http://www.waiwiki.org/api.php?action=feedcontributions&feedformat=atom&user=DimeWaiWiki - User contributions [en]2026-04-26T10:04:13ZUser contributionsMediaWiki 1.31.0http://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=1309Male Pattern Baldness2013-01-27T16:50:59Z<p>Dime: </p>
<hr />
<div><blockquote>Male pattern baldness (or androgenic alopecia) is the main cause of hairloss in men. Minimally, male pattern baldness (MPB) is related to androgens (which regulate hair growth), particularly dihydrotestosterone (DHT). [http://www.waiworld.com/waitalk/phpBB3/viewtopic.php?f=17&t=3236&start=0 Male Pattern Baldness discussed on WaiTalk]<br />
<br />
==Cause==<br />
* It is speculated that MPB is caused by a genetic sensitivity to DHT of the hair follicles on top of the scalp only.<br />
* It has been suggested that the anabolic effect of androgens leading to structural changes in skin and scalp cause hair loss.<br />
* Locally elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles may prevent them from maturing and growing hair.<br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** 7.5 months treatment with alfatradiol increased the proportion of frontal anagen hair statistically significantly, in women from 69 % to 77 % (means) and in men from 56 % to 65 % [https://www.thieme-connect.com/ejournals/abstract/10.1055/s-2005-870188 Wozel et al.]<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction [http://www.ncbi.nlm.nih.gov/pubmed/2469708 Charlesworth et al.]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
=== COX ===<br />
# COX converts arachidonic acid (AA, an omega-6 PUFA) to prostaglandin H2 (PGH2), the precursor of the series-2 prostanoids.<br />
## COX-2 expression in skin is induced by UVB exposure [http://www.ncbi.nlm.nih.gov/pubmed/9635856 Buckman et al.]<br />
# Lipocalin-type PGD2 synthase (L-PGDS) or hematopoietic (H)-PGDS converts PGH2 to PGD2<br />
# PGD2 undergoes sequential non-enzymatic dehydration reactions to form 15d-PGJ2 [http://www.ncbi.nlm.nih.gov/pubmed/15639643 Scher and Pillinger]<br />
# 15d-PGJ2 is deomonstrated to suppress hair growth and is implicated in male pattern baldness.<br />
## Toxicity of 15d-PGJ2 to mOP cells is related to intracellular Glutathione levels [http://www.jneuroinflammation.com/content/4/1/18 Zhongmin et al.]<br />
<br />
* Topical Ibuprofen could be another alternative for fixing inflammation, Ibuprofen is COX inhibitor.<br />
** Topical Ibuprofen penetrates 0.5cm in the skin<br />
* COX/LOX and general information of prostaglandins [http://www.itmonline.org/arts/lox.htm link]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== PTH ==<br />
Parathyroid hormone seems to have an effect on hair growth. Blocking PTH receptors in the skin stimulate hair growth in mice.<br />
* A topical parathyroid hormone/parathyroid hormone-related peptide receptor antagonist stimulates hair growth in mice. [http://www.ncbi.nlm.nih.gov/pubmed/17170098]<br />
* A parathyroid hormone antagonist stimulates epidermal proliferation and hair growth in mice. [http://www.ncbi.nlm.nih.gov/pubmed/17170098]<br />
<br />
== Diet ==<br />
The wai diet seems to have positive aspects regarding male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=135Dandruff2012-11-03T20:27:35Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
### Blood group O subjects may be the most susceptible, followed by AB group. [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2002;volume=47;issue=1;spage=21;epage=23;aulast=Shankar;type=0 Shankar et al.]] Also it's more common in males.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
* ''Note 3:'' a collection of a lot of research: [http://healthypixels.com/?p=960 link]<br />
<br />
= Treatment =<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]<br />
* Avoid putting fats on the scalp. Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.<br />
* Avoid using alkaline soap, baking soda, and similar, as the fungus grows optimally in pH 7-9 [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar Vijayakumar et al.]]<br />
** Consequently, raising the acidity on the scalp may be helpful; there are plenty of reports that apple cider vinegar on the scalp relieves itching.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=134Dandruff2012-11-03T20:07:09Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
### Blood group O subjects may be the most susceptible, followed by AB group. [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2002;volume=47;issue=1;spage=21;epage=23;aulast=Shankar;type=0 Shankar et al.]] Also it's more common in males.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]<br />
* Avoid putting fats on the scalp. Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.<br />
