I haven't posted on this forum for about 5 yr, but I have been following new developments and I have tried a number of treatments. The results have given me insights into what does and doesn't work, so I can narrow down what might cause EC in my case.
About 4-5 yr ago, an overgrowth of Candida albicans in my oral cavity was confirmed. It was not until the start of January this year that I went on a very strict anti-Candida diet. A stool test taken 1 week ago confirmed that there is NO more candida or sign of candida present. Another stool test to check for intestinal hyperpermeability ('leaky gut') is still in the works - I'll keep you posted.
I have rigorously tried the combined Constant moisture+ leave alone method using Aquaphor ("healing ointment/ advanced therapy) as recommended by Daniel Miller, which completely stopped the peeling cycle for as long as I applied it, and although this is a big change it ultimately caused no permanent improvement. A thin layer of differentiated skin cells seems to have developed after using it for about a year of this treatment, which exfoliated about 1 week after stopping Aquaphor cold-turkey.
I have tried Gloves in a Bottle as described by Cottonmouth (application of 2 layers before bed on RAW skin, religiously avoiding getting them wet, rince and repeat after 4 days). This really helps to moisturize my lips (they don't feel dry at all during these 4 days), however, skin exfoliation does proceed unabated albeit at a much slower pace and far thinner peels of dead skin. GIAB really helps restore more normal (normal pink) color to my generally pink/reddish lips, which helps a lot psychologically.
Taken together, I think that the results of these strict treatments (i.e. EC not cured, although temporarily effective treatments) allow us to narrow down the cause of EC in my case. I think my EC started in May 2007 due to a self-inflicted wound of chapped lips and biting thereafter.
One of the most important functions of our skin is the regulation of moisture and pathogenic factors into/ out of the skin. To accomplish this, skin cells (keratinocytes) have to undergo terminal differentiation. This process involves a degeneration of the cell nucleus and the formation of a so-called Cornified Envelope (C-E). The C-E consists mostly of keratin and permeates the entire cell. Cell-adhesion molecules at the outlines of the cell ensure that the whole layer of differentiated skin cells adhere to eachother.
The formation of a C-E depends on skin pH and on an anaerobic environment. Exfoliative Cheilitis, being an inflammatory condition, greatly increases the vascularization of the skin due to inflammatory processes. The increased blood supply support the massive demand for oxygen and nutrients by the basal layer of keratinocytes (at the deepest part of the epidermis).
Note that I mentioned that the formation of the cornified envelope depends on an anaerobic environment - I think that the presence of numerous blood vessels in our lips prevent the differentiation of keratinocytes.
In a few cases of EC that appear to be more closely related to contact dermatitis (allergy), the process of vascularization can be reversed and skin differentiation resumes as normal after some time. In other cases, it is not and EC remains uncured.
Therefore, my theory is that EC in these latter cases that appear to be refractory to dietary changes, artificial moisturization and where, untimately, the differentiation of keratinocytes (nearly-) does not occur, is ultimately causes by excessive oxygenation of the upper layers of skin.
Treatments to combat excessive vascularization do exist. Antibodies against vascular endothelial growth factor (anti-VEGF) are a common therapy against the same process in the retina of the eye (via injection).
I don't know how anti-VEGF might be administered to treat EC, but I think that it adresses a problem that no other treatments posted on this forum has adressed yet.
Let me know your thoughts.
I think anti-VEGF therapy against excessive blood vessels in the skin of EC patients (that are refractory to other treatments) can help the formation of a normal skin barrier.
PS. In my case, a biopsy confirmed that skin cells in the upper-most layer of my lip skin do possess a nucleus (this is called parakeratosis), which is evidence that these cells are not terminally differentiated. The differentiation of skin cells, and by extension the formation of a normal skin barrier, appears to be absent.