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Things That Are Different In Acne Prone Skin: The Differences Between Us And Them

genes genetics deficient deficiency sebum dht linoleic acid androgen retinoids estrogen

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#1 alternativista

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Posted 30 April 2012 - 09:18 AM

These things have been found to be different in acne prone skin.

This is specifically about what's going on in our skin, not about the various other factors going on elsewhere in our bodies that worsen the acne condition. For the most part, other people have those things happening too, they just don't get the symptom of acne. These are the differences between us and all your friends that can eat all the junk they want and make whatever other unhealthy lifestyle choices and even have other hormonal or other health problems, yet still have clear skin while you get acne.

-A tendency towards follicular hyperkeratosis or abnormal follicular keratosis (genetic tendency affected by many things such as high glycemic diet, IGF1 in diary, etc  More about hyperkeratinization/hyperproliferation of cells & what to do about it. http://www.acne.org/...acne/?p=2580171


-A deficiency in linoleic acid (applies to skin prone to all kinds of problems and all mammals) Linoleic acid is an important part of normal sebum and all of it's many functions in mammalian skin. This Affects almost all of the other things on this list. It's the root. Acne Prone Skin/sebum Deficient In Linoleic Acid, Possible Topical Solution: http://www.acne.org/...pical-solution/ which contains links to studies and papers that show that at least 3 genes/enzyme mutations are involved in the linoleic acid deficiency found in mammalian skin prone to skin irritations. But there are also many ways diet affects fat metabolism and fatty acid composition of sebum.  What to do about the linoleic acid deficiency:  http://www.acne.org/...20#entry3303681  Diet & lifestyle habits to improve metabolism of fats and improve sebum quality: http://www.acne.org/...acne/?p=2637530

-Fewer llamelar granulars that contain the desquammation enzymes and lipids (the things that make cells exfoliate normally without clogging pores. Affected by linoleic acid deficiency more info & research in the above link)

-More permeable around sebaceous glands and follicles. (affected by linoleic acid deficiency)

-There are more estrogen/androgen receptors in skin of the acne prone, especially in males per the research. http://www.ncbi.nlm....pt=AbstractPlus And http://www.ncbi.nlm..../pubmed/6448587

-Higher levels of dehydroepiandrosterone (DHEA) are found in the sebaceous glands. This in turn is converted by 5-alpha reductase into DHT (possibly due to the deficiency in linoleic acid in sebum which inhibits the conversion) 5-alpha reductase can be inhibited by some nutrients, i.e. beta sito sterol, obtained in food, supplements, and can be topically applied)

-More of the enzymes that convert androgens and estrogens - (promoted by  dairy, high GI diets, inhibited by linoleic acid)

-Deficient in retinoids, possible due to mutations in CYP26AI gene that causes it to be metabolized too fast to be used. These have a huge impact on hyperkeratinization and exfoliation, which would be why they are prescribed for acne treatments.  http://www.acne.org/...n/#entry3229786   (may be boosted with beta carotene consumption & UVB exposure. This mutation may also impair ability to make vitamin D, an important factor in normal cell proliferation/desquammation)
 
-A subspecies of P. Acnes bacteria that may be more problematic that the species inhabiting normal skin.  http://www.acne.org/...-2#entry3257204


More info:
http://www.acne.org/...rmation/
/>http://www.acne.org/...pical-solution/
http://www.acne.org/...dpost&p=2637530

 

 

There's also chronic inflammation, various hormones, stress, function of various organs such as liver, thyroid, adrenals, digestive tract and more. All affected by diet and lifestyle habits.

 

I.E. Some foods are anti-inflammatory such as omega 3 fats and just about any plant food, herb, tea or spice that isn't a seed and that you don't have an intolerance for.  Other foods are pro-inflammatory such as sugars, trans fats & hydrogenated oils, omega 6 from seeds, seed oils, products from grain fed animals and anything you have an intolerance for.

 

Even Melatonin affects cell proliferation. And your melatonin levels are affected by your diet and your daily exposure to light and dark. You should be in bright light in the daytime. And darkness at night. Avoid artificial light as much as possible.  This also affects hormones, and carb/glucose metabolism and is just about as big a factor in developing diabetes as diet. http://www.acne.org/...tion/?p=3216466


Edited by alternativista, 11 July 2014 - 04:08 PM.


