Vitamin D and Fertility: Why Ontario Women Are at Particular Risk

By Dr. Pamela Frank, BSc(Hons), ND – Published July 2026

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Vitamin D is the nutritional deficiency I find most consistently in fertility patients – and the one that is most consistently undercorrected even in patients who are already supplementing.

It is also one of the few nutritional variables in reproductive medicine where the mechanistic rationale, the observational data, and the clinical logic all point in the same direction clearly enough to act on – even while the randomized controlled trial evidence on supplementation remains mixed. This post explains why D matters for fertility at a biological level, what the research actually shows, what the right target level is for fertility (which differs from the general health target), and why women in Ontario face a specific, compounding problem with this nutrient.

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Vitamin D Is Not Just a Vitamin

The first thing to understand about D3 is that it does not behave like other vitamins. Vitamins are cofactors – they support enzymatic reactions. Vitamin D is a steroid hormone precursor. Once converted to its active form (calcitriol, or 1,25-dihydroxyvitamin D), it binds to vitamin D receptors (VDRs) in the nucleus of cells and directly regulates gene expression – turning genes on and off in the same way other steroid hormones do.

This distinction matters for fertility because steroid hormone action in reproductive tissue is not peripheral. Vitamin D receptors have been identified in the ovary, endometrium, fallopian tubes, pituitary gland, testes, and sperm – every tissue directly relevant to reproduction.¹ When D is deficient, gene expression in all of these tissues is altered. This is not a subtle nutritional effect. It is a hormone deficiency affecting reproductive organs.

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How It’s Made – and Why It’s a Problem in Ontario

Vitamin D is produced in the skin when ultraviolet B (UVB) radiation from sunlight converts 7-dehydrocholesterol to previtamin D3, which is then converted to vitamin D3 (cholecalciferol). This dietary- and skin-produced form is first converted in the liver to 25-hydroxyvitamin D (the form measured in blood tests), and then in the kidneys and other tissues to the active form, calcitriol.

The critical point for anyone living in Ontario: UVB radiation sufficient to produce D in the skin requires the sun to be at an angle of at least 45 degrees above the horizon. At Toronto’s latitude (43.7°N), this condition is met only between approximately April and September – and only during midday hours even in those months. From October through March, no amount of time outdoors in Ontario produces meaningful levels of D, regardless of how clear the sky is or how warm it feels.²

This means that for approximately five months of the year, Ontarians produce next to no D from sun exposure. Dietary sources – fatty fish, egg yolks, fortified milk and plant milks – provide only 100–400 IU per serving, far below the amounts required to maintain optimal levels. The result is that D deficiency is endemic in this province across all demographics, worsening through the winter, and rarely fully corrected by standard-dose supplementation.

Studies of Canadian adults consistently find 25-OH vitamin D levels below 50 nmol/L in 25–40% of the population during winter months, and below 75 nmol/L – the threshold most fertility-specific research uses to define insufficiency – in well over half.³ This is not a fringe problem or a dietary failure in any individual patient. It is a structural consequence of living at this latitude.

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The Fertility-Specific Mechanisms

The mechanisms by which this vitamin affects reproductive function are specific and operate across multiple levels of the reproductive system simultaneously.

Granulosa Cell Function and Ovarian Reserve

Vitamin D receptors (VDR) are expressed on granulosa cells – the cells that surround and nourish the developing follicle, produce estradiol, and respond to FSH stimulation. VDR activation in granulosa cells regulates FSH receptor expression, estradiol production, and anti-Müllerian hormone (AMH) secretion.⁴

The AMH relationship is particularly important clinically. AMH is produced by granulosa cells of small antral follicles and is the primary clinical marker of ovarian reserve. D deficiency is associated with altered AMH signalling in granulosa cells, with studies showing that VDR activation in granulosa cells directly stimulates AMH gene transcription. This provides a mechanistic pathway through which vitamin D deficiency could impair ovarian reserve signalling, independently of the number of remaining follicles.⁵

