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Acne Prone Skin/sebum Deficient In Linoleic Acid, Possible Topical Solution

vitamin d vitamin a vitamin e biotin fish oil omega-3 zinc

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#1 alternativista

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Posted 15 April 2012 - 12:29 PM

Linoleic acid is a vital component in normal sebum that does what it is supposed to: Protect the skin. Skin/sebum in people (and other mammals) prone to acne and other skin problems have been found to be deficient in linoleic Acid. Sebum deficient in linoleic acid is hard and sticky and clogs pores. It looks greasy and has fewer protective and anti-inflammatory properties.

Key points:

  • Acne and other problem prone skin (in people and animals) are lacking in linoleic acid.
    Linoleic acid is a component in the ceramides that make skin strong and impermeable and thus less easily ruptured and less sensitive to irritations.
  • This can be changed with topical application.
  • Grape seed and Safflower oil are over 70% linoleic acid.
  • Linoleic Acid inhibits the enzymes that convert Testosterone to DHT. Both types. So it can help with hirsutism, hairloss and acne.
  • Linoleic Acid is anti-inflammatory and protects the skin from UV damage.
  • Linoleic Acid inhibits melatonin and thus fades hyperpigmentation.
  • Linoleic acid is anti-microbial as the P. Acnes blamed for acne.
  • Linoleic acid deficiency causes an increase in interluekin -1a which is a factor inflammatory response.
  • Tretinoin (Retin A & the like) alters the lipid profile improving the linoleic acid composition.
  • Linoleic Acid improves the peroxisome proliferator-activated receptors (PPAR) and retinoid X receptor (RXR) situation that regulates sebum production and hyperkeritinization/differenciation (and is what accutane affects)
  • Linoleic acid is involved in the formation of Lamellar granules that produce the enzymes involved in normal exfoliation. They also form the armor that makes your skin strong. Acne prone skin has been found to contain fewer lamellar granules.
  • Ceramide in a deficient skin barrier is lacking a protein called sphingosine. In winter our skin produces less sphingosine which is one reason acne often worsens in winter. Topical application of live cultured yogurt can boost production.
  • Thyroid hormone affects lipid profile. One way that perhaps both hypo and hyperthyroid conditions affect acne.
  • We don't necessarily have a dietary or systemic deficiency in linoleic acid. Just in the sebum and thus a topical application is the best course of action. This tendency is genetic.

 

Examples of skin problems affected by a deficiency in linoleic acid include acne, eczema, psoriasis, keratosis pilares, hypersensitivity to allergens, and dry itchy sensitive skin of all types--aka dermatitis. 

 

A What To Do About This Post
: http://www.acne.org/...20#entry3303681

It also might repel pests like the mites responsible for many skin irritations. And hopefully mosquitos, fleas and ticks for your pets sake.

Excerpt from a good paper:

Healing fats of the skin: the structural and immunologic roles of the omega-6 and omega-3 fatty acids.
Linoleic acid (18:2omega6) and alpha-linolenic acid (18:3omega3) represent the parent fats of the two main classes of polyunsaturated fatty acids: the omega-6 (n-6) and the omega-3 (n-3) fatty acids, respectively. Linoleic acid and alpha-linolenic acid both give rise to other long-chain fatty acid derivatives, including gamma-linolenic acid and arachidonic acid (omega-6 fatty acids) and docosahexaenoic acid and eicosapentaenoic acid (omega-3 fatty acids). These fatty acids are showing promise as safe adjunctive treatments for many skin disorders, including atopic dermatitis, psoriasis, acne vulgaris, systemic lupus erythematosus, nonmelanoma skin cancer, and melanoma. Their roles are diverse and include maintenance of the stratum corneum permeability barrier, maturation and differentiation of the stratum corneum, formation and secretion of lamellar bodies, inhibition of proinflammatory eicosanoids, elevation of the sunburn threshold, inhibition of proinflammatory cytokines[/b] (tumor necrosis factor-alpha, interferon-gamma, and interleukin-12), inhibition of lipoxygenase, promotion of wound healing, and promotion of apoptosis in malignant cells, including melanoma. They fulfill these functions independently and through the modulation of peroxisome proliferator-activated and Toll-like receptors.

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

Nearly all the items in the list of roles played by linoleic acid in sebum above affect acne. i only bolded the ones that most here would recognize as causes of acne i.e. the inflammation. 


Note: These oils are not stable and should be stored in the refrigerator. Get a small, preferably dark colored bottle to keep a small amount at a time in your medicine cabinet.

------------------------
So, my dog is prone to itchy skin and is extremely sensitive to flea bites. Which attracts more fleas. They like dry, irritated, easily permeated skin. Most healthy animals aren't that bothered by fleas and some don't get fleas. My brother had an indoor/outdoor cat that didn't. And I have a friend with a dog and cat that don't get fleas which is amazing in this climate. So, there's probably something different about these animals. Just like there's something different about we acne prone people that makes the SAD diet leads to acne in us, but not everyone else.

I've been looking in to what I could do to improve his skin and have found information on some dogs having a deficient skin barrier because their skin is lacking a ceramide. That lead to me finding info on them lacking linoleic acid, just like acne prone skin.

And I discovered there is a topical 'spot on' treatment called Allerderm Spot on Lipid Complex For damaged epidermal barriers that involves putting a blend of lipids in a spot on the dog, usually the neck, where he won't lick it off just like with the spot on flea treatments.

That means you must be able to change your lipid profile with topically applied lipids!!!!
And you might not necessarily need to apply it directly to your acne prone skin if you don't want to. The way allerderm is not applied to the itchy skin but to some spot where the dog won't lick it off.

Since dogs can't have grapes, I'm trying safflower oil instead of my preferred grapeseed for now. The rest of you should try grapeseed. Grapeseed is a little more potentially comodogenic.

Here's some of the info and a study on dogs and Allerderm:

 

 

Dogs with allergic skin disease are missing a protein in their protective skin barrier that means water escapes from the skin making it very dry. Ceramide in a deficient skin barrier is lacking a protein called sphingosine. The sphingosine deficient ceramide is like aged, crumbling mortar between the skin cells in the dogs' skin. The skin barrier is permeable or "leaky".

