Progestins, Natural Progesterone, and Libido

Status: draft (compiled 2026-04-28)

The casual claim that "progestins lower libido" is true on average and false in detail, and the way it is wrong matters. "Progestin" is a regulatory and pharmacological category, not a single molecule. It picks out any synthetic compound that activates the progesterone receptor with enough fidelity to imitate progesterone's endometrial effect, but the scaffolds used to get there were assembled from very different parent steroids, each dragging its own affinities for the androgen, glucocorticoid, mineralocorticoid, and estrogen receptors. The accepted classification, summarized in García-Sáenz et al. 2023, J Clin Med, doi:10.3390/jcm12103388, splits progestins into progesterone-related compounds (pregnanes — MPA, megestrol, chlormadinone, cyproterone, dydrogesterone — plus norpregnanes such as nomegestrol acetate and trimegestone), testosterone-related compounds (estranes such as norethisterone, gonanes such as levonorgestrel, desogestrel, gestodene, etonogestrel, norgestimate, and the hybrid dienogest), and the spironolactone-derived drospirenone. Lumping every member under one libido prediction is like predicting how much a "diuretic" lowers blood pressure without specifying loop versus thiazide versus MR antagonist. Sources: García-Sáenz 2023, PMC10218893, Schindler 2003, Maturitas, PMID 14670641, Stanczyk 2003 review, PMID 12600226. Confidence: C1 for class existence, C2 for receptor-affinity tables because animal binding data do not always translate cleanly to humans.

The four off-target activities that drive the divergence are (i) residual AR androgenic activity, retained in graded amounts by the older 19-nortestosterone progestins (norethisterone, levonorgestrel, then weakly desogestrel/gestodene/norgestimate); (ii) outright AR antagonism, concentrated in cyproterone acetate, chlormadinone acetate, dienogest, and more mildly drospirenone; (iii) glucocorticoid agonism, possessed by MPA and CPA and contributing to their cushingoid side-effect histories at higher doses; and (iv) mineralocorticoid receptor antagonism, essentially unique to drospirenone and responsible for its spironolactone-like profile. Oelkers 2004, Mol Cell Endocrinol, PMID 15134826 describes drospirenone as the synthetic progestin closest to natural progesterone in pharmacodynamic profile because it shares the antimineralocorticoid behavior the 19-nortestosterone progestins lack. Nomegestrol acetate is a 19-norprogesterone derivative deliberately engineered for high PR selectivity with negligible AR/ER/GR/MR activity — the opposite design philosophy from levonorgestrel — marketed in modern combined pills such as Zoely. "Progestins" do not have a single libido coefficient because they do not have a single hormonal fingerprint. Sources: Oelkers 2004, PMID 15134826, Sitruk-Ware 2008, PMID 12600226, Ruan & Mueck 2012, PMID 22364709. Confidence: C1-C2.

The specific question the user asked — "do progestins lower libido by lowering testosterone?" — has a more precise answer than the popular literature usually concedes: in the highest-dose clinical settings, the bulk of the libido suppression comes from HPG-axis collapse and the resulting hypogonadal testosterone, but at contraceptive doses the picture is murkier, and at least one key animal experiment shows that medroxyprogesterone acetate suppresses sexual behavior even when systemic testosterone is held in the normal range. Michael & Zumpe 1993, Physiol Behav, doi:10.1016/0031-9384(93)90189-m, PMID 8511186 gave castrated cynomolgus monkeys subcutaneous testosterone implants to maintain plasma T in the upper-normal intact-male range, then added 40 mg/week intramuscular MPA in six animals and vehicle in two. By weeks 5–6 the MPA-treated monkeys were ejaculating and mounting significantly less, despite physiologically normal androgen exposure. The authors concluded that MPA acts on hypothalamic and preoptic mechanisms directly, not only through testosterone depletion. That is a small primate study, but it is the cleanest experimental dissociation in the literature, and it is one of the reasons forensic-psychiatric clinicians describe MPA's antilibidinal effect as having both a "subtractive" component (less circulating androgen) and a "central" component (direct CNS action through PR/AR-expressing hypothalamic neurons). Sources: Michael & Zumpe 1993, PMID 8511186. Confidence: C2.

