Finasteride, a 5-alpha reductase inhibitor, widely used in the medical management of male pattern hairloss, has been reported to cause sexual side effects. This article critically examines the evidence available and makes recommendations as to how a physician should counsel a patient while prescribing the drug. Some of the commonly faced questions by a physician while treating a patient of pattern hairloss are about the possible sexual side effects caused by finasteride. Reports in the press, internet sites, and misinformation by practitioners of alternative medicine, all have contributed to this image of the drug, and has lead to apprehension in the minds of patients. Often even dermatologists seem to hesitate to prescribe the drug on a long term basis.
All rights reserved. Arch Dermatol ; However, there is a concern over chronic use of finasteride and development of prostate cancer. Scand J Urol Nephrol Suppl. Although several rat studies have shown detrimental changes to erectile function caused by 5 alpha reductase inhibitors, the persistent nature of these changes is an area of active Libido proscar.
Doctor facial muscle. What is Propecia (finasteride)?
I apologize if you don't. Finasteride is a Libido proscar and competitive inhibitor of Type II 5—AR, and has therefore a selective action on hair follicles. Libido proscar fact I was basically not able to have sex for quite a while, and it caused some major relationship issues with my girlfriend at the time. It's certainly better now than when I quit, but I'm losing hope that I'll ever fully recover. BPH is an enlargement of the prostate gland. Testosterone to Estrogen Ratio While the 15 percent Strip club white plains in circulating testosterone and estrogen levels in men taking Finasteride 1mg per day does not seem much to me, it is important to also Libido proscar out for the testosterone to estrogen ratio in case you ever get blood tests done. The matter needs further systematic investigation and documentation. After Libido proscar week of finasteride, I've decided to stop taking it. Only those patients tolerating at least 4 mg were kept on doxazosin. The role of nocebo effect in the causation of ED due to finasteride has been investigated. Epstein encourages physicians who treat hair loss to be thorough in their explanation to patients in regard to the lack of definitive, consistent evidence for the risk of permanent sexual dysfunction with finasteride. Our team periodically reviews articles in order to ensure content quality. How did it go for you? Forgot your password? Caution should be exercised in the administration of Proscar in those patients with liver function abnormalities, as finasteride is metabolized extensively in the liver.
New reports based on patient questionnaires suggest finasteride Propecia , used for male pattern baldness, leads to permanent — rather than temporary— sexual side effects.
- I therefore decided to be cautious and take around half the recommend dose i.
- Finasteride, a 5-alpha reductase inhibitor, widely used in the medical management of male pattern hairloss, has been reported to cause sexual side effects.
- A very common misconception about Finasteride also known as Propecia and Proscar is the belief that it lowers testosterone levels.
I have read several news reports that claim finasteride, which I take for my prostate problem, can cause permanent impotence. Should I be concerned? Finasteride sold as Proscar and generic brands is prescribed for symptoms of an enlarged prostate; it's also used at a lower strength under the name Propecia for male pattern baldness. Finasteride blocks the metabolism of testosterone. It can prevent hair loss and decrease prostate enlargement, but not surprisingly, it can also suppress sexual function.
However, the side effects of a medication usually go away when you stop taking it. In April , the FDA issued a warning on finasteride. It stated that sexual side effects could persist even after stopping the medication. Those side effects include decreased sex drive and ejaculation problems. The warning was based on about reports the FDA received over nearly 20 years.
This is not proof that finasteride was to blame, since a variety of medical conditions and prescription drugs could explain the sexual symptoms the men reported while taking finasteride. Irreversible sexual side effects from finasteride are probably rare, since millions of men have taken these medications during the time period surveyed. The significance of this finding is also debated.
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Proscar and Depression. In particular, Dr. While 0. Proscar is a medication used to treat symptoms of benign prostatic hyperplasia BPH in men with an enlarged prostate. Even if someone has in range Total Testosterone levels, a significant amount of that may be bound up by sex hormone-binding globulin SHBG , which would have otherwise been freed up if their endogenous DHT was present to liberate it into usable Free Testosterone. Even men suffering from conditions such as hypogonadism severe decrease in Testosterone production often respond well to sexual counselling.
