Good news, I don't have VAIDS (but I also don't have eyebrows and eyelashes).

My T and B cell counts were normal and my lymphocyte panel was normal. Autoimmune thyroid problems and Alopecia areata - not normal. Pomegranate peel is still the answer...

Other news - Many Autoimmune diseases have become more common, and in association with CoV booster history. Long-term risk of autoimmune diseases after mRNA-based SARS-CoV2 vaccination in a Korean, nationwide, population-based cohort study. (Jung, et al., 2024) There was an increased risk for systemic lupus erythematosus (SLE) and Bullous pemphigoid. See Figure 2, Jung, et al., 2024.

What is Bullous pemphigoid? The Monkeypox like skin rash condition that is autoimmune based and more common in the CoV injected than the control group in the Korean based study.

“Bullous pemphigoid (a type of pemphigoid) is an autoimmune pruritic skin disease that typically occurs in people aged over 60, that may involve the formation of blisters (bullae) in the space between the epidermal and dermal skin layers.” Wikipedia.

~~ The rest of the post is about ‘My labs the continued story’ - a follow up to aprior post - Ginger, my autoimmune Kryptonite. This post gets into pecans, almonds, pistachios, Brazil and hazelnuts…my other Kryptonite I guess. They are also plant sources of albumin like proteins. However, pomegranate peel is still my Underdog Secret Energy Pill - microRNA became a part of this post, in a dipping the toes in way. It is a huge topic and I let Mother Nature handle most of the details for me. I just need to prep the pomegranate instead of over-eating pecans and not cooking healthy meals. We do tend to know which habits are helping and which aren’t.

My autoimmune disease is no longer invisible though, a win? I could tell that I hadn't removed all the causal factors because the hair follicles hurt with the swelling and itched. Rubbing too much, like dry seasonal allergy eyes but it was the eyebrows and eyelash area specifically. Since stopping all ginger, they feel better but my eyelids still look a little swollen. Scary photo later in the post.

My digging around in microRNA minutia could be a long time, so I am posting this - it has been in draft mode for a few days.

This post follows one that has my thyroid lab results, except for Reverse T3 which still isn’t available. (Substack)

Ginger is my autoimmune thyroiditis Kryptonite. Castor oil may be too

Excerpt from that post: The autoimmune thyroid panel is not looking good however.

• TSH - 14.43 High (Normal range: 0.40-4.50 mIU/L)

• T4 free is low normal at 0.8, range 0.8-1.8 ng/dL

• T3 free is also low normal at 2.5, range 2.3-4.2 pg/mL

• T3 Reverse is Pending

• Thyroglobulin antibodies - 61 High, anything equal to or over 1 is high.

• Thyroid Peroxidase antibodies - 836 High, over 9 IU/mL is high

I didn't heed my own advice to not mess with autoimmune disease. I knew I should avoid ginger but didn't avoid it consistently and then binged when I did buy it - addict style use.

Plant albumin may also be in almonds, so a nut allergy might be involved in my autoimmune thyroiditis and the hair loss. Pru du 2S is an albumin like protein and may cause food allergy IgE binding but might not cause typical allergy symptoms in all patients.

(Mandalari, et al., 2018)

Do pecans have it too? Yes.

• Cloning and characterization of 2S albumin, Car i 1, a major allergen in pecan (Sharma, et al., 2011)

I knew my Squirrelly diet had some problems, in theory or reality. (previous post) I knew that I was eating too many nuts for a balanced diet or life, at the time, because I wasn’t cooking often enough. And I had cut out tofu for a while to see if that was a problem. However, the ginger definitely was linked to flair ups in pain or itchiness of the hair follicles of my eyebrows and eyelids. 🤔 I will cut out or reduce the nuts too and see if that helps. Six months clear of a molecular mimicry autoimmune protein and the body’s level of autoimmune antibodies can drop back down.

Cutting out the ginger has improved the occasional painful feeling in the eyebrows. The eyelids are still a little swollen - inflamed with too many white blood cells ‘fighting’ the hair follicles it seems like.

What role does albumin have in thyroid follicles or hair follicles?

Well, albumin and prealbumin - transthyretin, plays a big role in thyroid hormone availability throughout the body, as it is a carrier protein. “Circulating T4 is almost entirely (99%) bound to plasma proteins: approximately 70% bound to TBG, 20% to transthyretin (prealbumin), and 10% to albumin....” (ScienceDirect/Thyroid Follicle)

“Outside the hypothalamic-pituitary-thyroid axis, the major regulator of thyroid hormone production is the concentration of thyroid hormone globulin (TBG). Circulating T₄ is almost entirely (99%) bound to plasma proteins: approximately 70% bound to TBG, 20% to transthyretin (prealbumin), and 10% to albumin.”

