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Is it possible that mewing will constrict the blood flow to the scalp and cause hair loss? Sometimes I worry about this…
If you are chronically tensing the muscles in your skull, it would be plausible. But then you would not be mewing correctly. If anything, reversing craniofacial dystrophy has high potential for reversing some of hair loss too. Here is an interesting article regarding the topic: https://tmdocclusion.com/2018/07/14/more-on-hair-loss/
I believe mewing and posture correction brought my hairline down and possibly also filled in the temples area with new hair. Complimentary practices I do to help digestion, assist driving blood to my head and clearing wastes may have contributed. Mewing won’t constrict blood flow when done correctly, but it may not increase it sufficiently, so complimentary practices such as chewing, face massage, inversion therapy, posture correction, nutritional approaches and lymphatic drainage may help.
Remember this pain… and let it activate you.
Is it possible that mewing will constrict the blood flow to the scalp and cause hair loss? Sometimes I worry about this…
How would mewing constrict blood flow to the head?
If you are chronically tensing the muscles in your skull, it would be plausible. But then you would not be mewing correctly. If anything, reversing craniofacial dystrophy has high potential for reversing some of hair loss too. Here is an interesting article regarding the topic: https://tmdocclusion.com/2018/07/14/more-on-hair-loss/
Tensing what muscles in the skull would lead to baldness? Have not heard of this
What gave me this impression was from issues I deal with in other parts of my body, specifically the quads and iliopsoas. I have dealt with debilitating pelvic and back pain for 7 years following a sports accident. This is actually how I discovered mewing: a means of reprogramming the neurological pathways of the head/spine/pelvis relationship. From what my pain management specialist has told me, intense muscle spasms can contract hard enough to prevent adequate blood flow in and out of the tissue.
Also I wonder why Mike Mew is bald and has great forward growth. I always figured he could have greatly exposed himself to the estrogenic compounds found in most chewing gums.
If you are chronically tensing the muscles in your skull, it would be plausible. But then you would not be mewing correctly. If anything, reversing craniofacial dystrophy has high potential for reversing some of hair loss too. Here is an interesting article regarding the topic: https://tmdocclusion.com/2018/07/14/more-on-hair-loss/
Tensing what muscles in the skull would lead to baldness? Have not heard of this
I imagine chronic tension in the scalp musclutaure would lead to lessened bloodflow (= oxygen & nutrients), which in turn would result in inferior function of follicle, and possibly fibrosis. Chewing and certain facial expressions with a dystrophied skull could also lead to imbalanced activation between temporalis, occipitalis and frontalis, possibly stretching the galea in unfavourable ways. Just speculating here. I have read a few anecdotes about hair growing back after postural & structural improvements, which has convinced me that something must be happening. Whether the change happens on hormonal or mechanical level, I can only guess, but I’m leaning towards the latter. It’s also interesting to note how the last places people lose their hair from are on top of the occipitalis and temporalis muscles, areas which are also oxygenated by strong arteries:
If oxygenation is relevant, perhaps improved nose breathing could be a factor too?
Chronic tension might be an issue, but exercising the scalp muscles actually improves blood flow. Wiggling ears and pulling back the scalp in reps. Some people claim it’s actually reversed their greying hair color and regenerated growth.
My hair was beginning to recede when I started to Mew and I didn’t think that was a coincidence. It wasn’t the oral posture that was affecting me it was my body posture. In Kyphosis&Lordosis(hunchback posture) The back muscles and the Neck Extensors(back neck muscles) Becomes short and tight while the abs, pecs, and frontal neck muscles get short. Since the muscles are already tight in just a normal slouched position, they become even tighter while trying to stand or sit upright. Rather than properly trying to fix my Kyphosis I just stood and sit up straight.
