Acne: could hormones or gut health be the root cause?

Androgens and sebum production

Androgens (male sex hormones, including testosterone and its more potent derivative DHT) are the primary biological driver of acne in both men and women. Androgens activate sebaceous (oil) glands in the skin, increasing sebum production. Excess sebum combines with dead skin cells to block follicles, creating the environment in which Cutibacterium acnes bacteria proliferate and trigger inflammation, producing the papules, pustules, and cysts characteristic of acne. Even small increases in androgen levels, or increased skin sensitivity to normal androgen levels, can produce significant sebaceous gland activation.

In women, free testosterone (the biologically active fraction not bound to proteins) is particularly relevant. The amount of free testosterone available to androgen receptors in the skin is determined by both total testosterone and SHBG (sex hormone binding globulin). When SHBG is low, more testosterone is biologically active, even when total testosterone appears within normal range. This is why testing testosterone alongside SHBG is more informative than testosterone alone for understanding androgen-driven acne.

Insulin resistance and its effect on androgen production

Insulin resistance is one of the most important and most commonly overlooked contributors to adult acne. Elevated insulin drives the ovaries and adrenal glands to produce more androgens, directly worsening the hormonal picture that drives sebum production. In women with PCOS (polycystic ovary syndrome, which affects around 1 in 10 women in the UK), insulin resistance and elevated androgens operate together as a self-reinforcing cycle: insulin drives androgen production, androgens worsen insulin resistance, and both together produce acne, irregular periods, and other PCOS features.

The relationship between diet, insulin, and acne is well supported. High glycaemic load diets (those high in refined carbohydrates and sugar) produce significant post-meal insulin spikes that stimulate androgen production through the same mechanism. This is one reason why dietary change is often effective for acne, and why blood markers of insulin regulation (HbA1c, fasting glucose) are clinically relevant to a comprehensive acne assessment.

Gut dysbiosis and the skin-gut axis

The connection between gut health and skin health is mechanistically established. A disrupted gut microbiome (dysbiosis) contributes to acne through several pathways. Gut dysbiosis increases intestinal permeability, allowing bacterial components to enter circulation and trigger systemic inflammation that worsens skin inflammation. The gut microbiome also influences the metabolism and circulation of sex hormones: bacteria in the gut regulate the enterohepatic recycling of oestrogen and androgens, meaning that microbiome imbalances can alter circulating hormone levels independently of production. Research in the journal Frontiers in Endocrinology has found that elevated levels of specific bacterial genera (including Bacteroides) correlate with higher testosterone concentrations in women, pointing to a direct role for microbiome composition in androgen regulation.

Additionally, the gut produces a significant proportion of the body's serotonin and other neurotransmitters, and gut-brain axis disruption amplifies the stress response that worsens cortisol-driven sebaceous gland activity. People who notice their skin worsens under stress often have both elevated cortisol and gut dysbiosis working together.

PCOS and acne

PCOS is the most common hormonal cause of persistent adult acne in women. The Rotterdam criteria for PCOS diagnosis require two of three features: oligo-ovulation (irregular or absent periods), clinical or biochemical signs of androgen excess (including acne), and polycystic ovarian morphology on ultrasound. Acne alone, particularly in women with otherwise regular cycles, may reflect PCOS even without the other features being immediately apparent. Blood testing in suspected PCOS should include testosterone, SHBG, LH, FSH, and HbA1c as a minimum, with DHEA-S providing context for adrenal androgen contribution.

Between 50 and 80% of women with PCOS have insulin resistance, which is the central metabolic feature driving the androgen elevation. Testing the metabolic picture alongside the hormonal picture is essential because the most effective interventions for PCOS-related acne (dietary changes, weight management, and metformin in some cases) target the metabolic root cause rather than the skin directly.

Cortisol and stress-driven acne

The adrenal glands produce both cortisol and androgens, and sustained cortisol elevation stimulates adrenal androgen output alongside the primary stress hormone response. This is why stress produces acne flares even in people whose hormonal profile is otherwise well-balanced. Cortisol also worsens insulin resistance through its effects on blood glucose regulation, creating an additional pathway from stress to sebum production. Measuring cortisol alongside androgens and metabolic markers provides a more complete picture of the combined hormonal drivers.

