The UV Index (UVI) is a valuable tool for assessing the strength of ultraviolet (UV) radiation from the sun at any given location and time. The UVI values are determined using the STAR (System for Transfer of Atmospheric Radiation) model. This model takes into account various atmospheric conditions to estimate UV radiation levels. The values provided reflect typical conditions for each location and serve as reference points. Actual UV Index readings can vary due to local factors, such as temporary changes in ozone levels and other atmospheric conditions. The values range from 0 to 11+, serving as a standardized guide for sun protection measures. This helps us understand the potential for skin damage based on UV exposure levels. They are specified for the 21st of each month across different regions. Higher UVI values indicate a greater risk of harm, particularly concerning sunburn, DNA damage, premature skin aging and hyperpigmentation [1][2].
 
HIGHEST AND LOWEST UV INDEX VALUES
Highest UV Index
The highest recorded UV Index values can reach 12 or more, especially in regions near the equator, high-altitude areas, and places with low ozone levels. The Atacama Desert in Chile has documented peaks as high as 20, highlighting the extreme UV exposure possible in certain environments [2]. 
Lowest UV Index
The lowest values are typically observed at night or during winter months in polar regions, where solar angles are significantly reduced, often resulting in readings close to zero [2][3].
 
GEOGRAPHIC INFLUENCES ON UV LEVELS
UV exposure varies widely across different geographical regions and withing the regions:
 
▌Europe: Generally experiences moderate UV levels due to higher latitudes and frequent cloud cover [4].
▌Asia: Significant variability; tropical areas encounter high UV levels while northern regions have lower indices [2].
▌Australia: Known for high UV exposure, particularly during summer months, due to its proximity to the equator and clearer skies.
▌USA: Southern states typically report higher UV indices compared to their northern counterparts.
▌Latin America: High UV indices are prevalent near the equator, while southern regions like Argentina experience lower values [2][3].
 
▌Altitude: Higher altitudes receive more intense UV radiation due to a thinner atmosphere [2].
▌Reflection: Beaches can experience increased UV levels due to sunlight reflecting off water and sand [3].
▌Northern vs. Southern hemisphere: The Southern hemisphere generally has higher UV levels attributed to less atmospheric pollution and ozone depletion [2].
▌Equatorial regions: These areas maintain consistently high UV indices throughout the year due to direct sunlight [2][3].

INDOOR vs OUTDOOR UV EXPOSURE
The UV Index indoors is significantly lower than outdoor levels on a sunny day. This is primarily due to the filtering effect of window glass, which blocks most UVB radiation. On a clear day, outdoor UV levels can reach up to 8,000 µW/cm², while indoor levels near a window may be as low as 250 µW/cm², dropping further with distance from the window.

The indoor UVI reduction is primarily due to the filtering effect of glass windows, which block most UVB (320–400 nm) radiation while allowing some UVA (320–400 nm) rays to penetrate and can still contribute to premature skin aging, hyperpigmentation and DNA damage. Blue Light (400–495 nm): Part of visible light spectrum; penetrates glass easily. High energy Visible Light is responsible for 50% of the free radical activity [5] and like UV radiations contributes to premature skin aging, hyperpigmentation and  DNA damage. Factors influencing indoor UV exposure include window size, orientation, and surrounding obstructions like trees.
 Direct and indirect exposure
▌Direct exposure occurs when sunlight directly enters through windows.
▌Indirect (Diffuse) exposure results from sunlight scattering off surfaces or atmospheric particles. While diffuse exposure is reduced by walls and roofs, it can still penetrate through windows [3].
 
Factors affecting indoor exposure
1. Window glass: Standard glass blocks most UVB but allows some UVA and High energy Visible Light  through.
2. Sky view: More visible sky from indoors increases diffuse UV exposure.
3. Distance from windows: The intensity of UV radiation decreases with distance from windows due to the inverse square law [3].
4. Window orientation and size: Larger windows facing south (in the Northern Hemisphere) or north (in the Southern Hemisphere) allow more sunlight into indoor spaces [3].
5. Scattering (indirect – diffuse exposure)

CHANGING UVI OVER TIME
There is scientific evidence indicating that the UV Index (UVI) is influenced by various environmental factors, including changes in ozone levels and climate conditions, which can affect UV radiation exposure over time. 
 
