Dribbling Urine: A Sign of Hypothyroidism
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As some of you may know, Danny Roddy posted this on his Telegram not too long ago "Dribbling urine can be a sign of hypothyroidism." and a lot of people seemed confused. https://t.me/dannyroddy/1568
This study that I found does a good job laying out the pathology of prostate issues and may explain why something such as dribbling urine would develop in the first place.
"Available evidence shows that a three-hit hypothesis can be drawn. An overt, or even a subclinical, bacterial or viral infection could induce prostatic inflammation (first hit) that could be autosustained or exacerbated by the presence of an altered metabolism and in particular by hypercholesterolemia (second hit). Hypogonadism and/or hyperestrogenism could act as a third hit, favoring the maintenance of this inflammatory state. The combined action of all three hits, or even two of them, may result in overexpression of Toll-like receptors (TLRs), transformation of prostatic cells into antigen-presenting cells and activation of resident human prostate-associated lymphoid tissue ending in overproduction of growth factors which, in turn, will induce prostate remodeling and further prostate enlargement."
Bacterial infection (caused by slow gut motility) seems to be a key factor leading to prostate inflammation, and as many of us know, endotoxin (LPS) is also highly involved in this.
As noted in the study; prostate inflammation, hypercholesterolemia, hypogonadism and/or hyperestrogenism (all connected to hypothyroidism) may activate the TLRs, further feeding this vicious cycle.
I also found a Haidut post on the old forum discussing how "Prostate Enlargement (BPH) May Be Due To Endotoxin"
https://raypeatforum.com/community/threads/prostate-enlargement-bph-may-be-due-to-endotoxin.11377/Vitamin D, vitamin K2, aspirin, pregnenolone, progesterone, methylene blue, carrot salad, may be useful in treating prostate issues through several mechanisms. Although, supplemental thyroid would probably be the best thing to look into.
Vitamin D and K2 both antagonize TLR4, oppose estrogen, lower inflammation. Vitamin K2 helps to dissolve calcification, vitamin D is androgenic.
https://pubmed.ncbi.nlm.nih.gov/33540416/
https://pubmed.ncbi.nlm.nih.gov/28587577/
https://pubmed.ncbi.nlm.nih.gov/19906814/
https://pubmed.ncbi.nlm.nih.gov/15763078/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070857/
https://raypeatforum.com/community/threads/vitamin-d-inhibits-the-deactivation-of-androgens.12411/Aspirin can lower inflammation by opposing the COX enzymes, antagonizes TLR4, and promotes proper blood flow.
https://pubmed.ncbi.nlm.nih.gov/14592543/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599518/
https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-017-0198-7Pregnenolone and progesterone are both anti-inflammatory, antagonists of TLR4, anti-estrogen, reinforce metabolism, lower cholesterol and promote steroid synthesis.
https://raypeatforum.com/community/threads/prostate-enlargement-bph-may-be-due-to-endotoxin.11377/
https://raypeatforum.com/community/threads/pregnenolone-is-a-potent-functional-endotoxin-tlr4-antagonist.27846/
https://pubmed.ncbi.nlm.nih.gov/21407165/Methylene blue lowers inflammation and serves as an anti-microbial.
https://en.m.wikipedia.org/wiki/Methylene_blue
https://raypeatforum.com/community/threads/methylene-blue-is-a-potent-anti-inflammatory-with-possibly-the-broadest-spectrum.22156/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9795775/
https://aacrjournals.org/cancerres/article/79/13_Supplement/2958/635047/Abstract-2958-Evaluating-the-therapeutic-effectsAs many may know, Ray's carrot salad is anti-microbial, improves gut motility, can lower estrogen by supporting the liver and digestion, which can lower inflammation and LPS.
And most notably... thyroid supports this entire framework of lowering inflammation, promoting gut motility, lowering cholesterol, promoting steroid synthesis, and ultimately improving metabolism.
I may have missed a bit, so please feel free to correct me on anything and/or add your own thoughts/experience/feedback.
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@nate very interesting. Times when i have low blood sugar from after a workout or very stressful days i have many symptoms like this
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Interesting post, thank you for sharing Nate
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@Hitler thank you Hitler
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Hi Nate, will preface by saying I enjoy your content on Xwitter, and your video with Georgi was very helpful for me to get situated with the principles of bioenergetics. This dribble has been an issue for me for a while now and I honestly feel that since Peating it has become a bit worse. Still, I feel markedly better in basically every other category. Will thyroid (I have been meaning to by IdeaLabs T3 and T3 + T4 for a bit, am broke college student) address this? I know there is seldom a one-stop solution to things as complex as thyroid but it is an area I am a bit deficient in more advanced knowledge.
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Hey thank you for that. I think thyroid would help a lot long term, but it seems that it may take a while to see improvement. I’ve been dealing with this issue personally and I’ve seen benefit from the things I’ve mentioned, but haven’t noticed much improvement from thyroid in particular quite yet. Been trying to find the right dose of T3 and T4 for a while now, my focus with thyroid is mainly on improving digestion (which seems to be where a lot of this starts, as mentioned above)
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@nate Overexpression of Toll-like receptors (TLRs) in prostate tissue represents a key element in the pathogenesis of benign prostatic hyperplasia (BPH), possibly functioning as an interface between inflammatory signals and pathological processes such as hyperplasia and fibrosis. These receptors, which are an integral part of the innate immune system, are able to recognize specific pathogen-associated molecular patterns (PAMPs) and damage (DAMPs), initiating a signaling cascade leading to the production of pro-inflammatory cytokines and inflammatory mediators.
