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Prof. Art Ayers On Autoimmunity; Celiac and Hashimoto’s Version

I had a chance to discuss this previous post with Art Ayers of Cooling Inflammation. Now, apparently, someone thinks my light, layman’s description of the basics of thyroid function wasn’t exhaustive. Duh! again. It wasn’t intended to be. Once again, for Who?-ever may be listening: I am interested in hacking at the root, not treating the various downstream consequences of that root.

The root is an autoimmune condition, specifically thyroid peroxidase (TPO) antibody. One is supposed to have no more than 35 IU/mL (i.e., some level of antibody is normal, just like some level of inflammation is normal) whereas, mine is 216. Now, it’s entirely possible that I might still have elevated Thyroid Stimulating Hormone (TSH) being produced by my pituitary glad without these out-of-range antibodies. Alternatively, I could just take Levothroid (synthetic T4) in an appropriate dose as I did for nearly a decade (I believe it was about 100mcg) and just ignore all possible root causes. People who make their money from the medical profession seem to have a bias toward the latter approach.

In short, whatever is at play in the entire hormonal / enzymatic signal process to generate appropriate levels of thyroid is mediated in most people (including me) by simply—duh—supplementing the hormone directly (Armour), even synthetic T4. Accordingly, I see no need in doing a copy/paste job from Wikipedia in order to dazzle you about all of it. Rather, I want to hash-imoto out the possible root cause, after a brief introduction about why some simpleton fucktards wave hands, call you quacks, and most importantly, tell you not to look any deeper.

Here’s what Art had to say about my previous post and the emails exchanged (with Gemma and Gabriella in tow as well).

Richard,

I fear these may be fighting words, but alas you seem too timid in your characterization of gut microbiome evolution. Please be not the biofilm wuss that you appear.

Chimera are constructed by the minute. The only stability is that of the physiological niches crudely defined by metabolic functions that are necessarily simultaneously species definitions, but if you pop the hood, an E. coli from Paris is a very different beast from an E. coli made in Caldwell, Idaho. On a DNA sequence basis, they would be as different as dogs and cats.

Richard, I know E. coli and my E. coli are nothing like your E. coli, even though you vainly claim homology by differential agar plates. Your poop will remain your poop.

Bacteria in gut biofilms aggressively extrude their DNA and actively pick up environmental DNA. Recombination produces chimeric new species, and niche selection perpetuates those with advantageous functions, including filling empty niches damaged by antibiotics. It also permits rescue of orphan genes from the diet, e.g. probiotics with beta galactosidase activity to repair lactose intolerance.

Well, for once I didn’t OVERSTATE something. 🙂 As I told Art, I try to stick to my pay grade, which is to say: understand all the essentials I can, and rephrase them in a way that inquisitive laymen will understand. At base, I consider my role as one of a promoter of curiosity in areas most people don’t otherwise give much thought to (or just regurgitate party lines), not as a therapist or clinician…or even a professor.

Art continues:

But I wish to return to Hashimoto’s thyroiditis. I am not interested in the management of thyroid defects. That is for doctors. I am interested in curing Hashimoto’s by reversing the damage and fixing the cause. The fix is diet to feed body and soul/gut flora.

I have written several posts on the link between celiac and Hashimoto’s. Celiac is initiated by wheat-based trypsin inhibitor and gluten, which cause gut inflammation, Treg deficiency and antigen presentation. The result is anti-tTG antibodies that promote a cellular immune attack on the thyroid gland. The ongoing Treg deficiency promotes presentation of TPO and the production of additional anti-thyroid antibodies. The result is vacillating hypo/hyper thyroidism and Hashimoto’s.

The cure for Hashimoto’s is to:

  1. minimize autoantigen exposure by wheat elimination,
  2. minimize inflammation by vitamin D and fish oil supplementation and
  3. enhance Treg production by repair of gut flora, e.g. resistant starch and other soluble fiber (prebiotics/low glycemic plant polysaccharides), and feeding back lost gut bacteria, e.g. probiotics, fermented vegetables, etc.

…i.e., a general cure for autoimmune diseases, plus consideration of the unusual wheat poly Q toxin, gluten.

Also note that antibiotics or damaging diets may have contributed to the original gut flora damage. Thus a prerequisite of cure is cessation of antibiotic onslaught. As a corollary, since essentially all pharmaceuticals have substantial antibiotic activity, drugs must be avoided and vigilance in gut micro biome defense is required to reverse Hashimoto’s.

Demurely,
Art

What a great guy. Not at all like those Who? sneer at the role of the microbiome out of ignorance, by yelling pewp, for LOLs. And, it’s pretty much the protocol I’ve started, with the added dimension of eliminating alcohol for 3 months. Also, I’ll just up my seafood intake for the omega-3. I love all seafood. Just had a nice plate of sushi the other day—a particularly good, non oxidized way to get the 3s.

So, without further ado, here’s some posts from Art on the whole gluten, celiac, Hashimoto’s, autoimmune connection (or, you can just listen to Who? rant about her complete ignorance in these matters—your choice). If you go to Cooling Inflammation, you can just search ‘hashimoto’s’ to see all posts where he’s mentioned it going all the way back to 2009.

I think the connections started here for him:

The Cause of Allegies and Autoimmune Diseases (June 2009)

Keyhole Limpet Hemocyanin (KLH): Internalized Antigen

Scanning the literature for a common protein that can be used as an experimental antigen, it becomes quickly obvious that a favorite is KLH. This would seem to be an odd choice — why a keyhole limpet protein? But that is the wrong question.

Why is KLH such a good antigen, i.e. why is it readily presented to the host immune system? If you have been reading my posts, you might be thinking about triplets of basic amino acids and that is the answer.

As soon as I remembered the prominent use of KLH as an antigen, I checked the NCBI protein database and immediately found an unusual KKK (triple lysine) near the amino terminus of hemocyanin II ( it comes in two pieces). This triplet explains why KLH is such a good experimental antigen, because it is internalized into antigen presenting cells by its strong heparin-binding domain. Other components, adjuvants, are typically added to the KLH for injection to make sure that a strong local inflammation occurs.

Autoantigens Have Strong Heparin-Binding Triplet

I also learned that Hashimoto’s thyroiditis is an autoimmune disease mediated by the autoantigen thyroid peroxidase. A quick search reveals that thyroid peroxidase is an autoantigen, because it also has a triplet of basic amino acids that can enhance presentation under inflammatory conditions. Grave’s disease of hyperthyroidism is an autoimmune disease in which the thyroid receptor (with a basic triplet) is an autoantigen. The same kind of triplet of basic amino acids was found when I searched today for fire ant antigens and mosquito antigens.

Celiac Causes Allergies and Autoimmune Diseases (July 2009)

Basic Triplets in Hasimoto’s Autoantigens

One of my hobbies is checking for the unusual occurrence of basic triplets in autoantigens and allergens. I have found dozens of examples. The most recent is associated with Hashimoto’s Thyroiditis. I knew that attack on the thyroid was common in celiacs, because the celiac autoantigen tTG (it has a basic triplet) is also present in the thyroid and the celiac autoantibodies to tTG also cause an attack on the thyroid. But the autoantigen for Hashimoto’s Thyroiditis is thyroid peroxidase (TPO).

I was momentarily perplexed, but then examined the TPO amino acid sequence and immediately found a couple of basic triplets (KKR and KRK).

MRALAVLSVTLVMACTEAFFPFISRGKELLWGKPEESRV
SSVLEESKRLVDTAMYATMQRNLKKRGILSPAQLLSFSK
LPEPTSGVIARAAEIMETSIQAMKRKVNLKTQQSQHPTD
ALSEDLLSIIANMSGCLPYMLPPK…

Autoimmune Diseases, Bacteria and GALT (Gut Associated Immune System) (July 2010)

Celiac, Oxidative Stress, Peroxiredoxin, Alopecia

Grain/gluten intolerance, celiac is an immunological attack on the small intestines with increased risk for numerous autoimmune diseases. Hashimoto’s thyroiditis is a common sequela of celiac and the two diseases share the same autoantigen, tissue transglutaminase (tTG). Thus, the development of celiac and the production of antibodies to the tTG produced in the intestines, results in a subsequent immunological attack on other tissues that produce lots of tTG, e.g. the thyroid. Gluten intolerance, because of its attack on the intestines and the proximity of a major part of the immune system (GALT), may play a major role as the foundation for autoimmune diseases.

Antibiotics, Gluten, Hashimoto’s Thyroiditis and Baldness (December 2013)

My impression is that Hashimoto’s is caused by a combination of an initial immune attack on the thyroid and incompetent regulatory T cells. In most cases the immune attack on the thyroid is a secondary consequence of celiac/gluten intolerance, in which anti-transglutaminase antibodies attack transglutaminase bound to gluten in the intestines. Transglutaminase is an enzyme that is also produced by the thyroid (and hair follicles) and attack by celiac antibodies can enhance or inhibit thyroid hormone production (or baldness.) Both Hashimoto’s and celiac do not occur if the suppressive part of the immune system, i.e. regulatory T cells, is functioning.

Health Diagrams II — Curing Autoimmunity and Allergies (March 2014)

Gut Flora to Tregs to Suppression of Autoimmunity

It is important to understand at the outset that autoimmunity and allergies are caused by a damaged immune system, and repairing the damage cures the diseases. Damage to the immune system typically represents a break in the continual development of immune cells in the lining of the intestines. Immune cell development in the gut is dependent on bacteria, the gut flora. Damage to the gut flora, e.g. by antibiotics, processed foods that lack flora feeding fiber or extreme diets, disrupts development of immune cells. Typically, loss of the immune cells that keep the aggressiveness of the immune system in check, regulatory T cells or Tregs, results in autoimmunity. Fix the gut flora and autoimmunity recedes.

Autoimmunity
Autoimmunity

Health Requires Suppression of the Aggressive Immune System

For simplicity, I am focusing on the T cells of the immune system that develop in the intestines and either kill other human cells that are dangerous, e.g. virus-infected or cancer cells, or provide protection by regulating the aggression, Tregs. Normal functioning of the immune cells permits elimination of damaged or dangerous human cells, while at the same time avoiding rampages of lethally armed T killers. Examples of untamed T killers in action are degenerative autoimmune diseases, such as arthritis, asthma, prostatitis, celiac, Hashimoto’s thyroiditis, type I diabetes, inflammatory bowel diseases and atherosclerosis.

Here’s a final one and perhaps, the most important one because it demonstrates that Professor Art just doesn’t profess, he professes to keep thinking.

Celiac, Gluten and Trypsin Inhibitor (October 2014)

Summary

Forget the gluten. Celiac is caused by trypsin inhibitors (ATI) that were increased in wheat fifty years ago to combat pests. Immune response to ATI spreads to include gluten and transglutaminase that perpetuates the disease. Celiac is an unexpected consequence of traditional plant breeding that could be fixed with GMO approaches.

Plants Target the Nerves, Immune Cells and Intestines

Plants have evolved chemicals and proteins that attack and punish plant-eating animals. A single molecule of caster bean toxin protein, for example, can kill a human cell. Plants produce some of the most toxic molecules on earth. The nervous system of insects and other herbivores is typically targeted by plants. Many recreational drugs, e.g. opioids, THC, nicotine, caffeine, etc., for example, are made by plants in self defense. Human nerves respond to these natural pesticides and the bitter taste and the vomit reflex help us to detect and avoid toxic phytochemicals. Gluten proteins contain polyglutamine stretches of amino acids that resist digestion and bind to intestinal cells. Seed lectins bind to the glycoproteins on the surface of the intestines and inhibit digestion. Wheat seeds also contain an inhibitor of starch and protein digestion, the amylase/trypsin inhibitor, ATI. ATI binds to the receptors on immune cells that trigger general inflammatory responses to pathogens, e.g. TLR4. It is the ATI in wheat that starts an immune response to gluten and celiac.

Celiac Causes Numerous Autoimmune Diseases

Celiac is often associated with other autoimmune diseases, because it causes them. Antibodies to tTG are diagnostic for celiac and the autoimmune attack on the intestines is mediated by anti-tTG antibodies. But anti-tTG antibodies of celiac don’t just attack the intestines, they attack any other tissues that have tTG, such as the thyroid gland and hair follicles. Thus, it should not be a surprise that celiacs are at high risk for autoimmune disease, e.g. Hashimoto’s thyroiditis, of the thyroid gland, including both hypothyroid and hyperthyroid diseases, depending on which region of the thyroid is attacked. Some forms of hair loss, alopecia, are also initiated by autoimmune attack on the tTG in hair follicles. Persistent exposure of celiacs to gluten will result in a cascade of autoimmune diseases as other body antigens are presented to the immune system and tissues with those antigens are targeted and attacked to produce arthritis, vitiligo, etc.

Cure for Celiac and Autoimmunity

Celiac and other autoimmune diseases are perpetuated by the presence of the corresponding autoantigen/allergen, in this case tTG and gluten proteins, and a deficiency of Tregs. Oddly enough, some pathogens (Helicobacter pylori) and parasites (Helminth worms) stimulate Treg development in the lining of the intestines, in addition to normal gut flora, Clostridium spp. It may be the relative absence of pathogens and parasites in affluent societies that reduces Tregs and enhances the incidence of allergies and autoimmunity. Antibiotics and the antibiotic activity of pharmaceuticals in general may also contribute to Treg deficiencies by damage to gut flora. Clearly, the repair of gut flora and reestablishment of the associated immune system will go a long way toward curing autoimmune diseases such as celiac. Celiac, however, provides the added complexity that it damages the ability of the intestines to maintain a functional gut flora. Thus, the cure for celiac would require simultaneous repair of both the gut and its flora, e.g. by a fecal transplant and supportive diet containing numerous soluble fibers to which the donor flora have been previously adapted, i.e. lacking antigenic triggers.

OK, so, the heckler (Who?) is irrelevant to all of this—and not just because she’s a 30-something narcissist virgin who had liposuction and pretended it was low carb, who used to publish about 30 selfies per day on her Twitarded feed (now by invitation only). That just makes it all the more fun to me, to have her lipo-induced tiny parties in a bunch. Guy has to have his misogynistic fun, yo!

No. It’s about always asking questions, above asserting answers. Hell, about a week ago I wan’t even seeking questions, and I had no answers. Since then, I have tons of the former and only hints at the latter, so I keep pursuing it, drilling down, and cataloging all of it, just in case any of you find similar proclivities suitable.

The very essential difference between me and all the promoters of conventional wisdom—including those who feign same, but then defend to the death their own versions of “myth busting” (e.g., keto crowd) that’s no more revelatory than conventional wisdom itself—is that I question them, too.

I’m agnostic toward all answers. Questions too.

Is this a question, statement, or both: who is being honest, and Who? is being dishonest?

Richard Nikoley

I'm Richard Nikoley. Free The Animal began in 2003 and as of 2021, contains 5,000 posts. I blog what I wish...from health, diet, and food to travel and lifestyle; to politics, social antagonism, expat-living location and time independent—while you sleep—income. I celebrate the audacity and hubris to live by your own exclusive authority and take your own chances. Read More

40 Comments

  1. Groker on December 16, 2014 at 19:59

    Richard

    I have been at woo’s blog. How come you can’t just come to understanding and talk about science? You critizice woo for a wikipedia copying, but you copy mr Ayers, as one commenter pointed out.

    • Richard Nikoley on December 16, 2014 at 20:06

      Groker:

      Yes, I know you’ve been there. Thanks, I think.

      It’s complicated. I tried long time ago to have a dialogue with Woo, even accepting whatever. She doesn’t do that. Even Robb Wolf reached out, the easiest guy on Planet Earth to get along with. Rejected.

      She’s a crazy bitch. It just is. She has sycophants. It just is. They all have the protection of distance and relative anonymity, which feeds the pathology.

      That’s not why Im engaging this. Wanna know? It’s because I saw Peter…Peter of hyperlipid mention her as some sort of confidant. I pay attention to little details.

      Anyway, feel free to to what you like to do. I’ll do what I know I’m doing. Be well.

  2. Jane Karlsson on December 17, 2014 at 06:06

    “Hashimoto’s. Celiac is initiated by wheat-based trypsin inhibitor and gluten, which cause gut inflammation, Treg deficiency and antigen presentation. The result is anti-tTG antibodies that promote a cellular immune attack on the thyroid gland.”

    The origin of Hashimoto’s is actually failure to clear dead cells and other cellular debris, as this paper you linked in an earlier post pointed out.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4115591/

    • Richard Nikoley on December 17, 2014 at 08:38

      I think he said initiated, so maybe too quibble. But Art is aware of that paper so let’s see if it enhances his view any. Or, perhaps it’s the clearance issue that caused by these other things.

      In any case, it’s all closer to the truth, I think, and a lot closer than simply take your meds.

    • damndirtyape - on December 17, 2014 at 16:27

      Interesting paper.. I wonder if it’s one more reason to engage in frequent fasting. Wouldn’t cellular clearing be accelerated by autophagy?

    • Gemma on December 18, 2014 at 00:00

      @Jane Karlsson

      “Clearance of Apoptotic Bodies, NETs, and Biofilm DNA: Implications for Autoimmunity”

      I am glad this paper is getting attention!

    • Gemma on December 18, 2014 at 00:04
    • Jane Karlsson on December 18, 2014 at 03:37

      Richard
      Yes, it’s all closer to the truth. Let’s see what Art has to say. He may not know that the phagocytes which clear cellular debris are very sensitive to copper deficiency.

      “We evaluated the function of peritoneal macrophages from rats fed a standard diet containing about 55% of the National Research council-recommended level of copper. Hepatic copper was only slightly decreased in this group, and other abnormalities often observed in the severely copper-deficient rats, including reduced hematocrit and enlarged heart, were absent. Therefore, this group was classified as marginally copper deficient. Candidacidal activity of elicited macrophages from such rats was significatly lower than that of cells for control animals. This observation provides support for Mills’ proposal that phagocytic cell function may provide a sensitive indicator of copper status (34). Furthermore, we have found that the copper content and function of rat neutrophils were reduced at levels of dietary copper that had minimal impact on tissue copper and no effect on erythrocyte SOD activity (29).”
      http://jn.nutrition.org/content/120/12/1692.full.pdf

      Wooo tells us she is ‘highly skeptical ANYONE can heal hypothyroidism that isn’t purely nutritional (e.g. iodine, zinc deficiency, selenium deficiency).’

      You forgot copper, Wooo.

    • Jane Karlsson on December 18, 2014 at 05:50

      Hi Gemma
      So it was you who gave Richard that paper. Nice work.

    • Gemma on December 18, 2014 at 07:05

      @Jane Karlsson

      On copper: you are surely aware of this paper:
      Copper at the Front Line of the Host-Pathogen Battle

      and this one too.

      Next, is there a link thyroid – Nrf2 – Kupffer cells? What is controlling the copper deposition in liver?

    • Jane Karlsson on December 18, 2014 at 08:21

      Gemma
      Could you expand on your question please? What copper deposition?

    • Richard Nikoley on December 18, 2014 at 08:43

      “Wooo tells us…”

      Who? 🙂

      Then you say Wooo, and I say Who? ….

      WoooWho!

      Cracks me up. That’s how silly I am.

    • Gemma on December 19, 2014 at 05:30

      @Jane Karlsson

      It is a complex puzzle. Got my email?

    • Jane Karlsson on December 19, 2014 at 05:36

      There’s a new paper on clearance of apoptotic cells in celiac. Makes it look like wheat is just the trigger, not the root cause. I think you said something like that.

      “Here, we have examined whether in CD there is a defective clearance of apoptotic cells/bodies, a phenomenon that helps promote tolerogenic signals thus limiting pathogenic responses. Accumulation of apoptotic cells and bodies was more pronounced in the epithelial and lamina propria compartments of active CD patients as compared to inactive CD patients and normal controls. Expression of scavenger receptors, which are involved in the clearance of apoptotic cells/bodies, namely thrombospondin (TSP)-1, CD36 and CD61, was significantly reduced in active CD as compared to inactive CD and normal mucosal samples. Consistently, lamina propria mononuclear cells (LPMC) of active CD patients had diminished ability to phagocytose apoptotic cells. Interleukin (IL)-15, IL-21 and interferon-γ, cytokines over-produced in active CD, inhibited the expression of TSP-1, CD36, and CD61 in normal intestinal LPMC. These results indicate that CD-related inflammation is marked by diminished clearance of apoptotic cells/bodies, thus suggesting a role for such a defect in the ongoing mucosal inflammation in this disorder.”
      http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0100980

    • Jane Karlsson on December 19, 2014 at 05:38

      @Gemma
      Yes, thanks. Will reply soon.

    • Gemma on December 19, 2014 at 05:52

      @Jane Karlsson

      From your link:

      “Moreover, in CD, there is enhanced production of IL-17A by gluten non-reactive T cells, thus raising the possibility that additional factors other than gluten are involved in the amplification and perpetuation of the ongoing mucosal inflammation in this disorder [9], [10].”

      Thanks, fits nicely.

    • ProfAyers on December 29, 2014 at 15:02

      Jane and Richard,
      I am making a big quibble as Richard indicated. I am leaving treatment of the symptoms of celiac/Hashimoto’s to medicos. I am limiting my attentions to the molecular events that initiate celiac, and approaches to cure. I also point out the obvious immune interactions that link celiac to numerous related autoimmune diseases, including Hashimoto’s.

      Clearing of debris from apoptosis and NETosis is a big piece in the grand puzzle and is especially relevant to my idea of a consensus sequence of three basic amino acids, a basic triplet, found in all allergens and autoantigens. In this case, the debris is loaded with nucleic acid binding proteins, and binding requires basic amino acids and in most cases nuclear translocation signals of four basic amino acids. I can easily read protein amino acid sequences and predict whether a protein can be an autoantigen. Related sequences are involved in heparin binding associated with most of the cytokine interactions, etc. involved in CD. It is interesting that the histocompatibility antigen that predisposes to celiac has a unique heparin binding domain and inflammation blocks heparan sulfate production.

      The point here is that initiation involves conditions, inflammation and Treg deficiency, that precede the debris clearing defects of established CD. Suppressing inflammation and replenishing Tregs (e.g. RS + Clostridium) could cure Hashimoto’s/CD. Diet is supportive of a cure, but insufficient since it leaves the debris clearing defect.

      I know next to nothing about copper deficiency, but it is interesting.

    • Jane Karlsson on December 30, 2014 at 08:32

      Hi ProfAyers
      Does the inflammation precede the debris clearing defects or is it a consequence of it? Clearance of apoptotic cells is supposed to be antiinflammatory and tolerogenic, whereas clearance of necrotic cells is inflammatory and immunogenic. I think there are exceptions to this rule, but in general it seems to hold.

      There also seems to be a connection with oxidative stress, which leads to apoptosis if it’s lower and necrosis if it’s higher. This would mean, oxidative stress is the key in autoimmune disease as in metabolic disease.

      Oxidative stress is confusing because ‘antioxidant cocktails’ have been tried in metabolic disease and failed. They contained vitamins A, C and E, with selenium and sometimes zinc. There are two problems here. First, the antioxidant vitamins can lower ROS too low. Second, people who eat meat regularly will not be deficient for selenium or zinc, but they might very well be deficient for copper and manganese, which activate the most important of the antioxidant enzymes, the superoxide dismutases. The antioxidant cocktails never contained manganese or copper, astonishingly.

    • ProfAyers on December 30, 2014 at 17:48

      Hi Jane,
      I think that in the wheat, celiac, Hashimoto’s string of causality, that the wheat amylase trypsin inhibitor (ATI) initiates the inflammation that promotes the gliaden/tTG mediated damage that triggers anti-tTG/gliaden antibody production due to compromised Tregs, and the resulting celiac continues the tTG-mediated attack on the thyroid, to produce Hashimoto’s with additional tissue-specific antibodies as a result of compromised debris clearance in the gut and other tissues.

      From my plant products background in phytoalexins, I give little credence to antioxidants. After all, the external environment is awash in free radicals used for free radical polymerization of lignin in plant cell walls and phytochemical antioxidants are polymerized along with phenyl propanoic monomers. I see little benefit in dietary phytochemicals, mostly natural antibiotics, and lots of benefit in prebiotic plant polysaccharides. That actual issue is what is causing the oxidative stress. Is it immune attack or hypernutrition?

      Gene mutations that predispose to autoimmune diseases seem to involve inflammation or antigen presentation/histocompatibility antigens. What do you think starts the inflammation? ATI does. What is the impact of gliaden, a polyQ, on insects? Is it an insecticide directed at inactivation of TG? The seed contents are like eggs, filled with nutrients that have a second major function of being antimicrobial. Embryos/milk are protected by numerous natural antibiotic nutrients that are inflammatory in adults. Babies can survive eating formula that disrupts natural baby gut flora, because formula causes gut inflammation that protects against infection. So, formula plus wheat, would be a recipe for celiac in susceptible individuals. Other disruptions of gut flora might also produce inflammation, but compromise of tolerance inducing cytokines/Tregs is also required for autoimmunity.

      NFkB inhibits apoptosis while it promotes proliferation, so I would say that apoptosis occurs in the absence of inflammation, whereas ROS and oxidative stress triggers inflammation, as in metabolic syndrome driven by excess glucose and fatty acids leading to superoxide production. Apoptosis and NETosis precede debris clearance, which in turn is the basis for antigen presentation. Antigen presentation in conjunction with inflammation can lead to autoimmunity. Absent inflammation, the result can be tolerance. Tregs make the difference.

      I know the metal content of SODs, but am still not convinced that mineral deficiencies are a big deal in autoimmune disease, even though current crops are deprived. I guess that just means that I am more impressed by initial events that trigger inflammation and ROS, rather than the accumulation of ROS that swamp cellular antioxidant capacity. That is also why I think dietary antioxidants are unnecessary for healthy people, but may be important for chronic, mismanaged inflammation in autoimmune disease. The cause of autoimmune disease is very different from the symptoms and healthy inflammation is a cycle that restores the initial conditions.

    • Jane Karlsson on December 31, 2014 at 07:20

      Hi ProfAyers,
      Yes, ATI is clearly a problem. It activates TLR4.

      “Here, we identified the nongluten ATIs CM3 and 0.19 and likely other homologous ATI variants as potent activators of TLR4. Based on our data, we believe that this interaction of ATI with TLR4 is a major signaling pathway in innate immune reactions to wheat. We did not find activity in gliadins, and reduction of disulfide bonds completely abolished TLR4-stimulating activity in ATI-enriched fractions.”
      http://www.ncbi.nlm.nih.gov/pubmed/23209313

      To my mind, that last sentence is highly significant. Protease inhibitors are toxic because of their disulfide bonds, which I believe can only be broken (reduced) in lysosomes. If enterocyte lysosomes are not working well, ATI will be a problem. Autophagy will be compromised too, which means ROS-damaged mitochondria won’t be replaced. These systems are dependent on minerals, and the minerals are removed from refined wheat. We need to know whether people who eat wheat but no refined wheat get celiac disease.

    • ProfAyers on December 31, 2014 at 13:28

      Hi Jane,
      The sensitivity of ATI to reduction merely means that the structure of ATI required for binding and triggering TLR4, requires disulfide bonds. ATI-TLR4 interactions all take place prior to reaching lysosomes, so the mineral needs for ROS handling enzymes seems to be after the fact. Reducing ROS production is more important than enhancing antioxidants.,

      My point is that ATI causes enough inflammation to make gliadin/tTG interactions result in antigen presentation via debris clearance, and celiac. ROS production is probably only important in the maintenance of celiac as immune cells produce ROS to kill other cells. I am only trying to explain the cause/initiation leading to anti-gliadin/tTG antibodies that then initiate Hashimoto’s and numerous other autoimmune diseases, assuming continuing Treg deficiency (gut flora defect).

      I don’t think that simply supplementing wheat flour with minerals will stop development of celiac/Hashimoto’s. I think that reducing ATI content, altering starch grain/flour processing and repairing gut flora to avoid Treg deficiencies will minimize autoimmune diseases.

      Reversing Hashimoto’s is dependent on extent of thyroid damage, but repair of the gut flora/immune system is a prerequisite, so I promote tolerance. I think of ROS/antioxidants and hormones as part of therapy, which I am not addressing.

    • Jane Karlsson on January 1, 2015 at 07:00

      ProfAyers
      The problem with disulfide bonded proteins is that they don’t get denatured in the acid of the stomach, so they have to be degraded by some other route. I expect ATI will be OK unless it builds up due to malfunctioning of the endocytosis/vesicle trafficking system. There is a very important enzyme in this system called vps34, which in vitro cannot be activated by magnesium, only by manganese. Another manganese-requiring enzyme important in trafficking is PP2A, which prevents neurofibrillary tangles in Alzheimer’s.

      I imagine that ATI in reasonable amounts would be beneficial, in that it would induce tolerance. As long as the gut is working properly and gut bacteria are delivering what Tregs need, as you say.

  3. TomS on December 17, 2014 at 09:38

    Richard, Art is particular of probiotic type. Can’t find any brands on his site. He favors some milk-based but I will avoid due to current histamine intolerance (that may be corrected with fixed biome). Any probiotic thoughts other than the usual FTA suspects?

    • Richard Nikoley on December 17, 2014 at 11:00

      More of that later. Amazon is in process of delivering lots of prebiotic powders and I’m going to be doing a bunch of different formulas and testing them, towards making an easy to scoop powder product with everything i like.

    • TomS on December 17, 2014 at 21:59

      After perusing Art’s site, it appears he preaching Clostridium spp./butyricum (AOR P-3), “soil bacteria”, RS et al, and fermented veggies.

  4. Frida on December 17, 2014 at 11:31

    Hi Richard,
    if the cure of autoimmunity is so easy: wheat elimination, vit.d/omega3, pre- and probiotics, why aren’t you already healthy? I thought you do these things already for a long time?
    Tatertot also takes T4 while doing all the above things. So even if you could heal autoimmunity with these steps, how could the thyroid grow back? Chris Kresser said as far as we know no healthy thyroid tissue can grow back.
    But after all, I wish you luck, I’m struggling with hashimoto myself and don’t want to take hormones. The pre- and probiotics helped me much with autoimmune-symptoms but free t4 and free t3 are still low and tsh high. By the way I got hashimoto after two years of gluten-free low carb, so for me, gluten wasn’t the cause.

    • Richard Nikoley on December 17, 2014 at 11:55

      ” why aren’t you already healthy? I thought you do these things already for a long time?”

      No, not at all. There were levels and I was never gluten free, just LC and grain avoidance. Pre and probiotics didn’t begin until within last two years. TSH is better now than 7 years ago so maybe something to this.

      In terms of you hashi, no idea. I have a comment on another post from a guy who said going gluten free was all it took to rid his. And now, we have Jimmy Moore, the guy who says find what works for you, going after a guy who wrote personal paleo code.

    • ProfAyers on December 31, 2014 at 13:48

      Frida,
      It seems clear to me that your celiac and Hashimoto’s occurred well before you were diagnosed or had profound symptoms. Your gluten-free LC diet didn’t repair your ongoing autoimmune disease, because it didn’t fix your gut flora and immune system. The gluten caused the initial damage perhaps a decade earlier. Your gut flora remains damaged and continues to promote autoimmunity regardless of your diet.

      Probiotics provide, at most, a couple of dozen species of bacteria that my contribute to your gut flora community of 200 species. Dairy probiotics, that mimic the baby gut flora that can provide many of the functions of a healthy, complex adult flora, are a supplement or temporary solution. Those same lactobacilli species are also present in fermented foods and are also supplements. These temporary gut flora fixes can be very effective in fixing damaged immune systems — krauts are emergency medicine for the immune system — but they still can’t supply the hundreds of species of bacteria in a healthy gut flora.

      Most pharmaceuticals and especially those labelled antibiotics, damage the gut flora and reverse efforts to repair the immune system.

  5. Thomas on December 17, 2014 at 14:30

    “Twitarded” LOL

    If this is your own neologism you win the internet again.

    • Richard Nikoley on December 17, 2014 at 14:44

      Sadly, it’s not. Quite common I think and if not mistaken she’s used it too.

      My best neologism is sycodouche, a combo of sycophant and douchebag, typically used to denote some screed, as in, “now let me adress Her sycodouche,”

      Came up with that in 1992, still hasn’t caught on. 🙂

  6. David on December 17, 2014 at 22:58

    “As a corollary, since essentially all pharmaceuticals have substantial antibiotic activity, drugs must be avoided”

    How substantial are we talking? I’ve been wondering about this myself lately but haven’t found much info on it. Looking for a good strategy to accommodate daily probiotics/RS and Adderall XR type stimulants. Hopefully most of the drug gets metabolized in the liver before the emptied capsule gets down to the main home of the biome but it sounds like that’s not the case…

    • ProfAyers on December 30, 2014 at 18:04

      David,
      Pharmaceuticals are repurposed plant antibiotics, so I would say that most drugs could also be labelled and used as antibiotics. They have about the same antibiotic activity as commonly used antibiotics purchased by prescription. There are some drug exceptions, but I think it is safe to assume that most drugs have major impacts on gut flora. I would say that many drugs have their physiological impact via their antibiotic impact on gut flora. It may be that Adderall, for example, treats ADHD by attacking gut flora to reduce the aggressive, inflammation causing part of the immune system in the same way that antibiotics are used to treat autoimmune diseases. I am just speculating.

      BTW, omega-3s have been used effectively in the treatment of ADHD, so that suggests that ADHD is a symptom of chronic inflammation similar to depression and obesity. That suggests that diet and gut flora interventions may be very effective in eliminating the ADHD symptoms.

  7. Anand Srivastava on December 18, 2014 at 02:50

    I just have one question. I understand that T4/Armour is not the cure. But it does help reduce pressure on the remaining Thyroid cells. I would think reduced stress on the Thyroid cells will help them recover.

    I am not sure why you are not taking T4/Armour in addition to whatever you are doing.

  8. Charlene on December 18, 2014 at 16:17

    Hey Richard,

    The thyroid issue might be behind your back/shoulder pain, too, as I’m sure you already realize.

