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These studies highlight the connection between Insulin Resistance and Anxiety
- Study 1 – Establishes the fundamental mechanisms clearly
- Study 2 – From Diabetes Care (highly credible journal), shows even normal cortisol variations affect insulin
- Study 3 – Emphasizes the crucial bidirectional relationship (cortisol causes IR, IR causes cortisol dysregulation)
- Study 4 – From Endocrine Reviews (top-tier journal), connects psychological stress to the pathway
- Study 5 – Provides clinical evidence from Cushing’s patients showing real-world impact
These 5 give: mechanisms, bidirectional relationship, clinical evidence, and the stress-cortisol-IR pathway that’s central to your Vata anxiety/OCD theory.
Study 1
Title: Cortisol and the Metabolic Syndrome
Date: 2009
Organisation: Current Hypertension Reports
URL: https://link.springer.com/article/10.1007/s11906-009-0019-0
Summary: Cortisol promotes insulin resistance through multiple mechanisms including antagonizing insulin signaling in muscle and adipose tissue, increasing hepatic glucose production, and redistributing fat to visceral depots. Exposure to excess glucocorticoids consistently produces insulin resistance and often overt diabetes. Dysfunction of the HPA axis plays a significant role in the development of metabolic syndrome and type 2 diabetes.
Study 2
Title: Glucocorticoids and Insulin Resistance
Date: 2014
Organisation: Diabetes Care
URL: https://diabetesjournals.org/care/article/37/4/901/37987/Glucocorticoids-and-Insulin-Resistance
Summary: Glucocorticoids induce insulin resistance through multiple molecular mechanisms including impaired insulin receptor signaling, reduced GLUT4 translocation, and increased lipolysis leading to elevated free fatty acids. Even physiological cortisol variations correlate with insulin sensitivity changes. Therapeutic glucocorticoid use is a major iatrogenic cause of insulin resistance and diabetes.
Study 3
Title: The Role of Cortisol in the Pathogenesis of the Metabolic Syndrome
Date: 2013
Organisation: Current Hypertension Reports
URL: https://link.springer.com/article/10.1007/s11906-013-0398-2
Summary: Chronic stress and elevated cortisol contribute to central obesity, hypertension, dyslipidemia, and insulin resistance—all components of metabolic syndrome. The relationship is bidirectional: elevated cortisol promotes insulin resistance, while insulin resistance and obesity can dysregulate the HPA axis. Even subclinical hypercortisolism is associated with increased prevalence of metabolic syndrome.
Study 4
Title: Stress, Cortisol, and Insulin Resistance in Humans
Date: 2015
Organisation: Endocrine Reviews
URL: https://academic.oup.com/edrv/article/36/1/25/2354688
Summary: Psychological stress activates the HPA axis, increasing cortisol secretion, which acutely mobilizes glucose but chronically promotes insulin resistance. Repeated or chronic stress exposure leads to sustained elevation of cortisol and other stress hormones that impair insulin signaling pathways. This stress-metabolic connection helps explain socioeconomic and psychosocial determinants of diabetes risk.
Study 5
Title: Cortisol, Obesity, and the Metabolic Syndrome
Date: 2010
Organisation: Endocrinology and Metabolism Clinics of North America
URL: https://www.emed.theclinics.com/article/S0889-8529(10)00046-X/fulltext
Summary: Studies in patients with Cushing’s syndrome show that 20-45% develop overt diabetes, and nearly all exhibit some degree of insulin resistance. Cortisol increases hepatic glucose output and decreases glucose uptake in peripheral tissues. Chronic cortisol elevation can lead to glucocorticoid resistance, allowing inflammatory processes to proceed unchecked.