Checklist for Managing the Chronic Canine AD
Allerderm Spot On:
Tretter,S ,Mueller, RS. The influence of topical unsaturated fatty acids and essential oils on normal and atopic dogs- a pilot study. Vet Derm 2010, 21 311-328
Seven dogs with atopic dermatitis and five normal dogs were treated with a spot-on containing essential oils and unsaturated fatty acids once weekly for 8 weeks. In all dogs, transepidermal water loss (TEWL) was measured before and after treatment. In atopic dogs, lesions and pruritus were assessed before and after treatment. The mean CADESI and pruritus scores and TEWL in atopic [u]dogs decreased.

http://www.avsg.net/...MuseDVMACVD.pdf


More info on Allerderms informaton sheet. Explains some of the ways a linoleic deficiency causes many skin conditions. (but i've found more, including acne) : http://www.virbacvet...OCT09.sflb.ashx


Dosage for Dogs and cats
6 pipettes of 2 mL each (0.068 oz) for small dogs and cats ≤ 20 lb 6 pipettes of 4 mL each (0.135 oz) for medium and large dogs ≥ 20 lb

I've been trying to find the ingredients in the spot on treatment for dogs and cats. So far, all I've found is that it contains ceramides, free fatty acids, and cholesterol without specifying which. I'm pretty sure it includes some omega 3 in addition to the linoleic acid. I've found info on capsules to be taken orally. They have a couple of formulas:

Allerderm EFA-Caps Guaranteed Analysis (per capsule): Eicosapentaenoic Acid (EPA) 80 mg, Docosahexaenoic Acid (DHA) 50 mg, Linoleic Acid (LA) 30 mg, Gamma Linolenic Acid (GLA) 18 mg, Vitamin A 800 IU, Vitamin D 25 IU, Vitamin E 11 IU
Allerderm EFA-Caps Ingredients: Fish oil, borage seed oil and sunflower seed oil (sources of fatty acids), glycerin, purified water, d-alpha tocopherol (source of vitamin E), vitamin A palmitate
Allerderm EFA-Z Plus Guaranteed Analysis (per mL): Linoleic Acid 510 mg, Vitamin A 136 IU, Vitamin E 1.9 IU, Zinc 2.1 mg, Pyridoxine HCI 0.10 mg, Biotin 2.0 µg, Inositol 0.38 mg
Allerderm EFA-Z Plus Ingredients: Sunflower seed oil, fish oil and borage seed oil (sources of fatty acids), zinc sulfate, natural and artificial flavoring, alpha tocopherol acetate (source of vitamin E), silica, propylparaben, inositol, pyridoxine HCl, vitamin A palmitate, methylparaben, biotin

A pretty good paper: Atopy, pyoderma and the skin: Barrier function and beyond....... About dogs and cats, but there's lots of reference to human skin problems and research and products for humans. http://www.avsg.net/...MuseDVMACVD.pdf There's quite a few citations at the bottom that I haven't looked at yet.


Edited by alternativista, 11 July 2014 - 02:46 PM.


#2 alternativista

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Posted 15 April 2012 - 01:07 PM

Ok, I was just posting all kinds of links and other great stuff when weirdness happened and my post was lost. I'll have to re-find it all. In the meantime, start with the Sebum quality section of my good things thread and the Recent Advances in the pathogenesis of acne thread.
http://www.acne.org/...30#entry2637530
http://www.acne.org/...__fromsearch__1
http://www.acne.org/...54#entry2581754

Since I still have this open, the wikipedia page on linoleic acid says:

A diet only deficient in linoleate causes mild skin scaling, hair loss,[7] and poor wound healing in rats.[8] However, achieving a deficiency in linoleic acid is nearly impossible consuming any normal diet and is thus not considered to be of clinical concern.

Along with oleic acid, linoleic acid is released by cockroaches upon death which has the effect of preventing other roaches from entering the area. This is similar to the mechanism found in ants and bees, in which oleic acid is released upon death.[9]



So, I'm thinking linoleic acid also repels fleas maybe and the lack of it is why my dog gets so many and I'm having a hell of a time getting rid of them. Also, I wonder what mosquitos release as they don't bother me much. They prefer other people. And I imagine this or something like it affects mites as well. We all have them, but only some animals scratch their fur off.

Also, the issue isn't whether we we have a dietary or systemic deficieny in linoleic acid, but that our skin/sebum is deficient. some of the info cited mentions that.

Edited by alternativista, 17 April 2012 - 08:13 AM.


#3 alternativista

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Posted 15 April 2012 - 01:42 PM

'Recent' Advances in Acne Pathogenesis Information

http://www.acne.org/...__fromsearch__1
A report from 2009. there's a link to a PDF of the entire report in that thread.

On page 5:

Jeremy et al23 investigated the initiating events for acne lesions, and found that immune changes and inflammatory responses occur before hyperproliferation of keratinocytes, with a pattern similar to a type IV delayed hypersensitivity response. The
immune response is led by CD41 lymphocytes and macrophages.23 These researchers hypothesize that
the subsequent production of cytokines activates local endothelial cells, up-regulating inflammatory vascular markers (E-selectin, vascular cell adhesion
molecule-1 [VCAM-1], intercellular adhesion molecule-1 [ICAM-1], and human leukocyte antigen-DR [HLA-DR]) in the vasculature around the pilosebaceous follicle.23 They further have postulated that the entire process is initiated by interleukin (IL)-1a up-regulation in response to a relative linoleic acid deficiency caused by excess sebum and perturbationof barrier function within the follicle.23


So, apparently a linoleic acid deficiency causes an increase in interluekin -1a which is a factor inflammatory response. So it makes you more prone to irritation, allergic reaction and so on.

Also. numerous things deficient in acne prone skin:


Researchers have found that there are fewer lamellar granules in the Stratum Granulosum of acneic skin. As the lamellar granules contain the desquamation of enzymes and lipids that comprise the barrier layer in the intercellular spaces, this could account for the accumulation of cells in the follicle canal. Likewise, acneic skin is more permeable around the sebaceous gland and follicle, which may lead to leakage and inflammation into surrounding tissues. Studies have shown that linoleic acid, an essential fatty acid that is a component of the barrier lipid layer, is indeed deficient in acneic clients.
http://www.dermalins...t_is_Acne_.html



So, acne prone skin is more permeable, just like in dogs. (Also, those lamellar granulars mentioned release components that are required for skin shedding (desquamation) in the uppermost epidermal layer, the stratum corneum)


Also, I found info on how tretinoin alters the lipid profile affecting the linoleic acid composition, which I'll have to find again. But here's a post on how beta carotene and sunlight affects our natural ability to produce retinoids in the skin:http://www.acne.org/...ost__p__3229786

Also, I found info on the involvement of PPARs, receptors whose involvement I never fully researched. and I'll have to find that again. Some of the studies in the sidebars of the pages with the linoleic acid and tretinoin studies were about PPARs.


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

Related Threads:

When Linoleic acid isn't available...
http://www.acne.org/...hl__cholesterol


Healing fats of the skin: the structural and immunologic roles of the omega-6 and omega-3 fatty acids.

http://www.acne.org/...78#entry3168178



Diminished concentrations of linoleic acid have been demonstrated in individuals with acne and, interestingly, these levels normalize after successful treatment with isotretinoin. This relative decrease in linoleic acid may be what initiates comedone formation.


http://www.emedicine...DERM/topic2.htm

Also in the above emedicine article, on genetics:

The pathogenesis of acne vulgaris is multifactorial. The key factor is genetics.