In PCOS specifically, where AMH is characteristically elevated and follicular arrest is a central feature, VDR-mediated regulation of granulosa cell function is particularly relevant. Multiple studies have found that vitamin D supplementation in vitamin D-deficient women with PCOS improves follicular development, reduces AMH, and supports more regular ovulation – consistent with this mechanism.⁶

Endometrial Receptivity and Implantation

This is where the evidence is strongest and most directly relevant to clinical fertility outcomes. D receptors are densely expressed in the endometrial stroma and glandular epithelium. VDR activation in endometrial tissue regulates:

Homeobox (HOX) gene expression:

The HOXA10 and HOXA11 genes are essential regulators of endometrial receptivity – they govern the molecular changes that open the window of implantation. D directly upregulates HOXA10 expression in endometrial stromal cells, and HOXA10 deficiency is associated with implantation failure.⁷ This is one of the most direct mechanistic links between vitamin D and implantation: VDR activation in the endometrium turns on the gene that opens the implantation window.

Uterine immune regulation:

Successful implantation requires a precisely calibrated immune response – tolerant enough to allow the embryo to invade, active enough to support trophoblast development and placentation. D shifts the uterine immune environment toward tolerance by suppressing Th1-mediated pro-inflammatory cytokines (IL-1, IL-6, TNF-α) and promoting regulatory T-cell activity.⁸ Disruption of this immune balance – including from vitamin D deficiency – is associated with implantation failure and recurrent miscarriage.

Endometrial decidualization:

Decidualization – the transformation of endometrial stromal cells in preparation for embryo invasion – is a D-dependent process. VDR activation in stromal cells directly supports the differentiation required for normal decidualization, and impaired decidualization is associated with implantation failure and early pregnancy loss.

The Thyroid Autoimmunity Connection

Vitamin D has direct immunomodulatory effects on thyroid autoimmunity – relevant to fertility because anti-thyroid antibodies are present in 14–33% of women with infertility and recurrent miscarriage, and independently impair implantation and increase pregnancy loss risk.

D deficiency is consistently more prevalent in women with Hashimoto’s thyroiditis and autoimmune thyroid disease than in euthyroid controls. VDR polymorphisms are associated with susceptibility to autoimmune thyroid disease. And D3 supplementation has demonstrated reductions in anti-TPO antibody titers in some trials – though the evidence here is less consistent than for selenium.⁹

The practical implication: correcting vitamin D deficiency is part of the management of thyroid autoimmunity in the fertility context, not separate from it.

Sperm Function

Vitamin D receptors are expressed on spermatozoa and in the male reproductive tract, and vitamin D deficiency in men is associated with reduced sperm motility, reduced progressive motility, and impaired sperm morphology in multiple observational studies.¹⁰

The proposed mechanisms include: VDR-mediated regulation of calcium influx into sperm (required for the acrosome reaction and fertilization), regulation of sperm mitochondrial function relevant to motility, and modulation of testosterone production in Leydig cells through VDR-dependent pathways.

A 2016 RCT found that D supplementation in vitamin D-deficient men improved sperm motility significantly compared to placebo – one of the more direct trial-level evidence pieces for male fertility specifically.¹¹

Pregnancy Maintenance and Miscarriage Risk

Beyond conception, D plays direct roles in early placentation – supporting trophoblast invasion, angiogenesis of the developing placental vasculature, and immune tolerance of the embryo. Vitamin D deficiency in early pregnancy is associated with increased miscarriage risk in observational studies, consistent with the endometrial immune and decidualization mechanisms described above.¹²

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What the IVF and Vitamin D Research Shows

The IVF literature on vitamin D is where I need to present the evidence carefully, because it is genuinely more nuanced than the clear mechanistic story above.

Observational data: consistent and meaningful

A 2022 meta-analysis by Iliuta et al., pooling data from multiple cohort studies, found that women with sufficient vitamin D status (above 75 nmol/L) had significantly higher implantation, clinical pregnancy, and live birth rates in IVF using their own eggs compared with vitamin D-deficient women.¹³ A 74% higher live birth rate in sufficient versus deficient women is a clinically large effect size.

