Progesterone

What it is

Progesterone is a steroid hormone made mainly by the corpus luteum of the ovary and by the placenta. The medicine is manufactured from a plant starting material and is chemically the same molecule as the hormone the ovary makes. Taken by mouth it is poorly absorbed unless the particles are made very small (micronised), and it is also given vaginally, by injection into muscle and by injection under the skin. Oral capsules in the United States are suspended in peanut oil.

What the research says

The evidence is strongest for two things. Taken with estrogen after menopause, progesterone protects the lining of the womb: in a three-year randomised trial, endometrial hyperplasia occurred in 6 per cent of women on estrogen plus progesterone against 64 per cent on estrogen alone. Given vaginally in a singleton pregnancy at high risk, it reduced birth before 34 weeks (relative risk 0.78) in an individual-participant meta-analysis of 31 trials. It failed in two large, well-run tests: it did not raise live births in women bleeding in early pregnancy (PRISM, 4,153 women), and it did not reduce preterm birth in twins. Progesterone causes breast tenderness, dizziness, bloating and vaginal discharge more often than placebo.

Evidence grade: Disputed.

How it works

Drug class: Progestogen: progesterone receptor agonist, chemically identical to the progesterone made by the ovary

Progesterone acts on progesterone receptors inside cells, which switch genes on and off - in the womb lining this turns a proliferating, estrogen-driven lining into a secretory one and stops it overgrowing. It also acts at receptors on the cell surface, and the liver and brain convert part of it into allopregnanolone-type metabolites that act on GABA-A receptors, the same receptors that sedatives act on, which is the likely reason bedtime dosing causes drowsiness and dizziness. (Source 1)

What it is used for

• A three-year randomised trial in 358 women found hyperplasia in 6 per cent on estrogen plus cyclical progesterone against 64 per cent on estrogen alone. This is the use the oral capsule is licensed for. Evidence: established. (Source 2)
• In a randomised double-blind study, 10 days of oral progesterone produced a withdrawal bleed within 7 days of the last dose in 80 per cent of women against 10 per cent on placebo. The trial was small (41 women analysed). Evidence: established. (Source 3)
• A Cochrane review of 94 trials found higher live birth or ongoing pregnancy with progesterone than with placebo or no treatment (odds ratio 1.77), but rated the evidence very low quality and based that estimate on five trials and 642 women. No route or regimen beat another. Evidence: limited. (Source 4)
• In the EPPPIC individual-participant meta-analysis, vaginal progesterone reduced birth before 34 weeks (relative risk 0.78, 95% CI 0.68-0.90, nine trials, 3,769 women). The authors said the absolute benefit is larger for women with a short cervix and that analyses questioned whether it works in women without one. Vaginal progesterone is not FDA-approved for this indication in the United States. Evidence: limited. (Source 5)
• EPPPIC found no reduction in birth before 34 weeks in twins (relative risk 1.01, 95% CI 0.84-1.20, eight trials, 2,046 women) and concluded that treating unselected multiple pregnancies is not supported. Evidence: not-supported. (Source 6)
• The PRISM trial randomised 4,153 women to 400 mg vaginal progesterone twice daily or placebo and found live births after 34 weeks in 75 per cent versus 72 per cent, a relative rate of 1.03 (95% CI 1.00 to 1.07), which did not reach significance. Evidence: not-supported. (Source 7)
• One placebo-controlled randomised trial in 133 healthy women found oral progesterone 300 mg at bedtime beat placebo on a vasomotor symptom score (adjusted difference -4.3). It is one trial, in early postmenopause, in women screened to be at low cardiovascular risk. Evidence: limited. (Source 8)

