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Swimmy

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Posts posted by Swimmy

  1. 1. the infection and itching on my scalp is only on front and crown not in sides and back , so i am confused how this resveratrol + Curcumin oral pills will give exact solution to my affected scalp ?

     

    Where the itch is, is where hair loss occurs. On the top. Usually never on the sides or back. So that's why you aren't getting a itch in those places. Curcumin+resveratrol together have a anti inflammatory properties. This includes every part of your body not just your scalp. It will selectively block the CB1 receptor. Curcumin by itself (downregulates androgen receptor, TGF-Beta), inhibits PLA-2, MMP-9, COX-2, TNF-a. But with Res protects against neurogenic inflammation.

     

    Not sure if its a full solution! It could be a full solution to your inflammation and itching..However, by itself it won't stop MPB. Make sure you order from a good source! Jarrows Curcumin 95 is recommended. Country life or Now foods resvertral are preferred. I ran out of supply on mine two weeks ago and was waiting to reorder. Without it my scalp went inflamed so I know it works for me.

     

     

     

     

    "2. my point on this itching in my head may be due to DHT ,because i am using finasteride and nizorol only for one and a half months , so i think this period of usage is not enough to stop the DHT effect in itching , may be it will take some time to cure the DHT infection . This is the thought running in my mind but i don't know its true or not , please tell me whether my guess is correct or not ? :(:(:("

     

     

     

    No, that would be plenty of time to see some kind of improved result on your inflammation.

     

     

    IMO, I wouldn't take any of those things. First cause I don't have a problem with scalp itch or inflammation with what I'm taking. All those things you mention are harsh on your scalp and can dry out your hair. Another thing you might want to try is get a sls free shampoo like i mentioned. Order some DMSO liquid and lithium orotate and add some to your shampoo. Its scientifically shown to be more effective than nizoral and can be used everyday. That will help with the scalp itch and inflammation.

     

     

    Give it some time. About a month.If none of it works you might want to see a doctor. It could also be possible that you have demodex or some kind of scalp fungus.

     

     

     

     

  2. 6 weeks ? You've got to be kidding, right ?

     

    6 weeks is not even enough time for your body to adjust to the drug. Most likely what you were feeling was exactly that, your body adjusting to the new experience of the lower DHT levels.

     

    Depression ? Maybe I'm from the old school (41 years), but when I used to tell my parents I was depressed and didn't feel like getting up out of bed to go to school my father would whip out his belt and smack me a good one on the ass. It's truly amazing what a sharp pain sensation like that can do to get rid of depression.

     

    I take 1.25 mg of finasteride daily. Brain fog ? I can still remember phone #s from ex-girlfriends in the early 1990s. I can also play Beethoven's most complicated piano compositions from memory without missing a single note! Lethargy ? I'm 41 years old and I'm in the best shape of my life; I ride 20 miles every day on a bicycle and leave guys in their mid 20s panting and gasping for air trying to keep up with me. I think they watch too much TV which is another MAJOR cause of depression!

     

    Are there days when I wake up and it's hard to even get out of bed ? You bet! But do you know what I do to GET MYSELF OUT OF BED ? I smack myself on the ass and FORCE myself to get up !! Try it -- it works !

     

    My motto: no pain, no gain. You either REALLY WANT to keep your hair and look your best, or you're mamby pamby about it. Also, the MIND is a much more powerful tool than 99.9% of people realize. You can overcome anything IF you have the WILL POWER to do it.

     

    Spending too much time hanging out on hairloss forums can also be an EXTREME source of depression !!!

     

    Yikes, 20 miles a day? That's really not good for you. A lot of oxidative stress. Are you taking anything after your work out?

  3. thank you very much for your help Swimmy , but i have few doubts please clarify my doubts dude ,

     

    1 . i am in india , where can i get this resveratrol and curcumin ?

    2. resveratrol and curcumin = is it a tablet or it is cream that has to apply on the scalp ?

    3. I saw some few medication for scalp inflammation in some site , they are

    a.T-gel

    d. Dermovate

    c. Lobate cream (temovate(dermovate) generic chobetasol propionate) - it is available in india

     

    will the above medicine a,b,c really helps in curing scalp inflammation completely ?

     

    4. I am using Nizoral shampoo . so do i have to use "Natural HERBAL SLS " Alone or i can use this shampoo along with Nizoral ? ....thank you . waiting for your reply

     

     

    1.Curcumin is of course Turmeric. Isn't india where that stuff comes from? You can buy the stuff online at multiple places. Like Iherb

     

    2. Its internal so its in pill form

     

    3- I don't know much about those other things. They may help but probably won't cure it.

     

    You can use both. Use Nizoral once or twice a week and then your choice of shampoo the rest of the days Preferably SLS free.

     

     

     

  4. Hope you feel better...I think a lot of people will go throught depression on or off Fin or any other drugs. When someone starts a drug, and have a medical change, they automatically assume it is the med, but it is not always.

     

    Especailly with a drug like Fin....becasue I think most men losing hair go through heavy emotions about it (the loss of the hair).

     

     

    Um no. I don't if you are trying to defend fin or not...It seems when someone on this forum posts their feedback that they are getting bad symptoms from fin, everyone goes into 'say ain't so" mode. An act all surprised, when sides from fin are very common. More common than the supposed only 3%.

     

    You can automatically assume if you suddenly feel really depressed while in Fin..Well then its more than likely its the fin.

  5. You are suffering from Scalp inflammation....Or its possible you have demodex. DHT shouldn't be a issue if you're taken niz and fin. It could be a variety of things.

     

     

    From first hand experience resveratrol + Curcumin synergistically is good for inflammatory responses and should help your scalp. It neutralizes neurogenic inflammation

     

     

    This is a good shampoo for fungal, inflammation, and dandruff. So it should help

     

    Natural HERBAL SLS FREE SHAMPOO with Organic Aloe Vera & Jojoba - Normal/Oily Hair - HAIR CARE

  6. thanks Swimmy, i appreciate your lightning quick responses! it is really nice to have someone to talk about particularly around this topic haha...

     

     

    #2. i think i did see a shed but i don't know if it was a different hair style or stress (currently under lots of stress). what are known saw palmetto sides? i heard rumors of it was sex related but i don't know if it has been confirmed.

     

     

     

     

    I think the sides are similar Fin but to a lesser extent.

     

     

    i never really paid attention to brands, i focused mostly on the dosage and volume. but i think i will try different things because i think it does make a difference whether your body can absorb or not. can you point me to where the supplement link is? i cant find it in the forum. thanks!

     

    Brand is very important. No brand is the same. Some use crappy ingredients.ETC. Now Foods Brand seems to be the best overall brand for supplements and price.

     

    Here's the link

     

    http://www.hairrestorationnetwork.com/eve/157775-what-top-hair-supplements-swimmy.html

     

     

     

    i actually never heard of magnesium oil + Potassium, is this something that you need to mix on your own or there are solutions out there ? i'll do a bit reading on those because the dizziness hits me like crazy.

