Archives for 2014

No wonder it’s so popular, the “ideal” way to organize society—into ideological factions where the “winners” get to loot from the “losers.”

Now and then I get a comment on the blog and I just know I have to blog something about it.

Recent research explains the paradox of why VLCers/Ketoists see the evidence that Eskimos were never in ketosis as a good reason for everyone to eat a ketogenic diet and was summed up with: “When people are misinformed, giving them facts to correct those errors only makes them cling to their beliefs more tenaciously.” (Marty Kaplan). This cartoon illustrates the problem.

Kaplan’s article isn’t perfect, as toward the end, he uses “climate change” as an example, without noting that there are lots and lots of people, like myself, who are skeptical of some of the [fraudulent] data, conclusions, predictions, asserted causes, outcomes, all without denying that warming appears to be taking place.

After posting this morning about “winding down,” I ended up wanting to add a sub-section to the Autoimmune Diseases section in Chapter 8 of the book: The Gut Microbiome In Disease Pathology (html version). Thanks to Tim Steele for his major contributions to this as well. Hopefully you’ll see that the intended style is layman accessible, but well referenced for the geeks. Didn’t take the time to make it pretty for the blog (the link above has footnote links and links to citations), so here’s just a plain text:

AUTOIMMUNE DISEASES

A well established aspect of the gut microbiome is its close relationship with host immunity, essentially comprising 70% of the immune system.[1] It’s no longer mere speculation that the composition of our gut microbes have a profound effect on the creation, training, maintenance, and actions of our immune system. An imbalance of intestinal microbes can cause an imbalance in our immune system, leading it to attack us instead of the pathogens it’s supposed to eradicate or keep in check. Here’s a partial list of autoimmune conditions that have been linked to disruptions in gut microbes:

* Addison’s Disease
* Alopecia
* Ankylosing Spondylitis
* Antiphospholipid Syndrome (APS)
* Autoimmune Hepatitis
* Behcet’s Disease
* Bullous Pemphigoid
* Castleman’s Disease
* Celiac Disease
* Chronic Fatigue Syndrome
* Chronic Inflammatory Demyelinating Neuropathy (CIDP)
* Churg Strauss Syndrome
* Crohn’s Disease
* Endometriosis
* Fibromyalgia
* Infertility
* Giant Cell Arteritis
* Glomerulonephritis (Autoimmune Kidney Disease)
* Graves’ Disease
* Guillain-Barre Syndrome
* Hashimoto’s Thyroiditis
* Idiopathic Pulmonary Fibrosis
* IgA Nephropathy
* Interstitial Cystitis
* Kawasaki Disease
* Lichen Planus
* Lupus
* Meniere’s Disease
* Mixed Connective Tissue Disease (MCTD)
* Multiple Sclerosis
* Myasthenia Gravis
* Narcolepsy
* Pemphigus
* Pernicious Anemia
* Polyarteritis Nodosa
* Polymyositis
* Primary Biliary Cirrhosis
* Psoriasis
* Raynaud’s Disease
* Reiter’s Syndrome
* Rheumatoid Arthritis
* Sarcoidosis
* Scleroderma or CREST Syndrome
* Silicone Immune Toxicity Syndrome
* Sjogren’s Syndrome
* Stiff-Man Syndrome
* Type 1 Diabetes
* Ulcerative Colitis
* Vascular Dementia
* Vasculitis
* Vitiligo
* Wegener’s Granulomatosis

Those with one or more of these autoimmune conditions are likely to have a diet high in modern, industrial Frankenfoods or one lacking in sufficient fibers our gut bugs recognize as food—but most likely both. The immune system keeps the body healthy by providing a fine balance between attacking invaders and maintaining healthy tissues. In autoimmune diseases, this delicate balance fails and the immune system attacks healthy tissue.

Let’s take a brief look at a few autoimmune conditions positively identified with altered gut microbes.

Rheumatoid Arthritis –

In rheumatoid arthritis, the immune system attacks membranes that line the joints, causing painful swelling, stiffness, and a loss of function in fingers, wrists, or other joints. Often thought to be triggered by factors such as smoking and stress, it’s now known to be related to gut health; i.e., diet related, ultimately.

