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1 wed later by ovariectomy (OVX; as a model of menopause).
2 elatively late), and 55 years or older (late menopause).
3 food intake is associated with risk of early menopause.
4 p in 1991 were followed until 2011 for early menopause.
5 skeletal fragility that operate long before menopause.
6 opause and 644 (0.4%) had surgical premature menopause.
7 communities in a rat model that mimics human menopause.
8 le) in relation to the number of years since menopause.
9 hat are unmasked by loss of estradiol during menopause.
10 previously been investigated in relation to menopause.
11 apacity, known as the ovarian reserve, until menopause.
12 of pubertal onset, hormone levels and age at menopause.
13 woman's reproductive lifespan, resulting in menopause.
14 ce arteries were attenuated by aging and the menopause.
15 nce subjective executive difficulties during menopause.
16 er and nonsignificant for surgical premature menopause.
17 the increased cardiovascular risk of earlier menopause.
18 subgroups or by timing of intervention after menopause.
19 destly associated with a lower risk of early menopause.
20 nd FEV1, is accelerated in women who undergo menopause.
21 s and how they may be altered with aging and menopause.
22 aused by a withdrawal effect of oestrogen at menopause.
23 y and secondary amenorrhoea as well as early menopause.
24 focusing on behaviors that are modifiable at menopause.
25 n and did not have breast cancer or surgical menopause.
26 omen who experience premature or early-onset menopause.
27 in the aging process, as they transition to menopause.
28 parity, lower PCOS risk, and earlier age at menopause.
29 pause and 887 (4.5%) with surgical premature menopause.
30 ze of the oocyte pool and thus the timing of menopause.
31 when it was initiated 10 or more years after menopause.
32 wer chronic systemic inflammation even after menopause.
33 sexual dimorphism declines with the onset of menopause.
34 women with a lower incidence in women before menopause.
35 was incidence of chemotherapy-induced early menopause.
36 was significantly associated with premature menopause.
37 a for subsequent malignancies and the age at menopause.
38 ts except MTX-FA increased the risk of early menopause.
39 GRS1 for age at menarche and GRS2 for age at menopause.
40 ted in pregnancy and one who presented after menopause.
41 t hormone measures and experienced a natural menopause.
42 risk for breast cancer, especially prior to menopause.
43 verse normal AMH per one-year earlier age at menopause.
44 my and women who did not report their age at menopause.
45 for species management and the evolution of menopause.
46 ry-food intake was not associated with early menopause.
47 pausal women was shown for increasing age at menopause (0.98; 0.96-0.99 [67,434 unique participants;
48 pression revealed similar results for age at menopause (0.98; 0.96-1.00 [48,894 unique participants;
49 use (HR 1.88, 1.62-2.20; p<0.0001) and early menopause (1.40, 1.27-1.54; p<0.0001), but were attenuat
50 uctive helping could in principle select for menopause [1, 2, 5], but the magnitude of these benefits
51 n were diagnosed with AAA, 134 had premature menopause (11.9%), 93 underwent surgical intervention an
52 se 43.7 +/- 8.6 years), women with premature menopause (29.3%) were younger at enrollment (P < 0.001)
53 000 woman-years) (difference vs no premature menopause, +3.08/1000 woman-years [95% CI, 2.06-4.10]; P
54 menopausal, younger than 40 years (premature menopause), 40-44 years (early menopause), 45-49 years (
56 rs (premature menopause), 40-44 years (early menopause), 45-49 years (relatively early), 50-51 years
57 000 woman-years) (difference vs no premature menopause, +5.57/1000 woman-years [95% CI, 2.41-8.73]; P
58 on with increasing (2-year increment) age at menopause (52,736 unique participants; 3 studies); sensi
62 tenuation compared with men (P < .008) until menopause, after which both groups had similar values.