Interactions

• Ketoconazole and other CYP3A4 inhibitors (which includes grapefruit juice as a CYP3A4 inhibitor in principle, though not tested here) (pharmacokinetic study): Progesterone is broken down by the liver enzyme CYP3A4. Blocking that enzyme can raise how much progesterone reaches the bloodstream. This was shown in liver microsomes in the laboratory, not in people, and the label says the clinical meaning is unknown. (Source 9)
• Food (any meal) (pharmacokinetic study): Taking oral progesterone capsules with food raises the amount absorbed compared with an empty stomach, which can mean more effect and more drowsiness from the same capsule. (Source 9)
• Peanut (label): The US oral capsules are suspended in peanut oil, so they are a problem for anyone with peanut allergy. Vaginal and injectable forms use other vehicles. (Source 10)
• Wild yam (Dioscorea villosa) cream and other diosgenin supplements (clinical trial): These are sold as natural progesterone. In a randomised crossover trial they did not change serum or salivary progesterone at all, so they are not a source of the hormone and do not add to a progesterone prescription. Limit: This was a crossover trial in 23 women with no power calculation reported, so "no change" means no change was detected in a very small study, not that an effect has been ruled out. The authors put it as the study "suggests" wild yam cream has little effect. (Source 11)

Stopping it

• Progesterone is not habit-forming and no withdrawal syndrome is described. What does happen on stopping is a withdrawal bleed: in a randomised double-blind study, 80 per cent of women bled within 7 days of the last of 10 daily doses, against 10 per cent on placebo. Cyclical use for endometrial protection is built around this, with the drug taken for 12 days in every 28-day cycle. (Source 3)
• When progesterone is stopped while estrogen continues, the protection against overgrowth of the womb lining goes with it: in the three-year trial, 64 per cent of women on estrogen alone developed hyperplasia against 6 per cent on the combination. (Source 2)

What goes wrong

Oral progesterone with estrogen caused breast tenderness, dizziness, bloating and vaginal discharge several times more often than placebo. (Source 12)

• Randomized trial, Moderate certainty.
• Size: 875 postmenopausal women in the trial; 178 on progesterone plus estrogen and 174 on placebo in the reported table.
• Who: postmenopausal women.
• How long: 3 years.
• Result: Progesterone 200 mg plus conjugated estrogens versus placebo: breast tenderness 27 versus 6 per cent, dizziness 15 versus 9 per cent, abdominal bloating 12 versus 5 per cent, vaginal discharge 10 versus 3 per cent, depression 19 versus 12 per cent, breast carcinoma 2 versus under 1 per cent.
• Funding: not stated (trial reported in the manufacturer's label)

Headache 31 27 Breast Tenderness 27 6 Joint Pain 20 29 Depression 19 12 Dizziness 15 9 Abdominal Bloating 12 5

At the higher 400 mg dose used for amenorrhoea, dizziness was reported by 24 per cent against 4 per cent on placebo. (Source 13)

• Randomized trial, Low certainty.
• Size: 49 women (25 progesterone, 24 placebo)
• Who: estrogen-primed postmenopausal women.
• How long: short course.
• Result: Dizziness 24 versus 4 per cent, abdominal cramping 20 versus 13 per cent, headache 16 versus 8 per cent, breast pain 16 versus 8 per cent, nausea 8 versus 0 per cent.
• Funding: not stated (trial reported in the manufacturer's label)

Fatigue 8 4 Headache 16 8 Dizziness 24 4 Abdominal Distention (Bloating) 8 8 Abdominal Pain (Cramping) 20 13

The preterm birth meta-analysis raised, without settling, a signal of more maternal complications with progestogens. (Source 5)

• Meta-analysis, Low certainty.
• Size: 31 trials, 11,644 women.
• Who: asymptomatic women at risk of preterm birth.
• How long: pregnancy to delivery.
• Result: A composite of serious maternal outcomes was examined; the authors reported a possible increase that remained uncertain, and reported increased preterm premature rupture of membranes with 17-OHPC in multifetal pregnancies.
• Funding: Patient-Centered Outcomes Research Institute (independent of manufacturers)

A possible increase in maternal complications was suggested, but this was uncertain.