     

     

    Not sure if you mix it. I think you apply one that day and then the other the next.

     

    i hope you are doing well yourself. i also tried lots of different things before until i just settled for the approved and proven approaches. the problem i see was the evaluation period is too long, it often takes 6 month+ to see if it works or not and it's quite a bit of investment with your time and money.

     

    Too early to tell. Started a month ago. But it seems like my front hairs are getting a darker pigment

  7. #1 i don't think it was stress related, i think it had to do more with a crazy life that i had during that 1 month. lots of all nighters, too much intimacy ....lol ( i know how some people say they can be unrelated but that's really all it was)

    now i look back, i believe my MPB was very gradual just that 1 month it spiked significantly where density in my hair changed quite a bit.

     

    healthier eating was really just including more supplements that targets at preventing hair loss such as the ones i've mentioned.

     

    #2 i will definitely check it out, would you recommend to start saw palmetto again? i dropped it because i just dont really feel like it was of any help and i dont know if it's mental but it seems to have some sexual side effects on me such as low sex drive and i don't get my morning wood as i would before. i've taken saw palmetto for almost 5 years before the recent drop.

     

    #3 i've used minox for about 1 year and half. i think my hair is a little bit thicker than before but i got mix feedback from people. never touched fina because im afraid of the potential side effects.

     

    minox makes my hair really dried out and it leaves residue on my hair which makes it look like i have gray hair, any recommendations on that? (after i wash it out, my hair is very shiny and healthy without it on). im also suffering dizziness and a little bit of black eye from it.

     

    i also agree with you that just letting it sit and do nothing about it is probably a bad idea unless you dont care much at all about at least maintaining what's left.

     

    i guess my real question is do people's hair grow back from a thinning state to near where it once was because it doesn't seem to be the case unless for those adverstisements and scams.

     

     

     

    1- Staying up late and a lack of sleep can result in hair loss.. I actually think this in itself raises stress levels in your body. Too much intimacy shouldn't be a problem. . Studies show that only masturbation rasie DHT levels. Not sex itself.

     

     

     

    2. Its possible it was helping you. If you ever got a shed after dropping it then its most likely it was helping. If you don't think the side effects are worth the risk of taking it then don't. If you take fish oil. Take Neptune Krill Oil. Its about as good as you can get and 9 times more absorb-able. Its about 18-20 dollars for 60 gel caps. However, I think the price evens out since you only have to take one a day and still be more effective than the likely 2-4 a day you have to take of generic fish oil. So in actuality the cost difference is very little, but a better product.

     

     

     

    3- Have you stopped using minox? Hairs becoming minox dependent so you can get a shed from that. Oh and yes you are experiencing the common side effects of Minox. It can make you look sick.If you want to try something similar without the same side effects .You can try magnesium oil + Potassium chloride alternating topically . Just like minox it opens up the potassium channels in the scalp.

     

     

    The earlier you catch it the better. But Its possible to turn miniaturized hairs into healthy hairs again. Right now I'm experimenting with different products on my hairline to see if I can get them unminiaturized

  8. its all about your genetics man. don't think too much about it.

     

    Its all genetics is a lazy answer. "don't think too much about it" is definitely the wrong approach to take. Inherent predispositions are only part of the problem..The point is to work on them so they aren't as susceptible or so as not to trigger them.

     

  9. When MPB started for me, my hair was coming out at a faster rate than usual. It usually tapers some as you age. Mine started at 17. It seems like more and more younger people are fighting MPB these days. I've seen 17 year olds who are already NW4!

     

     

    Why do you think that is? Maybe something to do with the ever increasing unhealthy western diet?

     

     

    Japanese have the lowest rate of MPB..And is the healthiest nation in the world. However, after WW2 when nations like Japan were opened to the western diet MPB actually spiked.

  10. Hi All,

     

    just a little bit about myself

     

    i've been losing hair since 5 years ago at age 21 (WTF!) which was shocking to me espeically at such a young age. it occurred almost in 1 month duration where i lost an extensive amount of hair to the point where i was able to tell something was wrong. since it happened so fast, i assume it wasn't MPB, and it was going to grow it back so i decided to just let it sit naturally, after 6 months, it did grew back a little bit but it was no where near where it was. Base on the hairloss , i believe i do have MPB

     

    i've been trying several things but mostly on the natural end such as eating healthier, sleeping earlier and took supplements such as fish oil, vitamin B, saw palmetto(recently dropped).

     

    2 years ago, i decided to take things up a notch and started applying generic minoxidil (5%) which i saw very little results.

     

     

    Current routine minoxdil (5%) twice a day, supplements: fish oil,vitamin b.

    Current progress: definitely not more than before, and it feels like the hair loss cycle is going to start again

     

    i am just wondering are there any success stories where people grew back a good amount of their hair from a thinning state?

     

    feels like most proven approaches (minoxdil and propecia) only helps you to maintain, and transplant can't really be done to to thinning patients.

     

    what other alternatives are there for people that are thinning ?

     

    sorry about the vent, appreciate your help in advance

     

     

     

    #1 What was the cause for your initial hair loss? Do you believe it was stress related? It can be numerous things outside of MPB..Or just MPB. Its possible that a event in your life triggered the switch to start your hair loss. Also what do you mean by healthier eating? Some things you eat you think may be "healthy" really aren' healthy for hair. Like high Glucoser foods, or those that spike insulin.

     

     

    #2 I wouldn't just taken random supplements for your hair loss. If you go that route you need to do lots of research. For starters you can visit the thread on top supplementations for hair loss that was made on here. Secondly the type of brand is all the more important.

     

    3# How long did you use minox and fin for? You should use it for about 6 months to see any progress

     

    4# Alternatives- Laser Helmet, experimental treatments. Things like that.

  11. swimmy likes to confuse and try to baffle every one by overcomplicating matters and posting irrelevant studies that only just touch on the subjects we are discussing, to the extreme!!!

     

     

    There's a lot of info out there that correlates:cool:

     

     

    changing ur diet to opose the effects of dht will take alot longer and will never have the same direct effect or be as effective as finest has so it its a no brainer.......

    diet is important and should be correct in all people not just balding men but even then the healthiest man in the world could still go bald due naturally high androgen levels no matter how good his diet is!

     

     

    It will be quicker. But in the long run addressing the underlying causes is a more permanent solution. No offense but you seem to have a more simplistic apporach to MPB. Most people do. But that is the problem. MPB is one of the most complex. Its not just DHT. Anyone who's done deeper research on it can tell you that DHT is only the tip of the iceberg...And yes if you can commit fully to the required diet changes and the appropiate supplementation that your body calls for you can completely halt your hair loss. You you would be addressing the underlying causes. Such as lowering your DHT safely and naturally. Its a lot easier said cause there is trial and error behind it. And it takes a lot of discipline.

