Submitted on July 12, 2006
Accepted on August 30, 2006
Association of Hormonal Dysregulation with Metabolic Syndrome in Older
Women (Data from the InCHIANTI Study)
Marcello Maggio1*, Fulvio Lauretani2, Gian Paolo Ceda3, Stefania Bandinelli4, Shehzad Basaria5, Giuseppe Paolisso6, Alessandro Ble1, Josephine M Egan1, E jeffrey Metter1, Angela M Abbatecola6, Giovanni Zuliani7, Carmelinda Ruggiero1, Giorgio Valenti3, Jack, M Guralnik8, and Luigi Ferrucci1
1 Clinical Research Branch, National Institute on Aging, Baltimore, Maryland, United States
2 Tuscany Regional Health Agency, Florence, Italy
3 Internal Medicine and Biomedical Sciences, School of Endocrinology, Section of Geriatrics, University of Parma, Parma, Italy
4 Geriatric Rehabilitation Unit, Azienda Sanitaria di Firenze (ASF), Florence , Italy
5 Department of medicine, Division of Endocrinology, Johns Hopkins University, School of Medicine, Bayview Medical Center, Baltimore, Maryland, United States
6 Department of Geriatric Medicine and Metabolic Disease II, University of Naples, Naples, Italy
7 7 Department of Clinical and Experimental Medicine, Section of Internal Medicine,, University of Ferrara, Ferrara, Italy
8 Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Bethesda, Maryland, United States
* To whom correspondence should be addressed. E-mail: maggiom{at}grc.nia.nih.gov.
The metabolic syndrome (MetS) is a strong risk factor for type 2 diabetes and cardiovascular disease. Hyperandrogenism is often associated with features of MetS in young women. Since the prevalence of MetS increases with age, it is reasonable to hypothesize that age-related changes in androgens and other hormones might contribute to the development of MetS in older women.
We hypothesized that high levels of testosterone, dehydroepiandrosterone sulphate (DHEAS), cortisol, and low levels of sex hormone binding globulin (SHBG) and insulin like growth factor-1 (IGF-1), would be associated with MetS in a representative cohort of older Italian women, independent of confounders (including inflammatory markers).
After excluding participants on hormone replacement therapy and with history of bilateral oophorectomy, 512 women aged 65 years or older had data on testosterone, cortisol, DHEAS, SHBG, fasting insulin, total and free IGF-1, IL-6 and C-reactive protein. MetS was defined according to ATP-III criteria. Insulin resistance was calculated according to the homeostasis model assessment (HOMA).
MetS was found in 145 women (28.3 %). Participants with MetS had higher age-adjusted levels of bioavailable testosterone (p<0.001), IL-6 (p<0.001), C-reactive protein (p<0.001), HOMA (p<0.001), and lower levels of SHBG (p<0.001). After adjusting for potential confounders, participants with decreased SHBG had an increased risk of MetS (p<0.0001). In a further model including all hormones and confounders, log (SHBG) was the only independent factor associated with MetS (OR: 0.44, 95 % CI 0.21-0.91; p=0.027).
In older women, SHBG is negatively associated with MetS independent of confounders, including inflammatory markers and insulin resistance.
