The coronary risk for women with android obesity
who are taking sex steroids was recently reviewed in the journal Climacteric Reviewers in Denmark sought “to summarize recent findings providing mechanistic insight into why the relative presence of central to peripheral fat mass is a critical determinant of atherogenesis and why postmenopausal women with android obesity represent a risk population with increased susceptibility to the cardiovascular harm of estrogen plus progestin therapy (EPT).” L.B. Tanko and C. Christiansen from the Center for Clinical & Basic Research conducted a review of their own research “and related literature in PubMed.”

“In postmenopausal women, android obesity characterized by excessive upper-body combined with relatively poorly developed lower-body fat mass is frequently associated with insulin resistance, low-grade inflammation, and early atherosclerosis. Underlying mechanisms involve disequilibrium between proinflammatory cytokines (high interleukin-6/C-reactive protein) and the anti-inflammatory adipokine (low adiponectin),” the researchers reported.

“Recent findings point out that women with abnormal glucose tolerance, a metabolic alteration closely linked to android adiposity, respond with increases in low-grade inflammation and accelerated atherogenesis to EPT that collectively may promote acute complications,” they stated. “We recently pointed out that a progestin could exert a dose-dependent inhibitory effect on circulating adiponectin.”

“Thus, when EPT is prescribed to women with android obesity, further decreases in the protective adiponectin pool may become critical and act as a promoter of thromboembolic complications via its effects on plaque formation and stability,” they advised. “Since android obesity is associated with the highest levels of free estradiol, women with this phenotype might not be trivial candidates for EPT.”

The authors concluded, “The herein summarized findings shed light on important interactions between sex steroids and body fat mass, with functional implications for cardiovascular risk. Since previous trials have not optimized the dose of the progestin for its effect on circulating adiponectin, utmost caution should be exercised in the prescription of available estrogen plus progestin therapies to women with android obesity and/or symptoms of the insulin resistance syndrome.”

Tanko and Christiansen published their report in Climacteric (Adipose tissue, insulin resistance and low-grade inflammation: Implications for atherogenesis and the cardiovascular harm of estrogen plus progestogen therapy. Climacteric, 2006;9(3):169-180).

For additional information, contact L.B. Tanko, Center for Clinical and Basic Research, Ballerup byvej 222, 2750 Ballerup, Denmark.

Publisher contact information for the journal Climacteric is: Taylor & Francis Ltd., 4 Park Square, Milton Park, Abingdon OX14 4RN, England.