A specific type of gut bacteria, Prevotella copri, is found in over 75% of those newly diagnosed. When lab animals were implanted with Prevotella copri, they developed symptoms of rheumatoid arthritis. While this is not enough for scientists to develop a cure, it does give them clues toward developing new treatments, treatments that will almost certainly target gut microbial dysbiosis.

Ankylosing Spondylitis –

Ankylosing Spondylitis is an autoimmune disease that attacks the spaces between vertebrae in the spinal column, hip joints, and other locations throughout the body. It’s a disfiguring, painful disease that’s closely associated with the gut microbe Klebsiella pneumoniae. Beneficial microbes Bifidobacteria, Lactobacilli, and other core species prevent Klebsiella from turning invasive.

While Klebsiella pneumoniae is a normal inhabitant of the human gut, it’s often associated with urinary tract infections, upper respiratory tract infections, and wound site infections. When it grows uncontrollably in the respiratory tract it can lead to deadly pneumonia.

The microbe’s association with ankylosing spondylitis has a clear genetic factor, with 90% of patients expressing the HLA-B27 genotype.[2] One hypothesis put forth is that this genetic signal could trigger the disease by enhancing the growth and perpetuation of the Klebsiella microbes in the bowel. In an attempt to slow the growth of the now pathogenic bacteria, the immune system mistakenly attacks the human tissues, thus causing the disease. Strings of protein in Klebsiella bear resemblance to human joint tissue. This molecular mimicry is the underlying mechanism behind all autoimmune disease and a growing number of modern diseases that heretofore had no clear medical pathophysiology—such as essential hypertension.[3] [4]

A common treatment for ankylosing spondylitis is to restrict all fermentable fiber from the diet in order to starve the gut microbes, achieving results similar to the overuse of antibiotics, or the practice of very low carbohydrate and ketogenic diets.[5] [6] This approach may have short-term therapeutic value but an unforeseen drawback may be further damaged immunity and gut health in the long term, leading to unintended consequences. The immune system lines the entire gut and atrophies without butyrate and contact from the beneficial microbes that regularly consume fermentable fiber.[7]

Type 1 Diabetes Mellitus (T1D) –

Type 1 diabetes results from autoimmune destruction of insulin-producing beta cells in the pancreas. As has been harped on plenty, factors that influence gut health—for better or worse—are factors that ultimately influence the function of the immune system—for better or worse. It’s so closely tied together, it’s a testament to the intricacies of the gut, gut microbes, and our resulting immune system. Gut bugs modulate its function through what is essentially training the immune system—in particular T cells—as mentioned earlier.[8]

The gut and pancreas also share several critical links and so problems with the gut are often reflected in the pancreas. Altered gut microflora have been linked to T1D in animal and human studies, and are normally thought to be a function of intestinal inflammation, gut permeability, and food allergies.[9] Children with T1D are more susceptible to certain infections and do not normally develop tolerance to cow’s milk. These complex interactions are currently the target of new approaches to prevention and treatment.

Hashimoto’s Thyroiditis –

“Hashi’s” is a condition where the thyroid gland is attacked by a combination of immune processes that can manifest as high or low thyroid levels, but most usually the latter. It has the distinction of being the very first disease to be recognized as an autoimmune condition.

Mounting evidence suggests that not only intestinal pathogens, but symbiotic ones can influence an overblown immune response against thyroid tissue. And more recent studies reveal that not only the gut commensals, but also oral microorganisms such as periodontal bacteria, may play a role.[10]

To muddy the waters even further, an association between celiac disease or gluten sensitivity and autoimmune thyroid disorders is well established, with about ten times as many with gluten issues also having thyroid issues than is observed in the general population.[11] Curiously but not surprisingly, this link may exist due to a molecular similarity between gliadin, the protein portion of gluten and thyroid tissue.[12] In all, one intuitive way to regard the process is that a leaky gut, as addressed previously, allows gliadin into the bloodstream where it’s attacked by the immune system as a foreign invader, with “similar looking” thyroid tissue getting caught in the crossfire.

