Vitamin D and Fertility: Why Deficiency Matters

By Dr (TCM) Attilio D'Alberto | Traditional Chinese Medicine Practitioner, Wokingham

Vitamin D deficiency reduces fertility by lowering ovarian reserve (AMH), worsening egg quality, reducing implantation rates, lowering IVF success and impairing sperm quality in men. The optimal serum 25(OH)D level for fertility is 75–125 nmol/L (30–50 ng/mL) — significantly higher than the UK NHS sufficiency threshold of 50 nmol/L. Most adults trying to conceive need 2,000–4,000 IU of vitamin D3 daily through autumn and winter to reach this range, alongside vitamin K2 (100 mcg) to direct calcium correctly. Test before supplementing; vitamin D is fat-soluble and toxicity is possible at very high doses.

Vitamin D deficiency is one of the most prevalent micronutrient deficiencies in the developed world — estimated to affect over 40% of the UK population and significantly higher proportions in winter months or in individuals who spend little time outdoors. Its relevance to fertility has become increasingly clear over the past decade, with research demonstrating associations between vitamin D status and ovarian reserve, egg quality, implantation rates, IVF success, sperm quality, and pregnancy outcomes. Yet it remains inadequately addressed in most fertility consultations, and many women trying to conceive have never had their vitamin D levels measured.

This post covers what vitamin D does in the reproductive system, what deficiency means for fertility, how to test and interpret levels, how much to supplement, and how vitamin D fits into the broader landscape of nutritional support for conception.

On this page

1. What vitamin D is and how it works
2. Deficiency: how common and why
3. Vitamin D and female fertility
4. Vitamin D and IVF outcomes
5. Vitamin D and male fertility
6. Vitamin D in pregnancy
7. Vitamin D, thyroid and immune function
8. Testing and interpreting levels
9. How much to supplement
10. Food sources
11. My Fertility Guide
12. References

1. What vitamin D is and how it works

Vitamin D is technically a steroid hormone that binds nuclear vitamin D receptors (VDR) in the ovaries, uterus, placenta, testes, pituitary and hypothalamus — explaining why vitamin D status affects fertility, implantation and pregnancy at every level of the reproductive axis.

Vitamin D is technically a steroid hormone rather than a vitamin — it acts on nuclear receptors (the vitamin D receptor, VDR) to regulate gene expression in virtually every tissue of the body. The vitamin D receptor has been identified in the ovaries, uterus, placenta, testes, pituitary gland, and the hypothalamus — in other words, in every major component of the reproductive axis. This tissue distribution explains why vitamin D status has such broad effects on fertility and pregnancy.

The primary form we produce (through sun exposure on skin) and obtain from food is vitamin D3 (cholecalciferol), which is converted in the liver to 25-hydroxyvitamin D (25-OH-D or calcidiol) — the circulating form that is measured in blood tests. This is then further converted in the kidneys and other tissues to the active form, 1,25-dihydroxyvitamin D (calcitriol), which binds to the VDR and exerts biological effects.

Key roles of vitamin D in the reproductive context include: regulation of reproductive hormone synthesis, modulation of immune function (particularly relevant to implantation), anti-inflammatory effects, calcium metabolism, and support of mitochondrial function in eggs and sperm.

2. How common is vitamin D deficiency and why?

Vitamin D deficiency (serum 25-OH-D below 50 nmol/L) affects 40–60% of the UK population at some point each year, with the proportion rising sharply between October and April when UVB sun exposure above 50° latitude is insufficient to drive skin synthesis.

Vitamin D deficiency is defined differently in different guidelines, but a serum 25-OH-D level below 50 nmol/L (20 ng/mL) is widely accepted as deficiency, and levels below 75 nmol/L are considered insufficient for optimal health. Studies in the UK and Northern Europe consistently show that 40–60% of the population has levels below 50 nmol/L at some point during the year, with the proportion rising significantly in winter and spring (October to April in the UK).

Risk factors for vitamin D deficiency include:

• Living above 50 degrees latitude (most of the UK is above this threshold, meaning UVB sun exposure is insufficient for vitamin D synthesis for approximately 6 months of the year)
• Dark skin pigmentation (melanin reduces UVB absorption)
• Spending little time outdoors (office work, indoor lifestyle, cultural practices)
• Consistent use of high-SPF sunscreen
• Obesity (vitamin D is fat-soluble and can be sequestered in adipose tissue)
• Malabsorption conditions (Crohn's disease, coeliac disease, inflammatory bowel disease)
• Very low dietary fat intake
• Exclusively breastfed infants (breast milk is low in vitamin D)

3. Vitamin D and female fertility

Vitamin D supports female fertility by raising AMH and ovarian reserve, supporting follicle development and ovulation through granulosa-cell VDR, regulating HOXA10 and the endometrial implantation window, improving outcomes in PCOS, and reducing inflammatory disease activity in endometriosis.

