Thyroid and Cortisol Response

* I am not a doctor and am only sharing my experience, I am also working with a doctor and have had labs run, please work with a doctor if you suspect something similar *

I wanted to share my experience with thyroid supplementation and low cortisol. My oral waking and midday temperatures were sitting around 97F and 97.5F respectively. As an aside, my axillary is always 0.5-1F warmer, yes warmer, than my oral temperature. I think what I am about to describe could have a part in that but I am unsure of the mechanism yet. My oral temperature has been in the low 96F but lifestyle interventions, supplements, and some topical thyroid were able to increase it.

I was taking 6ug T4 and 3ug T3 on waking and before bed, plus 8ug T3 only around midday, in my navel. Having done some research on T3 monotherapy, I decided to give the experiment a try due to high revT3, still high tsh, low temperatures, etc. I did 1 drop of the 8ug T3 on my navel upon waking, midday, and before bed. This exposed a low cortisol or improper cortisol response – for example, I may have had sufficient cortisol but due to cortisol binding globulin, an issue at the receptor level, etc. the response wasn’t adequate. This brought on days of blood glucose regulation issues, a decreased desire to eat, diarrhea, a wired but tired feeling, insomnia, blood pressure regulation issues, achy feeling around my kidney/ adrenal area, a mild cough, drop in body temperature, shivers, achy feeling around my sternum, achy feeling around my thyroid and the anterior cervical nodes, feeling strung out like I just had some coffee, frequent urination, body water swings (I sit around 116lbs but swung up to 121lbs then down to 114.6lbs over 2 days), achy muscles not recovering as they normally do from my workout, brain fog, and a general unwell feeling. I stopped the thyroid cold turkey, which arguably was not the best idea, but if it was pushing my adrenal glands harder than they could function, continue to stress them does not follow. I also figured this would be safe given I took the doses topically and was not taking even 1 grain of thyroid.

What I am grateful for about this experience, is the response elucidated many of my prior health issues. Low cortisol is implicated in: allergies – I used to have really bad MCAS; postural orthostatic tachycardia syndrome (POTs) – all the salt cravings, graying out upon standing, lower blood pressure in general, etc.; hypoglycemia – I had ketotic hypoglycemia and the ketotic part was basically non-existent due to supplementing vitamins B2 and B5 (B5 is especially important for the adrenals), and ALCAR+allicin (for possible TMAO issues), now I usually only have issues with hypoglycemia near my period and given the progesterone drop and cortisol’s relationship to estrogen, this makes more sense; recurring rhabdomyolysis – this can be due to too low or too high cortisol; hypermobility/ hEDS – including thin skin and bruising; anxiety; insomnia; night sweats; frequent colds; inability to handle stress – almost craving the stress to feel normal; some hyperpigmentation; freezing hands, feet, nose, and butt; etc. What I find truly crazy is I used to live my life with this strung out, on edge feeling 24/7, the type A, go-go-go personality, then I would crash and sleep for a few days and repeat the process.

I am recovering with Thorne’s adrenal cortex, pantethine (vitamin B5), salt in tangerine juice, sun and grounding for the SCN, trying to relax as much as possible, licorice tea topically, and continuing to eat sufficient protein and nutrient dense food even though I feel nauseous, etc.

Resources

Effects of pantothenic acid supplementation on adrenal steroid secretion from male rats: https://pubmed.ncbi.nlm.nih.gov/18520055/

Vitamin B5 and hypotension: https://altmedrev.com/wp-content/uploads/2019/02/v16-3-263.pdf

Low levels of skin cortisol leads to acne (many thing can as well like vitamin B5 deficiency): https://www.acne.org/what-is-cortisol-and-does-it-affect-acne.html

https://upload.wikimedia.org/wikipedia/commons/a/a6/Adrenal_Steroids_Pathways_-_edited.svg

High estrogen levels increase cortisol binding globulin, making cortisol inactive: https://anabolicminds.com/community/threads/cortisol-and-estrogen-relationship.59334/

Stop the thyroid madness has a lot of information on the thyroid-aldosterone-cortisol relationship

Shingles, lysine, and FAO

Lysine is usually brought up when discussing non-pharmaceutical responses to things like shingles and other viruses. Lysine being a crucial component to making carnitine. Does this point to a fatty acid oxidation issue?

