Newly Discovered Factor in Androgenetic Alopecia. The Cure is Near?
- Thread starter yassin
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2020
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Re: A recently discovered new factor in AA, the cure is near 
it doesn't matter.... if he grows hair that it means that cetrizine works and that would also confirm this "theory" about PGD2 being a main problem in Androgenetic Alopecia :whistle:
odalbak said:
it doesn't matter.... if he grows hair that it means that cetrizine works and that would also confirm this "theory" about PGD2 being a main problem in Androgenetic Alopecia :whistle:
odalbak
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Re: A recently discovered new factor in AA, the cure is near
No. The topical solution could do most of the job, or it could also be a balanced combination of both oral and topical solutions. If it works that would also mean continuing both products for years without being sure which one is the real cure. Especially since we have no clear knowledge of how the various prostaglandins work systemically and locally.
2020 said:
No. The topical solution could do most of the job, or it could also be a balanced combination of both oral and topical solutions. If it works that would also mean continuing both products for years without being sure which one is the real cure. Especially since we have no clear knowledge of how the various prostaglandins work systemically and locally.
Sparky4444
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Re: A recently discovered new factor in AA, the cure is near
I've always thought that a topical solution is the only way we will get our hair back...but thinking about it more, when we lose our hair, it isn't happening because of impact topically -- it's happening because something else is happening internally..
...applying topical solutions is like lancing a boil -- you treat it that way, but the boil comes from below and you're just managing the problem
:hump:
I've always thought that a topical solution is the only way we will get our hair back...but thinking about it more, when we lose our hair, it isn't happening because of impact topically -- it's happening because something else is happening internally..
...applying topical solutions is like lancing a boil -- you treat it that way, but the boil comes from below and you're just managing the problem
:hump:
Re: A recently discovered new factor in AA, the cure is near
Does it have to be citrizine, or will any second generation antihistamine do? I ask because I have azelastine nasal spray. Azelastine is also a histamine H1 antagonist. Would be easy to apply as its already in liquid form
Does it have to be citrizine, or will any second generation antihistamine do? I ask because I have azelastine nasal spray. Azelastine is also a histamine H1 antagonist. Would be easy to apply as its already in liquid form
fighting-baldness
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Re: A recently discovered new factor in AA, the cure is near
20mg cetrizine treatment
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; this was significant by analysis of variance (p less than or equal to 0.04). The inhibition was most marked during the fifth hour of the reaction when there was a 50% suppression of the PGD2 level by cetirizine (0.193 ng/ml to 0.075 ng/ml [p less than or equal to 0.03])
jp88 said:
20mg cetrizine treatment
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; this was significant by analysis of variance (p less than or equal to 0.04). The inhibition was most marked during the fifth hour of the reaction when there was a 50% suppression of the PGD2 level by cetirizine (0.193 ng/ml to 0.075 ng/ml [p less than or equal to 0.03])
BrightonBaldy
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Re: A recently discovered new factor in AA, the cure is near
I know its early days but any feedback from the other cetrizine lab rats?
I seem to remember having good regrowth when using miconazole in the past (stopped using it after losing my job a couple of years ago) but according to google it decreases PGE2 (one of the good post androgens)..
Are we trying to block/promote the wrong thing?
I know its early days but any feedback from the other cetrizine lab rats?
I seem to remember having good regrowth when using miconazole in the past (stopped using it after losing my job a couple of years ago) but according to google it decreases PGE2 (one of the good post androgens)..
Are we trying to block/promote the wrong thing?
BrightonBaldy
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Re: A recently discovered new factor in AA, the cure is near
any ideas why mico works for some people then?
any ideas why mico works for some people then?
squeegee
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Re: A recently discovered new factor in AA, the cure is near
Prostaglandins and platelet aggregation.
Smith JB.
Abstract
Prostaglandins may induce or inhibit platelet aggregation and constrict ro dilate blood vessels. Recent interest has focused on prostaglandins which are derivatives of arachidonic acid including prostaglandin, endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation whose enhanced production by vessel walls should be beneficial. It now appears that the circulating levels of PGI2 in man are extremely low and little is known about the manner in which to increase them. Furthermore, aspirin, in doses of as little as 4 mg/kg inhibits prostacyclin as well as thromboxane formation. Thromboxane A2 may be involved in coronary ischemia because it is a potent vasoconstrictor that is biosynthesized during platelet aggregation. Although thromboxane A2 is very unstable indirect evidence obtained by using thromboxane A generating systems or a stable analogue called carbocyclic thromboxane A2 (CTA2) suggests that it exacerbates ischaemic damage because of a selective increase in vascular resistance due to coronary vasospasm and platelet aggregation which acts to decrease myocardial blood flow. The stable prostaglandins PGD2 and PGE2 are also of interest as both are formed during platelet aggregation. Like PGI2, PGD2 inhibits platelet aggregation.
