Hair Loss: The Real Underlying Causes Are Not Androgenetic

[Deleted member 1973]

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

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 encouraging success rates, leading to a delay for baldness rather than a complete stop. The underlying causes of baldness has to be searched somewhere else. Let us see where.
Androgenetic alopecia is a common form of hair loss in both men and women. In men, this condition is also known as male-pattern baldness and hair on side of the head are not interested, leading to the typical male-pattern hair loss depicted in the Norwood Scale of Figure 1 [1].

Figure 1 – Norwood Scale for male-pattern baldness. (From [1])Current theories see the hormone dihydrotestosterone (DHT) as the main responsible for hair loss. As the name suggests, two are the supposed causes for androgenetic alopecia: the action of hormones (androgens) and action derived from genetic.

The androgen hormone dihydrotestosterone (DHT) is synthesized from the testosterone by the enzyme 5α-reductase into the hair follicle and it is believed to be the responsible for hair loss. The DHT reacts with the androgen receptor, interfering with the DNA of the cells, inhibiting the follicle from growing healthy hair. Nevertheless, DHT stimulates the production of pigmented terminal hair in many areas after puberty, including pubic and axillary hair in both sexes and beard growth in men. Both beard growth and balding can occur on the same person demonstrating a paradox. How does the same hormone stimulate hair growth on the face while taking it away on the scalp?
The given explanation is that androgen action within individual follicles is specific to the individual follicle i.e. relates to its gene expression. This is also the explanation given to the male baldness pattern: hair follicles in the temple areas and crown are genetically programmed to have receptors that are more sensitive to the DHT action, while hair on side are genetically programmed to be immune to the DHT. Hair transplantation is based on this fact: hair follicles on side and back are considered genetically programmed to be immune to the DHT action, so transplanting them into another region should be a valid solution. But why, once transplanted, these hair start to fall again after some time, leaving patients as in Figure 2?

Figure 2 – Head with hair loss and scar from hair transplant. (From [29])There are also many other lacks that the androgenetic theory cannot answer, such as:
​

• Scalp sensitivity (burning, stinging, dry scalp, vague discomfort in the scalp, and sometimes, trichodynia) is associated with hair loss [2,3,4]. Why?​
• The last layer of the skin, called stratum corneum, consists of dead cells (corneocytes). Corneocytes are regularly replaced through desquamation and renewal from lower epidermal layers, protecting from pathogenic bacteria, fungi, parasites, viruses, heat, UV radiation and water loss. Replacement of the cells in the outermost layer of the scalp happens regularly, on a monthly base. However, certain conditions trigger a more rapid turnover, leading to a large shedding recognised as dandruff. Excessive dandruff is linked to hair loss [5]. Why?​
• Minoxidil is an antihypertensive vasodilator medication, meaning that the main action is the widening of blood vessels, and it has been found to be effective in treating baldness [6]. Also, low level laser therapy has some effectiveness on hair loss [7]. These treatments have no correlation with androgenetic factors, so why are they effective?​
• It has been found that in non-bald scalp regions, 1) each region has a uniform skin
  thickness and it is thin; 2) the skin is soft; 3) the human head is in flat shape. As for bald scalp regions, 1) each scalp region has a non-uniform skin thickness and it is thick; 2) the skin is hard; 3) the human head is in dome shape [8]. How can be this explained?​

So, are androgenetic factors the real main underlying cause of baldness?
To answer this, let us have a look to the scalp layers composition in Figure 3. Just below the scalp skin (epidermis) there is the subcutaneous tissue, where hair follicles, sweat glands, and rich vascular networks lie. Scalp vessels travel within the subcutaneous layer just superficial to the aponeurotic layer called galea. The layer below is the loose areolar connective tissue (subgaleal space) that is so named because its fibers are far enough apart to leave ample open space for interstitial fluid and abundant blood vessels in between. Then there is the periosteum, that in the skull is called pericranium. This is a membrane that covers the outer surface of the bones and it provides nourishment by providing the blood supply to the body. Blood vessels pass through all the scalp layers arriving to the hair follicles.

Figure 3 – Layers of the scalp. The epidermis, dermis, and galea glide over the pericranium as a fixed unit. Scalp vessels travel within the subcutaneous layer superficial to the galeal layer. (From [30])The galea aponeurotica is attached to the occipitofrontalis muscles, as shown in Figure 4. The temporalis muscles are also connected to the galea aponeurotica via the temporalis fascia. The galea aponeurotica can be stretched by the forces of muscular contraction.

Figure 4 – The galea aponeurotica is attached to the occipitofrontalis muscles and to the temporalis muscle via the temporalis fascia. (From [31])With the rise of civilizations, we are assisting to a down-siding of the entire craniofacial structure, with the maxilla that drops down and back. This reduces the eye support, flattens the cheekbones, narrows the nasal airway, lengthens the mid facial third, and lowers the palate, which narrows and create malocclusion [9]. As shown in Figure 5, a vertical growth of the maxilla forces the mandible to swing back. As compensatory mechanism, a retruded mandible causes the head to tilt forward in a forward head posture [10,11]. Also, vertical growth of the maxilla promotes asymmetrical craniofacial development, referred as cranial distorsions (e.g. sidebending) [12].

Figure 5 – If the maxilla grows vertically, the mandible swings back. As a compensatory mechanism, the head is extended in a forward head posture. (From [32])Abnormal posture, like in the case of forward head posture and cranial distortions, affects muscle length/tension relationships [13]. This usually leads to pain and overuse injury where small focal, degenerative changes in the insertion fibers can occur [14].

The concept of trigger points provides a framework that can be used to help address certain musculoskeletal pain. In particular, they are useful for identifying pain patterns that radiate from these points of local tenderness to broader areas, sometimes distant from the trigger point itself. As Figure 6 suggests, neck muscles’ action propagates through the entire head.

Figure 6 – Referred pains from upper trapezius, sternocleidomastoid, suboccipital, splenius capitis, splenius cervicis, semispinalis capitis,temporalis and masseter muscle trigger points. (From [15])Indeed, whatever else they may be doing individually, muscles also influence functionally integrated body-wide continuities in the fascial webbing [16]. Since muscles throughout the body are connected via myofascial meridians, their action cannot be seen in isolation. This explains why intensity of neck pain, forward head posture, chronic tension-type headache and migraine are strictly correlated [17,18,19,20].

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).

