- Reaction score
- 490
I have plenty of other information in my previous posts, but I will make a summary here.
I performed the TrichoTest back in May, but I did it differently. I did the test while I was already on Topical Minoxidil(3 years) plus Topical Finasteride(2 years) and Oral Finasteride (16 months). So, I would be able to see if it was somehow "correct" because all the 3 above worked very well for me, but I was, and I am losing ground again steadily from January. Guess what? The test showed that Finasteride was needed (elevated 5AR2-not Duta-My 5AR1 was normal, but still, 5AR1 can form DHT as well. So, I was confused here because 5AR1 still can produce negative effects..), SULT1A1 were positive, so Minoxidil would work for me well (as it did), and I got some other factors that contribute, like low Aromatase, mildly elevated PGD2, low IGF-1, etc. Despite my combination of current treatments, my 5AR2 level, according to the test, is still elevated and this is concerning. Because I am losing ground, I needed to check other factors, so this test came in handy. All in all, I want to say that for my situation, it seems that the test came back correct. I do not know how biased the results were. The dermatologist included the treatments that I am taking, but not pictures, and added a high Norwood scale, as it should because of my aggressive hair loss. To summarize:
PGD2: Mildly Elevated
SULT1A1: Response to Minoxidil: Positive
5AR1: Activity Normal
5AR2: Mildly Elevated
Aromatase Activity: Mildly Reduced
IGF-1 Activity: Mildly Reduced
ACE Acitivity: Mildly Elevated (More Vasoconstriction-Vasodilation Needed: Arginine, Carnitine, etc.)
CRABP2: Mildly Reduced (Vitamin A not properly absorbed into the cells. Noteworthy: Vitamin A was in the low-end levels when I checked it before the test.)
PTGFR-1,-2,-3: 1,3: Mildly Reduced->Latanoprost can act-2: Negative Response to Latanoprost. So, here it's a bit of a mix.
Suggestions that would help:
Finasteride, Saw Palmetto (They mention this but not Duta? There are studies indicating that Saw Palmetto inhibits both isoforms.), 17a-Estradiol, Tretinoin, Vitamin A, Minoxidil, Arginine, Ginko Biloba, Igrantine-F1( Contains Cepharanthine which is meant to increase IGF-1 topically: https://www.longdom.org/open-access...leandrogenetic-alopecia-2167-0951-1000145.pdf), Cetirizine, and Latanoprost.
Another factor that connects with the Test. My DHT levels, which last time I checked them, before the test of course, they came back to my baseline levels. I know that hormones have many fluctuations, and the tests can’t be accurate sometimes, but it’s still something to consider:
August 2019: Started Topical Finasteride:Baseline levels of DHT: 541 pg/ml
Otober 2019: DHT levels:302 pg/ml
January 2020: DHT levels:298 pg/ml-After starting Oral Finasteride as well ( I was already on it for about 3 weeks-0.5mg 3 times/week)
May 2020: DHT levels:313 pg/ml-I jumped into 1mg daily from 31st of March. I jumped to 0.5mg everyday from mid February
June 2020: DHT levels:283 pg/ml- I even tested 3a-Diol-G which is far a strongest indicator than DHT alone. 3a-Diol-G is a major DHT metabolite and it can converts back to DHT as well. It came low at 1.3 ng/ml while the range is: 3.4-22.
September 2020: DHT levels: 383 pg/ml
January 2021: DHT levels: 550 pg/ml !!! Back to baseline!
May 2021 (Latest): I skipped DHT this time and tested only 3a-Diol-G. I got a result of: 16.1 this time!!! It makes sense, doesn't it? Higher DHT->Higher metabolite->Higher Androgenicity overall. I assume that my DHT is still high!
The DHT is not being targeted properly right now. Probably the high 5AR activity+Backdoor Pathway which requires 5AR1 enzyme, are still making the things worse. Plus, the low aromatase, and the 3a-Diol-G levels. 3a-Diol-G is very important indicator:
"3α-Androstanediol glucuronide (3α-ADG) is a metabolite formed from human androgens; compounds involved in the development and maintenance of sexual characteristics. It is formed by the glucuronidation of both dihydrotestosterone and testosterone, and has been proposed as means of measuring androgenic activity.