#2 alternativista

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Posted 07 May 2012 - 03:20 PM

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


Edited by alternativista, 12 February 2013 - 11:25 AM.


#3 alternativista

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Posted 07 May 2012 - 05:02 PM

Possible lower levels of antioxidant enzymes such as superoxide dismutase (SOD) and GSH-Px

In recent years there has been renewed interest in the influence of oxidative stress and the operations of the antioxidant defense system in acne. Many of these investigations have examined the extent to which a potential oxidative stress burden in the skin might be reflected in the blood of acne patients. In a study involving 52 patients with papulopustular acne, researchers reported that blood antioxidant enzyme activities, including superoxide dismutase (SOD) and GSH-Px, were significantly lower vs. controls [30].

Emerging studies indicate that low blood SOD, GSH-Px and elevated MDA are characteristic of acne vs. healthy controls [32-35]. These differences are not minute; indeed the GSH-Px activity in adults with acne is reported to be 42 percent lower than healthy controls [34]. Some investigators have not found a blanket decrease in SOD and increase in MDA among all acne patients. One investigative group noted that patients with the more severe forms of acne have the lowest SOD and highest MDA levels vs. other milder cases and controls [36].

and

Patients with inflammatory acne had significantly higher production of hydrogen peroxide, 43% more than healthy controls.



And higher levels of Squalene and thus oxidized squalene in our sebum

it has become increasingly clear that squalene production is highly upregulated in acne. Overall acne patients have 59% more sebum than healthy controls, yet it is squalene that emerges as the specific lipid that is being produced in abundance - 2.2-fold higher vs. controls [44]. As expected, an increase in squalene sets the stage for significantly higher levels of squalene peroxides and diminished vitamin E in the sebum of acne patients [45]. Squalene peroxides also diminish the important skin antioxidant glutathione, while pre-treatment with glutathione depleting agents (DL-buthionine sulfoximine and diethyl maleate) makes the comedogenic potential of squalene peroxides even worse [46]. In smokers with acne the squalene peroxidation and vitamin E reduction is even more pronounced [47]. Not only are the squalene peroxides confirmed to be highly comeodogenic [48], they have recently been reported to set an inflammatory cascade in motion. Specifically, exposure of peroxidated squalene products to human keratinocyte cells stimulates production of inflammatory cytokines and upregulates lipoxygenase (LOX) activity

http://www.ncbi.nlm....32/?tool=pubmed

It's a really interesting article citing research into inflammation/oxidation, all kinds of antioxidants and acne. There's also a lot of talk about oxidative stress caused by mental health issues for those interested.

Also:

The global aspects of diet are also worthy of brief mention. In recent years it has become evident that there may indeed be a connection between dietary components and the risk of acne. For example, regional diets low in processed foods and sugars (with an overall low glycemic load) are associated with decreased acne risk [133]. Intervention studies using similar low glycemic load meals have reported improvements [134]. One of the features of these intervention studies is that they tend to be higher in 'nutrient-dense' foods, and this would include greater intake of plant-based antioxidants from whole grains, vegetables and fruits. Adherence to the so-called South Beach diet, similar to the Mediterranean diet which reduces depression risk by 30%, has been associated with the reduction and discontinuance of acne medications [135].


A possible role for squalene in the pathogenesis of acne. I. In vitro study of squalene oxidation.

Saint-Leger D, Bague A, Cohen E, Chivot M.



Abstract

An in vitro study of the oxidation of squalene, and a description of factors acting on this transformation are presented. Thin layer chromatography was used to quantify the products generated by different oxidation processes. The results clearly show that squalene is a highly effective oxygen-scavenging agent. Its oxidation may first induce comedogenesis and, as a secondary event, cause a large reduction in oxygen tension in the human pilo-sebaceous duct. Porphyrins were confirmed to be highly efficient catalytic factors in the squalene oxidation process. The relationships between comedogenesis, bacterial colonization, and the role of sebum in the pathogenesis of acne are discussed in the light of these findings.


http://www.ncbi.nlm..../pubmed/2941049

Edited by alternativista, 07 May 2012 - 05:02 PM.


#4 alternativista

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Posted 12 February 2013 - 11:46 AM

Bump, because I revised a little. 