“When neck muscles are in continuous tension, their action propagates to the head, stretching and tightening the galea against the underlying layers of the scalp. The underlying structure is rich of blood vessels that are compressed, blocking blood flow towards the hair follicles. The restriction in blood supply to tissues is called ischemia: this leads to insufficiency of oxygen (hypoxia), reduced availability of nutrients and inadequate removal of metabolites. This obviously leads to the death of tissues, thus including the hair follicles (hair loss) and surrounding structures. This is also reflected in the presence of dandruff (excessive shedding of dead cells from the scalp).” https://tmdocclusion.com/home/connection-to-other-diseases-and-syndromes/hair-loss/
Mewing will raise cortisol if not done sunconsciously.
Nope. Hair loss is caused by a genetic defect of the androgen receptor at the hair follicle, and nothing else. The galea theory has largely been discredited, and if it were at all true, then 5-alpha reductase inhibitors like finasteride and dutasteride would not stop hair loss. Furthermore, given recent research by Dr. Cotsarelis, this type of hair loss, like shock loss/telogen effluvium, would be temporary at worst given that *actual* male pattern baldness aka hair follicle “death” is caused by androgen-mediated PGD2 (there are now MBP drugs in development specifically blocking the PGD2 receptor known as CRTH2) -> PGJ2 killer inflammation as a result of DHT, and to a much lesser degree testosterone, binding to the defective receptors at the hair follicle.
In short, I wouldn’t worry about it at all my dude 🙂 if you want to be absolutely certain though, you can always grab a knife and stab yourself in the scalp a few times — if it bleeds, there’s probably blood coming to it 😉
Nope. Hair loss is caused by a genetic defect of the androgen receptor at the hair follicle, and nothing else. The galea theory has largely been discredited, and if it were at all true, then 5-alpha reductase inhibitors like finasteride and dutasteride would not stop hair loss. Furthermore, given recent research by Dr. Cotsarelis, this type of hair loss, like shock loss/telogen effluvium, would be temporary at worst given that *actual* male pattern baldness aka hair follicle “death” is caused by androgen-mediated PGD2 (there are now MBP drugs in development specifically blocking the PGD2 receptor known as CRTH2) -> PGJ2 killer inflammation as a result of DHT, and to a much lesser degree testosterone, binding to the defective receptors at the hair follicle.
In short, I wouldn’t worry about it at all my dude 🙂 if you want to be absolutely certain though, you can always grab a knife and stab yourself in the scalp a few times — if it bleeds, there’s probably blood coming to it 😉
What would in your view explain hair loss increasing with age in spite of androgen activity decreasing?
DHT seems to be a scapegoat, or at the very least not the full explanation. Its presence in a struggling follicle is not a proof of it being the driving force behind hairloss. Why does DHT raise in the follicle in the first place? Does not happen spontaneously – it would have to occur as a response to some change, such as weakened circulation. Can you come up with a more fitting explanation?
As for your quip about stabbing the scalp, doing such would not be illuminating, since we are talking about microcirculation, not overall circulation of the scalp. Blood is still coursing throughout the major arteries and veins of the scalp, regardless of whether or not individual follicles are sufficiently plugged in to the blood flow.
Nope. Hair loss is caused by a genetic defect of the androgen receptor at the hair follicle, and nothing else. The galea theory has largely been discredited, and if it were at all true, then 5-alpha reductase inhibitors like finasteride and dutasteride would not stop hair loss. Furthermore, given recent research by Dr. Cotsarelis, this type of hair loss, like shock loss/telogen effluvium, would be temporary at worst given that *actual* male pattern baldness aka hair follicle “death” is caused by androgen-mediated PGD2 (there are now MBP drugs in development specifically blocking the PGD2 receptor known as CRTH2) -> PGJ2 killer inflammation as a result of DHT, and to a much lesser degree testosterone, binding to the defective receptors at the hair follicle.
