people here think about a sports medicine MD? I'm not an athlete and don't participate in anything like that but I'm thinking that they might at least be in the rough ballpark, at least with regard to hormones. After all, many of our concerns here are similar to that of the athlete: functional performance.

I see many people posting here about their numbers; they seem to be going to these doctors all the time. Where do you find these MDs?

 

[lollipop]

i want to be able to present my situation as clearly as possible, what my needs are, that I'm looking for someone to work with on a one to one basis while at the same time respecting the doctor's position. "You catch more flies with honey than vinegar."

+1

 

[sweetpeat]

All it is for me is bloating when consuming carbohydrate, and increased gut irritation from spicy foods that I didn't have before.

I had these symptoms last year after a 2nd round of antibiotics for strep. I remember that I craved Jello like crazy. Not gelatin like Peat recommends but regular fruity Jello like you buy in the supermarket. Gelatin bloats me, but I found the Jello very soothing. I ate tons of it, and tried to avoid foods that made me feel bad. I also used lysine, a 500mg capsule once or twice a day. It took a few weeks before I felt normal and could eat without issues. And my craving for Jello went away. Weird.

Anyway, just thought I would share since the symptoms sounded so similar.

 

[CLASH]

Hey Kyle M,
I think I may be of some help as I have dealt with this situation personally, both with doctors and with the same medical issue. For context I am a 22 year old male, I was breast fed only 4- 6 months (amount of time changes based on how much alcohol is in my moms system when I ask her), had multiple courses of antibiotics as a kid, adenoids removed, and gallbladder removed at 17.... (thank you modern medicine; jokes on me I'm a nurse haha). My symptoms where bloating after eating carbohydrates, brain fog, depression and irregular stools with some bleeding (more recently) all depending on what I ate. I tried herbal protocols, dietary adjustments, supplemental protocols with biofilm disruptors, enzymes and antibiotics (rifaximin and tetracycline). Nothing had a lasting effect, tetracycline actually made things much worse. I am going to try to organize my thoughts for you:

1) As for SIBO, I don't think its a main diagnosis, I think it secondary to a colonic dysbiosis (negative bacteria effecting colonic function and migrating up through the ileocecal valve into the small intestine.) Thus in order to treat this you have to establish the correct flora in the colon. Purely cleaning out your small intestine won't solve the issue hence all the people who don't recover from SIBO. This is also why antibiotics will never truly solve the problem, along with other reasons. The way to solve the issue is to raise the metabolic rate to increase immune function and allow the body to maintain the optimal flora , but at this point, this can only be done by establishing a normal colonic flora.

2) As for antibiotics, I think they are the source of the issue, as well as formula feeding and c-sections. There are stories all over the internet of people having issues (Autoimmune diseases) after antibiotics (penicillin and tetracyclines aren't that bad, many studies show the flora isn't largely effected by these. Cephalosporins, vancomycin, carbapenems etc. are the real issues, many studies show this). I think the reason antibiotics cause such an issue is because they permeate the tissues of the body including the intestinal epithelium. This causes the bacteria that are bound to the intestinal wall to die and dislodge as opposed to the bacteria in the lumen. Thus, the bacteria in the lumen which are inducing pathogenesis now have an opening in the ecosystem to bind to the intestinal epithelium setting you up for dysbiosis down the road. Also, antibiotic usage creates an environment for selective adaptation to antibiotic resistance and up regulates toxic genes within bacteria (toxic to us) due to the pressure put on them. i.e. if you try to kill a bunch of people, you'd probably piss them off and they would in return arm themselves. Also the weak people would die and the strong and possibly dangerous would survive. Rifaximin (the drug for SIBO) is somewhat unique in this instance in that it isn't absorbed so it only effects bacteria in the lumen. (Interestingly enough I developed the ulcer in my intestine after my round of tetracycline) So I don't think rifaximin is as detrimental. Nystatin is good in this sense as well. I have ordered rifaximin from Number 1 MEXICAN PHARMACY|BRANDS & GENERICS|WHOLESALE PRICES with success twice (I have used it for one 14 day course 400mg TID with interphase plus and lactoferrin and tetracycline; no lasting improvement). Regardless of this, I do think the medication is real. The tetracycline I received from them was real; I got antibiotic associated diarrhea from it. I think phages are useful as well, though I have yet to try. I have ordered phages from Редкие и уникальные лекарства | Фармалад | Поиск, заказ, доставка в Украине, Крым, страны СНГ, Балтии, Грузии. +38(044) 22-765-22 however I have not received them yet and it was expensive, I'll let you know if I received them. I had to make a DHL account to ship them to the US. I have been in contact with a representative from the company for over a month with almost daily emailing back and forth, so I do feel the the company is legit. With phages the issues is they are thermolabile, so they have to be kept below a certain temperature during transit so the DHL shipping from Russia is about 200$ and thats not including the phage cost. If the product is seized at customs your screwed (pardon my english), so keep in mind the monetary risk.

