From the Guidelines
In PCOS, excess fatty tissue contributes to increased unopposed estrogen through several mechanisms, including the conversion of androgens to estrogens by aromatase in adipose tissue and decreased production of sex hormone-binding globulin (SHBG), leading to higher estrogen levels and increased risk of endometrial hyperplasia and cancer. The relationship between fatty tissue and unopposed estrogen in PCOS is complex and multifaceted. Adipose tissue contains the enzyme aromatase, which converts androgens like testosterone into estrogens like estradiol 1. As fat mass increases in PCOS patients, this conversion becomes more pronounced, leading to higher estrogen levels. Furthermore, fat cells produce less SHBG, the protein that normally binds and inactivates estrogen in the bloodstream, resulting in more free estrogen circulating and exerting its effects 1. This unopposed estrogen, without adequate progesterone to balance it due to anovulation common in PCOS, stimulates continuous endometrial growth without the normal shedding that occurs during menstruation. The result is irregular menstrual cycles, endometrial hyperplasia, and increased risk of endometrial cancer. Weight loss of even 5-10% can help reduce this excess estrogen production by decreasing the amount of aromatase-containing adipose tissue and improving ovulation, which restores the normal estrogen-progesterone balance 1. Key factors to consider in managing PCOS include lifestyle modifications, such as diet and exercise, which can help achieve and maintain a healthy weight, improving metabolic, reproductive, and psychological health outcomes 1. Overall, the management of PCOS requires a comprehensive approach that addresses the complex interplay between hormonal, metabolic, and lifestyle factors, with a focus on reducing excess fatty tissue and promoting a healthy balance of estrogen and progesterone.
From the Research
Fatty Tissue and Unopposed Estrogen in PCOS
- Fatty tissue, particularly visceral adiposity, is a common feature in women with polycystic ovary syndrome (PCOS) 2
- The relationship between fatty tissue and increased unopposed estrogen in PCOS is complex and multifaceted
- Insulin resistance, which is often associated with excess fatty tissue, can contribute to increased androgen production and unopposed estrogen 3, 4
- Metformin, a medication commonly used to treat insulin resistance, may help improve insulin sensitivity and reduce androgen levels, potentially decreasing unopposed estrogen 3, 5
- Lifestyle modifications, such as diet and exercise, can also improve insulin resistance and reduce fatty tissue, which may help decrease unopposed estrogen 2
Mechanisms of Fatty Tissue and Unopposed Estrogen
- Excess fatty tissue can lead to chronic low-grade inflammation and oxidative stress, which can contribute to insulin resistance and increased androgen production 2
- Insulin resistance can also lead to increased glucose availability, which can stimulate androgen production and contribute to unopposed estrogen 6
- The endometrium in women with PCOS may be more sensitive to the effects of unopposed estrogen, which can increase the risk of endometrial hyperplasia and cancer 5
Treatment Options
- Metformin may be beneficial in reducing unopposed estrogen and improving insulin sensitivity in women with PCOS 3, 5
- Lifestyle modifications, such as diet and exercise, can also improve insulin resistance and reduce fatty tissue, which may help decrease unopposed estrogen 2
- Combination therapy with metformin and spironolactone may be more effective than monotherapy in reducing insulin resistance and androgen levels 4