The sebocyte is a major component of the skin’s barrier defence systems and its primary role is to manufacture sebum to contribute in building the first line of skin barrier defence; the Acid Mantle/Microbiome.

The sebocyte is situated within a basal membrane surrounding the sebaceous gland cell where it migrates towards the interior of the sebaceous gland within around 14-20 days (age/lifestyle dependant) where it fills up with more and more lipids (mainly triglycerides) until coming to the end of its timely lifecycle. The sebocytes contents (sebum) are released into the sebaceous gland interior and this cell itself must undergo disintegration where its components contribute to the secretions of the skin.

Depending on the health of the sebocyte, the cellular debris left over from the cells disintegration is removed by enzymes and macrophage cells before it poses any problems. Sometimes, and even in healthy skins, these built in defence systems fail and cellular debris becomes mixed with the sebum causing cutaneous blockages as the secretions move up through the narrow passageway of the hair shaft.

The quality of the sebaceous gland sebum is highly dependant on Essential Fatty Acids for improving the health of the sebocyte. When the quality of sebum is affected by Essential Fatty Acid Deficiency (EFAD), blockages of the hair follicle can occur as the sebum and cellular debris secreted literally becomes so thick, viscous and gluggy that it simply cannot migrate up through the narrow passageway of the hair shaft and onto the surface of the skin.

To improve the health of the sebocyte, one must consume Omega 3 + 6 topically and nutritionally to which will improve the viability of the cell membrane and the quality of the sebum. Lipid-peroxidation is a compounded form of oxidative stress to which will have a negative impact on the cells regenerative lifecycle and to fight off aggressive free radical damage to which will further impair cell membranes.

Essential Fatty Acid Deficiency is a very common skin condition and effects majority of the population due to the ‘Western Diet’ that we are exposed too… (more on that later).


P.acnes bacteria is responsible for converting all of the triglyceride sebum from the sebaceous gland interior as it migrates up through the hair shaft and pilosebaceous duct entrance. P.acnes metabolises this sebum by releasing a specialized enzyme of the protease family called lipase; and this enzyme is responsible for creating the acidic pH of the skin due to the sebum being converted into free fatty acids.

When the Acid Mantle has been disrupted and the ecosystem of the microflora has been compromised, p.acnes bacteria can in turn migrate down into the sebaceous gland interior and generate an inflammatory response by converting the triglycerides sebum into free fatty acids; and this substance is considered a foreign body due to the difference in pH of the sebaceous gland and dermal matrix.

P.acnes bacteria has the ability to send out chemical messengers to which can alert specific immune system defense cells (macrophages and neutrophils) to breakdown epithelial cell walls and contribute to the inflammatory process. Whenever you see pus within a breakout, that’s an indication of dead neutrophils from fighting the battle of infection.

P.acnes bacteria is not just one bacteria as there is approximately 66 strains of this bacteria and not all have pro-inflammatory properties as they are vital to the health of the skin. An interesting fact is that p.acnes is often treated by antibiotics, but studies were conducted back in 2001 where these particular strains of acne causing bacteria have become more and more resistant to the prescribed drugs overtime; not treating the actual cause and disappointing those affected by acne.

Working to repair all built in defense systems is essential before embarking down this treatment journey if necessary.


Whenever you see post inflammatory hyperpigmentation left behind from a pustule, papule or cyst, do you know what cells and systems have been affected? When there is inflammation taking place with the pilosebaceous unit, the fascia septa (loose connective tissue) that surrounds all appendages of the dermis becomes traumatised around the sebaceous gland; and if someone has repeatedly squeezed a pustule, papule or cyst, scarring will occur to the fascia septa and in clinic treatments such as LED and Collagen Induction Therapy are required to make vast changes to this skin condition.

When a pustule for example begins forming, the sebaceous gland swells which in turn causes trauma to the epithelium and this can lead to scarring due to abnormal stretching. The inflammation makes its way up to the Dermal/Epidermal Junction towards the basal layer of the epidermis and from here, 1 in every 10 cells of this layer is a melanocyte cell; and these cells are melanin constructing defence systems that are designed to protect the skin from UV radiation through the process of melanogenesis (more discussion on this further along).

The melanocyte cell becomes highly reactive when there is underlying inflammation and an increase in Reactive Oxygen Species (free radical production) begins to take effect which in turn activates inflammatory cytokines, prostaglandins 1 & 2 (inflammatory hormones) and stem cell growth factors along with excessive amounts of the Melanin Stimulating Hormone; triggering a vast increase in the production of melanin and melanin transfer to the surrounding keratinocytes and leading to post inflammatory hyperpigmentation.


