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Dan

Made a new page on acne.org

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http://www.acne.org/mightalsohelp.html

I am very reluctant to post any info on glycolic acid and omega-3s on this page because there are no studies backing them up, and I very well may take the information down, but I wanted to put this stuff out there anyway. I have not posted anything on acne.org in the past 10 years or so that doesn't have scientific studies backing it up, but since I don't see any studies on the horizon for glycolic acid or omega-3s and since I've personally seen glycolic acid work on people and since Omega-3s are rated so well, I'm breaking my rule.

Are there any other remedies you guys know about that a concensus of people claim helps acne and can be used in conjunction with the Clear Skin Regimen that I should add to the page? Perhaps I can make a separate part of the mightalsohelp.html page for unstudied but potentially helpful remedies.

Thanks,

Dan

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You can find both flaxseed and fish oil in pill form at most drugstores.

You might want to change this sentence because flax and fish oils in pills at a drugstore are mostly likely going to be rancid/oxidized, and taking rancid/oxidized oils does a lot of harm (maybe to the skin, and to one's health in general).

http://www.jeancarper.com/newsflash/1600

The best thing to do is buy a bottle of fish oil that is nitrogen-flushed and has added antioxidants.

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You can find both flaxseed and fish oil in pill form at most drugstores.

You might want to change this sentence because flax and fish oils in pills at a drugstore are mostly likely going to be rancid/oxidized, and taking rancid/oxidized oils does a lot of harm (maybe to the skin, and to one's health in general).

http://www.jeancarper.com/newsflash/1600

The best thing to do is buy a bottle of fish oil that is nitrogen-flushed and has added antioxidants.

I second what leah says.

You could show scientifically how omega-3's turn into less inflammitory leukotrines and Prostaglandins and how omega-6's turn to more inflamitory leukotriens and prostglanelnins (i can't spell for shit) via the AA cascade but you'd be hard pressed to find some form of subjective proof that acne is an inflamitory disease, personally i think omega-3's help but only if they're reet out of wack to start with, IMO excercise (aerobic) is far more effective for a much wider spectrum of people, it has tonnes of health benefits, many of which help lessen acne, you could add in white/green tea, stress, insulin management...

maybe you could make a pseudo science page and put in H202, candida, sequential eating, liver flushing Chinesse foot patches... just joking.

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Yeah, definitely include something about stress and low glycemic foods, SweetJade can get at you with plenty of science behind the low-glycemic connection / insulin sensitivity.

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I think the liver flushing is one of the widly accepted treatments aswell.

As is all detoxing. I dont know about scientific backup tho.

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^ ^ ^ While those have plenty of anecdotal evidence there's no science behind it so I don't think Dan would be down with that.

I myself have been seeing help with probiotics and liver flushing... Can't say that the latter has any scientific merit beyond theories, hypothesises, and anecdotes though.

Wouldn't it be nice if a scientist would actually devise a controlled study for it? There'd be nothing to profit off though... We can dream.

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Are there any other remedies you guys know about that a concensus of people claim helps acne and can be used in conjunction with the Clear Skin Regimen that I should add to the page? Perhaps I can make a separate part of the mightalsohelp.html page for unstudied but potentially helpful remedies.

Mandelic acid?

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I second what leah says.

You could show scientifically how omega-3's turn into less inflammitory leukotrines and Prostaglandins and how omega-6's turn to more inflamitory leukotriens and prostglanelnins (i can't spell for shit) via the AA cascade but you'd be hard pressed to find some form of subjective proof that acne is an inflamitory disease, personally i think omega-3's help but only if they're reet out of wack to start with, IMO excercise (aerobic) is far more effective for a much wider spectrum of people, it has tonnes of health benefits, many of which help lessen acne, you could add in white/green tea, stress, insulin management...

maybe you could make a pseudo science page and put in H202, candida, sequential eating, liver flushing Chinesse foot patches... just joking.

In reference to the bolded areas above, Melbourne actually wrote something that while people have read it, not many have felt compelled to respond to. http://www.acne.org/messageboard/index.php?showtopic=100399 The boy who cried wolf syndrome may be at play here and it's unfortunate because it's definately among his better articles! Anyway, this was part of my comment regarding what he posted (with addition of extra abstracts):

From reading these scientific articles I've noticed that antibiotics work to kill certain types of inflammation,

Initiated to clog the pores and then to kill the inflammation caused by overgrown TRAPPED bacteria,

which is why it's prescribed for acne, except these SAME sources of inflammation can be inhibited or prevented, in acne sufferers, by using:

* Anti-fungals (and they don't kill p.acnes)

* Anti-parasitics

* NAC

* ALA

* Green, White, Red Tea

* Boswellia

* among other HIGH powered antioxidants

These supplements, which are usually antioxidants, can multitask by lowering our testosterone levels, our IGF-1 levels, and boosting our Glutathione Levels, or SOD levels, and our PGE1 Anti-inflammatory Prostaglandins, among other things.