63 isease was higher in women who had premature menopause (age <40 years; HR 1.55, 95% CI 1.38-1.73; p<0
64 HR 1.55, 95% CI 1.38-1.73; p<0.0001), early menopause (age 40-44 years; 1.30, 1.22-1.39; p<0.0001),
65 , 1.22-1.39; p<0.0001), and relatively early menopause (age 45-49 years; 1.12, 1.07-1.18; p<0.0001),
67 ted lifetime ovulatory years (LOY) as age at menopause (age at blood collection for premenopausal wom
69 age at menopause of <40 years) and time from menopause (age at study enrollment - age at menopause, y
71 occurring before adulthood in 11,781 cases (menopause aged under 45) and 173,641 controls (menopause
72 sociations were larger for natural premature menopause (all CHIP: odds ratio, 1.73 [95% CI, 1.23-2.44
75 e analyzed PFOA in relation to self-reported menopause among women (n = 9,192) 30-65 years old and in
77 er 10,000 (9.4%) women experienced premature menopause and 22,240 (22%) experienced early menarche.
78 4] years), 4904 (3.4%) had natural premature menopause and 644 (0.4%) had surgical premature menopaus
79 including 418 (2.1%) with natural premature menopause and 887 (4.5%) with surgical premature menopau
82 ed to discuss the contemporary literature on menopause and CVD risk with the intent of increasing awa
84 ies evaluating the effect of age at onset of menopause and duration since onset of menopause on inter
85 nalling could inhibit hot flushes during the menopause and during treatment for sex-steroid dependent
86 sex-specific risk factors, such as premature menopause and early menarche, with risk of AAA in a larg
88 5% CI 1.15-1.61; P = 0.0003); age at natural menopause and endometrioid carcinoma (OR per year later
89 iated with MHT in women experiencing natural menopause and for late age at natural menopause warrant
91 e risk include HDP for ischemic stroke, late menopause and gestational hypertension for hemorrhagic s
94 sess the associations between age at natural menopause and incidence and timing of cardiovascular dis
95 lity; however, the association between early menopause and incidence and timing of cardiovascular dis
97 ogenous estrogens, expressed as older age at menopause and longer reproductive period, is associated
99 riectomized-osteoporosis rats were used as a menopause and menopause-osteoporosis model, respectively
100 ped by transitional periods such as puberty, menopause and pregnancy, while daily fluctuations in mic
101 conjecture that in previous studies, earlier menopause and reduced kidney function are the causes rat
103 no significant association between premature menopause and risk of AAA amongst women who have never s
106 increase in the risk for this disease after menopause and typically develop coronary heart disease s
107 en women between 50 and 54 years at onset of menopause and women younger than 50 years at onset; ther
108 oss-sectional) that assessed age at onset of menopause and/or time since onset of menopause as exposu
109 ctional studies; reported on age at onset of menopause and/or time since onset of menopause as exposu
113 being premenopausal, having an older age at menopause, and never taking HRT, both in cases and contr
115 n) and ovariectomized (induction of surgical menopause) animals that show reduced Runx2 and enhanced
118 ogically impactful events of parturition and menopause are recorded in dental cementum microstructure
120 ductive features, e.g., ages at menarche and menopause, are found to be associated with endometrial c
122 nset of menopause and/or time since onset of menopause as exposures as well as risk of cardiovascular
123 nset of menopause and/or time since onset of menopause as exposures; and assessed associations with r
124 hytoestrogen-rich soy is known to ameliorate menopause-associated obesity and metabolic dysfunction f
125 sing their reproduction and/or going through menopause (assuming that these traits are easier to sele
129 were 2.24 (95% CI, 1.19-4.21) in women with menopause at the age of at least 55 years vs 50 to 54 ye
130 Among women who were less than 6 years past menopause at the time of randomization, the mean CIMT in
131 Among women who were 10 or more years past menopause at the time of randomization, the rates of CIM
134 Recent guidelines endorse using history of menopause before age 40 years to refine atherosclerotic
139 n therapy was initiated within 6 years after menopause but not when it was initiated 10 or more years
140 nt of fecal incontinence (FI) in women after menopause by altering neuromuscular continence mechanism
143 Declines in endogenous estrogen levels after menopause can lead to systemic bone loss, including loss
145 through January 1, 2015) using the key terms menopause, climacteric, reproductive period, depression,
146 hat has been previously shown to mimic human menopause compared to sham-operated (SHM) intact control
147 3) and 1.06 (95% CI: 0.87, 1.30) >=5 y after menopause compared with 0.50 (95% CI: 0.31, 0.81) in pre
148 ty associated with premature and early-onset menopause could be an important factor affecting risk of
149 ew that grandmother effects alone select for menopause coupled with long post-reproductive lifespan.
