HumbleMTNN
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Exposing corticosteroids, (hydrocortisone, betamethasone, clobetasol, etc.)
High effort post
It's over for corticosteroid copers
some of you wont like to hear this but it has to be said. stop using corticosteroids thinking they are some advanced tool for nose shrinkage or skin thinning
after i acquired some betamethasone i stole from my grandparents medicine cabinet for nose shrinkage and did more research into them i discovered how shit and overrated they are and that is why im making this post
corticosteroids as a whole (hydrocortisone, betamethasone, clobetasol, mometasone, triamcinolone and the rest of the class) all share the same core mechanisms. they are lipophilic molecules that cross the cell membrane and bind the intracellular glucocorticoid receptor. the ligand-receptor complex translocates to the nucleus where it acts primarily through transrepression: it interferes with the activity of pro-inflammatory transcription factors such as NF-κB and AP-1, reducing transcription of cytokines (IL-1, IL-6, TNF-α, IL-8), chemokines, and adhesion molecules. this produces the anti-inflammatory and anti-edema effect people notice as reduced redness and soft-tissue volume. at the same time the complex can transactivate genes that upregulate anti-inflammatory proteins like annexin A1 and IκBα, further damping the local inflammation
the vasoconstriction that contributes to the temporary “smaller” or smoother look is mediated by inhibition of endothelial nitric oxide synthase and reduced prostaglandin and leukotriene synthesis, plus direct effects on vascular smooth muscle responsiveness. these effects are only temporary while you are using the steroids. the moment tissue levels drop, nitric oxide and vasodilatory mediators rebound and the vessels dilate again.
the skin thinning that looksmax users chase is also strictly pharmacologic and reversible in principle but often damaging in practice. glucocorticoids suppress keratinocyte proliferation by inhibiting cyclin D1 and other cell-cycle drivers, leading to epidermal atrophy. in the dermis they inhibit fibroblast proliferation and collagen synthesis by down-regulating TGF-β signaling and type I and III collagen gene expression while simultaneously increasing matrix metalloproteinase activity. glycosaminoglycan and hyaluronic acid production falls, reducing dermal ground substance and turgor. sebaceous and sweat gland activity is also suppressed. all of these changes require continuous receptor occupancy. these effects are only temporary while you are using the steroids. once receptor stimulation ceases, the suppressed pathways attempt to restart, but the barrier has usually been compromised (reduced ceramides, free fatty acids, and cholesterol in the stratum corneum), so the recovery is disordered.
that disordered recovery is the core of topical steroid withdrawal. after prolonged suppression the local hypothalamic-pituitary-adrenal-like feedback is altered, tachyphylaxis develops, and sudden withdrawal produces a rebound surge in cytokines, substance P, and other mediators. clinically this presents as intense erythema, burning, stinging, scaling, and sometimes oozing or papulopustular eruptions that can last weeks to many months. barrier failure amplifies transepidermal water loss and allows further irritation, creating a self-perpetuating cycle. higher-potency agents simply occupy more receptors more completely and therefore produce deeper suppression and more violent rebound, but the mechanism is identical across the class.
compare that to tretinoin and isotretinoin. tretinoin binds retinoic acid receptors (primarily RAR-γ in epidermis), directly modulating transcription of genes involved in keratinocyte differentiation, epidermal hyperplasia followed by normalization of thickness, and upregulation of collagen I and III via TGF-β and AP-1 pathways. it also increases hyaluronic acid and improves barrier lipid organization over time. the structural improvements accumulate and persist because they are anabolic and remodeling rather than purely catabolic and suppressive. isotretinoin induces sebocyte apoptosis through RAR/RXR and FOXO1 pathways, permanently reduces sebum output in a large percentage of users, decreases Propionibacterium density, and produces long-term dermal remodeling that does not rely on continuous receptor occupancy to maintain the benefit. when you stop isotretinoin the sebum suppression and collagen changes largely remain; there is no equivalent of the corticosteroid rebound.
the net result is that corticosteroids deliver small, receptor-occupancy-dependent reductions in inflammation, volume, and thickness that vanish as soon as the drug leaves the tissue and frequently leave behind a damaged barrier and withdrawal state. tretinoin and isotretinoin produce slower but mechanistically superior remodeling that does not collapse into TSW when dosing stops. the gap in durability and risk profile is obvious once the receptor biology and matrix effects are examined in detail.
