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NO i havent tried. Do you think it can work?
NO i havent tried. Do you think it can work?
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A reduction in PGD2 is what we want so if OL does decrease it - even better!
On the topic of Swiss, I think his methodology is off. His belief that DHT/AR is irrelevent and PGD2 is the only factor we need to address is inaccurate. Theres insurmountable evidence that Androgens significantly blunt hair growth by inhibiting β-Catenin accumulation. Sure he's seen some progress, but with the amount of β-Catenin he's increasing by inhibiting GSK3β (with VA + LiCl) and wounding (PGE2) I'm not surprised he believes he's on the right track. Alot of people can achieve regrowth with aggressive growth agonists. If he incorporates some form of AR/5ar suppressor then he'd be nw0 already. Hes trying to make his car go faster while having his foot still on the brakes (logic?).
You can get away with not targeting PGD2 itself by attacking its downstream cascades: GSK3β and PKC (references in new thread soon) with EGCG, Valproic Acid, OL, Anything that activates PKA (GSK3β inhibitors) + Apple polyphenols (procyanidin mediated PKC inhibition). Or if you suppress 5ar/AR you can prevent the PTGDS rise from the top.
Your hair doesnt look too bad. Unfortuneately alot of us including myself dont look good with a shaved head. I'm getting tired of seeing treatments that are always 2-5 years away. People on forums have been saying this for years, I remember when I first started receding at 17 there were cures supposedly 2-3 years away and it's still the same. The only cure I can think of is transplanting sideburn hair along the nw0 hairline evenly spaced out. The sideburn hairs are the first to respond to androgens so they have greater potential to secrete IGF-1 to nearby follicles which should slow down the effects of T/DHT. Then you can just get away with the occasional topical 5ar suppressor like GLA (more on this later) or keto or some other mild maintenance treatment. Thats the best cure I can realistically think of atm. A hair transplant is out of the question, the density and natural direction of growth is never the same. All these cell replication treatments dont look too promising either - how are they going to create a functioning ORS to form the hair canal itself? The DPC is useless without a canal/surrounding epithelial cells.
It would be useful if it worked topically without going systemic. I've known about tomatoes being bad for men, but I hadnt thought about its applications in AGA. Will do more research on this.
Taken orally Oleuropein can increase systemic WNT10b levels and reduce adipogenesis/increase osteogenesis. In the case of skin, this translates to enhanced keratinocyte proliferation and hair growth. It has the potential to work to increase hair if taken systemically - especially seeing as you were spacing it out throughout the day. (high doses have been shown not to have any effect so your single teaspoon might have been perfect). If it did prolong anagen then you're seeing the catch-up shed which happens when the anagen cycle is artificially extended. I dont fully understand how the feedback cycle works but the BMP signals try to reset the cycle to telogen as the hair progresses into late anagen. This is all speculation, it could all be coincidence.
I share his view that AR is root cause. His idea of viral gene transfection is not new but the application is the interesting part. The cost is a concern too. If he has figured out what he claims he has then I think it'll be revolutionary. A few injections to permanently turn off the AR gene is a cure imo. Executing it is easier said then done. Alternatively if we can permanently downregulate an AR coactivator to blunt the effects of AR by 50%+ thats kind of a semi cure too. There might even be a supplement out there that does this already but we havent found it yet.
Have you tried zinc pyrithione shampoos (H&S classic) or selenium sulfide (selsun blue) shampoos to at least manage the symptoms?
I've done a fair bit of research on HGH and its conflicting as to whether HGH modulates the HPTA axis. I've not read anything that mentions HGH physically interfering with 5ar or AR, but the possibility of it effecting the LH/HPTA loop is there (testosterone production).
Anyways. I'm sorry I havent been posting lately, I've been busy gathering all the research into one big easy to read pile which I'll be posting in a separate read-only thread.
