Learner1
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I took LL-37 along with thymosin alpha 1. Didn't feel any different at all with the LL37 so stopped it.
What were your dosages of Mors-c btw ? @Learner1I used MOTS-C for a couple of weeks. It was fine the first week, but I got increasingly tired on it, I believe because it stops folate from working, which is not a good idea.
I mixed today IV IgG with TB500. But would not mix with TA. Maybe tomorrow, or in a few days. If I will find a difference, will let you knowIm wondering that too. I did 250mcg a day for 1 and a half month or so. I dont know if I noticed anything or not. I didnt get any allergic reactions from birch pollen. That was interesting, though they said it was very little birch pollen where I live also. Im def going to try Ta1 longterm. I think they fused the ta1 in a study with immunoglobulin and made the half life increase to almost 20 hours or something. wonder if it does the same if I take Gammanorm and ta1 at the same time, and the same spot. Probably not? Or mix them.. Maybe thats not safe. or Maybe it is... Ta1 is super interesting and I think the ideal scenario is to use it longterm to see effects.
Edit: its called Thymosin alpha 1-Fc and here is the source https://www.nature.com/articles/s41598-018-30956-y
Among the strategies of extending serum half-life in the body, adding an immunoglobin G (IgG) Fc fragment is one of the most effective technologies. Result shows that the serum half-life of Tα1-Fc was 24.58 h, which is almost 13 times longer than of Tα1
Thank you for sharing a results. My IgM also grew a bit with TB and TA.I got my bloodwork in from the rHGH - its "immune" effects should be similar to those of Thymosin Alpha-1 as it helps to maintain the thymus gland.
rHGH started in April. First blood was taken about 10 days after starting rHGH every other day 8iu
My results:
2019 baseline
2020 April 10 days after starting rHGH 8iu eod
2020 July 3 months after starting rHGH 8iu eod and having increased to 15iu eod 20 days before.
2019 May: B-cells 213 Cells/per yl
2020 April: B-cells 238 Cells/per yl
2020 July: B-cells 520 Cells/per yl
2019 May: T-cells 1626 Cells/per yl
2019 May: T-helper cells 929 Cells/per yl
2020 April: T-cells 1682 Cells/per yl
2020 July: T-cells 2547 Cells/per yl
2020 July: T-helper cells 1534 Cells/per yl
I have mito issues and see two doctors who prescribe peptides, but nobody has recommended it.Has anyone heard of 5-Amino 1MQ? Supposedly good for mitos and can be taken in oral form...
I got my bloodwork in from the rHGH - its "immune" effects should be similar to those of Thymosin Alpha-1 as it helps to maintain the thymus gland.
rHGH started in April. First blood was taken about 10 days after starting rHGH every other day 8iu
My results:
2019 baseline
2020 April 10 days after starting rHGH 8iu eod
2020 July 3 months after starting rHGH 8iu eod and having increased to 15iu eod 20 days before.
2019 May: B-cells 213 Cells/per yl
2020 April: B-cells 238 Cells/per yl
2020 July: B-cells 520 Cells/per yl
2019 May: T-cells 1626 Cells/per yl
2019 May: T-helper cells 929 Cells/per yl
2020 April: T-cells 1682 Cells/per yl
2020 July: T-cells 2547 Cells/per yl
2020 July: T-helper cells 1534 Cells/per yl
I will probably first start with adding TB-500 and LL-37 to my existing BPC-157 stack to try and heal my gut issues.
For those taking BPC157 to cure gut problems, I found some info in the two links below that may help provide better results. Apparently, oral dosing of BPC157 is suggested to heal the gut. Also, there are now different versions of BPC157 and some versions are more stable than others in passing through the stomach. The most common version of BPC157 is acetate-BPC157, while the most stable form is arginine-BPC157. See the two links below for more info (reddit's /r/peptides is very good resource):10 days in with TB-500 500mcg daily and still using BPC-157 500mcg since May.
But no real success with BPC-157 alone. Maybe things will change with TA-1 and TB-500 in the mix now.
This product:@Learner1 which brand of resveretrol and what symptoms did it improve please?
This product:
https://www.zhounutrition.com/collections/all-products/products/resveratrol?utm_medium=ppc&utm_source=google&utm_campaign=1041851993&utm_term=zhou resveratrol&e&gclid=Cj0KCQjwpNr4BRDYARIsAADIx9xdcIKwYQFHAocjmsf_W80xcgdQsbaA_tRfzpzmTHpNk2B2u40ZhRAaAieMEALw_wcB
I don't take most supplements for immediate symptom relief. It's what they do over time.
This describes the benefits of resveratrol:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2546476/
David Sinclair advises taking it with fat and NMN, which is what I do. The NMN does have an immediate effect. The metformin is not wise - it impairs complex I, which is typically impaired in ME/CFS patients.
https://fastlifehacks.com/david-sinclair-supplements/
One of the most fascinating resveratrol aspects for its future development as a promising drug is that, it does not appear to have debilitating or toxic side effects. A wide range of resveratrol doses has been used in various in vivo and in vitro studies. However, it is imperative to find out the most appropriate dose and administration route. Also, it was documented that resveratrol induces cell death in tumor tissues with relatively no effect in normal adjacent tissues [
52]. Resveratrol cell uptake disparity between normal and tumor cells may be attributed to differences in available cellular targets and gene expression in cancer cells, which makes resveratrol tumor-specific. Mukherjee et al. [139] have suggested that lower resveratrol doses could be associated with health benefits, while higher doses devastate tumor cells via pro-apoptotic effects.
