Characteristics of Men Who Report Persistent Sexual Symptoms After Finasteride Use for Hair Loss
Shehzad Basaria; Ravi Jasuja; Grace Huang; Whitney Wharton; Hong Pan; Karol Pencina; Zhuoying Li; Thomas Travison; Jag Bhawan; Renaud Gonthier; Fernand Labrie; Alain Dury; Carlo Serra; Allen Papazian; Michael O'Leary; Sami Amr; Thomas Storer; Emily Stern; Shalender Bhasin
The Journal of Clinical Endocrinology & Metabolism2016
In plain terms
Researchers in Boston compared 25 men who had ongoing sexual problems after stopping finasteride for hair loss with 13 men who had taken it without such problems and 18 men who had never taken it. The men with ongoing problems had much poorer sexual function and higher depression scores. But their testosterone, DHT (a stronger form of testosterone) and other hormone levels were similar to the other groups, and no relevant gene differences were found. In brain scans of a small number of the men, activity in some areas linked to sexual arousal and mood rose or fell with how severe their symptoms were.
What it doesn’t show: It can't show that finasteride caused the symptoms or the low mood: everyone was measured once, after the fact, the groups were small, and each brain-scan task included only about 20 men.
Summary (paraphrased)
Basaria's group compared three groups of men: 25 finasteride users with persistent sexual symptoms, 13 asymptomatic finasteride users, and 18 men who never used the drug. Assessments covered hormones, body composition, cognition, and brain activity via fMRI. Men with persistent symptoms had normal testosterone and DHT and no explanatory variants in the androgen receptor or SRD5A genes, yet showed markedly worse sexual function and higher depression scores. In small fMRI subsets (6 symptomatic men in the erotic-image task, 7 per group in the emotional-word task), worse symptom scores among finasteride users correlated with activity in brain regions tied to sexual arousal and mood. The authors concluded the symptoms are unlikely to reflect simple androgen deficiency and may instead involve neurobiological changes. They suggested treatment focus on mood and sexual function rather than testosterone replacement.
Evidence
Extracted from the full text; page numbers refer to the paper. The library’s own notes are labelled as such.
- Design
- Case–control studyCase-control comparison at a single visit of three groups (symptomatic former finasteride users, asymptomatic former users, never-users): hormones, genes, skin androgen markers, body composition, sexual function, mood, cognition and functional MRI
- Setting
- Brigham and Women's Hospital, Boston, USA; enrolment June 2013 to October 2014
- Population
- Men aged 18–50. Group 1: used finasteride for hair loss for at least 7 days, none in the preceding 4 months, with erectile dysfunction (IIEF erectile function score of 25 or less) but normal blood tests and examination. Group 2: former finasteride users without sexual symptoms after stopping. Group 3: healthy men who never used finasteride. Excluded: depression before finasteride, recent androgens or related drugs, cancer, diabetes, BMI over 40.
- Size
- 56 · 25 symptomatic users, 13 asymptomatic users and 18 never-users, from 282 men screened by telephone and 132 in person. fMRI in subsets only: erotic-image task 6 symptomatic, 4 asymptomatic and 10 never-users; emotional-word task 7 per group
- Exposure
- Finasteride for hair loss, median 1.0 mg/day; median 1.7 years (IQR 0.5–6.0) in group 1 vs 1.0 (0.7–2.0) in group 2; median 3.5 vs 3.0 years since the last dose
- Compared with
- Asymptomatic former users and never-users
- Outcome
- Serum hormones by LC-MS/MS (testosterone, DHT, estradiol, glucuronide metabolites as markers of 5α-reductase activity); sequences of the AR, SRD5A1 and SRD5A2 genes; skin androgen markers; IIEF and Male Sexual Health Questionnaire; PHQ-9, Beck Depression Inventory, Hamilton Depression Scale; Positive and Negative Affect Scale; cognitive tests; body composition by DXA; fMRI during erotic images and emotional words.
