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    aspirin and kidney function

    Scheduled Pinned Locked Moved Bioenergetics Discussion
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    • M Offline
      mag me
      last edited by

      @LucH said:

      Andiroba Oil

      Is a Highly polyunsaturated fat

      sunsunsunS LucHL 2 Replies Last reply Reply Quote 1
      • sunsunsunS Offline
        sunsunsun @mag me
        last edited by

        i think bpc157 might reduce aspirin’s effect on platelets

        C LucHL 2 Replies Last reply Reply Quote 0
        • C Offline
          CrumblingCookie @sunsunsun
          last edited by

          @sunsunsun The sartans losartan and olmesartan are protective for kidney tissues and functions even though they may make routine serological kidney markers fall even lower (it's a known phenomenon). Don't do the other sartans.

          1 Reply Last reply Reply Quote 1
          • LucHL Offline
            LucH @mag me
            last edited by LucH

            @mag-me said:

            Andiroba Oil

            Is a Highly polyunsaturated fat

            Are you serious 😉 No need to answer ...
            Short answer: Mainly oleic acid. 1 /100 of a gram for LA. A very, very tiny amount...
            NB: Andiroba is used as part of a mixture.

            Detailed answer: Andiroba oil combo
            Andiroba oil is an excellent, quick-penetrating carrier oil for massages known for its potent anti-inflammatory and analgesic properties. It relieves muscle aches, soothes joint discomfort, and deeply moisturizes dry skin. [1, 2, 3, 4, 5]
            Andiroba oil (Carapa guianensis) is mainly oleic acid (52%), while LA is 11 %. (3)
            As there is 20-24 drops in one ml, we could say 4 drops andiroba brings 0.0352 g PUFA. Not even 0.04 g linoleic acid!

            Detailed calculation (you can bypass):
            An average drop size of 0.02 ml
            0.32 g×11%=0.0352 g.

            You’re looking at less than 4/100ths of a gram of PUFA. That is a minuscule amount.
            Dismissing Andiroba oil for arthritis because of a tiny 11% fraction of PUFA completely misses the forest for the trees.
            Topical vs. Dietary: The "anti-PUFA" argument is heavily centered on dietary ingestion. When applied topically for arthritis, the oil isn't being metabolized by your liver in the same way; it is acting locally on the skin and joint tissue.
            The Active Anti-Inflammatory Compounds: The reason Andiroba oil is highly effective in arthritis mixes isn't even about its basic fatty acid profile. It contains potent non-fatty bioactive compounds called limonoids (specifically andirobin and gedunin). Studies show these specific compounds actively inhibit inflammatory biomarkers and provide the pain-relieving, anti-rheumatic benefits the oil is famous for.

            References

            1. Fatty Acid Amides Synthesized from Andiroba Oil (Carapa guianensis Aublet.) Exhibit Anticonvulsant Action with Modulation on GABA-A Receptor in Mice:
              doi: 10.3390/ph13030043 Pharmaceuticals (Basel). 2020 March.
              =>endocannabinoid effects in short.
            2. Traditional use in treating inflammation, joint pain, insect bites, and other skin conditions. (7,8) This oil is rich in a variety of bioactive compounds, such as limonoids, triterpenes, and unsaturated fatty acids, mostly in oleic acid.
              February 4, 2026. ACS Omega.
              => In short a local NO effect (anti-inflammatory activity)
            3. Andiroba oil (Carapa guianensis): Descriptive analysis and applicability
              10.1016/j.indcrop.2023.117004
              https://www.sciencedirect.com/science/article/abs/pii/S0926669023007690
              The major cations were Ca, K, and Na. Oleic acid was the major fatty acid in the lipid fraction.
              The chemical constitution of the seeds and oil of species of the genus Carapa contains saponifiable compounds, such as oleic acid (± 52 %), palmitic acid (± 28 %), stearic acid (± 10 %), and linoleic acid (± 11 %), and unsaponifiable compounds, such as steroids, triterpene, and mainly tetranortriterpenes or limonoids (2–5 %), which are chemotaxonomic markers of the Meliaceae family (AMBROZIN et al., 2006, MARTINBOROUGH, 2003).
            1 Reply Last reply Reply Quote 0
            • LucHL Offline
              LucH @sunsunsun
              last edited by LucH

              @sunsunsun said:

              i think bpc157 might reduce aspirin’s effect on platelets

              Short answer:
              I won't say it so. BPC-157 as a preventive way. But the factory is still locked for new platelets.
              Here is a detailed explanation, after a search on internet to try to understand in details how it functions.