Keratinocytes of the basal layer of the epidermis are programed to undergo an event called ‘terminal differentiation’ and this event is a type of controlled, programmed journey which slowly takes place as the keratinocyte changes its structure to create a flat, hydrophobic corneocyte. The Stratum Corneum (top layer of skin) does not finish sharply as you might think; it actually runs slightly down into the pilosebaceous duct entrance. The basal layer of the epidermis contains dividing stem cells to which can contribute to blockages if this duct and the lifecycle of the keratinocyte fails to complete the cellular compaction process as it matures into a corneocyte.


Over exfoliating causes abrasive removal of the Stratum Corneum which can trigger inflammation and hyperproliferation of the keratinocyte due to the cell-to-cell communication process between the corneocyte and keratinocyte. When the Acid Mantle/Microbiome, Stratum Corneum and Permeability Barrier have been compromised, you have on your hands an unprotected skin which means you get an increase in oxidative stress, a decrease in cell protection, an increase in lipid-peroxidation and all of this is going to accelerate the cellular senescence of the cell.

The Acid Mantle contains Urocanic Acid formed by a protein called filaggrin found within the Stratum Corneum and is part of skin barrier defence against UV radiation. Urocanic Acid functions as an endogenous sunscreen against UVB induced DNA damage and when there is an increase in UV radiation, keratinocyte stem cells are programmed to upsend these epithelial cells due to the increase in melanogenesis. This results in melanosomes (pigment granules) released from the melanocyte which are needing to be picked up by the keratinocytes of the epidermis which in turn results in the increased dispersion of melanosomes due to an unprotected skin. This activates the need for more keratinocytes to pick up the melanosomes which results in a thickened epidermis; contributing to poor corneocyte compaction/desquamation and blockages of the pilosebaceous duct entrance.


The cornified cell envelope of the corneocyte is a physical barrier surrounding corneocytes which formed during the keratinocytes differentiation cycle and is part of the process of changing this very important cell into a flat, hydrophobic corneocyte. The cornified cell envelope is heavily dependant on intracellular calcium as it serves as a scaffold for the multilamellar lipid structure while also providing effective physical and water barrier functions in the skin by slowing down transepidermal water loss.

Why is this important? The cornified cell envelope if not developed accurately can cause cutaneous xerosis (dry skin) and allow for microorganisms to penetrate into the deeper layers of the skin causing a response from the innate/adaptive immune system; triggering poor corneocyte compaction/desquamation, closed comedones and inflammation. Having a properly formed Stratum Corneum with intact intra/extracellular water fluid within the epidermis is essential for enzyme activity to dissolve the cutaneous tethering desmosomes; enabling vital detachment from other neighbouring keratinocytes and corneocytes which will prevent the corneocyte from migrating over hair follicles and causing blockages.

Having an impaired barrier function causes high transepidermal water loss and impairs the metabolic enzymatic activity of the epidermis; causing the desmosomal protein bonds to remain attached rather than being dissolved and this results in hyperkeratinization (poor corneocyte compaction), closed comedones and inflammation.


The sebaceous gland and overall skin integrity is actually influenced by the endocrine system, and in relation to this topic of discussion, my thought process is around the androgen testosterone hormone and the enzyme 5a Reductase Type 1.

The enzyme 5a Reductase Type 1 is located within the sebaceous gland cell and is responsible for converting the testosterone from the bloodstream into dihydrotestosterone which ultimately can pose a problem for those who have an androgen sensitivity or dominance. Testosterone is a lipid soluble hormone composed of cholesterol that has the ability to merge with the bi-layer alignment of the plasma membrane of the sebaceous gland and ultimately change the cells activity once that hormone has been accepted.

Receptors are located within the plasma membrane for this particular steroid (lipid soluble) hormone and ultimately acts as a docking station for not only hormones but nutrients, oxygen, growth factors, cytokines and the removal of cellular waste. If receptors become impaired due to a compromised cell membrane, hormones will also be affected and can trigger forceful entry of substances (hormones) triggering fluctuations and sensitivities of cell membranes causing an inflammatory response.

All biological cells within the body are bounded by thin membranes composed primarily of phospholipids which protect the viability of the cell. Of course we are not indestructible and our body’s natural built in defence systems decline with age; causing damage or disease to cell membranes and accelerating the cellular senescence of the cell.

