Lets put together a compilation of evidence against the donor dominance theory; CS your input requested

SlowMoe wrote:

9rugrats5 wrote:
Some local factor must be making that area of the head susceptible to DHT to begin with.

Did you read my posts in other topics where low oxygen levels allow more DHT to be produced locally?

What it looks like to me is that the low oxygen level causes the DHT/ estradiol ratio to increase (2 times the DHT/ 3 times less estradiol). This hormonal slurry is what causes the cells to go haywire and ultimately overloads the follicle.

No, probably missed it- could you please link to the post?

Testosterone synthesis in MPB subjects should not be affected by scalp hypoxia, since the majority of testosterone in males is produced in the testis. In the hypoxic environment of the bald scalp, DHT synthesis should not be significantly impaired. Schweikert and Wilson have documented that 5-?-reduction of testosterone to DHT was increased in hair roots from the frontal scalps of balding individuals as compared to other hair bearing scalp sites in the same individuals or to frontal hair roots from women and non-balding men. Schweikert, H. U. et al., JCE&M 1974:38(5):811-89. Estradiol synthesis, however, should be stoichiometrically decreased in a hypoxic environment. Three moles of oxygen are required to convert one mole of testosterone to one mole of estradiol. In a hypoxic region, the ratio of DHT to estradiol (DHT/estradiol) should be increased. Sawaya has shown that men with MPB have nearly a two fold increase in 5-?-reductase activity of hair follicles in balding frontal scalp, than in hair bearing occipital scalp. However, hair follicles in the frontal region had nearly three times less aromatase activity than hair follicles in the occipital region in men with MPB. Sawaya, M. E. Ann. N.Y. Acad. Sci. 1991:642:376-383. Finding that the DHT/estradiol ratio is elevated in bald scalp as compared to hair bearing scalp in MPB subjects, is consistent with what would be expected in a hypoxic tissue environment.

If one were to develop a gradual local tissue hypoxia of the frontal scalp, the DHT/estradiol ratio might increase locally to a critical level at which point receptor hormone interactions might result in down regulation or inhibition of hair follicle cell function. In turn, this might result in the ultimate conversion of terminal hair to villus hair, and the development of MPB. This inhibition may take the form of altering the number of hair follicle cells in anagen phase as compared to telogen phase.


One of the early manifestations of vascular insufficiency of the lower extremities is hair loss. The mechanism by which vascular insufficiency causes hair loss is not known. However, Hunt and Pai showed that collagen syntheses by fibroblasts is significantly compromised when tissue PO.sub.2 <40 mm Hg. Hunt T. K. et al., Surg. Gynecol. Obstet. 1972:135:351. Ther may be an analogous situation with keratin production by hair follicle cells.


As shown, resting transcutaneous PO.sub.2 (PtcO.sub.2) was significantly lower in bald frontal scalp (32.2 mm Hg.+-.2.0) than hair bearing temporal scalp (51.8 mm Hg.+-.4.4) in men with MPB. In controls, there was no statistically significant difference in PtcO.sub.2 of frontal scalp (53.9 mm Hg.+-.3.5) and temporal scalp (61.4 mm Hg.+-.2.7). Further, in bald subjects the frontal scalp PtcO.sub.2 was also significantly lower (32.2 mm Hg.+-.2.0) than in either frontal or temporal scalp of the controls (53.9 mm Hg.+-.3.5 & 61.4 mm Hg.+-.2.7, respectively). Finally, the PtcO.sub.2 of the temporal scalps was not significantly different between bald and control subjects (51.8 mm Hg.+-.4.4 & 61.4 mm Hg.+-.2.7, respectively).

Hair Follicle Genetics. In contrast to the "Donor Dominance" theory, hair follicles in the frontal and crown regions of the scalp may not be genetically different from those in the temporal and occipital regions. Rather, a local tissue hypoxia may alter the local hormonal milieu, specifically the DHT/estradiol ratio, and thus account for the androgen stimulated difference in hair production in these regions in MPB subjects.

We would like to present the results of an open-label pilot study using botulinum toxin type A (Botox; Allergan, Inc., Irvine, Calif.) for the treatment of androgenetic alopecia.

This form of alopecia is believed to be caused by a genetically predisposed sensitivity of hair follicles to the toxic effects of dihydrotestosterone, a metabolite of testosterone. Medical treatment of androgenetic alopecia has previously only been moderately effective using systemic drugs such as finasteride, a 5?-reductase inhibitor.1

In this ethically approved study, 50 male subjects aged between 19 and 57 years with Norwood/Hamilton ratings of II to IV participated.2 The study was 60 weeks in duration, with 12 weeks of run-in followed by two treatment cycles of 24 weeks each. Subjects were injected with 150 units of Botox (5 units per 0.1 ml saline) into the muscles surrounding the scalp, including frontalis, temporalis, periauricular, and occipitalis muscles in equally divided doses over 30 injection sites.