1. UV radiation: A study by Fountoulakis et al. (2020) analyzed long-term changes in UV-B radiation and found that variations in UV levels are primarily driven by changes in aerosols and total ozone, with significant regional differences observed. The study indicates that while some areas have experienced increases in UV-B irradiance, others have shown decreases, particularly during summer months in polar regions due to improvements in ozone levels [6].
 
2. Impact of ozone depletion: Research has shown that the decline of stratospheric ozone has historically led to increased UV radiation at certain wavelengths. For instance, a study by Bais et al. (2011) projected that UV irradiance would likely return to its 1980 levels by the early 21st century at northern mid-latitudes and high latitudes, suggesting ozone recovery influences UV radiation levels [7].While standard windows block most harmful UVB rays, damaging UVA and blue light (or HEVIS) can still penetrate indoors, affecting skin´s beauty and health. Awareness of these factors and UV Index enables you to take appropriate protective measures against harmful effects of sunlight even indoors while considering the benefits of controlled exposure for vitamin D synthesis [3].
 
Take care
Anne-Marie
 
References
[1] Federal Office for Radiation Protection (BfS). (n.d.). What is the UV Index? Retrieved December 7, 2024, from bfs.de/EN/topics/opt/uv/index/introduction/introduction_node.html
[2] Fioletov V, Kerr JB, Fergusson A. The UV index: definition, distribution, and factors affecting it. Can J Public Health. 2010;101(4):I5-9. doi: 10.1007/BF03405303.
[3] Heckman CJ, Liang K, Riley M. Awareness and impact of the UV index: A systematic review of international research. Prev Med. 2019;123:71-83. doi: 10.1016/j.ypmed.2019.03.004.
[4] World Health Organization. (n.d.). Radiation: The UV index. Retrieved December 7, 2024, from who.int/news-room/questions-and-answers/item/radiation-the-ultraviolet-(uv)-index
[5] Albrecht S et al. Effects on detection of radical formation in skin due to solar irradiation measured by EPR spectroscopy. Methods. 2016;109:44-54.
[6] Fountoulakis I et al. Long-term changes in UV-B radiation. Atmos Chem Phys. 2020;20(5):3075-3091.
[7] Bais AF et al. Projections of UV radiation changes in the 21st century: impact of ozone recovery and cloud effects. Atmos Chem Phys. 2011;11(20):7533-7545. doi: 10.5194/acp-11-7533-2011
[8] Eleftheratos K et al. Ozone, DNA-active UV radiation, and cloud changes due to enhanced greenhouse gas concentrations. Atmos Chem Phys. 2022;22:12827–12855. doi: 10.5194/acp-22-12827-2022

The widespread belief that the epidermis renews itself every 28 days is inaccurate. Epidermal turnover primarily involves keratinocytes, the predominant cell type in the epidermis with 90%. These cells originate in the basal layer (stratum germinativum) and progressively move upward through the epidermal layers, undergoing various changes before being shed from the skin's surface as dead, flaky cells - a process known as desquamation [1].

The keratinocyte journey has several stages:

1. 1. Formation in the basal layer
2. 2. Migration through epidermal layers
3. 3. Maturation and differentiation
4. 4. Transformation into corneocytes (fully differentiated keratinocytes without nuclei or organelles)
5. 5. Shedding from the stratum corneum (outermost epidermal layer) [1]

This continuous cycle of cell production, maturation, and shedding is called epidermal turnover [1]
 
Epidermal turnover rates vary significantly with age:
▌In young adults: approximately 28-40 days [2]
▌In more mature adults: 60+ days [2]
This age-related slowdown is attributed to decreased cell proliferation [3]

KERATINOCYTE LIFESPAN 
The keratinocyte lifecycle can be divided into two main phases:
1. Active life: Approximately 8 to 10 days from mitosis (in the basal layer) to arrival in the stratum corneum [1].
2. Stratum corneum transit: The period spent in the outermost layer as corneocytes (dead keratinocytes) before shedding [1].

Balancing Health, Beauty, and vitamin D
 
Like many who promote skin health and beauty, I often find myself navigating the delicate balance between the benefits and risks of sun exposure. Moderate exposure to sunlight is essential for vitamin D production, triggers beneficial stress responses and DNA repair mechanisms in our bodies through hormesis, promoting overall health and well-being. However, excessive sun exposure can overwhelm these protective systems, leading to harmful effects such as skin damage and increased cancer risk.

Vitamin D is a crucial prohormone that plays a vital role in numerous functions, including:
1. Bone health and calcium absorption [1]
2. Immune system modulation [1]
3. Regulation of up to 2,000 genes involved in various biological processes [1] – more details below
4. Potential cancer prevention [1]
 
THE SUNLIGHT PARADOX: HEALTH BENEFITS VS. RISKS

Benefits of sunlight exposure
1. Vitamin D production (80-90%) [1]
2. Regulation of circadian rhythms and improved sleep quality [1]
3. Mood enhancement and potential alleviation of depressive symptoms [1]
4. Lowering of blood pressure through nitric oxide production in the skin [1]

Risks of excessive sun exposure
1. DNA damage, including the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs) [2]
2. Oxidative stress and generation of reactive oxygen species (ROS) [2]
3. Premature skin aging and hyperpigmentation [2]
4. Increased risk of skin cancers, including melanoma [2]
 
Health benefits of vitamin D
1. Bone health: Promotes calcium absorption and bone mineralization, preventing conditions like rickets and osteoporosis [3]
2. Muscle strength and function: Helps maintain muscle strength and reduce the risk of falls, especially in older adults [4]
3. Immune system support: Modulates immune responses and may reduce the risk of autoimmune diseases [5]
4. Heart health: Low vitamin D levels have been linked to increased risk of heart diseases, though the exact relationship is unclear [6]
5. Reduced risk of severe illnesses: May make severe flu and COVID-19 infections less likely [7]
6. Mood regulation: May play a role in regulating mood and decreasing the risk of depression [8]
7. Weight management: There is a relationship between (low) vitamin D levels and (over)weight, though the exact nature is not fully understood [9]
8. Reduced risk of multiple sclerosis (MS): Low levels of vitamin D are linked with an increased risk of MS [10]
9. Brain health: Supports brain cell activity and may have neuroprotective properties 
10. Anti-inflammatory effects: Has anti-inflammatory properties that support overall health 

Skin health and beauty benefits of Vitamin D
1. Skin barrier function: Regulates the generation of keratinocytes, which are critical for maintaining the skin barrier [11]
2. Skin immunity: Indispensable for the activation of immune cells in the skin, supporting its protective function [12]
3. Antimicrobial effects: Has direct antimicrobial effects in the skin, helping to fight off pathogens [13]
4. Regulation of sebaceous glands: Important for growth regulation and optimum functioning of sebaceous glands [14]
5. Photoprotective effects: Topical application may offer some protection against UV-induced skin damage [15]
6. Wound healing: Promotes repair of damaged tissue and restoration of the skin's barrier mechanism [16]
7. Anti-aging effects: May have antiaging effects on the skin, though more research is needed in this area [17]
8. Skin cell differentiation and growth: Plays a role in the proliferation and differentiation of skin cells [18]
9. Melanin regulation: Protects the epidermal melanin unit and restores melanocyte integrity [19]
10. Potential role in skin conditions: May play a role in managing conditions like psoriasis, atopic dermatitis, and vitiligo [20]
11. Skin hydration: Topical application of vitamin D improves skin hydration and symptoms of dry skin [21]

VITAMIN D AND PARP
A study published in the International Journal of Molecular Medicine demonstrated that the active form of vitamin D inhibits poly(adenosine diphosphate-ribose) polymerase (PARP). PARP is an enzyme that plays a crucial role in DNA repair. PARP acts like a cellular "first responder" for DNA damage, initiating the repair process to keep our genetic material intact.

1. Function: PARP detects and helps repair damaged DNA in cells.
2. Mechanism: When DNA is damaged, PARP attaches to the damaged site and creates a signal (called PAR chains) to attract other repair proteins.
3. Energy use: PARP uses NAD+ (a cellular energy molecule) to create these signals.
4. Importance: PARP helps maintain genetic stability and cell survival.
5. Cancer connection: Some cancer cells rely heavily on PARP for survival, which is why PARP inhibitors are used as cancer treatments.​

VITAMIN D SYNTHESIS IN THE SKIN 
When UVB rays from sunlight hit the skin, they trigger the production of vitamin D [22]:
 
1. UVB radiation converts 7-dehydrocholesterol in the skin to previtamin D3
2. Previtamin D3 then isomerizes to vitamin D3
3. Vitamin D3 is transported to the liver and converted to 25-hydroxyvitamin D [25(OH)D] 
4. Finally, 25(OH)D is converted to the active form, 1,25-dihydroxyvitamin D (calcitriol), in the kidneys 
 
