If it is that simple then why does birth controls, avoiding stress, omega-3, digestive/liver cleanse, avoiding certain foods work?? That doesn't have anything to do with the logic above right?? Also if it is that simple, then a simple topical retinoids/BP can work for all of us acne sufferers right? But then again some people get clear while some people isn't lucky enough to be cured from those retinoids/BP.
Too much sebum -dead skin clogs pores -bacteria causes inflammation
#1
Posted 15 February 2007 - 08:31 AM
If it is that simple then why does birth controls, avoiding stress, omega-3, digestive/liver cleanse, avoiding certain foods work?? That doesn't have anything to do with the logic above right?? Also if it is that simple, then a simple topical retinoids/BP can work for all of us acne sufferers right? But then again some people get clear while some people isn't lucky enough to be cured from those retinoids/BP.
#2
Posted 15 February 2007 - 10:22 AM
#3
Posted 18 February 2007 - 09:40 AM
#4
Posted 19 February 2007 - 07:38 PM
If it is that simple then why does birth controls, avoiding stress, omega-3, digestive/liver cleanse, avoiding certain foods work?? That doesn't have anything to do with the logic above right?? Also if it is that simple, then a simple topical retinoids/BP can work for all of us acne sufferers right? But then again some people get clear while some people isn't lucky enough to be cured from those retinoids/BP.
Yes, it is just as you said.
And as for your question
That actually goes to support the oil + dead skin cells + bacteria formula for acne. Let me explain. Avoid stress, omega 3 help reduce oil production. Liver cleansing and proper digestion help with expelling toxins (that would have otherwise been expelled through our skin helping to clog pores). This also goes for avoiding foods because high sugar foods also contribute to excess sebum production.
Make sense?
Took me many many years to learn that the hard way. Always question "why". I looked into articles, such as the "milk makes acne happen" articles and found the main conection they state. "Milk may increase sebum production, so may the hormones in the milk, which leads to acne. It's that indirect connection
#5
Posted 19 February 2007 - 07:44 PM
#6
Posted 19 February 2007 - 08:35 PM
There is likely a genetic component that makes some people more susceptible to these triggers than others.
#7
Posted 19 February 2007 - 08:59 PM
#8
Posted 19 February 2007 - 10:34 PM
likely have very efficient and consistent removal of dead skin cells at their pores due to genetics
#9
Posted 19 February 2007 - 10:56 PM
Exactly! Some people dont even clean their face daily still have perfect clear skin!!
Do you happen to know the exact genetic? or is it even known yet??
#10 Guest_~Wolfy~_*
Posted 20 February 2007 - 12:43 AM
#11
Posted 20 February 2007 - 12:45 AM
Exactly! Some people dont even clean their face daily still have perfect clear skin!!
Do you happen to know the exact genetic? or is it even known yet??
you are asking some really good questions buddy!!!!
One theory of acne is that there is a master enzyme system in our bodys called cyp450 http://en.wikipedia.org/wiki/Cytochrome_P4...450s_in_Animals and that specifically cyp21ai is responsible for the regulation of retinoic acid in epithelial cells. And is partly why isotretinoin works so well, isotretinoin creates retinoic acid in sebaceous glands causing them to atrophy and normalize to decrease sebum. So many people that suffer from acne have could have a defect in this enzyme.
Skin Retinoid Concentrations Are Modulated by CYP26AI Expression Restricted to Basal Keratinocytes in Normal Human Skin and Differentiated 3D Skin Models. june 2006
1Department of Dermatology and Allergology, University Hospital of the RWTH Aachen, Aachen, Germany.
