New Dermaroller Study; Thoughts, comments?

[BeliefISKEY]

That some good ****ing work!! bad ***!

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Lack of blood flow=inflammation..???????? BeliefISKEY.. I really hope that you're not another immigrant from Immortal forum with that stupid galea theory? Chronic inflammation= impairment of blood flow not the other way around.. destruction of blood vessels,capillaries, calcification, fibrotic & sclerotic tissues..etc..your hair and galea was fine before DHT and inflammation decided to be involved!

Sorry the first part came out wrong.... It is the other way around, you're absolutely right. I kinda meant that inducting blood flow to an inflamed area helps eliminate inflammation and help the area(s) heal more rapidly/efficiently.

& nope, people that loosened their scalp up cured their hair loss (all test subjects did), a great amount regrow, and dht and estradiol levels around the scalp (galea area) were regulated. You seem to know a lot about hair loss but always speculate on how the problem starts.

The galea gets tight, lack of blood+hypoxia occurs, dht tends to accumulate in hypoxic areas & estradiol tends to not flourish as well, then all of the sh** you talk about happens. 2 studies validate the tight gales theory already.

It's not your galea that's tightening by itself you genius, it's the muscles around it that get tight & pull on it. Once you relax these muscle there will be no more tightness, blood flow will no longer be impaired/disrupted, and everything else will be regulated overtime for the MOST PART.

Lots of Men that have high DHT levels don't go bald & you yourself said that it wasn't the main problem, yet you made the idiotic statement at the end of your response to me? There are even some male pattern baldness studies that show that bald/banding men have low serum DHT levels. One of the many things that can explain the DHT triggered inflammation is the Galea theory.. After all, it only happens AROUND THE GALEA AREA.

 

[squeegee]

Hey squeegee, that was a very fine ****ing post man!... thanks!

I might even try the 3 mm dermaroller now...

This is probably why our regimen works.. Minoxidil is antifibrogenic.. paired with with the derma roller.. you got results.. BTW good idea about stepping up a notch with the 3.0mm.. The problem is way deeper that people think.. Keep on rolling!!

 

[BeliefISKEY]

This is probably why or regimen works.. Minoxidil is antifibrogenic.. paired with with the derma roller.. you got results.. BTW good idea about stepping up a notch with the 3.0mm.. The problem is way deeper that people think.. Keep on rolling!!

http://s37.photobucket.com/user/set..._787144789_n_zps1631076f.jpg.html?sort=3&o=22

But the study, nor Joseph (the poster child for DR in your opinion) never used a 3.0 has he?...... You are very confusing and all over the place sometimes. You should go back to useful mode.

 

[squeegee]

Sorry the first part came out wrong.... It is the other way around, you're absolutely right.

& nope, people that loosened their scalp up cured their hair loss (all test subjects did), a great amount regrow, and dht and estradiol levels around the scalp (galea area) were regulated. You seem to know a lot about hair loss but always speculate on how the problem starts.

The galea gets tight, lack of blood+hypoxia occurs, dht tends to accumulate in hypoxic areas & estradiol tends to not flourish as well, then all of the sh** you talk about happens. 2 studies validate the tight gales theory already.

It's not your galea that's tightening by itself you genius, it's the muscles around it that get tight & pull on it. Once you relax these muscle there will be no more tightness, blood flow will no longer be impaired/disrupted, and everything else will be regulated overtime for the MOST PART.

Lots of Men that have high DHT levels don't go bald & you yourself said that it wasn't the main problem, yet you made the idiotic statement at the end of your response to me? There are even some male pattern baldness studies that show that bald/banding men have low serum DHT levels. One of the many things that can explain the DHT triggered inflammation is the Galea theory.. After all, it only happens AROUND THE GALEA AREA.

Belief.. The problem with Androgen Alopecia is that people only focus on the obvious, the scalp and the esthetic problem of thinning /missing hair.

The problem starts at the cellular level.. not at the physical level. DHT is a powerful steroid sex hormone than can or cannot trigger a chronic inflammation. This is why some people go bald or not going bald.

There are several studies out there proving a relation between early balding and signs of atherosclerosis or dyslipidemia.

DHT promotes VCAM-1 and NF-KB expression . Both related to theses diseases. The tight Galea theory has nothing to do with this. It is maybe a side-effect of the local chronic inflammation, no the problem itself. LOL

http://www.ncbi.nlm.nih.gov/pubmed/14684616
http://www.ncbi.nlm.nih.gov/pubmed/18941467


Is androgenetic alopecia a risk for atherosclerosis?

