“While pimples are not as simple as too much milk or sugar in your diet, both have a significant impact. Nutritional deficiencies as well as excesses can worsen acne”Mark Hyman.

Acne is a common disorder of the pilosebaceous glands in the skin. The causes of acne result from excess sebum production, presence of the Propionibacterium acnes, abnormal production of androgens, follicular hyperkeratinization and inflammatory mediators.

Acne is a common disease with prevalence up to 80 % during adolescence and affects more than 40-50 million Americans. A recent estimate indicates that about 85% of people will experience acne at some point in their life time, with huge impacts on their physical and psychological well being in terms of depression, low self-esteem, scarring and anxiety. Twin studies provide solid evidence of a genetic background for this disease. Similarly, available evidence suggests a link between androgens and acne. Less clear, however, is the data on other risk factors such as smoking, diets and other acne causes.


How Propionibacterium acnes causes Acne 

This gram-positive anaerobic bacteria are present in increased numbers in sebaceous follicles of most patients with acne vulgaris. P.acnes secrets a protective substance; a glycocalyx polymer, around itself that makes its ingestion and degradation by neutrophils difficult. Propionibacterium acnes overgrowth engenders potential follicular rupture initiating a host of inflammatory reactions.
Release of many enzymes by Propionibacterium acnes such as lipases, hyaluronidases, proteinases and other potential chemotactic factors serve as major modulators of the inflammatory process that leads to pimple formation.

Acne and Hormones
At the core of sebaceous gland activity and sebum production is hormonal regulation. Development of acne has long been linked to elaboration of hormones, which exert their effects on sebaceous glands and also play a role in follicular hyperkeratinization.
Examples of the hormones implicated in the pathogenesis of acne are androgens, growth hormone, Insulin, glucocorticoids, corticotropin-releasing hormone (CRH), eostrogns, melanocortins, insulin growth factor-1 and adrenocorticotropic hormone (ACT). The most important class of hormones involved in the development and progression of acne vulgaris is the androgens, which are produced in the adrenal glands, gonads and skin. They exert their effect on the sebaceous gland in the skin which is richly endowed with androgen receptors.

Acne and Follicular Growth

Though the precise mechanism behind comedo is still unclear, there are reliable pointers linking excessive elaboration of keratin in the follicles. Exogenous compounds have been proven to cause irritation of the follicular lining and sebaceous ducts. In addition, a similar endogenous phenomenon involves hormonal and neurological stimuli. In a nutshell, pimple severity can arise from hyper-proliferation of ductal keratinocytes. This excessive growth of the follicles can plug the pores which in the presence of bacteria and stasis provides a favorable medium for acne formation and progression. This is one of the fundamental mechanism behind acneiform eruptions and other similar skin lesions, like Acne Conglobata, Folliculitis, Acne Keloidalis Nuchae, Rosacea, Acne Fulminans and Sebaceous Hyperplasia.

How Inflammation Causes Acne
According to research, inflammatory responses involving the elaboration of immune mediators like macrophages and certain T-cells precede hyperkeratinization. This initial reaction primes the local endothelial cells to accentuate the action of other inflammatory mediators like vascular cell adhesion molecules, human leukocyte antigen and inter-cellular antigen. These inflammatory mediators are found in the vessels around the pilosebaceous follicles, a prime location for acne formation.


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Excess Sebum Production Causes Acne

Evidence supports the strong correlation between comedonal acne in prepubertal females and the circulating concentration of dehydroepiandrosterone sulphate (DHEA-S). The development of acne vulgaris is almost directly proportional to sebum production and excretion, which is also regulated by hormones and other immune mediators.


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