SickeningSkittles
New Member
what is the deal with people saying not to use finasteride with deca? Is this a myth?
MESO-Rx
Anabolic Steroids
Finasteride [5ARI] Induced/Associated Effects
- Thread starter madclown
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- finasteride
Allegedly, the reason nandrolone has low androgenic sides is because of conversion to DHN which blocks some anabolic signaling. Finasteride blocks this conversion and leaves nandrolone to exert androgenic effects that it would normally not. That's the prevailing "board" theory. I have no idea if it is true.
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SickeningSkittles
New Member
Ive been trying to figure this out for awhile. Half of people say no fina and half people say fina. Also the same for nolvadex but im not worried about that
MitchFit
New Member
Finasteride made me slow and my thoughts were always scrambled. It disrupts neurosteroid activity in the brain. Not worth the risk for me at least.
SickeningSkittles
New Member
I havent noticed that effect. ive been on for over a year and i want to know the truth in regards to deca/nandrolone
So i am guessing in your practice you must have cured a lot of people with PFS already?
If not go on the forums, you could make heaps of money curing them. They are commiting suicide over there because neither trt neither anti depressives work........
Many are also left handed, ambidextrous, many gays and bisexual, thats also a risk factor. Is there a pill you prescribe in your practice to correct that functional disorder ?
(Irony)
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1) Nope bc I'm NOT a psychiatrist
2) I dont practice medicine to make "heaps of money" and pity those who do!
3) "Suicide" bc of PFS, and what blog did you have the time to diligently search for such utter nonsense.
4) My suggestion, get a life outside of forums, boards and self help go nowhere boards!
Adios
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First of all writing Dr. Before your nickname, doesnt give you a medical degree, which at this point im doubtful you have, or that you are a good one, since you seem to lack the sensitivity of a good doctor, and the wisdom to admit you are wrong.
Im going to go ahead and say that a successful doctor, who loves his profession and is good at it, is not spending his days either on internet forums telling others to get a life, going against patients and discrediting established, serious diseases. You know, just because it doesnt show in blood exams yet, doesnt mean it doesnt exist or that we wont have a blood marker soon. Or a genetic marker involving possibly the androgen receptor.
Doctors dont usually comment on others specialties, so if you arent specialized in psychiatric medicine, neither have you cured someone from PFS, why are you commenting that it is a case for a psychiatric doctor? That this is an established psych disease that was there before hand? Because for a moment there, i thought you could actually cure this disease!!
Seems like most PFS patients are also left handed, whats your suggestion for that? Start writing with the right hand to solve it? Lol
You clearly are diminishing a disease that is incapacitating, has registered suicides on suicide watch database and up there from your high horse, you speak of what you dont understand. Get off of it.
Sad example of a doctor, really.
Adios
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Finasteride-Induced Suicidal and Self-Injurious Behavior Rises 33% in WHO Database of Adverse Drug Reactions - The Post-Finasteride Syndrome FoundationThe Post-Finasteride Syndrome Foundation
59 registered suicides, because no doctor can help !!
The PFS foundation's founder is also a doctor in case you didnt know. If that gives it any more credibility...
There's at least 4 more suicides since January this year.
Its counting, and if the drug is pulled of the market more will die since most of the side effects, show up during withdrawal phase.
Yet here you are, saying people should visit a psychiatrist...Correlation doesnt mean causation, you should know that! Any doctor does...
59 registered suicides, because no doctor can help !!
The PFS foundation's founder is also a doctor in case you didnt know. If that gives it any more credibility...
There's at least 4 more suicides since January this year.
Its counting, and if the drug is pulled of the market more will die since most of the side effects, show up during withdrawal phase.
Yet here you are, saying people should visit a psychiatrist...Correlation doesnt mean causation, you should know that! Any doctor does...
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Jonny Craig
New Member
Any Doctor, who in 2016, with the amount of research and clinical data out there, would scoff at 'PFS' and say it's all in someone's head, is a complete and utter fool.
