In our Western culture, the journey from pre-adolescent to teenager into adulthood unveils numerous hormone changes that strongly affect the pilosebaceous unit (the hair follicle).The appearance of pimples, whiteheads, blackheads, or inflamed cysts accompanies the active life of 79 to 95 percent of teenagers.2 It begins around age 11 in females and a little later in males.3 After age 25, some degree of facial acne may continue in 40 to 54 percent of men and women. Facial acne persists into middle age in 12 percent of women and three percent of men.2 For women, the hormone changes that occur prior to menstruation also become evident in slight breakout. Additionally, sebaceous gland hyperplasia may develop on elderly skin that appears as isolated nodules of yellowish color found on the front and cheeks of men with very oily skin.4
Studies of non-Western societies have found that there is a lower rate of acne within those cultures. Kitavan Islanders of Papua New Guinea and the Arché hunter-gatherers of Paraguay have an absence of acne.2 More recent research suggests that there is more to acne that goes beyond a genetic disposition. Environmental factors may very well contribute to the occurrences of acne in a Western society. 
There are a growing number of theories surrounding this condition and why it has become so prevalent in our culture. Researchers found evidence as far back as the 1930s linking acne to carbohydrates and impaired glucose toleration.5 A form of treatment discussed in dermatology textbooks of the 1800s recommended dietary restrictions to control acne breakouts.
In a published article, Jennifer Burris of New York University and her colleagues reviewed 27 studies on the correlation between nutrition and acne.6 Participants following a low-glycemic-load diet experienced decreases in inflammatory acne lesions.5 Burris’ 2012 study suggests that diet, particularly glycemic index diet, saturated fat, trans fat, milk, and fish, may influence or aggravate acne development.7
There are also misconceptions concerning the cause of acneic conditions such as dirty blood or lack of good hygiene. Harsh scrubbing, or even excoriation, ends up exacerbating this condition.1
EXPLORING THE PATHOLOGY OF ACNE
The Hair Follicle
To understand acne, the structure and function of the pilosebaceous unit (the hair follicle), a very active apparatus residing within the dermis and epidermis, should be examined first. There are two kinds of follicles: A hair follicle and a sebaceous follicle, both having sebaceous glands attached. There may be microscopic hair in the follicle called rudimentary hair. When acne develops, this hair usually 
coils up, gets lost in the rest of the debris, and never gets to the surface.
Sebum inside the follicle plays an important role in the building of the acid mantle. The environment within the follicle normally contains anaerobic bacteria (growing without oxygen). Bacteria feed off the triglycerides produced by the sebaceous glands, leaving fatty acid
by-products.
The stratum corneum curves into the top of the follicle where the opening serves as an exit/entrance to the pilosebaceous duct.
Epithelial cells inside the follicle are an extension of the stratum corneum. They are interspersed with melanocytes and line the entire pilosebaceous unit. At the base of the follicle is the papilla that supports the various stages of the hair growth cycle. Also known as the bulge, it houses several types of stem cells that supply the follicle with new cells.
Just as cells desquamate off the stratum corneum, the same process occurs inside the follicle where the movement of sebum washes cellular debris upward to the opening of the follicle, spilling its contents onto the surface of the skin. Hair acts as a wick inside the follicle.
Home of the Sebocyte
Sebaceous glands consist of lobes connected by ducts and are found over most of the body. The sebaceous gland (duct) contains sebocytes that are filled with lipids called sebum. The sebocyte cell has a lifespan from mitosis to bursting into the interior of the sebaceous gland of around 14 to 20 days. During the migration of this cell into the interior of the gland, it transforms into lipids, releasing its contents into the sebaceous gland. Referred to as the holocrine method of secretion, the release of the cell contents involves the complete breakdown and loss of the entire cell. Sebum moves from the sebaceous gland interior and flows up the hair shaft to the surface of the skin, becoming an integral part of the acid mantel and contributing to the first line of skin barrier defense.8 The pH of the sebum is transformed into a more acetic state by bacteria at the top of the follicle.
Sebum quality is dependent on the essential fatty acids omega 3 and 6. The quantity and quality of oil will be as good as the immature sebocyte cell membrane. Poor cell health may result in less oil and a large amount of cellular debris. This debris can easily contribute to a blocked duct with a viscous, sluggish oil flow that contributes to the formation of comedones and pustules.
Health of the Acid Mantle
The first line of defense for the skin is the acid mantle, which should maintain a pH level between 4.5 and 6.5. Normal sebaceous lipid composition is made up of squalane, sterols, wax esters, sterol esters, and triglycerides. However, during chronic inflammation, the composition of pustules and papules, as well as comedones, contain a high level of free fatty acids.
