Trans-Specific Libido Changes During HRT and Testosterone Supplementation in Cis Women

Status: draft (compiled 2026-04-28)

The trans HRT literature is one of the cleanest natural experiments human endocrinology has on which sex steroid actually drives libido in adults, because it is the rare situation where dominant-axis hormones are deliberately swapped or suppressed in a population large enough to study prospectively. Read carefully, however, that experiment is messier than the headline. The two largest longitudinal cohorts that actually measure desire — Wierckx's ENIGI work at Ghent and Defreyne's three-year ENIGI follow-up — agree that initiating feminizing hormone therapy is followed by a short-term drop in self-reported sexual desire, that initiating masculinizing testosterone is followed by a short-term rise, and that the relationship between absolute serum testosterone or estradiol and individual desire scores is much weaker than the populist "T = libido" framing assumes. The cleanest summary line is in Defreyne 2020, which found "no correlation between sexual desire and absolute serum testosterone" inside either cohort while still showing the population-level trajectories that match the popular impression. Sources: Defreyne 2020 J Sex Med, PMID 32008926, Wierckx 2014 ENIGI short-term, PMID 24828032, Wierckx 2014 sexual desire cross-sectional, PMID 24165564. Confidence: C1 for the existence of the population-level signal in both directions, C2 for the more nuanced "no within-person correlation with absolute T" claim because it is one cohort's analysis.

The transfeminine drop is real but is best described in two different magnitudes depending on which question is being asked. In Wierckx 2014's one-year ENIGI prospective study of 53 trans women on cyproterone acetate plus estradiol valerate or transdermal estradiol, "low sex drive" emerged as a statistically significant new symptom within the first year (P ≤ 0.02 versus baseline). In the same group's larger cross-sectional Wierckx 2014 sexual desire paper, 62.4% of 214 trans women reported a decrease in desire after starting sex reassignment treatment, 73% reported never or rarely experiencing spontaneous and responsive sexual desire, and the prevalence of full DSM hypoactive sexual desire disorder reached 22%, more than four times the 5% prevalence in trans men. The Defreyne 2020 longitudinal ENIGI follow-up of 401 trans women using the Sexual Desire Inventory showed total, dyadic, and solitary SDI scores all dropping during the first three months, then partially rebounding such that by 36 months total and dyadic SDI scores were higher than baseline while solitary scores had returned to baseline. That last finding is the most interesting one for the user's "regaining feminine-style libido" question, because it is the only longitudinal SDI data point that arguably captures it. Sources: Wierckx 2014 J Sex Med 11:1999, PMID 24828032, Wierckx 2014 J Sex Med 11:107, PMID 24165564, Defreyne 2020, PMID 32008926, Defreyne 2020 ENIGI abstract PMC7207496. Confidence: C1 for the prevalence numbers and the SDI trajectory, C3 for the inference that the 36-month rebound represents a "feminine-style" reorganization rather than partial habituation or relationship-status confounding.

The decomposition of this drop into "spontaneous" versus "receptive" components is more often invoked than measured, but two pieces of evidence support it. The Wierckx 2014 cross-sectional paper reports that 73% of trans women never or rarely experience spontaneous and responsive sexual desire, framing the symptom as disappearing autochthonous urges rather than disappearing receptivity. The AUA 2025 abstract on erection function in trans women on HRT and after orchiectomy found that "neither GAHT nor GABO significantly reduced erections caused by sexual arousal or physical stimulation" while orchiectomy further suppressed spontaneous erections. Mechanistically, that loss of T-driven nocturnal and morning tumescence is independent of the cortical pathway used during partnered or stimulus-elicited arousal. The clinical pattern is: spontaneous, intrusive, T-driven urges drop fast and hard; stimulus-elicited arousal is preserved more often than people expect; subjective desire is more dependent on context, mood, body satisfaction, and relationship variables than on absolute hormone levels. Sources: Wierckx 2014 PMID 24165564, AUA 2025 erection-function abstract. Confidence: C2.

