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[QUOTE=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.[/QUOTE]

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:

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


[B]Pathogenesis of acne.[/B]

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. [B]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.[/B] 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 [U]hypercornification[/U]. The[U] increased activity of sebaceous glands [B]elicited by androgen [/B] causes proliferation of P. acnes[/U], 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. [U][B]Substance P[/B], which can be elicited by stress[/U], 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. [/QUOTE] [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&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.


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


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

[Article in German]

Melnik B, Plewig G.

Universitats-Hautklinik Dusseldorf.

[B]Follicular hyperkeratinization [/B] 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.[/QUOTE] [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2973184[/url]


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


[B]Current concepts of the pathogenesis of acne: implications for drug treatment.[/B]

Gollnick H.

University Clinic for Dermatology and Venereology, Otto-von-Guericke-University, Magdeburg, Germany. [email][email protected][/email]

The pathogenesis of [B]acne is complex, with strong evidence supporting the involvement of sebaceous hyperplasia, follicular hyperkeratinisation, bacterial hypercolonisation, as well as immune reactions and inflammation[/B]. High sebum concentrations and follicular hyperkeratinisation lead to a change of the follicular milieu with consecutive proliferation of bacteria, chiefly Propionibacterium acnes. This [B]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 [/b]. [U]Follicular keratinocytes fail to differentiate by apoptosis and produce hypergranulosis similar to the impermeable skin outer layer, resulting in the formation of microcomedones.[/U] Further inflammatory responses lead to the development of increasing degrees of severity in inflammatory forms of acne. [B]Retinoids aid the differentiation and reduce the hyperproliferation of keratinocytes, and can inhibit the migration of leucocytes.[/B] 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.
[/QUOTE] [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12887264[/url]

Of course, increased growth of bacteria & other [B]trapped[/B] 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.
[QUOTE=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.[/QUOTE]

I never said you made it up. I love how you ignored everything else I said though. Oh and, if you do happen to end up being hypothyroid, just know that there are foods that are goitrogens, meaning they can contribute/aggrivate or be the sole cause of your hypothyroid problems by inhibiting the enzyme neccessary to make T3/Triiodothyronine (which raises SHBG so it can bind Free Testosterone). Thus, you may indeed need to reduce or avoid, if you aren't already doing so these foods.

Yup, I've run into a members on here that found they were eating these foods that they thought were healthy, and these [I]are[/I] some healthy foods such as soybeans (certain fruits & veggies) that ended up making them hypothyroid (when the condition didn't run in the family) and that's when their acne developed for the first time. Unfortunately even after ceasing consumption of some of these foods, they found they needed to also avoid other foods and/or take medication. Eitherway, I wish you the best in figuring it out.
[QUOTE=indy gal]SweetJade - This is totally off-topic, but you mentioned it earlier and made me curious. What foods can cause hypothyroidism?

And by the way, I was one of the non-believers that diet affected my acne. But, I was willing to give it a try and discovered that it really does trigger my acne. The healthier I eat, the better my skin is. These boards really helped me with that.[/QUOTE]

LOL, well I don't think it's totally off topic, as these foods have sugars too, but for thoe most part that is not an issue when consuming vegetables so maybe it is a wee bit ;-) Anyway, the foods that [B]Goitrogens[/B], especially when [U]raw[/U], are:

[B]Brassica Family [/B] (anti-cancerous, increase glutathione levels something that acne sufferers may be lacking, high fiber, calcium, etc):

Broccoli
Cauliflower
Brussel Sprouts
Cabbage
Spinach
Mustard
Kale
Collard
Turnips
Radishes
Rutabega
Horseradish
Kohlrabi
Canola Oil (Rapeseed)


[B]Misc. Legumes[/B]
Soybeans
Peanuts
Lima Beans
Peas

[B]Misc. Grains:[/B]
Millet
Corn

[B]Misc. Nuts:[/B]
Pine Nuts
Walnuts

[B][I]genus Prunus[/I] (of Rose Family) [/B]
Almonds
Peaches
[Nectarines]
Apricots
Cherries
[Plums]

[B]Others:[/B]
Strawberries
Sweet Potato
Cassava
Watercress

As you can see these are some very healthy foods, some of which most of us rarely eat (enough of). So if you don't eat tons of it raw, it's not a problem, but if you do eat tons of these foods you may want to cut back some or cook them more often. This is particularly true of soybean consumption as members have stated that after becoming vegans or increasing their soy content (it can work for or against you) their acne got worse OR it [B]GAVE[/B] them acne. Out of all of these foods, soybeans is something that Americans can consume daily and in a variety of ways (as a bean, protein, seasoning, "milk", "cheese" etc), so it makes sense that soybeans could be a big factor for members that chose to go vegan.

Of course the possiblity with soy is that it's being either overconsumed (compared to consumption in other countries), it's refined soy, or it's genetically modified as to why it may affect some members negatively. As for the other foods, well the ones I eat & have started increasing my intake of are brocolli, cauliflower, cabbage, and greens (spinach, turnips, kale, collard & mustard) but I eat brocolli the most, usually steamed, and none of these on a daily basis. Based on former thyroid tests I am high-normal for T4 hormone (converts into T3) so I guess i can afford to add some of these into my diet, especially since I wasn't eating these foods as often before (but I NEED the fiber & nutrients).

LOL, just added more to the list and I honestly had no idea how many foods could be goitrogens, but again, some people that are hypothyroid don't have problems with ALL of these foods. Sometimes it's only certain foods and if you cook them, this will further decrease or deactivate this ability. Cooking for legumes & nuts & grains may simply mean sprouting, soaking or fermenting them. In fact one source said that soybean consumption should be avoided entirely unless fermented (Leo's Last Acne solution also reccomends this) and members of a rawfood community that are hypothroid have also noted problems with soy. I would suggest that if you wanted to know if it's a problem I would avoid those that fall under being the top allergens first and then work your way through the rest of these. I actually eat corn almost every day, but I do avoid the Genus [I]Prunus[/I], nuts, & peanuts as I get cystic acne from them =( I used to think that it was due to an intolerance to the nuts (from possibly a leaky gut), but since those fruits involved also gave me the acne, then it may be a cross reaction or since they were raw, they may have been affecting my T3 levels....hmm.

Are you hypothyroid or suspect that you may be?
[QUOTE]Are you hypothyroid or suspect that you may be?[/QUOTE]

Well I had one of those biofeedback tests done at my local health food store. I don't know whether to believe what it said or just take it with a grain of salt, but my thyroid came up as my main concern. I haven't gone to the doctor to have it tested with blood tests yet (mainly because I have been fighting off the flu and other bad things for 2 months now), but I had it tested once like 6 years ago and it was fine then.

Curiously enough, I eat broccoli, cauliflour, and/or spinach on a daily basis and also consume a lot of raw almonds, use almond milk on my cereal, etc...





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