Importantly, this association was present only in autologous oocyte cycles – not in donor egg cycles. This is mechanistically consistent: if D’s primary reproductive role is in endometrial receptivity and uterine immune regulation, the effect should be observable when the egg is from the same woman (where both oocyte quality and endometrial factors vary together) but should be attenuated in donor cycles where the endometrium is the primary variable.

A 2025 prospective cohort study of FET cycles found that D supplementation in women with insufficient D status significantly improved clinical pregnancy rates compared with unsupplemented women with insufficient D status, with no difference between supplemented and naturally sufficient women.¹⁴ This is a practically important finding: correction of deficiency appears to restore outcomes toward those of naturally sufficient women.

Supplementation RCTs: mixed but trending positive

The randomized controlled trial evidence on vitamin D supplementation and IVF outcomes is more heterogeneous. A 2023 meta-analysis found that moderate daily vitamin D supplementation significantly increased clinical pregnancy rates. The 2020 Cochrane review found no significant difference in live birth rates – but included only two RCTs, both with methodological limitations. Heterogeneity across trials in dosing protocols, baseline vitamin D levels, supplementation duration, and population characteristics complicates pooled analysis.

The clinical interpretation: the observational evidence that vitamin D sufficiency is associated with better IVF outcomes is consistent and mechanistically supported. The RCT evidence that supplementation improves outcomes in already-sufficient women or with short supplementation windows is less compelling. The practical conclusion – correct deficiency before a cycle, target adequacy rather than just sufficiency – is supported by the best available evidence even where the RCT data is mixed.

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The Standard Lab Range Is Not the Fertility Target

This is one of the most important practical points in the entire post, and it is where most patients – and most conventional workups – go wrong.

Standard Ontario laboratory reference ranges for 25-OH vitamin D flag deficiency at below 25 nmol/L and sufficiency at or above 75 nmol/L. Most fertility-relevant research uses a higher threshold – 75–80 nmol/L as the minimum for sufficiency in the reproductive context – and clinical optimization targets in reproductive medicine are typically set at 100–150 nmol/L.

A patient whose lab result shows 76 nmol/L will receive a normal report from most Ontario labs. She is, by fertility-relevant standards, insufficient – and her endometrial HOXA10 expression, uterine NK cell regulation, granulosa cell FSH receptor expression, and sperm DNA integrity in her partner may all be compromised by a level that the lab considers acceptable.

I interpret 25-OH vitamin D results with the fertility target in mind, not the standard lab reference range. The practical target is 100–150 nmol/L for women actively trying to conceive or preparing for IVF.

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How Much Vitamin D Is Needed

Dosing is entirely dependent on the measured baseline level and should not be estimated. The same dose that corrects deficiency in one woman may maintain insufficiency in another, depending on body weight, fat distribution (D is fat-soluble and accumulates in adipose tissue), baseline sun exposure, dietary intake, inflammation, co-factor adequacy, and genetic VDR polymorphisms.

General dosing guidance from the fertility-specific literature:

Maintenance dose of Vitamin D3 in a sufficient person (above 100 nmol/L):

2,000 IU/day vitamin D3 (cholecalciferol), taken with a fat-containing meal.

Correction of insufficiency (50–100 nmol/L):

3,000–4,000 IU/day vitamin D3, taken with fat. Retest at 8–10 weeks.

Correction of deficiency (below 50 nmol/L):

4,000–6,000 IU/day vitamin D3 under monitoring, or a loading protocol followed by maintenance dosing. Retest at 10-12 weeks to confirm the level is moving toward the target.

The fat-soluble nature of D is clinically important in two directions. First, it must be taken with a fat-containing meal for meaningful absorption – taking it on an empty stomach substantially reduces bioavailability. Second, excess D accumulates in fat tissue and can cause toxicity at very high doses sustained over time. Testing before dosing and retesting to confirm response is the correct approach – not guessing.

