Acne: Causes and Treatment Options
Clearer skin starts with a correct diagnosis and a calm, structured plan.
Acne (acne vulgaris) is a very common inflammatory skin condition that causes blackheads, whiteheads, pimples, and sometimes deeper painful lumps on the face, chest, back, and jawline. It often begins in adolescence, but adult acne is extremely common — especially in women. Acne is treatable at every age, and most patients improve significantly once the key drivers are identified and treated consistently. (1,2)
If you’re unsure what type of acne you have or what to try next, the fastest path to improvement is a doctor-led assessment and a staged plan.
Acne Guides and Treatment Pathways
If you’d like to go deeper, choose the section most relevant to you:
What Is Acne?
Acne is an inflammatory disorder of the pilosebaceous unit — the hair follicle and its oil (sebaceous) gland. Acne develops when pores become blocked and inflammation builds inside the follicle. (1,3)
You may see:
- Comedones: blackheads (open comedones) and whiteheads (closed comedones)
- Inflammatory lesions: papules and pustules (“red pimples”)
- Deeper lesions: nodules (deep, tender lumps). True cysts are uncommon. (1)
Acne is not “caused by dirty skin”. In fact, harsh scrubbing and irritating products often make acne worse. (1)
Why Acne Happens
Acne develops through a combination of interacting factors. Modern research describes four core drivers:
1.Follicular plugging (hyperkeratinisation)
2.Increased oil (sebum) production
3.Changes within the follicle microbiome (especially Cutibacterium acnes)
4.Inflammation and immune activation (1,3)
These factors interact, and the sequence can vary between people — which is why there is no single best treatment for everyone.
The “Microcomedo”: Where Acne Begins
The earliest acne lesion is microscopic: a microcomedo, a tiny plug formed by sticky keratin cells inside the lower part of the follicle. Over time, this can evolve into visible acne lesions:
- When sebum and keratin accumulate behind the plug, it becomes a closed comedo (whitehead).
- As the pore opening stretches, it can become an open comedo (blackhead). The dark colour comes from oxidised material and pigment — not dirt.
- If inflammation escalates, papules and pustules develop. If the follicle wall ruptures, inflammation can spill into the deeper skin and form a nodule, increasing scarring risk. (1)
This is why acne treatment focuses on preventing plugs and calming inflammation early.
The Role of Hormones and Oil Glands
Hormones (especially androgens) increase acne risk because they stimulate sebaceous glands to grow and produce more oil. More sebum can promote follicle blockage and provide a favourable environment for acne bacteria within the follicle. (3,4)
Most people with acne have normal hormone levels, but acne can be more severe with androgen excess (for example in polycystic ovary syndrome) and acne commonly flares with hormonal cycling. (1)
A classic observation shows how central androgens are: people with complete androgen insensitivity do not produce sebum and do not develop acne. (4)
If you suspect a hormonal pattern (jawline acne, cyclical flares), see: Hormonal Acne in Women.
The Follicle Microbiome: Not “Too Much Bacteria”, But the Wrong Balance
Cutibacterium acnes is a normal part of skin flora — acne is not simply an infection. What appears to matter is dysbiosis (an imbalance) and differences between bacterial strains. (3,5)
Research suggests:
- Some C. acnes strains are more associated with acne, while others are more associated with healthy skin. (5)
- Acne-related strains may stimulate stronger inflammatory immune responses, including pathways linked with IL-17. (6)
- C. acnes can form biofilms in follicles, which may contribute to persistence and treatment resistance in some patients. (7)
This helps explain why acne can be stubborn — and why treatment usually needs to address follicle blockage, inflammation, and oil production together.
Inflammation: Why Pimples Become Red, Tender, and Persistent
Inflammation is what turns a blocked pore into a red pimple. C. acnes and follicle contents can activate immune pathways that increase inflammatory cytokines (including IL-1) and recruit inflammatory cells. (6,8,9)
Some studies show inflammatory and tissue-remodelling genes increase in acne lesions, which helps explain why deep, prolonged inflammation increases the risk of scarring. (10)
Genetics: Why Acne Runs in Families
If close relatives had acne, your risk is higher. Twin studies support a strong heritable component to acne susceptibility, although environment and hormones still play major roles. (11)
Factors That Can Worsen Acne
These factors don’t “cause” acne by themselves, but can aggravate it:
Skin trauma and irritation
Harsh scrubbing, strong astringents, and irritant routines can rupture comedones and worsen inflammation. (1)
Diet (evolving evidence)
Diet is not the cause of acne for most people, but evidence suggests it can influence acne severity in some individuals:
- Milk intake has been associated with acne in large observational studies, especially skim/low-fat milk in some cohorts. (12)
- High glycaemic load diets may worsen acne in some people; randomised trials suggest improvement with lower glycaemic load approaches, although weight change can be a confounder. (13)
The practical approach is not extreme restriction — it’s trialling sensible adjustments if you notice a pattern.
Stress
Stress appears to correlate with increased acne severity in some studies, even when sebum production doesn’t change substantially. (14,15)
Insulin/IGF-1 signalling (selected patients)
Insulin resistance and higher IGF-1 levels have been linked with acne in some studies, particularly in post-adolescent acne patterns. (16–18)
Common After-Effects: Marks and Scars
Even when pimples settle, acne can leave changes behind:
Post-inflammatory hyperpigmentation (brown marks)
Common after inflammation, especially in darker skin types, and may persist for months without treatment.