What remains to understand is which strains of intestinal flora help, and which hurt. As we’ve seen a number of times thus far, it’s not as simple as good guy vs. bad guy. “Good guys” can be bad if there are too many of them or they’re out of proportion with other “good guys.” And “bad guys” can be non pathologic if still other “bad guys” (or “good guys”) are keeping them in check. A 2012 paper demonstrates just how complex the picture is.

Multiple lines of evidence have demonstrated that probiotic organisms such as Bifidobacterium and Lactobacillus confer health benefits on the host. For instance, oral administration of probiotics to mice induced IL-10 production and prevented the development of autoimmune diseases including type 1 diabetes and colitis. This probiotic-induced anti-inflammatory effect is reportedly mediated by dendritic cells. However, series of in vivo and in vitro studies have demonstrated that certain probiotic strains exacerbated colitis and encephalomyelitis, enhanced interferon-γ (IFNγ) production and reduced regulatory T cell (Treg) activity, indicating that attention should be paid when choosing a probiotic strain to treat autoimmune disorders. In experimental autoimmune thyroiditis (EAT), a murine model of Hashimoto’s thyroiditis, probiotic strains Lactobacillus rhamnosus HN001 and Bifidobacterium lactis HN019, which had been shown to enhance splenocyte IFNγ production in mice, exhibited neither stimulatory nor inhibitory effect on the disease development. Taken collectively, the presence and the role of intestinal dysbiosis and the effect of alteration in the gut microbial composition remain to be investigated in Hashimoto’s thyroiditis.[13]

Unfortunately, the standard of treatment for low thyroid (hypothyroidism) is effective enough for most people by the administration of synthetic thyroid hormone to treat the symptom, that little has been done in the mainstream to investigate the underlying cause: in order to develop more fundamental therapies or recommended lifestyle changes for better management, or even a cure.
________________
[1] Wu, Hsin-Jung, and Eric Wu. “The role of gut microbiota in immune homeostasis and autoimmunity.” Gut Microbes 3.1 (2012): 4-14.
[2] “HLA-B27 – Wikipedia, the free encyclopedia.” 2004. 17 Aug. 2014 <http://en.wikipedia.org/wiki/HLA-B27>
[3] Schwimmbeck, PETER L, DT Yu, and MB Oldstone. “Autoantibodies to HLA B27 in the sera of HLA B27 patients with ankylosing spondylitis and Reiter’s syndrome. Molecular mimicry with Klebsiella pneumoniae as potential mechanism of autoimmune disease.” The Journal of experimental medicine 166.1 (1987): 173-181.
[4] Tervaert, JWC. “Hypertension: an autoimmune disease[quest] – Nature.” 2011. <http://www.nature.com/hr/journal/v34/n4/full/hr201115a.html>
[5] “LOW STARCH DIET.” 2012. 3 May. 2014 <http://www.spondylitis.org/about/low_starch_diet_summer2012_spondylitis_plus.pdf>
[6] Ebringer, A, and C Wilson. “The use of a low starch diet in the treatment of patients suffering from ankylosing spondylitis.” Clinical rheumatology 15.1 (1996): 62-66.
[7] Rashid, T. “The Link between Ankylosing Spondylitis, Crohn’s Disease …” 2013. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678459/>
[8] Vaarala, O. “Gut microbiota and type 1 diabetes.” The review of diabetic studies: RDS 9.4 (2011): 251-259.
[9] Jaimie Dalessio. “Gut Bacteria May Prevent Type 1 Diabetes – Digestive Health Center …” 2013. 19 Jan. 2014 <http://www.everydayhealth.com/digestive-health/gut-bacteria-may-prevent-type-1-diabetes-2306.aspx>
[10] Mori, K. “Does the gut microbiota trigger Hashimoto’s thyroiditis?.” 2012. <http://www.ncbi.nlm.nih.gov/pubmed/23200063>
[11] Sategna-Guidetti, C. “Autoimmune thyroid diseases and coeliac disease.” 1998. <http://www.ncbi.nlm.nih.gov/pubmed/9872614>
[12] “The Gluten-Thyroid Connection – Chris Kresser.” 2011. 18 Dec. 2014 <http://chriskresser.com/the-gluten-thyroid-connection>
[13] Mori, K. “Does the Gut Microbiota Trigger Hashimoto’s Thyroiditis …” 2012. <http://www.discoverymedicine.com/Kouki-Mori/2012/11/27/does-the-gut-microbiota-trigger-hashimotos-thyroiditis/>

I’m up here at my brother’s place in Placerville. View from my office window this morning.

