By Krystle Alves | Naturopath, Nutritionist & Yoga Therapist | B.HSc, Adv. Dip. Naturopathy
If you've been told you have PCOS, you've almost certainly been handed one of a few standard explanations: your hormones are out of balance, your periods are irregular, you may have trouble with weight, and if you want to conceive, there are things you can try. What you may not have been told is what's actually driving it, or that the drivers are considerably more complex, and more systemic, than a single hormonal imbalance.
PCOS is one of the most common endocrine conditions, affecting an estimated 8–13% of people of reproductive age. Yet despite its prevalence, it remains poorly understood in mainstream clinical settings, frequently managed with oral contraceptives or metformin and monitored rather than investigated. The research is telling a very different story: one involving insulin resistance, gut microbiome dysbiosis, environmental chemical exposures, adrenal stress pathways, and chronic low-grade inflammation operating in tightly interlocked feedback loops.
Understanding those drivers matters, not for academic interest, but because the management approach that follows from this picture is substantially different from the one that focuses on hormones alone.
Not One Condition: A Cluster With a Common Core
PCOS presents differently across individuals, and this is one reason it has been so difficult to characterise cleanly. Some presentations are metabolic, dominated by insulin resistance, weight gain, and cardiovascular risk factors. Others are androgenic, driven primarily by excess androgen production, with acne, hirsutism, and hair thinning as the most visible features. A third subtype is adrenal in origin, where elevated androgens are produced by the adrenal glands in response to chronic stress, rather than by the ovaries at all.
What recent research has identified is that underlying all of these presentations is a core triad: hyperandrogenism, insulin resistance, and chronic inflammation. These three elements drive each other in positive feedback loops, each one amplifying the others, with multiple organ systems implicated in sustaining the cycle. The gut, the adrenal glands, the liver, adipose tissue, and the immune system are all active participants. The ovaries are often the most visible site of dysfunction, but they are frequently downstream.
Insulin Resistance: The Central Metabolic Driver
Insulin resistance is present in 50–70% of people with PCOS, and critically, it is not confined to those who are overweight. Lean individuals with PCOS demonstrate insulin resistance at rates that challenge the assumption that this is simply a consequence of weight. It is, for a significant proportion of people, a primary feature.
Insulin resistance in PCOS operates through a specific mechanism: insulin directly stimulates the theca cells of the ovaries to produce androgens, primarily testosterone. At the same time, elevated insulin suppresses sex hormone-binding globulin (SHBG), the protein that binds and inactivates testosterone in circulation. The result is both more testosterone being produced and less being bound and neutralised. This drives the hyperandrogenism that characterises so many PCOS presentations.
There is also a neuroendocrine dimension. High insulin disrupts the normal pulsatile release of GnRH (gonadotropin-releasing hormone) from the hypothalamus, which in turn skews the ratio of LH to FSH, favouring LH-driven ovarian androgen production over FSH-driven follicle maturation. This is why cycles become irregular and ovulation is disrupted: the hormonal signalling cascade required for ovulation is being interrupted upstream.
Insulin resistance in PCOS is not a peripheral metabolic inconvenience. It is a central driver of the reproductive and hormonal dysfunction that defines the condition.
The Gut Microbiome: A Bidirectional Relationship
The relationship between the gut microbiome and PCOS is now among the most active areas of research in this field, and the findings are consistent: gut dysbiosis both reflects and amplifies PCOS pathophysiology.
People with PCOS show reduced overall microbial diversity, a depletion of short-chain fatty acid (SCFA)-producing bacteria, and an enrichment of endotoxin-producing species. Specific findings from 2024–2025 research include:
Bacteroides vulgatus and bile acid disruption. Bacteroides vulgatus is elevated in PCOS and has been shown to drive PCOS-like phenotypes in animal models by suppressing bile acid levels through the BSH pathway. Bile acids are not simply digestive compounds; they act as signalling molecules that regulate glucose metabolism, insulin sensitivity, and immune function. When their levels are suppressed, insulin resistance worsens and reproductive hormone signalling is disrupted.
