Avoiding Negative Interactions Between Medications

What Does Contraindicated Mean?

A medication is contraindicated when there is an existing condition that makes its use inadvisable. Certain medications can be contraindicated in specific groups of people (eg. pregnant women) or in combination with other medications (eg. aspirin and warfarin).

Some medications are contraindicated with one another because taking them together is known to cause potentially serious problems. Before using any medication, it is important to verify (preferably through consultation with a licensed medical provider) that the medication is not contraindicated with any medical conditions you may have, or with any medications you may already be taking.

Educate Yourself About Your Medications

The more you learn about a particular topic, the more likely you are to make good decisions and avoid mistakes when dealing with that topic. This is especially true for medical conditions and medications. At the end of the day, it is your body and you are responsible for what you put in it (or on it). It is the patient’s responsibility to educate themselves as best as possible about any medications they are taking, or are considering taking.

An excellent way to start educating yourself about the medications that you are taking is by reading the patient inserts that come with a medication. This information outlines many of the important features, and risks, of a medication. For more detailed information, the physician’s insert for the medication is a good start. These can be found online by using google to search for the term Physician Insert plus the name of your medication. The Physicians’ Desk Reference is another excellent resource to learn more about medications and their contraindications.

The Physician’s Desk Reference (PDR)

The Physicians’ Desk Reference (PDR) is a an annually updated compilation of manufacturers’ prescribing information for prescription medications. It is designed to provide physicians with the all of the legally mandated information relevant to available prescription medications. While it is widely used by medical professionals, it is also a valuable resource for patients and consumers. The Physician’s Desk Reference is available in many libraries, bookstores and online from sources like Amazon.com.

The Antibacterial Activity of Essential Oil


Many essential oils and other plant extracts have antimicrobial properties which can be helpful for health and wellness applications.There is an incredible diversity of essential oils and other plant extracts available on the market today. Both professional and casual practitioners of Naturopathic remedies have a plethora of options for the treatment of acne.

Antimicrobial Properties of Essential Oil

Much of what makes up an essential oil are molecules which are part of a plant’s natural defense system. These molecules have been designed by millions of years of evolution to protect the plant against potential enemies. These enemies can be bacteria, fungi, viruses, other plants, insects and other animal predators.

Some components of essential oil have antibacterial, anti-viral and anti-fungal activity. Other components in the essential oil are designed to prevent predation by insects and other animals. Some essential oils may even be toxic to other plants and are designed to help inhibit the growth of competing plants.

In the last twenty years, a great deal of scientific research has been done to characterize the antimicrobial activity of many essential oils. Using this knowledge can help guide better decisions when designing effective Naturopathic treatments for acne.

The Antibacterial Activity of an Essential Oil Depends on the Species of Bacteria

Some essential oils are highly toxic to certain species of bacteria, but are harmless to others. While some essential oils are effective against a broad spectrum of different bacteria, others are only useful against very specific types of bacteria.

When designing a Naturopathic acne treatment that includes essential oils, it is important to be aware of these differences. To better improve the design of acne treatments, we have compiled scientific reports from many sources in order to help identify which essential oils are likely to be most effective against acne-causing bacteria, such as Propionibacterium acnes (P. acnes) and Staphylococcus aureus (S. aureus).

Many essential oils also have anti-inflammatory properties which may also help in the treatment of acne symptoms.

What Essential Oils are Effective Against Propionibacterium acnes Bacteria?

Scientific research reports indicate that there are many types of essential oil that are active against P. acnes bacteria. Tea Tree essential oil is one of the most popular essential oils for skin care applications, and the research shows that it is indeed toxic to P. acnes bacteria (although not as much as some other essential oils). Thyme, Clove and Cinnamon essential oil have broad spectrum antibacterial properties, and are also effective against P. acnes as well.

Unfortunately, many of the essential oils with significant antibacterial activity against P. acnes bacteria can also be fairly irritating to the skin, particularly at high concentrations. However, there are several essential oils which have excellent antibacterial properties and a lower risk of skin irritation. For example, several different kinds of Citrus essential oils, were highly toxic to P. acnes bacteria but tend to be fairly mild to the skin. Lemongrass essential oil is another a potentially useful option for acne treatments.

Antibacterial Activity of Essential Oil Against Other Bacterial and Fungal Infections

There have been many research studies which examine the ability of different essential oils to inhibit or kill different kinds of infectious bacteria and fungi. No matter what kind of application you have in mind – whether it is designing a Naturopathic acne treatment or developing a natural disinfectant – understanding the antimicrobial properties of different essential oils is a critical first step. To help improve the understanding of these properties, we are working on developing a comprehensive database that about essential oils and their antimicrobial activities.


Activities of Ten Essential Oils towards Propionibacterium acnes and PC-3, A-549 and MCF-7 Cancer Cells. Zu, et al. 2010.
Antimicrobial Activity of Essential Oils Against Five Strains of Propionibacterium acnes. Luangnarumitchai, et al. 2007.
Antimicrobial activity of essential oils and other plant extracts. Hammer, et al. 1999.
Antioxidant Activities and Volatile Constituents of Various Essential Oils. Wei, et al. 2007.
Antimicrobial activity of the essential oil of Melaleuca alternifolia. Carson, et al. 1993.
A comparative study of tea-tree oil versus benzoylperoxide in the treatment of acne. Bassett, et al. 1990.
Preliminary Clinical Tests on Topical Preparations of ocimum gratissimum Linn Leaf Essential Oil for the Treatment of Acne Vulgaris. Orafidiya, et al. 2003.
Antimicrobial Activity of Ternary Essential Oil Mixtures in Topical Cosmetic Preparations Against Acne Vulgaris-Associated Bacteria. Owen, et al. 2017.
The in vitro antimicrobial evaluation of commercial essential oils and their combinations against acne. Orchard, et al. 2018.
Aromatherapy, botanicals, and essential oils in acne. Winkleman, 2018.
Chemical diversity and anti-acne inducing bacterial potentials of essential oils from selected Elsholtzia species. Phetsang, et al. 2017.

How Do Bacteria Become Resistant to Antibiotics?

Answer: Bacteria adapt, evolve and acquire antibiotic resistance.

The extensive use of antibiotics in human patients does contribute to increased antibiotic resistance among infection-causing bacteria. But, the short-term use of antibiotics to treat infections in an outpatient setting is not the primary cause of the increase in antibiotic-resistant bacteria.

There are several factors which contribute to the growing problem of antibiotic-resistant bacteria. This post discusses the many ways that antibiotic resistance may occur, as well as the conditions and environments that promote the development of antibiotic-resistant bacteria.

What is Antibiotic Resistance?

Antibiotics are molecules that inhibit the growth and/or kill bacteria. Antibiotics are small molecules that disrupt essential biological processes that are unique to bacteria.

Antibiotic resistance refers to a situation where a strain of bacteria becomes less sensitive to a particular antibiotic (or class of antibiotics). Antibiotic resistance occurs because the resistant bacteria have developed or acquired an ability to prevent the normal function of the antibiotic.

There are many types of antibiotics, and there are many types of bacteria. Most antibiotics are only good at killing certain types of bacteria. Some bacteria are naturally resistant to certain antibiotics. It is important to select antibiotics which are toxic to the specific type of bacteria that is causing an infection.

Adaptation and Evolution of Antibiotic Resistance

Epigenetic Adaptation (No Genetic Mutation)

Bacteria that consistently encounter sub-inhibitory levels of an antibiotic (concentrations of the antibiotic that are too low to kill it) can develop a temporary resistance to that antibiotic. This type of resistance is called Epigenetic Adaptation. This type of antibiotic resistance does not produce permanent genetic changes that can be inherited by subsequent generations of bacteria.

Epigenetic Adaptation is roughly equivalent to an athlete who develops large muscles from weight lifting and physical training. Bacteria exposed to sub-inhibitory levels of an antibiotic can mobilize defenses such as pumps to expel the antibiotics, enzymes to break them down, or they can simply decrease the permeability of their cell wall to decrease their exposure to the antibiotic molecules.

Genetic Adaptation (Genetic Mutation and Selection)

Genetic mutations are permanent changes in an organisms genetic code. Most mutations are very small and involve the change of a single nucleotide (an individual letter in the genetic code). Some mutations involve large rearrangements of the genome.

Genetic mutations occur naturally during DNA replication. Mutations can also occur as a result of exposure to mutagens like ionizing radiation (UV light) or chemicals. Many genetic mutations happen in regions of the genome that are not essential for the organism and don’t significantly change how that organism functions. When a mutation does occur in something important, it is usually disruptive and weakens the organism. Mutations that improve the fitness of an organism are rare.

Some antibiotics are more likely than others to become less effective as the result of genetic mutations in the target bacteria. This is because resistance to some antibiotics can be acquired as a result of a single genetic mutation, while other antibiotics require a bacteria to develop multiple mutations in order to become resistant.

One example of a class of antibiotics that are susceptible to single mutation resistance is the Quinolone family of antibiotics (eg. Ciprofloxacin, Nadifloxacin). Antibiotics in the Quinolone family target a bacterial enzyme called DNA gyrase. The antibiotic binds very tightly to this enzyme, which prevents the bacteria from reading and replicating its own DNA. A single mutation at a specific site in this enzyme can stop the antibiotic from binding. This specific mutation allows the bacteria to become resistant to that antibiotic. Antibiotics that can be inactivated by simple genetic mutations, such as Ciprofloxacin, are not generally recommended for long-term use because of the increased risk of generating resistant bacteria.

Genetic Acquisition (Plasmids, Transposons, Viruses, Conjugation, Naked DNA)

Bacteria can acquire large pieces of DNA from other bacteria, viruses and the environment. Genetic Acquisition is the mechanism by which bacteria acquire high-level resistance to many types of antibiotics. This is especially true for antibiotics which can not be inactivated by simple genetic mutations.

It is virtually impossible for a bacteria to randomly evolve a brand new gene or enzyme that provides resistance against a particular antibiotic (at least within a time-frame of weeks, months and years). But what does happen is that bacteria acquire big chunks of foreign DNA that contain many genes. Bacteria have many ways to acquire these large pieces of DNA that contain the genes that confer high-level antibiotic reistance:

  • Plasmids are mobile pieces of DNA (often circular) that bacteria can easily trade amongst themselves or simply acquire from the environment. Many bacteria have multiple plasmids. Plasmids can contain genes that inactivate a particular antibiotic. For example a gene called Beta Lactamase provides resistance to Penicillin family antibiotics and is commonly shared by bacteria via plasmid.
  • Transposons are sections of DNA that can jump from one place in the genetic code to another, or even to the genetic code of another organism.
  • Viruses (Bacteriophages) can infect bacteria and these viruses can copy and paste genetic code into the genomes of the bacteria they infect.
  • Conjugation is where two bacteria that are directly adjacent to one another create a direct connection and share DNA (think “”conjugal visit””). Conjugation is probably the closest thing that bacteria have to sex.
  • Naked DNA is DNA that bacteria find in the environment and internalize. This DNA can be from bacteria that have been killed, or part of a biofilm structure (some bacteria use DNA as a scaffold structure to anchor themselves to a surface).

Bacteria can utilize one of these techniques (or all of them) to acquire pieces of genetic code that provide resistance to a specific antibiotic (or a whole family of antibiotics).

Conditions That Allow Antibiotic Resistance To Develop

The Necessity of Selective Pressure

The average bacterial genome (a bacteria’s entire genetic code) is approximately 1000 times smaller than the genome of an animal (including humans). This is not because bacteria are smaller than human cells (although they usually are).

Bacterial genomes tend to be very small because of competition and a concept called genomic streamlining. A genome is not free. It takes energy and resources to maintain and replicate a genome. The bigger the genome, the more energy it takes to keep it up and running, and to duplicate it during reproduction. At the same time, the competition between bacteria for resources is incredibly intense.

Bacteria grow much faster, and in much larger numbers, than most other organisms. For example, in a single handful of dirt there are more bacteria than the entire human population of the world. The huge bacterial population and intense competition is like “survival of the fittest” on steroids. Weak and inefficient bacteria are quickly squeezed out by stronger, more efficient bacteria. Excess DNA is “dead weight” in this competition and it is quickly eliminated. If a section of bacterial DNA is not essential for survival or does not confer a consistent selective advantage, it is rapidly mutated and removed from the genome by the quickly evolving bacterial population.

How Does Selective Pressure Impact Antibiotic Resistance?

In order for a gene to remain functional and a part of a bacteria’s genome for any extended period of time, that gene must help improve the survival and/or competitiveness of the bacteria. If a gene stops being helpful it will eventually become non-functional and will be removed from the genome.

This means that the development and maintenance of antibiotic resistance is usually dependent on the bacterial population being frequently exposed to non-lethal doses of the antibiotic (note: some bacteria are intrinsically resistant to particular antibiotics). This process eliminates those bacteria that have lost resistance, and increases the percentage of resistant bacteria. From a big picture perspective, this means that antibiotic resistance is likely to develop and persist in specific environments where bacteria are frequently exposed to antibiotics. On an individual level, this means that a person is more likely to develop an antibiotic resistant infection from undergoing long-term or prophylactic antibiotic treatment, as opposed to short-term antibiotic treatments of acute infections. This also means that bacteria may lose resistance to antibiotics that are no longer frequently used.

Environments that Facilitate the Development of Antibiotic Resistance

If you have read the above sections, you now know that infectious bacteria do not randomly become resistant to antibiotics. The development of antibiotic resistance requires an environment that provides a good source of hosts (people/animals to infect), consistent selective pressure (frequent antibiotic use) and ideally, lots of other bacteria with which to share antibiotic resistance genes. It is because of this combination of factors that antibiotic resistance is not simply about using antibiotics too much, but also about where and how antibiotics are used. That said, there are some environments which uniquely support the development of antibiotic resistance:


Hospitals are often the perfect environment for bacteria to develop, acquire and maintain high-level antibiotic resistance. Hospitals have a many of the features that are necessary for antibiotic resistance to emerge. including:

  • A lot of infected people and contaminated surfaces (lots of bacteria hanging around).
  • A high density of potential hosts for bacteria infection (lots of new people to infect).
  • The frequent and sustained use of antibiotics (consistent selective pressure).