FACTORS INFLUENCING VITAMIN D PRODUCTION
1. Latitude: Higher latitudes receive less UVB radiation, especially during winter months [23]
2. Time of day: UVB rays are strongest at solar noon [23]
3. Season: Vitamin D production is lower in winter due to reduced UVB radiation [23]
4. Skin pigmentation: Darker skin requires longer sun exposure to produce the same amount of vitamin D as lighter skin [24]
5. Age: Older adults produce less vitamin D from sun exposure [23]
6. Sunscreen use: High SPF sunscreens can significantly reduce vitamin D production [25]
7. Air pollution: Reducing UVB radiation reaching the earth's surface

EPIGENETICS
Vitamin D regulates up to 2000 genes, involving both direct genomic effects and epigenetic mechanisms. 
1. Vitamin D receptor (VDR) binding
The active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], binds to the vitamin D receptor (VDR). This liganded VDR then forms a heterodimer with the retinoid X receptor (RXR) [26][27].
2. Direct gene regulation
The VDR/RXR complex binds to specific DNA sequences called vitamin D response elements (VDREs). These VDREs can be located in promoter regions, introns, or even far from the transcription start sites of target genes [26][27][28].
3. Epigenetic mechanisms

• Vitamin D signaling involves epigenetic modifications, including changes in DNA methylation and histone modifications [26][29].
• The VDR protein interacts with chromatin modifiers and remodelers, influencing the epigenetic landscape [26].
• Liganded VDR can regulate the expression of several chromatin modifiers and remodelers [26].

4. Coregulatory proteins
VDR interacts with numerous coregulatory proteins that can either activate or repress gene transcription [26][28].
5. Genome-wide effects
Genome-wide studies have shown that VDR can bind to hundreds of genomic loci, regulating gene activity at various locations, including many kilobases upstream or downstream of transcription start sites [26][28].
6. Primary and secondary target genes
Vitamin D regulates both primary target genes (directly controlled by VDR) and secondary target genes (controlled by transcriptional regulators encoded by primary targets) [26][30].
7. Cell-specific regulation
The effects of vitamin D on gene expression are highly cell-specific, depending on the epigenetic landscape of each cell type [26][31].
8. Dose-dependent effects
Higher doses of vitamin D supplementation have been shown to affect the expression of more genes in a dose-dependent manner [32].
 
RECOMMENDATIONS FOR SUN EXPOSURE 
Factors such as latitude, season, cloud cover, and individual skin type can all affect vitamin D synthesis [33][34]. Additionally, morning and evening sun contains less UVB radiation, which is necessary for vitamin D production, so longer exposure times may be needed [34]. Health experts often recommend midday sun exposure for optimal vitamin D production, while dermatologists typically advise against it due to increased UV intensity. 
 
Considerations
1. Midday sun (higher UVB) is more efficient for vitamin D production, requiring shorter exposure times [35]
2. Shorter exposure times may reduce overall UV damage risk [35]
3. Individual factors, such as skin type and location, should be considered when making recommendations [35]
 
Impact of skin type
Darker skin requires longer exposure times due to higher melanin content [1][36]

• For 1000 IU/day, average annual estimated times:

          Type I: 5.05 minutes
          Type VI: 25.25 minutes [37]

• Fair: 30 minutes of summer sun exposure in a bathing suit can produce 50,000 IU of vitamin D within 24 hours [38] 
• Tan: Same exposure produces 20,000–30,000 IU of vitamin D [38] 
• Dark: Same exposure produces only 8,000–10,000 IU of vitamin D [38] 

Recommendation fair skin (Fitzpatrick Types I-III)

1. Aim for 10-15 minutes of sun exposure to arms, legs, and torso 2-3 times per week during spring and summer months [3]. Wear sunscreen on face, neck and décolletage. 
2. This may need to be increased to 30-40 minutes if the sun is less intense, or in shadow (less UVB)
3. Expose approximately 25% of your body surface area (e.g., arms and legs) [39]
4. Avoid peak UV hours (10 am to 4 pm) to minimize skin damage risk [39]
5. Or 3 minutes during peak hours with 25% of body exposed (summer)
6. Winter: 45-60 minutes of morning or late afternoon sun with 25% of body exposed, or 23 minutes at noon with 25% of body exposed, or 2-3 hours if only 5% of body is exposed due to cold weather