Fungal dysbiosis. A 2025 study identified that Aspergillus tubingensis, a fungal species, is significantly elevated in the gut of PCOS patients. This species secretes a metabolite that suppresses interleukin-22 (IL-22) signalling in the gut, a pathway central to gut barrier integrity and immune regulation. This finding points toward the fungal microbiome as a dimension of PCOS pathology that is almost entirely overlooked in standard assessment.
Leaky gut and LPS-driven inflammation. Depletion of SCFA-producing bacteria compromises the integrity of the gut lining. Lipopolysaccharides (LPS) from gram-negative bacteria enter the bloodstream through the compromised barrier, triggering a sustained low-grade inflammatory response. This systemic inflammation further impairs insulin signalling and amplifies androgen production, feeding directly back into the core PCOS triad.
The estrobolome. The gut microbiome also regulates estrogen metabolism in PCOS. When the estrobolome is dysregulated, estrogen is either insufficiently cleared or excessively recirculated, contributing to the hormonal imbalances that affect menstrual cycle regularity and ovulatory function.
A 2025 systematic review in Physiological Genomics assessed microbiome alterations across body sites in PCOS and confirmed consistent patterns of dysbiosis, while also noting that the bidirectionality of the relationship means gut health both contributes to and is affected by the hormonal and metabolic environment of PCOS.
Hormone-Disrupting Chemicals: An Environmental Driver That Is Largely Invisible
One of the most underappreciated contributors to PCOS in the research literature is exposure to endocrine-disrupting chemicals (EDCs): synthetic compounds that interfere with the body's hormonal signalling systems.
Bisphenol A (BPA) and phthalates have received the most research attention in relation to PCOS. Both are pervasive in modern environments: BPA in plastics, food and drink packaging, and thermal paper; phthalates in personal care products, fragrances, food packaging, and flexible plastics. Both have been shown to disrupt ovarian function, stimulate androgen production, impair insulin sensitivity, and alter epigenetic programming.
A 2025 systematic review found a positive association between BPA exposure and PCOS across multiple studies, with mechanisms including direct stimulation of androgen-producing cells, disruption of insulin receptor signalling, and interference with the hypothalamic-pituitary axis. Phthalate exposure has been independently associated with impaired endocrine function in PCOS, with research showing correlations between phthalate metabolite levels and elevated androgens and disrupted ovarian follicular development.
A 2024 study comparing urban and rural populations found significantly higher concentrations of BPA and DEHP (a phthalate) in urban participants, highlighting that EDC exposure is not evenly distributed; it correlates with environmental and lifestyle factors in ways that intersect with PCOS risk.
The mechanism is not simply hormonal mimicry. EDCs alter gene expression through epigenetic modification, changing which genes are switched on or off in ovarian, adrenal, and hypothalamic tissue, in ways that can persist across cell generations and potentially be passed on. This is an emerging area that is likely to become significantly more prominent in PCOS research over the next decade.
The HPA Axis and the Adrenal Subtype
Stress is not a psychological detail in PCOS. For a specific subset of people, estimated at 20–30% of PCOS presentations, elevated androgens originate not from the ovaries but from the adrenal glands, driven by chronic activation of the HPA axis.
Under sustained stress, the brain releases adrenocorticotropic hormone (ACTH), which signals the adrenal glands to produce cortisol. The adrenals also produce DHEA and DHEA-S in response to ACTH, androgen precursors that convert downstream to testosterone. In people with adrenal-pattern PCOS, this adrenal androgen output is the primary driver of the androgenic symptoms: elevated DHEA-S on testing, with relatively normal or mildly elevated ovarian androgens.