The transmasculine surge is the cleanest part of the natural experiment and also the one most often overstated. Wierckx 2014's one-year ENIGI study of 53 trans men on quarterly testosterone undecanoate found a statistically significant rise in sexual desire (P ≤ 0.01) that emerged within weeks, alongside the expected clitoral pain and voice changes. The Wierckx 2014 cross-sectional paper found 71.0% of 138 trans men reporting an increase in sexual desire after starting hormones; HSDD prevalence in trans men was 5%. Defreyne 2020's longitudinal ENIGI showed total, dyadic, and solitary SDI all rising sharply over the first three months and then plateauing, which already complicates the "relentless surge" framing. By 36 months, total and dyadic SDI in trans men were comparable to baseline; only solitary desire scores remained elevated above baseline. That is consistent with both physiological tachyphylaxis and partner-context regression to the mean, and it is the kind of detail that the popular "T turns the libido knob to eleven" account misses. The Wierckx 2011 single-center cross-sectional follow-up of 45 trans men post-SRS reported 73.9% endorsing increased desire retrospectively, but found no direct correlation between absolute testosterone and dyadic or solitary desire scores; instead, elevated LH (a marker of suboptimal androgen replacement) predicted lower solitary desire (P=0.007). The right reading is that trans men reliably move into a higher-desire range when androgenized, but absolute serum T inside the typical replacement window does not titrate desire in a 1:1 way. There are even published case reports of trans men needing to stop or reduce testosterone because of disruptively high libido. Sources: Wierckx 2014 PMID 24828032, Wierckx 2014 PMID 24165564, Defreyne 2020 PMID 32008926, Wierckx 2011 Eur J Endocrinol 165:331, PMID 21602316, EPATH "Too much sexual desire" trans man case study. Confidence: C1 for the population direction, C2 for the absence of within-person T-libido titration.

The "regaining a more feminine-style libido on long-term estrogen" claim is the part of the user's framing that is most defensible from a population-level reading but most poorly characterized at the individual level. The Defreyne 2020 ENIGI finding that trans women's total and dyadic SDI scores at 36 months exceeded their pre-HRT baseline, while solitary scores returned to baseline, is the only solid prospective longitudinal evidence for a partial rebound in self-reported desire after the initial drop. Defreyne and colleagues' explicit phrasing in the abstract is that "over a longer period of time, other factors contribute to sexual desire, which results in a net increase in sexual desire in transgender women receiving feminizing hormone therapy." That said, the study cannot disentangle hormone-mediated reorganization of arousal pathways from confounders that systematically improve over the same horizon, including transition-related body satisfaction, relationship acquisition, mental-health improvement, escape from pre-transition gender dysphoria, and the simple fact that respondents who stay in a long-term cohort tend to be doing better than those lost to follow-up. The Nikkelen and Kreukels 2018 cross-sectional Dutch survey of 325 transfeminine and 251 transmasculine respondents reaches the same general conclusion from the other direction: body satisfaction explains a larger share of variance in sexual feelings than hormonal status does, particularly for trans women. The honest summary is that the rebound pattern is real in aggregate but should not be presented as a confirmed neuroendocrine reorganization toward a "cis-female-style" arousal architecture. Sources: Defreyne 2020 PMID 32008926, Nikkelen & Kreukels 2018 J Sex Marital Ther 44:370, Kerckhof 2019 J Sex Med 16:2018, PMID 31668732. Confidence: C2 for the population-level rebound, C4 for any stronger neuroendocrine claim about a "feminine pattern."

Community lore on r/asktransgender, r/MtF, and r/transtimelines treats the rebound as common knowledge: libido "comes back differently after a year or two on E," shifts from constant pressure to something one has to invite, becomes more about being touched than about chasing release. The SDI is a frequency-and-intensity instrument and does not capture that qualitative shift, which is part of why community lore and the longitudinal literature appear to disagree without actually contradicting each other. Treat the qualitative restructuring claim as C4 self-report convergence and the SDI U-shape as C2. Sources: Defreyne 2020 PMID 32008926, TransfeminineScience progestogens review. Confidence: C4 for the qualitative restructuring, C2 for the SDI U-shape.