Hospital Acquired Infections (HAIs) are often the most difficult types of infection to treat because they are can be highly resistant to standard antibiotic treatments. Hospitals are a reservoir for antibiotic resistance, and in many cases are the primary source of antibiotic resistant bacteria in the surrounding population.

In the United States, and other highly developed countries, hospitals are reasonably sterile and there are a number of systems in place to prevent hospital acquired infections. Despite these safeguards, HAIs are one of the leading causes of morbidity among patients admitted to hospitals in the United States. In many other countries hospital conditions are less sanitary, which encourages the transmission of disease from patient to patient. In hospitals that have a high rate of antibiotic use but poor sterility, the development of antibiotic resistant bacteria is accelerated.

It is not a coincidence that outbreaks of virulent antibiotic-resistant bacteria, such as Multi-drug Resistant Staphylococcus Aureus (MRSA) and Mycobacterium tuberculosis(XDR-TB), often originate in hospitals in countries like South Africa and Russia. In these places and others like them, high patient density, poor sterility, HIV/AIDs (see below) and high antibiotic usage combine to drive the rapid evolution of drug resistant bacteria.

Feedlots and Industrial Animal Farms

Many people may do not realize that industrial animal farming operations are among the largest consumers of antibiotics in the world. Industrial operations involve large amounts of animals, packed densely into enclosed spaces. In this type of environment, disease transmission is a major problem. To prevent disease outbreaks, many operations treat their animals prophylactically (continuously) with antibiotics. In fact, in the United States animal farming consumes more antibiotics than are used in human medicine.

Like highly unsanitary and overcrowded hospitals, the high level of antibiotic use in industrial animal farming drives the evolution of antibiotic resistance in bacteria. In addition, the sewage produced by these operations can contain significant levels of un-metabolized antibiotics. These residual antibiotics combined with the huge and diverse population of bacteria living in the untreated sewage encourages the transfer of antibiotic resistance genes among different species of bacteria. Industrial animal farms can also cause the spread of antibiotic resistant bacteria to neighboring wildlife. It also partly explains why detectable levels of antibiotics are found in many rivers, lakes and other waterways.

Nursing Homes, Sanitoriums and Other Residential Institutions

Many countries around the world place people who are elderly, infirm or disabled into various types of institutions. While the United States has started to moved away from the large-scale housing of these individuals, the practice is still common in many places around the world. In wealthier countries, these people are often placed into assisted living facilities, retirement homes and hospices.

These environments contain dense populations of people who have weakened immune systems, which allows for more frequent and longer lasting infections. Antibiotic use can be very high in many of these environments and prophylactic antibiotic use is common. The combination of large populations of immune-compromised people and extensive antibiotic use can contribute to the emergence of antibiotic resistant bacteria.


HIV and AIDS lead to higher rates of antibiotic resistance for two closely related reasons. First, because people who suffer from HIV and AIDS have an impaired immune system they are often highly susceptible to bacterial infection. As a result, many physicians place these patients on a permanent course of antibiotics to prevent infection. (Note: This is becoming less of a factor in places where effective anti-retrovirals are available, because they mitigate the need for prophylactic antibiotic treatment.)

The second reason HIV and AIDS foster antibiotic resistant bacteria is that they cause more infections to happen and they make antibiotics less effective (indirectly). Even in a person with a healthy immune system, a bacterial infection may not be completely eliminated by a course of antibiotics. However, in most cases the antibiotic weakens and kills most of the bacteria and the immune system is able to target and eliminate the surviving bacteria. But in a person with HIV, this small population of bacteria that remain after antibiotic treatment are not cleared by the immune system. This process selects for those bacteria that are slightly more resistant to the antibiotic treatment. Over time this process can drive Epigenetic Adaptation and select for Genetic Mutations that confer resistance.

Antibiotic Resistance and Acne Treatment

In the last ten years numerous studies have been done profiling the antibiotic susceptibility of the acne-causing bacteria, Propionibacterium acnes. The results tell a fascinating story. In countries where antibiotics are more frequently used to treat individuals with acne, antibiotic-resistant P. acnes bacteria tend to be more common. This means that in places like the United States and Europe, a significantly higher percentage of P. acnes bacteria have high-level antibiotic resistance than in places like Mexico, Chile and India.

Interestingly, the frequency of P. acnes bacteria resistant to a particular antibiotic varies from country to country, and this appears to reflect the differences in prescribing frequencies of different antibiotics for acne treatment between countries. In the United States, laboratory testing indicates that P. acnes bacteria that are resistant Macrolide and Tetracycline family antibiotics (the two antibiotic families most commonly used to treat acne) are becoming more common. But this trend is not true for all countries.


The Antibiotic Families


There are many different families of antibiotics. Each antibiotic family targets bacteria in a unique way. Each antibiotic family tends to be more effective against certain types of bacteria, and less effective against others.

Antibiotics and Acne Treatment

Antibiotics from several different families are used for the treatment of acne. The antibiotic families most commonly used in acne treatment are Macrolides, Tetracyclines, Pleuromutilins, Sulfonamides and Quinolones. Antibiotics can be used applied topically or ingested orally. The route of delivery, the ability of an antibiotic to accumulate in the skin and the susceptibility of P. acnes bacteria to an antibiotic all impact the efficacy of a given antibiotic treatment.

For more information about the sensitivity of Propionibacterium acnes (P. acnes) to specific antibiotics, visit our Antibiotic Susceptibility of Propionibacterium acnes page. For more information about the P. acnes bacterium, visit our What Is Propionibacterium acnes? page.

Antibiotic Families

Below is a summary of the different antibiotic families that are used in the treatment of acne:


Aminoglycoside Family Members: Gentamicin (Garamycin), Neomycin (Neosporin), Paromomycin (Gabbroral), Tobramycin (Tobrex).
Frequency of Use For Acne Treatment: Uncommon.
General Efficacy as Acne Treatments: Poor.
Frequency of High-Level Antibiotic Resistance: Very Common.

Aminoglycoside antibiotics tend to be ineffective treatments for acne vulgaris. The acne-causing P. acnes bacterium is naturally resistant to most antibiotics in the Aminoglycoside family.

Aminoglycoside antibiotics are modified sugar molecules that are pimarily effective against gram-negative bacteria (P. acnes bacteria are gram-positive). Aminoglycoside antibiotics work by binding to bacterial ribosomes and inhibiting the bacteria’s ability to synthesize new proteins. Aminoglycosides are popular antibiotics for topical first-aid treatments (the primary ingredient in Neosporin is neomycin, an aminoglycoside). Topical aminoglycoside ointments (eg. Neosporin) may help prevent secondary infections of damaged skin and/or popped pimples. Therefore, they may help prevent mild acne scarring and accelerate the healing process.


Amphenicol Family Members: Chloramphenicol (Clorin), Thiamphenicol (Biothicol).
Frequency of Use For Acne Treatment: Rare.
General Efficacy as Acne Treatments: Unknown.
Frequency of High-Level Antibiotic Resistance: Rare.

Amphenicols are a family of broad spectrum antibiotics that are used in many topical antibacterial medications, such as opthalmic solutions (eye drops). Amphenicols work by disrupting the ability of bacteria to synthesize new proteins. Antibiotic susceptibility testing indicates that P. acnes bacteria tend to be moderately susceptible to Amphenicols, and P. acnes bacteria with high-level resistance to Amphenicols are rare.

Amphenicols are rarely used for the treatment of acne. But topical formulations of Amphenicols (eg. Chloramphenicol) may be a useful acne treatment for some individuals. Topical Amphenicols may complement other types of acne treatments.


Cephalosporin Family Members: Cefaclor (Ceclor), Cefadroxil (Duricef), Cefdinir (Omnicef), Cefixime (Suprax), Cefpodoxime (Cefpo), Cefprozil (Cefzil), Cefradine (Cefradune), Ceftibuten (Cedax), Cephalexin (Keflex).
Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: OK.
Frequency of High-Level Antibiotic Resistance: Uncommon.

Cephalosporins are occasionally used as oral antibiotic treatments for moderate to severe acne symptoms (Acne Types: 2-4). Many individuals with acne have reported positive results from treatment with various Cephalosporin antibiotics. But not all acne patients achieve significant improvement with Cephalosporins.

Cephalosporins are type of beta-lactam antibiotic and they are structurally-related to the Penicillins. Cephalosporins kill bacteria by disrupting their cell walls via inhibition of peptidoglycan layer assembly. In contrast to Penicillins, Cephalosporins are effective against a broader range of bacteria and are more resistant to a bacterial antibiotic-resistance enzyme called Penicillinase. In antibiotic susceptibility testing, Cephalosporins were effective against P. acnes bacteria, but they tend to be less toxic to P. acnes than Penicillins.

Fusidic Acid

Fusidic Acid Family Members: Fusidic Acid (Fucidin).
Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: OK.
Frequency of High-Level Antibiotic Resistance: Uncommon.

Fusidic Acid is an antibiotic that prevents bacteria from synthesizing proteins by disrupting the function of a bacterial protein, Elongation Factor G (EF-G). Fusidic acid is available in oral and topical formulations. Topical Fusidic Acid is the form of this antibiotic that is generally used for the treatment of acne.

Antibiotic susceptibility testing indicates that the acne-causing P. acnes bacterium tends to be moderately susceptible to Fusidic Acid. Many patients have reported positive results with the use of topical Fusidic Acid. Fusidic Acid is generally used in combination with a complementary antibiotic.


Lincosamide Family Members: Clindamycin (Cleocin).
Frequency of Use For Acne Treatment: Very Common.
General Efficacy as Acne Treatments: Good.
Frequency of High-Level Antibiotic Resistance: Occasional (Increasing).

One member of the Lincosamide family, Clindamycin, is frequently used for the treatment of acne. Clindamycin is generally used as a topical medication, but oral versions of this antibiotic are also available. Topical Clindamycin can be an effective treatment for mild to moderate acne symptoms (Acne Types: 1-3).

Lincosamides are structurally related to the Macrolide family of antibiotics. Lincosamides work by binding to the bacterial 23S ribosome, which inhibits the ability of the bacteria to synthesize new proteins. Lincosamides are generally very toxic to P. acnes bacteria, but Lincosamide-resistant P. acnes bacteria are becoming increasingly common. Research reports indicate that Clindamycin-resistant P. acnes bacteria are especially common in the United States and Europe.


Macrolide Family Members: Azithromycin (Zithromax), Clarithromycin (Biaxin), Dirithromycin (Dynabac), Erythromycin (E-Mycin), Josamycin (Josalid), Pristinamycin (Pyostacine), Roxithromycin (Roximycin), Spiramycin (Spirex), Telithromycin (Ketek).
Frequency of Use For Acne Treatment: Common.
General Efficacy as Acne Treatments: Good.
Frequency of High-Level Antibiotic Resistance: Occasional (Increasing).

Macrolides are a diverse class of antibiotics that includes several medications that are commonly used for the treatment of acne. Macrolides work by preventing bacteria from synthesizing new proteins. They do this by binding to a bacterial enzyme called Peptidyltransferase and/or binding to the bacterial 50S ribosome subunit. Macrolides are structurally related to Lincosamide antibiotics.

Macrolides are commonly used to treat infections caused by gram-positive bacteria. Topical macrolide antibiotics (eg. Erythromycin) are a very common treatment for acne, but oral Macrolides are also widely used. Antibiotic susceptibility testing indicates that Macrolides are usually very toxic to acne-causing P. acnes bacteria. However, Macrolide-resistant P. acnes bacteria are becoming increasingly common in many areas. Current research now indicates that a significant proportion of acne-associated P. acnes bacteria in the United States and Europe have now acquired some level of resistance to Macrolide antibiotics.


Nitroimidazole Family Members: Metronidazole (Flagyl).
Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Poor.
Frequency of High-Level Antibiotic Resistance: Very Common.

Nitroimidazole antibiotics are used to treat infections that are caused by both bacteria and parasites. Nitroimidazoles work by disrupting the ability of microbes to synthesize new DNA.

Metronidazole is the only member of the Nitroimidazole family that is routinely used in the treatment of acne. Topical Metronidazole is also a common treatment for Rosacea. Antibiotic susceptibility testing indicates that P. acnes bacteria are naturally resistant to Metronidazole. However, many individuals with acne report improvements in their symptoms following use of Metronidazole. These improvements may be the result of Metronidazole’s ability to kill other types of bacteria that can contribute to acne symptoms (eg. S. aureus).


Oxazolidinone Family Members: Linezolid (Zyvox) and Tedizolid (Sivextro).
Frequency of Use For Acne Treatment: Rare.
General Efficacy as Acne Treatments: Unknown.
Frequency of High-Level Antibiotic Resistance: Rare.

Oxazolidinones are a relatively new class of antibiotics that are used to treat certain types of inections caused by gram-positive bacteria. Oxazolidinones prevent bacteria from synthesizing new proteins by preventing N-formylmethionyl-tRNA from binding to the bacterial ribosome.

Oxazolidinones are rarely used in the treatment of acne. However, antibiotic susceptibility testing indicates that they are active against the acne-causing P. acnes bacteria. These antibiotics may become more widely used as acne treatments in the future.


Penicillin Family Members: Amoxicillin (Amoxil), Ampicillin (Polycillin), Ampicillin + Clavulanic Acid (Augmentin), Cloxacillin (Cloxapen), Dicloxacillin (Diclocil)Flucloxacillin (Floxapen), Penicillin G (BenzylPenicillin), Penicillin V (Phenoxymethylpenicillin).
Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Good.
Frequency of High-Level Antibiotic Resistance: Rare.

Penicillin was discovered in 1920s by the Nobel Prize winning scientist Alexander Fleming. The discovery of Penicillin revolutionized the treatment of bacterial infections and initiated the modern era of antibiotics. Penicillins are beta lactam antibiotics that are structurally related to the Cephalosporins. Penicillin antibiotics work by damaging the cell wall of susceptible bacteria. They are most effective against gram positive bacteria, a group that includes the acne-causing P. acnes bacterium.

Penicillins are available in topical and oral formulations, both of which are occasionally used for the treatment of acne. Individuals with acne have generally reported positive results from treatments with Penicillin family antibiotics. Antibiotic susceptibility testing has shown that most P. acnes bacteria are extremely sensitive to Penicillins.


Pleuromutilin Family Members: Retapamulin (Altabax).
Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Good.
Frequency of High-Level Antibiotic Resistance: Rare.

