Vitamin D, often referred to as the "sunshine vitamin," is a fat-soluble secosteroid that plays a critical role in numerous physiological processes. Unlike most vitamins, Vitamin D functions as a prohormone — it is synthesised in the skin upon exposure to ultraviolet B (UVB) radiation and subsequently undergoes hepatic and renal hydroxylation to form its biologically active metabolite, 1,25-dihydroxyvitamin D (calcitriol).
During winter months, reduced solar angle and shorter daylight hours significantly diminish UVB availability, making cutaneous synthesis insufficient for maintaining adequate serum 25-hydroxyvitamin D [25(OH)D] levels. This seasonal decline has important clinical implications across multiple body systems.
Physiology of Vitamin D Synthesis
Vitamin D3 (cholecalciferol) is produced in the epidermis when 7-dehydrocholesterol is exposed to UVB radiation (wavelength 290–315 nm). It is then transported to the liver, where it is hydroxylated to 25(OH)D — the primary circulating form used to assess Vitamin D status — and subsequently to the kidneys, where it is converted to the active form, 1,25(OH)₂D (calcitriol).
Optimal serum 25(OH)D levels are generally considered to be ≥75 nmol/L (30 ng/mL), with deficiency defined as <50 nmol/L (20 ng/mL) and severe deficiency as <25 nmol/L (10 ng/mL).
Why Winter Increases Deficiency Risk
Several factors converge during winter to reduce Vitamin D synthesis:
- Reduced UVB exposure: At latitudes above 35°N or below 35°S (New Zealand sits between 34°S and 47°S), the solar zenith angle during winter months means UVB rays must travel through more atmosphere, significantly reducing their intensity at ground level.
- Behavioural changes: Colder temperatures lead to more time spent indoors and greater skin coverage with clothing.
- Reduced skin surface area exposed: Heavy winter clothing limits the skin area available for photosynthesis.
- Cloud cover and shorter days: Both reduce cumulative UVB exposure throughout the day.
Clinical Consequences of Vitamin D Deficiency
Musculoskeletal Health
Vitamin D is essential for calcium and phosphate homeostasis. Deficiency impairs intestinal calcium absorption, leading to secondary hyperparathyroidism, increased bone resorption, and reduced bone mineral density. In adults, prolonged deficiency can result in osteomalacia, characterised by bone pain, muscle weakness, and increased fracture risk. In children, severe deficiency causes rickets.
Immune Function
Vitamin D receptors (VDRs) are expressed on virtually all immune cells, including T lymphocytes, B lymphocytes, macrophages, and dendritic cells. Calcitriol modulates both innate and adaptive immune responses — enhancing the production of antimicrobial peptides (such as cathelicidin and defensins) while simultaneously dampening excessive inflammatory responses.
Epidemiological data consistently associate lower 25(OH)D levels with increased susceptibility to acute respiratory tract infections, including influenza. A 2017 meta-analysis published in the BMJ (Martineau et al.) demonstrated that Vitamin D supplementation reduced the risk of acute respiratory infection, with the greatest benefit observed in those with baseline deficiency.
Mental Health and Seasonal Affective Disorder (SAD)
VDRs are widely distributed throughout the brain, and Vitamin D plays a role in the synthesis of serotonin and dopamine. Low 25(OH)D levels have been associated with increased rates of depression, anxiety, and Seasonal Affective Disorder (SAD). While causality remains under investigation, supplementation trials in deficient individuals have shown modest improvements in mood outcomes.
Cardiovascular and Metabolic Health
Emerging evidence links Vitamin D deficiency with increased risk of hypertension, insulin resistance, and cardiovascular disease, though large-scale randomised controlled trials (e.g., VITAL trial) have produced mixed results. Current consensus supports maintaining sufficiency as part of overall cardiometabolic health management.
Assessment and Testing
Vitamin D status is assessed via serum 25(OH)D measurement. Testing is recommended for individuals with:
- Limited sun exposure (indoor workers, elderly, institutionalised individuals)
- Darker skin pigmentation (reduced cutaneous synthesis efficiency)
- Obesity (Vitamin D sequestration in adipose tissue)
- Malabsorption syndromes (Crohn's disease, coeliac disease, bariatric surgery)
- Chronic kidney or liver disease
- Use of medications that affect Vitamin D metabolism (e.g., anticonvulsants, glucocorticoids)
Supplementation Guidelines
For individuals unable to maintain adequate levels through sun exposure alone — which includes the majority of New Zealanders during winter — supplementation is clinically appropriate.
- Maintenance dose (general population): 1,000–2,000 IU (25–50 mcg) of Vitamin D3 daily
- Correction of deficiency: 3,000–5,000 IU daily under practitioner supervision, with repeat testing after 8–12 weeks
- Upper tolerable intake level: 4,000 IU/day (general population); higher doses may be used therapeutically under clinical supervision
Vitamin D3 (cholecalciferol) is preferred over D2 (ergocalciferol) due to superior bioavailability and more effective elevation of serum 25(OH)D. Co-administration with Vitamin K2 (MK-7) is increasingly recommended to support appropriate calcium deposition in bone rather than soft tissue.
Our Recommended Vitamin D Supplements
At The Wellness Store, we stock a range of practitioner-quality Vitamin D3 formulations:
- Solgar Vitamin D3 1000IU — a convenient chewable form, ideal for daily maintenance
- Biotrace Phyto D3 Complex — a plant-sourced D3 with enhanced absorption
- Nordic Naturals Vitamin D3 Gummies — a great-tasting option for those who prefer gummies
- Nordic Naturals Arctic-D Cod Liver Oil — provides Vitamin D alongside omega-3 fatty acids EPA and DHA
Dietary Sources
Dietary Vitamin D is limited but includes:
- Oily fish (salmon, mackerel, sardines) — 300–600 IU per serving
- Egg yolks — approximately 40 IU per yolk
- Fortified foods (milk, cereals) — variable
- Cod liver oil — approximately 400–1,000 IU per teaspoon
Dietary sources alone are generally insufficient to maintain optimal 25(OH)D levels, particularly during winter.
Conclusion
Vitamin D deficiency during winter is a clinically significant and largely preventable condition. Given New Zealand's latitude, seasonal UVB limitations, and the broad physiological roles of Vitamin D — spanning immune defence, musculoskeletal integrity, mental health, and metabolic function — proactive supplementation during the winter months is a well-supported, evidence-based intervention.
We recommend discussing your Vitamin D status with a qualified health practitioner, particularly if you fall into a higher-risk category. At The Wellness Store, our team can guide you toward practitioner-quality Vitamin D supplements tailored to your individual needs.
This article is intended for educational purposes only and does not constitute medical advice. Please consult your healthcare provider before commencing supplementation.