* Avoid using alkaline soap, baking soda, and similar, as the fungus grows optimally in pH 7-9 [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar Vijayakumar et al.]]<br />
** Consequently, raising the acidity on the scalp may be helpful; there are plenty of reports that apple cider vinegar on the scalp relieves itching.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=133Dandruff2012-11-03T19:39:49Z<p>Dime: /* Treatment */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]<br />
* Avoid putting fats on the scalp. Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.<br />
* Avoid using alkaline soap, baking soda, and similar, as the fungus grows optimally in pH 7-9 [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar Vijayakumar et al.]]<br />
** Consequently, raising the acidity on the scalp may be helpful; there are plenty of reports that apple cider vinegar on the scalp relieves itching.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=132Dandruff2012-11-03T19:29:47Z<p>Dime: /* Treatment */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]<br />
* Avoid putting fats on the scalp? Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.<br />
* Avoid using alkaline soap, baking soda, and similar, as the fungus grows optimally in pH 7-9 [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar Vijayakumar et al.]]<br />
** Consequently, raising the acidity on the scalp may be helpful; there are plenty of reports that apple cider vinegar on the scalp relieves itching.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=131Dandruff2012-11-03T19:29:37Z<p>Dime: /* Treatment */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]<br />
* Avoid putting fats on the scalp? Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.<br />
* Avoid using alkaline soap, baking soda, and similar, as the fungus grows optimally in pH 7-9 [[http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar Vijayakumar et al.]]<br />
* Consequently, raising the acidity on the scalp may be helpful; there are plenty of reports that apple cider vinegar on the scalp relieves itching.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=130Dandruff2012-11-03T19:26:36Z<p>Dime: /* Treatment */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]<br />
* Avoid putting fats on the scalp? Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=129Dandruff2012-11-03T19:25:23Z<p>Dime: /* Treatment */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
* Avoid putting fats on the scalp? Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.<br />
<br />
[[File:M.furfur.jpg|frame|right|Original source: [http://www.e-ijd.org/article.asp?issn=0019-5154;year=2006;volume=51;issue=2;spage=145;epage=148;aulast=Vijayakumar link]]]</div>Dimehttp://www.waiwiki.org/index.php?title=File:M.furfur.jpg&diff=128File:M.furfur.jpg2012-11-03T19:18:12Z<p>Dime: Growth of M.furfur as supported by different fats.</p>
<hr />
<div>Growth of M.furfur as supported by different fats.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=127Dandruff2012-11-03T17:46:09Z<p>Dime: /* Treatment */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =<br />
* Avoid putting fats on the scalp? Saturated fat feeds the fungus, and unsaturated (oleic acid) directly trigger dandruff in susceptible people.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=126Dandruff2012-11-03T17:45:01Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals.<br />
## The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=125Dandruff2012-11-03T17:44:19Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
## This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals. The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=124Dandruff2012-11-03T17:30:32Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
* This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals. The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
Some notes<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=123Dandruff2012-11-03T17:30:16Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind.<br />
# The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
** This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals. The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=122Dandruff2012-11-03T17:29:59Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind. # The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
** This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals. The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.<br />
<br />
= Treatment =</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=121Dandruff2012-11-03T17:27:55Z<p>Dime: /* Causes */</p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.]]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind. # The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
** This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals. The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=120Dandruff2012-11-03T17:27:34Z<p>Dime: </p>
<hr />
<div>Dandruff is increased turnover of skin cells on the scalp, leading to large amounts of flaking, and possibly redness and itching. In people with dandruf, skin cells develop and die in 2-7 days, in contrast to a cycle of one month in people with no dandruf. It is a condition that can fluctuate depending on the season, usually becomming worse in winter. Half of the population is affected by dandruff at some point; in people older than 50 it is not very common.<br />
<br />
'''There is no real cure for dandruff yet.'''<br />
<br />
= Causes =<br />
<br />
Three factors are required for dandruf to appear [[http://www.ncbi.nlm.nih.gov/pubmed/16382662 Ro and Dawson]]:<br />
# sebum<br />
# metabolic waste of skin bacteria (specifically [http://en.wikipedia.org/wiki/Malassezia Malassezia] [http://news.bbc.co.uk/2/hi/health/7080434.stm globosa] yeast) [[http://www.ncbi.nlm.nih.gov/pubmed/15523360 Gupta et al.], []]<br />
# individual susceptibility (above two combined will not necessarily cause dandruff in non-susceptible people)<br />
<br />
M. globosa has no ability to manufacture its own fatty acids, which are essential for life, and so relies on human sebum for its source. The way it causes dandruf:<br />
# The fungus produces 8 types of lipase and 3 types of phospholipase enzymes, which help to break down sebum into free fatty acids and glycerol.<br />
# It feeds on the satirated fatty acids, while it leaves irritating unsaturated '''oleic acid''' behind. # The oleic acid then penetrates the scalp, irritates the skin and triggers faster turnover of skin cells in susceptible people.<br />
** This has been proven by removing all of the fungus and treating the scalp with pure oleic acid in susceptible and non-susceptible individuals. The difference between susceptible and non-susceptible individuals is unclear.<br />
<br />
* ''Note:'' olive oil is extremely high in oleic acid, does this mean that putting olive oil on the scalp will exacerbate dandruff?<br />
* ''Note 2:'' the fungus research seems to be mainly done by Head & Shoulders, so likely a some details of it is not revealed.</div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=119Dandruff2012-11-01T08:20:44Z<p>Dime: /* Dandruf */</p>
<hr />
<div></div>Dimehttp://www.waiwiki.org/index.php?title=Dandruff&diff=118Dandruff2012-11-01T08:20:34Z<p>Dime: Created page with '= Dandruf ='</p>
<hr />
<div>= Dandruf =</div>Dimehttp://www.waiwiki.org/index.php?title=Research_Sandbox&diff=117Research Sandbox2012-11-01T08:20:18Z<p>Dime: </p>
<hr />
<div>Temporary space for research on various topics.<br />
<br />
== Hair ==<br />
* [[Male Pattern Baldness]]<br />
* [[Dandruff]]</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=91Male Pattern Baldness2012-10-29T10:15:17Z<p>Dime: /* Inhibition */</p>
<hr />
<div><blockquote>Male pattern baldness (or androgenic alopecia) is the main cause of hairloss in men. Minimally, male pattern baldness (MPB) is related to androgens (which regulate hair growth), particularly dihydrotestosterone (DHT). [http://www.waiworld.com/waitalk/phpBB3/viewtopic.php?f=17&t=3236&start=0 Male Pattern Baldness discussed on WaiTalk]<br />
<br />
==Cause==<br />
* It is speculated that MPB is caused by a genetic sensitivity to DHT of the hair follicles on top of the scalp only.<br />
* It has been suggested that the anabolic effect of androgens leading to structural changes in skin and scalp cause hair loss.<br />