In humans, the dose-response for HPG suppression is well characterized for MPA and CPA. Oral MPA suppresses serum testosterone by ~30% at 20 mg/day, 45–75% at 60 mg/day, and 70–75% at 100 mg/day; intramuscular depot MPA at 150 mg pushes T into the castrate range (<58 ng/dL) within a week and holds it for three months, with forensic dosing reaching 400–500 mg IM weekly to drive T below 100 ng/dL. The clinical literature is unambiguous about the consequence: paraphilic urges, masturbation frequency, fantasy intensity, and sexual responsiveness all drop in tandem. CPA compresses the same outcome into a smaller dose because it adds direct AR antagonism on top of gonadotropin suppression. The ENIGI study, Kuijpers et al. 2021, JCEM, PMID 34125226 followed 882 trans women across 0, 10, 25, 50, and 100 mg daily and found median total T of ~0.9 nmol/L from 10 mg upward, indistinguishable from higher rungs — CPA is maximally suppressive at 10 mg/day in trans-feminine HRT, with anything above adding side-effect burden but not extra T reduction. Higher oncologic/forensic doses (50–300 mg/day) push the AR-blockade contribution to the foreground. The user's instinct that "lowering testosterone" is the dominant pathway is broadly correct for high-dose progestin antilibidinal therapy. Sources: MPA pharmacology summary, ENIGI Kuijpers 2021, PMC8571811, Sauter et al. 2021, PMC8072038, WFSBP summary, PMID 29289377. Confidence: C1 for dose-response numbers, C2 for HPG-vs-central weighting.

That high-dose picture, however, is not the picture that applies to ordinary combined oral contraceptive (COC) users, where the libido story is more equivocal and the mechanism is partly ethinylestradiol's, not the progestin's. EE induces hepatic SHBG production in a dose-dependent way, which lowers free testosterone disproportionately to total testosterone — the meta-analytic estimate from Zimmerman et al. 2014, Hum Reprod Update, PMID 24082040 (PMC3845679) is that COCs reduce total T modestly, free T more steeply, and SHBG roughly two- to fourfold. This is the route through which COCs that are not particularly antiandrogenic still pull "androgen-dependent" symptoms (libido, lubrication, mood, body composition) into the discussion. The classic forensic worry, articulated in older Goldstein-group work, is that this SHBG elevation may persist for months after pill discontinuation in some users, plausibly producing a subset who experience genuine sustained low-androgen symptoms. The contemporary view is more measured: most users do not report libido decline, but a real minority does, and SHBG elevation is the single most consistent biochemical marker of risk. Sources: Zimmerman et al. 2014, PMC3845679, Panzer et al. 2006, J Sex Med, summary in Pastor 2013. Confidence: C2.

The best survey of the broader COC-libido literature remains Pastor, Holla & Chmel 2013, Eur J Contracept Reprod Health Care, doi:10.3109/13625187.2012.728643, PMID 23320933. They synthesized 36 studies covering 13,673 women, including 8,422 COC users specifically, and reported that 85% of COC users experienced increased or unchanged libido and 15% experienced a decrease. They also noted that the only formulation that consistently emerged as more libido-suppressive was the very low-dose 15 µg ethinylestradiol pill, plausibly because the relatively higher progestin-to-estrogen ratio worsens the SHBG/free-T outcome. The Pastor review is the right citation to attach to any sweeping claim that "the pill kills libido": at the population level, the most defensible statement is that COCs do not reliably lower libido in most users, but they reliably lower free testosterone and reliably produce a noticeable minority who report sexual-desire problems. Sources: Pastor et al. 2013, PMID 23320933, Casado-Espada et al. 2019, J Clin Med, PMID 31242625 for a more recent overview of the same conclusion. Confidence: C1 for Pastor's headline numbers, C2 for the mechanistic interpretation.

The cleanest randomized evidence on a specific COC formulation is Zethraeus, Dreber, Ranehill, … Hirschberg 2017, J Clin Endocrinol Metab, doi:10.1210/jc.2016-2032, PMID 27525531, a double-blind, placebo-controlled trial of 340 women aged 18–35 randomized to 30 µg ethinylestradiol/150 µg levonorgestrel or placebo for three months. The pill produced no detectable effect on the global Profile of Female Sexual Function score, but the desire, arousal, and pleasure subscales each fell significantly versus placebo. Levonorgestrel is one of the more androgenic progestins, so this trial is particularly damaging to a "more androgenicity should rescue libido" narrative; on net, even an androgenic-leaning COC depressed three sexual-function domains in healthy young women. That is methodologically important because it is one of the only RCTs in this entire literature that randomized hormone-naïve women, used a validated multidomain instrument, and detected a real signal. The signal is small, but it is real. Sources: Zethraeus et al. 2017, PMID 27525531. Confidence: C1.