     

     

    swimmy in regards to the nizoral lithium debate yes you are correct it may be 20% more effective than nizoral each to there own,

     

    but me personaly i dont wanna waste my time looking silly by hunting down and purchasing LITHIUM then crushing them in to bottles,

    when i can just by nizoral of the shelf........

    and 20% better than nizoral again is minute an yes these shampoos help oppose dht but in the smallest teeny way its almost irelavent when you look at the big picture. i think the difference isnt worth the hassle of crushing tabs as it wont make any difference, if anything it will only aid the finest! everything else is doing the work in regards to the hair loss.

    with the shampoos its this simple why use a normal shampoo when you can use a shampoo that is proven to help hairs..... thats it plain and simple! its not a cure and with out fenist you will still go bald no matter how much nizoral or lithium you have.... its even debatable whether it works on every man?

     

    so its up to the individual user but for me the risk of looking like you have mental issues seeking out lithium as well as the humility of going bald already isnt worth the rediculously small 20% of the tiny 1% good any shampoo will be doing any way in the grand scheme of things?

     

     

    Well actually you can go online and buy the lithium.

     

    It only takes a few minutes out of your day to put it in a bottle. Only once and it last the whole bottle. About Tbsp of it. So I really don't think its that big of a hassle.

     

    20% is actually a huge difference. Why not take any edge you can get in the fight against hair loss.

  12. Background:Vitamin‐D deficiency and vitamin‐D receptor genotype (VDR) are risk factors for several disorders with inflammatory components, including coronary heart disease (CHD) and diabetes, though the mechanisms involved are unclear.

    Aim:  To examine the hypothesis that vitamin D status modulates the matrix metalloproteinase (MMP) system in a population with a high prevalence of vitamin D deficiency, a situation affecting susceptibility to CHD and diabetes.

    Design:  Prospective cross‐sectional, interventional and embedded studies.

    Methods:  Circulating MMP2,9, the inhibitor TIMP‐1 and C‐reactive protein (CRP) were measured during studies of vitamin‐D deficiency as a risk factor for type 2 diabetes and CHD in 171 healthy British Bangladeshi adults, free of known diabetes or major illness. Vitamin D status, VDR genotype, body‐build, blood pressure, lipid and insulin profiles, glucose tolerance, fibrinogen, PAI‐1, folate and homocysteine were measured. Vitamin‐D‐deficient subjects were re‐assessed after 1 years' supplementation. MMP, TIMP‐1 and CRP levels were measured in 41 subjects halfway through 5‐year follow‐up. Independent determinants of circulating concentrations of MMP9, TIMP‐1 and CRP were assessed by multiple regression analysis.

    Results:  Vitamin D status was the sole determinant of circulating MMP9 (inversely) and an independent determinant of CRP (inversely). Determinants of TIMP‐1 were MMP9, systolic blood‐pressure (directly) and VDR genotype (TaqI). Significant reductions in MMP9 (−68%), TIMP‐1 (−38%) and CRP (−23%) concentrations followed vitamin‐D supplementation.

    Discussion:  Vitamin‐D insufficiency is associated with increased circulating MMP2,9 and CRP, correctable by supplementation. This finding provides a possible mechanism for tissue damage in chronic inflammatory conditions, including CHD and diabete

  13. Oh here's a nice little study

     

    Androgenetic alopecia and microinflammation Yann F. Mah?,PhD, Jean-Fran?ois Michelet,MSc, Nelly Billoni, MSc, Fran?oise Jarrousse, BTS , Bruno Buan, BTS , Stephane Commo, BTS, Didier Saint-L?ger,PhD and Bruno A. Bernard,PhD

    International Journal of Dermatology

    Volume 39 Issue 8 Page 576 - August 2000

     

     

    Today, androgenetic alopecia (AGA) is considered to be an alteration of hair growth and/or a premature aging of the pilosebaceous unit with a multifactorial and even polygenic etiology. 1 The fact that the success rate of treatment with either antihypertensive agents, or modulators of androgen metabolism, barely exceeds 30% means that other pathways may be envisioned. The implication of various activators of inflammation in the etiology of AGA has progressively and recently emerged from several independent studies. 2,3,4,5,6,7,8,9,10,11 A fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the miniaturization and involution of the pilosebaceous unit in AGA. 2 8 We review here several observations underlining the possible implication of a slow, silent, and painless process in AGA. Because we think that it should not be confused with a classical inflammatory process, we have called it microinflammation. An early study referred to an inflammatory infiltrate of mononuclear cells and lymphocytes in about 50% of the scalp samples studied. 2 Another more recent study by Jaworsky et al . 3 confirmed an inflammatory infiltrate of activated T cells and macrophages in the upper third of the hair follicles from transitional regions of alopecia (i.e. which are characterized by actively progressing alopecia). This study also reported the occurrence of a developing fibrosis of the perifollicular sheath, together with the degranulation of follicular adventitial mast cells. The miniaturization of the hair follicles was found to be associated with a deposit of so-called "collagen or connective tissue streamers" beneath the follicle, 2,7 as well as a 2 2.5 times enlargement of the follicular dermal sheath composed of densely packed collagen bundles. 3 This thickening of the dermal sheath in progression zones of AGA has also recently been observed in our laboratory using immunohistochemical staining ( Fig. 1 ).

    Horizontal section studies of scalp biopsies indicate that the so-called perifollicular fibrosis is generally mild, consisting of loose, concentric layers of fibrotic collagen that must be distinguished from cicatricial alopecia. 4 It is unclear whether or not the fibrosis seen in follicular streamers (stelae or fibrous tracts) is permanent and/or alters the downgrowth of anagen hair follicles. Only 55% of male pattern AGA patients with microinflammation had hair regrowth in response to minoxidil treatment, which was less than the 77% of patients with no signs of inflammation, 4 suggesting that, to some extent, perifollicular microinflammation may account for some cases of male pattern AGA which do not respond to minoxidil. 4 Another study on 412 patients (193 men and 219 women) confirmed the presence of a significant degree of inflammation and fibrosis in at least 37% of AGA cases. 5 The upper location of the infiltrate near the infrainfundibulum 2 7 clearly distinguishes AGA from alopecia areata (AA), the latter disease being characterized by infiltrates in the bulb and dermal papilla zone. 12

    The aim of this review is to determine the location and chronology of the microinflammation process within the complex pathophysiology of the human pilosebaceous unit in order to improve the possible approaches for the reduction or prevention of the development of AGA.