In twin and triplet pregnancies, the injected synthetic progestogen 17-OHPC increased preterm rupture of the membranes; this was 17-OHPC, not progesterone itself. (Source 6)

• Meta-analysis, Moderate certainty.
• Size: 8 trials, 2,253 women for 17-OHPC in twins or triplets, within a 31-trial individual-participant dataset of 11,644 women.
• Who: women with multifetal pregnancies, mostly without additional risk factors.
• How long: pregnancy to delivery.
• Result: Preterm premature rupture of membranes before 34 weeks: relative risk 1.59 (95% CI 1.15 to 2.22) with 17-OHPC exposure. No consistent evidence of benefit or harm on other outcomes with either vaginal progesterone or 17-OHPC in these pregnancies.
• Funding: Patient-Centered Outcomes Research Institute (independent of manufacturers)

Limit of this finding: 17-OHPC (17-hydroxyprogesterone caproate) is a synthetic progestogen given by injection, not the micronised progesterone this entry is about. The harm was found with 17-OHPC in multifetal pregnancies; the same meta-analysis found no equivalent signal for vaginal progesterone.

Preterm premature rupture of membranes was increased with 17-OHPC exposure in multifetal gestations (rupture <34 weeks RR 1·59, 95% CI 1·15-2·22)

What the evidence supports

Adding cyclical oral progesterone to estrogen cut endometrial hyperplasia from 64 per cent to 6 per cent over three years. (Source 2)

• Randomized trial, Moderate certainty.
• Size: 358 postmenopausal women with an intact uterus (117, 115 and 116 analysed)
• Who: postmenopausal women with a uterus taking conjugated estrogens 0.625 mg daily.
• How long: up to 36 months.
• Result: Hyperplasia 7/117 (6 per cent) with progesterone 200 mg for 12 days per 28-day cycle plus estrogen versus 74/115 (64 per cent) with estrogen alone and 3/116 (3 per cent) on placebo; atypical hyperplasia 1 per cent versus 12 per cent.
• Funding: not stated (trial reported in the manufacturer's label)

A comparison of the PROMETRIUM Capsules plus conjugated estrogens treatment group to the conjugated estrogens only group showed a significantly lower rate of hyperplasia (6 percent combination product versus 64 percent estrogen alone)

Vaginal progesterone reduced birth before 34 weeks in high-risk singleton pregnancies, but the meta-analysis questioned whether it works without a short cervix. (Source 5)

• Meta-analysis, Moderate certainty.
• Size: 9 trials, 3,769 women (vaginal progesterone) within 31 trials, 11,644 women and 16,185 offspring overall.
• Who: asymptomatic women at risk of preterm birth, mostly with previous spontaneous preterm birth or short cervix.
• How long: pregnancy to delivery.
• Result: Preterm birth before 34 weeks: vaginal progesterone RR 0.78 (95% CI 0.68-0.90); 17-OHPC RR 0.83 (0.68-1.01); oral progesterone RR 0.60 (0.40-0.90) from only 2 trials and 181 women.
• Funding: Patient-Centered Outcomes Research Institute (independent of manufacturers)

Preterm birth before 34 weeks was reduced in such women who received vaginal progesterone (nine trials, 3769 women; relative risk [RR] 0·78, 95% CI 0·68-0·90)

Progesterone for luteal phase support raised live birth or ongoing pregnancy compared with placebo, on very low quality evidence. (Source 4)

• Systematic review, Very low certainty.
• Size: 5 RCTs, 642 women for the live birth outcome (94 RCTs, 26,198 women in the whole review)
• Who: subfertile women undergoing assisted reproduction.
• How long: single treatment cycles.
• Result: Live birth or ongoing pregnancy OR 1.77 (95% CI 1.09 to 2.86), I2 = 35 per cent; the review said most studies had unclear or high risk of bias.
• Funding: independent (Cochrane)

Limit of this finding: The published abstract of this review misprints its own study count as "Ninety-four women RCTs (26,198 women)". The review included 94 randomised trials in 26,198 women. The result itself is very low certainty: the review says most studies had unclear or high risk of bias, with poor reporting of methods and imprecision from small sample sizes, so the size of any benefit is not established.

