PCOS: Understanding What Is Really Driving Polycystic Ovary Syndrome
- Lauren Dyer
- 5 days ago
- 6 min read

Polycystic Ovary Syndrome (PCOS) is one of the most common endocrine conditions affecting women of reproductive age. Despite its prevalence, it remains one of the most misunderstood conditions in women’s health.
Many women are told they have “cysts on their ovaries” and are prescribed hormonal contraception without ever being given a clear explanation of what is actually happening within the body.
The reality is far more complex.
PCOS is not simply an ovarian condition. It is a heterogeneous metabolic and hormonal disorder involving communication between the brain, ovaries, adrenal glands, insulin signalling pathways and the reproductive hormone axis.
Understanding these mechanisms is essential if we want to move beyond symptom management and begin addressing the factors contributing to the condition.
What Is PCOS?
PCOS is characterised by two key features:
Excess androgen production (male-type hormones such as testosterone)
Ovulatory dysfunction
Women with PCOS commonly experience:
Irregular or absent periods
Acne
Excess facial or body hair (hirsutism)
Scalp hair thinning
Difficulty conceiving
Weight gain or difficulty losing weight
Ovarian changes visible on ultrasound
Importantly, acne, unwanted hair growth and obesity do not cause PCOS. They are symptoms resulting from the underlying hormonal disturbances.
The condition is most commonly diagnosed during a woman’s twenties and thirties, although the underlying processes often begin much earlier.
Why Ovulation Matters
Many discussions around PCOS focus on fertility, but ovulation influences far more than the ability to conceive.
Regular ovulatory cycles contribute to:
Healthy progesterone production
Bone integrity
Mood regulation
Metabolic health
Mitochondrial energy production
Cardiovascular health
Neurotransmitter function
When ovulation becomes irregular or absent, progesterone production is reduced.
This creates a hormonal environment where oestrogen remains relatively unopposed and androgen production often increases.
Over time, this can affect everything from mood and energy levels to metabolic function and endometrial health.
Understanding A Normal Menstrual Cycle
To understand PCOS, it helps to understand what should happen during a healthy cycle.
At the beginning of the menstrual cycle, levels of oestradiol and progesterone are low.
In response, the hypothalamus and pituitary gland signal the ovaries through the release of:
Follicle-stimulating hormone (FSH)
Luteinising hormone (LH)
Each month, a group of ovarian follicles begins developing.
Although hundreds of follicles are recruited, only one typically becomes dominant and proceeds to ovulation.
Within the ovary:
Theca cells produce androgens
Granulosa cells convert those androgens into oestrogen via the aromatase enzyme
As the dominant follicle grows, oestradiol levels rise.
This eventually triggers the mid-cycle LH surge responsible for ovulation.
Following ovulation, the follicle transforms into the corpus luteum, which produces progesterone.
Progesterone prepares the uterine lining for pregnancy and helps regulate the second half of the menstrual cycle.
If pregnancy does not occur, progesterone falls and menstruation begins.
What Happens In PCOS?
In PCOS, this finely tuned communication system becomes disrupted.
Instead of the normal rhythmic release of GnRH from the hypothalamus, abnormal pulse patterns develop.
These altered signals favour LH production.
As a result:
LH levels become chronically elevated
FSH remains relatively lower
Theca cells produce excessive androgens
Follicle development slows or stalls
Ovulation becomes delayed or absent
Rather than progressing to ovulation, many follicles remain trapped in a partially developed state.
These are often described as “cysts”, but they are not true cysts.
They are immature follicles that have failed to complete development.
This distinction is important because PCOS cannot be ruled in or ruled out solely on the basis of an ultrasound scan.
Why Excess Androgens Matter
Excess androgen production is one of the defining features of PCOS.
Higher androgen levels can contribute to:
Facial hair growth
Acne
Oily skin
Hair thinning around the crown of the head
Irregular cycles
Impaired ovulation
The most potent androgen, dihydrotestosterone (DHT), is produced through the action of the enzyme 5-alpha reductase.
This enzyme is often a therapeutic target when addressing androgen-related symptoms.
The Role of Insulin Resistance
One of the most important drivers of PCOS is insulin resistance.
Research suggests that approximately 75-80% of women with PCOS demonstrate some degree of impaired insulin sensitivity.
When insulin levels remain elevated:
Insulin directly stimulates ovarian theca cells
Insulin mimics some of the actions of LH
Sex hormone binding globulin (SHBG) decreases
Free testosterone increases
This creates a cycle where elevated insulin drives greater androgen production, which then further disrupts ovulation.
For many women, hyperinsulinaemia sits at the centre of the condition.
It is one reason why blood sugar regulation and metabolic health are often critical components of treatment.
