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:
- It evolves at a rate of up to many generations every 24 hours.
- 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. The populations reached the milestone of 50,000 generations in February 2010 and 60,000 in in April 2014.
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.
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.]