https://www.hairlosstalk.com/intera...es-and-one-new-one.12832/?p=647686&viewfull=1
Galea theory is crap
Come on ideal, it was debunked long time ago
Galea theory is crap
Come on ideal, it was debunked long time ago
Why The Galea Is The Fundamental Cause Of Male Pattern Balding (& Androgens Are Secondary)
- Thread starter IdealForehead
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It's not crap, it's very legitimate. In fact, it's the best theory we have today.
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I tried to comment on transplant experiements and how they can be best made sense of within my original post in this thread.
I think the galeal tension theory can absolutely still explain why hairs continue to bald even when moved away from the galeal region if we consider a major mechanism of galeal tension to be exerted epigenetically over the course of early developmemt.
We know the galeal tension pattern mirrors the Norwood pattern very well. We also know mechanical stress proteins can upregulate genes for androgen sensitivity. We don't know how early epigenetic changes in the follicles may result from these factors, but conceivably it may then be from the very beginning of our development.
Ie. Galeal stress patterns may be what determine the androgen sensitivity of our scalp follicles and program them into the Norwood distribution that determines their androgen sensitivity for life.
Someone asked in an another thread why then some men lose their temporal points first. I found this diagram of anatomy which shows we may have a temporal fascia in the temporal region that balds first in some men:
This fascia would be expected to act the same as the galea in inducing higher androgen sensitivity in these areas. Also note at the back of the scalp where some people get retrograde nape thinning there is yet another fascia binding the occipitalis to the scalp, which could yet again have the same effect as the galea. We all have natural variations in our anatomy.
I don't know enough about monkeys to comment on why they bald as they do. I also don't have all the answers to all questions of human development. I don't think anyone does. But I think this is the best current theory we can apply based on current evidence to understand why our human hair has the Norwood androgen sensitivity pattern and where the fundamental trigger for that comes from.
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A new user (@VonMises just joined and posted some of his own 2D models he made based on this research here. They are 2D models so not perfect representations, but they still can be used to manifest the Norwood pattern well enough. He also modeled what I was discussing yesterday about applying anchors to the galea to surgically unload it. At least with this simplified model, it suggests you only really need a few anchors at the corners on each side to almost completely de-load the galea.
This is mostly just useful from a conceptual standpoint. Again, if androgenic sensitivity patterns are set early in development, then even if you set the anchors in adulthood, your hair might remain androgen sensitive and be at risk of balding even despite removing the galeal stress. But in theory, based on this model as well as the Botox study, we should expect such an approach would still reduce the balding progression considerably.
His basic model I think implies an excessive degree of forelock preservation (pink zone) at the bottom than what is actually expected. This may be due to his model being rather simply 2D in its design. Either way, it is very useful from a theoretical standpoint.
Here is his original model:
And here is the same model with galeal anchors placed behind the frontotemporal zones:
With the anchors placed (red dots on the bottom left white grid), the entire scalp is deloaded (becomes pink) and the galeal tension is relieved.
Obviously this model is an oversimplification of the real world condition, but it does illustrate that if this type of galeal anchoring was possible to be performed, it might reduce the stress considerably and we may not need to anchor the entire perimeter of the galea to do it.
(Please don't try DIY stapling your galea to your skull...)
This is mostly just useful from a conceptual standpoint. Again, if androgenic sensitivity patterns are set early in development, then even if you set the anchors in adulthood, your hair might remain androgen sensitive and be at risk of balding even despite removing the galeal stress. But in theory, based on this model as well as the Botox study, we should expect such an approach would still reduce the balding progression considerably.
His basic model I think implies an excessive degree of forelock preservation (pink zone) at the bottom than what is actually expected. This may be due to his model being rather simply 2D in its design. Either way, it is very useful from a theoretical standpoint.
Here is his original model:
And here is the same model with galeal anchors placed behind the frontotemporal zones:
With the anchors placed (red dots on the bottom left white grid), the entire scalp is deloaded (becomes pink) and the galeal tension is relieved.
Obviously this model is an oversimplification of the real world condition, but it does illustrate that if this type of galeal anchoring was possible to be performed, it might reduce the stress considerably and we may not need to anchor the entire perimeter of the galea to do it.