Pleuromutilins are new class of antibiotics that are used to treat certain types of infections caused by gram-positive bacteria. Pleuromutilins work by preventing bacteria from synthesizing new proteins via inhibition of a bacterial enzyme called Peptidyl Transferase.

Antibiotic susceptibility testing indicates that P. acnes bacteria are highly sensitive to Pleuromutilin antibiotics, such as Retapamulin. Retapamulin is the only antibiotic in this family that is currently approved for human use. Retapamulin is used as a topical treatment for several kinds of skin infections, including acne. Patient reports and clincal research indicate that topical Retapamulin can significantly improve acne symptoms for most patients. The use of topical Retapamulin as a treatment for acne is likely to become more common as this medication becomes more widely available.


Quinolone Family Members: Ciprofloxacin (Cipro), Gatifloxacin (Tequin), Gemifloxacin (Toplon), Levofloxacin (Levaquin), Moxifloxacin (Avelox), Nadifloxacin (Nadixa), Nalidixic Acid (Wintomylon), Norfloxacin (Norflox), Ofloxacin (Floxin) and Sparfloxacin (Zagam).
Frequency of Use For Acne Treatment: Uncommon.
General Efficacy as Acne Treatments: Good.
Frequency of High-Level Antibiotic Resistance: Rare.

Quinolones are a class of broad-spectrum antibiotics that were discovered in the 1960s. Quinolones inhibit bacterial growth by preventing bacteria from reading and duplicating their DNA. Quinolones are effective against both gram-negative and gram-positive bacteria.

Quinolones are commonly used in combination with other antibiotics. They are rarely used for long term treatments or prophylaxis. This is because bacteria can develop resistance to Quinolones easire than they can to most other antibiotics. Quinolones also tend to have higher rates of side effects than other antibiotics.

Laboratory testing indicates that P. acnes bacteria are generally susceptible to most antibiotics in the Quinolone family. However, Quinolones are not commonly used for the treatment of acne vulgaris. Patient reports indicate that oral Quinolones can improve acne symptoms in many patients, at least temporarily. Most Quinolones are only available in oral formulations, but there is one fairly new Quinolone for topical use that is gaining some buzz – Nadifloxacin. Topical Nadifloxacin is not available in all countries, but several studies suggest that this medication can significanly improve acne symptoms in some individuals. Because it is administered topically, Nadifloxacin has a much better safety profile than most oral antibiotics.


Rifamycin Family Members: Rifabutin (Mycobutin), Rifampicin (Rifampin), Rifapentine (Priftin).
Frequency of Use For Acne Treatment: Rare.
General Efficacy as Acne Treatments: Unknown.
Frequency of High-Level Antibiotic Resistance: Rare.

Rifamycins were discovered in the 1950’s. Rifamycins work by preventing bacteria from reading their own DNA (they block RNA synthesis). Rifamycins are important components of the combined antibiotic therapies used to treat tuberculosis. Because Rifamycins are an essential part of anti-tuberculosis therapy, their use in the treatment of other infections has been restricted in some places. Antibiotic resistance to Rifamycins tend to develop faster than resistance to other antibiotics.

Antibiotic susceptibility testing indicates that Rifamycins are very toxic to most strains of P. acnes bacteria. However, Rifamycins are rarely used for the treatment of acne vulgaris. Several research and patient reports suggest that Rifamycins (Rifampicin in particular) can be very effective at improving acne symptoms for some individuals. More research is needed on the utility of Rifamycin family antibiotics in the treatment of acne. Rifamycines are generally only available in oral formulations.


Sulfonamide Family Members: Co-Trimoxazole (Bactrim), Dapsone (Aczone), Mafenide (Sulfamylon), Silver Sulfadiazine (Silvadene), Sulfacetamide (Clenia), Sulfadimethoxine (Albon), Sulfadoxine (Sulphadoxine), Sulfafurazole (Sulfisoxazole), Sulfamethoxazole (SMX) and Sulfathiazole (Sulfatiazol).
Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Good.
Frequency of High-Level Antibiotic Resistance: Rare.

Sulfonamides are a class of antibiotics whose molecules all contain sulfur atoms. They were among the first oral antibiotics to be used in human medicine and their use became widespread in the 1930s. Sulfonamides work by preventing bacteria from synthesizing an essential vitamin, Folate (Vitamin B9).

Antibiotics in the Sulfonamide family are available in many oral and topical formulations. Sulfonamides are also widely used in veterinary medicine. Antibiotic susceptibility testing indicates that ance-causing P. acnes bacteria tend to be moderately susceptible to Sulfonamides. Topical sulfonamides (eg. Dapsone, Mafenide, Silver Sulfadiazine and Sulfacetamide) are occassionally used for the treatment of mild to moderate acne symptoms (Acne Types: 1-3) and many individuals have reported positive results with these medications. Because Sulfonamides have a unique mechanism of action, they can be combined with many other acne medications.

Only one oral Sulfonamide antibiotic is routinely used as an acne treatment – Co-Trimoxazole. Co-Trimoxazole is a combination of two antibiotics Sulfamethoxazole and Trimethoprim. These two antibiotics work synergistically and are substantially more effective in together than either is alone. Co-Trimoxazole is an important acne treatment because it can be very effective for individuals with moderate to severe inflammatory acne (Acne Types: 3-4). However, Co-trimoxazole is not routinely prescribed for the treatment of acne vulgaris in many places. This is primarily the result of two factors. First, allergic reactions to oral Sulfonamides can be more severe than allergic reactions caused by other antibiotics. Second, the use of Co-Trimoxazole as an acne treatment is considered “”off-label”” in many countries, including the United States. As a result, many physicians do not feel comfortable considering Co-Trimoxazole for the treatment of acne. But for those patients without allergies to Sulfonamides, Co-trimoxazole treatments may yield substantial improvements in difficult-to-treat acne cases.


Tetracycline Family Members: Demeclocycline (Declomycin), Doxycycline (Vibramycin), Lymecycline (Tetralysal), Minocycline (Minocin), Oxytetracycline and Tetracycline (Sumycin).
Frequency of Use For Acne Treatment: Very Common.
General Efficacy as Acne Treatments: OK.
Frequency of High-Level Antibiotic Resistance: Common.

Tetracyclines were discovered in the 1940s by the plant scientist Benjamin Duggar. Tetracyclines are a class of broad-spectrum antibiotics that work by inhibiting protein synthesis in susceptible bacteria via disruption of the 30S Ribosome. In the past, Tetracyclines were frequently used for the treatment of many different types of infections. But in the last thirty years, the efficacy of Tetracyclines has decreased substantially due to the spread of Tetracycline-resistant bacteria.

Tetracyclines are the antibiotic family of choice for many dermatologists when treating acne. Oral Tetracyclines are commonly used for the treatment of moderate to severe acne symptoms (Acne Types: 2-4). However, antibiotic susceptibility reports clearly demonstrate that Tetracycline-resistant P. acnes bacteria are common, particularly in certain regions of the world (eg. United States and Europe).

When acne is caused by Tetracycline-susceptible bacteria, treatment with Tetracyclines (particularly Minocycline) can be very effective. But current patient reports and clinical research indicate that Tetracyclines yield little to no improvement in acne symptoms for many individuals. The likely reason why Tetracyclines are so frequently used for the treatment of acne, despite their mediocre efficacy and the prevalence of Tetracycline-resistant P. acnes bacteria, is that many of the prescribing guidelines now in use for the treatment of acne were developed decades ago, when the patterns of antibiotic resistance among P. acnes bacteria were different.

Additional Antibiotics


Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Unkown.
Frequency of High-Level Antibiotic Resistance: Common.


Frequency of Use For Acne Treatment: Rare.
General Efficacy as Acne Treatments: Unkown.
Frequency of High-Level Antibiotic Resistance: Very Common.


Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Unkown.
Frequency of High-Level Antibiotic Resistance: Common.


Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: Poor.
Frequency of High-Level Antibiotic Resistance: Very Common.


Frequency of Use For Acne Treatment: Rare.
General Efficacy as Acne Treatments: Unknown.
Frequency of High-Level Antibiotic Resistance: Rare.


Frequency of Use For Acne Treatment: Occasional.
General Efficacy as Acne Treatments: OK.
Frequency of High-Level Antibiotic Resistance: Rare.

The Antibiotic Susceptibility of Propionibacterium acnes


Antibiotics are medications that are used to treat bacterial infections, including acne. The acne-causing Propionibacterium acnes (P. acnes) bacterium is naturally resistant to some antibiotics, and naturally susceptible to others. For the past 50 years, physicians and researchers have been screening the susceptibility of P. acnes bacteria to different antibiotics. The results from these studies clearly demonstrate that in many places, P. acnes bacteria are becoming more resistant to certain classes of antibiotics.

The Rise of Antibiotic Resistance in P. acnes Bacteria

In many countries, a significant percentage of the P. acnes bacteria isolated from acne patients are now resistant to the some of the antibiotics that are commonly used in acne treatment (eg. Clindamycin, Erythromycin, Tetracycline, Doxycycline and Minocycline). The patterns of antibiotic resistance among acne-causing P. acnes bacteria tend to vary between countries. These variations are influenced by many factors. Not all of these factors are directly associated with acne vulgaris.

What Does Antibiotic Resistance and Susceptibility Mean?

Not all antibiotics are created equal. The same is true for bacteria. Some types of antibiotics are highly effective against certain types of bacteria, but useless against other types of bacteria. Antibiotic susceptibility and resistance is a dynamic process that is constantly changing. Over time, certain types of bacteria may gain or lose resistance to particular antibiotics. The general trend is that over time, bacterial resistance to commonly-used antibiotics increases, but this is not a uniform process.

How Does Antibiotic Susceptibility Testing Work?

Antibiotic susceptibility testing is usually conducted by growing bacteria in special petri dishes with small disks that contain known amount of antibiotics. When scientists test the susceptibility of bacteria to different antibiotics, they generally focus on the Minimum Inhibitory Concentration (MIC) of an antibiotic. The MIC is defined as the lowest concentration of an antimicrobial compound that will inhibit the visible growth of a microorganism after overnight incubation.

The Limitations of Antibiotic Resistance Testing

The primary limitation of conventional antibiotic resistance testing is that the susceptibility of a bacteria to an antibiotic is often different when it is growing on a petri dish versus when it is growing in the body. There are 2 main reasons for this:

The first reason for these differences are because bacteria adapt to their environment. P. acnes bacteria that is growing in a hair follicle and feeding on sebum from the sebaceous glands has a different metabolic profile than one growing on a petri dish and feeding on a bacterial nutrition supplement. In addition, bacteria can modulate expression of surface proteins, cell wall structures and antibiotic resistance genes in response to changes in their environment. The adaptation of a bacteria to its specific environment can have a profound effect on its susceptibility to a particular antibiotic.

The second major limitation with antibiotic susceptibility testing is that antibiotics are not evenly dispersed throughout the different tissues in the body. Different types of antibiotics tend to accumulate in different tissues. Many antibiotics do not effectively accumulate in the skin, which means that they may not inhibit acne-causing bacteria growing deep inside follicles. Even if a bacteria is highly susceptible to a particular antibiotic in laboratory testing, if that antibiotic does not make it to the site of infection at a sufficient concentration, it is not going to be an effective treatment.

What Causes Antibiotic Resistance?

A commonly held belief is that the over-use of antibiotics in an outpatient setting and patients that fail to complete their prescribed antibiotic treatments are the primary causes of emerging antibiotic resistance. While these two factors do contribute to the growing incidence of antibiotic resistant infections, they are far from the only causes. Other sources of antibiotic-resistant bacteria include antibiotic use in commercial livestock farming, unsatisfactory hygiene in institutional settings (hospitals, nursing homes, prisons) and HIV/AIDS. For an in-depth discussion of both the mechanisms and causes of antibiotic resistance read – How Do Bacteria Become Resistant to Antibiotics?

The Emergence of Antibiotic Resistant Strains of P. acnes

Starting in the 1990’s some popular antibiotics started becoming less effective for the treatment of acne. This change was particularly pronounced in places where acne vulgaris was routinely treated with antibiotics (eg. North America and Europe). A 2001 study by Ross, et al examined P. acnes isolated from acne patients and found that the bacteria was much more likely to be resistant to commonly used anti-acne antibiotics than they had been in the past. In particular, they found that most of the bacteria was resistant to Macrolide Family (eg. Erythromycin, Azithromycin, Clindamycin) and Tetracycline Family (Minocycline, Doxycycline) antibiotics. It is unlikely to be a coincidence that these two families of antibiotics include the most commonly used anti-acne antibiotics.

Antibiotic resistance testing clearly indicates that acne-causing P. acnes bacteria are becoming increasingly resistant to the antibiotics commonly used as acne treatments. Particularly in places like Europe and the United States, a significant percent of bacteria isolated from acne patients are now show an elevated level of antibiotic resistance. Generally speaking, the data indicates that in Europe, resistance to Macrolide antibiotics is very high, and resistance to Tetracycline antibiotics is also elevated. The situation is similar in the US, but Tetracycline resistance appears to be more common.

The scientific research also clearly shows that some of the antibiotic treatments that have been the mainstay of dermatologists in the fight against acne, are now becoming ineffective. As a result, for patients who have P. acnes infections that are resistant to these common treatments, it may be helpful to explore alternative types of anti-acne medications, such as Retinoids, Hormonal Treatments, Naturopathic Treatments and Light & Laser Therapies.

Antibiotic Resistance and Susceptibility Test Results for Propionibacterium acnes

Scientists have been testing antibiotics against P. acnes bacteria for over forty years. To summarize this history of testing into a single document, we have compiled a composite chart that includes the results of many of these research studies on the antibiotic susceptibility screens of P. acnes bacteria.

How To Read Our Composite Antibiotic Susceptibility Chart

Many studies use different standards and measurements. We have translated these various results into a simple 1 (Worst) to 5 (Best) scale. The lower the value the LESS effective the antibiotic was in testing. The higher the value the MORE effective the antibiotic was. The average score for each medication is listed on the left hand side of the chart and is color coded (red = least effective, yellow = moderately effective, green = most effective). The average score for each family of antibiotic is also listed next to the name of that family. On the chart itself, a box that is highlighted in red indicates that scientists detected P. acnes bacteria that were highly resistant to that particular antibiotic.

