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  • Author: Irene Lambrinoudaki x
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Irene Lambrinoudaki, George Kaparos, Dimitra Papadimitriou, Theodoros N Sergentanis, Maria Creatsa, Andreas Alexandrou, Emmanuel Logothetis, George Christodoulakos and E Kouskouni

Objective

To assess the association of genetic polymorphisms related to cardiovascular disease (CVD) risk with anthropometric parameters and indices of androgenicity in healthy postmenopausal women.

Design

Cross-sectional study in a University Menopause Clinic.

Methods

The following polymorphisms were assessed in 84 healthy postmenopausal women: glycoprotein IIIa Leu33Pro, apolipoprotein E2/E3/E4, methylenetetrahydrofolate reductase (MTHFR) Ala222Val, apolipoprotein B Arg3500Gln, paraoxonase 1 Gln192Arg, plasminogen activator inhibitor 1 4G/5G, cholesterol-7 α-hydroxylase A-204C, and cholesterol ester transfer protein (TaqIB) B1/B2. Hormonal assays included FSH, LH, 17-β-estradiol, testosterone, sex hormone-binding globulin (SHBG), DHEA sulfate, Δ-4-androstenedione (Δ4A), free androgen index (FAI), free estrogen index (FEI), and homocysteine (Hcy). The anthropometric components were body mass index (BMI) and waist-to-hip ratio (WHR).

Results

MTHFR Ala222Val polymorphism was positively associated with testosterone, FAI, and FEI (P=0.001, P=0.0004, and P=0.014 respectively) and negatively with SHBG (P=0.047). Furthermore, women bearing this polymorphism had higher BMI and WHR compared with women with the wild-type variant (P=0.027 and P=0.044 respectively).

Conclusions

MTHFR Ala222Val polymorphism is associated with increased androgenicity and elevated BMI and WHR in healthy postmenopausal women. The significance of this association with respect to the CVD risk of postmenopausal women remains to be elucidated in future studies.

Free access

Irene Lambrinoudaki, George Christodoulakos, Demetrios Rizos, Emmanuel Economou, John Argeitis, Sofia Vlachou, Maria Creatsa, Evangelia Kouskouni and Dimitrios Botsis

Objective: To assess the association between endogenous sex hormones and risk factors for atherosclerosis in healthy postmenopausal women.

Design: Cross-sectional study in a university menopause clinic.

Methods: Serum sex hormones and lipid–lipoprotein profile, arterial pressure, homocysteine and insulin resistance, measured by the homeostasis model assessment of insulin resistance (HOMA-IR), were assessed in 598 healthy postmenopausal women not on hormone therapy.

Results: Compared with women in the lowest testosterone quartile (Q), women in the highest testosterone quartile had higher total cholesterol (Q1: 225.2 ± 41.3 vs Q4: 246.2 ± 38.4 mg/dl, P < 0.01), low-density lipoprotein (LDL)-cholesterol (Q1: 146.9 ± 37.2 vs Q4: 171.8 ± 35.3 mg/dl, P < 0.001), atherogenic index of plasma (AIP) (Q1: −0.224 ± 0.238 vs Q4: −0.087 ± 0.254, P < 0.01), apolipoprotein B (ApoB) (Q1: 100.7 ± 23.1 vs Q4: 113.9 ± 23.8 mg/dl, P < 0.001) and higher high-density lipoprotein (HDL)-cholesterol (Q1: 60.7 ± 14.5 vs Q4: 52.9 ± 13.0 mg/dl, P < 0.01). Accordingly, women in the highest free androgen index (FAI) quartile had higher AIP (Q1: −0.232 ± 0.254 vs Q4: −0.078 ± 0.243, P < 0.001) and ApoB (Q1: 102.4 ± 25.5 vs Q4: 114.2 ± 25.8 mg/dl, P < 0.01) and lower HDL-cholesterol (Q1: 62.0 ± 15.7 vs Q4: 51.9 ± 11.6 mg/dl, P < 0.001) and apolipoprotein A (Q1: 159.6 ± 25.6 vs Q4: 147.9 ± 24.1 mg/dl, P < 0.01) compared with women in the lowest FAI quartile. These differences remained significant after adjustment for age, body mass index (BMI), insulin resistance and social habits. The free estrogen index (FEI) exhibited similar associations to the FAI. HOMA-IR showed an independent positive association with total testosterone (Q1: 2.00 ± 1.36 vs Q4: 2.66 ± 1.60, P < 0.01), FAI (Q1: 1.70 ± 1.12 vs Q4: 3.04 ± 1.66, P < 0.001) and FEI (Q1: 1.70 ± 0.91 vs Q4: 3.08 ± 1.77, P < 0.001).

