Vitamin D occupies a unique position in human physiology, functioning both as a vitamin and as a hormone. Technically classified as a prohormone, vitamin D is converted by the body into calcitriol, an active steroid hormone that regulates gene expression throughout multiple organ systems. Unlike traditional vitamins, which must be obtained from the diet, vitamin D can be synthesised endogenously when skin is exposed to ultraviolet B radiation from sunlight. This dual nature explains why vitamin D deficiency affects bone health, immune function, and other physiological processes. Understanding whether vitamin D is a hormone helps clarify supplementation recommendations and clinical management strategies.

Is Vitamin D a Hormone or a Vitamin?

Vitamin D occupies a unique position in human physiology, functioning both as a vitamin and as a hormone. Technically, vitamin D is classified as a prohormone — a substance that the body converts into an active hormone. This dual nature often causes confusion, but understanding this distinction is crucial for appreciating how vitamin D works in the body.

Traditionally, vitamins are defined as essential organic compounds that the body cannot synthesise in sufficient quantities and must obtain from dietary sources. However, vitamin D challenges this definition because the human body can produce it endogenously when skin is exposed to ultraviolet B (UVB) radiation from sunlight. Once synthesised or ingested, vitamin D undergoes two hydroxylation steps — first in the liver to form 25-hydroxyvitamin D (calcidiol), then in the kidneys to produce the active hormone 1,25-dihydroxyvitamin D (calcitriol).

Calcitriol functions as a steroid hormone, binding to vitamin D receptors (VDRs) that are widely expressed throughout the body. These receptors regulate gene expression, influencing numerous genes involved in calcium homeostasis, immune function, cell growth, and other physiological processes. This hormonal action distinguishes vitamin D from conventional vitamins, which typically serve as cofactors for enzymatic reactions rather than acting as signalling molecules.

The NHS and UK Health Security Agency (UKHSA) recognise vitamin D's importance, recommending supplementation during autumn and winter months when sunlight exposure is insufficient for vitamin D synthesis. Understanding vitamin D as both a nutrient and a hormone helps explain why deficiency can have widespread effects throughout the body, affecting bone health and potentially influencing immune function and other systems, though many non-skeletal effects remain under investigation.

The Difference Between Vitamin D and Traditional Vitamins

Traditional vitamins function primarily as coenzymes or cofactors that facilitate specific biochemical reactions. For example, B vitamins assist enzymes in energy metabolism, whilst vitamin C acts as an antioxidant and cofactor for collagen synthesis. These vitamins must be obtained regularly from the diet because the body cannot manufacture them, and they are typically required in small amounts to prevent deficiency diseases.

Vitamin D differs fundamentally in several key aspects:

• Endogenous synthesis: Unlike true vitamins, vitamin D can be produced by the body through a photochemical reaction when 7-dehydrocholesterol in the skin is exposed to UVB radiation (wavelengths 290–315 nm). However, in the UK, particularly from October to early March, UVB radiation is insufficient for adequate vitamin D synthesis, making dietary sources or supplements necessary during these months.

• Hormonal mechanism: After conversion to calcitriol, vitamin D binds to nuclear receptors (VDRs) throughout the body, directly influencing gene transcription. This mechanism resembles that of steroid hormones like cortisol or oestrogen, rather than the catalytic role of conventional vitamins.

• Systemic regulation: The body tightly regulates vitamin D metabolism through feedback mechanisms involving parathyroid hormone (PTH), calcium, and phosphate levels. The kidneys adjust calcitriol production based on physiological needs, demonstrating hormonal control rather than simple nutrient utilisation.

• Storage capacity: Vitamin D is fat-soluble and can be stored in adipose tissue and liver for extended periods, unlike water-soluble vitamins that require regular replenishment.

These distinctions explain why vitamin D deficiency manifests differently from other vitamin deficiencies. Rather than causing a single, specific deficiency disease, inadequate vitamin D affects multiple organ systems due to its widespread hormonal actions. NICE guidance (PH56: Vitamin D – supplement use in specific population groups) acknowledges this complexity in recommendations for at-risk populations.

It's important to note that while sun exposure is a natural source of vitamin D, you should spend time outdoors safely and avoid sunburn. The NHS advises against using sunbeds as a source of vitamin D.

How Your Body Produces and Regulates Vitamin D

The production and regulation of vitamin D involves a sophisticated multi-organ system that maintains calcium homeostasis and supports numerous physiological functions. Understanding this process illuminates why vitamin D is considered a hormone rather than simply a dietary nutrient.

