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Premature Aging Skin

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The skin is the largest, most complex, immune organ that challenges the practicing aesthetician today. Due to its interface function between the body and the environment, the skin is chronically exposed to both endogenous and environmental pro-oxidant agents, leading to premature aging and impaired cellular function.

Compelling evidence of premature aging suggests that oxidative stress is the major cause involved in the damage of the skin’s cellular constituents i.e.; keratinocytes, melanocytes, Langerhans, Merkle, mast, fibroblasts, etc. and their DNA, cell membrane lipids, and proteins.

The skin’s natural antioxidant network protects these cells against oxidative injury and prevents the production of oxidation products such as 4-hydroxy to 2-nonenal or malonadehyde, which are able to induce protein damage, apoptosis or release of pro-inflammatory mediators, such as cytokines. Inflammatory cytokines exist within the interstitial space in normal and inflamed skin, and are protein mediators. Cytokines govern the inflammatory phase that clears cellular and extra cellular matrix debris. However, the repair process is not always 100 percent, and when oxidative stress overwhelms the skin’s natural antioxidant capacity and the subsequent modifications of cellular redox apparatus lead to an alteration of cell homeostasis and a generation of degenerative processes.

One common fear is premature aging of the skin. Aging is a basic biological process common to all living organisms. Its biological mechanisms have yet to be elucidated in detail; however aging is usually understood as an irreversible, progressive loss of homeostatic (cellular balance) capacity. Given this fact, let it not be said the most influential generation dedicated to combating this issue is the infamous Baby Boomer age group. It is this powerful generation fueling the energy to battle aging and demanding skin care products and treatments that produce results.

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The Science Behind Aging

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The 101 of Aging

Aging is a 24/7 biological process that results in cellular wear and tear and cellsenescence, eventually lapsing into decreased viability and then eventual cell death. This unavoidable, redundant aging syndrome is also affected by a pre-programmed genetic agenda (intrinsic) superimposed on cumulative environmental (extrinsic) and endogenous insults that take place throughout the cellular organism’s lifespan. Chronological skin aging comprises unwanted changes in the skin that occur as a result of a passage of time and, in part, as the consequence of cumulative damage from continuous formation of reactive oxygen species (ROS) generated during oxidative cellular metabolism. Despite inherent cellular antioxidant defense systems, generated ROS damages several cellular constituents including membranes, enzymes and DNA.

Telomeres, the terminal portions of eukaryotic chromosomes, have been established as a culprit of chronological aging. Simply put, with each cell division, human telomere length shortens. Even in relatively inactive skin, fibroblast cells, more than 30 percent of the telomere length, have vanished during adulthood. Perilously short telomeres signal cell hindrance or apoptosis, or cell suicide, (programmed cell death is a developmental process that usually proceeds apoptosis) and depending on cell type, contributes to cellular depletion.

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