Abstract
Background:
Women experience adverse changes in cardiovascular health in mid-life; whether the menopausal transition influences these remains strongly debated. The aim of this study was to examine associations of reproductive age (time since final menstrual period (FMP)) with change in carotid intima media thickness (CIMT) and cardiovascular risk factors and determine the role of chronological and reproductive age.
Methods:
We used data from 1,702 women from a pregnancy-based UK cohort who had up to four repeat cardiovascular health measures between mean age 51 (SD=4.0) and 56 (SD=3.6) and experienced a natural menopause. Multilevel models were used to assess the relationship between cardiovascular measures and time since FMP (reproductive age), while adjusting for the underlying effects of chronological age and confounders (socioeconomic factors, body mass index, smoking, alcohol, parity, menarche age). In addition, we looked at the relationship between cardiovascular measures by chronological age according to menopausal stages (pre-menopause, peri-menopause and post-menopause) using information from women who had and had not experienced menopause (N=3,892).
Results:
There was no strong evidence that reproductive age was associated with CIMT (difference in mean 0.8 μm/year, (95%CI -0.4, 2.1), whereas there was a strong positive association of chronological age (7.6 μm/year, 95%CI 6.3, 8.9). Consistent with this, we found weaker linear associations of reproductive compared with chronological age for atherosclerotic risk factors, such as with systolic blood pressure (-0.1 mmHg/year, 95%CI -0.3, 0.1, and 0.4 mmHg/year, 95%CI 0.2, 0.5, respectively) and non-HDL-cholesterol (0.02 mmol/l/year, 95%CI 0.005, 0.03, and 0.06, 95%CI 0.04, 0.07, respectively). In contrast associations with fat mass (0.06 kg/m2/year, 95%CI 0.03, 0.10, and 0 kg/m2/year, 95%CI -0.04, 0.04, respectively) and C-reactive protein (0.01, 95%CI 0.001, 0.02, and 0.01, 95%CI -0.001, 0.02 natural logged mg/l/year, respectively) were stronger for reproductive compared with chronological age. Both reproductive and chronological age were (weakly) positively associated with glucose (0.002, 95%CI 0.0001, 0.003, and 0.002, 95%CI 0.0001, 0.003 natural logged mmol/l/year, respectively)
Conclusions:
Our results suggest that going through the menopausal transition does not further increase women’s risk of atherosclerosis (measured by CIMT) beyond effects of aging. Menopausal transition may, in additional to aging, modestly increase adiposity and higher glucose levels and therefore a possible associated diabetes risk.
Women experience adverse changes in cardiovascular health in mid-life; whether the menopausal transition influences these remains strongly debated. The aim of this study was to examine associations of reproductive age (time since final menstrual period (FMP)) with change in carotid intima media thickness (CIMT) and cardiovascular risk factors and determine the role of chronological and reproductive age.
Methods:
We used data from 1,702 women from a pregnancy-based UK cohort who had up to four repeat cardiovascular health measures between mean age 51 (SD=4.0) and 56 (SD=3.6) and experienced a natural menopause. Multilevel models were used to assess the relationship between cardiovascular measures and time since FMP (reproductive age), while adjusting for the underlying effects of chronological age and confounders (socioeconomic factors, body mass index, smoking, alcohol, parity, menarche age). In addition, we looked at the relationship between cardiovascular measures by chronological age according to menopausal stages (pre-menopause, peri-menopause and post-menopause) using information from women who had and had not experienced menopause (N=3,892).
Results:
There was no strong evidence that reproductive age was associated with CIMT (difference in mean 0.8 μm/year, (95%CI -0.4, 2.1), whereas there was a strong positive association of chronological age (7.6 μm/year, 95%CI 6.3, 8.9). Consistent with this, we found weaker linear associations of reproductive compared with chronological age for atherosclerotic risk factors, such as with systolic blood pressure (-0.1 mmHg/year, 95%CI -0.3, 0.1, and 0.4 mmHg/year, 95%CI 0.2, 0.5, respectively) and non-HDL-cholesterol (0.02 mmol/l/year, 95%CI 0.005, 0.03, and 0.06, 95%CI 0.04, 0.07, respectively). In contrast associations with fat mass (0.06 kg/m2/year, 95%CI 0.03, 0.10, and 0 kg/m2/year, 95%CI -0.04, 0.04, respectively) and C-reactive protein (0.01, 95%CI 0.001, 0.02, and 0.01, 95%CI -0.001, 0.02 natural logged mg/l/year, respectively) were stronger for reproductive compared with chronological age. Both reproductive and chronological age were (weakly) positively associated with glucose (0.002, 95%CI 0.0001, 0.003, and 0.002, 95%CI 0.0001, 0.003 natural logged mmol/l/year, respectively)
Conclusions:
Our results suggest that going through the menopausal transition does not further increase women’s risk of atherosclerosis (measured by CIMT) beyond effects of aging. Menopausal transition may, in additional to aging, modestly increase adiposity and higher glucose levels and therefore a possible associated diabetes risk.
| Original language | English |
|---|---|
| Article number | 299 |
| Pages (from-to) | 1-13 |
| Number of pages | 1 |
| Journal | BMC Medicine |
| Volume | 20 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 17 Aug 2022 |
Bibliographical note
Funding Information:AF and KT report funding from UK Medical Research Council, for work unrelated to that presented here. DAL reports receiving support from several national and international government and charity research funders, and grants from Medtronic Ltd for work unrelated to that presented here. SMN has received speaker’s fees and participated in medical advisory boards for Roche. GLC, ALGS, FK, PIW, and NS declare that they have no competing interests.
Funding Information:
Roche Diagnostics provided support for the reproductive hormone measures that are used in this paper. The European Union’s Horizon 2020 research and innovation programme under grant agreement No 733206 (LifeCycle), funds GLC’s salary. FK, ALGS, AF, KT, and DAL work in, or are affiliated with, a Unit that is funded by the UK Medical Research Council (Grant Refs: MC_UU_00011/6 and MC_UU_00011/3) and University of Bristol. DAL is a National Institute for Health Research Senior Investigator (NF-0616-10102) and BHF Chair (CH/F/20/90003). AF is funded by a UK MRC fellowship (MR/M009351/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Funding Information:
This study was funded by the British Heart Foundation (Grant Refs: SP/07/008/24066 and AA/18/7/34219), Wellcome Trust (Grant Ref: WT092830M), and UK Medical Research Council (Grant Ref: G1001357).
Funding Information:
The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC, with additional support from a wide range of national and international funders (a comprehensive list of grant funding is available on the ALSPAC website; http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf ). This publication is the work of the authors and all authors will serve as guarantors for the contents of this paper. This research was funded in whole, or in part, by the Wellcome Trust [Grant Ref: 102215/2/13/2]. For the purpose of Open Access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission.
Funding Information:
The data that support the findings of this study are available from the ALSPAC executives, but restrictions apply to the availability of these data, which were used under licence for the current study, and so are not publicly available. The ALSPAC study website ( http://www.bristol.ac.uk/alspac/researchers/our-data/ ) contains details of all the data that are available through a fully searchable data dictionary and variable search tool. The analysis plan can be found on the github: https://github.com/gc13313/Menopause-and-CV-health . The European Union’s Horizon 2020 research and innovation programme under grant agreement No 874739 (LongITools) funds AGS' salary.
Publisher Copyright:
© 2022, The Author(s).
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