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 .
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?
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 . 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 . Also, low level laser therapy has some effectiveness on hair loss . 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 . 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.
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.
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 . 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) .
Abnormal posture, like in the case of forward head posture and cranial distortions, affects muscle length/tension relationships . This usually leads to pain and overuse injury where small focal, degenerative changes in the insertion fibers can occur .
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.
Indeed, whatever else they may be doing individually, muscles also influence functionally integrated body-wide continuities in the fascial webbing . 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).
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.
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.
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 .
- 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 .
- 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 .
- It has been found that Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth .
- By relieving tension at the vertex in the scalp, cutaneous blood flow rate increases, promoting hair regrowth .
- Minoxidil is less effective in subjects with significant inflammation in the scalp than in subjects with no significant inflammation .
- 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.
- 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 .
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?
 Norwood, O. T. “Male pattern baldness: classification and incidence.” Southern medical journal 68.11 (1975): 1359-1365.
 Godse, Kiran, and Vijay Zawar. “Sensitive scalp.” International journal of trichology 4.2 (2012): 102.
 Misery, Laurent, et al. “Sensitive scalp: does this condition exist? An epidemiological study.” Contact Dermatitis 58.4 (2008): 234-238.
 Willimann, Barbara, and Ralph M. Trüeb. “Hair pain (trichodynia): frequency and relationship to hair loss and patient gender.” Dermatology 205.4 (2002): 374-377.
 ALEXANBER, SUZANNE. “Loss of hair and dandruff.” British Journal of Dermatology 79.10 (1967): 549-552.
 Rossi, Alfredo, et al. “Minoxidil use in dermatology, side effects and recent patents.” Recent patents on inflammation & allergy drug discovery 6.2 (2012): 130-136.
 Avci, Pinar, et al. “Low‐level laser (light) therapy (LLLT) for treatment of hair loss.” Lasers in surgery and medicine 46.2 (2014): 144-151.
 Choy, H. “Detumescence Therapy of Human Scalp for Natural Hair Regrowth.” J Clin Exp Dermatol Res 3.138 (2012): 2.
 Mew, M. “Craniofacial dystrophy. A possible syndrome?.” British dental journal 216.10 (2014): 555-558.
 Gonzalez, Humberto E., and Arturo Manns. “Forward head posture: its structural and functional influence on the stomatognathic system, a conceptual study.” CRANIO® 14.1 (1996): 71-80.
 Solow, Beni, and Antje Tallgren. “Head posture and craniofacial morphology.” American Journal of Physical Anthropology 44.3 (1976): 417-435.
 Strokon, Dennis. “Correction of Dental and Cranial Sidebend with ALF.” IJOM 21 (2010): 3.
 Darnell, Michael W. “A proposed chronology of events for forward head posture.” Journal of craniomandibular practice1.4 (1983): 49-54.
 Ernest III, Edwin A., and W. Ernest. “Splenius Capitis.”
 Simons, David G., Janet G. Travell, and Lois S. Simons. Travell & Simons’ myofascial pain and dysfunction: upper half of body. Vol. 1. Lippincott Williams & Wilkins, 1999.
 Myers, Thomas W. “The ‘anatomy trains’.” Journal of Bodywork and Movement Therapies 1.2 (1997): 91-101.
 Haughie, Laura J., Ira M. Fiebert, and Kathryn E. Roach. “Relationship of forward head posture and cervical backward bending to neck pain.” Journal of Manual & Manipulative Therapy 3.3 (1995): 91-97.
 Fernández‐de‐las‐Peñas, César, et al. “Trigger Points in the Suboccipital Muscles and Forward Head Posture in Tension‐Type Headache.” Headache: The Journal of Head and Face Pain 46.3 (2006): 454-460.
 Fernández-de-las-Penas, César, et al. “Referred pain areas of active myofascial trigger points in head, neck, and shoulder muscles, in chronic tension type headache.” Journal of bodywork and movement therapies 14.4 (2010): 391-396.
 Fernández‐de‐las‐Peñas, César, Maria L. Cuadrado, and Juan A. Pareja. “Myofascial trigger points, neck mobility, and forward head posture in episodic tension‐type headache.” Headache: The Journal of Head and Face Pain 47.5 (2007): 662-672.
 Freund, Brian J., and Marvin Schwartz. “Treatment of male pattern baldness with botulinum toxin: a pilot study.” Plastic and reconstructive surgery 126.5 (2010): 246e-248e.
 Klemp, Per, Kurt Peters, and Birgitte Hansted. “Subcutaneous blood flow in early male pattern baldness.” Journal of investigative dermatology 92.5 (1989): 725-726.
