While I have not seen the studies that found that the tendency towards hyperkeratinization is genetic, absolutely everything you find about hyperkeratinization and any condition that involves hyperkeratinization in the skin or elsewhere states that the tendency is genetic. It seems to be a given accepted by every researcher doing any research on any condition involving hyperkeratinization.
And here's a patent request involving an enzyme encoded by gene UGCG that is involved in keratinocyte differentiation. They want to use it as a treatment for acne and any other condition that involves hyperkeratinization:
More info on UGCG: http://en.wikipedia.org/wiki/UGCG
And here: http://www.genecards...sp.pl?gene=UGCG Where it includes a chart with its genomic location.
And under Epigenetics it says:
'QIAGEN PyroMark CpG Assay predesigned Pyrosequencing DNA Methylation assays for UGCG'
I, of course, have no idea what that means, but epigenitics are things that we change in our life time due to environment and the things we do to ourselves that become part of our genetic makeup and can get passed down to our kids. And it seems they've identified something.
Good Things for Hyperkeratinization:
Also, there's at least 3 genes/enzyme mutations identified as being involved in the linoleic acid deficiency found in mammalian skin prone to skin irritations of all sorts. http://www.acne.org/...pical-solution/
-Acne prone skin has found to be deficient in retinoids, possible due to mutations in CYP26AI gene that causes it to be metabolized too fast to be used.
Polymorphisms in the human cytochrome P-450 1A1 gene (CYP1A1) as a factor for developing acne.
Paraskevaidis A, Drakoulis N, Roots I, Orfanos CE, Zouboulis CC.
Department of Dermatology, University Medical Center Benjamin Franklin, Free University of Berlin, Germany.
Cytochromes P-450 are a supergene family of enzymes involved in the metabolism of a wide range of endogenous and foreign compounds. The existing genetic variations of the distinct isozymes lead to interindividually different metabolic capacity. Since vitamin A, endogenous retinoids and their natural metabolites are morphogenic for the sebaceous gland, we investigated the polymorphisms of cytochrome P-450 1A1, as being one of the most active isozymes involved in their interconversion. From the known mutations, two were investigated; an additional cleavage site for MspI in the 3'-flanking region identified as a thymine-to-cytosine transition 1,194 bp downstream of exon 7 (m1) and an adenine-to-guanine transition at position 4889 in exon 7 (m2). We studied 96 acne patients for m1 and m2 mutations by restriction fragment length polymorphism and allele-specific polymerase chain reaction, respectively, and compared the results with 408 reference individuals. No statistically significant difference was found in the distribution of m2 alleles; the frequency was 3.13 and 3.06% of the alleles, respectively (odds ratio = 1.02, confidence limits 0.41-2.52, p = 0.96). In contrast,a trend to an overrepresentation of m1 alleles in acne patients was observed; allele frequency was 8.33 in the patients and 6.99% in the control subjects, respectively (odds ratio 1.21, 95% confidence limits 0.68-2.16, p = 0.52). As the m1 mutation might define a marker for alterations on regulatory sites, the biological efficacy of natural retinoids could be greatly impaired by their rapid metabolism to inactive compounds. The resulting deficit of active natural retinoids may lead to abnormal sebocyte differentiation and hyperkeratinization of the follicular canal implicating the development of acne in some patients.
Also, according to this article, the genome of p acnes has been mapped. or at least that of P. acnes strain KPA171202 http://www.acne.org/...#entry3257204..
This study on the genetics of P acnes finds that there we might have a subspecies of the bacteria that causes acne as opposed to the bacteria present in normal skin:
Population genetic analysis of Propionibacterium acnes identifies a subpopulation and epidemic clones associated with acne.
The involvement of Propionibacterium acnes in the pathogenesis of acne is controversial, mainly owing to its dominance as an inhabitant of healthy skin. This study tested the hypothesis that specific evolutionary lineages of the species are associated with acne while others are compatible with health. Phylogenetic reconstruction based on nine housekeeping genes was performed on 210 isolates of P. acnes from well-characterized patients with acne, various opportunistic infections, and from healthy carriers. Although evidence of recombination was observed, the results showed a basically clonal population structure correlated with allelic variation in the virulence genes tlyand camp5, with pulsed field gel electrophoresis (PFGE)- and biotype, and with expressed putative virulence factors. An unexpected geographically and temporal widespread dissemination of some clones was demonstrated. The population comprised three major divisions, one of which, including an epidemic clone, was strongly associated with moderate to severe acne while others were associated with health and opportunistic infections. This dichotomy correlated with previously observed differences in in vitro inflammation-inducing properties. Comparison of five genomes representing acne- and health-associated clones revealed multiple both cluster- and strain-specific genes that suggest major differences in ecological preferences and redefines the spectrum of disease-associated virulence factors. The results of the study indicate that particular clones of P. acnes play an etiologic role in acne while others are associated with health.
Full article: http://www.ncbi.nlm....82/?tool=pubmed
And that's just a few. See also this thread:
Edited by alternativista, 08 January 2014 - 03:41 PM.