Figure 7 – Drawing explaining muscles action on the galea aponeurotica. When the galea is stretched and tightened, blood vessels are compressed impeding blood flow to reach the hair follicle. (From [33])When tissues are damaged, an inflammatory response is activated. The function of inflammation is to clear out necrotic cells and damaged tissues. The classical signs of inflammation are heat, pain and redness. These elements describe symptoms of scalp sensitivity and trichodynia.

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, promoting ulterior cells death, leading to a closed-loop chain of events depicted in Figure 8, reason why hair loss progresses with individuals becoming older.

Figure 8 – Closed-loop chain of events leading to hair loss and related symptoms.
Furthermore, the role of bones must be taken into account. Indeed, bones remodel under the presence of forces, with sutures acting growth site. The neurocranium may also expand under the compression forces generated by the above layers as a form of protection for the brain. This creates further restriction for the blood vessels, feeding the closed-loop chain of events described before.
The typical pattern of male baldness is characterized by bald frontal and vertex regions that overlie the galea, while temporal and occipital regions that overlie muscles do not lose hair, as shown in Figure 9. Muscles provide a richer network of musculocutaneous blood vessels, with larger arteries, and a softer environment than the galea, thus a compression in these regions do not cause a missing blood flow with consequent hypoxia.

Figure 9 – The typical pattern of male baldness is characterized by bald frontal and vertex regions that overlie the galea, while temporal and occipital regions that overlie muscles do not lose hair.
The confirmation of this explanation for hair loss can be found in several studies:​

• Bald subjects had a positive response when injected with Botox into the muscles surrounding the scalp, including frontalis, temporalis, periauricular, and occipitalis muscles. Conceptually, Botox “loosens” the scalp, reducing pressure on the perforating vasculature, thereby increasing blood flow and oxygen concentration. This leads to reduced hair loss and new hair growth [21].​
• The subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower than the values found in the normal individuals [22].​
• Men suffering from androgenic alopecia have significantly lower oxygen partial pressure (meaning microvascular insufficiency and hypoxia) in the areas of their scalp affected by balding (frontal and vertex regions) versus unaffected areas (temporal and occipital regions). Moreover, balding men have significantly lower oxygen partial pressure in the areas of balding scalp than the same areas of non-bald people [23].​
• It has been found that Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth [24].​
• By relieving tension at the vertex in the scalp, cutaneous blood flow rate increases, promoting hair regrowth [25].​
• Minoxidil is less effective in subjects with significant inflammation in the scalp than in subjects with no significant inflammation [26].​
• In women, significant degrees of inflammation and fibrosis is present in cases of androgenetic alopecia. Even if less significant, inflammation and fibrosis is present also in chronic telogen effluvium cases[27].​
• Dr. Frederick Hoelzel of Chicago reported the observations he made in 1916-17 while he served as a technician in gross anatomy at the College of Medicine of the University of Illinois. During that time, he removed the brains of around 80 cadavers and noticed an obvious relation between the blood vessel supply to the scalp and the quantity of hair: “baldness occurred in people where calcification of the skull bones apparently not only firmly knitted the cranial sutures but also closed or narrowed various small foramens through which blood vessels pass“. He thought this would also explain why men suffer baldness more than women, since bone growth or calcification is generally greater in males than females [28].​

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. Look around and try yourself! So, do you still believe in the androgenetic theory?​

 

[looksmaxxed]

cliffs?

 

[Deleted member 1973]

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

More on Hair Loss: Part I
Posted on July 14, 2018 by TmdOcclusion
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 craniofacial development affects total body posture. The second most popular was the article on hair loss (available here), where the current androgenetic theory is questioned and a new model has been proposed. Let us clarify some concepts expressed in there.
Current theories see the dihydrotestosterone (DHT) hormone as the main responsible for hair loss. As the name suggests, there are two supposed causes for androgenetic alopecia: the action of hormones (androgens) and action derived from genetic.
The theory started to arise after observations made on Eunuchs (i.e. men who have been castrated). Already in 400 BCE, Hippocrates noticed that Eunuchs do not become bald [1], with formal conclusions made by James B. Hamilton between 40s and 60s: eunuchoid and prepubertally castrated men fails to achieve sexual maturation and show complete retention of head hair [2]. Baldness can then be induced by following administration of male hormone substances to sexually immature men who otherwise would not have become bald [3]. In 1974, a study has generally observed a higher formation of 5α-reduced metabolites and 17-ketosteroid metabolites at all sites of the scalp of bald men as compared to hair obtained from the corresponding sites of women and nonbalding men [4]. So, from here it has been assumed the importance of DHT in baldness.
However, many arguments are against the role of DHT as primary cause in hair loss:

• DHT stimulates the production of pigmented terminal hair in many areas after puberty, including pubic and axillary hair in both sexes and beard growth in men. But both beard growth and balding can occur on the same person demonstrating a paradox [5,6].
• Serum androgen concentrations in men with a disposition to balding is lower than in men with no reduction of scalp hair [7].
• The prevalence of Male Pattern Baldness increases with age [8]. However, serum testosterone production declines with aging [9], together with lower serum DHT [10].
• Female androgenetic alopecia can develop in the absence of detectable levels of circulating androgens or other signs of postpubertal androgenization, showing that this pattern of hair loss is not necessarily androgen dependent [11]. Not only, female patients with androgen deficiency reports hair regrowth on testosterone therapy [12].

By looking to Figure 1, we can see that Male Pattern Baldness only affects hair on top of the head, while hair on sides and back does not fall. So, how can DHT cause hair in one area of the scalp to fall out but have no effect on hair follicles just a few millimeteres further down?

Figure 1 – Male Pattern Baldness, Norwood 7. Androgenetic alopecia affects only hair on top of the head. If DHT is the main cause of baldness, why hair on the sides and back are not susceptible to DHT? (From [60])Here is where the genetic part comes into action. According to the current theory, hair follicles on top of the head show increased expression of the androgen receptor gene [13], i.e. the top of the head is more sensitive to androgens action than hair on the sides and back of the head. However, higher levels of androgen receptors are also found in follicles of beard, scrotum and pubis, reinforcing the paradox [14]. Genetics also suggests that the probability of male pattern hair loss is dependent on family history and age [15]. However, in case of identical male twins, one can bald significantly faster than his counterpart [16]. These together with many other unknowns bring the necessity to define a new model for the explanation of baldness.