- Follow-up
- None; a single assessment, a median 3.5 years after the last dose in group 1
Key results
- Total and free testosterone, DHT, LH, FSH, estradiol and SHBG did not differ among groups (P > .1) and were in the normal range for young men; the testosterone-to-DHT ratio, 3α-diol glucuronides and the ADT-G to ETIO-G ratio were also similar · p. 8; Fig. 1, p. 9
- No potentially harmful variants in the AR, SRD5A1 or SRD5A2 genes; AR CAG repeat length 22.2, 21.8 and 21.0 (P = .236) · p. 10
- IIEF composite score median 30.0 (IQR 23.0–35.0) vs 67.0 (65.0–68.0) vs 68.5 (67.0–71.0), P < .001; not related to treatment duration (r = 0.059, P = .725) or time since stopping (r = −0.215, P = .194) · p. 10
- PHQ-9 depression score median 11.0 (7.0–17.0) vs 1.0 (1.0–2.0) vs 1.0 (0–2.0), P < .001, in the moderate range for group 1; Beck and Hamilton scores also higher, more negative and less positive affect. Objective cognitive tests did not differ; memory complaints were higher (MAC-Q 20.8 vs 18.4 vs 16.9, education-adjusted overall P = .02, no significant pairwise difference) · pp. 12, 14; Table 2, p. 15
- fMRI, correlations across finasteride users in small subsets: lower IIEF scores went with more activity in the hypothalamus and thalamus and less in cingulate and other cortical areas during erotic images; higher Beck negative-attitude subscores went with more activity in the nucleus accumbens, anterior cingulate and other regions linked to depression · pp. 16–18; Fig. 4, pp. 17–18
Limitations the authors note
- Cross-sectional design, so a causal link between finasteride and the symptoms, mood changes, cognitive complaints or fMRI findings cannot be inferred
- Low mood may be coincidental, related to hair loss itself or a nocebo effect, or may contribute to the sexual dysfunction
- No control group of profoundly hypogonadal men
- Normal blood DHT does not rule out local 5α-reductase inhibition in specific brain regions
- Variation in other genes, gene expression in other tissues or brain regions, or epigenetic effects cannot be excluded
- Findings need confirmation in larger prospective studies
Also worth weighing (library’s note)
- Groups differed in race (white 88%, 61.5%, 50%; Black 4%, 15.4%, 50%; P < .001) and years of education (19.3, 19.3, 16.2; P = .03), and were recruited differently (physician referral for group 1, newspaper advertising and mailing for never-users)
- The fMRI covered only small subsets and was analysed mainly as correlations between symptom scores and brain activity across finasteride users (symptomatic and asymptomatic together), not as a direct comparison of symptomatic men with never-users
- The text says acne and androgen-responsive markers did not differ, but Table 1 shows back acne (P = .02) and haemoglobin (15.4 vs 14.9 vs 14.6 g/dL, P = .02) differing, both highest in group 1
- The asymptomatic group was small (13), and entry required only 7 days of finasteride use
- Hormones were measured in one morning fasting sample
Funding: In part the Post-Finasteride Syndrome Foundation; also Harvard Catalyst and the Center for Clinical Investigation at Brigham and Women's Hospital Interests: S. Basaria: grant support from Abbott for unrelated studies, previously consulted for Eli Lilly. S. Bhasin: research grants from AbbVie, Transition Therapeutics, Takeda and Eli Lilly for unrelated research; consultant to AbbVie, Regeneron, Novartis and Eli Lilly; financial interest in Function Promoting Therapies, LLC. Other authors nothing to disclose.
What it can support (library’s note): That men with persistent sexual symptoms after finasteride, in this sample, had normal circulating androgen levels and markers alongside poorer sexual function and depressed mood. It cannot show that finasteride caused the symptoms, it tested no treatment, and its brain-scan findings come from small subsets.
Why it’s in the corpus
Three-group cross-sectional study (symptomatic users, asymptomatic users, never-users) arguing persistent post-finasteride sexual symptoms are not explained by androgen deficiency, pointing instead to central neurobiological mechanisms. The groups differed in race and education and were recruited by different routes.
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