Dr Jorge Zafra discusses the different ways the body is affected by sunlight.
The importance of understanding the impact of sunlight exposure and vitamin D is crucial to be able to recommend appropriate skincare and assess our patients’ health from an antiageing perspective. Ageing is a multifactorial process, which depends on both intrinsic and extrinsic factors. The main extrinsic factor is sun exposure; ultraviolet (UV) rays have positive effects on our body predominantly through the activation of vitamin D.1,2,3,4 However, UV rays also have negative effects on the skin, increasing the risk of skin cancers and photoageing. Healthy lifestyle recommendations are key to minimising the signs of ageing and maximising the outcome of aesthetic treatments.
Living organisms began to evolve in the oceans more than one billion years ago. Emiliania huxleyi, which is a type of photosynthetic plankton that forms the basis of virtually all marine food webs, has existed unchanged for millions of years. When exposed to sunlight, not only does it photosynthesise glucose, but it also produces vitamin D2, which is essential for their exoskeleton. Since life on earth has evolved from these type of organisms this could explain why vertebrates, including humans, have depended on sun exposure for the maintenance of their calcium metabolism.5
UV rays emitted by the sun are divided into three major subtypes: UVA (320-400 nm), UVB (290-320 nm), and UVC (200-290 nm). UVA and UVB reach the earth and penetrate the skin; UVA makes up approximately 95% of the total UV rays, while UVB only makes up about 5%. UVC meanwhile is effectively absorbed in the upper atmosphere, preventing it from reaching the earth.1,6
Only UVB has a role in vitamin production and it mainly acts on the epidermal basal layer of the skin. It has a beneficial and essential impact in humans due to the production of Vitamin D3. UVB acts on subcutaneous 7-dehydrocholestrol (7-DHC) to convert it into pre-vitamin D3, after which it is thermally converted into 25-hydroxycholecalciferol (25(OH)D3) (calcifediol).2 Calcifediol is then converted primarily in the kidneys and liver into its most hormonally-active form, 1α,25- dihydroxvitamin D3 or calcitriol. Calcitriol, the active form of vitamin D3, regulates nearly 60 genes, through which it can down-regulate proto-oncogenes such as c-myc, c-fos and c-jun, as well as up-regulate genes responsible for cell cycle arrest. Calcitriol can also stimulate DNA repair, affect the immune system and is found to be implicated in regulating our mood. The increase in serum 25(OH)D attained from exposure to UVB radiation is often more effective than ingesting 1000 IU vitamin D. Exposing 20% of the body surface to sunlight is equivalent to ingesting approximately 1400-2000 IUs of vitamin D3.6
Although UVB has positive effects on vitamin D production, it is also thought to be most responsible for skin cancers as it is the typical source of sunburn, inflammation, DNA damage, oxidative stress, free radical production, immunosuppression and photoageing.2,6
The degree of skin pigmentation and age influences vitamin D production as larger amounts of melanin on the epidermal layer protect from the UV rays, however reduce the skin’s ability to produce vitamin D and the production also decreases with age.6,7,8,9 The definition of vitamin D deficiency, based on 25 (OH) D serum levels, is a motive for controversy in literature. Levels above 30 ng/ml (> 75 nmol/l) are considered satisfactory by a number of authors like Trummer et al.10 in their review of beneficial effects of UV radiation. Levels lower than 20 ng/ml (< 50 nmol/l) may be consensually considered as vitamin D deficiency, since 97.5% of the population is above this level.7,10
The following are considered as risk factors for the development of vitamin D deficiency:9
Daily doses of vitamin D recommended by the Food and Nutrition Board for deficiency prevention in individuals at risk are:9,11
Intoxication by vitamin D, associated with hypercalcemia and hyperphosphatemia, is extremely rare and may be caused by doses greater than 50,000 UI per day and a level of (25 (OH) D) above 150 ng/mL. Photodegradation of vitamin D3 produced by the skin avoids intoxication by vitamin D through sun exposure.9,10
Our skin is the first line of defense against environmental toxicants and consequently suffers directly from the deleterious effects of UV radiation. UV radiation is the primary source for the development of cutaneous cancers, which affects the Caucasian population more frequently.4,6 Most skin cancers diagnosed are non-melanoma skin cancers, consisting of squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs), accounting for around 96% of all skin cancers, while cutaneous malignant melanoma (CMM) for the remaining 4%.6 Most skin cancers develop on sun-exposed areas of the skin. The non-melanoma skin cancers are more easily treatable as they are diagnosed earlier whereas melanoma, the least common form of skin cancer, is often lethal.6
The lifetime risk assessments demonstrate that those with lower exposures rates to UV rays, like the average UK holiday maker, have an increased risk for developing CMM. The pattern of SCCs is the accumulated UV exposure that determines the risk for development. Studies demonstrate that around 83% of children have sunburn in the summer, a percentage that drops to 36% among teenagers.6 The incidence of melanoma and non-melanoma skin cancer in patients with sunburn history is well documented in meta-analysis; this was the base for a mathematical model by Schalka et al. in 2014 that concluded that the habit of applying sunscreen in the first 18 years of life reduced the incidence of skin cancer by 78% during lifetime, attributing this possibility due to the number of sunburn episodes in childhood and adolescence.3
Practically, ageing signs can be classified into four main categories: wrinkles/texture, loss of firmness of cutaneous tissues (ptosis), vascular disorders, and pigmentation heterogeneities.
