saintsfan92344
Established Member
- Reaction score
- 25
wow you can really see them little bugars Opti, congrats. refresh my memory how long have you been rolling?
New Dermaroller Study; Thoughts, comments?
- Thread starter Jlyncher
- Start date
- Status
wow you can really see them little bugars Opti, congrats. refresh my memory how long have you been rolling?
tomorrow is my 3. or 4. session with 1,5mm. .Im rolling since about 7-8 weeks?i did 2-3 rolling sessions with 0,5mm 540 before but many hair got grabbed by so much needles .192 needles and 1,5mm alot better in my opinion
hairregrowth21
Established Member
- Reaction score
- 7
Way to step up- these are much better results than you would get doing anything else and you are still early on in the process.
unk:
squeegee
Banned
- Reaction score
- 132
Hair follicle bulge: a fascinating reservoir of epithelial stem cells.
Ohyama M.
Source
Department of Dermatology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. maboym@sc.itc.keio.ac.jp <maboym@sc.itc.keio.ac.jp>
Abstract
Hair follicles reconstitute themselves though the hair cycle, suggesting the presence of intrinsic stem cells. In contrast to the previous belief that stem cells reside in the bulbar region of hair follicles, stem cells were detected in the bulge area, a contiguous part of outer root sheath, that provides the insertion point for arrector pili muscle and marks the bottom of the permanent portion of hair follicles. The bulge cells are morphologically undifferentiated and slow-cycling under the normal conditions. Later, studies successively demonstrated that bulge cells possess stem cell properties such as high proliferative capacity and multipotency to regenerate not only hair follicles but also sebaceous glands and epidermis. Our knowledge of the bulge cell biology is rapidly increasing because of the identification of novel cell surface markers, the ability to isolate living bulge cells, and microarray analysis of multiple gene expression. Importantly, novel cell surface markers were identified on human bulge cells using precise laser capture microdissection and microarray analyses. Use of these markers enabled the successful enrichment of living human bulge cells, raising the possibility of future treatments of hair disorders using stem cells. Additional clinical relevance of bulge cell biology includes the importance of bulge cells as a gene therapy target and their possible roles in tumorigenesis.
Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.
Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, Stanton DC, Carrasco L, Spiegel JH, Tobias JW, Cotsarelis G.
Source
Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Abstract
Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia.
Folliculitis is defined histologically as the presence of inflammatory cells within the wall and ostia of the hair follicle, creating a follicular-based pustule. The actual type of inflammatory cells can vary and may be dependent on the etiology of the folliculitis, the stage at which the biopsy specimen was obtained, or both. The inflammation can be either limited to the superficial aspect of the follicle with primary involvement of the infundibulum or the inflammation can affect both the superficial and deep aspect of the follicle. Deep folliculitis can eventuate from chronic lesions of superficial folliculitis or from lesions that are manipulated, and this may ultimately result in scarring.
Perifolliculitis, on the other hand, is defined as the presence of inflammatory cells in the perifollicular tissues and can involve the adjacent reticular dermis. Folliculitis and perifolliculitis can manifest independently or together as a result of follicular disruption and irritation.
The role of inflammation and immunity in the pathogenesis of androgenetic alopecia.
Magro CM, Rossi A, Poe J, Manhas-Bhutani S, Sadick N.
Source
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY, USA.
Abstract
BACKGROUND:
Female pattern hair loss affects many women; its pathogenetic basis has been held to be similar to men with common baldness.
OBJECTIVE:
The objective of this study was to determine the role of immunity and inflammation in androgenetic alopecia in women and modulate therapy according to inflammatory and immunoreactant profiles.
MATERIALS AND METHODS:
52 women with androgenetic alopecia (AA) underwent scalp biopsies for routine light microscopic assessment and direct immunofluroescent studies. In 18 patients, serologic assessment for antibodies to androgen receptor, estrogen receptor and cytokeratin 15 was conducted.
RESULTS:
A lymphocytic folliculitis targeting the bulge epithelium was observed in many cases. Thirty-three of 52 female patients had significant deposits of IgM within the epidermal basement membrane zone typically accompanied by components of complement activation. The severity of changes light microscopically were more apparent in the positive immunoreactant group. Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group.