Guo M, Heran B, Flannigan R, Kezouh A, Etminan M. Persistent Sexual Dysfunction with Finasteride 1mg Taken for Hair Loss. Pharmacotherapy. Persistent Sexual Dysfunction with Finasteride 1mg Taken for Hair Loss - Guo - 2016 - Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy - Wiley Online Library
PURPOSE: To examine the risk of persistent sexual dysfunction (PSD) with finasteride 1mg.
METHODS: We conducted a retrospective cohort study using the IMS U.S. health claims database. From an original cohort of 6,110,723 patients, we identified 1390 men who had stopped using finasteride 1mg and 20,000 randomly selected age- and calendar time-matched users of omeprazole from 2006 to 2014.
First PSD event was defined as
1) the first PSD diagnosis through the first International Classification for Diseases, Ninth Revision Clinical Modification [ICD-9-CM]) code for sexual dysfunction and
2) use of a phosphodiesterase inhibitor (sildenafil, tadalafil, or vardenafil).
RESULTS: In the primary analysis, we identified 1,390 men taking finasteride 1mg and 20,000 omeprazole users. The median time to first PSD event after discontinuation of a finasteride 1mg prescription was 339 days (SD, 334 days). The rate of PSD for finasteride 1mg users and omeprazole users was 37.9 and 15 per 1000-person-years, respectively.
For the primary analysis of sexual dysfunction, the adjusted hazard ratio (HR) comparing finasteride 1mg users to omeprazole users was 1.62 (1.14-2.29). Adjusted HR in the secondary analysis comparing finasteride users to omeprazole users with respect to the first phosphodiesterase inhibitor was 2.73 (2.01-3.69).
CONCLUSIONS: The risk of PSD in men who stopped finasteride 1mg therapy was higher than for omeprazole users. Patients who stopped finasteride therapy sought physician visits for sexual dysfunction up to 1 year after stopping finasteride.
PURPOSE: To examine the risk of persistent sexual dysfunction (PSD) with finasteride 1mg.
METHODS: We conducted a retrospective cohort study using the IMS U.S. health claims database. From an original cohort of 6,110,723 patients, we identified 1390 men who had stopped using finasteride 1mg and 20,000 randomly selected age- and calendar time-matched users of omeprazole from 2006 to 2014.
First PSD event was defined as
1) the first PSD diagnosis through the first International Classification for Diseases, Ninth Revision Clinical Modification [ICD-9-CM]) code for sexual dysfunction and
2) use of a phosphodiesterase inhibitor (sildenafil, tadalafil, or vardenafil).
RESULTS: In the primary analysis, we identified 1,390 men taking finasteride 1mg and 20,000 omeprazole users. The median time to first PSD event after discontinuation of a finasteride 1mg prescription was 339 days (SD, 334 days). The rate of PSD for finasteride 1mg users and omeprazole users was 37.9 and 15 per 1000-person-years, respectively.
For the primary analysis of sexual dysfunction, the adjusted hazard ratio (HR) comparing finasteride 1mg users to omeprazole users was 1.62 (1.14-2.29). Adjusted HR in the secondary analysis comparing finasteride users to omeprazole users with respect to the first phosphodiesterase inhibitor was 2.73 (2.01-3.69).
CONCLUSIONS: The risk of PSD in men who stopped finasteride 1mg therapy was higher than for omeprazole users. Patients who stopped finasteride therapy sought physician visits for sexual dysfunction up to 1 year after stopping finasteride.
Basaria S, Jasuja R, Huang G, et al. Characteristics of Men Who Report Persistent Sexual Symptoms after Finasteride Use for Hair Loss. The Journal of Clinical Endocrinology & Metabolism:jc.2016-726. http://press.endocrine.org/doi/abs/10.1210/jc.2016-2726
Context: Some men who use finasteride for hair loss report persistent sexual and other symptoms after discontinuing finasteride therapy.
Objective: To determine whether these persistent symptoms after discontinuation of finasteride use are due to androgen deficiency, decreased peripheral androgen action, or persistent inhibition of steroid 5α-reductase (SRD5A) enzymes.
Participants: Finasteride-users, who reported persistent sexual symptoms after discontinuing finasteride (group 1); age-matched finasteride-users who did not report sexual symptoms (group 2); and healthy men who had never used finasteride (group 3).
