We need doctors, not merchants!

 

 

 

 

'Lessons not Iearnt in blood are soon forgotten'  —Clyde Shelton

 

 

I really hope not...

 

Years ago, doctors were responsible for causing me SIBO and overall gut microbiome dysbiosis with overuse of antibiotics. Not long after that, most of them called me crazy because I was complaining of neurotoxicity with occasions of feeling drunk, nausea, fatigue, and a profound feeliing of illness. A couple of them were strongly against me and convinced I should be committed to a mental hospital. It’s the usual stuff you normally get from low, dogmatic and closed minds, which stink of arrogance and self-infatuation. However, some doctors gained my respect because their answer was 'I believe you, but this is beyond my knowledge'. But who were these doctors? Exactly the ones who should know, in the 21st century, how dangerous a dysbiotic gut microbiome is for our general health: gastroenterologists and infectionists.

 

 

But they don’t know because the whole medical system is focused on the categorization of symptoms and the promotion of drugs, and not on causality. And this is the main goal for this manifesto, to change the medical view towards causality which actually leads to the gut microbiome!

 

 

'The hardest choices require the strongest wills'  —Thanos

 

Neuroimmunity, Autoimmunity, Autism, Anxiety, Depression, IBS, SIBO, Neurotoxicity, Fibromyalgia, Fatigue...All cute and useless labels! But what do they all have in common? What’s their main cause? Our dysbiotic and infected gut microbiome! And all of them can be easily proven these days with PubMed publications.

 

The research exploded the last decade and new PubMed appears every day now. Google is full of them! Hundreds...But our MDs are still trained in the same old dogma to deny the microbiota and they act as merchants because this system still holds its grounds severely in the hundreds of billions of dollars made with symptom suppressing drugs!

 

Did you know that at the end of 2020, the market, just for Inflammatory bowel diseases, was more than $200 billion? And that's just from steroids alone...

 

So, why am I writing this? Well, this is my appeal to doctors to change the system. Or to at least to put some effort towards this cause. It's your moral obligation as a doctor and only doctors have the power and ability to make these changes. Even though the solutions are still limited, if the medical view radically changes, then more effort will be put into microbiome research, thus finding better ways to really 'cure' these modern comorbidities! Obviously, this appeal is not for the stereotypes mentioned earlier, but for open minded doctors who are willing to act for the 'general good'. I doubt the FDA or Big Pharma will come across a strong majority of doctors who stand up for this! At this point, where the system is right now, antibiotics are becoming less effective, and in the majority of cases, they are actually the ones responsible for causing these comorbidities. And from this point further, the sick people are just victims of the market mentioned!

 

 

‘This is a joke, it’s all a joke’  —The comedian

 

I could probably fill several pages with examples of people I know that have been prescribed antibiotics for various reasons from their MDs, and now they are victims of the comorbidities mentioned! This is the real epidemic of the 21st century! Every year, more people get sick, but the salaries for the guys running the pharmaceutical companies are only getting bigger...I don’t have a problem with the drugs developed by Big Pharma for terminal illnesses like cancer, HIV, or whatever...They are doing a fine job. But overall these markets are lower than the ones for depression, autoimmunity, or neuroimmunity! It does bother me, when sick people reach higher numbers every year, the drugs for the comorbidities mentioned are not meant to target their real cause, and they are getting richer every year!

 

 

'Health care decisions should be made by doctors and their patients'  —John Kramer

...and not governed in the background by FDA and Big Pharma!!!

 

The part that comes next can be disgusting, I agree, but the short demo I’ve put on this page is necessary to show how easy it is to prove these comorbidities are rooted in the microbiome. If I, armed only with the recent PubMed, wrote this page in just a couple of months, I'm pretty sure most of you out there can do it! Keep in mind, this may not look ‘professional’ since I'm not an immunologist, microbiologist, pharmacologist, or an MD. Changing the medical communities’ beliefs, especially when there is so much proof, should be the ‘professionals’ job, not mine or sick people in general! Why is this happening? Mostly because, like most systems these days, this is a corrupt system.

