Skin Aging and Physiology

Three Factors in Aging
Many factors, both extrinsic and intrinsic, cause the skin to age. Those causes can easily be divided into three main categories: biological aging, environmental aging, and mechanical aging. Let's look at each cause individually to understand ways they can be minimized.

The first category is biological aging. Biological aging is the result of changes—often genetically determined—that occur naturally within the body. Everyone has a biological clock or chronological age determined by genetic makeup. This applies to the skin as well. As our biological clock ticks, our skin gradually loses its ability to function as it once did. Biological aging occurs as a result of natural changes within the body that manifest themselves in outward signs of aging on the skin. Frequently, changes associated with biological aging are the result of a gradual shift in the balance of certain hormones and messenger molecules excreted by other glands and organs within the body. Many of these changes are genetically determined and cannot be stopped.

Fortunately, some of the factors contributing to biological aging can be controlled. Scientists are beginning to understand how free radicals (unstable molecules) damage proteins, lipids, and the DNA within cells, and, in turn, accelerate the biological aging process. Antioxidants are molecules with the ability to neutralize free radicals in the skin. A healthful diet full of antioxidant-rich fruits and vegetables, along with nutritional supplementation and topical application of key nutrients, may help decrease the intensity and delay the onset of many changes that are a result of biological aging.

The second category of factors that cause the skin to age are all results of extrinsic sources in the environment. Environmental aging occurs as a result of daily exposure to trillions of free radicals from a variety of sources: the sun's ultraviolet rays, pollution, smoke, harsh weather, and external stress. These free radicals damage lipids, proteins, and DNA, all of which limit the ability of cells to function and cripple the integrity of overall cell composition. Years of accumulated environmental stress on cellular structures results in the premature aging of the skin.

Sun exposure is the primary environmental stressor leading to damaged skin. The damage to skin components caused by both prolonged and incidental sun exposure is called photoaging. Although cigarette smoke, exposure to harsh weather conditions, and pollution are prolific contributors to environmental aging, UV damage from the sun's rays accounts for 90 percent of premature skin aging. Photoaging damages collagen, elastin, melanocytes, and the moisture barrier, resulting in wrinkles, sagging, uneven skin tone, dark spots, and a rough, dry skin texture.

While sun exposure is the environmental stressor that accounts for most premature skin aging, there are others. Pollution damages skin by increasing free radical production and increasing the effects of UV radiation. Harsh weather (dry air, wind, and cold) depletes skin of essential moisture, resulting in a rough texture and fine, dry lines. Cigarette smoke increases free radical production and may decrease collagen and elastin production. Cigarettes also significantly decrease the supply of oxygen to skin cells.

The third category of aging is called mechanical aging. Mechanical aging is the result of continually repeated wrinkle causing behaviors, muscle movements repeated day after day and year after year. Although it is unrealistic to avoid some wrinkle causing behaviors such as smiling and frowning, the following behaviors should be avoided to help prevent premature signs of mechanical aging:

• Squinting.
• The thinker stance (resting chin or cheek in the hand).
• Sleeping on your side or stomach.
• Scrubbing with hot water.
• Weight fluctuation.
• Unbalanced diet and lack of sleep.
• Pursing the lips while smoking or drinking from a straw.

Evidence of Aging: Changes in Physiology
Skin aging results from the deterioration of structures in the skin and the slowing of healthy skin functions. Let's take a closer look at several of the visible signs of skin aging and what is happening inside the skin to cause these changes.

Dry skin is a visible sign of skin aging. Healthy, young skin maintains appropriate moisture levels through the sealing properties of the moisture barrier, which is composed of keratin-filled keratinocytes (skin cells) surrounded by and sealed together with interspersed epidermal lipids (ceramides, lipids, and fatty acids). As we age, the skin produces fewer ceramides, lipids, and fatty acids to seal the moisture barrier, resulting in an increase in transepidermal water loss and dryness.

A natural decline in hormone levels is usually the cause of this decreased production; however, several other preventable factors can also strip epidermal lipids, causing excessive dryness. Consider the following:

• Improper skin care. Using harsh cleansers and neglecting to supplement the skin with rich, nourishing moisturizers.
• Harsh weather conditions. Enduring extreme temperatures and wind without adequate moisturizers and protection.
• UV radiation. Neglecting to protect skin from the sun's UV rays with sunscreen.

A dull, rough complexion is another visible sign of skin aging. Healthy, young skin remains smooth and radiant because fresh, new cells are brought to the surface as older cells are continuously shed. The skin cells in the bottom layer of the epidermis (stratum basale) constantly divide through cell division, forming new keratinocytes. This regenerative process is called skin cell renewal. As we age, the rate of skin cell renewal decreases, causing cells to become more sticky and not shed as easily. As a result of cell renewal decreasing, the skin becomes thinner and more susceptible to environmental damage, especially photodamage from the sun's UV rays. Eventually, the skin appears dull and rough in texture.

Several factors contribute to the process of skin cell renewal declining as we age. For example, weakened blood vessels in the dermis and a flattening of dermal papillae decreases the surface area between the dermis and epidermis across which nutrients can diffuse. This process decreases nutrient and oxygen supplies to the basal cells in the lower epidermis. UV exposure can also penetrate the epidermis, damage basal cells, and slow the rate of cell division. Finally, failure to exfoliate the surface of the skin with physical and chemical exfoliates for the purpose of smoothing the skin and stimulating cell renewal contributes to the decline in renewal.