Outcomes: Sexual function, mood, affect, cognition, hormone levels, body-composition, functional magnetic resonance imaging (fMRI) response to sexually and affectively-valenced stimuli, nucleotide sequences of androgen receptor (AR), SRD5A1 and SRD5A2; expression levels of androgen-dependent genes in skin
Setting: Academic medical center
Results: Symptomatic finasteride-users were similar in body composition, strength, and nucleotide sequences of AR, SRD5A1 and SRD5A2 genes to asymptomatic finasteride-users and nonusers. Symptomatic finasteride-users had impaired sexual function, higher depression scores, a more negative affectivity balance, and more cognitive complaints than men in groups 2 and 3, but had normal objectively-assessed cognitive function. Testosterone, DHT, 5α-androstane-3α,17|gb-diol glucuronide, testosterone-to-DHT and androsterone glucuronide-to-etiocholanolone glucuronide ratios, and markers of peripheral androgen action, and expression levels of AR-dependent genes in skin did not differ among groups. fMRI BOLD responses to erotic and nonerotic stimuli revealed abnormal function in brain circuitry linked to sexual arousal and major depression.
Conclusions: We found no evidence of androgen deficiency, decreased peripheral androgen action, or persistent peripheral inhibition of SRD5A in men with persistent sexual symptoms after finasteride use. Symptomatic finasteride-users revealed depressed mood and fMRI findings consistent with those observed in depression.
Context: Some men who use finasteride for hair loss report persistent sexual and other symptoms after discontinuing finasteride therapy.
Objective: To determine whether these persistent symptoms after discontinuation of finasteride use are due to androgen deficiency, decreased peripheral androgen action, or persistent inhibition of steroid 5α-reductase (SRD5A) enzymes.
Participants: Finasteride-users, who reported persistent sexual symptoms after discontinuing finasteride (group 1); age-matched finasteride-users who did not report sexual symptoms (group 2); and healthy men who had never used finasteride (group 3).
Outcomes: Sexual function, mood, affect, cognition, hormone levels, body-composition, functional magnetic resonance imaging (fMRI) response to sexually and affectively-valenced stimuli, nucleotide sequences of androgen receptor (AR), SRD5A1 and SRD5A2; expression levels of androgen-dependent genes in skin
Setting: Academic medical center
Results: Symptomatic finasteride-users were similar in body composition, strength, and nucleotide sequences of AR, SRD5A1 and SRD5A2 genes to asymptomatic finasteride-users and nonusers. Symptomatic finasteride-users had impaired sexual function, higher depression scores, a more negative affectivity balance, and more cognitive complaints than men in groups 2 and 3, but had normal objectively-assessed cognitive function. Testosterone, DHT, 5α-androstane-3α,17|gb-diol glucuronide, testosterone-to-DHT and androsterone glucuronide-to-etiocholanolone glucuronide ratios, and markers of peripheral androgen action, and expression levels of AR-dependent genes in skin did not differ among groups. fMRI BOLD responses to erotic and nonerotic stimuli revealed abnormal function in brain circuitry linked to sexual arousal and major depression.
Conclusions: We found no evidence of androgen deficiency, decreased peripheral androgen action, or persistent peripheral inhibition of SRD5A in men with persistent sexual symptoms after finasteride use. Symptomatic finasteride-users revealed depressed mood and fMRI findings consistent with those observed in depression.
[OA] Hagberg KW, Divan HA, Persson R, Nickel JC, Jick SS. Risk of erectile dysfunction associated with use of 5-alpha reductase inhibitors for benign prostatic hyperplasia or alopecia: population based studies using the Clinical Practice Research Datalink. BMJ 2016;354:i4823. Risk of erectile dysfunction associated with use of 5-α reductase inhibitors for benign prostatic hyperplasia or alopecia: population based studies using the Clinical Practice Research Datalink | The BMJ
OBJECTIVE: To estimate the risk of erectile dysfunction in men who used 5-alpha reductase inhibitors to treat benign prostatic hyperplasia or alopecia.
DESIGN: Cohort studies with nested case-control analyses.
SETTING: UK Clinical Practice Research Datalink.