Dogramaci AC, Balci DD, Balci A, Karazincir S, Savas N, Topaloglu C, Yalcin F.
Author information


Abstract

BACKGROUND:

Several studies have demonstrated the presence of an association between androgenetic alopecia (Androgenetic Alopecia) and cardiovascular disease. The aim of this study was to evaluate subclinical atherosclerosis in patients with Androgenetic Alopecia and healthy controls by the incorporation of carotid intima-media thickness (IMT) and high-sensitive C-reactive protein (hs-CRP) along with echocardiography (ECHO) and exercise electrocardiography (ExECG).
METHODS:

We performed a case-control study in 50 male patients with Androgenetic Alopecia and 31 age-matched healthy male controls with normal hair status. Both the Androgenetic Alopecia patients and controls with a history of diabetes mellitus, cigarette smoking, hypertension, cardiovascular or cerebrovascular disease, and renal failure were excluded. Androgenetic Alopecia was classified according to the Hamilton-Norwood scale. Serum lipids, serum hs-CRP, total testosterone, and dehydroepiandrosterone sulphate were examined in all study subjects. Carotid ultrasonography was used to measure the IMT of the common carotid arteries (CCA). ECHO and ExECG were performed in all subjects.
RESULTS:

IMT of the CCA was found to be significantly higher in patients with severe vertex pattern Androgenetic Alopecia when compared to patients with other patterns of Androgenetic Alopecia and healthy controls (P < 0.05). Hs-CRP in patients with any group of Androgenetic Alopecia was not significantly different from those healthy controls (P > 0.05). ECHO showed that cardiac structural and functional measures were in normal ranges. ExECG was also normal in all subjects.
CONCLUSION:

Severe vertex pattern Androgenetic Alopecia should be considered to have an increased risk of subclinical atherosclerosis. For this reason, CCA IMT measurement can be recommended as a non-invasive and early diagnostic method.


Early onset of androgenetic alopecia associated with early severe coronary heart disease: a population-based, case-control study.

Matilainen VA, Mäkinen PK, Keinänen-Kiukaanniemi SM.
Author information


Abstract

CONTEXT:

The relationship of ischaemic heart disease (IHD) with androgenic alopecia (Androgenetic Alopecia) has been demonstrated, but no differentiation between early and late onsets of alopecia with regard to the risk and severity of IHD has been made.
OBJECTIVE:

To test if the early onset of alopecia is a risk factor for early severe, coronary artery disease (CAD) requiring surgery and to test if the early onset of Androgenetic Alopecia differs in this respect from the late onset of Androgenetic Alopecia.
DESIGN:

Population-based case-control study.
SETTING AND PARTICIPANTS:

All the 85 male persons living on 31 December 1999 in a Finnish town with total population of 7200, who had had a coronary revascularization procedure between March 1987 and January 1999, were drawn from the discharge register. For each case, an individually selected age-matched control person living in the same town was drawn from the official census register.
MAIN OUTCOME MEASURE:

Alopecia defined as grade 3 vertex or more on the alopecia classification scale of Hamilton, modified by Norwood South Med J, 68:1359-1365, 1975.
RESULTS:

The unadjusted odds ratio (OR) for coronary revascularization under the age of 60 years was 3.57 (95% confidence interval (CI) 1.19-10.72) in men with an early onset of Androgenetic Alopecia compared with men with normal hair status or late Androgenetic Alopecia. After multivariate adjustment for the traditional CAD risk factors, the corresponding OR was 3.18 (95% CI, 1.01-10.03). The unadjusted OR for the coronary revascularization procedure at any age was 2.14 (95% CI, 1.08-4.23) in the subgroup of the men with early Androgenetic Alopecia compared to those with late Androgenetic Alopecia or normal hair status. After adjustment for traditional risk factors this OR was 1.84, being nearly significant (95% CI, 0.90-3.77).
CONCLUSION:

Our results support the hypothesis that the early onset of Androgenetic Alopecia is a risk factor for an early onset of severe coronary heart disease.


A comparative study of dyslipidaemia in men and woman with androgenic alopecia.

Arias-Santiago S, Gutiérrez-Salmerón MT, Buendía-Eisman A, Girón-Prieto MS, Naranjo-Sintes R.
Author information


Abstract

Several studies have analyzed the relationship between androgenetic alopecia and cardiovascular disease (mainly heart disease). However few studies have analyzed lipid values in men and women separately. This case-control study included 300 patients consecutively admitted to an outpatient clinic, 150 with early onset androgenetic alopecia (80 males and 70 females) and 150 controls (80 males and 70 females) with other skin diseases. Female patients with androgenic alopecia showed significant higher triglycerides values (123.8 vs 89.43 mg/dl, p = 0.006), total cholesterol values (196.1 vs 182.3 mg/dl, p = 0.014), LDL-C values (114.1 vs 98.8 mg/dl, p = 0.0006) and lower HDL-C values (56.8 vs 67.7 mg/dl, p <0.0001) versus controls respectively. Men with androgenic alopecia showed significant higher triglycerides values (159.7 vs 128.7 mg/dl, p = 0.04) total cholesterol values (198.3 vs 181.4 mg/dl, p = 0.006) and LDL-C values (124.3 vs 106.2, p = 0.0013) versus non-alopecic men. A higher prevalence of dyslipidemia in women and men with androgenic alopecia has been found. The elevated lipid values in these patients may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia.