Cellular levels of all-trans retinoic acid (RA) are meticulously regulated utilizing an array of systems to balance uptake, biosynthesis, catabolism, and efflux transport. Metabolic transformation of all-trans RA to 4-hydroxylated RA appears to be primarily catalyzed by the cytochrome P450 (CYP) 26AI. Analysis of monolayer cultures of normal human epidermal keratinocytes (NHEKs) and dermal fibroblasts by quantitative real-time PCR and reverse transcription-PCR revealed no basal levels of CYP26AI mRNA expression, whereas specific transcripts were detectable following addition of 10(-6) M all-trans RA. Immunofluorescence and Western blot analysis showed a weak expression of CYP26AI in NHEK, which was increased by stimulation with all-trans RA. Using a newly developed peptide antibody, we further examined the localization of CYP26AI expression in normal skin and three-dimensional (3D) skin models. In contrast to cell culture monolayers where CYP26AI was only weakly detectable, strong constitutive expression of CYP26AI in vivo and in organotypic culture was found to be restricted to basal epidermal keratinocytes, as well as eccrine sweat glands and sebaceous glands. These studies verify the capacity of human skin to metabolize RA, although substantial differences exist in CYP expression between normal skin and 3D skin models compared to monolayer cultures. Complex metabolic processes that maintain retinoid homeostasis may therefore be better studied in model systems more closely resembling in vivo skin. In light of our prior studies documenting the functional activity of RA metabolites, expression of CYP26 in the sebaceous gland epithelium supports the suggestion that altered RA metabolism may be involved in the pathogenesis of acne.Journal of Investigative Dermatology advance online publication, 15 June 2006; doi:10.1038/sj.jid.5700432.
and here is another i would rather not try to explain!!
: J Invest Dermatol. 2006 Sep;126(9):2002-9. Epub 2006 May 4.FPRIVATE "TYPE=PICT;ALT=Click here to read" Links
Peroxisome proliferator-activated receptors increase human sebum production.
The Jake Gittlen Cancer Research Institute, Hershey, Pennsylvania 17033, USA.
Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPARalpha agonist-GW7647, PPARdelta agonist-GW0742, PPARalpha/delta agonist-GW2433, PPARgamma agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.
PMID: 16675962 [PubMed - indexed for MEDLINE]
i also have read evidence that eicosanoids can modulate ppars, eicosanoids http://en.wikipedia.org/wiki/Image:EFA_to_Eicosanoids.svg are made from essential fatty acids.
i could go on but its getting late.
#12
Posted 20 February 2007 - 01:43 PM
just some random thoughts
from wiki:
Regulation of gene expression (gene regulation) is the cellular control of the amount and timing of appearance of the functional product of a gene. Although a functional gene product may be an RNA or a protein, the majority of the known mechanisms regulate the expression of protein coding genes. Any step of gene expression may be modulated, from the DNA-RNA transcription step to post-translational modification of a protein. Gene regulation gives the cell control over structure and function, and is the basis for cellular differentiation, morphogenesis and the versatility and adaptability of any organism.
as i read more into genetics(i dont know much right now) and also into factors for gene expression i find much evidence for relation between dietary conditions and how they influence gene expression. and right now i think that everyone has different hardwired genetic codes and that all we need is to provide to right dietary conditions and we can modify our gene expression. such is the way accutane may cause long remissions through the modulation of genes. up-regulated some and downregulating others to effect how the cells replicate. thats pretty much what topical tretinoin does too binds to retinoid receptors to make cells replicate at a normal rate.
But with genetic diseases the hardwiring is there, but every gene can be modulated to a certain degree(according to wiki and many studies) and this all has to do with the dietary environment we provide our bodys with what we eat consistently over a period of time.
So provide the right dietary environment, and maximize our genetic potential.
but right now im slowly learning what the right dietary environment is for my body.
What i know:
a good balance of complex carbs vs. simple carbs-otherwise it could lead to many diseases like diabetes etc. and also just plain make you fat.
also a good balance of protein to carbs.
get vitamins and minerals
eat lots of vegetables and a good amount of fruit
what im learning and have not incorporated yet:.
the healthy ratios of good fats to bad fats
omega 3s to omega 6s and being able to indentify sources of omega 6s in my diet
this is something ive never thought of before and when i think back over the period of my entire life i have never had optimum 6-9 ratios.
and then i realize that ive been taking better care of my car then i've been taking care of my own body!!!!!!!