 
Recommendation darker skin (Fitzpatrick Types IV-VI)
1. Longer sun exposure times are needed, typically 15-30 minutes 3-5 times per week [40]
2. Consider exposing larger body surface areas when possible [40]
3. Sun exposure during midday hours may be more effective for vitamin D production [35]
 
Variations based on location and season

• In Tsukuba, Japan at noon in July: 3.5 minutes of solar exposure to produce 5.5 μg vitamin D3 per 600 cm2 skin
• ​In Sapporo, Japan in December at noon: 76.4 minutes for the same amount [41]
• 9:00 AM in December in Tsukuba (36°N latitude), it took 106.0 minutes to produce 5.5 μg of vitamin D3 per 600 cm2 of skin, compared to 22.4 minutes at noon under the same conditions  [41]

This illustrates the significant difference in vitamin D production efficiency between midday and morning/evening sun exposure. 
  
Sunscreen and vitamin D production
Sunscreen can decrease vitamin D3 formation in the skin. The effect varies based on coverage, thickness, and SPF. [36] Nevertheless, I would highly recommend the always use sunscreen on face, neck and décolletage as and expose skin surface areas to sunlight in the shortest amount possible to minimise DNA damage and the risk of sunburn and skin cancer.  [1][36]
 
ALTERNATIVE STRATEGIES FOR VITAMIN D SUFFICIENCY
For many people, especially those living at higher latitudes, with darker skin, or those unable to obtain adequate sun exposure, or at high risk for skin damage, vitamin D supplementation may be necessary to maintain optimal levels, particularly during winter months [33][42]. However, excessive vitamin D3 levels can have negative health effects.

1. Dietary sources: Fatty fish, egg yolks, and fortified foods
2. Vitamin D3 supplements: The recommended dose is 1000 units per 25 pounds bodyweight (>4000 IU or 100 micrograms only under medical supervision) and taken alongside vitamin K2 and magnesium for a synergistic effect. Best is to take it in the morning in line with circadian rhythms. Consult with a healthcare provider for appropriate dosage and monitor your levels.
3. UVB lamps: Under medical supervision, these can be used for controlled vitamin D production.
 
​For the average adult a range of 30-50 ng/mL (75-125 nmol/L) is seen as optimal, 50 ng/mL (125 nmol/L) may be too high and below 20 ng/mL (50 nmol/L) are generally considered deficient. Achieving optimal vitamin D levels while protecting skin health requires a personalised approach. I hope that the information provided will help you to navigate the delicate balance between sun exposure benefits, risks and the use of sunscreens. Always consult a healthcare professional, especially if you have a history of skin cancer or are at risk for vitamin D deficiency.
 