Evidence suggests a higher rate of live birth or ongoing pregnancy in the progesterone group (OR 1.77, 95% CI 1.09 to 2.86, five RCTs, 642 women, I2 = 35%, very low-quality evidence)

Oral progesterone 300 mg at bedtime reduced hot flushes and night sweats more than placebo in one randomised trial. (Source 14)

• Randomized trial, Low certainty.
• Size: 133 women randomised, 114 analysed.
• Who: healthy community women 1 to 10 years after their final period, screened to exclude cardiovascular risk.
• How long: 3 months.
• Result: Vasomotor symptom score: mean adjusted difference -4.3 (95% CI -6.6 to -1.9); reductions of 10.0 with progesterone versus 4.4 with placebo; discontinuation with adverse events 9 per cent (8 progesterone, 4 placebo)
• Funding: not stated.

The VMS scores of women taking progesterone were better than placebo (mean adjusted difference, -4.3 (95% CI, -6.6 to -1.9), with mean reductions of 10.0 (95% CI, -12.0 to -8.1) and 4.4 (95% CI, -6.6 to -2.2) in the progesterone and placebo arms, respectively.

What the evidence does not support

Vaginal progesterone did not increase live births in women who bled in early pregnancy. (Source 15)

• Randomized trial, High certainty.
• Size: 4,153 women at 48 UK hospitals.
• Who: women presenting with vaginal bleeding in early pregnancy.
• How long: from presentation with bleeding to 16 weeks of gestation.
• Result: Live birth after at least 34 weeks 75 per cent (1513/2025) with progesterone versus 72 per cent (1459/2013) with placebo; relative rate 1.03 (95% CI 1.00 to 1.07), P = 0.08; an absolute difference of about 3 percentage points that did not reach significance.
• Funding: UK National Institute for Health Research (independent of manufacturers)

The incidence of live births after at least 34 weeks of gestation was 75% (1513 of 2025 women) in the progesterone group and 72% (1459 of 2013 women) in the placebo group

Vaginal progesterone did not reduce preterm birth in twin pregnancies. (Source 6)

• Meta-analysis, Moderate certainty.
• Size: 8 trials, 2,046 women (vaginal progesterone in twins); 8 trials, 2,253 women for 17-OHPC in twins or triplets.
• Who: women with multifetal pregnancies, mostly without additional risk factors.
• How long: pregnancy to delivery.
• Result: Preterm birth before 34 weeks: vaginal progesterone RR 1.01 (95% CI 0.84-1.20); 17-OHPC RR 1.04 (0.92-1.18)
• Funding: Patient-Centered Outcomes Research Institute (independent of manufacturers)

For twins, vaginal progesterone did not reduce preterm birth before 34 weeks (eight trials, 2046 women: RR 1·01, 95% CI 0·84-1·20)

Neither the route of progesterone nor micronised versus synthetic progestogen changed live birth rates in assisted reproduction. (Source 16)

• Systematic review, Low certainty.
• Size: 45 RCTs, 13,814 women across the progesterone regimen comparisons.
• Who: subfertile women undergoing assisted reproduction.
• How long: single treatment cycles.
• Result: Micronised versus synthetic OR 0.90 (95% CI 0.53 to 1.55, two RCTs, 470 women); low-dose versus high-dose vaginal OR 0.97 (0.84 to 1.11, five RCTs, 3,720 women, moderate quality); subcutaneous versus vaginal gel OR 0.92 (0.74 to 1.14)
• Funding: independent (Cochrane)

Limit of this finding: Two things to keep in mind. The review reports harms for only two of these nine comparisons (intramuscular versus oral, and low versus high-dose vaginal), so the regimens were compared on pregnancy rates with almost no safety data. And the abstract prints some intervals to one decimal place, so "OR 1.24, 95% CI 1.03 to 1.5" means an upper bound of 1.50, not a dropped digit.

micronised versus synthetic: OR 0.9, 95% CI 0.53 to 1.55 (two RCTs, 470 women, I2 = 0%, low-quality evidence)

Menopausal hormone therapy containing progesterone did not change body weight or waist and hip measurements compared with other regimens. (Source 17)

• Randomized trial, Moderate certainty.
• Size: 875 women in the PEPI trial.
• Who: postmenopausal women.
• How long: 3 years.
• Result: Women on estrogen with or without a progestogen gained on average 1.0 kg less than placebo (P = 0.006); no significant differences in weight or girth change between the four active regimens, one of which was micronised progesterone 200 mg on days 1-12.
• Funding: not stated.

