Lab Library

Fertility -- Women

Fertility -- Women is a lab panel for trying to conceive, cycle irregularity, or a pre-conception baseline. It covers 13 markers. This page explains what each one measures, what it does NOT measure, and which nutrients are known to move it.

The markers, and what they actually tell you

Each marker below carries its technical name, what it measures in plain language, the limits of what it can tell you, and the nutrients known to move it. Where a framework and mainstream practice disagree, both views are shown rather than one being hidden.

Anti-Mullerian Hormone (AMH)

Cellular Six: Sense

This marker sits in Sense -- signals being produced, detected and acted on.

A hormone secreted by small growing ovarian follicles, used as a proxy for how many eggs remain (ovarian reserve/quantity). It does **not** measure egg quality, and it is a poor predictor of natural per-cycle fertility in women without other risk factors -- its main clinical use is guiding IVF stimulation dosing.

Typical range: Highly age-dependent with no single universal "normal" number; rough lab bands (assay-dependent): >3.0 ng/mL runs high (sometimes PCOS-associated), 1.0-3.0 ng/mL "normal," 0.5-1.0 ng/mL "low-normal," <0.5 ng/mL "low." No legitimate functional-optimal target exists -- AMH is expected to decline with age, and that decline is normal, not a deficiency to correct.

Nutrients that move it

  • No nutrient in controlled human trials has been shown to raise AMH itself or meaningfully "restore" ovarian reserve -- the follicle pool AMH reflects is essentially fixed and non-renewable. (mechanism/expert opinion, uncited -- included to be explicit that no real lever exists here)
  • CoQ10emerging -- doesn't move AMH, but in women with diminished ovarian reserve undergoing IVF, CoQ10 pretreatment (commonly 200-600 mg/day for 6-8 weeks before stimulation) increased the number of oocytes retrieved, fertilization rate, and top-quality embryos in a prospective RCT, and a pooled meta-analysis of 6 RCTs (1,529 DOR patients) found consistent improvements in ovarian response and embryo quality -- though live-birth data across these trials is still limited. This is an egg-quality/ovarian-response signal, distinct from AMH itself. (cite: Xu Y et al., Reproductive Biology and Endocrinology, 2018, PMC5870379; systematic review/meta-analysis of 6 RCTs, Annals of Medicine, 2024, PMC11321116)
  • DHEA supplementation (distinct from the endogenous DHEA-S marker)contested -- widely marketed for diminished ovarian reserve based on smaller, older positive trials, but the largest and most rigorous RCT to date (821 women with DOR, randomized to DHEA vs. placebo for 4-12 weeks before ART) found **no difference** in oocytes retrieved, live birth rate, or cumulative live birth rate between groups -- directly contradicting the supplement's popular reputation. (cite: Wang et al., large multicenter RCT summarized in Fertility and Sterility systematic review/meta-analysis of DOR therapies, 2024, fertstert.org S0015-0282(24)02256-8)
  • Melatoninemerging -- plausible antioxidant protection of oocytes from follicular oxidative stress; small RCTs show improved oocyte/embryo quality markers, and one pilot RCT in unexplained infertility found a higher pregnancy/live-birth rate with melatonin, but the trial was underpowered for that endpoint and results are inconsistent across studies. (cite: pilot double-blind RCT, Assisted Reproductive Technology, PMC6157331; melatonin in unexplained infertility, PMID 31450726)

Food first: Nothing reliably raises the number itself. General preconception nutrition -- vitamin D sufficiency, adequate antioxidant intake, healthy body weight, not smoking -- supports overall egg quality even though the AMH number won't change.

When to see someone: Be skeptical of any product marketed to "boost AMH" or "reverse ovarian aging" -- this is not supported by reproductive endocrinology evidence. DHEA is a real hormone with androgenic side effects (acne, hair growth/loss, mood changes, voice changes at high doses) and should only be used under a reproductive endocrinologist's supervision, especially given the large null trial above.