As for my progress update. I'm going through a shed which I'm not happy about. It could mean new hairs? But then I'd have to wait 2 months for the density to come back so whats the frickin point of new hairs. I've bought a 6 months supply of minox because I keep forgetting to but more. I've also bought some Valproic acid which'll be here next week. I plan to use 5% mixed with minox, that should definitely speed up growth. I've been using the following solution for the past 10 days:
Minox
OL 1mg/ml
EGCG ~8mg/ml
GLA 2.6mg/ml
I'm seeing more terminal hairs pop up along my nw1 hairline, not visible on camera but I can feel/see them (will post pics soon). The hairs I regrew on my left side are seem to be getting thicker but I cant tell for sure. The GLA might actually be doing something... I've come across some new research regarding safflower oil and theres a genetically modified version (Sonova 400) that has 400mg of GLA per 1000mg. Normal safflower doesnt contain GLA at all lol. The EPO I'm using only has a measly 80mg so I think a higher dose is what I need to really inhibit 5ar. I'm going to get my hands on this GLA, and also because safflower (what sonova uses) also has the ability to grow hair independent of GLA. I'll be posting an analysis soon.
I was going over the research on EGCG and it seems it might not be as strong as I'd anticipated so I'm going to get some Rosemary too. Chuck in apple polyphenols for good measure. I'm going all out because I really dont want to have to wait 2 months just to get my density back.Comment
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Thoughts on thymosin beta 4?Comment
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Hi, thanks for your work, I'm vary fascinated by your and swisstemle's work. I just wanted to add two things that I noticed:
1: Swiss posted this on reddit, and ask.fm: "Oleuporin is a dud I discussed this with a very helpful guy on my ask.fm. Beta catenin is not the only way in which pge2 works, not at all", and "Oleic acid is a precursor to PGE2/PGF2a. It doesn't however really boost the snythesis itself from what I see." Maybe you can do something with this information, I certainly can't
2: Swiss is on dutasteride to my best knowledge, so he does have the AR/DHT pathway covered.Comment
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I couldnt find where he discussed oluropein. It would be nice if he referenced his comments. However he does have Oleuropein listed in his protocols table.
Sadly he hasnt stated "the other mechanisms" by which PGE2 works. But regardless, whatever other mechanism PGE2 uses, all pathways that grow hair converge on β-Catenin. Every single treatment that grows hair stops working in the presence of a β-Catenin inhibitor. Be it DKK-1 which inhibits WNT induced β-Catenin, or PGD2 which inhibits β-Catenin via GSK3β/PKC, to grow hair you need β-Catenin. If people are going to deny this fact then at least clarify how you think this whole thing works.
You are right, he is on DUT for 3 years. Not sure if he still is. But if he is then it sure as hell is helping his results. This is dutasteride we're talking about.
I think with zero DHT you will have alot less PGD2 - judging from that diagram. No DHT doesnt mean no Testosterone so its AR that needs to be blocked. And plus not everyone is sensitive to PGD2 anyway.Dut won't inhibit PGD2. Even with zero DHT you will still have PGD2 in your scalp which keeps you from regrowing hair.
Do you understand what I mean? Here's a diagram. http://i.imgur.com/ujqSDHS.pngComment
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Chemical, thank you for all of your hard work and for sharing it with everyone here. Not only that, but you take the time to respond to everyone's questions without any arrogance.
It seems that your regiment has evolved since you began this thread and that it continues to change. Do you think you're near a point where you will have finalized the regiment or do see it being a work in progress indefinitely?
Also, what is your opinion on the current pipeline of treatments? Which do you think will have the greatest chance of success if any? (Replicel, histogen, SM, CB, etc.)
Thanks again. I wish I were half as knowledgable as you on this.Comment
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Thanks Chemical, much appreciate the in depth response. Really is fascinating stuff.Comment
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Hi Chemical,
You have a lot of information posted on here. I haven't been able to read all of it, a bit overwhelmed reading all of fgf11. It seems like a lot of interesting assumptions but as others pointed out in his post, they are skeptical if he is really correct. Then again I don't know why someone would put that much time to type something fake.
I was curious how can you for sure that your assumptions are working? For example hair loss may be a factor of many complex things so how do you go about it? Also I somewhat agree with you regarding how companies indicate they are only a few years away but do you really think Replicel / Histogen / other treatments aren't going to work or be available soon? (They mentioned in 2018)
Also im curious about some of your pics, do you have any better pics to share? I try to stay away from forums because a lot of times people can manipulate their pics etc.
Can you make a post on the exact supplements you are taking and dosages? I know one of them was Oleuropein.
BTW what is your take on biotin, saw palmetto with Beta-Sitosterol, pumpkin seed oil extract? Some have calimed saw palmetto did nothing but i wonder if they took it with the beta sitosterolComment
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Chemical apologize for previous post, my edit didn't go through and some remarks don't make sense.