So it's interesting because chronic inflammation can cause biochemical imbalances and those biochemical imbalances can cause (further) inflammation...Hmm :think:

When I speak of inflammation, with regards to acne sufferers, I'm referring to biomolecules such as:

* Histamine

* Free Radicals

* ROS - Reactive Oxygen Species

* PGE2- Proinflammatory Prostaglandins

* Leukotriene B4

* Cytokines (Interleukines 1 - 12a/b sometimes, TNF-a/Tumor Necrosis Factor-a, etc)

* NO - Nitric Oxide

* Peroxide (from lysed PMN/Polymorphonuclear leukocytes (white blood cells/neutrophils))

* Lactic Acid

* PPAR beta/delta - Peroxisome Proliferator Activated Receptors beta/delta

* Substance P

etc...

For example:

Skinmed. 2003 Jul-Aug;2(4):222-8. Related Articles, Links

Assessment of etiologic agents in acne pathogenesis.

Burkhart CN, Gottwald L.

The Department of Microbiology, Medical College of Ohio at Toledo, Toledo, OH 43623, USA. [email protected]

Acne is a chronic inflammatory disease of the pilosebaceous units. Traditional etiologic factors include increased sebum production, ductal hyperkeratosis, abnormality of the microbial flora within the pilosebaceous unit, and mediators of inflammation. Recent developments do not refute these familial elements, but rather refine particular aspects. Interleukin-1a influences hypercornificationof the infundibulum as well as the inflammatory responseby inducing the production of vascular endothelial growth factor in dermal papilla cells and follicular keratinocytes of the pilosebaceous unit. New retinoids have been developed based on controlling cellular proliferation and differentiation in the pilosebaceous unit by their action on nuclear receptors of cells. Dermal inflammation is not due to presence of bacteria, but from biologically active mediators produced by Propionibacterium acnes. The environment within the pilosebaceous unit is probably more important than the absolute number of P. acnes organisms. Indeed, the major role of the sebaceous gland appears to be supplying P. acnes needed nutrients. Moreover, the microbiologic principle of biofilms appears to be applicable to P. acnes in acne.

Publication Types:

Review

PMID: 14673275

(Thankfully further studies refine THIS study as well)

Rev Med Chir Soc Med Nat Iasi. 2004 Apr-Jun;108(2):319-24. Related Articles, Links

[immunohistochemical evidence of chronic inflammation in acne vulgaris]

[Article in Romanian]

Branisteanu D, Cianga C, Cianga P, Petrescu Z, Carasevici E.

Universitatea de Medicina si Farmacie Gr.T. Popa Iasi, Facultatea de Medicina, Clinica Dermatologica.

The etiology and pathogenesis of acne vulgaris are not yet completely understood. Therefore we have investigated 5 patients with different clinical forms of disease, including therare form of acne fulminans. Taking into consideration the four factors that are currently incriminated in the development of acne, sebaceous hypersecretion, hyperkeratosis of the pilosebaceous infundibulum, bacterial colonisation and perifollicular inflammation, we have focused our study on a set of cells involved in the chronic inflammatory process. We have evidenced by immunohistochemistry methods, using appropriate monoclonal antibodies, the presence of T lymphocytes and macrophages, while the B cells could be evidenced only in the severe forms. We were also interested to investigate the occurrence of new capillary formation, as an accompanying phenomenon of the inflammatory process. The presence and histological distribution of these cells highly supports the hypothesis that the mechanisms underlying the development of acne vulgaris belong to the Delayed Type Hypersensitivity.

PMID: 15688807 http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

(This was one I had been looking to post again for awhile and I thought they had removed this article! This is a Type IV Hypersensitivity Reaction and was a key part of my arguement for WHY, sometimes, there's such a huge variance among the anti-inflammatory/anti-acne diets.)

Acta Dermatovenerol Alp Panonica Adriat. 2005 Jun;14(2):39-42. Related Articles, Links

Superoxide dismutase and myeloperoxidase activities in polymorphonuclear leukocytes in acne vulgaris.

Kurutas EB, Arican O, Sasmaz S.

KSU Medical Faculty, Department of Biochemistry, TR-46000 Kahramanmaras, Turkey.