3) As for Nathan Hatch's SIBO article, I don't think he knows what he is talking about in some respects. A2 milk, chewing food, aspirin, biotin and vit C make sense (these are all very generally and non-specific toward SIBO). His info on acetic acid bacteria vs lactic acid bacteria was either not elaborated well or he hasn't done his research. Also, his comment on bacteria conjugation linoleic acid or the creation of trans fatty acid by bacteria being negative was very misinformed (the trans fatty acid created is generally CLA or conjugated linoleum acid; a component of dairy that is seen as extremely beneficial on multiple physiologic fronts. Basically, bacteria are taking the PUFA you eat, and making it into a trans-fatty acid with health effect; talk about depleting PUFA) Bioproduction of Conjugated Linoleic Acid by Probiotic Bacteria Occurs In Vitro and In Vivo in Mice. The bacteria that naturally (From breastmilk) inhabit our colon, as well as small intestine, are both lactic acid and acetic acid produces. Bifidobacteria and Lactobacillus bacteria both can produce both lactic acid and acetic acid and utilize both of them as a substrate for fermentation. The beneficial bacteria you want in the colon is lactobacillus and bifidobacteria. If you drink milk at all you are promoting the development of these bacteria to some extent. Also, lactic acid bacteria produce lactic acid that is then cross fed to butyrate producing bacteria. I think taking a butyrate based probiotic is a waste of money considering that its not solving the ecology issue in your colon. The butyrate producers are maintained by the lactic acid bacteria that we receive from breast milk as well as fermentable fibers, but in the beginning I think they are established by the breast milk bacteria Bifidobacteria and Butyrate-Producing Colon Bacteria: Importance and Strategies for Their Stimulation in the Human Gut. Breast milk is the originator of our intestinal ecosystem, not obscure industrial probiotics. So to say that you want acetic acid bacteria and not lactic acid bacteria is a poorly educated statement, especially in the context of promoting milk. Also, some of the logic and information around the use of sodium acetate is poorly discussed. I have never used the substance or have read extensively about it but based on the information he provided I really don't see the point of the substance for SIBO. Overall I think, besides chewing well, switching to A2 milk and taking some vit C, aspirin and maybe some biotin the article is full of misinformation and not one of his better articles. If anyone would like, I will elaborate more on what I have said. I generally enjoy Nathan's articles but I think this article was filled with misinformation. Lastly, I posted a comment on Nathan's article with these same points and he deleted my comment. The comment wasn't offensive or directed at him, it was directed at the information.