(Please don't try DIY stapling your galea to your skull...)
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It doesn't explain any of these things because it's bullshit.
InBeforeTheCure posted no shortage of research in the RepliCel hype thread that disproved this whole galea thing.
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That's not actually correct. The evidence he posted involved studies showing that:
- Transplanted hair from the NW7 donor zone retains its characteristics once moved elsewhere in the body.
- Hair from the Norwood galeal zone retains its sensitivity to androgens when moved away from the galea.
Both of these points were addressed in my original post and repeatedly in replies since. These transplantation studies can be explained within the galeal tension model if galeal tension upregulates and induces epigenetic changes to androgen sensitivity genes early in development, thus establishing the Norwood pattern of androgen sensitivity as part of our developmental process. Such early epigenetic change would not be easily reversed later in life even with hair follicle relocation.
This, again, is why I am suggesting that although Botox helps the problem, and we should expect any therapy that reduces tension on the galea to do so, surgically deloading the galea with anchors in adulthood may not solve the fundamental process.
Individual and racial differences in balding propensity would be genetically determined by the degree of androgen sensitivity upregulation the galeal stress induces, which just like all individual factors, would be expected to vary from one person to another. Again, I explained that in the original post.
I addressed retrograde and temple point androgenic alopecia above as possibly resulting based on natural variations in the fascia of the skull with a diagram supporting such variations.
A good hypothesis and theory integrates the most known scientific information into one cohesive whole. If you are aware of any newer or more comprehensive theories to explain the findings I reviewed in my original post of this thread, I would be interested to read it. I have always sought to adapt and adjust my belief system to whatever has the best evidence and makes the most sense.
Currently, I think this is the best model we can use to understand the pathogenesis of androgenic alopecia as an integrated whole.
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You could get some gold threads implanted:
https://www.ncbi.nlm.nih.gov/pubmed/29399026
Then there is carboxyl therapy:
https://onlinelibrary.wiley.com/doi/abs/10.1111/jocd.12501
Or the classic scalp tension relaxer!
pdf-archive.com/2017/07/11/scalp-relaxer-study/scalp-relaxer-study.pdf
And dont forget to take care about your fibrosis, you dont wanna your scalp to look like this, do you?
https://www.ncbi.nlm.nih.gov/pubmed/29399026
Then there is carboxyl therapy:
https://onlinelibrary.wiley.com/doi/abs/10.1111/jocd.12501
Or the classic scalp tension relaxer!
pdf-archive.com/2017/07/11/scalp-relaxer-study/scalp-relaxer-study.pdf
And dont forget to take care about your fibrosis, you dont wanna your scalp to look like this, do you?
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There is no way to directly relax the galea since it's not a muscle - it's just fibrous tissue. So you'd have to manifest the muscle relaxation in the same muscles that surround and attach to it that were targeted in the botox study: "frontalis, temporalis, periauricular, and occipitalis".
This basically means forehead, and the entire NW7 zone.
It's an interesting idea - applying a topical to your NW7 horseshoe in order to save the rest of the hair.
In theory it would provide the same potential benefit as Botox. I just searched and cyclobenzaprine and baclofen are two muscle relaxants that come up. I'm not sure if you'd get woozy or feel funny from those going systemic.
It would seem much simpler and more efficient to just get Botox injections if you wanted this effect once every 6 months and be free from needing to apply muscle relaxers to your forehead and NW7 scalp daily.
How about scalp massaging? I understand its effectiveness is controversial but if balding was due to scalp tension, doesn't massaging introduce more tension, or is it because it actually relieves tension build up and hence helps to alleviate balding.
the smoking baby
Established Member
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I would love to see more research into Botox and hairloss. In January, I contacted Brian Freund, one of the researchers who did the Botox study, to find out if there were plans for expanding the study's parameters (number of patients, number of injections, duration). He told me that no further research could be done, not because there weren't results worth further investigation, but because the cost of these small studies have gone up significantly in costs due to increased regulations. I believe that the study was financed through the NIH and not the makers of Botox.
Look man, you can keep telling yourself whatever you want; it doesn't change what actually went down.
I urge everyone to go over and actually read that thread if they haven't — He responded to each of the points and shot them down with studies that have solid data and pointed out how this theory contradicts proven medical practices.