I was curious how can you be sure that your mixtures / suggestions are working and it isn't because of the Minoxidil only?
I have read some people have bad experience with keta shampoo / nizoral and experience massive hair falling out. I don't want to risk having clumps of my hairs gone
Also there was a lot of users that got on the RU wagon but later on people experienced side effects with RU too and now CB is suppose to be the miracle...Comment
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Any Update Chemical?Comment
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To Seek : Modulation of Androgen Receptor Activity by P160
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Thoughts? More than thoughts. Thymosin beta 4 is an absolute goldmine. (Thanks for sharing this)
Thymosin beta 4 induces hair growth via stem cell migration and differentiation.
Without looking too hard I found this. TB4 acts directly on the stem cells to induce hair follicle growth. Sadly the abstract doesnt go over the mechanism of TB4 that they discovered.
Thymosin beta4 upregulates the expression of hepatocyte growth factor and downregulates the expression of PDGF-beta receptor in human hepatic stellate cells.
HGF is a known stem cell pluripotency maintainer providing further evidence of TB4's stem cell effects.
Thymosin β4 induces the expression of vascular endothelial growth factor (VEGF) in a hypoxia-inducible factor (HIF)-1α-dependent manner.
We know that VEGF expression leads to increased hair follicle size and growth rate.
Regulation of glycogen synthase kinase-3 by thymosin beta-4 is associated with gastric cancer cell migration.
And it also inhibits GSK3β which leads to more β-Catenin. However the study mentioned they noticed a decrease in β-Catenin in response to TB4.
Over-expression of thymosin beta4 promotes abnormal tooth development and stimulation of hair growth
Looking at the deeper mechanisms of TB4 we see that it interacts with laminin 5. I've never heard of laminin 5 so I did some research:Accelerated hair growth in thymosin β4 transgenic mice The effect of thymosin β4 on hair growth was analyzed in the transgenic mice. We watched the hair growth pattern of transgenic mice after birth but could not detect any differences in the onset of hair growth when compared with the wild type mice. However, we found significant difference in the speed of hair re-growth after shaving. Shaved mice were observed and the speed of hair re-growth was compared by measuring the hair area on the shaved spot at 2 weeks using an image analysis program. The speed of hair growth on the skin of the transgenic mice was accelerated as shown in Fig. 3. These data suggest that the increased expression of thymosin β4 in the hair follicles (Fig. 1B) promoted hair re-growth in the transgenic mice. To analyze the expression pattern of thymosin β4 on the hair follicle, we stained for thymosin β4 in the skin of transgenic mice. As shown in Fig. 3B, thymosin β4 was expressed on surface of the hair follicles especially in the external root sheath.
Induced expression of laminin-5 in thymosin β4 transgenic mice
We examined the expression of laminin-5 in the thymosin β4 over-expressing mice since laminin-5 was one of the candidate genes associated with hair growth among the proteins upregulated by thymosin β4. Western blot analysis and immunohistochemistry were used with the skin of wild type and transgenic mice to characterize the expression of laminin-5. As shown in Fig. 4A, Western blot shows that the expression of laminin-5 was increased approximately 5-fold in the transgenic mice relative to the wild type mice. Immunohistochemistry showed that the expression of laminin-5 was specifically increased in the root of the hair follicles and this staining pattern is different from that of thymosin β4 (Fig. 4B). The expression of laminin-5 around the root of the hair follicle suggests that laminin-5 is induced by the over-expression of thymosin β4 and that this induced laminin-5 expression may stimulate hair follicle stem cells and play a role in the thymosin β4- stimulated hair growth.