The Role of Propionibacterium (P.acnes bacteria)8
The normal role of P.acnes bacteria is to support the formation of the acid mantle. They have evolved to be both anaerobic and aero-tolerant and reside at the top of the pilo sebaceous duct and on the skin surface near the exit. As sebum moves up the follicle, the triglycerides are transformed into free fatty acids. P.acnes use sebum as an energy source and ingest the abundant triglycerides in the sebum and excrete specialized enzymes (lipases) required to create the free fatty acids. This action also creates a pH of 5.5 for the acid 
mantle.
It is important to mention that P.acnes does not directly cause significant damage to the follicle and surrounding skin when it is functioning normally. Most of the damage caused by acne is due to an inflammatory process of the immune system.9 Whenever there is an impairment of the acid mantle, including being stripped by harsh chemicals, the P.acnes move away from their normal environment and seek the next highest source of triglycerides, the sebaceous gland interior down inside the follicle. It is here where the bacteria continue to breakdown triglycerides into free fatty acids. Unfortunately, this location is very close to the dermis that has a pH of around 7. The acidic nature of the free fatty acids now becomes pro-inflammatory and comedogenic. Due to the arrival of the cells from the immune system to combat the inflammation and infection, irritation soon causes pustules. The immune system looks at the bacteria components of the P.acnes as adversary molecules. Immune cells also release large amounts of inflammatory cytokines that induce more white blood cells to release destructive enzymes and free radicals at the infection site.9
Some individuals with acne vulgaris have a faulty and oversensitive immune response that causes the arrival of more inflammatory cytokines to induce additional white blood cells that continue to fight infection. This vicious cycle begins to affect the surrounding tissue with more damage, continuing the propagation of bacteria. Furthermore, it is not uncommon to have ruptured glands that form fibrotic tissue. They can be shallow or deep, creating permanent pitting and scarring.
Genetic Traits Leading to Poor Function
A genetic predisposition in the makeup of the follicle structure can occur during embryonic development. Some individuals may inherit more sebaceous glands on the face and other areas or have inherited a higher sensitivity to circulating androgens. A hereditary factor called retention hyperkeratosis may be present whereby the keratinocytes do not shed off the surface on the stratum corneum and out of the follicle as in normal skin.
Androgens and Their Role in Sebum Production
Androgens are hormones that are important for normal male sexual development during embryonic development and during puberty. The AR gene provides instructions for making a protein called the androgen receptor. Androgens and their receptors help direct the 
development of male sexual characteristics. They also have important functions in both males and females such as hair growth and sex drive.10
Androgen receptors located within the sebaceous follicle stimulate an upsurge of sebum production. At the onset of puberty, androgen hormones are produced, beginning with testosterone. An enzyme called 5-alphareductase converts testosterone to di-hydrotestosterone. Di-hydrotestosterone stimulates the sebaceous glands to begin the production of sebum.
Retention hyperkeratosis is a result of the buildup of epithelial cells. Continuous overproduction of sebum causes a distention of the gland and a notable enlargement of the follicle. Essentially, the process of pimple formation is a result of an obstruction in the follicle. Cellular debris mixes with sebum, dries out, and creates a plug that obstructs the drainage of the sebum.
Other circumstances that affect and modulate sebum production include: Pregnancy and use of oral contraceptives; Low levels of circulating androgens in women; Hormonal changes during menopause; and drugs, such as corticosteroids, lithium, Adderall®, anticonvulsants, barbiturates, androgenic steroids, didehydroepiandrosterone, chemotherapy drugs, and other medications.
Environmental Exposure
Acne and comedones tend to manifest in areas of sun exposure. Ultraviolet exposure depletes vitamin A, an important nutrient that helps control sebaceous gland activity, along with maintaining the quality of the sebum. A component called CIS retinoic acid helps reduce the sensitivity of the sebocytes to circulating androgens.1
Furthermore, overexposure and sun bathing creates a thickening of the stratum corneum that contributes to acne formation. A thickened horny layer can obstruct the follicle of the sebaceous glands.
Primary Causes of Hyperkeratinization1
A lack of free water or low humidity within the skin causes impairment of the enzymes required for dissolution of the desmosomes that tether the keratinocytes together. Poor desquamation ends up blocking the pilosebaceous duct leading to comedones. Lack of free water also interferes with the alignment of the epidermal bilayer lipids, causing them to crystalize and affect the desquamation process, which shows an uneven appearance.
Essential fatty acid deficiency causes an alteration in the viscosity of the lipids found in the bilayers of the corneocytes resulting in “sticky” cells leading to poor desquamation. Essential fatty acid deficiency also affects sebum quality within the follicle. Individuals with acne have a reduced amount of the essential fatty linoleic acid.
