Some thoughts about wounding and soliciting ideas

waynakyo

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Let's take stock of few facts:

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1- No other method has created de novo hair follicles thus far except for wounding. A string of publication starting in 2007 or so (Ito, Garza, Jahoda, Cotsarelis,...) . However, they found that a signaling process is needed for this to work nicely, and did so in mice.

2- Numerous recent studies showing that wounding ALONE (through bi-weekly dermarolling) can compete in some people achieve results similar to minoxidil.You can find these publications under the sub-forum.

3- some scattered evidence that some people on reddit have managed to see significant regrowth with dermarolling alone. The combination with minoxidil is super impressive, but minoxidil is not for everyone.

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There are many anecdotal findings as well. A guy I follow on twitter went from slick bald to showing growth and he said the only thing he added recently was wounding. I was stunned by the results. No minoxidil. But has been taking finasteride. finasteride is not known for growing hair from slick bald area.

For the last year I have been doing two things only. Scalp massage (the tedious protocol) and over the last 5 months or so bi-weekly wounding of scalp with dermapen + PDRN (called BIo antiaging PDRN ampoule from dermaline) in one area only (right ridge, between temple and top) few hours after. I know that ridge has grown some hair with some coverage that I look tiny bit better in mirror but for me to show by pictures I have to find some before pictures of that specific area...



Any ideas of what other substances we can try to combine with wounding?

Minoxidil is one, but has side effects that some people do not like. Me included. Hair popping everywhere on face, sunken eyes, aging skin, etc. The PDRN I am trying is better than nothing but not good enough to grow full thickness hair all over.

What we know and researchers such as Ralph (?) Paus said: "Anything good for healing wounds is good for hair regeneration"

So this post is soliciting ideas of substances that we can try.
 

waynakyo

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Thanks @pegasus2
I am copying it below for the sake of discussion. But I think they basically threw the kitchen sink at this patent, which is usually what they do in patents not to keep any option off the table... they have RU, estrogen, finasteride, caffeine...
But there are some good candidates obviously. I have seen studies about copper peptides and wound healing for example




"2018-10-18 Application filed by Follica Inc"
This is a broad patent application that includes every conceivable method and degree of wounding. The Most recent trial data from Follica provides a more concise description of the initial treatment.

"In one aspect, a method of integumental perturbation described herein disrupts skin to a depth of between 30 μm to 200 μm,... and preferably to approximately 100-150 μm."

"the microneedle array can disrupt skin at a depth of 100 microns to 4000 microns."

"In certain aspects the methods described herein are used to replenish hair in scalp that was used or could be used as a donor site for hair transplant surgery."

"In an embodiment, the treatment regimen is repeated multiple times to build up hair density over time."

The patent is a catch all, and most of it has not been tested:

"In some embodiments, integumental perturbation is to a skin depth of 100-500 μm. In some embodiments, integumental perturbation is to a skin depth of less than 500 μm. In some embodiments, integumental perturbation is to a skin depth of 500-1000 μm. In some embodiments, integumental perturbation is to a maximum skin depth of about 1 mm. In some embodiments, integumental perturbation is to a skin depth of about 1 mm or more. In some embodiments, integumental perturbation is to a maximum skin depth of about 2 mm. In some embodiments, integumental perturbation is to a skin depth of about 2 mm or more. In some embodiments, integumental perturbation is to a skin depth of 1 mm to 3 mm. In some embodiments, integumental perturbation is to a skin depth of 1 mm to 5 mm. In a particular embodiment, the depth of integumental perturbation does not exceed 500 μm. In a particular embodiment, the depth of integumental perturbation does not exceed 1 mm. In a particular embodiment, the depth of integumental perturbation does not exceed 2 mm."

For those of you who can't tolerate minoxidil here is an exhaustive list of alternatives:

"Hair growth-promoting agents for use, alone or in combination, in accordance with this aspect include but are not limited to: agents affecting prostaglandins, such as Prostaglandin F2α analogs, e.g. latanoprost (trade name Xalatan), travoprost (trade name Travatan), tafluprost, unoprostone, dinoprost (trade name Prostin F2 Alpha), AS604872, BOL303259X, PF3187207, carboprost (trade name Hemabate); Prostamides, e.g., bimatoprost (trade names Latisse, Lumigan); Prostanoid receptor agonists, e.g. fluprostenol; Prostaglandin D2 receptor antagonists, e.g. laropiprant, AM211; Prostglandin E2 analogs, e.g. sulprostone; and EP 2 receptor agonists, e.g. butaprost; 5α-reductase inhibitors, such as, e.g., finasteride, dutasteride, turosteride, bexlosteride, izonsteride, epristeride, epigallocatechin, Fluridil (Sovak et al, Dermatol Surg. 2002; 28(8):678-685), RU 58841 (Pan et al. Endocrine. 1998; 9(1):39-43), N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 beta-carboxamide (Rittmaster et al., J Clin Endocrinol Metab. 1987; 65(1):188-193), MK-386, azelaic acid, FCE 28260, SKF 105,111; Minoxidil; ATP-sensitive potassium channel openers, e.g. diazoxide; and the hair growth-promoting agents described herein or otherwise known in the art, such as, e.g., kopexil (for example, the product Keranique™), CaCl2, botilinum toxin A, adenosine, ketoconazole, DoxoRx, Docetaxel, FK506, GP11046, GP11511, LGD 1331, ICX-TRC, MTS-01, NEOSH101, HYG-102440, HYG-410, HYG-420, HYG-430, HYG-440, spironolactone, CB-03-01, RK-023, Abatacept, Viviscal®, MorrF, ASC-J9, NP-619, AS101, Metron-F-1, PSK 3841, Targretin (e.g., 1% gel), MedinGel, PF3187207, BOL303259X, AS604872, THG11331, PF-277343, PF-3004459, Raptiva, caffeine, and coffee. Other hair-growth promoting agents include arginine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine, gamma linoleic acid and polyphenol catechins, copper peptides. Other hair-growth promoting agents that can be formulated as a hair wash tonic could include but are not limited to, jojoba oil, extract of apple, saw palmetto, emu oil, beta carotene and green tea. In one aspect, an integumental perturbation method of the invention is used in combination with drugs for alopecia being developed by SWITCH Biotech LLC."

