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1.
Tomato Phytonutrients Balance UV Response: Results from a Double-Blind, Randomized, Placebo-Controlled Study.
Groten, K, Marini, A, Grether-Beck, S, Jaenicke, T, Ibbotson, SH, Moseley, H, Ferguson, J, Krutmann, J
Skin pharmacology and physiology. 2019;(2):101-108
Abstract
BACKGROUND Our previous double-blinded, placebo-controlled cross-over study indicated that a nutritional supplement named lycopene-rich tomato nutrient complex (TNC) can protect from UVA1-induced (340-400 nm) and UVA- (320-400 nm)/UVB-induced (280-320 nm) upregulation of molecular markers associated with oxidative stress, inflammation, and ageing. OBJECTIVES in the current double-blind, randomized, placebo-controlled multicenter study, we analyze whether a similar, synergistic carotenoid-rich TNC can protect from broadband UVB-induced threshold erythema formation assessed as increase in minimal erythemal dose (MED) reading, the intensity of erythema formation, and the upregulation of molecular markers associated with inflammation and immunosuppression, and whether this correlates with carotenoid blood levels. METHODS One hundred and forty-nine healthy volunteers were randomized to two groups and subjected to a 5-week washout phase, followed by a 12-week treatment phase receiving either 15 mg lycopene, 5.8 mg phytoene and phytofluene, 0.8 mg β-carotene, 5.6 mg tocopherols from tomato extract, and 4 mg carnosic acid from rosemary extract per day or placebo made from medium-chain triglycerides. At the end of each phase, MED determination, UVB irradiation, chromametry, biopsies, and blood samples were undertaken. RESULTS The active supplement was well tolerated. Interestingly, no significant difference was seen in the MED between the active-supplement and placebo groups, as determined by visual grading by expert assessors. Of note, the carotenoid-containing supplement significantly protected against UVB-induced erythema formation measured as Δa* after the intervention minus Δa* after the washout phase as compared to the placebo. Moreover, intake of the active supplement significantly protected against UVB-induced upregulation of IL6 and TNFα as compared with the intake of placebo. Lastly, carotenoid plasma levels were significantly increased. CONCLUSION This well-tolerated carotenoid-containing supplement significantly protected against UVB-induced erythema formation and upregulation of proinflammatory cytokines in healthy volunteers.
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2.
The potential role of antioxidants in mitigating skin hyperpigmentation resulting from ultraviolet and visible light-induced oxidative stress.
Nahhas, AF, Abdel-Malek, ZA, Kohli, I, Braunberger, TL, Lim, HW, Hamzavi, IH
Photodermatology, photoimmunology & photomedicine. 2019;(6):420-428
Abstract
Oxidative stress is an integral element that influences a variety of biochemical reactions throughout the body and is known to play a notable role in melanogenesis. Exogenous triggers of oxidative stress, such as ultraviolet radiation (UVR) and visible light (VL), lead to pigment formation through somewhat different pathways, but both share a common endpoint-the potential to generate cosmetically undesirable hyperpigmentation. Though organic and inorganic sunscreens are available to protect against the UVR portion of the electromagnetic spectrum, coverage is lacking to protect against the VL spectrum. In this manuscript, we review the phases of tanning, pathways of melanogenesis triggered by UVR and VL, and the associated impact of oxidative stress. We also discuss the known intrinsic mechanisms and paracrine regulation of melanocytes that influence their response to UVR. Understanding these mechanisms and their role in UVR-induced hyperpigmentation should potentially lead to identification of useful targets that can be coupled with antioxidant therapy to alleviate this effect.
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3.
Serum 25(OH)D levels after oral vitamin D3 supplementation and UVB exposure correlate.
Datta, P, Philipsen, PA, Olsen, P, Andersen, JD, Morling, N, Wulf, HC
Photodermatology, photoimmunology & photomedicine. 2019;(5):344-353
Abstract
BACKGROUND The inter-individual variation in 25(OH)D3 increase (Δ25(OH)D3 ) after vitamin D3 supplementation was determined and compared with the UVB irradiation response. METHODS Nineteen Danish participants received 85 μg vitamin D3 (cholecalciferol) daily for nine weeks with regular serum 25(OH)D3 measurements. These participants had three years earlier taken part in a 9-week controlled UVB study. The Δ25(OH)D3 was not confounded by ambient UVB, BMI or ethnicity. RESULTS Δ25(OH)D3 was 53 nmol L-1 and almost identical to Δ25(OH)D3 (52 nmol L-1 ) after UVB. Δ25(OH)D3 ranged from 17 to 91 nmol L-1 (span 74 nmol L-1 ) and was about half of that observed after UVB irradiation (span 136 nmol L-1 ). The interquartile ranges for vitamin D3 supplementation (38.8-71.4 nmol L-1 , span: 32.6 nmol L-1 ) and UVB irradiation (35.7-65.4 nmol L-1 , span: 29.7 nmol L-1 ) were similar indicating a comparable response of the two interventions. As the 25(OH)D3 start levels (R2 = 0.398, P = 3.8 × 10-3 ), 25(OH)D3 end levels (R2 = 0.457, P = 1.5 × 10-3 ) and Δ25(OH)D3 (R2 = 0.253, P = 0.028) between both interventions were correlated, this suggested a possible common individual background for the variation. Four pigment SNPs influenced the variation in the vitamin D3 -induced and UVB-induced Δ25(OH)D3 . A combined model including the influence of these four SNPs and the 25(OH)D3 start level explained 86.8% (P = 1.6 × 10-35 ) of the individual variation after vitamin D3 supplementation. CONCLUSION The inter-individual variation in the two interventions was comparable and had no common demographic but a partly common genetic background.