As you can see, it comes completely decorated and includes a resident Shih Tzu named Kobe.

Arrived last evening after a day and night at the cabin in Arnold, where “Groker” (Jaime Perez), “Nicole Ocampo,” and “Stark Soze” amused themselves trolling Wooo’s blog (Who? Wooo. Who? Wooo. WoooWho). Jaime was the avoid conflict, understanding, peacemaker, questioning kinda dude. Nicole’s mom knew Richard in Olongapo, PI way back. Stark is an asshole misogynist who always gets carried away and in that vein, blew up the whole deal. I was saving it up for a YHBT (you have been trolled, in ASCII art) post, but Soze always ruins everything he touches.

Plus, I didn’t bother to light up a proxy server to spoof IP addresses. Clever one, that Who. Oh for the USENET days, where nobody with an AOL account knew the Unix shell commands to find out that stuff. On the other hand, the whole troll did have the desired result of keeping a bunch of hens cackling about what an evil and loathsome man Richard is.

Bea—who has nothing but sympathy from cackling hens—is still in San Jose, last day of school, headed up here tomorrow AM with the two rat killer brats. Then, we head to South Lake Tahoe for three nights with my parents.

…I made another batch of Horchata de Chufa, my version. Soak the Tiger Nuts for a couple of days, until they swell up and have a water chestnut consistency, then dump in blender, add more water, pulverize, strain through cheesecloth. No sugar. Plenty sweet as it is. This is 12 oz bag of nuts to a full quart of water.

Funny thing about that sediment. I think it’s mostly raw resistant starch, RS2 to be more precise. You know, that stuff that’s so bad for you while RS3 is manna from heaven—in spite of the fact that human ancestors have been eating raw Tiger Nuts for eons before RS3 was even possible from cooking and cooling. Baboons are chowing down on them to this day.

If you were to take a few tablespoons of raw potato starch, add water, shake it up, let it settle and turn the bottle on its side, it’s going to look a lot like this. Non-Newtonian Fluid time.

I Googled for ‘spaniards drop dead from horchata consumption.’ No hits. Nonetheless, be very careful out there, in spite of admonitions that it’s probably safe to go in the water.

…I took a 5-minute hang glider flight vicariously this morning. Among the best vids I’ve ever seen, professionally shot by the Red Bull team from a helicopter. The scenery is breathtaking—wish I knew what location. Oh, it’s done to Pink Floyd music. Hard to go wrong: hang gliding and Pink Floyd. Oh, there’s great aerobatics, too

Louder than words from Matjaz Klemencic on Vimeo.

I may blog some more substantive stuff over the next couple of weeks but not going to worry about it if I don’t feel the compelling urge.

Happy festivities, wherever you may be.

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

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?

Well, I ended up revealing the secret I was saving up for drama, and I did so in comments, so here’s the deal.

I was so very impressed with Todd Dosenberry‘s handling of the Buck Books Promotion and so liked the sane, a-la-carte value proposition, that it didn’t take long to find out that Matt Stone is a driving force behind it. Matt and I have a history, and this is just one of those posts.

I got in contact, we lafed about history, and he and Rob—after some reservations that took long enough to check out the draft and the market—have agreed to front one hell of a lot of sweat in terms of paying people, in order to get this book out there. We’re looking at end of Feb timeframe. Plus, Todd has some list building to do via his continuing promotions. Archangel Ink. Check them out.

Here’s another tidbit. Matt and I actually had an exchange last April 1, when people pointed me to his newsletter release on that day, thinking I’d get pissed or something. Actually, I busted a gut and told him so. He invited me to get back at him this next April, and I assure you: I’ve had it outlined for months.

Anyway, these guys are very legit and I’ve even bounced their offerings off people who generally hate everything. And even they say, impressive.

Isn’t life stranger than fiction?

