What Causes Acne?

Inflammatory Acne Papules Skin and Cellular View
Healthy and Infected Follicle
Healthy and Infected Follicle

Acne is a complex disease and many factors can contribute to the development of acne symptoms. Every case of acne is unique and the blend of factors that cause acne varies between individuals. A detailed discussion about What Is Acne? can be found here. Below is a list of things that are major contributors to the development of acne:

Genetics

Genetic Information is Encoded in DNA
Genetic Information is Encoded in DNA

An individual’s genetic makeup is a dominant factor in determining the likelihood of developing acne and how severe their acne symptoms will be. People inherit their genes from their parents. If either of your parents experienced significant acne symptoms, you are substantially more likely to develop acne yourself.

Genetics impact the structure of the hair follicle, sebaceous gland activity, hormone levels and the immune response to bacteria. For example, many people who suffer from inflammatory acne have immune cells that are less effective at killing the acne bacteria or produce more inflammatory molecules than the general population.  As a result of genetic differences, their body responds more vigorously (but less effectively) to acne causing bacteria than the average person. This can result in more frequent and more severe acne breakouts.

Hormones

Androgens Drive Muscle Growth
Androgen Hormones Drive Muscle Growth and Acne

Hormones are an important factor in the development of acne. Hormones regulate many of the factors that are involved in acne, including the activity of the sebaceous glands, the production of sebum and the immune system’s response to acne-causing bacteria (eg. P. acnes). Hormones largely explain why women tend to experience worsening acne symptoms during certain times of their menstrual cycle, or during/after pregnancy. Hormones also explain why acne symptoms tend to peak during adolescence for males.

Pregnancy
Pregnancy can Trigger Acne Symptoms

Men and women tend to experience acne differently and much of this difference can be explained by hormones. Men are more likely to develop acne during puberty and are more likely to develop severe and inflammatory forms of the disease. Acne symptoms tend to peak during adolescence and recede during a male’s mid 20’s. In contrast, women tend to experience less acne and less severe acne than men, but rates of acne actually increase for women in the 20-40 age range. Many women who have never had complexion problems begin to experience acne symptoms during pregnancy, and sometimes acne continues to persist after completion of the pregnancy.

Men, particularly adolescent males, produce abundant quantities of male hormones called androgens. Androgens include hormones like testosterone. Among other things, androgens stimulate the growth of sebaceous glands, which increases the amount of sebum produced by the skin. Increased sebum production fosters the growth of bacteria that feed on sebum, such as P. acnes. Additionally, high levels of sebum production can increase the incidence of hyper-keratinized follicular plugs (clogged pores) that encourage the development of acne symptoms like pimples, nodules and cysts.

Bacteria

Propionibacterium acnes (Toyoda, et al)
Propionibacterium acnes (Toyoda, et al)

Acne, and inflammatory acne in particular, is usually connected to bacteria growing deep within pores and hair follicles in the skin. The bacteria most commonly associated with acne symptoms is Propionibacterium acnes (P. acnes). These bacteria produce molecules which cause an immune response, leading to inflammation and acne symptoms.

High levels of bacterial growth within follicles is associated with a higher incidence of acne and more severe symptoms.  Although P. acnes bacteria are generally thought of as a causative agent of acne, other bacteria (eg. Staphylococcus aureus) can also live in the skin and may also contribute to the development of acne. Antibiotics are commonly used to control the growth of bacteria and can greatly improve symptoms for many acne sufferers.

There are many different strains of P. acnes bacteria and many of these strains have developed resistance to one or many different antibiotics. As a result, some antibiotics, including erythromycin and tetracycline, are becoming less effective in some countries (eg. United States) because many people who suffer from acne carry strains of bacteria that are resistant. Fortunately, there are still many antibiotics available that do not have this shortcoming.

Environment

UV Light is an Environmental Condition
UV Light is an Environmental Condition

Environmental conditions, like temperature, sun exposure, humidity and allergens can play a big role in acne outbreaks. Low temperatures may decrease the fluidity of the sebum passing through the follicle and increase the risk of developing a plug. Or low humidity levels can dry the skin, causing the body to increase sebum production in a bid to protect the skin, which then increases the formation of clogged pores and the growth of acne-causing bacteria. Sunlight can affect both the bacteria and the skin, causing physiological changes or damage to various structures. Allergic reactions may exacerbate skin problems, or cause new ones.

Many people notice that their acne tends to improve or worsen depending on the weather, and this is because the environmental conditions can directly affect the way the body functions. The effect of specific environmental conditions on acne symptoms varies greatly between individuals.

Stress

Stressed Out
Stress

Stress is well known to disrupt normal hormonal balance and depress the immune system. Both of these changes can lead to a worsening of acne symptoms. Acne is a type of infectious disease, and elevated levels of stress can make people more susceptible to all types of infection, including acne.

