The Holy Grail Of Acne Information

Previous Blog Postings

In my last posts we discussed what causes retention hyperkeratosis  
and the the roll of p-acnes bacteria and biofilms on acne 

As I stated in my first blog on acne, My Journey To Fully Understanding Acne, I had no idea what some of these people were talking about on these message boards. My first question on the message board was a simple one about acne inflammatory responses.

 This was the first response I got

1. increased 5a reductase in the folicle.
2. abnormal stickiness in the keratinocytes.
3. deficiency of linoleic acid
4. elevated levels of interleukin-1a
5. MMP-8 elevated levels.
6. p. acnes bacteria

Some of these overlap. The abnormal stickiness is from a local deficiency of linoleic acid, p.acnes, and biofilm. Interleukin-1a is also known to increase proliferation of keratinocytes, another contributing factor. MMP-8 is released which breaks down the follicle and allows for the inflammatory process to occur.

5a reductase - in the pores of acne sufferers is 2-7 times higher than those who don't have acne. 

My Response                                                

I thought to myself 'WOW, what does this even mean'? So after my frustration fit was over, I decided to take it slow and research one thing at a time. And as you all know, with research, if you don't understand one thing it leads to something else, then to something else. This one message from a wonderful lady in Australia by the name of Jacine Greenwood, CEO of Roccoco Cosmetics, led me down a month long path of acne research and discovery.

 

Let's Break It Down

5a reductase is an enzyme responsible for the conversion of testosterone into DHT (dihidrotestosterone). There are 2 types of 5a reductase enzymes - type 1 and type 2. Type 2 predominates in the hair follicles and type 1 resides in the sebaceous glands.

5a reductase is the cause of hormonal mediated acne. So basically when you inhibit it you stop the effects of testosterone working in the sebaceous follicle.

MMP (Matrix Metalloproteinases) are enzymes that destroy collagen. Specifically MMP-8 is involved with acne. The follicular wall ruptures as a result of MMP-8 being released. This is what degrades the structure of the follicle wall. If you inhibit MMP-8 then you will get less inflammatory lesions.

Interleukin-1a is an inflammatory mediator. It has been shown to be present in high concentrations in the skin of acne sufferers. Interleukin-1a has also been shown to promote hyper Keratinization.

 

The Protocol

Some of you maybe saying "okay that's interesting what can I do to stop this." Well I am glad you asked. Here are a few ingredients that are know to help each one of these steps.  

1. 5a reductase inhibitors - green tea, resveratrol, saw palmetto, bellamcanda chinensis root, zinc, evening primrose oil, and linolenic acid.

2. linoleic acid deficiency - decrease oil flow through 5a reductase inhibitors and cleanser that is high in linoleic acid to correct the deficiency. Sunflower oil his high in linoleic acid.

3. Reduce interleukin-1a expression in the skin - Nettle extract, magnolia extract, black cumin oil.

4. kill p.acnes bacteria - type 1 and type 2. There are 2 types of p.acnes bacteria and tea tree oil only kills type 1( gram-positive), not type 2 (gram negative). For this I use black cumin oil, magnolia, chaulmoogra oil, Manuka oil. Licorice also has anti-bacterial and anti-inflammatory properties. Magnolia extract kills type 1 and 2 p acne.

5. mmp-8 - I inhibit this with pine needle extract which has a strong inhibition against mmp-8.

Jacine Greenwood CEO of Roccoco Cosmetics writes:
Everyone else focuses on exfoliation rather than preventing the cells getting sticky in the first place. I don't like benzoyl peroxide because of the free radical component and it also causes epidermal hyperplasia which contributes to follicular hyper keratinization. I exfoliate the skin with papain and bromelain. I also use desincrustation solutions to facilitate extraction.

I get them to prep with their products. The oil cleanser helps loosen impacted blackheads along with the serum packed with interleukin-1a inhibitors as well. They literally start to wiggle their way out easily. They also get a serum full of 5a reductase inhibitors.  
  
The difference between the non-inflammatory and inflammatory is simply the products I select.

I tend to focus on more 5a reductase inhibitors for the inflammatory and ingredients that have been shown to be highly anti-inflammatory such as licorice, green tea extract. This works very successfully.

With clients who have a lot of blackheads, etc. I ensure that they are using a proteolytic enzyme at home to eat the dead skin cells and keep the skin smooth, along with the 5a reductase inhibitor and a toner with a natural blend of fruit extracts in it. This is not an AHA but has a similar effect. 

 

In Conclusion

As I have stated, acne is an inflammatory skin disease.  It is because of the inflammation that a cascade of events occur. If you control the inflammation you control the breakdown of the follicle, bacteria, and hyperkeratosis in the follicle. Dead p.acnes bacteria still promote acne formation because they promote inflammation. So p.acnes are really only part of it. The problem is inflammation.