152 tment for weight, height, physical activity, menopause duration, calcium intake, and the interaction
155 g 25 years of follow-up, 1,045 women reached menopause (for NM, n = 588; for HOC, n = 304; and for HB
156 l women experience genitourinary syndrome of menopause, for which many use lubricating vaginal produc
158 50-51 years, women with premature and early menopause had a substantially increased risk of a non-fa
161 rs, longitudinal studies of women traversing menopause have contributed significantly to our understa
162 was associated with 23% lower risk of early menopause (hazard ratio = 0.77, 95% confidence interval:
163 (based on 67 cases) than women with natural menopause (hazard ratio = 1.51, 95% confidence interval:
164 BCC was associated with late age at natural menopause (hazard ratio [HR] for >/= 55 years v 50 to 54
165 before age 60 years for women with premature menopause (HR 1.88, 1.62-2.20; p<0.0001) and early menop
166 borderline significantly lower risk of early menopause (HR: 0.87; 95% CI: 0.76, 1.00; P-trend = 0.03)
167 parity, age at first and last births, age at menopause, hysterectomy, oophorectomy, hormone therapy u
168 orted their menopause status, age at natural menopause (if postmenopausal), and cardiovascular diseas
172 hese boutons form are altered with aging and menopause in rhesus monkeys and that these metrics may b
173 m are associated with the incidence of early menopause in the prospective Nurses' Health Study II (NH
174 size the challenge in determining definitive menopause in women with chemotherapy-induced amenorrhea.
175 and 49 women (7.6%) with surgical premature menopause (incidence, 11.27/1000 woman-years) (differenc
176 urred in 5415 women (3.9%) with no premature menopause (incidence, 5.70/1000 woman-years), 292 women
177 rs), 292 women (6.0%) with natural premature menopause (incidence, 8.78/1000 woman-years) (difference
179 n, reductions in circulating oestrogens with menopause interact with ageing processes to induce vascu
186 Furthermore, genetic susceptibility to later menopause is associated with higher PCOS risk (P=1.6 x 1
190 omen may suggest that decreased oestrogen at menopause is partially responsible for the gender-relate
191 served association between measured PFOA and menopause is subject to reverse causation for this outco
193 ture menopause, especially natural premature menopause, is independently associated with CHIP among p
194 s of protracted childhood and prolonged post-menopause longevity as derived human characteristics.
195 omen were stratified according to time since menopause (<6 years [early postmenopause] or >/=10 years
198 oup analyses by age, age at menarche, age at menopause, menopausal status, number of pregnancies, bre
200 monitoring in clinical practice, and age at menopause might also be considered as an important facto
201 e hypothesis that the decline of estrogen at menopause might contribute to the pathogenesis of HFpEF
204 cular disease (CVD) before and after natural menopause (NM), hysterectomy with at least 1 ovary conse
205 at menarche, first and last live birth, and menopause; number of live births; hormonal contraceptive
208 ple birth was strongly associated with early menopause (odds ratio = 1.42, confidence interval: 1.11,
209 associations of premature menopause (age at menopause of <40 years) and time from menopause (age at
210 non-fatal cardiovascular disease event after menopause, of whom 9369 (3.1%) had coronary heart diseas
212 set of menopause and duration since onset of menopause on intermediate CVD end points, CVD outcomes,
213 investigated the influence of aging and the menopause on the acute vasodilatory effects of estrogen
215 it can be expected to successfully bridge to menopause or allow for a less-invasive intervention.