Endocrine Disturbances Affecting Reproduction, Alice Y. Chang, Richard J Auchus, in Yen & Jaffe's Reproductive Endocrinology (Sixth Edition), 2009, viewable at (ScienceDirect/Thyroid Follicle)

My “Thyroglobulin antibodies” were elevated - so I may be autoimmune attacking the TBG too.

Transthyretin (TRR or prealbumin) is also involved with the transport of retinol to the liver for activation into Retinoic Acid or other retinoids. (Brave AI Summary) Loss of TRR in knockout mice causes rapid loss of Retinol Binding Protein (RBP) in the urine - which would likely mean the mice/patient would have insufficient vitamin A or activated retinoids for optimal health. (Newcomer and Ong, 2000-2013)

“Whether vitamin A is to be ultimately utilized as retinoic acid, 11-cis-retinal or another retinoid, [retinol binding protein] RBP delivers only all-trans-retinol, and only retinol can trigger secretion of RBP.⁴ In the plasma, RBP binds to the larger protein, transthyretin (TTR, previously referred to as thyroxine binding prealbumin). The binding of RBP to TTR was suggested to prevent extensive loss of the low molecular weight RBP through glomerular filtration.³ This hypothesis was supported by the much later experiments of Blaner and colleagues with TTR “knockout” mice that demonstrate that RBP is rapidly clearly from the plasma in TTR deficient mice.^11” (Newcomer and Ong, 2000-2013)

Autoimmune antibodies against transthyretin (prealbumin) may be involved in Rheumatoid arthritis (Sharma, et al, 2014, retracted for a data image questions) and Juvenile Rh. arthritis. (Clement, et al., 2016) Rh. arthritis is considered an autoimmune disease but may also have an intracellular pathogen as a causal factor. (Lida Mattman/Stealth Pathogen) I am having early symptoms of Rh. arthritis in my thumbs and toes but I haven’t seen the doctor about it.

Albumin - egg white, can also be an autoimmune antibody concern. Antibodies against human or bovine albumin have been associated with presence and severity of SLE, an autoimmune disease also known as Lupus. (Nehring, et al., 2018) Auto-antibodies against albumin has also been observed in chronic liver disease and was associated with severity of chronic hepatitis. (Lenkai, et al., 1981) Treatment with interferon is linked to formation of auto-antibodies in chronic hepatitis and greater oxidative stress is likely causal in more auto-antibody formation in liver disease. They are common in liver disease even when it is not called autoimmune liver disease. (Himoto and Nishioka, 2013)

Brave AI really flubbed on that question - It said albumin didn’t appear to have a causal role in multiple autoimmune conditions based on the search results, which included those in previous paragraph. (summary) And the subpoints it shared are not unexpected. A higher albumin level would likely support a better immune response (Jang, et al., 2018) as it is also an indicator of the person being a healthier/less frail patient. the other subpoint - low albumin level is associated with more severe myasthenia gravis (MG) - also not unusual - sicker/frailer people tend to have lower albumin levels. (Weng, et al., 2016)

The symptoms of Lupus are vague enough that I do fit within them and hair loss is one of them. Sun sensitivity skin rashes or reddening of the face is common - a ‘butterfly rash’ over the cheeks and nose - I don’t have that but my sun-exposed neckline is reddened and rashy and has a few tiny shingles; and Raynaud’s - cold/blue fingertip symptoms. I have tingling LongCovid or B12 deficiency type finger symptoms, mild, not a severe pain level - which I had when off of medical marijuana for a while in 2020 when traveling. (SLE symptoms, Brave AI)

I napped today (Thursday). I have been generally fatigued this summer and overdid it once or twice trying to get things done in my old style. A moderate pace is not my style but that is what is needed to reduce the risk of inflammatory myokine excess. Myokines are like cytokines except they are produced by muscles during exercise. Some are good, but an excess would be like oxidative stress - a problem the body has to cope with or it leads to worse inflammation.

Autoimmune disease is a puzzle. My goal - Six months of strict avoidance of a triggering protein can reduce the antibody flair up. Continue to avoid it after that though, no little tastes or binges later. The memory B cells would remain active, ready to make more antibodies if the protein was present again.

Knowledge is power, but it has to be put in action - practiced in daily routine.

Uh, oh, no eyebrows. Or eyelashes. And allergy/adrenal fatigue dark rings under my eyes. Need a suntan? Not really, I have been burning too easily and currently have a bit of sunburn pox on my neck.

Yes, it is weird to not have eyelashes and eyebrows. I use eyebrow makeup sometimes but adding anything artificial to my sore eyelids is not in my plans.

I shared the thyroid labs in a previous post. (Ginger…Substack) Excerpt - The autoimmune thyroid panel is not looking good, however.

• TSH - 14.43 High (Normal range: 0.40-4.50 mIU/L)

• T4 free is low normal at 0.8, range 0.8-1.8 ng/dL

• T3 free is also low normal at 2.5, range 2.3-4.2 pg/mL

• T3 Reverse is Pending

• Thyroglobulin antibodies - 61 High, anything equal to or over 1 is high.

• Thyroid Peroxidase antibodies - 836 High, over 9 IU/mL is high

Ginger is my autoimmune thyroiditis Kryptonite. Castor oil may be too

Thyroid follicular cells are the main cell type in the thyroid and they make the enzyme thyroperoxidase and thyroglobulin which is involved in thyroid hormone production (Brave AI summary, excerpt below) but thyroglobulin is different from the thyroid binding protein, also called the thyroxine binding globulin, (TBG) or thyroid hormone globulin, (TBG), which is made in the liver. (different question, Brave AI Summary) So my immune system is making antibodies against the proteins being made by the thyroid follicular cells - the thyroglobulin and thyroid peroxidase - but the T3 and T4 levels were in the low normal range - a little more towards hypothyroid - which I had been feeling and had added seaweed back to my diet and then high dose iodine again (Iodoral, 12.5 mg). My blood albumin level was tested with the CBC panel and it was okay.

Thyroid Follicular Cells’ Interaction with Albumin

• Thyroid follicular cells take up iodide and amino acids from the blood circulation on their basolateral side.

• They synthesize thyroglobulin and thyroperoxidase, which are then secreted into the follicular lumen along with iodide.

• The follicular cells subsequently take up iodinated thyroglobulin by endocytosis, extract thyroid hormones from it, and release them into the bloodstream.

• Albumin is involved in the transport of thyroid hormones produced by the follicular cells, carrying them away from the thyroid gland and delivering them to target tissues. (Brave AI summary)

What does all that have to do with hair follicles? …. plenty. Thyroid stimulating hormone can affect hair follicle stem cell growth and T3 thyroid hormone has regulatory function over hair growth - lack of T3 is going to lead to a lack of hair growth. (excerpt below, Brave AI summary)

Thyroid Hormone Regulation of Hair Follicle Stem Cell Dynamics

Based on the provided search results, thyroid hormones (T3) regulate hair follicle biology and stem cell function through several mechanisms:

1. Epigenetic alterations: T3 deficiency leads to epigenetic changes in bulge stem cells, including aberrant activation of Smad signaling and reduced nuclear activity (Contreras-Jurado et al., 2015).

2. BMP-Smad signaling: Excessive BMP-Smad signaling, triggered by T3 deficiency, contributes to reduced stem cell proliferation (Contreras-Jurado et al., 2015).

3. Wnt/β-catenin signaling: T3 regulates Wnt/β-catenin signaling, which is essential for stem cell maintenance and hair follicle homeostasis (Ruiz-Llorente et al., 2018).

4. Nuclear thyroid hormone receptors (TRs): TRs directly regulate the expression of microRNAs with key roles in skin homeostasis, including those involved in hair follicle development and maintenance (Ruiz-Llorente et al., 2018).

5. Cellular quiescence: T3 regulates the balance between stem cell quiescence and activation, with excessive signaling leading to exhaustion of the stem cell reservoir (Contreras-Jurado et al., 2015).

6. Epigenetic profile: Quiescent stem cells in the hair follicle bulge are enriched in H3K9me3, which is regulated by T3 (Frye et al., 2007).

7. Thyroid hormone receptor-mediated transcriptional regulation: TRs regulate the expression of genes involved in hair follicle development, maintenance, and cycling, including those involved in stem cell self-renewal and differentiation (Takeda et al., 2013). (Brave AI summary)

A microRNA, miR-218-5p, has been identified that promotes hair follicle growth:

Based on the provided search results, the following microRNAs are associated with hair follicle development and maintenance:

1. miR-218-5p: Regulated by T3, miR-218-5p plays a crucial role in promoting hair follicle growth and regeneration. It enhances the molecular pathway responsible for promoting hair follicle growth and could be a candidate for future drug development (North Carolina State University research*). *MicroRNA shows promise for hair regrowth, July 27, 2020, (sciencedaily.com)