Resveratrol does not appear to have side effects at short-term doses (1.0 g). Otherwise, at doses of 2.5 g or more per day, side effects may occurs, like nausea, vomiting, diarrhea and liver dysfunction in patients with non-alcoholic fatty liver disease [140]. Interestingly, no major side effects were stated in long-term clinical trials [141]. In fact, resveratrol has been found to be safe and well-tolerated at up to 5 g/day, either as a single dose or as fraction of multiple-day dosing schedule [142]. However, it is imperative to mention that these studies were done in healthy populations, and that may vary in sick patients. Our understanding of resveratrol dose-dependency and administration route is further complicated, since orally administrated resveratrol gets metabolized by gut microbiota [143], which makes it difficult to determine which effects are solely due to resveratrol or both resveratrol and its metabolites.
To investigate the assumption, whether resveratrol inhibit atherosclerotic development in hypercholesterolemic rabbits, Wilson et al. [144] supplemented rabbits with or without oral resveratrol (1mg/kg), and found that resveratrol treatment did not adversely affect rabbits health other than promoting atherosclerosis. Plasma LDL electrophoretic mobility was not different between groups. Atherosclerotic lesions staining in control and resveratrol-treated groups revealed that resveratrol-treated rabbits had significantly more aortic surface area covered by atherosclerotic lesions. Therefore, resveratrol promoted atherosclerotic development, rather than protect against it, by an independent mechanism of differences observed in gross animal health, liver function, plasma cholesterol concentrations, or LDL oxidative status [144]. Ferry-Dumazet et al. [145] aiming to analyze resveratrol nephrotoxicity effects, given orally 3000 mg/kg b.w. to rats for 28 days. It resulted in nephrotoxicity documented as elevated serum blood urea nitrogen and creatinine levels, increased kidney weights, gross renal pathology changes, and an increased incidence and severity of histopathological changes in kidneys. Kidneys microscopic evaluation identified lesions whose pathogenesis could be increased by resveratrol concentration (or its metabolite) as a function of renal osmotic concentration gradients, resulting in toxic levels in renal pelvis. This would result in necrosis, renal tubules obstruction and thus tubules dilation behind obstructed region. Indeed, inflammation and pelvic epithelium hyperplasia are expected responses to the presence of necrotic tissues. Therefore, administration of 1000 or 300 mg resveratrol/kg b.w./day did not result in nephrotoxic findings. The predominant clinical signs of toxicity at 3000 mg/kg b.w./day dose group were dehydration, piloerection, and red material in cage/urine, body weight gain reduction, hyperalbuminemia, anemia (due to renal injury, which reduced erythropoietin synthesis), white blood cell counts increase due to renal pelvic inflammation. Moreover, increased ALT, ALKP and total bilirubin levels suggest liver toxicity, but this was not histologically supported. Similarly, organs evidencing weight change did not evidenced histological changes [146].
Resveratrol has been reported to both reduce cell growth and induce apoptosis in normal cells, when administered at high doses, which confirm its biphasic effects over low to high concentrations spectrum [145]. Resveratrol rapidly activate mitogen-activated protein kinase (MAPK) in a MEK-1, Src, matrix metalloproteinase, and epidermal growth factor receptor in a dependent manner. It activates MAPK and endothelial nitric-oxide synthase (eNOS) at nanomolar concentrations (i.e., magnitude less than that required for ER genomic activity) and at concentrations possibly/transiently achieved in serum following oral red wine consumption [147]. Additionally, resveratrol consumption at modest doses result in a life span increase in 1-year old mice. However, when mice consumed larger resveratrol doses (1800 mg/kg), animals were shown to die within 3–4 months [148]. Studies on steady-state pharmacokinetics and tolerability of 2000 mg trans-resveratrol, administered twice daily with food, quercetin and alcohol (ethanol) showed that trans-resveratrol was well-tolerated by healthy subjects, although diarrhea was frequently observed [149].
Very true... good clues for you to investigate.is imperative to mention that these studies were done in healthy populations, and that may vary in sick patients. Our understanding of resveratrol dose-dependency and administration route is further complicated, since orally administrated resveratrol gets metabolized by gut microbiota
I heard this too. I had read that you could reconstitute the TA-1, then fill up all your syringes and put them in the freezer. Just take one out and thaw when you need to inject. It's supposed to degrade slower when frozen, so that's what I did.Does anyone know the storage life of TA1 once reconstituted? I need to go back and look but I thought I saw some lit that said it degrades rather quickly and a vial needed to be used within a few days from reconstitution.
Has anyone tried higher doses for short durations?
Zadaxin is actually a different "compound" in the sense that it is Thymosin-a1, attached to a very long PEG chain. That keeps it much longer in the blood, which makes it much more potent and not requiring as frequent doses.