The cis-female testosterone-supplementation story sits beside this naturally because it tests what happens when androgen levels are deliberately moved into the upper female range or just above it. The most rigorous synthesis is the Islam et al. 2019 Lancet Diabetes & Endocrinology individual-trial-data meta-analysis covering 36 RCTs and 8480 participants, which found that testosterone increased the frequency of satisfying sexual events by a mean of 0.85 per month (95% CI 0.52-1.18) and improved sexual desire by a standardized mean difference of 0.36 (95% CI 0.22-0.50) versus placebo, with no serious adverse events recorded across the trials. Achilli 2017's earlier meta-analysis of seven trials and 3035 mostly postmenopausal participants reached the same direction: short-term improvement in sexual function with transdermal testosterone, no serious adverse events, increased androgenic events such as acne and hirsutism. Both reviews converge on a "real but modest" effect — about one extra satisfying sexual event per month above placebo — which is exactly the magnitude reported in the original APHRODITE (Davis 2008 NEJM) and INTIMATE (Shifren 2006) Phase III trials of the 300 µg/day testosterone patch in surgically and naturally menopausal women. That magnitude is meaningful at the public-health level but is not the libido transformation that consumer marketing implies. Sources: Islam 2019 Lancet Diabetes Endocrinol 7:754, PMID 31353194, Achilli 2017 Fertil Steril 107:475, PMID 27916205, Davis 2008 NEJM 359:2005 (APHRODITE), Shifren 2006 INTIMATE NM1 Menopause 13:770, PMID 16932240. Confidence: C1.

The Davis 2019 Global Consensus Position Statement endorsed by the Endocrine Society, IMS, NAMS, ISSWSH, and a dozen other bodies is the cleanest current synthesis of what testosterone should and should not be used for in cisgender women. Its conclusions are deliberately narrow: the only evidence-based indication is HSDD; the recommendation applies to postmenopausal women; the target is to "approximate physiological testosterone concentrations for premenopausal women" rather than to push above that range; injectables, pellets, and supraphysiologic regimens are explicitly not recommended; "there are insufficient data to make any recommendations regarding the use of testosterone in premenopausal women for treatment of sexual function or any other outcome." That last sentence matters because it is exactly the indication for which testosterone is most often hyped in functional-medicine and online wellness markets. The 2021 ISSWSH Clinical Practice Guideline (Parish 2021) adds a more practical layer: dose to keep total testosterone in the physiological premenopausal range — quoted as roughly 27-58 ng/dL depending on age decade — using either off-label male transdermal gel at one-tenth of a sachet daily or, where available, the Australian-licensed AndroFeme 1% cream at 0.5 mL daily (5 mg starting dose, titratable to 10 mg). The "upper female range, no masculinization" target the user describes is therefore a real clinical aim, just one that the consensus literature treats as approximately total T 30-70 ng/dL (≈1.0-2.4 nmol/L) rather than the much higher numbers some compounding practices use. Sources: Davis 2019 Global Consensus Position Statement, PMID 31488288, PMC6821450, Parish 2021 ISSWSH CPG, PMC8064950, AndroFeme 1 TGA registration / Lawley Pharmaceuticals. Confidence: C1 for the consensus framing, C2 for the precise numerical "upper female" target because the consensus deliberately resists publishing one specific cutoff.

The FDA story is one of regulatory caution, advisory-committee-driven safety conservatism, and trial design problems rather than a clean "the drug failed." Procter & Gamble's Intrinsa 300 µg/day testosterone patch went to the FDA's Reproductive Health Drugs Advisory Committee in December 2004 with a narrow indication for surgically menopausal women on concurrent estrogen who had developed HSDD; the committee voted overwhelmingly that long-term cardiovascular and breast safety data were insufficient and recommended against approval, despite agreeing the patch was efficacious. The same product was approved in Europe in July 2006, then withdrawn from the EU market in 2012 after Warner Chilcott declined to expand the indication for commercial reasons. BioSante's LibiGel testosterone gel ran into a different problem in its 2011 Phase III: an unexpectedly high placebo response made the active arm fail on the primary efficacy endpoint, even though a pre-specified cardiovascular safety study (the LibiGel CV study with 3656 high-risk women) showed no signal of harm. Bremelanotide / PT-141, finally approved in 2019 for premenopausal HSDD, took a non-hormonal route around the same regulatory landscape. The honest causal story is that the FDA's stance reflects a mixture of unresolved cardiovascular and breast cancer safety questions inherited from the Women's Health Initiative era, advisory-committee preference for stronger long-term data than two-year trials provide, sponsor unwillingness to fund the multi-thousand-patient cardiovascular outcomes trials needed to settle those questions definitively, and the political optics of approving a "female libido drug" on weaker safety data than the FDA used to approve men's testosterone. Marketing politics is a real factor but is not, by itself, the explanation. Sources: FDA briefing document Intrinsa 2004, White 2012 Am J Cardiol LibiGel CV study, PMID 22172433, EMA Intrinsa withdrawal page, Kingsberg 2019 J Womens Health bremelanotide, PMC6819021. Confidence: C2 for the integrated regulatory narrative, C1 for the individual events.

