Understanding Acne: A Dive into the Hidden Causes Behind this Skin Condition

Acne is a skin condition that occurs when your skin pores are blocked by oil, bacteria, dead skin cells, and/or dirt. The oil glands under our skin release sebum(oil), which normally travels up hair follicles (also known as our pores) and onto the surface of our skin, keeping our skin soft. However, a build-up of oil, bacteria, or dead skin cells trapped in our pores can lead to inflammation. Acne is a physical manifestation of this inflammation.

Main Factors that Cause Acne

• Excess Sebum Production
• Hyperkeratosis (excess skin cell shedding in the hair follicle or pore)
• Over-Colonization of Propionibacterium Acnes (P.Acnes bacteria)
• Inflammation as part of the immune response to the bacteria
• Hormonal Influence
• Immune Response

Acne Pathogenesis

Excess Sebum Production - Hormone Imbalance

The sebaceous gland is located next to the hair follicle. Ideally, the sebum it produces moves along

the hair shaft to the skin’s surface, where it contributes to the lipid barrier that both lubricates and

protects the skin from environmental damage. Since sebum production is influenced by hormones,

particularly androgens such as testosterone, hormonal imbalances which can occur monthly or at

certain life stages, (ie. puberty) can lead to excessive sebum production. While most sebum reaches

the surface, in acneic skin, the sebum becomes trapped within the follicle.

Hyperkeratosis (excess skin cell shedding)

People with acne-prone skin shed up to five times more dead skin cells (corneocytes). These dead

skin cells should shed naturally, however in acne-prone skin, the process of shedding dead skin

cells (keratinocytes) becomes disrupted. Acne-prone pores are stickier, making it harder to shed

dead cells. This condition is known as retention hyperkeratosis, where dead cells accumulate in the

hair follicles and mix with sebum, leading to clogged pores. The trapped oil serves as a nutrient for

bacteria, creating an ideal environment for Cutibacterium Acnes (C.Acnes, formerly known as

Propionibacterium Acnes or P. Acnes) to increase and cause inflammation.

C. Acnes Bacterial Proliferation

Cutibacterium Acnes (C.Acnes) is a type of bacteria commonly found on the skin. Under normal

conditions, it exists as part of the skin's natural microbiome. When pores are blocked with excess

sebum and dead skin cells, C. acnes can multiply in this anaerobic environment, contributing to

inflammation, causing the characteristic redness, swelling, and pus associated with acne lesions.

Inflammation

When Cutibacterium Acnes (C.Acnes) bacteria overpopulate the hair follicles, it contributes to the

genesis of inflammatory acne. Our body’s natural response to this bacteria is to send white blood

cells to the source in order to ‘fight’ it and prevent any nasty infections. Once our white blood cells

have ‘killed’ the bacteria, they remain in your pores and are, essentially,

‘dead’ (pus is literally just a bunch of dead white blood cells).

Hormonal Influence

Hormonal fluctuations, especially an increase in androgens, further stimulate sebaceous gland

activity, making hormonal changes a key driver of acne, particularly during puberty, menstrual

cycles, pregnancy, or due to certain medications.

Immune Response

The body's immune system reacts to the bacterial activity and clogged pores, resulting in further

inflammation. The immune response can exacerbate the severity of acne, particularly in individuals

with inflammatory acne types such as cystic or nodular acne.

When Does Acne Begin?

Acne commonly begins during puberty, typically between the ages of 10 and 13, although it can start

earlier or later for some individuals. The onset is influenced by hormonal changes that occur during

this time, leading to increased sebum production and skin cell turnover.

While puberty is the most common period for acne to develop, it can also appear:

• In Early Childhood: Some infants may experience a form of acne known as neonatal acne,

which usually resolves on its own.

• In Young Adults: Many people experience acne into their late teens and early twenties, and for

some, it can persist into their thirties or beyond.

• Hormonal Fluctuations: Acne can also be triggered by hormonal changes related to menstrual

cycles, pregnancy, or conditions like polycystic ovary syndrome (PCOS).

Overall, while puberty is the primary phase for the onset of acne, various factors can influence its

development at different life stages.

Let’s talk about the most common time for acne to appear: puberty, when the body starts producing androgens such as testosterone. In the skin, an enzyme converts testosterone into dihydrotestosterone, which stimulates the sebaceous glands (oil-producing glands) to produce sebum (an oil-like substance). Boys experience a significant increase in testosterone levels during puberty, typically beginning around ages 9 to 14. Girls in their teens also experience an increase in testosterone, but to a greater extent in estrogen. Both of these hormone increases lead to more sebum production.

In individuals prone to acne, the increase in sebum triggers a condition called retention hyperkeratosis, where dead skin cells don't shed properly, leading to clogged follicles.

So, with all of this happening, it's time to look at the genesis of a pimple! Oil production is increasing, and dead skin cells are not shedding properly, leading us to the first stage: the formation of the microcomedone. As the dead skin cells begin to accumulate inside the pore, they become sticky and get trapped. Acne is an inflammatory condition, and the severity of the condition will determine the type of acne lesion that forms.

Below is an illustration of the life cycle of pimples.