skin & beauty

DDB2

The Link Between DNA Repair, Oily Skin & Acne (DDB2)

Written by Jasmine Foster, BSc, BEd on October 7th, 2020

DDB2 regulates cell repair & death and promotes the antimicrobial activity of sebocytes. How does it affect acne? Read on to learn more.

Summary

DDB2 encodes damage-specific DNA binding protein 2. Variants of DDB2 may play a role in acne by improving the antimicrobial effects of sebocytes. Lifestyle and supplement modifications may counteract the effects of these variants by supporting DDB2 activity.

DDB2 and Acne

DDB2 encodes damage-specific DNA binding protein 2. When the DNA inside of a cell becomes damaged, DDB2 helps decide whether the cell is marked for repair or programmed for death [R].

This gene also plays a role in the antimicrobial activity of a type of cell called a sebocyte. Sebocytes are skin cells that make up the sebaceous glands and produce sebum, a fatty substance that protects the skin from water, damage, and infection. In other words, sebum is that oily stuff on your nose [R, R, R, R].

Sebocytes are a double-edged sword in acne. Depending on its composition, or if too much is produced, sebum can end up clogging pores and promoting the growth of bacteria. On the other hand, healthy sebocytes can kill Cutibacterium acnes [R, R].

DDB2 sends signals by altering structures called histones H3 and H4. Of these, H4 has direct antibacterial activity; researchers believe that DDB2’s connection to acne goes through H4 [R, R].

The DDB2 gene on its own is associated with relative incidence of severe acne. However, its effect becomes even stronger in combination with variants in other genes, including TP63 and CACNA1H [R, R].

DDB2 mainly regulates cell repair and death. However, it also interacts with H4, a histone that can kill acne bacteria.

Your DDB2 Results for Acne

SNP Table

variant	genotype	frequency	risk allele
rs747650

DDB2 rs747650

‘C’ = More common in people with severe acne
‘T’ = Possibly protective against severe acne
The ‘T’ allele may increase the activation of antimicrobial histone H4 [R, R].

Recommendations

Light Therapy

Light therapy applies light of specific wavelengths through human skin to elicit certain effects in the underlying tissue.

Ultraviolet light is a major trigger of DDB2 activity; in most people, UV light exposure will increase DDB2 [R].

People with certain serious mutations that make DDB2 ineffective should avoid UV light altogether. If you have xeroderma pigmentosum, for example, then you already know to avoid UV light. However, mutations in DDB2 alone do not usually cause this disease. To be sure about your risk level from UV exposure, talk to your doctor [R, R, R].

Red light, blue light, and their combination have all been shown to improve acne. In one study, the combination was more effective than not only either wavelength alone, but also the FDA-approved medication benzoyl peroxide [R, R, R, R].

Most of red light’s effects are through the cells’ mitochondria absorbing light. In cell studies, the cytochrome c oxidase in the mitochondria absorbs red light, which causes it to release nitric oxide, increase ATP, and decrease oxidative stress [R].

Blue light activates proteins that contain light-sensitive molecules (porphyrins and flavones) and increase mitochondrial activity and oxidative stress. Skin cells respond by releasing molecules that promote inflammation and control skin growth. Additionally, blue light killed the acne-causing bacteria Cutibacterium acnes in test tubes [R, R, R].

Various wavelengths of light may increase DDB2 activity and have been shown to improve acne.

Milk Thistle

Silymarin, an active compound of milk thistle, increased DDB2 expression in cells exposed to ultraviolet light [R].

In a clinical trial, silymarin reduced acne severity when taken by mouth daily for 2 months. However, it was less effective than the antibiotic doxycycline [R].

In another trial, a combination of silymarin, N-acetylcysteine, and selenium reduced acne after 8 weeks by 53% [R].

Silymarin from milk thistle increased DDB2 in cells and may improve acne when taken as a supplement.

Jasmine Foster

BSc, BEd

Jasmine received her BS from McGill University and her BEd from Vancouver Island University.

Jasmine loves helping people understand their brains and bodies, a passion that grew out of her dual background in biology and education. From the chem lab to the classroom, everyone has the right to learn and make informed decisions about their health.

Disclaimer

The information on this website has not been evaluated by the Food & Drug Administration or any other official medical body. This information is presented for educational purposes only, and may not be used to diagnose or treat any illness or disease.

Also keep in mind that the “Risk Score” presented in this post is based only on a select number of SNPs, and therefore only represents a small portion of your total risk as an individual. Furthermore, these analyses are based primarily on associational studies, which do not necessarily imply causation. Finally, many other (non-genetic) factors can also play a significant role in the development of a disease or health condition — therefore, carrying any of the risk-associated genotypes discussed in this post does not necessarily mean you are at increased risk of developing a major health condition.

Always consult your doctor before acting on any information or recommendations discussed in this post — especially if you are pregnant, nursing, taking medication, or have been officially diagnosed with a medical condition.

More skin & beauty blogs

Genetic Link Between Acne and Inflammation (TNF) Is Your Skin Prone to Trapping Acne Bacteria? (TGFB2) A Gene Linking Bacteria, Inflammation, and Acne (IL4R) A Surprising Genetic Factor for Acne (FST) The Link Between DNA Repair, Oily Skin & Acne (DDB2) A Genetic Link Between an Immune System Protein & Acne (IL8) How a Metabolic Gene Contributes to Acne (PPARG) Cortisol Genetics in Acne Development (HSD11B1) Can Skin Inflammation Cause Acne? (SELL) The Relationship Between Clogged Pores & Acne (IL1A)

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