Libido proscar. Proscar Sexual Side Effects: An Overview
According to Dr. Wolverton, the study by McClellan and Markham demonstrated that there was a slightly increased risk of sexual side effects in patients taking finasteride for male pattern baldness , including decreased libido, erectile dysfunction and ejaculation disorders, but, he adds, there are a couple of points in the article that are particularly important to the current debate about long-term side effects.
In a report from the Finasteride Male Pattern Hair Loss Study Group, a slightly higher proportion of finasteride users compared to patients on placebo reported drug-related adverse events AEs that related to sexual function, but only 11 men 1. Epstein encourages physicians who treat hair loss to be thorough in their explanation to patients in regard to the lack of definitive, consistent evidence for the risk of permanent sexual dysfunction with finasteride. The ISHRS also encourages transparency, recommending that all members discuss the risks and benefits of finasteride with patients.
The role the media plays in publicizing studies and the inability of patients to fully comprehend what the studies are saying are both factors that may relate to why the topic gained such widespread attention.
The sensitivity of the side effects and the possibility of lawsuits may have also impacted the level of attention the issue received, experts added. A study in the Journal of Sexual Medicine examined the prevalence of sexual dysfunction in patients taking finasteride. While continued difficulty having erections after discontinuing finasteride has been reported in post-marketing surveillance the incidence of this problem remains unknown. McMichael agrees this new evidence for long-term sexual side effects with finasteride has raised some intriguing — and complicated — questions.
The Bottom Line. However, the labeling changes were announced in conjunction with advice from the administration on how to counsel patients with hair loss who are considering treatment with finasteride. Information about these adverse events may be important to individual patients. Therefore, prescribers and patients need to be aware of them, as part of a discussion of risk and benefits of finasteride when determining the best treatment options.
Topic Centers. Actinic Keratosis. Hidradenitis Suppurativa. These adjustments preserve the utility of PSA to detect prostate cancer in men treated with Proscar.
If clinicians elect to use percent free PSA as an aid in the detection of prostate cancer in men undergoing finasteride therapy, no adjustment to its value appears necessary.
Women should not handle crushed or broken Proscar tablets when they are pregnant or may potentially be pregnant because of the possibility of absorption of finasteride and the subsequent potential risk to a male fetus. Proscar is not indicated for use in pediatric patients [see Use in Specific Populations 8.
Treatment with Proscar for 24 weeks to evaluate semen parameters in healthy male volunteers revealed no clinically meaningful effects on sperm concentration, mobility, morphology, or pH. These parameters remained within the normal range and were reversible upon discontinuation of therapy with an average time to return to baseline of 84 weeks.
Prior to initiating treatment with Proscar, consideration should be given to other urological conditions that may cause similar symptoms. In addition, prostate cancer and BPH may coexist. These patients may not be candidates for finasteride therapy. Proscar is generally well tolerated; adverse reactions usually have been mild and transient.
In PLESS, patients treated with Proscar and patients treated with placebo were evaluated for safety over a period of 4 years. In years of the study, there was no significant difference between treatment groups in the incidences of impotence, decreased libido and ejaculation disorder. Of these, the incidence of abnormal ejaculation in patients receiving combination therapy was comparable to the sum of the incidences of this adverse experience reported for the two monotherapies.
Combination therapy with finasteride and doxazosin was associated with no new clinical adverse experience. Three of these patients were on finasteride only and one was on combination therapy. The MTOPS Study was not specifically designed to make statistical comparisons between groups for reported adverse experiences. In addition, direct comparisons of safety data between the MTOPS study and previous studies of the single agents may not be appropriate based upon differences in patient population, dosage or dose regimen, and other procedural and study design elements.
Men received either Proscar finasteride 5 mg or placebo daily. Patients were evaluated annually with PSA and digital rectal exams. Biopsies were performed for elevated PSA, an abnormal digital rectal exam, or the end of study. The incidence of Gleason score prostate cancer was higher in men treated with finasteride 1. During the 4- to 6-year placebo- and comparator-controlled MTOPS study that enrolled men, there were 4 cases of breast cancer in men treated with finasteride but no cases in men not treated with finasteride.