Direct comparisons among progestins are scarcer and noisier. Oranratanaphan & Taneepanichskul 2006, J Med Assoc Thai, PMID 17726807 randomized women to drospirenone- or gestodene-containing COCs and found no detectable difference in libido and no decrement on either arm, which is consistent with drospirenone's milder antiandrogenic profile and gestodene's mild androgenicity roughly cancelling at low contraceptive doses. Other small trials have produced inconsistent results, and at least one observational study reported lower desire and arousal subscale scores on a drospirenone-containing COC after three months. The honest reading is that no progestin's libido profile in COC has been shown to be reliably superior to another's in head-to-head RCTs of adequate power, although high-androgenicity older 19-nortestosterone formulations are not, on the available data, more libido-protective than the supposedly "antiandrogenic" newer ones. The androgenic-progestin "rescue" hypothesis sounds plausible mechanistically and is not supported by the trial evidence. Sources: Oranratanaphan & Taneepanichskul 2006, PMID 17726807, Caruso et al. 2005 drospirenone observational study, overview in Casado-Espada 2019, PMID 31242625. Confidence: C2-C3.

Long-acting and progestin-only methods, which strip out the ethinylestradiol confound, isolate the progestin's contribution more cleanly, and the signal there is real. The Boozalis, Tutlam, Robbins & Peipert 2016, Obstet Gynecol, doi:10.1097/AOG.0000000000001286, PMID 26855094 cross-sectional analysis of 1,938 Contraceptive CHOICE Project participants found that 37.3% of DMPA users reported lack of interest in sex at six months, compared with 18.3% of copper-IUD users (adjusted OR 2.61), with the etonogestrel implant (28.6%, aOR 1.60) and the etonogestrel-releasing ring (27.6%, aOR 2.53) elevated as well, while combined oral contraceptive pills, the levonorgestrel IUD, and the patch did not reach significance against the copper-IUD reference. The Boozalis authors framed the finding as plausibly mediated by progestin-induced suppression of ovarian estradiol, since DMPA, the implant, and the ring share systemic ovarian-suppressive activity. The ECHO secondary analysis, Hofmeyr et al. 2024, PLoS One, doi:10.1371/journal.pone.0299802, PMID 38722832 randomized 7,829 sub-Saharan African women across DMPA-IM, the levonorgestrel implant, and the copper IUD and found a smaller but directionally consistent gradient: 1.6% versus 1.1% versus 0.5% reporting decrease in sexual desire. The ECHO numbers are smaller because the outcome was a single-question side-effect prompt rather than a structured sexual-function instrument, but the gradient survives randomization, which is the strongest possible inferential design. The honest summary is that DMPA in particular and to a lesser degree etonogestrel-based methods do produce a modest, real, and dose-related reduction in self-reported sexual desire in a non-trivial minority of users. Sources: Boozalis et al. 2016, PMID 26855094, Hofmeyr et al. ECHO 2024, PMID 38722832. Confidence: C1.

The Mirena (LNG-IUS) sits awkwardly in this picture because systemic plasma levonorgestrel is much lower than oral progestin-only pills, ovulation continues in a substantial fraction of users, and observational data are mostly neutral-to-positive. A 2024 systematic review (Soares et al. PMC10903617) reports a positive-to-neutral effect on desire and a positive effect on dyspareunia, while acknowledging some users do report decline. The Mirena should not be assumed equivalent to DMPA on this axis. Sources: Soares et al. 2024, PMC10903617, Skrzypulec & Drosdzol 2008, PMID 19149209. Confidence: C2-C3.

A separate and clinically important window onto progestin antilibidinal effect is the forensic-psychiatry literature on paraphilic disorder. The clearest contemporary synthesis is Sauter, Turner, Briken & Rettenberger 2021, Sex Abuse, doi:10.1177/1079063220910723, which formalizes the European/Anglo-American split: Europe and Canada have favored cyproterone acetate, the United States has favored MPA, and GnRH agonists (triptorelin, leuprolide) have increasingly displaced both for the most severe cases because they produce faster, deeper, and more reliable testosterone suppression. The WFSBP guidelines, summarized in Turner & Briken 2018, J Sex Med, PMID 29289377 propose a stepped scheme: SSRIs first, then CPA for medium-high-risk cases, then GnRH agonists for the most severe. The trials are mostly observational and small, but the convergent clinical reality is that male sexuality can be substantially turned off at sufficient progestin dose, with the pathway dominantly HPG-axis testosterone suppression plus the CNS contribution Michael & Zumpe documented in primates. Sources: Sauter et al. 2021, PMC8072038, Turner & Briken 2018, PMID 29289377, Maletzky 1991, J Interpers Violence. Confidence: C2.