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But the study, nor Joseph (the poster child for DR in your opinion) never used a 3.0 has he?...... You are very confusing and all over the place sometimes. You should go back to useful mode.

See.. go back to the beginning of this page.. http://www.hairlosstalk.com/interac...w-Dermaroller-Study-Thoughts-comments/page387 read the whole deal about the Fibrosis and the studies... then you'll get a better grasp of why I am using a 3.0mm during my derma rolling sessions. Useful mode? Not because we don't share the same vision, that I am not useful.. I could care less about the galea theory madness. I have actual studies, biopsies to back up my claims. The Indian study was only for me a good starting point. This is it.

 

[Plyschapan]

So Squeege, what are you saying? Roll deep and go right ahead with Nizoral, Emu oil and those anti-inflammatories?

 

[squeegee]

So Squeege, what are you saying? Roll deep and go right ahead with Nizoral, Emu oil and those anti-inflammatories?

Just a 3.0mm derma roller. with minoxidil twice a day. no topical anti inflammatory yet. Derma rolling session trigger acute inflammation needed for proper remodeling.
4 Stages of Healing

How Do Wounds Heal?

Research work on acute wounds in an animal model shows that wounds heal in four phases. It is believed that chronic wounds must also go through the same basic phases. Some authors combine the first two phases.

The phases of wound healing are:

• Hemostasis
• Inflammation
• Proliferation or Granulation
• Remodeling or Maturation

Hemostasis:
Once the source of damage to a house has been removed and before work can start, utility workers must come in and cap damaged gas or water lines. So too in wound healing damaged blood vessels must be sealed. In wound healing the platelet is the cell which acts as the utility worker sealing off the damaged blood vessels. The blood vessels themselves constrict in response to injury but this spasm ultimately relaxes. The platelets secrete vasoconstrictive substances to aid in this process but their prime role is to form a stable clot sealing the damaged vessel. Under the influence of ADP (adenosine diphosphate) leaking from damaged tissues the platelets aggregate and adhere to the exposed collagen. They also secrete factors which interact with and stimulate the intrinsic clotting cascade through the production of thrombin, which in turn initiates the formation of fibrin from fibrinogen. The fibrin mesh strengthens the platelet aggregate into a stable hemostatic plug. Finally platelets also secrete cytokines such as platelet-derived growth factor (PDGF), which is recognized as one of the first factors secreted in initiating subsequent steps. Hemostasis occurs within minutes of the initial injury unless there are underlying clotting disorders.
Inflammation Phase:
Clinically inflammation, the second stage of wound healing presents as erythema, swelling and warmth often associated with pain, the classic “rubor et tumor c*m calore et dolore”. This stage usually lasts up to 4 days post injury. In the wound healing analogy the first job to be done once the utilities are capped is to clean up the debris. This is a job for non-skilled laborers. These non-skilled laborers in a wound are the neutrophils or PMN’s (polymorphonucleocytes). The inflammatory response causes the blood vessels to become leaky releasing plasma and PMN’s into the surrounding tissue. The neutrophils phagocytize debris and microorganisms and provide the first line of defense against infection. They are aided by local mast cells. As fibrin is broken down as part of this clean-up the degradation products attract the next cell involved. The task of rebuilding a house is complex and requires someone to direct this activity or a contractor. The cell which acts as “contractor” in wound healing is the macrophage. Macrophages are able to phagocytize bacteria and provide a second line of defense. They also secrete a variety of chemotactic and growth factors such as fibroblast growth factor (FGF), epidermal growth factor (EGF), transforming growth factor beta (TGF-__ and interleukin-1 (IL-1) which appears to direct the next stage.


Proliferative Phase ( Proliferation, Granulation and Contraction):
The granulation stage starts approximately four days after wounding and usually lasts until day 21 in acute wounds depending on the size of the wound. It is characterized clinically by the presence of pebbled red tissue in the wound base and involves replacement of dermal tissues and sometimes subdermal tissues in deeper wounds as well as contraction of the wound. In the wound healing analogy once the site has been cleared of debris, under the direction of the contractor, the framers move in to build the framework of the new house. Sub-contractors can now install new plumbing and wiring on the framework and siders and roofers can finish the exterior of the house. The “framer” cells are the fibroblasts which secrete the collagen framework on which further dermal regeneration occurs. Specialized fibroblasts are responsible for wound contraction. The “plumber” cells are the pericytes which regenerate the outer layers of capillaries and the endothelial cells which produce the lining. This process is called angiogenesis. The “roofer” and “sider” cells are the keratinocytes which are responsible for epithelialization. In the final stage of epithelializtion, contracture occurs as the keratinocytes differentiate to form the protective outer layer or stratum corneum.
Remodeling or Maturation Phase:
Once the basic structure of the house is completed interior finishing may begin. So too in wound repair the healing process involves remodeling the dermal tissues to produce greater tensile strength. The principle cell involved in this process is the fibroblast. Remodeling can take up to 2 years after wounding and explains why apparently healed wounds can break down so dramatically and quickly if attention is not paid to the initial causative factors.