    Classically, an inflammatory process is ascribed to a central major mediator or pathway. Such a monofactorial vision has been historically well exemplified by the famous interleukin-1 (IL-1) scheme developed by Oppenheim et al . 13 which is still valid even after 13 years. In fact, many inflammatory agents are at the center of a huge array of effects, involving cells, enzymes, adhesion molecules and other biological mechanisms. The identification of the effects of isolated factors is only part of the problem; it may be more important to determine when and where the individual factors are involved in the complex sequence. This pathway has been clearly identified, and several inhibitory anti-inflammatory drugs acting on this aspect of inflammation have been developed and clinically evaluated. 14,15 , 16,17

    The cytokine/chemokine side of microinflammation

    Why does microinflammation take place in the pilosebaceous unit and for what benefit and purpose? Fig. 2 and Fig. 3 show, in a simplified sequence, that inflammation is a multistep process which may start from a primary event. Let us look at the clues at the "crime scene" of AGA: we observe a perifollicular infiltrate in the upper follicle near the infundibulum. 2 7 This suggests that the primary causal event for the triggering of inflammation might occur near the infundibulum. 3,7 Supporting this point of view, improvement of the inflammatory aspect of AGA has been reported in a pilot study with an antimicrobial lotion. 7 One could speculate that several inhabitants of the scalp, such as the "triad" ( Propionibacterium sp.; Staphylococcus sp.; Malassezia ovalis ) or other members of the transient flora, could be involved in this complex inflammatory process. 7 The presence of porphyrins (produced by Propionibacterium sp.) in the pilosebaceous duct of 58% of AGA patients (compared with 12% of control subjects), which are able to induce the production of complement (C5) chemotactic factor, is considered to be a possible cofactor of this initial pro-inflammatory stress. 6,7 Keratinocytes are also known to respond within minutes to chemical stress, pollutants, UV irradiation or even mechanical stress. 37 Not only are radical oxygen species, 38 NO, 39 PGs, and histamine 40 produced, but also intracellularly stored IL-1 is released 37,41 (see Fig. 2 and step 1 of Fig. 3 ). By itself, this pro-inflammatory cytokine (as well as IL-1 which binds to the same receptor) is able to inhibit the growth of isolated hair follicles in culture in vitro. 9 11 This concentration-dependent inhibition of human hair elongation and survival indicates a high sensitivity to IL-1 of the isolated organ in culture in vitro (IC 50 = 10 pg/mL 11 ). In vivo , transgenic mice which overexpress IL-1 in the basal epidermis and in the outer root sheath of their pelage hair follicles exhibit a spontaneous cutaneous phenotype characterized by a sparseness of hair. 42 As a response to an IL-1 signal, adjacent keratinocytes which express receptors for IL-1 start to engage the transcription of IL-1 responsive genes 41 ( Fig. 3 , step 2). In vitro , following IL-1 stimulation, this transcriptional activation cascade is induced within 6 h in plucked human hair follicles. 11

     

    Alternatively, skin keratinocytes, which may also have antigen presenting capabilities, could theoretically induce T-cell proliferation in response to bacterial antigens. 51 These antigens, once they have been "tagged," are then selectively destroyed by infiltrating macrophages, Langerhans cells, or natural killer cells. 50,52 On many occasions, however, the causal agent persists, resulting in sustained inflammation ( Fig. 3, step 4). This corresponds partly to the situation which has been pictured in the progression zone of roughly one-third of alopecia cases: infiltrating T lymphocytes, together with mastocytes and macrophages, located in the upper perifollicular adventitial dermal sheath perpetuate a local inflammatory stage. 27 This phase of inflammation often results in tissue remodeling, where collagenases, such as matrix metalloproteinase (MMP)-9 (transcriptionally activated by pro-inflammatory cytokines) or MMP-8 (directly produced by infiltrating cells), may play an active role. 5355 Thus, collagenases are suspected to contribute to the tissue changes and the so-called "perifollicular fibrosis" by "preparing" tissue matrix and basal membranes for macrophages and T-cell adhesion. Accordingly, this scenario facilitates the secretion of membrane-anchored cytokines, such as TNF-. 55 Other factors, such as MCP-1, have been directly suspected to contribute to organ fibrosis in an experimental model of renal inflammation. 56 As MCP-1, together with other chemokines, was found to be expressed in human hair follicles in vitro, 11 as well as in the eccrine ducts of sebaceous glands in vivo, 57 it might also be actively involved in the progression of perifollicular fibrosis detected in AGA. 26 The development of perifollicular fibrosis might thus appear as the signature of a disequilibrium between pro-and anti-inflammatory pathways.

     

    Relations between inflammation and steroidogenesis: the missing link

     

    There is no question that androgens are major modulators of hair loss. Recently, it was shown that testosterone inhibited the growth of outer root sheath keratinocytes only when they were cocultured with dermal papilla cells derived from the bald scalp of an adult macaque, 58 reinforcing the hypothesis of an androgen influence on hair growth via the dermal papilla. 59 The potent metabolite of testosterone (i.e. 5-dihydrotestosterone, 5-DHT) is considered as a "culprit". 60 5-DHT is generated from testosterone through the activity of 5-reductase (5-R). Two active isoforms of 5-R, which differ both in tissue site distribution as well as in optimal pH for enzymatic activity, have been identified and cloned. 61,62, 63 While the type II isoform is considered to be the major isozyme in genital tissues, 61 the type I isoform is considered to be the major isoform expressed in skin and in the pilosebaceous unit. 64,65 Isoform II, however, has recently been detected in the inner root sheath of the pilosebaceous unit by immunohistochemistry, 66,67 Northern blotting, 67 and the pH dependence of optimal enzymatic activity. 67 Thus, the contribution of both isoforms in the regression of the pilosebaceous unit is still a matter of debate. Recently, a clinical study using finasteride, a strong inhibitor of 5-RII (and weak inhibitor of 5-RI), showed that intervention in androgen metabolism could, to some extent, modulate the progression of AGA, when the drug was given by the oral route, 68 but not topically. 69 After oral ingestion, an improvement of hair growth was observed, which was associated with a drastic reduction of serum levels of 5-DHT, corresponding to those observed in castrates. 68 Despite such a reduction of circulating 5-DHT levels, however, a number of individuals (60-70%) still remained unresponsive to this treatment, indicating again that simple dysregulation of 5-DHT synthesis levels or a genetic polymorphism of 5-R genes cannot account for all cases of AGA, and a polygenic etiology should be considered. 1

     

    Thus, to date, the only evident link that can be established between androgen metabolism and the complex inflammatory process is sebum production which is controlled by androgens. 70 As sebum harbors a large amount of microorganisms which use lipids as nutrients, 8 it cannot be excluded that, at least for some individuals, androgen metabolism might facilitate the colonization of the sebaceous infundibulum and sebaceous ducts by such microorganisms which may be involved in the first steps of pilosebaceous unit inflammation.