Sebaceous Glands

Sebaceous glands produce sebum, which is responsible for moisturizing and protecting skin and hair. Sebaceous glands are essential components of healthy skin. Damaged or malfunctioning sebaceous glands contribute to many dermatological conditions, including acne vulgaris.

Structure of the Sebaceous Glands

Sebaceous glands are clusters of specialized cells in the skin. These specialized cells are called sebocytes. Sebocytes are responsible for the synthesis and secretion of sebum. Sebum is a complex blend of fatty acids, waxes, lipids and other molecules that are responsible for moisturizing, lubricating and protecting the skin.

Sebocytes are similar to adipose cells (fat cells) because they accumulate large amounts of fats and lipids. But unlike adipose cells, sebocytes do not store energy. Rather, like true patriots, they sacrifice themselves for the greater good and undergo apoptosis (commit suicide). The death of the sebocyte releases the sebum stored within the cell and this sebum is exported through the hair follicle to the skin surface. Once at the skin surface, the sebum then diffuses into the epidermis where it moisturizes and protects the tissue.

Sebocyte Development

Sebaceous glands are composed of two main types of sebocyte cells – Peripheral Sebocytes and Central Sebocytes. Peripheral Sebocyte Cells (PCs) line the outer edge of the sebaceous gland. Peripheral sebocytes are where the cellular reproduction happens, and where the sebaceous gland originates and grows. Peripheral sebocytes accumulate relatively little sebum compared to their more mature counterpart, Central Sebocyte Cells (CCs). Central sebocytes originate from proliferating peripheral sebocytes.

As central sebocytes mature, they migrate from the edges to the center of the sebaceous gland. During this process they begin to synthesize and accumulate large reserves of sebum, which they store in specialized storage structures inside the cell, called vacuoles. As they continue to mature, they migrate towards the hair follicle. When completely mature sebocytes reach the follicle opening, they undergo cellular suicide and spill their contents (sebum) into the follicle. This sebum then travels up the follicle to the surface of the skin, where it is essential for the maintenance of the epidermis.

Sebaceous Glands and Acne

Sebaceous glands can contribute to the development of acne in several ways. One of the most common problems faced by acne sufferers involves overactive sebaceous glands and sebaceous hyperplasia (enlarged sebaceous glands). These conditions can lead to an overproduction of sebum. Excess sebum can facilitate the growth of bacteria (eg. Propionibacterium acnes) that contribute to acne symptoms. These bacteria can utilize sebum as a food source and large food supplies encourage bacterial growth.

Excess sebum production by overactive sebaceous glands can also cause the formation keratinized plugs (clogged pores) that block the follicle and spur the development of inflammatory lesions. Sebum itself and the byproducts of its breakdown can also be directly comedogenic (acne-causing) because byproducts of sebum metabolism can cause inflammation.

Sebaceous Glands and Hormones

Androgen (male) hormones stimulate the growth and activity of the sebaceous glands. Hormonal changes are largely responsible for the increase in acne that can occur during adolescence, particularly among males. Women with elevated androgen levels can also experience problems with androgen-dependent sebaceous hyperplasia. Excessive levels of androgen hormones can be treated with androgen inhibitors, which suppress their effects. Sebaceous glands also appear to respond to non-androgen hormones, like Insulin Growth Factor (IGF), a hormone that has been loosely tied to milk consumption.

Sebaceous Glands and Retinoids

Retinoids are a class of acne treatment that can reduce the activity of sebaceous glands. When sebocytes are exposed to retinoid medications, it initiates a cascade of changes that dramatically alter their growth pattern. Retinoids cause sebaceous glands to slow their frowth rate and decrease in overall size. These changes can result in a significant reduction of sebum production. In some cases, treatment with oral retinoids (such as Accutane/Isotretinoin) can decrease the production of sebum by up to 90%.

Retinoids can also affect the proliferation of other types of cells. The broad activity of retinoids on a diverse range of cells contributes to many of the possible side effects of this class of medication. The most dangerous side effect of retinoid treatment is potential damage to a developing fetus. Retinoids dramatically disrupt normal embryonic development and leads to severe birth defects. For this reason, oral retinoids (eg. Isotretinoin/Accutane) are tightly controlled in many countries, particularly for women.

Retinoid Medications

Retinoids are available in both oral and topical formulations. Isotretinoin (Accutane) is the only retinoid widely available as an oral treatment. Isotretinoin, Tretinoin, Adapalene and Tazarotene are all retinoids that are available as topical treatments. Topical retinoids tend to be less effective acne treatments than oral retinoids, but have fewer side effects.

Additional Treatments for Sebaceous Hyperplasia

Emerging therapies that utilize Light and Laser Treatments are becoming increasingly popular options for dealing with problematic sebaceous glands. Specialized Photodynamic Therapy (PDT) and Diode Lasers can be used to specifically target, damage and destroy sebaceous glands. While these treatments can be quite expensive and incompletely effective, their development offers the promise of additional treatments for acne sufferers.


Sebaceous Gland Lipids: Friend or Foe? Smith, et al. 2008.
Sebaceous Gland Receptors. Zouboulis. 2009.
Differentiation of the Sebaceous Gland. Niemann. 2009.
The Sebocyte Culture: A Model to Study the Pathophysiology of the Sebaceous Gland in Sebostasis, Seborrhoea and Acne. Zouboulis, et al. 2008.
The Role of Specific Retinoid Receptors in Sebocyte Growth and Differentiation in Culture Kim, et al. 1999.
Sebaceous Gland Lipids Picardo, et al. 2009.
Isotretinoin Revisited: Pluripotent Effects on Human Sebaceous Gland Cells Zouboulis. 2006.
Selective photothermolysis of the sebaceous glands for acne treatment. Lloyd, et al. 2002.
Significant reduction of inflammation and sebaceous glands size in acne vulgaris lesions after intense pulsed light treatment. Barakat, et al. 2017.
Role of sebaceous glands in inflammatory dermatoses. Shi, et al. 2015.
Beyond acne: Current aspects of sebaceous gland biology and function. Zouboulis, et al. 2016.
Photodynamic Therapy for Acne Vulgaris and Sebaceous Gland Hyperplasia. Taub, et al. 2016.
The role of androgen under normal and pathological conditions in sebaceous glands: the possibility of target therapy. Azmahani, et al. 2016.
Modulation of Toll Like Receptor-2 on sebaceous gland by the treatment of adult female acne. Rocha, et al. 2017.

Acne at a Cellular Level

Most people can recognize acne when it presents on the face or body. Most people also have the vague understanding that acne is associated with oily skin and an excess production of sebum. But beyond that, few people really grasp what is actually happening at the microscopic level of a pimple.

Understanding the physiological and pathological processes behind acne can help you sort out what treatments and advice can help you make positive changes in your acne. A better understanding of the science of acne can also help you identify the claims that have no basis in scientific reality and should be ignored.

What Causes Acne?

Acne is caused by a combination of factors that result in blocked pores, an accumulation of sebum, bacterial growth and inflammation. Acne generally occurs within the hair follicle, when excess sebum is produced by the sebaceous glands and creates a plug that blocks the follicle.

Clogged follicles create a micro-environment that favors the growth of certain types of bacteria, such as Propionibacterium acnes and Staphylococcus aureus. The presence of this bacteria triggers an immune response, which is characterized by inflammation, increased blood flow (redness) and the recruitment of white blood cells to the follicle.

The initial inflammation of an acne lesion can cause damage to the follicle and surrounding tissue. This inflammation can then increase the growth of bacteria, which creates a positive feedback loop of additional inflammation. In some individuals, this process becomes a vicious cycle and leads to extensive acne and significant damage to the skin and the subcutaneous matrix that supports healthy skin. Severe and repeated damage that is caused by inflammatory acne lesions can cause permanent acne scars.

Sebum and a Healthy Follicle

Sebum is a mixture of fatty acids and lipids that is essential for lubricating and protecting healthy skin. Sebum is produced by Sebaceous Glands, which are attached to the base of hair follicles. In a healthy follicle, the sebaceous gland produces the appropriate amount of sebum to maintain the health of the surrounding skin, and the sebum is efficiently extruded along with the hair.

For individuals with acne, several things can happen that disrupt the delicate balance of sebum production. Normal sebaceous glands are relatively small and produce a minimal amount of sebum. However, excessive growth of the sebaceous glands (sebaceous hyperplasia) and overproduction of sebum can be an important contributor to acne symptoms. Sebaceous hyperplasia can be triggered by increases in androgen hormones, which is common for males during puberty.

Sebum itself is created by the breakdown of the cells that form the sebaceous gland. Sebaceous cells replicate at the base of the gland and move up towards the hair follicle as the new cells proliferate. As the maturing cells approach the hair follicle, they undergo apoptosis and die. The cells are lipid rich (oil) and the byproducts left over as the cells dissolve composes the sebum that lubricates and protects the hair. Proliferation of the sebaceous glands causes an increase in the production of sebum, which can present as oily skin and hair.

Sebum can also serve as a nutrition source for bacteria that reside inside the hair follicle, such as P. acnes and S. aureus. Excess amounts of sebum can encourage bacterial growth and lead to inflammation, redness and an infiltration of white blood cells (pus). If a hair follicle is plugged near the surface, this process can often lead to the formulation of a surface pustule (whitehead). However, for many people who suffer with inflammatory acne, the pustules are often formed deep in the tissue and away from the surface. These deep-seated pustules are responsible for nodular and cystic acne symptoms (Acne Types: 3-4).

The deep-seated pustules that form in nodular and cystic acne lesions are surrounded by tissue and it is difficult to drain the pus and bacteria to the surface (eg. “pop” or lance the pimple). Individuals with acne lesions that are significantly inflamed or painful should generally avoid trying to pop these pimples at home. Effectively and safely draining these lesions can reduce symptoms and accelerate healing, but these procedures should be performed by a trained medical professional. Many times, continued sebum production, bacterial growth and inflammation within a plugged follicle can cause the follicle to rupture and drain into the surrounding tissue. This process can lead to further inflammation, dissemination of the bacterial infection, worsening acne symptoms and the formation of acne scars.


The human sebocyte culture model provides new insights into development and management of seborrhoea and acne. Zouboulis, et al. 1998.
Severity of acne and sebum excretion rate. Cotterill, et al. 1971.
Genetic control of sebum excretion and acne—a twin study. Walton, et al. 1988.
A review of the role of sebum in the mechanism of acne pathogenesis. Li, et al. 2017.
From new findings in acne pathogenesis to new approaches in treatment. Gollnick. 2015.
A systematic review and meta-analysis on Staphylococcus aureus carriage in psoriasis, acne and rosacea. Totte, et al. 2016.
Evolving perspectives on the etiology and pathogenesis of acne vulgaris. Eichenfield, et al. 2015.

What is Propionibacterium acnes?

Answer: Propionibacterium acnes (P. acnes) is a bacteria that can colonize the the skin and hair follicles. Excessive growth of this bacteria in the skin contributes to acne vulgaris.

Propionibacterium acnes – The Basics

Propionibacterium acnes (P. acnes) is a bacteria that grows deep inside of pores, where it feeds on the sebum that is produced by the sebaceous glands that surround the base of the hair shaft. Most individuals with acne symptoms have an overgrowth of P. acnes bacteria in their skin. Several research studies have indicated that specific strains of P. acnes bacteria are commonly associated with acne vulgaris. However, other bacteria (e.g. Staphylococcus and Corynebacterium) can also reside in the skin and contribute to acne.

Biology of Propionibacterium Acnes

P. acnes are a type of “gram-positive” bacteria. Gram-positive bacteria produce a positive result in the Gram stain test, which is a common way to test for bacterial infections. Gram positive bacteria have thick cell walls that that help protect them from their environment. There are many other types of gram-positive bacteria that cause infections, such as Staphylococcus (MRSA), Streptococcus (Strep Throat) and Listeria (food poisoning).

P. acnes is an oxygen-tolerant, anaerobic bacteria that prefers to grow in low oxygen environments (like deep within a plugged follicle). P. acnes bacteria can form sticky clumps of bacteria known as biofilms that help them to attach to surfaces and modulate their environment. In many cases, bacterial biofilms have been shown to contribute to long term infections, and may play a role in the persistence of P. acnes infection in some individuals.

The Relationship Between Sebum and Propionibacterium acnes

P. acnes bacteria use sebum as an energy source (food). Sebum production is partially controlled by hormones (androgens) and sebum production is elevated in many people with acne. The excess production of sebum increases the growth of P. acnes bacteria, causes oily skin and creates plugs that block the opening of the hair follicle. In a plugged follicle, the low oxygen levels and accumulating sebum create an excellent environment for the growth of P. acnes bacteria.

P. acnes bacteria produce specialized enzymes that help them digest the fatty acids and triglycerides that are abundant in sebum. In an anaerobic environment, P. acnes ferments the fatty acids and triglycerides, and releases short chain fatty acids and propionic acid as metabolic byproducts (that’s why it’s called Propionibacterium). Research indicates that the breakdown of sebum by P. acnes can create comedogenic byproducts, and this may be a contributing factor to the severity of acne symptoms. There is also some evidence that presence of P. acnes bacteria may directly stimulate the sebaceous glands to produce additional sebum. If this is true, it is possible that the bacteria has adapted to the environment of the follicle, and part of this adaptation includes a mechanism to get more food (sebum) from the surrounding tissue.

Propionibacterium acnes, Inflammation and Acne

The P. acnes bacteria itself does not directly cause significant damage to the skin. Instead, most of the damage caused by inflammation that results from the body’s own immune response to the presence of the P. acnes bacteria.

Particularly for individuals who suffer from inflammatory acne (Acne Types: 2-4), the immune system over-reacts to the presence of bacteria and sends in lots of white blood cells. Each person’s immune system is different, and some immune systems are more sensitive to P. acnes bacteria than others. People with a naturally strong immune response to P. acnes bacteria have an increased risk of developing acne symptoms.

Many of the individual components that make up the bacteria are easily recognized by the immune system as “foreign” molecules. This material includes components of the bacterial cell wall, like peptidoglycans, lipopolysacharides and proteins. Even the DNA from P. acnes bacteria is recognized as foreign by the immune system. The bacteria doesn’t even have to be alive to trigger a powerful immune response, dead bacteria can also set off alarms within the immune system.