Many people observe that they tend to break out especially bad after pulling an all-nighter, drug/alcohol consumption or other activities that put stress on the body. Inadequate sleep is a very common form of stress. Avoiding stress and identifying strategies to reduce stress (eg. Exercise, Yoga, Meditation, etc) are important components of a holistic approach to treating acne.

Diet

High Glycemic Foods can Increase Risk of Acne
High Glycemic Foods can Increase Risk of Acne

Scientific evidence does not appear to support the common claims that there is a connection between eating greasy foods or chocolate and the development of acne. However, scientific research has identified a connection between high glycemic index diets and increased incidence of acne. High glycemic diets are those that are high in sugar and simple carbohydrates.

Excessive consumption of sugar and starch is the primary cause of high blood sugar levels, and blood sugar levels are the primary regulator of metabolic function. Consistently elevated blood sugar levels are a type of stress, and they appear to negatively affect the body in ways that are similar to other forms of stress. This type of metabolic stress may cause or worsen acne symptoms in some individuals. Besides increased acne symptoms, high blood sugar levels can lead to other problems, like type 2 diabetes.

Eating a balanced, healthy diet that is rich in protein, whole grains and vegetables is important for overall health and can help minimize acne symptoms. There is some evidence that specific dietary plans (eg. Mediterranean or Vegan diets) may help improve acne for some individuals, but these claims require further scientific investigation.

References

Pathogenesis of Acne. Toyoda, et al. 2001.
Correlation Between Serum Levels of Insulin-like Growth Factor 1, Dehydroepiandrosterone Sulfate, and Dihydrotestosterone and Acne Lesion Counts in Adult Women. Cappel, et al. 2005.
Acne in Victorian adolescents: Associations with age, gender, puberty and psychiatric symptoms. Kilkenny, et al. 1997.
Post-adolescent acne: a review of clinical features. Goulden, et al. 1997.
Prevalence of facial acne in adults. Goulden, et al. 1999.
Neuroimmunology of Stress: Skin Takes Center Stage. Arck, et al. 2006.
Neuroendocrine regulation of sebocytes and a pathogenetic link between stress and acne. Zouboulis, et al. 2004.
Sebaceous glands in acne patients express high levels of neutral endopeptidase. Nakamura, et al. 2002.
The Response of Skin Disease to Stress. Chiu, et al. 2003.
Stress, Acne and Skin Surface Free Fatty Acids. Kraus. 1970.
Transient Receptor Potential Vanilloid-1 Signaling as a Regulator of Human Sebocyte Biology. Toth, et al. 2009.
Comparative Chemistry of Sebum. Nikkari. 1974.
Comprehensive analysis of the major lipid classes in sebum by rapid resolution high-performance liquid chromatography and electrospray mass spectrometry. Camera, et al. 2010.
Quantitative evaluation of sebum lipid components with nuclear magnetic resonance. Robosky, et al. 2008.
Sebaceous gland lipids. Picardo, et al. 2009.
Variation in Sebum Fatty Acid Composition Among Human Adults. Green, et al. 1984.
Sebaceous gland lipids: friend or foe? Smith, et al. 2007.
Sebum analysis of individuals with and without acne. Pappas, et al. 2009.
Does facial sebum excretion really affect the development of acne? Youn, et al. 2005.
Sebum output as a factor contributing to the size of facial pores. Roh, et al. 2006.
Comparison of sebum secretion, skin type, pH in humans with and without acne. Kim, et al. 2006.
Can sebum reduction predict acne outcome? Janiczek-Dolphin, et al. 2010.
Human Neutrophils Convert the Sebum-derived Polyunsaturated Fatty Acid Sebaleic Acid to a Potent Granulocyte Chemoattractant. Cossette, et al. 2008.
Peroxisome Proliferator-Activated Receptors Increase Human Sebum Production. Trivedi, et al. 2006.
Sebum Free Fatty Acids Enhance the Innate Immune Defense of Human Sebocytes by Upregulating b-Defensin-2 Expression. Nakatsuji, et al. 2010.
Control of Human Sebocyte Proliferation in Vitro by Testosterone and 5-DHT is Dependent on the Localization of the Sebaceous Glands. Akamatsu, et al. 1992.
Differentiation of the sebaceous gland. Niemann. 2009.
Correlation of facial sebum to serum insulin like growth factor-1 (IGF-1) in patients with acne. Vora, et al. 2008.
The Role of Specific Retinoid Receptors in Sebocyte Growth and Differentiation. Kim, et al. 2000.
The Effect of Marked Inhibition of Sebum Production with 13-Cis-Retinoic Acid on Skin Surface Lipid Composition. Strauss, et al. 1980.
Regional and seasonal variations in facial sebum secretions: a proposal for the definition of combination skin type. Youn, et al. 2005.
Study of Psychological Stress, Sebum Production and Acne Vulgaris in Adolescents. Yosipovitch, et al. 2007.

Inflammatory Acne Papules Skin and Cellular View