     

    We propose here working hypotheses which do not invalidate the contribution of a hereditary genetic androgen imbalance in AGA, 60 but rather attempt to integrate the neglected microinflammatory aspects of alopecia into the complex etiology of AGA. On the one hand, excessive local and/or endocrine, genetically exacerbated 5-DHT synthesis results in sebaceous gland enlargement; 2,60 as a consequence, some scalps might offer more comfortable niches to harbor the previously mentioned pro-inflammatory microorganisms. 6,7 On the other hand, androgen imbalance and metabolism may be locally exacerbated by pro-inflammatory cytokines. For example, gingival fibroblasts have been reported to modify their androgen metabolism through the action of several growth factors, such as epidermal growth factor (EGF), transforming growth factor beta (TGF-), and the pro-inflammatory cytokines IL-1 and TNF-. 71 Therefore, one could speculate that, once the inflammatory process has been triggered, the androgenetic mechanism of alopecia could subsequently be locally amplified. This upregulation of androgen metabolism by pro-inflammatory cytokines remains, however, to be established at the pilosebaceous unit level.

    Our visit to the "crime scene" of AGA yielded many clues ( Fig. 4 ). We know now that, at least in about one-third of cases, the tool which causes the lethal damage is a microinflammatory process. Several factors are present, however, which are suspected to have handled the tool: androgens, microbial flora, endogenous or exogenous stress, genetic imbalance, and possibly others. Although other suspects or tools are likely to be discovered in the future, it cannot be excluded that, for each individual, the causal agent, as well as the sequence of events or combined factors, may be different. The large number of molecules claimed to be active and patented in this field, 89 and their limited efficacy in offering a definite and extensive cure of AGA, confirm that the mechanism of AGA is highly complex. Accordingly, it appears that, due to the complexity and multiple interactivities and cooperations involved throughout the distinct inflammatory pathways (partly described in Fig. 2 ), an anti-inflammatory strategy should be targeted to the appropriate effector(s) at the right moment. For this purpose, we have developed a simple assay to evaluate individuals with potentially affected hair follicles. 11 We observed that plucked hair specimens of 33% of the 116 volunteers evaluated could be classified as highly inflammatory in terms of spontaneous IL-1 production. 11 Consequently, the identification of the "inflammatory alopecic individuals" may help to adapt the right answer to the right cause. Such a selective approach might be valuable for other parameters, such as an imbalance in 11 HSD activity, 5-DHT synthesis, or microorganism colonization. Encompassing individual diversity is thus a prerequisite for appropriately addressing the biological conditions contributing to AGA. Our findings and a review of the literature suggest that inflammation in its diversity is a potentially active player to consider in this approach.

  14. scalp inflamation results in itching which results in damaged hair being lost most often in irregular patterns or patches,how ever the author reports of hair not being the same quality in the MPB pattern ie on top in the high risk areas or area more sensitive to DHT,this eqyuates to minaturisation to me and if a dht blocker is not used now when the hairs can still be saved or some quality improved they will shed and most likely continue to decrease in quality untill they are gone for good as the dht cuts off blood flow and attacks the follicles........ that is the nature of it!!!!!!! eating diff food wont prevent this if he is predisposed!!!!

     

     

     

     

     

     

     

    Really? How about you go ask this question over to the link I gave you? There's hundreds of people there who have stopped or slowed their hair loss by simply changing their diet. DIET plays a huge factor in HAIRLOSS! It plays every part in how much DHT your body is regulating!

    Don't be ridiculous, Its for people who are predisposed MPB. Again, this is what the problem aims at. All of the mention below are the cause of MPB

     

    Reducing insulin producing foods or the impact of such foods on glucose and insulin.

    Controlling over expressed DHT

    Removing heavy metals

    Correcting metabolic conundrums

    Reducing oxidative stress

    Improving glucose metabolism

    Optimizing thyroid function

    Normalizing estrogen metabolism

    Balancing prostaglandins

    Curtailing inflammation

    Balancing intestinal microflora.

     

    Now there's nothing wrong with what you're taking. Fine by me me

    If we made a check list I wonder what areas on here your route is covering.

     

     

    its not an assumption dietry changes are so slight that by the time nay signifcant chnage in the diet has been esyablished the effects of MPB onset are so fast and sometimes harsh the difference will be irrelivent!!!

    !

     

     

    Yes that is a assumption. Diet plays a part in every aspect of our life. From how we feel, mentallly, and physically. To how long we live. So I would like to see research that dietary changes are a slight.

     

     

     

     

    Nizoral 1% can be used up to every other day and why would you want to wash your hair more than that? with out the need to buy lithium?? and the benefits from both shampoos or potion is again minute hardly nothing at all so why bother crushing pills etc just by off the shelf and use in combo with more effective proven treatments ie minox and finest? just seems like overcomplicating matters keep it simple........ as the benefits are both small it aint going to stop hair loss at all far from it if anything.... it just backs up the finest!

     

    Oh really? Lithium has shown be 22% more effective than ketoconazole .

     

     

     

     

     

     

    dietry and supplemtaion being correct is called healthy living and should be normal practice for both hairloss suferrers and non balding men alike not marathon cure for androgenic alopecia as im affraid you will just go bald!!!

     

     

    Oh geez there you go. Do some research. I'll get you started off with a few.

     

     

     

    Human Scalp Dermal Papilla and Fibrous Sheath Cells have a different expression profile of Matrix Metalloproteinases in vitro when compared to Scalp Dermal Fibroblasts.

     

    Arch Dermatol Res. 2005 Sep;297(3):121-126.

     

    Anti-inflammatory and antipyretic activities of beta-sitosterol.

     

    Planta Med. 1980 Jun;39(2):157-63.

     

    Taraxasterol and beta-sitosterol: new naturally compounds with chemoprotective/chemopreventive effects.

     

    Neoplasma 2004;51(6):407-14.

     

    Effect of beta-sitosterol as inhibitor of 5 alpha-reductase in hamster prostate.

     

    Proc West Pharmacol Soc. 2003;46:153-5.

    ?-Sitosterol, ?-Sitosterol Glucoside, and a Mixture of ?-Sitosterol and ?-Sitosterol Glucoside Modulate the Growth of Estrogen-Responsive Breast Cancer Cells In Vitro and in Ovariectomized Athymic Mice

     

    American Society for Nutritional Sciences J. Nutr. 134:1145-1151, May 2004

     

    The Importance of Sitosterol and Sitosterolin

    in human and animal nutrition

     

    Department of Chemistry and Applied Chemistry of Natal, Durban, 4041 South Africa

    Published in the South African Journal of Science Vol 93 June 1997

     

    New aspects in rheumatism therapy. Experiences with a sitosterin preparation in chronic polyarthritis

     

    Med. Welt. 1981 Jan 23;32(4):135-8.

    Plant-Based Fat Inhibits Cancer-Cell Growth By Enhancing Cell's Signaling System, UB Researchers Show

     

    University of Buffalo 1998-10-26

     

    Comparison of intestinal absorption of cholesterol with different plant sterols in man.

     

    Eur J. Clin Invest 1993 Dec;23(12):827-31. Anti-inflammatory and immunomodulating properties of a sterol fraction from Sideritis foetens Clem.

