Skin as an immune organ
It has been well over 40 years since the aesthetic medicine industry, as we know it today, became a unified establishment with a singular purpose: to make the skin look, and hopefully
behave, like its younger self. However, in our beautification efforts, have we inadvertently ignored skin structure and function, and created a model of theoretical cellular regeneration that has no long-term sustainability to the health of our skin? To fully understand the relevance of this concept, it is essential we start at the beginning of a movement whose ideology has remained mired in an antiquated understanding of skin physiology. The general consensus on aging is that, by definition, it is a progressive accumulation of damage at the molecular and cellular level. Barring any chronological and genetic factors, it is extrinsic aging that the movement in question was founded. When the integument is exposed to harsh environmental aggressors, including but not limited to, UV overexposure, chemical toxins, carcinogens and pollutants— a cascade of biological processes are activated that become the catalyst to the acceleration of the aging cell. The mechanism of action pioneered in the late 1960s to rejuvenate classically aged skin was based on the premise that further injury of this damaged tissue, and its subsequent wound healing response, would provide a method of cellular regeneration that, in theory, was therapeutic enough to reward a statistically significant change in its appearance, while being seemingly gentle enough as to not cause major harm.
What I propose is that the gold standard mentioned above, actually does more harm to cutaneous health than good, as it completely disregards the skin’s most basic function, to protect and defend. Since the birth of this aesthetic medicine specialty, our comprehension of skin physiology has evolved at an exponential rate. Given this fact, our approach at treating hallmark photo aging symptoms has yet to catch up. The disconnect between mainstream modalities and providing the skin with what it needs to maintain homeostasis, has never been more heightened. Historically, our skin was categorized as simply being a physical-mechanical barrier between the environment and the body, contributing no other purpose than serving as the body’s proverbial brick wall. And, that two things in particular would turn back the clock on the aging process: removal of the compacted layer of surface corneocytes, thought to be of as non-viable and “dead,” and to directly injure the dermal fibroblast in order to stimulate production of structural protein. We now know this is far from the truth. This misconception has been perpetuated to the point where convoluted marketing practices have undermined empirical data and verified skin science. The skin is the largest organ of the body, and aside from acting as a literal shield of armor, it is a powerful immunologic organ, maintaining and mounting a host defense system when facing foreign threats and unwelcome invasion. In fact, our skin has an estimated 20 billion T cells, outnumbering the amount in the circulatory system, proving that the skin’s number one priority is defense. This, in addition to the billions of commensal microbes that take up residence in our skin, part of the collective microbiome, show that immunosuppression is not the answer to sustainable anti-aging methodologies. Disruption of barrier homeostasis ignites a strong inflammatory and immune suppressive response, that when left in a chronic state, leads to an imbalance in cellular communication, cutaneous microbiome ecology and ultimately cellular senescence. This is the epitome of the pathophysiology behind aging skin. It then begs the question, why is our industry encouraging a cutaneous rejuvenation approach that injures, suppresses and forces the skin to make change, versus supporting and augmenting this immune organ, in our favor, to ignite a regenerative and reparative response, void of inflammation? Inflammation is NOT a prerequisite to repair, as has been proven in the fetal wound-healing model. Direct injury to the fibroblast is NOT required to synthesize new structural protein, as has been proven by cellular cross-talk, with the keratinocyte being the appropriate target for stimulation. And the skin’s barrier has a far more powerful role in dermal health than previously thought, with its integrity being vital to the overall performance, function and homeostasis of the skin as a whole. When we know, definitively, that aging is a direct result of damage, in what context would damaging the skin further produce an opposite effect? The most promising research for cellular regeneration, without insult or injury, leads us to tapping into the skin’s defense system, augmenting and supporting its ability to do what it does best, and maintaining the viability of microbiome symbiosis. The skin and the body are remarkable and fascinating organs that deserve far more respect than they have been given for the latter part of the 20th century. Using targeted skin care technologies that provide a synergistic and coordinated effort, affording us a true partnership with skin function and design, will allow us to finally break free from industry complacency and give us the most sensible and sustainable way to achieve our collective anti-aging objectives.