BACKGROUND AND DESIGN: Acne vulgaris frequently occurs in the second decade of life. The pathogenesis of the disease is multifactorial and in the present study, we aimed to investigate the role of reactive oxygen species in the inflammation of acne by determining the activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) in polymorphonuclear leukocytes (PMN).

MATERIALS AND METHODS: Forty-three patients with acne vulgaris and 24 healthy controls were enrolled. The severity of the acne was categorized from mild (subjects with only comedonic lesions) to severe (subjects with nodulocystic lesions). SOD and MPO activities in PMN were measured spectrophotometrically.

RESULTS: There was no significant difference in the activity of MPO between the patients and controls.However, SOD activity in PMN was significantly lower in the patientsthan in the controls (p<0.001). Nocorrelation was detected between the activities of enzymes and the severity of the disease.

CONCLUSION: Propionibacterium acnes may not play a primary role in the pathogenesis of acne as a bacterium. However, the low activity of SOD in PMN may be responsible for the increased levels of superoxide anion radicals in the epidermis. New anti-acne drugs should include substances with lymphocyte stimulating and anti-oxidative properties.

PMID: 16001098 [PubMed - indexed for MEDLINE]

http://www.mf.uni-lj.si/acta-apa/acta-apa-05-2/1.pdf (full text)

And excerpts from "What is the pathogenesis for acne?"

Zouboulis CC, Eady A, Philpott M, Goldsmith LA, Orfanos C, Cunliffe WC

Rosenfield R. What is the pathogenesis of acne?

Exp Dermatol 2005: 14: 143–152. # Blackwell Munksgaard, 2005

Abstract: For a long time, the mantra of acne pathogenesis debates has been that

acne vulgaris lesions develop when (supposedly largely androgen-mediated)

increased sebum production, ductal hypercornification, and propionibacteria come

together with local inflammatory process in the unlucky affected individual. And

yet, the exact sequence, precise interdependence, and choreography of pathogenic

events in acne, especially the ‘match that lights the fire’have remained surprisingly

unclear, despite the venerable tradition of acne research over the past century.

However, exciting recent progress in this – conceptually long somewhat stagnant, yet

clinically, psychologically, and socioeconomically highly relevant – everyday battlefield

of skin pathology encourages one to critically revisit conventional concepts of acne

pathogenesis. Also, this provides a good opportunity for defining more sharply key

open questions and intriguing acne characteritics whose underlying biological basis has

far too longremained uninvestigated, and to emphasize promising new acne research

avenues off-the-beaten-track – in the hope of promoting the corresponding

development of innovative strategies for acne management.

Inflammatory signalling is involved in the initiation

of acne lesions

Hyperproliferation of the follicular epithelium leads to formation

of microcomedones, which are the first acne lesions and

can be found in normal-looking skin (23). The sebaceous

follicle undergoes a cycling process which may explain a natural

resolution of microcomedones and also comedones and,

on a longer term, the resolution of the disease itself (24)

(Fig. 1). The very early stage of acne lesion development,

namely the beginning of microcomedones, is associated with

vascular endothelial-cell activation and involvement of inflammatory

events (25) which corroborates the suggestion that acne

may represent a genuine inflammatory disorder withoutinvolvement

of bacteria in its initiation(26).

Similar results have been reported by Ingham et al. (27) who found bioactive interleukin

(IL)-1a-like material in the majority of open acne comedones

from untreated acne patients. There was no correlation

between levels of any cytokine, in particular IL-1a, and the

numbers of follicular microorganisms. It seems that healthy

sebaceous glands also express various cytokines. In our laboratories,

we stressed sebocytes in vitro by maintaining them in

serum-free medium and detected IL-1a expression at the

mRNA and protein levels (28). Antilla et al. (29) showed that

IL-1 is present in normal sebaceous glands and Boehm et al.

(30) detected mRNA for IL-1a, IL-1b, and tumor necrosis

factor-a in normal sebaceous glands by in situ hybridization.

Interestingly, IL-1a induced hyperproliferation of follicular

keratinocytes in isolated sebaceous follicle infundibula maintained

ex vivo (31).

Which factors interrupt cycling of the sebaceous

follicle?

Overstimulation of the initiation of the preclinical inflammatory

process or defect negative feedback regulation may be major

reasons for the interruption of the normal cycling of the sebaceous

follicle and be responsible for the initiation of the clinical

inflammatory process in acne (Fig. 1). As mentioned above, hereditary

factors and excess androgen activity, e.g. in puberty, may

cause overstimulation, thus triggering sterileinflammatory phenomena

(Fig. 2). Neuroendocrinologic regulation and environmental

factors, such as dietary lipids and smoking, have also

been suggested to represent trigger mechanisms.

