Changes in Cardiovascular Risk Factors During the Peri- and Postmenopausal Years

Matthews, Karen A.; Kuller, Lewis H.; Sutton-Tyrrell, Kim

doi:10.1007/978-0-387-21628-7_14

Cited by 5 publications

(4 citation statements)

References 35 publications

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“…The analyses showed no evidence of FMP on blood pressure, insulin, glucose, Lp(a), and hemostatic and inflammatory factors. These null menopause results are consistent with other SWAN analyses of relationship between reproductive hormones and changes in risk factors, and with earlier reports of changes in menopause based on bleeding patterns (6–10, 24). Taking these findings together, it is unlikely that the acceleration of CHD risk in the postmenopausal years is due to menopause-induced increases in these factors.…”

Section: Discussionsupporting

confidence: 91%

“…Epidemiological studies suggest that the menopause is associated with increases in total cholesterol and low density lipoprotein cholesterol (LDL-C), while increases in blood pressure and weight during midlife are more linear and appear to reflect chronological aging (6–11). However, almost all studies were based on Caucasian samples and did not measure risk factors simultaneously with changes in menopausal status.…”

Section: Introductionmentioning

confidence: 99%

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Are Changes in Cardiovascular Disease Risk Factors in Midlife Women Due to Chronological Aging or to the Menopausal Transition?

Matthews

Crawford

Chae

et al. 2009

Journal of the American College of Cardiology

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547

399

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OBJECTIVES This prospective study examined if changes in traditional and novel coronary heart disease (CHD) risk factors are greater within a year of the final menstrual period (FMP), relative to changes that occur before or after that interval, in a multi-ethnic cohort. BACKGROUND Understanding the influence of the menopause on CHD risk remains elusive and has been evaluated primarily in Caucasian samples. METHODS The Study of Women’s Health across the Nation (SWAN) is a prospective study of the menopausal transition in 3302 minority (African American, Hispanic, Japanese, or Chinese) and Caucasian women. After 10 annual exams, 1054 women had achieved a FMP not due to surgery and without HT use prior to FMP. Measured CHD risk factors included lipids and lipoproteins, glucose, insulin, blood pressure, fibrinogen, and C-reactive protein. We compared which of two models provided a better fit to the observed risk factor changes over time in relation to FMP: a linear model, consistent with chronological aging, or a piece-wise linear model, consistent with ovarian aging. RESULTS Only total cholesterol, LDL-C, and apolipoprotein-B demonstrated substantial increases within the 1 year interval before and after FMP, consistent with menopause-induced changes. This pattern was similar across ethnic groups. The other risk factors were consistent with a linear model, indicative of chronological aging. CONCLUSIONS Women experience a unique rise in lipids at the time of FMP. Monitoring lipids in perimenopausal women should enhance primary prevention of CHD.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Are Changes in Cardiovascular Disease Risk Factors in Midlife Women Due to Chronological Aging or to the Menopausal Transition?

Matthews

Crawford

Chae

et al. 2009

Journal of the American College of Cardiology

Self Cite

547

399

View full text Add to dashboard Cite

show abstract

“…Oestrogen has numerous biological effects including those on reproductive tissues, bone, liver, pituitary and brain, and its importance in complicated processes such as bone and mineral metabolism, cardiac and vascular function and neuroprotection are just beginning to be understood (1–4). As each physiological system is studied, it is clear that there are general mechanisms of the action of oestrogen, particularly those relating to gene transcription.…”

mentioning

confidence: 99%

Oestrogen Receptors, Receptor Variants and Oestrogen Actions in the Hypothalamic‐Pituitary Axis