In short, I wouldn’t worry about it at all my dude 🙂 if you want to be absolutely certain though, you can always grab a knife and stab yourself in the scalp a few times — if it bleeds, there’s probably blood coming to it 😉
What would in your view explain hair loss increasing with age in spite of androgen activity decreasing?
DHT seems to be a scapegoat, or at the very least not the full explanation. Its presence in a struggling follicle is not a proof of it being the driving force behind hairloss. Why does DHT raise in the follicle in the first place? Does not happen spontaneously – it would have to occur as a response to some change, such as weakened circulation. Can you come up with a more fitting explanation?
As for your quip about stabbing the scalp, doing such would not be illuminating, since we are talking about microcirculation, not overall circulation of the scalp. Blood is still coursing throughout the major arteries and veins of the scalp, regardless of whether or not individual follicles are sufficiently plugged in to the blood flow.
In regards to hair loss becoming more prevalent with age, there is progressive androgen-mediated damage occurring to the follicles of those predisposed to MBP. Androgen-mediated PGD2 expression in the scalp results not only follicle “death”, but also progressive epigenetic changes in scalp tissue, most importantly, increased PTGDS (Prostaglandin D2 synthase) expression which itself leads to elevated PGD2, which then further increases PTGDS expression, in a vicious cycle which results in the progressive synthesis of ever-more PGD2 in the scalp — which is why it’s so difficult to actually regrow hair on slick bald scalp, even by nuking DHT with finasteride, dutasteride, and etc — the epigenetic changes (+PGDS -> +PGD2 -> ++PGDS …) in scalp tissue have already manifested, so even if you remove the original source of the inflammation cascade (DHT), you are still left with an environment that cannot support healthy hair follicles. Likewise, despite androgens decreasing in old age, you must also take into account changes in androgen receptor sensitivity, which can upregulate in certain tissues in the relative absence of androgens. Additionally, while androgens result in a negative signal cascade in those predisposed, there are numerous positive growth factors and signaling pathways involved in hair loss that diminish in old age which are to a degree contributory.
Actually DHT at the site of the hair follicle tends to be no more or less significantly present in individuals with or without male pattern baldness, nor does it increase in those with MBP, but you are partially right in that it is not the full explanation, nor is it THE #1 driving force (more like #2) behind hair loss. As mentioned, the driving force is the genetically defective androgen receptor at the site of the hair follicle, which reacts negatively to the binding of ALL androgens, but especially DHT, which is the “culprit” molecule here as it is the most abundant highly androgenic hormone in the human body (10-17x more binding affinity for the androgen receptor than regular testosterone).
The scalp stabbing was a joke and hyperbole. Regardless, circulation will not diminish significantly in regular, healthy scalp tissue — lack of circulation and hypoxia becomes an issue in unhealthy/bald scalp tissue due to fibrosis resultant of the chronic inflammation cascades I discussed previously.
Nope. Hair loss is caused by a genetic defect of the androgen receptor at the hair follicle, and nothing else. The galea theory has largely been discredited, and if it were at all true, then 5-alpha reductase inhibitors like finasteride and dutasteride would not stop hair loss. Furthermore, given recent research by Dr. Cotsarelis, this type of hair loss, like shock loss/telogen effluvium, would be temporary at worst given that *actual* male pattern baldness aka hair follicle “death” is caused by androgen-mediated PGD2 (there are now MBP drugs in development specifically blocking the PGD2 receptor known as CRTH2) -> PGJ2 killer inflammation as a result of DHT, and to a much lesser degree testosterone, binding to the defective receptors at the hair follicle.
In short, I wouldn’t worry about it at all my dude 🙂 if you want to be absolutely certain though, you can always grab a knife and stab yourself in the scalp a few times — if it bleeds, there’s probably blood coming to it 😉
What would in your view explain hair loss increasing with age in spite of androgen activity decreasing?