4) testing for SIBO that may actually help address the root of the issues:
-doctors data parasitology x3: stool test to show pathogenic bacteria. I did this one and had klebsiella, staph, and strep in my stool and no lactobacillus and +1 bifiodbacteria haha..... (this was after carrot salad, coffee attempts, aspirin, 2 years of strict peat inspired diet and 6 years of gluten free and vegetable oil free diet, tetracycline, dhea, pregnenolone, androsterone, energin, tocovit, estroban, kuinone, glycine, taurine etc. etc. etc.)
-biohealth laboratories GI 401H: stool test to show pathogenic bacteria (more expensive test)
-ELISA/ ACT LRA: a test for delayed hypersensitivity allergies (these are caused by leaky gut). The test is very expensive, but very helpful. I was allergic to orange juice, took it out and my temps went up and lost weight haha (I really miss it).

5) Treatment:
in order to reestablish normal flora which is an ecosystem, I think you have to go back to the beginning. You have to basically breast feed yourself. But you have to use A2 RAW milk or RAW goats milk. Also, I think raw goat kefir is essential (since using kefir, no bloating anymore and blood in stool has gone down dramatically). While doing this, nothing in your diet should ferment (just as with breastfeeding). In order to do this, the diet should be all animal products (shellfish, ruminant meat, I don't eat any fowl or poultry, haven't for 4 years now) and invert syrup (I mentioned this on other threads but Invert syrup is the only thing that hasn't bother my gut even when sucrose has). I think invert syrup is much easier to digest due to it being free monosaccharides. I make it with ascorbic acid from nutrabio and organic cane sugar by bringing it close to a boil in a pan with water. You can also maybe try the "milk cure". I don't due eggs because they cause me digest distress (interestingly eggs contain trypsin inhibitors as well as other digestive inhibitors i.e. avidin) the diet is essentially as follows:
-grass fed ruminant meat (liver, kidney, muscle meat)
-shellfish (shrimp, mussels, oysters, scallops)
-raw grass fed A2 cows milk or goats milk
-raw grass fed A2 cow or goats kefir (made from kefir grains)
-invert syrup made from sucrose and ascorbic acid from nutrabio (I use nutrabio because they manufacture in house and I think their products are pretty pure, haven't had any bad reaction from impurities from them)

Hope this helps man, digestive troubles really suck, I've struggle with them since I was in 8th grade (I am now 22). The Goat kefir and Goat milk have helped me the most (I just started them 2 weeks ago and my change has been significant; no depression, no bloating, no blood in stool, no pain in LLQ).

 

[lollipop]

If anyone would like, I will elaborate more on what I have said.

Pretty fascinating post @CLASH. I am interested. Would you mind elaborating?

 

[Kyle M]

Thanks for the thoughtful post @CLASH , if my antibiotic course doesn't work I will look into some of that. I have had some of those stool tests and nothing ever showed up.

 

[CLASH]

@lisaferraro
1)The article is sound in these areas for the most part:

- The introductory paragraphs,

-The “what is SIBO” paragraphs except for the location of vit k2 in endotoxin (not sure where this came from, would love to see a reference, from what I understand this is false, I could be wrong though so if anyone has the research I’d love to see it)

-The “lysozyme” paragraphs

-The milk and SIBO paragraphs (the exception is that the substitution of histidine in place of the proline is what allows the BCM-7, a morphine like peptide present in A1 milk, to be more easily hydrolyzed and exert its inflammatory effect. I’m not sure what exactly he is referring to specifically, it was a bit unclear to me, but the mechanism is documented in research:


“In humans, digestion of bovine A1 beta-casein, but not the alternative A2 beta-casein, releases beta-casomorphin-7, which activates μ-opioid receptors expressed throughout the gastrointestinal tract and body. Studies in rodents show that milk containing A1 beta-casein significantly increases gastrointestinal transit time, production of dipeptidyl peptidase-4 and the inflammatory marker myeloperoxidase compared with milk containing A2 beta-casein. Co-administration of the opioid receptor antagonist naloxone blocks the myeloperoxidase and gastrointestinal motility effects, indicating opioid signaling pathway involvement. In humans, a double-blind, randomized cross-over study showed that participants consuming A1 beta-casein type cows’ milk experienced statistically significantly higher Bristol stool values compared with those receiving A2 beta-casein milk. Additionally, a statistically significant positive association between abdominal pain and stool consistency was observed when participants consumed the A1 but not the A2 diet.”

