Polycystic ovary syndrome and its multidimensional impacts on women's mental health: A narrative review.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects approximately 8% to 13% of women of reproductive age worldwide. It is characterized by a range of symptoms, including hirsutism, acne, and menstrual irregularities, and poses a significant psychological burden, including anxiety and depression. The evolving definition of PCOS, from the 1990 NIH conference to the 2003 Rotterdam conference, highlights its multifaceted nature, encompassing metabolic, reproductive, and psychological aspects. This overview aims to elucidate the complex interplay between PCOS's physiological and psychological dimensions. It focuses on understanding the heightened risk of psychiatric disorders, including depression and anxiety, among women with PCOS and explores the contributing factors, such as obesity, body image issues, and stress. The etiology of PCOS involves a complex mixture of genetic, hormonal, and lifestyle factors that contribute to its pathophysiology and the associated mental health challenges. Stress, in various forms, including metabolic, inflammatory, oxidative, and emotional, is identified as a significant contributor to the pathogenesis of PCOS. Management strategies highlighted include lifestyle modifications, dietary and exercise interventions, and psychological therapies, underscoring the need for comprehensive and integrated care approaches that address the broad spectrum of PCOS effects. A multifaceted treatment approach that goes beyond just the physical symptoms of PCOS to also include its significant psychological effects is emphasized, reinforcing the necessity for a comprehensive, integrated care strategy to manage this complex condition effectively.

Diabetic neuropathy: Pathogenesis and evolving principles of management.

The global rise of prediabetes and diabetes has spawned an epidemic of complications associated with these conditions. Neuropathy is the most common consequence, with distal symmetric polyneuropathy (DSP) being the most prevalent. Diabetic neuropathy (DN) is a debilitating consequence of diabetes mellitus resulting in the highest morbidity and death, besides imposing a substantial financial burden on the patient. Loss of sensory function commencing distally in the lower limbs, accompanied by discomfort and considerable morbidity, characterizes diabetic neuropathy. The clinical evaluation and therapeutic options for diabetic peripheral neuropathy are multifaceted. At least fifty percent of people with diabetes acquire diabetic neuropathy over time. Good glycemic control halts the evolution in individuals with Type 1 diabetes mellitus. These results have prompted fresh attempts to comprehend the origin and develop new guidelines for prevention and treatment. New recommendations have also been established for the treatment of painful DN using separate classes of medications, with an emphasis on avoiding the use of opioids. Although our comprehension of the intricacies of diabetic neuropathy has progressed significantly over the past decade, the unique processes driving the neuropathy in type 1 and type 2 diabetes remain unexplained. Currently, glycemic control and pain management are the only effective therapies. While glucose management significantly reduces neuropathy development in type 1 diabetics, the effect is considerably lower in type 2 diabetics. Evidence supports the use of anticonvulsants and antidepressants for diabetic peripheral neuropathy pain treatment. However, the absence of disease-modifying medications for diabetic DSP necessitates the identification of unrecognized modifiable risk factors. It is imperative to identify the 'missed' risk factors and targets, allowing comprehensive, individualized care for patients.