Violeta
Senior Member
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I think finasteride causes hypoxia. That's what cause mariovitali's ME/CFS.
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My guess is hypoxemia is involved as a root cause in a lot of cases. It’s a direct cause of ER stress
Excellent. Yes, I remembered seeing HIF1A in one of your messages but didn't remember the specifics.Yes if that wasnt clear from earlier posts, HIF1a induces expression of WASF3 under hypoxic conditions. I mentioned HIF1A is also upregulated with the itaconate shunt leading to increase in WASF3.
HIF1A induces expression of the WASF3 Metastasis Associated Gene under hypoxic conditions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629704/
Violeta- High glucose treatment, but not the osmotic control mannitol, induces csGRP78 expression through an ER stress–dependent mechanism. There are many 'roads' to increase NLRP3 and/or ER Stress. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6514638/ GRP78 levels were positively correlated with HbA1c and AGEs. https://pubmed.ncbi.nlm.nih.gov/34591271/
I think finasteride causes hypoxia. That's what cause mariovitali's ME/CFS.
HIF-1a helps a cell adapt to hypoxia. That might be good if you want apoptosis, but what if you don't want apoptosis?Maybe not - Finasteride administration in benign prostatic hyperplasia results in statistically significant suppression of MVD, VEGF, and HIF-1alpha in a time-dependent manner. https://pubmed.ncbi.nlm.nih.gov/16904480/
Maybe this AI helps a little.with respect to finasteride
I was just looking at finasteride's side effects. Yikes.Maybe this AI helps a little.
Apoptosis is a programmed cell death process that occurs naturally in the body to eliminate damaged or unnecessary cells. Hypoxia, on the other hand, refers to a condition where there is a reduced level of oxygen in the tissue or organ. When it comes to finasteride, it is important to understand how these two concepts are related, especially in the context of the drug's potential effects on the body.
Finasteride is a medication primarily used to treat conditions related to the prostate gland, such as benign prostatic hyperplasia (BPH) and male pattern baldness. It works by inhibiting an enzyme called 5-alpha-reductase, which converts testosterone into dihydrotestosterone (DHT). DHT is a hormone that can contribute to the enlargement of the prostate gland and male pattern baldness.
Now, let's discuss apoptosis and hypoxia in the context of finasteride:
It's worth noting that the relationship between finasteride, apoptosis, and hypoxia is complex and not fully understood. Finasteride's mechanisms of action are primarily related to hormonal changes, and any effects on apoptosis or hypoxia are secondary and may vary among individuals.
- Apoptosis and Finasteride:
- Finasteride may have an impact on apoptosis in tissues where it reduces DHT levels. DHT is known to influence cell growth and proliferation in certain tissues, including the prostate and hair follicles.
- By inhibiting 5-alpha-reductase and reducing DHT levels, finasteride may slow down cell proliferation in the prostate, which can be beneficial for conditions like BPH.
- In some cases, finasteride may help promote apoptosis in prostate cells, leading to the shrinkage of the prostate gland, which can relieve symptoms associated with BPH.
- Hypoxia and Finasteride:
- Hypoxia, or reduced oxygen supply to tissues, can occur in various parts of the body, including the prostate. This can be due to factors like inflammation, obstruction, or inadequate blood supply.
- In the context of BPH, the enlarged prostate can compress blood vessels, reducing oxygen delivery to the prostate tissue and causing localized hypoxia.
- Finasteride's ability to reduce the size of the prostate can potentially improve blood flow to the area and alleviate hypoxia by relieving the compression on blood vessels.
Here 10 more - no fun at all:finasteride's side effects
LXR has been in the conversation lately. HIF1-a is involved.Indeed check this out yall;
“Neonatal rat ventricular myocyte cultures subjected to hypoxia (16 hours) exhibited increased XBP1 mRNA splicing, XBP1 protein expression, GRP78 promoter activation, and GRP78 protein levels; however, the levels of these UPR markers declined during reoxygenation, suggesting that the UPR is activated during hypoxia but not during reoxygenation. When cells were infected with a recombinant adenovirus (AdV) encoding dominant-negative XBP1 (AdV-XBP1dn), UPR markers were reduced; however, hypoxia/reoxygenation-induced apoptosis increased. Confocal immunocytofluorescence demonstrated that hypoxia induced GRP78 in neonatal rat and isolated adult mouse ventricular myocytes. Moreover, mouse hearts subjected to in vivo myocardial infarction exhibited increased GRP78 expression in cardiac myocytes near the infarct, but not in healthy cells distal to the infarct. These results indicate that hypoxia activates the UPR in cardiac myocytes and that XBP1-inducible proteins may contribute to protecting the myocardium during hypoxic stress.”
My guess is hypoxemia is involved as a root cause in a lot of cases. It’s a direct cause of ER stress
It will take me a while to understand this, but a quick question, it looks as if this is saying saturated fatty acids are detrimental to muscle cells. Is that what is means?@Violeta yeah I remember studying LXR a few years ago and it’s a double edge sword. It’s involved in the immune response to viruses and helps to kick off inflammatory responses.
I found a super interesting paper that just was published about AMPK, master metabolic regulator, being involved in kicking off the UPR response to high dose saturated fatty acid (SFA) Palmitate in muscles.
https://www.imrpress.com/journal/FBL/28/8/10.31083/j.fbl2808159/htm#S4
“In summary, we have provided evidence of bidirectional crosstalk between AMPK signaling and early activation of the UPR in muscle cells exposed to SFAs (Fig. 6). We also showed that pharmacologic activation of AMPK was sufficient to induce mild UPR in skeletal muscle cells. These findings demonstrate an essential role for the AMPK pathway in restoring ER homeostasis via activation of the UPR in response to metabolic stress. Furthermore, they may guide the development of new strategies for the treatment of diseases such as obesity and diabetes through improvements in skeletal muscle metabolism.”
They tested an AMPK agonist, a closely related drug to Metformin (also an AMPK agonist) and depending on dose timing it increased the UPR and made ER stress worse. I would be careful with Metformin if anyone was thinking of taking it
This is what I understand.it looks as if this is saying saturated fatty acids
Do you have a theory about why the crash happened after you stopped Finasteride?Thanks for all of your posts and this is correct. I ended up having ME/CFS after taking finasteride. Please note that the crash happened AFTER I stopped Finasteride.