Jump to content
Acne.org
Search In
Find results that contain...
Find results in...
Madworld

Anti-inflammatories are NOT for ACNE.

Recommended Posts

I've been pondering if anti-inflammatories, whether it's the topical cream you apply, the corticosteroid you inject, the oral medications you take or the foods you ingest are even the correct way to approach acne.

Now, the current model suggests that ACNE has causes, the hyperkeratinisation of the skin causing the build-up for dead-skin, enforcing the proliferation of P.acne bacteria. This initiate the inflammation cascade (which physically appears as acne spots) to kill the bacteria and remodel the skin.

So, inflammation is not the cause but rather the effector of the process.

The process of inflammation is complicated, but the part of the cycle involves the redness and swelling you get (i.e, acne) and tissue destruction and healing at the same time. The endpoint involves a termination of the inflammation cycle.

Now, anti-inflammatories, despite its name, do not completely stop but instead prolongs the natural cycle. As a result, you do notget the adequate and timely response to remove the cause(P.acnes bacteria) and although you may have prevented the physical manifestation (redness and swelling) you have prevented the body to eliminate the cause and also delaying the endpoint (thus the healing part). As long as the cause is there, there will always be a repeating cycle in attempts to eliminated it.

Also, since inflammation is contributed to not only tissue destruction and also healing, anti-inflammatories may retard the healing of existing acne. Redmarks anyone?

I'm not here to advocate a pro-inflammatory diet. I'm just feeling skeptical on the anti-inflammatory this and anti-inflammatory that that's been spewing around way too much in the internet.

What's useful is the same old dietary advices, just eat a regular diet, sleep plentiful, avoid stress, excerise and the let the body do its job and allow the quicker completion of the inflammatory cycles. No need for any strict, 'special'/'acne-free' diet.

Share this post


Link to post
Share on other sites

I'll go along, since we're both speculating.

I would distinguish between sub-clinical inflammation (pre-micro-comedo) and acute inflammation (acne).

The first one is very likely the trigger of hyper-keratinization, and it is poorly understood. An interplay of genetics, androgens, and sebocyte proliferation. Nothing really targets that, except isotretinoin to some extent, by modulating gene expression, and androgen suppression in women. It's like the first sign of the train wreck to come.

When acute inflammation comes to fore (lipase by-products of P. Acne inducing inflammation), one would be a self-flagellating not to intervene with a potent anti-inflammatory, be it antibiotic or corticosteroid or something else.

Since sub-clinical inflammation is by definition ... non-noticeable, anything visible is to be actively managed, or should I say contained. My POV.

Share this post


Link to post
Share on other sites
I'll go along, since we're both speculating.

I would distinguish between sub-clinical inflammation (pre-micro-comedo) and acute inflammation (acne).

The first one is very likely the trigger of hyper-keratinization, and it is poorly understood. An interplay of genetics, androgens, and sebocyte proliferation. Nothing really targets that, except isotretinoin to some extent, by modulating gene expression, and androgen suppression in women. It's like the first sign of the train wreck to come.

When acute inflammation comes to fore (lipase by-products of P. Acne inducing inflammation), one would be a self-flagellating not to intervene with a potent anti-inflammatory, be it antibiotic or corticosteroid or something else.

Since sub-clinical inflammation is by definition ... non-noticeable, anything visible is to be actively managed, or should I say contained. My POV.

Inflammation is a natural process to elicit pathogen control. Suppressing it will mount to more aggressive inflammatory responses as the P. Acne population is not controlled.

Share this post


Link to post
Share on other sites
Inflammation is a natural process to elicit pathogen control. Suppressing it will mount to more aggressive inflammatory responses as the P. Acne population is not controlled.

Your logic is backwards. Everyone has P. Acne on their skin, and the body doesn't react to it as to a pathogen. When acne develops, IT IS because P. Acne growth is not naturally controlled, due to finding rich feeding ground in trapped sebum. Remove/reduce sebum and acne subsides, at least in inflamed form.

Inflammatory acne is due to waste products of P. Acne metabolism. These waste products, among which is lipase, are highly inflammatory.

