Vitamin D & Hormones: The Missing Link on Every Hormone Test

What follows is a proper look at what the research says about vitamin D's role in hormonal health, who's most at risk, what the numbers actually mean, and why our Ultimate Hormone Checks include vitamin D as a standard biomarker — when most panels quietly leave it off the list.

Wait - is vitamin D actually a hormone?

Technically, yes. The term "vitamin" is something of a historical accident. Vitamin D is synthesised in the skin via a UVB-triggered photochemical reaction, then converted in the liver to 25-hydroxyvitamin D (25(OH)D — the form we measure in blood tests), and further activated in the kidneys to its biologically potent form: 1,25-dihydroxyvitamin D, also known as calcitriol.

Calcitriol behaves like a classical steroid hormone. It binds to the vitamin D receptor (VDR) — a nuclear receptor that belongs to the same superfamily as receptors for glucocorticoids, sex hormones, and thyroid hormone (Bouillon et al., 2019; NCBI Bookshelf). And because VDR is found in tissues throughout the body — from the ovaries and testes to the adrenal glands, thyroid, brain, and immune cells — its influence extends far beyond calcium and bones.

 

How common is vitamin D deficiency in the UK — and who's most at risk?

The UK sits at a latitude where UVB radiation is insufficient to trigger meaningful skin synthesis of vitamin D between October and March. For roughly half the year, even sunny days won't get you there. That's not a minor inconvenience — it's a structural problem that affects the whole population (UK Government; Public Health England).

According to large-scale UK Biobank analyses, approximately 17–23% of White European adults are vitamin D deficient at any given time, rising sharply in winter and spring. For people of South Asian ancestry, the figure climbs to over 57% in winter. For Black African populations, it's around 38–40% (Darling et al., 2021; Constructive et al., ScienceDirect, 2020).

The SACN (Scientific Advisory Committee on Nutrition) recommends that all UK adults consider supplementing with 10 micrograms (400 IU) of vitamin D daily, particularly from October to March. Despite this, only around 17% of UK adults regularly take supplements — suggesting a significant and largely silent deficiency is baked into the population (Donin et al., 2025).

Where does vitamin D actually come from?

Does vitamin D actually affect testosterone?

This is the big one for men, and the evidence is compelling. Vitamin D receptors (VDRs) are expressed in Leydig cells — the cells in the testes responsible for testosterone production. This is not a theoretical link; it's a direct mechanistic pathway. When vitamin D status is low, Leydig cell function appears to be sub-optimal (Holt et al., 2024).

A 2024 systematic review and meta-analysis published in Diseases (MDPI, Abu-Zaid et al.) searched four major medical databases and evaluated randomised controlled trials on vitamin D supplementation and male reproductive hormones. The findings pointed to significant improvements in total testosterone, free testosterone, and the free androgen index (FAI) following vitamin D supplementation in adult men. SHBG and LH were also measured as part of the picture (Abu-Zaid et al., 2024).

A complementary Danish clinical study (Holt et al., 2024, Andrology) found that vitamin D-insufficient men who received supplementation showed significantly higher testosterone-to-LH ratios compared to placebo — suggesting improved Leydig cell responsiveness. In plain English: their testes were better at converting the hormonal signal into actual testosterone.

What about oestrogen and progesterone — does vitamin D affect women's hormones too?

Absolutely. The VDR is present on the granulosa cells and theca cells of the ovary — the very cells responsible for producing oestrogen and progesterone. Animal studies have shown that VDR-null mice (mice without functional vitamin D receptors) have impaired folliculogenesis and lower oestrogen levels. In humans, activated vitamin D (1,25-dihydroxyvitamin D) has been shown to directly stimulate oestrogen and progesterone production in ovarian cells (Sodhi & Shah, 2019; Frontiers in Endocrinology, 2021).

A comprehensive 2021 study published in Frontiers in Endocrinology measured vitamin D alongside a full panel of female reproductive hormones — including FSH, LH, oestradiol, progesterone, testosterone, prolactin, DHEAS, SHBG, AMH, and thyroid markers — finding meaningful relationships between vitamin D status and reproductive hormone balance in reproductive-aged women. This is exactly the kind of joined-up thinking that's missing from most testing approaches.

Vitamin D has also been shown to stimulate aromatase activity — the enzyme responsible for converting testosterone into oestrogen. This has implications not just for fertility, but for hormonal balance throughout the menstrual cycle, perimenopause, and beyond.