The theory has been investigated and it has been debunked.
The effects of DHT upon genetic "defects" of the follicle itself are undeniably the cause of male pattern baldness; the decades of scientific study and the effectiveness of Anti-Androgens have proven this.
Studies using human cells like Jahoda, Tsuji, etc. have demonstrated for 20 years that it not only works to create hair but is a viable option for treating hairloss when it can be brought to market and their results further debunk the Galea theory.
What does all this mean? No matter how bad you want to believe it, anti-androgens like finasteride or transplants are your only chance of fighting this and your only future options are going to be cultivated cells that grow primordial hair follicles in-vitro and wounding protocols — like it or not.
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The Galeo theory does seem to imply that male pattern baldness is an isolated condition. However, I'm inclined to think that it's a general correlate of the distribution of androgen receptors within the body, given the associations with heart disease and prostate cancer.
The similarity in shape, though, is interesting.
The similarity in shape, though, is interesting.
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From what you're saying, I don't think you actually read this thread, which was written and put together with the discussion from the other preliminary thread taken into account. This is the best purpose of an open forum like this. It allows us to learn from one another and form more comprehensive views. But only if you go into it with a good spirit.
To make it simple, basically, the only thing new things this theory would suggest are:
1) Galeal tension is mechanism for how the Norwood pattern epigenetic programming of androgenic hair sensitivity occurs.
2) This programming likely occurs very early in our development, and is at least relatively permanent once set.
3) Reducing scalp tension can reduce some of the progression of male pattern baldness, but likely not change the basic Norwood programming once established.
It does not in any way refute that DHT damages hair or that finasteride is an important treatment strategy. Those mechanisms and how they fit together are covered in my original post.
The studies that you refer to on transplantation were very useful to determining "when" the galea most likely exerts its influence on the follicles and how permanent that influence is. Given that transplanted hair does not quickly change characteristics based on where you put it (at least for up to a few years), it suggests the tension-mediated androgen sensitivity epigenetic programming is set during early development, and it is relatively permanent once set.
Please consider reading the first post and thread in its entirety before you comment further. I don't mean that in a rude way. I mean it sincerely. It's just hard to discuss when you seem to be making false assumptions about what I am or am not saying in this thread.
For example, I was very, very, very clear about the importance of androgens and anti-androgens like finasteride in the pathogenesis and treatment of this problem. And I also made the same point as you, which is that people should stick with conventional treatments (plus perhaps Botox) unless stem cells possibly offer something new.
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Unfortunately it's actual very difficult to think of an ideal interventional methodology to determine in a concrete sense whether galeal tension is what induces the androgen sensitivity or not. I'm not sure if there are already sufficient studies to know.
We would first need be understand at what stage of life the androgen sensitivity is programmed into the hair. I'm not sure if this has already been done. To do this, you would need to biopsy hair follicles and scalp from humans/macaques at various stages of development and perform analyses to evaluate their androgen sensitivity related gene expression/epigenetics.
This would mean first likely comparing a newborn to an adult. If the newborn has not yet established a "Norwood pattern" of epigenetic programming to their scalp, then it suggests, the programming occurs some time after birth and during development. Further analyses could be done to narrow down when in childhood or adolescence this occurs. If this programming occurs during childhood or adolescence, then theoretically an approach like illustrated above with galeal anchors to unload the scalp in advance of this "programming age" could be done to prevent sufficient galeal stress from being exerted (and thus prevent androgen sensitivity from developing).
I have been pondering this the past two days and think this is unlikely though. I think more likely, just like all many other features of our development, the programming is occurring even in the womb. Babies make facial expressions even in utero. Galeal pressures will be exerted even before birth. The timing of development could only then be established then by biopsying scalps of fetuses at various points of embryonic development. I suppose studies on embryonic development are probably done in science with aborted fetuses, but this would be completely grotesque and pointless as it's just for curiosity's sake at that point.
So the only way to "prove" that galeal stress induces the androgenic programming in a real sense will be through cell biologists publishing more data on how integrins and mechanical stress proteins upregulate genes for androgen sensitivity. Ie. Wait for more studies to on the different pathways by which mechanical stress upregulates androgen sensitivity and androgen production in the galeal regions.
