Menstrual irregularities, clinical and biochemical signs of hyperandrogenism, and polycystic appearing ovaries are all symptoms of PCOS, a diverse, multifactorial, complicated hereditary and endocrine condition.
The negative and widespread effects of PCOS on the body’s physiology and metabolism have led to its classification as a metabolic syndrome with detectable abnormalities such as insulin resistance, hyperinsulinemia, obesity, dyslipidemia [low HDL cholesterol and hypertriglyceridemia], all of which lead to serious long-term consequences such as an increased risk of type 2 diabetes mellitus, endometrial hyperplasia, and hypertension.
PCOS affects 5–10 per cent of women of reproductive age, with approximately 60 per cent of PCOS women reporting menstrual abnormalities and biochemical and clinical hyperandrogenism. There is evidence of familial aggregation of this condition, and there are ethnic and racial differences in the incidence of the illness and its symptoms.
PCOS was first identified as an endocrine ailment affecting premenopausal women, but its definition has now been broadened from a condition that begins at menarche and ends at menopause to one that can affect women from birth until senescence. Mumbai & Dubai based IVF expert and consultant. Following specific exclusion criteria like the Rotterdam ESHRE/ASRM guidelines for validating the diagnosis of PCOS. While the ultrasound morphological characteristics of PCOS ovaries may be typical, this finding is not specific, as it can occur in more than 20 per cent of healthy girls.
The clinical indications and symptoms of PCOS vary greatly among women with the condition, and they can also change over time within the same woman in the presence of specific triggering circumstances, the most significant of which is a change in body weight. A history of weight increase appears to typically precede the beginning of clinical signs of PCOS, particularly obese PCOS. In comparison to normal-weight women, women with severe hyperandrogenism had a much higher prevalence of anovulatory cycles, oligomenorrhea, and/or hirsutism.
Furthermore, the influence of PCOS on metabolism is evident in its widespread negative effects on the body’s physiology, as well as the long-term implications that arise. Obesity, aberrant gonadotropin dynamics, excessive androgen production, and insulin resistance are all significant hallmarks of multi-system dysfunctions, and environmental factors play a big role in them. Though the pathophysiology of these individual illnesses strongly link the multi-system dysfunctions in PCOS, they can be genetically characterised as endocrine dysfunction, reproductive dysfunction, metabolic dysfunction, and biochemical dysfunction.
The expert informs, “Although the exact cause of PCOS is unknown, a variety of neuroendocrine abnormalities have been identified as a key component of the condition. Recent research suggests that PCOS is characterised by abnormalities in GnRH/LH and ovarian androgen signalling, both feedforward and feedback.” Accelerated GnRH pulsatile activity, hypersecretion of LH, theca-stromal cell hyperactivity, and hypofunction of the FSH-granulosa cell axis are the main endocrine disorders of the reproductive axis.
An increase in GnRH pulse frequency during the follicular phase supports LH synthesis, whereas a reduction in GnRH pulse frequency during the luteal phase favours FSH production due to the progesterone impact. In PCOS, a steroid-permissive environment and decreased sensitivity of the GnRH pulse generator to feedback inhibition by ovarian steroids result in a persistently rapid GnRH pulse frequency and gonadotropin secretion perturbations, such as LH hypersecretion, a hallmark of the disorder and a cause of hyperandrogenism. This could also explain how PCOS develops during puberty.