Introduction
The sun has always had a basic place in the world where we live as humans, not just as a provider of light and warmth, but as a natural instrumentation of human health. Of the many biological roles, the production of vitamin D through sunlight exposure is among the most fundamental. Vitamin D is a fat-soluble vitamin known as the “sunshine vitamin.” Vitamin D is supportive of a variety of physiological processes including bone health, immunity, and mental health.
The following article will discuss the science of vitamin D, its production through sun exposure, its functions and benefits, deficiency and risks, and the contemporary discussion of balancing adequate sun exposure along with vitamin D synthesis.
1. Knowing More About Vitamin D
1.1 What is Vitamin D?
Vitamin D is a fat-soluble prohormone; it behaves more like a hormone rather than a vitamin. The body can produce vitamin D when exposed to ultraviolet B (UVB) rays from the sun – which is unique compared to other vitamins, requiring vitamin D to be consumed mostly from the diet and food options.
There are two primary forms of Vitamin D:
. Vitamin D2 (ergocalciferol) – present in limited plant-based sources and fortified foods.
. Vitamin D3 (cholecalciferol) – produced in human skin and also consumed from eating more animal-based foods such as fish, liver, and eggs.
Generally, vitamin D3 is considered to be more effective at increasing and maintaining blood levels of vitamin D.
1.2 How Vitamin D Works
Once vitamin D is made in the skin or consumed it undergoes a two-step conversion:
1. The first conversion occurs in the liver to form 25-hydroxyvitamin D [25(OH)D] being the primary circulating form measured in blood tests.
2. The second conversion occurs in the kidneys producing 1,25-dihydroxyvitamin D [1,25(OH)2D] being the active form that helps regulate calcium absorption, bone metabolism, and immune function.
2.1 The Physics of Sunlight
Sunlight consists of ultraviolet rays separated into three types:
. UVA (320–400 nm): Aging/damaging the skin without making vitamin D.
. UVB (290–320 nm): Signaling the skin to convert 7-dehydrocholesterol into previtamin D3.
. UVC (100–280 nm): Absorbed by the ozone layer and does not reach the earth.
2.2 The Function of the Skin
When the skin absorbs UVB rays, one of the precursors of vitamin D, 7-dehydrocholesterol, which is in the epidermis, transfers this energy, becoming previtamin D3, which then becomes vitamin D3. The process is affected by:
. Distance from the equator and season (UVB is more intense closer to the equator and in the summer than winter).
. Time of day (the peak time for vitamin D is mid-day sun).
. Skin color (darker skin has a higher amount of melanin and lowers UVB).
. Age (the older skin produces less vitamin D).
. Sunscreen and clothing (prevents UVB).
3. Roles of Vitamin D in the Body
3.1 Bone and Skeletal Health
. Promotes the absorption of calcium and phosphorus within the intestines.
. Helps in preventing rickets in youngsters and osteomalacia in adults.
. Aids in bone remodeling and density and decreasing the risk of osteoporosis.
3.2 Immune System Regulation
. Enhances innate immunity by boosting antimicrobial peptides.
. Inhibits human adaptive immunity to reduce the responses of the autoimmune immune system.
. Contributes to reducing the infection’s risk, including tuberculosis, flu, and likely, COVID-19.
3.3 Cardiovascular Health
. Aids in blood pressure regulation.
. May decrease heart disease risk.
3.4 Brain and Mental Health
. Vitamin D receptors are found in brain tissues.
. Deficiency levels are directly associated with mental outcomes such as depression, seasonal affective disorder (SAD) and cognitive loss over time.
3.5 Other Roles
. May regulate insulin levels and lower the risk of developing type 2 diabetes.
. May help in muscle strength and balance development.
. Some evidence exists suggesting anticancer actions due to its ability to regulate cells’ growth.
4. Vitamin D Deficiency: A Global Issue
Vitamin D deficiency, in the face of excess sunlight, is classified as a global public health issue.
4.1 Statistics
. Approximately one billion people throughout the world are estimated to have low vitamin D levels.
. This problem is noticeable in geographic regions characterized by limited sun exposure, including those that the sun does not directly reach (high latitude areas) and those with limited sunlight due to pollution or clothing style.
. Normal findings would suggest that vitamin D deficiency is prevalent in the elderly, females, and people with darker skin or limited sun exposure.
4.2 Reasons for vitamin D deficiency
. Reasons for vitamin D deficiency include a limited amount of time being in the sunlight due to living in urban settings or being indoors when engaged in daily activities (e.g., working or attending school).