There were no significant differences in weight or girth changes among any of the four active hormone regimens.

Where the evidence is mixed

Observational studies suggest progesterone carries a lower breast cancer risk than synthetic progestins when either is combined with estrogen, but this is not evidence that progesterone is risk-free. (Source 18)

• Systematic review, Very low certainty.
• Size: 3 studies (2 cohorts, 1 population-based case-control), 86,881 postmenopausal women.
• Who: postmenopausal women using menopausal hormone therapy, mean age 59 years.
• How long: follow-up 3 to 20 years.
• Result: Breast cancer relative risk 0.67 (95% CI 0.55-0.81) for progesterone versus synthetic progestins; no data on cardiovascular events; the review rated overall risk of bias in the pooled cohorts as moderate.
• Funding: not stated.

Progesterone was associated with lower breast cancer risk compared to synthetic progestins when each is given in combination with estrogen, relative risk 0.67; 95 % confidence interval 0.55-0.81.

The FDA removed the cardiovascular, breast cancer and dementia boxed warning from menopausal hormone therapy labels, so current progesterone capsule labelling carries no boxed warning. (Source 19)

• Official position, Certainty not rated.
• Size: six products in the first batch; 29 companies asked to submit changes.
• Who: menopausal hormone therapy products including systemic progestogen-alone therapy.
• How long: labelling action dated 12 February 2026.
• Result: Risk statements on cardiovascular disease, breast cancer and probable dementia removed from the boxed warning; the underlying Women's Health Initiative numbers (for conjugated estrogens plus medroxyprogesterone, not progesterone) remain in the body of the label.
• Funding: regulatory action, not a study.

Specifically, risk statements related to cardiovascular disease, breast cancer and probable dementia were removed from the

Where the research disagrees

Whether the cardiovascular, breast cancer and dementia risks that came from the Women's Health Initiative trial of conjugated estrogens plus medroxyprogesterone apply to micronised progesterone

• US Food and Drug Administration (February 2026), position: Specifically, risk statements related to cardiovascular disease, breast cancer and probable dementia were removed from the (Source 19)
• Asi and colleagues, systematic review and meta-analysis (2016), systematic-review of observational studies: Progesterone was associated with lower breast cancer risk compared to synthetic progestins when each is given in combination with estrogen, relative risk 0.67; 95 % confidence interval 0.55-0.81. (Source 18)

Whether progesterone helps women who are bleeding in early pregnancy or at risk of preterm birth

• EPPPIC collaboration (2021), individual participant data meta-analysis, meta-analysis of individual participant data: Preterm birth before 34 weeks was reduced in such women who received vaginal progesterone (nine trials, 3769 women; relative risk [RR] 0·78, 95% CI 0·68-0·90) (Source 5)
• PRISM trial investigators (2019), rct: The incidence of live births after at least 34 weeks of gestation was 75% (1513 of 2025 women) in the progesterone group and 72% (1459 of 2013 women) in the placebo group (Source 15)

How much

• Reference intake: Dosing is set by the prescriber, not by a reference intake. As a position, the US label for oral micronised progesterone capsules states 200 mg at bedtime for 12 days per 28-day cycle for endometrial protection in a woman also taking conjugated estrogens (rev. 02/2026). (Source 20)
• Upper limit: There is no upper limit in the nutrient sense. The highest dose in the oral capsule label is 400 mg at bedtime for 10 days, for secondary amenorrhoea (label rev. 02/2026). (Source 20)
• Studied: PRISM gave vaginal suppositories of 400 mg progesterone twice daily from presentation with bleeding to 16 weeks. (Source 7)
• Studied: The vasomotor symptom trial gave oral micronised progesterone 300 mg daily at bedtime. (Source 8)
• Studied: The endometrial protection trial gave 200 mg per day for 12 days per 28-day cycle with conjugated estrogens 0.625 mg per day. (Source 2)

A common belief, and what the research shows

The belief: Wild yam or diosgenin creams give you natural progesterone, and yams are a food source of it.