The primary outcome measure was a change in hair count in a fixed 2-cm area using a method described by Canfield.3 Secondary outcome measures included hair loss, measured by having subjects collect loose hair from their pillow with a sticky lint roller, and subjective efficacy using a validated questionnaire. Statistical analysis entailed paired t tests of group means.


Forty subjects completed the study, and no adverse effects were reported. The treatment response rate was 75 percent.

Mean hair counts for the entire group showed a statistically significant (p < 0.0001) increase of 18 percent between baseline and week 48 (Table 1), similar to the results reported with Propecia (Merck, Whitehouse Station, N.J.).1 Hair regrowth was objectively visible in some subjects (Fig. 1).

Secondary outcome measures were also significantly improved. The reduction in hair loss and increase in hair count did not show a statistically significant correlation. This suggested that longer retention of terminal hairs did not account for the increase in hair count.



Mechanistically, the scalp behaves like a drum skin with tensioning muscles around the periphery. These muscle groups - the frontalis, occipitalis, and periauricular muscles and to a minor degree the temporalis - can create a "tight" scalp when chronically active.

Because the blood supply to the scalp enters through the periphery, a reduction in blood flow would be most apparent at the distal ends of the vessels, specifically, the vertex and frontal peaks. Areas of the scalp with sparse hair growth have been shown to be relatively hypoxic, have slow capillary refill, and to have high levels of dihydrotestosterone.4

Conceptually, Botox "loosens" the scalp, reducing pressure on the perforating vasculature, thereby increasing blood flow and oxygen concentration. The enzymatic conversion of testosterone to dihydrotestosterone is oxygen dependent. In low-oxygen environments, the conversion of testosterone to dihydrotestosterone is favored; whereas in high-oxygen environments, more testosterone is converted to estradiol.4 Blood flow may therefore be a primary determinant in follicular health.
Strategically placed Botox injections appear able to indirectly modify this variable, resulting in reduced hair loss and new hair growth in some men with androgenetic alopecia.

Thanks, SlowMoe, I wasn't aware of the first study- it's an interesting find. Topical application of phytoestrogens may be beneficial after all.

9rugrats5 wrote:Thanks, SlowMoe, I wasn't aware of the first study- it's an interesting find. Topical application of phytoestrogens may be beneficial after all.

It appears that any method used to bring the tissue oxygen pressure above, say, 40mmhg should be sufficient to bring the DHT/estradiol ratio bsck to normal, and stop hair loss. Theoredically

A few years ago, I would have been extremely skeptical of the idea of hair loss from sleeping, but between the oxygen theory and this...
Other contributing factors: excessive sleeping
http://healthland.time.com/2011/09/27/the-stress-of-divorce-writ-on-womens-heads/

Only as a minor factor of course. But how to avoid such hair loss while still getting enough sleep? Side sleeping, eh? What about the type of pillow and mattress? Not that it's practical, but would be multiphasic sleeping be better for hair?

We use our muscles by selectively contracting them. On the biochemical level muscle contraction is triggered by calcium ions flowing into muscle cells. To relax the muscle calcium is pumped out again. However, as we age, more and more calcium remains trapped in the muscles and these become more or less permanently contracted, leading to increasing muscle tension and spasms.

And this is why scalp tension and hairloss often starts in an older age.

ferox wrote:

We use our muscles by selectively contracting them. On the biochemical level muscle contraction is triggered by calcium ions flowing into muscle cells. To relax the muscle calcium is pumped out again. However, as we age, more and more calcium remains trapped in the muscles and these become more or less permanently contracted, leading to increasing muscle tension and spasms.

And this is why scalp tension and hairloss often starts in an older age.

Yep...Good stuff

Besides the usual info such as lack of K2, etc. here is additional info:

When the immune system perceives abnormal cell growth or invading organisms as threats, dystrophic calcification usually occurs as the immune system responds by walling off the affected area.

more info = http://www.wisegeek.com/what-is-dystrophic-calcification.htm

In addition, would want to look into the sodium and potassium pump. There is old information from years ago on this to help here such as magnesium deficiency, food intolerance, being hypothyroid. I personally have mentioned 16 Hz for a possible minoxidil effect.

“16Hz frequency opens potassium ion channels of cell membranes. Opening these channels reduces the influx of calcium ions, which reduces the need for oxygen"

“Reducing calcium also causes the smooth muscle layer of blood vessels to relax so more blood is being pumped to the heart.”

http://israel21c.org/health/israeli-device-harnesses-electromagnetic-healing-power/

rdkml wrote:Besides the usual info such as lack of K2, etc. here is additional info:

When the immune system perceives abnormal cell growth or invading organisms as threats, dystrophic calcification usually occurs as the immune system responds by walling off the affected area.

more info = http://www.wisegeek.com/what-is-dystrophic-calcification.htm

In addition, would want to look into the sodium and potassium pump. There is old information from years ago on this to help here such as magnesium deficiency, food intolerance, being hypothyroid. I personally have mentioned 16 Hz for a possible minoxidil effect.

