TGF-Beta Inhibition - Another angle?

[DrGrow]

So TGF-b is the Immune systems way of having a go at the genetic-disposed hair follicles which makes us bald.

So obviously, theres a way to tackle hair loss at the last line of defence. I'm thinking, and maybe Bryan could shed some light, that by throwing force at TGF instead of DHT, we leave our systems as they are, and simply get to the problem right before the last domino.

Some inhibitors include

- apple poly
- green tea extract
- apple cidar vinegar

minoxidil - I believe this is also a TGF-b.. I don't believe it "stimulates" hair growth. I don't think anything can stimulate hair growth, rather it blocks the very substance that stops it growing.

If this is the case, then minoxidil could very well be preventative alongside apple poly, green tea etc? Unless I'm missing something else here?

 

[DrGrow]

This is perhaps why also minoxidil grows alot more than finasteride does and quicker.

finasteride simply stops the chemical that activates the chemical that stops your hair growing, whereas minoxidil stops the latter chemical, skipping a process and speeding things up.

 

[Guest]

This is perhaps why also minoxidil grows alot more than finasteride does and quicker.

finasteride simply stops the chemical that activates the chemical that stops your hair growing, whereas minoxidil stops the latter chemical, skipping a process and speeding things up.

this doesn't make sense because minoxidil regrew more hairs in studies than finasteride did. minoxidil gives more regrowth than finasteride on average. it's not a time thing.

 

[michael barry]

I'll be interested in some of the responses on this thread from Bryan and Doctor.


I had a list of the dermal papilla growth inhibitors on a link.


Here are the dermal papilla mediated inhibitors:
TGF-beta 1 and 2 ...................................(inbited by gt, ap, bp)
Inerleukin 1-alpha .........................................(silica inhibits this)
Fiberblast growth factor-five (FGF-5)
Epidermal growth factor (EGF)
thrombospondin
DPPK
IL-5 and 6 ...............................(roxythromicyn inhibits both of these)




Here is a list of dermal papilla growth factors that we know of in humans:

Basic fibroblast growth factor (bFGF)
Platelet-derived growth factor (PDGF)
Insulin-like growth factor (IGF-1)
Its unknown if vitamin D3 might increase hair cell activity....but its there.




Also we know that inflammatory cytokines that hurt hair growth that are sent by the immune system from the outside include Protien Kinease C and TNF-alpha. Grape seed proanthocyaindins and apple proanthocyanidins can take care of PKC, while green tea, borage, black currant, ginko biloba, stinging nettle, fish oil all can take care of TNF-alpha.

Superoxide dismutases can help with superoxides.
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DrGrow,
2 things. If youve ran into any of my posts on here, you know Ive been looking at things that just block the androgen receptor. Ive posted a study concerned with female transexuals who took testosterone injections that found that they end up going male pattern bald at about the same incidence that men do. Ive looked for substances that will block or occupy androgen receptors as a "first base" to begin treatment based on that and the fact that castration stops further baldness (and one does regrow some hair in anti-androgen theray if you look at the finas and dutas pictures available).
Its my contention that stopping androgens binding should stop the negative growth factors from being overexpressed over time and stop the reason for the immuno attack. It will not, obviously, kick start dying apoptic hair cells however, so even if I find that tea tree oil or lavendar (they cause gyno in young boys who bathe in bodywashes that have the stuff) can sit on androgen receptors and inhibit androgen uptake almost completely, one would still need some sort of stimulation of the hair cells.
The alanine/histidyl/lysine copper complex was tested by korean researchers (used to have the link) and shown to stimulate hair cells directly.....................so we can conclude that its a stimulant.

In the pre-clinicals with roxythromicyn, it was shown to stimulate hair cells and delay apoptosis directly, so there must be some stimulative properties with it. There must also be some stimulative properties of caffeine.

Dr. Proctor has experimented with other hypertrichotics and includes them in his products (pheynytoin, etc).