Conclusions: Increased androgenicity in healthy postmenopausal women is associated with an unfavorable cardiovascular risk profile. High endogenous estradiol is related to a pro-atherogenic lipid profile, an association which may, in part, be mediated by insulin resistance.

Free access

Irene Lambrinoudaki, Eleni Armeni, Demetrios Rizos, Georgios Georgiopoulos, Foteini Athanasouli, Nikolaos Triantafyllou, Konstantinos Panoulis, Areti Augoulea, Maria Creatsa, Andreas Alexandrou, Maria Alevizaki and Kimon Stamatelopoulos

Objective

We aimed to evaluate the association between thyroid hormones and indices of obesity in a sample of euthyroid postmenopausal women.

Design

Cross-sectional study.

Methods

Serum levels of TSH, free triiodothyronine (FT3), and free thyroxine (FT4) as well as BMI and waist:hip ratio (WHR) were evaluated in 194 healthy euthyroid postmenopausal women. Ultrasonography was used to assess abdominal fat layers (subcutaneous fat (SF), preperitoneal fat (PF), and SF:PF ratio). Indices of adiposity were defined as high vs low depending on the median value of the assessed parameters.

Results

After multivariate adjustment for traditional risk factors, lower FT4 levels and a higher FT3:FT4 ratio predicted higher SF mass (FT4, Exp(β)=0.035, P=0.020 and FT3:FT4, Exp(β)=2.374, P=0.018), whereas higher FT3 predicted higher PF mass (Exp(β)=2.815, P=0.032). Women with FT3:FT4 above the highest quartile had a significantly higher SF mass as compared to women in the lowest quartile (1.81±0.62 cm vs 1.54±0.46 cm, P=0.027). BMI had a positive independent association with TSH (Exp(β)=1.829, P=0.018). Finally, FT3 was significantly associated with SF mass among women with higher BMI (FT3, β=0.259, P=0.040) and women with higher WHR (β=0.309, P=0.020) but not among women with lower BMI or WHR values.

Conclusion

Thyroid hormone levels, and in particular FT3, were independently associated with SF and PF in euthyroid postmenopausal women, and this association was mainly evident in women with higher BMIs. On the other hand, among traditional indices of adiposity, only TSH was positively associated with BMI. Larger prospective studies are needed to evaluate the significance of the present findings.

Restricted access

Panagiotis Anagnostis, Konstantinos Christou, Aikaterini-Maria Artzouchaltzi, Nifon K Gkekas, Nikoletta Kosmidou, Pavlos Siolos, Stavroula A Paschou, Michael Potoupnis, Eustathios Kenanidis, Eleftherios Tsiridis, Irene Lambrinoudaki, John C Stevenson and Dimitrios G Goulis

Objective/Design

Menopausal transition has been associated with a derangement of glucose metabolism. However, it is not known if early menopause (EM, defined as age at menopause <45 years) or premature ovarian insufficiency (POI, defined as age at menopause <40 years) are associated with increased risk of type 2 diabetes mellitus (T2DM). To systematically investigate and meta-analyze the best evidence regarding the association of age at menopause with the risk of T2DM.

Methods

A comprehensive search was conducted in PubMed, CENTRAL and Scopus, up to January 31, 2018. Data are expressed as odds ratio (OR) with 95% confidence intervals (CI). The I 2 index was employed for heterogeneity.

Results

Thirteen studies were included in the qualitative and quantitative analysis (191 762 postmenopausal women, 21 664 cases with T2DM). Both women with EM and POI were at higher risk of T2DM compared with those of age at menopause of 45–55 years (OR: 1.15, 95% CI: 1.04–1.26, P = 0.003; I 2: 61%, P < 0.002 and OR: 1.50, 95% CI: 1.03–2.19, P = 0.033; I 2: 75.2%, P < 0.003), respectively). Similar associations emerged when women with EM and POI were compared with those of age at menopause >45 years (OR: 1.12, 95% CI: 1.01–1.20, P < 0.02; I 2: 78%, P < 0.001 and OR: 1.53, 95% CI: 1.03–2.27, P = 0.035; I 2: 78%, P < 0.001), respectively).

Conclusions

Both EM and POI are associated with increased risk of T2DM.

Free access

Evanthia Diamanti-Kandarakis, Maurizio Dattilo, Djuro Macut, Leonidas Duntas, Efstathios S Gonos, Dimitrios G Goulis, Christina Kanaka Gantenbein, Marianna Kapetanou, Eftychia Koukkou, Irene Lambrinoudaki, Marina Michalaki, Shahla Eftekhari-Nader, Renato Pasquali, Melpomeni Peppa, Marinella Tzanela, Evangeline Vassilatou, Andromachi Vryonidou and COMBO ENDO TEAM: 2016

Aging and its underlying pathophysiological background has always attracted the attention of the scientific society. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Endocrine function undergoes major changes during aging, as well. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. As hypothalamic–pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity.