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).
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.
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:
- minimize autoantigen exposure by wheat elimination,
- minimize inflammation by vitamin D and fish oil supplementation and
- 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.
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).
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.
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)
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?