Milk Intolerance, Beta-Casein and Lactose


“The A1 and A2 variants of beta casein differ at amino acid position 67 with histidine (CAT) in A1 and proline (CCT) in A2 milk as a result of single nucleotide difference. This polymorphism leads to a key conformational change in the secondary structure of expressed β-casein protein. Gastrointestinal proteolytic digestion of A1 variant of β-casein (raw/processed milk) leads to generation of bioactive peptide, beta casomorphin 7 (BCM7)”

Milk proteins and human health: A1/A2 milk hypothesis


2)The rest of the article, gets a bit obscure especially with lack of references, some of the statements are conjecture, over simplification and some seem to be just pure misinformation. I’m going to focus on the lactic acid bacterial portion specifically because I think this is the most relevant to SIBO. As for the claims about sodium acetate, and other metabolic claims he makes, I think they are secondary to the conversation on SIBO and I’m not going to address them in a direct metabolic sense. I can’t address every aspect of the article because there are too many claims, zero references to what he is saying, and the metabolic pathways are all over the place. As for the claims directly relating to SIBO that I find to be a bit of misinformation these include:




- “One strain of lactic acid bacteria was found to alter dietary fats, turning them into more toxic trans-fatty acids.”

· "Conjugated linoleic acids (CLA) are a group of isomers of linoleic acid (LA) possessing anti-inflammatory and anticarcinogenic properties, which can be produced from LA by certain bacterial strains. In this study, the ability of probiotic bacteria to exert anticarcinogenic effects through the production of CLA was assessed. Incubation of probiotic bacteria (VSL3, Lactobacillus acidophilus, L. bulgaricus, L. casei, L. plantarum, Bifidobacterium breve, B. infantis, B. longum, and Streptococcus thermophilus) in the presence of LA yielded CLA production as measured by gas chromatography."Bioproduction of Conjugated Linoleic Acid by Probiotic Bacteria Occurs In Vitro and In Vivo in Mice




-“unlike other bacterial metabolic products like acetic and butyric acids, lactic acid is not used for anything”


- “where lactic acid simply suppresses the growth of all others and provides no useful nutritive products”


-“ It also suppresses the growth of other species of bacteria, namely the ones we rely on to make acetic and butyric acid”


-“ During SIBO the overgrowth of lactic acid bacteria suppress strains which produce acetic acid, lowering the amounts of those other important down-stream products”

(all are drastically oversimplified claims borderline straight false. )

· “Examples of functions carried out by bifidobacteria include the production and/or liberation of B vitamins, antioxidants, polyphenols, and conjugated linoleic acids; maturation of the immune system during early life and preservation of immune homeostasis during life; preservation of gut barrier functions and protection against pathogens by producing bacteriocins, decreasing luminal pH by the production of acids, and blocking the adhesion of pathogens to the intestinal mucosa”

· “Another important function of the bifidobacterial genus that contributes to gut homeostasis and host health is the production of acetate and lactate during carbohydrate fermentation, organic acids that in turn can be converted into butyrate by other colon bacteria through cross-feeding interactions”

· “Once internalized into the cytoplasm, hexose monosaccharides (e.g., fructose and glucose) are converted into acetate and lactate by the fructose 6-phosphate phosphoketolase pathway or bifid shunt”

· Bifidobacteria and Butyrate-Producing Colon Bacteria: Importance and Strategies for Their Stimulation in the Human Gut

