PCOS May Not Be One Condition - But Two Distinct Biological Patterns

Two Main Patterns Identified

Researchers separated women with PCOS into two groups:

• Hyperandrogenic (HA) - higher levels of androgens such as testosterone 

• Non-Hyperandrogenic (Non-HA) - meeting PCOS criteria, but without elevated testosterone

Roughly 1 in 4 women with PCOS fall into the non-hyperandrogenic group.

These patterns were not simply “mild” versus “severe.”
They appeared to reflect different dominant biological drivers.

Pattern One: When Metabolism Drives Hormones

In the hyperandrogenic group, the strongest signal was insulin resistance.

Women in this group had:

• Higher insulin resistance
• Stronger links between insulin levels and testosterone
• Longer menstrual cycles
• More pronounced ovarian changes

Importantly, insulin resistance predicted androgen excess even after accounting for BMI.

This tells us something clinically important:

It is not body weight alone driving hormonal disruption.
It is the metabolic dysfunction underneath - particularly how the body handles insulin.

Biologically, here’s what happens:

When cells become resistant to insulin, the pancreas produces more of it.

Elevated insulin then:

• Directly stimulates ovarian theca cells to produce more androgens
• Amplifies LH signalling to the ovary
• Reduces liver production of SHBG (a protein that binds testosterone)

The result? Higher circulating free testosterone and disrupted ovulation.

In this phenotype, the metabolic and reproductive systems are closely intertwined.

Pattern Two: When Brain–Ovary Signalling Dominates

The non-hyperandrogenic group looked different.

They showed:

• Less metabolic disturbance
• Minimal link between insulin resistance and reproductive hormones
• Stronger association between LH (luteinising hormone) and cycle disruption

In this group, ovarian dysfunction appeared to be driven more by altered signalling along the hypothalamic–pituitary–ovarian (HPO) axis - essentially the communication pathway between the brain and the ovaries.

The metabolic “engine” seen in the hyperandrogenic group was largely absent here.

This reinforces an important idea:

Not all PCOS is primarily insulin-driven.

Why This Distinction Matters

If insulin resistance is the primary driver (as in the hyperandrogenic phenotype), metabolic support becomes central - regardless of body size.

If neuroendocrine signalling is more dominant (as in the non-hyperandrogenic phenotype), strategies may need to focus more on cycle regulation and stress–brain–ovary dynamics.

Understanding the biology allows care to become more precise.

Menstrual and Ovarian Differences

Women in the hyperandrogenic group had longer average cycle lengths and more classic polycystic ovarian morphology.

The non-hyperandrogenic group showed ovarian changes as well, but without the same metabolic–androgen amplification.

Again, this supports the idea of distinct biological pathways rather than one uniform disorder.

What This Means for Women with PCOS

This research offers a reassuring message:

If your PCOS looks different from someone else’s - that makes biological sense.

For some women, PCOS is primarily a metabolic condition that presents through reproductive symptoms.

For others, altered brain–ovary signalling appears more central.

Both are real.Both are valid.But they may require different support strategies.