216 ly determined as the period from menarche to menopause or lifetime number of ovulatory cycles after a
217 lifespan, roughly age of menarche to age of menopause or lifetime ovulatory cycles after accounting
219 EMENT Estrogen replacement therapy following menopause or surgical removal of the ovaries is a widesp
220 ostmenopausal includes patients with natural menopause or that induced by ovarian suppression or abla
221 ncome, nativity, smoking, physical activity, menopause, oral contraceptive use, hormone therapy, and
224 esus macaques, soon after surgically-induced menopause [ovariectomy (OVX)], on tests of memory and at
227 cline in ovarian estradiol production during menopause plays a significant role in shaping memory cir
228 nopause aged under 45) and 173,641 controls (menopause/pre-menopausal at >/= 45 years), in models con
229 symptoms and quality of life measured by the Menopause Quality of Life (Men-QoL), Insomnia Severity I
232 s16991615, previously associated with age at menopause, reached genome-wide significance at P = 3.48
233 nonhuman primates are vulnerable to age- and menopause- related decline in working memory, a cognitiv
234 us monkeys and women are subject to age- and menopause-related deficits in working memory, an executi
235 .02, Cohen's d = 0.51), and improved overall menopause-related quality of life (- 2.53 [- 4.17; - 0.8
236 AMH-by chronological age and time around the menopause (reproductive age) in mid-life women and explo
239 Classic life-history theory predicts that menopause should not occur because there should be no se
241 in any MENQOL domain or, especially, overall menopause-specific QOL, was associated with early treatm
242 stics and clinically meaningful worsening in menopause-specific quality of life (QOL) with treatment
243 ating exemestane, participants completed the Menopause-Specific Quality of Life Questionnaire (MENQOL
244 vestigated the association between worsening menopause-specific quality of life, baseline participant
246 amine the impact of patient factors (such as menopause status, body mass index, and vaginal pH) in th
247 sociation of SHBG with T2D did not change by menopause status, whereas the associations of ESH and T2
248 cess underlying PD symptoms may begin before menopause, suggests that estrogen-based hormone therapy
249 d) had a significant 17% lower risk of early menopause than women with the lowest intake [quintile me
252 the aging process, as women transition into menopause, to identify neuronal and cognitive changes th
253 the etiology of depression with onset in the menopause transition ("perimenopausal depression") invol
254 s observation led to the hypothesis that the menopause transition (MT) contributes to the increase in
255 ich the changing hormonal environment of the menopause transition may interact with the psychosocial
258 levels increased for the first 7 years after menopause (trend test, p < 0.0001), providing further ev
260 fication by age, body mass index, time since menopause, use of hormone replacement therapy, use of ca
263 n with versus without a history of premature menopause was 8.8% versus 5.5% (P<0.001), respectively.
264 age 40 or more years compared with premature menopause was associated with a 50% decreased risk for d
266 , and hormone replacement therapy, premature menopause was associated with an increased likelihood of
268 association but genetically-predicted age at menopause was associated with lower AMH levels by 0.18 S
271 nterval 1.3-2.7, P = 0.001), while time from menopause was directly associated with an increased like
272 After multivariable adjustment, premature menopause was independently associated with CHIP (all CH
275 ea (which has been associated with premature menopause) was associated with a significantly lower ris
277 mary outcome, natural and surgical premature menopause were associated with hazard ratios of 1.36 (95
281 reproductive duration [time from menarche to menopause]) were self-reported at study baseline in 1993
285 ssociation between multiple births and early menopause, which connects events pre-birth, when the ooc
287 ory (n = 19,286), 2148 (11.1%) had premature menopause, which was associated with greater risk of AAA
288 of vitamin D and calcium and incident early menopause while accounting for potential confounding fac
289 n at higher risk for depression due to early menopause who could benefit from psychiatric interventio
290 most increased among women reporting natural menopause who used MHT for 10 or more years versus women
291 g of the mechanisms linking seizures and the menopause will help to develop effective therapeutic str
293 gression tested the association of premature menopause with CHIP, adjusted for age, race, the first 1
294 hed men, but this advantage disappears after menopause with disrupted glucose homeostasis, in part ow
296 sociations of age at menopause and time from menopause with fibrosis severity in postmenopausal women
298 menopause (age at study enrollment - age at menopause, years) with fibrosis severity (stage 0-4) wer
300 were compared between women who experienced menopause younger than 45 years and women 45 years or ol