[1]

If both parents had acne, 3 of 4 children will have acne. If 1 parent had acne, then 1 of 4 of the children will have acne. However, similar to other genetic conditions, not every family will have the same pattern, with acne vulgaris sometimes skipping generations.

What is inherited is the propensity for follicular epidermal hyperproliferation

with subsequent plugging of the follicle. Additional aggravating factors include excess sebum, the presence and activity of


Propionibacterium acnes,

and inflammation.



It seems that the amount of linoleic acid content stays the same, but the more sebum is produced, the more it gets diluted by oleic acid due to how much free fatty acid (linoleic) is in the blood

I typed out the important aspects of the book on the linoelic acid portion:


A link between comedogensis and a low sebum level of linoleic acid was proposed by Downing and co-authors. They found that patients with acne had a significantly lower level of linoleic acid in their skin surface lipids that normal individuals. Subsequent studies have suggested that this effect relates to the higher sebum secretion rates characteristic of acne, since there is an inverse relationship between the secretion rate and the linoleate content of the surface wax esters, which are purely of sebaceous origin. Conversely, a reduction in the rate of sebum secretion by treatment by treatment with the ant-androgen cyproterone acetate, or with oral isotretinoin, cause a corresponding increase in the linoleic acid content of the sebaceous lipds.

Once sebum synthesis begins, no further lipids are accepted from circulation, so that the more sebum that is synthesized per cell, the more initial linoleate content will be diluted.

It is proposed that when the secretion rate of sebum is high, as in acne, and, as a result, its linoleate concentration is low, the cells of the follicular epithelium might thereby be subjected to lipds that are deficient in essential fatty acids.



Note: cyproterone acetate, is what's in the BCP Diane that many people out side the U.S. take for acne. I wonder if spiro does the same thing.


Acne is characterized by hyperkeratosis of the follicular epithelium, leading to horny impactions that may lie dormant as open or closed comedones or may cause inflammation of the follicle. Although persons with acne have consistently been observed to have elevated levels of sebum secretion, no mechanism relating sebum secretion rates to comedogenesis is known. Acne patients have also been shown to have low levels of linoleic acid in their skin surface lipids. To explain this observation, the hypothesis is advanced that the linoleate concentration in human sebum depends on the quantity of linoleic acid present in each sebaceous cell at the commencement of its differentiation and on the extent to which this initial charge is diluted by subsequent endogenous lipid synthesis in each sebaceous cell. A corollary hypothesis holds that low concentrations of linoleate in sebum impose a state of essential fatty acid deficiency on the cells of the follicular epithelium and induce the characteristic response of hyperkeratosis. Both hypotheses could hold, without there being a systemic deficiency of linoleic acid, simply as the result of elevated lipogenesis in individual sebaceous cells.



PMID: 2936775 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm....;indexed=google


Patent for a treament for acne using linoleic acid topically

Linoleic acid preparations for topical treatment of acne vulgaris

http://www.freepaten...om/5443844.html
Abstract:
A preparation for topical application of linoleic acid, for treatment of acne, and Propionibacteriem acnes, contains between about 0.1% and about 10%, preferably between about 1% and about 5% and specifically about 2% of linoleic acid. This acts both as an antibiotic and as a means for correcting the essential fatty acid imbalance in sebum which causes follicular plugging and triggers the process.



These people sell topicals that include linoleic acid.

http://www.skintacti...fatty_acids.htm

Edited by alternativista, 19 April 2012 - 09:09 AM.


#4 alternativista

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Posted 16 April 2012 - 09:04 AM

-

PPAR and RXR receptors


- peroxisome proliferator-activated receptors

PPAR alpha receptor is involved in regulating the sebaceous glands.PPAR's are responsible for lipid metabolism in the body as well as sebaceous control in the skin.

see resveratrol link below, also this discussion in Healthboards


PPAR beta and delta cells increase sebum production
PPAR alpha and gamma cells reduce sebum production
An imbalance between receptors can cause acne.

And this study: http://www.acne.org/...dpost&p=2740146 that indicates that 'PPAR-beta/delta activation stimulates keratinocyte differentiation, is anti-inflammatory, improves barrier homeostasis, and stimulates TG accumulation in keratinocytes.'

- PPAR situation improved by linoleic acid and derivatives, sesamin, chloropyll, fish oil and resveratrol (see the resveratrol thread. Seriously. Read it!) and is affected by insulin/insulin sentitivity.


retinoid X receptor (RXR) accutane (or other retinoids) binds to RXRs blocking PPAR

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

Healing fats of the skin: the structural and immunologic roles of the omega-6 and omega-3 fatty acids.


Linoleic acid (18:2omega6) and alpha-linolenic acid (18:3omega3) represent the parent fats of the two main classes of polyunsaturated fatty acids: the omega-6 (n-6) and the omega-3 (n-3) fatty acids, respectively. Linoleic acid and alpha-linolenic acid both give rise to other long-chain fatty acid derivatives, including gamma-linolenic acid and arachidonic acid (omega-6 fatty acids) and docosahexaenoic acid and eicosapentaenoic acid (omega-3 fatty acids). These fatty acids are showing promise as safe adjunctive treatments for many skin disorders, including atopic dermatitis, psoriasis, acne vulgaris, systemic lupus erythematosus, nonmelanoma skin cancer, and melanoma. Their roles are diverse and include maintenance of the stratum corneum permeability barrier, maturation and differentiation of the stratum corneum, formation and secretion of lamellar bodies, inhibition of proinflammatory eicosanoids, elevation of the sunburn threshold, inhibition of proinflammatory cytokines[/b] (tumor necrosis factor-alpha, interferon-gamma, and interleukin-12), inhibition of lipoxygenase, promotion of wound healing, and promotion of apoptosis in malignant cells, including melanoma. They fulfill these functions independently and through the modulation of [u]peroxisome proliferator-activated and Toll-like receptors. Copyright © 2010 Elsevier Inc. All rights reserved.



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

Lipid mediators in acne.


Ottaviani M, Camera E, Picardo M.


Multiple factors are involved in acne pathogenesis, and sebum secretion is one of the main ones. The role sebum plays in acne development has not been completely elucidated yet; however, increasing amounts of data seem to confirm the presence of alterations in sebum from acne patients. Altered ratio between saturated and unsaturated fatty acids has been indicated as an important feature to be considered in addition to the altered amount of specific fatty acids such as linoleic acid. Furthermore, particular attention has been focused on squalene peroxide that seems to be able to induce an inflammatory response beyond cytotoxicity and comedones formation. Moreover, recent data suggest that lipid mediators are able to interfere with sebocytes differentiation and sebogenesis through the activation of pathways related to peroxisome proliferators-activated receptors. Understanding the factors and mechanisms that regulate sebum production is needed in order to identify novel therapeutic strategies for acne treatment.
--------------------------


Essential fatty acids and acne.

