TheCalciumCad
Member
- Joined
- Mar 28, 2019
- Messages
- 1,297
"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.
Since the muscle tension that tight the galea is always present, the inflammation is long-term and chronic, causing fibrosis and calcification. This further decreases the blood flow into the scalp.
Craniofacial development plays an important role in hair loss: indeed it is the real underlying cause that gives predisposition to baldness. Predisposition means that it is possible to see people with a poor craniofacial development and no signs of hair loss, but it is not possible to see bald people with a good craniofacial development. If spotting a bald person, you will be 100% sure that he has jaw problems to some extent."
"Hair follicles on top of the scalp are affected by androgenetic alopecia, while those on the sides are not.
Androgenetic model: hair follicles on top of the head show increased expression of the androgen receptor gene. However, DHT stimulates the production of pigmented terminal hair in many other areas after puberty and higher levels of androgen receptors are also found in these follicles which remain healthy, e.g. like in those in men’s beard. So, this is a paradox and thus the androgenetic model does not offer a clear explanation.
New model: neck muscular tension propagates through the myofascia to the galea, which tightens and compresses blood vessels going to the hair follicles. Instead on the sides of the head, the underlying tissue is made of muscles so it is softer and richer of blood vessels. Thus, a compression in those areas does not block blood reaching the follicles.
The scalp of bald men show higher formation of 5α-reduced metabolites and 17-ketosteroid metabolites.
Androgenetic model: although DHT is considered playing the main role in baldness, this model does not give any explanation of why DHT and other metabolities should be present in higher concentration in bald scalps. So, no explanation.
New model: when blood vessels are compressed, blood cannot reach hair follicles causing reduced availability of nutrients and inadequate removal of metabolites, damaging tissues. Then, an inflammatory response is activated and DHT is an important regulator of its activity.
Subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower.
Androgenetic model: no explanation.
New model: galea compresses blood vessels, blocking blood flow.
Miniaturization of hair follicles has been associated with deposits of densely packed collagen bundles in the follicular dermal sheath, called perifollicular fibrosis.
Androgenetic model: no explanation.
New model: when the inflammation is long-term and chronic, it causes fibrosis and calcification."
Since the muscle tension that tight the galea is always present, the inflammation is long-term and chronic, causing fibrosis and calcification. This further decreases the blood flow into the scalp.
Craniofacial development plays an important role in hair loss: indeed it is the real underlying cause that gives predisposition to baldness. Predisposition means that it is possible to see people with a poor craniofacial development and no signs of hair loss, but it is not possible to see bald people with a good craniofacial development. If spotting a bald person, you will be 100% sure that he has jaw problems to some extent."
Hair Loss: The Real Underlying Causes Are Not Androgenetic
Although there are many unknowns, the current medical world has accepted androgenetic factors as the main underlying cause of hair loss. However, all the available treatments fail to have encouragi…
tmdocclusion.com
"Hair follicles on top of the scalp are affected by androgenetic alopecia, while those on the sides are not.
Androgenetic model: hair follicles on top of the head show increased expression of the androgen receptor gene. However, DHT stimulates the production of pigmented terminal hair in many other areas after puberty and higher levels of androgen receptors are also found in these follicles which remain healthy, e.g. like in those in men’s beard. So, this is a paradox and thus the androgenetic model does not offer a clear explanation.
New model: neck muscular tension propagates through the myofascia to the galea, which tightens and compresses blood vessels going to the hair follicles. Instead on the sides of the head, the underlying tissue is made of muscles so it is softer and richer of blood vessels. Thus, a compression in those areas does not block blood reaching the follicles.
The scalp of bald men show higher formation of 5α-reduced metabolites and 17-ketosteroid metabolites.
Androgenetic model: although DHT is considered playing the main role in baldness, this model does not give any explanation of why DHT and other metabolities should be present in higher concentration in bald scalps. So, no explanation.
New model: when blood vessels are compressed, blood cannot reach hair follicles causing reduced availability of nutrients and inadequate removal of metabolites, damaging tissues. Then, an inflammatory response is activated and DHT is an important regulator of its activity.
Subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower.
Androgenetic model: no explanation.
New model: galea compresses blood vessels, blocking blood flow.
Miniaturization of hair follicles has been associated with deposits of densely packed collagen bundles in the follicular dermal sheath, called perifollicular fibrosis.
Androgenetic model: no explanation.
New model: when the inflammation is long-term and chronic, it causes fibrosis and calcification."
More on Hair Loss: Part I
So far, two months and 6000 views. What can I say? Thank you! The article with greater interest has been the one on body posture (read it here), about the importance of body alignment and how crani…
tmdocclusion.com