Polycystic ovary syndrome (PCOS) is not a recent disorder, but it seems to be very old. Going back to the early history, Hippocrates and Soranus of Ephesus reported that “many women with masculine and robust aspect don’t menstruate and they don’t become pregnant” [1, 2].

Some authors suggest that the origin of PCOS began in Paleolithic communities, in which environmental stressful factors favored the survival of the “thrifty genotype”: it was represented by males and females with the greatest capacity for energy storage necessary to face fasting periods [3, 4].

Moreover, subfertility among nomadic hunters gave some benefits: women could care only for one child, and a lower parity may have reduced the death rates of these women and the risk of progeny abandonment, as delivery-related complications were a major cause of mortality in reproductive-age women.

On the other hand, during the Neolithic revolution, when communities started to be sedentary, PCOS genotype may have survived because of its robustness, with some gene variants over the years, as well shown by the heterogeneity of PCOS phenotypes and genotypes.

Moreover, since the eighteenth century it was noticed that signs of hyperandrogenism were associated with metabolic abnormalities, such as increased visceral fat [5].

Jean Vague, physician and professor at University of Marseille, introduced the term “android obesity” to define the abdominal fat accumulation, which is the typical male pattern of body fat distribution, associated with increased diabetes and cardiovascular risk [6]. Later, it was realized that lots of hyperandrogenic women were obese with increased visceral fat; they had increased insulin response during OGTT (oral glucose tolerance test), and they presented with acanthosis nigricans [7, 8]: all of these are signs of insulin resistance, and these observations were the starting point for the study of the association between insulin resistance and PCOS.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine and metabolic disorder, characterized by chronic anovulation/oligomenorrhea, hyperandrogenism, and insulin resistance.

In accordance with the most used guidelines drawn in Rotterdam in 2003 by ESHRE/ASRM (European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine) [9], PCOS diagnosis can be raised only after the exclusion of other known causes of hyperandrogenism and amenorrhea (hyperprolactinemia, non-classic congenital adrenal 21-hydroxylase deficiency, thyroid dysfunction, androgen-secreting neoplasm, Cushing’s syndrome) and when there are at least two of the three following parameters:

The previous criteria processed by NIH (National Institute of Health) in 1992 included both:

Τhe most recent (2006) AES (Androgen Excess Society) criteria [10] includes all of the following conditions:

Approximately 85–90 % of women with oligomenorrhea have PCOS, while 30–40 % of women with amenorrhea suffer from PCOS [11].

More than 80 % of women showing symptoms of androgen excess have PCOS [12]. Roughly 90–95 % of anovulatory women presenting to infertility clinics have PCOS. The syndrome is present in approximately 5–10 % of reproductive-age women, and it is considered the most frequent endocrine abnormality in females.

As there are significant variations in the clinical appearance of PCOS, its prevalence may be different among populations.

It is 4.8 and 8 % in white and black women in southeastern United States [13], 6.8 % in white women in Greece [14], 6.5 % in white women in Spain [15], 6.3 % in South Asian in Sri Lanka [16], and 5 % in Thai women [17].

Some groups have showed that the frequency of PCOS varies depending on the diagnostic criteria used: for example, the prevalence estimations using the Rotterdam criteria are two to three times greater than those achieved using NIH criteria [18–21].