  • "In some embodiments, the hair growth-promoting agent treatment comprises treatment with one or more of the following hair growth-promoting agents: kopexil (for example, the product Keranique™), CaCl2, botilinum toxin A, adenosine, ketoconazole, DoxoRx, Docetaxel, FK506, GP11046, GP11511, LGD 1331, ICX-TRC, MTS-01, NEOSH101, HYG-102440, HYG-410, HYG-420, HYG-430, HYG-440, spironolactone, CB-03-01, RK-023, Abatacept, Viviscal®, MorrF, ASC-J9, NP-619, AS101, Metron-F-1, PSK 3841, Targretin (e.g., 1% gel), MedinGel, PF3187207, BOL303259X, AS604872, THG11331, PF-277343, PF-3004459, Raptiva, caffeine, an coffee. In some embodiments, the hair growth-promoting agent treatment comprises drugs for alopecia being developed by SWITCH Biotech LLC.
  • [0351]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with one or more of the following: herbs (such as, e.g., saw palmetto, glycine soja, Panax ginseng, Castanea Sativa, Arnica Montana, Hedera Helix Geranium Maculatum), triamcinolone acetonide (e.g., suspension of 2.5 to 5 mg/ml for injection), a topical irritant (e.g., anthralin) or sensitizer (e.g., squaric acid dibutyl ester [SADBE] or diphenyl cyclopropenone [DPCP]), clomipramine, unsaturated fatty acids (e.g., gamma linolenic acid), a fatty acid derivative, thickeners (such as, e.g., carbomer, glycol distearate, cetearyl alcohol), a hair loss concealer, niacin, nicotinate esters and salts, adenosine, and methionine. In some embodiments, the hair growth-promoting agent treatment comprises treatment with nitroxide spin labels (e.g., TEMPO and TEMPOL). See U.S. Pat. No. 5,714,482, which is incorporated herein by reference.
  • [0352]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with an androgen receptor inhibitor, which have been shown to be useful for stimulating scalp hair growth (Hu L Y, et al., 2007, Bioorg Med Chem Lett. 2007 17:5983-5988).
  • [0353]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with a copper peptide(s), preferably applied topically, or another compound with superoxide dismutation activity. In some embodiments, the hair growth-promoting agent treatment comprises treatment with an agent that increases nitric oxide production (e.g., arginine, citrulline, nitroglycerin, amyl nitrite, or sildenafil (v****)). In preferred embodiments, such compounds are administered further in combination with a catalase or catalase mimetic, or other antioxidant or free radical scavenger.
  • [0354]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with a compound that mobilizes bone marrow-derived stem cells (e.g., growth factors such as G-CSF and/or chemical agents such as plerixafor (Mozobil®)); and/or that regulates the differentiation of these stem cells into gender-specific specialized human hair follicles (e.g., using agents such as finasteride, fluconazole, spironolactone, flutamide, diazoxide, 11-alpha-hydroxyprogesterone, ketoconazole, RU58841, dutasteride, fluridil, or QLT-7704, an antiandrogen oligonucleotide, cyoctol, topical progesterone, topical estrogen, cyproterone acetate, ru58841, combination 5α-reductase inhibitors, oral contraceptive pills, and others in Poulos & Mirmirani, 2005, Expert Opin. Investig. Drugs 14:177-184, incorporated herein by reference, or any other antiestrogen, an estrogen, or estrogen-like drug (alone or in combination with agents that increase stem cell plasticity; e.g., such as valproate), etc., known in the art), that can result in, e.g., the appearance of specialized follicles having features that are different from natural follicles in the target location of skin.
  • [0355]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with one or more agents that counteract age-related hair thinning and/or hair follicle cell senescence (also referred to herein as “anti-senescence agents”) for example, antioxidants such as glutathione, ascorbic acid, tocopherol, uric acid, or polyphenol antioxidants); inhibitors of reactive oxygen species (ROS) generation, such as superoxide dismutase inhibitors; stimulators of ROS breakdown, such as selenium; mTOR inhibitors, such as rapamycin; or sirtuins or activators thereof, such as resveratrol, or other SIRT1, SIRT3 activators, or nicotinamide inhibitors.
  • [0356]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with one or more agents that induce an immune response or cause inflammation, such as, e.g., tetanus toxoid, topical non-specific irritants (anthralin), or sensitizers (squaric acid dibutyl ester [SADBE] and diphenyl cyclopropenone [DPCP]). While not intending to be bound by any theory, it is thought that by contacting these agents to the skin, lymphocytes and hair follicle stem cells may be recruited to skin. In some embodiments, the hair growth-promoting agent treatment comprises treatment with a chemical or mechanical (such as those discussed infra) treatment that induces an inflammatory process in the skin. While not intending to be bound by any theory, inducing inflammation in the site where hair growth is desired helps to recruit stem cells to the tissues that drive the formation of new follicles.
  • [0357]
    In some embodiments, the hair growth-promoting agent treatment comprises treatment with an antiapoptotic compound. In one embodiment, the antiapoptotic compound is not a Wnt or a Wnt agonist."
 

pegasus2

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The most promising candidates there have some of the same side effects as minoxidil. Defactinib and verteporfin reduce scarring. Defactinib in particular might be worth combining with wounding
 

5minutesbeforemiracle

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Has it been figured out yet if dermarolling + minoxidils great efficacy is due mostly to increased absorption? From quick search it looks like the jury's still out on that.

Secondly, if dermarolling+minoxidil effect is mostly due to some other effect of minoxidil on the wound healing process, would it be a solid idea to just apply minoxidil for the next few days after wounding only (then have 11 to 18 days without any minoxidil application)? This strategy might help you avoid the side-effects of minoxidil, @waynakyo.
 

pegasus2

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Has it been figured out yet if dermarolling + minoxidils great efficacy is due mostly to increased absorption? From quick search it looks like the jury's still out on that.

Secondly, if dermarolling+minoxidil effect is mostly due to some other effect of minoxidil on the wound healing process, would it be a solid idea to just apply minoxidil for the next few days after wounding only (then have 11 to 18 days without any minoxidil application)? This strategy might help you avoid the side-effects of minoxidil, @waynakyo.
Yes, It has nothing to do with absorption
 
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Emu oil, quercetin and copper peptides. I got all those ideas from your post on Chinese herbs. I've combined all three and apply for a couple of days after rolling. Not sure if it's doing anything though (it's been a few months)...
 

Jakejr

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Good question…dermarolling is only a path to what we are looking for. It definitely increases blood flow/growth factors to struggling hairs. But if our hair was growing ideally we wouldn’t need to.
So what is causing the regression of hair growth? We have many answers, but few solutions. But this is the correct question.
Yes, I’ve had some results, BUT WHAT NOW? Trial & error at this point my friend..
 
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