Polycystic Ovary Syndrome (PCOS) is a very common endocrine disorder of young women.
The proper treatment of PCOS requires a thorough understanding of the underlying cause of disease. In this article, we review the extent to which hyperinsulinemia contributes to the development of PCOS.
The goal of this review was to assess the current literature on the contribution of hyperinsulinemia to the hyperandrogenism of polycystic ovary syndrome in hopes of promoting future research and advancements in clinical treatments for women with PCOS focusing on this major contributing factor, hyperinsulinemia.
A review of published peer-reviewed literature was conducted by searching the keywords.
Excessive insulin causes both the overproduction of testosterone and decreased sex hormone binding globulin (SHBG) levels seen in PCOS, both of which collaborate in creating an increased testosterone effect.
The majority of research and evidence shows that the hyperandrogenism of PCOS is likely caused by hyperinsulinemia. Yet the conventional treatment of hyperandrogenic symptoms in women with PCOS is not directed towards correcting this underlying hyperinsulinemia. Further research is needed to assess how the treatment of the hyperinsulinemia through lifestyle would compare to the current treatment of hyperandrogenemia through testosterone-lowering drugs.
Polycystic Ovary Syndrome (PCOS) has now evolved into the most common endocrine disorder of young women, involving multiple organ systems. Newer estimates of the prevalence suggest it affects 15% – 20% of women, making it the most common endocrine disorder of young women by far.
The goal of this review was to assess the current literature on the contribution of hyperinsulinemia to the hyperandrogenism of polycystic ovary syndrome in hopes of promoting future research and advancements in clinical treatments for women with PCOS focusing on this major contributing factor, hyperinsulinemia.
A review of published peer-reviewed literature was conducted by searching the keywords: PCOS, polycystic ovary syndrome, polycystic ovarian syndrome, hyperandrogenemia and hyperinsulinemia. Additional articles were suggested by the authors and clinicians involved in this review. Studies were first selected based on title and abstract. A full text assessment was then utilised to ensure relevance. Studies were included if the title and abstract focused on the contribution of hyperinsulinemia to hyperandrogenemia.
This article followed all ethical standards for research without direct contact with human or animal subjects.
Excessive androgen production, specifically testosterone, has been extensively linked to many symptoms of PCOS.
Testosterone is produced in both the ovaries and the adrenal glands in roughly equal proportions.
By 1989, studies firmly pointed towards the ovary as the key source of excessive testosterone production in women with PCOS. Specifically, it is the theca cells within the ovary that are responsible for the overproduction of hormones.
This suspicion is further strengthened by Drs Stein and Leventhal’s research, who performed ovarian wedge resection surgery on patients with PCOS, which often restored normal ovulation and normal menstrual cycles.
Direct measurement of blood testosterone levels is not part of the diagnostic criteria for hyperandrogenemia
Testosterone in high levels starts to exert its masculinising effects on the neighbouring organs because of the lack of SHBG,
Insulin and testosterone blood levels have showed a strong 85% correlation, highly suggestive that one hormone is directly stimulating the other.
In vivo studies have confirmed that high insulin does indeed increase androgen levels. Direct insulin infusion measurably increases androgen production by binding to insulin or insulin-like growth factor-1 receptors in the ovary.
Insulin plays another role as the major regulator of SHBG production in the liver; hyperinsulinemia has been linked to hyperandrogenemia and lack of SHBG.
Particularly with diabetics, type 1 diabetics, with very low insulin levels, have very high SHBG, and type 2 diabetics, with very high insulin levels, have very low SHBG.
Insulin directly inhibits liver production of SHBG, and therefore increases the levels of free and bioavailable androgens.
Thus, excessive insulin causes both the overproduction of testosterone and decreased SHBG levels, both of which collaborate in creating an increased testosterone effect.
The majority of research and evidence shows that the hyperandrogenism of PCOS is likely caused by hyperinsulinemia. Yet the conventional treatment of hyperandrogenic symptoms in women with PCOS is not directed towards correcting this underlying hyperinsulinemia. Rather, conventional treatments focus on lowering testosterone levels, with moderate success. This is symptomatic treatment only, and therefore would not be expected to be very successful. Instead, decreasing insulin levels through weight loss, diet and lifestyle might have greater success in overall signs and symptoms of PCOS as well as preventing associated conditions such as type 2 Diabetes, Obesity and Cardiovascular Disease.
Further research is needed to assess how the treatment of the hyperinsulinemia through lifestyle would compare to the current treatment of hyperandrogenemia through testosterone-lowering drugs. More research is also warranted to gain a better understanding of evidenced-based guidelines for treatment of PCOS, especially when considering specific dietary recommendations.
The authors have declared that no competing interest exists.
N.B.P. was responsible for conceptualisation, methodology and writing. N.B.P. and A.J. were responsible for investigation. Both authors reviewed the final manuscript.
This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Data sharing is not applicable to this article as no new data were created or analysed in this study.
The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of any affiliated agency of the authors.