Read the studies on Anti-Mullerian Hormone (AMH)

FSH & LH (early-follicular / cycle day 2-4 baseline)

Pituitary gonadotropins -- FSH drives follicle development, LH triggers ovulation and supports corpus luteum function. Day 2-4 FSH was historically used as an ovarian-reserve screen; it has largely been superseded by AMH and antral follicle count because it's less sensitive and more cycle-variable.

Typical range: Conventional: day 2-4 FSH <10 mIU/mL is reassuring, >10-15 mIU/mL suggests diminished reserve (assay-dependent); LH runs similarly in the early follicular phase. An LH:FSH ratio >2-3:1 is sometimes invoked as PCOS-suggestive in older literature, but it is **not** part of the current Rotterdam diagnostic criteria for PCOS and shouldn't be over-weighted.

Nutrients that move it

  • No nutrient reliably lowers an elevated FSH -- an elevated FSH reflects reduced ovarian reserve, a largely fixed biological state, not a correctable deficiency. (mechanism/expert opinion, uncited -- included to set realistic expectations)
  • Adequate energy availabilitysolid -- chronic low energy intake relative to expenditure (very restrictive dieting, high training load without enough fueling) suppresses GnRH pulsatility and can lower LH/FSH, causing hypothalamic amenorrhea; correcting the energy deficit restores normal pulsatile signaling. This is a real nutrition lever, but it works by *not suppressing* the hormones rather than boosting them.

Food first: For anyone with signs of hypothalamic amenorrhea (low LH/FSH, absent or irregular periods, low body fat, high exercise volume), the fix is adequate total energy and carbohydrate intake -- not a supplement. There is no dietary way to lower a truly elevated FSH that reflects diminished ovarian reserve.

When to see someone: Don't chase an elevated FSH with supplements. A low LH/FSH picture with amenorrhea needs a full medical and nutritional workup -- it can reflect serious chronic under-fueling (relative energy deficiency in sport) that carries its own bone-health and cardiovascular risks beyond fertility.

Read the studies on FSH & LH (early-follicular / cycle day 2-4 baseline)

Estradiol (E2)

The primary circulating estrogen, produced by the developing ovarian follicle; rises through the follicular phase, peaks just before ovulation, and supports endometrial lining development.

Typical range: Highly cycle-day dependent (approximate, assay-dependent): early follicular ~20-75 pg/mL, periovulatory peak ~150-750 pg/mL, luteal ~30-450 pg/mL; postmenopausal <20 pg/mL. No single "optimal" number applies outside a specific cycle-day context.

Nutrients that move it

  • Omega-3 fatty acids (EPA/DHA)emerging -- in the EARTH prospective cohort of couples undergoing infertility treatment, women's higher intake of omega-3-rich foods was associated with a lower risk of pregnancy loss; this is a diet-outcome association from an observational cohort, not randomized proof that omega-3 changes estradiol levels themselves. (cite: Mínguez-Alarcón L, Chavarro JE, et al., American Journal of Obstetrics and Gynecology, 2022, PMC9308672)
  • Adequate energy intake and body fatsolid -- estradiol production requires sufficient energy substrate and an intact hypothalamic-pituitary-ovarian axis; both very low and very high body fat can disrupt estradiol levels (low body fat toward suppression, high body fat toward excess peripheral aromatization).

Food first: A Mediterranean-style dietary pattern, adequate healthy fat intake, and a healthy body-fat range support normal estradiol physiology better than any single nutrient.

When to see someone: A single estradiol value only means something in the context of the specific cycle day it was drawn -- don't over-interpret one number without that context.

Read the studies on Estradiol (E2)

Progesterone (mid-luteal, ~cycle day 21)

Produced by the corpus luteum after ovulation; sustains the endometrial lining and early pregnancy. A mid-luteal draw is used mainly to confirm that ovulation occurred.

