100Rings

I'm not understanding the bias here. Why is it unsubstantiated when there is studies backing him up and half baked when valid logic is being used? Literally what is the problem here?

Did you even watch the video? This point is addressed. Also no I have not used botox as cost is an issue at the moment.

Just go to my profile and scroll to the latest thread I made under my activity. I bring up the fact that women develop pattern hairloss when taking AIs. Why it develops in the male pattern could likely be due to the fact that women have an overabundance of aromatase in the frontal scalp whereas men do not. So when AIs take effect, it promarily effects those areas first, forming the familiar norwood patern. Granted this is just a theory but it makes sense. give this a watch

1. The muscle is tense. Not the dermis. Unless you had surgery done on your galea, this is a non-point. 2. Women lose their hair due to hormonal shifts and the same is heavily implied for men. For men, this hormonal shift is mediated by tension. For women, it is mediated by menopause. Two different causes occurring at two different rates of frequency for completely different reasons. Same underlying change pushed forward by totally different mechanics. 3. No you wouldn't. The tension is not constantly at the same level at all ages or even at all norwood stages. And why are you assuming kids would bald with little to no DHT present in the scalp? You do understand that without sexual maturation there can be no threat of excess DHT? Are you aware of what the muscle tension theory even posits? 4. DHT upregulation via oxygen restriction would be a gradual occurrence, not a sudden snap. Tension gradually restricts blood-oxygen from getting to the scalp which then downregulates estradiol and upregulates DHT. The tension isn't a static, unchanging force. 5. Speculating on presidents (one of which is nearly bald all over the top of his head where he got transplanted) without knowing their personal regiment or hair loss stack is a complete waste of time. Lastly, consider the following: https://perfecthairhealth.com/hair-transplants-debunk-scalp-tension-hair-loss/ Answer honestly; how much research have you done on scalp tension as a whole? Because from the way you speak, it seems to me you don't really understand the mechanics of it.

Read my latest post for the answer.

uh, never said it wasn't a theory? has nothing to do with anything. Edit: also this is frankly a stupid statement as it implies all theories are equivalent in validity which is hilariously wrong.

