What Causes Acne?
Acne is an inflammatory skin condition caused by the western diet and its impact on metabolic pathways and the skin microbiome. It appears at puberty but increasingly extends into the mid-’30s in men and women. It is a metabolic disease caused by the western diet, as it does not occur in populations outside this dietary habit.
Acne affects the hair follicles and pores in the skin. Under the skin’s surface, these connect to oil glands that produce sebum. Acne’s primary cause is increased turnover of skin cells and blockage of the pores, increased oil production, and bacteria overgrowth.
- Increased cell turnover and accumulation of exfoliated cells lead to obstruction of the hair/oil follicle. In addition, high sebum production builds up in the obstructed follicle to form a plug or comedones (blackheads, whiteheads).
- This obstructed oil-rich follicle is the perfect environment for the Cutibacterium acnes (C. acnes)bacteria to overgrow, creating inflamed papules or pustules (pimples).
- As the inflamed contents of the now obstructed hair/oil follicle cannot escape, painful nodules can form deep in the skin: nodular acne.
- Or result in the destruction of the follicle with the release of inflamed contents into the dermis.
- With further destruction, inflamed, tender cysts with slow healing with scarring, the result; is cystic acne.
Cutibacterium acnes the bacteria are formally known as Propionibacterium acnes – even bacteria can change their name!
Acne results in dysbiosis in the skin microbiome. However, the driving cause is not the bacteria but changes to the skin, which allows the bacteria to overgrow. The skin environment that allows this to happen is the overstimulation of metabolic pathways (mTORC1). How the skin dysbiosis develops – and results in the destructive elements.
- C. acnes bacteria live abundantly on healthy skin, principally deep within the hair/oil follicles and the surface. Its preferred source of energy is obtained from oil and cell debris. In return, it produces by-products that may maintain the skin’s acid surface and protect it from harmful bacteria. However, when the hair/oil follicle becomes blocked and oil production increases, the C. acnes proliferates, and different strains of the C acnes become more dominant. This imbalance or dysbiosis is believed to drive the formation of pimples, cysts and nodules. In addition, the increased concentration of by-products produced by the ordinarily helpful skin microbe creates a toxic environment that contributes to cystic acne’s more destructive elements – inflammation, destruction, and scarring.
How does diet affect the skin changes that cultivate C. acnes dysbiosis?
A western diet is high in low GI carbohydrates (sugar, refined and processed grains), dairy and animal protein. The high sugar load promotes insulin and insulin-like growth factor (IGF-1), which stimulates the mTORC1 pathway (mTORC1 determines cell proliferation and growth). Usually, at puberty, the mTORC1 is activated as it is, after all, a time of change. However, regular mTORC1 activity is sent into overdrive with an excessively sugar-loaded diet.
MTORC1 increases cell turnover in the hair/ oil follicle (results in blockage) and increases oil production, starting comedo formation. The mTORC1 also causes early inflammation (accumulation of T immune cells and cytokines) even before overgrowth by C. acnes. That’s right; inflammation occurs even before dysbiosis and overgrowth. (Melnik, 2015; Agamia et al., 2016; Zaenglein et al., 2016). So, of course, the blocked, obstructed hair/oil follicle is the perfect feeding and breeding ground for C. acnes overgrowth and dysbiosis.
C. acne is a normal bacteria of your skin; therefore, acne should not be considered an infection.
The Western diet underlies acne formation and explains why acne increasingly persists for years. Though not physically harmful, it has a severe psychosocial impact, causing low self-esteem, depression and social withdrawal. The resulting stress has a further negative impact back on both the gut and skin. Stress is a well know precipitant of breakouts in its own right (gut-brain-skin axis).
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