Cardiovascular safety at supraphysiological doses is the legitimate end of the FDA's caution and is also where most "T for women, no downside" sales talk falls apart. Islam 2019's meta-analysis specifically flagged that oral testosterone — but not transdermal — produced a significant rise in LDL-cholesterol and reductions in total cholesterol, HDL-cholesterol, and triglycerides; the consensus and ISSWSH guidelines therefore recommend non-oral routes only. None of the placebo-controlled trials in the meta-analysis were long or large enough to detect rare cardiovascular events at the population level, which is exactly the gap the FDA flagged in 2004 and which ISSWSH 2021 still describes as "limited and inconclusive." Pellet implants and intramuscular injections used in some US compounding-clinic practices routinely produce supraphysiological serum T (often >150 ng/dL trough, with peaks substantially higher), well above the consensus target, and these regimens have not been shown safe or effective for HSDD. Sources: Islam 2019 PMID 31353194, Davis 2019 Global Consensus PMC6821450, Parish 2021 ISSWSH CPG PMC8064950. Confidence: C1 for the lipid signal and consensus warning, C2 for the practical observation that pellet/IM clinics routinely overshoot.

DHEA as an alternative to direct testosterone is best understood through Labrie's intracrinology framework, in which adrenal DHEA is converted intracellularly to active androgens and estrogens at the tissue site of action. Vaginal DHEA (prasterone, sold as Intrarosa) at 6.5 mg daily has good evidence for moderate-to-severe dyspareunia and vulvovaginal atrophy and was FDA-approved in 2016 on that indication. Oral DHEA for systemic libido enhancement is a much weaker proposition: most randomized trials in postmenopausal women without adrenal insufficiency have not shown reliable improvements in sexual function, and ISSWSH and the Global Consensus do not recommend it as a primary HSDD treatment. The fact that vaginal but not oral DHEA works mainly tells us that the local androgen-and-estrogen tissue effect on genital atrophy is real, not that DHEA is a hidden libido lever. Sources: Labrie 2017 J Steroid Biochem Mol Biol intracrinology, PMID 28098598, Labrie 2018 Climacteric PMID 30130283, Cleveland Clinic Journal of Medicine androgen review. Confidence: C2.

Within trans care, the choice of androgen blocker is itself a libido variable that is often underplayed. Cyproterone acetate is a strong progestogen with both antiandrogen and antigonadotropic effects; in the Burinkul 2021 RCT comparing CPA 25 mg/day to spironolactone 100 mg/day in trans women, CPA achieved female-range total testosterone (<50 ng/dL) in 90% versus 19% on spironolactone, which means the typical CPA-based regimen drives more profound androgen suppression and is more likely to produce the deepest end of the libido drop. Cyproterone is also explicitly antilibidinal at higher doses and has been used for that purpose in cis men with paraphilic disorders. Spironolactone, even at 100-200 mg/day, often leaves total T at 100-200 ng/dL while still producing some receptor blockade, which correlates with milder reported drops in subjective desire among community accounts. Bicalutamide is a peripheral androgen receptor antagonist that does not lower androgen levels (and may actually raise total T modestly via feedback), and is therefore the antiandrogen with the lowest expected effect on libido and erectile function — although the trans-specific clinical evidence base for bicalutamide is small, mostly case series and adolescent cohort reports. GnRH agonists such as triptorelin and leuprolide produce near-complete pituitary-gonadal axis shutdown after the initial flare and are functionally analogous to medical orchiectomy, with the deepest libido suppression of any reversible regimen. Orchiectomy itself is the irreversible endpoint of that axis: post-orchiectomy trans women routinely report further reductions in spontaneous erections and morning tumescence, with preserved partner-elicited arousal in most. The clinical implication for the user's framing is that "trans HRT lowers libido" is not a single hormone exposure; it is a family of exposures with very different completeness of androgen suppression, and the deepest drops are seen with the combinations that suppress the HPG axis most thoroughly (CPA, GnRH agonists, post-orchiectomy). Sources: Burinkul 2021 J Sex Med 18:1299, PMID 34274044, Angus 2021 ENIGI lowest effective dose CPA, PMC8571811, Neyman 2019 bicalutamide adolescents PMC6431559, TransfeminineScience bicalutamide adoption review, AUA 2025 / Smith J Sex Med 21 Supp 5 erection function abstract. Confidence: C2.