* Locally elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles may prevent them from maturing and growing hair.<br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** 7.5 months treatment with alfatradiol increased the proportion of frontal anagen hair statistically significantly, in women from 69 % to 77 % (means) and in men from 56 % to 65 % [https://www.thieme-connect.com/ejournals/abstract/10.1055/s-2005-870188 Wozel et al.]<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction [http://www.ncbi.nlm.nih.gov/pubmed/2469708 Charlesworth et al.]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
=== COX ===<br />
# COX converts arachidonic acid (AA, an omega-6 PUFA) to prostaglandin H2 (PGH2), the precursor of the series-2 prostanoids.<br />
## COX-2 expression in skin is induced by UVB exposure [http://www.ncbi.nlm.nih.gov/pubmed/9635856 Buckman et al.]<br />
# Lipocalin-type PGD2 synthase (L-PGDS) or hematopoietic (H)-PGDS converts PGH2 to PGD2<br />
# PGD2 undergoes sequential non-enzymatic dehydration reactions to form 15d-PGJ2 [http://www.ncbi.nlm.nih.gov/pubmed/15639643 Scher and Pillinger]<br />
# 15d-PGJ2 is deomonstrated to suppress hair growth and is implicated in male pattern baldness.<br />
## Toxicity of 15d-PGJ2 to mOP cells is related to intracellular Glutathione levels [http://www.jneuroinflammation.com/content/4/1/18 Zhongmin et al.]<br />
<br />
* Topical Ibuprofen could be another alternative for fixing inflammation, Ibuprofen is COX inhibitor.<br />
** Topical Ibuprofen penetrates 0.5cm in the skin<br />
* COX/LOX and general information of prostaglandins [http://www.itmonline.org/arts/lox.htm link]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet seems to have positive aspects regarding male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados.</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=31Male Pattern Baldness2012-10-18T21:32:43Z<p>Dime: /* COX */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction [http://www.ncbi.nlm.nih.gov/pubmed/2469708 Charlesworth et al.]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
=== COX ===<br />
# COX converts arachidonic acid (AA, an omega-6 PUFA) to prostaglandin H2 (PGH2), the precursor of the series-2 prostanoids.<br />
## COX-2 expression in skin is induced by UVB exposure [http://www.ncbi.nlm.nih.gov/pubmed/9635856 Buckman et al.]<br />
# Lipocalin-type PGD2 synthase (L-PGDS) or hematopoietic (H)-PGDS converts PGH2 to PGD2<br />
# PGD2 undergoes sequential non-enzymatic dehydration reactions to form 15d-PGJ2 [http://www.ncbi.nlm.nih.gov/pubmed/15639643 Scher and Pillinger]<br />
# 15d-PGJ2 is deomonstrated to suppress hair growth and is implicated in male pattern baldness.<br />
## Toxicity of 15d-PGJ2 to mOP cells is related to intracellular Glutathione levels [http://www.jneuroinflammation.com/content/4/1/18 Zhongmin et al.]<br />
<br />
* Topical Ibuprofen could be another alternative for fixing inflammation, Ibuprofen is COX inhibitor.<br />
** Topical Ibuprofen penetrates 0.5cm in the skin<br />
* COX/LOX and general information of prostaglandins [http://www.itmonline.org/arts/lox.htm link]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=30Male Pattern Baldness2012-10-18T21:22:16Z<p>Dime: /* COX */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction [http://www.ncbi.nlm.nih.gov/pubmed/2469708 Charlesworth et al.]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
=== COX ===<br />
# COX converts arachidonic acid (AA, an omega-6 PUFA) to prostaglandin H2 (PGH2), the precursor of the series-2 prostanoids.<br />
## COX-2 expression in skin is induced by UVB exposure [http://www.ncbi.nlm.nih.gov/pubmed/9635856 Buckman et al.]<br />
# Lipocalin-type PGD2 synthase (L-PGDS) or hematopoietic (H)-PGDS converts PGH2 to PGD2<br />
# PGD2 undergoes sequential non-enzymatic dehydration reactions to form 15d-PGJ2 [http://www.ncbi.nlm.nih.gov/pubmed/15639643 Scher and Pillinger]<br />
# 15d-PGJ2 is deomonstrated to suppress hair growth and is implicated in male pattern baldness.<br />
## Toxicity of 15d-PGJ2 to mOP cells is related to intracellular Glutathione levels [http://www.jneuroinflammation.com/content/4/1/18 Zhongmin et al.]<br />
<br />
* Topical Ibuprofen could be another alternative for fixing inflammation, Ibuprofen is COX inhibitor.<br />
** Topical Ibuprofen penetrates 0.5cm in the skin<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=29Male Pattern Baldness2012-10-18T21:21:55Z<p>Dime: /* PGD2 */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction [http://www.ncbi.nlm.nih.gov/pubmed/2469708 Charlesworth et al.]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
=== COX ===<br />