   1. The same microRNA, miR-218-5p, may be aberrant in atherosclerosis and arthritis. Upregulation of it occurs during chronic stress (study on rats). (Yoshino, et al., 2022)

2. miR-214: This microRNA modulates the activity of the Wnt pathway, controlling skin and hair follicle development (Ahmed et al., 2014). Although not directly regulated by T3, its involvement in hair follicle development and maintenance is mentioned. (Brave AI Summary)

Also from that search:

• Downregulation of microRNA 31 is related to hair loss with aging, (Zhang and Yi, 2021), and stress can cause upregulation of it and is associated with skin aging. (Yu, et al., 2021)

• ‘Thyroid hormone action in epidermal development and homeostasis and its implications in the pathophysiology of the skin’, Open access, (Mancino, et al., 2021) Alopecia, hair loss and skin conditions of eczema or vitiligo (melanin loss - albino white skin patches) are associated with autoimmune thyroid conditions.

• ‘Thyroid hormones directly alter human hair follicle functions: anagen prolongation and stimulation of both hair matrix keratinocyte proliferation and hair pigmentation’. (van Beek, et al., 2008)

“The skin of hyperthyroid patients is dry and thinner than the skin of euthyroid subjects, as well as patients frequently experience flushing of the face, erythema of the palms and hyperhidrosis of the palms and soles (Tables 1 and 2) [46]. The skin in hypothyroid subjects, caused by Hashimoto’s thyroiditis or congenital hypothyroidism in pediatric population, appears thicker, colder and has classical myxoedema respect a euthyroid subjects (Tables 1 and 2).” (Mancino, et al., 2021)

*Myxoedema: “non-pitting edema caused by increased deposition of mucopolysaccharides in the skin” - Wikipedia

The term “myxedema” can mean severely advanced hypothyroidism. But it’s also used to describe skin changes in someone with severely advanced hypothyroidism. The classic skin changes are:

• swelling of your face, which can include your lips, eyelids, and tongue

• swelling and thickening of skin anywhere on your body, especially in your lower legs. (Healthline)

“The most widely accepted hypothesis explaining the wide variety of cases in which skin diseases are associated with chronic autoimmune thyroiditis is the autoimmune hypothesis, which argues that thyroid antibodies as thyroglobulin (TgAb) and thyroperoxidase (TPOAb), are among the serum autoantibodies that react with and destroy melanocytes [48]. A fascinating hypothesis by Li et al., [52] proposes that, autoantibodies such as TgAb and TPOAb can induce a sustained oxidative stress, which in turn can result in enhanced apoptosis and senescence of melanocytes [52].” (Mancino, et al., 2021)

Plant polyphenols or other phytonutrients can be a solution to varied health issues

The nice thing about plant polyphenols or other phytonutrients and microRNA modulation is that they tend to up or down regulate as needed - when present in therapeutic amounts, too much can be an irritant or may ecom Plants intuitively are designed to react very quickly to changes in the weather, to prevent cell damage from extremes of temperature or sun, and changes in microRNA can rapidly lead to big changes in what the cells are doing. Oxidative stress is the negative signaling ~ “too hot”, “too cold”, “too sunny”, “too dark”, and the plant responds somehow to reduce the negative inputs from the environment. Flowers or leaves may open or close or turn in response to the sun or temperature changes. How does the plant “know”? Chemicals react or they don’t react based on environmental inputs of temperature or solar UV radiation.

“Using transgenic and conditional knockout mouse models plus a lineage-tracing technique, we show that miR-31 acts as a key driver of HFSC aging by directly targeting Clock, a core circadian clock gene whose deregulation activates a MAPK/ERK cascade to induce HFSC depletion via transepidermal elimination.” (Yu, et al., 2021)

From my pomegranate paper, I know that pomegranate/peel would be helpful for inhibiting a MAPK cascade:

Mitogen-activated protein kinase (MAPK) is inhibited by phytonutrients in pomegranate peel extract (PPE) by the regulation of Fox03, which would decrease unwanted phosphorylation of proteins, observed in an animal-based study in which PPE reduced ototoxicity caused by amikacin (AMK). (Liu, et al, 2017) Ototoxicity, damage to Hair cells within the inner ear, is associated with certain medications like amikacin and also seems to be caused by CoV/chimeric spike subunit S1 disrupting ankyrin binding domains of TRP channels in the Hair cells. (Liviero, et al, 2021)

• ‘Pomegranate Products for the Pain of Histamine Excess.’ copyright Jennifer Depew, RD (Pom pdf in my sync file)

Other microRNA involved in the MAPK pathway

MAPK signaling is aberrant in myeloid leukemia, a review article looked at the microRNA that are involved in the MAPK pathway. (Chakraborty, et al., 2016)