If this is your main issue, see: Post-Inflammatory Hyperpigmentation.
Post-inflammatory erythema (red marks)
Persistent redness can remain after acne lesions heal and may respond to targeted vascular strategies in selected cases.
Scarring
Inflammatory acne is more likely to scar than purely comedonal acne. Scars can be:
- atrophic (ice-pick, rolling, boxcar)
- hypertrophic or keloid (more common on chest/back/jawline in predisposed patients) (1)
If scarring is your main concern, see: Acne Scarring Treatments.
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Your Next Step
If acne is affecting your confidence, leaving marks, or not responding to your current routine, a structured plan can make a major difference.
References
1.Zaenglein AL, Pathy AL, Schlosser BJ, et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2016;74(5):945–973.e33. https://pubmed.ncbi.nlm.nih.gov/26897386/
2.Collier CN, Harper JC, Cafardi JA, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol. 2008;58(1):56–59. https://pubmed.ncbi.nlm.nih.gov/18029084/
3.O’Neill AM, Gallo RL. Host-microbiome interactions and recent progress into understanding the biology of acne vulgaris. Microbiome. 2018;6:177. https://pubmed.ncbi.nlm.nih.gov/30285861/
4.Imperato-McGinley J, Gautier T, Cai LQ, et al. The androgen control of sebum production. J Clin Endocrinol Metab. 1993;76(2):524–528. https://pubmed.ncbi.nlm.nih.gov/8381804/
5.Fitz-Gibbon S, Tomida S, Chiu BH, et al. Propionibacterium acnes strain populations in the human skin microbiome associated with acne. J Invest Dermatol. 2013;133(9):2152–2160. https://pubmed.ncbi.nlm.nih.gov/23337890/
6.Agak GW, Qin M, Nobe J, et al. Propionibacterium acnes induces an IL-17 response in acne vulgaris that is regulated by vitamin A and vitamin D. J Invest Dermatol. 2014;134(2):366–373. https://pubmed.ncbi.nlm.nih.gov/23924903/
7.Jahns AC, Lundskog B, Ganceviciene R, et al. An increased incidence of Propionibacterium acnes biofilms in acne vulgaris: a case-control study. Br J Dermatol. 2012;167(1):50–58. https://pubmed.ncbi.nlm.nih.gov/22356121/
8.Kim J, Ochoa MT, Krutzik SR, et al. Activation of toll-like receptor 2 in acne triggers inflammatory cytokine responses. J Immunol. 2002;169(3):1535–1541. https://pubmed.ncbi.nlm.nih.gov/12133981/
9.Li ZJ, Choi DK, Sohn KC, et al. Propionibacterium acnes activates the NLRP3 inflammasome in human sebocytes. J Invest Dermatol. 2014;134(11):2747–2756. https://pubmed.ncbi.nlm.nih.gov/24820890/
10.Trivedi NR, Gilliland KL, Zhao W, et al. Gene array expression profiling in acne lesions reveals marked upregulation of genes involved in inflammation and matrix remodeling. J Invest Dermatol. 2006;126(5):1071–1079. https://pubmed.ncbi.nlm.nih.gov/16543895/
11.Bataille V, Snieder H, MacGregor AJ, et al. The influence of genetics and environmental factors in the pathogenesis of acne: a twin study of acne in women. J Invest Dermatol. 2002;119(6):1317–1322. https://pubmed.ncbi.nlm.nih.gov/12485434/
12.Adebamowo CA, Spiegelman D, Danby FW, et al. High school dietary dairy intake and teenage acne. J Am Acad Dermatol. 2005;52(2):207–214. https://pubmed.ncbi.nlm.nih.gov/15692464/
13.Smith RN, Mann NJ, Braue A, et al. The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: a randomized controlled trial. J Am Acad Dermatol. 2007;57(2):247–256. https://pubmed.ncbi.nlm.nih.gov/17448569/
14.Yosipovitch G, Tang M, Dawn AG, et al. Study of psychological stress, sebum production and acne vulgaris in adolescents. Acta Derm Venereol. 2007;87(2):135–139. https://pubmed.ncbi.nlm.nih.gov/17340019/
15.Chiu A, Chon SY, Kimball AB. The response of skin disease to stress: changes in the severity of acne vulgaris as affected by examination stress. Arch Dermatol. 2003;139(7):897–900. https://pubmed.ncbi.nlm.nih.gov/12873885/
16.Vora S, Ovhal A, Jerajani H, et al. Correlation of facial sebum to serum insulin-like growth factor-1 in patients with acne. Br J Dermatol. 2008;159(4):990–991. https://pubmed.ncbi.nlm.nih.gov/18652583/
17.Nagpal M, De D, Handa S, et al. Insulin resistance and metabolic syndrome in young men with acne. JAMA Dermatol. 2016;152(4):399–404. https://pubmed.ncbi.nlm.nih.gov/26720707/
18.Di Landro A, Cazzaniga S, Parazzini F, et al. Family history, body mass index, selected dietary factors, menstrual history, and risk of moderate to severe acne in adolescents and young adults. J Am Acad Dermatol. 2012;67(6):1129–1135. https://pubmed.ncbi.nlm.nih.gov/22386050/