POPULATION: Two populations of men free of risk factors for erectile dysfunction and other sexual dysfunction or its treatment: men aged 40 or more with benign prostatic hyperplasia who received a prescription for a 5-alpha reductase inhibitor (finasteride or dutasteride) or alpha blocker, or both, and men aged 18-59 with alopecia.
EXPOSURES: In the benign prostatic hyperplasia study, exposures were classified as 5-alpha reductase inhibitors only, 5-alpha reductase inhibitors+alpha blockers, or alpha blockers only. In the alopecia study, exposures were finasteride 1 mg or no treatment.
MAIN OUTCOME MEASURES: Cases were men with a diagnosis of erectile dysfunction or treatment (procedure or prescription for a phosphodiesterase type 5 inhibitor) during follow-up. We calculated incidence rates and adjusted incidence rate ratios with 95% confidence intervals. We also conducted nested case-control analyses to control for major confounders, and calculated adjusted odds ratios with 95% confidence intervals.
RESULTS: In the population with benign prostatic hyperplasia (n=71 849), the risk of erectile dysfunction was not increased with use of 5-alpha reductase inhibitors only (incidence rate ratio 0.92, 95% confidence interval 0.85 to 0.99; odds ratio 0.94, 95% confidence interval 0.85 to 1.03) or 5-alpha reductase inhibitors+alpha blocker (1.09, 0.99 to 1.21, 0.92; 0.80 to 1.06) compared with alpha blockers only, and remained null regardless of number of prescriptions or timing of use.
The risk of erectile dysfunction increased with longer duration of benign prostatic hyperplasia, regardless of exposure. For the alopecia population (n=12 346), the risk of erectile dysfunction was not increased for users of finasteride 1 mg compared with unexposed men with alopecia (1.03, 0.73 to 1.44; 0.95, 0.64 to 1.41).
CONCLUSION: 5-alpha reductase inhibitors do not seem to significantly increase the risk of incident erectile dysfunction, regardless of indication for use. Risk of erectile dysfunction increased with longer duration of benign prostatic hyperplasia.
OBJECTIVE: To estimate the risk of erectile dysfunction in men who used 5-alpha reductase inhibitors to treat benign prostatic hyperplasia or alopecia.
DESIGN: Cohort studies with nested case-control analyses.
SETTING: UK Clinical Practice Research Datalink.
POPULATION: Two populations of men free of risk factors for erectile dysfunction and other sexual dysfunction or its treatment: men aged 40 or more with benign prostatic hyperplasia who received a prescription for a 5-alpha reductase inhibitor (finasteride or dutasteride) or alpha blocker, or both, and men aged 18-59 with alopecia.
EXPOSURES: In the benign prostatic hyperplasia study, exposures were classified as 5-alpha reductase inhibitors only, 5-alpha reductase inhibitors+alpha blockers, or alpha blockers only. In the alopecia study, exposures were finasteride 1 mg or no treatment.
MAIN OUTCOME MEASURES: Cases were men with a diagnosis of erectile dysfunction or treatment (procedure or prescription for a phosphodiesterase type 5 inhibitor) during follow-up. We calculated incidence rates and adjusted incidence rate ratios with 95% confidence intervals. We also conducted nested case-control analyses to control for major confounders, and calculated adjusted odds ratios with 95% confidence intervals.
RESULTS: In the population with benign prostatic hyperplasia (n=71 849), the risk of erectile dysfunction was not increased with use of 5-alpha reductase inhibitors only (incidence rate ratio 0.92, 95% confidence interval 0.85 to 0.99; odds ratio 0.94, 95% confidence interval 0.85 to 1.03) or 5-alpha reductase inhibitors+alpha blocker (1.09, 0.99 to 1.21, 0.92; 0.80 to 1.06) compared with alpha blockers only, and remained null regardless of number of prescriptions or timing of use.
The risk of erectile dysfunction increased with longer duration of benign prostatic hyperplasia, regardless of exposure. For the alopecia population (n=12 346), the risk of erectile dysfunction was not increased for users of finasteride 1 mg compared with unexposed men with alopecia (1.03, 0.73 to 1.44; 0.95, 0.64 to 1.41).