Thats unbelievable!!!
#13
Posted 20 February 2007 - 04:17 PM
#14
Posted 20 February 2007 - 04:21 PM
Do you happen to know the exact genetic? or is it even known yet??
It all starts with a genetic predisposition and the ability to convert testosterone to dihydrotestosterone in the sebaceous gland due to the presence of the enzyme 5 alpha-reductase.
Sebaceous glands enlarge, produce more oil, the skin start shedding more skin cells and clog the pores, and when bacteria enter the scene, things really get going. Now its only a matter of breakage of the follicles and inflammation and you have full-blown acne.
#15
Posted 20 February 2007 - 05:47 PM
Thanks Marton
I know how difficult it is to change your genetics, but can anything be done to correct the defect in this enzyme?
#17
Posted 20 February 2007 - 06:18 PM
This thread is too good for General Acne .... moved to Acne Research forum.
Thanks for the awesome posts, guys!
#18
Posted 20 February 2007 - 08:00 PM

this is a very good outline of events that lead to acne.
it would be a mistake to claim that we know exactly how acne works, because as you can see in the latest reseach articles ive posted (all published in 2006), that nobody has that clear of a picture as to what the main cause of acne is genetics is gotta be the first factor for the disease though i cant argue with that. its all very debatable and complex.
and im not too sure that 5 alpha reductase and dht is the main cause for sebum production. I thought that was ruled out a long time ago.
why are you so convinced that this is the reason? Im very curious.
#19
Posted 20 February 2007 - 08:35 PM
so far I've boiled it down to:
5-alpha reductase and dht, retinoic acid production, or arachidonic acid via eicosanoids from omega-3 efas.
#20
Posted 20 February 2007 - 08:44 PM
J Steroid Biochem Mol Biol. 2002 Nov;82(4-5):393-400. Links
5 alpha-reductase-catalyzed conversion of testosterone to dihydrotestosterone is increased in prostatic adenocarcinoma cells: suppression by 15-lipoxygenase metabolites of gamma-linolenic and eicosapentaenoic acids.Pham H, Ziboh VA.
Department of Dermatology, School of Medicine, University of California at Davis, TB-192, One Shields Avenue, 95616, USA.
Although the androgens, testosterone (T) and its highly active metabolite dihydrotestosterone (DHT) play a role in the development and progression of prostate cancer, the mechanism(s) are unclear. Furthermore, 5 alpha-reductase which catalyze the conversion of T to DHT, has been a target of manipulation in the treatment of prostatic cancer, hence synthetic 5 alpha-reductase activity inhibitors have shown therapeutic promise. To demonstrate that nutrients derived from dietary sources can exert similar therapeutic promise, this study was designed using benign hyperplastic cells (BHC) and malignant tumorigenic cells (MTC) derived from Lobund-Wistar (L-W) rat model of prostatic adenocarcinoma to test the effects of gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and their 15-lipoxygenase metabolites on cellular 5 alpha-reductase activity. Our data revealed: (i) that incubation of MTC with [3H]-T resulted in marked conversion to [3H]-DHT when compared to similar incubation with BHC; (ii) that DHT-enhanced activity of 5 alpha-reductase was inhibited 80% by 15S-hydroxyeicosatrienoic acid, the 15-lipoxygenase metabolite of GLA, when compared to 55% by 15S-hydroxyeicosapentaenoic acid, the 15-lipoxygenase metabolite of EPA; and (iii) that their precursor fatty acids, respectively, exerted moderate inhibition. Taken together, the study underscores the biological importance of 15-lipoxygenase metabolites of polyunsaturated fatty acids (PUFAs) in androgen metabolism.
so even though dht can stimulte sebaceous glands, so can factors such as inflammatory eicosanoids of arachidonic acid.
so i guess ive managed to unify these two theorys with efas being a good contender for an acne treatment or acne cause,even though this study wasnt on acne i think it would be safe to hypothesize that this could also be applied to cells all over the body that depend on efas and their products such as sebaceuos glands.
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