 

[BeliefISKEY]

Belief.. The problem with Androgen Alopecia is that people only focus on the obvious, the scalp and the esthetic problem of thinning /missing hair.

The problem starts at the cellular level.. not at the physical level. DHT is a powerful steroid sex hormone than can or cannot trigger a chronic inflammation. This is why some people go bald or not going bald.

There are several studies out there proving a relation between early balding and signs of atherosclerosis or dyslipidemia.

DHT promotes VCAM-1 and NF-KB expression . Both related to theses diseases. The tight Galea theory has nothing to do with this. It is maybe a side-effect of the local chronic inflammation, no the problem itself. LOL

http://www.ncbi.nlm.nih.gov/pubmed/14684616
http://www.ncbi.nlm.nih.gov/pubmed/18941467


Is androgenetic alopecia a risk for atherosclerosis?

Dogramaci AC, Balci DD, Balci A, Karazincir S, Savas N, Topaloglu C, Yalcin F.
Author information


Abstract

BACKGROUND:

Several studies have demonstrated the presence of an association between androgenetic alopecia (Androgenetic Alopecia) and cardiovascular disease. The aim of this study was to evaluate subclinical atherosclerosis in patients with Androgenetic Alopecia and healthy controls by the incorporation of carotid intima-media thickness (IMT) and high-sensitive C-reactive protein (hs-CRP) along with echocardiography (ECHO) and exercise electrocardiography (ExECG).
METHODS:

We performed a case-control study in 50 male patients with Androgenetic Alopecia and 31 age-matched healthy male controls with normal hair status. Both the Androgenetic Alopecia patients and controls with a history of diabetes mellitus, cigarette smoking, hypertension, cardiovascular or cerebrovascular disease, and renal failure were excluded. Androgenetic Alopecia was classified according to the Hamilton-Norwood scale. Serum lipids, serum hs-CRP, total testosterone, and dehydroepiandrosterone sulphate were examined in all study subjects. Carotid ultrasonography was used to measure the IMT of the common carotid arteries (CCA). ECHO and ExECG were performed in all subjects.
RESULTS:

IMT of the CCA was found to be significantly higher in patients with severe vertex pattern Androgenetic Alopecia when compared to patients with other patterns of Androgenetic Alopecia and healthy controls (P < 0.05). Hs-CRP in patients with any group of Androgenetic Alopecia was not significantly different from those healthy controls (P > 0.05). ECHO showed that cardiac structural and functional measures were in normal ranges. ExECG was also normal in all subjects.
CONCLUSION:

Severe vertex pattern Androgenetic Alopecia should be considered to have an increased risk of subclinical atherosclerosis. For this reason, CCA IMT measurement can be recommended as a non-invasive and early diagnostic method.


Early onset of androgenetic alopecia associated with early severe coronary heart disease: a population-based, case-control study.

Matilainen VA, Mäkinen PK, Keinänen-Kiukaanniemi SM.
Author information


Abstract

CONTEXT:

The relationship of ischaemic heart disease (IHD) with androgenic alopecia (Androgenetic Alopecia) has been demonstrated, but no differentiation between early and late onsets of alopecia with regard to the risk and severity of IHD has been made.
OBJECTIVE:

To test if the early onset of alopecia is a risk factor for early severe, coronary artery disease (CAD) requiring surgery and to test if the early onset of Androgenetic Alopecia differs in this respect from the late onset of Androgenetic Alopecia.
DESIGN:

Population-based case-control study.
SETTING AND PARTICIPANTS:

All the 85 male persons living on 31 December 1999 in a Finnish town with total population of 7200, who had had a coronary revascularization procedure between March 1987 and January 1999, were drawn from the discharge register. For each case, an individually selected age-matched control person living in the same town was drawn from the official census register.
MAIN OUTCOME MEASURE:

Alopecia defined as grade 3 vertex or more on the alopecia classification scale of Hamilton, modified by Norwood South Med J, 68:1359-1365, 1975.
RESULTS:

The unadjusted odds ratio (OR) for coronary revascularization under the age of 60 years was 3.57 (95% confidence interval (CI) 1.19-10.72) in men with an early onset of Androgenetic Alopecia compared with men with normal hair status or late Androgenetic Alopecia. After multivariate adjustment for the traditional CAD risk factors, the corresponding OR was 3.18 (95% CI, 1.01-10.03). The unadjusted OR for the coronary revascularization procedure at any age was 2.14 (95% CI, 1.08-4.23) in the subgroup of the men with early Androgenetic Alopecia compared to those with late Androgenetic Alopecia or normal hair status. After adjustment for traditional risk factors this OR was 1.84, being nearly significant (95% CI, 0.90-3.77).
CONCLUSION:

Our results support the hypothesis that the early onset of Androgenetic Alopecia is a risk factor for an early onset of severe coronary heart disease.