 

There are 4 ideas I follow in this demo: 1) an inflammatory response is always present in these comorbidities; 2) basic bacterial metabolites are ligands for basic receptors, contributing to general health; 3) the condition most ignored by doctors could be the one to start this change; and 4) why the current situation won’t change if we don’t stand up to it?!

 

1) An inflammatory response is always present in these comorbidities!

 

In my head, it all started with this question: "Why the known pathogens seen in most infections outside the gut are not seen as pathogens in our dysbiotic guts by the medical community? Because obviously, such pathogens are responsible for triggering inflammatory cytokines, thus an inflammatory response. And this idea’s been around for decades: diseases have an inflammatory response present. CRP, measured in our blood it’s a basic reflection of inflammatory cytokines. And more and more recent papers, show us that there’s a low level of inflammatory cytokines in depression, autism, anxiety, SIBO, and so on. All of them, if our doctors will test us, have a high sensitive CRP present, which is the reflection of a low inflammatory response. From here it’s not hard to point out the microbiome pathogens responsible for triggering this response, as they have the same generic names as the ones responsible for triggering infections outside the gut: Enterobacteria, pathogenic gram positives like Enterococcus, SFB Clostridia, and so on! Practically, the bugs producing inflammatory cytokines as a result of their strong PAMPs!

 

These comorbidities could be easily prevented if our doctors always look for a low inflammatory response!

 

Once you understand how an immune response starts, you look for other basic responses from immune or secretory cells, besides inflammatory cytokines. And you’ll find something like this: Antimicrobial Peptides (produced by secretory Paneth and Goblet cells), Immunoglobulins with Siga (produced by lymphocytes plasma B cells), Lysozyme (produced by all phagocytes like macrophages, monocytes, neutrophils, dendritic, and mast cells), Lactoferrin (stored like Calprotectin in Neutrophils, Macrophages) counteract strong PAMPs, and in our dysbiotic guts immunity suffers from a dysregulated activity. Lysozyme is used by phagocytes in the process of phagocytosis, particularly effective against peptidoglycans. All of them have abnormal levels, in the comorbidities mentioned. In a recent study, children with Autism had low SCFA and Lysozyme levels, high sensitivity CRP, abnormal IGGs, and increased levels of inflammatory cytokines (Il–17) and chemokines (Cxcl8) in plasma. Imagine our MDs using this in diagnosis from now on!

 

 

'Doctors...their power is in jargon so you study up, you do your best'  —David Aames

 

2) Basic bacterial metabolites are ligands for basic receptors, contributing to general health!

 

All microbiome bugs metabolize carbs and proteins or peptides. As a result, they produce the same things or a complex made from them (the difference is that some of them are more proteolytic, others more carbs oriented). The most beneficial products are SCFA (butyrate, acetate, propionate) and Tryptophan (indole, indole derivatives). PAMPs (Lipoteichoic acids, Lipopolysaccharides, Lipoproteins, Peptidoglycans, etc.) are probably more important, as they suppress inflammation and oxidative stress. Neuropeptides could be considered as next important because they regulate various metabolic functions. In these comorbidities, SCFA, Tryptophan derivatives, and neuropeptides have lower and abnormal levels, and the overgrown pathogens which take the place of beneficial species, will always trigger an inflammatory response because of their strong PAMPs. There's much more metabolism taking place in our guts, but the ones mentioned are more than enough to prove these comorbidities as gut microbiome dysbiosis. There's nothing more abundant and multilayered than SCFA and Tryptophan metabolism in our guts. More, proper metabolized tryptophan will upregulate the production of some neuropeptides and maintain the proper tryptophan/kynurenine ratio in our system. It's simple...we stick with the most basic ones and we can make our point!

