6 replies to this topic

[alternativista]

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 (affected by many things such as high glycemic diet, IGF1 in diary, etc http://www.acne.org/...dpost&p=2581754)

-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. Affects most of the other things on this list.
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.

-Fewer llamelar granulars that contain the desquammation enzymes and lipids (the things that make cells exfoliate normally without clogging pores. Affected by linoleic acid)

-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. 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)

-More of the enzymes that convert androgens and estrogens - (promoted by/in 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)
 
-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

Edited by alternativista, 28 February 2013 - 02:56 PM.

[alternativista]

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.

[alternativista]

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.

[alternativista]

Bump, because I revised a little. 

[alternativista]

See also this thread on genes involved in acne:

 

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

[gingergirl22]

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

[alternativista]

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-alpha, IL-1 alpha, CYP1A1 among others.^[19]