# COX converts arachidonic acid (AA, an omega-6 PUFA) to prostaglandin H2 (PGH2), the precursor of the series-2 prostanoids.<br />
** COX-2 expression in skin is induced by UVB exposure [http://www.ncbi.nlm.nih.gov/pubmed/9635856 Buckman et al.]<br />
# Lipocalin-type PGD2 synthase (L-PGDS) or hematopoietic (H)-PGDS converts PGH2 to PGD2<br />
# PGD2 undergoes sequential non-enzymatic dehydration reactions to form 15d-PGJ2 [http://www.ncbi.nlm.nih.gov/pubmed/15639643 Scher and Pillinger]<br />
# 15d-PGJ2 is deomonstrated to suppress hair growth and is implicated in male pattern baldness.<br />
** Toxicity of 15d-PGJ2 to mOP cells is related to intracellular Glutathione levels [http://www.jneuroinflammation.com/content/4/1/18 Zhongmin et al.]<br />
* Topical Ibuprofen could be another alternative for fixing inflammation, Ibuprofen is COX inhibitor.<br />
** Topical Ibuprofen penetrates 0.5cm in the skin<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=28Male Pattern Baldness2012-10-18T20:40:04Z<p>Dime: /* PGD2 */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction [http://www.ncbi.nlm.nih.gov/pubmed/2469708 Charlesworth et al.]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=27Male Pattern Baldness2012-10-18T20:36:31Z<p>Dime: /* PGD2 */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
* Topical [http://en.wikipedia.org/wiki/Cetirizine Cetirizine] may be an appropriate solution to fight PGD2 in the scalp. [http://www.hairlosstalk.com/interact/showthread.php/64012-Exciting-results-from-Minoxidil-Pantostin-Cetirizine?p=1103255&viewfull=1#post1103255 idea]<br />
** Recipe to make at home: 50 tabs cetirizine, 50 ml of distilled water, 30 ml of ethanol (70%), Propylene glycol 20 ml<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=26Male Pattern Baldness2012-10-18T14:01:07Z<p>Dime: /* DHEA(S) */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin. Excess DHEA is related to oily skin, immune hyperactivity and insulin resistance.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=25Male Pattern Baldness2012-10-18T13:55:10Z<p>Dime: </p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT, as well as androstenedione to 5alpha-androstanedione. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== 17beta-HSD ==<br />
High enzyme activity may be related to higher degrees of balding (Hodgins et al.)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=24Male Pattern Baldness2012-10-18T13:48:05Z<p>Dime: /* 5-alpha-reductase */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
* On the same scalp, balding skin has more 5-AR activity than non-balding skin. [http://www.ncbi.nlm.nih.gov/pubmed/2091154 Puerto and Mallol]<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=23Male Pattern Baldness2012-10-18T13:40:31Z<p>Dime: </p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== 3beta-HSD ==<br />
The 3beta-HSD isoenzymes catalyze an obligatory step in the biosynthesis of androgens, estrogens, mineralocorticoids and glucocorticoids.<br />
* There is substantially increased activity of 3beta-HSD in balding than in non-balding scalps [http://www.ncbi.nlm.nih.gov/pubmed/3165109 Sawaya et al.]<br />
** The increased conversion of DHEA to 3H-delta 4-androstenedione may be a critical step for androgenic action and may be responsible for excessive androgenicity in male-pattern baldness.<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=22Male Pattern Baldness2012-10-18T13:28:35Z<p>Dime: /* DHEA(S) */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS). STS deficiency manifests with dry, scaly skin.<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=21Male Pattern Baldness2012-10-18T13:24:55Z<p>Dime: /* DHEA(S) */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
The skin is capable of synthesizing active androgens, such as DHT, from the systemic precursor DHEA-S. The first step in this pathway is the desulfatation of DHEA-S by the enzyme steroid sulfatase (STS).<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=20Male Pattern Baldness2012-10-18T13:22:28Z<p>Dime: /* DHEA(S) */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