Methylation, lysine, vitamin B6, vitamin C, Fe, vitamin B3, and Zn are all required.

10 February 2021

Na has a larger hydrated radius and it’s harder to remove the water molecules (takes more energy) then potassium (K). This seems to be why K is intracellular and Na predominately extracellular. When there’s a phase change Na (and Ca) come in and K and Mg leave. However, this is supposed to reverse again as the cytoplasm restructures. The monovalent cations can then bind to proteins (again why K would be desirable) the divalent hold different proteins together, etc.

So, B1, helping to structure the cellular water (increased ATP, etc) should allow for thins like K and Mg to stop being wasted. This then will cause aldosterone to normalize, etc so yes, the need for Na should decrease.

10 February 2021

Na has a larger hydrated radius and it’s harder to remove the water molecules (takes more energy) then potassium (K). This seems to be why K is intracellular and Na predominately extracellular. When there’s a phase change Na (and Ca) come in and K and Mg leave. However, this is supposed to reverse again as the cytoplasm restructures. The monovalent cations can then bind to proteins (again why K would be desirable) the divalent hold different proteins together, etc.

So, B1, helping to structure the cellular water (increased ATP, etc) should allow for thins like K and Mg to stop being wasted. This then will cause aldosterone to normalize, etc so yes, the need for Na should decrease.

30 September 2020

I think TTFD causes more oxalate dumping because this form of B1 is fat soluble. Lipid metabolism occurs in the peroxisome which is also the site where a lot of oxalate is formed. I think the cell probably stored oxalate here.

3 September 2020

I think it’s the inability to properly oxidize those calories that leads to aging. I don’t think our heart has a finite number of beats and our cells are limited to the Hayflick limit. I don’t think the goal is to suppress metabolic rate for a long life. A high functioning metabolic rate allows for cleanup, etc which leads to a long, healthy life.

Endogenous Oxalate

Sally Norton posted about potassium oxalate in blood tubes. She said the Mg binds the oxalate which causes metabolic enzymes to not be activated. My comments: does the body make endogenous oxalate then to keep glucose from entering the cell? There could be many reasons why it would want to do this. Especially if there aren’t enough carrier proteins, vitamins, and minerals to go through glycolysis, TCA, and ETC.
This would also explain the oxalate dumping seen with either reducing glucose intake, or taking vitamins and minerals that ensure proper metabolism.

14 June 2020

Just like minerals have decreased due to farming activity, so have vitamins. Also, our microbiome used to supply us with some Bs as well. With the increase use of antibiotics, etc these are obviously compromised too. Sometimes supraphysiologic doses are needed to fix deficiencies especially when you flood the system with a high dose of one vitamin, B1 for example. Doing this will put more strain on B2. B2 is needed for many things like methylation so this will stress B12 for example.
All of the Bs are important for proper metabolic activity (PPP, TCA, ETC, glycolysis, etc). Restoring ATP and CO2 production is what causes the cytoplasm to be structured correctly. When it is, protein synthesis, DNA folding, all fundamental cellular processes work appropriately. This is what makes sure enough ferritin, ceruloplasmin, etc are made. And this is why B1 (and other vitamins and minerals but especially B1 because of much it’s needed as a rate limiting step in these processes) helps get Fe out of the body.
It’s something to watch out for. My edema clears up immediately with B1. But if I don’t take B2 with it then my POTs continues. I eat liver, use bee keepers naturals b powered, and take a ton of the ancestral supplements organs.