But the HPA axis connection extends beyond the adrenal subtype. In PCOS more broadly, chronic HPA activation contributes to the inflammatory environment, worsens insulin resistance (cortisol directly impairs insulin signalling), and dysregulates hypothalamic GnRH pulsatility, further disrupting the reproductive axis. A 2025 review in PMC confirmed that the HPA axis plays a pivotal role in PCOS pathophysiology, and that standard lifestyle interventions frequently fail because they do not directly address the neuroendocrine dysregulation driving the condition.
The practical implication is significant: if chronic stress and HPA dysregulation are primary drivers, managing PCOS without addressing the nervous system will consistently produce incomplete results.
Chronic Low-Grade Inflammation: The Thread That Connects Everything
Across all subtypes and all drivers, chronic low-grade inflammation appears as the common thread in PCOS pathophysiology. A 2025 review in Endocrinology titled "Unpacking PCOS Inflammation" characterised the condition as one defined by multi-system immune dysfunction, not simply as an inflammatory response to hormonal or metabolic changes, but as a driver of them.
In PCOS, visceral adipose tissue secretes pro-inflammatory cytokines that impair insulin signalling and stimulate androgen production. Gut dysbiosis drives LPS-mediated inflammation that further destabilises insulin and immune function. Chronic HPA axis activation maintains an elevated inflammatory tone. And elevated androgens themselves promote inflammatory signalling in ovarian and adipose tissue, completing the loop.
This interconnected picture explains why PCOS so frequently co-occurs with other inflammatory conditions, including thyroid autoimmunity, irritable bowel syndrome, skin conditions, and mood disorders, and why managing it through a single pathway consistently fails to resolve the full picture.
Investigating the Drivers Clinically
Understanding the research is essential. Translating it into what is actually driving an individual's presentation requires investigation, and the standard workup for PCOS (ultrasound, LH/FSH ratio, total testosterone, fasting glucose) is often insufficient to reveal the full picture.
In my practice, I use a combination of advanced functional testing to assess the key systems the research has implicated:
DUTCH hormone testing maps not only estrogen, progesterone and androgen levels but the specific pathways through which androgens are being produced and metabolised. This distinguishes ovarian androgen excess from adrenal androgen excess, a distinction that changes the entire management approach, and reveals how hormones are being processed through the liver and gut. Progesterone status, cortisol metabolites, and markers of hormonal oxidative stress are all captured in a single test, giving a far more complete hormonal picture than a serum panel alone.
Cortisol rhythm testing assesses the diurnal cortisol pattern across the day. Given that HPA axis dysregulation is both a driver of adrenal PCOS and an amplifier of insulin resistance and inflammation across all subtypes, understanding where someone's cortisol rhythm sits is clinically essential, particularly in presentations where stress, fatigue, and anxiety are prominent features alongside the reproductive symptoms.
Advanced microbiome screening provides detailed characterisation of gut bacterial and fungal composition, SCFA production capacity, markers of intestinal permeability, and inflammatory species abundance. Given the strong research linking specific microbial patterns (Bacteroides vulgatus, SCFA depletion, fungal dysbiosis) to PCOS pathology, this level of assessment goes considerably beyond what standard stool testing reveals.
Genetic reports identify individual variations in androgen metabolism pathways, insulin signalling genes, inflammatory cytokine genes, and detoxification capacity. These variations help explain why two people with identical hormone levels can have very different symptom experiences, and they inform which interventions are most likely to be effective for that individual's specific biology.
When this functional investigation is deployed alongside any medical management being provided, whether that is hormonal contraception, metformin, or fertility support, it addresses the systemic drivers that pharmacological management alone does not reach. The two approaches are not in competition; they work at different levels of the same problem.
If you have PCOS and feel that the management approach you've been offered is not reaching the root of what's driving it, that instinct is worth following.
This post is for educational purposes only and does not constitute medical advice. If you have PCOS or suspect you may, please consult a qualified health practitioner for personalised assessment and support.
Krystle Alves is a naturopath, nutritionist and yoga therapist with over 17 years of clinical experience. She works with clients navigating complex hormonal and metabolic conditions including PCOS. Consultations are available via telehealth Australia-wide. Book a consultation →