Prostaglandins and platelet aggregation.
Smith JB.
Abstract
Prostaglandins may induce or inhibit platelet aggregation and constrict ro dilate blood vessels. Recent interest has focused on prostaglandins which are derivatives of arachidonic acid including prostaglandin, endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation whose enhanced production by vessel walls should be beneficial. It now appears that the circulating levels of PGI2 in man are extremely low and little is known about the manner in which to increase them. Furthermore, aspirin, in doses of as little as 4 mg/kg inhibits prostacyclin as well as thromboxane formation. Thromboxane A2 may be involved in coronary ischemia because it is a potent vasoconstrictor that is biosynthesized during platelet aggregation. Although thromboxane A2 is very unstable indirect evidence obtained by using thromboxane A generating systems or a stable analogue called carbocyclic thromboxane A2 (CTA2) suggests that it exacerbates ischaemic damage because of a selective increase in vascular resistance due to coronary vasospasm and platelet aggregation which acts to decrease myocardial blood flow. The stable prostaglandins PGD2 and PGE2 are also of interest as both are formed during platelet aggregation. Like PGI2, PGD2 inhibits platelet aggregation.
squeegee
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Re: A recently discovered new factor in AA, the cure is near
The potencies of prostaglandins (PG) I2, PGD2 and PGE1 as inhibitors of human platelet aggregation induced by threshold concentrations of four aggregating agents were determined in platelet-rich plasma from normal individuals who had not ingested aspirin. The order of activity against ADP, adrenaline and collagen was always PGI2 greater than PGD2 greater than PGE1. However, PGD2 and PGE1 were almost equipotent with PGI2 when tested against arachidonic acid (AA). The threshold inhibitory effects of PGD2, PGE1 and PGI2 could be over come by increasing the concentrations of the aggregating agents AA, collagen or ADP. Adrenaline was found to be different from the other aggregating agents. It could overcome inhibition of platelet aggregation by PGD2 but could not overcome inhibition by PGI2 or PGE1. These facts support the hypothesis that platelet receptors for PGI2 and PGE1 are similar to each other and different from the receptor(s) for PGD2. PRP obtained from normal subjects after the ingestion of aspirin exhibited only one wave of aggregation in response to ADP, adrenaline or collagen, PGI2, PGD2 and PGE1 were all powerful inhibitors of this single wave of aggregation. The inhibitory activity of all three prostaglandins at threshold concentrations was overcome by increasing the concentration of ADP or collagen but not by increasing the concentration of adrenaline.
The potencies of prostaglandins (PG) I2, PGD2 and PGE1 as inhibitors of human platelet aggregation induced by threshold concentrations of four aggregating agents were determined in platelet-rich plasma from normal individuals who had not ingested aspirin. The order of activity against ADP, adrenaline and collagen was always PGI2 greater than PGD2 greater than PGE1. However, PGD2 and PGE1 were almost equipotent with PGI2 when tested against arachidonic acid (AA). The threshold inhibitory effects of PGD2, PGE1 and PGI2 could be over come by increasing the concentrations of the aggregating agents AA, collagen or ADP. Adrenaline was found to be different from the other aggregating agents. It could overcome inhibition of platelet aggregation by PGD2 but could not overcome inhibition by PGI2 or PGE1. These facts support the hypothesis that platelet receptors for PGI2 and PGE1 are similar to each other and different from the receptor(s) for PGD2. PRP obtained from normal subjects after the ingestion of aspirin exhibited only one wave of aggregation in response to ADP, adrenaline or collagen, PGI2, PGD2 and PGE1 were all powerful inhibitors of this single wave of aggregation. The inhibitory activity of all three prostaglandins at threshold concentrations was overcome by increasing the concentration of ADP or collagen but not by increasing the concentration of adrenaline.
squeegee
Banned
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Re: A recently discovered new factor in AA, the cure is near
I bet that the major problem in Male pattern baldness is platelet aggregation which is inhibited by PGD2..this is why PGd2 is 3x the norm and PA is boosted by androgen.