So what have we learned? That's right, corticosteroids are not to be misused for nose shrinkage
High effort post
It's over for corticosteroid copers
some of you wont like to hear this but it has to be said. stop using corticosteroids thinking they are some advanced tool for nose shrinkage or skin thinning
after i acquired some betamethasone i stole from my grandparents medicine cabinet for nose shrinkage
and did more research into them i discovered how shit and overrated they are and that is why im making this postcorticosteroids as a whole (hydrocortisone, betamethasone, clobetasol, mometasone, triamcinolone and the rest of the class) all share the same core mechanisms. they are lipophilic molecules that cross the cell membrane and bind the intracellular glucocorticoid receptor. the ligand-receptor complex translocates to the nucleus where it acts primarily through transrepression: it interferes with the activity of pro-inflammatory transcription factors such as NF-κB and AP-1, reducing transcription of cytokines (IL-1, IL-6, TNF-α, IL-8), chemokines, and adhesion molecules. this produces the anti-inflammatory and anti-edema effect people notice as reduced redness and soft-tissue volume. at the same time the complex can transactivate genes that upregulate anti-inflammatory proteins like annexin A1 and IκBα, further damping the local inflammation
the vasoconstriction that contributes to the temporary “smaller” or smoother look is mediated by inhibition of endothelial nitric oxide synthase and reduced prostaglandin and leukotriene synthesis, plus direct effects on vascular smooth muscle responsiveness. these effects are only temporary while you are using the steroids. the moment tissue levels drop, nitric oxide and vasodilatory mediators rebound and the vessels dilate again.
the skin thinning that looksmax users chase is also strictly pharmacologic and reversible in principle but often damaging in practice. glucocorticoids suppress keratinocyte proliferation by inhibiting cyclin D1 and other cell-cycle drivers, leading to epidermal atrophy. in the dermis they inhibit fibroblast proliferation and collagen synthesis by down-regulating TGF-β signaling and type I and III collagen gene expression while simultaneously increasing matrix metalloproteinase activity. glycosaminoglycan and hyaluronic acid production falls, reducing dermal ground substance and turgor. sebaceous and sweat gland activity is also suppressed. all of these changes require continuous receptor occupancy. these effects are only temporary while you are using the steroids. once receptor stimulation ceases, the suppressed pathways attempt to restart, but the barrier has usually been compromised (reduced ceramides, free fatty acids, and cholesterol in the stratum corneum), so the recovery is disordered.
that disordered recovery is the core of topical steroid withdrawal. after prolonged suppression the local hypothalamic-pituitary-adrenal-like feedback is altered, tachyphylaxis develops, and sudden withdrawal produces a rebound surge in cytokines, substance P, and other mediators. clinically this presents as intense erythema, burning, stinging, scaling, and sometimes oozing or papulopustular eruptions that can last weeks to many months. barrier failure amplifies transepidermal water loss and allows further irritation, creating a self-perpetuating cycle. higher-potency agents simply occupy more receptors more completely and therefore produce deeper suppression and more violent rebound, but the mechanism is identical across the class.
compare that to tretinoin and isotretinoin. tretinoin binds retinoic acid receptors (primarily RAR-γ in epidermis), directly modulating transcription of genes involved in keratinocyte differentiation, epidermal hyperplasia followed by normalization of thickness, and upregulation of collagen I and III via TGF-β and AP-1 pathways. it also increases hyaluronic acid and improves barrier lipid organization over time. the structural improvements accumulate and persist because they are anabolic and remodeling rather than purely catabolic and suppressive. isotretinoin induces sebocyte apoptosis through RAR/RXR and FOXO1 pathways, permanently reduces sebum output in a large percentage of users, decreases Propionibacterium density, and produces long-term dermal remodeling that does not rely on continuous receptor occupancy to maintain the benefit. when you stop isotretinoin the sebum suppression and collagen changes largely remain; there is no equivalent of the corticosteroid rebound.
the net result is that corticosteroids deliver small, receptor-occupancy-dependent reductions in inflammation, volume, and thickness that vanish as soon as the drug leaves the tissue and frequently leave behind a damaged barrier and withdrawal state. tretinoin and isotretinoin produce slower but mechanistically superior remodeling that does not collapse into TSW when dosing stops. the gap in durability and risk profile is obvious once the receptor biology and matrix effects are examined in detail.
So what have we learned? That's right, corticosteroids are not to be misused for nose shrinkage
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usually people use things like hydrocortisone which is a bit lighter strength but you can still get unlucky so don’t just assume you’re all good