CONCLUSION:
A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia and could point toward an immunologically driven trigger. Cases showing a positive immunoreactant profile respond well to combined modality therapy compared to those with a negative result.
- - - Updated - - -
Perifollicular fibrosis: pathogenetic role in androgenetic alopecia.
Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH.
Source
Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University, Seoul, Korea.
Abstract
Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 microg/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia.
Androgenetic alopecia in males: a histopathological and ultrastructural study.
El-Domyati M, Attia S, Saleh F, Abdel-Wahab H.
Source
Department of Dermatology, Al-Minya University, 2 Obour Buildings, Salah Salem St, Apt. 53, Nasr City, Cairo 11371, Egypt. moetazeldomyati@yahoo.com
Abstract
BACKGROUND:
Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process.
AIMS:
To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (Androgenetic Alopecia). Patients/methods Fifty-five subjects were included in this study (40 with Androgenetic Alopecia and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study.
RESULTS:
The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant inverse correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases.
CONCLUSION:
Follicular microinflammation plays an integral role in the pathogenesis of Androgenetic Alopecia in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases
During the hair cycle the follicle has to be rebuilt from stem cells,” explains Dr Bruno Bernard, director of research for life sciences at L’Oreal. “Stem cells in human hair follicles are localised in two different reservoirs – one is in the upper part of the follicle and the other in the lower part. “The cells in the lower part are required to activate the cells in the upper part and so help to maintain the follicle function. The thickening of collagen in the connective tissue sheath, which sits around the base of the hair follicle, prevents the movement of stem cells from the lower reservoir to the upper reservoir. Bit by bit, the follicle is squeezed and causes the follicles to grow smaller and smaller.” Indeed, research from The Rockefeller University in New York suggests movement between the two groups of stem cells is crucial in normal hair growth.
Another recent study, at the University of Pennsylvania, has shown that bald areas of scalp contain the same number of stem cells as hairy areas. It disproved theories that hair loss in androgenic alopecia was due to a loss of follicle stem cells suggesting that they have just become inactive.
Ohyama M.
Source
Department of Dermatology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. maboym@sc.itc.keio.ac.jp <maboym@sc.itc.keio.ac.jp>
Abstract
Hair follicles reconstitute themselves though the hair cycle, suggesting the presence of intrinsic stem cells. In contrast to the previous belief that stem cells reside in the bulbar region of hair follicles, stem cells were detected in the bulge area, a contiguous part of outer root sheath, that provides the insertion point for arrector pili muscle and marks the bottom of the permanent portion of hair follicles. The bulge cells are morphologically undifferentiated and slow-cycling under the normal conditions. Later, studies successively demonstrated that bulge cells possess stem cell properties such as high proliferative capacity and multipotency to regenerate not only hair follicles but also sebaceous glands and epidermis. Our knowledge of the bulge cell biology is rapidly increasing because of the identification of novel cell surface markers, the ability to isolate living bulge cells, and microarray analysis of multiple gene expression. Importantly, novel cell surface markers were identified on human bulge cells using precise laser capture microdissection and microarray analyses. Use of these markers enabled the successful enrichment of living human bulge cells, raising the possibility of future treatments of hair disorders using stem cells. Additional clinical relevance of bulge cell biology includes the importance of bulge cells as a gene therapy target and their possible roles in tumorigenesis.
Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.
Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, Stanton DC, Carrasco L, Spiegel JH, Tobias JW, Cotsarelis G.
Source
Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Abstract
Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia.
Folliculitis is defined histologically as the presence of inflammatory cells within the wall and ostia of the hair follicle, creating a follicular-based pustule. The actual type of inflammatory cells can vary and may be dependent on the etiology of the folliculitis, the stage at which the biopsy specimen was obtained, or both. The inflammation can be either limited to the superficial aspect of the follicle with primary involvement of the infundibulum or the inflammation can affect both the superficial and deep aspect of the follicle. Deep folliculitis can eventuate from chronic lesions of superficial folliculitis or from lesions that are manipulated, and this may ultimately result in scarring.
Perifolliculitis, on the other hand, is defined as the presence of inflammatory cells in the perifollicular tissues and can involve the adjacent reticular dermis. Folliculitis and perifolliculitis can manifest independently or together as a result of follicular disruption and irritation.
