Vitamin D and Bone Health

Vitamin D and bone health are fundamentally connected: without adequate vitamin D, the body cannot absorb calcium efficiently from food, and calcium is the structural mineral that gives bone its density and strength. Vitamin D deficiency is among the most prevalent nutritional deficiencies in the UK — estimates suggest 20–30% of UK adults have insufficient vitamin D levels, rising to higher proportions in winter, in those with darker skin, in older adults who go outside less, and in people who cover most of their skin for cultural or other reasons. Understanding what vitamin D does, where it comes from, how to know if you are deficient, and when supplementation is needed is important for anyone managing their bone health.

What Vitamin D Does

Vitamin D is not a single compound but a group of fat-soluble secosteroids, of which vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol) are the most clinically relevant. Vitamin D3 is produced in human skin when ultraviolet B (UVB) radiation from sunlight converts 7-dehydrocholesterol to pre-vitamin D3, which is then isomerised to vitamin D3. Vitamin D2 comes from UV-irradiated fungi and plants. Both are metabolised in the liver to 25-hydroxyvitamin D (25-OHD, or calcidiol) — the main circulating form and the marker used to assess vitamin D status — and then in the kidney to 1,25-dihydroxyvitamin D (calcitriol), the biologically active form.

Calcitriol’s principal function in bone health is to upregulate calcium and phosphate absorption in the small intestine. It activates vitamin D receptor (VDR)-dependent transcription of intestinal calcium transport proteins (calbindin-D, TRPV6) that move calcium from the gut lumen into the bloodstream. Without adequate calcitriol, dietary calcium absorption efficiency falls from approximately 30–40% to 10–15% or less. Calcitriol also promotes phosphate absorption, which is required alongside calcium for hydroxyapatite crystal formation.

When vitamin D is deficient, blood calcium tends to fall. Parathyroid hormone (PTH) rises in response, stimulating osteoclast-mediated bone resorption to release calcium from bone into the bloodstream (maintaining serum calcium at the expense of bone mass), and also stimulating the kidney to produce more calcitriol. Chronically elevated PTH — secondary hyperparathyroidism — drives ongoing bone resorption and is one mechanism by which vitamin D deficiency contributes to osteoporosis over years.

Vitamin D Deficiency and Bone Consequences

The clinical consequences of vitamin D deficiency on bone range in severity with the degree and duration of deficiency:

• Osteomalacia (adults) — severe, prolonged vitamin D deficiency causes failure of bone mineralisation, resulting in soft, painful, deformable bone. Osteoid (unmineralised bone matrix) accumulates at bone surfaces because the calcium and phosphate required for hydroxyapatite formation are not available. Osteomalacia presents with diffuse bone pain (particularly in the spine, pelvis, and legs), proximal muscle weakness, and characteristic Looser’s zones (stress fractures) on X-ray. It is entirely preventable with adequate vitamin D and is treated with high-dose loading regimens.
• Secondary hyperparathyroidism — even moderate vitamin D insufficiency (25-OHD 25–50 nmol/L) can cause a modest PTH rise, increasing osteoclast activity and contributing to bone density loss over time; this is a more common clinical scenario than full osteomalacia
• Accelerated bone loss — vitamin D insufficiency in postmenopausal women and older adults compounds the existing oestrogen-deficient and age-related bone loss pathways, increasing fracture risk above what would be expected from BMD alone
• Impaired fracture healing — vitamin D is required for callus formation during fracture repair; deficiency slows healing and increases the risk of non-union

Sources of Vitamin D

Vitamin D sources fall into two main categories: sunlight and diet (including supplements).

Sunlight: UVB radiation from sunlight (wavelength 280–315 nm) striking bare skin triggers vitamin D3 synthesis. In the UK, this synthesis is only possible when the sun is above approximately 45° elevation angle — typically from late March to early September, between approximately 10 am and 3 pm. From October to March, the UVB component of sunlight in the UK is insufficient for vitamin D production regardless of how much time is spent outdoors. This “vitamin D winter” of 5–6 months is the fundamental reason why supplementation matters in the UK.

Even during the productive months, synthesis is impaired by: factor-50+ sunscreen (which blocks most UVB), glass windows (which filter UVB), indoor work, and melanin pigmentation (which absorbs UVB, reducing skin vitamin D3 production — meaning individuals with darker skin need substantially more sun exposure to produce the same amount of vitamin D3 as those with lighter skin).