Vitamin B1 biosynthesis in plants requires the essential iron–sulfur cluster protein, THIC

Thoughts

I think the most important statement in this paper is de novo biosynthesis is not found in animals. That means we must acquire it from the animals who eat these things, the plants/ fungi themselves, and/ or have the right bacteria (prokaryote) strains. The plants need to have functioning mitochondria and sources of bioavailable Fe and S for thiamine’s synthesis.

Notes

Vitamin B1, in the form of thiamin diphosphate (TPP), acts as a cofactor for several enzymes in key cellular metabolic path- ways such as glycolysis, the pentose phosphate pathway and the citric acid cycle (TCA), in addition to amino acid and nonmeval- onate isoprenoid biosynthesis, respectively (1). More recently, it has been implicated in tolerance to DNA damage (2) and as an activator of disease resistance in plants (3, 4). It is an essential compound in all-living systems, but de novo biosynthesis is only found in pro- karyotes, fungi, and plants; therefore, animals must acquire it from dietary sources.

proteins involved in thiamin biosynthesis in plants have been reported to have differential subcellular localizations. For example, THI1 involved in the syn- thesis of the thiazole moiety, is targeted to both mitochondria and plastids (24), whereas the recently described thiamin pyrophos- phokinase is reported to be cytosolic (25). To assemble the site(s) of synthesis of the thiamin molecule, it is thus of interest to know the subcellular localization of THIC [Fe-S containing protein].

Vitamin B1 was discovered in 1932, its structure was elucidated in 1936, and it was the first such compound to be recognized as an essential metabolic cofactor. Yet, surprisingly many facets of its metabolism still remain unresolved. Nowhere is this more apparent than in plants. In this study, we show that THIC plays an essential role in the synthesis of vitamin B1 and moreover is necessary for plant viability. The presence of a Fe-S cluster in THIC suggests that it must be coupled with a reductant to enable catalytic activity. In bacteria, this can be accomplished by the flavodoxin/flavodoxin reduc- tase/NADPH system as for the non-mevalonate isoprenoid biosynthesis proteins, IspG and IspH (37). However, flavodoxin is absent from the plastids of phototrophic organisms, but reduction could be achieved by ferredoxin, which can supply the electrons either in the presence of light or in the dark via ferrredoxin-NADP􏰊 reductase and NADPH (38). In plants, many chloroplastic enzymes are also activated and deactivated through oxidation/reduction reactions via the thioredoxin sys- tem. THIC has been found as a potential thioredoxin target protein in chloroplasts (39) and could influence the protein at several levels, including activity, oxidative regulation, and as- sembly or folding (40). Thus, the regulation of thiamin biosynthesis in plants may occur at several levels, i.e., riboswitch and redox.

https://www.pnas.org/content/104/49/19637

11 June 2020

I bet the PUFAs inhibiting the thyroid is why people seem to gain weight first. Then they start messing with cytoplasm structure (ROS). This then messes with amino acids. Which then causes skeletal muscle wasting.

“The enzymes which break down proteins are inhibited by unsaturated fats, and these enzymes are needed not only for digestion, but also for production of thyroid hormones, clot removal, immunity, and the general adaptability of cells. The risks of abnormal blood clotting, inflammation, immune deficiency, shock, aging, obesity, and cancer are increased. Thyroid and progesterone are decreased. Since the unsaturated oils block protein digestion in the stomach, we can be malnourished even while “eating well.”“ – RP

“[UF] best understood effect is their interference with the function of the thyroid gland. Unsaturated oils block thyroid hormone secretion, its movement in the circulatory system, and the response of tissues to the hormone. When the thyroid hormone is deficient, the body is generally exposed to increased levels of estrogen. The thyroid hormone is essential for making the “protective hormones” progesterone and pregnenolone, so these hormones are lowered when anything interferes with the function of the thyroid. The thyroid hormone is required for using and eliminating cholesterol, so cholesterol is likely to be raised by anything which blocks the thyroid function.” – RP

100iu of vitamin E per day