Role Of TGF-b1 In Hair Loss

ddjd

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Danny Roddy published this very interesting article a few years ago about TGF-b1 and IGF-1 in relation to hair loss. There doesn't seem to be much discussion about it on the forum so i wanted to create a thread.

The Mysterious Conductor of the Hair Cycle Clock

Here's an excerpt:

"
TGF-b1 stimulates the formation of collagen, and overtime this overproduction leads to “perifollicular fibrosis” further reducing the hair follicles’ access to oxygen, sugar, and other nutrients. Levels of TGF-b1 are closely related to the progression of pattern baldness,[23] and alongside hypoxia, the accumulation and activation of mast cells,[24] and an increased concentration of prostaglandins reinforce the view that the defining feature of pattern baldness, a decreased anagen to telogen ratio, is the result of chronic scalp inflammation and an inability to repair.[25] The development of fibrosis in baldness might explain why accidentally setting fire to one's scalp can result in a new head of hair.[26, 27]

TGF-b1 appears to share an inverse relationship with the liver's production of IGF-1,[28,29] and in one experiment supplementary IGF-1 stimulated hair follicle development leading the researchers to say that it might be “a promising drug candidate for baldness therapy.”[30] In the 1990s, Keaely et al. demonstrated that IGF-1 inhibits the catagen and telogen phases of the hair growth cycle favoring anagen.[31, 32] More recently, it was discovered that balding hair follicles secreted “significantly less” IGF-1 and “that the downregulation of IGF-1 may be one of the important mechanisms contributing to male pattern baldness.”[33]

Progesterone is generally supportive of hair growth and has been shown to increases IGF-1[34] and lower aldosterone.[35] The historical treatments for pattern baldness cyproterone acetate and spironolactone are both progesterone-like,[36,37] and spironolactone has been shown to reduce TGF-b1.[38] The harzadous drug, finasteride has been shown to lower TGF-b1,[39] and in a small study, its efficancy was related to the upregulation of IGF-1.[40]

Working in the opposite direction of "the most powerful antifibromatogenic steroid" progesterone,[41] estrogen appears to lower IGF-1 and increases aldosterone and TGF-b1.[42,43,44]"


Having researched substances which antagonise TGF-b1, here are some options:

- methyl palmitate (DeFibron)
- taurine
- green tea extract
- gingko Biloba
- curcumin
- apigenin
- naringenin
- apple cide vinegar
- sage
- aspirin
 

Arrade

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Apr 29, 2018
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1,496
Danny Roddy published this very interesting article a few years ago about TGF-b1 and IGF-1 in relation to hair loss. There doesn't seem to be much discussion about it on the forum so i wanted to create a thread.

The Mysterious Conductor of the Hair Cycle Clock

Here's an excerpt:

"
TGF-b1 stimulates the formation of collagen, and overtime this overproduction leads to “perifollicular fibrosis” further reducing the hair follicles’ access to oxygen, sugar, and other nutrients. Levels of TGF-b1 are closely related to the progression of pattern baldness,[23] and alongside hypoxia, the accumulation and activation of mast cells,[24] and an increased concentration of prostaglandins reinforce the view that the defining feature of pattern baldness, a decreased anagen to telogen ratio, is the result of chronic scalp inflammation and an inability to repair.[25] The development of fibrosis in baldness might explain why accidentally setting fire to one's scalp can result in a new head of hair.[26, 27]

TGF-b1 appears to share an inverse relationship with the liver's production of IGF-1,[28,29] and in one experiment supplementary IGF-1 stimulated hair follicle development leading the researchers to say that it might be “a promising drug candidate for baldness therapy.”[30] In the 1990s, Keaely et al. demonstrated that IGF-1 inhibits the catagen and telogen phases of the hair growth cycle favoring anagen.[31, 32] More recently, it was discovered that balding hair follicles secreted “significantly less” IGF-1 and “that the downregulation of IGF-1 may be one of the important mechanisms contributing to male pattern baldness.”[33]

Progesterone is generally supportive of hair growth and has been shown to increases IGF-1[34] and lower aldosterone.[35] The historical treatments for pattern baldness cyproterone acetate and spironolactone are both progesterone-like,[36,37] and spironolactone has been shown to reduce TGF-b1.[38] The harzadous drug, finasteride has been shown to lower TGF-b1,[39] and in a small study, its efficancy was related to the upregulation of IGF-1.[40]

Working in the opposite direction of "the most powerful antifibromatogenic steroid" progesterone,[41] estrogen appears to lower IGF-1 and increases aldosterone and TGF-b1.[42,43,44]"


Having researched substances which antagonise TGF-b1, here are some options:

- methyl palmitate (DeFibron)
- taurine
- green tea extract
- gingko Biloba
- curcumin
- apigenin
- naringenin
- apple cide vinegar
- sage
- aspirin
Correct me if I’m wrong. Green tea and curcumin are potentially anti androgenic
Ginkgo Biloba feels like adderall

Serrapeptase also rids the body of fibrosis, TGIF-1 is that simply a fibrotic agent?

Once again, lower estrogen and improve liver function. Taurine is able to improve liver function and lower fibrosis
 

Muckl3

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The best condition my hair was ever in was when I was running peptides, mod Grf and impamorelin that raises your natural gh out put without shutting it down over time like synthetic Hgh, I dident connect the dots at first but realised later that was the cause.
 
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ddjd

ddjd

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ddjd

ddjd

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The best condition my hair was ever in was when I was running peptides, mod Grf and impamorelin that raises your natural gh out put without shutting it down over time like synthetic Hgh, I dident connect the dots at first but realised later that was the cause.
Very interesting .Are you saying that they raised your IGF-1 levels?
 
