Can a Hormonal Imbalance Cause Miscarriage?

Several types of hormonal imbalance can raise the risk of miscarriage, though hormones are far from the most common explanation for pregnancy loss. Chromosomal abnormalities in the embryo account for the majority of first-trimester miscarriages, dwarfing all other causes combined. Still, thyroid disorders, progesterone deficiency, insulin resistance, and elevated androgens each have credible evidence linking them to pregnancy loss, and understanding where that evidence is strong and where it is thin matters for anyone navigating recurrent losses or weighing treatment options.

Chromosomal Problems Still Dominate

Before diving into hormones, the single most important piece of context is that roughly half to four-fifths of first-trimester miscarriages involve chromosomal abnormalities in the embryo, most commonly an extra or missing chromosome that prevents normal development.¹ That means most isolated miscarriages have nothing to do with the mother’s hormone levels. Hormonal imbalances become a more meaningful part of the conversation when losses recur, when an endocrine condition is already known, or when a pattern suggests something beyond random chromosomal bad luck.

Thyroid Disorders and Miscarriage

Of all the hormonal connections to pregnancy loss, thyroid dysfunction has the most consistent evidence. Even mildly elevated thyroid-stimulating hormone (TSH) in early pregnancy is linked to a higher miscarriage rate. A large nested case-control study found that women whose first-trimester TSH fell between 2.5 and about 4.9 had roughly one and a half times the odds of miscarriage compared with women whose TSH was in the lower-normal range, and those with TSH above 4.9 had about twice the odds.² A separate prospective cohort looking at subclinical hypothyroidism alongside thyroid autoimmunity found even steeper increases, with women who had both conditions facing adjusted odds roughly five to ten times higher than euthyroid women, depending on the severity of the TSH elevation.³

Thyroid autoantibodies add a layer of risk beyond TSH levels alone. A meta-analysis of cohort studies found that the presence of thyroid autoantibodies was associated with more than triple the odds of miscarriage, even when thyroid function appeared normal.⁴ Seven studies across six countries have consistently shown this association in women screened during the first trimester, ruling out other explanations like anticardiolipin antibodies.⁵ Because of this strength of evidence, major guidelines recommend TSH and thyroid antibody screening for women with recurrent pregnancy loss.⁶

The mechanisms are not entirely pinned down. Thyroid hormones regulate metabolism in virtually every tissue, and an underactive thyroid can impair implantation and early placental development. Thyroid autoantibodies may also reflect a more broadly overactive immune system that treats the pregnancy as foreign. What is clear is that thyroid screening is one of the few hormonal tests with enough evidence behind it to be universally recommended in the recurrent-loss workup.

Progesterone and the Luteal Phase

Progesterone is often called the “pregnancy hormone” because it prepares the uterine lining for implantation and helps maintain early pregnancy until the placenta takes over hormone production. It makes intuitive sense that too little progesterone could lead to miscarriage, and there is evidence supporting the connection. Women with recurrent pregnancy loss are more likely to have short luteal phases (the window between ovulation and the next period) and low mid-luteal progesterone levels. One study found that a progesterone concentration below 10 ng/mL and a luteal phase shorter than 10 days were strongly associated with recurrent loss.⁷

But here is where the story gets complicated. Just because progesterone levels are lower in pregnancies that fail does not prove the low progesterone caused the failure. A failing pregnancy with chromosomal abnormalities may produce less progesterone as a consequence, not a cause, of the problem. Research looking at endometrial tissue has found that women with unexplained recurrent miscarriage can have normal blood levels of progesterone and estrogen yet abnormal receptor activity in the uterine lining itself, suggesting the issue may sometimes be how the tissue responds to the hormone rather than how much hormone is circulating.⁸

This distinction matters for treatment. The large PROMISE trial, which randomized over 800 women with recurrent miscarriage to vaginal progesterone or placebo, found only a small and statistically uncertain improvement in live birth rates with progesterone.⁹ However, both PROMISE and the subsequent PRISM trial showed that the benefit of progesterone supplementation grew larger as the number of prior miscarriages increased.¹⁰ A separate analysis confirmed a meaningful reduction in miscarriage rate following progesterone supplementation in women who had experienced four or more previous losses.¹¹ In other words, progesterone therapy does not seem to help everyone broadly, but it may genuinely help the subgroup whose losses are most likely to have a hormonal contribution.