              BPC 157 peptide used as healing against aspirin effects on Cox-1
              The Aspirin vs. COX-1 Problem
              COX-1 is responsible for producing cytoprotective prostaglandins (PGE₂) in the stomach wall.
              Aspirin blocks Cox-1 and 2.
              How BPC-157 Heals Without Changing COX-1
              BPC-157 upregulates Vascular Endothelial Growth Factor (VEGF) and the egr-1 gene. [1]

              • It bypasses standard vascular collapse by initiating rapid blood vessel growth (angiogenesis).
              • It triggers "vessel recruitment," dynamically bypassing occluded or damaged microvessels to route oxygenated blood directly to the damaged gastric lining. [1, 2, 3]
                In Short: BPC-157 stabilizes and stimulates healing of damage linens.
                Now let's focus strictly on the platelet kinetics.
                Regeneration is impeached and new platelets do not emerge fully functional while aspirin is continuously present.
                Part 1: The Aspirin Problem (The Broken Tools)
                Think of platelets as a fleet of tiny construction trucks floating in your blood. Their only job is to rush to a leak (a cut or a wound), stick together, and form a patch to stop the bleeding.
                When you take aspirin, the blood cells aren’t allowed to stick together, your blood gets "thin," and you bleed for a longer time if you get a cut.
                -The Reality: Aspirin only blocks one specific pathway (Thromboxane A₂).
                -The Result: The platelet is handicapped, not broken. It can still stick to a damaged blood vessel wall using other pathways (like collagen and ADP), but it loses its ability to rapidly recruit other platelets to build a massive, stable plug quickly.
                The Regeneration Lock: Short & Direct
                As long as aspirin is taken daily, regeneration is completely locked because the factory floor is poisoned.

              New platelets cannot be born healthy on a broken field.
              Where BPC-157 Actually Fits
              Since the factory is locked and platelets are handicapped, BPC-157 acts purely as an external workaround. It doesn't unlock the factory or fix the platelet pathways. It changes the chemistry of the blood vessel wall itself to compensate for the handicap.

              Additional comment
              Still to be re-said: BPC-157 helps to dampen side-effects when taken previously. Platelet formation is still on an underperformed way. Not totally prevented (nothing to do with BPC). Mind in case of a virus like covid-19.

              Comment asked to AI (Google) :
              Exactly. Let's lock down those final critical details, especially regarding a viral scenario like COVID-19.
              1. BPC-157 Dampens the Blow (If Taken Beforehand)
              Pre-treating with BPC-157 helps cushion the body against the damage aspirin causes. It functions as a protective shield, allowing the stomach lining and blood vessel walls to withstand the drug's harsh side effects before the injuries can even take root.
              2. Platelet Formation Remains Impaired
              You are completely spot on—BPC-157 has zero control over platelet manufacturing.
              • As long as aspirin is in the system, new platelet formation remains strictly underperforming and handicapped.
              • BPC-157 cannot override this factory lock. The newly released platelets will continue to emerge from the marrow with their internal pathways pre-blocked. [1]
              3. The Wildcard: Enter a Virus Like COVID-19
              This is where the combination of daily aspirin, a locked platelet factory, and BPC-157 becomes highly unpredictable—and potentially dangerous. To fight the virus, the body shifts into a state of hyper-coagulation, forcefully triggering massive clotting and thrombosis inside microvessels.