Typical range: Conventional: >3 ng/mL is generally used to confirm ovulation occurred; many clinicians prefer >10 ng/mL as more robust evidence of adequate luteal function. Functional-medicine opinion sometimes cites >15 ng/mL as an ideal target -- not an established consensus cutoff.

Nutrients that move it

  • Vitex/chasteberry (Vitex agnus-castus)contested -- widely used in herbal/functional medicine for "hormone balance" and luteal-phase symptoms via a proposed dopaminergic/prolactin-modulating mechanism; small trials exist but effects on measured serum progesterone are inconsistent across studies, and it is far short of the rigor applied to actual progesterone supplementation (a prescription medication) in confirmed luteal insufficiency.

Food first: General reproductive health support -- healthy body weight, adequate energy intake -- rather than a specific "progesterone food." Vitex is popular but shouldn't be relied on as a proven progesterone booster.

When to see someone: Low luteal progesterone with recurrent pregnancy loss or confirmed luteal phase defect is a medical management question (progesterone supplementation is a real, evidence-based treatment in specific contexts) -- don't substitute herbs for that conversation with a reproductive endocrinologist.

Read the studies on Progesterone (mid-luteal, ~cycle day 21)

Prolactin

A pituitary hormone whose primary role is lactation; mild elevation can suppress GnRH pulsatility and ovulation, while marked elevation suggests a prolactinoma or a medication side effect.

Typical range: Conventional: roughly 4-23 ng/mL in nonpregnant, non-lactating women (assay-dependent); mild, transient elevations are common with stress, recent breast stimulation/exam, or sleep.

Nutrients that move it

  • Vitex/chasteberrycontested -- traditionally used for mild hyperprolactinemia and cycle irregularity via a proposed dopaminergic effect in small trials, but evidence is thin and inconsistent compared with the evidence-based pharmaceutical treatment (dopamine agonists such as cabergoline or bromocriptine) for clinically significant hyperprolactinemia.
  • Zinc, vitamin B6 -- popular in functional-medicine circles for "balancing" prolactin; weak direct human trial evidence for changing serum prolactin specifically.

Food first: Stress management and adequate sleep are reasonable general support; food does not reliably move a truly elevated prolactin level.

When to see someone: A significantly elevated prolactin needs medical workup (including pituitary imaging if very high) -- don't rely on herbal approaches to manage what could be a prolactinoma or medication effect.

Read the studies on Prolactin

Total & Free Testosterone

Cellular Six: Sense

This marker sits in Sense -- signals being produced, detected and acted on.

Testosterone is physiologically important in women too, at much lower levels than in men; elevated levels (often with low SHBG) are a hallmark of PCOS-related hyperandrogenism.

Typical range: Conventional: total testosterone roughly 15-70 ng/dL, free testosterone roughly 0.1-6.4 pg/mL (both highly assay-dependent -- standard immunoassays are notoriously imprecise at the low female range; mass spectrometry-based assays are more reliable).

Nutrients that move it

  • Myo-inositolemerging -- in PCOS-related hyperandrogenism, several small RCTs pooled in meta-analysis show myo-inositol supplementation reduces testosterone and improves the broader hyperandrogenic/metabolic profile. (cite: meta-analysis of 9 RCTs, 247 vs. 249 PCOS patients, PMC5655679)
  • Zincemerging -- relevant mainly in confirmed zinc-deficient states, not as a general androgen-lowering agent in replete women.

Food first: For PCOS-driven elevation, weight management and a lower-glycemic-load dietary pattern (improving insulin sensitivity, since insulin resistance drives ovarian androgen production) are the most evidence-backed levers -- see the Fasting Insulin/HOMA-IR section below.

When to see someone: Elevated testosterone accompanied by rapidly progressive virilizing signs (fast hair growth, voice deepening, clitoromegaly) needs prompt medical evaluation to rule out an androgen-secreting tumor -- don't assume "it's just PCOS" without that workup.

