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With intrinsic biological aging, the skin’s outer layer is thinned (over time by about 20 percent). The surface of the skin remains smooth. The border between the epidermis and the dermis becomes flattened, making the skin less resistant to friction (you get more blisters in snug shoes!). In contrast, extrinsic photoaging causes a thickening of the outer skin layer, with up to 50 percent more cells being accumulated onto the skin’s surface, making it feel rough and dry. Think of the grainy, thickened skin on the backs of the hands of a gardener, for example. With photoaging, accumulation of pigment in the basal cells is more markedly irregular than in intrinsic aging, causing the so-called “liver spots” or “age spots” (medically called solar lentigos), the unattractive dark spots especially prevalent on the hands, arms, face and chest.

Even greater differences between intrinsic and extrinsic aging are seen in the skin’s inner layer, the dermis. The most noticeable distinction is that in photoaged skin, the elastic fibres are markedly increased and thickened. This is not seen in normal, protected skin, in which elastic fibres may increase slightly in quantity and thickness but maintain the normal candelabra-like pattern of fibres.

This so-called solar-elastosis effect is readily observed on the thick, leathery skin on the neck of a fisherman: deep wrinkles are fixed and prominent, and the skin is not very pliable. At the same time, the amount of mature collagen in photoaged skin decreases and the dermis is filled with degenerated elastic fibres and increased amounts of the gel-like substance — the mucopolysaccharide — that surrounds these fibres. The composition of this gel is different from youthful skin. With normal, biologic aging, these mucopolysaccharides decrease.

Another major difference in photoaged skin is the presence of many cells. Fibroblasts, white blood cells and mast cells abound, all working overtime to repair the extrinsic damage they encountered. As mentioned, the presence of all of these cells means that photoaged skin is chronically red and inflamed. In contrast, with natural aging there are fewer cells because all this activity has slowed down.

Blood circulation in the skin also suffers from both natural aging and sun exposure. In protected aged skin, the number of small blood vessels declines, but those remaining are not unnaturally expanded and are normal. With photoaging, these micro-blood vessels become misshapen. With normal aging, the decline in the efficiency of the skin’s “drainage system” (its “lymphatics”) is just moderate, whereas with photodamage, this loss is so marked that the lymphatics are practically absent.

Hair follicles normally degenerate with age, as do sebaceous glands. In contrast, after photodamage through sun exposure, follicles expand and fill with debris from the sun-thickened layer of outer skin. This in turn makes the sebaceous glands become greatly enlarged, leading to more oily secretion and unsightly blackheads.

Certain marks or growths become more visible with aging. The dominant marking normally associated with age is a little red dot or soft, red raised papule, the so-called senile angioma, occurring most frequently on the trunk of the body. Rarely do other growths occur in sun- protected skin.

Wrinkles and aging

Even young children have wrinkles! All skin has folds corresponding to the way the skin envelops and moves with the body. To minimize the appearance of scars, when surgeons make incisions in the skin they follow the direction of these so-called Langer’s lines whenever possible.

When you look closely at your skin, you can see tiny furrows that intersect in complex ways, creating delicate skin-surface patterns which vary with age and differ from one part of the body to another. In unexposed areas of young people’s skin, these patterns are orderly and regular. With intrinsic aging, the furrows become shallower and the pattern becomes more irregular in shape. Where skin has been exposed to the sun, there is a loss of skin-surface pattern with age.

With both intrinsic and extrinsic aging, the amount of fat under the skin steadily decreases. The degree of fat absorption varies in different parts of the body. The combination of decreased thickness of the dermis, decreased resilience of the skin, and the loss of subcutaneous fat makes sagging skin and jowl-like wrinkles become more apparent.

We all shrink from the moment we stop growing. This contraction of bone usually accelerates in our late 50s or early 60s. Particularly prominent is some contraction of our facial structure causing sagging jowls and wrinkles; this is further accentuated by the later loss of teeth. Our skin can then begin to fold away from the underlying muscle and bone, and gravity pulls that excessive, non-resilient skin down.

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