“16Hz frequency opens potassium ion channels of cell membranes. Opening these channels reduces the influx of calcium ions, which reduces the need for oxygen"

“Reducing calcium also causes the smooth muscle layer of blood vessels to relax so more blood is being pumped to the heart.”

http://israel21c.org/health/israeli-device-harnesses-electromagnetic-healing-power/

So whats the best way to remove calcifications?

I couldn't tell you the best way to remove calcification but can say what I used.

Topical nutribiotic grapefruit seed extract full strength. There was a university study showing extremely acidic substances are able to remove tissue calcification.

LLLT, strong PEMF device, a possibly certain Rife frequencies may be helpful.

K2, magnesium, etc..

Fix the sodium potassium pump. Some have resorted to drinking braggs apple cider vinegar or similar with the mother (floating particles) in it as well as topical ACV or topical potassium chloride.


I'm sure there is much more and someone better can answer as I'm very rusty regarding hair loss info.

Other forums use DHT inhibition and minoxidil is used here but we all know the side effects from those on this forum.

SlowMoe wrote:So whats the best way to remove calcifications?

how about this script, found at the curezone rife forum? it targets Nanobacterium Sanguineum, which is suspected to be involved in calcification and arteriosclerosis. I believe its from Jeff Sutherland.

repeat 5
dwell 360
duty 66.6
#For F160 change program c to program a in next line
program c
#For F160 comment out next line
vbackfreq a 0.002478752 0 66.6
vbackfreq b 0.049787068 0 66.6
duty 66.6
43644.3 #mercury release
converge 0 0
5333.7 #toxic protein
converge 6 .01
4202.30 #DNA database
converge 12 1
127724
converge 30 1
6746544
4665553
4663426
2765636
3535546
3645647
3467055
3467235
converge 5 1
3467330
3467390
3467900
3468000
converge 10 1
3467415
converge 40 1
3467575
3468020
3426676
2666776
2666448
2474235
2464447
2344442
converge 4 0.01
1902 317 #CAFL list freqs that work
label last
end repeat

Guys I sleep with no pillow and always on my side. I never sleep on my back. My crown hair is very thick It's my temples that are receding.

ferox wrote:

We use our muscles by selectively contracting them. On the biochemical level muscle contraction is triggered by calcium ions flowing into muscle cells. To relax the muscle calcium is pumped out again. However, as we age, more and more calcium remains trapped in the muscles and these become more or less permanently contracted, leading to increasing muscle tension and spasms.

And this is why scalp tension and hairloss often starts in an older age.

And why does it get trapped? Depleting tissue thickness and fibrosis probably...
H/Ts are just another mainstream money maker symptom treatment, but without catering to the cause, the transplanted hair will fall out just like the native hair to that area. Cells die the same way, hair is hair is hair, the energy supply (i.e. tissue and capillary thickness) to the hair is what makes it a different size or growth capacity, which is why all organs of the body miniaturize as blood flow decreases.. Left unchecked, after awhile the transplated hair will go through the same process if it even successfully grew to begin with.

We know theres already studies proving calcification blocks certain small passages of those suffering mpb, and possibly is relevant to skull expansion (see: child/teen head size versus mature adult) which is just one more negative for a failing capillary bed.. If the blood flow that is reaching is low on oxygen moles then hair death even quicker, which is actually what started your inflammation to begin with.. So as has already been discussed numerous times here, local tissue deprivation is the real culprit ( And that deprivation is caused by some of or all of what c/s has informed of depending person )...

Without over complicating my thoughts, on a cellular level the distance from a balding temple to thick robust hair growth on the sides could be equivalent to hundreds of miles of highways... Correction, slow traffic jammed highways... No hair growth at all then call it a road block if you catch my drift... I believe we are all genetically programmed to continue growing most of our hair like our child selves, I'm starting to see all of this aggressive balding as more of a mutation due to multiple conflicting events damaging the hair follicles environment and power supply so to speak. Certainly escalated in modern times...

Slowmoe->
It appears that any method used to bring the tissue oxygen pressure above, say, 40mmhg should be sufficient to bring the DHT/estradiol ratio bsck to normal, and stop hair loss. Theoredically

Would be nice to know these numbers and be able to gauge it based on what things specifically increase and decrease it in an significant way individually.. Hey there'd never be any surprises at least if you suddenly went through a shed...