A comparative study of dyslipidaemia in men and woman with androgenic alopecia.

Arias-Santiago S, Gutiérrez-Salmerón MT, Buendía-Eisman A, Girón-Prieto MS, Naranjo-Sintes R.
Author information


Abstract

Several studies have analyzed the relationship between androgenetic alopecia and cardiovascular disease (mainly heart disease). However few studies have analyzed lipid values in men and women separately. This case-control study included 300 patients consecutively admitted to an outpatient clinic, 150 with early onset androgenetic alopecia (80 males and 70 females) and 150 controls (80 males and 70 females) with other skin diseases. Female patients with androgenic alopecia showed significant higher triglycerides values (123.8 vs 89.43 mg/dl, p = 0.006), total cholesterol values (196.1 vs 182.3 mg/dl, p = 0.014), LDL-C values (114.1 vs 98.8 mg/dl, p = 0.0006) and lower HDL-C values (56.8 vs 67.7 mg/dl, p <0.0001) versus controls respectively. Men with androgenic alopecia showed significant higher triglycerides values (159.7 vs 128.7 mg/dl, p = 0.04) total cholesterol values (198.3 vs 181.4 mg/dl, p = 0.006) and LDL-C values (124.3 vs 106.2, p = 0.0013) versus non-alopecic men. A higher prevalence of dyslipidemia in women and men with androgenic alopecia has been found. The elevated lipid values in these patients may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia.

Please tell me why when the scalp is loosened 1) Hair loss is cured 2) all noticable inflammation (itchiness, redness etc.) is eliminated, 3) Good Regrowth occurs.

Please tell me why when the scalp is loosened, the DHT/ESTRADIOL ratio is regulated and all of sh** I said above is eliminated...

You know, the scalp gets tighter when you stress out... That fibrosis is pretty tricky huh? Also, DHT is very tricky as well! Some fuc**** guys have a sh** load of it when younger but DHT decided to say NO, I will fuc* you up when you're 42 years old... NOT NOW! I will fuc* you up when I start declining. damn that DHT is tricky... So tricky that it decides WHEN it wants to fuc* your scalp hair up. You can go half a lifetime with DHT FILLED BLOOD circulating throughout your whole scalp without a problem until it just decides to fu** u up... And only in the GALEA REGION! The SAME REGION that is basically cured of the symptoms this badass DHT decides to wreck, at the time it chooses to, AFTER you loosen the scalp. Damn that tricky DHT, DAMN IT!

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So Squeege, what are you saying? Roll deep and go right ahead with Nizoral, Emu oil and those anti-inflammatories?

Emu oil is great for fibrosis & other stuff so KEEP THAT!

But yea according to him you should now make an attempt to loose your manhood & puncture your follicles.

I love it how lasers (don't worry, I won't mention the violet ray for all of you "quackwatchers out there!) aren't talked about too much on this thread since the word "fibrosis" gets thrown around much.

 

[squeegee]

Please tell me why when the scalp is loosened 1) Hair loss is cured 2) all noticable inflammation (itchiness, redness etc.) is eliminated, 3) Good Regrowth occurs.

Please tell me why when the scalp is loosened, the DHT/ESTRADIOL ratio is regulated and all of sh** I said above is eliminated...

You know, the scalp gets tighter when you stress out... That fibrosis is pretty tricky huh? Also, DHT is very tricky as well! Some fuc**** guys have a sh** load of it when younger but DHT decided to say NO, I will fuc* you up when you're 42 years old... NOT NOW! I will fuc* you up when I start declining. damn that DHT is tricky... So tricky that it decides WHEN it wants to fuc* your scalp hair up. You can go half a lifetime with DHT FILLED BLOOD circulating throughout your whole scalp without a problem until it just decides to fu** u up... And only in the GALEA REGION! The SAME REGION that is basically cured of the symptoms this badass DHT decides to wreck, at the time it chooses to, AFTER you loosen the scalp. Damn that tricky DHT, DAMN IT!

Why don't you go massage your galea if you know the cure already?



DHT no only trigger the scalp area. That can be the whole endothelium in your body. DHT is related to VCAM-1 expression which is monocyte adhesion in the endothelium.

DHT is related to a lot of inflammation diseases in males and pro-androgenic females for a reason.

DHT is pro-inflammatory.period.

http://en.wikipedia.org/wiki/Endothelium

 

[BeliefISKEY]

and because i am more sexy eventually with hair short. i will not buzz sorry. but here is a pic of hair grown a month after buzz and hair now. its difference is slightly more than a month.

same angle/same camera/same position/same settings/same lighting.

generally from slightly back or side you cant notice i thin anymore and that my friends is awesome.
View attachment 23063

Not doubting your progress or anything but that second pic is hiding some of your prior thinning areas and your grown out hair is just covering your hairline. Maybe you should take pics from the front while holding your hair back?