Role of neuropeptides for regulation of clinical

inflammation in acne

There is current evidence that regulatory neuropeptides with

hormonal and non-hormonal activity may control the development

of clinical inflammation in acne. Numerous substance P

immunoreactive nerve fibers were detected in close apposition to

the sebaceous glands, and expression of the substance P-inactivating

enzyme neutral endopeptidase was observed within sebaceous

germinative cells of acne patients (32). In vitro experiments

using an organ culture system demonstrated that substance P induced

expression of neutral endopeptidase in sebaceous glands

in a dose-dependent manner. On the other hand, treatment of

sebocytes with IL-1b which resulted in marked increase of IL-8

release (33) was partially blocked by co-incubation of the cells

with a-melanocyte-stimulating hormone in a dose-dependent

manner (34). Corticotrophin-releasing hormone induces the

synthesis of sebaceous lipids in vitro (33), and adrenocorticotropic

hormone evokes adrenal dehydroepiandrosterone [DHEA androgen] to regulate skin

inflammation (35). These current findings indicate that central

(36) or topical stress (33,37) may, indeed, influence the feedback

regulation, thus inducing the development of clinical inflammation

in early acne lesions.

Dietary lipids and inflammatory process in acne

Topically applied linoleic acid was shown to induce an almost

25% reduction in the overall size of microcomedones over a

1-month treatment period (38). On the other hand, arachidonic

acid, an essential, long-chain, pro-inflammatory o-6 fatty acid,

stimulates IL-8and IL-6synthesis in cultured human sebocytes

(39) and enhances synthesis of sebaceous lipids (21). Leukotriene

B4 inhibition in vivo reduces concomitantly pro-inflammatory

sebaceous fatty acids and inflammatory acne lesions (22). Inuit

Eskimos, the inhabitants of the Okinawa island and Chinese have

been observed to develop acne with the changing of their nutrition

habits (20,40,41). Westernized nutrition includes low

amounts of o-3-fatty acids and antioxidant vitamins and higher

amounts of the pro-inflammatory o-6 and trans-fatty acids. The

ratio o-6/o-3 fatty acids in westernized nutrition is 20 : 1, in

contrast to a 1 : 1 ratio in traditional nutrition (42).

Overall, the role of nutrition in acne still remains controversial. A

current study reported that the Kitavan islanders of Papua New

Guinea and the Ache hunter-gatherers of Paraguay do not present

acne (43), however, other authors suggested that these population

studies may have detected a genetic background rather than a nutritional

effect (44).

Smoking and acne

Smoking was currently reported to be a clinically important

contributor to acne prevalence and severity (45). Recent investigations

revealed that cigarette smoke contains high amounts of

arachidonic acid and polycyclic aromatic hydrocarbons which

induce a phospholipase A2-dependent inflammatory pathway

(46); this effect may further stimulate arachidonic acid synthesis

(37). On the other hand, smokers have a higher saturated fat

intake with their food and much lower polyunsaturated fat

intake, principally due to a lower linoleic acid intake compared

with nonsmokers (47).

Are Propionibacterium acnes (P. acnes) and tolllike

receptors involved in the initiation of acne

lesions?

Toll-like receptors 2 and 4 as well as CD14 are expressed in

human monocytes. Chemokine/cytokine synthesis in these cells

is induced through activation of Toll-like receptor 2 by P. acnes

(48). These findings in combination with the expression of active

Toll-like receptors 2 and 4 and of CD14 in human keratinocytes

(49) have implicated P. acnes and Toll-like receptors in acne

inflammation. However, P. acnes was unable to induce IL-1a

expression in human keratinocytes in vitro (50), therefore,

P. acnes seems to induce later events not being involved in

the initiation of acne lesions. The successful therapeutic

action of antibiotics in acne has been attributed to an antibacterial

activity but it may also be seen as a para-antibiotic,

anti-inflammatory effect.

Conclusion

Acne vulgaris is likely to be a genuine inflammatory disease with

androgens, PPAR ligands, regulatory neuropeptides, and environmental

factors being agents able to interruptthe natural

cycling of the sebaceous follicles and lead microcomedones to

form comedones and inflammatory lesions (Figs. 1 and 2). Proinflammatory

lipids and chemokines/cytokines seem to act as

mediators for the initiation of acne lesions. P. acnes is not initially

involved but may mediate later inflammatory events leading to

worsening of the lesions. This concept of acne pathogenesis may be controversially discussed,

however, it initiates a fruitful discussion for better understanding

this most common disease.

http://www.blackwellpublishing.com/dermato.../cont_feb05.pdf Full Text

(Funny Splenda/Sucralose is a Chlorinated/Halogenated Polycyclic Aromatic Hydrocarbon (LabGirl, True or False) and based on reports on this board as well as on the web, just as with Dioxin, it is capable of increasing acne in those prone and initiating acne in those not prone.)

