Alright, I have the ingredients for the recipe and will begin mixing it up soon, with tests on the back of my hands and sun-damaged neck.
If I am an outlier, there are a LOT of us. Use of retin-A skin treatments may explain why more women than men have autoimmune conditions like Lupus and Fibromayalgia.
Does the skin really act as a barrier to prevent the absorption of vitamin A? It all eventually breaks down to retinoic acid and goes to the liver to be detoxed. When the liver canât handle any more, it is wrapped in Retinal Binding Protein, made by fat cells, to prevent it from coming into contact with and burning tissues. More fat may be necessary to handle the overload, which may contribute to obesity.
Look at the insert (iPLEDGE REMS) that comes with prescriptions for the acne medication, Accutane, to read about the serious side effects of the drug (Accutane is really just pure retinoic acid, the end metabolite of vitamin A). They are like those of Thalidomide, the drug for morning sickness that caused babies to be born with multiple abnormalities, including missing limbs. The Accutane brochure carries this warning: âThere is an extremely high risk that severe birth defects will result if pregnancy occurs while taking isotretinoin in any amount, even for a short period of time.â You must sign 2 legal documents to acknowledge that you are aware of the danger before you can even buy it.
Please cite any studies that show any studies that show what you say is true.
A systematic review says the side effects are minimal.
Topical tretinoin for treating photoaging: A systematic review of randomized controlled trials
I highly doubt thatâs true. We already know that one reason women are more prone to autoimmune diseases than men is because they tend to have a stronger and more aggressive immune system.
As far as the accutane risks such as severe birth defects. Thatâs because accutane is taken orally. Thatâs very different from applying vitamin A derivatives to your skin.
Just curious, why not just use topical tacromilus gel or better yet, Pimecrolimus Topical, which does not have as many sides instead of creating a topical sirolimus? These meds cannot be used on a regular basis, but maybe used intermiitently just as we use the oral rapamycin.
Hyftor which is sirolimus topical gel 2% is another option, if one can find a way to get a script for it. I would only use this once weekly as with oral rapa.
Tacrolimus and Pimecrolimus are calcineurin inhibitors. Sirolimus/Rapamycin is an mTOR inhibitor. Despite having similar sounding names, they are quite different and have different effects, ie you cannot substitute Tacrolimus/Pimecrolimus for Sirolimus/Rapamycin.
Tac also inhibits mTOR Inhibition of the mTOR pathway: A new mechanism of β cell toxicity induced by tacrolimus - PubMed
Yes - but I donât think it inhibits mTOR nearly much as the rapamycin and the rapalogs like everolimus and temsirolimus. Iâm not sure of the exact comparison, but if you want to inhibit mTOR you probably want the main mTOR inhibitors:
Thanks for pointing this out. Will look into it.
The only reason to use it would be because it is available as a topical. Hyftor is the only sirolimus topical that I am aware of, and it seems like the logical choice. Hyftor appears on Indiamart by various sellers, but not on Oddwayâs portal.
How is the topical senolytics experiment going?
I have all the compounds⌠just have been busy with kids starting school, etc.
Iâll start it soon and will report progress, take photos, etc.
Topical ABT-263 (navitoclax) treatment reduces aged skin senescence and improves subsequent wound healing
Senescent cells (SnC) accumulate in aging tissues, impairing their ability to undergo repair and regeneration following injury. Previous research has demonstrated that targeting tissue senescence with senolytics can enhance tissue regeneration and repair by selectively eliminating SnCs in specific aged tissues. In this study, we focused on eliminating SnC skin cells in aged mice to assess the effects on subsequent wound healing. We applied ABT-263 directly to the skin of 24-month-old mice over a 5-day period. Following topical ABT-263, aged skin demonstrated decreased gene expression of senescent markers p16 and p21, accompanied by reductions in SA-β-gal and p21-positive cells compared to DMSO controls. However, ABT-263 also triggered a temporary inflammatory response and macrophage infiltration in the skin. Bulk RNA sequencing of ABT-263-treated skin revealed prompt upregulation of genes associated with wound healing pathways, including hemostasis, inflammation, cell proliferation, angiogenesis, collagen synthesis, and extracellular matrix organization. Aged mice skin pre-treated with topical ABT-263 exhibited accelerated wound closure. In conclusion, topical ABT-263 effectively reduced several senescence markers in aged skin, thereby priming the skin for improved subsequent wound healing. This enhancement may be attributed to ABT-263-induced senolysis which in turn stimulates the expression of genes involved in extracellular matrix remodeling and wound repair pathways.