Downing DT, Stewart ME, Wertz PW, Strauss JS.

Abstract

Acne is characterized by hyperkeratosis of the follicular epithelium, leading to horny impactions that may lie dormant as open or closed comedones or may cause inflammation of the follicle. Although persons with acne have consistently been observed to have elevated levels of sebum secretion, no mechanism relating s
ebum secretion rates to comedogenesis is known. Acne patients have also been shown to have low levels of linoleic acid in their skin surface lipids. To explain this observation, the hypothesis is advanced that the linoleate concentration in human sebum depends on the quantity of linoleic acid present in each sebaceous cell at the commencement of its differentiation and on the extent to which this initial charge is diluted by subsequent endogenous lipid synthesis in each sebaceous cell. A corollary hypothesis holds that low concentrations of linoleate in sebum impose a state of essential fatty acid deficiency on the cells of the follicular epithelium and induce the characteristic response of hyperkeratosis. Both hypotheses could hold, without there being a systemic deficiency of linoleic acid, simply as the result of elevated lipogenesis in individual sebaceous cells.

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

Dilutional effect of increased sebaceous gland activity on the proportion of linoleic acid in sebaceous wax esters and in epidermal acylceramides.

Stewart ME, Grahek MO, Cambier LS, Wertz PW, Downing DT.

Abstract


Sebaceous wax esters and epidermal acylceramides were isolated from skin surface lipid obtained from children and from young adults. Fatty acid methyl esters (FAME) were prepared from the esterified fatty acids of these lipid classes and analyzed to ascertain the proportions of methyl linoleate (18:2 delta 9,12), methyl sebaleate (18:2 delta 5,8), and methyl sapienate (16:1 delta 6). On the same subjects, 2 measures of sebum secretion rate were obtained, namely the sustainable wax ester secretion rate (WESR) on the forehead and the ratio of wax esters/(cholesterol + cholesterol esters) [WE/(CH + CE)] in the surface lipid. The proportions of methyl linoleate in FAME from the wax esters decreased, and the proportions of methyl sebaleate increased, with increased rates of sebum secretion. For both methyl linoleate and methyl sebaleate, a better correlation was obtained when the ratio of WE/(CH + CE) was used as a measure of sebum secretion rather than the WESR. The proportions of methyl linoleate in the FAME from the acylceramides were also inversely related to ratios of WE/(CH + CE). In acylceramides, linoleate was replaced by sapienate, a major fatty acid of human sebum. It appears, therefore, that sebum fatty acid composition may change with changes in sebaceous gland activity, and that sebum fatty acids can enter the epidermis and be incorporated into epidermal lipids.
PMID: 2946783 [PubMed - indexed for MEDLINE]

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

Increasing retinoids in our skin??

See also this post in which I started gathering info on retinoids in our skin, our possible deficiency and that beta carotene plus sunlight might improve that. http://www.acne.org/...n/#entry3229786

Edited by alternativista, 21 May 2012 - 05:06 PM.


#5 alternativista

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Posted 16 April 2012 - 02:45 PM

Thyroid hormone affects the composition of lipids:

The effect of thyroid hormones, phorbol esters, and sphingosine on incorporation of linoleic acid in liver lipids of white rats/
http://www.ncbi.nlm..../pubmed/8600996


Perhaps it impacts the lipid composition in the skin/sebum

-----------------------------------------------
Another study about how a deficiency of linoleic acid coincides with acne formation:

The composition of the ceramides from human stratum corneum and from comedones.


Human epidermal surface lipids were collected by an ethanol wash and the ceramides were quantified by thin-layer chromatography-photodensitometry. Six ceramide fractions were isolated and the structural components of each were analyzed in detail. The most unusual of the epidermal ceramides contained a sphingosine base with amide-linked 30- and 32-carbon omega-hydroxyacids and an ester-linked nonhydroxyacid, 41% of which was linoleic acid. The proportion of linoleic acid in the analogous ceramide from comedones was 6%. This supports the hypothesis that a localized insufficiency of linoleic acid in the follicular epithelium is an etiologic factor in comedogenesis.

http://www.ncbi.nlm..../pubmed/3158712

Edited by alternativista, 18 January 2013 - 09:30 AM.


#6 alternativista

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Posted 17 April 2012 - 09:20 AM

Studies have discovered links that propose that Trans fats may break down the body's own supply of linoleic and alpha-linoleic acids. This is why a deficiency of linoleic and alpha-linoleic acids affects people making them prone to acne breakouts.
Sebum output with lack of omega 3 fatty acids begins to be produced with oleic acid and can cause irritation to the skin which is why acne can show up. It has also been suggested that oleic acid sebum is drier, stiffer, hardened, and thus more prone to create lesions to the cells lining the walls of the sebum ducts and to form follicular plugs which lead to acne inflammation. (in our more permeable skin)

From an article. I haven't yet found the studies on the trans fats, but I imagine that our problem is that the linoleic acid gets metabolized into inflammatory substances too for it to do its anti-inflammatory stuff.

Due to low consumption of essential fatty acids or high consumption of trans-fats or hereditary factors that frequently involve digestive enzyme issues, some people have systemic deficiency of essential fatty acids and linoleic acid.

from http://www.acne.org/...and-skin-sebum/ So someone thinks we might have a systemic deficiency. I haven't found where they are getting this from though. I'd particularly like to know about the genetic factors for my collection of genetic differences between us and them.

Also " One hypothesis is that when sebum increases, linoleate content is diluted, and this decrease in linoleate signals overproduction of cells."


"To explain this observation, the hypothesis is advanced that the linoleate concentration in human sebum depends on the quantity of linoleic acid present in each sebaceous cell at the commencement of its differentiation and on the extent to which this initial charge is diluted by subsequent endogenous lipid synthesis in each sebaceous cell. A corollary hypothesis holds that low concentrations of linoleate in sebum impose a state of essential fatty acid deficiency on the cells of the follicular epithelium and induce the characteristic response of hyperkeratosis. Both hypotheses could hold, without there being a systemic deficiency of linoleic acid, simply as the result of elevated lipogenesis in individual sebaceous cells."

http://www.acneq.com/




Essential fatty acids and acne.
J American Academy of Dermatology. 1986 Feb;14(2 Pt 1):221-5.