My studies on the subject started after a terrible personal experience (you can read my story here): a wrong splint therapy lead many symptoms to appear, among them tremendous muscular tensions in the neck. Muscles were so tight that I was exactly feeling their action propagating to the head and compressing the galea. This is when I started to lose hair at an incredible pace (Figure 2).

Figure 2– On the left, healthy hair. On the right, my hair started to thin and to fall as a consequence of the muscle stiffness in the scalp.
I will then discover that muscles are connected together through myofascial connections and their action can be propagated in distal areas [17]. This is also what the trigger point model proposes: pain frequently radiates from points of local tenderness in muscles to broader areas, sometimes distant from the muscle itself [18]. By looking to Figure 3, we can clearly understand how action of neck muscles propagate to the head, so my feelings were actually right.

Figure 3 – Referred pains from upper trapezius, sternocleidomastoid, suboccipital, splenius capitis, splenius cervicis, semispinalis capitis,temporalis and masseter muscle trigger points. Crosses represents the location of the trigger point. Red area is the referred pain pattern for that specific trigger point. (From [18])Then another particular event happened. Neck muscles tensions kept increasing up to a point that they were so severe and unbearable that lying down on a bed was the only partial pain remedy. This is how I was forced to spend three months lying down on a bed, trying every possible remedy to relax the muscles. One of the most effective method was the transcutaneous electrical nerve stimulation (usually referred as TENS). I used it applied to neck muscles and it did relax them, although its benefits were very short in time. But I noticed an incredible fact: every time my 10-minute session ended, my hair was in a really good health. It was kind of surreal for me, how was this possible? Nevertheless, muscles were tightening again after a short time period and so my hair was affected too.

This gave me more inputs on where to look for to explain the mysteries behind hair loss: I understood that action of neck muscles propagates to the galea and that there was some connection. At that point, I did not know the actual mechanisms to explain how a compressed galea was causing hair loss but I understood it was the key. Galea’s key role can be simply guessed by looking to Figure 4: balding areas of Norwood 7 pattern exactly matches galea’s anatomy. Was this just a coincidence?

Figure 4– On the left, Norwood 7 androgenetic alopecia. On the right, head and neck anatomy. Notice the bald area exactly matches the galea aponeurotica. (From [61])No, it was not a coincidence. As Figure 5 shows, blood vessels pass through all the scalp layers arriving to the hair follicles and one of these layers is the galea aponeurotica. If the galea is tightened, the blood vessels in the underlying tissues are compressed, i.e. blood cannot reach hair follicles causing reduced availability of oxygen, nutrients and inadequate removal of metabolites.

Figure 5 – Layers of the scalp. The epidermis, dermis, and galea glide over the pericranium as a fixed unit. Scalp vessels travel within the subcutaneous layer superficial to the galeal layer. (From [62])Not surprisingly, it has been found that subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower than the values found in the normal individuals [19]. This would explain the aforementioned higher formation of 5α-reduced metabolites and 17-ketosteroid metabolites at all sites of the scalp of bald men at the basis of the androgenetic theory.

The restriction in blood supply to tissues is called ischemia: this leads to insufficiency of oxygen (hypoxia). Not surprisingly again, men suffering from androgenic alopecia have significantly lower oxygen partial pressure (meaning microvascular insufficiency and hypoxia) in the areas of their scalp affected by balding (frontal and vertex regions) versus unaffected areas (temporal and occipital regions). Moreover, balding men have significantly lower oxygen partial pressure in the areas of balding scalp than the same areas of non-bald people [20].
Minoxidil solution, which is one of the commercially available medications for hair loss, stimulates the microcirculation of the bald scalp, effectively promoting hair growth [21]. Patients should be warned about increased shedding in the first months of treatment, that is seen as a positive response to the treatment [22]. How can this increased shedding be explained? Could it be the so called reperfusion injury, i.e. the tissue damage caused when blood supply returns to the tissue after a period of ischemia [23]?
In case of reduced blood supply, tissues are damaged and die, thus including the hair follicles and surrounding structures. A proof of this is the associated excessive dandruff found in hair loss [24]: the last layer of the skin, called stratum corneum, consists of dead cells (corneocytes) that are regularly replaced through desquamation. However, certain conditions trigger a more rapid turnover, leading to a larger shedding recognized as dandruff (Figure 6).

Figure 6 – Topical presentation of normal scalp and dandruff scalp. (From [25])When tissues are damaged, an inflammatory response is activated. The function of inflammation is to clear out necrotic cells and damaged tissues. The classical signs of inflammation are heat, pain and redness, situation recognized as scalp sensitivity (burning, stinging, dry scalp, vague discomfort in the scalp, and sometimes, trichodynia) that is associated with hair loss [26,27,28]. And guess what? Many studies have shown DHT plays an important role in inflammations, regulating its activity [29,30,31,32]. Could be this the explanation of why increased DHT levels are found in bald scalps?

When the inflammation is long-term and chronic, it causes fibrosis and calcification. Indeed, miniaturization of hair follicles has been associated with deposits of densely packed collagen bundles in the follicular dermal sheath, called perifollicular fibrosis [33,34,35]. This further decreases the blood flow into the scalp, promoting ulterior cells death.
So, I came to a conclusion: hair loss was not a problem of the hair itself but was a problem of the surrounding tissues. Take two seeds of a genetically identical corn, place one seed in a temperate climate and one in an arid climate: the one in the arid climate only grows to half the height of the one in the temperate climate due to lack of water and nutrients in its environment. This is exactly what happens with our hair and there are studies confirming it: miniaturized hair follicles of pattern alopecia can quickly regenerate once removed from the human scalp and can grow as well as or better than terminal follicles from the same individual [36]. And not only miniaturized hair can regrowth, but also terminal hairs can shrink in difficult recipient sites, impacting their growth and survival rates [37].
At this point, for me everything was clear. Only one thing was missing: where does this muscular tension come from? I will found out that craniofacial development has a huge impact on body posture and muscular balance. And actually all my symptoms were originating from a cranial distortion. Bingo! Now everything had an explanation!
Apparently, poor craniofacial development is a problem of civilized modern societies and not surprisingly also hair loss has widespread in the modern era. Figure 7 shows Native Sioux people that lived in the 19th Century. Their craniofacial development is something that would be considered extraordinary in our era, however at their time it was the normality. Also notice their perfect hair despite their old age. In Figure 8 we have instead a Sioux lived in our era, between the 20th and 21st Century: notice the difference in craniofacial development and the presence of hair loss.

