ReviewThe vitamin D questions: How much do you need and how should you get it?
Section snippets
The controversy
The vitamin (vit) D controversy is nearly 100 years old. It pits established risks of sun exposure against established benefits of cutaneous production of vit D and, more recently, against a variety of potential unproven benefits.
Two discoveries in the 1920s reinforced Coco Chanel's trendy new “tanned is beautiful” message1 and led to the public opinion that unprotected sunshine exposure was beneficial to health: (1) vit D is the active compound in cod liver oil that prevents childhood rickets2
Nomenclature and sources
Vit D obtained its name in the early part of the 20th century after the discovery of the antirachitic effect of cod liver oil. The suspected vit in cod liver oil was designated “D,” as vits A, B, and C had already been identified.2 The nomenclature for vit D precursors and metabolites is provided in Table I. The sources and production of vit D are summarized briefly in Fig 1 and extensively reviewed elsewhere.9 The term “vitamin D” specifically refers to two biologically inert precursors: vit D3
Established vit D hormonal function and the consequences of deficiency or excess
The principal physiologic function of the active vit, 1,25-(OH)2 vit D, is to maintain calcium homeostasis. In this essential role, vit D functions as a hormone, synthesized far from the sites of its biologic action (GI tract and bone) and reaching these distant sites through the blood stream. Vit D is indeed a member of the superfamily of steroid hormones that also includes corticosteroids, all trans-retinoic acid (vit A), and thyroid hormone, and act in the nucleus by binding their cognate
Vit D deficiency versus insufficiency
Vit D differs from most other vits and essential nutrients in having a large precursor pool in the body that varies over a wide range in healthy individuals and a small tightly regulated range of the active compound. By consensus, the circulating level of the inactive precursor 25-OH vit D is the universally accepted indicator of vit D status because it is easily measured, has the longest half-life in circulation (approximately 2 or 3 weeks), and the levels of 25-OH vit D correlate with
Does vit D insufficiency affect skeletal homeostasis?
Although randomized clinical trials of vit D supplementation have failed to clearly support clinical benefits of treating insufficiency (see below), some authorities have chosen to blur the distinction between insufficiency and deficiency. They suggest that the normal range for 25-OH vit D should be redefined as that required to minimize PTH levels (Table II).34, 38, 39, 40, 41 This change in definition causes individuals with 25-OH vit D levels in the insufficient range to be counted as
Skeletal muscle strength
1,25-(OH)2 vit D, a secosteroid hormone, enters the target cell, then binds and activates a nuclear receptor, the vit D receptor (VDR). This complex, which may form heterodimers with non-VDRs, then binds to specific DNA sequences (vit D–responsive elements), altering transcription of effector genes.9, 65 Thus, VDR-expressing tissues comprise a population of cells theoretically able to respond to 1,25-(OH)2 vit D. As would be expected for the classic hormonal function of 1,25-(OH)2 vit D in
The case for diet/supplementation versus UV exposure
Overwhelming evidence asserts that vit D through dietary supplementation can correct both deficiency and insufficiency, except for those patients with GI malabsorption as the cause of vit D deficiency. The endocrine community, through its consensus groups, and journal editorials, reviews, and letters, recognizes the carcinogenic potential of UV radiation and calls for more dietary vit D supplementation, not more sun exposure or tanning bed usage.25, 30, 105, 106, 107, 108 Dietary
The case against promoting reliance on photosynthesis
The action spectra for previt D3 formation, erythema, and formation of cyclobutane pyrimidine dimers in DNA all peak in the UVB range (Fig 2). Hence, vit D photosynthesis cannot be dissociated from acute and chronic photodamage, including photocarcinogenesis.121, 122, 123, 124, 125 As few as 6 sunburns in a lifetime have been shown to increase an individual's risk for nonmelanoma and melanoma skin cancer.125, 126, 127, 128 Moreover, in fair-skinned individuals maximum possible vit D synthesis
Conclusion
Given the scarcity of naturally occurring vit D in many otherwise adequate diets, human beings may once have depended on unprotected exposure to natural sunlight as the primary environmental source of vit D, at least during those periods of the year when sunlight can produce previt D3 in the skin.30 However, chronic unprotected exposure to carcinogenic UV radiation in sunlight not only results in photoaging, but also greatly increases the risk of skin cancer. This risk is further exacerbated by
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Anti-sunshine vitamin A
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The war against skin cancer: the time for action is now
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Photoprotection: a 21st century perspective
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Tanning devices–fast track to skin cancer?
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Spectral character of sunlight modulates photosynthesis of previtamin D3 and its photoisomers in human skin
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The UV advantage
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Sunscreens: Misconceptions and Misinformation
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2021, Clinical NutritionCitation Excerpt :The ideal amount of daily sun exposure needed to balance out vitamin D requirements and sun skin damage prevention is therefore difficult to estimate. Many authors consider that sun exposure to the face, arms and legs for 10–15 min twice a week, below the erythemal level [14,51–53], could provide adequate amounts of vitamin D. However, increasing the time or intensity of exposure does not enhance vitamin D synthesis while it does increase the risk of skin cancer [54]. For dark skinned subjects, this could be lengthened to 30 min twice a week.
Light sensing in plant- and rock-associated black fungi
2020, Fungal BiologyDeciphering the role of vitamin D on skin cancers and tumour microenvironment
2024, Indian Journal of Dermatology, Venereology and Leprology
Funding sources: None.
Conflicts of interest: None identified.