How much does finasteride reduce dht in scalp/ follicle and serum?
Finasteride reduces TGF beta expression in the scalp by 30%, could this be the hidden reason why finisteride works
Genes Regulating Inflammation, Stress, And Fibrosis Were Massively Overexpressed In All Androgenetic Alopecia Groups
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How much does finasteride reduce dht in scalp/ follicle and serum?
Finasteride reduces TGF beta expression in the scalp by 30%, could this be the hidden reason why finisteride works
The inflammation is pushing it. 1 inflammation 2 dht as an anti inflammatory but the hair susceptible genetically to miniaturising when dht is present.
I say stop the inflammation as best as you can through diet and environmental factors, then actually get some tests done to check c reactive protein,fasting insulin,Hemoglobin A1C (HbA1c),serum ferritin and red blood cell with.
I’m sure everyone is different in what causes inflammation
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Genetic analysis of large European male population had revealed AR gene and hair related genes are main culprits. If inflammation was the case then reaseachers would have found genes related to immune system and antiinflammatory like aspirin or ibuprofens would do the job of deadly finasteride. DHT is upstream and it caused inflammation after doing their dirty job.
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One of our TGF-β receptor antagonists is a natural small-molecule organic compound. This antagonist in solution and foam formulations has been shown to promote hair growth in animals and human volunteers. Its efficacy and strength in promoting hair growth and preventing hair loss are much more potent than RogaineR (minoxidil) in animals and human volunteers. It promotes hair growth by suppressing TGF-β in follicles, which plays an important role in initiating and maintaining the catagen phase in the hair growth cycle. The other natural small-molecule TGF-β antagonist (in lotion formulation) is capable of beautifying human skin by stimulating collagen synthesis in skin cells. This has provided superior cosmetic results in many human volunteers. These products represent a novel hair-growth and skin-care agent.
One of our TGF-β receptor antagonists is a natural small-molecule organic compound. This antagonist in solution and foam formulations has been shown to promote hair growth in animals and human volunteers. Its efficacy and strength in promoting hair growth and preventing hair loss are much more potent than RogaineR (minoxidil) in animals and human volunteers. It promotes hair growth by suppressing TGF-β in follicles, which plays an important role in initiating and maintaining the catagen phase in the hair growth cycle. The other natural small-molecule TGF-β antagonist (in lotion formulation) is capable of beautifying human skin by stimulating collagen synthesis in skin cells. This has provided superior cosmetic results in many human volunteers. These products represent a novel hair-growth and skin-care agent.
Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells.
Vignozzi L, et al. J Endocrinol. 2012.
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Abstract
Progression of benign prostatic hyperplasia (BPH) involves chronic inflammation and immune dysregulation. Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether, in humans, hypogonadism was associated with more severe BPH inflammation and the in vitro effect of the selective androgen receptor agonist dihydrotestosterone (DHT) on cultures of stromal cells derived from BPH patients (hBPH). Histological analysis of inflammatory infiltrates in prostatectomy specimens from a cohort of BPH patients and correlation with serum testosterone level was performed. Even after adjusting for confounding factors, hypogonadism was associated with a fivefold increased risk of intraprostatic inflammation, which was also more severe than that observed in eugonadal BPH patients. Triggering hBPH cells by inflammatory stimuli (tumor necrosis factor α, lipopolysaccharide, or CD4(+)T cells) induced abundant secretion of inflammatory/growth factors (interleukin 6 (IL6), IL8, and basic fibroblast growth factor (bFGF)). Co-culture of CD4(+)T cells with hBPH cells induced secretion of Th1 inducer (IL12), Th1-recruiting chemokine (interferon γ inducible protein 10, IP10), and Th2 (IL9)- and Th17 (IL17)-specific cytokines. Pretreatment with DHT inhibited NF-κB activation and suppressed secretion of several inflammatory/growth factors, with the most pronounced effects on IL8, IL6, and bFGF. Reduced inflammatory cytokine production by T-cells, an increase in IL10, and a significant reduction of T cells proliferation suggested that DHT exerted a broad anti inflammatory effect on testosterone cells [corrected]. In conclusion, our data demonstrate that DHT exerts an immune regulatory role on human prostatic stromal cells, inhibiting their potential to actively induce and/or sustain autoimmune and inflammatory responses.