I know you're making progress because 1) I take your word and most importantly 2) I've seen some good progress on other "better" pics you've uploaded. Just my 2c bro.

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Why don't you go massage your galea if you know the cure already?



DHT no only trigger the scalp area. That can be the whole endothelium in your body. DHT is related to VCAM-1 expression which is monocyte adhesion in the endothelium.

DHT is related to a lot of inflammation diseases in males and pro-androgenic females for a reason.

DHT is pro-inflammatory.period.

http://en.wikipedia.org/wiki/Endothelium

THAT'S THE PROBLEM WITH YOU... If you would have looked at the study or paid attention to anything I've been saying you would understand that you DO NOT DO ANYTHING TO YOUR GALEA... IT'S THE MUSCLES AROUND IT THAT ARE THE PROBLEM. In the Botox study, people loosened their scalp via receiving Botox injections to the sides and back of their heads where there is NO BALDNESS... And that resulted in less local/scalp dht and regulated DHT/ESTRADIOL levels. This was also similarly demonstrated in the German study as well.

I love you.

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Why don't you go massage your galea if you know the cure already?



DHT no only trigger the scalp area. That can be the whole endothelium in your body. DHT is related to VCAM-1 expression which is monocyte adhesion in the endothelium.

DHT is related to a lot of inflammation diseases in males and pro-androgenic females for a reason.

DHT is pro-inflammatory.period.

http://en.wikipedia.org/wiki/Endothelium

Also I'm not claiming DHT doesn't fuc* u up... I know it does... But only when it's accumulated/overproduced in the Galea area, i explained myself on my last response in regards to this. You're not looking at the bigger picture... You just wanna see what you wanna see.

Jesus Christ squeege.. You do know that people with completely shaved heads still have hair on the sides and back, right? Godamn DHT is even more trickier than i thought. It decides when AND WHERE it wants to fuc* you up.

 

[squeegee]

Not doubting your progress or anything but that second pic is hiding some of your prior thinning areas and your grown out hair is just covering your hairline. Maybe you should take pics from the front while holding your hair back?

I know you're making progress because 1) I take your word and most importantly 2) I've seen some good progress on other "better" pics you've uploaded. Just my 2c bro.

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THAT'S THE PROBLEM WITH YOU... If you would have looked at the study or paid attention to anything I've been saying you DO NOT DO ANYTHING TO YOUR GALEA... IT'S THE MUSCLES AROUND IT THAT ARE THE PROBLEM. In the Botox study, people loosened their scalp via receiving Botox injections to the sides and back of their heads where there is NO BALDNESS... And that resulted in less local/scalp dht and regulated DHT/ESTRADIOL levels. This was also demonstrated in the German study as well.

I love you.

I know about the frigging galea theory. This is horse ****! People achieves respective results with finasteride/minoxidil without masturbating their galea all day!!! Masturbating the galea will probably help adding fresh blood the hypoxic area.. this is it. It won't reverse the physical damages done by the inflammation. People with hair transplant have results without masturbating the galea! This is horse ****.. Follica achieves results without any surgery done to the galea! **** the GALEA!!! DHT trigger an endothelial dysfunction on your scalp! this is it! I wasn't masturbating my galea region in my teens.. I had more hair than lady gaga for ****sakes! Cardiovascular diseases had nothing to do with the friggin galea! **** the galea.. I hate that word too! It is the endothelium on your scalp not the friggin galea!

Belief.. are your from the Planet Galea? hahaahha


Even the BBQ guy will disagree with the stupid galea theory! The real problem is at the endothelium level.. **** the galea!

Notice how they temple are still not grown yet?

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http://en.wikipedia.org/wiki/Endothelium
Endothelium:

The endothelium is the thin layer of cells that lines the interior surface of blood vessels and lymphatic vessels,[SUP][1][/SUP] forming an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. The cells that form the endothelium are called endothelial cells. Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells.
Vascular endothelial cells line the entire circulatory system, from the heart to the smallest capillaries. These cells have very distinct and unique functions that are paramount to vascular biology. These functions include fluid filtration, such as in the glomeruli of the kidney, blood vessel tone, hemostasis, neutrophil recruitment, and hormone trafficking. Endothelium of the interior surfaces of the heart chambers are called endocardium.