     

    Biol Pharm Bull 2001 May; 24(5): 470-3. Navarro A, De las Heras B, Villar A.

     

    Beta-Sitosterol, an Explanation of Benefits, Including Anti-Inflammatory Activity

    Early Onset Baldness and Prostate Cancer Risk

     

    Cancer Epidemiology Biomarkers & Prevention Vol. 9, 325-328, March 2000

     

    Age-associated deficit of mitochondrial oxidative phosphorylation in skeletal muscle: Role of carnitine and lipoic acid.

    Mol Cell Biochem 2005 Dec;280(1-2):83-9.

     

    Inhibition of gelatinase B (matrix metalloproteinase-9) by dihydrolipoic acid.

    Can J Physiol Pharmacol. 2005 Mar;83(3):301-8.

     

    Differential activity of lipoic Acid enantiomers in cell culture.

     

    J Herb Pharmacopher 2005;5(3):43-54.

     

    Flaxseed supplementation significantly increased urinary 2-hydroxyestrone secretion

     

    American Journal of Clinical Nutrition, Vol. 79, No. 2, 318-325, February 2004

    Intestinal Bacterial Communities That Produce Active Estrogen-Like Compounds Enterodiol and Enterolactone in Humans

     

    Applied and Environmental Microbiology, October 2005, p. 6077-6085, Vol. 71, No. 10

     

    Phylogeny of human intestinal bacteria that activate the dietary lignan secoisolariciresinol diglucoside.

     

    FEMS Microbiol Ecol. 2006 Mar;55(3):471-8.

     

    Polymorphisms in the CYP19 gene may affect the positive correlations between serum and urine phytoestrogen metabolites and plasma androgen concentrations in men.

     

    J Nutr 2005 Nov;135(11):2680-6.

     

    Oxidative stress as a mechanism of diabetes in diabetic BB prone rats: effect of secoisolariciresinol diglucoside (SDG).

    Mol Cell Biochem 2000 Jun;209(1-2):89-96.

     

    Secoisolariciresinol diglucoside from flaxseed delays the development of type 2 diabetes in Zucker rat.

     

    J. Lab Clin Med 2001 Jul;138(1):32-9.

    The Effect of Flax Seed Cultivars with Differing Content of Alpha Linolenic Acid and Lignans on Responses to Mental Stress

     

    Journal of the American College of Nutrition, Vol. 22, No. 6, 494-501 (2003)

    Pharmacokinetics of Enterolignans in Healthy Men and Women Consuming a Single Dose of Secoisolariciresinol Diglucoside

     

    American Society for Nutritional Sciences J. Nutr. 135:795-801, April 2005

    The Relative Bioavailability of Enterolignans in Humans Is Enhanced by Milling and Crushing of Flaxseed

     

    American Society for Nutritional Sciences J. Nutr. 135:2812-2816, December 2005

     

    Studies on the metabolism of the plant lignans secoisolariciresinol and matairesinol.

    J. Agric Food Chem 2003 Oct 8;51(21):6317-25

     

    Antioxidant activity of the flaxseed lignan secoisolariciresinol diglycoside and its mammalian lignan metabolites enterodiol and enterolactone.

     

    Mol Cell Biochem1999 Dec;202(1-2):91-100.

     

    Mammalian lignans and genistein decrease the activities of aromatase and 17beta-hydroxysteroid dehydrogenase in MCF-7 cells.

     

    J Steroid Biochem Mol Biol. 2005 Apr;94(5):461-7. Epub 2005 Mar 16.

    Androgenetic alopecia in women and Coronary Heart Disease in Women

     

    Androgenetic alopecia and coronary artery disease in women

    Androgenetic alopecia in women.

     

    J Investig Dermatol Symp Proc. 2003 Jun;8(1):24-7.

     

    Different levels of 5alpha-reductase type I and II, aromatase, and androgen receptor in hair follicles of women and men with androgenetic alopecia.

     

    J. Invest Dermatol 1997 Sep;109(3):296-300.

     

    Current understanding of androgenetic alopecia. Part I: etiopathogenesis

     

    Eur J. Dermatol 2000 Jun;10(4):319-27.

     

    Different gene expression profile observed in dermal papilla cells related to androgenic alopecia by DNA macroarray analysis.

     

    J. Dermatol Sci.2004 Oct;36(1):25-32.

     

    The relation of smoking, age, relative weight, and dietary intake to serum adrenal steroids, sex hormones, and sex hormone-binding globulin in middle-aged men.

     

    J. Endocrinol Metab. 1994 Nov;79(5):1310-6.

     

    Cigarette smoking is associated with elevated adrenal androgen response to adrenocorticotropin.

     

    J. Steriod Biochem Mol Biol1993 Aug;46(2):245-51.

     

    Carnosine and carnosine-related antioxidants: a review.

     

    Curr Med. Chem. 2005;12(20):2293-315.

     

    The effect of finasteride on the prostate gland in men with elevated serum prostate-specific antigen levels.

     

    British Journal of Cancer, 78 (3) August 1998.

     

    CD200, a "no danger" signal for hair follicles.

     

    J Dermatol Sci. 2005 Dec 28

     

    Photochemopreventive Effect of Pomegranate Fruit Extract on UVA-mediated Activation of Cellular Pathways in Normal Human Epidermal Keratinocytes.

    Photochem Photobiol June 2005

     

    Pomegranate as a cosmeceutical source: Pomegranate fractions promote proliferation and procollagen synthesis and inhibit matrix metalloproteinase-1 production in human skin cells.

     

    J Ethnopharmacol2005 Oct 8

    Pomegranate juice reduces oxidized low-density lipoprotein downregulation of endothelial nitric oxide synthase in human coronary endothelial cells

    Nitric Oxide 2006 Jan 11

     

    Pomegranate flower extract diminishes cardiac fibrosis in Zucker diabetic fatty rats: modulation of cardiac endothelin-1 and nuclear factor-kappaB pathways.

     

    J Cardiovasc Pharmacol 2005 Dec;46(6):856-62.

    Development and progression of alopecia in the vitamin D receptor null mouse.

     

    J. Cell Physiol 2006 Jan 17

    Prevention of bone loss by phloridzin, an apple polyphenol, in ovariectomized rats under inflammation conditions.

     

    Calcif Tissue Int. 2005 Nov;77(5):311-8.

    Investigation of the topical application of procyanidin oligomers. from apples to identify their potential use as a hair-growing agent.

     

    http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1473-2165.2005.00199.x

    BMP signaling in the control of skin development and hair follicle growth.

     

    Differentiation 2004 Dec;72(9-10):512-26.

     

    5alpha-reductase 2 inhibition impairs brain defeminization of male rats: reproductive aspects.

     

    Pharmacol Biochem Behave 2005 Sep;82(1):228-35.