· "Although lactic acid bacteria are named after their ability to form lactic acid, many are able to degrade lactic acid as well, especially if O2 is available as electron acceptor (21, 23). Some lactic acid bacteria are also able to degrade lactic acid under anoxic conditions in the presence of alternative electron acceptors. For example, Lactobacillus plantarum and L. pentosus can use citrate as electron acceptor (11, 19). The products of this cofermentation of lactic acid and citrate are succinic acid, acetate, formate, and CO2. Other lactic acid bacteria, such as L. brevis and L. buchneri, can degrade lactic acid by using glycerol as an electron acceptor, while producing acetate, 1,3-propanediol, and CO2 (26). L. bifermentans is thus far the only species known to ferment lactic acid, i.e., without requiring an external electron acceptor. This bacterium can form acetic acid, ethanol, CO2 and H2 from lactic acid at a pH of >4.0"

· Anaerobic Conversion of Lactic Acid to Acetic Acid and 1,2-Propanediol by Lactobacillus buchneri




- “Apples are especially effective at raising acetate and lowering lactic acid, because lactic acid bacteria are unable to feed on apple fiber yet acetic acid bacteria do so readily” (I cite this one, just to exemplify the misinformation related to some of the claims, I admit it is a bit nitpicky in the scheme of things, but the statement is just blatantly unfounded)

· "apple juice from four cultivars were fermented for 0, 24, 48 and 72 h using Lactobacillus acidophilus and their effects related to management of hyperglycemia, hypertension, inhibition of Helicobacter pylori and proliferation of probiotic Bifidobacterium longum were evaluated using in vitro models"

· "Overall, α-glucosidase inhibition and hypertension-relevant angiotensin-converting enzyme inhibition decreased after 72 h for pH-adjusted samples, whereas contrasting results were obtained for fermented acidic pH samples. Only at 48- and 72-h fermented acidic pH samples had H. pylori inhibitory activity."

· FERMENTATION OF WHOLE APPLE JUICE USING LACTOBACILLUS ACIDOPHILUS FOR POTENTIAL DIETARY MANAGEMENT OF HYPERGLYCEMIA, HYPERTENSION, AND MODULATION OF BENEFICIAL BACTERIAL RESPONSES



· "Administration of extraction juices from apples increased fecal counts of Lactobacillus and Bifidobacterium. More acetate and total short-chain fatty acids appeared in intestinal contents of the apple and red beet group"

· Physiological effects of extraction juices from apple, grape, and red beet pomaces in rats. - PubMed - NCBI


- “Citrus fruit and peels help raise butyric acid.” (The verdict on butyric acid is absent. It seems to depend on concentration and which bacteria are producing it. More research needs to be done. Citrus fruits contain a high amount of pectin, pectin is implicated in advancing cancer. Goes hand in hand with peats low fermentable fiber diet. The only things that seem protective of colon cancer are dairy (vit D, calcium, bacteria, bioactive peptides), cellulose and in some studies wheat bran (wholly indigestible and pretty un-fermentable; basically a colonic brillo pad).

· " 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."

· "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."

· Relationship between dietary fiber and cancer: metabolic, physiologic, and cellular mechanisms. - PubMed - NCBI


Also, in conjunction with all of this, the bacteria present in breast milk and the breast fed infants colon is mostly “lactic acid bacteria” lactobacillus and bifidobacteria. It seems to me the optimal bacteria, if living on milk are lactobacillus and bifidobacteria. Also, it seems that these are the optimal bacteria overall in conjunction with clostridia group XIVa and some other clostridia groups which include faecalibacterium prausnitzii, roseburia intestinalis, akkermensia muciniphia, and eubacterium rectale among others that can cross feed on lactic acid and other substrate and produce butyrate in necessary quantities. It seems that breast milk sets this dynamic up. Formula and antibiotics destroy it. Starch, legumes, vegetables, nuts, seeds, plant toxins etc. can only be consumed safely with the right gut bacteria to dispose of them, if not inflammation occurs. This is not too mention that, T-regs and the immune system are directly dependent on gut bacteria and wiping them out with antibiotics leads directly to auto-immunity, hair loss and hormonal issues. (I don’t want to find all the studies linking all of these things, it would take me forever to draw all the lines through the studies).