Kligman and Kligman introduced the term ‘photoageing’ in 1986 so to differentiate intrinsic from extrinsic ageing of the skin.1,12
Intrinsic ageing is the ‘natural’ process, caused by the accumulation of reactive oxygen species (ROS), resulting from oxidative cellular metabolism and influenced by genetic factors (ethnicity), anatomic variations and hormonal changes (natural decline of hormone and growth factor levels). Despite the identification and understanding of the causes of chronological ageing, this process is considered incontrollable.1,2,3,4 Extrinsic ageing is responsible for 80% of the visible signs of skin ageing, which include the aesthetic signs of ageing and the clinical injuries like the non-melanoma skin cancers. It is a result of chronic exposure to various environmental elements, such as sun and UV exposure (the main extrinsic factor),1,2,3,4 pollution, smoking, diet, repetitive muscle movements (squinting, frowning, pursing, etc), sleeping position and cutaneous or general diseases.1 This type of ageing is mediated by two processes that disrupts the skin collagen matrix: decreased collagen synthesis and increased collagen degradation. The main traits of photoaged skin is the accumulation of damage to the extracellular matrix fibres of collagen and elastin, by accumulation of elastotic material composed of aggregated elastin fibres.4 Photoageing ultimately simulates a typical wound-healing response with deposition of collagen type I, which is seen in scars, rather than the usual mixture of collagen type III and I that gives skin resilience and pliability.13
The most important products used for skincare are sunscreens (physical or chemical) because of their ability to prevent photoageing.14
The elements present in sunscreens are called UV filters. These interfere directly with the incident solar radiation through absorption, reflection or dispersion of energy. From the structural viewpoint, UV filters can be organic/chemical or inorganic/physical.14 The chemical filters absorb UV ray photons, promoting an alteration in their molecular structure. The physical filters have a mineral origin and promote the reflection of UV radiation to the external part of the tissue.6,15
An SPF15 sunscreen filters out 93% of UV radiation, SPF30 a 96% and SPF50 a 98%.15 The general guideline for sunscreen application is to use 2mg of sunscreen per cm2 of skin surface.16 Evidence suggests that most users apply insufficient amounts of sunscreen; moreover, individuals may overestimate the amount of time that they can stay in the sun after applying sunscreen relative to their skin type.6,15 It is therefore important to advise patients accordingly. Patients should be advised to avoid sun exposure without adequate protection, especially in the period of greater risk between 10:00am and 3:00pm.3,9 Children younger than six months of age should not be directly exposed to the sun and should not make regular use of sunscreen to allow adequate synthesis of vitamin D.3,9
Knowledge about vitamin D, skin cancer risk and motivation to prevent sunburn does not seem to play a role on the perceived importance of tanning, while implementing sun-safe practices have been viewed as interfering with people’s recreational experiences. UVB exposure is necessary for maintaining a healthy lifestyle due to its important role in the synthesis of vitamin D3. However, UVB also causes a number of adverse health effects ranging from sunburn to skin cancer. The use of sunscreen with SPF higher than 30 is recommended to everyone older than six months when exposed to the sun, it should be applied in recommended amount and reapplied accordingly.3,15 Oral supplementation of vitamin D is indicated for all the population with risk factors to develop vitamin D deficiency.9
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