Can vitamin D affect cortisol and the stress response?

This one's more nuanced — and that's exactly why we're not going to oversimplify it. The relationship between vitamin D and cortisol is real but context-dependent. Here's what the evidence says.

Vitamin D receptors are expressed in the brain's stress-responsive regions — including the hypothalamus, pituitary gland, and adrenal glands — all of which are central players in the HPA (hypothalamic-pituitary-adrenal) axis, the system that governs your cortisol response (GrassrootsHealth, 2025; ScienceDirect, 2025).

A 2025 focused review in ScienceDirect confirmed that vitamin D has a significant influence on neuroendocrine regulation by modulating cortisol through both genomic and non-genomic HPA axis mechanisms. Some studies suggest cortisol levels decrease after vitamin D supplementation in cases of obesity, depression, or chronic inflammation — while effects in otherwise healthy populations are more modest. The relationship also varies with age and sex.

Additionally, research has noted that vitamin D deficiency is associated with activation of the RAAS (renin-angiotensin-aldosterone system) — a pathway involved in blood pressure regulation but also closely tied to adrenal hormone output (Frontiers in Endocrinology, 2022). Patients with Cushing's disease — characterised by excess cortisol — consistently show lower 25(OH)D levels, and the correlation between vitamin D deficiency and cortisol overproduction has been observed in multiple clinical studies.

Is there a link between vitamin D and thyroid hormones?

Yes — and it's particularly relevant for anyone dealing with thyroid symptoms or Hashimoto's. The VDR belongs to the same nuclear receptor superfamily as the thyroid hormone receptor, and research has explored links between vitamin D status and autoimmune thyroid conditions including Hashimoto's thyroiditis and Graves' disease (Giallauria et al., 2022; Frontiers in Endocrinology).

Vitamin D's role in modulating the immune system — downregulating pro-inflammatory Th1 and Th17 cells while promoting regulatory T cells — may help reduce the autoimmune attack on thyroid tissue that characterises Hashimoto's. Several observational studies have found that people with autoimmune thyroid disease tend to have lower vitamin D levels than matched controls. Correlation isn't causation, but given the mechanistic plausibility, it's a relationship worth knowing about when you test.

The 2021 Frontiers in Endocrinology study measuring vitamin D alongside reproductive hormones in women also included free T3, T4, TSH, and TPO antibodies — reinforcing the clinical logic of looking at these biomarkers together rather than in siloed panels.

What are the symptoms of vitamin D deficiency — and why do they look like hormone imbalance?

This is where things get genuinely tricky. The symptoms of vitamin D deficiency overlap almost perfectly with those of hormonal imbalance — which is exactly why identifying each component in isolation, through a comprehensive test, matters so much.

So why does vitamin D keep getting left off hormone panels?

A few reasons, none of them great. Vitamin D has historically been categorised as a "bone health" nutrient, siloed into orthopaedic and geriatric medicine long before its endocrine significance was properly established. Standard GP hormone panels were designed in an era when vitamin D's receptor distribution - and its role across the endocrine system - wasn't well characterised.

The result is that you can go for a hormone test, get your testosterone, oestrogen, progesterone, LH, FSH, SHBG, cortisol, and thyroid markers all measured - and still have a deficiency quietly undermining every single one of those results. You'd never know, because nobody checked.

This is one of the most important reasons Vitall built vitamin D into our Ultimate Hormone Checks as a standard biomarker - not an optional add-on. Because you cannot meaningfully interpret a hormone panel without understanding the vitamin D status of the person you're looking at.

What should you actually do about vitamin D?

First: test, don't guess. Symptoms are useful signals, but they're not diagnostic. The only way to know your vitamin D level is to measure it in blood - ideally as part of a comprehensive panel that also captures your hormone picture so you can see everything in context.

If your result comes back deficient (below 25 nmol/L), supplementation is usually recommended - typically under guidance, as the dose and duration depend on your baseline. For insufficiency (25–50 nmol/L), most people will benefit from a daily supplement of 1,000–2,000 IU (25–50 µg) of vitamin D3 (cholecalciferol), taken with a fatty meal for absorption. Vitamin K2 is often co-supplemented to support calcium directionality.

For those in the optimal range (75–100 nmol/L), maintenance supplementation of 400–1,000 IU daily through winter months is a sensible baseline. And then — retest. Because optimising without measuring is just guesswork.