To further clarify something here about the whole Diet & Acne connection (taken from above study). "Follicular keratinocytes fail to differentiate
by apoptosis and produce hypergranulosis similar to the impermeable skin outer layer, resulting in the formation of microcomedones." and this is a result of something called Peroxisome Proliferator-Activated Receptor Cells (mentioned in a prior article about acne). These are genes that can be upregulated (turned on) or downregulated (turned off) by our diets (or supplements) and they also happen to interact/bind with the retinoid X receptors!
In fact Avandia, an Insulin Sensitizer binds to PPAR-gamma to help our bodies become more insulin sensitive, thus decreasing our insulin resistance. Yet if we eat foods that support insulin resistance we can increase our production of PPAR-beta/delta receptors cells that are responsible for 95% sebum production, inflammation, as well as hyperkeritinization. Yet if we eat in a way that decreases Insulin Resistance we can also upregulate PPAR-alpha & PPAR-gamma (oppose PPAR-beta/delta) and the cells will differentiate normally! This is why I say that you MUST understand the human body before you can begin to use diet in a therapeutic way to help you! You don't need to understand to follow it, but if you want to change the world you do ;-)
Dermatology. 1998;196(1):171-5. Related Articles, Links |
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.
I know that this is what you want to hear about, the genetic defect, but as of yet, we can not fix this defect. Thus, we intercept the pathway for acne in a multitude of ways: Diet (1st Level of Interception), Oral Drugs or Supplements (2nd Level of Interception), and/or Topicals (3rd Level of Interception). Based on what level of interception & method you use, your will results will vary. Most people can get away with only using the 3rd level, Topicals, but others like myself found that THE most effective level was the one where we can stop it pretty much before it can start and that began with our diets. Our diets provide the fuel neccessary for the defect to be present or expressed physically, so we just ceased providing the fuel, while still allowing enough fuel to grow & functionally normally elsewhere.
I honestly shouldn't bother with you anymore, but doesn't that show how MUCH I care about wanting you to be free of acne, even if I don't agree at all with the way you think (it's a bit self-defeating). Yet, I have nothing to prove, this effort is for YOU, not for me. I dont need you to believe me, but I do need for you to BELIEVE. If you are openseason, I want sooo badly for you to believe that there is something out there that could help you, but I'm not going to exhaust myself for your benefit, especially when you aren't willing to put in just a little bit of effort on your part to do the work & research for yourself. If you don't think that you are worth enough to do the work, to get the tests run, to try the diets, then why should anyone else?