** Like cortisol, DHEAS concentrations showed a diurnal rhythm with higher concentrations in the morning compared to the evening and a decrease in response to dexamethasone (DEX) administration.<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=19Male Pattern Baldness2012-10-18T13:21:10Z<p>Dime: /* DHEA(S) */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Acute and chronic stress increase DHEAS concentrations in rhesus monkeys [http://www.ncbi.nlm.nih.gov/pubmed/20153584 Maninger et al.]<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=18Male Pattern Baldness2012-10-18T13:16:36Z<p>Dime: </p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
=== Inhibition ===<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
=== Promotion ===<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=17Male Pattern Baldness2012-10-18T13:16:02Z<p>Dime: </p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
=== What affects 5-AR? ===<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
==== Inhibition ====<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
==== Promotion ====<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== DHEA(S) ==<br />
* Elevation of DHEA-S is associated with male pattern baldness in young men The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that '''adrenal hyperactivity''' may initiate alopecia in young men who are genetically susceptible. [http://www.ncbi.nlm.nih.gov/pubmed/2950147 Pitts]<br />
* Regular exercise and calorie restriction increase DHEA.<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=16Male Pattern Baldness2012-10-18T12:37:54Z<p>Dime: /* Diet */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
=== What affects 5-AR? ===<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
==== Inhibition ====<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
==== Promotion ====<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.<br />
* Beta-sitosterol is found in avocados and cashews (wai foods), and pumpkin seeds (non-wai that might be somewhat acceptable)</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=15Male Pattern Baldness2012-10-18T12:31:11Z<p>Dime: </p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
=== What affects 5-AR? ===<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
==== Inhibition ====<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
==== Promotion ====<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]<br />
<br />
== Diet ==<br />
The wai diet for now seems like a very good diet for managing male pattern baldness.<br />
* High-frequency, low glycemic meals of OJ + olive oil would avoid insulin spikes (shown to stimulate 5-AR)<br />
* Oleic/linoleic acids, as well as polyphenols in olive oil would inhibit 5-AR to an extent.<br />
* Antioxidants in fruits would help to cope with inflammation, which is present in the scalp of those with androgenic alopecia as shown by the higher levels of PGD2.<br />
* Vitamin E (or any other vitamin) deficiency is unlikely.</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=14Male Pattern Baldness2012-10-18T12:16:21Z<p>Dime: /* 5-alpha-reductase */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
=== What affects 5-AR? ===<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
==== Inhibition ====<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
==== Promotion ====<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=13Male Pattern Baldness2012-10-18T12:15:59Z<p>Dime: /* PGD2 */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
=== What affects 5-AR? ===<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
==== Inhibition ====<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
<br />
==== Promotion ====<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al] <br />
** TFC-007 is a selective H-PGDS inhibitor. [http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=12Male Pattern Baldness2012-10-18T12:14:12Z<p>Dime: /* 5-alpha-reductase and DHT */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase ==<br />
5-alpha-reductase (5-AR) is an NADPH-dependent enzyme which converts testosterone to DHT. Three isoenzymes of 5 alpha-reductase enzyme are recognised<br />
* [http://en.wikipedia.org/wiki/SRD5A1 type 1] - which is located on the short arm of chromosome 7 and occurs in non genital skin, '''scalp''', in the sebaceous gland, in the liver and in the brain<br />
* [http://en.wikipedia.org/wiki/SRD5A2 type 2] - which is located on the short arm of chromosome 2 and occurs mainly in the prostate, genital skin, seminal vesicles and in the '''dermal papilla''' [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
