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  • Scientific papers, books, blog posts. Discussion of whatever you find interesting and notable.

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    M

    Again, TLR 4 /Endo­toxin implicated inInfections, not just bac­terial ones, but also viral.

    "TLR4-dependent viral entry was further validated by an anti-TLR4 antibody-mediated blocking experiment. It was noticed that TLR4 is necessary for the early events of viral infection, especially during the attachment and entry stages."

    https://pmc.ncbi.nlm.nih.gov/articles/PMC10157217/

  • Websites, newsletters, articles, podcasts, interviews, explainers, books, and other resources that relate to the work of Dr. Raymond Peat.

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    @dapose haha yes I remember the smart part

  • Do you have a question? You can post it here, but you will only receive unqualified personal opinions and NOT medical advice in any shape or form. If something seems like medical advice but it's posted in this category, it's actually a personal opinion.

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    @BearWithMe said in Mysterious gallbladder disease - can't digest fat for no apparent reason:

    Cholagogues, choleretics, and bile salt supplements doesn't relieve the symptoms (they sometimes make the symptoms worse), and cause constipation.

    Pressure and pain aside, does TUDCA and the other bile helpers also increase or decrease this:

    Also floating stool and undigested food in stool.

    So far it sounds as if any expediting of bowel movements alleviates your symptoms whereas those things that others think would support "proper" digestion, or any foods which require and trigger "proper" digestion in all its harshness, worsen your symptoms. Hypothetically you could be in dire need of the latter but aren't fit for it.
    From that there could be either something seriously wrong with forward peristalsis,
    or it could be a matter of chronic mucosal infection. Or both in a mutually supportive way.
    Have you tested for H.pylori and gastric/duodenal ulcers as well as for blood, calprotectin, bacterial intestinal pathogens (PCR on stool specimen)?
    Was there mild hepatic or splenic enlargments seen in the ultrasound?
    I'd bet on an infectious background also messing with thirst & glucose metabolism & renal functions.

  • From medical devices to supplements. Red lights, CO2 tanks, large trash bags, kuinone, and more.

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    @samson Why would you need more dietary cholesterol? If anything supplementing with an end-point androgen would initiate feedback loops leading to less steroidogenesis, thus lowering the dietary requirement for cholesterol, right?

    Or maybe you're referring to the fact that androsterone is a thyroid mimetic, thus increasing metabolism in steroid-producing organs, thus leading to a higher requirement of dietary cholesterol?

    Perhaps you would need more cholesterol because androsterone or its metabolites, being 5AR androgens, stimulate their own synthesis, thus increasing the need for dietary cholesterol to fuel the enhanced steroidogenesis?

    I don't know which possibility is correct, but if you know which is correct, please enlighten us.

  • Recipes, food, meal prep, brands. Discuss them all here.

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    @herenow said in Has anyone managed a liquid diet long term?:

    @Jennifer said in Has anyone managed a liquid diet long term?:

    , cumin would sabotage my best effort to moderate,

    There are few thoughts more comforting than that we are not alone🤗

    So true. 😊

  • Discussing pistol squats, concentric exercise, resting, and other forms of strength training.

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    J

    @cs3000

    According to the first link you posted, forskolin dephosphorylates the androgen receptor, not phosphorylates. There is an increase in the 110 kDa AR isoform and a decrease in the 112 kDa AR isoform. The latter is the phosphorylated isoform.

    Specifically, it was with the phosphorylation of serines 641 and 653 that Forskolin interfered.

    When the dephosphorylated AR was analyzed in terms of its transcriptional activity, it was observed that the regulation of two genes: PSA and the beta 1-subunit of Na,K-ATPase was inhibited relative to control.

    They also claim that the 110kDa AR had only 40% of the maximum ligand binding of the 112kDa phosphorylated AR. I suppose that means that its ligands (androgens) did not bind as effectively to the dephosphorylated AR, thus limiting the amount of gene transcription that androgens could cause relative to interaction with the 112kDa isoform.

    Now, that all looks quite troubling, except that the AR has a half life of only a few hours. So, if you take Forskolin, it seems consistent with what we know that the AR that your cells synthesize within a few hours of peak serum levels will be the 110kDa isoform, but that doesn't mean that the next AR that is synthesized will not be the 112kDa isoform.

    Increased cAMP also turns on genes associated with ramping up steroid hormone production, so the net outcome is ... who knows

    That's why we need people to actually try it and report back. You will never be able to figure out the net effect on paper alone.

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