Shupnik

2002

J Neuroendocrinology

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Information on oestrogen action has grown exponentially in the past decade, and recent studies have begun to de®ne the mechanism of ligand-dependent activation and cell-speci®c effects. Oestrogenmediated gene transcription in a speci®c tissue depends on several factors, the most important of which is the presence of at least one of the two nuclear oestrogen receptor (ER) isoforms, ERa and ERb. The presence and levels of speci®c ER isoform variants, along with receptor coactivator, corepressor and integrator proteins, directly modulate overall nuclear ER activity. The structure of the ligand, including both physiological oestrogens and synthetic oestrogen receptor modulators, in¯uences ER interactions with these other proteins and thus determines the biological response. Furthermore, peptide and neurotransmitter-stimulated intracellular signalling pathways activate speci®c enzyme cascades and may modify the receptors and their interacting proteins, resulting in either independent or ligand-enhanced ER-mediated responses. Finally, several rapid effects of oestrogen probably occur at the membrane through nongenomic pathways that may or may not require the same ER proteins that are found in the nucleus. This review concentrates on the pituitary-hypothalamic axis and the genomic effects of oestrogen, and discusses the current knowledge of each of these factors in determining oestrogen actions in the neuroendocrine system.Oestrogen has numerous biological effects including those on reproductive tissues, bone, liver, pituitary and brain, and its importance in complicated processes such as bone and mineral metabolism, cardiac and vascular function and neuroprotection are just beginning to be understood (1±4). As each physiological system is studied, it is clear that there are general mechanisms of the action of oestrogen, particularly those relating to gene transcription. However the expression of oestrogen receptor (ER) forms and other proteins interacting with the receptor, as well as the activation of other intracellular signalling pathways that cross-talk with the ER, can profoundly in¯uence the overall response to oestrogen in a given cell or tissue. Physiological effects of oestrogen on the neuroendocrine system include direct actions on hypothalamic neurones and pituitary cells and indirect effects through glia and endothelial cells (4). These ultimately result in altered rates of synthesis and secretion of nearly all pituitary hormones, particularly prolactin and the gonadotropins luteinizing hormone (LH) and follicle stimulating hormone (5±7). There are both positive and negative effects of oestrogen on pituitary hormones, occurring either though the hypothalamus or directly at the level of the pituitary gland. Stimulatory effects of oestrogen are noted on prolactin, which acts in females to promote mammary gland development and lactation or milk production. Positive oestrogen feedback on the reproductive axis occurs at the time of the proestrus surge of oestrogen and LH prior to ovulation. Negative fee...

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“…[1][2][3]. The intense interest in understanding the circumstances under which estradiol protects and the mechanisms of it protective actions results from three converging areas of understanding.…”

mentioning

confidence: 99%

Minireview: Neuroprotective Effects of Estrogen—New Insights into Mechanisms of Action

et al. 2001

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An accumulating body of evidence clearly establishes that estradiol is a potent neuroprotective and neurotrophic factor in the adult: it influences memory and cognition, decreases the risk and delays the onset of neurological diseases such as Alzheimer's disease, and attenuates the extent of cell death that results from brain injuries such as cerebrovascular stroke and neurotrauma. Thus, estradiol appears to act at two levels: 1) it decreases the risk of disease or injury; and/or 2) it decreases the extent of injury incurred by suppressing the neurotoxic stimulus itself or increasing the resilience of the brain to a given injury. During the past century, the average life span of women has increased dramatically, whereas the time of the menopause has remained essentially constant. Thus, more women will live a larger fraction of their lives in a postmenopausal, hypoestrogenic state than ever before. Clearly, it is critical for us understand the circumstances under which estradiol exerts protective actions and the cellular and molecular mechanisms that underlie these novel, nonreproductive actions.

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Changes in Cardiovascular Risk Factors During the Peri- and Postmenopausal Years

Cited by 5 publications

References 35 publications

Are Changes in Cardiovascular Disease Risk Factors in Midlife Women Due to Chronological Aging or to the Menopausal Transition?

Are Changes in Cardiovascular Disease Risk Factors in Midlife Women Due to Chronological Aging or to the Menopausal Transition?

Oestrogen Receptors, Receptor Variants and Oestrogen Actions in the Hypothalamic‐Pituitary Axis

Minireview: Neuroprotective Effects of Estrogen—New Insights into Mechanisms of Action

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