Clinical Practice Considerations: A Systems-Based Approach to Acne Assessment for Allied Health Practitioners

Acne is one of the most common skin presentations in allied health, yet persistent or recurrent cases almost always point to underlying systemic drivers. When topical strategies aren’t enough, it’s often because deeper hormonal, metabolic, gut, nutritional, immune, or neuroendocrine patterns are influencing the skin.

For practitioners using integrative or functional models, recognising how these systems interact is key to building truly effective, root-cause treatment plans.

Below, we explore the major physiological contributors to acne, with clinical indicators and recommended testing included for easy application.

1. Hormonal Drivers of Acne

Hormones play a major role in adult acne, particularly when breakouts follow a cyclical pattern or appear in hormonally sensitive areas like the jawline, chin, and neck. Many patients describe deeper, more cystic lesions that flare premenstrually.

Polycystic Ovary Syndrome (PCOS) is a common endocrine condition underpinning androgenic acne. Excess androgens (testosterone, DHEAS) increase sebaceous activity, contributing to clogged pores and inflammation. Testing helps clarify this picture and guides targeted intervention.

Clinical Indicators of Hormonal Acne

• Cyclical flares (especially premenstrual)
• Jawline, chin, neck distribution
• Deep, tender, cystic lesions
• Irregular cycles, PMS, mood swings -Signs of androgen excess (oily skin, hirsutism)

Recommended Hormone Testing

• Hormone Imbalance Test (including Total & free testosterone, DHEA-S. LH & FSH, Prolactin, Thyroid function tests, Insulin, Cortisol)

2. Metabolic Health, Blood Sugar Regulation & IGF-1 Pathways

A substantial body of research links high-glycaemic diets, insulin resistance, and elevated insulin-like growth factor 1 (IGF-1) with acne severity. High-GI/GL diets lead to insulin spikes, which elevate IGF-1, increasing sebaceous gland activity and accelerating keratinocyte proliferation, promoting comedogenesis. Hyperinsulinemia amplifies androgen activity in the skin.

Patients with metabolic-driven acne often describe feeling tired after meals, craving sugar or carbs, gaining weight around the midsection, or noticing their skin gets oilier throughout the day.

Clinical Indicators of Metabolic-Driven Acne

• Fatigue after meals
• Sugar or carbohydrate cravings
• Central weight gain
• Higher BMI
• Oily, inflamed acne on cheeks or jawline

Recommended Metabolic Testing

• Insulin Resistance Test
• HbA1c Test
• Cholesterol Test

Addressing metabolic dysfunction may lead to notable improvements in skin clarity and inflammation.

3. Gut–Skin Axis & the Microbiome

The gut significantly influences systemic inflammation, hormonal regulation, nutrient absorption, and immune responses. Dysbiosis (imbalanced gut bacteria), leaky gut (intestinal permeability), food sensitivities (especially dairy, gluten, and high-glycaemic foods), and infections like H. pylori or parasitic infections can elevate systemic inflammation, affect nutrient absorption, and disrupt hormone metabolism.

Dysbiosis Research shows two key patterns: higher levels of Bacteroides are linked to an increased risk of acne, while higher levels of Lactobacillus are associated with a reduced risk. This matters because Bacteroides produce inflammatory compounds such as LPS, which can weaken the intestinal barrier and promote systemic inflammation. In contrast, Lactobacillus supports gut barrier integrity, regulates immune function, and reduces inflammatory signalling, providing a protective effect against acne-related inflammation.

Intestinal Permeability ("Leaky Gut") The intestinal epithelial layer serves as a physical and functional barrier between the microbe-rich lumen and the immunologically active submucosa. When this barrier is compromised, microbial products such as lipopolysaccharides (LPS) can translocate into the systemic circulation, leading to immune activation and chronic low-grade inflammation. This systemic inflammation can exacerbate acne.