Laminin-10 is crucial for hair morphogenesis
So it seems laminin 5 is crucial for cellular adhesion. But what does cellular adhesion do?Our results, as well as the results of a number previous studies, suggest that laminin-10 supports hair follicle development through a mechanism other than the maintenance of dermal–epithelial cohesion. A comparison between inhibition of laminin-5 and laminin-10 in the skin illustrates this point. In human skin xenografts, laminin-5 antibodies induced extensive epidermal detachment within 24 h of application, while in our studies, skin treated with laminin-10 antibodies did not show blisters or epidermal detachment even after 3 weeks. Similarly, extensive blistering is seen in patients with HJEB, who lack laminin-5. Absence of laminin-5 in Lama3 –/– mice produced extensive epidermal detachment as well as detachment-associated cell death (anoikis). In contrast, in our studies, we were unable to demonstrate significant epidermal detachment or anoikis in Lama5 –/– mouse skin. On the other hand, while inhibition of laminin-10 in both human and murine skin produced marked effects on hair follicle development, no hair follicle defects were demonstrated in laminin-5/6 null mouse skin, and hair follicle development is typically normal in HJEB patients. In conclusion, laminin-5 and laminin-10 appear to have non-overlapping functions in the skin, with laminin-5 promoting epidermal adhesion and laminin-10 promoting epithelial development.
Cellular adhesion is necessary for epithelial mesenchymal transition to take place and it also increases intracellular β-Catenin. You can read more about E-cadherins role in hair growth here:
E-cadherin controls adherens junctions in the epidermis and the renewal of hair follicles
It looks like TB4 is designed for the sole purpose of growing hair, nearly everything it does is directly promotes the development of hair follicles. I will doing more research on ways of increasing TB4 (endogenously or exogenously).
While I was researching laminin 5 I came across this excerpt which talks about DPC regeneration by "growth of papilla cells in 3D spheroid cultures" implanted into skin:
I dont know what to say. Just let that sink in.Microenvironmental reprogramming by three-dimensional culture enables dermal papilla cells to induce de novo human hair-follicle growth
The observation of hair follicles within grafts, as described above, suggests that the 22% restoration of papilla signature is sufficient for follicle neogenesis. However, as complete hair-follicle morphogenesis involves epithelial:mesenchymal interactions, it is likely that external paracrine signals will be required for full signature restoration and development of external hairs. Importantly, in this study, we have demonstrated that dermal spheroids are, by themselves, capable of initiating the hair induction process in non-hair-bearing human skin, where there are no previous epidermal “hair-follicle” signals.
You are very welcome.
I started off using minox, emu oil, oleuropein, Saw palmetto and ketoconazole. Now I'm using Minox, EGCG, OL, GLA, ketoconazole and miconazole. I'm going to add Valproic acid, apple polyphenols, Rosemary and a different brand of GLA in the form of safflower oil. I think this is as far as I will go and this should be more than enough to see steady regrowth. The problem is I'm being impatient and thats a bad trait to have when watching hair to grow (or a tree to grow). If I were to choose a few core treatments to stick to I'd say minox, egcg, ol, keto, rosemary and gla. We keep discovering new studies and pathways that enhance or inhibit hair growth so its inevitable that in a few months time this protocol will change. This is still an experiment in progress so nothing is fixed yet until I've become nw0. Moreover, treating AGA is an optimisation problem where we have to find the treatments that have the best cost to effectiveness ratio and ease of acquisition/application - which takes trial and error. And even after complete regrowth, we have to find a maintenance protocol that doesnt require aggressive planning or time. I firmly believe in never settling for less. There is always room for improvement.
Looking at histogens preliminary results and theory I would say their treatment has potential to grow hair in less aggressive AGA. This idea of using cultured stem cell/growth factors (?) injected only once into scalps is definitely more convenient than daily topical use. The only problem is AR.
Replicels methodology is better that histogens on paper:
I previously stated that these implanted DPC cells might fail to create a functional hair canal with outer root sheath cells but that was ignorant of me to say without fully understand how follicular neogenesis works.
Instead of occipital hair cells I think replicel might have more success with beard DPC since they actually thrive in the presence of DHT and release IGF-1 to nearby follicles. I realise that culturing these cells is not an easy task so atm its all looking really good on paper. But just because it seems to work on paper and mice doesnt mean it'll translate the same in human balding scalp.Human DP cells isolated from temporal scalp dermis (Promocell, Heidelberg, Germany) from six donors were propagated in vitro according to manufacturer's recommendations. Alkaline phosphatase activity, a DP marker which correlates with hair-inducing capacity, was measured in vitro using the BCIP/NBT substrate on passage 5 DP cells. Alkaline phosphatase activity was variable between samples, with cells from 3 of the donors showing alkaline phosphatase activity in more than 50% of the cells (Table 1). DECs were constructed by combining DP cells with rat tail collagen type 1, adding NFKs on top and bringing the constructs to the air-liquid interface for 2 days before grafting onto female nude mice. Eight weeks after grafting, HFs were observed in mice grafted with the 3 human DP cells with higher alkaline phosphatase activity (Table 1, Figure 1a). HFs had a bulb, dermal sheath, hair matrix and cortex (Figure 1b). Epithelial compartments of the HFs were intact with concentric layers of inner and outer root sheaths, sebaceous glands and hair shaft (Figure 1c-e).
