PCOS Hormones Debunked: Why Women with PCOS Actually Make Too Little Estradiol (E2)

Introduction: Turning the Narrative Upside Down

When most people hear about Polycystic Ovary Syndrome (PCOS), they assume it means women have too much estrogen. For decades, the term “estrogen dominance” has circulated in medical conversations and health blogs, leaving many women terrified that their bodies are flooded with estrogen.

But here’s the shocking truth: women with PCOS don’t actually make enough of the most important estrogen—estradiol (E2).

If you’ve been told your body is “overloaded with estrogen,” this blog will set the record straight.

Estradiol (E2) vs. Estrone (E1): The Two Faces of Estrogen

To understand the PCOS estrogen puzzle, you first need to know that estrogen isn’t just one hormone. There are three main types:

• Estradiol (E2): The “gold standard” estrogen. It’s the most potent and biologically active form, critical for bone health, metabolism, brain function, fertility, and cardiovascular protection.
  
  

• Estrone (E1): A weaker estrogen, made in fat tissue, that acts differently than E2. High levels of E1 can drive inflammation and abnormal tissue growth.
  
  

• Estriol (E3): A pregnancy-related estrogen with a minor role outside of gestation.
  
  

Here’s the kicker: women with PCOS often have too little estradiol (E2) and too much estrone (E1). That imbalance—not an “estrogen surplus”—is at the root of many symptoms.

Why Do Women with PCOS Have Low Estradiol?

The problem lies in how the ovaries respond to brain signals:

1. Hormonal Miscommunication (LH vs. FSH):
   
   

   • In PCOS, luteinizing hormone (LH) is often much higher than follicle-stimulating hormone (FSH).
     
     

   • This imbalance overstimulates theca cells, leading to too much testosterone production.
     
     

   • Meanwhile, the low FSH means the ovary isn’t producing enough aromatase, the enzyme that converts testosterone into estradiol.
     
     

2. The Aromatase Roadblock:
   
   

   • Without enough aromatase, testosterone lingers in the ovary instead of turning into estradiol.
     
     

   • This is why women with PCOS often have high testosterone symptoms (acne, hair growth, hair loss) and low estradiol symptoms (irregular cycles, inflammation, metabolic issues).
     
     

3. Fat Tissue’s Role:
   
   

   • Fat cells have aromatase too—but instead of making estradiol, inflamed fat tissue tends to convert testosterone and androstenedione into estrone (E1).
     
     

   • This creates a double-whammy: too little estradiol (the “good” estrogen) and too much estrone (the “bad” one).
     
     

Symptoms of Estradiol Insufficiency in PCOS

Low estradiol doesn’t always show up on routine labs, but its effects are noticeable:

• Irregular or absent periods
  
  

• Low energy and brain fog
  
  

• Chronic inflammation and insulin resistance
  
  

• Bone and joint issues over time
  
  

• Mood swings, depression, or anxiety
  
  

• Difficulty conceiving
  
  

Many of these symptoms overlap with “high testosterone” issues, which is why PCOS can feel like a confusing storm of contradictions.

Why “Estrogen Dominance” Misses the Mark

When women are told they’re “estrogen dominant,” the real issue—low estradiol—gets ignored. This mislabeling leads to:

• Wrong treatment approaches: Some patients are placed on medications or supplements that lower estrogen, which can worsen the problem.
  
  

• Patient confusion: Women may think they need to “detox” estrogen when in reality, their body is crying out for more estradiol support.
  
  

• Missed opportunities for health: Estradiol plays a key role in protecting against diabetes, heart disease, and osteoporosis—risks that are already higher in PCOS.
  
  

How to Support Estradiol Balance in PCOS

1. Get the right labs: Request estradiol (E2), estrone (E1), testosterone, LH, and FSH—not just “estrogen” as a blanket test.
   
   

2. Address insulin resistance: High insulin fuels ovarian testosterone production. Lowering insulin levels helps restore balance.
   
   

3. Support ovulation: Regular ovulation boosts estradiol and progesterone naturally. Lifestyle changes, supplements, or medical therapies can help.
   
   

4. Reduce inflammation: Anti-inflammatory nutrition, exercise, and targeted therapies help fat tissue produce less estrone and improve hormone balance.
   
   

5. Work with a hormone-literate provider: Precision matters—find someone who sees beyond the myth of estrogen dominance.
   
   

Takeaways

• Women with PCOS produce too little estradiol (E2), not too much.
  
  

• Estrone (E1) often rises in fat tissue and drives inflammation, worsening symptoms.
  
  

• The LH-to-FSH imbalance prevents the ovary from making enough aromatase, leading to high testosterone and low estradiol.
  
  

• Correct terminology—estradiol insufficiency, estrone excess, androgen excess—is more accurate than “estrogen dominance.”
  
  

• Supporting ovulation, lowering insulin resistance, and reducing inflammation are key to restoring estradiol balance.
  
  

Final Word

The myth of estrogen dominance has caused confusion for far too long. The truth is that women with PCOS are often dealing with too little estradiol, too much testosterone, and excess estrone from fat tissue.

When you understand this, the path forward becomes clearer: supporting estradiol levels, improving ovulation, and tackling inflammation. Knowledge is power—and in PCOS, precision is everything.

References

• Azziz, R., Carmina, E., Chen, Z., Dunaif, A., Laven, J. S., Legro, R. S., ... & Yildiz, B. O. (2016). Polycystic ovary syndrome. Nature Reviews Disease Primers, 2(1), 1-18. https://doi.org/10.1038/nrdp.2016.57
  
  

• Legro, R. S. (2013). Obesity and PCOS: implications for diagnosis and treatment. Seminars in Reproductive Medicine, 31(6), 496–506. https://doi.org/10.1055/s-0033-1356480
  
  

• Pasquali, R., & Gambineri, A. (2018). Mechanisms of disease: obesity and PCOS. Nature Reviews Endocrinology, 14(6), 337–350. https://doi.org/10.1038/s41574-018-0007-8
  
  

• Rosenfield, R. L., & Ehrmann, D. A. (2016). The pathogenesis of polycystic ovary syndrome (PCOS): the hypothesis of PCOS as functional ovarian hyperandrogenism revisited. Endocrine Reviews, 37(5), 467–520. https://doi.org/10.1210/er.2015-1104