 

SCFA (butyrate, acetate, propionate) lowers pH and promotes our gut epithelial cells and brain endothelial cells (BBB). Germ-free mice suffer from the gut and blood-brain barrier permeability because SCFAs are essential for occludin and claudins (the same thing for tight junctions in our guts). Proper SCFA metabolism is important because various good bugs produce different quantities (ex: Bacteroides producing more acetate, Clostridias producing more propionate). By definition, the blood-brain barrier (BBB) is permeable with a dysbiotic gut because of abnormal SCFA (according to an old PubMed paper).

 

Indole derivatives (IPA, IAA, IA, ILA, Tryptamine), metabolized from Tryptophan are equally important to SCFAs. Tryptamine, a precursor to serotonin and dopamine, releases 5HT from Chromaffin cells (a type of enteroendocrine cells) which acts on Enteric Neurons promoting gastric motility. Enteric Neurons respond to SCFA and Tryptophan derivatives and secrete neurotransmitters like acetylcholine and norepinephrine which are used for neurotransmission in the gastrointestinal tract. Overall, indole derivatives promote intestinal barrier and brain health. Low and abnormal tryptophan metabolism will trigger many symptoms related to gastric motility and brain health.

 

The Portal Vein provides 80% of the liver blood flow, and almost 40% of our blood can probably be bacterial metabolites. That’s the ‘leaky gut’ idea, denied by conventional medicine, and blabbered by morons, aka functional doctors. Your gut’s always leaky, either with a healthy microbiome, or a dysbiotic and infected one. The problem is, with a dysbiotic one the ratio changes in favor of bad metabolites, which are agonists or antagonists for basic receptors, and because of that, you’ll get dysregulated activity in various cells. Germ-free mice are proof we can’t be in a healthy state without our microbiome. Those basic receptors are called G protein, Aryl hydrocarbon, Toll-like, Pregnane X...I know, so many bulshit names, but stick with me and you'll get it eventually! This page is for everyone out there, thus iIm forced to put this shit in it!

 

Neurotransmitters (acetylcholine, dopamine, serotonin aka 5HT, norepinephrine) produced in the gut, which sometimes can be even higher than the ones produced in the brain, will not cross the BBB (Blood Brain Barrier). The main pathway is different: Vagus Nerve upregulates the brain after it gets stimulated from the gut. Vagus Nerve has a lot of G protein receptors responding to neurotransmitters, especially serotonin (Google for vagal afferents and 5HT). When i was in acute phase with SIBO, i had strong and very sudden episodes of negative feelings (e.g. fear, anxiety), which obviously don't represent me. This happened because vagal afferents are highly responsive to 5HT, both in the gut, and in the brain. As a general rule, serotonin is responsible for emotions, while dopamine is known for overall motivation, happiness and 'feelling good'. Most people try to numb their physical or psychological pain by increasing dopamine, thus addictions and various drugs! In my case, to numb a bit of my strong neurotoxicity, i abused the hell out of pepsi becoming more than addicted to it! But without knowing it back then, i shot myself in the foot. I needed caffeine yes, because caffeine stimulates the primary excitatory receptors in the brain, NMDA, which were really fucked up by gut neurotoxocity. But, caffeine also increases epinephrine which stimulates the adrenergic receptors in your veins and aortas! In long run, this abuse will fuck up your circulatory system, because that's a vasodilator!

 

But let's continue with this microbiology bulshit, shall we?

 

Low tryptophan in plasma triggers the kynurenine pathway, which works something like this: tryptophan and its derivatives get converted in our system by two enzymes IDO (in tissues) and TDO (in the liver) into quinolinic and kynurenic acid and probably a bunch of others with fancy names. Usually, the balance is in favor of kynurenic acid. Quinolinic acid does not cross the BBB, however, the others do and can act as precursors for quinolinic acid in the brain, if inflammatory cytokines are present even at a low level. Having IDO in them, macrophages and microglia (which are macrophages in the brain) produce quinolinic acid when they are stimulated by inflammatory cytokines. Neuroinflammation and all neurogenerative diseases are directly correlated with quinolinic acid, which is an agonist for NMDA receptors (kynurenic acid is an antagonist). Inflammatory cytokines and quinolinic acids are the main causes for brain neurotoxicity and emotional symptoms: mood, anxiety, depression. Even Wikipedia, which can't be considered a fully reliable source, has very good info about quinolinic acid! And for fatigue and overall 'sickness' feeling, again, inflammatory cytokines are to blame because they distort the metabolic rates in neurotransmitters.