Figure 7 – On the left, Red Cloud (1822-1909), leader of a Native American tribe (Sioux). In this picture he was 78 years old. Notice his excellent craniofacial development and how not surprisingly he has all his hair. On the right, another example of a good craniofacial development from the Sioux tribe lived in the same years. (From [63] and [64])

Figure 8– Russell Charles Means (1939-2012) was a Native American Oglala Sioux born in modern era. We can notice his poorer craniofacial development compared to his ancestors and his hair loss. (From [65])If we look to photographs taken over 100 years ago of Somalis in Figure 9, we can notice the excellent craniofacial development of the two individuals on the left and their perfect hair. However, the individual on the right has a poor craniofacial development and, not surprisingly, hair loss. In Figure 10, Barkhad Abdi, a Somali-American actor living in our era. Do you notice any difference with his ancestors?

Figure 9 – On the left, Warsame Yonis, 24 years old. In the middle, Igge Karbaashe, 20 years old and on the right Ali Gaboose, 20 years old. Notice the difference in Ali’s maxilla development and his hair loss. (From [66])

Figure 10 – Barkhad Abdi is a Somali-American actor. Notice his much poorer craniofacial development compared with his ancestors and his hair loss. (From [67])Already in 1939 Weston A. Price wrote about his travel around the world where he discovered that jaw problems were not present in tribes of isolated areas far from civilization [38]. In a simplistic view, maxilla is primarily remodeled by forces coming from the tongueand teeth (through masseter muscles) and the causes of a poor craniofacial development have to be found in modern lifestyle, in particular in:

• Increasing of bottle-feeding over breast-feeding that influences the swallowing pattern and all oral muscles [39,40,41,42].
• Use of pacifiers/dummies that mainly affect tongue posture [43,44,45,46].
• Trend towards industrial soft high-calorie food that hits chewing effort and muscles action [47,48,49].
• Reduced nasal airways, increasing of allergies and nasal congestion that leads to mouth breathing affecting both tongue posture and muscles action [50,51,52,53,54].
• Trend towards an earlier or too early weaning, influencing swallowing pattern [55,56].

When one or more of these factors are present, the maxilla drops down and back, reducing the eye support, flattening the cheekbones, narrowing the nasal airway, lengthening the mid facial third, and lowering the palate, which narrows and create malocclusion [57].
After discovering what a poor craniofacial development means for the hair, I started to look to every single person I was meeting, investigating their hair loss and the correlation with their jaws development: I never found a single bald person with a good craniofacial development! I also started to ask questions to people, curious to know the truth.
The first person I spoke with was my Portuguese housemate of that period. He had a very poor craniofacial development and he was bald. So I asked him: “Do you know if you used pacifiers or if you were bottle-fed when you were a child?”. His reply: “When I was a child, in Portugal it was almost a shame to breast-feed a child, so many mothers were opting to bottle-feed for this reason. My mother was one of those.”. No other comments are needed. Thus, I also started to ask the same questions to other people close to me: some have been breast-fed because their mother had not breast milk, some used pacifiers, some have been through a too early weaning and so on. There were no doubts that the correlation was clear.
I would like to show here some examples of famous people, so that everybody can understand what I am talking about. Figure 11 shows Prince William, Duke of Cambridge. On the left picture, you can clearly see his very narrow palate (i.e. a consequence of a poor craniofacial development). Also, if you pay attention, you will notice a cross-bite on one side and the dental midline that is shifted, sign of a cranial distortion. On the right picture, you can instead better appreciate his vertical growth of the maxilla, with missing cheekbones, missing support for the eyes, little lips, aquiline nose with little nostrils. I would not be surprised if he is a mouth-breather.

Figure 11– Prince William, Duke of Cambridge. Notice in these two pictures his poor craniofacial development: vertical growth of maxilla, narrow palate, cross-bite on one side with dental midline shifted, little lips, aquiline nose with little nostrils. (From [68])In observing other people with hair loss problems, the more severe cases I have seen were for two reasons: either their craniofacial development was extremely poor or they had an impressive cranial distortion. Now, I want to show you what I mean. In Figure 12 we can observe Angelino Alfano (an Italian politician) and his really poor craniofacial development. On the left picture we can notice his really narrow palate and the midline that is not completely centered. On the right one, we can observe his excessive vertical growth of the maxilla, with consequences on his eyes, lips and nose shape.

Figure 12– Angelo Alfano (Italian politician). Notice in these two pictures his extremely poor craniofacial development, notable from his excessive vertical growth of the maxilla, missing cheeckbones, eyes, nose and lips shape.
An example of an impressive cranial distortion is Jeff Bezos, current CEO of Amazon (Figure 13). In the left picture we can notice his narrow palate and also another important detail: look at his tongue, he has teeth signs on it. This means he has a tongue between the teeth posture, i.e. low tongue posture. In the right picture it is possible to notice his cranial distortion: asymmetrical face, asymmetrical ears, asymmetrical eyes, asymmetrical nasal philtrum and his mandible that deviates on one side.

Figure 13– Jeff Bezos, CEO of Amazon. In the left picture notice his narrow palate and the teeth signs on the tongue, meaning a tongue between the teeth posture. On the right, notice his cranial distortion. with asymmetrical face, asymmetrical ears, asymmetrical eyes and his mandible that deviates on one side. (From [69])If craniofacial development is the key for hair loss, can we predict who will have predisposition for baldness once older? My answer is yes, however predisposition does not mean that hair loss will actually happen. Let us take an example, Dwayne Douglas Johnson, an American actor also known as The Rock (Figure 14). We can see him in his younger days on the left and notice his poor craniofacial development, highlighted by a vertical facial growth, missing eyes support, missing cheekbones. These clues are signs of his predisposition to baldness. Indeed, we better know him now with his bald head, as in the photo on the right, where we can also appreciate his asymmetric smile with a shifted midline.

Figure 14– Dwayne Douglas Johnson, aka The Rock. On the left, we can notice his poor craniofacial development, highlighted by a vertical facial growth, missing eyes support, missing cheekbones when he was young and still with hair. On the right, we can appreciate a more recent photo and his teeth asymmetry with a shifted midline. (From [70])The Rock played some movies with Jason Statham and I think he is also a good example for this theory. Notice in Figure 15 his posture with an increased kyphotic curve. Also notice the tightened muscles on the side of the neck while he turns his head, i.e. reduced neck mobility. If you investigate yourself, you will also find his excessive vertical growth of the maxilla, with a narrow palate, cross-bite on both side of the teeth and a cranial distortion.