Cutaneous synthesis begins when UVB radiation penetrates the epidermis and converts 7-dehydrocholesterol to previtamin D₃, which then isomerises to cholecalciferol (vitamin D₃) through a temperature-dependent process. The amount produced depends on several factors: latitude, season, time of day, skin pigmentation, age, and sunscreen use. In the UK, particularly at latitudes above 50°N, UVB radiation is insufficient for vitamin D synthesis between October and March, necessitating reliance on dietary sources or supplements during these months.

Once formed or ingested (as vitamin D₂ from plants or D₃ from animal sources), vitamin D enters the circulation bound to vitamin D-binding protein. The first hydroxylation occurs in the liver, where the enzyme 25-hydroxylase converts vitamin D to 25-hydroxyvitamin D [25(OH)D], also called calcidiol. This is the major circulating form and the biomarker measured in blood tests to assess vitamin D status. The Scientific Advisory Committee on Nutrition (SACN) established a population protective threshold of 25 nmol/L, while UK clinical practice generally considers levels above 50 nmol/L as sufficient, though optimal levels remain debated.

The second hydroxylation takes place primarily in the kidneys, where 1α-hydroxylase produces the active hormone 1,25-dihydroxyvitamin D [1,25(OH)₂D] or calcitriol. This step is tightly regulated by parathyroid hormone, serum calcium and phosphate levels, and fibroblast growth factor 23 (FGF23). When calcium levels fall, PTH stimulates renal 1α-hydroxylase activity, increasing calcitriol production to enhance intestinal calcium absorption and mobilise calcium from bone.

Negative feedback mechanisms prevent excessive calcitriol production. High calcitriol levels suppress PTH secretion and induce 24-hydroxylase, an enzyme that catabolises both 25(OH)D and 1,25(OH)₂D into inactive metabolites. This sophisticated regulation exemplifies hormonal control, distinguishing vitamin D from nutrients that lack such homeostatic mechanisms.

It's worth noting that certain conditions, such as sarcoidosis and other granulomatous diseases, can cause extrarenal 1α-hydroxylation, potentially leading to hypercalcaemia in affected individuals taking vitamin D supplements.

Why Understanding Vitamin D Matters for Your Health

Recognising vitamin D's dual nature as both nutrient and hormone has important implications for health management, disease prevention, and clinical practice. This understanding shapes how healthcare professionals approach screening, supplementation, and treatment of deficiency.

Bone health remains the most established role of vitamin D. Calcitriol maintains serum calcium and phosphate concentrations necessary for bone mineralisation. Severe deficiency causes rickets in children and osteomalacia in adults, conditions characterised by inadequate bone mineralisation. Ensuring vitamin D sufficiency is important for bone and muscle health, though vitamin D supplementation alone is not recommended for fracture prevention. NICE guidance on osteoporosis (NG246) and falls prevention (NG160) addresses the broader approach needed for these conditions.

Immune function represents an increasingly recognised aspect of vitamin D's hormonal actions. VDRs are expressed on immune cells including T lymphocytes, B lymphocytes, and antigen-presenting cells. Calcitriol modulates both innate and adaptive immunity, influencing antimicrobial peptide production and inflammatory responses. Whilst observational studies suggest associations between vitamin D deficiency and increased infection risk, randomised controlled trials have shown mixed results, and supplementation should not replace evidence-based preventive measures.

Screening and supplementation strategies should be targeted rather than universal. The NHS does not recommend routine vitamin D testing for the general population. However, testing may be appropriate for individuals with:

• Symptoms or signs of deficiency (bone pain, muscle weakness, frequent fractures)

• Conditions affecting vitamin D metabolism (chronic kidney disease, malabsorption disorders)

• Increased risk factors (limited sun exposure, darker skin, obesity)

The NHS recommends that most adults take a daily supplement containing 10 micrograms (400 IU) of vitamin D during autumn and winter. People at higher risk of deficiency should take this supplement year-round. Note that 1 microgram equals 40 IU of vitamin D.

Patient safety considerations include recognising that vitamin D toxicity can occur with excessive supplementation. The NHS advises not exceeding 100 micrograms (4,000 IU) daily unless prescribed by a doctor. Toxicity can cause hypercalcaemia with symptoms including nausea, vomiting, weakness, and kidney problems. Patients should consult their GP before taking high-dose supplements, particularly if they have kidney disease, hypercalcaemia, renal stones, or granulomatous conditions like sarcoidosis. Certain medications can interact with vitamin D, including thiazide diuretics, orlistat, cholestyramine, and some antiepileptics.

Seek urgent medical advice if you develop symptoms of hypercalcaemia while taking vitamin D supplements. Contact your GP if you experience unexplained bone pain, muscle weakness, or low-trauma fractures. Suspected adverse reactions to vitamin D products can be reported through the MHRA Yellow Card scheme.

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