Nutritional factors

Zinc plays a direct role in regulating sebaceous gland activity and has anti-inflammatory effects in skin tissue. Zinc deficiency has been associated with acne severity, and zinc supplementation in deficient individuals has shown benefit in some clinical studies. Vitamin D deficiency is associated with impaired immune regulation in the skin and higher rates of inflammatory acne. Both markers are worth including in an acne blood test panel, particularly for people whose diet is low in these nutrients or who have absorption impairments.

A GP assessment for acne rarely includes hormonal or metabolic testing beyond a basic check for PCOS if periods are irregular. For adults with persistent acne, particularly women with acne alongside other features such as irregular cycles, excess facial hair, or weight management difficulty, a comprehensive hormonal acne test provides the biological context for targeted rather than symptomatic treatment.

Testosterone establishes androgen levels. In women, total testosterone may appear normal while free testosterone (determined by SHBG) is elevated enough to drive sebaceous gland overactivity.

SHBG (sex hormone binding globulin) determines how much testosterone is biologically active. Low SHBG is common in PCOS and insulin resistance, and significantly amplifies androgenic effects on skin even when total testosterone is within range.

LH and FSH provide context for ovulatory function and the LH-to-FSH ratio that characterises PCOS.

HbA1c reflects average blood glucose over three months and provides the clearest picture of insulin regulation. Elevated HbA1c indicates insulin resistance, the metabolic driver that amplifies androgen production.

Cortisol measured in the morning establishes the baseline adrenal hormone output that contributes to both androgen production and insulin dysregulation.

CRP (C-reactive protein) measures systemic inflammation. In people whose acne is driven by gut dysbiosis and elevated intestinal permeability, CRP is often mildly elevated even in the absence of other inflammatory conditions.

Vitamin D and zinc (where available) complete the nutritional picture, since deficiency in either can worsen inflammatory acne.

Dietary glycaemic load reduction

The most consistently evidence-supported dietary intervention for acne is reducing dietary glycaemic load. Foods that produce rapid glucose spikes (white bread, processed cereals, sugar-sweetened foods and drinks) drive insulin peaks that stimulate androgen production and worsen sebum output. Replacing these with complex carbohydrates (oats, legumes, vegetables), adequate protein, and healthy fats reduces the insulin burden while maintaining energy. This is a sustained dietary pattern rather than a temporary elimination, and tracking HbA1c at 3 months provides an objective measure of whether blood sugar regulation is improving.

Supporting a diverse gut microbiome

Dietary diversity is the most evidence-supported strategy for improving gut microbiome composition. The 30 plants per week target, encompassing a varied range of vegetables, fruits, legumes, wholegrains, nuts, and seeds, provides the range of prebiotic fibres that different beneficial bacterial species require. Fermented foods including natural yoghurt, kefir, kimchi, and sauerkraut introduce beneficial bacteria and support microbiome diversity. Reducing ultra-processed food consumption reduces the dietary environment that promotes dysbiosis and the inflammation associated with it. Retesting gut microbiome composition after a 3-month dietary change provides an objective picture of how the microbiome has responded.

Stress management and cortisol regulation

For acne that flares predictably with stress, the adrenal androgen pathway is likely involved alongside direct cortisol-driven sebaceous gland activation. Interventions that measurably reduce cortisol output, including adequate sleep, structured recovery within the day, and practices that activate the parasympathetic nervous system, reduce the adrenal contribution to androgen production. Tracking cortisol at baseline and after a period of structured stress management quantifies whether the intervention is producing a biological response, independent of the subjective experience of feeling less stressed.

Zinc and vitamin D support

For people with confirmed zinc or vitamin D deficiency, supplementation has a more direct evidence base for acne improvement than for those with adequate levels. Zinc supplementation in deficient individuals at doses of 30-45mg of elemental zinc daily has shown benefit in several clinical studies. Correcting vitamin D deficiency supports immune regulation in the skin and reduces the inflammatory component of acne. Both should be tested before supplementation and retested at 3 months to confirm that target levels are being achieved.