In wound healing and many pathologic conditions, keratinocytes become activated: they turn into migratory, hyperproliferative cells that produce and secrete extracellular matrix components and signaling polypeptides. At the same time, their cytoskeleton is also altered by the production of specific keratin proteins. These changes are orchestrated by growth factors, chemokines, and cytokines produced by keratinocytes and other cutaneous cell types. The responding intracellular signaling pathways activate transcription factors that regulate expression of keratin genes. Analysis of these processes led us to propose the existence of a keratinocyte activation cycle, in which the cells first become activated by the release of IL-1. Subsequently, they maintain the activated state by autocrine production of proinflammatory and proliferative signals. Keratins K6 and K16 are markers of the active state. Signals from the lymphocytes, in the form of Interferon-gamma, induce the expression of K17 and make keratinocytes contractile. This enables the keratinocytes to shrink the provisional fibronectin-rich basement membrane. Signals from the fibroblasts, in the form of TGF-beta, induce the expression of K5 and K14, revert the keratinocytes to the healthy basal phenotype, and thus complete the activation cycle.


your skin produces hydrogen peroxide to fight each acne infection and this may continue for weeks, until the infection is resolved?
Hydrogen peroxide is a free radical which causes skin damage and skin aging. Over a period of time the volume of hydrogen peroxide acts just like continual sun exposure, damaging skin components such as collagen and causing the skin to sag and wrinkle.
Additionally, the healing process of acne infections involves thousands and thousands of chemical processes. These chemical processes produce more free radicals as a natural by-product and add to the volume of free radical damage (aging).
The skin has a supply of antioxidants that reduce the volume of free radicals and their damage. It is believed that moderate to severe acne literally depletes the skin's level of antioxidants, leaving it nearly defenseless against free radicals that are created by normal skin functions.


Your skin produces aging free radicals in response to acne infection.

Edited by alternativista, 18 January 2013 - 09:37 AM.


#7 Sarnon

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Posted 17 April 2012 - 10:28 AM

Thanks for all of the useful research info. Needless to say I'm overwhelmed, which isn't surprising since I'm 38 years old and still fighting acne. So do you think a supplement rich in linoleic acid such as borage seed oil might be helpful?

#8 alternativista

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Posted 17 April 2012 - 10:48 AM

Thanks for all of the useful research info. Needless to say I'm overwhelmed, which isn't surprising since I'm 38 years old and still fighting acne. So do you think a supplement rich in linoleic acid such as borage seed oil might be helpful?



A lot of people have claimed improvement with supplements. But we might not, and likely don't have a dietary or systemic deficiency. Most people get too much omega 6. I think the issue is entirely in our skin and topical application is the way to go. I'm trying to find info on why we our skin/sebum is deficient.

Unless you have an issue metabolizing fats, in which case you should look into lipase and pancreatic health and possibly take lipase supplements.

--------------------------------
On the involvement of enzyme stearoyl-CoA desaturase 1 (SCD1) and retinol metabolism

http://www.ncbi.nlm....les/PMC2835892/

Constituents of the lipid metabolism have been shown to be important for sebaceous gland morphogenesis. Targeted deletion of stearoyl-CoA desaturase 1 (SCD1) or mutations within the gene coding for this key enzyme of mammalian lipid metabolism (asebia mouse) result in atrophy of sebaceous glands of the skin and Meibomian glands of the eyelid as well as abnormal hair growth.6,3335 SCD1 converts saturated fatty acids into monounsaturated fatty acids using palmitoyl- and stearoyl-CoA as preferred substrates to generate palmitoleic (Δ9-16:1) and oleic acid (Δ9-18:1), respectively. Both are essential components of triglycerides and more complex lipids found in lipoproteins and eukaryotic membranes. Interestingly, SCD1 deficiency leads to disruption of the epidermal lipid barrier most likely caused by the strong reduction of epidermis-specific ceramides, one of the crucial lipid fraction in mammalian skin.6The dramatic phenotype seen in SCD1 mutants highlights the importance of unsaturated fatty acids for sebaceous gland formation and functional skin barrier. Furthermore, the SCD1 mouse mutants are representative for the interdependence of hair follicle structures and sebaceous glands. Particularly, it has been observed that damaging one of the two organs results in disturbance of homeostasis of the other one. In the future, it will be important to analyse crucial signals responsible for this tight interaction between hair follicle and sebaceous gland and their mutual dependence for tissue homeostasis.
Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor family and emerged as important mediators of the lipid metabolism in adipocytes but also in sebaceous glands.5,36 Analysis of mutant mice chimeric for PPARγ expression revealed that PPARγ is required for proper sebaceous gland differentiation.37 A set of different in vitro studies demonstrated the important function of PPARs for cell differentiation, lipid synthesis and fatty acid uptake into the cells.5,36 Additionally, like SCD1, PPARs have also been implicated in the regulation of keratinocyte differentiation and the formation of a functional skin barrier.38,39 These interesting results provoke the speculation that the effects observed following PPAR activation are accomplished in close coordination between PPARs and signalling pathways known to be important for regulating skin development and epidermal homeostasis.





I'm just posting this because it's a summary of factors in acne pathogenesis. Though it's not really relevant to this thread, notice how it says estrogens & thyroid hormone influence sebaceous gland activity:



Acne and sebaceous gland function.


 

Zouboulis CC.



Source

Department of Dermatology, Charité University Medicine Berlin, Campus Benjamin Franklin, Fabeckstrasse 60-62, 14195 Berlin, Germany. christos.zouboulis@charite.de



Abstract

The embryologic development of the human sebaceous gland is closely related to the differentiation of the hair follicle and the epidermis. The number of sebaceous glands remains approximately the same throughout life, whereas their size tends to increase with age. The development and function of the sebaceous gland in the fetal and neonatal periods appear to be regulated by maternal androgens and by endogenous steroid synthesis, as well as by other morphogens. The most apparent function of the glands is to excrete sebum. A strong increase in sebum excretion occurs a few hours after birth; this peaks during the first week and slowly subsides thereafter. A new rise takes place at about age 9 years with adrenarche and continues up to age 17 years, when the adult level is reached. The sebaceous gland is an important formation site of active androgens. Androgens are well known for their effects on sebum excretion, whereas terminal sebocyte differentiation is assisted by peroxisome proliferator-activated receptor ligands. Estrogens, glucocorticoids, and prolactin also influence sebaceous gland function. In addition, stress-sensing cutaneous signals lead to the production and release of corticotrophin-releasing hormone from dermal nerves and sebocytes with subsequent dose-dependent regulation of sebaceous nonpolar lipids. Among other lipid fractions, sebaceous glands have been shown to synthesize considerable amounts of free fatty acids without exogenous influence. Sebaceous lipids are responsible for the three-dimensional skin surface lipid organization. Contributing to the integrity of the skin barrier. They also exhibit strong innate antimicrobial activity, transport antioxidants to the skin surface, and express proinflammatory and anti-inflammatory properties. Acne in childhood has been suggested to be strongly associated with the development of severe acne during adolescence. Increased sebum excretion is a major factor in the pathophysiology of acne vulgaris. Other sebaceous gland functions are also associated with the development of acne, including sebaceous proinflammatory lipids; different cytokines produced locally; periglandular peptides and neuropeptides, such as corticotrophin-releasing hormone, which is produced by sebocytes; and substance P, which is expressed in the nerve endings at the vicinity of healthy-looking glands of acne patients. Current data indicate that acne vulgaris may be a primary inflammatory disease. Future drugs developed to treat acne not only should reduce sebum production and Propionibacterium acnes populations, but also should be targeted to reduce proinflammatory lipids in sebum, down-regulate proinflammatory signals in the pilosebaceous unit, and inhibit leukotriene B(4)-induced accumulation of inflammatory cells. They should also influence peroxisome proliferator-activated receptor regulation. Isotretinoin is still the most active available drug for the treatment of severe acne.

http://www.ncbi.nlm....pubmed/15556719




Metabolic changes in skin caused by Scd1 deficiency: a focus on retinol metabolism.
 