Read the studies on Total & Free Testosterone

DHEA-Sulfate (DHEA-S)

An adrenal androgen precursor hormone that declines steadily with age; also frequently elevated as part of the PCOS hyperandrogenic picture.

Typical range: Highly age-dependent, roughly 35-430 mcg/dL in adult women, declining through the 30s-60s; no consensus "optimal" replacement target outside diagnosed adrenal insufficiency.

Nutrients that move it

  • See the AMH section above for DHEA *supplementation* evidence -- the largest RCT to date found no ovarian-reserve or live-birth benefit in women with diminished ovarian reserve. No nutrient has been shown to reliably raise *endogenous* DHEA-S.

Food first: General metabolic health (healthy weight, exercise, stress management, sleep) is reasonable, but nothing reliably restores a lower DHEA-S to a younger baseline.

When to see someone: DHEA is sold over-the-counter in the US and has real androgenic effects. Given the null 821-woman RCT above, and the fact that many women being told to take it for fertility already have some degree of PCOS-related androgen excess, it should only be used under reproductive-endocrinology guidance, not self-prescribed.

Read the studies on DHEA-Sulfate (DHEA-S)

Sex Hormone-Binding Globulin (SHBG)

Cellular Six: Sense

This marker sits in Sense -- signals being produced, detected and acted on.

A liver-made protein that binds testosterone and estradiol, controlling how much circulates "free" and biologically active; low SHBG is common in PCOS and insulin resistance and raises free androgen exposure.

Typical range: Conventional: roughly 20-130 nmol/L in women, highly lab- and assay-dependent.

Nutrients that move it

  • Boroncontested -- popular claim that 5-10 mg/day boron lowers SHBG and raises free testosterone; human trial evidence for this specific effect is thin (small, short, inconsistent studies) despite heavy supplement marketing.
  • Cruciferous vegetables / DIM (diindolylmethane)contested -- shifts estrogen metabolism pathways in mechanistic studies; the claim that this meaningfully lowers SHBG or "detoxifies" estrogen in a clinically important way is plausible biochemistry without strong human RCT outcome support.
  • Improving insulin sensitivity (via myo-inositol, weight management, or lower-glycemic eating)emerging -- insulin directly suppresses hepatic SHBG production, so anything that improves insulin resistance (see HOMA-IR section) tends to raise SHBG indirectly, which is a more evidence-grounded lever than boron or DIM.

Food first: Weight management and a lower-glycemic dietary pattern for insulin-resistant women; treat boron/DIM supplement marketing claims skeptically.

When to see someone: Same caution as above -- don't rely on boron or DIM supplements to meaningfully change SHBG or symptoms.

Read the studies on Sex Hormone-Binding Globulin (SHBG)

TSH -- Fertility-Specific Interpretation

Cellular Six: Sense

This marker sits in Sense -- signals being produced, detected and acted on.

Pituitary signal to the thyroid; central to preconception and pregnancy screening because maternal thyroid hormone drives early fetal brain development before the fetal thyroid becomes functional (~week 12).

Typical range: Conventional nonpregnant upper limit is roughly 4.0-4.5 mIU/L (or 4.12 mIU/L using the reference population in the 2024 ASRM guideline). Older functional-medicine guidance and the 2011 ATA pregnancy guideline popularized a stricter <2.5 mIU/L preconception target. **Important honest update:** ASRM's 2024 practice guideline (Fertil Steril 2024;121:765-82), after a fresh systematic review that explicitly screened out lower-quality and data-integrity-flagged studies, concluded there is moderate evidence that **TSH levels between 2.5 and 4.0 mIU/L are NOT associated with increased miscarriage risk**, and found only weak evidence that subclinical hypothyroidism is associated with infertility at all. Universal preconception TSH screening is not recommended; the guideline reserves screening for higher-risk patients (autoimmune disease, thyroid symptoms, personal/family thyroid history, prior thyroid surgery/radiation). This directly contradicts the popular "get your TSH under 2.5 before trying to conceive" advice still common in functional-medicine circles. (cite: ASRM Practice Committee, Fertility and Sterility, 2024, subclinical hypothyroidism in the infertile female population guideline)

Nutrients that move it

  • Iodine** and **seleniumsolid -- see `Function-Health-Hyman.md` Thyroid section and `Thyroid.md` for full detail; both are legitimate thyroid-hormone-synthesis cofactors, but excess of either can worsen thyroid autoimmunity.