Getting back on track regarding the enzyme 5a Reductase Type 1, this enzyme changes the quality of the sebum to be quite defective and highly aggravating for those with hormonal mediated acne; and those with hormonal mediated acne will most definitely have an androgen sensitivity or dominance.

Androgen hormones have the ability to trigger poor corneocyte compaction/desquamation of the keratinocyte during its differentiation cycle from mitosis (cell division) all the way to the Stratum Corneum. Androgens not only have the ability to increase sebum production, but they also thicken up the epidermis/dermis which can contribute to interfollicular compaction, comedones and inflammation.

Androgen hormones are responsible for changing a vellus hair (soft baby hair) into a terminal hair (corse adult hair) which unfortunately can cause further blockages of the pilosebaceous duct further aggravating the acneic skin. P.acnes bacteria is always present at the site of response so do be keeping this in the back of your mind at all times.

Hormones in general are all literally like an orchestra. If one instrument goes out of tune, it will have a profounding effect to the viability of the entire epidermis/dermis as the skin essentially is an endocrine system of its own.


Refined carbohydrates are quickly absorbed into the bloodstream which in turn causes a resurgence in blood sugar levels. When blood sugars rise, insulin levels also rise to help shuttle the blood sugars out of the bloodstream and into your cells; and high levels of insulin are an aggravating factor for those with acne.

One study found those who frequently consume added sugars had a 30% greater risk of developing acne, while those who regularly consumed pastries and cakes had a 20% greater risk of developing the skin condition. This increased risk may be explained by the effects carbohydrates have on blood sugar and insulin levels.

Due to our overbearingly cytotoxic western diet, human beings are eating far too much glucose and this in turn is having a detrimental effect to not just our skin, but to our bodies! In regards to hormones, insulin makes androgen hormones more active and increases insulin-like growth factor 1 (1GF-1) and this contributes to acne development by making cells grow more quickly and by boosting sebum production… hello 5a Reductase enzyme!

Foods rich in refined carbohydrates include:

  • Bread, crackers, cereal or desserts made with white flour
  • Pasta made with white flour
  • White rice and rice noodles
  • Sodas and other sugar-sweetened beverages
  • Sweeteners like cane sugar, maple syrup and honey

Studies have also shown that those who consume a low-glycemic diet, which do not dramatically raise blood sugars or insulin levels, are associated with a reduction in their acne symptoms.


Skincare of course can be a recipe for disaster when it comes to an acneic skin as the microbiome residing within the acidic pH of the Acid Mantle can become compromised or even causing them to die off due to external physiological changes. Unfortunately many of the skincare products that people use are often exacerbating this condition and as I like to say, playing ‘Russian Roulette’ with the first three lines of skin barrier defence.

If you haven’t read my blog titled, ‘Do Not Remove Your Skin Barrier’ I suggest you do as I go into detail about the importance of preserving the integrity of the Acid Mantle/Microbiome and all of the other related skin barrier defence systems.

Always avoid skincare products that contain fragrances, emulsifiers, preservatives, parabens, silicones, amines, colours and dyes as they do NOT work with the physiological functions of the skin and thus must be avoided at all times to prevent not only the development of acne, but other cutaneous disorders such as atopic dermatitis, psoriasis and rosacea.

Will the microbiome survive the personal skincare industry? That is the question.

The global market for personal care products is expected to increase to a total market value of 500 US billion dollars by 2020 and the market for product ingredients is more likely to grow even faster. Supermarkets for example contain thousands of chemicals that have the potential to damage our microbiome along with our health, and thus need to be analysed for contraindications before one directly applies a possible comedogenic substance or worse a DNA mutating toxin to the skin; and side effects of ingredients can be either instant or accumulative until they eventually display a multitude of cutaneous side effects.

To summarise, acne is a multifaceted condition that often has more than just one offending cause and the key is to find the offending cause so the symptom can be alleviated. My professional recommendations is to seek out a Corneotherapist (Skin Treatment Therapist) and a Naturopath; particularly one who specialises in DUTCH testing as there is always a hormonal component when it comes to treating the acneic skin.

There is more to the acneic story than just being prescribed antibiotics or Accutane; and just to be clear here I am not discriminating against these forms of treatment modalities as there is indeed a time and place for them; and I personally believe doctors and dermatologists need to dig a little deeper to find the offending cause rather than just alleviate the symptom which often result having the condition bounce back once the medication has been discontinued.

Written by Kai Atkinson (Corneotherapist)