Dysfunctional Immune Responses and Acne vulgaris

In some people who suffer from moderate to severe acne (Acne Types: 2-4), the root of the problem can be traced back to a faulty immune response. There are two main types of immune system malfunctions that can lead to acne symptoms:

Hyper-Sensitive Response

In a hyper-sensitive immune response, an individual’s immune system reacts over-aggressively to the presence of the bacteria and produces large amounts of inflammatory signals. These inflammatory cytokines induce white blood cells to release large amounts of digestive enzymes and free radicals into the site of infection.

For individuals with acne, this immune response is often poorly-targeted against the infectious agent and it causes a lot of unnecessary collateral damage to the surrounding tissue. This collateral damage can actually make it more difficult for the immune system to fight off the infection. The damage often stimulates the production of more inflammatory signals and this can become a vicious cycle. This type of inflammatory cycle is responsible for the symptoms observed in moderate-to-severe inflammatory acne. This inflammation can also permanently damage the skin and lead to acne scars.

Impaired Bacterial Killing Ability

Another type of dysfunctional immune response can occur when an individual’s white blood cells do not effectively destroy and process the bacteria that they encounter. In an ideal situation, white blood cells called Macrophages capture (phagocytose) all of the bacteria that they come in contact with. Once captured, the Macrophage isolates the bacteria into an special intracellular compartment called a phagosome. It then pumps antibacterial molecules and digestive enzymes into this compartment. These molecules and enzymes kill the bacteria and break it down into small pieces. Some of these pieces are then used by the immune system to design antibodies that target the bacteria and prevent future infections. The immune system uses certain pieces of the digested bacteria to train specialized white blood cells to identify and respond to infections caused by that bacteria.

Some individuals who suffer from chronic inflammatory infections (eg. acne) have white blood cells that are able to ingest bacteria normally, but are not able to efficiently kill certain types of bacteria that they ingest. In this situation, the white blood cell will often continue to secrete lots of inflammatory signals till it exhausts itself and dies in a process called apoptosis. After the white blood cell dies, the bacteria may not be dead, in which case it can sometimes escape and continue proliferating.


Both of the above examples of immune system dysfunction are usually genetic in origin. The susceptibility to acne vulgaris is appears to be partially hereditary. Individuals whose parents experienced difficulty with acne have an increased risk of developing acne symptoms.

How to Treat P. acnes Bacteria

Antibiotics and Other Antibacterial Compounds

Extensive screening has been done to test the susceptibility of P. acnes bacteria to different classes of antibiotics. In general, what researchers have found is that P. acnes is moderately susceptible, when directly exposed, to many classes of antibiotics.

Researchers have also found that P. acnes bacteria is becoming increasingly resistant to some of the common antibiotics used to treat acne, like erythromycin and tetracycline family drugs (tetracycline, doxycycline and minocycline). Interestingly, numerous studies have shown that P. acnesbacteria is extremely sensitive to Penicillin, which was one of the first antibiotics ever developed.

It is important to keep in mind that these tests are primarily done on a Petri dish in a laboratory. When asking whether an antibiotic is effective when treating a clinical acne infection there are additional factors that need to be considered. The biggest question is whether the antibiotic makes it to the site of infection. Many antibiotics may be effective at killing P. acnes bacteria on a Petri dish, but they do not accumulate in sufficient concentration in the follicle and sebaceous glands to be effective at treating active acne infections.

Several Over-The-Counter medications, like benzoyl peroxide and triclosan, are also directly toxic to P. acnes bacteria. However, these topically applied medications have difficulty penetrating to the base of the hair follicle, which is where the P. acnes bacteria are causing problems.

Retinoids and Hormonal Treatments

P. acnes bacteria use the fatty acids and triglycerides found in sebum as its primary food source. Limiting the amount of sebum production can suppress the growth of P. acnes bacteria by reducing its food supply.

Treatment with retinoids can decrease the production of sebum in the skin. This is true for both oral retinoids (eg. Isotretinoin/Accutane) and topical retinoids (eg. Tretinoin/Retin-A, Adapalene/Differin). Hormonal treatments such as androgen inhibitors (eg. Spironolactone, Cyproterone) and birth control pills may also decrease sebum production.

Light and Laser Treatments

Certain light and laser therapies can also decrease the production of sebum. Diode lasers can be used to treat overactive sebaceous glands, thereby reducing the amount of sebum.

Blue light phototherapy and Photodynamic Therapy (PDT) can be used to directly kill P. acnes bacteria growing in the skin. These therapies work by using high intensity light of a specific color (wavelenght) to excite a bacterial molecule called a porphyrin. Porphyrin is produced in large quantities by P. acnes bacteria. Excitation of porphyrins with blue light causes them to release free radicals into the bacteria and killing them.

Essential Oils

Many essential oils have been shown to contain antibacterial molecules that are toxic to P. acnes bacteria. Some essential oils, such as Tea Tree Essential Oil and Thyme Essential Oil are commonly used as topical acne treatments.

Other Naturopathic Treatmens

Besides essential oil, many natural compounds (eg. Aloe vera gel and natural honey) have been shown to have antibacterial properties against P. acnes. Certain metals (eg. silver and copper) and other elements (eg. sulfur) are also toxic to P. acnes bacteria in pure form. There are numerous Naturopathic treatments for acne.


The complete genome sequence of Propionibacterium acnes, a commensal of human skin. Brüggemann, et al. 2004.
Acne and Propionibacterium acnes. Bojar, et al. 2004.
Induction of proinflammatory cytokines by a soluble factor of Propionibacterium acnes: implications for chronic inflammatory acne. Vowels, et al. 1995.
Propionibacterium acnes resistance: a worldwide problem. Eady, et al. 2003.
Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light. Ashkenazi, et al. 2003.
Propionibacterium acnes strain populations in the human skin microbiome associated with acne. Fitz-Gibbon, et al. 2013.
Induction of toll‐like receptors by Propionibacterium acnes. Jugeau, et al. 2005.
Propionibacterium acnes and lipopolysaccharide induce the expression of antimicrobial peptides and proinflammatory cytokines/chemokines in human sebocytes. Nagy, et al. 2006.
Formation of Propionibacterium acnes biofilms on orthopaedic biomaterials and their susceptibility to antimicrobials. Ramage, et al. 2003.
Biofilm formation by Propionibacterium acnes is associated with increased resistance to antimicrobial agents and increased production of putative virulence factors. Coenye, et al. 2007.
The role of Propionibacterium acnes in acne pathogenesis: facts and controversies. Dessinioti, et al. 2010.
A comparative study of Cutibacterium (Propionibacterium) acnes clones from acne patients and healthy controls. Lomholt, et al. 2017.
Propionibacterium acnes: an update on its role in the pathogenesis of acne. Beylot, et al. 2014.
Antagonism between Staphylococcus epidermidis and Propionibacterium acnes and its genomic basis. Christensen, et al. 2016.

Anabolic Steroids and Acne

What are Anabolic Steroids?

Anabolic Steroids (aka Roids, Juice, AAS, etc) are molecules that mimic the shape and function of androgen hormones (eg. Testosterone). Anabolic Steroids are generally used to stimulate protein synthesis and muscle growth.

The Difference Between Anabolic Steroids and Corticosteroids

Anabolic steroids should not be confused with corticosteroids, which are immune suppressants and can actually inhibit muscle growth. Corticosteroid injections are sometimes used to treat acute inflammation in severe acne lesions. Anabolic Steroids are never used as an acne treatment, and their use can cause or worsen acne symptoms.

Anabolic Steroids as Performance Enhancing Drugs

There are numerous medical conditions for which Anabolic Steroids are legitimately used as treatments, but Anabolic Steroids are better known for their use as performance enhancing drugs. All major sporting leagues ban the use of Anabolic Steroids, although this doesn’t necessarily prevent their use by athletes. Anabolic Steroids use by individuals for aesthetic purposes is also common in some populations.

Risks and Side Effects of Anabolic Steroid Use

There is widespread concern and controversy about the danger posed by both aesthetic and performance enhancing use of Anabolic Steroids. While some of the danger may be overstated, there are many well-known side effects associated with the use of Anabolic Steroids, including: Growth disruption in adolescents, hormone balance problems, accelerated male pattern balding, cardiovascular problems, contaminated/counterfeit medications, psychological problems (e.g. roid rage) and acne vulgaris.

Research shows that negative side effects of Anabolic Steroid use tend to occur in a dose dependent fashion. Higher and more frequent dosing of Anabolic Steroids is generally associated more frequent and severe side effects. The side effect profile is also dependent on the precise type of Anabolic Steroid being used. With the rapid expansion in designer Anabolic Steroids over the last two decades, a tremendous diversity of options now exists in the marketplace.

How Anabolic Steroids Work

Androgens are the primary hormones responsible for many of the masculine characteristics that differentiate males and females. While females naturally produce androgen hormones like testosterone, they tend to produce much less than males. Anabolic Steroids are usually compounds that are structurally similar to the testosterone.

Focused scientific development of Anabolic Steroids was pioneered by the Soviet Union to improve their competitiveness in international athletic competitions (e.g. the Olympics. The first Anabolic Steroids were simple blends of testosterone and its naturally occurring derivatives. However, these first generation steroids not only increased muscle growth but also had potent masculinizing effects on the user. These effects were most evident in female athletes, with the women of the East German Olympic teams of the 1970’s and early 80’s being the most famous examples. Starting in the 1970’s doctors and scientists began researching new testosterone derivatives that would encourage muscle growth with fewer side effects, so called “designer steroids”.

Many of the cells that compose the human body have sensors called “androgen receptors” that mediate cellular responses to androgen hormones. When the androgen hormone is detected by the cell it stimulates changes in gene expression and metabolism in the cell. However, not all cells respond the same way when they are activated by an androgen hormone. Whereas muscle cells may be stimulated to grow and multiply, other cells, like those in the testes, may actually slow their growth.

Androgen receptors are not exactly the same from cell to cell. There are slight differences between the androgen receptors (and their downstream signalling pathways) depending on the type of cell. The androgen receptors on certain have a high affinity for some androgen hormone derivatives, but a low affinity for others. Over the last thirty years, scientists have been working to develop “designer steroids” that preferentially stimulate the androgen receptors on muscle cells. Significant progress has been made in this pursuit, and today’s designer steroids have far fewer androgenic side effects than those used by the Soviet Union thirty years ago. That said, virtually all Anabolic Steroids still have some level of negative side effects.

Anabolic Steroids and Acne

One of the most common side effects of Anabolic Steroid use is the development of acne on the face, chest and back. The development of acne symptoms is generally caused by the increased activity of the sebaceous glands in response to elevated levels of androgen hormones. High concentrations of androgens (eg. Testosterone) in the body can increase the size and growth rate of the sebaceous glands.

The increase in sebaceous gland activity generally leads to a corresponding increase in sebum production. High levels of sebum production can increase the incidence of clogged pores and induce the growth of acne-causing bacteria, such as Propionibacterium acnes. P. acnes bacteria use sebum as a nutritional source. Increased sebum levels can also contribute to increased inflammation in and around the follicle, worsening acne symptoms, contributing to tissue damage and increasing the risk of acne scarring.

Different types of designer Anabolic Steroids have different profiles of androgenic side effects. Anabolic steroids like testosterone and dihydrotestosterone have a relatively high androgenic to anabolic (muscle building) profile, while some synthetics like Oxandrolone tend to have fewer androgenic side effects, relative to the dose.

Sebaceous gland activity is not only regulated by androgens, but also by other compounds that may be used in “performance enhancement” applications. For example, Human Growth Hormone (hGH) is a commonly used muscle building supplement that can also potentially contribute to acne symptoms. Human growth hormone stimulates the production of another growth factor Insulin-Like Growth Factor 1 (IGF-1) which has also been shown to increase sebaceous gland activity.

There are a lot of variables and cross-reacting factors when it comes to Anabolic Steroids and their side effects, like acne. As always, it is strongly recommended that any steroid therapy be done under the supervision of a qualified medical professional. Illicit steroid use can be quite dangerous not only because of the known side effects and legal restrictions (in many countries), but also because of the high incidence of poorly labeled, impure and counterfeit product being sold as Anabolic Steroids in the unregulated market.

Treatment of Anabolic Steroid Induced Acne

Obviously, stopping the use of Anabolic Steroids is the best solution, although maybe not realistic in all cases. Additionally, stopping use might not actually be enough to completely resolve acne symptoms that were caused by prior Anabolic Steroid use. In most cases of acne (steroid-induced acne included), a central feature of acne is a persistent infection of P. acnes bacteria within hair follicle. Once established, this infection may persist long after steroid use is stopped. Fortunately, individuals with steroid related acne have many treatment options available to them, including:


Both oral retinoids and topical retinoids can help decrease sebaceous gland activity and improve acne symptoms in many individuals. However, there is some research that indicates that oral retinoids (Accutane) may negatively impact athletic performance and recovery times. As a result, oral retinoids are rarely prescribed to competitive athletes who are in active competition. Topical retinoids are effective in some cases, but they tend to be less effective against inflammatory, nodular and cystic forms of acne. Unfortunately, inflammatory acne is fairly common with steroid use.


There are a wide range of topical and oral antibiotics that have been shown to be viable anti-acne treatments. Like topical retinoids, topical antibiotics usually have reduced efficacy against inflammatory forms of acne. Some oral antibiotics have been shown to have both antibacterial and anti-inflammatory properties.

Androgen Inhibitors

While it is unlikely that an individual who is using Anabolic Steroids would be interested in using a systemic androgen inhibitor, there are some topical androgen inhibitors available which have a minimal systemic impact. These topical androgen inhibitors have been used to decrease the effect of anabolic steroids on the skin in a targeted fashion. However, there is not much research on this approach and minimal evidence about its efficacy.

Over The Counter (OTC) Medications

For mild cases of steroid induced acne, Over The Counter (OTC) medications that contain benzoyl peroxide, salicylic acid and other antibacterial/keratolytic compounds may be helpful in improving acne symptoms. These medications are generally most effective with mild, non-inflammatory (Acne Types: 1-2) and are less effective against moderate and severe acne symptoms (Acne Types: 3-4).