Food first: Adequate iodine without megadosing; selenium sufficiency, particularly if autoimmune thyroiditis (elevated TPO/Tg antibodies) is present.

When to see someone: The "under 2.5" TSH target came from older guidance and is not an agreed treatment threshold -- chasing it with high-dose iodine can worsen autoimmune thyroid disease specifically. The band is the target, not the floor.

Read the studies on TSH -- Fertility-Specific Interpretation

Fasting Insulin, Glucose & HOMA-IR

HOMA-IR = (fasting glucose mg/dL x fasting insulin uIU/mL) / 405, a calculated estimate of insulin resistance. Insulin resistance and compensatory hyperinsulinemia drive ovarian androgen production in a large subset (not all) of PCOS patients.

Typical range: No single universal HOMA-IR cutoff exists -- research studies commonly use thresholds ranging from 1.67 to 2.5+ depending on the population studied. Fasting insulin: <10 uIU/mL is often called "normal" on a standard lab report; functional-medicine opinion favors <5-7 uIU/mL, which is not a consensus clinical cutoff.

Nutrients that move it

  • Myo-inositol +/- D-chiro-inositolemerging -- multiple RCTs and meta-analyses show inositol improves insulin sensitivity markers, ovulation rate, and menstrual regularity in PCOS, and a meta-analysis of ART-outcome trials found higher clinical pregnancy rates (RR 1.64, 95% CI 1.25-2.15) and more top-grade embryos (RR 1.12) with myo-inositol/D-chiro-inositol supplementation. **However**, the 2024 update to the international evidence-based PCOS guideline reviewed this same literature and graded the overall body of inositol evidence as limited and inconsistent, explicitly calling for shared decision-making with patients rather than routine recommendation -- so despite its popularity, treat inositol as promising-but-unsettled rather than a proven PCOS treatment. (cite: meta-analysis of 9 RCTs, PMC5655679; ART-outcomes meta-analysis, PMC12413536; International Evidence-Based PCOS Guideline update, JCEM, 2024, PMC11099481)
  • N-acetylcysteine (NAC)emerging -- a meta-analysis of 8 RCTs (910 women with PCOS) found NAC improved ovulation rate (OR 4.49), pregnancy rate (OR 3.97), and live birth rate (OR 3) versus placebo, though NAC underperformed metformin in head-to-head comparisons within the same analysis, and a separate, more recent RCT found no difference between NAC and L-carnitine in clomiphene-resistant PCOS. (cite: Thakker D et al., Obstetrics and Gynecology International, 2015, PMC4306416)
  • Chromium, magnesiumemerging -- see `Function-Health-Hyman.md` Metabolic section for the general glycemic-control evidence; the mechanism applies similarly in PCOS but hasn't been rigorously isolated as PCOS-specific.

Food first: A lower-glycemic-load eating pattern, adequate fiber and protein, regular physical activity (resistance training especially improves insulin sensitivity), and weight management if BMI is elevated remain more consistently evidence-backed than any single supplement -- metformin is the best-studied pharmaceutical comparator in this space.

When to see someone: Inositol is generally well tolerated, but anyone combining it with metformin or other glucose-lowering medication should loop in their clinician. NAC can cause GI upset at higher doses. None of these supplements substitute for an actual PCOS diagnostic workup (androgen levels, pelvic ultrasound, glucose tolerance testing) or ruling out other causes of anovulation.