Research into vitamin D and female fertility has grown substantially in recent years. Key findings include:

Ovarian reserve: Several studies have found positive associations between vitamin D levels and AMH (anti-Müllerian hormone), a key marker of ovarian reserve. Women with higher vitamin D levels tend to have higher AMH and larger antral follicle counts, suggesting that vitamin D supports the maintenance of the follicular pool.

Follicle development and ovulation: Vitamin D receptors are expressed in granulosa cells — the cells that surround and nourish the developing follicle. In vitro studies have shown that vitamin D supports granulosa cell oestrogen and progesterone synthesis, suggesting a direct role in follicular development and ovulation.

Endometrial receptivity: Vitamin D regulates the expression of several genes involved in endometrial receptivity, including HOXA10 — a gene critical to the implantation window. Deficiency may impair the opening of the implantation window, contributing to unexplained infertility and recurrent implantation failure.

PCOS: Women with PCOS have significantly higher rates of vitamin D deficiency than the general population. Studies have shown that vitamin D supplementation in women with PCOS improves insulin sensitivity, menstrual regularity, and hormonal parameters including AMH and testosterone.

Endometriosis: Vitamin D has anti-inflammatory and anti-proliferative effects on endometrial tissue. Studies have found that women with endometriosis have lower vitamin D levels than controls, and some research suggests supplementation may reduce disease activity and pain.

4. Vitamin D and IVF outcomes

Women with sufficient vitamin D levels (≥75 nmol/L) have significantly higher IVF clinical pregnancy rates than deficient women — a 2014 meta-analysis of four studies found a 46% greater likelihood of clinical pregnancy per IVF cycle in vitamin D sufficient women.

Multiple observational studies and several meta-analyses have examined the relationship between vitamin D status and IVF outcomes. The most consistent findings are:

• Women with sufficient vitamin D levels (typically defined as ≥75 nmol/L or ≥30 ng/mL) have significantly higher clinical pregnancy rates per IVF cycle than deficient women
• Vitamin D sufficiency is associated with better quality embryos and higher blastocyst conversion rates
• Endometrial vitamin D receptor expression is associated with improved implantation
• A 2014 meta-analysis of four studies found that women with sufficient serum vitamin D were 46% more likely to achieve a clinical pregnancy per IVF cycle compared to deficient women

These findings have led many fertility specialists to recommend testing and optimising vitamin D levels before IVF, and supplementation to achieve levels above 75 nmol/L is now a standard recommendation in many integrative fertility practice settings.

5. Vitamin D and male fertility

Vitamin D supports male fertility independently of testosterone: deficient men have lower sperm motility, and 3,000 IU vitamin D3 daily for 12 weeks in deficient men improved total sperm count, motility and morphology in a randomised controlled trial. Vitamin D also supports Leydig-cell testosterone synthesis.

Vitamin D receptors are present in sperm and testicular tissue, and vitamin D plays a role in sperm function independent of testosterone. Research has shown:

• Vitamin D-deficient men have lower sperm motility than vitamin D-sufficient men
• Supplementation of 3000 IU vitamin D3 daily for 12 weeks in deficient men improved total sperm count, motility, and morphology in a randomised controlled trial
• Vitamin D supports testosterone synthesis in Leydig cells and may improve total testosterone levels in deficient men

These findings support the inclusion of vitamin D assessment and supplementation in the male partner's fertility preparation as well as the female's.

6. Vitamin D in pregnancy

Optimal vitamin D in pregnancy supports fetal bone development, immune regulation, blood-pressure regulation (reducing pre-eclampsia risk), healthy birth weight, and infant vitamin D stores at birth. UK NICE recommends 400 IU daily but many practitioners and the Endocrine Society recommend 1,500–2,000 IU guided by testing.

Vitamin D requirements increase in pregnancy. Optimal levels support:

• Healthy bone development in the fetus (calcium absorption and mineralisation)
• Immune regulation — reducing the risk of autoimmune complications of pregnancy
• Blood pressure regulation — vitamin D deficiency is associated with increased risk of pre-eclampsia
• Healthy birth weight and reduced risk of preterm birth
• Infant vitamin D stores at birth (exclusively breastfed infants receive limited vitamin D from breast milk)

Current UK guidance (NICE) recommends that all pregnant women take 400 IU vitamin D3 daily. However, given that this level is insufficient to correct deficiency in most people, many practitioners recommend higher doses (1000–2000 IU) during pregnancy, guided by testing. The Endocrine Society recommends 1500–2000 IU as a minimum for pregnant and lactating women.

7. Vitamin D, thyroid and immune function

Vitamin D deficiency drives autoimmune thyroid disease (Hashimoto's, elevated anti-TPO antibodies) and impairs implantation tolerance — the development of tolerogenic T-regulatory cells that allow the mother to accept the genetically half-foreign embryo. Both pathways contribute to implantation failure and early miscarriage.