A plausible explanation for an association between baldness and CHD may be elevated androgen levels. Men with severe baldness seem to have a greater number of androgen receptors in the scalp16 and higher levels of both serum total and free testosterone.17 In a recent trial with finasteride,18 a drug that inhibits the conversion of testosterone to dihydrotestosterone in scalp and other tissue by blocking the 5? reductase enzyme, arrest of hair loss and substantial hair regrowth were noted among men receiving the agent. High levels of androgens may directly contribute to both atherosclerosis and thrombosis, and may adversely influence risk factors such as hypertension and high cholesterol. Receptors for dihydrotestosterone have been found in mouse and baboon heart muscle and endothelial cells.19 - 20 In rats, dihydrotestosterone may directly accelerate atherosclerosis by stimulating the proliferation of vascular smooth muscle cells.21 Administration of testosterone was associated with a significant increase in platelet thromboxane A2 receptor density in rodents.22
A similar effect—an increase in platelet aggregation—was observed in young men receiving clinical replacement doses of testosterone following orchiectomy.23 Complete androgen deprivation for 6 months or more after orchiectomy has been associated with improved endothelial function compared with men having normal androgen levels.24 Testosterone exacerbates hypertension in spontaneously hypertensive rats by reducing pressure-natriuresis25 and by increasing levels of 11-deoxycorticosterone through inhibition of 11?-hydroxylase activity.26 - 27
Taken from Male Pattern Baldness and Coronary Heart Disease
http://archinte.jamanetwork.com/article ... 2&page=165
I bet that the major problem in Male pattern baldness is platelet aggregation which is inhibited by PGD2..this is why PGd2 is 3x the norm and PA is boosted by androgen.
A plausible explanation for an association between baldness and CHD may be elevated androgen levels. Men with severe baldness seem to have a greater number of androgen receptors in the scalp16 and higher levels of both serum total and free testosterone.17 In a recent trial with finasteride,18 a drug that inhibits the conversion of testosterone to dihydrotestosterone in scalp and other tissue by blocking the 5? reductase enzyme, arrest of hair loss and substantial hair regrowth were noted among men receiving the agent. High levels of androgens may directly contribute to both atherosclerosis and thrombosis, and may adversely influence risk factors such as hypertension and high cholesterol. Receptors for dihydrotestosterone have been found in mouse and baboon heart muscle and endothelial cells.19 - 20 In rats, dihydrotestosterone may directly accelerate atherosclerosis by stimulating the proliferation of vascular smooth muscle cells.21 Administration of testosterone was associated with a significant increase in platelet thromboxane A2 receptor density in rodents.22
A similar effect—an increase in platelet aggregation—was observed in young men receiving clinical replacement doses of testosterone following orchiectomy.23 Complete androgen deprivation for 6 months or more after orchiectomy has been associated with improved endothelial function compared with men having normal androgen levels.24 Testosterone exacerbates hypertension in spontaneously hypertensive rats by reducing pressure-natriuresis25 and by increasing levels of 11-deoxycorticosterone through inhibition of 11?-hydroxylase activity.26 - 27
Taken from Male Pattern Baldness and Coronary Heart Disease
http://archinte.jamanetwork.com/article ... 2&page=165
squeegee
Banned
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Re: A recently discovered new factor in AA, the cure is near
Effect of minoxidil on platelet function and the synthesis of prostaglandins in platelets.
O'Barr TP, Swanson EW, Fitzpatrick JE, Corby DG.
Source
Department of Clinical Investigation, Fitzsimons Army Medical Center.
Abstract
At the 12.5 micrograms level, minoxidil prevents the irreversible aggregation of platelets by 2 x 10(-6) mol/L adenosine diphosphate (ADP). Levels of minoxidil greater than 12.5 micrograms cause a reversal of primary aggregation by 2 x 10(-6) mol/L ADP. Aggregation of platelets in response to 125 micrograms of arachidonic acid is measurably reduced by 12.5 micrograms of minoxidil and totally suppressed by 30 micrograms. Concurrent with the inhibition of platelet aggregation, increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2) and thromboxane B2 (TxB2). In the presence of 100 micrograms of minoxidil, PGE2 is reduced from a control value of 87.7 +/- 2.2 pg/ml to 23.9 +/- 3.2 pg/ml. At this level of minoxidil, TxB2 drops from 105 +/- 3.3 ng/ml to 10.5 +/- 2.6 ng/ml. The effect of minoxidil on platelet aggregation is not associated with increased cyclic adenosine monophosphate synthesis. All data support the conclusion that minoxidil functions (in platelet metabolism) primarily as a cyclooxygenase inhibitor.
