DHT influencing the pathways of CD34+ progenitor cells?

CD34+ progenitor cells have been found to be lacking in the scalp follicles of balding men; these stem cells are derived from bone marrow, and higher bone marrow density has been proven to produce more PC's. According to research, bone marrow increases via exercise and good protein sources, so one would conclude that increasing bone marrow would be the logical step to curing MPB. Yet, it isn't as simple as that... there are countless body builders who no doubt have very strong bones, higher levels of bone marrow, and also progenitor cells, yet they continue to go bald. So this must suggest that these growth factors are purposely switched off within galea follicles.

What is this influencing factor that prevents progenitor cells from migrating to scalp follicles? It could be high levels of DHT influencing the pathways of these PC's. When you think about it, androgenic hairs were just micro-vellus hairs up until androgen receptors began to upregulate at puberty; when this happens progenitor cells begin to migrate to these follicles and cause them to produce terminal hair, in the same way they cause the scalp follicles to start growing terminal hair.

So could it be that DHT causes most bone marrow derived progenitors to migrate to androgenic follicles, thereby leaving the scalp deficient in growth factors? This may partially explain it, but why does the galea lose out on growth factors and not the hair at the lower back and sides of the head? It would seem that the galea specifically is more prone to inflammation due to a myriad of reasons, so i can only conclude that reduced growth factors + inflammation = slow wound healing.

I have read countless cases about long term use of anti-DHT drugs and how they either slow down the growth of body hair or cause it to diminish altogether. When body hair is reduced, it seems that head hair growth increases. I can only surmise this is because there is an abundance of circulating progenitors when androgenic hairs no longer need them, and this allows scalp follicles to utilize more of them.

But one could also argue that there are lots of men who are as hirsute as werewolves and still have thick heads of hair (cue Alec Baldwin as a prime example). I wonder why guys like Baldwin don't go bald, even though his last name is bald, but you get my point   

Maybe poor scalp circulation (due to tightness) plays some sort of role in reduced growth factors, also. i mean, if progenitors circulate in the blood stream and travel to target tissues, then perhaps the scalp can't acquire enough of them due to the capillary network being so constricted AND because DHT programs the majority of them to move towards tissues displaying high androgenic activity?

Here's something else to consider regarding the information in the original post... my 6 month old niece was initially born with all over head hair, albeit very thin. Because she cannot yet crawl, she spends a great deal of time laying on her back with the back of her head pressed against a pillow. She now has a bald patch at the back of her head which is reminiscent of a man who is suffering hairloss at the crown. interestingly there is no hair loss where the occipital muscles exist -- just the galea.

Obviously it is a stretch to compare new born's follicles to that of an adult MPB sufferer, but the common thread they both share are lack of growth factors. The very fact that my niece has developed a bald patch in the very area she has had her head compressed against a pillow, makes me think that there is a similar pathology with adults who also experience thinning hair. I have no doubt at all that pillow compression accelerates MPB... the fact that most of us lay on our sides with our temples pressed against a pillow for several hours per night, without doubt accelerates hairline recession. But this likely only happens if growth factors are already weak, hence my baby niece.

The only solution I can think of to combat pillow compression is to sleep with the lower back and sides of the head on a draft excluder, so that more blood can flow to the galea as we sleep.

The compression theory is always interesting.

However, I find at least according to the research that dealing with the inflammation is important. Especially fibrinogen levels.

J Am Acad Dermatol. 2010 Sep;63(3):420-9. doi: 10.1016/j.jaad.2009.10.018. Epub 2010 Jul 8.
Androgenetic alopecia and cardiovascular risk factors in men and women: a comparative study.
Arias-Santiago S1, Gutiérrez-Salmerón MT, Castellote-Caballero L, Buendía-Eisman A, Naranjo-Sintes R.

BACKGROUND:
Numerous studies in recent decades have associated male androgenetic alopecia (AGA) with the risk of cardiovascular disease. However, only 3 studies have addressed this association in female patients. Most studies considered the risk of myocardial infarction or mortality as a result of heart disease, without analyzing cardiovascular risk factors.
OBJECTIVES:
The objectives of this study were to analyze the presence of cardiovascular risk factors included in the Adult Treatment Panel-III criteria for metabolic syndrome, the prevalence of carotid atheromatosis, hormonal (aldosterone, insulin, testosterone, and sex hormone-binding globulin) factors, and acute phase reactant (C-reactive protein, fibrinogen, D-dimers, erythrocyte sedimentation rate) variables in male and female patients with AGA and in a control group, and to analyze differences among the groups.
METHODS:
This case-control study included 154 participants, 77 with early-onset AGA (40 male and 37 female) and 77 healthy control subjects (40 male and 37 female) from the dermatology department at a university hospital in Granada, Spain.
RESULTS:
Metabolic syndrome was diagnosed in 60% of male patients with AGA (odds ratio [OR] = 10.5, 95% confidence interval [CI] 3.3-32.5), 48.6% of female patients with AGA (OR = 10.73, 95% CI 2.7-41.2), 12.5% of male control subjects, and 8.1% of female control subjects (P < .0001). Atheromatous plaques were observed in 32.5% of male patients with AGA (OR = 5.93, 95% CI 1.5-22.9) versus 7.5% of male control subjects (P = .005) and 27% of female patients with AGA (OR = 4.19, 95% CI 1.05-16.7) versus 8.1% of female control subjects (P = .032). Aldosterone and insulin levels were significantly higher in the male and female patients with AGA versus their respective control subjects. Mean values of fibrinogen were significantly higher in male patients with AGA, whereas values of fibrogen, C-reactive protein, and D-dimers were significantly higher in female patients with AGA versus their respective control subjects.
LIMITATIONS:
The study of a wider sample of patients with AGA would confirm these findings and allow a detailed analysis of the above factors as a function of the degree of alopecia or between menopausal and premenopausal women.
CONCLUSION:
The determination of metabolic syndrome and ultrasound study of the carotid arteries may be useful screening methods to detect risk of developing cardiovascular disease in male and female patients with early-onset AGA and signal a potential opportunity for early preventive treatment.