Additionally, a weakened gut barrier can impair the absorption of essential nutrients, including zinc, B vitamins, and fat-soluble vitamins (A, D, E, K). These nutrients are crucial for maintaining skin health, immune function, and reducing inflammation. Deficiencies in these nutrients can further contribute to the pathogenesis of acne.

Food Sensitivities Research shows that dairy and high glycaemic foods increase insulin-like growth factor 1 (IGF-1) activity, thereby amplifying hormonal and metabolic acne drivers. High glycaemic index (GI) and glycaemic load (GL) diets lead to insulin spikes, which elevate IGF-1 levels. IGF-1 stimulates sebaceous gland activity and keratinocyte proliferation, contributing to acne pathogenesis. Dairy consumption has been shown to increase serum insulin and IGF-1 levels, further exacerbating acne.

Gluten sensitivity may worsen gut inflammation and dysbiosis. Gluten can increase intestinal permeability, leading to the translocation of endotoxins such as lipopolysaccharides (LPS) into the bloodstream. This process triggers systemic inflammation, which can exacerbate acne. Dysbiosis, or an imbalance in gut microbiota, is also linked to increased gut permeability and systemic inflammation, further contributing to acne severity.

GI Infections (e.g., H. pylori) H. pylori infection can increase systemic inflammation, raising pro-inflammatory cytokines like IL-1β, IL-6 and TNF-α, which may worsen acne by amplifying inflammatory skin pathways. A study in Archives of Dermatological Research found that people with severe acne were more likely to test positive for H. pylori antigens and antibodies than those with mild acne or healthy controls, highlighting a clear association between the infection and acne severity.

Clinical Indicators of Gut-Related Acne

• Bloating, IBS symptoms, reflux
• Acne flares after dairy, sugar, or gluten
• History of antibiotic use
• Coexisting fatigue or nutrient deficiencies
• Skin that worsens with stress (gut–brain axis involvement)

Recommended Gut Testing

• Microbiomix Advanced Gut Test
• SIBO Breath Test
• Helicobacter Pylori Stool Test or Helicobacter Pylori Breath Test
• Intestinal Permeability Test
• Food Intolerance Test
• Platinum Gut Health Test (includes Microbiomix, SIBO, H Pylori, Intestinal Permeablity & Food Intolerance tests)

4. Nutrient Deficiencies

Several nutrients are essential for healthy skin turnover, hormonal signaling, and inflammation regulation, and deficiencies in these nutrients commonly appear in patients with chronic or treatment-resistant acne.

Zinc: Zinc is crucial for maintaining skin integrity, modulating inflammation, and supporting immune function. Zinc deficiency can lead to increased inflammation, impaired wound healing, and overproduction of sebum. Studies have shown that zinc supplementation can alleviate acne by reducing inflammatory responses and oxidative stress.

Vitamin A: Vitamin A is vital for skin cell differentiation and turnover. Deficiency in vitamin A can lead to hyperkeratinization, which contributes to clogged pores and acne formation. Retinoids, derivatives of vitamin A, are commonly used in acne treatment due to their ability to normalize skin cell shedding and reduce inflammation.

Vitamin D: Vitamin D has anti-inflammatory and antimicrobial properties. Low levels of vitamin D are associated with increased acne severity. Vitamin D deficiency can impair immune function and increase inflammation, exacerbating acne.

Omega-3 Fatty Acids: Omega-3 fatty acids have anti-inflammatory effects and can help reduce the production of pro-inflammatory cytokines. Deficiency in omega-3 fatty acids can lead to increased inflammation and sebum production, worsening acne.