During the 4-year, placebo-controlled PLESS study that enrolled men, there were 2 cases of breast cancer in placebo-treated men but no cases in men treated with finasteride. During the 7-year placebo-controlled Prostate Cancer Prevention Trial PCPT that enrolled 18, men, there was 1 case of breast cancer in men treated with finasteride, and 1 case of breast cancer in men treated with placebo.
The relationship between long-term use of finasteride and male breast neoplasia is currently unknown. There is no evidence of increased sexual adverse experiences with increased duration of treatment with Proscar. New reports of drug-related sexual adverse experiences decreased with duration of therapy.
The following additional adverse events have been reported in postmarketing experience with Proscar. Because these events are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure:.
The following additional adverse event related to sexual dysfunction that continued after discontinuation of treatment has been reported in postmarketing experience with finasteride at lower doses used to treat male pattern baldness. Because the event is reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate its frequency or establish a causal relationship to drug exposure:. No drug interactions of clinical importance have been identified.
Finasteride does not appear to affect the cytochrome Plinked drug metabolizing enzyme system. Compounds that have been tested in man have included antipyrine, digoxin, propranolol, theophylline, and warfarin and no clinically meaningful interactions were found.
Proscar is contraindicated for use in women who are or may become pregnant. In animal studies, finasteride caused abnormal development of external genitalia in male fetuses. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the male fetus. Women who are pregnant or may become pregnant should not handle crushed or broken Proscar tablets because of possible exposure of a male fetus.
In an embryo-fetal development study, pregnant rats received finasteride during the period of major organogenesis gestation days 6 to At maternal doses of oral finasteride approximately 0.
Exposure multiples were estimated using data from nonpregnant rats. Days 16 to 17 of gestation is a critical period in male fetal rats for differentiation of the external genitalia. At oral maternal doses approximately 0. Decreased anogenital distance occurred in male offspring of pregnant rats that received approximately 0. No abnormalities were observed in female offspring at any maternal dose of finasteride. No effects on fertility were seen in female offspring under these conditions.
However, this study may not have included the critical period for finasteride effects on development of male external genitalia in the rabbit. No other abnormalities were observed in male fetuses and no finasteride-related abnormalities were observed in female fetuses at any dose. Of the total number of subjects included in PLESS, and subjects were 65 and over and 75 and over, respectively. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients.
No dosage adjustment is necessary in the elderly [see Clinical Pharmacology Caution should be exercised in the administration of Proscar in those patients with liver function abnormalities, as finasteride is metabolized extensively in the liver [see Clinical Pharmacology No dosage adjustment is necessary in patients with renal impairment [see Clinical Pharmacology The empirical formula of finasteride is C 23 H 36 N 2 O 2 and its molecular weight is Its structural formula is:.
It is freely soluble in chloroform and in lower alcohol solvents, but is practically insoluble in water. DHT induces androgenic effects by binding to androgen receptors in the cell nuclei of these organs. This has been demonstrated both in vivo and in vitro. Finasteride has no affinity for the androgen receptor. In man, a single 5-mg oral dose of Proscar produces a rapid reduction in serum DHT concentration, with the maximum effect observed 8 hours after the first dose.
The suppression of DHT is maintained throughout the hour dosing interval and with continued treatment. In healthy volunteers, treatment with Proscar did not alter the response of LH and FSH to gonadotropin-releasing hormone indicating that the hypothalamic-pituitary-testicular axis was not affected. In patients with BPH, Proscar has no effect on circulating levels of cortisol, prolactin, thyroid-stimulating hormone, or thyroxine.
No clinically meaningful effect was observed on the plasma lipid profile i. These individuals have a small prostate gland throughout life and do not develop BPH. Intraprostatic content of PSA was also decreased.
Bioavailability of finasteride was not affected by food. Mean steady-state volume of distribution was 76 liters range, liters.