Oh…yes; for a time, Mark Sisson and I were planning to deal together. As you may know, Mark also participates the the Buck Book deals. Anyway, Mark and I are perfectly cool about this, just in case you were wondering.

…In the meantime, I now have both Beatrice and Tim asking me, “aren’t you supposed to be working on a book?”

One last thing: Buck Flogging.

Over the last days, given my activities, I have had tons of comments. None got through, except those known to The Club.

So you haven’t seen them. Unlike folks like Dr. Michael Eades and jimmy moore, I have never, ever not put through or deleted a comment that was on the science, no matter how it may disagree. Never, not once, and there are replete examples of the former doing that.

Rather, I have what’s called 1st comment moderation. Think of it as going up to the doorman of a popular nightclub. How do you behave? I’d guess better than you actually have to, all the time, once you get in.

Here’s how stupid the people who hang out at Grace’s and Who’s blog are. They give me one line insults. They don’t even exercise any effort beyond writing a single sentence. It’s like saying to the doorman, “just let me in, you ugly stupid cunt!”

But, lots who read Grace and Who, and begin to do so sycophantically, are fucktards. They don’t even know that little bit much. That to get in here and then have a little dispensation in comments, including being able to tell me I’m fucked up, you have to get in the door first. It would be pretty stupid of me to just let anyone in…and another way to think of it is that once you’re in, you aren’t burdened by what stranger fucktards do. I keep them out so you can be real.

Have fun and be careful and thoughtful out there. I’m going to see The Exodus tonight, because I hear tell it’s written by an atheist and doG is portrayed as a spoiled little cunt-brat, like me. About time we had a The Ten Commandments remake, though I did love the film as a kid. Thing is, I’m not omnipotent, so can’t harm you…and more importantly, all those people you suck up to can’t make you believe I can hurt you, cunty as I may be…

In other news, I saw (Bea and I do movies come Holiday season) The Theory of Everything Saturday, Foxcatcher last night. I predicted McConauhey would get best actor for Dallas Buyer’s Club last year. This year, gonna be competition between Eddie Redmayne as Stephen Hawking (must see), and Steve Carell as John DuPont. I think Steve edges out. I looked for a single sign of That Steve Carell all the fucking film. It’s almost a distraction, but that cannot be his fault. Go Steve. I’ve never been a particular fan, but I know fucking hard work applied to a talent when I see it.

Here’s what I’m up to in terms of drilling down on my Hashimoto’s Thyroiditis. I’m reasonably familiar with the hormonal / enzymatic “pathways.” Duh that the principle TSH feedback is T4, which is why the synthetic T4 I was on from about 1998 – 2007 brought the TSH right down.

However, assuming I had the TPO antibody that antagonizes this enzyme, that basically “makes” T4, then the synthetic T4 supplementation was merely large enough to overcome it and bring down TSH. Easy peasy. It stands to reason that addressing the root, i.e., the antibody, then T4 production might be sufficient on its own and TSH will come down to normal.

A little background. I stopped the T4 sometime in 2007, along with sinus allergy meds and PPIs for GERD, in order to see how well LC paleo, intermittent fasting, and my workout program worked to eliminate those needs. It worked for the other two (and my BP came down so meds for that was no longer on the table), but a TSH in 2008 had it at 16, so no joy there (2-3 outta 3-4 ‘aint bad), and instead of going back on the synthetic T4, I opted for Armour, with subsequent tests putting me in range. I then stopped that a couple of years ago, while increasing carbs, and then later, the whole resistant starch and gut stuff happened. I tested last week with an improved THS in an untreated state.

Am I onto something? I think it’s a legitimate question, not kookiness or quackery. And plus, I’m asymptomatic, in spite of 30-something-crazy-virgin-bitch’s fucktarded but  ”authoritative” assertion  that life is a shambles because of untreated hypothyroidism. More plus, I can start meds any time I want. If this doesn’t pan out, I will, and I’ll just do the synthetic.

70% of the immune system is in the gut. There are enormous associations between autoimmune conditions and the state of the gut and the resident biome. I’ve come to think a bit differently about the gut in terms of resident species. Two primary reasons:

1. It evolves at a rate of up to many generations every 24 hours.
2. Horizontal gene transfer is another layer of this evolution.