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Actually, NSAID drugs do not reduce inflammation in blood vessels, they make it worse. So taking something like ibuprophen actually increases the risk of heart attacks and strokes. Studies show that NSAIDs also have effects on the lining of blood vessels, which is similar to the effects of inflammation (i.e hardening, possibly causing clots). This is also similar to the blood vessels in a balding scalp. So if you’re worried about your hair, it might be wise to avoid NSAIDs and find other ways to reduce inflammation for arthritis, back pain, etc. Actually, aspirin is an NSAID, but studies have shown that they do not increase the chance of heart attack or stroke, they actually help in that area. So it’s probably best to take aspirin rather than ibuprofen. On the other hand, I’m not convinced that these types of NSAIDs (particularly aspirin) can reduce inflammation in blood vessels and arteries.
https://www.health.harvard.edu/blog/nsaids-how-dangerous-are-they-for-your-heart-2019010715677
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Autoimmune diseases are wide spread and common. And vast antiinflammatory agents have been in use for years,so someone would have found some of them working for androgenic alopecia also ,but they didn't find. So inflammation comes after dht poisoning. If inflammation is of that concern then eunuchs would also loose some hairs.
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I've never said inflammation is the root cause of hair loss, it's a side effect. Otherwise, minoxidil wouldn't work (i.e. vasodilator used to dilate blood vessels that have been tightened due to inflammation). Both DHT and inflammation cause hair loss, but neither is the root cause. The only answers we have so far about a "root cause" is that our follicles genetically inherit a sensitivity to DHT. Remember, 50 year old men with a full head of hair have DHT in their system as well. One of the questions is why do balding men have higher levels of DHT in their follicle than non balding men? Why do our genes interact with DHT in that way vs a non balding person?
My initial point is that pattern baldness seems to have similarities to an autoimmune disorder. Our follicles are emitting signals that cause this whole process, which could explain why our hair follicles have more DHT than a non balding person.
https://www.sciencedaily.com/releases/2017/05/170525125626.htm
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even if that is true it doesn't explain why hair follicles in non balding areas are protected from dht . hair from sides and back never falls despite having same genes like hair on the top.
Why non balding region has less androgen and 5AR receptors? Why non balding region has less dht than balding region
It is a very tissue specific disease that why galea and skull expansion theories are popular.
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I think baldness could be sets in in the womb ,the fetal development is crucial. That's why we generally see one brother bald and other doesn't .
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All point a genetic autoimmune disorder i agree, linked to an hypersensitivity to androgens from some follicles
Bushi
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One thing I noticed is that my hairloss was paired with the start of hair on my back and my eyebrows growing. I recently asked a guy at work, who is the same age as me with no hairloss, if he also had to cut his eyebrows from time to time. In which he replied "never". So i doubt it's only in the scalp that something changed.
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Eyebrows final length are controlled by a whole other system, but you're right on the fact that it can fail as you age
Wait until you have hair on your ears...human body is not perfect but don't search link where clearly there's not
Bushi
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Hair on your ears? How frustrating when it falls out on top of your head and is growing everywhere else.
Clearly? Don't know if it's that clearly. I can easily think of a couple a guys in my surroundings with hairloss and hair on their back growing and guys with no hairloss with no hair on their back growing. Maybe am seeing ghosts here and it's all coincidence.
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A study already said 5)/5 the pattern happens due to the way the erector pilli muscle is layed out on the skull.
Skull expansion theory is bogus. The skull reshapes it’s self yes. But it doesn’t cause hairloss
This is really over complicating the issue.
DHT culprit or hero? Just look at a crowd of people over 21, especially women and notice how their hair is many times thicker, denser, longer than yours & most males. Why? Women as a rule have little to no facial/body hair. Why? Much lower male hormones; ie DHT. Excess DHT causes excess sebum, excess hair loss. I think that’s a fair assumption. Hair growing on scalp, like any living organism is sensitive to toxins or negative growth factors. Therefore for starters keeping scalp clean is often neglected. I find even after shampooing hair there is still buildup of residue on my scalp. I microneedle so I see the gunk on needles. Inflammation or micro inflammation is really a vague term & is not the cause but a byproduct at best. There are many people offering theories. Some have perfectly normal hair. Some bald as cue ball.
Seems we should concentrate on those individuals who have experienced significant regrowth. Who had lost their hair, but regrew it, as the strongest evidence.