Obviously P.acnes doesn't play a PRIMARY role in acne development, otherwise why the use of RetinA, Accutane, Spironolactone, other antiandrogens, anti-fungals, and Insulin Sensitizers (some are PPAR-gammas), etc???

Acne has been called an Inflammatory Skin Disease for decades. Furthermore, based on available articles, science and the medical community have known about some of these immunological events preceeding Type III and Type IV Hypersenstivity Reactions which initiate the inflammatory response found in the development of acne since the 1970s! Yet, for the most part, they never bothered to do anything beyond throwing overprescribed antibiotics our way as a quick way of dealing with our CHRONIC (silent & systemic) inflammation.

As a result, a percentage of us are worse off because of it either mentally (people still think it's about bacteria or sebum) or at least physically, thanks to the side effects of antibiotics. :naughty:

I'd also like add that this would apply to a host of other drugs or topicals used in the treatment of acne. Omega 3s are obviously anti-inflammatory. AHAs (Glycolic, Mandelic, etc) are anti-inflammatories. Salicylic Acid/BHA is an anti-inflammtory. Retinoids and Accutane are anti-inflammatories. Benzoyl Peroxide is an anti-inflammatory. Hydrocortisone and Glucocorticoids (to a point) are anti-inflammatory. Tylenol, Asprin, & Motrin which some members use (and SHOULDN'T) are anti-inflammatories. B5 Therapy...Anti-inflammatory..........

The list goes on, some do it directly and others indirectly by inhibiting or regulatingour ability, in some way, to make inflammatory products. Most of these drugs, topicals, supplements, and specialized diets have other abilities as well and due to this, or the fact that some have stronger anti-inflammatory properties, make certain "treatments" a better choice than other methods.

Peace :angel:

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Sweetjade I completely agree acne is an inflamitory disease (mainly becuase of what ive read in your posts :D ) its just i thought it would be hard to prove becuase of the traditional dogma about sebum/p.acnes etc... i was unaware that "real" evidence existed, i'll have a read of those studies but i suspect most of it will be too complicated for me. btw check your PM i sent you a message about a week ago.

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YES Sweet Jade ACNE IS AN INFLAMMATORY DISEASE.

i know this is a fact and I created this thread

http://www.acne.org/messageboard/index.php?showtopic=101083

Melbourne,

LOL, yup, I saw it. :) It's a shame your wisdom sometimes goes unnoticed! In fact some of those foods are actually incoropated in a few of these specific anti-acne diets (ex: nightshades are avoided in "Evil" Lectin Free diet) and of course, sometimes the foods can also be very much so based on individual sensitivities.

Take Care!

Sweetjade I completely agree acne is an inflamitory disease (mainly becuase of what ive read in your posts :D ) its just i thought it would be hard to prove becuase of the traditional dogma about sebum/p.acnes etc... i was unaware that "real" evidence existed, i'll have a read of those studies but i suspect most of it will be too complicated for me. btw check your PM i sent you a message about a week ago.

NotaDr,

Unfortunately, quite a few people are unaware that real evidence exists. In part it's because of how one may be doing their research or because they are looking for studies that specifically state that "acne is an inflammatory disease" or something of that nature. Well, now we have such studies! :D

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Good idea Dan,

I see you put Zinc at the top.

I would hate for readers / acne sufferers to rush out and buy Zinc and to take it improperly, it can lead to serious stomach aches if taken improperly. I would just add one line saying: "If you take any Zinc, take it with food!!"

If taken with food, you'll be perfectly fine, but without food, there have been many people, including myself that have found zinc produces stomach aches.

Also, I would recommend adding: Green tea to the list of things that help,

The medicinal action of androgens

And lemon water, freshly squeezed lemon juice mixed in a water bottle seems like a universal helper, it has helped me a lot, although it takes 2-3 days of drinking 1 water bottle per day to take effect. It stimulates liver function, improves digestion, cleans the digestive tract and prevents infections. Although I haven't found any medical studies on lemon juice.

- Personally the Omega 3/6/9 fat supplements break me out, I think I might be allergic to something in them, everytime I try them I break out more. This is not to say it doesn't belong on the page however.

Things that seem to surface in the holistic forum seem to be teas, flushes & detoxes, improving digestion and reducing stress (mental, when you're happy you get less acne & physical, moderate regular exercise relieves stress and improves digestion)

- Kaybee

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