What the research shows: They do not. Progesterone medicine is made in a factory from a plant starting material; the human body cannot do that conversion. In a double-blind crossover trial of wild yam cream in 23 menopausal women, blood and saliva progesterone did not move: the investigators reported "there were no changes in weight, systolic or diastolic blood pressure, or levels of total serum cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, FSH, glucose, estradiol, or serum or salivary progesterone". The pharmaceutical is "synthesized from a starting material from a plant source and is chemically identical to progesterone of human ovarian origin".

Questions and answers

What is it?

Progesterone is a steroid hormone normally made by the ovary after ovulation and by the placenta in pregnancy. The medicine is the identical molecule, manufactured from a plant starting material rather than extracted from anyone. Oral capsules contain progesterone ground very fine (micronised) so that enough survives the gut and liver; it is also given as vaginal pessaries and gels and by injection. (Source 10)

What does it do in the body?

Progesterone works through progesterone receptors inside cells, turning the estrogen-driven, proliferating lining of the womb into a secretory lining and stopping it overgrowing. It also acts at receptors on the cell membrane. Part of it is converted in the body to neurosteroid metabolites that act on GABA-A receptors, the receptors sedative drugs act on, which is why it is usually taken at bedtime and why dizziness and drowsiness are common. (Source 1)

Is it good or bad for you?

It depends entirely on the situation, and the same drug is clearly useful in some and clearly useless in others. Alongside estrogen after menopause it protects the womb lining, and in a singleton pregnancy with a short cervix or a previous preterm birth vaginal progesterone lowered the risk of early birth. In twin pregnancies and in women bleeding in early pregnancy, large trials and meta-analyses found no benefit. It also causes breast tenderness, dizziness and bloating well above placebo rates. (Source 21)

How do you get more of it?

Progesterone is prescription-only; there is no food or over-the-counter product that raises it. In studies it was given as oral micronised capsules, vaginal pessaries or gel, or injections. As a position, the US capsule label sets 200 mg at bedtime for 12 days in each 28-day cycle for endometrial protection. Only a prescriber can decide whether and how much anyone should take. (Source 20)

If it is harmful, what reduces it?

Progesterone is cleared by the liver within hours to a day or two, so stopping the drug is what reduces it; there is nothing to flush out. The visible sign that levels have fallen is a withdrawal bleed, which in a randomised study followed the last dose within 7 days in 80 per cent of women against 10 per cent on placebo. (Source 3)

Why might someone be low in it or missing it?

Natural progesterone is only made after ovulation, so it is low in anyone who does not ovulate that cycle, after the menopause, and in pregnancy loss. Cycles can look normal and still be anovulatory. In a study of 107 women having ovarian stimulation and insemination, the anovulation rate was 18.7 per cent, judged on a mid-luteal progesterone above 3 ng/mL. (Source 22)

Which whole foods contain it or feed it?

No whole food contains usable progesterone and no food or supplement raises it. Yams and wild yam creams are the common claim: they contain diosgenin, which chemists can turn into progesterone in a factory but the human body cannot. A double-blind crossover trial of wild yam cream in menopausal women found no change in serum or salivary progesterone. (Source 11)

What happens if you do not have it?

The clearest consequence is in the womb. When women took estrogen after menopause without a progestogen, 64 per cent developed endometrial hyperplasia within three years, including 12 per cent with atypical hyperplasia, against 6 per cent when cyclical progesterone was added. Low progesterone in a cycle also means no ovulation happened, which matters for fertility. (Source 2)

How can you test for it?