 

If you want a short dose of realism, I dare you to spend a couple of weeks on Facebook groups related to the gut (SIBO, autoimmunity, etc.). All the people there, including teenagers, suffer with systemics like brain fog, neurotoxicity described in various ways, and emotional issues, all because of their messed-up guts. You will also see examples of the harsh mistreatment from doctors these days. It kind of breaks your heart! Which is ironic, because 'kynurenine pathway' has been around for one decade, and the whole 'inflammatory cytokines' idea, probably since the beginning. Or even better, Google now for 'gut microbial metabolites in depression' as it reviews basic gut metabolites in general, and ask yourself why the people who wrote this PubMed paper don't give a shit about changing the medical view! Even in most dreadful conditions like Parkinson's, Multiple Sclerosis or Autism, although there can be additional dysmetabolism involved (ex: amyloids, α-synuclein), there’s always SCFA and Tryptophan dysmetabolism, strong PAMPs which will initiate inflammatory cytokines (probably gene expressions because of them), and abnormal neuropeptides production.

 

 

‘The world deserves more than you have been able to provide’  —Adrian Veidt

 

Autoimmunity it’s the biggest lie we are living! And it's probably been like this for the last two decades since they've come up, and marketed, corticosteroids!

 

Every immune response starts with macrophages, as part of our innate immune cells. They initiate this response in form of inflammatory cytokines (Il–1, 2, 6, 8, 12, 15) and probably a bunch of other chemokines. They recognize PAMPs (bacterial lipids, flagellins, peptidoglycans, etc.) via Pattern Recognition Receptors (notable TLRs, NODs). A strong PAMP will trigger inflammatory cytokines and chemokines. Bacterial lipids stimulate probably around half of our TLRs (1,2,4,6). Strong endotoxins and lipoproteins promote an inflammatory response (inflammatory cytokines), while weak ones suppress that. PAMPs are anti-inflammatory, and strong PAMPs are inflammatory.

 

Enterobacteria LPS promote inflammatory cytokines, while Bacteroides LPS has an opposite effect. Same for lipoteichoic acid coming from gram positives. For example, Pathogenic Staphylococcus or Enterococcus promote inflammatory cytokines while good bugs like Lactobacillus or Clostridium Butyricum can suppress that, promoting anti-inflammatory cytokines (Il-10 or derivatives from it, like Il-22). The same thing happens from all PAMPs including flagellin which stimulates TLR5. TLR2 and NODs are peptidoglycan receptors.

 

Inflammatory cytokines usually open the door for genes expressions or mutations (ex: hla-dqa, hla-b27, and dozens more), and various pathways in immune and epithelial cells. Some of them are receptors themselves. For example, there are three NOD2 mutations associated with Crohn's. Furthermore, your liver responds to inflammatory cytokines with acute-phase proteins. C reactive protein, which is an opsonin, is such an example. High CRP suggests infection. Amyloids A is the other acute-phase proteins regulated in the liver by inflammatory cytokines. Calprotectin can be high because it's an antimicrobial peptide upregulated by anti-inflammatory cytokines (ex: Il-22) in response to infection. Calprotectin (abundant in neutrophils) is released to bind metals, preventing their utilization by pathogens (this has been demonstrated in a paper against various Enterobacteria and Staphyloccocus).

 

In short, Ileal Crohns is mostly TLR2 and NOD activation with Il-17 or Il-23 as main inflammatory agents. This means bugs that do inflammatory polysaccharides, which can be found in strong peptidoglycans. That's why Ruminoccocus Gnavus is mentioned in the latest papers. Most likely, more can be blamed as instigators because of their strong peptidoglycans!