The problem with speciation is that the xyz species of bacteria you have today may not be precisely the same genetically as the one you had yesterday. So, why not just think of it as a massive genome containing about 300 times the number of genes as your human cells? I understand that species classification is helpful, but it’s not fundamentally what’s going on.

Or, to think of it another way: when you introduce different bacteria via probiotics, and then target feeding them—understanding species are engaged in chemical warfare, are in competition for food—you’re essentially practicing genetic engineering on yourself. Not your human genes, but a genome that affects your own gene expression or repression in various ways.

Neither do I want to overemphasize. After all, it took about 20 years and 50,000 generational turnovers for some of 12 strains of E. coli to emerge into what might be classified a new species.

The E. coli long-term evolution experiment is an ongoing study in experimental evolution led by Richard Lenski that has been tracking genetic changes in 12 initially identical populations of asexual Escherichia coli bacteria since 24 February 1988.[1] The populations reached the milestone of 50,000 generations in February 2010 and 60,000 in in April 2014.[2]

Since the experiment’s inception, Lenski and his colleagues have reported a wide array of genetic changes; some evolutionary adaptations have occurred in all 12 populations, while others have only appeared in one or a few populations. One particularly striking adaption was the evolution of a strain of E. coli that was able to use citric acid as a carbon source in an aerobic environment.[3]

If you drill down, you’ll find it’s that use of citric acid where it arguably emerges as a new species classification.

Of course, given the number and the exponential combinations of potential interactions, all within a framework of rapid evolution given their high generational turnover, it’s too complex to consciously engineer in a precise manner. So we go with associations: what do lean healthy people eat? What does their microbial genetic profile look like? And yes, classification in terms of species is yet another way we simplify or break down the problem into chunks.

I’ve been scrounging a lot of stuff (thanks people), but here’s a couple of papers and a link I’ve been chewing on today.

• Clearance of Apoptotic Bodies, NETs, and Biofilm DNA: Implications for Autoimmunity – add cell death and clearance to the list of things that effect the evolution of cells and hence, autoimmunity.
• Molecular Mimicry, the Hygiene Hypothesis, Stealth Infections and Other Examples of Disconnect between Medical Research and the Practice of Clinical Medicine in Autoimmune Disease – “Physicians should look for immune dysregulatory conditions with a strong emphasis on: 1) very early detection with predictive auto-antibodies; 2) a focus on optimizing gastrointestinal mucosal immune function and the microbiome; 3) the eradication of infectious triggers with antimicrobial therapy; 4) the detection and elimination of food sensitivities; and 5) the promotion of an anti-inflamatory lifestyle.”
• RHR: Pioneering Researcher Alessio Fasano M.D. on Gluten, Autoimmunity & Leaky Gut – Cool fun fact: “mortality — because you could die of celiac disease at that time — for celiac disease dropped from 35%-40% to zero during the war [WWII]. And then when the war was over, the mortality rate for celiac disease went back to pre-war era. And when he tried to understand what was the connection between the war environment and this swing in mortality, he realized that possibly it was the availability of grains containing gluten that really was changing in parallel. So during war, there was no wheat available, and flour was made with potato starch, and that was the time in which the mortality went pretty much to zero. And when after the war, gluten was again available, the disease came back.”

Alright, or just take your thyroid meds and don’t be quacky or stupid… Above all, don’t think for yourself. Listen to crazy bitches, conventional MD’s, and all who present as an authority. You can’t just stop your thyroid meds, you know. You just can’t! Well, I fucking did, twice. So far, I’m better, but still drilling down.

[Insert pussy-ass “disclaimer,” here. Or, you’re on your own.]

I like quiet Saturday and Sunday mornings. It’s for this reason that I often find myself getting my ass out of bed earliest—about 5am this particular Sunday morning. Began catching up on emails, Google alerts, etc.

Low & behold, I got a complete education on myself I had no idea of, courtesy of a rather crazy person and her solipsist readers.