              The Angiogenesis/VEGF Risk: BPC-157 forces blood vessel growth (angiogenesis) and heavily activates Nitric Oxide (eNOS) pathways. During the peak of a "cytokine storm" or severe viral lung inflammation, forcing rapid vascular changes can sometimes worsen vascular permeability—meaning blood vessels leak fluid into surrounding tissues more easily.

              sunsunsunS 1 Reply Last reply Reply Quote 0
              • B Offline
                bio3nergetic
                last edited by

                The answer to this is same as in most cases and as I always say: bullshit studies.

                In a euvolemic or hydrated state, renal blood flow is maintained by multiple redundant vasodilatory pathways. Prostaglandins are present but not critical; inhibiting them with aspirin has negligible hemodynamic impact.

                In a hypovolemic or dehydrated state, the kidney loses all redundant vasodilatory capacity and becomes 100% dependent on prostaglandins to keep the afferent arteriole open. Here, aspirin removes the only remaining mechanism for blood flow, causing immediate vasoconstriction and ischemia.

                The primary flaw here is, essentially ALL these studies have this confounder. And the other subsequent flaw - most likely also intentional mind you - is they put out in the public eye an average of these two distinct physiological states. So they can report a "small average risk" which obscures the binary reality: zero risk in hydration vs. high risk in depletion.

                Aspirin is not inherently nephrotoxic in a metabolically competent, hydrated host. The "detrimental" label is largely an artifact of studying compromised systems: dehydrated, elderly, poly-medicated, and then of course projecting those risks onto the general population.

                sunsunsunS 1 Reply Last reply Reply Quote 1
                • sunsunsunS Offline
                  sunsunsun @LucH
                  last edited by sunsunsun

                  @LucH bpc157 has study on it where it lowers aspirin effect on platelets. i think i saw something about the NOS effect and how it actually regulates it instead of just boosting the presumably bad side of it.

                  LucHL 1 Reply Last reply Reply Quote 0
                  • sunsunsunS Offline
                    sunsunsun @bio3nergetic
                    last edited by sunsunsun

                    @bio3nergetic nice explanation . the messaging on aspirin is like this. i see vets warn against it and people repeat it but i found a study showing 50mg/kg 2x a day (so 100mg/kg total, some subjects even went higher to 89mg/kg 2x a day) showed no noticeable negative GI effect as long as the aspirin was crystal form and mixed with food. Even the merck manual says it’s reasonably ok at 25mg/kg but vets always warn against it and reccomend other NSAIDs.

                    the results in study showed that every single dog went from really bad arthritis / pain issues to good or very good with no side effects in the 9 months of the study

                    given with glycine/gelatin and putting baking soda in drinking water (both glycine and bicarbonates are required for processing aspirin) and with bpc157 (anti arthritic/anti pain and gut protective) i think its probably the best oral nsaid treatment for arthritis

                    interestingly the study says slow release aspirin is worse in dogs for promoting gastric ulcers. plain old powder aspirin is the best

                    B 1 Reply Last reply Reply Quote 1
                    • LucHL Offline
                      LucH @sunsunsun
                      last edited by

                      @sunsunsun said:

                      bpc157 has study on it where it lowers aspirin effect on platelets. i think i saw something about the NOS effect

                      Yes, you're right. There is protection but the brake is still there. The lifespan of blood platelets is limited. Their renewal is impaired.

                      1 Reply Last reply Reply Quote 0
                      • B Offline
                        bio3nergetic @sunsunsun
                        last edited by

                        @sunsunsun Usually slow release has a reason it is "slow release;" a chemical reason. That is most likely what is causing disturbances in pup's guts. When used properly, with the right cofactors, which you aptly listed, aspirin is fantastic. Hence, why they paint it in a bad light! This isn't new however.

                        During the first fake pandemic: start of industrializing-rothchildism take-overs-celebrating birth of hypodermic needle-polluting of true medical texts, etc, namely the so-called "spanish flu," which was actually and also vaccine injuries of that time, they totally demonized aspirin. Later as publications were discovered supporting anti-aspirin sentiment, they noticed that upwards of 30 grams!!! of aspirin was used in those studies!

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