Figure 15– Jason Statham, English actor. Notice his posture with an increased kyphotic curve and the tightened muscles on the side of the neck while he turns his head, i.e. reduced neck mobility. (From [71])Another example: one day I was reading a newspaper and there was an article on the death of Danny Kirwan, guitarist of a British band named Fleetwood Mac. I did not know the band and neither him, but there was his picture when he was young that captured my attention (Figure 16).

Figure 16– A young Danny Kirwan (1950-2018), known as guitarist of the Fleetwood Mac. In this picture we can notice his long hair but his poor craniofacial development. Once older, which implications this brings to his hair? (From [72])He had perfect long hair, but a pretty poor craniofacial development. So, will he be affected by hair loss once older? According to everything I knew, yes he will! So, curious to know the answer I searched a picture of him older and guess what? He suffered of baldness (Figure 17).

Figure 17– An older Danny Kirwan (1950-2018), known as guitarist of the Fleetwood Mac. We can notice his baldness, that can be related to his poor craniofacial development. (From [73])Are you still with doubts? Then, I would like to put here a challenge. In Figure 18 there is Gianluigi Donnarumma, an Italian goalkeeper currently playing for AC Milan (2018), where we can notice his poor craniofacial development. He was born in 1999, so he is now 19 years old. Will he suffer of hair loss? Let us go back to this page in 10 or 15 years time, when he will be in his 30s, and we will probably have something new to discuss on.

Figure 18 – Gianluigi Donnarumma, Italian goalkeeper playing for AC Milan. He has a poor craniofacial development. In 10 or 15 years time, will he still have his hair? (From [74])Summary: what this new model can explain
Now, let us put everything together and let us see how this new model can better explain predisposition to baldness, comparing it with the deficits of the androgenetic model, where DHT is thought to play a main role in the disease.
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 incidence of Male Pattern Baldness increases with age. However, serum testosterone production declines with aging, together with lower serum DHT.
Androgenetic model: no explanation.
New model: neck muscular tensions that compress the galea are caused by an abnormal posture. Posture is determined by craniofacial development which depends on bone remodeling. Bone remodeling is a lifelong process, so an increase in age means a poor craniofacial development can worsen over time, with an impact on the posture. This creates higher predisposition to baldness with age.
Baldness have significantly spread in the modern era and isolated tribes are less likely to suffer of hair loss.
Androgenetic model: no explanation.
New model: craniofacial development depends on forces coming from orofacial muscles (among them, the tongue). The causes of a poor craniofacial development have to be found in modern civilized lifestyle (e.g. use of pacifiers, bottle-feeding, soft high-calorie diet, early weaning).
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.
Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth.
Androgenetic model: no explanation.
New model: minoxidil acts as a vasodilator through membrane hyperpolarization caused by opening potassium channels [58,59]. This promote blood flow, thus hair growth.
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.
Excessive dandruff and scalp sensitivity are often associated with hair loss.
Androgenetic model: no explanation.
New model: dandruff consists of dead cells (corneocytes) from the last scalp layer that are regularly replaced through desquamation. In case of reduced blood supply, cells die more rapidly triggering an excessive turnover, i.e. the dandruff. When tissues are damaged, an inflammatory response is activated. The classical signs of inflammation are heat, pain and redness, situation recognized as scalp sensitivity (burning, stinging, dry scalp, vague discomfort in the scalp, and sometimes, trichodynia).
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.
Conclusion
The model proposed on this website can explain many more things on baldness than the current androgenetic model can do. I am not here to say that it can fulfill all the unknowns of this disorder, but if the androgenetic model is accepted despite all its gaps then I do not see why this new model would not be considered and investigated. Anyway, the answer is in front of your eyes: just observe the craniofacial development and neck mobility of bald people and you will understand what I am talking about. You can contribute saying your opinion at the bottom of this page. I will try to clarify other aspects of hair loss in the second part of the article.​

 

[looksmaxxed]

just read the thesis at the end. disproven by simple google search of bald athletes

just lol at all that text for nothing

 

[currymax]

cliffs?

iqcel falls for charlatan shit

 

[Tiddlywink]

cliffs?

Lazy fuck.

 

[Effortless]

Well done!

But read, I did not.

 

[slime]

My father is bald because the government forces him to be.

 

[Deleted member 1973]

Well done!

But read, I did not.

Of course you didn't

 

[Effortless]

Of course you didn't

Ok, I read a bit now.

Brutal buddy.

 

[diggbicc]

yes I have seen this blog, seems legit.

 

[Deleted member 1464]

You should make your post more concise and to the point.
What the fuck no is reading all of this

 

[ChoSeungHui]

 

[diggbicc]

You should make your post more concise and to the point.
What the fuck no is reading all of this

TLDR: scalp tension is what restricts blood flow and causes buildup of DHT. The balding pattern for males exactly coincides with the galea of the scalp.

Also I think some experiment was done where a metal sheet was stretched and the stress pattern of the metal was mapped and it resembled that of the balding pattern of males(idk the exact study)

Certain experiments were done where botox was injected in the scalp of totally bald men to relieve the muscle tension, and noticeable hair growth was seen where hair seemed to have disappeared from, due to new blood flow.

 

[Deleted member 1973]

“baldness occurred in people where calcification of the skull bones apparently not only firmly knitted the cranial sutures but also closed or narrowed various small foramina through which blood vessels pass“. He thought this would also explain why men suffer baldness more than women since bone growth or calcification is generally greater in males than females

Could explain why people with big foreheads correlating to baldness.