Well, at least I now know that:

– My plan to do a 3-month experiment to see how much, if any, I can improve hypothyroidism (here and here) is plain quackery. And here I thought that my Kaiser primary physician, Haas, MD, had blessed the experiment, said he’s seen stranger things, so why not, and already approved the next round of lab work. And while I thought I’d consulted Chris Kresser, not to contradict my mainstream doc, but to see if the approach my doc had already said sounded good, jived with his clinical experience, but apparently not. Oh, well. Back to the drawing board.

– I’m having suicidal thoughts. And here I thought that was five years ago, back in the winter of 2010 where, for the first time in my life, I had months of chronic pain as a result of a herniated cervical disc (likely from pulling heavy deadlifts at #325 for reps), confirmed by MRI. I’d thought that I’d worked that out and this time around, no such thing because the pain doesn’t worry me anymore in terms of putting up with it for life. But what do I know?

– My current back, hip, and leg pain—along with tingling in my left foot—is linked to my hypothyroidism, general ill health, and a slew of other conditions I wasn’t aware of until today. And here I thought that, save for the thyroid panel (with untreated TSH better today than 7 years ago), I just had the best blood work I’ve ever had. And what a surprise to learn that the radiologist’s report from the MRI I had a week ago is unrelated to my pain.

Individual axial levels as follows:

T12-L1: Normal

L1-L2: Normal

L2-L3: Normal

L3-L4: Normal

L4-L5: There is loss of disc height with disc desiccation. There
is presence of a left posterior lateral to far lateral disc
protrusion measuring 5 mm. This abuts the left L4 and L5 nerve
roots. Correlate for appropriate nerve symptoms. There is moderate
left neural foraminal narrowing and mild central canal stenosis.
There is no right neural foraminal narrowing.

L5-S1: Normal

Additional findings: None.

– S

** IMPRESSION **:
Left posterior lateral to far lateral L4-L5 disc protrusion abuts
the left L4 and L5 nerve roots. Correlate for appropriate nerve
root symptoms.

And won’t longtime reader Rick Mehaffy of Peninsula RSI be surprised to learn that the hour and a half I spent in his chamber of horrors yesterday as he poked, prodded, stretched, put me in traction, and hung me upside-down, was not about the MRI report, but about my thyroid. Perhaps I should get another thyroid panel, since I had measurable relief all the rest of the day. Or, perhaps there’s something to this notion that spinal alignment underlies all disease and Rick is just very clever, making me believe he was actually treating an apparent spinal injury! Clever man!

And next, I’m going to have to let my dad and two younger brothers know that those 2″ scars they all sport on their lower backs has nothing to do with the conspiracy underlying an MRI finding identical to mine, but that it’s actually a revolutionary new technique to conduct surgery on the thyroid glad, cure depression, anxiety, and/or whatever else may ail you, according to the exclusive authority of people who’ve never met you. Won’t they be surprised!

– I live apart from my wife. And here I thought the woman in the next room here in San Jose is my wife—including time spent in Mexico, SoCal, and Las Vegas over Thanksgiving with her parents and looking forward to a Tahoe trip with my parents next weekend. I hope she doesn’t find out the truth!

– I don’t make any money anymore, and even have to clean my own cabin vacation rental because occupancy is down and I can’t afford a cleaner. And here I thought that I was finishing up 2014 with the highest income for that property in the four years since renting it out. I was also pretty sure that I was dissatisfied with the level of cleanliness, had a parting of the ways, and that while looking for another cleaning vendor and I did it myself, that it was a good way to move around, given the back and leg pain that’s all in my head…or was it hypothyroid…can’t remember.

And what a shock to find out that after selling out my 2014 right to occupy contract with The Grand Solmar in Cabo (10 weeks per year) by the end of March, then popping for an additional contact, then selling that one out for 2014 (another 10 weeks per year), it’s only because of poverty.

I sure wish that 89 bookings in 2014, and 19 so far for 2015 between the three rentals was enough to keep me out of the poor house.

…The truth about yourself is out there, folks. You just have to stop hiding and accept it!

[“Clown car” indeed.]

 It’s so Paleo Anarchy.

2:00 PM “Break Fast”

…Makes me feel sorry for the paleo Rabbits with their bales of greens and a side of hubris. Could this kinda thing help you break through that “LC Stall?“