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Microvascular Hypoxia in MPB Study

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LawOfThelema
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Microvascular Hypoxia in MPB Study Empty Microvascular Hypoxia in MPB Study

Post  LawOfThelema Thu Jun 14, 2012 3:45 pm

False.

Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.
Goldman BE, Fisher DM, Ringler SL.
Source

Department of Plastic Surgery, Butterworth Hospital, Grand Rapids, Mich., USA.
Abstract

Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.

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Post  LawOfThelema Thu Jun 14, 2012 5:03 pm

lol admin?

i dont remember posting this topic, but nice play!

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Post  a<r Thu Jun 14, 2012 5:18 pm

Haha, yeah, I was going to delete the entire thread but that study is worth having its own topic so I just deleted 2020's fascist sociopath ravings and changed the title, I hope you don't mind.

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Post  LawOfThelema Thu Jun 14, 2012 5:21 pm

its good. warrants a topic for sure

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Microvascular Hypoxia in MPB Study Empty Is androgenic alopecia a result of endocrine effects on the vasculature?

Post  LawOfThelema Thu Jun 14, 2012 5:25 pm

http://www.medical-hypotheses.com/article/S0306-9877%2803%2900342-6/abstract

Abstract

Androgenic alopecia is a condition of concern for many patients. Though much has been learned about this condition, the exact pathophysiological mechanism is yet to be established. Currently most study concerning androgenic alopecia has focused on the effects of androgens on the pilosebaceous unit itself. An area of study that has received considerably less attention is that of androgens inducing baldness by indirect effects, that is, effects on tissues other than the pilosebaceous unit.

In this paper, the author offers a novel hypothesis in which androgenic hair loss is mediated via the effects of androgens on the vasculature supplying the scalp. In this new hypothesis androgens effect anatomical changes in the vasculature of susceptible individuals, resulting in an environment in which hair growth is hindered and eventually ceases. The author discusses past studies demonstrating the effects of androgens on vessels and how these effects may relate to anatomical changes in the vasculature leading to hair loss. Also included is a discussion on future experimentation to test this new hypothesis.

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Post  ppm Thu Jun 14, 2012 7:13 pm

However, one has to keep in mind that transplanted hair will grow nonetheless; therefore, the inabillity to sustain growth (still) is a feature of the follicles in question.

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Post  SlowMoe Thu Jun 14, 2012 10:50 pm

Implanted hair papilla are robust, vigorously producing new hair. They can be implanted almost anywhere in the body and survive, my theory is that the wounding action of the procedure stimulates angiogenesis to the region, providing a new blood highway for the hair to tap into.
There have been reports that simply wounding the scalp has caused dormant vellus hairs on a slick bald scalp to transform into robust terminal hairs.
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Post  987 Fri Jun 15, 2012 2:41 am

SlowMoe wrote:Implanted hair papilla are robust, vigorously producing new hair. They can be implanted almost anywhere in the body and survive, my theory is that the wounding action of the procedure stimulates angiogenesis to the region, providing a new blood highway for the hair to tap into.

I agree ^ and many of the hair transplant patients who do have success are still likely so scared of hair loss that they are still doing everything they can to prevent further loss, or loss of the transplants... Therefor remember that HT's are not always successful, or permanent, and I think the more years that go by, there will be more reports of this coming to front, which will eventually lead the mainstream hair loss drug/surgery industry into being forced to abandon their current ( possibly deceptive) stance that blood flow is a non factor in mpb.. This is of course after they've made countless billions of dollars, and literally destroyed the prosperity, and fertility of numerous men world wide ...


In this paper, the author offers a novel hypothesis in which androgenic hair loss is mediated via the effects of androgens on the vasculature supplying the scalp. In this new hypothesis androgens effect anatomical changes in the vasculature of susceptible individuals, resulting in an environment in which hair growth is hindered and eventually ceases. The author discusses past studies demonstrating the effects of androgens on vessels and how these effects may relate to anatomical changes in the vasculature leading to hair loss.

Yea!^ Ive put a LOT of thought into this subject along with many of you here, and in efforts to try to tie in all the major factors in mpb ( most of which have been identified due to this site) my current conclusion, I personally think that some individuals have a genetically less robust/with-standing, micro capillary network in their scalps supplying their 'galea' , with a persons natural head shape/size in mind in regards to susceptibility also. I agree with the notion that the reason the sides and the back of head do not go bald is due to the sides and back having a more adequate blood network due to the muscles on the sides of the head, and less resistance from gravity which makes more sense to me now when understanding there are no muscles in the galea. Less muscle/movement = less blood flow, stagnation, inferior angiogensis rebuilding!? Also consider that the typical unheathly diet of bad fats, oils and junk, along with transfats/chlorine etc scaring and plaquing arteries walls enough to cause heart issues, imagine what this plaque could do if its having a similar effect on small feeble micro capillaries in the scalp. Having clean smooth flowing pipes and good blood pressure probably at least helps...