COX-1 is inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin. TXA2, the major product of COX-1 in platelets, induces platelet aggregation
Effect of minoxidil on platelet function and the synthesis of prostaglandins in platelets.
O'Barr TP, Swanson EW, Fitzpatrick JE, Corby DG.
Source
Department of Clinical Investigation, Fitzsimons Army Medical Center.
Abstract
At the 12.5 micrograms level, minoxidil prevents the irreversible aggregation of platelets by 2 x 10(-6) mol/L adenosine diphosphate (ADP). Levels of minoxidil greater than 12.5 micrograms cause a reversal of primary aggregation by 2 x 10(-6) mol/L ADP. Aggregation of platelets in response to 125 micrograms of arachidonic acid is measurably reduced by 12.5 micrograms of minoxidil and totally suppressed by 30 micrograms. Concurrent with the inhibition of platelet aggregation, increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2) and thromboxane B2 (TxB2). In the presence of 100 micrograms of minoxidil, PGE2 is reduced from a control value of 87.7 +/- 2.2 pg/ml to 23.9 +/- 3.2 pg/ml. At this level of minoxidil, TxB2 drops from 105 +/- 3.3 ng/ml to 10.5 +/- 2.6 ng/ml. The effect of minoxidil on platelet aggregation is not associated with increased cyclic adenosine monophosphate synthesis. All data support the conclusion that minoxidil functions (in platelet metabolism) primarily as a cyclooxygenase inhibitor.
COX-1 is inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin. TXA2, the major product of COX-1 in platelets, induces platelet aggregation
Ace Ventura
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Re: A recently discovered new factor in AA, the cure is near
How have you made your solution?
- Cetirizine from tablets or as a liquid?
- Which vehicle? in minoxidil?
mj9 said:
How have you made your solution?
- Cetirizine from tablets or as a liquid?
- Which vehicle? in minoxidil?
Re: A recently discovered new factor in AA, the cure is near
So in short you think:->platelet aggregation (due to androgens or what ever the cause is.. the body tries to inhibit it, by producing PGD2. PGD2 binds on PGDr receptor + CRTH2. --> hairloss.
also take a look at this:->http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=100447&enterthread=y
http://www.ncbi.nlm.nih.gov/pubmed/948626
The study 22 march shows us an higher level of PGF2alpha. pgf2alpha causes 2times higher levels of androgens, by triggering the LH hormone...
now we have an elevated level of PGf2a in the scalp.. which leads to more androgens and also platelet aggregation... -> more PGD2-> hairloss. Its a whole chain reaction man.
So I think its more then you suspect.. PGF2alpha has a big role in the process is what I think. Just read the study and my experience on HLH with Bimatoprost(PGF2alpha)
So in short you think:->platelet aggregation (due to androgens or what ever the cause is.. the body tries to inhibit it, by producing PGD2. PGD2 binds on PGDr receptor + CRTH2. --> hairloss.
also take a look at this:->http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=100447&enterthread=y
http://www.ncbi.nlm.nih.gov/pubmed/948626
The study 22 march shows us an higher level of PGF2alpha. pgf2alpha causes 2times higher levels of androgens, by triggering the LH hormone...
now we have an elevated level of PGf2a in the scalp.. which leads to more androgens and also platelet aggregation... -> more PGD2-> hairloss. Its a whole chain reaction man.
So I think its more then you suspect.. PGF2alpha has a big role in the process is what I think. Just read the study and my experience on HLH with Bimatoprost(PGF2alpha)
squeegee said:
Re: A recently discovered new factor in AA, the cure is near
I guess, we are beginning to understand our Androgenetic Alopecia...
this is possible because we read studies and Lay the links between things.. Good work squeegee.
I think we should avoid higher PGF2 + PGD2 levels. the best way to do this(what I think) is targetting the CRTH2 by an antagonist. and increasing the PGE2 somehow.
I guess, we are beginning to understand our Androgenetic Alopecia...
this is possible because we read studies and Lay the links between things.. Good work squeegee.
I think we should avoid higher PGF2 + PGD2 levels. the best way to do this(what I think) is targetting the CRTH2 by an antagonist. and increasing the PGE2 somehow.
squeegee said:Boldy said:
Bad *** post Boldy!!!
BrightonBaldy
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Re: A recently discovered new factor in AA, the cure is near
if thats the case, why hasnt minoxidil cured baldness?
squeegee said:
if thats the case, why hasnt minoxidil cured baldness?