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The general peaterian viewpoint is that DHT is far from the culprit when it comes to hair loss. How do we explain young teenagers with sky high DHT and full heads of hair vs. old men with barely a follicle left and non existent levels of DHT

DHT is THE main END-culprit that shrinks the hair follicle, but that is most definitely happening in the context of high estradiol, so if we go back up one step it’s definitely years/decades of low SHBG + high Androgens that end up atrophying the hair. Just look at modern steroid users.

That said, the other topic on growth hormone and igf1:igfbp3 is very interesting too.

DHT and T each increased IGF-I (7-fold) and decreased IGFBP-3 (2-fold) mRNA expression and protein secretion in a dose- and time-dependent manner and increased IGFBP-2 (2-fold) mRNA in a dose- and time-dependent manner. DHEA and E2 did not significantly alter these measures.

Here Tadalafil seems to block TGFb1 so there again, there’s more to the story than NO good/bad - DHT good/bad. The TGF+IGF science is much more interesting imo.

Attenuated Proliferation and Trans -Differentiation of Prostatic Stromal Cells Indicate Suitability of Phosphodiesterase Type 5 Inhibitors for Prevention and Treatment of Benign Prostatic Hyperplasia | Endocrinology | Oxford Academic
 

Muckl3

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Very interesting .Are you saying that they raised your IGF-1 levels?
Oh defiantly. My skin, hair, nails quality jumped leaps and bounds. You can uses peptides every 3 hours or so at 100mcg each of mod grf(ghrh) & ipamorlin (ghrp) this is the saturation dose, so bodybuilders use 3+ a day but for anti ageing purposes 1 dose pre bed is all that’s needed and all I used.

I think peps are better as they use your own growth hormone not synthetic like Hgh.
 

Kray

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Oh defiantly. My skin, hair, nails quality jumped leaps and bounds. You can uses peptides every 3 hours or so at 100mcg each of mod grf(ghrh) & ipamorlin (ghrp) this is the saturation dose, so bodybuilders use 3+ a day but for anti ageing purposes 1 dose pre bed is all that’s needed and all I used.

I think peps are better as they use your own growth hormone not synthetic like Hgh.

Would peptides as in collagen hydrolysate be the same? (green can)
 

mujuro

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Mk677 probably works better than the injectable ones

I think in a Peat context, the key distinction to point out with peptides vs rHGH/ghrelin agonists is that peptides (any GHRP + Mod GRF 1-29 as the GHRH of choice) do not chronically elevate serum growth hormone or hepatic IGF-1. They are acutely elevated and then decrease to baseline. Mod GRF lasts only 30 minutes in the body, and the GHRPs are just somatostatin blockers, but in effect they are very short acting compared to the normal 191aa HGH or MK677. They also powerfully stimulate local IGF-1 splice variants in muscle tissue, IGF-1Ea and IGF-1Ec (MGF), which actually affect muscle tissue development. There does exist GHRHs with longer biological half lives, like CJC-1295 with the lysine linker, but that’s not at all surprising, since keeping blood levels of x elevated around the clock is regarded as a positive thing in bodybuilding circles, no matter what the substance. The chronic elevation of hepatic IGF-1 is worrying on account of its antiapoptotic, mitogenic activity, and it generally affects insulin sensitivity in a negative way.
 
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I do believe that people take way too much mk677, don’t understand that the effects last much longer than its half life, and low doses will be much more physiological than high doses. In that regards, i take 25mg every 5th day. Igf-1 is good enough in the upper half of the range, and that’s where mk use will keep it. The same way people use too many drugs in general, high doses of hormones and so on.

It also raises igf binding proteins so that’s important to consider. All in all the only issue would be insulin resistance + increased lipolysis. Which should be dose dependent?
 

Muckl3

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I do believe that people take way too much mk677, don’t understand that the effects last much longer than its half life, and low doses will be much more physiological than high doses. In that regards, i take 25mg every 5th day. Igf-1 is good enough in the upper half of the range, and that’s where mk use will keep it. The same way people use too many drugs in general, high doses of hormones and so on.

It also raises igf binding proteins so that’s important to consider. All in all the only issue would be insulin resistance + increased lipolysis. Which should be dose dependent?

I’m going to look into this more as it’s very interesting, I took mk677 everyday for a short time and my god the lethargy about killed me but it’s a awesome product. Use my peps ed and look into mk677 every 5 days or so.
 
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e5d is based on personal feels, I've read on another forum that e2d was studied in children and yielded similar IGF-1 results with less desensitizing. Couldn't find the study myself...

Some more data on chronic use of MK677:

The stimulatory effect of MK-677 on mean GH concentrations in the 8 h after drug administration declined between the first and fourth day of drug administration, although the fourth day value was still significantly greater than baseline. This decline may indicate desensitization to the GH stimulatory effects of the drug and foreshadow an eventual loss of stimulatory effect. Alternately, and probably more likely, it may result from negative feedback effects of IGF-I on GH secretion. There is evidence that IGF-I acts at pituitary and/or hypothalamic sites to suppress GH secretion

The negative feedback effects of IGF-I would be expected to increase as circulating IGF-I concentrations increase in the days to weeks after starting MK-677 treatment. This would eventually result in a new set point at which IGF-I and GH concentrations are higher than at baseline, but GH concentrations are lower than immediately after initiation of treatment. Such changes have been reported in beagle dogs treated with oral MK-677 for 2 weeks (40).

Ergo, every other day at least could make sense.
 

Arrade

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If you want IGF-1 drink pasteurized whole milk and start doing squats
 
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