Flowers MT, Paton CM, O'Byrne SM, Schiesser K, Dawson JA, Blaner WS, Kendziorski C, Ntambi JM.



Source

Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, United States of America. mflowers@biochem.wisc.edu



Abstract

We previously reported that mice with skin-specific deletion of stearoyl-CoA desaturase-1 (Scd1) recapitulated the skin phenotype and hypermetabolism observed in mice with a whole-body deletion of Scd1. In this study, we first performed a diet-induced obesity experiment at thermoneutral temperature (33°C) and found that skin-specific Scd1 knockout (SKO) mice still remain resistant to obesity. To elucidate the metabolic changes in the skin that contribute to the obesity resistance and skin phenotype, we performed microarray analysis of skin gene expression in male SKO and control mice fed a standard rodent diet. We identified an extraordinary number of differentially expressed genes that support the previously documented histological observations of sebaceous gland hypoplasia, inflammation and epidermal hyperplasia in SKO mice. Additionally, transcript levels were reduced in skin of SKO mice for genes involved in fatty acid synthesis, elongation and desaturation, which may be attributed to decreased abundance of key transcription factors including SREBP1c, ChREBP and LXRα. Conversely, genes involved in cholesterol synthesis were increased, suggesting an imbalance between skin fatty acid and cholesterol synthesis. Unexpectedly, we observed a robust elevation in skin retinol, retinoic acid and retinoic acid-induced genes in SKO mice. Furthermore, SEB-1 sebocytes treated with retinol and SCD inhibitor also display an elevation in retinoic acid-induced genes. These results highlight the importance of monounsaturated fatty acid synthesis for maintaining retinol homeostasis and point to disturbed retinol metabolism as a novel contributor to the Scd1 deficiency-induced skin phenotype.


http://www.ncbi.nlm....pubmed/21573029



The role of stearoyl-CoA desaturase in obesity, insulin resistance, and inflammation.
 

Sampath H, Ntambi JM.



Source

Center for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, Portland, Oregon, USA.



Abstract

Stearoyl-CoA desaturase 1 (SCD1) is an essential lipogenic enzyme that has been shown to play an intrinsic role in the development of obesity and related conditions, such as insulin resistance. Through the generation of various mouse models of SCD1 deficiency, we have come to understand that SCD1 plays a role, directly or indirectly, in diverse metabolic processes, including lipogenesis, fatty acid oxidation, insulin signaling, thermogenesis, and inflammation. This review will address recent advances in our understanding of this key regulator of cellular metabolic processes, including the role of SCD1 in maintaining skin barrier integrity and the role of skin SCD1 in the metabolic phenotype elicited by global SCD1 deficiency. http://www.ncbi.nlm....pubmed/22211892


Edited by alternativista, 22 April 2014 - 10:42 AM.


#9 alternativista

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Posted 17 April 2012 - 11:14 AM

The dog is much, much better already, in case anyone is interested. I'd already been applying my olive oil with a little grape seed that I use in my skin before starting this and then i went out and bought the safflower oil Sunday, I think. He scratches much less. Any sores he scratched are healed and he has fewer fleas. He had always stopped to roll around in an asphalt parking lot we pass through. It looked like he enjoyed it a great deal, apparently because it felt so good to scratch his itchy skin. And now he doesn't do it anymore.

I've also given him some orally as he's willing to lick it out of a dish.

He'd been given Advantage Multi, a spot on flea and heartworm preventative at the first of the month, btw. But still suffered from fleas even though I was also combing him daily (finding dozens each time) and changing his bedding daily, spraying him with herbal repellents, mopping the floor. I don't have carpet for them to live in.

#10 dejaclairevoyant

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Posted 17 April 2012 - 11:15 AM

Interesting you mentioned grapeseed oil, I've been doing the "oil cleansing method" with grapeseed oil and castor oil mixed and it's doing great things for my skin!

#11 alternativista

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Posted 17 April 2012 - 11:28 AM

Interesting you mentioned grapeseed oil, I've been doing the "oil cleansing method" with grapeseed oil and castor oil mixed and it's doing great things for my skin!


Yeah and it has a lot of anti-oxidant nutrients. I would prefer it, but I didn't want to compound my dog's problems with something that has a remote possibility that it's toxic to him. And safflower has a bit more linoleic acid. It's nearly 80%.

These oils aren't stable though and should be stored in the refrigerator. Get a small, preferably dark colored bottle to keep a small amount at a time in your medicine cabinet.

Edited by alternativista, 17 April 2012 - 12:34 PM.


#12 alternativista

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Posted 17 April 2012 - 12:32 PM

Her's a lot about the metabolism of PUFAs in the skin and the enzymes involved, but in normal skin.

Metabolism of polyunsaturated fatty acids by skin epidermal enzymes: generation of antiinflammatory and antiproliferative metabolites.

In the skin epidermis, the metabolism of polyunsaturated fatty acids (PUFAs) is highly active. Dietary deficiency of linoleic acid (LA), the major 18-carbon n-6 PUFA in normal epidermis, results in a characteristic scaly skin disorder and excessive epidermal water loss. Because of the inability of normal skin epidermis to desaturate LA to gamma-linolenic acid, it is transformed by epidermal 15-lipoxygenase to mainly 13-hydroxyoctadecadienoic acid, which functionally exerts antiproliferative properties in the tissue. In contrast, compared with LA, arachidonic acid (AA) is a relatively minor 20-carbon n-6 PUFA in the skin and is metabolized via the cyclooxygenase pathway, predominantly to the prostaglandins E(2), F(2)(alpha), and D(2). AA is also metabolized via the 15-lipoxygenase pathway, predominantly to 15-hydroxyeicosatetraenoic acid. At low concentrations, the prostaglandins function to modulate normal skin physiologic processes, whereas at high concentrations they induce inflammatory processes. PUFAs derived from other dietary oils are also transformed mainly into monohydroxy fatty acids. For instance, epidermal 15-lipoxygenase transforms dihomo-gamma-linolenic acid (20:3n-6) to 15-hydroxyeicosatrienoic acid, eicosapentaenoic acid (20:5n-3) to 15-hydroxyeicosapentaenoic acid, and docosahexaenoic acid (22:6n-3) to 17-hydroxydocosahexaenoic acid, respectively. These monohydroxy acids exhibit antiinflammatory properties in vitro. Thus, supplementation of diets with appropriate purified vegetable oils, fish oil, or both may generate local cutaneous antiinflammatory and antiproliferative metabolites which could serve as less toxic in vivo monotherapies or as adjuncts to standard therapeutic regimens for the management of inflammatory skin disorders.