There is a slow accumulation phase for finasteride after multiple dosing. Finasteride has been shown to cross the blood brain barrier but does not appear to distribute preferentially to the CSF.
Finasteride is extensively metabolized in the liver, primarily via the cytochrome P 3A4 enzyme subfamily. Finasteride is not indicated for use in pediatric patients [see Warnings and Precautions 5. Finasteride is not indicated for use in women [see Contraindications 4 , Warnings and Precautions 5. No dosage adjustment is necessary in the elderly.
Although the elimination rate of finasteride is decreased in the elderly, these findings are of no clinical significance. The effect of hepatic impairment on finasteride pharmacokinetics has not been studied. Caution should be exercised in the administration of Proscar in those patients with liver function abnormalities, as finasteride is metabolized extensively in the liver.
No dosage adjustment is necessary in patients with renal impairment. In patients with chronic renal impairment, with creatinine clearances ranging from 9. Urinary excretion of metabolites was decreased in patients with renal impairment. This decrease was associated with an increase in fecal excretion of metabolites. A positive correlation between the proliferative changes in the Leydig cells and an increase in serum LH levels 2- to 3-fold above control has been demonstrated in both rodent species treated with high doses of finasteride.
These concentrations correspond to times the peak plasma levels in man given a total dose of 5 mg. No drug-related effect on testes or on mating performance has been seen in rats or rabbits. This decrease in fertility in finasteride-treated rats is secondary to its effect on accessory sex organs prostate and seminal vesicles resulting in failure to form a seminal plug.
The seminal plug is essential for normal fertility in rats and is not relevant in man. Symptoms were quantified using a score similar to the American Urological Association Symptom Score, which evaluated both obstructive symptoms impairment of size and force of stream, sensation of incomplete bladder emptying, delayed or interrupted urination and irritative symptoms nocturia, daytime frequency, need to strain or push the flow of urine by rating on a 0 to 5 scale for six symptoms and a 0 to 4 scale for one symptom, for a total possible score of Patients in PLESS had moderate to severe symptoms at baseline mean of approximately 15 points on a point scale.
See Figure 1. BPH-related urological events were defined as urological surgical intervention and acute urinary retention requiring catheterization. Compared with placebo, Proscar was associated with a significantly lower risk for acute urinary retention or the need for BPH-related surgery [ Compared with placebo, Proscar was associated with a significantly lower risk for surgery [ In the patients in PLESS who remained on therapy for the duration of the study and had evaluable urinary flow data, Proscar increased maximum urinary flow rate by 1.
There was a clear difference between treatment groups in maximum urinary flow rate in favor of Proscar by month 4 1. In patients treated with Proscar who remained on therapy, prostate volume was reduced compared with both baseline and placebo throughout the 4-year study.
Finasteride and sexual side effects
In adults, DHT acts as primary androgen in prostate and hair follicles. The only FDA-approved dermatological indication of finasteride is androgenetic alopecia. But, apprehension regarding sexual dysfunction associated with finasteride deters dermatologists from prescribing the drug and patients from taking the drug for androgenetic alopecia.
Testosterone, through its humoral endocrine and local paracrine effects is relevant in central and peripheral modulation of sexual function than locally acting DHT. Several large population-based long-term placebo-controlled studies, using International Index of Erectile Function-5 questionnaire and objective method Nocturnal Penile Tumescence to assess the erectile function have demonstrated no clear evidence of the negative effect of finasteride on erectile function. Reduction in ejaculatory volume is the only established causal relationship between finasteride and sexual dysfunction.
Though finasteride causes significant reduction in all the semen parameters except sperm morphology, they did not fall below the threshold levels to interfere with fertility. Therefore, the sexual adverse effects associated with finasteride should be viewed in relation to normal prevalence and natural history of erectile dysfunction in the population, age of the patient, other confounding factors and also nocebo effect.
