The Study
UV increases skin-derived 1α,25-dihydroxyvitamin D3 production, leading to MMP-1 expression by altering the balance of vitamin D and cholesterol synthesis from 7-dehydrocholesterol.
This study looked at skin cells in a dish and saw that when you shine UV light on them, they make more of a certain protein. But it didn't test this in real people, so we don't know if the same thing happens in your skin when you're outside.
Analysis score
Maximum 44 for a cross-sectional study.
Where the score came from
When your skin gets sunburned, it makes a special form of vitamin D that accidentally triggers a protein that breaks down collagen, the stuff that keeps skin firm.
Where does this study sit?
Reviews of RCTs (Meta-analyses)
Max 100Randomized Trials
Max 90Reviews of Cohort Studies
Max 85Cohort Studies
Max 72Reviews of Case-Control Studies
Max 63Case-Control Studies
Max 58Cross-Sectional & Case Series
Max 50Expert Opinion
Max 527 / 100
Quality score
Snapshots of a population at a single point in time, or descriptions of small groups. Can identify correlations and prevalence, but cannot determine cause and effect.
Key takeaways
Summary
Based on the study abstract and findings.
- 1Yes — this suggests sun exposure may accelerate skin aging by triggering collagen breakdown through a vitamin D pathway.
- 2UV light reduces DHCR7 (a cholesterol-making enzyme) and increases CYP27B1 (a vitamin D-making enzyme), leading to more active vitamin D and more MMP-1 (a collagen-breaker).
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
The Journal of steroid biochemistry and molecular biology
Year
2019
Authors
M. Shin, Yuri Lee, Min-Kyoung Kim, Dong Hun Lee, J. Chung
Related Content
Claims (6)
Cholesterol is a molecule that is necessary for maintaining the structure of cell membranes and for producing steroid hormones and vitamin D.
Ketoconazole and CYP27B1 siRNA reduce the production of MMP-1 protein in human skin cells exposed to UV light by preventing the formation of 1α,25-dihydroxyvitamin D3.
When DHCR7 is inhibited in skin cells, cholesterol production decreases and 7-dehydrocholesterol becomes more available to produce vitamin D3, which leads to higher levels of MMP-1 protein after UV light exposure.
UV light exposure on human skin cells increases the production of a specific form of vitamin D, which directly increases the activity of an enzyme that breaks down collagen through a biochemical pathway involving reduced DHCR7 activity and more available 7-dehydrocholesterol.
The active form of vitamin D, 1α,25-dihydroxyvitamin D3, increases the production of MMP-1 protein in human skin cells, while its precursor molecules 7-dehydrocholesterol and 25-hydroxyvitamin D3 do not.
Exposure to ultraviolet light in human skin increases the activity of the CYP27B1 gene and reduces the activity of the DHCR7 gene.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.