 

For Coeliac, we can blame again TLR2 and Il-15, which upregulates the Nkg2d pathway. Interaction of Nkg2d with Mica (another receptor in enterocytes) induces villous atrophy. A recent paper even explained the gluten immunoreactivity because of Enterobacteria overgrowths: Pseudomonas degrade gluten differently than our normal bugs, like Lactobacillus. The resulting gliadin peptide interacting with the Hla-dq receptor (found in some immune cells) will trigger the antibodies for it! Multiple Sclerosis it's also about Peptidoglycans, TLR2, but with Myd88 pathways involved!

 

A recent immunology paper showed that TLR2 and TLR5 activation is more representative for small bowel, while TLR4 had very low or no activation! Autism is also about Il-17, that's why many papers name SFB Clostridia and that's why Vancomycin works in flare-ups or acute phases. Most autoimmune (ex: MS, Lupus, Arthritis, Psoriasis, Sjogren's, Diabetes) are happening because of TLR 2 and 4 activation. Probably if I dig deep enough, I'll be able to specifically explain all autoimmune, because the basic idea is the same: inflammatory cytokines, different gene expressions, with various pathways triggered!

 

Small bowel dysbiosis sufferers (aka SIBO) or large bowel dysbiosis sufferers (aka IBS) have an inflammatory response present, but if a gene mutation won’t take place then there will be no autoimmunity! However, a low CRP does not mean you don't have an infection! Like mentioned, you may not have the standard CRP but the high sensitive one is there because Enterobacteria and pathogenic gram-positive overgrowths are there in various proportions! For example, Early Lupus, Coeliac, RA, Pillory, SIBO can miss the standard CRP!

 

The immune response it’s triggered by strong PAMPs, and according to one paper, the most violent are probably Endotoxins. In one, a rat’s small bowel was infused with large quantities of E.coli LPS. In just a few hours, the rat ended up with an inflamed small bowel and with severe diarrhea! An increase of inflammatory cytokines in plasma was also noted. Because of strong PAMPs, Enterobacteria induced colitis in rats, while Bacteroides had the opposite effect. Crohn's or Ulcerative Colitis was triggered in rats promoting Enterobacteria, with Antibiotics and Urease. Fusobacterium, which reside only in the large bowel, is more closely related to Enterobacteria because they have stronger Endotoxins than Bacteroides. Because of its slippery coating, LPS can sometimes escape phagocytosis (macrophages have a hard time tracking them down).

 

The immune response initiated by macrophages is mostly fever from Il-1 and Tnfa, CRP from Il-6 and Tnfa, activation of Natural killer cells from Il-2, Il-12, and Il-15, Neutrophils from Il-8, and Mast cells and Monocytes from most inflammatory cytokines just mentioned. That’s how an immune response starts and it gets further perpetuated by these cells. Most likely, if you don't have a fever or a high CRP, you could probably have a low level of natural killer cells, Neutrophils, Monocytes (precursors to macrophages), and Mast cells in your blood. By far, the best answer that you actually are in a low inflammatory state even if your standard CRP doesn't show it, comes from Mast cells. They release histamine, and that feeling is usually described by people as 'feeling hot' or in a low inflammatory state. LBP (Lps binding protein) will probably be another good marker to prove enterobacteria overgrowths in some of these comorbidities (according to an old paper, commensal Enterobacteria are more correlated with LBP in blood, and not always with the standard CRP).

 

A healthy gut is associated with good bugs, SCFA, PAMPs, anti-inflammatory cytokines, and proper production of antimicrobial peptides, while a damaged and inflamed one with commensal pathogens, strong PAMPs, low SCFA, inflammatory cytokines, oxygen, nitrate, and abnormal production of antimicrobial peptides. In a healthy gut, antimicrobial peptides regulate anti-inflammatory cytokines and vice versa! Usually, these are produced by secretory and immune cells and promoted by the basic metabolites mentioned! Both, the peptides and the anti-inflammatory cytokines counteract the small amounts of bacterial toxins and inflammatory cytokines still coming from low-level commensal pathogens. Il-10, which is a well-known anti-inflammatory cytokine, is low in IBD, IBS, or Autism. In IBS, SIBO, or Autoimmunity, antimicrobial peptides (cathelicidin 37, alpha, and beta-defensins) have abnormal levels.