     

    Terminalia arjuna (Roxb.) protects rabbit heart against ischemic-reperfusion injury: role of antioxidant enzymes and heat shock protein.

    J Enthopharmacol 2005 Jan 15;96(3):403-9. Epub 2004 Nov 21.

     

    Aminophospholipid glycation and its inhibitor screening system: A new role of pyridoxal 5'-phosphate and pyridoxal as lipid glycation inhibitor.

    J. Lipid Res.2006 Feb 9

     

    The hair growth promoting effect of ascorbic acid 2-phosphate, a long-acting Vitamin C derivative.

     

    J. Dermatol Sci. 2006 Feb;41(2):150-2. Epub 2006 Jan 9.

    Human Scalp Hair Follicles Are Both a Target and a Source of Prolactin, which Serves as an Autocrine and/or Paracrine Promoter of Apoptosis-Driven Hair Follicle Regression

     

    American Journal of Pathology. 2006;168:748-756.

     

    The effects of a special Agnus castus extract (BP1095E1) on prolactin secretion in healthy male subjects.

     

    Exp Clin Endocrinol Diabetes 1996;104(6):447-53.

     

    Benfotiamine prevents the vascular accumulation of advanced glycation end products and the induction of pro-apoptotic caspase-3

    Diabetologia 2006 Feb;49(2):405-20. Epub 2006 Jan 17.

     

    Increased circulating levels of matrix metalloproteinase-2 and -9 in women with the polycystic ovary syndrome.

     

    J. Clin Endocrinol Metab. 2006 Mar;91(3):1173-7. Epub 2005 Dec 6.

     

    Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?

    Endocr Regul. 2005 Dec;39(4):127-31.

     

    Inhibitory autocrine factors produced by the mesenchyme-derived hair follicle dermal papilla may be a key to male pattern baldness.

     

    Br J. Dermatol 2006 Apr;154(4):609-18.

     

    Biological characterization of cultured dermal papilla cells and hair follicle regeneration in vitro and in vivo.

    Chinese Medical Journal, 2006, Vol. 119 No. 4 : 275-281

     

    Induction of versican by ascorbic acid 2-phosphate in dermal papilla cells.

     

    J Dermatol Sci. 2006 Apr 4

     

    Focus on prolactin as a metabolic hormone.

     

    Trends Endocrinol Metab. 2006 Apr;17(3):110-6

     

    Epithelial-mesenchymal interaction and hair cycling

    Shiseido Life Science Research Center, MGH/Harvard Cutaneous Biology Research Center

     

    PDGF isoforms induce and maintain anagen phase of murine hair follicles.

     

    J Dermatol Sci. 2006 May 22

     

    Fibroblast growth factor 5 inhibits hair growth by blocking dermal papilla cell activation.

    Biochem Biophys Res Commun. 2002 Jan 11;290(1):169-76.

     

    Exploring link between Estrogen and hair growth

     

    Dermatology Times 2003

    Suppression of Estrogen Biosynthesis by Procyanidin Dimers in Red Wine and Grape Seeds

     

    Cancer Research 63, 8516-8522, December 1, 2003

    Pathomechanism of androgenetic alopecia and new treatment

    Nippon Ronen Igakkai Zasshi. 2004 Nov;41(6):598-600.

     

    Interleukin-1beta is differentially expressed by human dermal papilla cells in response to PKC activation and is a potent inhibitor of human hair follicle growth in organ culture.

     

    J Interferon Cytokine Res. 1997 Mar;17(3):151-7.

     

    Hormone studies in females with androgenic hairloss.

    Gynecol Obstet Invest. 1991;31(4):235-9.

     

    P35 HAIR CARE FORMULATIONS CONTAINING CARNITINE DERIVATIVES ACTIVATE CELLULAR ENERGY METABOLISM AND BOOST THE ATP CONTENT IN HUMAN HAIR FOLLICLES

     

    Hair Loss Research Society 2005

     

    Researchers Indentify Signals that Cause Hair Follicles to Sprout

     

    Howard Hughes Medical Institute March 20th, 2003

    In vitro assays for bioactivity-guided isolation of endocrine active compounds in Vitex agnus-castus.

     

    Maturitas. 2006 Aug 21

    A hot new twist to hair biology: involvement of vanilloid receptor-1 (VR1/TRPV1) signaling in human hair growth control.

     

    Am J Pathol. 2005 Apr;166(4):985-98.

    Stress Inhibits Hair Growth in Mice by Induction of Premature Catagen Development and Deleterious Perifollicular Inflammatory Events via Neuropeptide Substance P-Dependent Pathways.

     

    American Journal of Pathology. 2003;162:803-814

    p53 Involvement in the Control of Murine Hair Follicle Regression

     

    American Journal of Pathology. 2001;158:1913-1919.

    Stress and the Hair Follicle

     

    American Journal of Pathology. 2003;162:709-712.

    Prolactin and Its Receptor Are Expressed in Murine Hair Follicle Epithelium, Show Hair Cycle-Dependent Expression, and Induce Catagen

     

    American Journal of Pathology. 2003;162:1611-1621.

    Cyclosporin A-induced hair growth in mice is associated with inhibition of calcineurin-dependent activation of NFAT in follicular keratinocytes

     

    Am J Physiol Cell Physiol 284: C1593-C1603, 2003; doi:10.1152/ajpcell.00537.2002

    Neurogenic Inflammation in Stress-Induced Termination of Murine Hair Growth Is Promoted by Nerve Growth Factor

     

    American Journal of Pathology. 2004;165:259-271.

     

    Hair growth inhibition by psychoemotional stress: a mouse model for neural mechanisms in hair growth control.

     

    Exp Dermatol. 2006 Jan;15(1):1-13.

    Control of human hair growth by neurotrophins: brain-derived neurotrophic factor inhibits hair shaft elongation, induces catagen, and stimulates follicular transforming growth factor beta2 expression.

     

    J Invest Dermatol. 2005 Apr;124(4):675-85.

    Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders?

    Q J Med 2002; 95: 787-796

    favicon.icofavicon.icowiki-favicon-sharpened.pngoneriot-favicon.ico

  15. swimmy you always seem to come out with some far out left field answerr for everything instead of the obviouse!!!!!

     

    DHT in the scalp causes inflamation and itching and sensitivity i had it myself, its a fact!!!!!!!

     

    also in regards to diet, dietry requirments or lack of can act as a precurser for dht spikes which would also explain why he gets the symptoms on and off as i did also when i first notice the onset of my MPB,

     

    regardless of his dietry shortfalls the author of the post is complaining a disatsisfaction for HAIRLOSS...... which we all know is caused by DHT!!!!

     

    so your statement "I don't know why people are telling you to take hair loss treatment for this. None mentioned will help you with this problem" is silly..

    Its silly cause we don't know. He said he experienced scalp itch and was suddenly losing hair.. This doesn't automatically means he has MPB or whatever and should take a bunch of stuff. He could simply be losing hair soley on scalp inflammation and not DHT. Scalp inflammation does not need DHT and most times than not can occur without it.