The role of inflammation and immunity in the pathogenesis of androgenetic alopecia.
Magro CM, Rossi A, Poe J, Manhas-Bhutani S, Sadick N.
Source
Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY, USA.
Abstract
BACKGROUND:
Female pattern hair loss affects many women; its pathogenetic basis has been held to be similar to men with common baldness.
OBJECTIVE:
The objective of this study was to determine the role of immunity and inflammation in androgenetic alopecia in women and modulate therapy according to inflammatory and immunoreactant profiles.
MATERIALS AND METHODS:
52 women with androgenetic alopecia (AA) underwent scalp biopsies for routine light microscopic assessment and direct immunofluroescent studies. In 18 patients, serologic assessment for antibodies to androgen receptor, estrogen receptor and cytokeratin 15 was conducted.
RESULTS:
A lymphocytic folliculitis targeting the bulge epithelium was observed in many cases. Thirty-three of 52 female patients had significant deposits of IgM within the epidermal basement membrane zone typically accompanied by components of complement activation. The severity of changes light microscopically were more apparent in the positive immunoreactant group. Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group.
CONCLUSION:
A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia and could point toward an immunologically driven trigger. Cases showing a positive immunoreactant profile respond well to combined modality therapy compared to those with a negative result.
- - - Updated - - -
Perifollicular fibrosis: pathogenetic role in androgenetic alopecia.
Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH.
Source
Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University, Seoul, Korea.
Abstract
Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 microg/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia.
Androgenetic alopecia in males: a histopathological and ultrastructural study.
El-Domyati M, Attia S, Saleh F, Abdel-Wahab H.
Source
Department of Dermatology, Al-Minya University, 2 Obour Buildings, Salah Salem St, Apt. 53, Nasr City, Cairo 11371, Egypt. moetazeldomyati@yahoo.com
Abstract
BACKGROUND:
Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process.
AIMS:
To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (Androgenetic Alopecia). Patients/methods Fifty-five subjects were included in this study (40 with Androgenetic Alopecia and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study.
RESULTS:
The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant inverse correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases.
CONCLUSION:
Follicular microinflammation plays an integral role in the pathogenesis of Androgenetic Alopecia in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases
During the hair cycle the follicle has to be rebuilt from stem cells,” explains Dr Bruno Bernard, director of research for life sciences at L’Oreal. “Stem cells in human hair follicles are localised in two different reservoirs – one is in the upper part of the follicle and the other in the lower part. “The cells in the lower part are required to activate the cells in the upper part and so help to maintain the follicle function. The thickening of collagen in the connective tissue sheath, which sits around the base of the hair follicle, prevents the movement of stem cells from the lower reservoir to the upper reservoir. Bit by bit, the follicle is squeezed and causes the follicles to grow smaller and smaller.” Indeed, research from The Rockefeller University in New York suggests movement between the two groups of stem cells is crucial in normal hair growth.
Another recent study, at the University of Pennsylvania, has shown that bald areas of scalp contain the same number of stem cells as hairy areas. It disproved theories that hair loss in androgenic alopecia was due to a loss of follicle stem cells suggesting that they have just become inactive.
2young2retire
Experienced Member
- Reaction score
- 163
squeege we tear apart these bulges and stem cells travel around huge needles kill these fellas lol.....
[video=youtube;eU4ZvfkmOck]http://www.youtube.com/watch?v=eU4ZvfkmOck[/video]
huge needles kill these fellas lol.....[video=youtube;eU4ZvfkmOck]http://www.youtube.com/watch?v=eU4ZvfkmOck[/video]
2young2retire
Experienced Member
- Reaction score
- 163
two applications for me on nw6 thinning area
squeegee
Banned
- Reaction score
- 132
=2young2retire;1148763]squeege we tear apart these bulges and stem cells travel aroundhuge needles kill these fellas lol.....
Totally bros! The length of the needles are really important.. This is why we need to put some weight on the derma roller! still waiting for some 3.0mm 192 needles derma rollers from China LOL L'Oreal was on the money with their study.