 

In a recent paper, good bugs like Bifidobacterium and Clostridium were depleted after antibiotic infusions and associated with altered intestinal homeostasis and with E.coli overgrowth in the small bowel. As result: inflammatory cytokines and dysregulated responses from Enterocytes, Goblet, Paneth, and Dendritic cells. And, this was recorded as decreased SCFA, Serum Igg, Siga, Dao, Zonulin (occludins). I started researching PubMed after reading this paper because it made me question myself: what we lose from these bugs, and how it will affect our cells. A simple Google search after that revealed to me our basic epithelial cells: Enterocytes, Colonocytes, Secretory cells (Paneth cells, Goblet cells, Enteroendocrine cells), Immune cells (Dendritic cells, Macrophages, Monocytes, Natural Killer cells, Mast cells, Lymphoid cells), Stem cells, Enteric Neurons...and the fact that some have the basic receptors mentioned in them!

 

 

‘Good men mean well, we just don’t always end up doing well’  —Isaac Clarke

 

3) The condition most ignored by doctors could be the one to start the change!

 

SIBO may be the condition that will eventually push the medical view towards the gut microbiome. Why? Because small bowel dysbiosis has a few particularities over large bowel dysbiosis, which show how important the microbiota is in that environment, and our MDs, especially gastroenterologists, still have no idea or care about it! And these particularities have to do with our ability to process nutrients. Ironic, don’t you think?!

 

First, and probably the most important one is bile metabolism. Bile dysmetabolism as a result of dysbiosis will eventually lead to malabsorption of fat-soluble vitamins. Unlike stomach or upper small bowel, which are populated only by Firmicutes and Proteobacteria, Ileum has a higher pH than 5. Because of that, it is populated, like the large bowel, by the most important species. Clostridia (with Clostridium) and Bacteroides are also a part of it. In a recent paper, depleted good bugs that metabolize bile in the ileum (like Lactobacillus, Bifidobacterium, Clostridium clusters, Bacteroides, Parabacteroides) promoted an overgrowth of Enterobacteria, while abnormal dehydroxylation (second bile metabolism) can be a cause for Enterobacteria overgrowths. I know many people who had these symptoms, and their gastroenterologists had no idea about their causality or just called it IBS. As a result, some of them ended up with bones problems from malabsorption!

 

Second, the activity in your enterocytes gets messed up and this will lead to altered border enzymes, lactoferrin receptors, glut 5, and so on. Generally, it means, incapacity to break down food, and more malabsorption.

 

Third, the largest endocrine system in terms of cells it's located in the small bowel. Enteroendocrine cells secrete around 20 gut hormones (Ex: GLP, PYY, and more) involved in gastric emptying and different metabolic functions. In normal conditions, they are stimulated by proper SCFA and bile metabolites. They express the basic receptors mentioned. For example, L-cells have G protein receptors in them and when they are activated by SCFA the secretion of GLP and PYY increases. These hormones impact the function of the pancreas (insulin secretion) and brain (appetite). Beta cells from the pancreas, which produce and store insulin, respond to SCFA. In a recent paper, beta cells in response to SCFA also produced cathelicidin suppressing inflammation.

 

Fourth, in extreme and rare chronic cases it can affect gastric motility to the point where your intestines will stop functioning. Like mentioned previously, proper tryptophan metabolism is essential for gastric motility, being a direct gateway for the enteric nervous system. I personally know about two cases like this: a polish guy who is now on TPN, and a girl in the UK who eventually recovered. In both cases gastroenterologists didn't know why that happened to them!

 

 

‘You’re a chemical whore, they make you beg on your knees for more’  —Peter Tagtgren

 

4) Why the current situation won’t change if we don’t stand up to it ?!

