The incidence of metabolic syndrome increases substantially during perimenopause and early menopause. Postmenopausal women are at a higher risk of hypertension, proatherogenic lipid changes, diabetes, and severe cardiovascular disease as compared with their premenopausal counterparts. Whether or not menopause has a causative contribution to the deteriorating metabolic profile that is independent of chronological aging has been a subject of many studies. Menopausal transition is associated with significant weight gain (2 to 2.5 kg over 3 years on average), which is not dissimilar to that in premenopausal women of like age. Concomitantly, there is an increase in abdominal adiposity and a decrease in energy expenditure, phenomena that have been postulated to explain the higher risk of metabolic syndrome and increases in cholesterol and triglycerides. Hypertension and diabetes become more prevalent with age and should be timely diagnosed and treated. Lifestyle changes including moderately decreased caloric intake and aerobic exercise could prevent proatherogenic changes and weight gain observed with aging. Accurate prediction of cardiovascular risk in midlife women is essential to help identify the subset of women who are likely to benefit from intensive management of metabolic risk factors. This review focuses on metabolic changes associated with menopausal transition, specifically alterations in weight, waist circumference, body fat distribution, energy expenditure, and circulating biomarkers including adipokines.
Context:Female obesity is linked to abnormal menstrual cycles, infertility, reproductive wastage, and deficient LH, FSH, and progesterone secretion. Objective and Design:To elucidate the reproductive defects associated with obesity, we sampled 18 eumenorrheic (nonpolycystic ovary syndrome) women with a mean Ϯ SEM body mass index of 48.6 Ϯ 1.4 kg/m 2 with daily, first morning voided urine collections, seven of whom also had early follicular phase 12-h, every 10-min blood sampling to assess LH pulses. Daily hormones were compared with 11 eumenorrheic, normal-weight controls. A separate control group of 12 eumenorrheic, normal-weight women was used for the LH pulse studies. Main Outcome Measures:Assays for LH (serum and urine) and FSH, and estradiol and progesterone metabolites (estrone conjugate and pregnanediol glucuronide; urine) were performed. Daily hormones were meaned and normalized to a 28-d cycle length. LH pulsations were determined using two objective methods. Group means were compared using t tests. Results:Reduced whole-cycle mean, normalized pregnanediol glucuronide was observed in obese (38.2 Ϯ 2.1 g/mg creatine) compared with normal-weight women (181.3 Ϯ 35.1 g/mg creatine; P ϭ 0.002), without significant differences in LH, FSH, or estrone conjugate. Early follicular phase LH pulse frequency did not differ from normalweight women, but both amplitude and mean LH were dramatically reduced in obese women (0.8 Ϯ 0.1 and 2.0 Ϯ 0.3 IU/liter) compared with controls (1.6 Ϯ 0.2 and 3.4 Ϯ 0.2 IU/liter; P Ͻ 0.01). 10 -15% induces reversible deficits in reproductive function that have been well characterized (1). The effects of increased body weight on the reproductive axis are not as well understood, but the association of obesity with lower gonadotropins and reduced levels of sex steroids has been established (2, 3). One large, recent epidemiological study of 848 women used daily urinary sampling over the course of a menstrual cycle and observed longer follicular phases, lower LH and FSH, lower estradiol metabolites, and lower progesterone metabolites by 33% in overweight/obese [body mass index (BMI) of Ͼ25 kg/m 2 ] compared with normalweight women (4). Conclusions:We hypothesized that the reduced reproductive hormones in ovulatory, regularly cycling obese women are attributable to a deficient central neural reproductive drive. We studied morbidly obese (baseline BMI of Ͼ35 kg/m 2 ) women scheduled to undergo bariatric surgery before weight loss and compared menstrual cycle urinary hormone excretion and serum LH secretory patterns using frequent blood sampling to infer the characteristics of GnRH secretion. In this study, we compared our findings in the high-BMI women with normal-weight historical controls. Patients and Methods ParticipantsNineteen participants were recruited through a weight-loss surgery support group at the Montefiore Medical Center and Beth Israel Medical Center (New York, NY). Participants were aged 35-50 yr at enrollment and had to meet the following criteria: 1) BMI of at least 35 kg/m ...
Objective To determine whether obesity related reproductive endocrine abnormalities in ovulatory women are reversible with weight loss Design Observational cohort study. Setting Healthy volunteers in an academic research environment. Patients Women age 18–48 with regular menstrual cycles 21–40 days with a BMI ≥ 35 kg/m2 planning to undergo bariatric surgery were recruited. Intervention 25 eumenorrheic (non-PCOS) women with a mean BMI of 47.3 +/− 5.2 kg/m2 were sampled with daily menstrual cycle urinary hormones prior to (n=25) and 6 months after (n=9) weight loss surgery resulting in >25% reduction initial body weight. Daily hormones were compared pre- and post-operatively, and to 14 normal weight controls. Main Outcome Measures LH, FSH, estradiol and progesterone metabolites measured daily for one menstrual cycle. Group means were compared using t-tests among ovulatory cycles. Results Luteal Pdg increased from 32.8 ± 10.9 to 73.7 ± 30.5 ug/mgCr (p<0.001) and whole cycle LH increased from 168.8 ± 24.2 to 292.1 ± 79.6 mIU/mgCr (p<0.001) after surgically induced weight loss. Luteal Pdg remained lower than normal weight controls (151.7 ± 111.1 ug/mgCr). Obese women took longer to attain a postovulatory Pdg rise >2mcg/mg creatinine than controls (3.91 ± 1.51 versus 1.71 ± 1.59 days); this improved post-operatively (2.4 ± 1.82 days, p=0.046). Whole cycle E1c was similar to controls at baseline, but decreased after weight loss (from 1026.7 ± 194.2 to 605.4 ± 167.1 ng/mgCr, p<0.001). FSH did not relate to body size in this sample. Conclusions Women of very high BMI have deficient luteal LH and Pdg excretion and a delayed ovulatory Pdg rise compared to normal weight women. Although all of these parameters improved with weight loss, Pdg did not approach levels seen in normal weight women. LH may be less effective in stimulating the corpus luteum in obesity. The large postoperative decrease in E1c may reflect the loss of estrone-producing adipose tissue after weight loss.
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