@alfredoolivas something that could help is HUGE amounts of milk, or something else with a lot of bulk and liquid

@wester130 This is great news. Do you know what vehicle they're using?

Still coughing Over the night my tube fills up with mucus so I start to cough because of that then once that clears out I have a more dry type of cough I think. Either way it usually turns into a fit and it takes me some time to calm down and stop. Will try sodium bicarb rn.

@engineer I have been doing that with great results.

@sunsunsun The Japanese had found increased susceptibility to severe fungi infetion and mortality thereof in liver injuries. Additional transferrin negated the extra mortality from liver injury in rodent studies. I.e., liver injuries lead to less transferrin (and UIBC (unbound iron binding capacity) and TIBC (total iron binding capacity) and it is that decrease of transferrin which enhances fungal infections. https://pubmed.ncbi.nlm.nih.gov/2960898/ https://pubmed.ncbi.nlm.nih.gov/2975353/ Copper (and retinol) are therefore very essential in prevention of fungal infections. Not sure about any treatment efficacy after infection has already occured, though. Surely more free iron will stimulate fungal growth - but does iron restriction assist when aiming for fungal eradication from tissues? I have been trying to raise my ceruloplasmin (and thus functional transferrin) by regular copper intake since late last year. Also, in this paper from 2000 a strong clinical distinction was suggested between acute disseminated candidiasis and chronic disseminated candididiasis: Again, in CDC, there's typically no candidemia and whereas ADC involves several organ system, CDC predominantly befalls the spleen and liver. Typical findings are hepatosplenomegaly, and focal hepatic lesions by ultrasound imaging and recurrent fevers although I reckon the presentation of the latter two will be subject to the mentioned individual immunological response and existence of an even more latent phenotype of CDC (as abundantly shown in other publications in this thread). Interestingly, cultures and histophathology of liver biopsies again frequently failed to detect fungi proven to be present by clinical signs and PCR of liver biopsies (no positive fungi PCR in healthy control group). In this 1992 publication intrabiliary Amphotericin B was successfully used in a child after (typical) failure of priorly administred systemic AmB to clear the biliary infection. Good for her. Yet only downstream of the hepatic tumor she had been hospitalized for.

Talk with AI (Claude) How efficient is the intake of a MK4 supplement, (with enough fat, hereby 25 g fat with some MUFAs), when taking 1 mg (1 000 mcg) K2 MK4? Question of vehicle only? No intermediate change into menadione, I suppose, since there is no digest process. Need a confirmation, whenever there is a target amount limited to 2-3 mg K2 supplement. Note: 2 takes of 1 mg MK4 at breakfast and midday meal, with 1 000 UI D3 (both at the same time, AKA 2 x 1 000 UI D3). Brain target. AI says (Claude): Summary: A moderate amount of D3 and K2 are co-absorbed in the same chylomicron pathway; so simultaneous intake is fine. Brain target and dose adequacy: 2 mg/day total is a reasonable range for a brain-focused protocol. Step 1 — Chylomicrons (intestinal phase, 0–4h postprandial) Step 2 — Chylomicron remnants → liver (4–6h) Step 3 — VLDL → IDL → LDL (hepatic re-export, hours to days) A possible route for extra-hepatic tissue supply is that part of the K-vitamins are re-packed into LDL, which forms a major transport system from the liver to peripheral tissues. ScienceDirect This is the key insight for your brain target — the liver processes the chylomicron-delivered MK4 and re-exports it via VLDL, which is then progressively remodeled into IDL and LDL for peripheral tissue delivery. Agarose gel electrophoresis of lipoprotein fractions after K2 supplementation revealed distinct chylomicron bands and variations in VLDL and HDL mobility, influenced by dietary lipids and VK2 supplementation. Wiley Online Library

COX-2 is overexpressed in advanced stages of tumors. Aspirin starts inhibiting COX-2 meaningfully after dosages of about 500mg (better would be >1g). Aspirin vindicated as an anti cancer drug. "Most solid tumors express the cyclooxygenase-2 (COX-2) protein, a target of NSAIDs. COX-2 overexpression in tumorsis considered a predictor of more advanced stage disease and of worse prognosis in a number of studies investigating solid malignancies. Therefore, NSAIDs are evaluated as anti-cancer drugs." Artificially overexpressing COX-2 makes mice more prone to developing tumors and knocking it out makes them less likely to develop tumors. "Both COX-1 and COX-2 are involved in tumor vascularization. COX inhibitors can directly affect angiogenesis [47]. " "Thus, COX-2 may be the cause of progression of estrogen-dependent breast cancer either directly by stimulating tumor cell proliferation, or indirectly by upregulating aromatase activity [60]. " "Part of the rationale for combining NSAIDs with chemotherapy involves circumvention of chemotherapy resistance mechanisms." https://pubmed.ncbi.nlm.nih.gov/16945549/ COX-2 inhibition makes chemotherapy (5-fluorouracil) more effective in vitro. https://pubmed.ncbi.nlm.nih.gov/21163769/