Interestingly, despite the widespread clinical attention to progesterone, the European Society of Human Reproduction and Embryology (ESHRE) does not recommend routine luteal phase insufficiency testing as part of the standard recurrent-loss workup. The evidence that measuring it changes outcomes is not strong enough to justify routine screening.⁶

PCOS, Insulin Resistance, and Androgens

Polycystic ovary syndrome brings together several hormonal disruptions that each independently raise miscarriage risk. Women with PCOS who experience recurrent pregnancy loss tend to have higher testosterone, higher fasting insulin, higher fasting glucose, and lower insulin sensitivity than women with PCOS who carry pregnancies successfully.¹² Two systematic reviews have found that PCOS women with hyperandrogenism specifically face a higher relative risk of miscarriage.¹²

Animal research suggests a plausible mechanism: the combination of high androgens and insulin resistance appears to cause defects in the uterus during pregnancy, involving mitochondrial dysfunction, oxidative stress, and inflammation.¹³ High BMI and insulin resistance are also independently linked to miscarriage risk in the PCOS population.¹² Yet ESHRE guidelines do not currently recommend routine testing for PCOS, fasting insulin, or androgens as part of the recurrent loss workup, because the evidence that identifying these factors changes the next pregnancy’s outcome remains thin.⁶

Uncontrolled blood sugar, whether from PCOS or pre-existing diabetes, is its own risk factor. In one retrospective study comparing women with well-controlled and poorly controlled diabetes in pregnancy, the miscarriage rate in the poorly controlled group was about seven times higher.¹⁴ This is one of the few hormonal-metabolic risk factors where the intervention is straightforward: getting blood sugar under control before and during pregnancy clearly improves outcomes.

Cortisol and the Stress Question

The idea that stress can cause miscarriage is one of the most emotionally loaded questions in this space, and the evidence pulls in different directions. One carefully designed study measured cortisol in women’s urine during the earliest weeks of pregnancy, before they even knew they were pregnant. Pregnancies that coincided with elevated cortisol were roughly 2.7 times more likely to end in loss, and about 90% of the high-cortisol pregnancies failed compared with about a third of normal-cortisol pregnancies.¹⁵ That is a striking result that suggests cortisol can disrupt pregnancy at its most vulnerable stage.

But a separate study using validated psychological stress scales alongside cortisol measurements found no relationship between psychosocial stress and miscarriage risk.¹⁶ The important distinction may be between the biological event of cortisol elevation, which can stem from illness, sleep disruption, physical stress, or other physiological causes, and the subjective feeling of being stressed. Perceived stress does not reliably translate into the kind of sustained cortisol surge that the biological research implicates. Reviews of the broader literature note that stress hormones like cortisol and corticotropin-releasing hormone can interact with immune cells in ways that destabilize the delicate immune tolerance pregnancy requires, but call for more research before drawing firm conclusions.¹⁷

The practical upshot: telling someone their miscarriage happened because they were “too stressed” is not supported by the evidence, and it adds guilt to grief. But the biological finding that cortisol elevations correlate with very early pregnancy loss is real and points toward mechanisms that future research may clarify.

Prolactin and Pituitary Hormones

Elevated prolactin, the hormone best known for stimulating milk production, has a plausible connection to miscarriage through its effects on ovarian function. High prolactin levels can suppress ovulation and shorten the luteal phase, which may create conditions unfavorable for early pregnancy.¹⁸ Some clinicians treat elevated prolactin with dopamine agonist medications in the hope of reducing future miscarriages, but the evidence base for this practice is limited. ESHRE recommends against prolactin testing in women with recurrent loss unless they show clinical symptoms of hyperprolactinemia, such as irregular or absent periods.⁶

What hCG Patterns Actually Tell You

Human chorionic gonadotropin (hCG) is produced by the developing placenta and is the hormone that pregnancy tests detect. A sluggish rise in hCG is associated with miscarriage, and clinicians have long used hCG doubling rates to monitor early pregnancies that seem uncertain. A recent retrospective analysis found that specific hCG doubling-rate thresholds could help predict which pregnancies were at higher risk of early loss, including in women with a history of recurrent miscarriage.¹⁹ A prospective cohort study tracking urinary hCG trajectories in women who had undergone embryo transfer identified three distinct patterns, and women whose hCG followed the lowest and slowest trajectory had dramatically higher odds of miscarriage compared with those in the highest trajectory.²⁰

It is worth understanding that low hCG is usually a marker of a pregnancy that is already failing rather than a hormonal cause of the failure itself. A chromosomally abnormal embryo or one that implanted poorly will produce less hCG. So while hCG levels are useful for monitoring, they do not typically point to a treatable hormonal imbalance the way thyroid problems or insulin resistance might.