TLRs on prostate cells can be activated by pathogen-specific ligands as well as endogenous ligands secreted during tissue damage.
Once activated, TLRs initiate a signaling cascade through adapters such as MyD88, activating NF-κB, MAPK and other pathways, leading to the transcription of pro-inflammatory cytokine genes (e.g. IL-6, TNF-α).
Overexpression of TLRs in the prostate may be correlated with other pathological processes, such as dysregulation of lipid and hormonal metabolism. TLR-induced inflammation may synergize with the effects of hypercholesterolemia and hormonal imbalance, further modulating the prostate environment.
Overexpression of TLRs and the resulting inflammation may contribute to the pathological proliferation of prostate cells and fibroblasts, as well as the accumulation of extracellular matrix (ECM), leading to prostate hyperplasia and fibrosis.
TLR activation and associated proinflammatory signaling can induce the overproduction of various growth factors, such as fibroblast growth factor (FGF) and transforming growth factor beta (TGF-β), which are key mediators in prostate tissue remodeling.
It is possible that hypothyroidism can indirectly cause prostate disorders.
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@Fructose said in Dribbling Urine: A Sign of Hypothyroidism:
@nate Overexpression of Toll-like receptors (TLRs) in prostate tissue represents a key element in the pathogenesis of benign prostatic hyperplasia (BPH), possibly functioning as an interface between inflammatory signals and pathological processes such as hyperplasia and fibrosis. These receptors, which are an integral part of the innate immune system, are able to recognize specific pathogen-associated molecular patterns (PAMPs) and damage (DAMPs), initiating a signaling cascade leading to the production of pro-inflammatory cytokines and inflammatory mediators.
TLRs on prostate cells can be activated by pathogen-specific ligands as well as endogenous ligands secreted during tissue damage.
Once activated, TLRs initiate a signaling cascade through adapters such as MyD88, activating NF-κB, MAPK and other pathways, leading to the transcription of pro-inflammatory cytokine genes (e.g. IL-6, TNF-α).
Overexpression of TLRs in the prostate may be correlated with other pathological processes, such as dysregulation of lipid and hormonal metabolism. TLR-induced inflammation may synergize with the effects of hypercholesterolemia and hormonal imbalance, further modulating the prostate environment.
Overexpression of TLRs and the resulting inflammation may contribute to the pathological proliferation of prostate cells and fibroblasts, as well as the accumulation of extracellular matrix (ECM), leading to prostate hyperplasia and fibrosis.
TLR activation and associated proinflammatory signaling can induce the overproduction of various growth factors, such as fibroblast growth factor (FGF) and transforming growth factor beta (TGF-β), which are key mediators in prostate tissue remodeling.
It is possible that hypothyroidism can indirectly cause prostate disorders.
https://pubmed.ncbi.nlm.nih.gov/37143736/
,,Studies indicate that THs regulate different aspects of growth, metabolism, and prostate pathology, whose global effect depends on total and/or free concentrations of THs in serum, local bioavailability, and the endocrine androgen/thyronine context."
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@donovan I notice the same. I could be wrong but I think Ray said something like the benefit of taking a substance to prevent inflammation from occurring in the first place usually outweighs the downsides. Sometimes I’ll preemptively take aspirin or something on a day I know I’ll be stressed and I find that helps.
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@nate i do the exact same thing. Usually aspirin and some pregnenolone if i know i have a stressful or workload heavy day
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@Fructose thanks for this, nice share
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@Fructose said in Dribbling Urine: A Sign of Hypothyroidism:
Overexpression of TLRs in the prostate may be correlated with other pathological processes, such as dysregulation of lipid and hormonal metabolism. TLR-induced inflammation may synergize with the effects of hypercholesterolemia and hormonal imbalance, further modulating the prostate environment.
Just to be clear. Thyroid hormone deficiency is a contributing factor to TLR overexpression. There is a known direct relationship between TLR and the progression of Hashimoto's disease (a self-perpetuating mechanism?). Because thyroid hormones regulate the proliferation and differentiation of T and B lymphocytes. Reduced T cell proliferation is observed in the hypothyroid state; : Thyroid hormone deficiency may affect the phagocytic functions of macrophages, which changes their ability to eliminate pathogens and present antigens.
Coming back to the point. Thyroid hormones modulate the expression of Toll-like receptors (TLRs) on immune cells, which are key elements of pathogen recognition in the innate immune system. In hypothyroidism, changes in TLR expression and function are observed, which may lead to a modified response to infections and potentially to dysregulation of inflammatory processes.
The indication of TLR in the context of the development of prostate disorders is really interesting and it interested me. Maybe soon I will gather all the information and write a post about it.
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@Fructose I was just about to mention T cells. The connection between thyroid, immunity, and TLR is starting to become a lot more clear to me. It really is amazing to see Peat's work reinforced.
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@nate Do you experience this just in the morning before eating or throughout the day too?
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@zeal actually notice it most at night, it seems to fluctuate with the state of my gut and stress