Enzymes involved in the biosynthesis of leukotriene B4 and prostaglandin E2 are active in sebaceous glands.

The expression of enzymes involved in leukotriene and prostaglandin signalling pathways, of interleukins 6 and 8 and of peroxisome proliferator-activated receptors in sebaceous glands of acne-involved facial skin was compared with those of non-involved skin of acne patients and of healthy individuals. Moreover, 5-lipoxygenase and leukotriene A(4) hydrolase were expressed at mRNA and protein levels in vivo and in SZ95 sebocytes in vitro (leukotriene A(4) hydrolase > 5-lipoxygenase), while 15-lipoxygenase-1 was only detected in cultured sebocytes. Cyclooxygenase-1 and cyclooxygenase-2 were also present. Peroxisome proliferator-activated receptors were constitutively expressed. Enhanced 5-lipoxygenase, cyclooxygenase 2 and interleukin 6 expression was detected in acne-involved facial skin. Arachidonic acid stimulated leukotriene B(4) and interleukin 6 release as well as prostaglandin E(2) biosynthesis in SZ95 sebocytes, induced abundant increase in neutral lipids and down-regulated peroxisome proliferator-activated receptor-alpha, but not receptor-gamma1 mRNA levels, which were the predominant peroxisome proliferator-activated receptor isotypes in SZ95 sebocytes. In conclusion, human sebocytes possess the enzyme machinery for functional leukotriene and prostaglandin pathways. A comprehensive link between inflammation and sebaceous lipid synthesis is provided.


http://www.ncbi.nlm....pubmed/16388388


lipoxygenase and lipoxygenase inhibitors

A lipoxygenase with dual positional specificity is expressed in olives (Olea europaea L.) during ripening. http://www.ncbi.nlm....pubmed/19268561

Doesn't say anything about skin or acne, but maybe olive oil has the enzymes needed for normal metabolism. Or it looks like maybe we don't it.
I keep coming across a study on a lipozygenase inhibitor as a novel approach to acne treatment, but there's no text whatsoever. It's about Zileuton which is a treatment for asthma that inhibits leukotriene formation. A healthboards member posted this:

"lipoxygenase inhibitors. It appears that Zyflo (aka Zileuton) is one such inhibitor. A [font=inherit !important][font=inherit !important]herbal [/font][font=inherit !important]alternative[/font][/font][font=verdana, geneva, lucida,] for those without medical insurance (i.e. me) is Boswellia. I have seen several articles and posts where people have noted a significant decrease in sebum production and [/font][font=inherit !important][font=inherit !important]inflammation[/font][/font][font=verdana, geneva, lucida,]. "[/font]

Inhibition of PPAR-mediated keratinocyte differentiation by lipoxygenase inhibitors
Full paper: http://www.biochemj..../BJ20020377.pdf

[font=arial, helvetica, clean, sans-serif][/font]

[font=sans-serif]LA is a [/font]polyunsaturatedfatty acid[font=sans-serif] used in the biosynthesis of [/font]arachidonic acid[font=sans-serif] (AA) and thus some [/font]prostaglandins[font=sans-serif].[/font]
[font=sans-serif]The first step in the metabolism of LA is performed by [/font]Δ6desaturase[font=sans-serif], which converts LA into[/font]gamma-linolenic acid[font=sans-serif] (GLA).[/font]
[font=sans-serif]GLA is converted to [/font]Dihomo-gamma-linolenic acid[font=sans-serif] (DGLA), which in turn is converted to arachidonic acid (AA). One of the possible fates of AA is to be transformed into a group of metabolites called [/font]eicosanoids[font=sans-serif], a class of [/font]paracrine hormones[font=sans-serif]. The three types of eicosanoids are prostaglandins, thromboxanes, and leukotrienes. Eicosanoids produced from AA tend to be inflammatory.[/font][11]

From wikipedia

[font=sans-serif]This says that AA can't be synthesized in the epidermis because it lacks the enzymes: [/font]http://books.google...... skin&f=false

http://www.dermavidu...nd-outside.html

[font=arial, helvetica, geneva, sans-serif]Thus, with the help of enzymes the body - not our skin however - converts part of the linoleic acid assimilated with nutrition into gamma linolenic acid (GLA) which is a triunsaturated omega-6 fatty acid and among others can be found in primrose oil, borage oil and in the seed oil of black currants. Neurodermatitis patients sometimes suffer from an enzyme defect which prevents the formation of GLA as well as of secondary substances essential for the body and the physiology of the skin. Consequently, products of the above mentioned oils may be very helpful for internal and external use.[/font]
[font=arial, helvetica, geneva, sans-serif]Within the skin, linoleic acid either is integrated into ceramide I which is skin barrier active or it will be oxidized through enzymes to a fatty acid with anti-prolific effect. Through chain extension the GLA converts into dihomo-gamma-linolenic acid (DGL) and subsequently to the triunsaturated arachidonic acid (AA). Inter alia, arachidonic acid is intermediately stored in epidermal phospholipids and there it comes up to 9 % of the fatty acid percentage. Arachidonic acid is the vital base material for many of the tissue hormones with regulatory functions which are effective already in microscopic amounts right in situ of formation with various specific features. Just to mention a few examples:[/font]

  • Prostacyclins are anticoagulants
  • Thromboxanes are coagulants and support the closure of wounds
  • Prostaglandins play a major role in inflammations among others also in the skin
  • Leukotriens are responsible for immune responses and control allergic reactions for example
[font=arial, helvetica, geneva, sans-serif]DGL also forms a prostacyclin which has tissue-specific effects, thromboxanes, prosta­glandins ("series 1"), with various compositions and effects which however widely differ from the products developed from arachidonic acid ("series 2"). They may even prove to be opposing and competing. Hence the prosta­glandin E2(from arachidonic acid) promotes inflammations whereas the prostaglandin E1 (from DGL) will prevent them. As arachidonic acid is found in egg yolk and lard in concentrations from 0.3 % and 1.7 % respectively and high doses of linoleic acid prevent the natural formation of arachidonic acid, it is obvious that an adequate adjustment of the nutrition to appropriate vegetable oils may have a positive influence on various different skin problems.[/font]


the non-steroidal anti-inflammatory drugs (NSAIDs; antirheumatic drugs) like aspirin interfere with the complicated fatty acid metabolism via enzyme in­hibition it is recommended to take into account any possible side effects of medication.
By means of the enzyme phospholipase A2, arachidonic acid is released from phospho­lipids. Prescriptions containing cortisone act as enzyme inhibitors and thus will prevent the formation of arachidonic acid metabolites which support inflammations. Any inflammatory processes in the skin can thus be treated immediately and also very effectively. The other side of the coin is, however, that the skin will develop deficiencies in the supply of other important fatty acids, a fact that will consequently result in atrophic skin.