Ovarian Reserve and Egg Quality

Anti-Müllerian hormone (AMH) is produced by developing follicles in the ovary and serves as a marker of ovarian reserve. A meta-analysis pooling data from retrospective and prospective studies found that women with low AMH had roughly 35% higher odds of miscarriage in assisted-reproduction pregnancies, and naturally conceiving women with low AMH showed a similar increase in risk.²¹ One study found that women with very low AMH (at or below 0.4 ng/mL) had about 2.2 times the risk of miscarriage compared with women whose AMH was above 1 ng/mL.²² Women with recurrent miscarriage have also been found to have higher FSH and lower AMH than controls, consistent with a diminished ovarian reserve.²³

The connection is likely about egg quality rather than hormone levels per se. As ovarian reserve declines, the remaining eggs are more likely to carry chromosomal errors, circling back to the dominant cause of miscarriage. Low AMH does not mean the hormonal environment itself is hostile to pregnancy; it means the supply of healthy eggs is running low. ESHRE does not recommend routine ovarian reserve testing in the recurrent-loss workup for this reason: it tells you something about prognosis but does not point to a treatment that changes outcomes.⁶

Environmental Chemicals That Disrupt Hormones

One angle that often gets overlooked in discussions of hormonal imbalance and miscarriage is the role of environmental endocrine-disrupting chemicals (EDCs). These are synthetic compounds found in plastics, personal care products, food packaging, and industrial settings that can mimic or interfere with the body’s own hormones. A systematic review and meta-analysis found that maternal exposure to phthalate esters was associated with about 55% higher odds of miscarriage, and specific chemicals including BPA and several individual phthalate metabolites showed statistically significant links to pregnancy loss.²⁴ Per-and polyfluoroalkyl substances (PFAS) and BPA exposure were also tied to other adverse pregnancy outcomes like preterm birth and low birth weight.

These chemicals may create a kind of “hormonal imbalance” that no blood test would flag as an endocrine disorder. They operate at low doses and through subtle disruption of estrogen signaling, progesterone action, and thyroid function. Research in this area is still maturing, and we are far from being able to tell an individual patient whether their exposure level played a role in a specific loss. But the population-level data is concerning enough to warrant basic precautions: limiting use of plastic food containers (especially with heat), choosing fragrance-free personal care products, and filtering drinking water are sensible steps during pregnancy planning.

When the Father’s Hormones Matter

Almost all discussion of hormonal causes of miscarriage focuses on the mother, but there is emerging evidence that the male partner’s endocrine function can contribute. A study comparing male partners of women with recurrent miscarriage to partners of women with uncomplicated pregnancies found that the recurrent-loss group had impaired reproductive endocrine function, higher levels of reactive oxygen species in semen, and more sperm DNA fragmentation.²⁵ In essence, reduced steroid production in the testes may lead to lower-quality sperm, which in turn may contribute to embryos that are more likely to fail after implantation.

This line of research is relatively new, and no guidelines currently recommend hormonal testing for male partners in the recurrent miscarriage workup. But it challenges the default assumption that miscarriage is entirely a maternal problem and opens up a potential avenue for future intervention.

Vitamin D and Uterine Immune Tolerance

Vitamin D occupies an interesting gray zone. The uterine lining has receptors for vitamin D and the enzyme needed to activate it locally, meaning the endometrium can use vitamin D as a signaling molecule independent of what circulates in the bloodstream. Disrupted vitamin D signaling in the uterus has been linked to increased inflammation, impaired transformation of the lining for implantation, and shifts in the immune cell balance that pregnancy requires for survival.²⁶ Despite these plausible mechanisms, ESHRE found no evidence that vitamin D deficiency is a contributing factor for recurrent pregnancy loss and does not recommend testing for it.⁶ The biology is suggestive, but the clinical data connecting low vitamin D to actual miscarriage outcomes has not materialized convincingly enough to change practice. This is a space to watch rather than act on aggressively.

Why So Few Hormonal Tests Are Actually Recommended

One of the most counterintuitive findings in this area is how many hormonal tests the major guidelines recommend against for women with recurrent pregnancy loss. The ESHRE guideline, one of the most respected in the field, advises against routine testing of androgens, luteinizing hormone, fasting insulin, prolactin (unless symptoms are present), ovarian reserve markers, and luteal phase progesterone in the standard recurrent-loss workup.⁶ The sole hormonal screen they do endorse is for thyroid function and thyroid antibodies.

This is not because the other hormones are irrelevant. It is because the bar for recommending a test in clinical guidelines is high: the test must identify something that, when treated, actually improves outcomes in the next pregnancy. For most hormonal factors besides thyroid disease, the evidence that treatment changes the prognosis simply is not robust enough yet. Progesterone supplementation may help women with many prior losses, and blood sugar control clearly matters for women with diabetes, but these situations can often be identified from medical history alone rather than from a panel of hormone tests. The gap between “this hormone is biologically involved in pregnancy” and “measuring and treating it prevents miscarriage” is wider than most people expect, and it is the reason many women feel frustrated after a loss when their doctor does not order every test imaginable. The restraint is evidence-based, even if it does not feel satisfying.

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