DHT seems to be a scapegoat, or at the very least not the full explanation. Its presence in a struggling follicle is not a proof of it being the driving force behind hairloss. Why does DHT raise in the follicle in the first place? Does not happen spontaneously – it would have to occur as a response to some change, such as weakened circulation. Can you come up with a more fitting explanation?
As for your quip about stabbing the scalp, doing such would not be illuminating, since we are talking about microcirculation, not overall circulation of the scalp. Blood is still coursing throughout the major arteries and veins of the scalp, regardless of whether or not individual follicles are sufficiently plugged in to the blood flow.
In regards to hair loss becoming more prevalent with age, there is progressive androgen-mediated damage occurring to the follicles of those predisposed to MBP. Androgen-mediated PGD2 expression in the scalp results not only follicle “death”, but also progressive epigenetic changes in scalp tissue, most importantly, increased PTGDS (Prostaglandin D2 synthase) expression which itself leads to elevated PGD2, which then further increases PTGDS expression, in a vicious cycle which results in the progressive synthesis of ever-more PGD2 in the scalp — which is why it’s so difficult to actually regrow hair on slick bald scalp, even by nuking DHT with finasteride, dutasteride, and etc — the epigenetic changes (+PGDS -> +PGD2 -> ++PGDS …) in scalp tissue have already manifested, so even if you remove the original source of the inflammation cascade (DHT), you are still left with an environment that cannot support healthy hair follicles. Likewise, despite androgens decreasing in old age, you must also take into account changes in androgen receptor sensitivity, which can upregulate in certain tissues in the relative absence of androgens. Additionally, while androgens result in a negative signal cascade in those predisposed, there are numerous positive growth factors and signaling pathways involved in hair loss that diminish in old age which are to a degree contributory.
Actually DHT at the site of the hair follicle tends to be no more or less significantly present in individuals with or without male pattern baldness, nor does it increase in those with MBP, but you are partially right in that it is not the full explanation, nor is it THE #1 driving force (more like #2) behind hair loss. As mentioned, the driving force is the genetically defective androgen receptor at the site of the hair follicle, which reacts negatively to the binding of ALL androgens, but especially DHT, which is the “culprit” molecule here as it is the most abundant highly androgenic hormone in the human body (10-17x more binding affinity for the androgen receptor than regular testosterone).
The scalp stabbing was a joke and hyperbole. Regardless, circulation will not diminish significantly in regular, healthy scalp tissue — lack of circulation and hypoxia becomes an issue in unhealthy/bald scalp tissue due to fibrosis resultant of the chronic inflammation cascades I discussed previously.
Thanks for your input. I will have to mull over this.
Not at the moment. I have had what could be called a mature hairline (norwood 1-2) since I was 16. I had a period of shedding last winter while I was doing daily scalp massages, a process which overall did not move the hairline into either direction. Scalp did get less rigid though, indicating that some level of fibrosis probably existed within the scalp tissue.
Perhaps the various massages contribute toward helping blood flow and/or create micro-injuries to help induce growth factors. Probably many different ways to restore hair loss; I’ve experienced a few it seems. I remember when I had my daughter and was dosed with some PGE2 (for labour induction): my hairline returned to NW0 for about 6 months. There’s a hair loss protocol that delves in to how the PGE2 may have helped there. Funnily enough, part of that protocol is stabbing your scalp (by microneedling). Another factor I suspect is at play is gut bacteria. I experienced some hair regrowth at the temples after I began eating homemade sauerkraut before each meal with some prebiotics (just honey and apple cider vinegar, but I also want to experiment with inulin). A bacteria that’s supposed to be in sauerkraut is l. reuteri which is being connected to hair regrowth. It’s also found in vaginal flora, and I kind of wonder if the way we are born has any impact on hair loss later on in life, as cesarean babies and those formula fed are found to have a different gut microbiome than those vaginally born and breastfed, and aren’t subjected to the skull-shaping forces of a vaginal birth.
Remember this pain… and let it activate you.