Cyproterone acetate's specific role as the classic transfeminine antiandrogen also clarifies a recurring confusion in lay writing. CPA is a progestin in pharmacological taxonomy: it activates the progesterone receptor, suppresses gonadotropins, and is used clinically for endometriosis, prostate cancer, and feminizing HRT. But unlike MPA, CPA is also a direct competitive androgen-receptor antagonist with substantial intrinsic AR-blocking activity (IC50 ≈ 7 nmol/L), which is why it works at lower dose than MPA for testosterone suppression and provides additional peripheral antagonism even when residual testosterone is present. That dual mechanism is the reason CPA is so effective at trans-feminine doses around 10 mg/day, and the reason it produces the libido-and-erection reductions that are routinely listed in CPA's side-effect profile and in clinical guidance such as UCSF's transgender care guidelines. The libido reduction in trans-feminine HRT is generally welcomed clinically (reduced spontaneous erections, less dysphoric arousal), but it is not a zero-cost feature: over-suppression of testosterone or AR signaling on CPA can produce energy, mood, and pleasure decrements that some patients describe as worse than the dysphoria the drug was started to relieve. Sources: CPA Wikipedia pharmacology summary citing primary references, Wikipedia CPA side-effect compendium, Angus et al. 2021 systematic review, doi:10.1111/cen.14329, UCSF feminizing HRT guideline. Confidence: C1-C2.

Bicalutamide, while sometimes confused with progestins in trans-feminine practice, is not a progestin. It is a nonsteroidal AR antagonist with selective AR activity and essentially no progestogenic, glucocorticoid, or mineralocorticoid action (Krasniqi et al. 2025, PMC11980709; Transfeminine Science bicalutamide summary). It does not suppress gonadotropins at typical doses; it tends to raise gonadal testosterone via feedback, with feminizing effects driven by peripheral AR blockade. That predicts a different libido profile from CPA: bicalutamide can blunt androgen-driven sexual drive through AR antagonism without deep HPG suppression, though users commonly report reduced erections and libido anyway. Lumping bicalutamide into "the progestins lower libido" garbles the mechanism. Sources: Krasniqi 2025, PMC11980709, Neyman et al. 2019, PMC6431559. Confidence: C2.

Beyond HPG suppression, AR blockade, and SHBG elevation, there is a fourth real mechanism by which progestins can shift sexual desire: the central nervous system effects of progesterone itself and its 5α-reduced metabolite allopregnanolone, plus whatever fraction of synthetic-progestin behavior arises from PR signaling in the hypothalamus and limbic system. Natural progesterone is rapidly reduced to allopregnanolone, which is a positive allosteric modulator of GABA-A receptors, behaving acutely like a benzodiazepine in many assays. The classical neurosteroid story is well laid out by Bitran, Shiekh & McLeod 1995, J Neuroendocrinol, PMID 7606242, who showed progesterone's anxiolytic effect was mediated by allopregnanolone at brain GABA-A. The PMDD literature, including Bäckström et al. 2014 and Hantsoo & Epperson 2020 (PMC7231988), turns this into a biphasic model: at endogenous luteal-phase concentrations, allopregnanolone produces an inverted-U mood response in some women, with mid-range concentrations causing the worst negative mood and irritability — a counterintuitive but well-replicated dose-response. That mood story directly intersects sexual desire. A woman experiencing GABA-A-mediated negative affect, irritability, and emotional blunting in response to her own luteal-phase progesterone is also more likely to score lower on desire and arousal during that phase, and the same pharmacology likely contributes to the subset of progestin-pill users who experience flattened affect along with reduced libido. Sources: Bitran et al. 1995, PMID 7606242, Hantsoo & Epperson 2020, PMC7231988, Schumacher et al. 2014 review, doi:10.1016/j.jsbmb.2013.02.012. Confidence: C2.

