The Science Behind Dry Skin

As the summer fades into winter and the autumn sets in weather will get cooler, wind will get stronger and my skin will get dryer. As a skin-care enthusiast this concerns me because I know that dry skin causes split hands, itchy legs, red faces, and alligator scales- not a pretty picture.  What's worse is according to most skin care companies, dry skin results in early wrinkles! So what really happens when our skin dries out? According to indianapublicmedia.org, the outer most layer of our skin is composed of dead cells called the stratum corneum. These cells are cemented together to form a protective barrier for the alive cells underneath. Normally this layer of skin has the same surface area as our epidermis (the layer directly underneath the stratum corneum). However, when our skin dries out, the stratum corneum shrinks creating that cracked alligator skin I talked about earlier. This process is perfectly normal and preventable in healthy skin- but what about eczema and chronic dry skin victims? What is going  on beneath the surface that makes topical creams and lotions seem to have no effect?

According to skincarephysicians.com, other than certain types of ecxema caused by allergic reaction, dermatologists don't really know why some people have chronic eczema. They claim it could be many factors coming together such as genes, a barrier defect (gaps in the skin that allow water to escape faster and bacteria to enter easier), an overactive immune system, and climate. A recent study featured in Cell Press in the October issue, Immunity may have shed some light on the dry skin dilemma.  Underneath our stratum corneum is the epidermis. In the epidermis there are cells called keratinocytes, and in these keratinocytes there are proteins that may be related to dry skin called FADD, RIP1 and RIP3. All of these proteins are responsible for activating death receptors in our cells which triggers a multistep cell death. The difference is that FADD triggers a cell death called apoptosis and RIP1 and 3 cause cell death called necroptosis. A study at the University of Cologne found that when the FADD protein was removed from the epidermis of mice, necroptosis occurred and created inflammation and skin liaisons. The senior study author Dr. Manolis Pasparakis says the discovery was that FADD not only causes cell death but also, "performs and essential pro-survival function in keratinocytes that is crucial for the maintenance of a balanced skin immune response and the prevention of skin inflammation."

I think these findings are very significant! In my church there is a small girl who has suffered from skin rashes and severe dry skin since birth. She is constantly uncomfortable and her skin is always dry, cracked and scaly. Her parents have done everything they know to do including taking her to slues of doctors and dermatologists. Nothing has worked and she lives on itchy and sore. What if doctors could find a way to mitigate cell death by necroptosis? What if they could identify a lack of FADD in her skin and find a way to give her more of it? What if she didn't have to live in discomfort now and embarrassment when she's 13 and the other middle school kids wonder why she has rashes all over her body? What if there was a simple topical ointment or pill that could cure her and others that suffer like she does? And what implications does this finding have on chemotherapy patients who also get dry skin? Is the chemotherapy killing the FADD along with the cancer cells? I think this calls for more research!