A blood progesterone level is the test, taken in the middle of the luteal phase, roughly a week after ovulation. It is a snapshot of a hormone that swings through the day and the cycle, so it answers a narrow question. Above about 3 ng/mL is taken as evidence that ovulation happened, but in the same study the level had no value in predicting whether a pregnancy followed. (Source 22)

References

1. International Journal of Molecular Sciences. Progesterone in the Brain: Hormone, Neurosteroid and Neuroprotectant. 2020. PMID 32722286, DOI 10.3390/ijms21155271. Read the source
2. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - CLINICAL STUDIES, Effects on the endometrium. 2026. Read the source
3. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - CLINICAL STUDIES, Effects on secondary amenorrhea. 2026. Read the source
4. Cochrane Database of Systematic Reviews. Luteal phase support for assisted reproduction cycles. 2015. PMID 26148507, DOI 10.1002/14651858.CD009154.pub3. Read the source
5. The Lancet. Evaluating Progestogens for Preventing Preterm birth International Collaborative (EPPPIC): meta-analysis of individual participant data from randomised controlled trials. 2021. PMID 33773630, DOI 10.1016/S0140-6736(21)00217-8. Read the source
6. The Lancet. Evaluating Progestogens for Preventing Preterm birth International Collaborative (EPPPIC): meta-analysis of individual participant data from randomised controlled trials. 2021. PMID 33773630, DOI 10.1016/S0140-6736(21)00217-8. Read the source
7. The New England Journal of Medicine. A Randomized Trial of Progesterone in Women with Bleeding in Early Pregnancy. 2019. PMID 31067371, DOI 10.1056/NEJMoa1813730. Read the source
8. Menopause. Oral micronized progesterone for vasomotor symptoms--a placebo-controlled randomized trial in healthy postmenopausal women. 2012. PMID 22453200, DOI 10.1097/gme.0b013e318247f07a. Read the source
9. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - CLINICAL PHARMACOLOGY, Food-Drug and Drug Interactions. 2026. Read the source
10. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - DESCRIPTION and CLINICAL PHARMACOLOGY. 2026. Read the source
11. Climacteric. Effects of wild yam extract on menopausal symptoms, lipids and sex hormones in healthy menopausal women. 2001. PMID 11428178, DOI 10.1080/cmt.4.2.144.150. Read the source
12. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - ADVERSE REACTIONS, Table 7. 2026. Read the source
13. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - ADVERSE REACTIONS, Table 8. 2026. Read the source
14. Menopause. Oral micronized progesterone for vasomotor symptoms--a placebo-controlled randomized trial in healthy postmenopausal women (Results section). 2012. PMID 22453200, DOI 10.1097/gme.0b013e318247f07a. Read the source
15. The New England Journal of Medicine. A Randomized Trial of Progesterone in Women with Bleeding in Early Pregnancy (Results section). 2019. PMID 31067371, DOI 10.1056/NEJMoa1813730. Read the source
16. Cochrane Database of Systematic Reviews. Luteal phase support for assisted reproduction cycles. 2015. PMID 26148507, DOI 10.1002/14651858.CD009154.pub3. Read the source
17. The Journal of Clinical Endocrinology and Metabolism. Effect of postmenopausal hormone therapy on body weight and waist and hip girths. Postmenopausal Estrogen-Progestin Interventions Study Investigators. 1997. PMID 9141548, DOI 10.1210/jcem.82.5.3925. Read the source
18. Systematic Reviews. Progesterone vs. synthetic progestins and the risk of breast cancer: a systematic review and meta-analysis. 2016. PMID 27456847, DOI 10.1186/s13643-016-0294-5. Read the source
19. U.S. Food and Drug Administration. FDA Approves Labeling Changes to Menopausal Hormone Therapy Products. 2026. Read the source
20. DailyMed / Acertis Pharmaceuticals, LLC. PROMETRIUM (progesterone, USP) Capsules, US prescribing information (rev. 02/2026) - DOSAGE AND ADMINISTRATION. 2026. Read the source
21. The Lancet. Evaluating Progestogens for Preventing Preterm birth International Collaborative (EPPPIC): meta-analysis of individual participant data from randomised controlled trials (Interpretation section). 2021. PMID 33773630, DOI 10.1016/S0140-6736(21)00217-8. Read the source
22. Medicine. Does mid-luteal progesterone predict pregnancy in intrauterine insemination cycles following sequential clomiphene citrate and gonadotropin treatment?. 2023. PMID 37657005, DOI 10.1097/MD.0000000000034754. Read the source