If, like many women, you find the face in the mirror doesn’t match the image in your head, skin aging is likely the driving factor. The primary culprits of the aging process of skin are divided into two categories: extrinsic aging caused by chronic exposure to the sun’s UVA and UVB rays, pollution, ionizing radiation, chemicals, toxins and intrinsic aging (influenced by genetics factors, cellular metabolism, hormone and metabolic processes).
Many of the changes that occur in skin structure as a result of aging are expressed prematurely in sun damaged skin, a phenomenon known as photoaging. In fact, up to 80% of skin’s aging is due to sun damage.
As sunlight penetrates the skin, it batters your DNA.
UVB attacks DNA directly, damaging cells in the epidermis. UVA is dubbed the silent wrinkler, as it penetrates layers of skin deeper than other rays causing a delayed tan, delayed wrinkling, and delayed skin cancer.
Melanocytes naturally defend the body against UVB radiation through the production of melanin, a brown colored pigment, that surround nearby epidermal cells. Melanin absorbs incoming UVB light, preventing it from damaging tissues located in skin layers underneath the epidermis. The amount of melanin produced is dependent on the length of time we are exposed to the sun; not only deepening the hue of our suntan but temporarily thickening the epidermal layer of skin.
DNA cells found in the epidermis directly absorb UVB radiation, meaning that these cells are vulnerable injury directly caused by UVB radiation. UVA radiation enhances facial aging through an intermediate step, the induction of free radical formation.
Free radicals damage everything they contact; contributing to photoaging by causing oxidative stress to cells in every layer of the skin –disrupting proper cell function by preventing proper cellular repair, allowing for prolific cellular damage, decay and abnormal cellular growth.
The dermal layer contains crisscrossing collagen fibers that form a strong elastic network. Elastin, a fibrous protein, weaves in between collagen fibers, supporting collagen movement, allowing it to stretch back and forth. Elastin and collagen provide the skin with structure, elasticity and durability, keeping it firm and resilient. The integrity and production of collagen and elastin naturally decline with age, causing skin to sag and wrinkle.
UV exposure prematurely deteriorates the structure of collagen and elastin. Free radicals and UV exposure further degrade these structural proteins by altering the function of fibroblasts. Fibroblasts not only repair damaged collagen and elastin, they also produce new collagen.
Fibroblasts that are not functioning optimally increase abnormal elastin structure and the decay of collagen structure. Additionally damaged fibroblasts diminish the overall presence of collagen decreasing collagen synthesis at a higher rate than chronological aging.
Ultimately, the dermal layer thins as damaged collagen and elastin fibers are improperly remodeled. Resulting in disorganized networks of damaged collagen and fragmented elastin fibers called solar scars.
All of these effects are cumulative on the appearance of aging skin. The combination of uneven thickening and thinning of the skin’s layers combined with a lack of sub structural support in the dermis layer leads to loose, sagging skin. Skin is no longer able to resist permanent wrinkle formation due to abnormal elastin. This is most apparent as facial wrinkles develop where the skin is folded by expressive muscles. Degradation of the dermis layer increases dryness giving rise the leathery appearance of skin. UVB radiation damages melanocytes, resulting in the overproduction of melanin resulting in brown “age spots”. Telangiectasias, the appearance of red spider web like lines, can also emerge due as UV exposure affects blood vessel dilation.
Most importantly photodamage increases your risk of developing skin cancer because UV exposure causes cellular mutation and inhibits the body’s ability to repair itself! It is estimated that UV is causative for nearly 65% of melanoma and 90% of non-melanoma skin cancers.