Common Anabolic Steroids and Their Chemical Structures

Diagram of how steroid modifications affect anabolic vs androgenic
Diagram of how steroid modifications affect anabolic vs androgenic
Chemical Structures of Common Anabolic Steroids (Fragkaki)
Chemical Structures of Common Anabolic Steroids (Fragkaki)


A league of their own: demographics, motivations and patterns of use of 1,955 male adult non-medical anabolic steroid users in the United States. Cohen, et al. 2007.
Adverse health effects of anabolic androgenic steroids. Amsterdam, et al. 2010.
Anabolic steroid abuse: Psychiatric and physical costs. Talih, et al. 2007.
Pharmacology of anabolic steroids. Kicman. 2008.
Social capital: Implications from an investigation of illegal anabolic steroid networks. Maycock, et al. 2007.
Structural characteristics of anabolic androgenic steroids contributing to binding to the androgen receptor and to their anabolic and androgenic activities: Applied modifications in the steroidal structure. Fragkaki, et al. 2009. 
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.
Anabolic-Androgenic Steroids (AAS) Related Disorders. Hassan, et al. 2017.
The cutaneous bacterial microflora of the bodybuilders using anabolic-androgenic steroids. Zomorodian, et al. 2015.
A qualitative study of anabolic steroid use amongst gym users in the United Kingdom: motives, beliefs and experiences. Kimergård. 2015.
Drug-induced acne. Kazandjieva, et al. 2017.
Acute and chronic adverse reaction of anabolic–androgenic steroids. van Amsterdam, et al. 2014.
Sex hormones and acne. Ju, et al. 2017.

What is the Relationship Between Pregnancy and Acne?

Answer: There are many changes that take place in the female body during pregnancy and these changes can have both positive and negative effects on acne symptoms.

Many women experience dramatic changes in their acne both during and after pregnancy. Hormones that control the natural processes of menstruation and pregnancy have wide-ranging effects throughout the body. Onset of acne or a worsening of acne symptoms is very common during pregnancy. At the same time, a smaller percentage of women report an improvement in their acne symptoms during pregnancy.

Pregnancy and Hormones

Hormones can play a major role in the development of acne symptoms. Pregnancy causes large changes in hormone balance. During pregnancy, women produce increasing amounts of the female hormones progesterone and estrogen. In addition, blood sugar levels rise to provide additional energy to the growing fetus. These blood sugar changes also affect hormone balance. The fetus itself and the placenta produce additional hormones.

Sex Hormones and Acne

The fundamental regulators of pregnancy are the sex hormones. These sex hormones include both female hormones (progesterone and estrogen) and male hormones (testosterone and other androgens). Both sets of hormones cause major physiological and metabolic changes in the body. During pregnancy, levels of all of these hormones tend to rise. Increasing levels of progesterone and estrogen help to stabilize the uterus, direct nutrients to the placenta and facilitate growth of the fetus.

The role of male sex hormones (androgens) in the process of pregnancy is less well understood. What is known is that androgen levels increase throughout pregnancy and spike in the third trimester. Androgen hormones tends to stimulate proliferation of the sebaceous glands and the production of sebum, both of which can worsen acne symptoms. Elevated levels of androgens are strongly correlated with increased frequency and severity of acne symptoms. Signs of elevated androgen levels in women include increased body and facial hair growth (hirsutism), hair thinning (on the head) and masculinization of features (in severe cases).

The Role of Post-Pregnancy Sex Hormones

Research indicates that pregnancy can induce long-lasting changes in a woman’s hormonal balance. This can include elevated levels of both male and female sex hormones. Many women report experiencing problems with acne that began with a pregnancy and continued long after the birth of their child.

Lasting acne symptoms that began during pregnancy could be the result of semi-permanent changes in sex hormone levels. It could also be a result of continuing infection with acne causing bacteria that began during pregnancy. For women who are not pregnant, there are several medications available to modulate hormone levels and to treat acne directly. These include androgen inhibitors, which can block the effect of elevated androgen levels.

Common Changes in the Skin during Pregnancy

In most cases, pregnancy induces noticeable changes in the appearance of the skin, especially in facial skin. People often refer to a “glow” in the skin of pregnant women. These changes result from vascular (blood vessel) dilation and proliferation which results in increased blood flow to the skin. Another very common change is hyper-pigmentation, which occurs in approximately 90% of women. Approximately 50% of women experience pregnancy induced melasma, which is increased pigmentation of patches of skin, primarily found on the nose, cheeks and upper lip. Some of these effects subside after completion of pregnancy, but some remain permanently.

Acne Medications and Pregnancy

Pregnant women have limited acne treatment options, compared to men or non-pregnant women. Because pregnancy is such a delicate process, it is essential that pregnant women maintain a healthy diet and limit their exposure to substances that may effect the development of the fetus. Some acne medications, like Retinoids (eg. Isotretinoin, Accutane) are highly toxic to the fetus and even small amounts of these drugs can cause birth defects or death of the fetus. Other medications like Tetracyclines (eg. Doxycycline, Minocycline) or Androgen Inhibitors (eg. Spironolactone, Cyproterone) can disrupt normal fetal development.

Allergic reactions to medications can also be dangerous to the fetus. Even homeopathic treatments, such as Herbal and Mineral supplements (eg. Zinc, Copper), can be dangerous to a developing embryo. It is important to thoroughly discuss any medication or homeopathic treatment with your physician or Ob/Gyn before beginning treatment.

Acne Treatment Options for Pregnant Women

In general, topical treatments are significantly safer for pregnant women than oral medications. Most Topical Antibiotics and Topical Naturopathic Treatments do not enter the body in concentrations high enough to risk harm to the developing fetus. Light and Laser Treatments, such as Blue Light Phototherapy, are also generally safe for use by pregnant women.


Physiologic Skin Changes During Pregnancy: A study of 140 Cases. Muzaffar, et al. 1998.
Acne and Pregnancy. O’Connell, et al. 2000.
Maternal serum androgens in human pregnancy: early increases within the cycle of conception. Castracane, et al. 1998.
Treatment of acne in pregnancy. Chien, et al. 2016.
Inflammatory facial acne during uncomplicated pregnancy and post‐partum in adult women: a preliminary hospital‐based prospective observational study of 35 cases from Taiwan. Yang, et al. 2016.
Acne in pregnant women: a French survey. Dreno, et al. 2014.
Dermatologic therapy in pregnancy. Tyler, 2015.
Sex hormones and acne. Ju, et al. 2017.
An overview of pregnancy dermatoses. McNulty-Brown, et al. 2016.
Inflammatory and glandular skin disease in pregnancy. Yang, et al. 2016.
Acne and rosacea in pregnancy. Bechstein, et al. 2017.

Can Stress Cause Acne?

Answer: Yes. Stress can trigger and/or worsen acne symptoms.

It is well known that putting an organism under stress makes it more susceptible to infection. This is true for humans, animals and even plants. The same neural and biochemical pathways that make stress feel uncomfortable can also disrupt the delicate balance of a properly functioning immune system, which increases your susceptibility to acne.

In the words of the experts:

“Activation of neurohormones by psychological stress occurs largely via the hypothalamic (pituitary) adrenal (HPA) axis, with subsequent upregulation of key stress hormones, such as corticotropin-releasing hormone (CRH), ACTH, and glucocorticoids (Cacioppo et al., 1998; Glaser and Kiecolt-Glaser, 2005). Via these stress-related hormones, accompanied by additional stress response mediators such as neuropeptides or neurotrophins (Webster, 2002), immune responses are profoundly altered (Glaser and Kiecolt-Glaser, 2005). For example, glucocorticoids inhibit the production of IL-12, IFN-y, and tumor necrosis factor by antigen-presenting cells and T helper 1 (Th1) cells but upregulate the production of IL-4, IL-10, and IL-13 by Th2 cells (Wonnacott and Bonneau, 2002).”Arck, et al. 2006.

To summarize that for non-scientists:

Stress causes changes in hormonal balance and that negatively impact your immune system. These changes appear to suppress immune functions that encourage the direct killing of pathogens (like the acne-causing Propionibacterium acnes bacteria), instead shifting the immune response to a more passive approach.

Glucocorticoids and Stress

One of the most well known stress hormones is cortisol (aka hydrocortisone). Cortisol is released by certain tissues in the body in response to stress. Many people have heard the claims on late night infomercials about the effect of stress on weight gain (and how they have a product that can fix it).

Specifically, these infomercials are referencing research that shows that stress induces the release of a molecule called cortisol, which can potentially induce the growth of adipose cells (fat cells). Cortisol is part of a group of molecules called glucocorticoid steroids (corticosteriods). These molecules have many functions, but one of their primary functions is to suppress the immune system.

The release of corticosteroids by the body in response to stress could explain why immune function is diminished in stressed individuals. Corticosteroids are often medically administered to treat severe allergic reactions (eg. poison oak) and inflammation. Corticosteroids are also occasionally injected directly into acne nodes and cysts in order to immediately reduce inflammation. However, because corticosteroids have a suppressive effect on the immune system, long-term use of these mediccations is generally discouraged.

Stress and Acne Symptoms

The hormonal changes that are induced by stress can cause or worsen acne symptoms. Stress can increase the production of sebum by sebaceous glands and suppress the immune system. This combination of effects provides conditions that increase the likelihood of acne. It is well-known that stress relief and relaxation can improve overall health. This also applies to acne. Decreasing psychological and physical stress (e.g. binge drinking, high-sugar diets, insufficient sleep, anxiety, drug use, injuries, etc) can improve acne and general health.


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: changes in the severity of acne vulgaris as affected by examination stressChiu, et al. 2003.
Stress, Acne and Skin Surface Free Fatty Acids. Kraus. 1970.
Exploring the relationship between stress and acne: a medical student’s perspective. Maleki, et al. 2018.
Effects of stress on immune function: the good, the bad, and the beautiful. Dhabhar, et al. 2014.
Exercise, immune function and respiratory infection: An update on the influence of training and environmental stress. Walsh, et al. 2016.
Repeated Social Defeat Stress Changes Peripheral Immune Status in Rats: Potential Effects on Basolateral Amygdala Function. Munchi, et al. 2017.
A systematic review and meta-analysis of the effort-reward imbalance model of workplace stress with indicators of immune function. Eddy, et al. 2016.
The effects of stress hormones on immune function may be vital for the adaptive reconfiguration of the immune system during fight-or-flight behavior. Adamo. 2014.

What Does Non-Comedogenic Mean?

Answer: Comedogenicity refers to the potential of a substance to cause a comedo, a plugged or inflamed pore.

Non-comedogenic means that in testing, the substance or product has not been shown to cause comedos (clogged or inflamed hair follicle). Some substances (eg. coal tar) are highly comedogenic and produce a type of allergic, acne-like reaction. There is not a clear consensus when it comes to the comedogenicity of many substances, with different tests yielding different results.

How is comedogenicity determined?

The large majority of comedogenicity testing is done on animals, often using a rabbit ear model. In this test, the substance is applied to the inside of the rabbit’s ear, which has a similar structure as human facial skin. The development of comedos is quantified to evaluate the relative comedogenicity of a substance. In some cases, human volunteers are used to evaluate substances. In these tests, the most common treatment area is the skin on the back.

What kinds of things determine comedogenicity?

Comedogenicity is a complicated process that can vary from individual to individual. One interesting observation is that human sebum is itself comedogenic. A substance can be comedogenic for several reasons. It can contribute directly to the formation of a plug in the hair follicle. This could potentially occur with a substance that triggers the coagulation of free sebum.

A substance could also be comedogenic because it triggers an allergic reaction and/or inflammation. Substances like SLS (sodium lauryl sulfate) are common ingredients in topical preparations and but can cause allergic reactions in some individuals and are generally considered comedogenic.

Additionally, a substance can serve as a direct food source for the bacteria responsible for acne, Propionibacterium acnes. P. acnes bacteria eat fatty acids as one of their primary food sources and certain substances like olive oil or other vegetable oils could potentially serve as food sources for these bacteria and encourage their growth. Increased bacteria levels in the skin can then stimulate a local immune response, inflammation and comedogenecity.

Lastly, relatively harmless substances can be converted into allergens and comedogens by the enzymes present in the skin, or even by UV light.

Common Comedogenic Substances

There are several lists of comedogenic substances available in different places on the internet. However, a review of the scientific literature reveals a serious lack of actual testing on commonly used substances. This may be because many companies do their own testing and do not publish the results, but it also casts some doubt on some of these online comedogenic substances lists.

We are currently working to compile a comprehensive comedogenic substance lists from published scientific journal articles. Until then, we have included this table from the original comprehensive comedogenicity testing done by Dr. Fulton, et al. Comedogenicity and irritancy are graded on a scale of 0 to 5, with 0 being no effect and 5 being highly comedogenic:

Comedogenicity Testing Results of Common Substances – Part 1
Comedogenicity Testing Results of Common Substances – Part 2
Comedogenicity Testing Results of Common Substances – Part 3


Comedogenicity and Irritancy of Commonly Used Ingredients in Skin Care Products. Fulton, et al. 1989.
A re-evaluation of the comedogenicity concept. Draelos, et al. 2006.
Comedogenicity of Squalene Monohydroperoxide in the Skin after Topical Application. Chiba, et al. 2000.
An Experimental Study on the Comedogenicity of Several External Contactants. Ahn, et al. 1985.
Relationship between acne vulgaris and cosmetic usage in Sri Lankan urban adolescent females. Perera, et al. 2017.
Analysis of comedone, sebum and porphyrin on the face and body for comedogenicity assay. Baek, et al. 2016.
A Clinical Appraisal of Endogenous and Exogenous Factors of Acne Vulgaris in Adolescents and Adults from a Tertiary Care Teaching Hospital in Central Kerala. VG, et al. 2016.
Isopropyl Myristate and Cocoa Butter are not Appropriate Positive Controls for Comedogenicity Assay in Asian Subjects. Lee, et al. 2015.
Enhancement of comedogenic substances by ultraviolet radiation. Mills, et al. 1978.
Comedogenicity of current therapeutic products, cosmetics, and ingredients in the rabbit ear. Fulton, et al. 1984.
An improved rabbit ear model for assessing comedogenic substances. Kligman, et al. 1979.
A reevaluation of fatty acids as inflammatory agents in acne. Puhvel, et al. 1977.

Does Greasy Food, Milk or Chocolate Cause Acne?

Answer: Not exactly. At least not in the way you might think.