The upper tolerable limit from Health Canada is 4,000 IU/day for adults without medical supervision. Higher doses used to correct significant deficiency should be done under monitoring.

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Vitamin D3 Versus D2: Which Form to Take

Vitamin D comes in two supplemental forms:

Vitamin D3 (cholecalciferol):

This is the form produced in human skin from sun exposure. It more effectively raises and maintains serum 25-OH vitamin D levels than vitamin D2. Vitamin D3 is the preferred form for supplementation.

Vitamin D2 (ergocalciferol):

This is the plant-derived form, used in some prescription D preparations. It is less potent at raising serum levels than equivalent doses of vitamin D3.

For fertility purposes, vitamin D3 is the supplement form of choice. Most over-the-counter D supplements in Canada contain D3, almost never D2; check the label to confirm.

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Vitamin D and Fertility Diagnosis-Specific Considerations

PCOS:

D deficiency is significantly more prevalent in women with PCOS than in the general population – studies report rates of 67–85% deficiency in PCOS cohorts.¹⁵ D deficiency in PCOS is associated with more severe insulin resistance, higher androgen levels, more irregular cycles, and worse metabolic markers – independently of BMI. Correcting vitamin D is one of the first and most impactful interventions in PCOS management for fertility. See the PCOS page →.

Endometriosis:

Vitamin D has anti-inflammatory and anti-proliferative effects on endometrial tissue through VDR-mediated pathways. Observational studies have found lower D levels in women with endometriosis than in controls, and VDR polymorphisms are associated with susceptibility to endometriosis. There is emerging evidence that vitamin D supplementation may reduce disease activity markers in endometriosis, though trial data is limited.¹⁶

Recurrent miscarriage:

Through its roles in endometrial immune regulation, decidualization, and trophoblast function, vitamin D deficiency is a biologically plausible and clinically supported contributor to recurrent miscarriage. Testing and correcting D is part of the comprehensive recurrent miscarriage workup I conduct. See the recurrent miscarriage page →.

Thyroid autoimmunity:

As described above, correcting vitamin D deficiency is part of the management of Hashimoto’s thyroiditis alongside selenium and anti-inflammatory dietary support.

Fertility over 40:

Vitamin D synthesis efficiency in the skin declines with age, as does renal conversion of 25-OH to active calcitriol. Women over 40 are at compounded risk of D insufficiency from both reduced production and reduced activation. Checking and correcting vitamin D is particularly important in this age group. See the fertility over 40 page →.

Male factor infertility:

Partners of women undergoing fertility treatment should have vitamin D status assessed – particularly in the context of abnormal sperm motility or elevated sperm DNA fragmentation, where the VDR-calcium-acrosome mechanism is most directly relevant.

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What Adequate Vitamin D Cannot Do

Correcting D deficiency is not a fertility treatment in isolation. It does not replace investigation of structural causes, immunological causes, or other hormonal and nutritional factors. In a patient with blocked fallopian tubes, vitamin D status is irrelevant to the primary mechanical obstruction. In a patient with confirmed antiphospholipid syndrome, vitamin D optimization is supportive but not the primary intervention.

Vitamin D is one variable in a comprehensive fertility workup – the most commonly deficient one, the most consistently undertested for fertility-appropriate targets, and one of the most practically correctable. It is worth taking seriously for those reasons. It is not a magic bullet.

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Frequently Asked Questions About Vitamin D and Fertility

How do I know if my vitamin D level is adequate for fertility?

You need a blood test – specifically a serum 25-OH vitamin D (25-hydroxyvitamin D) test. The standard Ontario lab reference range for sufficiency is above 75 nmol/L; the fertility-relevant target is 100–150 nmol/L. A result that your GP considers normal may still be suboptimal for reproductive purposes.

Can I get enough vitamin D from sunlight in Ontario?