DHT culprit or hero? Just look at a crowd of people over 21, especially women and notice how their hair is many times thicker, denser, longer than yours & most males. Why? Women as a rule have little to no facial/body hair. Why? Much lower male hormones; ie DHT. Excess DHT causes excess sebum, excess hair loss. I think that’s a fair assumption. Hair growing on scalp, like any living organism is sensitive to toxins or negative growth factors. Therefore for starters keeping scalp clean is often neglected. I find even after shampooing hair there is still buildup of residue on my scalp. I microneedle so I see the gunk on needles. Inflammation or micro inflammation is really a vague term & is not the cause but a byproduct at best. There are many people offering theories. Some have perfectly normal hair. Some bald as cue ball.
Seems we should concentrate on those individuals who have experienced significant regrowth. Who had lost their hair, but regrew it, as the strongest evidence.
Bushi
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Not only that it raises the chance of glaucoma.
Novel ALK5 inhibitor TP0427736 reduces TGF-β induced growth inhibition in human outer root sheath cells and elongates anagen phase in mouse hair follicles
Author links open overlay panelTakumiNaruseaAkikoIkedad
https://doi.org/10.1016/j.pharep.2017.01.024Get rights and content
Abstract
Background
Androgenic alopecia (Androgenetic Alopecia) occurs as a result of the contraction of the anagen phase because of the action of androgens on hair follicles. TGF-β production from dermal papillae is enhanced by androgens, and growth inhibition of hair-follicle cells is induced by TGF-β, and the hair cycle progresses from the anagen phase to the catagen phase. We investigated both the in vitroand in vivo potency of the newly identified ALK5 inhibitor TP0427736 {6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole}.
Methods
For in vitro study, kinase inhibitory activity was evaluated with ELISA, and inhibitory activity against TGF-β-induced Smad2/3 phosphorylation in A549 cells and TGF-β-induced growth inhibition of human outer root sheath cells were assayed using ELISA. For in vivo study, we used a mouse model that had been synchronized through dorsal hair depilation.
Results
TP0427736 inhibited ALK5 kinase activity with an IC50of 2.72 nM; this effect was 300-fold higher than the inhibitory effect on ALK3. In cell-based assays, TP0427736 inhibited Smad2/3 phosphorylation in A549 cells and decreased the growth inhibition of human outer root sheath cells. The topical applicationof TP0427736 significantly decreased Smad2 phosphorylation in mouse skin, and its repeated application suppressed the shortening of average hair follicle length during the transition from the late anagen phase to the catagen phase.
Conclusions
TP0427736, a potent ALK5 inhibitor with appropriate in vitro and in vivo profiles, may serve as a potential new therapy for Androgenetic Alopecia.
Author links open overlay panelTakumiNaruseaAkikoIkedad
https://doi.org/10.1016/j.pharep.2017.01.024Get rights and content
Abstract
Background
Androgenic alopecia (Androgenetic Alopecia) occurs as a result of the contraction of the anagen phase because of the action of androgens on hair follicles. TGF-β production from dermal papillae is enhanced by androgens, and growth inhibition of hair-follicle cells is induced by TGF-β, and the hair cycle progresses from the anagen phase to the catagen phase. We investigated both the in vitroand in vivo potency of the newly identified ALK5 inhibitor TP0427736 {6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole}.
Methods
For in vitro study, kinase inhibitory activity was evaluated with ELISA, and inhibitory activity against TGF-β-induced Smad2/3 phosphorylation in A549 cells and TGF-β-induced growth inhibition of human outer root sheath cells were assayed using ELISA. For in vivo study, we used a mouse model that had been synchronized through dorsal hair depilation.
Results
TP0427736 inhibited ALK5 kinase activity with an IC50of 2.72 nM; this effect was 300-fold higher than the inhibitory effect on ALK3. In cell-based assays, TP0427736 inhibited Smad2/3 phosphorylation in A549 cells and decreased the growth inhibition of human outer root sheath cells. The topical applicationof TP0427736 significantly decreased Smad2 phosphorylation in mouse skin, and its repeated application suppressed the shortening of average hair follicle length during the transition from the late anagen phase to the catagen phase.
Conclusions
TP0427736, a potent ALK5 inhibitor with appropriate in vitro and in vivo profiles, may serve as a potential new therapy for Androgenetic Alopecia.