Take care

Anne-Marie

References
[1] Holick MF. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr. 2004
[2] Cadet J, Douki T. Formation of UV-induced DNA damage contributing to skin cancer development. Photochem Photobiol Sci. 2018
[3] Holick MF. Vitamin D deficiency. N Engl J Med. 2007
[4] Bischoff-Ferrari HA et al. Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Archives of Internal Medicine. 2009
[5] Prietl B et al. Vitamin D and immune function. Nutrients. 2013
[6] Wang TJ et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation. 2008
[7] Martineau AR et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. 2017
[8] Anglin RE et al. Vitamin D deficiency and depression in adults: systematic review and meta-analysis. British Journal of Psychiatry. 2013
[9] Vimaleswaran KS et al. Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization analysis of multiple cohorts. PLoS Medicine. 2013
[10]  Munger KL et al. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA. 2006
[11]  Bikle DD. Vitamin D metabolism and function in the skin. Molecular and Cellular Endocrinology. 2011
[12]  Schauber J. et al.  Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D–dependent mechanism. Journal of Clinical Investigation. 2007
[13] Liu PT et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006
[14] Krämer C et al. Characterization of the vitamin D endocrine system in human sebocytes in vitro. Journal of Steroid Biochemistry and Molecular Biology. 2009
[15]  Dixon KM, Deo SS, Wong G, Slater M, Norman AW, Bishop JE, Posner GH, Ishizuka S, Halliday GM, Reeve VE, Mason RS. Skin cancer prevention: a possible role of 1,25dihydroxyvitamin D3 and its analogs. Journal of Steroid Biochemistry and Molecular Biology. 2005
[16] Oda Y, Uchida Y, Moradian S, Crumrine D, Elias PM, Bikle DD. Vitamin D receptor and coactivators SRC2 and 3 regulate epidermis-specific sphingolipid production and permeability barrier formation. Journal of Investigative Dermatology. 2009
[17]  Rinnerthaler M, Bischof J, Streubel MK, Trost A, Richter K. Oxidative stress in aging human skin. Biomolecules. 2015
[18]  Bikle DD. Vitamin D regulated keratinocyte differentiation. Journal of Cellular Biochemistry. 2004
[19] Ranson M, Posen S, Mason RS. Human melanocytes as a target tissue for hormones: in vitro studies with 1α-25, dihydroxyvitamin D3, α-melanocyte stimulating hormone, and beta-estradiol. Journal of Investigative Dermatology. 1988
[20]  Mostafa WZ, Hegazy RA. Vitamin D and the skin: Focus on a complex relationship: A review. Journal of Advanced Research. 2015
[21]  Russell M. Assessing the relationship between vitamin D3 and stratum corneum hydration for the treatment of xerotic skin. Nutrients. 2012
[22] Wacker M, Holick MF. Vitamin D - effects on skeletal and extraskeletal health and the need for supplementation. Nutrients. 2013
[23] Webb AR, Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status. Photochem Photobiol. 2006
[24] Farrar MD, et al. Efficacy of a dose range of simulated sunlight exposures in raising vitamin D status in South Asian adults: implications for targeted guidance on sun exposure. Am J Clin Nutr. 2013
[25] Matsuoka LY, et al. Sunscreens suppress cutaneous vitamin D3 synthesis. J Clin Endocrinol Metab. 1987
[26] Fetahu IS, Höbaus J, Kállay E. Vitamin D and the epigenome. Front Physiol. 2014 
[27] Carlberg C. Vitamin D and Its Target Genes. Nutrients. 2022 
[28] Christakos S et al. Vitamin D: Metabolism, Molecular Mechanism of Action, and Pleiotropic Effects. Physiol Rev. 2016 
[29] Voltan G et al. Vitamin D: An Overview of Gene Regulation, Ranging from Metabolism to Genomic Effects. Genes (Basel). 2023
[30] Veijo Nurminen et al. Front. Physiol., 05 March 2019 Sec. Integrative Physiology Primary Vitamin D Target Genes of Human Monocytes
[31] Vassil Dimitrov et al. Vitamin D-regulated Gene Expression Profiles: Species-specificity and Cell-specific Effects on Metabolism and Immunity, Endocrinology, Volume 162, Issue 2, February 2021
[32] GrassrootsmHealth Nutrient Research Institute. Vitamin D Supplementation Amount Influences Change in Genetic Expression. [Internet]. 2018
[33] Wacker M, Holick MF. Sunlight and Vitamin D: A global perspective for health. Dermatoendocrinol. 2013 
[34] Nagaria TD et al. The Sunlight-Vitamin D Connection: Implications for Patient Outcomes in the Surgical Intensive Care Unit. Cureus. 2023 
[35] Rhodes LE, et al. Recommended summer sunlight exposure levels can produce sufficient (≥20 ng ml(-1)) but not the proposed optimal (≥32 ng ml(-1)) 25(OH)D levels at UK latitudes. J Invest Dermatol. 2010
[36] Ashley, R. (n.d.). Ask the Doctors - How much sunshine do I need for enough vitamin D? UCLA Health.
[37] Yilmaz, B., & Karakas, M. (2024). UV index-based model for predicting synthesis of (pre-)vitamin D3 in human skin. Scientific Reports, 14(1), 3188.
[38] Mead MN. Benefits of sunlight: a bright spot for human health. Environ Health Perspect. 2008 
[39] American Academy of Dermatology. Sunscreen FAQs. 
[40] Farrar MD, et al. Efficacy of a dose range of simulated sunlight exposures in raising vitamin D status in South Asian adults: implications for targeted guidance on sun exposure. Am J Clin Nutr. 2013
[41] Miyauchi, M., & Nakajima, H. (2016). The solar exposure time required for vitamin D3 synthesis in the human body estimated by numerical simulation and observation in Japan. Journal of nutritional science and vitaminology, 62(5), 379-385.
[42] Healthline How to Safely Get Vitamin D From Sunlight Ryan Raman, MS, RD — Updated on April 4, 2023