What actually is PCOS? Understanding the 4 subtypes
- Dr Natalie Hutchins
- 15 hours ago
- 7 min read
For something so common, PCOS is still one of the most misunderstood conditions in women’s health. It’s often talked about as a “hormone imbalance” or a fertility issue, but the reality is far more complex.
New research shows PCOS isn’t just about the ovaries. It’s a whole-body condition that sits at the crossroads of metabolism, hormones, and brain-ovary communication. This helps explain why two women can share the same diagnosis yet experience it so differently.
In this article, we’ll explore the newly defined subtypes of PCOS, what drives each one, and how metabolism fuels the cycle of symptoms. Understanding exactly where the disruption begins in each case changes how we diagnose, treat, and manage PCOS effectively.
What PCOS actually is (and isn’t)
Polycystic Ovary Syndrome (PCOS) affects around 1 in 10 women worldwide. However, the real number is likely much higher, since research suggests up to 70% of people with PCOS don’t even know they have it.1
Why? Because despite how common it is, PCOS is still deeply misunderstood – both by patients and healthcare professionals. Many of us are told it’s “just a hormone imbalance”, “a period problem”, or caused by “too many cysts on the ovaries”.
The name PCOS is misleading because those “cysts” are actually enlarged, immature follicles that appear when the body isn’t ovulating properly.2 So, polycystic ovaries can be just one of the many symptoms of hormonal disruption in PCOS. We still don’t fully understand the exact causes behind PCOS, but new research is shedding light on just how complex the condition can be.
Navigating the PCOS diagnosis criteria
According to the 2023 International Evidence-Based Guidelines for PCOS, a diagnosis can be made when someone meets two out of three of the following criteria (after ruling out other causes of symptoms).3
Irregular or absent ovulation. This often shows up as missing or unpredictable periods.
High androgen levels. Androgens are often called “male-type” hormones (like testosterone). They can be measured on a blood test or seen through symptoms like acne, excess facial or body hair, or hair thinning.
Polycystic ovarian morphology (PCOM). This means the ovaries show lots of small, immature follicles on an ultrasound. Importantly, they’re not cysts – they just appear cyst-like because the follicles haven’t matured or released an egg.
The latest guidelines also allow Anti-Mullerian Hormone (AMH) testing as an alternative to ultrasound in adults. AMH is produced by ovarian follicles, so higher levels can suggest lots of active follicles, a key feature of PCOM.3
For teens, ultrasound and AMH testing aren’t recommended. During puberty, it’s completely normal for the ovaries to contain lots of small follicles and for cycles to be irregular for the first 1-3 years after menarche. The hypothalamic-pituitary-ovarian axis (the brain-ovary communication system) is still maturing, so an irregular cycle doesn’t suggest PCOS. If your symptoms continue beyond those early years, or there are clear signs of androgen excess, it might be time to speak to a doctor.4
Not all PCOS looks the same: The 4 subtypes
PCOS doesn’t follow a single pattern, it’s a spectrum, making it difficult to diagnose and even harder to manage. A recent study of nearly 12,000 women outlined four main subtypes, each with their own underlying cause.5
OB-PCOS (Obesity-related PCOS)
In this type, metabolism is the starting point. The body becomes less sensitive to insulin, the hormone that moves sugar (glucose) from your blood into your cells for energy. To compensate, the pancreas produces even more insulin.
High insulin levels tell the ovaries to make extra androgens and less sex-hormone binding globulin (SHBG) – the protein that normally keeps those hormones in check. With less SHBG, more androgens circulate freely, triggering symptoms like weight gain, irregular periods, and inflammation.6
HA-PCOS (Hyperandrogenic PCOS)
Here, the imbalance starts with the hormones themselves. The ovaries (and sometimes the adrenal glands) produce too many androgens because their hormone-producing cells are overly sensitive to insulin and luteinising hormone (LH).7
Even mild insulin resistance can worsen this imbalance, but excess androgens are the starting point. Women with this type of PCOS often notice visible symptoms like acne, oily skin or excess hair, even if they’re not overweight.
LH-PCOS (High-LH or High-AMH PCOS)
This type begins in the brain-ovary feedback loop. The hypothalamus (the brain’s hormone control centre) sends gonadotrophin-releasing hormone (GnRH) signals too quickly. This pushes LH levels high and follicle-stimulating hormone (FSH) low, disrupting the balance needed for healthy ovulation.5
The ovaries respond by producing more androgens and anti-Mullerian hormone (AMH), which stops follicles from maturing properly. Ovulation then becomes irregular or stops altogether, even when metabolism is normal. This type is more common in lean women and teenagers.