Anecdotal associations between acne and particular foods like chocolate, ice cream and pizza have been discredited by scientific research.  But research does point to a connection between overall diet and the development of acne symptoms.

The Connection Between Acne and Overall Diet

Researchers have presented compelling evidence that people whose diets include lots of high glycemic index foods (foods that are high in sugar and simple carbohydrates) tend to experience acne at a greater frequency than those who have low glycemic index diets. However, there is no clear scientific consensus on why this connection exists. Some experts believe that high glycemic index diets may have negative impacts on hormone balance and the immune system.

Common Assumptions About Acne and Diet

There many widely held beliefs about the relationship between certain types of food and acne symptoms. Three of the common are:

Assumption #1: Eating Greasy Food Causes Greasy Skin

True or False?: Mostly False. The grease that you eat is not the same grease that makes your skin oily. Genetics, hormones, stress and environmental factors are much more important players than consumption of fatty or greasy foods when it comes to oily skin.

The substance that makes your skin feel and look greasy is not actually grease at all – it is a natural substance called sebum. The purpose of sebum is to moisturize and protect the skin.

Sebum is produced by a specialized structures called sebaceous glands, which are located deep inside of hair follicles. Sebum is produced from the break-down of sebocytes, which are the specialized cells that make up the sebaceous gland. Sebocytes are rich in lipids (fatty acids) and triglycerides (fats and oils). The sebocytes nearest to the hair follicle die and then dissolve, releasing their contents into the hair follicle. The faster the sebaceous gland proliferates (grows), the faster this process of cell death and sebum production takes place, and the more oily the skin becomes. But eating more grease and fat does not necessarily cause this process to happen any faster.

It is also important to point out that oil is a generic term for a diverse class of molecules. The oils (lipids and triglycerides) in sebum are not the same as the oils that you consume when you eat things like fried foods. There are a lot of intermediate steps between the consumption of dietary oil and the synthesis of sebum, and this makes a direct connection between the two unlikely.

Assumption #2: Chocolate Causes Acne

True or False?: Mostly False. Chocolate itself has not been shown to have a direct connection with acne symptoms. There have been at least two studies that directly examined the relationship between chocolate and acne. In both of these studies, the researchers found no correlation between chocolate consumption and acne.

However, many chocolate-containing products are also high in sugar and/or high-fructose corn syrup, and are therefore high glycemic index foods. Research has shown that diets high in sugar and simple carbohydrates may contribute to acne symptoms.

Chocolate is generally a mixture of ingredients, and different kinds of chocolate can have a dramatically different composition of ingredients, such as sugar. It is also possible for people to develop allergic reactions to particular foods, including chocolate, and these reactions can produce acne-like symptoms. However, most cases an allergic reaction would also have additional symptoms including, itching, hives, throat swelling, fever, rash, joint pain, etc.

Assumption #3: Milk Causes Acne

True or False?: Possibly True. There are a handful of studies that suggest a relationship between high levels of milk consumption and increased incidence of acne. The authors of these studies suggest that it is possible that hormones in the milk (or hormones stimulated by milk consumption) may be to blame.

A particular hormone called Insulin Growth Factor 1 (IGF-1) is present in milk may cause changes in metabolism and hormone balance that can impact acne symptoms. IGF-1 is a naturally occurring hormone, and it is present in all animal milks (even products made from animals that have not been treated with hormones).

Whether or not milk consumption actually causes acne symptoms (and whether this is true for all people) remains to be scientifically proven. People have blamed a lot of medical conditions on milk consumption. There is a large group of people who swear that by stopping milk consumption they were relieved of a range of medical problems, from respiratory infections to acne vulgaris. Not all of these claims are going to be true (at lesat for most people).

Milk consumption may also impact the balance of sex hormones, such as androgens and estrogens (male and female sex hormones). Several studies have demonstrated that elevated androgen levels are associated with more severe acne symptoms in some patients. It is also possible that people with certain types of milk allergies could exhibit acne-like symptoms.

In conclusion, there is some evidence that milk may contribute to symptoms of acne vulgaris, but the exact relationship between milk and acne is not well understood. Regardless, for many people it’s worth a shot to cut milk out of their diet for a few weeks and see if that helps improve their acne symptoms.


Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health (Vintage). Taubes. 2008.
The Clear Skin Diet. Logan, et al. 2007.
Glycemic Index and Glycemic Load of Foods. DietGrail. 2011.
Eat, Drink, and Be Healthy: The Harvard Medical School Guide to Healthy Eating. Willett, et al. 2005.
A systematic review of the evidence for ‘myths and misconceptions’ in acne management: diet, face-washing and sunlight. Magin, et al. 2005.
Diet and acne: a review of the evidence. Spencer, et al. 2009.
A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Smith, et al. 2007.
Does diet really affect acne? Ferdowsian, et al. 2010.
Effect of Chocolate on Acne Vulgaris. Fulton, et al. 1969.
Milk consumption and acne in teenaged boys. Adebamowo, et al. 2008.
Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Melnik, et al. 2009.
Linking diet to acne metabolomics, inflammation, and comedogenesis: an update. Melnik, et al. 2015.
A Low Glycemic Index and Glycemic Load Diet Decreases Insulin-like Growth Factor-1 among Adults with Moderate and Severe Acne: A Short-Duration, 2-Week Randomized Controlled Trial. Burris, et al. 2018.
Significance of diet in treated and untreated acne vulgaris. Kucharska, et al. 2016.
Diet and acne update: carbohydrates emerge as the main culprit. Mi, et al. 2014.
The Effects of a Low Glycemic Load Diet on Acne Vulgaris in Adolescents and Young Adults. White. 2015.
The constellation of dietary factors in adolescent acne: a semantic connectivity map approach. Bonci, et al. 2016.
Diet and acne: an exploratory survey study of patient beliefs. Nguyen, et al. 2016.
Dietary Regimes for Treatment of Acne Vulgaris: A Critical Review of Published Clinical Trials. Norstedt, et al. 2016.
The possible role of diet in the pathogenesis of adult female acne. Romańska-Gocka, et al. 2016.

How Do Acne Scars Form?

Acne scars are the result of tissue damage caused by inflammatory acne.


The vast majority of acne scars are caused by from persistent cases of inflammatory acne affecting the same area of skin. Individuals who suffer from frequent nodular and cystic acne outbreaks (Acne Types: 3-4) are at a very high risk of developing permanent acne scarring. This is particularly true when a region is affected by overlapping acne outbreaks, with no opportunity for the skin to completely heal.

When an individual experiences persistent outbreaks of severe inflammatory acne, significant regions of the affected skin and underlying tissue can be damaged. Acne is an inflammatory process that usually involves an infection caused by bacteria (eg. Propionibacterium acnes).

The inflammation that occurs during severe acne prevents the body from mobilizing the cells and materials necessary for the normal healing process that is required to repair the skin. In this situation, the original (healthy) tissue can be replaced by fibrous scar tissue.

The Role of Inflammation in Acne Scarring

What many people may not realize is that acne scarring is primarily due to the body’s own immune response to infection, and not the infection itself. A major component of inflammatory acne is the migration of white blood cells to the hair follicle, sebaceous glands and surrounding tissue. These white blood cells compose much of the “pus” that comes out when you pop a zit.

The white blood cells that make up the pus in acne pimples, nodules and cysts are not uniform. Instead the pus contains a mixture of many different sub-types of white blood cells, such as macrophages, neutrophils, dendritic cells, T cells, granulocytes, mast cells and others. Neutrophils are one of the body’s front-line defenses against infection and these cells are usually the most abundant white blood cells in an acne lesion.

Many of the white blood cells (and especially neutrophils) produce powerful degradative enzymes that can damage health tissue. These cells also produce inflammatory molecules, super-oxides and free radicals. These weapons are designed to help neutralize pathogens and foreign invaders, but they can also cause damage to the surrounding healthy tissue.

In inflammatory acne, the damage caused by these white blood cells can actually cause the underlying bacterial infection to spread, leading to more inflammation and tissue damage. This can create a vicious, self-fulfilling cycle of tissue damage that leads to permanent acne scars.

Neutrophils and Acne Scars

When it comes to scarring, perhaps the most important type of white blood cell is the neutrophil. The neutrophil is one of the first responders to the infected follicle, and can accumulate in great numbers. Neutrophils are kind of like the suicide bombers of the cellular world. When they reach the site of infection they can undergo apoptosis (controlled suicide) and degranulation, which releases many anti-microbial molecules, DNA and proteases into environment. These proteases that can cause tremendous damage to the surrounding tissue, which ultimately results in scarring. The proteases digest the elastin and collagen matrix that provides support and elasticity to the skin.

The Structure of Scar Tissue

Healthy skin is supported by a complex matrix (scaffolding) that provides structural support and nutrients to the skin surface. When skin is damaged, this matrix helps guide the healing process. Without this matrix to guide healing, the body has a very difficult time properly repairing and re-creating the damaged tissue.

In cases of persistent infection and inflammation, the body is not able to repair the matrix fast enough to keep up with the damage. In these cases, the body begins to build scar tissue, which is simple and tough. The scar tissue can permanently replace the more complex and delicate healthy matrix. This process underlies not only the formation of acne scars, but of other diseases marked by chronic inflammation, such as chronic obstructive pulmonary disorder (emphysema) and rheumatoid arthritis.

Scar tissue is composed largely of collagen, which is the same material that comprises much of a healthy sub-cutaneous matrix. However, unlike the healthy matrix – which is a complex, spacious and interconnected web of collagen and other proteins – the collagen in scar tissue is much different. In scar tissue, the collagen becomes tightly bundled and tends to line up in a single direction, instead of the original, interconnected web pattern.

In scar tissue there is much less open space than healthy tissue, and many of the essential accessory proteins and molecules that are essential for the maintenance of healthy skin are absent. This alignment of the collagen fibers and their closely packed arrangement creates a denser, less elastic tissue.

Scar tissue becomes impermeable to migration by many cell types, preventing the formation of blood vessels and a regrowth of complex structures, such as hair follicles and sweat glands. This is why scar tissue is generally monotone, feels tough and dense to the touch, and is hairless. It also explains why the body has such a difficult time replacing scar tissue with healthy tissue.

Repairing Scar Tissue

Once scar tissue has been generated at a site of injury, it is relatively permanent (without medical intervention). In some cases, the body will gradually replace some scar tissue with the healthy tissue, but this process is so slow that is largely irrelevant. The single best treatment for acne scarring, is to prevent it in the first place. This means aggressively attacking the infection and treating the inflammation as it arises.

Fortunately, there are many different treatments available to help repair acne scar damage. The ideal type of treatment is largely dependent on the specific types of acne scarring. Acne scar treatment generally involves either surgically removing the scar tissue, or breaking it apart with laser, heat or surgical treatments.

Light and Laser treatments can be very effective treatments for many different kinds of acne scars. Invasive and non-invasive surgical treatments can also be very helpful.

Topical Retinoids may also be helpful for very mild acne scars and uneven skin tone.


Physiopathology of acne vulgaris: recent data, new understanding of the treatments. Pawin, et al. 2004.
Topical ALA Photodynamic Therapy for the Treatment of Acne Vulgaris. Hongcharu, et al. 2000.
Human b Defensin-1 and -2 Expression in Human Pilosebaceous Units: Upregulation in Acne Vulgaris Lesions. Chronnell, et al. 2001.
A prospective, randomized, placebo-controlled, double-blinded, and split-face clinical study on LED phototherapy for skin rejuvenation: Clinical, profilometric, histologic, ultrastructural, and biochemical evaluations and comparison of three different treatment settings. Lee, et al. 2007.
Acne scarring: a classification system and review of treatment options. Jacob, et al. 2001.
The role of elastic fibers in scar formation and treatment. Cohen, et al. 2017.
The pivotal role of inflammation in scar/keloid formation after acne. Shi, et al. 2017.
Mechanical stress and the development of pseudo‐comedones and tunnels in Hidradenitis suppurativa/Acne inversa. Boer, et al. 2016.
Effect of basic fibroblast growth factor combined with laser on content of a variety of cytokines in acne scar wound. Dong, et al. 2016.
Scar prevention and remodeling: a review of the medical, surgical, topical and light treatment approaches. Kerwin, et al. 2014.
Post acne scarring: a review. Goodman, et al. 2003.
The molecular basis of keloid and hypertrophic scar formation. Tuan, et al. 1998.
Postacne scarring: a review of its pathophysiology and treatment. Goodman, et al. 2000.
Acne scar treatment. Rusciani, et al. 2015.
Acne scar treatment: a multimodality approach tailored to scar type. Zaleski-Larsen, et al. 2016.
Atrophic scar formation in acne patients involves long‐acting immune responses with plasma cells and alteration of sebaceous glands. Carlavan, et al. 2018.
The pivotal role of inflammation in scar/keloid formation after acne. Shi, et al. 2017.
Prospective Study of Pathogenesis of Atrophic Acne Scars and Role of Macular Erythema. Tan, et al. 2017.
Expression of inflammatory and fibrogenetic markers in acne hypertrophic scar formation: focusing on role of TGF-β and IGF-1R. Yang, et al. 2018.
The role of elastic fibers in scar formation and treatment. Cohen, et al. 2017.
Current Concepts in Acne Pathogenesis: Pathways to Inflammation. Tan, et al. 2018.


Sebum is a naturally occurring substance that moisturizes, lubricates and protects the skin and hair.


Sebum is produced by the sebaceous glands of mammals. Healthy sebum production is essential for the integrity and normal function of the skin as a protective organ. Sebum is also an important source of energy (food) for acne-causing Propionibacterium acnes bacteria.

Sebum and Health Skin

Human skin is composed of three primary layers: the stratum corneum, the epidermis, and the dermis. The outermost layer of the skin, the stratum corneum, functions as the primary barrier to the external environment, preventing water loss and the invasion of microorganisms. Sebum is secreted to the stratum corneum from the sebaceous glands and helps maintain an effective, hydrophobic (water-resistant) barrier.

Normal sebum levels help to maintain healthy skin, but abnormal sebum production or composition can contribute to a variety of diseases, including acne.

Chemical Composition of Sebum

Sebum is a complex mixture of naturally produced fats, oils, waxes, cholesterols and other molecules. It is important to point out that the fats and oils present in sebum do not originate directly from the fats and oils consumed in the diet. Rather, sebum is manufactured and stored by the sebaceous glands under the direction of a highly specialized biological process.