 

Very simple answer...this market is getting consistently bigger every year, and none of these comorbidities, although they can cripple you, are 'legally' lethal! So, FDA and Big Pharma are not forced 'legally' to take a 'strong' position on the matter, which means they can afford to play with the whole thing like mobsters until a strong majority of people oppose it. I believe some form of collective action should be taken against the current system. In this world significant changes for the better always happened slow and with lots of collaterals. All of you sick right now are the collaterals! And the more you are, the richer they get! It's strictly up to you if you want to stand up to it, or remain an abused 'bitch' while they make tons of money on your so called 'medical condition'! Medicine is science only for cancers, lethal and severe diseases, for the rest it's just bulshit pseudoscience build around the biggest drug market while you are the lab rats for it. How do you think symptom supressing drugs are invented? The 'professionals' mentioned earlier have a good knowledge of cells receptors along with their agonists and antagonists, while being fully aware your microbiome is actually the biggest producer of metabolites in your body! And they push the drugs forward to your doctor, which takes them for granted and acts only as a statistician without digging or questioning for the real cause! In this reality, both the sick individual and the doctor, are just a little 'bitch'. But, you should judge for yourself which is which!

 

Here are just a few examples from this 'glorious' market:

 

IPA, which is a neuroprotective antioxidant, and a bacterial tryptophan metabolite, it's proposed now in new drugs for Alzheimer's. Laquinimod, which triggers AHR, is used in Multiple Sclerosis management to suppress inflammation, 5HT antagonists are used for depression, Esketamine, which is an antagonist for NMDA receptors, is used for resistant depression, Corticosteroids are used in general for IBD, Ustekinumab targeting a couple of inflammatory cytokines is used for Crohn’s, Psoriasis and Arthritis...and so on! Our gastroenterologists are 'managing' an autoimmune disease, but they have no idea about basic immunology or microbiology, which can explain it in a few words. Your psychologist, for example, is not different! Everything I mentioned earlier, about how microbiota impacts main neurotransmitters through tryptophan derivatives and the vagus nerve, are just hieroglyphs to him! And I can probably fill pages on how antidepressants failed to help people, not to mention their side effects...or, I can give you examples of 'lucky' depressed people cured with fecal transplants. I mentioned 'lucky', because stuffing shit in people's asses to cure them of IBD or other strong infections can put you on the same 'broken' pathway, if you don't know the basics mentioned on this page! If you're not testing the donors for high sensitivity CRP and MDRO's, you risk putting the patients in the same low inflammatory state, which can open the door for some of the comorbidities mentioned! And when our unknownledgeable doctors actually fucked up while experimenting with FMT, and one patient almost died after contracting MDRO's, FDA was forced to make a stand! Thus, the point I made earlier! If you don't have a lethal disease, they will always afford a 'window' of comfort to fuck with you! That will not happen anymore if the medical view will change! Sure, it will be a 'window', but not like it is now when the whole premise for these comorbidities is denied and intentionally overlooked! And, in long run, none of these symptoms supressing drugs really work, on the contrary they are damaging, unbalancing various other receptors in your body! My self destructive nature made me realise how big that 'window' can be, and how much comfort they have to fuck with you, selling you bulshit!

 

I think I've heard hundreds of stories from people with autoimmunity in situations where antibiotics don’t work for them anymore, and they are just victims of this market. For example, the last dude I spoke with faces colon removal because of IBD, and nothing works on him anymore. His doctors only switch between corticosteroids when he flares up. These infections become more and more resistant with time, because your microbiome has the tendency to adapt and tough it out. Proving this shouldn't be that hard if again we stick with the basics, like I mentioned in the beginning.