In women the adrenal steroids, dehydroepiandrosterone sulfate, androstenedione, and dehydroepiandrosterone are the major precursors of plasma 3α-ADG, accounting for almost the totality of circulating 3α-ADG. Levels of 3α-ADG decrease significantly with age.
3α-ADG is used as a marker of target tissue cellular action. 3α-ADG correlates with level of 5α-reductase activity (testosterone and 3α-androstanediol to dihydrotestosterone) in the skin. Concentrations of 3α-ADG are associated with the level of cutaneous androgen metabolism."
"Serum 3a-androstanediol glucuronide (3a-Adiol-G) is considered to be an indicator of peripheral tissue androgen metabolism. Precursor circulating androgens are converted in peripheral tissue to dihydrotestosterone (DHT), which is ultimately metabolized to 3a-Adiol-G and secreted from the cell. Elevated serum 3a-Adiol-G concentrations have been reported in women in hyperandrogenic states. We studied 44 consecutive male medical students for chest hair density, acne, and serum dehydroepiandrosterone sulfate (DHEA-S), total testosterone (total T), free and albumin-bound (bioavailable) T (bio T), and 3a-Adiol-G concentrations. Although there was a considerable overlap of serum 3a-Adiol-G values among the groups defined by hair density or acne scores, we found statistically significant correlations between serum 3a-Adiol-G and chest hairiness (P = 0.0034), acne (P = 0.0005), and a combined chest hairiness and acne score (P = 0.0018). There was no significant correlation between these clinical parameters and the levels of precursor androgens. There was, however, a strong correlation between serum 3a-Adiol-G and bio T (P = 0.0005), suggesting that in men serum 3a-Adiol-G levels may be dependent upon available free and albumin-bound T. The correlations in men of serum 3a-Adiol-G with chest hair density, acne, and the hairiness and acne index supports the hypothesis that the serum levels of 3a-Adiol-G reflect the extent of androgen action in peripheral tissues."
Study:https://pubmed.ncbi.nlm.nih.gov/2972739/
So, I would appreciate your opinions here and your interpretation of my results. I hope all of you are getting some helpful insights and get a benefit. I am trying to do as much as I can and help other members as well from my actions. Thank you so much!
I performed the TrichoTest back in May, but I did it differently. I did the test while I was already on Topical Minoxidil(3 years) plus Topical Finasteride(2 years) and Oral Finasteride (16 months). So, I would be able to see if it was somehow "correct" because all the 3 above worked very well for me, but I was, and I am losing ground again steadily from January. Guess what? The test showed that Finasteride was needed (elevated 5AR2-not Duta-My 5AR1 was normal, but still, 5AR1 can form DHT as well. So, I was confused here because 5AR1 still can produce negative effects..), SULT1A1 were positive, so Minoxidil would work for me well (as it did), and I got some other factors that contribute, like low Aromatase, mildly elevated PGD2, low IGF-1, etc. Despite my combination of current treatments, my 5AR2 level, according to the test, is still elevated and this is concerning. Because I am losing ground, I needed to check other factors, so this test came in handy. All in all, I want to say that for my situation, it seems that the test came back correct. I do not know how biased the results were. The dermatologist included the treatments that I am taking, but not pictures, and added a high Norwood scale, as it should because of my aggressive hair loss. To summarize:
PGD2: Mildly Elevated
SULT1A1: Response to Minoxidil: Positive
5AR1: Activity Normal
5AR2: Mildly Elevated
Aromatase Activity: Mildly Reduced
IGF-1 Activity: Mildly Reduced
ACE Acitivity: Mildly Elevated (More Vasoconstriction-Vasodilation Needed: Arginine, Carnitine, etc.)
CRABP2: Mildly Reduced (Vitamin A not properly absorbed into the cells. Noteworthy: Vitamin A was in the low-end levels when I checked it before the test.)
PTGFR-1,-2,-3: 1,3: Mildly Reduced->Latanoprost can act-2: Negative Response to Latanoprost. So, here it's a bit of a mix.
Suggestions that would help:
Finasteride, Saw Palmetto (They mention this but not Duta? There are studies indicating that Saw Palmetto inhibits both isoforms.), 17a-Estradiol, Tretinoin, Vitamin A, Minoxidil, Arginine, Ginko Biloba, Igrantine-F1( Contains Cepharanthine which is meant to increase IGF-1 topically: https://www.longdom.org/open-access...leandrogenetic-alopecia-2167-0951-1000145.pdf), Cetirizine, and Latanoprost.