Estradiol level is its own modulator. At physiological female-range levels (roughly 100-200 pg/mL trough on most modern transfeminine regimens) estradiol does much of the work of suppressing the gonadotropic axis, lowering testosterone, and producing the expected feminization. At supraphysiological levels (>300-400 pg/mL chronically, common with high-dose injection regimens) several mechanisms converge to deepen the libido suppression: strong gonadotropin suppression drives endogenous T even lower, hepatic SHBG production rises (especially with oral routes), reducing free testosterone further; and in some patients high estradiol itself appears to produce a sedating or mood-flattening effect that overlaps with low desire. Defreyne 2020 did not find an absolute-level estradiol-desire correlation, which is consistent with the broader pattern that population-level effects are real while within-person hormone-desire titration is weak. The takeaway is that some patients reporting persistent low desire on transfem HRT are over-suppressed, not under-suppressed, and dose reduction toward the physiological female range can sometimes rescue desire without reversing feminization. Sources: Defreyne 2020 PMID 32008926, Madsen 2024 review of E2 regimens in transgender adults, Endocr Pract, TransfeminineScience SHBG and transfeminine HRT review. Confidence: C2-C3.

The progesterone-for-trans-women hypothesis advanced by Jerilynn Prior in her widely circulated 2019 J Clin Endocrinol Metab editorial argued that adding oral micronized progesterone would improve breast development, mood, and possibly libido by completing the analogy to cis-female endogenous hormone exposure. The empirical evidence has not supported the libido part. The 2023 randomized trial of progesterone added to feminizing HRT (NCT04102449 reporting in JAPhA) found no statistically significant difference in patient-reported libido satisfaction between standard GAHT and GAHT plus progesterone arms. A retrospective 2024 cohort similarly found no discernable difference in libido satisfaction. TransfeminineScience's careful aggregate review reaches the same conclusion: progesterone, in cisgender women, in non-human primate models, and in the limited transfeminine evidence base, has shown either no effect or a mild inhibitory effect on sexual desire — the luteal-phase progesterone surge in cis women is itself associated with reduced desire. High-dose synthetic progestins such as cyproterone and medroxyprogesterone are used clinically to suppress libido. The honest reading is that the popular "progesterone might restore libido on E" claim is community optimism extrapolated from breast-development reports, not an evidence-supported intervention for desire. Sources: Prior 2019 JCEM 104:1181 editorial, Patel 2023 JAPhA progesterone GAHT trial, TransfeminineScience progestogens-and-sexual-desire review, Aly 2023 progesterone in transgender hormone therapy review PMC10558402. Confidence: C2.

Tucking is sometimes invoked as an additional androgen-suppressing factor — the claim that chronic testicular compression and elevated scrotal temperature partly shut down Leydig output. The mechanistic case is weaker than the spermatogenic case: heat-and-pressure damage to seminiferous tubules and spermatogonia is well documented, but Leydig cells are more thermotolerant and respond primarily to LH rather than local heat. The available trans-specific data document strong sperm-parameter effects but only weak associations with serum testosterone, and the studies are small and confounded by concurrent feminizing hormones. The "tucking suppresses libido independently of HRT" claim is therefore C4. Sources: Schneider 2017 Andrology, PMID 28914501, Yaish 2021 cryptozoospermia tucking case PMC8058914. Confidence: C4.