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4.
Overview on vitamin D and sunbed use.
Pierret, L, Suppa, M, Gandini, S, Del Marmol, V, Gutermuth, J
Journal of the European Academy of Dermatology and Venereology : JEADV. 2019;:28-33
Abstract
Vitamin D seems to be associated with a protective effect in a vast range of diseases, including cardiovascular, autoimmune and oncologic conditions. Since ultraviolet (UV) B light is the most important prerequisite for the cutaneous synthesis of vitamin D, sunbeds are able to increase serum vitamin D levels, although only transiently in most cases. In this scenario, the artificial tanning industry relentlessly tries to promote the use of sunbeds as a 'safe' therapeutic measure to achieve an adequate serum vitamin D status. The World Health Organization classified UV-emitting tanning devices, as well as the whole UV spectrum, as group-1 carcinogens, as they significantly increase the risk of melanoma and non-melanoma skin cancer. In case of vitamin D deficiency or insufficiency, the current risk-benefit ratio is therefore in favour of vitamin D supplementation instead of sunbed use. Artificial tanning devices should never be considered as an option to achieve an appropriate vitamin D status. Their supposedly beneficial effects, vastly publicised by the artificial tanning industry, are not worth the carcinogenic risk associated with sunbed use.
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5.
A Review of the Evidence Supporting the Vitamin D-Cancer Prevention Hypothesis in 2017.
Grant, WB
Anticancer research. 2018;(2):1121-1136
Abstract
The vitamin D-cancer prevention hypothesis has been evaluated through several types of studies, including geographical ecological studies related to indices of solar ultraviolet-B (UVB) dose (the primary source of vitamin D for most people), observational studies related to UVB exposure or serum 25-hydroxyvitamin D [25(OH)D] concentrations, laboratory studies of mechanisms, and clinical trials. Each approach has strengths and limitations. Ecological studies indirectly measure vitamin D production and incorporate the assumption that vitamin D mediates the effect of UVB exposure. Findings from observational studies with long follow-up times are affected by changing 25(OH)D concentrations over time. Most clinical trials have been poorly designed and conducted, based largely on guidelines for pharmaceutical drugs rather than on nutrients. However, three clinical trials do support the hypothesis. In general, the totality of the evidence, as evaluated using Hill's criteria for causality in a biological system, supports the vitamin D-cancer prevention hypothesis.
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6.
Sub-optimal Application of a High SPF Sunscreen Prevents Epidermal DNA Damage in Vivo.
Young, AR, Greenaway, J, Harrison, GI, Lawrence, KP, Sarkany, R, Douki, T, Boyer, F, Josse, G, Questel, E, Monteil, C, et al
Acta dermato-venereologica. 2018;(9):880-887
Abstract
The cyclobutane pyrimidine dimer (CPD) is a potentially mutagenic DNA photolesion that is the basis of most skin cancers. There are no data on DNA protection by sunscreens under typical conditions of use. The study aim was to determine such protection, in phototypes I/II, with representative sunscreen-user application. A very high SPF formulation was applied at 0.75, 1.3 and 2.0 mg/cm2. Unprotected control skin was exposed to 4 standard erythema doses (SED) of solar simulated UVR, and sunscreen-treated sites to 30 SED. Holiday behaviour was also simulated by UVR exposure for 5 consecutive days. Control skin received 1 SED daily, and sunscreen-treated sites received 15 (all 3 application thicknesses) or 30 (2.0 mg/cm2) SED daily. CPD were assessed by quantitative HPLC-tandem mass spectrometry (HPLC-MS/MS) and semi-quantitative immunostaining. In comparison with unprotected control sites, sunscreen significantly (p ≤ 0.001-0.05) reduced DNA damage at 1.3 and 2.0 mg/cm2 in all cases. However, reduction with typical sunscreen use (0.75 mg/cm2) was non-significant, with the exception of HPLC-MS/MS data for the 5-day study (p <0.001). Overall, these results support sunscreen use as a strategy to reduce skin cancer, and demonstrate that public health messages must stress better sunscreen application to get maximal benefit.