@Greensmoothies swisstemples is right on the money, prostaglandin manipulation along with the other angles of the protocol are crucial to hair loss and regrowth. I did his “ghetto protocol” and went from a norwood 2-3 to a native density nw1 and a pseudo nw0 (lacking full density from nw1-nw0 region) over the course of two years.
@darkindigo if your loss was from a vitamin deficiency and regrowth from correction of said deficiency then that’s pretty common – that’s not AGA, probably telogen effluvium. I think I remember reading that something like 80% of people with TE have a vit D deficiency actually. Congrats regardless, must feel good.
Is it possible that mewing will constrict the blood flow to the scalp and cause hair loss? Sometimes I worry about this…
Seriously? It is absurd and makes 0 sense.
Mewing is not some holy grail to end all ailments, it is just an experimental tool that might or might not work to some small extent. That’s it.
Male pattern baldness is caused by the person having 2 factors:
1) Follicles that are genetically sensitive to DHT
2) normal to high DHT
If you have normal or high DHT, but you don’t have follicles that are genetically sensitive to DHT, you won’t suffer from male patter baldness.
If you have low DHT, but follicles who are sensitive to DHT, you won’t suffer from male pattern baldness.
To suffer from male pattern baldness, you must have high or normal DHT range and sensitive follicles (genetic factor).
This can be easily prevented by anti androgen drugs that lower DHT such as finasteride and dutasteride.
How can your theory have any sense when it is only MEN who suffer from male pattern baldness. And what is the main difference between men and women? Hormonal development and higher DHT levels not head tensing.
30 yo, need to expand palate, move maxilla upward and forward, reduce gonial angle.
While I do disagree with varbro, we can agree to disagree. With that being said, I will just leave these links and articles here for you all to read them. All I ask is to keep an open mind.
Here is a quote from the comment section on the bottom page from the second link
” The model for hair loss proposed here explain the causes behind predisposition to hair loss. Predisposition means that, in presence of these factors (i.e. poor craniofacial development and its consequences), some people may suffer of hair loss, others may not. But still if you see a bald person, you will always find them. As I wrote in another article ( https://tmdocclusion.com/home/my-story/tmd-symptoms/ ): Please note that I am talking about predisposition. Why? Because every body is different and every body reacts differently under similar conditions. This means you can find the biggest jaw problems on Earth but no symptoms and at the same time a person can have the worst symptoms but just few millimeters problems in his jaw. However, if you find some of these symptoms, it is my believe that jaw problems are always present!”
https://tmdocclusion.com/home/connection-to-other-diseases-and-syndromes/hair-loss/
https://tmdocclusion.com/2018/07/14/more-on-hair-loss/
If hair loss is genetic, than why is Mike Mews father John Mew have a full head of hair while Mike is balding? Those first 2 links basically say that when your head is not right you will get tension in your head which restricts blood flow to your hair and thus you lose your hair.
I will also leave these 2 links here from a guy who has been researching hairloss for a while and managed to reverse his own hair loss even when he was told he was going to go bald because of his genetics
https://perfecthairhealth.com/genes-and-hair-loss-not-so-simple-anymore/
https://perfecthairhealth.com/the-leading-theories-of-pattern-hair-loss/
These are good reads.
@FutureModel cope. Hair loss science is well established and galea theory put forward on that tmdocclusion site has been debunked time and time again.
Mike Mew is bald because his father doesn’t reproduce asexually, like, he has a mom and genetic recombination is a thing. She more than likely has MBP genes which she passed on to Mike. And according to that ridiculous theiry John Mew should be the bald one here since he has worse craniofacial development?
Stop reading broscience articles written by people with zero understanding of biochem and pick up a scientific journal. Just because mainstream orthodontics gets things wrong doesn’t mean you have to be contrarian about literally everything else.
Never heard of a study that confirms that. Maybe you should apply as a test person :)!