Psoriasis and keratosis pilaris are also aggravating factors for the buildup of skin cells.
TREATMENT OBJECTIVES
The basic principles for acne formation are recapped as four major factors:4 follicle hyperkeratosis, sebaceous gland hyperplasia, microbial 
hypercolonization, and inflammation and immune reaction.
All grades of acne have a common theme – a hormonal component. The knowledge of the keratinocyte and sebocyte life cycle is essential to understanding the underlying causes of acne. It is also important to address the inflammation and the ensued disturbances created in the barrier function, the follicle, and the acid mantle. Correction and treatment must be carefully assessed and depends upon age, health history, medications, lifestyle, and the degree of the condition. Severe cases, as in Grades III and IV, or anything questionable may require medical intervention. Furthermore, acne can be painful, leaving scars and other forms of disfiguration.
There are several aspects in the pathogenesis of acne to be addressed when selecting the application of active agents, which have the following qualities: sebum-liquefying, sebum-suppressive, keratosis-impeding, antimicrobial, inflammation reduction, immune-suppressive, and repair and regenerating effects.
Educate and provide guidelines to clients regarding the care of their acne. Be mindful that even when acne gets under control or subsides, initial treatments should be gentle and work with the natural physiology of the skin. Phototherapy directed towards reducing the quantities of P.acnes bacteria may be used in tandem with in-clinic sessions. There are keratolytic, anti-inflammatory, and antimicrobial agents available in specialized products and treatments.
Biological active molecules and compounds are found in plant sources that are considered to be antimicrobial, antifungal, and calming. For example, tea tree, thyme, mahonia, and ribwort are but a few.
The application of topical vitamin A is effective in compacting and smoothing the stratum corneum. Linoleic acid and liposomal phosphatidylcholine are effective in the control of acne. The consumption of vitamin A, as well as other supplements, can be helpful.
Skin care professionals should provide the client with a list of aggravating substances that can make the situation worse. An effective management program can also be designed with regular sessions. Also, review dietary and lifestyle habits, and recommend that fast/refined foods and sugars, along with foods that are considered high glycemic and affect blood sugar and insulin, be eliminated. A gentle home care regimen should be recommended. Advise clients not to use scrubs or harsh ingredients.
Clients undergoing acne care require a good dose of understanding and compassion. This, along with proper treatment and homecare, can help clear up a client’s acne in no time!
References:
1 Fernandes, D., MD. (n.d.). Acne Vulgaris: Introducing an effective treatment regimen. Retrieved from http://www.beautymagonline.com/beauty-articles/953-acne-basics-3
2 Cordiain, L., Lindeberg, S., et al. (December 2002). Acne vulgaris: a disease of Western civilization. Arch Dermatol, 138(12):
1584-90.
3 Checkup on Health: Don’t let acne ruin those important teenage years. (n.d.). Retrieved from http://www.ucdmc.ucdavis.edu/welcome/features/20090909_teen_acne/
4 Lautenschläger, H., PhD. (2003). Acne – prevention and care. Kosmetik International, (5):27-31
5 Aubrey, A. (February 20, 2013). Diet and Acne: For a Clearer Complexion, Cut The Empty Carbs. NPR
6 Burris, J. MS, RD, Rietkerk, MD, Woolf, K., PhD. (March 2013). Acne: The Role of Medical Nutrition Therapy. J of the Academy of Nutrition and Dietetics, 113(3):416-30
7 Burris, J. MS, RD, et al. (January 2013). Relationships of Self-Reported Dietary Factors and Perceived Acne Severity in a Cohort of New York Young Adults. J of the Academy of Nutrition and Dietetics, 114(3):384-92
8 Barrett-Hill, F., (2011). Advanced Skin Analysis Course. Retrieved from www.pastiche.net.nz Pastiche Resources,
New Zealand.
9 What is Propionibacterium acnes? (n.d.). Retrieved from http://thescienceofacne.com/what-is-propionobacterium-acnes/
10 Genetics Home Reference: Your Guide to Understanding Genetic Conditions. (n.d.). Retrieved from http://ghr.nlm.nih.gov/gene/AR
Alexandra J. Zani is an international educator, researcher, and author with a background in cell biology and medical. Her passion for education resulted in receiving numerous advanced certifications, both in the United States and abroad. Zani earned an instructor license for aesthetics/cosmetology, is National Catholic Educational Society (NCEA) Nationally Certified, certified in Oncology Esthetics®, and the Pastiche Method® of Skin Analysis. She is a member of the International Association for Applied Corneotherapy (IAC). Zani presents education for advanced aesthetic technology, including microcurrents, LED, and non-ablative laser. She is a specialist in the anti-aging sciences, including the effects of nutrition, lifestyle, and the mind/body connection.
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