Edited by alternativista, 30 April 2012 - 08:56 AM.


#13 alternativista

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Posted 17 April 2012 - 03:15 PM

All about Fatty Acids:

The ABC of fatty acids
http://www.dermavidu...atty-acids.html

Things are different on and in the skin
The situation is rathe r different, though, if essential fatty acids aren't assimilated via daily nutrition but via skin surface. In case of topically applied oils, the fatty acids are released by epidermal ester-cleaving lipases or through hydrolysis (reaction with water) which is further intensified by humidity and heat. Unlike other body cells and above all the universally acting liver cells, only very few of the major metabolites will form. Linoleic acid, alpha and gamma-linolenic acid are used without modification of their fatty acid chain or alternatively oxidized by epidermal 15-lipoxygenase (15-LOX) into unsaturated hydroxy fatty acids with anti-inflammatory characteristics. In particular, the following processes are significant:


  • Linoleic acid is a substrate for ceramide I into which it is integrated without modifying the fatty acid chain. This process is beneficial for the recovery of the skin barrier.

  • 15-LOX at first peroxides linoleic acid into 13-hydroperoxy-9,11-octadecadienoic acid (13-HPODE) which then is immediately reduced into the anti-inflammatory 13-hydroxy-9,11-octadecadienoic acid (13-HODE).

  • Analogous to this process is the reaction of 15-LOX with gamma-linolenic acid from which the anti-inflammatory 13-hydroxy-6,9,11-octadecatrienoic acid (13-HOTrEg) is formed via hydroperoxy-6,9,11-octadecatrienoic acid (13-HOTrEg).

  • Alpha-linolenic acid is transformed by 15-LOX via 13-hydroperoxy-9,11,15-octadecatrienoic acid (13-HPOTrE) into 13-hydroxy-9,11,15-octadecatrienoic acid (13-HOTrE). This explains the strong anti-inflammatory effect of linseed oil which formerly used to be a component of bandages. Today it is used as watery nanoparticle dispersion.

Essential fatty acids and appropriate vegetable oils can be successfully used for the skin care of inflammatory skin conditions like neurodermatitis and psoriasis.
It is assumed that the excellent efficacy of linoleic acid for acne conditions can be ascribed to the anti-inflammatory 13-HODE, the formation of linoleic acid containing ceramide I (heals cornification disorders) as well as the liquefied sebum.



This is a good paper: E s s e n t i a l Fatty Acids & the Skin http://www.biorigina...les/file_42.pdf

Patients suffering from skin disorders have been found to have abnormal levels of EFAs. The evidence is consistent with a reduced rate of conversion of dietary EFAs to metabolites due to reduced activity of the delta-6-desaturase (D6D) enzyme.1 T


And we all might be interested in knowing that: linoleic acid and other PUFAs reduce hyperpigmentation, especially that caused by UV.

------------
In this study on piglets injected with linoleic acid, they found that linoleate may be rapidly redistributed throughout
the viable epidermis after initial uptake. And yes, two piglets were harmed for this study. http://www.jlr.org/c...0/1839.full.pdf

#14 alternativista

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Posted 19 April 2012 - 09:31 AM

Bump. see the first post. I've added a lot to the Key points listing the many, many ways linoleic is important for skin health and the many ways the lack of it contributes to acne formation.

Also:Researchers have found that many insects expel odors when they die to repel other members of their species from the area. Major components of these odors include linoleic and oleic acid. The articles I found named several critters like cockroaches, but not these biting insects. Other than one article about a relative of the mosquito that's a major pest in the Scottish Highlands. But that article only talked about researching the 'death scent' without naming anything.

#15 joe93

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Posted 19 April 2012 - 01:18 PM

Wow, you did a lot of research. Is there a specific brand and way to use linoleic acid that you recomend?

#16 alternativista

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Posted 19 April 2012 - 02:32 PM

Wow, you did a lot of research. Is there a specific brand and way to use linoleic acid that you recomend?


It should come in a dark bottle. And probably isn't found in your average supermarket. I buy a brand from California called Napa something that produces the olive oil I use and annoyingly packaged like wine with a cork. If they make a quality olive oil, there other products are probably good too.

You could oil cleanse and/or use it as a moisturizer. Apply to wet skin or with wet fingers to apply it thinly. And it should be stored in the refrigerator.

#17 FSAS

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Posted 19 April 2012 - 11:54 PM

wow long read, thankyou so much for the info !

I'm really interested in linoleic acid. what would your suggestion be? I think I have seen pills but I assume as you mentioned stafflower might be the way to go. topically or internally? :)
thanks

#18 alternativista

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Posted 20 April 2012 - 07:32 AM

wow long read, thankyou so much for the info !

I'm really interested in linoleic acid. what would your suggestion be? I think I have seen pills but I assume as you mentioned stafflower might be the way to go. topically or internally? :)
thanks


Topically. And I think grapeseed has more benefits. I only chose safflower to be safer for my dog

#19 Bruno C

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Posted 20 April 2012 - 12:16 PM

checking on weekpedia about grapeseed oil, I found that it has 4% of Stearic Acid, which is 2 in comedogenic rate. (According to http://www.zerozits..../acnedetect.htm)


Has anyone tried it?
I'm sorta affraid of changing my finacea to this and having a massive breakout =/

#20 alternativista

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Posted 20 April 2012 - 01:03 PM

checking on weekpedia about grapeseed oil, I found that it has 4% of Stearic Acid, which is 2 in comedogenic rate. (According to http://www.zerozits..../acnedetect.htm)


Has anyone tried it?
I'm sorta affraid of changing my finacea to this and having a massive breakout =/


so, it has a tiny percentage of a very mildly comedonegenic substance? Up to you. Safflower rates 0 on both [ comedonegenicity and irritancy according to that chart, if you want a safer choice.

Grapeseed has never bothered my skin, but neither does coconut or olive oil. I've never noticed anything topical breaking me out. Someone else posted above that she's been using it.




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