Sugar-acne is true?

[SweetJade1]

To HELP people. I do not have to be here and there are times when I don't hang around. I do this because I KNOW what it feels like. I know how it feels to search, and try, and fail over and over and over again. If you are openseason you've already heard my heartfelt plea and why I do what I do, so this my purpose here is irrelevant.

If you aren't openseason than I sincerely apologize but your mannerisms are very similar to his. You both like to make excuses for why you won't try something. You both won't share your acne problem, your diets, your health histories, etc. Yet you both are so full of opinions and assumptions about people and things that you have NEVER tried. Then when we take the time to try and explain it to you, nicely and then unfortunately, not so nicely, you both find a way to rationalize how it couldn't possibly apply to you.

Oh and my favorite is how you both demand proof of what causes acne, how it's formed etc, and when others, including myself, post scientific studies that tell you EXACTLY how it is formed, you still can't believe it. It's beyond your grasp that androgens could be doing all of it. Well it is. I suppose you can't grasp that concept because then you would have to admit that insulin can control the amount of androgens and inflammatory products needed in the development of acne. You can't admit that, because that is one of the main purposes for why we follow the diets that we do: The Sugar/Fat-Insulin-Androgen-Inflammatory Product-Acne Connection!

Yet you are still sitting there with your opinions, rationalizations, & excuses and you STILL have acne. I certainly do not want to sound mean, but those are the facts and until you are ready to try ALL possibilities, then.....I guess you are stuck with it. I guess you must want acne because you haven't bothered to try other options and I don't just mean diet, but prescription drugs or supplements as well. I've offered you so many suggestions and you've turned them ALL down. So, why is someone here on an acne board, with acne, but isn't interested in doing whatever it takes (safely) to try and annihilate their problem?

[SweetJade1]

Originally Posted by yelps

Sure I trust yor research. Acne is complex thats what I got from reading it. Maybe some people produce too much insulin. What is causing the oil gland to clog in the first place. Its hard to belive androgen level is causing that. Maybe acne is caused by malfuntioning thiroid, thats what I am going to check next, thats a simple body temperature check.

To test for a malfunctioning thyroid you must do more than just check your temperature. You must also get several blood tests run as well. Perhaps you aren't openseason as that's something he wouldn't have shared with us (the fact that he's considering that it may be some form of a hormonal disorder). If you aren't then check to see if you are Hypothyroid or have NCCAH (see prior posted studies). These both can cause Hyperandrogenism as well as increase your inflammatory products. So, it STILL comes back to androgens and there is no way that you are going to avoid this fact, so please stop trying to rationalize your way out of it. How many studies do you want that describes this for you? Did you even read the very last study I posted? I left it for last because I figured if nothing else you may read that one, but I guess you didn't. OK, here's another one for you that explains the whole "clogged pore" aspect of it:

Med Electron Microsc. 2001 Mar;34(1):29-40. Related Articles, Links


Pathogenesis of acne.

Toyoda M, Morohashi M.

Department of Dermatology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan.

Acne vulgaris is a skin disorder of the sebaceous follicles that commonly occurs in adolescence and in young adulthood. The major pathogenic factors involved are hyperkeratinization, obstruction of sebaceous follicles resulting from abnormal keratinization of the infundibular epithelium, stimulation of sebaceous gland secretion by androgens, and microbial colonization of pilosebaceous units by Propionibacterium acnes, which promotes perifollicular inflammation. The clinical presentation of acne can range from a mild comedonal form to severe inflammatory cystic acne of the face, chest, and back. At the ultrastructural level, follicular keratinocytes in comedones can be seen to possess increased numbers of desmosomes and tonofilaments, which result in ductal hypercornification. The increased activity of sebaceous glands elicited by androgen causes proliferation of P. acnes, an anaerobe present within the retained sebum in the pilosebaceous ducts. The organism possesses a ribosome-rich cytoplasm and a relatively thick cell wall, and produces several biologically active mediators that may contribute to inflammation, for instance, by promoting leukocyte migration and follicular rupture. In inflamed lesions, numerous neutrophils and macrophages infiltrate around hair follicles and sometimes phagocytose P. acnes. To examine the participation of neurogenic factors in the pathogenesis of acne, we quantitatively assessed the effects of neuropeptides on the morphology of sebaceous glands in vitro using electron microscopy. Substance P, which can be elicited by stress, promoted the development of cytoplasmic organelles in sebaceous cells, stimulated sebaceous germinative cells, and induced significant increases in the area of sebaceous glands. It also increased the size of individual sebaceous cells and the number of sebum vacuoles for each differentiated sebaceous cell, all of which suggests that substance P promotes both the proliferation and the differentiation of sebaceous glands. In this review, we introduce the general concept of pathogenic factors involved in acne, including typical electron microscopic findings and recent evidence of stress-induced exacerbation of acne from a neurological point of view. An improved understanding of the pathogenesis of acne should lead to a rational therapy to successfully treat this skin disease.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11479771[/url]


Do you see the large bolded section? That pretty much describes how a pore gets clogged. All of these aren't mentioned in this article but, Seborrhea (excess sebum), Skin Cell Proliferation (growth), Hyperkeritinization (thickening), Hypodesquamation (poor shedding), Hypercornification (hardening) are whats needed in the development of a clogged pore. When dealing with the same studies they don't always mention each and every one of those as it get tedious, but search pubmed and you will find them listed under acne.