 Goldman, Boris E., David M. Fisher, and Steven L. Ringler. “Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.” Plastic and reconstructive surgery97.6 (1996): 1109-16.
 Wester, Ronald C., et al. “Minoxidil stimulates cutaneous blood flow in human balding scalps: pharmacodynamics measured by laser Doppler velocimetry and photopulse plethysmography.” Journal of investigative dermatology 82.5 (1984): 515-517.
 Toshitani, Shoji, et al. “A New Apparatus for Hair Regrowth in Male‐pattern Baldness.” The Journal of dermatology 17.4 (1990): 240-246.
 Whiting, David A. “Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern androgenetic alopecia.” Journal of the American Academy of Dermatology 28.5 (1993): 755-763.
 Whiting, David A. “Chronic telogen effluvium: increased scalp hair shedding in middle-aged women.” Journal of the American Academy of Dermatology 35.6 (1996): 899-906.
 Hoelzel, Frederick. “Baldness and Calcification of the Ivory Dome.” Journal of the American Medical Association 119.12 (1942): 968-968.
 Repair: Old Plug Removal, SMP Into Hair Transplant Scar, by Balding Blog
 Incisions and Closures, by Clinical Gate
 Muscles Of The Face Diagram, by Anatomy Human
 The Cause and Cure of Malocclusion, by John Mew
 The Mechanics of Male Pattern Baldness, by David M. Hatch
32 thoughts on “Hair Loss: The Real Underlying Causes Are Not Androgenetic”
Yeah, if only jeremy meeks mewed more and mouthbreathed less in childhood, he wouldn’t be bald by now. Sure
Good point. I would love to hear an explanation for this case, why he is balding to some extent
I totally agreedwith all what you said.
Yeah totally agreed. So what should be th solution then . What will help in early stages of balding???
you need to press on the forehead consistnetly for a long time every day for months so that the bone remodeling process changes into a flatter shape which favors hair growth. But I believe you need to be doing this in conjunction with mewing or some other way to stop those forces originating in the face from acting on your frontal and parietal bones causing baldness.
so, why don’t women exhibit the same degree of hair loss? why did jocko willink go bald? (his forward growth I’d say is impressive). my driving school instructor is a NW0, despite being a chronic mouth breather with terrible posture.
also why is Mike Mew, ceo of forward growth, a baldcel??? what about SubhumanCurrycel??? why are two universally recognized and internationally acclaimed pillars of forward growth bald?? I’m not saying this theory is BS, but it’s incomplete AT BEST. it must be more than calcification and galea stretching… I’m sure most if it is endocrinological. we need a john mew tier aspiepilled scholar to connect the dots: DHT/testosterone/androstenol, CFD, stretched galea aponeurotica, diffuse thinning etc…
maybe it will be MPMD
maybe that annoying long hair coping baldcel on youtube
Women are different. They have different skulls and different hormones that cause bone to remodel differently. The lack of androgens does not grow and remodel bone the same way a man’s hormones would. They do have hairloss from the same cause as men. Their hairline usually don’t recede like a man’s would in the M shape, but it’s possible and happens sometimes. And they don’t get much loss on the crown. women’s hair loss from CFD usually just pushes their hairline back and it takes on a very curved upisde down U shape.
There is nothing incomplete with this theory, you just don’t understand it. Mike mew has hair loss because he has a flat mid face. He has a flat midface because he has chronic bad neck posture when he was growing and he still might have it. It’s very hard and takes a long time to undo things like this.
Chronic bad posture causes stress on the skull, the body compensates for this by building fibrosis in the place of chronic stress and the bone remodels to deal with the stress and takes on a rounder shape. Androgens accelerate and increase the growth of the skull bones. These cut off blood supply to the follicles slowly. All the bones of the skull are connected and movement of one can affect many.
There’s nothing more to elucidate.
Hey King Mog. I’m really impressed by your response, finally someone that understood the theory. I always wanted to reply exactly what you just wrote, but I never had the time. Keep up with the good work!
I for one have observed that bald men are subject to the extended influence of catecholamines. That is to say, stress. They seem to have been stressed, stress easily, stuttering may occur too. Irregular OCDs and love for sugar. Anterior pelvic tilt may be present as well quite often.
I am suffering from this.What to do about it then ? Kindly add a treatment section in ur blog
Funny i got a jaw problem and a pretty bad posture and balding since 22 or 23. I grew up playing games from age 14 i sat infront of the pc screen daily for years and fapped alot and noticed recession. I have receeded hairline in my family so its genetic but Im balding alot faster than my family.
Can pumping blood to scalp externally help rid of Balding ?