B Vitamins (B5 and B6): Vitamin B5 (pantothenic acid) is involved in lipid metabolism and can help reduce sebum production. Vitamin B6 (pyridoxine) is important for hormone regulation. Deficiencies in these vitamins can contribute to acne by promoting inflammation and altering oil production.7,8,9

Clinical Indicators of Nutrient-Related Acne

• Slow wound healing
• Recurrent or chronic inflammation
• Fatigue, low mood, or frequent illness
• Diet low in whole foods, healthy fats, or protein

Recommended Nutrient Testing

• Micronutrient Test (including zinc, vitamin D, vitamin A, B vitamins) - Omega-3 Index
• Organic Acids Test (OAT) (how your cells are using nutrients)

5. Stress, Cortisol & the Neuroendocrine System

Chronic stress activates the HPA axis, leading to elevated cortisol levels. This increase in cortisol stimulates sebaceous glands, resulting in higher sebum production, which is a key factor in acne development. Elevated cortisol also disrupts hormone metabolism, further exacerbating acne.

Stress-induced cortisol can compromise gut barrier integrity, allowing endotoxins to enter the bloodstream and promote systemic inflammation, which can worsen acne. Additionally, cortisol impairs wound healing by inhibiting keratinocyte migration and reducing collagen synthesis, causing acne lesions to persist longer and new ones to form more easily. Patients frequently report that their acne worsens during periods of high stress, such as exams, major life events, sleep deprivation, or emotionally demanding times.

Clinical Indicators of Stress-Related Acne

• Flares during high-pressure periods
• Coexisting anxiety, IBS symptoms, or poor sleep
• Breakouts that worsen before important events
• Slow healing lesions

Recommended Testing

• Hormone Imbalance Test (including Total & free testosterone, DHEA-S. LH & FSH, Prolactin, Thyroid function tests, Insulin, Cortisol)
• Advanced DUTCH Test

6. Thyroid Function: A Frequently Overlooked Contributor

Thyroid hormones are essential for healthy skin, supporting normal cell turnover, wound healing and hormonal balance. When thyroid levels are low, as in hypothyroidism, keratinocyte proliferation slows, leading to dry, congested skin and delayed healing of acne lesions. Thyroid dysfunction can also disrupt estrogen–androgen balance, potentially increasing androgen activity and worsening breakouts.

Research shows that reduced thyroid hormone signalling not only slows skin renewal but also heightens inflammation, contributing to more persistent and severe acne. While not a primary cause, thyroid dysfunction can meaningfully exacerbate acne through these combined effects.

Clinical Indicators of Thyroid-Related Acne

• Fatigue, cold intolerance
• Dry skin with concurrent congestion
• Weight gain
• Menstrual irregularities
• Slow healing or post-inflammatory hyperpigmentation

Recommended Thyroid Testing

• Comprehensive Thyroid Test (including TSH, Free T4, Free T3, Reverse T3, Thyroid antibodies (TPO & TGAb))

7. When Acne Isn’t Acne

Not all breakout-like eruptions are true acne. When lesions are itchy, rapidly worsening, or fail to improve with/ or worsen on antibiotics, other conditions should be considered.

Gram-negative folliculitis, often triggered by long-term antibiotic use, presents as uniform pustules and nodules around facial openings and is typically resistant to standard acne treatments, requiring targeted antibiotics or isotretinoin.

Malassezia (fungal) folliculitis appears as itchy, uniform papules and pustules on the upper trunk or face and is commonly mistaken for acne, especially after antibiotic therapy. Diagnosis is confirmed by identifying yeast in the follicles, and treatment involves topical or oral antifungals.

Clinical Indicators

• Itchy lesions
• Rapid worsening of symptoms
• Lack of response to conventional acne treatments
• Worsening of symptoms with antibiotic therapy

Recommended Microbiological Testing

• Bacterial cultures
• Fungal microscopy/culture

Final Clinical Perspective

Acne is rarely a stand-alone skin condition. More often, it reflects intricate disruptions across hormonal, metabolic, gut, nutritional, thyroid, microbiological, and neuroendocrine systems.

By using a systems-based, root-cause approach, allied health practitioners can move beyond surface-level interventions and support patients in achieving long-lasting improvements in skin health and overall wellbeing.