Haha we need to invite swisstemples to this discussion. Theres already at least 2 or 3 phg members in this thread alone
I’m a little late to this thread guys, but I have some info relevant to this issue.
First, I have recently come across some information on the resurfacing of the scalp tension theory of hair loss, which apparently, though not new in general as a theory, as it existed before the androgen theory, nonetheless has returned given new evidence. The idea here is that cronic scalp tension leads to inflammation, which leads to a cascade of effects including DHT as a component, that ultimately results in scar tissue that hinders further growth. I will provide a link bellow for more information.
One piece of evidence that supports this is that the areas on the scalp where the tension is the greatest, corresponds precisely to the Norwood progression patterns, and areas of loss, being around the temples, the forehead, the top, and even bellow the occipital region. The correlation there is very high to be coincidental. Note again, this theory doesn’t ignore the androgen component, but it is arguing that underlying imflamation, caused by chronic tension (though there could be other causes in principle) is the source of the cascade of effects.
The next part is anecdotal, but here me out. So, I have had hair loss for like over 20 years, but if you saw me, its hardly noticble unless I really pull my hairline back. I have a “slow” going rate of progression.
I want to note two coincidences. First, the hairloss has been a little worse on my left side, whereas, my right side has been for years, vertically untouched, or just not as bad, always lagging far behind by comparison. The right side of my face and skull is asymetrical compared to the left, with the left side being more developed facially. guess what, I sleep on my right side, so constantly sleeping on that side, I think, coupled with charnifacial dystrophy, has made that side more “pushed in”. Well guess what, that would result in less tension, as the regions where the tension is the greatest is the areas where the skin is pulled the most taught.
For a while I had wondered about the skull expansion theory of baldness and how that might have played a roll in my own case if true. Of course I always dismissed it due to the obvious effect on hair loss from taking anti-androgens, none of which I’ve ever taken, to help with the hair loss.
However, in leu of the scap tension theory, it makes a little more sense if one side of my face was simply not subject to as much tension, hence less baldness.
Now that much isn’t in my mind very strong.
However..this is interesting.
Like four years ago I received two injections of PRP and Extra cellular matrix for hair loss. This is the only hair loss treatment I have ever received. And they did do some regrowth, that was well evidenced from the pictures. My hair thicked a bit, and the hair line came forward slightly. So, definitely improvement.
Recently though, within the last two years, I have noticed some ‘mild’ temple recession, as in the temples are just starting to go. And this is WIERD.
Why?
Because it is strange that the hairless suddenly out of nowhere is accelerating in terms of the rate of progression, given that one of the determining factors is hair growth cycle according to the androgen theory. There are many factors, so that in itself isn’t astonishing by itself.
But I have been HARD mewing for the last two years. AND, I have felt it, and can feel it in my temples, like all the time. AND, I was even doing mastic gum for a while and my jaw got huge as did my temple muscles. I stopped it because I didn’t like the look of it.
But…the hair loss in exactly that region does correspond to the scalp tension model, and even though I received injections for hairloss, all of a sudden the hair loss gets worse corresponding exactly to that area.
So, I received more injections just the other week, but I am going to go get a botox injection to the scalp, as you can paralyze those muscles. Some doctors have been using this to treat hairloss, and it gets results, lending support to the scalp tension theory. The botox injections are like 750$ from one place that quoted me, and you need them like twice a year. But the good news is the muscles atrophy so you would need them less often in the future.
Of course that doesn’t correct the underlying problem, which is improper musculature. Much like myofucntional therapy, the underlying muscle pattern needs to be corrected. I need to find out what I have been doing wrong with Mewing as well.
Anyways, just wanted to add that.
Google secret of athleticism
It absolutely has nothing to do with balding in any way, shape or form. My 10 mewers and myself have all mewed our ways into Chad and myself Gigachad territory, and nobody has balded our hairlines are all the same but everyone we know who didn’t mew or do anything, balded. So the choice is yours
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