CONCLUSION: 5-alpha reductase inhibitors do not seem to significantly increase the risk of incident erectile dysfunction, regardless of indication for use. Risk of erectile dysfunction increased with longer duration of benign prostatic hyperplasia.
Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS. Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review. J Clin Aesthet Dermatol 2016;9(7):56-62. Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review
Finasteride and dutasteride, both 5-alpha reductase inhibitors, are considered first-line treatment for androgenetic hair loss in men and used increasingly in women. In each case, patients are expected to take the medications indefinitely despite the lack of research regarding long-term adverse effects.
Concerns regarding the adverse effects of these medications has led the United States National Institutes of Health to add a link for post-finasteride syndrome to its Genetic and Rare Disease Information Center.
Herein, the authors report the results of a literature search reviewing adverse events of 5-alpha reductase inhibitors as they relate to prostate cancer, psychological effects, sexual health, and use in women.
Several large studies found no increase in incidence of prostate cancer, a possible increase of high-grade cancer when detected, and no change in survival rate with 5-alpha reductase inhibitor use.
Currently, there is no direct link between 5-alpha reductase inhibitor use and depression; however, several small studies have led to depression being listed as a side effect on the medication packaging. Sexual effects including erectile dysfunction and decreased libido and ejaculate were reported in as many as 3.4 to 15.8 percent of men.
To date, there are very few studies evaluating 5-alpha reductase inhibitor use in women. Risks include birth defects in male fetuses if used in pregnancy, decreased libido, headache, gastrointestinal discomfort, and isolated reports of changes in menstruation, acne, and dizziness.
Overall, 5-alpha reductase inhibitors were well-tolerated in both men and women, but not without risk, highlighting the importance of patient education prior to treatment.
Finasteride and dutasteride, both 5-alpha reductase inhibitors, are considered first-line treatment for androgenetic hair loss in men and used increasingly in women. In each case, patients are expected to take the medications indefinitely despite the lack of research regarding long-term adverse effects.
Concerns regarding the adverse effects of these medications has led the United States National Institutes of Health to add a link for post-finasteride syndrome to its Genetic and Rare Disease Information Center.
Herein, the authors report the results of a literature search reviewing adverse events of 5-alpha reductase inhibitors as they relate to prostate cancer, psychological effects, sexual health, and use in women.
Several large studies found no increase in incidence of prostate cancer, a possible increase of high-grade cancer when detected, and no change in survival rate with 5-alpha reductase inhibitor use.
Currently, there is no direct link between 5-alpha reductase inhibitor use and depression; however, several small studies have led to depression being listed as a side effect on the medication packaging. Sexual effects including erectile dysfunction and decreased libido and ejaculate were reported in as many as 3.4 to 15.8 percent of men.
To date, there are very few studies evaluating 5-alpha reductase inhibitor use in women. Risks include birth defects in male fetuses if used in pregnancy, decreased libido, headache, gastrointestinal discomfort, and isolated reports of changes in menstruation, acne, and dizziness.
Overall, 5-alpha reductase inhibitors were well-tolerated in both men and women, but not without risk, highlighting the importance of patient education prior to treatment.
IwantToGetBig.Frank
Well-known Member
I use Finasteride during big cycles of test to minimize the hair loss. I have all my hair but I notice way less shedding with fina.
Test makes me very clear mentally, so I haven't had that type of effect - scrambled thoughts.
Frank
MitchFit
New Member
Yeah more power to ya. Honestly, finasteride is a wonder drug without the side effects. For a young man in his 20s, balding can be very damaging to your dating life and women. Finasteride can halt balding progression by many years, which can literally be life changing for a young guy.
[OA] Differences in Reproductive Toxicology Between Alopecia Drugs: An Analysis On Adverse Events Among Female and Male Cases
Alopecia is a dermatological condition with limited therapeutic options. Only two drugs, finasteride and minoxidil, are approved by FDA for alopecia treatment. However, little is known about the differences in adverse effects between these two drugs.
We examined the clinical reports submitted to the FDA Adverse Event Reporting System (FAERS) from 2004 to 2014. For both female and males, finasteride was found to be more associated with reproductive toxicity as compared to minoxidil.