    So the real question is would you be willing to try a fecal transplant for this?

    • Richard Nikoley on December 18, 2014 at 17:04

      That would be down the road, some.

  9. Gemma on December 19, 2014 at 05:31

    It is interesting to watch the evolving science:

    Thyroid Regeneration: How Stem Cells Play a Role? (2014)

    • VF on August 9, 2016 at 22:00

      Interesting! I can’t wait to see the potential role played by vitamin A for stem cell differentiation here (as it is already being used for bone marrow stem cell differentiation in leukemia).

      I could see vitamin A possibly tying in with autoimmunity and Hashimoto in a multitude of ways:

      According to the Linus Pauling Institute page on vitamin A, supplementation reduced TSH and thyroid volume.

      It’s necessary for healthy skin (or that specialized skin we call gut mucosa).

      Seems to modulate in Treg/T17 balance in intestinal inflammation (http://www.hindawi.com/journals/bmri/2015/137893/)

      And seems to stimulate ceruloplasmin production.

      Anyway, most of this conversation is over my head, but I’ll gladly try my best to understand it.

      Clearly, this Hashimoto business is caused by some fairly common circumstance given how widespread it is, and it just seems likely to me that a powerful fat-soluble vitamin that many Americans are deficient in could be a contributing factor.

  10. Sky on December 24, 2014 at 04:37

    Mass Murderers! I wonder how many of our little gut pets these researchers murdered just to prove a point?

    http://www.hcplive.com/publications/family-practice-recertification/2014/December2014/Low-Carb-Diet-Decreases-Weight-and-Improves-Framingham-Risk-Scores?utm_content=buffer38433&utm_medium=social&utm_source=twitter.com&utm_campaign=buffer

    Wasn’t sure which thread to post this in, so I just posted here in the latest thread.

  11. Ellen on December 28, 2014 at 11:02

    Hey Richard!
    Sorry you have to go down the Hashimoto’s/autoimmunity rabbit hole. I wish you luck and healing.

    I wanted to add a few things that I’ve learned through my own Hashi’s/autoimmune experience, if I may 🙂

    -Getting the Cyrex panel for gluten cross-reactive foods and food sensitivities was really valuable.
    There’s a ton of misinfo about it on the web, stating that there are x-number of gluten cross-reactive foods (not all of the foods in the panel are cross-reactors and this was never claimed by the lab/researchers) and that the panel isn’t legit. Dr. Vojdani met that last claim with a thoughtful and thorough explanation of the science.

    Anyway, it’s common for casein and whey to cross-react to gluten and when I did my panel, that was the case for me (soy and potato were also sensitivities, though not cross-reactors). Cutting dairy and doing the autoimmune protocol diet allowed me to finally easily lose the weight I had gained in the past year while eating my regular paleo+dairy/occasional gluten-free grains diet. I’m still figuring out what works for me, via reintroductions, but reducing my inflammatory foods load was invaluable.

    Cyrex has a new food sensitivity panel coming out that is of particular interest to Hashi’s patients because the researchers have identified foods (many paleo) that people with Hashi’s can specifically have cross-reactions to that involve mounting antibody attacks on, say, T3, for example. So, it becomes more complicated than just reacting to TPO. Vojdani and Kharrazian will be releasing a research paper this spring with all of those details. This panel will allow Hashi’s patients to customize their autoimmune diets in a really individual way.

    -Another thing that I think anyone with autoimmunity should look into is the multiple autoimmunity panel by Cyrex. Autoimmunity nearly never sticks to one organ. It’s kind of horrifying to see the panel’s results, but it shows you your weak links and also helps to shed light on individual symptoms.
    For example, a lot of Hashi’s patients also make parietel cell antibodies (hence all the anemias and deficiencies associated with it). Tubulin antibodies are common, too, as are different brain tissue antibodies. It’s good to know this stuff so you can decide how to proceed with extra nutritional support- and so you know where your symptoms are coming from. Not all of them are thyroid. I know know that my brain farts are probably not thyroid-related and more likely caused by my synapsin antibodies (yikes).

    -Something I’m not seeing mentioned that could be really helpful: TH17 modulation/eNOS support. High-dose curcumin/resveratrol combo is great for TH17 modulation and Apex Nitric Support increases eNOS- esp. if you take a dose and then do just a few minutes of intense exercise. This works synergistically with glutathione support/recycling and D3 optimization.

    -One last thing (not saying this applies to you, but it probably applies to someone with Hashi’s who is reading this): good blood sugar control. I’m seeing more and more about how blood sugar fluctuations directly fire up the immune system and many of the functional med. practitioners are saying this is a deal breaker for autoimmune healing, so I thought I’d mention it 🙂

    PS- google low-level laser treatments to regenerate thyroid tissue- there are promising studies (some patients eliminated the need for thyroid hormone meds and others reduced their requirements). Dave Asprey and Izabella Wentz are both experimenting with it.

    • Richard Nikoley on December 29, 2014 at 10:12

      Ellen:

      Thanks for all that info. I’ll dig into it.

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