Perhaps some real world galeal tension studies could be done to confirm the tension modelling is correct as well. Maybe such studies could be done on fresh cadavers. But this gets quite macabre (fetuses and cadavers) as you can see and is not any type of research anyone jumps to do. I'd rather just wait for more cell biology.
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Interestingly enough, the authors of the finite element analysis (here) commented on the connection to prostates in their study as follows:
Undoubtedly, the primary cause of Androgenetic Alopecia is intrinsic to hereditary predisposition, and a possible genetic factor could be the degree of response to mechanical stimuli in each individual. The pathology that presents greater association with Androgenetic Alopecia is benign prostatic hyperplasia (BPH)[30] and recent research links BPH pathogenesis with prostatic pressure.[31] Thus, the genes that regulate mechanosensitivity in androgen target tissues could be critically involved in Androgenetic Alopecia etiology.
In other words, pressure-related factors may play a mediating role in prostate problems too. Those of us who highly express androgen sensitivity genes in response to mechanical stress may upregulate these genes both in our Norwood distribution of hair follicles and prostates, creating a linked problem.
The article they link to suggesting prostate pathogenesis is also related to mechanical stress is here. An excerpt:
Benign prostatic epithelial cells demonstrate increased proliferation when cultured under pressure-induced stretch conditions. Benign prostatic epithelial cells increase their production of TGF-B under conditions of pressure-induced cyclic stretch.
Recall that increased production of TGF-beta was suggested as a fundamental part of the mechanically induced galeal stress pathway for hair as well. If prostatic cells and hair cells are in fact both "triggered" by mechanical pressures in similar pathways, it would give greater weight to the notion that mechanical stress is one of the fundamental underlying factors in the pathogenesis of male pattern baldness.
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H
Senior Member
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I think this really well thought out post. The shape similarity can't be ignored even in the front taking the shape of the widows peak. Although this would mean we are kinda screwed especially with the current direction our star companies are going I'd feel great if this was proven to be right and they could focus on that. "Most" people i guess, start going bald faster later in life despite the lowering dht production and this to me seems to fit nicely into that years of wear and tear from facial expressions deplete hair faster.
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This is a very interesting topic. Thank you for sharing. I would like your insight into a rare problem concerning hair transplants. Myself and a few others that I am aware of have experienced strange texture changes to our transplanted hair. It has become darker, thicker and more kinky than our donor hair. What do think is the cause of this in your opinion?
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I do not know too much about transplanted hair, but I have heard of some of the features you describe.
You can read some transplant surgeons opinions of this here:
https://www.realself.com/question/calgary-ab-hair-transplant-concerns
One thing I might be able to explain is the kinkiness issue. This article discusses the way curliness is imparted to a hair. They suggest hair curl is dictated by three factors:
1) The shape of the follicle when viewed from above (ie. round will make straight hair, oval will make curly)
2) The way protein bonding is performed in the hair itself
3) The shape of the tunnel path through which the follicle grows out of the skin
#3 is represented in the diagram above. If you had straight hair, but it gained a wave or curl after transplantation, perhaps this has happened because the surgical implantation and scarring/healing process has imparted a curve to the follicle's path out of the skin, and this has in turn given it a new characteristic shape to grow in.
Another possible explanation comes from the "corkscrew" type hairs that we see during androgenic alopecia. During Androgenetic Alopecia, damage to the follicles can lead them to become "corkscrews" before they eventually die. This suggests curling can be a response to trauma/damage, probably through abnormal protein bonding or degradative alterations the shape of the follicle. Damage from transplantation trauma could possible cause these alterations as well.
As for why they thicken, thickness is determined by the size (diameter) of the follicle. Perhaps if the incision slits the follicles are placed in are wider than needed, it gives the follicle a chance to "expand" as it heals, and take on this thicker appearance. I'm not sure about the darkening, as traumatized hairs often can do the opposite and lose their color.
In general, none of these factors I think have anything to do with the galea or the discussion in this thread, unless perhaps galeal stress is one of the mediating factors for these transformations. I think more likely these hairs transform due to the physical trauma the follicles go through during removal and transplantation, and that is just one of the risks of the procedure.
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