 

[Gaia262]

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

More on Hair Loss: Part I
Posted on July 14, 2018 by TmdOcclusion
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 craniofacial development affects total body posture. The second most popular was the article on hair loss (available here), where the current androgenetic theory is questioned and a new model has been proposed. Let us clarify some concepts expressed in there.
Current theories see the dihydrotestosterone (DHT) hormone as the main responsible for hair loss. As the name suggests, there are two supposed causes for androgenetic alopecia: the action of hormones (androgens) and action derived from genetic.
The theory started to arise after observations made on Eunuchs (i.e. men who have been castrated). Already in 400 BCE, Hippocrates noticed that Eunuchs do not become bald [1], with formal conclusions made by James B. Hamilton between 40s and 60s: eunuchoid and prepubertally castrated men fails to achieve sexual maturation and show complete retention of head hair [2]. Baldness can then be induced by following administration of male hormone substances to sexually immature men who otherwise would not have become bald [3]. In 1974, a study has generally observed a higher formation of 5α-reduced metabolites and 17-ketosteroid metabolites at all sites of the scalp of bald men as compared to hair obtained from the corresponding sites of women and nonbalding men [4]. So, from here it has been assumed the importance of DHT in baldness.
However, many arguments are against the role of DHT as primary cause in hair loss:

• DHT stimulates the production of pigmented terminal hair in many areas after puberty, including pubic and axillary hair in both sexes and beard growth in men. But both beard growth and balding can occur on the same person demonstrating a paradox [5,6].
• Serum androgen concentrations in men with a disposition to balding is lower than in men with no reduction of scalp hair [7].
• The prevalence of Male Pattern Baldness increases with age [8]. However, serum testosterone production declines with aging [9], together with lower serum DHT [10].
• Female androgenetic alopecia can develop in the absence of detectable levels of circulating androgens or other signs of postpubertal androgenization, showing that this pattern of hair loss is not necessarily androgen dependent [11]. Not only, female patients with androgen deficiency reports hair regrowth on testosterone therapy [12].

By looking to Figure 1, we can see that Male Pattern Baldness only affects hair on top of the head, while hair on sides and back does not fall. So, how can DHT cause hair in one area of the scalp to fall out but have no effect on hair follicles just a few millimeteres further down?

Figure 1 – Male Pattern Baldness, Norwood 7. Androgenetic alopecia affects only hair on top of the head. If DHT is the main cause of baldness, why hair on the sides and back are not susceptible to DHT? (From [60])Here is where the genetic part comes into action. According to the current theory, hair follicles on top of the head show increased expression of the androgen receptor gene [13], i.e. the top of the head is more sensitive to androgens action than hair on the sides and back of the head. However, higher levels of androgen receptors are also found in follicles of beard, scrotum and pubis, reinforcing the paradox [14]. Genetics also suggests that the probability of male pattern hair loss is dependent on family history and age [15]. However, in case of identical male twins, one can bald significantly faster than his counterpart [16]. These together with many other unknowns bring the necessity to define a new model for the explanation of baldness.

My studies on the subject started after a terrible personal experience (you can read my story here): a wrong splint therapy lead many symptoms to appear, among them tremendous muscular tensions in the neck. Muscles were so tight that I was exactly feeling their action propagating to the head and compressing the galea. This is when I started to lose hair at an incredible pace (Figure 2).

Figure 2– On the left, healthy hair. On the right, my hair started to thin and to fall as a consequence of the muscle stiffness in the scalp.
I will then discover that muscles are connected together through myofascial connections and their action can be propagated in distal areas [17]. This is also what the trigger point model proposes: pain frequently radiates from points of local tenderness in muscles to broader areas, sometimes distant from the muscle itself [18]. By looking to Figure 3, we can clearly understand how action of neck muscles propagate to the head, so my feelings were actually right.

Figure 3 – Referred pains from upper trapezius, sternocleidomastoid, suboccipital, splenius capitis, splenius cervicis, semispinalis capitis,temporalis and masseter muscle trigger points. Crosses represents the location of the trigger point. Red area is the referred pain pattern for that specific trigger point. (From [18])Then another particular event happened. Neck muscles tensions kept increasing up to a point that they were so severe and unbearable that lying down on a bed was the only partial pain remedy. This is how I was forced to spend three months lying down on a bed, trying every possible remedy to relax the muscles. One of the most effective method was the transcutaneous electrical nerve stimulation (usually referred as TENS). I used it applied to neck muscles and it did relax them, although its benefits were very short in time. But I noticed an incredible fact: every time my 10-minute session ended, my hair was in a really good health. It was kind of surreal for me, how was this possible? Nevertheless, muscles were tightening again after a short time period and so my hair was affected too.

This gave me more inputs on where to look for to explain the mysteries behind hair loss: I understood that action of neck muscles propagates to the galea and that there was some connection. At that point, I did not know the actual mechanisms to explain how a compressed galea was causing hair loss but I understood it was the key. Galea’s key role can be simply guessed by looking to Figure 4: balding areas of Norwood 7 pattern exactly matches galea’s anatomy. Was this just a coincidence?

Figure 4– On the left, Norwood 7 androgenetic alopecia. On the right, head and neck anatomy. Notice the bald area exactly matches the galea aponeurotica. (From [61])No, it was not a coincidence. As Figure 5 shows, blood vessels pass through all the scalp layers arriving to the hair follicles and one of these layers is the galea aponeurotica. If the galea is tightened, the blood vessels in the underlying tissues are compressed, i.e. blood cannot reach hair follicles causing reduced availability of oxygen, nutrients and inadequate removal of metabolites.

Figure 5 – Layers of the scalp. The epidermis, dermis, and galea glide over the pericranium as a fixed unit. Scalp vessels travel within the subcutaneous layer superficial to the galeal layer. (From [62])Not surprisingly, it has been found that subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower than the values found in the normal individuals [19]. This would explain the aforementioned higher formation of 5α-reduced metabolites and 17-ketosteroid metabolites at all sites of the scalp of bald men at the basis of the androgenetic theory.

The restriction in blood supply to tissues is called ischemia: this leads to insufficiency of oxygen (hypoxia). Not surprisingly again, men suffering from androgenic alopecia have significantly lower oxygen partial pressure (meaning microvascular insufficiency and hypoxia) in the areas of their scalp affected by balding (frontal and vertex regions) versus unaffected areas (temporal and occipital regions). Moreover, balding men have significantly lower oxygen partial pressure in the areas of balding scalp than the same areas of non-bald people [20].
Minoxidil solution, which is one of the commercially available medications for hair loss, stimulates the microcirculation of the bald scalp, effectively promoting hair growth [21]. Patients should be warned about increased shedding in the first months of treatment, that is seen as a positive response to the treatment [22]. How can this increased shedding be explained? Could it be the so called reperfusion injury, i.e. the tissue damage caused when blood supply returns to the tissue after a period of ischemia [23]?
In case of reduced blood supply, tissues are damaged and die, thus including the hair follicles and surrounding structures. A proof of this is the associated excessive dandruff found in hair loss [24]: the last layer of the skin, called stratum corneum, consists of dead cells (corneocytes) that are regularly replaced through desquamation. However, certain conditions trigger a more rapid turnover, leading to a larger shedding recognized as dandruff (Figure 6).

