The debate needs to start with a physiologic assessment of what happens to make skin age. At the epidermal level, research shows us that very little long-term aging occurs. The reason for this is simple, any aging event like an acid peel or a sunburn will create damage to the various layers of the epidermis but it very rarely creates changes that are not corrected within six weeks. The skin is well aware of the need to maintain a functional epidermal barrier because without it, we would all eventually die. Think about it… without an adequate epidermal barrier the body will ooze, bleed, and eventually develop a life-ending infection. That is why the epidermis is continually replacing itself and why sunburn (and other) damage is almost always self-corrected. For these reasons, I do not consider the treatment of the epidermis an "anti-aging" event. While there is no question plumping the epidermis makes fine lines look better, they are still the result of a thinning dermis. While inhibiting melanocytes will help to even skin tone, our problem still exists at the dermal/epidermal junction (loss of antioxidant absorption to support melanocytes) and in the dermis itself.
The dermis is the control center for what happens at both the dermal and epidermal level since it receives the nutrients for daily activity and repair. There are no capillaries in the epidermis but they receive their needed supplies through osmosis at the dermal/epidermal junction often using channels called rete ridges. The dermis has a choice every day. It can either utilize the "shipment" (from capillaries) of antioxidants, minerals, proteins, enzymes, and lipids to repair itself, to rebuild itself, or to maintain the epidermis. As we get older (and with stress, caffeine, UVR, smoking, etc.), our dermal circulation continually declines. Faced with a progressive starvation and often an increasing number of free radical episodes, the dermis struggles to maintain both itself as well as its partner, the epidermis. What research shows is that the dermis thins at a rate of about one percent a year which is likely the result of the combined events discussed above. In addition, a point not usually made, the dermis also slows the rate of epidermal turnover in an effort to conserve scarce remodeling components. In other words, it accommodates by slowing metabolism, which is how the rest of our body acts in poor nutritional states. There is also an additional aspect of aging that needs to be addressed; as a result of the increasing workload of the dermis, it has trouble remodeling and removing damaged collagen and elastin. Ultimately this leads to a progressive increase in "scar tissue bundles" within the dermis. The effect of these bundles is to interfere with normal collagen/elastin deposition and function as well as reducing new capillary formation.
In summary, epidermal slowing, dermal thinning, scar tissue build-up, and continual free radical overload are what lead to aged skin, which are all essentially dermal events. What are we doing about it? Most of the world has been offering traumatic treatments including peels, lasers, devices, etc. Less invasive procedures involve damaging the epidermis because, even though they do not address dermal aging, they produce a visibly improved epidermis in the way of temporary plumping and improved discoloration. Both of these strategies are flawed for reasons to be explained, but the important point on the growth of these treatments is this; the process of reversing aging, if possible, is a slow and tedious one because of the obstacles faced and most treatments need immediate visible improvement in order to justify their price. As a result, the industry has been continually designing new ways to plump and inflame to meet the growing demand for immediate results.
Let's take a look at what an exfoliation procedure (including the daily application of exfoliators like AHAs, Retinols, and vitamin C) does to the skin. Every time we exfoliate, we place a new demand on the dermis to fix the problem. The epidermis loses lipids and corneocytes which can only be replaced from the bottom up. The epidermal rate increases (e.g. 40 day cycle increases to a 30 day cycle) because the dermis goes into emergency repair mode to fix the newly developed damage. The critical point here is that the collagen, lipids, enzymes, and antioxidants that will now be diverted to the epidermis for repair efforts would have normally been utilized at the dermal level to either maintain it or even to add some of the lost dermal thickness. This occurs every time exfoliation occurs. I have heard the concept that the epidermis "needs exercise" or help with exfoliation… which sounds a little far fetched to me. If the epidermal turnover rate slowed because of an inability to exfoliate, we would have much bigger problems than we do. The reason I do not buy the idea that the skin needs exercise (exfoliation) is because the skin is already in a 24 hour a day exercise routine… it never stops. Using the exercise analogy, that would be like asking a marathon runner to diet beforehand and do several sprints during their race… it just doesn't make physiological sense. In summary, exfoliation, and in particular, chronic exfoliation, drains the dermis' resources and speeds aging as a result. I would suggest that any research that shows increased collagen production related to an exfoliating procedure or damage to the epidermis is simply reflecting the repair of what was damaged as opposed to increasing collagen production that can be used to rebuild the dermis. Therefore, my position is that any procedure based on treating the epidermis and/or exfoliating will not make the skin younger.
There is much more potential treating the dermis. At least that strategy includes the possibility of stimulating fibroblast activity that is not earmarked for the damage created by the procedure. Unfortunately, most dermal treatments today involve significant trauma to the epidermal and/or dermal layers. This once again creates an environment where it is almost impossible for dermal density gains to be made. Consider that the dermis is already overwhelmed with its daily routine and then look at how much extra work is involved in a traumatic peel or laser treatment. This is substantiated by research that has documented dermal thinning after the initial treatment, as much as 30 percent (a.k.a. 30 years of skin aging!) loss in dermal thickness after a TCA peel. To be fair, this loss was reportedly recovered over the next month in the study referenced. However, my own personal experience with certain lasers and TCA peels is that many people come away from the procedure with newly visible capillaries. When this happens, you know that permanent dermal thinning has occurred because the collagen that had been covering the capillaries in the dermis is no longer there.
My belief is that the dermis must be targeted with ingredients that communicate new collagen production (through fibroblast stimulators) while avoiding giving the skin more work if possible. It can be done with delivery mechanisms like liposomes, ultrasound, and other penetration enhancing strategies. There are several ingredients that talk to fibroblasts directly including retinoic acid, retinaldehyde, r-lipoic acid, chlorella, ghk copper peptides, 1,3 beta glucan, and epidermal growth factor. Again, these ingredients need to have enhanced delivery mechanisms or else they will end up stalling in the epidermis (and never doing their job) since the average penetration rate of most actives is two percent.
A second component to achieving a true anti-aging result is scar tissue removal. The only way to make the dermis an ideal "planting ground" for new collagen/elastin is to remove the debris that occupies more and more of the dermal layers. 1,3 beta glucan has been shown to enhance macrophage activity, which are the scavengers of the skin and will help to remove these bundles of debris.
A final aspect to the age reversing strategy is re-establishing the barrier. It is common sense that if we reduce the workload of the skin by reducing the need for collagen/nutrient diversion to the epidermis and we reduce the free radicals normally generated as a result of having a damaged barrier (more sun damage and more environmental toxin absorption), then the skin will handle the fibroblast stimulation much more efficiently. Through the invention of new "physiologic" peptides and the enhancement of dermal delivery of fibroblast stimulators, we may finally be reaching a point where anti-aging accurately describes the products we are using!
Ben Johnson MD is the current founder and formulator of Osmosis Skincare. Dr. Johnson began his career starting one of the first medical spa chains in the country along with founding/formulating Cosmedix. He is an established speaker, educator, and formulator who is well known for his unique approach to skin conditions by thinking outside of the box. Dr. Johnson's passion is creating tremendous change in the skin without constantly exfoliating away the protective benefits of the epidermis.