During the hair cycle the follicle has to be rebuilt from stem cells,” explains Dr Bruno Bernard, director of research for life sciences at L’Oreal. “Stem cells in human hair follicles are localised in two different reservoirs – one is in the upper part of the follicle and the other in the lower part. “The cells in the lower part are required to activate the cells in the upper part and so help to maintain the follicle function. The thickening of collagen in the connective tissue sheath, which sits around the base of the hair follicle, prevents the movement of stem cells from the lower reservoir to the upper reservoir. Bit by bit, the follicle is squeezed and causes the follicles to grow smaller and smaller.” Indeed, research from The Rockefeller University in New York suggests movement between the two groups of stem cells is crucial in normal hair growth.
Another recent study, at the University of Pennsylvania, has shown that bald areas of scalp contain the same number of stem cells as hairy areas. It disproved theories that hair loss in androgenic alopecia was due to a loss of follicle stem cells suggesting that they have just become inactive.
Another recent study, at the University of Pennsylvania, has shown that bald areas of scalp contain the same number of stem cells as hairy areas. It disproved theories that hair loss in androgenic alopecia was due to a loss of follicle stem cells suggesting that they have just become inactive.
[video=youtube;8gyLR4NfMiI]http://www.youtube.com/watch?v=8gyLR4NfMiI[/video]
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Been 3 application still have a lot.. You need a thick coat and 15 minutes roughly before your start rolling.. get your head wet with hot water.. skin get really permeable before application. You still going to feel the needles.. common sense.. but at least I can roll without having a towel in my mouth LOL I put some more on the temples.. Works really good!
Morinohtar
New Member
- Reaction score
- 0
squee, tsk tsk, not my hero anymore... at 1st i used a towel too, but the last few times i just try to put my mind somewhere else (the painless world lol) and bear with it. Still hurts and some strange liquid comes out of my eyes ahahahaha
saintsfan92344
Established Member
- Reaction score
- 25
Opti no sheds?? I am doing my 5th roll, minoxidil for 1.5 months and shedding at a rediculous pace, I know its part of the game but its daily now and scary
squeegee
Banned
- Reaction score
- 132
hahahahhahahahah! get a few drinks in!
int::beer: and fast roll it! Like a sewing machine!- - - Updated - - -
Get over it! Shedding can be part of the growing process! I made it and you will! Keep on rolling!
zombiehair
Member
- Reaction score
- 3
Just checking in ,haven't posted in a while but still rolling.
Think I'm on week 12 or 13 now.
Doing one main roll once a week and some times a less aggressive top up roll mid week.
I usually start my session with a 1.5mm 512 needle roller then go over the area again with a 2mm 192 needle roller.
The crunching popping sensation felt initially when I started rolling is all but gone apart from around the temple area.
Recently I have noticed more blood spots after rolling which I take as a positive as no mater how hard I rolled at the beginning my scalp wouldn't bleed.
As for results I notice a definite overall improvement.My hairloss has been quite advanced for the past 10 years or so.
It makes a nice change to see the tide turn and notice numerous terminal looking hairs appearing on previously bald areas of my scalp.
Nothing drastic so far but I believe I've caught a few people I know looking at my hair with a slightly puzzled look on there faces
Its Good to read the positive results roll in.
roll on
Think I'm on week 12 or 13 now.
Doing one main roll once a week and some times a less aggressive top up roll mid week.
I usually start my session with a 1.5mm 512 needle roller then go over the area again with a 2mm 192 needle roller.
The crunching popping sensation felt initially when I started rolling is all but gone apart from around the temple area.
Recently I have noticed more blood spots after rolling which I take as a positive as no mater how hard I rolled at the beginning my scalp wouldn't bleed.
As for results I notice a definite overall improvement.My hairloss has been quite advanced for the past 10 years or so.
It makes a nice change to see the tide turn and notice numerous terminal looking hairs appearing on previously bald areas of my scalp.
Nothing drastic so far but I believe I've caught a few people I know looking at my hair with a slightly puzzled look on there faces
Its Good to read the positive results roll in.
roll on
squeegee
Banned
- Reaction score
- 132
Just checking in ,haven't posted in a while but still rolling.
Think I'm on week 12 or 13 now.
Doing one main roll once a week and some times a less aggressive top up roll mid week.
I usually start my session with a 1.5mm 512 needle roller then go over the area again with a 2mm 192 needle roller.