read my latest post

Part 1: The Evidence While the behavior of estrogenic hormones are well documented in female pattern hair loss, their influence in the male pattern hair loss process is not as documented or emphasized within the academic literature. Therefore, I’d like to start things off by highlighting a bit of background on the functions of aromatase, as well as its sister compound estradiol, on pattern hair loss as a whole. I’ve also included some studies entailing what we know about scalp tension thus far. [Scalp Tension] 1. Data proves that the areas of muscular tension are the same exact areas of hair loss, suggesting that mechanical stress plays a deterministic role in the formation of the signature ‘Norwood’ balding pattern by triggering androgen activity (i.e. DHT overproduction [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4639964] 2. It is strongly implied that the signature inflammation seen in male pattern hair loss is mediated by tension. This inflammation is understood as the main causes for TGFB1 overexpression and DHT upregulation, both of which appear to be contributing factors to collagen buildup and fibrosis.[https://www.sciencedirect.com/science/article/pii/S0306987717310411] 3. In 1947, Researcher Moses Wharton Young demonstrated that monkeys, after having their scalps sutured to replicate the scalp tension seen in male humans, began to demonstrate a balding pattern remarkably similar to that which we see in male pattern hair loss. [https://journals.sagepub.com/doi/10.1177/0967772015622628?icid=int.sj-abstract.similar-articles.2#bibr12-0967772015622628] [Aromatase and Estradiol] 4. In a study involving pre and postmenopausal women with female pattern hair loss, finasteride was proven to cause a relative estradiol excess due to the reduction of DHT resulting in hair regrowth at rates of statistical significance. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5419033] 5. Further studies also confirmed that women who took aromatase suppressants (the estrogenic equivalent of 5AR suppressants) experienced accelerated hair loss, likely due to an unmitigated conversion of T into DHT in the absence of normal levels of aromatase [https://sci-hub.et-fine.com/10.1034/j.1600-0625.2002.110413.x] 6. This paper notes that aromatase appears to serve a regulatory role with DHT, both limiting and regulating its production. This makes sense when considering both aromatase and 5AR feed off testosterone to create estradiol and DHT, strongly implying a hormonal balancing act is at play. [https://www.jidonline.org/article/S0022-202X(15)42988-4/pdf] 7. A biological man with MPHL took oral estradiol and spironolactone for 6 months and regrew statistically significant amounts of hair. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5367483] 8. A study comparing the results of PRP injections treated with estradiol and those untreated with estradiol concluded that the estradiol treated injections were superior in efficacy to a staggering degree (those treated with estradiol-PRP at the 1 month mark showed results superior to those treated with just pure PRP at the 12 month mark) [https://academic.oup.com/asj/article/40/11/NP613/5854761?login=false] 9. This paper notes that aromatase and the subsequent production of estradiol mitigates and regulates the production of scalp tissue T conversion into DHT by acting as an adjacent androgenic process. Again, aromatase and 5AR appear to feed off of scalp T at rates that achieve a sort of hormonal equilibrium. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171668] 10. This paper speaks on the pathogenesis of FPHL stating that the markedly lesser severity of FPHL when compared to MPHL is more than likely due to the significantly higher levels of estradiol in female balding scalp areas since estradiol has a protective effect against hair loss in the vast majority of cases. It is theorized that the estradiol-DHT imbalance is less severe in women than it is in men [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769411] 11. Two teenage boys developed female pattern hair loss after taking aromatase inhibitors. They had no medical history of hair loss prior to the aromatase inhibition. [https://sci-hub.et-fine.com/10.1111/pde.14339] Part 2: The Role of Scalp Tension With a bit of context provided by the data, we can now discuss the muscle tension theory directly. As the theory goes, the scalps of men suffering from MPHL are observed to be under chronic, low level and perpetual tension sourced in the galea aponeurotica. This tension pinches off vital pathways for blood flow, creating a bloodless and, most importantly, hypoxic scalp environment. Due to this hypoxia, aromatase, the counterbalancing force against 5AR, cannot properly convert T into estradiol because estradiol is an oxygen dependent compound and the tension is limiting blood flow and thus sufficient oxygen supply. Less blood flow means less oxygen; less oxygen means less estradiol. This results in the downregulation of estradiol and the upregulation of DHT since 5AR now has unmitigated access to T, This dramatic upregulation of DHT occurs for two reasons: Aromatase cannot convert T into estradiol without at least a mole of oxygen. Testosterone has been shown to favor conversion into DHT when in hypoxic environments. (i.e. upregulation) [https://www.sciencedirect.com/science/article/pii/S0306987717310411][https://journals.lww.com/plasreconsurg/Abstract/1996/05000/TranscutaneousPo2of_the_Scalp_in_Male_Pattern.3.aspx] Part 3: How does Botulinum Toxin Fit Into All of This? Botulinum toxin thus works to repair the hormonal imbalance by reintroducing oxygen via blood flow back into the scalp. With proper oxygen levels restored, the counterbalancing effect of estradiol is brought back into play; Not only is 5AR forced to share scalp T with aromatase resulting in less DHT on average, estradiol’s anagen elongating effects also take effect, further strengthening the balance between the two forces. This conclusion is reached by several research groups given their findings of significantly low blood-oxygen levels inherent to the scalps of men with MPB, the affinity T has for conversion to DHT in hypoxic tissue and the very positive effect estradiol has on hair growth in both men and women in combination with estradiol's oxygen dependent nature. [https://drive.google.com/file/d/14qhsSXZ0kVeTPtXGNhPpRYavwt22hFIR/view?usp=sharing] We probably all agree that botulinum toxin has no direct effect on androgens. In other words, Botox itself does not fight against MPHL on a direct, androgenic level. However, research heavily suggests, 5AR works in tandem with aromatase to achieve an equilibrium between the DHT and estradiol in the scalp. When this balance is upset and estradiol production becomes restricted due to hypoxic scalp conditions triggered by galea tension, DHT upregulation begins; 5AR now has uninhibited access to all T in the scalp, competing with no adjacent T conversion processes. However, when botulinum toxin is administered to the galea, tension is released, blood flow is increased and oxygen levels are rejuvenated which then leads to higher levels of estradiol, lengthening of the anagen phase of the hair cycle and downregulation of DHT, achieving a hormonal equilibrium more conducive to hair growth rather than hair loss. Part 4: OK So The Theory Is Plausible…But What If It's True? The scalp muscle tension theory, if confirmed beyond all doubt as true, would answer why the scalp's area of tension, hypoxia DHT upregulation and the balding pattern itself are all one in the same. It would also account for DHT/5AR upregulation via T’s favoring of converting to DHT in hypoxic scalp environments. It would sufficiently address why intramuscular botulinum toxin is so effective, consistently bearing finasteride-esque results and why it cannot be compared to intradermal injections which, without exception, have vastly different results in, hair count, hair growth and even area of effect. The theory, while sorely needing more research, is the furthest thing from invalid. A strong hypothesis is present and it does not contradict any of the existing research on any fundamental levels. It does, however, directly challenge the DHT primacy narrative head on, calling into question if 5AR and DHT are truly the sole or even the most important players in the male pattern hair loss game.

I'm going to make a separate post about my findings, stay tuned

Especially when all follicles on the head are genetically identical. It is ASSUMED that "safe zone" follicales are DHT "immune" simply because they don't miniaturize. There is no hard evidence proving dht immunity theory true. In fact, it is quite the opposite actually.. mechanical stress of the scalp and skull expansion theory are by far the most logical answer given the evidence.

It's your head bro. Do you. But don't be surprised if things go south in some years.

There is no such thing as "dht resisitant" hairs lol get on fin rn.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8061642 How in the world on a hair loss forum are people still saying transplanted hair doesn't miniaturize is absolutely beyond me 💀💀💀 you are just straight up wrong my boy. Transplanted hairs are susceptible to DHT and to insit otherwise is to remain delusional. Do you even know the science behind MPB to begin with?

They absolutely don't and I'm shocked that this blatant misinformation is still passed off as common fact. Hairs transplanted to the balding areas minaturize just as any other hair will. The process may take a lifetime or it may take several years. The amount if time it takes varries from man to man but there is no such thing as DHT "immune" hair follicles. That literally does not exist whatsoever.