I posted some studies recently on inhibiting the enzyme 11b-HSD1, which is responsible for the synthesis of cortisol. Currently, despite the denials of medicine that elevated cortisol has a causative role in diabetes and obesity, behind the scenes both Pfizer and Merck have experimental drugs for obesity/diabetes whose primary mechanism of action is inhibition of 11b-HSD1. One of these experimental drugs (AZD6925) is mentioned in the study below. This latest study shows that adipose tissue has elevated expression of 11b-HSD1, which contributes to reduced mitochondrial activity and lower levels of adiponectin. Inhibiting 11b-HSD1 and thus lowering cortisol restored mitochondrial respiration and adiponectin synthesis. Supplements that inhibit 11b-HSD1 include vitamin A, DHEA, emodin (cascara, aloe), zinc and bark extracts of Magnolia (Relora).
So there you have it, high stress and thus high cortisol directly prevent you from losing fat by inhibiting oxidative metabolism in fatty tissue. Not to mention cortisol also increases storage of dietary fat and upregulates de novo synthesis of fat from carbs.
http://www.ncbi.nlm.nih.gov/pubmed/25869616
"...In conclusion, increased 11β-HSD1 expression in hypertrophic adipocytes is associated with reduced mitochondrial respiration and adiponectin synthesis. Administration of an 11β-HSD1 inhibitor increases mitochondrial respiration and adiponectin synthesis. These findings support and extend our previous finding that mitochondrial function is necessary for adiponectin synthesis and that mitochondrial dysfunction in adipocytes might explain the reduced plasma."
So there you have it, high stress and thus high cortisol directly prevent you from losing fat by inhibiting oxidative metabolism in fatty tissue. Not to mention cortisol also increases storage of dietary fat and upregulates de novo synthesis of fat from carbs.
http://www.ncbi.nlm.nih.gov/pubmed/25869616
"...In conclusion, increased 11β-HSD1 expression in hypertrophic adipocytes is associated with reduced mitochondrial respiration and adiponectin synthesis. Administration of an 11β-HSD1 inhibitor increases mitochondrial respiration and adiponectin synthesis. These findings support and extend our previous finding that mitochondrial function is necessary for adiponectin synthesis and that mitochondrial dysfunction in adipocytes might explain the reduced plasma."