For now all we can do guess when they will be ready to release their treatments. I think the main problem is the researchers like hyping their work before they can actually execute it properly. I think we should stop holding our breath for these companies and look for alternative treatments that we can use immediately, and when these do finally come out, it'll be a win-win. Otherwise you'll just be setting yourself up for disappointment.
Yes I'm nearly finished writing up the material for the new thread which will all the treatments with the relevant dosing and science, plus all the research in this thread formatted nicely so it's easy to find. Its proving to harder than I thought gathering all the research scattered all over this thread but I'm nearly done.
I've stated before that I fully believe my results were attributed to minox with the other treatments merely potentiating the rate of regrowth. When I tried minox, fin and keto back in april 2015 it took 2 months before I saw visible improvement and it wasnt anything spectacular. With OL + Minox and keto/mico I saw very fast terminal differentiation of vellus hairs when I was applying 3x a day for 2 weeks. (I will make a proper progress log too). I will talk more about testing methodology and gauging effectiveness of treatments in the new thread so I dont keep repeating myself however the point you raise about which treatment is actually working - is important.
I cant comment on keto and RU since their side effects are subjective and varying but personally I havent experienced anything bad with Keto (I use the cream form). This shedding that people experience could be a good sign of new anagen entry but it could also be coincidence - you will see more bad experiences because people dont post unless they see a change for the worst. Thats something to keep in mind when reading anecdotes.
Targeted disruption of the p160 coactivator interface of androgen receptor (AR) selectively inhibits AR activity in both androgen-dependent and castration-resistant AR-expressing prostate cancer cells.
Good find as always Seuxin.
Nearly forgot:
http://imgur.com/a/g6TdQ
http://imgur.com/a/aV65d - taken today.Comment
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The problem with TB500 (Thymosin beta 4) is it needsto be injected, and it's expensive ! In addition, i think some peoples already tried it
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I actually have been using tb500 for the past few weeks on and off. I have taken a few weeks off and now back on 8mg injected one a week. I bought enough this time to run it for at least 6 weeks at 8mg a week. It definitely has an impact on hair color and growth because my hair did look way healthier and darker when I only used it for a 3 weeks in the past . The only downside is the price as it's costing me $31 for 2mg vial but the stuff I have it 100% legit. I heal way quicker too from weight lifting. I just did my first shot again this past Wednesday and plan to keep going for another 5 weeks or more if I have the money.Thoughts? More than thoughts. Thymosin beta 4 is an absolute goldmine. (Thanks for sharing this)
Thymosin beta 4 induces hair growth via stem cell migration and differentiation.
Without looking too hard I found this. TB4 acts directly on the stem cells to induce hair follicle growth. Sadly the abstract doesnt go over the mechanism of TB4 that they discovered.
Thymosin beta4 upregulates the expression of hepatocyte growth factor and downregulates the expression of PDGF-beta receptor in human hepatic stellate cells.
HGF is a known stem cell pluripotency maintainer providing further evidence of TB4's stem cell effects.
Thymosin β4 induces the expression of vascular endothelial growth factor (VEGF) in a hypoxia-inducible factor (HIF)-1α-dependent manner.
We know that VEGF expression leads to increased hair follicle size and growth rate.
Regulation of glycogen synthase kinase-3 by thymosin beta-4 is associated with gastric cancer cell migration.
And it also inhibits GSK3β which leads to more β-Catenin. However the study mentioned they noticed a decrease in β-Catenin in response to TB4.
Over-expression of thymosin beta4 promotes abnormal tooth development and stimulation of hair growth
Looking at the deeper mechanisms of TB4 we see that it interacts with laminin 5. I've never heard of laminin 5 so I did some research:
Laminin-10 is crucial for hair morphogenesis
So it seems laminin 5 is crucial for cellular adhesion. But what does cellular adhesion do?