Read the studies on Fasting Insulin, Glucose & HOMA-IR

Ferritin

Cellular Six: Exchange

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

Reflects iron stores (though it also rises with inflammation, so it isn't iron-specific in isolation); relevant to fertility both through anemia's effect on energy/ovulation and through iron's cofactor role in cellular metabolism.

Typical range: Conventional: roughly 15-150 ng/mL in women (lab-dependent). Functional-medicine opinion often cites 50-100 ng/mL as a better fatigue/functional target than the low end of "normal" -- not an official diagnostic threshold.

Nutrients that move it

  • Iron intakesolid -- the Nurses' Health Study II found women who took iron supplements had a significantly lower risk of ovulatory infertility than nonusers (RR 0.60, 95% CI 0.39-0.92), and total nonheme iron intake was inversely associated with ovulatory infertility risk in a dose-response pattern; heme iron intake showed no such association. **However**, a more recent (2023) study looking specifically at ovarian reserve markers (AMH, antral follicle count) found no consistent association between iron intake and ovarian reserve, and the original ovulatory-infertility finding has not been consistently replicated in newer cohorts. Grade this as real, dated, mechanistically-plausible observational evidence -- not settled science that "more iron helps fertility." (cite: Chavarro JE et al., Obstetrics & Gynecology, 2006, PMID 17077236; iron intake and ovarian reserve, Human Reproduction, 2023, PMC10391310)
  • Vitamin Csolid -- enhances nonheme iron absorption; see `Function-Health-Hyman.md` Iron entry for the general iron-repletion evidence, which applies the same way here.

Food first: Heme iron sources (red meat, poultry, fish) are more bioavailable than plant iron; pair plant iron with vitamin C-rich foods; avoid pairing iron-rich meals with coffee, tea, or calcium supplements, which block absorption.

When to see someone: Confirm it before correcting it. Iron overload causes real organ damage, and ferritin doubles as an inflammatory marker, so a "normal" number can hide a deficiency -- interpret it with iron saturation and CRP rather than in isolation.

Read the studies on Ferritin

Homocysteine, Folate/Methylfolate, Vitamin B12, Vitamin B6

Cellular Six: Build

This marker sits in Build -- the raw material for making and renewing structure.

Homocysteine is an amino acid byproduct that rises when B-vitamin-dependent "remethylation" back to methionine is inadequate; elevated homocysteine is associated with cardiovascular risk and, observationally, with recurrent pregnancy loss.

Typical range: Conventional: roughly 4-15 micromol/L (lab-dependent); functional-medicine opinion favors <7-8 micromol/L, tighter than the standard upper limit.

Nutrients that move it

  • Folic acid / folate / methylfolate -- neural tube defect preventionsolid -- periconceptional folic acid supplementation is one of the best-established preventive interventions in medicine: the landmark MRC Vitamin Study RCT found folic acid reduced neural tube defect recurrence risk by 72% (RR 0.28, 95% CI 0.12-0.71) in high-risk women. This is genuinely solid evidence and the reason folic acid/folate is a standard preconception recommendation. (cite: MRC Vitamin Study Research Group, The Lancet, 1991, PMID 1677062)
  • Folic acid -- miscarriage prevention specificallyemerging -- a small but rigorous 2026 systematic review/meta-analysis (3 RCTs) found high-dose folic acid (4 mg/day) reduced miscarriage risk by about 27% compared with the standard 0.4 mg/day dose (RR 0.73, 95% CI 0.56-0.94) among women who achieved pregnancy. This is a new, promising finding based on only 3 trials -- treat it as an emerging signal needing replication, not an established reason to self-prescribe high-dose folic acid, since high-dose folic acid also has its own considerations (see safety note). (cite: Vinti et al., American Journal of Obstetrics & Gynecology MFM, 2026)
  • Methylfolate (5-MTHF) vs. folic acid for MTHFR variants -- women with MTHFR polymorphisms convert folic acid to its active form less efficiently, and methylfolate is often recommended as an alternative; this is biochemically plausible and widely practiced, but outcome-level trial evidence that methylfolate specifically improves fertility or pregnancy outcomes beyond standard folic acid is thin.
  • Vitamin B12solid -- B12 deficiency and hyperhomocysteinemia are both independently associated with recurrent pregnancy loss in case-control data (one study found ORs of 7.02 and 16.39, respectively), and B12/folate supplementation reliably lowers homocysteine. Whether correcting homocysteine itself (versus other factors correlated with poor B12/folate status) reduces miscarriage risk has not been proven in large RCTs. (cite: NIH Office of Dietary Supplements, Vitamin B12 Health Professional Fact Sheet; case-control study, recurrent pregnancy loss and B12/folate/homocysteine, PMC10480748)