“Several miRNAs play regulatory role in MAPK1 expression, of which, miR-17 and miR-19a can directly regulate the MAPK1.” […] “Several miRNAs play significant role in the MAPK signaling pathway and among them, the following miR-203, miR-196b, miR-29b, miR-30a, miR-138, miR-155, miR-19a, miR-17, miR-126, miR-128, miR-221, miR-15a, miR-188-5p and miR-181a are well studied (Table ​(Table1,1, ​,2)2) [39].” (Chakraborty, et al., 2016)

»> Daily reminder that pomegranate peel/extract is VERY effective against cancer, and against cancer metastasis in particular. It is also helpful for autoimmune conditions, is a broad spectrum antimicrobial while also promoting beneficial species (eat the inner pith for the benefit of pectin, rather than only using an extract is my synergistic tip) and it helps in many, many other health conditions as well as being effective as a mouthwash/tooth brushing substitute, (seriously, and isn’t that cool?)

I think pomegranate and its peel has a variety of phytonutrients that can modulate microRNA as needed to reduce oxidative stress and restore normal cell functions - as needed situationally. That is the magic of nature - let the phytonutrients modulate as needed to adjust to the environment they find themselves in. That makes our job to be eating the plants or extracts, so the nature magic can happen for us. Pomegranate will be in season in the US growing areas soon!

MicroRNA and hair follicles: (Brave AI summary) *I think this is linked earlier too, but I will leave it here.

Switching lab sections - do I have VAIDS? or Micro-clotting? - it seems not too bad yet.

My D-Dimer level is slightly elevated at 0.55, range below 0.50. That was an additional lab I ordered as a stand alone. It may be an early indication of microclotting within my blood vessels ~ potentially related to chimeric spike issues.

The T cell and B cell panel included Absolute CD19+ - 238, range 110-660 cells/uL; % CD19 (B cells) - 14, range 6-29%; Absolute CD3+ - 1275, range 840-3060 cells/uL; % CD3 (Mature…) - 74, range 57-85%.

I don’t know enough about the T and B cell counts. Is being towards the lower end of the range a bad thing? - lower immune function? Or would be being towards the higher end of the range be a bad thing — indicating an infection is being fought? Regarding diagnosis of VAIDS, not having enough of the cells is the concern, so my being towards the low end of the range is maybe not a great thing. My sunshine, less stress - but not too much sunshine either, I’m a little sun sensitive lately.

Self-pay, self-order labs through ultalabtests.com. Other companies exist for that service too.

Platitude: Today is a present to open with glee. Moving forward is the goal. I also have a baseline lab value now for my immune cells.

The lymphocyte panel looks normal, no infection or outrageous autoimmune excess of white blood cells.

My liver labs and uric acid levels were improved but kidney function had an improvement in my elevated creatinine, 262 dropped to 182, range 29-143. That can be a sign of muscle breakdown or tissue damage - or thyroid dysfunction, more on that is next.

Elevated creatinine and reduced kidney filtration is seen with low thyroid function

…in Hashimoto’s thyroiditis (hypothyroid typically but can fluctuate between high or low levels of thyroid hormone) or increased filtration and low creatinine was seen in Grave’s disease (a hyperthyroid condition).

The findings in the excerpt below, would suggest that I am functionally more hypothyroid currently than hyperthyroid, as my creatinine is elevated and my filtration reduced. I have had active Grave’s disease in the past ~ 2012/2013. More recently I had been feeling hypothyroid and increased my use of iodine rich foods and then added a high dose iodine supplement (Iodoral - 12.5 mg/day) and it seems to have helped. Trying a month of a loading dose (50 mg) might be worth trying to clear fluoride and bromide.

Case study: “Our patients demonstrate a remarkable effect of thyroid function on glomerular filtration rate.

• The creatinine clearance of the patient with hyperthyroidism was doubled,

• while the creatinine clearance of the hypothyroid patient was halved.

Both patients were treated, the hyperthyroid patient with β blockade and methimazole, and the hypothyroid patient with thyroid hormone. After several months, the creatinine clearance of both patients had returned to normal.” (Claus, et al., 2005) *Reformatting emphasis added by me.

My creatinine level might also be more elevated because I have been supplementing with creatine now, about 5 mg once or twice a day. Creatine is used in the muscles and creatinine is the breakdown product which is excreted by the kidneys. (Brave AI summary)

Disclaimer: This information is being provided for educational purposes within the guidelines of Fair Use and is not intended to provide individual health care guidance.

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