Two areas of particular relevance to fertility deserve specific mention. First, vitamin D deficiency is associated with autoimmune thyroid disease (Hashimoto's thyroiditis) and with elevated anti-TPO antibodies. Supplementation has been shown in several trials to reduce anti-TPO antibody levels and support thyroid hormone normalisation — with implications for both thyroid function and the associated increased miscarriage risk. See thyroid and fertility.

Second, vitamin D is a central regulator of immune tolerance — the mechanism by which the mother's immune system accepts the embryo (which is genetically half-foreign) rather than rejecting it. Adequate vitamin D is required for the development of tolerogenic T-regulatory cells at the implantation site. Deficiency may contribute to recurrent implantation failure and early miscarriage through immune dysregulation at the maternal-fetal interface.

8. How to test and interpret vitamin D levels for fertility

Vitamin D is measured by a serum 25-OH-D blood test, ideally once or twice a year (end of summer and end of winter). For fertility, the optimal range is 75–125 nmol/L (30–50 ng/mL) — significantly higher than the UK NHS sufficiency threshold of 50 nmol/L.

Vitamin D status is measured through a serum 25-OH-D test. This is available on the NHS (though often only requested when deficiency is suspected) and can be requested through private testing services. Testing once or twice per year (at the end of winter and end of summer) is a sensible approach for anyone trying to conceive.

Interpreting results:

• <25 nmol/L (<10 ng/mL): Severe deficiency
• 25–50 nmol/L (10–20 ng/mL): Deficiency
• 50–75 nmol/L (20–30 ng/mL): Insufficiency
• 75–150 nmol/L (30–60 ng/mL): Sufficiency — optimal range for fertility
• >150 nmol/L (>60 ng/mL): Potentially excessive (uncommon from supplementation alone)

For fertility purposes, the target range is 75–125 nmol/L. Most people achieving consistent supplementation of 2000–4000 IU daily during winter will reach and maintain this range; levels above 150 nmol/L from supplementation alone are uncommon without doses exceeding 10,000 IU daily.

9. How much vitamin D to supplement for fertility

For most adults trying to conceive in the UK, take 2,000 IU vitamin D3 daily year-round as baseline, rising to 3,000–4,000 IU if 25-OH-D is 50–75 nmol/L and 4,000–5,000 IU under supervision if below 50 nmol/L. Co-supplement vitamin K2 (MK-7, 100–200 mcg) to direct calcium correctly. Take with a fat-containing meal.

For most adults trying to conceive in the UK or Northern Europe:

• Maintenance (summer, regular sun exposure): 1000 IU vitamin D3 daily
• Baseline supplementation (year-round for most): 2000 IU vitamin D3 daily
• Correction of deficiency (50–75 nmol/L): 3000–4000 IU vitamin D3 daily until levels optimised, then maintenance
• Correction of significant deficiency (<50 nmol/L): 4000–5000 IU daily under supervision, for 8–12 weeks, then retest

Vitamin D3 (cholecalciferol) is more effective than vitamin D2 (ergocalciferol) at raising and maintaining serum levels — always choose D3. Taking vitamin D with a fat-containing meal improves absorption. Vitamin K2 (MK-7 form, 100–200mcg) is often co-supplemented with vitamin D3 to support calcium direction to bones rather than soft tissues — a sensible practice particularly at higher doses.

10. Food sources of vitamin D

The best food sources of vitamin D are oily fish (salmon, mackerel, sardines, herring, trout) at 400–600 IU per 100 g, cod liver oil (~400 IU per teaspoon), egg yolks, beef liver, fortified foods and UVB-exposed mushrooms — but diet alone cannot maintain optimal fertility levels in the UK without supplementation.

While supplementation is usually necessary in the UK to maintain optimal levels, food sources of vitamin D include:

• Oily fish (salmon, mackerel, sardines, herring, trout) — highest food source, providing 400–600 IU per 100g
• Cod liver oil — very high (approximately 400 IU per teaspoon)
• Egg yolks — small amounts (approximately 40 IU per egg), more in pasture-raised eggs
• Beef liver — moderate amounts
• Vitamin D-fortified foods (some milks, orange juices, cereals) — check labels
• Mushrooms exposed to UV light (UVB) — the only plant-based significant source

Diet alone is insufficient to maintain optimal levels in most people in northern latitudes — supplementation fills the gap that food and limited sun exposure cannot.

11. My Fertility Guide

12. References

• Paffoni A, et al. Vitamin D deficiency and infertility: insights from IVF cycles. J Clin Endocrinol Metab. 2014;99(11):E2372–E2376.
• Lerchbaum E, Obermayer-Pietsch B. Vitamin D and fertility: a systematic review. Eur J Endocrinol. 2012;166(5):765–778.
• Nandi A, et al. Vitamin D and male reproductive dysfunction. Clin Endocrinol (Oxf). 2017;86(4):480–487.
• Pilz S, et al. Effect of vitamin D supplementation on testosterone levels in men. Horm Metab Res. 2011;43(3):223–225.
• NICE. Vitamin D: supplement use in specific population groups. Public Health Guideline PH56. 2014.