Lastly, somewhat secondary taurine is mentioned often on the ray peat forum and by Nathan hatch in his articles. Please be careful using the substance, it is a GABA agonist and long term use can result in down regulation of GABA receptors. I took 1-2g semi-consistently for 5 months and now I am up at 1:45 A.M. writing this response post because of the insomnia of the withdrawal (never had insomnia like this before in my life). I posted on another thread about this but since stopping taurine I have had insomnia, anxiety, a lot of adrenaline rushes, and I feel emotions again (the GABA agonist thing is similar to bentos, they can cause a depression (more like a slight apathy and lack of emotion) which I experienced very slightly for the period of time taking taurine). As Peat has stated to some degree; the use of isolated amino acids is not necessarily a good idea. Be careful with your supplementation and your drug utilization, please (especially antibiotics, I only had blood in my stool and LLQ pain after taking tetracycline).

 

[CLASH]

The "-" were Nathan's statements quoted.
The "·" were my replies with studies.

 

[lollipop]

@lisaferraro
1)The article is sound in these areas for the most part:

- The introductory paragraphs,

-The “what is SIBO” paragraphs except for the location of vit k2 in endotoxin (not sure where this came from, would love to see a reference, from what I understand this is false, I could be wrong though so if anyone has the research I’d love to see it)

-The “lysozyme” paragraphs

-The milk and SIBO paragraphs (the exception is that the substitution of histidine in place of the proline is what allows the BCM-7, a morphine like peptide present in A1 milk, to be more easily hydrolyzed and exert its inflammatory effect. I’m not sure what exactly he is referring to specifically, it was a bit unclear to me, but the mechanism is documented in research:


“In humans, digestion of bovine A1 beta-casein, but not the alternative A2 beta-casein, releases beta-casomorphin-7, which activates μ-opioid receptors expressed throughout the gastrointestinal tract and body. Studies in rodents show that milk containing A1 beta-casein significantly increases gastrointestinal transit time, production of dipeptidyl peptidase-4 and the inflammatory marker myeloperoxidase compared with milk containing A2 beta-casein. Co-administration of the opioid receptor antagonist naloxone blocks the myeloperoxidase and gastrointestinal motility effects, indicating opioid signaling pathway involvement. In humans, a double-blind, randomized cross-over study showed that participants consuming A1 beta-casein type cows’ milk experienced statistically significantly higher Bristol stool values compared with those receiving A2 beta-casein milk. Additionally, a statistically significant positive association between abdominal pain and stool consistency was observed when participants consumed the A1 but not the A2 diet.”

Milk Intolerance, Beta-Casein and Lactose


“The A1 and A2 variants of beta casein differ at amino acid position 67 with histidine (CAT) in A1 and proline (CCT) in A2 milk as a result of single nucleotide difference. This polymorphism leads to a key conformational change in the secondary structure of expressed β-casein protein. Gastrointestinal proteolytic digestion of A1 variant of β-casein (raw/processed milk) leads to generation of bioactive peptide, beta casomorphin 7 (BCM7)”

Milk proteins and human health: A1/A2 milk hypothesis


2)The rest of the article, gets a bit obscure especially with lack of references, some of the statements are conjecture, over simplification and some seem to be just pure misinformation. I’m going to focus on the lactic acid bacterial portion specifically because I think this is the most relevant to SIBO. As for the claims about sodium acetate, and other metabolic claims he makes, I think they are secondary to the conversation on SIBO and I’m not going to address them in a direct metabolic sense. I can’t address every aspect of the article because there are too many claims, zero references to what he is saying, and the metabolic pathways are all over the place. As for the claims directly relating to SIBO that I find to be a bit of misinformation these include:




- “One strain of lactic acid bacteria was found to alter dietary fats, turning them into more toxic trans-fatty acids.”