The CNS picture also has a direct PR-mediated component independent of allopregnanolone. The ventromedial hypothalamus contains a dense population of progesterone-receptor-expressing neurons whose activation is required for the lordosis posture in rodents and which gate sexual receptivity through estradiol-dependent priming and progesterone facilitation. Mani et al., reviewed in Frontiers Sys Neurosci 2017, and more recent imaging work characterizing PR+ VMHvl neurons in Inoue et al. 2021, eNeuro document that progesterone's facilitation of female receptivity in rodents involves both classical genomic PR signaling and rapid membrane PR effects. Translating that to humans is non-trivial — humans do not lordose — but it provides a plausible neuroanatomical scaffold for the user's intuition that "natural progesterone in some people raises libido when E-only doesn't." In rodents, PR activation does increase receptivity, and the human menstrual-cycle data are consistent with the idea that progesterone's net effect on sexual motivation depends on context, dose, timing relative to estradiol, and individual neurosteroid sensitivity. Sources: McCarthy et al. 2017 Front Sys Neurosci review, Inoue 2021 eNeuro. Confidence: C2-C3.

The natural-cycle data themselves cut against the simple "progesterone raises libido" anecdote. Roney & Simmons 2013, Horm Behav, doi:10.1016/j.yhbeh.2013.02.013, PMID 23601091 collected daily saliva samples and daily diary reports across 1–2 menstrual cycles, fit within-cycle multilevel models, and reported a positive within-woman effect of estradiol on subjective desire and a negative within-woman effect of progesterone, with progesterone statistically mediating the fall in desire from mid-cycle to the luteal phase. Crucially, testosterone showed no significant within-cycle predictive effect once estradiol and progesterone were modeled, which is one of the more important challenges to the "testosterone is the female libido hormone" simplification. Subsequent work from the same group, including Grebe et al. 2016, Horm Behav, PMID 27049465, confirmed that within-cycle progesterone fluctuations negatively predict in-pair and extra-pair desire. Read literally, endogenous progesterone elevation is associated with lower desire on average, which complicates the trans-feminine and perimenopausal claim that adding micronized progesterone "boosts libido." Sources: Roney & Simmons 2013, PMID 23601091, Grebe et al. 2016, PMID 27049465. Confidence: C1-C2.

Against that, the human evidence on micronized progesterone (Prometrium) and libido is limited and underwhelming. The most cited comparison, Cumming et al. 2002, Fertil Steril, randomized 27 estrogen-treated postmenopausal women to add MPA 10 mg or oral micronized progesterone 200 mg for 15 days and found no difference in mood or libido — a small, short, underpowered study that only argues "progesterone is not worse than MPA" rather than "progesterone improves libido." Fitzpatrick 2000 (PMID 10868610), 176 women switched from MPA to micronized progesterone, found improved vasomotor/somatic/anxiety scores and 80% satisfaction but did not robustly characterize libido. Recent transgender data (Patel & Millet 2024, PMID 37549733, Stadler et al. 2025) find more reliable subjective improvements in breast development and femininity than in libido, with libido changes reported by a smaller subset in mixed directions. There is no high-quality RCT showing micronized progesterone reliably increases libido in any defined population. The "progesterone improved my libido" anecdotes are real but heterogeneous, plausibly reflect mood improvement, sleep improvement (via allopregnanolone), and partner/context confounding, and may be biased by self-selection. Sources: Cumming et al. 2002, Fitzpatrick et al. 2000, PMID 10868610, Patel & Millet 2024, PMID 37549733. Confidence: C2-C3.

The progestin-only pill (POP) is a useful intermediate test because it removes ethinylestradiol from the equation. Desogestrel-based POPs (e.g., Cerazette) ovulation-suppress in roughly 97% of cycles, meaningfully reducing estradiol, and libido decline is among the more commonly reported user complaints, though formal trial evidence remains thin. Older norethisterone POPs leave more cycles ovulatory and produce more bleeding irregularity than desire complaints. The general principle: any progestin regimen that suppresses ovulation enough to flatten endogenous estradiol — DMPA, implant, ring, desogestrel POP — carries more libido downside than progestin regimens that allow ovarian estradiol to continue cycling, regardless of the progestin's specific androgenic profile. The mechanism converges on the same lever as the SHBG story: low estradiol means low lubrication, lower vasocongestion, and reduced central reward sensitivity for sexual stimuli. Sources: Casado-Espada 2019, PMID 31242625, Boozalis 2016, PMID 26855094. Confidence: C2-C3.