#5 alternativista

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Posted 28 February 2013 - 02:36 PM

See also this thread on genes involved in acne:

 

http://www.acne.org/...volved-in-acne/

 

 

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:

http://www.freshpate...20100028878.php

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:
http://www.acne.org/...p...t&p=2580171

----------------------------------------
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.

http://www.ncbi.nlm....st_uids=9557256

----------------------------------
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

----------------------------------------------------------------------------


Edited by alternativista, 26 February 2014 - 04:13 PM.


#6 gingergirl22

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Posted 02 March 2013 - 12:09 AM

Alternamista - Thank you for all the excellent inofrmation you bring to this forum!



#7 alternativista

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Posted 14 March 2013 - 02:20 PM

I just noticed the wikipedia article has a couple more genes to look into:

 

The predisposition for specific individuals to acne is likely explained by a genetic component, which has been supported by twin studies as well as studies that have looked at rates of acne among first degree relatives. The genetics of acne susceptibility is likely polygenic, as the disease does not follow classic Mendelian inheritance pattern. There are multiple candidates for genes which are possibly related to acne, including polymorphisms in TNF-alphaIL-1 alphaCYP1A1 among others.[19]



#8 alternativista

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Posted 10 October 2013 - 01:36 PM

cathelicidin & vitamin D levels.  Affects rate of keratinization/cell proliferation.  Sorry, I closed the page I was looking at.  something to look into.

 

Anyway, cathelicidin is an antimicrobial peptide.



#9 LewisS

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Posted 11 October 2013 - 05:22 AM

The point about a deficiency in linoleic acid acid interests me. Could taking a supplement help or eating certain types of food? I think I'll do a search on foods that contain it.

 

I already take measures to inhibit DHT and still get mild acne, I know my diet certainly isn't helping.

 

Thanks a lot for these posts. They are the only posts on this forum that are factual and genuine. Most other threads just tell us to use a ton of different products and eat what we want. It's definitely your posts that converted me from external to internal/natural acne treatment!



#10 alternativista

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Posted 11 October 2013 - 06:41 AM

The point about a deficiency in linoleic acid acid interests me. Could taking a supplement help or eating certain types of food? I think I'll do a search on foods that contain it.
 
I already take measures to inhibit DHT and still get mild acne, I know my diet certainly isn't helping.
 
Thanks a lot for these posts. They are the only posts on this forum that are factual and genuine. Most other threads just tell us to use a ton of different products and eat what we want. It's definitely your posts that converted me from external to internal/natural acne treatment!


Use a high linoleic acid oil like safflower topically. But you could take gamma linoleic acid supplement like borage oil.

#11 nikkimixam

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Posted 11 October 2013 - 12:44 PM

I was using grapeseed oil for a couple of weeks and felt as if it were making my skin more dry, yet giving me small whiteheads that I never usually get. what explains this? I was using the Napa valley organics from whole foods as well.

Edited by nikkimixam, 11 October 2013 - 12:45 PM.


#12 alternativista

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Posted 11 October 2013 - 03:02 PM

I was using grapeseed oil for a couple of weeks and felt as if it were making my skin more dry, yet giving me small whiteheads that I never usually get. what explains this? I was using the Napa valley organics from whole foods as well.

 

 

I don't know.  Grapeseed is a little more comodegenic.  have you tried safflower?  And were you just applying or using it to oil cleanse?  

 

I know when I first began using oil, I got small closed comedones in the center of my forehead, but it was fine everywhere else.  And I don't have that problem anymore.  The first oils I ever tried include jojoba and almond.  So maybe the difference is the type of oil.  Or the quality, as the first oils I used were bottled for cosmetic use,in clear plastic bottles.


Edited by alternativista, 11 July 2014 - 04:11 PM.


#13 Gladiatoro

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Posted 11 October 2013 - 08:51 PM

Alternamista - Thank you for all the excellent inofrmation you bring to this forum!

Her tag name is Alternativista not Alternamista lol.... just wanted to clarify that . I would be upset about that ha.... she is a female after all.


Edited by Gladiatoro, 11 October 2013 - 08:52 PM.


#14 alternativista

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Posted 06 November 2013 - 10:23 PM

Bump.




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