     

     

    There's plenty of first hand experience that ..Foods high in gluten cause scalp inflammation/ itch. Hell, I notice it to. Gluten is intolerable. I had some fastfood today and my scalp is going crazy..It never does that.

     

    These are also strongly correlated with scalp inflammation/itch

     

    1. peroxynitrite,

    2. malassezia yeast, bacteria, etc.

     

     

     

     

     

     

     

    you can change and alter his diet all you like and give him advice on all the homeopathic remedies you liike also but the facts are is minturisation will continue.....as he is more than likely predisposed to dht sensitivity!!!]

     

    That's a assumption. Resvertral and Curcumin have plenty of studies that show it stops sinflammation and has high anti oxidant activity. I ran out a few days ago and have to order more. That's probably why my scalp is going crazy right now.

     

     

     

     

    i know wot i would do any way?? why mess around cruching lithium and buying potions when you can get the equivilant effect from ready to use nizoral with out half the hassel, and why concentrate soley on dietry requirements when in the mean time you continue to go balled and miniturise due to male androgenic patern alopecia?????

     

    It takes like 3 minutes to crunch the lithium and put it in a bottle.Huge hassle Secondly, studies have already shown that Lithium/DMSO is more effective than Nizoral. Guess what? It can be used everyday without the damaging effects. So is it equivalent? No not really. Lithium combo is more effective.

     

    Why concentrate soley on dietary matters? Cause thats the only way to get to the underlying cause. .So you can assume I'm "balding" Or maybe I have stopped my hair loss? What it all boils down to, you are putting a band aid on your head and will inevitably lose and problem remains with DHT blockers I'll keep taking my "magical potions' back by research to address the real cause of hair loss.

     

     

    For the sprint- DHT blocker, minox, etc

     

    For the marathon- Dietary, proper supplementation

  16. thanks very much :) , how long i use this treatment ?

     

     

     

     

    i didt understand u right , my top scalp get little sensitve like " twice or more" a week , it goes and comes time from time is this the problem ?

     

     

    It gets sensitive due to inflammation. Something in your diet is causing this . This is where most scalp inflammation comes Are you consuming any common allergenic foods like eggs or peanuts? Find a pattern. Other everyday foods like bread may cause this to.

     

    Curcumin+ Resevratral is good at counteracting inflammation .

    Or adding Lithium orotate/DMSO liquid to a shampoo.

     

    Haha, I don't know why people are telling you to take hair loss treatment for this. None mentioned will help you with this problem.

  17. Hi Swimmy

     

    Did you mean to say that you were only able to use it for one month and then discontinued!! if so, what was the reason to discontinue..

     

     

    Just ran into a money problem. I actually have a lot left. If you use it properly it should last longer. I just figured there's no point in making a commitment if I couldn't buy it when it empties at the time

  18. are any of these products organic (or close to it)?

     

    natural ingredients?

     

     

    are any of these products organic (or close to it)?

     

    natural ingredients?

     

     

    Dermaheal ingredients

    Full Ingredients

    • Rh-Oligopeptide-2 (IGF-1), Rh-Polypeptide-1 (bFGF), Rh-Polypeptide-9 (VEGF), Rh-Polypeptide-11 (aFGF), Copper Tripeptide-1, Octapeptide-2 (Prohairin ?4), Hyaluronic Acid, Biotin, Arginine, 2-O-Ethyl Ascorbic Acid, Polygala Tenuifolia Root Extract, Portulaca Oleracea Extract, Pleurotus Multiflorus Root Extract, Thuja Orientalis Extract, Ginkgo Biloba Leaf Extract, Multi-vitamins and Amino Acids

     

     

     

    As for the Stem C'rum I don't know the ingredients list. Its not listed but its from Dermaheal. This is all I found. So some of its listed

     

     

    Dermaheal Stem C’rum HL(Anti-hair Loss)

    Lyophilized Powder 5vials + Stem C’rum HL Solution 5ml, 5vials / set

    Length and thickness of hair have been increased in the hair root organ, when applied with Stem C’rum HL.

    Direction for Use: Use general mesotherapy and mesoroller (microneedle) method.

    Step 1. Remove both caps from the vials

    Step 2. Inject (or pour) the solution to powder vial

    Step 3. Gently mix well

    Main Ingredients: Insulin like Growth Factor-1 (IGF-1), basic Fibroblast Growth

    Factor (bFGF), Vascular Endothelial Growth Factor (VEGF)

    (10 ppm each / vial), Copper Tripeptide-1, Biotin,

    Human Adipocyte Conditioned Media Extract,

    Amino Acids, Minerals and Vitamins

     

     

    As for the Dermo

     

     

    DERMATOPOIETINTM is a 159 amino acid long

    polypeptide. It is constantly produced by skin almost

    exclusively onto the stratum corneum (upper skin layer)

    of the human epidermis. DERMATOPOIETINTM serves as

    an autocrine factor that initiates a cascade of events

    directed to deeper layers of skin.

    Activation of cell growth signaling cascade

    DERMATOPOIETINTM activates genes encoding growth

    factors such as keratinocyte growth factor (KGF)1-3,

    hepatocytes growth factor (HGF)1, granulocytemacrophage

    growth factor (GM-CSF)4, and transforming

    growth factor-alpha (TGF-alpha)5. These growth factors,

    in turn, initiate a cascade of events leading to fibroblast

    and keratinocyte proliferation, keratinocyte migration6,7,

    and entire skin renewal.

     

     

    DERMATOPOIETINTM suppress expression of

    connective tissue growth factor (CTGF), a major

    fibrogenic factor responsible for excessive scarring or

    keloid formation through promoting proliferation and

    collagen synthesis of mesenchymal cells12

     

     

     

    I'm not sure if these should be considered "natural". But I don't see any actual chemicals. They would be pretty gentle on your scalp and are absorbed quickly

  19. here's my story , about 3 to 4 years ago i started to grow my hair to be long and " i have very-good hair density " as time passes the first year and da second and the tird every thing is good i luv it:) and my hair is in very good density and natrual and from time to time i cut my hair to bottom of the nick to keep my hair in good strength..... to the forth year " 8 month ago " i start to lose hair in the Top scalp ! ! :eek: and i started to see difference in hair density , , the top scalp is less density from other sides :confused:

     

     

    so i decided to cut all of my hair :( to keep it all in the same range , and the hair stoped from fallin :o..... but when i take look deep in my hair i see diffrence in density , the top scalp is less density

     

    and time from time i have little itching in the top scalp .

     

     

    so i need help to get my hair to its natural density ? any advice .....

     

     

     

     

    sorry for the long story :rolleyes: , yea luv for all ;)

     

     

    If your scalp is itchy and you are losing hair its probably Scalp Inflammation. If you fix that it should help.

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