Wu M, Yu Q, Li Q. Differences in reproductive toxicology between alopecia drugs: an analysis on adverse events among female and male cases. Oncotarget. Differences in reproductive toxicology between alopecia drugs: an analysis on adverse events among female and male cases
Alopecia is a dermatological condition with limited therapeutic options. Only two drugs, finasteride and minoxidil, are approved by FDA for alopecia treatment. However, little is known about the differences in adverse effects between these two drugs.
We examined the clinical reports submitted to the FDA Adverse Event Reporting System (FAERS) from 2004 to 2014. For both female and males, finasteride was found to be more associated with reproductive toxicity as compared to minoxidil.
- Among male alopecia cases, finasteride was significantly more concurrent with several forms of sexual dysfunction.
- Among female alopecia cases, finasteride was significantly more concurrent with harm to fetus and disorder of uterus. In addition, drug-gene network analysis indicated that finasteride could profoundly disturb pathways related to sex hormone signaling and oocyte maturation.
Wu M, Yu Q, Li Q. Differences in reproductive toxicology between alopecia drugs: an analysis on adverse events among female and male cases. Oncotarget. Differences in reproductive toxicology between alopecia drugs: an analysis on adverse events among female and male cases
Reprint of "Steroid 5alpha-Reductase 2 Deficiency"
Highlights
Mutations in the type 2 isoenzyme cause a disorder of 46,XY sex development, termed 5alpha-reductase type 2 deficiency and that was described forty years ago.
Many mutations in the encoding gene have been reported in different ethnic groups. In affected 46,XY individuals, female external genitalia are common, but Mullerian ducts regress, and the internal urogenital tract is male.
Most affected males are raised as females, but virilization occurs at puberty, and male social sex develops thereafter with high frequency.
Fertility can be achieved in some affected males with assisted reproduction techniques, and adults with male social sex report a more satisfactory sex life and quality of life as compared to affected individuals with female social sex.
Mendonca BB, Batista RL, Domenice S, et al. Reprint of "Steroid 5alpha-reductase 2 deficiency". J Steroid Biochem Mol Biol. Reprint of “Steroid 5α-reductase 2 deficiency”
Highlights
- 46,XY due 5α-reductase type 2 deficiency subjects have a variable degrees of external genitalia virilisation but most of them have almost normal female external genitalia at birth leading to female sex assignment.
- All patients virilise at puberty and gynecomastia is rarely observed in 5α-reductase type 2 deficiency patients.
- 5α-reductase type 2 deficiency is caused by homozygous or compound heterozygous loss-of-function mutations of the SRD5A2 gene.
- Normal testosterone to dihydrotestosterone ratio in affected patients indicates mutational analysis of the SRD5A2 gene as the first approach to 5α-reductase type 2 deficiency diagnoses, especially in neonates.
- Mutational analysis of the SRD5A2 gene is clinically important as the diagnosis of SRD5A2 mutations in neonates with atypical genitalia suggest the choice of male sex-of-rearing considering: the frequent change to male social sex, the better quality of life and the possibility of fertility following assisted reproduction techniques in the male social sex individuals.
Mutations in the type 2 isoenzyme cause a disorder of 46,XY sex development, termed 5alpha-reductase type 2 deficiency and that was described forty years ago.
Many mutations in the encoding gene have been reported in different ethnic groups. In affected 46,XY individuals, female external genitalia are common, but Mullerian ducts regress, and the internal urogenital tract is male.
Most affected males are raised as females, but virilization occurs at puberty, and male social sex develops thereafter with high frequency.
Fertility can be achieved in some affected males with assisted reproduction techniques, and adults with male social sex report a more satisfactory sex life and quality of life as compared to affected individuals with female social sex.
Mendonca BB, Batista RL, Domenice S, et al. Reprint of "Steroid 5alpha-reductase 2 deficiency". J Steroid Biochem Mol Biol. Reprint of “Steroid 5α-reductase 2 deficiency”
Hello,
I have not taken Finasteride but I wanted to ask about this here because I have seen the
subject discussed on similar forums.
I'm looking for a test that can measure 5a-Reductase Activity.
From what I have read serum DHT levels may not be an accurate measurement.
Is 3a Androstanediol Glucuronide a reliable measure of 5a-Reductase Activity?