A third visible sign of aging is fine lines and deep wrinkles in the skin. The structural protein called collagen, which is found in the dermis, provides a mesh-like framework of support and strength for the skin. As we age, collagen production decreases and collagen fibers degrade at a faster rate than in earlier years. This results in an overall decrease in the amount of collagen in the dermis. Areas with less support begin to cave in and wrinkles begin to form.

Multiple factors lead to decreased collagen levels. First, with age there is a natural decline in messenger molecules that trigger collagen production. There is also an increase in the enzyme collagenase which breaks collagen down. Another factor contributing to decreased collagen levels is free radicals from UV exposure. These can damage collagen strands and stimulate collagenase activity, which leads to the formation of irregular collagen linkages that weaken the skin. In order to avoid UV damage to collagen fibers and fibroblasts, application of a consistent daily sunscreen is necessary. Research also indicates that chemical exfoliation may stimulate collagen production.

The following are factors that decrease collagen levels in the skin:

• UV rays can penetrate the skin and cause damage to collagen-producing fibroblast cells.
• Mechanical stress on the skin caused by repeated wrinkle causing behaviors can also break down collagen.
• With age, the synthesis of glycosaminoglycans (GAGs) decreases, affecting moisture levels in the dermis; collagen becomes brittle and prone to breakage.
• As skin renewal decreases, wounds heal more slowly and the skin thins, becoming more susceptible to environmental stressors; this can lead to damaged fibroblasts and a decrease in collagen levels.

Loss of firmness in the skin is another evidence of aging. All three types of skin aging—biological, environmental, and mechanical—contribute to the skin's loss of firmness. Biologically, our body naturally produces more of the hormone DHT as we age. As DHT levels increase, elastin production is inhibited. Elastin is another skin structural protein found in the dermis. This coil-like protein has the ability to snap back into place after stretching, giving the skin its elastic quality. As we age, elastin fibers lose much of their resilience and elastin production within the fibroblasts decreases. This overall decline in healthy elastin levels results in areas of decreased firmness, especially along the jaw line, neck, and around the eyes. Environmentally, UV rays can penetrate the skin to damage elastin-producing fibroblast cells. Also, as skin cell renewal decreases, wounds heal more slowly and the skin thins, becoming more susceptible to environmental damage. This can lead to damaged fibroblasts and decreased elastin levels. Finally, mechanical stress, due to repeated wrinkle causing behaviors, can permanently stretch out elastin fibers.

Enlarged pores are also a sign of aging skin. To a large degree, pore size is determined by genetics; however, as we age, our pores tend to appear larger. The pore's enlarged appearance is due to a buildup of dead cells around the pore. As more collagen breaks down and production slows, the supportive structures surrounding cells decrease and cells can appear stretched. Keeping the skin exfoliated and the pores clear will help reduce the appearance of pore size. Also, consistently using a sunscreen to protect collagen helps maintain pore size.

Age spots are the last evidence of aging that we're going to discuss. Normal skin pigmentation helps protect healthy skin from the stress of mild UV exposure. Melanin, the skin's photoprotective pigment, is produced in specialized melanocyte cells in the lowest layer of the epidermis (stratum basale). As we age, melanocyte activity decreases, making the skin more susceptible to UV damage. With age, melanocytes also tend to cluster together. This results in patches of pigmentation called age spots.

Many factors contribute to the production of age spots. First, hormone imbalances that occur with advanced age result in fewer melanocytes and can also trigger excessive melanin production. Second, UV light rays stimulate melanocytes to produce skin pigment. UV light can also penetrate the skin and damage melanocyte DNA, which can stimulate melanocytes to enlarge and cluster together. Third, as the cell renewal cycle decreases, wounds heal more slowly and the skin thins, becoming more susceptible to environmental damage. This can lead to damaged melanocytes and abnormal pigmentation. Finally, poor skin care habits can lead to skin irritation, which triggers melanin production.

Prevent Premature Skin Aging with Proper Skin Care
The majority of premature, avoidable skin aging is caused by UV radiation; thus, it is absolutely essential to use a daytime moisturizer with sunscreen. Even if you aren't in the sun for extended periods, effects of incidental sun exposure accumulate and show up on the skin.

Fortunately, you can turn back the clock on your skin. Even if you did not properly care for your skin in years past, there are many technologically advanced ingredients and exceptional botanicals that help repair sun damage and reverse some of the effects of both biological and mechanical aging. Because youthful, healthy skin portrays confidence and beauty, we are all concerned with what we assume is inevitable skin aging. The good news is that we have more control than we realize over the rate at which our skin ages. Maintaining youthful skin starts with good skin care. Using products specifically formulated for your skin type is the first step to preventing unnecessary skin damage.

Zoe Diana Draelos
M.D., F.A.A.D.

Dr. Draelos worked extensively with Nu Skin to create the Nu Skin® Profiler and conducted clinical research on the use of Tru Face™ Revealing Gel with Polishing Peel,™ as well as studies on Tru Face™ Line Corrector and Tru Face™ IdealEyes.® She serves on the board of directors for the American Academy of Dermatology and has a research interest in cosmetics, toiletries, and biologically active skin medications. Dr. Draelos is a practicing, board certified dermatologist in High Point, North Carolina, and a clinical associate professor of dermatology at Wake Forest University School of Medicine.