1 reply to this topic

[nutsinsack]

I never had acne in high school, but halfway through college, I started getting break-outs on my face and body. I had been dealing with it for years with mainly topical creams using salicylic acid, benzyl peroxide, and retin-a creams. Nothing seemed to work. Recently, I have been focusing on my diet, and my skin looks and feels much better. I cut out a lot of processed foods, avoid foods with high glycemic index such as candy, chocolate, etc., focus on eating fresh vegetables (lots of kale, broccoli, etc.) for every meal with lean protein and whole grains, and try to avoid foods laden with hormones (non-organic milk and red meat).

 

I am not a doctor, but I was curious why low glycemic diet would promote a reduction in acne. If sugar was the sole culprit, then diabetic patients would routinely be affected with break-outs. Acne, as I understand it, is an inflammatory response from the body when harmful bacteria are trapped in the sebaceous glands of your skin. The root cause of acne is a bacterial infection so topical creams such as salicylic acid or benzyl peroxide are used to inhibit growth of all micro-organism on your skin. Failing that, the last line of treatment is anti-biotics.

 

I believe you are more prone to break-outs when your blood glucose level is high because the harmful bacteria that reside under your skin can somehow access glucose. That gives them a carbon source for unmitigated growth. When you are stressed, your body produces glucocorticoids which increase blood sugar levels while inhibiting your immune system. That could also lead to break outs.

 

I suspect I started having acne after being prescribed anti-biotics for an ulcer. My memory is faulty so I can’t be too sure, but I don’t remember having trouble with acne before. It was a broad spectrum anti-biotic so that event may have significantly disturbed the micro-flora in my body. I remember having trouble with my digestive system for the longest time.  As far as I can tell, we don’t really understand the role of micro-organisms in our body even though they play a key role in our health (for example bacteria in your colon synthesize key vitamins that you need).

 

I guess the take-away here is to focus not on the chemicals, but the micro-biota for treating acne. I have tried the no washing technique after reading people rave about it, and it was a disaster. I realize now that it probably didn’t work for me because the composition of my micro-biota is not optimal. The holistic nutrition focused approach to combat acne is the only effective approach in the long run. Your body knows best how to regulate these problems so your job is to give it the tools it needs to fight the battle.

Be careful about what you consume. Do your research and be skeptical. FDA is great about toxicity, and America has the safest food supply in the world. But there is almost no research funded on long term effects of certain food additives/ hormones/ residuals aside from animal toxicity tests. No one has an incentive to fund those studies because food products are held at lower standards than drugs, and you can’t exactly patent hormones.   

 

 

[nutsinsack]

Summary:

 

The mechanism of acne is not clear to date. As far as we know, changes in the skin (hypercornification of the outer root sheath and the pilosebaceous duct, increased sebum production, etc.) seem to create ideal conditions for certain bacteria (P. acnes) to grow and proliferate. Healthy microbiota of our skin was mapped out using 5 volunteers in an interesting study by Grice et. al (2008). Seems like P.acnes made up less than 5% of the healthy microflora with the majority of these sequences derived from the Proteobacteria division and predominantly from the genera Pseudomonas and Janthinobacterium. These results point toward a common core skin microbiome among healthy human subjects Grice et al. (2008). 

 

Grice couldn't determine if the specific species were cultured or could be even cultured. However, this research has gotten me thinking of a novel treatment toward acne. 

 

What if you could transplant some of the healthy micro-organisms to your own skin? There has been great success with transplanting the microflora of healthy people to patients suffering from digestive problems using an edema. If you can find someone who is related to you with great skin, you can take a biopsy of their skin and transplant it on yours. I do not recommend doing this without consulting a medical professional and taking the necessary precautions. I have also never tried this so I do not know if it will work. 

 

*I don't advocate this. It is just a hypothesis with unproven results. It might also have unintended medical side effects as well as possibly of infections, blood borne pathogens, etc.*

 

Research on the role of microbiota on our skin:

http://www.scienceda...20726153947.htm

http://www.ncbi.nlm....les/PMC2746716/

http://www.nature.co...l/5601829a.html

http://www.ncbi.nlm....les/PMC2746716/

http://www.ncbi.nlm....pubmed/18502944

 

Interesting points about acne from Cogen (2008):

 

"Propionibacterium acnes is implicated in a variety of manifestations such as folliculitis, sarcoidosis and systemic infections resulting in endocarditis.^93,94 Occasionally, P. acnes causes SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis and osteitis), a chronic, inflammatory, systemic infection.⁹⁵ In the sebaceous gland, P. acnes produces free fatty acids as a result of triglyceride metabolism. These byproducts can irritate the follicular wall and induce inflammation through neutro-phil chemotaxis to the site of residence.⁹⁶ Inflammation due to host tissue damage or production of immunogenic factors by P. acnes subsequently leads to cutaneous infections"

 

"Proposed P. acnes virulence factors include enzymes that aid in adherence and colonization of the follicle. In particular, hyaluronate lyase degrades hyaluronan in the extracellular matrix, potentially contributing to adherence and invasion.¹¹¹ The genome of P. acnes also encodes sialidases and endoglyco-ceramidases putatively involved in host tissue degradation.⁹⁹ Propionibacterium acnes also produces biofilms, limiting antibiotic access to the site of infection.⁹⁶ Studies have shown that TLRs play an important role in inflammation associated with P. acnesinfection.

 

Propionibacterium acnes induces expression of TLR2 and TLR4 in keratinocytes,¹¹² and the bacterium can induce interleukin (IL)-6 release from TLR1^−/−, TLR6^−/− and wild-type murine macrophages but not from TLR2^−/− murine macrophages.¹¹³ These combined data show that P. acnesinteracts with TLR2 to induce cell activation. Propionibacterium acnes infection also stimulates production of proinflammatory cytokines such as IL-8 (involved in neutrophil chemotaxis), tumour necrosis factor-α, IL-1β and IL-12.^114,115

 

The major factors contributing to acne are the hypercornification of the outer root sheath and the pilosebaceous duct, increased sebum production and, potentially, the overgrowth of P. acnes. Some have suggested that P. acnes involvement in inflammation is relatively minor and the abnormal bacterial growth in the sebaceous ducts may be a side-effect of inflammation rather than a root cause (Fig. 4). Although the bacterium is commonly associated with acne pathogenesis, healthy and acne-prone patients alike are colonized.¹¹

 

Studies have also shown that antibiotics primarily reduce inflammation and only secondarily inhibit P. acnes growth.¹⁰⁶ These data suggest that P. acnes has a low pathogenic potential with a minor role in the development of acne. The prevalence of P. acnes on healthy skin suggests a relationship of commensalism or mutualism rather than parasitism."

Edited by nutsinsack, 07 February 2013 - 08:52 AM.