The impact of finasteride on the prevention of prostate cancer has been discussed extensively. Finasteride is found to be effective in significantly reducing the incidence of low-grade prostate cancer. But the paradoxical increase in high-grade cancer in the finasteride group has been attributed to increased sensitivity and improved performance of prostate specific antigen levels to detect all grades of prostate cancer.
Androgens, otherwise known as sex hormones, are essential for the development of external genitalia, testes, and maintenance of spermatogenesis and secondary sexual characters. Testosterone and dihydrotestosterone DHT are the main biologically active forms of androgens.
Testosterone is synthesized by both gonads and adrenal glands. In the testes, testosterone is synthesized by the Leydig cells in response to stimulation by lutenizing hormone. It exists in two isoenzyme forms. Type 1 is predominant in the sebaceous glands and liver, and Type 2 is predominant in the prostate, seminal vesicles, epididymes, hair follicles and liver. The average peak plasma concentration has been found to be 9. The bioavailability of finasteride is not related to food intake.
Finasteride is extensively metabolized in the liver by Cytochrome P 3A4 enzyme subfamily and excreted both in urine and feces. The FDA-approved dermatologic indication is male pattern androgenetic alopecia. Other dermatologic uses include hirsutism, acne vulgaris, and hidradenitis suppurativa. Various adverse effects of finasteride include sexual dysfunctions; hypersensitivity reactions such as rash, pruritus, urticaria, and swelling of the lips and face; breast tenderness and enlargement; severe myopathy and testicular pain.
It is also known to have teratogenic effects in animals. To understand the impact of finasteride on sexual function, it is important to know the normal physiology of male sexual function and the role of testosterone and DHT in erectile function.
Male sexual function normally requires intact libido; the ability to achieve and maintain penile erection; ejaculation; and detumescence. Androgens, especially testosterone increases the libido. A variety of visual, olfactory, tactile, auditory and imaginative stimuli can also influence the libido. The penile erection is mainly under the control of the parasympathetic nervous system.
The nitric oxide released from the non-adrenergic, non-cholinergic autonomic fibers causes relaxation of smooth muscles in the penis, leading to increased flow and accumulation of blood in the lacunar network of corpora which are converted into non-compressible cylinders resulting in erection.
The nitric oxide is synthesized in the cavernosal tissue of penis by nitric oxide synthetase. Ejaculation and detumescence require intact sympathetic system. The integrity of structural and cellular components of the penis, and veno-occlusive mechanism is essential for normal erectile function. In animal experiments on castrated rats, the importance of testosterone in normalizing erectile function and nitric oxide synthetase activity has been demonstrated.
However, in elderly males, normal testosterone levels appear to be important for erection. DHT is a paracrine hormone exerting its action in the tissue of origin. Thus, the testosterone, through its humoral endocrine and local paracrine effects is relevant in central and peripheral modulation of sexual function than locally acting DHT.
Review of the literature on ED in men taking finasteride revealed the incidence of ED to be between 0. However, randomized controlled studies reported ED to be between 0.
Therefore, large population-based long-term placebo-controlled clinical studies using a validated questionnaire and objective method of assessment of sexual function are required to establish the causal relationship between finasteride and ED. In a study, the group informed about the sexual adverse effects of finasteride reported increased incidence of ED when compared to the group without such information.
Several placebo-controlled studies have evaluated the efficacy and side-effects of dutasteride 0. The ED has been reported to be significantly higher in the dutasteride group than in the placebo group 6.
However, by the end of two years, the prevalence of ED was similar in both the groups 1. Therefore, ED occurring during finasteride therapy should be viewed in terms of normal prevalence and natural history of ED in the population, age of the patient, other confounding factors, and also the nocebo effect.
The effect of finasteride on ejaculatory volume and other semen parameters has not been reported in detail in the literature. The ejaculatory dysfunction associated with finasteride ranges from 2. The individuals received any one of these drugs for one year and semen analysis was performed at 26 weeks and 52 weeks of treatment, and also after 24 weeks of follow- up.
The finasteride group showed statistically significant reduction in sperm count However, at 52 weeks of treatment and after 24 weeks follow-up, the reduction of all the three semen parameters from the baseline was no longer statistically significant. But there was no significant change in sperm morphology anytime during the study. However, marked sensitivity of some individuals to finasteride may result in substantial reduction in semen quality leading to infertility.