. Another possible reason, one that has gained less attention, is poor diet. Those with limited sun exposure are often consuming fewer vitamin D-rich food diets.
. Certain medical conditions that affect the body’s ability to absorb vitamin D (e.g., Crohn’s disease and celiac disease).
. Some studies have indicated the relationship among obesity, limited sun exposure, and vitamin D deficiency, as vitamin D will accumulate in the fat tissue and is less available to the body.
5. Risks of Vitamin D deficiency ( risks associated with vitamin D deficiency)
5.1 In Children
. Rickets- characterized by soft bones, skeletal deformities, and delayed growth.
5.2 In Adults
. Osteomalacia- bone pain and muscle weakness.
. Osteoporosis- increased risk of fracture.
5.3 Other effects of vitamin D deficiency
. Increased susceptibility to infection.
. Increased susceptibility to autoimmune diseases (multiple sclerosis, rheumatoid arthritis).
. Increased risk may also be seen in certain types of cancers, cardiovascular disease, and neurodegenerative disorders.
6. Balancing Sun Exposure and Skin Health
6.1 Sunlight Benefits and Risks
. Benefits: production of vitamin D, mood elevation, regulation of circadian rhythm.
. Risks: skin aging, summer sunburn, DNA damage, skin cancers, literal skin cancers such as basal cell carcinoma, squamous cell carcinoma, melanoma.
6.2 Guidelines on Safe Sun Exposure
. Brief, regular exposure 10-30 minutes few times weekly. Times and durations will depend on your skin type.
. When possible, expose arms, legs and face.
. Avoid excessive exposure in the summer months, particularly during midday, to decrease risk of skin damage.
. once initial exposure occurs, sunscreen can be applied to balance vitamin D needs and UV exposure.
7. Alternatives to Sunlight for Vitamin D
7.1 Dietary Sources
. fatty fish (salmon, tuna, sardines, mackerel)
. cod liver oil
. egg yolks
. fortified foods (milk, cereals, fortified plant-based milks)
7.2 Supplements
. Vitamin D3 supplements are more effective than vitamin D2.
. Recommended dietary allowances (RDA):
. infants (0 -12 months): 400 IU (10mcg)
. children and adults under 70 years: 600 IU (15mcg)
. adults over 70: 800 IU (20mcg)
. supplements should be decided upon blood tests and medical advice.
8. Special Considerations
8.1 Pregnant and Lactating Women
. They need a higher Vitamin D for maternal well-being and developing fetus.
. Supplementation lowers the odds of preeclampsia and gestational diabetes.
8.2 Elderly Population
. Reduced skin synthesis and reduced dietary intake.
. Older adults find Vitamin D supplementation can lower fall and fracture chance.
8.3 Darker Skin
. Higher melanin reduces the body’s ability to produce Vitamin D.
. Higher risk of deficiency as you move higher latitude.
9. The Future of Research on Vitamin D
. Current studies are looking into prevention of cancer, autoimmune disease, and infectious diseases.
. The future recommendations for Vitamin D may include personalized nutrition and genomics.
. Global public health initiatives are trying to combat deficiency through fortification programs, campaigns, and policies.
10. Cutaneous The Synthesis of Vitamin D
The main natural source of vitamin D for humans is the endogenously synthesized vitamin D within the skin.
1. Precursor Molecule:
The first step in cutaneous vitamin D synthesis is a molecule, 7-dehydrocholesterol, which is a derivative of cholesterol found in the plasma membranes of keratinocytes in the epidermis.
2. UVB Absorption:
With exposure to UVB (290-320 nm) from the sunlight, the 7-dehydrocholesterol absorbs energy when it is photolyzed.
3. Formation of Previtamin D3:
7-dehydrocholesterol is converted through UVB into previtamin D3, an isomer that is thermodynamically unstable.
4. Thermal Isomerization:
Previtamin D3 then spontaneously undergoes thermal isomerization into vitamin D3 (cholecalciferol).
5. Transport to the Circulating Blood:
Vitamin D3 diffuses into the circulatory blood, transporting vitamin D3 bound to vitamin D-binding protein (DBP), a carrier protein in plasma providing stability and delivery to target organs and tissues.
Thus, distantly excessive UVB exposure does not result in vitamin D toxicity, as the body photodegrades previtamin D3 into biologically inert metabolites, lumisterol and tachysterol.