Endothelial cells are involved in many aspects of vascular biology, including:

• Barrier function - the endothelium acts as a semi-selective barrier between the vessel lumen and surrounding tissue, controlling the passage of materials and the transit of white blood cells into and out of the bloodstream. Excessive or prolonged increases in permeability of the endothelial monolayer, as in cases of chronic inflammation, may lead to tissue edema/swelling.
• Blood clotting (thrombosis & fibrinolysis). The endothelium normally provides a non-thrombogenic surface because it contains, for example, heparan sulfate which acts as a cofactor for activating antithrombin, a protease that inactivates several factors in the coagulation cascade.
• Inflammation
• Formation of new blood vessels (angiogenesis)
• Vasoconstriction and vasodilation, and hence the control of blood pressure
• Repair of damaged or diseased organs via an injection of blood vessel cells[SUP][5][/SUP]
• Angiopoietin-2 works with VEGF to facilitate cell proliferation and migration of endothelial cells

Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of nitric oxide, often due to high levels of asymmetric dimethylarginine, which interfere with the normal L-arginine-stimulated nitric oxide synthesis and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in reactive oxygen species, which can impair nitric oxide production and activity via several mechanisms.[SUP][6][/SUP] The signalling protein ERK5 is essential for maintaining normal endothelial cell function.[SUP][7][/SUP] A further consequence of damage to the endothelium is the release of pathological quantities of von Willebrand factor, which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.

 

[BeliefISKEY]

I know about the frigging galea theory. This is horse ****! People achieves respective results with finasteride/minoxidil without masturbating their galea all day!!! Masturbating the galea will probably help adding fresh blood the hypoxic area.. this is it. It won't reverse the physical damages done by the inflammation. People with hair transplant have results without masturbating the galea! This is horse ****.. Follica achieves results without any surgery done to the galea! **** the GALEA!!! DHT trigger an endothelial dysfunction on your scalp! this is it! I wasn't masturbating my galea region in my teens.. I had more hair than lady gaga for ****sakes! Cardiovascular diseases had nothing to do with the friggin galea! **** the galea.. I hate that word too! It is the endothelium on your scalp not the friggin galea!

Belief.. are your from the Planet Galea? hahaahha


Even the BBQ guy will disagree with the stupid galea theory! The real problem is at the endothelium level.. **** the galea!

Notice how they temple are still not grown yet?

- - - Updated - - -
http://en.wikipedia.org/wiki/Endothelium
Endothelium:

The endothelium is the thin layer of cells that lines the interior surface of blood vessels and lymphatic vessels,[SUP][1][/SUP] forming an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. The cells that form the endothelium are called endothelial cells. Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells.
Vascular endothelial cells line the entire circulatory system, from the heart to the smallest capillaries. These cells have very distinct and unique functions that are paramount to vascular biology. These functions include fluid filtration, such as in the glomeruli of the kidney, blood vessel tone, hemostasis, neutrophil recruitment, and hormone trafficking. Endothelium of the interior surfaces of the heart chambers are called endocardium.


Endothelial cells are involved in many aspects of vascular biology, including:

• Barrier function - the endothelium acts as a semi-selective barrier between the vessel lumen and surrounding tissue, controlling the passage of materials and the transit of white blood cells into and out of the bloodstream. Excessive or prolonged increases in permeability of the endothelial monolayer, as in cases of chronic inflammation, may lead to tissue edema/swelling.
• Blood clotting (thrombosis & fibrinolysis). The endothelium normally provides a non-thrombogenic surface because it contains, for example, heparan sulfate which acts as a cofactor for activating antithrombin, a protease that inactivates several factors in the coagulation cascade.
• Inflammation
• Formation of new blood vessels (angiogenesis)
• Vasoconstriction and vasodilation, and hence the control of blood pressure
• Repair of damaged or diseased organs via an injection of blood vessel cells[SUP][5][/SUP]
• Angiopoietin-2 works with VEGF to facilitate cell proliferation and migration of endothelial cells

Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of nitric oxide, often due to high levels of asymmetric dimethylarginine, which interfere with the normal L-arginine-stimulated nitric oxide synthesis and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in reactive oxygen species, which can impair nitric oxide production and activity via several mechanisms.[SUP][6][/SUP] The signalling protein ERK5 is essential for maintaining normal endothelial cell function.[SUP][7][/SUP] A further consequence of damage to the endothelium is the release of pathological quantities of von Willebrand factor, which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.

So that BBQ man grew terminals hairs on his temples? Let me guess, you don't have a follow up on his case to provide me with? I know he's dead and I also know those hairs went bye bye just like the vast majority of guys with overly overly tight scalps that get a hair transplant done.


I read the first half of your reply and noticed that you still don't get it...

Guys that have hair transplant done on their scalps experience formation of new new vascularity just like with DR only to have it die out on them if they don't take finasteride (Good hair transplant doctors always prescribe finasteride for life after undergoing a hair transplant procedure) or induce local BLOOD FLOW to the transplanted areas via massage/laser/violet ray , BECAUSE OF A TIGHT GALEA. The blood flow is disrupted dude & once that's taken care of male pattern baldness is reversed for the most part... Studies confirm it... Deal with it. I understand the validity in DR lol relax.... You're the one that doesn't understand here. DR is absolutely necessary after being bald for a long time since the networks DO DIE as a result of accumulated/overproduced DHT only around the (SPEAKING OF HORSES AND HORSESH**) HORESHOE AREA AKA GALEA.