** testosterone has a much higher affinity for this type 2 than for type 1<br />
* type3 is also required for the glycosylation, it converts polyprenol to dolichol<br />
<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
In 5 alpha-reductase deficiency (5-ARD), the ''type 2'' isoenzyme is that which is lacking. Men with this condition do not develop male-pattern baldness despite evidence that the type 1 isoenzyme is the dominant form in the adult male scalp, and in 5 alpha-reductase deficiency, this isoenzyme is present at normal levels. Thus, one must conclude that the '''type 2 5-AR is necessary to the development of male pattern baldness''' [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1953169455 ref]. This conclusion doesn't sound justified, and dutasteride which inhibits type 1 too is more effective than finasteride which inhibits type 2.<br />
<br />
=== What affects 5-AR? ===<br />
The only recognized, effective way for slowing down male pattern baldness is by inhibiting ''5-AR type 2'' via [http://en.wikipedia.org/wiki/Finasteride Finasteride] or similar drug. Therefore, it is important to have an overview on what inhibits or promotes 5-AR.<br />
<br />
==== Inhibition ====<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Finasteride Finasteride] inhibits type 2 and 3<br />
** 5 mg per day is able to reduce about 70% of the serum DHT concentration [http://www.ncbi.nlm.nih.gov/pubmed/15026079 Occhiato et al.]<br />
* Synthetic drug [http://en.wikipedia.org/wiki/Dutasteride Dutasteride] inhibits all types of 5-AR<br />
** Dutasteride is considered more effective at 0.1mg than Finasteride at 5mg doses, so it is possible that actually inhibiting ''type 1'' is more important than type 2<br />
** 90% reduction of serum DHT (dosage not mentioned)<br />
* [http://en.wikipedia.org/wiki/Alfatradiol Alfatradiol/Pantostin] is topical ethanolic solution that inhibits 5-AR when applied on the scalp. The ethanol can irritate the skin.<br />
** Minoxidil is more effective, but at least Alfatradiol decreases hair loss [http://www.ncbi.nlm.nih.gov/pubmed/17451383 Blume-Peytavi et al.]<br />
** No prescription is needed in Germany, so it's fairly safe, besides the possibility of skin irritation.<br />
<br />
* ''Zinc sulphate and azelaic acid'' inhibit 5-AR in human skin ''in vitro''. Adding ''B6'' increases the effect of zinc. A combination of the three in low amounts achieved 90% inhibition of 5-AR. [http://www.ncbi.nlm.nih.gov/pubmed/3207614 Stamatiadis et al]<br />
* ''Saw palmetto and beta-sitosterol'' [http://www.ncbi.nlm.nih.gov/pubmed/12006122 Prager et al.]<br />
* ''Unsaturated fatty acids'' gamma-linolenic, alpha-linolenic, linoleic, and oleic acid [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132824/ Liang and Liao]<br />
* ''Medium chain fatty acids'' found in coconut oil, palm kernel oil, as well as ''unsaturated'' alpha-linolenic and oleic [http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200800125/abstract Liu et al.]<br />
* Various ''polyphenols'' [http://www.ncbi.nlm.nih.gov/pubmed/11931850 Hiipakka et al.]<br />
** Green tea catechin (-)-epigallocatechin gallate (EGCG) shows potent inhibition in cell-free but not in whole-cell assays of 5-AR<br />
** type 1 inhibitors: myricetin, quercitin, baicalein, and fisetin; alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates<br />
** type 2 inhibitors: biochanin A, daidzein, genistein, and kaempferol<br />
* Cream containing ''honokiol'' [http://www.ncbi.nlm.nih.gov/pubmed/23049247 Bernard et al.]<br />
** [http://www.dreliaz.org/abstract/honokiol-research/ Collection] of research on honokiol, not necessarily related to hair loss<br />
* ''Ganoderic acid'' (in Reishi mushroom) [http://www.sciencedirect.com/science/article/pii/S0960894X0900287X Liu et al.]<br />
<br />
<br />
==== Promotion ====<br />
* 6-month dietary ''vitamin E (VE) deficiency'' in rats resulted in a twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7910314 Fischer et al.]<br />
* ''Hyperinsulinemia''<br />