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7.
A Critical Appraisal of the Recent Reports on Sunbeds from the European Commission's Scientific Committee on Health, Environmental and Emerging Risks and from the World Health Organization.
Reichrath, J, Lindqvist, PG, DE Gruijl, FR, Pilz, S, Kimball, SM, Grant, WB, Holick, MF
Anticancer research. 2018;(2):1111-1120
Abstract
The European Commission's Scientific Committee on Health, Environmental and Emerging Risks and the World Health Organization recently published reports which concluded that a large proportion of melanoma and non-melanoma skin cancer is attributable to sunbed use, and that there is no need to use sunbeds as there are no health benefits and they are not needed to achieve an optimal vitamin D level. The overall conclusion from both bodies was that there is no safe limit for UV irradiance from sunbeds. We are, however, deeply concerned that these assessments appear to be based on an incomplete, unbalanced and non-critical evaluation of the literature. Therefore, we rebut these conclusions by addressing the incomplete analysis of the adverse health effects of UV and sunbed exposure (what is 'safe'?) and the censored representation of beneficial effects, not only but especially from vitamin D production. The stance taken by both agencies is not sufficiently supported by the data and in particular, current scientific knowledge does not support the conclusion sunbed use increases melanoma risk.
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8.
Mechanisms and prevention of UV-induced melanoma.
Sample, A, He, YY
Photodermatology, photoimmunology & photomedicine. 2018;(1):13-24
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Abstract
Melanoma is the deadliest form of skin cancer and its incidence is rising, creating a costly and significant clinical problem. Exposure to ultraviolet (UV) radiation, namely UVA (315-400 nm) and UVB (280-315 nm), is a major risk factor for melanoma development. Cumulative UV radiation exposure from sunlight or tanning beds contributes to UV-induced DNA damage, oxidative stress, and inflammation in the skin. A number of factors, including hair color, skin type, genetic background, location, and history of tanning, determine the skin's response to UV radiation. In melanocytes, dysregulation of this UV radiation response can lead to melanoma. Given the complex origins of melanoma, it is difficult to develop curative therapies and universally effective preventative strategies. Here, we describe and discuss the mechanisms of UV-induced skin damage responsible for inducing melanomagenesis, and explore options for therapeutic and preventative interventions.
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9.
The Winding Path Towards an Inverse Relationship Between Sun Exposure and All-cause Mortality.
Lindqvist, PG
Anticancer research. 2018;(2):1173-1178
Abstract
For a long time, skin cancer has been known to be related to extensive UV exposure. New emerging data have, however, shown low UV exposure/low vitamin D levels to be related to increased mortality rate due to skin cancer. In addition, low sun exposure habits in regions of low solar intensity have been shown to be a major risk factor for all-cause mortality in the same range as that for smoking. This is mainly due to lower all-cause mortality due to cardiovascular disease (CVD) and non-CVD/non-cancer disease among women with active sun exposure. Women with active sun exposure habits were estimated to have a 1- to 2-year longer life-expectancy during the Melanoma in Southern Sweden study interval. These findings are in line with those to be expected from an evolutionary perspective and research findings, but in opposition to present guidelines and recommendations.
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10.
The Protective Role of Astaxanthin for UV-Induced Skin Deterioration in Healthy People-A Randomized, Double-Blind, Placebo-Controlled Trial.
Ito, N, Seki, S, Ueda, F
Nutrients. 2018;(7)
Abstract
Skin is a major safeguard tissue in humans. Because biological barrier function is deteriorated by several kinds of stresses including exposure to ultra-violet (UV) rays, the protection and treatment of skin conditions by dietary supplements are important. We therefore evaluated the effects of dietary supplementation with an algal food-derived antioxidant, astaxanthin, on UV-induced skin deterioration. Twenty-three healthy Japanese participants were recruited to a 10-week double-blind placebo-controlled study. They were assigned to the astaxanthin group supplemented with a capsule containing 4 mg of astaxanthin or the placebo group. To assess the protective role of astaxanthin for UV-induced skin deterioration, we determined the minimal erythema dose (MED) and analyzed UV-induced changes of moisture and transepidermal water loss (TEWL) at baseline and after 9 weeks of supplementation. Subjective skin conditions were assessed by the visual analog scale. The astaxanthin group showed increased MED compared with placebo. In addition, the astaxanthin group had a reduced loss of skin moisture in the irradiated area compared with placebo. Subjective skin conditions for “improvement of rough skin” and “texture” in non-irradiated areas were significantly improved by astaxanthin. Astaxanthin seems protective against UV-induced skin deterioration and helps maintain healthy skin in healthy people.