The post-vaginoplasty libido pattern has its own subliterature. Across modern series, 70-90% of trans women report orgasmic capacity within 6-12 months of penile-inversion or peritoneal vaginoplasty; FSFI scores remain lower than cis-female norms but improve over one to two years post-op. The Kerckhof 2019 ENIGI follow-up of 518 trans persons at 4-6 years found 26% of trans women citing difficulty initiating sexual contact and 29% citing difficulty achieving orgasm as their primary ongoing concerns; these issues persist across treatment groups including post-surgical, arguing against a model in which surgery alone is the libido-recovery lever. Surgery resolves erection-versus-vulva dysphoric mismatch but the desire trajectory tracks time on hormones, body satisfaction, partner relationships, and mental health more than surgical milestone. Sources: Kerckhof 2019 PMID 31668732, Kloer 2021 Andrology vaginoplasty review. Confidence: C2.

Pharmacologic libido rescue inside trans care has three main routes, none of which has high-grade trans-specific evidence. PDE5 inhibitors (sildenafil, tadalafil) are commonly used by trans women who want to maintain erectile function pre-vaginoplasty and can preserve responsive erections in the absence of meaningful spontaneous tumescence; they do not raise testosterone or reverse libido suppression and should be understood as performance medications rather than desire medications. Bremelanotide / PT-141 acts centrally on melanocortin receptors and is FDA-approved for HSDD in cis premenopausal women; community reports and a small case-series literature describe off-label use in trans women with persistent low desire post-HRT, with mixed effect and a meaningful nausea side-effect rate. Low-dose testosterone supplementation in trans women with persistent HSDD is the most theoretically obvious move and the most clinically contentious, because the entire feminizing pathway suppresses T deliberately. The Nolan 2021 management-of-HSDD-in-trans-women guide flags transdermal T as potentially useful but cautions against virilization risk and notes the absence of dose-response data in this population. The honest summary is that all three approaches lack the controlled trial base they would need to be recommended generally; PDE5 use is well-tolerated and reasonable; PT-141 and low-dose T should be considered off-label, individualized, and properly monitored. Sources: Nolan 2021 Int J Impot Res HSDD in trans women, PMID 33558671, Kingsberg 2019 J Womens Health bremelanotide RECONNECT, PMC6819021, UCSF Transgender Care feminizing HT overview. Confidence: C2-C3.

The user's broader framing — that the trans experience reveals which hormone is doing the work for libido — is useful but should be sharpened. The trans natural experiment shows that population-level desire moves predictably with the direction of androgen change: suppress testosterone in adults assigned male at birth and average desire drops in the short term; raise testosterone in adults assigned female at birth and average desire rises. That is consistent with sixty years of androgen-and-libido literature in cis populations of both sexes. What the same data also show is that the within-person, dose-response part of the story is much weaker than the population direction implies. Defreyne 2020 reported no correlation between absolute serum testosterone and SDI scores in either trans cohort; Wierckx 2011 found no T-desire correlation in trans men but did find an LH-desire correlation, suggesting that adequacy of replacement matters more than absolute level; the cis-female testosterone trials show only a modest one-extra-event-per-month effect at a target physiological range. The cleaner statement is: testosterone is necessary for typical adult desire in both sexes within reasonable limits, but it is not sufficient, and it does not titrate desire in a clean dose-response way once a person is in their replacement window. Estrogen does not appear to be doing nothing, but the trans-women rebound suggests its contribution is more about long-horizon arousal architecture than acute drive. The trans data are the right natural experiment to invoke; they just say something more interesting than "T is the libido hormone." Sources: Defreyne 2020 PMID 32008926, Wierckx 2011 PMID 21602316, Islam 2019 PMID 31353194, Davis 2019 Global Consensus PMC6821450. Confidence: C1 for the population-direction claim, C2 for the qualifications.