Figure 6 – Topical presentation of normal scalp and dandruff scalp. (From [25])When tissues are damaged, an inflammatory response is activated. The function of inflammation is to clear out necrotic cells and damaged tissues. The classical signs of inflammation are heat, pain and redness, situation recognized as scalp sensitivity (burning, stinging, dry scalp, vague discomfort in the scalp, and sometimes, trichodynia) that is associated with hair loss [26,27,28]. And guess what? Many studies have shown DHT plays an important role in inflammations, regulating its activity [29,30,31,32]. Could be this the explanation of why increased DHT levels are found in bald scalps?

When the inflammation is long-term and chronic, it causes fibrosis and calcification. Indeed, miniaturization of hair follicles has been associated with deposits of densely packed collagen bundles in the follicular dermal sheath, called perifollicular fibrosis [33,34,35]. This further decreases the blood flow into the scalp, promoting ulterior cells death.
So, I came to a conclusion: hair loss was not a problem of the hair itself but was a problem of the surrounding tissues. Take two seeds of a genetically identical corn, place one seed in a temperate climate and one in an arid climate: the one in the arid climate only grows to half the height of the one in the temperate climate due to lack of water and nutrients in its environment. This is exactly what happens with our hair and there are studies confirming it: miniaturized hair follicles of pattern alopecia can quickly regenerate once removed from the human scalp and can grow as well as or better than terminal follicles from the same individual [36]. And not only miniaturized hair can regrowth, but also terminal hairs can shrink in difficult recipient sites, impacting their growth and survival rates [37].
At this point, for me everything was clear. Only one thing was missing: where does this muscular tension come from? I will found out that craniofacial development has a huge impact on body posture and muscular balance. And actually all my symptoms were originating from a cranial distortion. Bingo! Now everything had an explanation!
Apparently, poor craniofacial development is a problem of civilized modern societies and not surprisingly also hair loss has widespread in the modern era. Figure 7 shows Native Sioux people that lived in the 19th Century. Their craniofacial development is something that would be considered extraordinary in our era, however at their time it was the normality. Also notice their perfect hair despite their old age. In Figure 8 we have instead a Sioux lived in our era, between the 20th and 21st Century: notice the difference in craniofacial development and the presence of hair loss.

Figure 7 – On the left, Red Cloud (1822-1909), leader of a Native American tribe (Sioux). In this picture he was 78 years old. Notice his excellent craniofacial development and how not surprisingly he has all his hair. On the right, another example of a good craniofacial development from the Sioux tribe lived in the same years. (From [63] and [64])

Figure 8– Russell Charles Means (1939-2012) was a Native American Oglala Sioux born in modern era. We can notice his poorer craniofacial development compared to his ancestors and his hair loss. (From [65])If we look to photographs taken over 100 years ago of Somalis in Figure 9, we can notice the excellent craniofacial development of the two individuals on the left and their perfect hair. However, the individual on the right has a poor craniofacial development and, not surprisingly, hair loss. In Figure 10, Barkhad Abdi, a Somali-American actor living in our era. Do you notice any difference with his ancestors?

Figure 9 – On the left, Warsame Yonis, 24 years old. In the middle, Igge Karbaashe, 20 years old and on the right Ali Gaboose, 20 years old. Notice the difference in Ali’s maxilla development and his hair loss. (From [66])

Figure 10 – Barkhad Abdi is a Somali-American actor. Notice his much poorer craniofacial development compared with his ancestors and his hair loss. (From [67])Already in 1939 Weston A. Price wrote about his travel around the world where he discovered that jaw problems were not present in tribes of isolated areas far from civilization [38]. In a simplistic view, maxilla is primarily remodeled by forces coming from the tongueand teeth (through masseter muscles) and the causes of a poor craniofacial development have to be found in modern lifestyle, in particular in:

• Increasing of bottle-feeding over breast-feeding that influences the swallowing pattern and all oral muscles [39,40,41,42].
• Use of pacifiers/dummies that mainly affect tongue posture [43,44,45,46].
• Trend towards industrial soft high-calorie food that hits chewing effort and muscles action [47,48,49].
• Reduced nasal airways, increasing of allergies and nasal congestion that leads to mouth breathing affecting both tongue posture and muscles action [50,51,52,53,54].
• Trend towards an earlier or too early weaning, influencing swallowing pattern [55,56].

When one or more of these factors are present, the maxilla drops down and back, reducing the eye support, flattening the cheekbones, narrowing the nasal airway, lengthening the mid facial third, and lowering the palate, which narrows and create malocclusion [57].
After discovering what a poor craniofacial development means for the hair, I started to look to every single person I was meeting, investigating their hair loss and the correlation with their jaws development: I never found a single bald person with a good craniofacial development! I also started to ask questions to people, curious to know the truth.
The first person I spoke with was my Portuguese housemate of that period. He had a very poor craniofacial development and he was bald. So I asked him: “Do you know if you used pacifiers or if you were bottle-fed when you were a child?”. His reply: “When I was a child, in Portugal it was almost a shame to breast-feed a child, so many mothers were opting to bottle-feed for this reason. My mother was one of those.”. No other comments are needed. Thus, I also started to ask the same questions to other people close to me: some have been breast-fed because their mother had not breast milk, some used pacifiers, some have been through a too early weaning and so on. There were no doubts that the correlation was clear.
I would like to show here some examples of famous people, so that everybody can understand what I am talking about. Figure 11 shows Prince William, Duke of Cambridge. On the left picture, you can clearly see his very narrow palate (i.e. a consequence of a poor craniofacial development). Also, if you pay attention, you will notice a cross-bite on one side and the dental midline that is shifted, sign of a cranial distortion. On the right picture, you can instead better appreciate his vertical growth of the maxilla, with missing cheekbones, missing support for the eyes, little lips, aquiline nose with little nostrils. I would not be surprised if he is a mouth-breather.

Figure 11– Prince William, Duke of Cambridge. Notice in these two pictures his poor craniofacial development: vertical growth of maxilla, narrow palate, cross-bite on one side with dental midline shifted, little lips, aquiline nose with little nostrils. (From [68])In observing other people with hair loss problems, the more severe cases I have seen were for two reasons: either their craniofacial development was extremely poor or they had an impressive cranial distortion. Now, I want to show you what I mean. In Figure 12 we can observe Angelino Alfano (an Italian politician) and his really poor craniofacial development. On the left picture we can notice his really narrow palate and the midline that is not completely centered. On the right one, we can observe his excessive vertical growth of the maxilla, with consequences on his eyes, lips and nose shape.

