A Primer on Acne: Natural and Holistic Strategies Prevent Eruptions
Tuesday, October 12, 2010 by: Andrew Kim, citizen journalistSee all articles by this author
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Acne is a disorder of EXCESSIVE GROWTH and INFLAMMATION, which is driven by hormonal changes.
1. The formation of acne begins in the hair follicle, with over proliferation and adhesion of epidermal cells called keratinocytes (dead surface skin cells). This process is driven by a growth factor (EGF) and a cytokine (IL-1).
2. An over active sebaceous gland empties sebum into the follicle, which mixes with the dead skin cells. This sticky mass inhibits normal skin exfoliation and creates a clogged pore (microcomedone).
3. Impaction and bacterial infiltration creates oxidative stress and the follicle eventually bursts, releasing its contents. Inflammation ensues and becomes visible in and around the clog. The lesion is now called a papule, pustule, or cyst.
Insulin influences every step in the formation of acne directly and indirectly.
1. First, insulin frees up IGF-1 and EGF, which are incredible promoters of growth. IGF-1 acts on and stimulates keratinocyte proliferation. It also decreases IGFBP-3, which regulates IGF-1, and acts on RXR to normalize cell growth. High insulin levels are also linked to chronic inflammation, triggering the release of IL-1 that starts the whole process.
2. Insulin increases sebum production in two ways: by stimulating androgen release in the testes and ovaries and by decreasing SHBG, which normally binds sex hormones in the bloodstream, regulating its availability to cells.
3. Insulin worsens acne by diverting essential fatty acid (EFA) derived eicosanoid production towards inflammation.
Recommendations
1. Diet
- Choose low-glycemic load , anti-inflammatory foods, which provoke less insulin, growth factor release, androgen production, and inflammation. These changes normalize follicular cell proliferation and reduce sebum.
- Avoid inflammatory foods like trans-fats, refined vegetable oils, grain-fed meats, and refined carbohydrates.
- Minimize inflammation by consuming foods rich in omega-3s and reducing Arachidonic acid (AA).
2. Lifestyle
- Increase quality and quantity of sleep. Inadequate sleep increases inflammation, stress, weight gain, and cortisol production. Cortisol may contribute to acne flare-ups by elevating blood sugar and stimulating the sebaceous glands, much like the androgens.
- Negative emotions and stress are linked to increased production of inflammatory cytokines. Stress also increases the production of cortisol.
- Chronic stress depresses the adrenal glands over time and leads to hypothyroidism. Hypothyroidism decreases SHBG, freeing up the androgens that increase sebum.
3. Supplements
- Vitamin D3: Regulates proper skin cell formation and modulates the inflammatory response.
- Alpha linolenic acid (ALA): Flooding the body with ALA reduces inflammation by outcompeting AA for delta-5-desaturase. Reducing AA, insulin surges, and boosting ALA will divert EFA production towards anti-inflammatory mediators.
- Methylsulfonylmethane
- N-acetyl cysteine: precursor to glutathione; prevents oxidative damage and inflammation and enhances Vitamins C and E.
Acne may have a genetic component, but as with most other diseases, the expression and severity of acne is influenced by lifestyle factors that are well within our control. Until dermatologists recognize the potential for natural, holistic solutions to modify the hormonal and inflammatory changes that cause acne, long-term success with conventional therapies will be elusive.
Author's note: the supplements listed above are neither comprehensive nor all the supplements necessary for everyone. Rather, it is a starting list worthy of consideration based on research.
Sources:
1."Implications for the Role of Diet in Acne" (Seminars in Cutaneous Medicine and Surgery, 2005).
2."Dietary Implications for the Development of Acne: A Shifting Paradigm" (US Dermatology Review, 2006).
3."Acne Vulgaris" (Archives of Dermatology, 2002).
4."Vitamin D analogs: mechanism of action and therapeutic potential" (Nagpal S, Boehm MF).
5."Noncalcemic actions of vitamin d receptor ligands" (Nagpal S, Rathnchalam R).
6."The vitamin D pathway: a new target for control of the skin's immune response?" (Experimental Dermatology, June 2008).
7."Oxidative Stress in the Pathogenesis of Skin Disease" (Journal of Investigative Dermatology, 2006).
About the author
Andrew KimAndrewkim21@gmail.com
Reposted From Andrew Kim of NaturalNews
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