11. Hepatic Hydroxylation
One vitamin D3 reaches the circulation, it is hydroxylated in the liver:
. Enzyme: Cytochrome P450 enzyme 25-hydroxylase (CYP2R1) “
. Reaction: Hydroxylation of vitamin D3 at the C–25 position to form 25-hydroxyvitamin D [25(OH)D], also called calcidiol “
This is the major circulating form of vitamin D, and is the best measure of vitamin D status in practice. It has a relatively long half life (2–3 weeks), so it is a stable measure “
12. Renal Hydroxylation
The next important step occurs in the kidneys “
. Enzyme: 1-alpha-hydroxylase (CYP27B1)
. Reaction: Hydroxylation at the C-1α position of 25(OH)D to produce 1,25-dihydroxyvitamin D [1,25(OH)2D], also called calcitriol “
Calcitriol is the biologically active hormone form of vitamin D. Its synthesis is tightly regulated by a variety of factors :
. Parathyroid hormone (PTH): Stimulates 1-alpha-hydroxylase activity when calcium is low.
. Fibroblast growth factor 23 (FGF23): Suppresses 1-alpha-hydroxylase to decrease calcitriol synthesis.
. Calcium and phosphate levels: feedback regulation based on levels.
The active hormone has a short half-life (~4–6 hours), indicative of its tightly controlled homeostatic role for calcium and phosphate levels .”
13. Inactivation and Catabolism
Calcitriol undergoes inactivation to remove excessive hormone activity :
. Enzyme: 24-hydroxylase (CYP24A1)
. Reaction: Hydroxylation of 25(OH)D and 1,25(OH)2D at the C-24 carbon.
. Products: Water-soluble metabolites (e.g., calcitroic acid) that are eliminated via bile .
This process allows activation, inactivation, and maintains a degree of homeostasis, avoiding deficiency and toxicity .
14. Transport and Binding
Calcium and vitamin D are circulated in the plasma bound to vitamin D binding protein (DBP, a glycoprotein produced in the liver)
. Affinity: highest for 25(OH)D, moderate for vitamin D3, and lower for calcitriol .
. Function :
. Protects vitamin D metabolites from degradation also
. Delivery of the metabolites to tissues .
. Regulates the free and bound vitamin D (the “free hormone hypothesis”)
15 .Vitamin D Receptor (VDR)
Vitamin D’s biological effects are mediated by a biological receptor (VDR), which belong to the superfamily of nuclear receptor.
1. The ligand-binding domain of VDR binds calcitriol
2. The VDR-calcitriol complex heterodimerizes with the RXR (retinoid X receptor) complex.
3. The heterodimer binds to specific DNA sequences, termed vitamin D response elements (VDREs), in the promoter regions of target genes.
4. Recruitment of coactivators or corepressors modifies gene transcription which alters protein synthesis.
VDR is shown to be expressed in many tissues such as the intestinal, kidney, bone, pancreatic, immune and brain tissues which should explain the multitude of effects of vitamin D.
16. Gene Regulation
Vitamin D regulates the transcription of over 200 genes that can affect many biological processes.
1. Calcium and Phosphate Homeostasis: The genes that encode calcium transporters (TRPV6), calbindin, and phosphate transport proteins.
2. Immune: Regulation of antimicrobial peptides such as cathelicidin (LL-37) and defensins.
3. Cell Proliferation and Differentiation: the regulation of genes that modulate apoptosis and growth, especially with respect to cancer biology.
4. Hormonal: Effects on insulin secretion, inhibition of renin secretion, and parathyroid hormone regulation.
17. Non-Genomic Effects
In addition to its established genomic effects, vitamin D also exerts a rapid, non-genomic effect, which includes :
. Interaction with membrane bound VDRs.
. Activation of secondary messengers, including phospholipase C and protein kinase C.
. Alteration of calcium channels in muscle and immune cells.
These rapid response activities take place within minutes and supplement the genomic effects.
18. Biochemical Regulatory Pathways
Vitamin D metabolism is controlled and regulated by a complex set of hormones and feedback mechanisms:
. Low calcium/phosphate: causes the release of PTH → stimulates renal 1-alpha-hydroxylase activity → increases calcitriol.
. High calcium/phosphate: suppresses PTH, increases FGF23, and ultimately suppress calcitriol levels.
. Autoregulation: calcitriol results in increased CYP24A1 and ultimately its own degradation may be regulated naturally >
This finely tuned system is critical to maintain a a precise mineral balance for neuromuscular function and bone health.
Conclusion
The sun to vitamin D is a remarkable example of nature integrated into human health. Exposure to sun is the #1 way to obtain adequate Vitamin D while being aware of the risks associated with overexposure to the sun. For individuals who cannot get sufficient sun exposure, dietary sources or supplementation provides the next best option.