Therefore, finasteride should be considered as a possible etiological agent while evaluating men for infertility. Recovery of semen parameters towards the baseline at 52 weeks of treatment and after 24 weeks of follow-up in the presence of significant decrease in DHT levels In these patients, the prostate and seminal vesicles were atrophic with resulting low semen volume.
Thus the only causal relationship between finasteride and sexual dysfunction is low semen or ejaculatory volume. Prostate cancer is one of the common causes of cancer deaths in men. The management of prostate cancer should be focused on early detection and treatment.
The prostate epithelial cells and the stromal cells express androgen receptors and depend on androgens for growth. PCPT compared the ability of finasteride 5 mg versus placebo in reducing the risk of prostate cancer. The study reported that finasteride prevents or delays the appearance of prostate cancer, thereby decreasing the overall incidence of prostate cancer.
Significantly, it was also found that there was an increase in the incidence of high-grade prostate cancer with finasteride compared to placebo.
This may be due to the finasteride induced alteration of intraprostatic androgen levels leading to morphologic changes in low-grade tumors. Selective inhibition of low-grade tumor by finasteride may also be another explanation for the increase in high grade cancer. The analysis of the PCPT study demonstrated that finasteride significantly increased the sensitivity of PSA levels in the detection of all grades of prostate cancer when compared to placebo.
Thus increased incidence of high-grade prostate cancer in the finasteride group has been attributed to improved performance of PSA screening in detection of prostate cancer.
However, there is a concern over chronic use of finasteride and development of prostate cancer. Through its effect on hormonal estrogens vs. In many studies it has been shown that the prostatic hyperplasia and cancer develop frequently in the hormonal milieu of estrogen excess over androgens. This hormonal imbalance is normally seen in aging males. Finasteride increases the circulating levels of testosterone which is peripherally aromatized to estrogens.
Thus the use of finasteride in older males further shifts the hormonal balance towards estrogen excess. The expression of aromatase is also up-regulated in prostatic hyperplasia and cancer.
Finasteride alters the immune surveillance of cancer in aging males and may predispose them to the risk of prostate cancer. The supplementation of DHT, a non-aromatizing androgen, restores the estrogen-androgen balance by decreasing the plasma levels of estradiol and testosterone. It has been reported that DHT has a favorable effect on sexual function and the cardiovascular system without any adverse effects on prostate. Although a relationship has been established between finasteride and sexual dysfunction in the literature, the analysis of the role of androgens in male sexual function and the evidences from large population-based long-term placebo-controlled studies using validated questionnaire and objective method for assessing sexual function suggested no substantial evidence of ED in men receiving finasteride.
Low ejaculatory volume is the only causal relationship between finasteride and sexual dysfunction. Finasteride has been an effective drug in preventing low-grade prostate cancer but its role in increased incidence of high-grade prostate cancer has been attributed to better performance of PSA screening in prostate cancer detection. So, as dermatologists, we should be aware of the potential risks and benefits while treating baldness in young men with long-term finasteride.
Source of Support: Nil. Conflict of Interest: None declared. National Center for Biotechnology Information , U. J Cutan Aesthet Surg. Author information Copyright and License information Disclaimer.
Address for correspondence: Dr. Arun C. E-mail: moc. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Keywords: Finasteride, prostate cancer, sexual function. Normal male sexual function Male sexual function normally requires intact libido; the ability to achieve and maintain penile erection; ejaculation; and detumescence.
Role of androgens in erectile function The integrity of structural and cellular components of the penis, and veno-occlusive mechanism is essential for normal erectile function. Erectile dysfunction Review of the literature on ED in men taking finasteride revealed the incidence of ED to be between 0.
Ejaculatory dysfunction The effect of finasteride on ejaculatory volume and other semen parameters has not been reported in detail in the literature. Canguven O, Burnett AL. J Androl. J Clin Endocrinol Metab. J Med Sci.