The crunching popping sensation felt initially when I started rolling is all but gone apart from around the temple area.
Recently I have noticed more blood spots after rolling which I take as a positive as no mater how hard I rolled at the beginning my scalp wouldn't bleed.
As for results I notice a definite overall improvement.My hairloss has been quite advanced for the past 10 years or so.
It makes a nice change to see the tide turn and notice numerous terminal looking hairs appearing on previously bald areas of my scalp.
Nothing drastic so far but I believe I've caught a few people I know looking at my hair with a slightly puzzled look on there faces
Its Good to read the positive results roll in.
roll on
Good stuff Zombiehair!!! :salut:
zombiehair
Member
- Reaction score
- 3
:salut:
- Reaction score
- 49
Why are there no before and after pictures? I've been taking lots of pics and I was sure I had regrowth but when I finally checked, there was no difference.....
- - - Updated - - -
Why are there no before and after pictures? I've been taking lots of pics and I was sure I had regrowth but when I finally checked, there was no difference.....
- - - Updated - - -
Why are there no before and after pictures? I've been taking lots of pics and I was sure I had regrowth but when I finally checked, there was no difference.....
saintsfan92344
Established Member
- Reaction score
- 25
where are yours, looked at your story and they were asking you the same on that thread
BeliefISKEY
Established Member
- Reaction score
- 5
If you're implying that people are just wishfully thinking that new hairs are popping up then you are stupid my friend.... Almost everybody here cries new hair regrowth after seeing it on a picture or seeing OBVIOUS new growth. Keep in mind that most of these guys have tried everything out there before trying this, & are some of the worse skeptics ever, YET they report drastic changes with this method. Stop fighting it.
How long have you been rolling for? Do you even roll?
How long have you been rolling for? Do you even roll?
squeegee
Banned
- Reaction score
- 132
Guys, if you have nothing positive to post on here, just keep it for yourself. No needs of negativity/pessimism.. If you don't have ****ing results yet..there is few options for you.
1: You're not doing it right. 1.5mm or + deep rolling with weight on the damn roller, blood everywhere with ground as much covered as possible. You want to stimulates angiogenesis ( new plumbing system) on your pumpkin and destroy fibrosis and hardened collagen. minoxidil 5% twice a day after the rolling day.
2: You are being an impatient b**ch, yes remodeling your damn scalp takes times. People have different stages of baldness, different ages...etc so different results will occur with different time-frame. Some have results within a month some others shed like a mofo, some takes month to see results.. you get the idea? Look at a newborn baby. It takes forever for the hair to grow. Losing your hair is a slow process, gaining them back is the same ****ing speed. Even hair transplant is a slow process. A lot of people posted pictures already with positive outcomes even if we are still early with this experimental treatment. Stop being a lazy POS and dig the forum for them.
Very cool that people are seeing regrowth. I am not successful YET. I actually lost a good bit of hair since I started. 9 weeks ago. I am happy that people are getting results. And this is very early in our discovery of this. When we get more knowledge of this it will be wondeful. There has to be a better compund out there than minoxidil that can really make our hairs grow. Cant wait until someone discovers it. Peace out everyone.
2young2retire
Experienced Member
- Reaction score
- 163
squeege i already feel the new plumbing system. the blood travels around my galea like a veyron.
guys if youdont roll hard then i dodnt expect magical results. thats why they should have made a study with 2.5mm rollers for people not pressing hard. anyway through numbing cream and drift your roller .
guys i am so happy now. if this truly truly works i am getting the hair transplant money on a vette. you know through some concaves on it and ofcourse the top is removable. so that the air messes my donkey roller hair
[video=youtube;H5JNfD2FNiI]http://www.youtube.com/watch?v=H5JNfD2FNiI[/video]
guys if youdont roll hard then i dodnt expect magical results. thats why they should have made a study with 2.5mm rollers for people not pressing hard. anyway through numbing cream and drift your roller . guys i am so happy now. if this truly truly works i am getting the hair transplant money on a vette. you know through some concaves on it and ofcourse the top is removable. so that the air messes my donkey roller hair
[video=youtube;H5JNfD2FNiI]http://www.youtube.com/watch?v=H5JNfD2FNiI[/video]
- Status