SHBG-PCOS (High SHBG, or more mild PCOS)
This type is a milder form of PCOS where metabolism stays mostly stable. High levels of SHBG help bind excess androgens, keeping active testosterone low and symptoms less severe. Women with this profile tend to have a lower BMI, more balanced insulin levels, and fewer or milder symptoms.5
The metabolic loop: How insulin and hormones feed each other
PCOS is now recognised as both a metabolic and reproductive condition – one that looks, feels and behaves differently in each woman. Even when metabolism isn’t the first thing to go wrong, it often becomes the engine that keeps PCOS running.8
Specifically, PCOS symptoms are shaped by how we process insulin, a hormone that moves glucose (sugar) from your blood into your cells to be used as energy. In a healthy system, insulin keeps blood sugar and energy levels steady. But when cells stop responding properly to insulin, a self-reinforcing cycle begins:
Insulin resistance: the body’s cells become less responsive to insulin, making it harder to move glucose into cells for energy.
Hyperinsulinaemia: to compensate, the pancreas works overtime, releasing even more insulin to keep blood sugar stable. This triggers a state called hyperinsulinaemia (chronically high insulin).9
Ovarian over-stimulation: While muscle and fat cells resist insulin, the ovaries remain super sensitive to it. High insulin works alongside luteinising hormone (LH) to push the ovaries to produce more androgens.10
Inflammation and fat changes: High androgens encourage the body to store fat around the abdomen (known as visceral fat). This tissue is more hormonally active and releases inflammatory chemicals which make insulin resistance even worse.11
The feedback loop: insulin resistance → high insulin → high androgens → more abdominal fat → more inflammation → worse insulin resistance
Because of this metabolic feedback loop, PCOS is linked not just to changes in ovulation and fertility – but also to wider health problems like type 2 diabetes, fatty liver disease and cardiovascular risks (even in women who appear healthy or lean).11
How the metabolic loop shapes PCOS symptoms
Once we understand where individual cases of PCOS start, the symptoms begin to make more sense.
Irregular or absent ovulation
High insulin and androgens disrupt how the ovaries grow and release eggs. Instead of one dominant follicle maturing and releasing an egg, lots of small follicles begin to develop but don’t finish the process. This can cause irregular or missing periods, making ovulation unpredictable and getting pregnant more difficult.9
Polycystic ovaries
Those same undeveloped follicles can build up on the ovaries, creating the “polycystic” look seen on ultrasound. They’re not cysts, just immature follicles that haven’t been released because the hormonal signals are out of balance. That’s why polycystic ovaries are a sign of disrupted ovulation, not the cause of it.9
Skin and hair changes
When there’s more free testosterone circulating in the blood, it can affect both skin and hair follicles. Sebum (oil) production increases, leading to acne or oily skin. Meanwhile, hair follicles become more sensitive, triggering hirsutism (excess facial or body hair), or hair thinning on the scalp.8
Weight and body shape
Many people with PCOS describe “stubborn belly fat” or difficulty losing weight. High insulin encourages the body to store more fat around the abdomen (visceral fat), which is more hormonally active and releases inflammatory chemicals.11 That inflammation makes insulin resistance worse, feeding the metabolic loop. It’s not just about willpower or diet; PCOS directly changes how the body stores and uses fat.
Energy and mood
When insulin and blood sugar fluctuate, so does energy. Sharp rises and falls can trigger fatigue, sugar cravings, or that “wired but tired” feeling that’s common in PCOS. High insulin and androgens can also affect brain chemicals like dopamine and serotonin, which regulate mood and stress, which helps explain why anxiety and low mood often appear alongside physical symptoms.9
Making sense of the evidence
Looking at PCOS through multiple lenses – metabolic, hormonal, and neuroendocrine – transforms how we understand it. It helps explain why two women with the same diagnosis can have entirely different experiences, and why what works for one might not work for another.
The discovery of these four PCOS subtypes marks a major step forward. It moves us beyond a vague, catch-all diagnosis toward a clearer picture of this whole-body condition. Even though PCOS has different starting points, understanding how metabolism, insulin resistance and inflammation interact gives us a practical framework for better symptom management.
There’s still a serious need for more research, but this new evidence lays a solid foundation for more personalised PCOS care.
Sources:
Insulin resistance, metabolic syndrome and polycystic ovaries: an intriguing conundrum
Data-driven subtypes of polycystic ovary syndrome and their association with clinical outcomes
Polycystic Ovary Syndrome as Metabolic Disease: New Insights on Insulin Resistance
Reappraising the relationship between hyperinsulinemia and insulin resistance in PCOS
Metabolic Syndrome and PCOS: Pathogenesis and the Role of Metabolites