Verdict

Claim 1: Transfeminine people often experience a HUGE drop in libido after lowering testosterone levels. KIND-OF-TRUE. The drop is real, prospective, and statistically robust. "Huge" is justified for spontaneous T-driven urges (morning erections, intrusive sexual ideation) and for the deeply suppressed combinations (CPA-based regimens, GnRH agonists, post-orchiectomy). It is overstated for partner-elicited arousal, for long-horizon dyadic desire (which actually exceeds baseline at 36 months in the ENIGI cohort), and for any single hormone-level threshold. Roughly 22% develop full HSDD versus 5% in trans men — meaningful but not universal. Sources: Wierckx 2014 PMID 24165564, Defreyne 2020 PMID 32008926. Confidence: C1 for the directional claim, C2 for the magnitude qualification.

Claim 2: Transmasculine people often experience a HUGE surge upon raising testosterone levels. TRUE, with one important nuance. The surge is reproducible across Wierckx 2014 (P ≤ 0.01), Wierckx 2011 (73.9%), Defreyne 2020 (sharp rise in first three months), and clinical case literature of trans men needing to reduce T because desire is disruptively high. The nuance is that by 36 months total/dyadic SDI scores have regressed to baseline; only solitary desire stays elevated. So "surge" is correct for the first months to year, more like "stable elevation versus pre-T baseline" in the longer term. Sources: Wierckx 2014 PMID 24828032, Wierckx 2011 PMID 21602316, Defreyne 2020 PMID 32008926. Confidence: C1.

Claim 3: Some transfem people regain a more "feminine-style" libido after long-term feminine hormone levels — others do not. KIND-OF-TRUE. The "regain" piece is supported by the Defreyne 2020 SDI U-shape (total/dyadic > baseline at 36 months). The "feminine-style" qualitative piece (more receptive, less spontaneous, more context-dependent) is consistent across community lore and a few qualitative studies but has not been operationalized in a primary endocrine study. The "others do not" part is also supported: 22% HSDD prevalence in Wierckx 2014, persistent low desire even years post-surgery in Kerckhof 2019. Treat the rebound as real at the population level (C2) and the qualitative restructuring as community-aligned but not yet pinned down (C4). Sources: Defreyne 2020 PMID 32008926, Kerckhof 2019 PMID 31668732, Nikkelen & Kreukels 2018. Confidence: C2-C4.

Claim 4: Some women supplement testosterone to upper female range for higher libido without masculinization. KIND-OF-TRUE. Yes, this is the explicit aim of the Davis 2019 Global Consensus and Parish 2021 ISSWSH guidelines, and Australia's AndroFeme 1% cream is licensed for exactly that indication (5-10 mg/day, 0.5-1.0 mL). The effect size is modest — about one extra satisfying sexual event per month above placebo (Islam 2019, Davis 2008, Shifren 2006). The "without masculinization" caveat is honest only at carefully titrated transdermal physiological-range dosing; meta-analyses still show acne and hirsutism increases versus placebo, and pellet/IM/oral regimens reliably push above the consensus range. Evidence is good for postmenopausal women and explicitly insufficient in premenopausal women per the consensus. The FDA has not approved any T product for women in the US; AndroFeme is Australia-only. Sources: Davis 2019 PMC6821450, Parish 2021 PMC8064950, Islam 2019 PMID 31353194, Achilli 2017 PMID 27916205. Confidence: C1 for the existence of the practice and the modest effect, C2 for the "without masculinization" framing because the evidence shows clear if minor androgenic side effects.

Claim 5: The trans experience reveals which hormone is doing the work for libido and is a useful natural experiment. KIND-OF-TRUE / USEFUL-BUT-OVERSIMPLIFIED. The trans experiment is genuinely informative: it confirms population-level androgen direction, it confirms that estrogen elevation in adult males does not substitute for the lost androgen drive in the short term, and it confirms that the cis-female baseline of low circulating T is compatible with active desire when the rest of the system has had time to reorganize. What it does not show is a clean hormone-by-hormone titration, because Defreyne 2020 explicitly reports no within-person correlation between absolute T and SDI scores in either cohort, and Wierckx 2011 reports the same in post-SRS trans men. The natural experiment is real, but its lesson is that desire is androgen-anchored at the population level and only loosely hormone-titrated at the individual level — it is not "T is the libido knob." Sources: Defreyne 2020 PMID 32008926, Wierckx 2011 PMID 21602316, Islam 2019 PMID 31353194. Confidence: C2.