I read it was but it was also disputed in one thread I saw.
Can the 3a Androstanediol Glucuronide test be ordered online without an MD order?
I found a urinary hormone test that I can order that measures
DHEA Testosterone Androsterone Etiocholanolone 5a-Androstanediol 5ß-Androstanediol and other hormones
Would the Androsterone/Etiocholanolone Ratio be better than 3a Androstanediol Glucuronide testing?
What would be the best test currently available to measure 5a-Reductase Activity?
Thanks,
Brian
I have not taken Finasteride but I wanted to ask about this here because I have seen the
subject discussed on similar forums.
I'm looking for a test that can measure 5a-Reductase Activity.
From what I have read serum DHT levels may not be an accurate measurement.
Is 3a Androstanediol Glucuronide a reliable measure of 5a-Reductase Activity?
I read it was but it was also disputed in one thread I saw.
Can the 3a Androstanediol Glucuronide test be ordered online without an MD order?
I found a urinary hormone test that I can order that measures
DHEA Testosterone Androsterone Etiocholanolone 5a-Androstanediol 5ß-Androstanediol and other hormones
Would the Androsterone/Etiocholanolone Ratio be better than 3a Androstanediol Glucuronide testing?
What would be the best test currently available to measure 5a-Reductase Activity?
Thanks,
Brian
Motofei IG, Rowland DL, Manea M, Georgescu SR, Paunica I, Sinescu I. Safety Profile of Finasteride: Distribution of Adverse Effects According to Structural and Informational Dichotomies of the Mind/Brain. Clin Drug Investig. Safety Profile of Finasteride: Distribution of Adverse Effects According to Structural and Informational Dichotomies of the Mind/Brain
Finasteride is currently used extensively for male androgenic alopecia and benign prostatic hyperplasia; however, some adverse effects are severe and even persistent after treatment cessation, the so-called 'post-finasteride syndrome'.
The following most severe adverse effects-sexual dysfunction and depression-often occur together and may potentiate one other, a fact that could explain (at least in part) the magnitude and persistence of finasteride adverse effects.
This paper presents the pharmacological action of finasteride and the corresponding adverse effects, the biological base explaining the occurrence, persistence and distribution of these adverse effects, and a possible therapeutic solution for post-finasteride syndrome.
The distribution of finasteride adverse effects is presented within a comprehensive and modern neuro-endocrine perspective related to structural and informational dichotomies of the brain.
Understanding the variation of finasteride side effects among different populations would be necessary not only to delineate the safety profile of finasteride for different subgroups of men (a subject may or may not be affected by a certain anti-hormonal compound dependent on the individual neuro-endocrine profile), but also as a possible premise for a therapeutic approach of finasteride adverse effects.
Such therapeutic approach should include administration of exogenous hormones, which are deficient in men with post-finasteride syndrome, namely dihydrotestosterone (in right-handed men) or progesterone/dihydroprogesterone (in left-handed subjects).
Finasteride is currently used extensively for male androgenic alopecia and benign prostatic hyperplasia; however, some adverse effects are severe and even persistent after treatment cessation, the so-called 'post-finasteride syndrome'.
The following most severe adverse effects-sexual dysfunction and depression-often occur together and may potentiate one other, a fact that could explain (at least in part) the magnitude and persistence of finasteride adverse effects.
This paper presents the pharmacological action of finasteride and the corresponding adverse effects, the biological base explaining the occurrence, persistence and distribution of these adverse effects, and a possible therapeutic solution for post-finasteride syndrome.
The distribution of finasteride adverse effects is presented within a comprehensive and modern neuro-endocrine perspective related to structural and informational dichotomies of the brain.
Understanding the variation of finasteride side effects among different populations would be necessary not only to delineate the safety profile of finasteride for different subgroups of men (a subject may or may not be affected by a certain anti-hormonal compound dependent on the individual neuro-endocrine profile), but also as a possible premise for a therapeutic approach of finasteride adverse effects.
Such therapeutic approach should include administration of exogenous hormones, which are deficient in men with post-finasteride syndrome, namely dihydrotestosterone (in right-handed men) or progesterone/dihydroprogesterone (in left-handed subjects).
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