Thanks CS, I've never heard of fibrinogen until you jut mentioned it. It is interesting that the AGA group tested positive metabolic syndrome. I read that metabolic syndrome is implicated in slow wound healing. At one time I thought that I suffered from metabolic syndrome, but since keeping fit over the last 5 months, I no longer feel lethargic or the need to retire to bed all the time. I can actually hold down a job now -- something I could never do since I left school.

And while I'm on the subject of retiring to bed all of the time, too much pillow compression throughout the day and night has likely suppressed growth factors in some way. In fact, I remember developing bald patches at the side of my head when I'd sleep in too often, so I think that this may have adversely affected temple growth.

I'm not entirely pinning the cause of my temple recession on pillow compression, but I think that it may have assisted in periodically weakening follicles in some way... perhaps inducing hypoxia and slow lymph drainage / wound healing.

Xenon - Your theories on compression and heat/sweating I really think have huge value.

Here is something that might relate to this thread title (CD34+ cells).

First though a quick background: One of the symptoms of vitamin D deficiency is head sweating.
I believe most people in the UK are prone towards D deficiency.

Also, in a somewhat unrelated study, here it shows that treatment of vitamin D, positively effects immunity of CD34+ cells.

Otolaryngol Head Neck Surg. 2009 Feb;140(2):235-40. doi: 10.1016/j.otohns.2008.11.011.
1alpha,25-Dihydroxyvitamin D(3) to skew intratumoral levels of immune inhibitory CD34(+) progenitor cells into dendritic cells.
Kulbersh JS1, Day TA, Gillespie MB, Young MR.

OBJECTIVES:
Prior studies showed that immune inhibitory CD34(+) progenitor cells, whose numbers are increased in head and neck squamous cell carcinoma (HNSCC) patients, can be differentiated into immune stimulatory dendritic cells by culture with 1alpha,25-dihydroxyvitamin D(3) (1,25[OH](2)D(3)). This was extended to a pilot study to diminish intratumoral levels of CD34(+) progenitor cells by inducing their maturation into dendritic cells with 1,25(OH)(2)D(3).
STUDY DESIGN:
Newly diagnosed HNSCC patients were untreated for 3 weeks or received 3 weeks of 1,25(OH)(2)D(3) treatment befoer surgical treatment.
SUBJECTS AND METHODS:
HNSCC tissue was collected by biopsy from six patients who had no prior 1,25(OH)(2)D(3) treatment and at the time of surgical treatment from six untreated patients and 11 patients who completed 1,25(OH)(2)D(3) treatment. Tissues were analyzed by immunohistochemistry for levels of CD34(+) cells and dendritic cells.
RESULTS:
After 1,25(OH)(2)D(3) treatment, intratumoral levels of CD34(+) cells and levels of immature dendritic cells declined. However, levels of intratumoral mature dendritic cells increased. Clinical effects of 1,25(OH)(2)D(3) treatment are premature to analyze.
CONCLUSIONS:
Treatment of HNSCC patients with 1,25(OH)(2)D(3) reduced levels of immune inhibitory CD34(+) cells while increasing maturation of dendritic cells. This supports added studies to determine the effect of 1,25(OH)(2)D(3) on intratumoral immune competence.

Just common sense dictates you first clear the fibrous scar tissue, otherwise stem cells have no place to attach. Next one needs to establish (for a prolonged period) the proper environment of reduced inflammation and lack of oxidation around cell membrane. Then the body needs the right nutritional building blocks to reassemble the entire DNA/RNA cellular network. I find that not focusing on nutritional deficiencies vs. the kitchen sink approach is one of the biggest last step mistakes in health.

Fibrinogen is a cardiovascular disease marker, one of which is ignored by mainstream medicine. In fact, they seem to ignore all of the most important markers in favor of the least important ones (such as cholesterol).

Fibrinogen is a substance that prevents blood from becoming too thin (protects from excess bleeding), however it seems to work too well, ultimately producing collagen strands/fibrosis all over, which binds to calcium (hence calcification).

Anyway, ways to combat Fibrinogen would include vitamin K2, Magnesium, Sulfur, and Ecklonia Cava.