Aging results from the interaction of a genetic program and the cumulative wear and tear of skin. This involves two phenomena: intrinsic aging and photoaging. A person’s genetic program controls his intrinsic aging. Skin will age because of the passage of time alone. This is best exemplified by buttock skin which is normally not exposed to the sun. This manifests with very subtle changes in skin appearance. On the other hand, photoaging is attributable to the cumulative effects of the ultraviolet radiation (UVR) of the sun. People who have more sun exposure, whether for work or pleasure, are more at risk for photoaging or for looking old.

Photoaging corresponds to the more popular notion of ‘old skin’. This presents in varying degrees but to picture old skin at its worst is the best example of photoaging. Photoaged skin is dry and rough. Melanocytes are cells specialized in producing melanin, the brown pigment of skin. The decrease in melanocyte number in photoaged skin leads to an uneven melanocyte distribution. The result is an uneven pigmentation. Freckles, lentigines, guttate hypomelanosis (<8mnn off-white spots), and persistent brown discolorations are due in part to this.

The dermis is the layer of skin beneath the epidermis. Despite its deeper location, the UVR of the sun is able to effect certain dermal changes. This includes damage to collagen fibers which normally provides the structural framework of the skin. This gives rise to non-functional collagen fibers. As a result, wrinkling occurs, initially with fine surface lines and in the more sun-exposed skin, with deep furrows. In severe cases, the skin appears coarse with nodularities.

UVR also induce damage to elastic fibers in the dermis making it non-functional. For this reason, the skin becomes less elastic. Severely sun-damaged skin does not return to its original position after being pulled, like a rubber band that has lost its elasticity. Tiny prominent blood vessels on sun-exposed skin termed telangiectasia, purpura (easy bruising), comedones (‘black heads’), and sebaceous hyperplasia (1-4mm lightly-colored bumps) are other signs of photoaging.

Skin cancers like basal cell carcinoma and squannous cell carcinoma also occur as a consequence of habitual sun exposure. Basal cell carcinoma often appears as darkly or fleshly-colored ulcerated nodules. Squamous cell carcinoma may appear as a firm eroded enlarging mass. Once suspected, consult a licensed dermatologist.

At present, there is some evidence that a specific skin deterioration observed in aging is accelerated in diabetes melllitus. This is linked to the damage brought about by abnormal collagen cross-linking. When collagen fibers are cross-linked or joined together in an abnormal fashion, major changes in its physical properties result. This is best likened to a brick wall. If bricks are put together in an abnormal manner such that holes are gaping through, the wall will not be as functional. This abnormal collagen cross-linking increase slowly with age but the rate is accelerated in diabetes due to high blood sugar levels. These can ultimately affect the repair of damaged blood vessels and wound healing in diabetes. These modifications are deleterious to collagen as structural supporting framework of the skin. Ultimately, these contribute to the cumulative wear and tear of skin that constitutes aging. Further clinical studies are warranted at this point to validate the interactive effect of high sugar levels and aging.

Skin darkening of the nape among diabetics must not be confused
with photoaging. This is acanthosis nigricans. It is due to increased insulin levels in the blood. Excess insulin leads to the abnormal epidermal and dermal tissue proliferation. The result is the brown to gray-black velvety thickening of the nape, armpits, and skin folds. Among obese patients, resolution may occur with weight loss to ideal body weight).

Diabetic dermopathy is another condition that presents with brown spots unrelated to photoaging. These are small (<1 I mm), brown, flat,
starlike lesions on the shins, hence the term shin spots. These are not painful or itchy and usually clear in a year or two leaving a residual lighter skin-colored mark or scar. New lesions often arise giving the impression that they are persistent. The lesions are brought about by trauma. In a study involving the induction of shin spots in diabetic and nondiabetic patients with heat and cold injury, nondiabetic patients healed without scarring. Hence, avoidance of trauma is important. Shin spots occur more often among those with longstanding diabetes and those with eye, kidney, and nerve diabetic complications. The recognition of diabetic dermopathy points to the possibility of these complications. Proper diet and sugar control is still the cornerstone in the therapy of diabetes mellitus and its skin complications.

A multicenter study on photoaging, involving more than 700 subjects, was published in a British journal. The investigator noted that patients were found to have statistically significant improvements in fine wrinkling, roughness, dyspigmentation, and overall appearance after six months of daily sunscreen and moisturizer use. This suggests an intrinsic repair capacity and a central role for sunscreen use in photoaging. In the same study, the ability of retinoic acid (also termed tretinoin) to improve photoaging changes was demonstrated.

There were statistically significant improvements in global appearance, fine and coarse wrinkling, surface roughness, and mottled pigmentation when compared with sunscreen use alone. These benefits increase with duration of use for at least 10 to 12 months.

Alpha-Hydroxy acids (AHAs) are derived from fruits (malic acid), and sugar cane (glycolic acid). Topical treatment of photoaged skin with AHAs has also been reported to result in subtle clinical improvements in wrinkling, roughness, and discolorations within months of daily application.

Vitamin A (retinol), C (ascorbic acid), and E (tocopherols), beta-carotene, and bioflavinoids are antioxidants. Their role against oxidative stress is well documented. However, the ability of topically applied antioxidants to modify damage in the skin still requires large, multicenter, controlled human studies.

Although intrinsic aging is universal, photoaging is evitable. The use of sunscreens cannot be overemphasized and this applies to all. It is always wise to consult an endocrinologist for the proper management of diabetes and avoid its complications. For proper skin therapy of photoaging, get the expert opinion of a licensed dermatologist. Ultimately, the choice is yours.

Related terms:

• basal cell carcinoma diabetes
• abnormal collagen elasticity diabetes
• acanthosis nigricans is also known as photoaging
• Are diabetics prone to acidity
• brown roughness in armpit
• dark spots on the nape obese
• diabetes photoaging
• diabetics prone to
• nape darkening due to sugar
• photoaging rubbery skin
• skin brown spot flat dermopathy

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