Z Hautkr. 1988 Jul 15;63(7):591-2, 595-6. Related Articles, Links


[New lipid biochemical aspects in the pathogenesis of a follicular keratinization disorder in acne vulgaris]

[Article in German]

Melnik B, Plewig G.

Universitats-Hautklinik Dusseldorf.

Follicular hyperkeratinization of the epithelium of the acroinfundibulum of sebaceous follicles is one of the primary events in the pathogenesis of acne vulgaris. Oral treatment with 13-cis-retinoic acid can reduce these hyperkeratoses. In order to determine whether follicular hyperkeratinization is related to disturbances of epidermal follicular lipids, we analyzed the lipids of initial comedones from 10 patients with nodulocystic acne before and after a 6th weeks oral therapy with 13-cis-retinoic acid (0.7 mg/kg body weight). The treatment with retinoid resulted in a significant increase of epidermal lipids (free sterols: +34%; ceramides: +19%, whereas the lipids of sebaceous origin decreased (glycerides: -36%). The mass ratio of free sterols to cholesterol sulfate increased by 86% compared to pre-treatment levels. These findings support the hypothesis that local follicular deficiencies of epidermal lipids due to increased sebum secretion might induce abnormal follicular keratinization.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2973184[/url]

Drugs. 2003;63(15):1579-96. Related Articles, Links


Current concepts of the pathogenesis of acne: implications for drug treatment.

Gollnick H.

University Clinic for Dermatology and Venereology, Otto-von-Guericke-University, Magdeburg, Germany. [email]harald.gollnick@medizin.uni-magdeburg.de[/email]

The pathogenesis of acne is complex, with strong evidence supporting the involvement of sebaceous hyperplasia, follicular hyperkeratinisation, bacterial hypercolonisation, as well as immune reactions and inflammation. High sebum concentrations and follicular hyperkeratinisation lead to a change of the follicular milieu with consecutive proliferation of bacteria, chiefly Propionibacterium acnes. This leads to further increased production of the pro-inflammatory cytokines interleukin-1alpha and tumour necrosis factor alpha by T cells and keratinocytes, leading to proliferation of both cell types . Follicular keratinocytes fail to differentiate by apoptosis and produce hypergranulosis similar to the impermeable skin outer layer, resulting in the formation of microcomedones. Further inflammatory responses lead to the development of increasing degrees of severity in inflammatory forms of acne. Retinoids aid the differentiation and reduce the hyperproliferation of keratinocytes, and can inhibit the migration of leucocytes. Combination therapy using retinoids plus benzoyl peroxide or antibacterials can treat existing acne lesions faster than the individual agents alone and can also prevent the development of new lesions. The new retinoids (e.g. adapalene) have not only the typical potent comedolytic activity but also anti-inflammatory effects. When added to antibacterial therapy, topical retinoids demonstrate faster and significantly greater reduction of inflammatory acne lesions and comedones than antibacterials alone.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12887264[/url]

Of course, increased growth of bacteria & other trapped microorganisms can lead to inflammation, but so can Substance P, and the prolonged prescence of Androgens, as well as a prolonged increase of insulin & IGF-1. These can all encourage the presence inflammatory products such as Interleukin-1 (IL-1), IL-6, IL-8, TNF, PGE2 (prostaglandin E2), & Leukotrienes that have been found in acne lesions.

[SweetJade1]

Yelps,

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.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9557256[/url]

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?

[yelps]

A low functioning thyroid can be checked by a simple body temperature check. It has to be performed in a certain way but it is foolproof. The test was developed by a medical professional with 30 years experience diagnosing diseases. Also a blood and nurtrition expert. He is a member of the board of Harvard Medical school. So its not something I made up.

[Zenfish]

[QUOTE=SweetJade1]
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 & function normally elsewhere.

The quote above nicely restates the initial metaphor that started this whole dialogue. Food is the fuel that allows acne, gas is the fuel that allows driving a car. In both cases, the most dramatic and permanent change is to cut off the fuel supply.

Thank you for caring SweetJade