Most mammals (but not whales and dolphins) produce some sort of sebum, and each animal has its own unique blend. In addition to sebaceous glands and sebum, there are other structures in the skin that produce a sebum-like mixture called “epidermal lipids”.

Human sebum is composed primarily of glycerides, free fatty acids, wax esters and squalenes. Glycerides are more commonly known as “fats” and are molecules of two or three free fatty acids connected together by a glycerol backbone. Free Fatty Acids are the building blocks of glycerides and other molecules. They are composed of a polar head group and a non-polar (aliphatic tail). Wax Esters are molecules composed of fatty acids linked to fatty alcohols by an ester bond. Squalenes are hydrophobic chains of carbon atoms that serve as the basic building block for naturally occurring steroids and other types of intercellular signaling molecules.

The Biological Role of Sebum in Acne Vulgaris

Several research studies have found a direct relationship between increased sebum secretion and increased acne symptoms. People with sebaceous gland disorders (e.g. sebaceous hyperplasia) that lead to very high sebum levels often have severe forms of acne and other skin diseases. However, there are several possible explanations for how sebum production may contribute to acne, and there is not unanimous agreement between experts when it comes to explaining this relationship.

The most common explanation for why elevated sebum production leads to acne symptoms is that increased sebum production leads to increased follicular plugs (clogged pores). Clogged pores create an low oxygen (hypoxic) environment that supports the growth of acne-causing P. acnes bacteria. Sebum is also a source of food for P. acnes bacteria. The accumulation of sebum within plugged follicles provides ideal growing conditions for P. acnes bacteria and can lead to large numbers of these bacteria growing in the skin.

Research has also found that sebum itself can lead to increased inflammation. Byproducts of the sebum metabolism may cause the accumulation of molecules that trigger an inflammatory immune response. It is possible that this mechanism is at work in some individuals with inflammatory acne.

Research has also shown that people with abnormally high sebum production tend to make sebum that has a different composition than the sebum from people with normal levels. Apparently, people with acne tend to have decreased levels of free fatty acids, but increased levels of glycerides and squalene. Some scientists have proposed that these compositional changes play a role in the development of acne symptoms.

The Regulation of Sebum Production

Acne symptoms are often associated with sebum overproduction, which can increase the incidence of clogged pores, stimulate inflammation, provide nutrients for bacterial growth. Overproduction of sebum is generally the result of excessive growth and activity of the sebaceous glands. Overactive sebaceous glands and sebum overproduction can be caused by many factors, such as hormones, genetics, stress and environmental stimuli.

The proliferation of sebaceous glands and production of sebum is directly regulated by a complex system of hormones and other cellular signals. At a deeper level, these hormonal signals are controlled by an even more complex balance that includes genetics, environmental conditions, metabolic conditions, stress, diet, injury and many other factors. Despite this extraordinary complexity, scientists have begun to unravel the central relationships in sebaceous gland biology.

Several of the central factors that control sebum production have been identified and are currently being investigated by scientists. The major regulators of sebaceous gland activity include:


Androgens are male sex hormones, like testosterone. Acne symptoms commonly develop in males during adolescence, when levels of androgen hormones in the body are their highest. Androgens drive the development of many male characteristics, like muscle and body hair growth. They also stimulate the proliferation of sebaceous glands, particularly those located on the face, chest and upper back.

Individuals with excessively high levels of androgen hormones tend to have higher levels of sebaceous gland proliferation, sebum production and acne vulgaris. Women with elevated androgen levels tend to have higher levels of acne and hirsuitism (excess body hair growth). The effect of androgens on sebaceous gland activity is also why the use of anabolic steroids, which increase androgen levels, can cause acne symptoms.


Estrogens are female sex hormones. In most cases, estrogens antagonize (suppress) the effects of androgen hormones. This relationship partially explains why acne symptoms tend to change over the course of a woman’s menstrual cycles, or during and after pregnancy. Men do not usually produce significant levels of estrogen hormones. Estrogens may also directly modulate sebaceous gland activity, although this relationship is not well studied.

Insulin-Like Growth Factor 1 (IGF-1)

IGF-1 is a protein hormone that is produced in the liver and is similar in structure to insulin. Researchers have reported that high IGF-1 levels correlate with elevated sebum production. Levels of IGF-1 tend to be highest during adolescence. Since insulin is similar in structure to IGF-1, it is possible that elevated levels of insulin could cause increased sebum production.

Insulin levels are often elevated in individuals who consume a high glycemic diet (high sugar/carbohydrate), or who have Type 2 diabetes. This relationship could explain the observed correlation between high glycemic diets, obesity and increased incidence of acne vulgaris. Increased IGF-1 has also been linked to milk consumption, although these studies are not necessarily conclusive. IGF-1 hormone production is stimulated by human growth hormone (hGH).


Retinoids are intercellular signalling molecules that are derived from Vitamin A. Retinoid is the generic name for a diverse class of related molecules that play essential roles in many human biological systems, including development of the human embryo. The proliferation of sebaceous glands and the production of sebum is directly controlled by specific retinoid signal molecules. Accutane (Isotretinoin, 13-cis-retinoic acid) is a retinoid that is a powerful anti-acne drug. Binding of Isotretinoin molecules to specialized receptors on the surface of sebocyte cells causes them to slow down their growth and sebum production. The natural balance of different retinoids in the body has a direct impact on sebaceous gland activity.

Environmental Conditions

Recent research has shown that sebum secretion levels change in response to seasonal and environmental changes. While the changes are not drastic, researchers observed that sebum secretion levels were highest during the summer. These changes may be due to the increased fluidity of sebum in warmer conditions, or something else entirely.

Generally speaking, acne sufferers tend to observe an improvement in their acne symptoms during the summer, although this could be more directly related to factors such as UV light exposure or stress levels, than to sebum production. Overall, the research indicates that sebum production is modulated by environmental conditions, although it is less clear whether these normal fluctuations play a role in the development of acne or other skin conditions.


Several research studies have reported that there is a direct correlation between stress and increased acne symptoms. However, other research studies have found that stress does not appear to increase the levels of sebum production. While it is well understood that stress can modulate levels of certain hormones, like cortisol, it does not appear that these pathways directly impact sebaceous gland activity.

Treatments for Excessive Sebum Production

Treatments that reduce the production of sebum are commonly used for the management of acne symptoms. Common sebum-reducing treatments include Retinoids (eg. Accutane, Differin), Androgen Inhibitors (eg. Spironolactone, Cyproterone) and Laser Treatments (eg. PDT, Diode Lasers).


Retinoids are the most common course of treatment for individuals with hyperactive sebaceous glands and abnormally high sebum production. Retinoids can be an effective acne treatment for many people. Retinoids cause side effects related to decreased sebum production, such as dry and sensitive skin.

The oral retinoid, Isotretinoin (Accutane), is a potent anti-acne medication that can dramatically reduce sebum production. For many individuals, treatment with isotretinoin can lead to significant, long-lasting improvement in their acne symptoms. However, Accutane can have significant side effects, causes severe birth defects in pregnant women, and is tightly controlled in many countries.

Topical retinoid medications are commonly used to treat acne and other skin conditions. Popular topical retinoids include tretinoin (Retin-A), adapalene (Differin), tazarotene (Tazorac) and isotretinoin (Isotrex). These treatments also decrease sebum production, although the effect is often less dramatic than that of oral retinoids.

Retinoids are also used in Naturopathic acne treatments. Retinoids are naturally present in some plant extracts, such as Rose Hip Seed Oil.

Androgen Inhibitors

Androgen Inhibitors can block the activity of the androgen hormones that stimulate sebum production. Androgen inhibitors like spironolactone (Aldactone) and cyproterone (Androcur) can partially block the effects of androgen hormones and decrease sebaceous gland activity. Androgen Inhibitors are available in both oral and topical formulations.

Hormonal Contraceptive medications can also block the effect of androgen hormones. Both anti-androgen medications and birth control medications are usually reserved for use in females, because their effects can disrupt the normal function of the male hormone system.

Light and Laser Treatments

Light and Laser Treatments have become increasingly popular for the treatment of acne and other skin disorders. Certain light and laser treatments, like Photo Dynamic Therapy (PDT) and Diode Laser Therapy, can be used to directly target the sebaceous glands. Damaging the sebaceous glands with laser treatments can decrease the production of sebum at the treatment site. Depending on the specific type of laser treatment, these effects can be semi-permanent.


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.
Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. Zouboulis, et al. 2014.
Use of lipidomics to investigate sebum dysfunction in juvenile acne. Camera, et al. 2016.
A Topical Medication of All-Trans Retinoic Acid Reduces Sebum Excretion Rate in Patients With Forehead Acne. Pan, et al. 2017.
The relevance of sebum composition in the etiopathogeny of acne. da Cunha, et al. 2018.
Evaluation of Seasonal Changes in Facial Skin With and Without Acne. Meyer, et al. 2015.
Sebum secretion of the trunk and the development of truncal acne in women: do truncal acne and sebum affect each other?. Kim, et al. 2015.
Relationship between sleep quality and facial sebum levels in women with acne vulgaris. Bilgiç, et al. 2016.
A review of the role of sebum in the mechanism of acne pathogenesis. Li, et al. 2017.
The relevance of sebum composition in the etiopathogeny of acne. da Cunha, et al. 2018.
Lipidomics reveals skin surface lipid abnormity in acne in young men. Zhou, et al. 2018.
Acne vulgaris: The metabolic syndrome of the pilosebaceous follicle. Melnik, et al. 2018.
Developing an in vitro artificial sebum model to study Propionibacterium acnes biofilms. Spittaels. 2018.

What Causes Acne?


Acne is a complex disease and many factors can contribute to the development of symptoms. Every case of acne is unique and the blend of factors that cause acne varies between individuals. Overall, the most important factors in the development of acne are:

  • Genetics
  • Hormones
  • Bacteria
  • Environment
  • Stress
  • Diet


A person’s genetic makeup is a dominant factor in determining their 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 the immune cells in their skin produce more inflammatory molecules than the general population. As a result of genetic differences, their body may respond 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 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.

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.


Acne (especially inflammatory acne) 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.  Many of these P. acnes 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 for acne sufferers, there are still many antibiotics available that do not have this shortcoming.


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 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.


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.


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.
New insights into acne pathogenesis: exploring the role of acne-associated microbial populations. Kumar, et al. 2016.
On the TRAIL to truth, or on a road to nowhere? van Steensel. 2017.

What Is Acne?


Acne is a difficult to treat and often debilitating disease that affects the skin, usually the face. The most common form of acne (acne vulgaris) is an infection within a hair follicle. This infection causes varying degrees of inflammation, which manifest as pimples, nodules and cysts. When the inflammation is severe, it can cause permanent damage to the skin and create acne scars.

Types of Acne

Acne can range from small patches of red skin with tiny bumps to large cysts that are painful to the touch. Different types of acne can have profoundly different underlying causes and understanding precisely what type of acne you have can help you identify what solutions are going to have the best chance of being effective.

Type 1 Acne

  • Minimal inflammation
  • Minimal affected area
  • Not painful
  • Irregular outbreaks

Type 1 Acne is the most mild form of acne and generally is the least damaging and easiest to treat form of the disease. It is characterized by a lack of inflammation and is usually not particularly painful. The area of the body affected by the acne is usually limited.

Type 1 acne is often transient and often resolves on its own after about a week. Non-inflamed blackheads and small red bumps (papules) are common with this form of acne. This form of acne appears to be particularly common in females and often affects the forehead, cheeks, nose and neck. Topical treatments are often effective at resolving the symptoms associated with Type 1 acne.

Type 2 Acne

  • Mild inflammation
  • Some painful pimples
  • Regular outbreaks

Type 2 Acne is similar to Type 1 acne, but is characterized by increased levels of inflammation and more frequent outbreaks. With Type 2 acne, pimples can range from small red bumps to medium sized whiteheads.

Unlike Type 1 acne blemishes, pimples associated with Type 2 acne are often painful to the touch. Over-The-Counter (OTC) topical treatments are often partially effective at decreasing the severity and duration of outbreaks, but are frequently inadequate for Type 2 acne. Topical antibiotics, Topical Retinoids and Light-Based Therapies can be quite effective for this type of acne. In some instances it may be necessary to explore oral antibiotics or oral retinoids, if the acne does not respond completely to topical treatments.

In general, Type 2 acne is minimally scarring if allowed to resolve on its own. However, it is important to practice good hygiene and avoid exacerbating the situation by “”popping”” pimples without cleaning and sterilizing the area before and after.

Type 3 Acne

  • Large, painful pimples
  • Nodular pimples
  • Frequent outbreaks

Type 3 Acne is characterized by the presence of medium to large nodules and pustules that are frequently painful. With Type 3 acne, pimples are often associated with significant amounts of inflammation. Large whiteheads and large, painful red bumps (nodules and cysts) are common. Individual pimples can take a long time to resolve, up to 10-14 days.

In type 3 acne, much of the inflammation and infection originates deeper in the skin tissue than in Acne Types 1 and 2. Because the source of the problem is deep within the skin, Type 3 acne is usually unresponsive to OTC medications, and many other topical treatments.

Topical antibiotics and topical retinoids are often innefective treatments for people with Type 3 acne. In many cases, oral antibiotics, oral retinoids (Isotretinoin) and laser-based therapies are the only effective treatments. The increased inflammation associated with Type 3 acne poses a significant risk of permanent scarring.

Type 4 Acne

  • Large and painful nodules.
  • Abundant Pustules and Cysts.
  • Persistent Outbreak.

Type 4 Acne is the most severe form of the disease. In most cases, Type 4 acne will cause permanent skin damage and scarring. Like Type 3 acne, Type 4 acne is characterized by inflammatory infections deep within the hair follicle and surrounding tissue. Large, painful cysts and nodules are a common feature in Type 4 acne.

Type 4 acne is generally non-responsive to OTC medications. Topical antibiotics, topical retinoids and naturopathic treatments are poorly effective in many cases. Type 4 acne is a serious medical condition that should be evaluated and treated immediately by a dermatologist, if possible. Treating Type 4 acne often requires aggressive treatment regimens that combine topical and oral pharmaceuticals. Type 4 acne is often extremely painful, both physically and psychologically.