Not reliably, and not for most of the year. From October through March, Toronto’s latitude means the sun is too low in the sky to produce meaningful vitamin D in the skin, regardless of how long you spend outdoors. Even in summer months, sunscreen use, time of day, skin pigmentation, and glass windows all reduce effective UVB exposure. Most people in Ontario need supplemental D year-round.

How long does it take to correct vitamin D deficiency?

At a corrective dose of 3,000–5,000 IU/day, significant deficiency typically takes 8–12 weeks to correct. Retesting at 8–10 weeks confirms whether the level is moving toward the target. For women preparing for IVF, starting D optimization as early as possible in the preparation window – ideally three months or more before a cycle – allows time for full correction before stimulation begins.

Is vitamin D safe during pregnancy?

Yes, at doses required to maintain optimal levels. Multiple RCTs and meta-analyses have confirmed the safety of D supplementation during pregnancy. Most prenatal vitamins contain only 400–1,000 IU of vitamin D – often insufficient to maintain optimal levels, particularly in women who enter pregnancy deficient. Measuring and supplementing to target is appropriate both before and during pregnancy.

What dose of vitamin D should I take?

Dosing should be based on your measured 25-OH vitamin D level, not on an estimate. Without testing, there is no reliable way to know whether you need 1,000 IU or 5,000 IU to reach the target. Testing first, supplementing to a specific dose, and retesting to confirm response is the clinically correct approach. As a general reference: 1,000 IU/day raises serum 25-OH vitamin D by approximately 15–25 nmol/L in most adults over 8–12 weeks, though individual response varies significantly.

Does my partner need to check their D level too?

Yes, if sperm motility or DNA fragmentation is a concern. VDR-mediated effects on sperm calcium signalling and motility are mechanistically supported, and supplementation RCT data in men with deficiency show improvement in motility. Testing in male partners is appropriate as part of a comprehensive preconception assessment.

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Vitamin D and Fertility Research References