It will be interesting when a TGF-beta inbibitor (hopefully effective on tgf-1 and 2) is synthesized and tested to see how much hair it can regrow and how long lasting the effects are. Perhaps its "the one" that gets the immuno attack started as Doctor has suggested. Or perhaps when negative growth factors outnumber positive ones in the papilla, the immune system just sees a "struggling organ" and assumes its a foreign body? Perhaps there is some microinflammation of a part of the follicle where different negative growth factors retard growth (epilitheal cells are slowed by different DP inhibitors than root sheath cells, etc.?). Here's to hoping science can find out.



By the way..........................I have a feeling the apple cider vinegar grandma advice and the beer and eggs shampoo grandma advice really did help...........as well as the lavendar and rosemary grandma advice.

 

[Strange Days]

I posted this in the new discoveries forum, they don't recommend systemic tgf-beta inhibition:

Topical Application of a Peptide Inhibitor of Transforming Growth Factor-bold beta1 Ameliorates Bleomycin-Induced Skin Fibrosis

Topical application of P144 significantly reduced skin fibrosis and soluble collagen content. Most importantly, in mice with established fibrosis, topical treatment with P144 lipogel for 2 wk significantly decreased skin fibrosis and soluble collagen content. Immunohistochemical studies in P144-treated mice revealed a remarkable suppression of connective tissue growth factor expression, fibroblast SMAD2/3 phosphorylation, and alpha-smooth muscle actin positive myofibroblast development, whereas mast cell and mononuclear cell infiltration was not modified. These data suggest that topical application of P144, a peptide inhibitor of TGF-beta1, is a feasible strategy to treat pathological skin scarring and skin fibrotic diseases for which there is no specific therapy.

Systemic inhibition of TGF-beta, however, raises important safety concerns, because this factor displays pleiotropic and potent effects in immunomodulation, inflammation, and tumor development (Akhurst, 2002). Consistently, in TGF-beta1-deficient mice, skin scarring is reduced but they develop a severe wasting syndrome accompanied by a generalized inflammatory response and tissue necrosis, resulting in organ failure and death.

Therefore, local rather than systemic TGF-beta inhibition, or targeting of downstream factors involved in TGF-beta profibrotic signaling represent alternative strategies for the development of anti-fibrotic therapies.

 

[docj077]

Minoxidil does many things in the scalp and two of the most important attributes it has are selective arterial dilation and inhibition of TGF-beta mediated apoptotic processes through activation of the SUR receptor and opening of the Kir 6.0 pore that is coupled with the receptor.

Minoxidil also raises the levels of pro-growth mediators like IGF-1, VEGF, and HGF.

The actions are faster than drugs like finasteride, which have their success directly correlated with a rise of IGF-1, as well. Minoxidil must just perform its effects faster.

I'm sure that pretty much any drug that we test will have its efficacy proven through the testing of scalp IGF-1 levels.

 

[DrGrow]

This is perhaps why also minoxidil grows alot more than finasteride does and quicker.

finasteride simply stops the chemical that activates the chemical that stops your hair growing, whereas minoxidil stops the latter chemical, skipping a process and speeding things up.

this doesn't make sense because minoxidil regrew more hairs in studies than finasteride did. minoxidil gives more regrowth than finasteride on average. it's not a time thing.

On the contrare JayMan.. thats my actual argument that it is a timing thing.

But furthermore, the TGF may be acting quicker than the DHT levels, so lowering the DHT levels may not necassrily be enough to maintain lower TGF.. either that or TGF is very sensitive to DHT, so having even 1% has some adverse effects.

 

[DrGrow]

Systemic inhibition of TGF-beta, however, raises important safety concerns, because this factor displays pleiotropic and potent effects in immunomodulation, inflammation, and tumor development (Akhurst, 2002). Consistently, in TGF-beta1-deficient mice, skin scarring is reduced but they develop a severe wasting syndrome accompanied by a generalized inflammatory response and tissue necrosis, resulting in organ failure and death.

So Green Tea taken orally could be a bad thing?