Dietary sources: Few foods are naturally rich in vitamin D. Key sources:

• Oily fish (salmon, mackerel, sardines, herring): 300–700 IU per 100 g — the richest natural food source
• Tinned sardines or pilchards: 200–400 IU per 100 g — practical and affordable; serve dual purpose as a calcium and vitamin D source (see our guide to calcium and bone health)
• Egg yolks: approximately 40 IU per egg — modest contribution; whole eggs also provide vitamin K2, which has roles in bone mineralisation
• Fortified foods: some cereals, margarines, and plant milks are fortified with vitamin D; levels vary by product; typically 40–80 IU per serving, contributing meaningfully to daily intake when consumed regularly
• Red meat and liver: 10–50 IU per 100 g; modest but present in a typical omnivore diet

The practical implication is that diet alone cannot reliably maintain adequate vitamin D status in most UK adults, particularly through winter — daily dietary intake from a typical UK diet is approximately 100–200 IU, well below the 400–800 IU needed to maintain adequate serum 25-OHD in the absence of sun exposure.

Vitamin D Status: Testing and Thresholds

Vitamin D status is measured by serum 25-hydroxyvitamin D (25-OHD). The reference ranges and interpretive thresholds used in clinical practice (noting that different organisations use slightly different cut-offs):

• Deficiency: 25-OHD below 25 nmol/L — associated with risk of osteomalacia, marked secondary hyperparathyroidism, and significant bone loss risk
• Insufficiency: 25-OHD 25–50 nmol/L — associated with modest secondary PTH elevation and suboptimal calcium absorption; bone density effects are less severe but clinically relevant over time
• Adequate: 25-OHD 50–75 nmol/L — generally considered sufficient for bone health in most adults
• Optimal: 25-OHD 75–125 nmol/L — the range often associated with additional non-skeletal benefits; the Royal Osteoporosis Society targets above 50 nmol/L as the minimum for bone health
• Toxicity risk: 25-OHD above 250 nmol/L — hypervitaminosis D with hypercalcaemia; virtually impossible from sun exposure; only occurs with very high supplemental doses (typically above 10,000 IU/day for extended periods)

Routine testing of vitamin D levels is not recommended for the general population by NHS guidelines — the advice to supplement 400 IU/day in autumn and winter applies regardless of measured status. Testing is appropriate for individuals at high risk of severe deficiency (darker skin, housebound, covered skin), those with conditions affecting vitamin D metabolism (CKD, liver disease, malabsorption), and those on loading regimens where confirmation of repletion is appropriate.

Supplementation Recommendations

The NHS recommends that all UK adults and children aged 4 and over consider taking a daily vitamin D supplement of 400 IU (10 micrograms) during autumn and winter (October to March). This recommendation applies to everyone, regardless of diet or lifestyle, because UK sunlight is insufficient for vitamin D synthesis during these months.

Higher doses are recommended or appropriate in specific groups:

• People at high risk of deficiency (darker skin, housebound, covering most skin outdoors): 400–1,000 IU/day year-round
• Adults over 65: 400–800 IU/day year-round; skin synthesis efficiency declines with age, and older adults typically spend less time outdoors
• Osteoporosis or osteopenia on pharmacological treatment: 800 IU/day (co-prescribed alongside bisphosphonates or denosumab in standard clinical practice in the UK)
• Confirmed vitamin D deficiency (25-OHD below 25 nmol/L): loading regimen (e.g. 300,000 IU over 6–12 weeks, typically as a series of high-dose weekly doses), followed by maintenance 400–1,000 IU/day
• Obese individuals: vitamin D is fat-soluble and distributes into adipose tissue, reducing circulating 25-OHD; higher maintenance doses (800–2,000 IU/day) may be needed to maintain adequacy

Vitamin D3 (cholecalciferol) is preferred over vitamin D2 (ergocalciferol) for supplementation — D3 raises and maintains serum 25-OHD more effectively than D2 at equivalent doses. Most UK supplements and co-prescribed preparations (Adcal-D3, Calcichew-D3) contain vitamin D3.

Vitamin D in Pregnancy, Infancy, and Childhood

Vitamin D requirements during pregnancy, infancy, and early childhood deserve specific attention because deficiency at these stages has lasting bone health consequences and because the populations at greatest risk are identifiable.