Why Heavy Periods Can Occur
Without regular ovulation, progesterone production is reduced.
Oestradiol continues stimulating growth of the endometrial lining, but the balancing effects of progesterone are absent.
Over time this can contribute to:
Endometrial hyperplasia
Heavy bleeding
Large clots
Irregular bleeding patterns
This is one reason prolonged absence of ovulation should never be ignored.
Diagnosing PCOS: Why It Can Be Confusing
Historically, diagnosis focused heavily on androgen excess and ovulatory dysfunction.
The Rotterdam Criteria introduced in 2003 broadened the definition.
Under these guidelines, PCOS could be diagnosed if two of the following three features were present:
Clinical or biochemical androgen excess
Ovulatory dysfunction
Polycystic ovaries on ultrasound
This change meant some women could receive a diagnosis based on irregular periods and ultrasound findings alone, even without clear evidence of androgen excess.
The 2023 international guidelines continue to use a two-out-of-three framework whilst recognising the role of Anti-Müllerian Hormone (AMH) as an additional diagnostic tool in adults.
Importantly, ultrasound and AMH are not recommended as diagnostic tools within eight years of menarche because the reproductive system is still maturing and irregular cycles are often physiological.
Laboratory Assessment
A thorough assessment should consider:
Total testosterone
Free androgen index
Sex hormone binding globulin (SHBG)
LH
FSH
Anti-Müllerian Hormone (AMH)
Fasting insulin
Blood glucose regulation
Prolactin
Thyroid function
17-hydroxyprogesterone
DHEA-S
When evaluating testosterone, laboratory methodology matters.
Liquid chromatography tandem mass spectrometry (LC-MS/MS) is generally considered the gold standard for measuring female androgens.
Conditions That Can Mimic PCOS
Not every woman with elevated androgens has PCOS.
Other causes must be considered, including:
Congenital adrenal hyperplasia
Elevated prolactin
Thyroid dysfunction
Adrenal androgen excess
Certain medications
Hormonal contraception
For example, deficiencies in the enzyme 21-hydroxylase can lead to increased androgen production and may resemble PCOS.
Likewise, elevated prolactin can suppress normal LH and FSH signalling and disrupt ovulation.
A Functional Medicine Perspective
PCOS is unlikely to be a single disease with a single cause.
Different women may present with different dominant drivers.
These commonly include:
Insulin-resistant PCOS
Characterised by:
Elevated insulin
Weight gain
Cravings
Difficulty losing weight
Elevated free testosterone
Adrenal PCOS
Characterised by:
Elevated DHEA-S
Stress-related symptoms
Anxiety
Sleep disruption
Relatively normal insulin levels
Post-pill PCOS
Symptoms may emerge following cessation of hormonal contraception, particularly after prolonged suppression of the hypothalamic-pituitary-ovarian axis.
Inflammatory PCOS
Low-grade inflammation may contribute to androgen production through inflammatory signalling pathways involving CRP, IL-6 and NF-kB.
Supporting Healthy Hormone Balance
Management should always be individualised and based on the underlying drivers.
Potential areas of support may include:
Improving insulin sensitivity
Supporting ovulation
Reducing excess androgen production
Addressing stress and adrenal dysfunction
Correcting nutrient deficiencies
Improving sleep quality
Supporting healthy body composition
Investigating gut and inflammatory contributors
Inositol
Myo-inositol plays an important role in insulin signalling, ovarian function and follicular development.
Research suggests it may:
Improve insulin sensitivity
Reduce androgen levels
Improve ovulation
Increase SHBG
Improve LH:FSH ratios
Products using a physiological 40:1 ratio of myo-inositol to D-chiro-inositol are commonly used in PCOS.
Nutrients and Botanicals
Several nutrients and plant compounds have been investigated for their effects on androgen metabolism, including:
Zinc
Spearmint tea
Green tea
Reishi mushroom
Liquorice root
Paeonia (Chinese peony)
Nettle root
Many work through mechanisms involving androgen production, aromatase activity or 5-alpha reductase inhibition.
Progesterone
For some women, cyclical micronised progesterone may be considered under medical supervision.
Potential benefits include:
Supporting regular withdrawal bleeds
Protecting the endometrium
Reducing DHT formation
Supporting more normal GnRH and LH signalling patterns
The Bigger Picture
PCOS is far more than a collection of ovarian cysts.
It is a complex hormonal and metabolic condition involving communication between the brain, ovaries, adrenal glands and insulin signalling pathways.
The presence of excess androgens, disrupted ovulation and metabolic dysfunction can influence fertility, mood, energy production, body composition and long-term health.
Understanding the underlying drivers allows for a more personalised approach that goes beyond symptom suppression and focuses on restoring healthy hormonal signalling, metabolic resilience and ovulatory function.




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