This is really basic stuff. I'm surprised it needs explaining. Where people get tripped up is that excess sebum does not automatically imply acne, and acne is not always a consequence of excess sebum.

Inflammatory acne is always associated with sebum though.

Share this post


Link to post
Share on other sites

No, P.Acnes is not the cause of acne.

I've been in situations where I have treated consistently and long enough, with powerful enough treatments, that there very clearly is not a single P.Acnes on my skin, but I still get spots. I've eradicated every last freaking one of them. And I still get spots, they're just a lot smaller and disappear a lot more quickly.

The deepest root cause that anyone know is poor shedding into the pore. It's not known what causes that, but when you get a blocked pore, P.Acnes makes it 4-5x worse, it grows out of control and causes massive inflammation, and produces enzymes that chew through the wall of the pore and then you get an infection with P.Acnes and other bacteria as well (staph, strep, molds, funghi etc. etc.).

It's also my experience that the inflammation tends to cause surrounding pores to grow poorly, and that can trigger nearby pores to block- a really ghastly cascade.

BUT P.Acnes IS NOT THE CAUSE.

Share this post


Link to post
Share on other sites

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 Ëœmatch 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.

Share this post


Link to post
Share on other sites

Hautarzt. 2008 May 18.

[Acne : Current pathophysiologic considerations.][Article in German]

Degitz K, Ochsendorf F.

Dermatologische Gemeinschaftspraxis, Pasinger Bahnhofsplatz1, 81241, München, Deutschland, [email protected]

Seborrhea, follicular hyperkeratosis, propionibacteria, and inflammatory reactions are the most important factors leading to acne. The combination of increased sebum producation and follicular hyperkeratosis facilitates an increased growth of Propionibacterium acnes. Its metabolic products lead to follicular inflammation and, in extreme cases, even to perifollicular abscesses. Sebum production is influenced by androgens, so that abnormalities in androgen levels can produce seborrhea and acne. Follicular hyperkeratosis may be triggered by a relative deficiency in linoleic acid, peroxides from sebum components, and especially by inflammatory mediators such as interleukin-1. Bacterial metabolic products such as lipases, proteases, or chemotactic factors lead to the perifollicular inflammation. This inflammation is not only a response to other pathogenetic factors, but also a cause of acne. An initial mild perifollicular infammation can induce comedogenesis via a variety of mediators. The influence of dietary factors on the initiation and course of acne has recently received increased recognition. A connection has been postulated between acne and a high nutrients with glycemic index, as well as with milk products. http://www.ncbi.nlm.nih.gov/pubmed/1848818...Pubmed_RVDocSum

Share this post


Link to post
Share on other sites

I'm totally in agreement with temp123 and SweetJade. Nowhere I claimed P.Acne is root cause, it just makes things 4-5x worse as temp123 said. So I was arguing with the OP that the trainwreck must be managed/contained, which he disagrees, as he "lets the nature take its course".

I also talked about sub-clinical inflammation as the root cause, leading to hyper-keratinization. Interestingly that isotretionin modulates both that and sebum production. If it wasn't just so damn dangerous.

So we're all in agreement, except with the OP.

PS: I firmly believe that the root cause (the poor shedding in the pore) is genetic. Coupled with varying degrees of sebum excretion it proportionally becomes a train wreck. The level of sebum excretion is speculated to be androgen regulated. So the disease needs a chain of events gone wrong to manifest itself.

Share this post


Link to post
Share on other sites

From what I can tell, anti-inflammatories *do* target the preclinical inflammation.

I've had pretty good success with minocycline, red light therapy and now topical ibuprofen myself. All three have a pretty substantial anti-inflammatory effect.

I've also found that sebum secretion seems to be a function of irritation, rather than the other way around. I think it's something skin does to try to protect itself. Reducing P.Acnes and some foods and using anti-inflammatories seems to greatly reduce sebum production for me- YMMV.

Share this post


Link to post
Share on other sites

Join the conversation

You can post now and register later. If you have an account, sign in now to post with your account.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.


  • Personalized Advice Quiz - All of Acne.org in just a few minutes

×