Pregnancy: Adequate vitamin D is needed for foetal bone mineralisation (particularly in the third trimester, when the greatest proportion of foetal bone is formed) and for normal neuromuscular development. The NHS recommends 400 IU/day supplementation throughout pregnancy. Women who are at high risk of deficiency (darker skin, covered skin, minimal sun exposure, BMI above 30) may need higher doses and blood level monitoring. Severe vitamin D deficiency in pregnancy is associated with neonatal hypocalcaemia and, in severe cases, neonatal rickets.

Infants: Breast milk contains very little vitamin D (typically less than 50 IU/L), meaning exclusively breastfed infants receive almost no vitamin D from their primary food source. The NHS recommends vitamin D supplementation of 340–400 IU/day for all breastfed infants from birth. Formula-fed infants consuming more than 500 ml/day of fortified formula typically receive adequate vitamin D and do not require additional supplementation. Vitamin D drops specifically designed for infants are available and should be used rather than adult capsules.

Children: Rickets — the childhood equivalent of osteomalacia — is caused by severe vitamin D (and/or calcium) deficiency during the years of active skeletal growth. It presents with bowed legs, knock knees, delayed walking, bone tenderness, and widening at the wrist growth plates on X-ray. Despite being largely preventable, rickets has been increasing in incidence in the UK, driven by inadequate supplementation in high-risk groups, dietary calcium insufficiency in some communities, and declining sun exposure in children who spend less time outdoors. Vitamin D supplementation at 400 IU/day for children aged 1–4 is NHS-recommended; higher doses are appropriate for children with confirmed deficiency or risk factors.

Vitamin D and Falls Risk in Older Adults

Beyond calcium absorption and bone density, vitamin D has direct effects on muscle function that are clinically important for fracture prevention in older adults. Vitamin D receptors (VDR) are present in skeletal muscle cells. Calcitriol activates VDR in muscle, promoting calcium transport into muscle cells, protein synthesis, and muscle fibre development (particularly fast-twitch type II fibres that are critical for postural reflex responses to perturbation). Vitamin D deficiency in older adults is associated with reduced muscle strength, slower reaction time, impaired balance, and increased falls frequency.

Meta-analyses of vitamin D supplementation trials in older adults show a 10–20% reduction in falls frequency with supplementation in those who are deficient or insufficient at baseline. This falls-reduction benefit is independent of the bone density effect — it translates into fracture risk reduction even in individuals whose BMD does not change significantly with supplementation. This dual mechanism (better calcium absorption for bone, and better muscle function for falls prevention) is the reason vitamin D supplementation is recommended across all pharmacological bone treatment guidelines, not just as a nutritional addendum but as a co-treatment with clinically relevant fracture-prevention value in its own right. The interaction between bone fragility and falls risk is explored further in our guide to osteoporosis risk factors.

Frequently Asked Questions

Summary

Vitamin D is essential for calcium absorption and bone mineralisation — without it, the skeleton cannot use dietary calcium effectively, and PTH-driven bone resorption compensates at the expense of bone density. UK sunlight is insufficient for vitamin D synthesis from October to March, making supplementation (400 IU/day) a public health recommendation for all UK adults during this period, with higher doses appropriate for those at elevated risk of deficiency. Dietary sources — oily fish, eggs, fortified foods — contribute meaningfully but are insufficient as the sole source for most people. Vitamin D3 is preferred over D2 for supplementation; it is most effective taken with a fat-containing meal. For those with confirmed osteoporosis or osteopenia on pharmacological treatment, ensuring 800 IU/day of vitamin D3 is standard practice. In older adults, vitamin D’s additional effect on muscle strength, reaction time, and balance adds an important falls-prevention benefit on top of its direct skeletal role. The companion to vitamin D is calcium — see our guide to calcium and bone health — and how these fit into overall bone protection is covered in our guides to osteoporosis: symptoms, causes, and prevention and osteoporosis risk factors.

Medical disclaimer: This article is for general educational purposes and does not constitute medical advice. Consult a qualified healthcare professional for personalised vitamin D and bone health advice.

References:
NHS. Vitamin D. nhs.uk. 2023.
NICE CG146. Osteoporosis: assessing the risk of fragility fracture. NICE. 2023.
Royal Osteoporosis Society. Vitamin D and bone health. theros.org.uk. 2023.
Tripkovic L, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status. Am J Clin Nutr. 2012;95(6):1357–1364.
Bjelakovic G, et al. Vitamin D supplementation for prevention of mortality in adults. Cochrane Database Syst Rev. 2014;(1):CD007470.