Cellular adhesion is necessary for epithelial mesenchymal transition to take place and it also increases intracellular β-Catenin. You can read more about E-cadherins role in hair growth here:
E-cadherin controls adherens junctions in the epidermis and the renewal of hair follicles
It looks like TB4 is designed for the sole purpose of growing hair, nearly everything it does is directly promotes the development of hair follicles. I will doing more research on ways of increasing TB4 (endogenously or exogenously).
While I was researching laminin 5 I came across this excerpt which talks about DPC regeneration by "growth of papilla cells in 3D spheroid cultures" implanted into skin:
I dont know what to say. Just let that sink in.
You are very welcome.
I started off using minox, emu oil, oleuropein, Saw palmetto and ketoconazole. Now I'm using Minox, EGCG, OL, GLA, ketoconazole and miconazole. I'm going to add Valproic acid, apple polyphenols, Rosemary and a different brand of GLA in the form of safflower oil. I think this is as far as I will go and this should be more than enough to see steady regrowth. The problem is I'm being impatient and thats a bad trait to have when watching hair to grow (or a tree to grow). If I were to choose a few core treatments to stick to I'd say minox, egcg, ol, keto, rosemary and gla. We keep discovering new studies and pathways that enhance or inhibit hair growth so its inevitable that in a few months time this protocol will change. This is still an experiment in progress so nothing is fixed yet until I've become nw0. Moreover, treating AGA is an optimisation problem where we have to find the treatments that have the best cost to effectiveness ratio and ease of acquisition/application - which takes trial and error. And even after complete regrowth, we have to find a maintenance protocol that doesnt require aggressive planning or time. I firmly believe in never settling for less. There is always room for improvement.
Looking at histogens preliminary results and theory I would say their treatment has potential to grow hair in less aggressive AGA. This idea of using cultured stem cell/growth factors (?) injected only once into scalps is definitely more convenient than daily topical use. The only problem is AR.
Replicels methodology is better that histogens on paper:
I previously stated that these implanted DPC cells might fail to create a functional hair canal with outer root sheath cells but that was ignorant of me to say without fully understand how follicular neogenesis works.
Instead of occipital hair cells I think replicel might have more success with beard DPC since they actually thrive in the presence of DHT and release IGF-1 to nearby follicles. I realise that culturing these cells is not an easy task so atm its all looking really good on paper. But just because it seems to work on paper and mice doesnt mean it'll translate the same in human balding scalp.
For now all we can do guess when they will be ready to release their treatments. I think the main problem is the researchers like hyping their work before they can actually execute it properly. I think we should stop holding our breath for these companies and look for alternative treatments that we can use immediately, and when these do finally come out, it'll be a win-win. Otherwise you'll just be setting yourself up for disappointment.
Yes I'm nearly finished writing up the material for the new thread which will all the treatments with the relevant dosing and science, plus all the research in this thread formatted nicely so it's easy to find. Its proving to harder than I thought gathering all the research scattered all over this thread but I'm nearly done.
I've stated before that I fully believe my results were attributed to minox with the other treatments merely potentiating the rate of regrowth. When I tried minox, fin and keto back in april 2015 it took 2 months before I saw visible improvement and it wasnt anything spectacular. With OL + Minox and keto/mico I saw very fast terminal differentiation of vellus hairs when I was applying 3x a day for 2 weeks. (I will make a proper progress log too). I will talk more about testing methodology and gauging effectiveness of treatments in the new thread so I dont keep repeating myself however the point you raise about which treatment is actually working - is important.
I cant comment on keto and RU since their side effects are subjective and varying but personally I havent experienced anything bad with Keto (I use the cream form). This shedding that people experience could be a good sign of new anagen entry but it could also be coincidence - you will see more bad experiences because people dont post unless they see a change for the worst. Thats something to keep in mind when reading anecdotes.
Targeted disruption of the p160 coactivator interface of androgen receptor (AR) selectively inhibits AR activity in both androgen-dependent and castration-resistant AR-expressing prostate cancer cells.
Good find as always Seuxin.
Nearly forgot:
http://imgur.com/a/g6TdQ
http://imgur.com/a/aV65d - taken today.Comment
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Chemical, could you please confirm how much OL and EGCG we should be using per ml? Thanks.Comment
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