 

First, inflammatory cytokines skew a couple of genes (Nox1, Duox2) in intestinal organoids, increasing the production of nitrogen and oxygen in the gut lumen and this favors enterobacteria. Unlike Enterobacteria, other commensals like Clostridia and Bacteroides don’t possess genes for nitrate and oxygen respiration. So, it’s like a vicious circle, they can contribute to an inflammatory response, and they are the best at thriving after that. In a paper, depleted butyrate-producing Clostridia elevated epithelial oxygenation leading to luminal expansion of Enterobacteria (through aerobic respiration). PPA receptor in colonocytes regulates oxygen bioavailability and responds to SCFA. More, these bugs are known to be at a low level in a healthy gut (no more than 10%), they don't produce SCFA and dislike a low pH. They produce Urease to lower the acidic environment, which is common with pathogens. In IBD, even if gram-positive pathogens are the main instigators, enterobacteria overgrowths will be present in some proportions because they flourish in an inflamed gut, which is abundant in nitrogen and oxygen! I've read in a paper that aminoglycosides targeting gram negatives calm IBD flares! This is why!

 

Second, indole metabolized from tryptophan is used by many beneficial and pathogenic species as a quorum-sensing molecule that coordinates collective behaviors like spore and biofilm formation, and drug resistance. They communicate through indole, and indole is produced by many tryptophanase Clostridium, Bacteroides, and Enterobacteria. So even if you have pathogenic overgrowths, they are still pretty good friends with good bugs, sharing some basic metabolism. From personal experience, I can tell you that your microbiome tends to get better by itself, but only to a certain point, which still translates into symptoms, but 'tolerable' ones. Without arrogance, I can say that over years of chronic dysbiosis, I never took anything...no antibiotics, no probiotics, no bulshit products from 'functional' doctors! Why? Because I was smart enough to realize that doctors, or private functional doctors, were always contradicting themselves. And, I didn't want to be this market's 'bitch', when no one could tell me exactly what the fuck was going on! At the same time, I knew people who spent small fortunes on these private functional doctors and with no significant results in the long run. Sick people should read about bugs resistance (MDRO, MIC, etc.) instead of dumping, in desperation, small fortunes on private nitwits. The majority of them lack basic knowledge, are mostly gold diggers, and they take advantage of desperate people who are let down by doctors!

 

The overall focus has to shift onto microbiota, and it will happen only if the medical system demands it, thus, doctors making a stand for it! And, my request to sick people out there is this: 'Stop paying private nitwits, because you're fuelling the wrong system and these guys have nothing in particular to offer you. We should work with our doctors to change the overall medical view towards causality'. Keep in mind, I'm far from being an extremist, and I don’t want symptom supressing drugs to be abolished! Their utility is valid for acute phases of various conditions. I want most of the effort to be put into causality, aka the microbiome! Not the other way around, as it is now. Fixing this mess should be both doctors' and sick peoples' responsability. I believe we lost it a couple of decades ago. Instead of following the basic ‘inflammatory response’ idea from the beginning, and building from it, we denied it, and built a fake 'route' that serves mostly Big Pharma and its markets! Obviously, it's good business, but not for sick people. A dude I knew used to say 'For every new pill, they invent a disease'...and I can add 'or, a category with fancy names which masks its real cause'! Vets are actually better trained than our doctors these days! And a simple example that comes to my mind is phages. Phages are approved and used by vets for many known infections. Do you know why? A sick cow means losing money. With humans it is the opposite: cured patients mean losing the market for symptom suppressing drugs! In our days, the medical system has become an 'archaic' common practice, not so different to a cult: '...You're only delusional, because your blood tests are ok!'

 

 

'You're on thin fucking ice my pedigree chums, and shall be under it when it breaks'  —Brick Top

 

 

I didn't write all this for nothing! I want two things!

One, I lost money when I was sick...lots! I want them back, but it's not about the money – it's more about the principle! My 'moronic' docs didn't do their jobs as they were meant to be! I was fucked up, not only that I felt fluish and with a terrible hangover, but I had this neurotoxicity that felt like venom in my nervous sytem and my neurons. I couldn't think, i couldn't focus or remember properly...Obviously, i couldn't work! And, this paper proved what caused this!

Two, I want that change to happen so that others in the future can really rely on this system when they fuck up their lives! What this system is currently doing is called 'passive' abuse!

This bulshit page was written before 2020! Don't believe anything in it, because is just a joke!

 

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