Why do we have EXTRA DHT around the top and not the sides SQUEEGERINA (and ironically the vast majority of baldies still have hair their =] )?? Why is it that when you loosen the muscles pulling on the galea the local ELEVATES DHT levels are lowered SQUUEGINA? & why is it that male pattern baldness is reversed as a result of this SQUEEGIANA??

http://m.youtube.com/watch?v=0-cpL--0AQA

 

[squeegee]

So that BBQ man grew terminals hairs on his temples? Let me guess, you don't have a follow up on his case to provide me with? I know he's dead and I also know those hairs went bye bye just like the vast majority of guys with overly overly tight scalps that get a hair transplant done.


I read the first half of your reply and noticed that you still don't get it...

Guys that have hair transplant done on their scalps experience formation of new new vascularity just like with DR only to have it die out on them if they don't take finasteride (Good hair transplant doctors always prescribe finasteride for life after undergoing a hair transplant procedure) or induce local BLOOD FLOW to the transplanted areas via massage/laser/violet ray , BECAUSE OF A TIGHT GALEA. The blood flow is disrupted dude & once that's taken care of male pattern baldness is reversed for the most part... Studies confirm it... Deal with it. I understand the validity in DR lol relax.... You're the one that doesn't understand here. DR is absolutely necessary after being bald for a long time since the networks DO DIE as a result of accumulated/overproduced DHT only around the (SPEAKING OF HORSES AND HORSESH**) HORESHOE AREA AKA GALEA.

Why do we have EXTRA DHT around the top and not the sides SQUEEGERINA (and ironically the vast majority of baldies still have hair their =] )?? Why is it that when you loosen the muscles pulling on the galea the local ELEVATES DHT levels are lowered SQUUEGINA? & why is it that male pattern baldness is reversed as a result of this SQUEEGIANA??

http://m.youtube.com/watch?v=0-cpL--0AQA

BeliefISKEY.. It is like am talking to a 5 years old. you have a tunnel vision on your stupid galea ! go loose your muscles on your galea then! ..not everybody balding end up with horseshoe pattern.. it is the degree of inflammation that makes the difference.. I am in the Military, I see bald ****ers everyday , only the worst case scenario of Androgenetic Alopecia sport the horses "hoe". I even see people with sides almost disappeared. DHT doesn't accumulates, it triggers inflammation. Fibrosis is the best proof. The horseshoe pattern is probably related to the endothelium distribution (blood vessels,capillaries) or the androgen receptors network on your scalp?? Derma rolling destroy local fibrosis, mediates angiogenesis locally. The same goes for cardiovascular diseases. The endothelium is the biggest organ of your body. You don't need to masturbates your galea to get results or reverse male pattern baldness. Your stupid galea theory has no relation with cardiovascular diseases. The endothelium does.

BeliefISKEY..this is not a frigging caterpillar..It is an hair transplant strip showing marked perifollicular fibrosis
This is where the ****ing problem is, not your stupid galea.

If you believes in unicorns theories and Santa Claus.. that is cool but keep it for yourself LOL

 

[saintsfan92344]

Im going to get popcorn this is getting good :argue:

 

[CharlesXavier]

Lawlz not gonna lie im lost as tits right now cX

- - - Updated - - -

Bring me some

 

[hellouser]

 

[RisingFist]

Get a girl to give you a galea job. Use some olive oil for lube. With time, the scalp will c*m hair and you'll feel good afterwards.

 

[squeegee]

Get a girl to give you a galea job. Use some olive oil for lube. With time, the scalp will c*m hair and you'll feel good afterwards.

:worthless:

hahaahaahahahah! this is awesome! KY warming/tingling oil would be more appropriates for the job..

BeliefISKEY.. here is a good video for you.. I know that you believes in unicorn theories. Relax.. and masturbates your galea while watching!

[video=youtube;h_a__AtNcbg]http://www.youtube.com/watch?v=h_a__AtNcbg[/video]

P.S: the guy running the video is also a balder!

 

[slam1523]

@saintsfan haha bro I respected you firstly because of your football fan hood, but now because of your posts! #respect... I'm going to get #respectthesqueeg trending! Do work dogg!

 

[squeegee]

But the study, nor Joseph (the poster child for DR in your opinion) never used a 3.0 has he?...... You are very confusing and all over the place sometimes. You should go back to useful mode.

Dr. Fernandez mentioned many times the use of 3.0mm for serious deeper problems.

http://www.medik8.es/documents/Combating_photoaging.pdf
http://owndoc.com/pdf/DermarollingScience.pdf


[video=youtube;uLCJ5VHTfiY]http://www.youtube.com/watch?v=uLCJ5VHTfiY[/video]

2:20

 

[saintsfan92344]

@saintsfan haha bro I respected you firstly because of your football fan hood, but now because of your posts! #respect... I'm going to get #respectthesqueeg trending! Do work dogg!

SQUEEGEE SQUEEGEE SQUEEGEE