1. Lerchbaum E, Obermayer-Pietsch B. Vitamin D and fertility: a systematic review. Eur J Endocrinol. 2012 May;166(5):765-78. doi: 10.1530/EJE-11-0984. Epub 2012 Jan 24. PMID: 22275473.
2. Webb AR, Kline L, Holick MF. Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J Clin Endocrinol Metab. 1988 Aug;67(2):373-8. doi: 10.1210/jcem-67-2-373. PMID: 2839537.
3. Langlois K, Greene-Finestone L, Little J, Hidiroglou N, Whiting S. Vitamin D status of Canadians as measured in the 2007 to 2009 Canadian Health Measures Survey. Health Rep. 2010 Mar;21(1):47-55. PMID: 20426226.
4. Irani M, Merhi Z. Role of vitamin D in ovarian physiology and its implication in reproduction: a systematic review. Fertil Steril. 2014 Aug;102(2):460-468.e3. doi: 10.1016/j.fertnstert.2014.04.046. Epub 2014 Jun 3. PMID: 24933120.
5. Dennis NA, Houghton LA, Jones GT, van Rij AM, Morgan K, McLennan IS. The level of serum anti-Müllerian hormone correlates with vitamin D status in men and women but not in boys. J Clin Endocrinol Metab. 2012 Jul;97(7):2450-5. doi: 10.1210/jc.2012-1213. Epub 2012 Apr 16. PMID: 22508713.
6. Wen X, Wang L, Li F, Yu X. Effects of vitamin D supplementation on metabolic parameters in women with polycystic ovary syndrome: a randomized controlled trial. J Ovarian Res. 2024 Jul 16;17(1):147. doi: 10.1186/s13048-024-01473-6. PMID: 39014475; PMCID: PMC11251207.
7. Vilarino FL, Bianco B, Lerner TG, Teles JS, Mafra FA, Christofolini DM, Barbosa CP. Analysis of vitamin D receptor gene polymorphisms in women with and without endometriosis. Hum Immunol. 2011 Apr;72(4):359-63. doi: 10.1016/j.humimm.2011.01.006. Epub 2011 Jan 26. PMID: 21277927.
8. Yu-Gyeong Lee, Danbi Lee, Hwijae Cha, Jungho Ahn, Hwa Seon Koo, Sun-Young Hwang, Gaeun Lee, Youn-Jung Kang, The therapeutic effects of vitamin D3 administration on embryo implantation, Biomedicine & Pharmacotherapy, Volume 176, 2024, 116853, ISSN 0753-3322. https://doi.org/10.1016/j.biopha.2024.116853.
9. Tamer G, Arik S, Tamer I, Coksert D. Relative vitamin D insufficiency in Hashimoto’s thyroiditis. Thyroid. 2011 Aug;21(8):891-6. doi: 10.1089/thy.2009.0200. Epub 2011 Jul 13. PMID: 21751884.
10. de Angelis C, Galdiero M, Pivonello C, Garifalos F, Menafra D, Cariati F, Salzano C, Galdiero G, Piscopo M, Vece A, Colao A, Pivonello R. The role of vitamin D in male fertility: A focus on the testis. Rev Endocr Metab Disord. 2017 Sep;18(3):285-305. doi: 10.1007/s11154-017-9425-0. PMID: 28667465.
11. Blomberg Jensen M, Gerner Lawaetz J, Andersson AM, Petersen JH, Nordkap L, Bang AK, Ekbom P, Joensen UN, Prætorius L, Lundstrøm P, Boujida VH, Lanske B, Juul A, Jørgensen N. Vitamin D deficiency and low ionized calcium are linked with semen quality and sex steroid levels in infertile men. Hum Reprod. 2016 Aug;31(8):1875-85. doi: 10.1093/humrep/dew152. Epub 2016 Jun 19. PMID: 27496946.
12. Pilz S, Zittermann A, Obeid R, Hahn A, Pludowski P, Trummer C, Lerchbaum E, Pérez-López FR, Karras SN, März W. The Role of Vitamin D in Fertility and during Pregnancy and Lactation: A Review of Clinical Data. Int J Environ Res Public Health. 2018 Oct 12;15(10):2241. doi: 10.3390/ijerph15102241. PMID: 30322097; PMCID: PMC6210343.
13. Iliuta F, Pijoan JI, Lainz L, Exposito A, Matorras R. Women’s vitamin D levels and IVF results: a systematic review of the literature and meta-analysis, considering three categories of vitamin status (replete, insufficient and deficient). Hum Fertil (Camb). 2022 Apr;25(2):228-246. doi: 10.1080/14647273.2020.1807618. Epub 2020 Aug 14. PMID: 32791871.
14. Christoforidis N, Papapanou M, Michalakis D, Dimitraki M, Chatziparasidou A, Siristatidis C. Effect of vitamin D supplementation on frozen embryo transfer cycle outcomes. Hum Fertil (Camb). 2025 Dec;28(1):2493251. doi: 10.1080/14647273.2025.2493251. Epub 2025 Apr 25. PMID: 40277196.
15. Krul-Poel YHM, Koenders PP, Steegers-Theunissen RP, Ten Boekel E, Wee MMT, Louwers Y, Lips P, Laven JSE, Simsek S. Vitamin D and metabolic disturbances in polycystic ovary syndrome (PCOS): A cross-sectional study. PLoS One. 2018 Dec 4;13(12):e0204748. doi: 10.1371/journal.pone.0204748. PMID: 30513089; PMCID: PMC6279035.
16. Miyashita M, Koga K, Izumi G, Sue F, Makabe T, Taguchi A, Nagai M, Urata Y, Takamura M, Harada M, Hirata T, Hirota Y, Wada-Hiraike O, Fujii T, Osuga Y. Effects of 1,25-Dihydroxy Vitamin D3 on Endometriosis. J Clin Endocrinol Metab. 2016 Jun;101(6):2371-9. doi: 10.1210/jc.2016-1515. Epub 2016 Apr 1. PMID: 27035829.