"Platelet COX inhibition was nearly complete already at 37.5 mg aspirin daily, as evidenced by >98% suppression of serum thromboxane B2 ..." https://pubmed.ncbi.nlm.nih.gov/16601836/

@alfredoolivas yeah im aware. Me and my son use this account. We are not on here though mainly the raypeat forum. And the reason i give him t3 is because his ATP production is bad.

skin surface way is capacitive coupling https://pubmed.ncbi.nlm.nih.gov/8200888/ this showed effect i dont have the info on their approach rn. non fusing fractures for 11+ months 6/10 fused vs 0 The non-union healed in six of the ten patients who had been managed actively but in none of the patients who had been managed with the placebo unit. https://www.semanticscholar.org/paper/Capacitively-coupled-electrical-stimulation-results-Abeed-Naseer/bc78f0db97ce86d9fc64d5487b91cee839744c8d 11 of non unions unified by 15 weeks applied through steel plates on the skin - healed if the plates were within 8cm of each other The only significant factor determining the success of healing was the distance between the plates; a distance of eighty millimeters or less resulted in healing in all cases https://pubmed.ncbi.nlm.nih.gov/8458140/ partial limb regeneration https://pmc.ncbi.nlm.nih.gov/articles/PMC4683620/ https://pmc.ncbi.nlm.nih.gov/articles/PMC3495370/

@engineer 5ar Society tweeted about developing new products, and even mentioned Peat and Haidut in a tweet. I wonder if we could convince them to make a transdermal. They're so expensive but I'd be willing to pay for that.

@Ray-Peat-Fanboy no politics allowed in my Christian ray peat forum

@engineer nop sadly not

@CrumblingCookie It also kills bacteria and fungus and parasites (e.g. demodex mites). The vasodilation was never the main use for me. And who cares if it's not the most potent vasodilator? It still produces some vasodilation. That's just a plus. Anti-inflammatory + anti-bacteria/fungus/parasite + vasodilation. No way that's not going to be beneficial to your hair health/growth.

@wester130 correct. I recollect not feeling good injesting the black cumin seed extract in certain therapeutic doses

@user73636 sounded like a gimmick at first but its well studied theres a lot on it, decent amount from japan , another way to get it without a machine is buying some elemental magnesium metal sticks or ribbons (safer to avoid as fine powder tho unless stored right). can add a stick or ribbon chunk to water and it will make hydrogen bubbles (added a small amount of malic acid to speed up getting past the oxide surface and a bit more hydrogen , then rinsing after drinking. i added it without malic and it still bubbled) https://bioenergetic.forum/topic/9291/hydrogen-dissolved-in-drinking-water-or-via-gastric-acid i reckon 200ug hydrogen at once would be good. trying to figure out how much a 10cm 130mg ribbon would give. max water saturation you can get is 1mg - 1.5mg per L but it reacts slow and without a lot of acid it forms a black layer. i read some papers where they dipped it for a short time and it had effect still

Here's a very peaty explanation of CO2 by a german doctor in bamberg. Might be worth a shot for some. https://dr-kersten.com/kann-die-co2-inhalation-den-energiestoffwechsel-normalisieren

https://youtu.be/0vzrJkJ-gQE

@GRay said in mk4 dosing?: isn't only the k1 that effect clotting? K1 and K2MK7 too affect clotting. For Chris Masterjohn, MK7 would even be better. Chris Masterjohn : « The ultimate vitamin K2 resource »). https://chrismasterjohnphd.com/blog/2016/12/09/the-ultimate-vitamin-k2-resource/ Excerpt 1: There is reason to think MK-7 would be better at supporting blood clotting. “MK-7 is not just three times better than K1 at reaching bone; it’s also five times better at supporting blood clotting (Schurgers, 2007). This may be because the greater fat-solubility of MK-7 makes it hold on more tightly to the membranes within liver cells, making it stay active in the liver much longer rather than being released and broken down (Shearer, 2008). The liver is where clotting proteins are made, so more extended activity in the liver would explain why MK-7 could better support blood clotting. If this is correct, other long-chain MKs such as MK-8 and MK-9 probably share this property as well.” Additional comment: The risk of improper clot formation is increased in cases of low vitamin K levels. Vitamin K (VK) does not cause or dissolve blood clots. However, VK enhances the function of both these systems. VK1 can therefore be seen as a facilitator: Procoagulant factors are VK-dependent. Remind that platelet formation requires 10-12 days after taking aspirin, whatever the dose is (baby or adult caps).

@gg12 increased adrenaline compensates for lower thyroid function. Increased adrenaline always made me want to make a million plans