I took accutane 5 years ago. It permanent dried up my face. I am wrinkling like crazy for someone my age (just 22 years old) -- both fine and deep wrinkles. My crow's feet look like accordions. My skin feels thin. I get extreme inflammation upon contact with water (even cold water).
I began taking adderall prescribed for ADHD last year. It has definitely worsened my skin. But to put it into perspective, I have a classmate who takes 10 times higher daily dose, and is 60 pounds lighter than me and a year older. I see her almost daily, and I have not noticed any skin symptoms remotely like mine. Hence, the accutane is the main culprit.
I have tried Omega 3, Biotin, I drink tons of water, shea butter, coconut oil, hiding from the sun...recently started MSM supplements. My dermatologist prescibed me Lac Hydrin (12% ammonia lactate) because my face was getting rough like sandpaper, and this has made my skin smooth. However, my skin is so thin, so when my skin feels smooth and freshly exfoliated, it also feels tight and thinner.
He prescribed me metronidazole cream for the redness. I haven't noticed any effects. And I don't understand the logic behind this, because I only have redness from inflammation (and I suspect the thinning of my skin makes this extremely more visible). And metro cream seems more for surface growths associated with rosacea (since it is anti-bacterial), not the inflammation redness, right?
He also recommended Nutraplus Urea cream (10%). It also makes my face smoother, but again, same limitations as Lac Hydrin.
I have seen 3 dermatologists, 1 with PHD/MD credentials. But these creams don't really seem to be getting to the root of the problem.
In my personal research, I am intrigued by PPAR stimulators. One study examined topical GW1514, and it supposedly helped the skin barrier repair processes and thickened some layers or the skin. PPAR stimulators in diabetic medication is known to have effects on the skin, including stimulating the sebaceous glands (the glands that accutane shrinks).
Another complication: I have moved to a dry climate from a more humid one. I am shopping for a humidifier (I picked up a cheapy one from walgreens and it does not seem to evaporate much water). Any recs or thoughts?
My situation is pretty severe. I feel like Benjamin Button. I am going to go off Adderall during winter break and see how my skin responds, but I am only taking 5 mg/day (and the smallest pill size is 10mg).
The damage is only to my face (and my hair as mentioned). But the rest of my body's skin I am very happy with. However, I did also experience permanent lessened saliva production and slightly more dry eyes.
In my research, the literature on skin barrier homeostasis and skin fragility seems centrally pertinent. My face's waterproofing is deteriorated (when water runs off it, it does not "bead up" like other skin on my body), there is dyshesion, my face feels like in a constant sloughing state (rough, "dusty" surface texture). My chin and my nose are the only regions on my face that feel preserved (chin feels thick and fine, and the nose can still get oily). By my forehead and cheeks etc. are dry as the desert. I constantly slap on moisturizer and creams, but my skin doesn't even seem to absorb these anymore.
Can someone please help me? I just don't know what to do. I have even tried emailing some of the researchers I have read about looking for advice or things to recommend my dermatologist look into (many are affiliated with UCSF, which I live near). Even if it can't be fixed, I would at least like to fully understand what happened and what is going on -- but even getting pertinent information is difficult...and my science background isn't sophisticated enough to easily sift through the literature, though I am getting better.
I thought my situation was so severe that it would take something internal to have any effects, but then I stumbled upon the topical PPAR stimulator (GW1514) study, so perhaps there are some topical solutions, beyond these futile creams I have been slapping on religiously to no avail.
Below is a link to the specific PPAR abstract:
Peroxisome proliferator-activated receptor (PPAR)-beta/delta stimulates differentiation and lipid accumulation in keratinocytes.
Schmuth M, Haqq CM, Cairns WJ, Holder JC, Dorsam S, Chang S, Lau P, Fowler AJ, Chuang G, Moser AH, Brown BE, Mao-Qiang M, Uchida Y, Schoonjans K, Auwerx J, Chambon P, Willson TM, Elias PM, Feingold KR.
Department of Medicine, University of California, San Francisco, California, USA.
J Invest Dermatol. 2004 Oct;123(4):806.
Peroxisome proliferator-activated receptor (PPAR) are nuclear hormone receptors that are activated by endogenous lipid metabolites. Previous studies have demonstrated that PPAR-alpha activation stimulates keratinocyte differentiation in vitro and in vivo, is anti-inflammatory, and improves barrier homeostasis. Recent studies have shown that PPAR-beta/delta activation induces keratinocyte differentiation in vitro. This study demonstrated that topical treatment of mice with a selective PPAR-beta/delta agonist (GW1514) in vivo had pro-differentiating effects, was anti-inflammatory, improved barrier homeostasis, and stimulated differentiation in a disease model of epidermal hyperproliferation [corrected]. In contrast to PPAR-alpha activation, PPAR-beta/deltain vivo did not display anti-proliferative or pro-apoptotic effects. The pro-differentiating effects persisted in mice lacking PPAR-alpha, but were decreased in mice deficient in retinoid X receptor-alpha, the major heterodimerization partner of PPAR. Furthermore, in vitro PPAR-beta/delta activation, aside from stimulating differentiation-related genes, additionally induced adipose differentiation-related protein (ADRP) and fasting induced adipose factor (FIAF) mRNA in cultures keratinocytes, which was paralleled by increased oil red O staining indicative of lipid accumulation, the bulk of which were triglycerides (TG). Comparison of differentially expressed genes between PPAR-beta/delta and PPAR-alpha activation revealed distinct profiles. Together, these studies indicate that PPAR-beta/delta activation stimulates keratinocyte differentiation, is anti-inflammatory, improves barrier homeostasis, and stimulates TG accumulation in keratinocytes.