So at puberty and beyond the scalp becomes saturated in androgen's, which cause detrimental effects to this 'susceptible' galea area of the head over time if conditions aren't matched to counter its affects. I believe that the less robust the head of hair is naturally, the less survivable the hair will be to the affects of androgen's, 'IF' a detrimental ratio of androgen's, and/or if inadequate dietary/lifestyle habits are present.. Apparently low shbg, low T to dht ratio's (hormonal imbalances, possibly upregulated from excessive estrogen exposure), poor thyroid functioning, sedentary lifestyle, poor general circulation, and mineral deficiencies which also exacerbates all of the above; will amplify the chances of mpb to occur in susceptible individuals.

The androgen's (dht namely) probably deteriorates the thin galea's micro vascular network, and fatty tissue health (tightness) through inflammation damage, which propentiates gradual reduction of necessary micro circulation pathways thus receding, thinning, then balding depending the severity of the androgen induced inflammation. I know that this is a strong factor, because countering inflammation through supplements was all I really needed myself to stop my hair thinning up top. I'm also getting more prone to believe in most of what I read about manual increasing blood flow, ( Messaging, brushing, S.E.) I have lately thought of how some African Americans with low cut hair styles and low hair lines tend to brush their hair for the waves look constantly throughout the day, and I wouldn't doubt that those that do will have a less likely hood of recession/balding due to that constant stimulation. Due to my hairstyle and length I cant really brush my hair all over, but I have started aggressively brushing the vellu's hairs around the temple/hair line throughout the day constantly with very noticeable sensation to the area...

I feel like if caught early enough in the process, hair loss likely is beat with perfecting an anti inflammatory diet, anti inflammatory supplements, lots of vitamin C and E for circulation, gingko biloba, organic teas to increase SHBG and boost antioxidants, IH top 6, correcting typical deficiencies (D3, Magnesium, Iodine) and last but not least aggressively exercising all of the manual blood flow stimulating methods, and for some mildly reducing dht through diet/herbs...With all of that in mind done daily, I really dont see how ones hair could continue to bald, and if it does it surely wont fall nearly as quickly. Feel free to disagree...


Last edited by J987 on Fri Jun 15, 2012 3:26 am; edited 1 time in total

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Post  SlowMoe Fri Jun 15, 2012 3:24 am

Very good post.
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Post  Mastery Fri Jun 15, 2012 2:31 pm

J987 wrote:

I feel like if caught early enough in the process, hair loss likely is beat with perfecting an anti inflammatory diet, anti inflammatory supplements, lots of vitamin C and E for circulation, gingko biloba, organic teas to increase SHBG and boost antioxidants, IH top 6, correcting typical deficiencies (D3, Magnesium, Iodine) and last but not least aggressively exercising all of the manual blood flow stimulating methods, and for some mildly reducing dht through diet/herbs...With all of that in mind done daily, I really dont see how ones hair could continue to bald, and if it does it surely wont fall nearly as quickly. Feel free to disagree...


That is essentially very correct.
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Post  dudebro Fri Jun 15, 2012 3:23 pm

great thread.

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Post  LawOfThelema Sat Jun 16, 2012 6:34 pm

Acemannan stimulates gingival fibroblast proliferation; expressions of keratinocyte growth factor-1, vascular endothelial growth factor, and type I collagen; and wound healing.
Jettanacheawchankit S, Sasithanasate S, Sangvanich P, Banlunara W, Thunyakitpisal P.
Source

Oral Biology Program, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
Abstract

Aloe vera has long been used as a traditional medicine for inducing wound healing. Gingival fibroblasts (GFs) play an important role in oral wound healing. In this study, we investigated the effects of acemannan, a polysaccharide extracted from Aloe vera gel, on GF proliferation; keratinocyte growth factor-1 (KGF-1), vascular endothelial growth factor (VEGF), and type I collagen production; and oral wound healing in rats. [(3)H]-Thymidine incorporation assay and ELISA were used. Punch biopsy wounds were created at the hard palate of male Sprague Dawley rats. All treatments (normal saline; 0.1% triamcinolone acetonide; plain 1% Carbopol; and Carbopol containing 0.5%, 1%, and 2% acemannan (w/w)) were applied daily. Wounded areas and histological features were observed at day 7 after treatment. From our studies, acemannan at concentrations of 2, 4, 8, and 16 mg/ml significantly induced cell proliferation (P<0.05). Acemannan concentrations between 2 - 16 mg/ml significantly stimulated KGF-1, VEGF, and type I collagen expressions (P<0.05). Wound healing of animals receiving Carbopol containing 0.5% acemannan (w/w) was significantly better than that of the other groups (P<0.05). These findings suggest that acemannan plays a significant role in the oral wound healing process via the induction of fibroblast proliferation and stimulation of KGF-1, VEGF, and type I collagen expressions.



ok its gingivial but maybe it would be effective on your dome as well


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Post  Amaranthaceae Mon Jun 18, 2012 10:33 pm


VERY interesting study result !!!!! Thanks for posting.

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Post  ferox Tue Jun 19, 2012 9:28 pm

cpio wrote:
VERY interesting study result !!!!! Thanks for posting.

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