· "Conjugated linoleic acids (CLA) are a group of isomers of linoleic acid (LA) possessing anti-inflammatory and anticarcinogenic properties, which can be produced from LA by certain bacterial strains. In this study, the ability of probiotic bacteria to exert anticarcinogenic effects through the production of CLA was assessed. Incubation of probiotic bacteria (VSL3, Lactobacillus acidophilus, L. bulgaricus, L. casei, L. plantarum, Bifidobacterium breve, B. infantis, B. longum, and Streptococcus thermophilus) in the presence of LA yielded CLA production as measured by gas chromatography."Bioproduction of Conjugated Linoleic Acid by Probiotic Bacteria Occurs In Vitro and In Vivo in Mice




-“unlike other bacterial metabolic products like acetic and butyric acids, lactic acid is not used for anything”


- “where lactic acid simply suppresses the growth of all others and provides no useful nutritive products”


-“ It also suppresses the growth of other species of bacteria, namely the ones we rely on to make acetic and butyric acid”


-“ During SIBO the overgrowth of lactic acid bacteria suppress strains which produce acetic acid, lowering the amounts of those other important down-stream products”

(all are drastically oversimplified claims borderline straight false. )

· “Examples of functions carried out by bifidobacteria include the production and/or liberation of B vitamins, antioxidants, polyphenols, and conjugated linoleic acids; maturation of the immune system during early life and preservation of immune homeostasis during life; preservation of gut barrier functions and protection against pathogens by producing bacteriocins, decreasing luminal pH by the production of acids, and blocking the adhesion of pathogens to the intestinal mucosa”

· “Another important function of the bifidobacterial genus that contributes to gut homeostasis and host health is the production of acetate and lactate during carbohydrate fermentation, organic acids that in turn can be converted into butyrate by other colon bacteria through cross-feeding interactions”

· “Once internalized into the cytoplasm, hexose monosaccharides (e.g., fructose and glucose) are converted into acetate and lactate by the fructose 6-phosphate phosphoketolase pathway or bifid shunt”

· Bifidobacteria and Butyrate-Producing Colon Bacteria: Importance and Strategies for Their Stimulation in the Human Gut

· "Although lactic acid bacteria are named after their ability to form lactic acid, many are able to degrade lactic acid as well, especially if O2 is available as electron acceptor (21, 23). Some lactic acid bacteria are also able to degrade lactic acid under anoxic conditions in the presence of alternative electron acceptors. For example, Lactobacillus plantarum and L. pentosus can use citrate as electron acceptor (11, 19). The products of this cofermentation of lactic acid and citrate are succinic acid, acetate, formate, and CO2. Other lactic acid bacteria, such as L. brevis and L. buchneri, can degrade lactic acid by using glycerol as an electron acceptor, while producing acetate, 1,3-propanediol, and CO2 (26). L. bifermentans is thus far the only species known to ferment lactic acid, i.e., without requiring an external electron acceptor. This bacterium can form acetic acid, ethanol, CO2 and H2 from lactic acid at a pH of >4.0"

· Anaerobic Conversion of Lactic Acid to Acetic Acid and 1,2-Propanediol by Lactobacillus buchneri




- “Apples are especially effective at raising acetate and lowering lactic acid, because lactic acid bacteria are unable to feed on apple fiber yet acetic acid bacteria do so readily” (I cite this one, just to exemplify the misinformation related to some of the claims, I admit it is a bit nitpicky in the scheme of things, but the statement is just blatantly unfounded)

· "apple juice from four cultivars were fermented for 0, 24, 48 and 72 h using Lactobacillus acidophilus and their effects related to management of hyperglycemia, hypertension, inhibition of Helicobacter pylori and proliferation of probiotic Bifidobacterium longum were evaluated using in vitro models"

· "Overall, α-glucosidase inhibition and hypertension-relevant angiotensin-converting enzyme inhibition decreased after 72 h for pH-adjusted samples, whereas contrasting results were obtained for fermented acidic pH samples. Only at 48- and 72-h fermented acidic pH samples had H. pylori inhibitory activity."