** elevated levels of 5α-reduced androgens seen in hyperinsulinemic conditions might be explained on the basis of a stimulatory effect of insulin on 5α-reductase in granulosa cells. [http://www.ncbi.nlm.nih.gov/pubmed/20810561 Kayampilly et al.], [http://www.biolreprod.org/cgi/content/meeting_abstract/81/1_MeetingAbstracts/563 Another paper]<br />
** acutely enhances ACTH effects on both the androgen and glucocorticoid pathways that suggest insulin stimulation of 5 α-reductase activity [http://www.eje-online.org/content/164/2/197 Tosi et al.]<br />
* A diet only ''deficient in linoleate'' causes mild skin scaling and hair loss in mice [http://www.jlr.org/content/38/4/805.full.pdf+html Cunnane and Anderson] (note: not clear if it's due to 5-AR promotion, move to some other section)<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [[http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [[http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [[http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al]] <br />
** TFC-007 is a selective H-PGDS inhibitor. [[http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [[http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al]] [[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [[http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]]</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=11Male Pattern Baldness2012-10-18T09:57:38Z<p>Dime: /* PGD2 */</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase and DHT ==<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [[http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]]<br />
<br />
* Prostaglandin D2 synthase (Prostaglandin-H2 D-isomerase (PTGDS) = H-PGDS) converts prostaglandin H2 (PGH2) into prostaglandin D2 (PGD2), so maybe a topical inhibitor of this enzyme will do the trick (to compensate for the elevated level of this enzyme).<br />
** HQL-79 is a well known, but relatively weak H-PGDS inhibitor. [[http://www.ncbi.nlm.nih.gov/pubmed/16547010 Aritake K et al]]<br />
** Scientists seem to have designed ''much more potent'' H-PGDS inhibitors. [[http://www.ncbi.nlm.nih.gov/pubmed/22068479 Kamauchi S et al]]<br />
** More H-PGDS inhibitors here, but no formulae are provided ''"The formulae of the inhibitors are proprietary information"''[[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898477 Takahashi S et al]] <br />
** TFC-007 is a selective H-PGDS inhibitor. [[http://www.ncbi.nlm.nih.gov/pubmed/21601002 Nabe T et al]]<br />
<br />
* H-PGDS levels also seem to decrease rapidly (through the ubiquitin-proteasome system) when intracellular calcium is increased [[http://www.ncbi.nlm.nih.gov/pubmed/22049022 Yazaki M et al]] [[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248891/ Free full text]]<br />
** but (the required) calcium ionophores (to increase intracellular calcium locally) also seem to promote tumors. [[http://www.ncbi.nlm.nih.gov/pubmed/10469622 Kumar S et al]]</div>Dimehttp://www.waiwiki.org/index.php?title=Male_Pattern_Baldness&diff=10Male Pattern Baldness2012-10-18T08:50:02Z<p>Dime: Created page with 'What is male pattern baldness? <blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniatur…'</p>
<hr />
<div>What is male pattern baldness?<br />
<blockquote>Male pattern baldness is caused by a genetic sensitivity of hair follicles to DHT. This hormone causes follicles to shrink or "miniaturize". In turn, this shortens their lifespan and prevents them from producing hair normally.</blockquote><br />
<br />
== 5-alpha-reductase and DHT ==<br />
Men with androgenic alopecia typically have higher levels of 5-alpha-reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.<br />
<br />
== PGD2 ==<br />
Recent research suggests that elevated levels of the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles causes androgenetic alopecia. [[http://stm.sciencemag.org/content/4/126/126ra34 Garza A et al]]</div>Dimehttp://www.waiwiki.org/index.php?title=Main_Page&diff=9Main Page2012-10-18T08:41:10Z<p>Dime: </p>
<hr />
<div>'''<br />
== WaiWiki ==<br />
'''<br />
<br />
The Wai Says articles are outdated. The Wai Wiki will deal with this, hopefully. :)<br />
<br />
* [[Research Sandbox]]</div>Dimehttp://www.waiwiki.org/index.php?title=Research_Sandbox&diff=8Research Sandbox2012-10-18T08:40:45Z<p>Dime: /* Research Sandbox */</p>
<hr />
<div>Temporary space for research on various topics.<br />
<br />
== Hair ==<br />
* [[Male Pattern Baldness]]</div>Dimehttp://www.waiwiki.org/index.php?title=Research_Sandbox&diff=7Research Sandbox2012-10-18T08:40:31Z<p>Dime: Created page with '= Research Sandbox = Temporary space for research on various topics. == Hair == * Male Pattern Baldness'</p>
<hr />
<div>= Research Sandbox =<br />
<br />
Temporary space for research on various topics.<br />
<br />
== Hair ==<br />
* [[Male Pattern Baldness]]</div>Dime