A practical takeaway for the user's draft: the simplest accurate sentence is that synthetic progestins as a class can lower libido through several non-mutually-exclusive mechanisms — HPG suppression and reduced endogenous testosterone (the main pathway for high-dose MPA, CPA, and progestin-only methods that suppress ovulation), direct AR antagonism (CPA, dienogest, drospirenone, chlormadinone), SHBG elevation when combined with ethinylestradiol (which lowers free testosterone disproportionately), suppression of ovarian estradiol production (which contributes more than people realize, especially for DMPA, the implant, and the ring), and direct CNS effects via PR-expressing hypothalamic and limbic neurons and via allopregnanolone-driven mood/affect changes. The "lowering testosterone" answer to the user's question is correct as the dominant mechanism in the high-dose forensic and trans-feminine contexts, but it is incomplete for combined-pill use and arguably wrong for DMPA/implant users in whom ovarian estradiol suppression appears to do at least as much work. The Pastor 85% no-change-or-increase versus 15% decrease distribution is not the profile of a "direct libido dampener" in the clean pharmacologic sense; it is the profile of a class with several plausible suppressive mechanisms whose effects are large only in subgroups (DMPA users, very-low-dose-EE COC users, the pre-existing low-androgen-symptomatic, the neurosteroid-sensitive). A more accurate evidence map splits progestins into (i) high-dose forensic/oncologic/anti-androgen contexts, where libido suppression is the desired and reliable outcome; (ii) ovulation-suppressing systemic contraception (DMPA, implant, ring, desogestrel POP), where modest decrement appears in a non-trivial minority and ovarian-estradiol suppression is the dominant proximate mechanism; (iii) combined oral contraceptives, where libido is unaffected in most users but a 10–20% minority reports decrement, with SHBG elevation as the most plausible biomarker; (iv) levonorgestrel IUD, where systemic exposure is low and the signal is mostly null-to-favorable; and (v) natural micronized progesterone, where the picture is mixed and the strongest within-cycle data point toward suppression rather than enhancement. Sources: Pastor 2013, PMID 23320933, Boozalis 2016, PMID 26855094, Hofmeyr 2024 ECHO, PMID 38722832, Michael & Zumpe 1993, PMID 8511186, Roney & Simmons 2013, PMID 23601091, Soares 2024 LNG-IUD review, PMC10903617. Confidence: C2.

Verdict on the draft's specific claims

1. "There exist synthetic variants of progesterone called 'progestins' which typically lower libido." KIND-OF-TRUE. The category exists and the directional claim is correct on average and in some subsets, but "typically lower libido" overstates the population-level signal: in most contraceptive-dose users, libido is unchanged, and the suppression is class- and context-dependent. Better wording would say "can lower libido, with effect size depending on dose and which progestin." Sources: Pastor 2013, PMID 23320933, Zethraeus 2017, PMID 27525531.

1. "One example is medroxyprogesterone acetate (MPA)." TRUE. MPA is the canonical pregnane progestin and the prototype antilibidinal progestin in forensic psychiatry.

1. "These [progestins] can lower libido — and the user asks 'how exactly? by lowering testosterone?'" TRUE that lowering testosterone is a mechanism — and the dominant one at high-dose anti-androgen/forensic settings — but it is one of several pathways. Other mechanisms include direct AR antagonism (CPA, drospirenone, dienogest), SHBG elevation with ethinylestradiol (lowering free T), suppression of ovarian estradiol (DMPA, implant), allopregnanolone-mediated mood effects, and direct CNS PR signaling (Michael & Zumpe primate experiment). Sources: Michael & Zumpe 1993, PMID 8511186, Boozalis 2016, PMID 26855094.

1. "Synthetic progestins are categorized as 'direct libido dampeners.'" KIND-OF-TRUE. The category is too coarse. CPA and high-dose MPA earn that label cleanly; combined-pill progestins do not at the population level; LNG-IUS arguably does not at all. A more careful evidence map should split high-dose anti-androgen progestins from contraceptive doses.

1. "Natural progesterone in some people raises libido when E-only doesn't." NOT-EVALUABLE from RCT evidence. The cleanest cycle data (Roney & Simmons 2013) show endogenous progesterone is negatively associated with desire within-cycle. The trans-feminine and perimenopausal user-survey data report subjective libido improvement in a subset, but no high-quality RCT has demonstrated that exogenous micronized progesterone reliably raises libido. The claim is plausible at the individual level but not supported by population-level evidence; it should be marked as anecdotal/heterogeneous.

What was searched and not found

A clean RCT of micronized progesterone vs. placebo with libido as a pre-registered primary endpoint, in either cis women or trans women, was not located. PubMed searches for "micronized progesterone RCT libido," "Prometrium sexual function trial," and combinations targeting trans-feminine HRT returned only retrospective/observational designs and small comparator trials such as Cumming 2002 that were not designed or powered to detect libido effects. Confidence: C5 for any positive claim that micronized progesterone raises libido above placebo in an RCT.