Another factor that connects with the Test. My DHT levels, which last time I checked them, before the test of course, they came back to my baseline levels. I know that hormones have many fluctuations, and the tests can’t be accurate sometimes, but it’s still something to consider:
August 2019: Started Topical Finasteride:Baseline levels of DHT: 541 pg/ml
Otober 2019: DHT levels:302 pg/ml
January 2020: DHT levels:298 pg/ml-After starting Oral Finasteride as well ( I was already on it for about 3 weeks-0.5mg 3 times/week)
May 2020: DHT levels:313 pg/ml-I jumped into 1mg daily from 31st of March. I jumped to 0.5mg everyday from mid February
June 2020: DHT levels:283 pg/ml- I even tested 3a-Diol-G which is far a strongest indicator than DHT alone. 3a-Diol-G is a major DHT metabolite and it can converts back to DHT as well. It came low at 1.3 ng/ml while the range is: 3.4-22.
September 2020: DHT levels: 383 pg/ml
January 2021: DHT levels: 550 pg/ml !!! Back to baseline!
May 2021 (Latest): I skipped DHT this time and tested only 3a-Diol-G. I got a result of: 16.1 this time!!! It makes sense, doesn't it? Higher DHT->Higher metabolite->Higher Androgenicity overall. I assume that my DHT is still high!
The DHT is not being targeted properly right now. Probably the high 5AR activity+Backdoor Pathway which requires 5AR1 enzyme, are still making the things worse. Plus, the low aromatase, and the 3a-Diol-G levels. 3a-Diol-G is very important indicator:
"3α-Androstanediol glucuronide (3α-ADG) is a metabolite formed from human androgens; compounds involved in the development and maintenance of sexual characteristics. It is formed by the glucuronidation of both dihydrotestosterone and testosterone, and has been proposed as means of measuring androgenic activity.
In women the adrenal steroids, dehydroepiandrosterone sulfate, androstenedione, and dehydroepiandrosterone are the major precursors of plasma 3α-ADG, accounting for almost the totality of circulating 3α-ADG. Levels of 3α-ADG decrease significantly with age.
3α-ADG is used as a marker of target tissue cellular action. 3α-ADG correlates with level of 5α-reductase activity (testosterone and 3α-androstanediol to dihydrotestosterone) in the skin. Concentrations of 3α-ADG are associated with the level of cutaneous androgen metabolism."
"Serum 3a-androstanediol glucuronide (3a-Adiol-G) is considered to be an indicator of peripheral tissue androgen metabolism. Precursor circulating androgens are converted in peripheral tissue to dihydrotestosterone (DHT), which is ultimately metabolized to 3a-Adiol-G and secreted from the cell. Elevated serum 3a-Adiol-G concentrations have been reported in women in hyperandrogenic states. We studied 44 consecutive male medical students for chest hair density, acne, and serum dehydroepiandrosterone sulfate (DHEA-S), total testosterone (total T), free and albumin-bound (bioavailable) T (bio T), and 3a-Adiol-G concentrations. Although there was a considerable overlap of serum 3a-Adiol-G values among the groups defined by hair density or acne scores, we found statistically significant correlations between serum 3a-Adiol-G and chest hairiness (P = 0.0034), acne (P = 0.0005), and a combined chest hairiness and acne score (P = 0.0018). There was no significant correlation between these clinical parameters and the levels of precursor androgens. There was, however, a strong correlation between serum 3a-Adiol-G and bio T (P = 0.0005), suggesting that in men serum 3a-Adiol-G levels may be dependent upon available free and albumin-bound T. The correlations in men of serum 3a-Adiol-G with chest hair density, acne, and the hairiness and acne index supports the hypothesis that the serum levels of 3a-Adiol-G reflect the extent of androgen action in peripheral tissues."
Study:https://pubmed.ncbi.nlm.nih.gov/2972739/
So, I would appreciate your opinions here and your interpretation of my results. I hope all of you are getting some helpful insights and get a benefit. I am trying to do as much as I can and help other members as well from my actions. Thank you so much!
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