Figure 12– Angelo Alfano (Italian politician). Notice in these two pictures his extremely poor craniofacial development, notable from his excessive vertical growth of the maxilla, missing cheeckbones, eyes, nose and lips shape.
An example of an impressive cranial distortion is Jeff Bezos, current CEO of Amazon (Figure 13). In the left picture we can notice his narrow palate and also another important detail: look at his tongue, he has teeth signs on it. This means he has a tongue between the teeth posture, i.e. low tongue posture. In the right picture it is possible to notice his cranial distortion: asymmetrical face, asymmetrical ears, asymmetrical eyes, asymmetrical nasal philtrum and his mandible that deviates on one side.

Figure 13– Jeff Bezos, CEO of Amazon. In the left picture notice his narrow palate and the teeth signs on the tongue, meaning a tongue between the teeth posture. On the right, notice his cranial distortion. with asymmetrical face, asymmetrical ears, asymmetrical eyes and his mandible that deviates on one side. (From [69])If craniofacial development is the key for hair loss, can we predict who will have predisposition for baldness once older? My answer is yes, however predisposition does not mean that hair loss will actually happen. Let us take an example, Dwayne Douglas Johnson, an American actor also known as The Rock (Figure 14). We can see him in his younger days on the left and notice his poor craniofacial development, highlighted by a vertical facial growth, missing eyes support, missing cheekbones. These clues are signs of his predisposition to baldness. Indeed, we better know him now with his bald head, as in the photo on the right, where we can also appreciate his asymmetric smile with a shifted midline.

Figure 14– Dwayne Douglas Johnson, aka The Rock. On the left, we can notice his poor craniofacial development, highlighted by a vertical facial growth, missing eyes support, missing cheekbones when he was young and still with hair. On the right, we can appreciate a more recent photo and his teeth asymmetry with a shifted midline. (From [70])The Rock played some movies with Jason Statham and I think he is also a good example for this theory. Notice in Figure 15 his posture with an increased kyphotic curve. Also notice the tightened muscles on the side of the neck while he turns his head, i.e. reduced neck mobility. If you investigate yourself, you will also find his excessive vertical growth of the maxilla, with a narrow palate, cross-bite on both side of the teeth and a cranial distortion.

Figure 15– Jason Statham, English actor. Notice his posture with an increased kyphotic curve and the tightened muscles on the side of the neck while he turns his head, i.e. reduced neck mobility. (From [71])Another example: one day I was reading a newspaper and there was an article on the death of Danny Kirwan, guitarist of a British band named Fleetwood Mac. I did not know the band and neither him, but there was his picture when he was young that captured my attention (Figure 16).

Figure 16– A young Danny Kirwan (1950-2018), known as guitarist of the Fleetwood Mac. In this picture we can notice his long hair but his poor craniofacial development. Once older, which implications this brings to his hair? (From [72])He had perfect long hair, but a pretty poor craniofacial development. So, will he be affected by hair loss once older? According to everything I knew, yes he will! So, curious to know the answer I searched a picture of him older and guess what? He suffered of baldness (Figure 17).

Figure 17– An older Danny Kirwan (1950-2018), known as guitarist of the Fleetwood Mac. We can notice his baldness, that can be related to his poor craniofacial development. (From [73])Are you still with doubts? Then, I would like to put here a challenge. In Figure 18 there is Gianluigi Donnarumma, an Italian goalkeeper currently playing for AC Milan (2018), where we can notice his poor craniofacial development. He was born in 1999, so he is now 19 years old. Will he suffer of hair loss? Let us go back to this page in 10 or 15 years time, when he will be in his 30s, and we will probably have something new to discuss on.

Figure 18 – Gianluigi Donnarumma, Italian goalkeeper playing for AC Milan. He has a poor craniofacial development. In 10 or 15 years time, will he still have his hair? (From [74])Summary: what this new model can explain
Now, let us put everything together and let us see how this new model can better explain predisposition to baldness, comparing it with the deficits of the androgenetic model, where DHT is thought to play a main role in the disease.
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 incidence of Male Pattern Baldness increases with age. However, serum testosterone production declines with aging, together with lower serum DHT.
Androgenetic model: no explanation.
New model: neck muscular tensions that compress the galea are caused by an abnormal posture. Posture is determined by craniofacial development which depends on bone remodeling. Bone remodeling is a lifelong process, so an increase in age means a poor craniofacial development can worsen over time, with an impact on the posture. This creates higher predisposition to baldness with age.
Baldness have significantly spread in the modern era and isolated tribes are less likely to suffer of hair loss.
Androgenetic model: no explanation.
New model: craniofacial development depends on forces coming from orofacial muscles (among them, the tongue). The causes of a poor craniofacial development have to be found in modern civilized lifestyle (e.g. use of pacifiers, bottle-feeding, soft high-calorie diet, early weaning).
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.
Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth.
Androgenetic model: no explanation.
New model: minoxidil acts as a vasodilator through membrane hyperpolarization caused by opening potassium channels [58,59]. This promote blood flow, thus hair growth.
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.
Excessive dandruff and scalp sensitivity are often associated with hair loss.
Androgenetic model: no explanation.
New model: dandruff consists of dead cells (corneocytes) from the last scalp layer that are regularly replaced through desquamation. In case of reduced blood supply, cells die more rapidly triggering an excessive turnover, i.e. the dandruff. When tissues are damaged, an inflammatory response is activated. The classical signs of inflammation are heat, pain and redness, situation recognized as scalp sensitivity (burning, stinging, dry scalp, vague discomfort in the scalp, and sometimes, trichodynia).
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.
Conclusion
The model proposed on this website can explain many more things on baldness than the current androgenetic model can do. I am not here to say that it can fulfill all the unknowns of this disorder, but if the androgenetic model is accepted despite all its gaps then I do not see why this new model would not be considered and investigated. Anyway, the answer is in front of your eyes: just observe the craniofacial development and neck mobility of bald people and you will understand what I am talking about. You can contribute saying your opinion at the bottom of this page. I will try to clarify other aspects of hair loss in the second part of the article.​

I have noticed this phenomenon too that poor craniofacial development leads to a high propensity to bald.

Whatever causes poor craniofacial development be It a recessed jaw doesn't effect it in isolation it stems everywhere.

The standard wimp skull

 

[Virgincel]

Redpill me on scalp massages.