· FERMENTATION OF WHOLE APPLE JUICE USING LACTOBACILLUS ACIDOPHILUS FOR POTENTIAL DIETARY MANAGEMENT OF HYPERGLYCEMIA, HYPERTENSION, AND MODULATION OF BENEFICIAL BACTERIAL RESPONSES



· "Administration of extraction juices from apples increased fecal counts of Lactobacillus and Bifidobacterium. More acetate and total short-chain fatty acids appeared in intestinal contents of the apple and red beet group"

· Physiological effects of extraction juices from apple, grape, and red beet pomaces in rats. - PubMed - NCBI


- “Citrus fruit and peels help raise butyric acid.” (The verdict on butyric acid is absent. It seems to depend on concentration and which bacteria are producing it. More research needs to be done. Citrus fruits contain a high amount of pectin, pectin is implicated in advancing cancer. Goes hand in hand with peats low fermentable fiber diet. The only things that seem protective of colon cancer are dairy (vit D, calcium, bacteria, bioactive peptides), cellulose and in some studies wheat bran (wholly indigestible and pretty un-fermentable; basically a colonic brillo pad).

· " 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."

· "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."

· Relationship between dietary fiber and cancer: metabolic, physiologic, and cellular mechanisms. - PubMed - NCBI


Also, in conjunction with all of this, the bacteria present in breast milk and the breast fed infants colon is mostly “lactic acid bacteria” lactobacillus and bifidobacteria. It seems to me the optimal bacteria, if living on milk are lactobacillus and bifidobacteria. Also, it seems that these are the optimal bacteria overall in conjunction with clostridia group XIVa and some other clostridia groups which include faecalibacterium prausnitzii, roseburia intestinalis, akkermensia muciniphia, and eubacterium rectale among others that can cross feed on lactic acid and other substrate and produce butyrate in necessary quantities. It seems that breast milk sets this dynamic up. Formula and antibiotics destroy it. Starch, legumes, vegetables, nuts, seeds, plant toxins etc. can only be consumed safely with the right gut bacteria to dispose of them, if not inflammation occurs. This is not too mention that, T-regs and the immune system are directly dependent on gut bacteria and wiping them out with antibiotics leads directly to auto-immunity, hair loss and hormonal issues. (I don’t want to find all the studies linking all of these things, it would take me forever to draw all the lines through the studies).


Lastly, somewhat secondary taurine is mentioned often on the ray peat forum and by Nathan hatch in his articles. Please be careful using the substance, it is a GABA agonist and long term use can result in down regulation of GABA receptors. I took 1-2g semi-consistently for 5 months and now I am up at 1:45 A.M. writing this response post because of the insomnia of the withdrawal (never had insomnia like this before in my life). I posted on another thread about this but since stopping taurine I have had insomnia, anxiety, a lot of adrenaline rushes, and I feel emotions again (the GABA agonist thing is similar to bentos, they can cause a depression (more like a slight apathy and lack of emotion) which I experienced very slightly for the period of time taking taurine). As Peat has stated to some degree; the use of isolated amino acids is not necessarily a good idea. Be careful with your supplementation and your drug utilization, please (especially antibiotics, I only had blood in my stool and LLQ pain after taking tetracycline).

Great information to chew on @CLASH. Appreciate your effort. When I read the article, I did not have the information you have or the experience. Not sure why exactly, something about the article raised red flags in me. This is why your detailed post sparked my interest.

 

[CLASH]

@lisaferraro
No problem, glad I could help.
Some of the things I said I didnt want to directly reference because of time, such as T-reg development and the gut, I just posted about in this thread if your interested:
https://raypeatforum.com/community/...hairloss-is-caused-by-immune-imbalance.19983/

 

[lollipop]

@lisaferraro
No problem, glad I could help.
Some of the things I said I didnt want to directly reference because of time, such as T-reg development and the gut, I just posted about in this thread if your interested:
Latest Hair Studies: Hairloss Is Caused By Immune Imbalance

Yes, interested. Thank you!