Food first: Leafy greens and legumes (folate), animal products/fortified foods (B12), poultry/fish/potatoes/bananas (B6); a standard prenatal vitamin covers this for most B-vitamin-replete women. Supplementing the *specific* deficient B-vitamin lowers homocysteine reliably; extra B-vitamins in an already-replete woman do not further lower homocysteine.

When to see someone: Very high-dose B6 (>100 mg/day long-term) can cause peripheral neuropathy. High-dose folic acid (as in the emerging miscarriage-prevention data above) can mask an underlying B12 deficiency by normalizing red-cell size while the neurological effects of B12 deficiency continue unchecked -- always check B12 alongside folate, especially in vegans/vegetarians or after bariatric surgery. Kidney disease independently raises homocysteine regardless of B-vitamin status.

Read the studies on Homocysteine, Folate/Methylfolate, Vitamin B12, Vitamin B6

Vitamin D (25-hydroxyvitamin D)

Cellular Six: Build

This marker sits in Build -- the raw material for making and renewing structure.

The standard clinical measure of vitamin D status; functions more like a hormone than a classic vitamin, with roles in calcium regulation, immune function, and (per emerging fertility data below) reproductive outcomes.

Typical range: Conventional (Endocrine Society): deficient <20 ng/mL, insufficient 20-29 ng/mL, sufficient >=30 ng/mL. Functional-medicine opinion often cites 40-60 ng/mL, but the Endocrine Society's own 2024 guideline update declined to set an optimal target for healthy adults, noting outcome-specific benefit levels haven't been established in trials.

Nutrients that move it

  • Vitamin D and IVF outcomesemerging -- a trial-sequential meta-analysis of 5 RCTs found vitamin D supplementation improved chemical pregnancy rate (RR 1.53, 95% CI 1.06-2.20) but **not** clinical pregnancy rate (RR 1.34, 95% CI 0.81-2.24). A separate meta-analysis of 12 studies (9 RCTs + 3 cohorts) found a significantly higher clinical pregnancy rate (OR 1.70, 95% CI 1.24-2.34) specifically among infertile women who were vitamin-D-deficient and got repleted -- so the benefit looks concentrated in women who start out deficient, not a general fertility booster for everyone. (cite: trial sequential meta-analysis of 5 RCTs, Frontiers in Endocrinology, 2022, PMC8969598; meta-analysis of 12 studies, 2023, PMC9896710)
  • Vitamin D and PCOSemerging -- meta-analyses show modest improvement in ovulation/menstrual regularity with repletion in vitamin-D-deficient PCOS patients; effect on live birth specifically is less established.

Food first: Fatty fish, egg yolks, fortified foods, sensible sun exposure; supplementation (typically 1000-4000 IU/day) is often needed to reach sufficiency, and correcting a true deficiency preconception is low-risk and low-cost even given the modest outcome data above.

When to see someone: Toxicity is rare but real above ~10,000 IU/day sustained without monitoring (causes hypercalcemia). People with granulomatous disease or hyperparathyroidism need medical supervision before supplementing.

Read the studies on Vitamin D (25-hydroxyvitamin D)

Food first, then fill the gaps

Every marker above lists the nutrients known to move it. Build a day around them first -- the Diet Builder shows which food groups you are consistently missing, inside the way you already eat.