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1 centrations due to decreased excretion after menopause).
2 wed later by ovariectomy (OVX; as a model of menopause).
3 ze of the oocyte pool and thus the timing of menopause.
4 le) in relation to the number of years since menopause.
5 when it was initiated 10 or more years after menopause.
6 sexual dimorphism declines with the onset of menopause.
7 women with a lower incidence in women before menopause.
8  was incidence of chemotherapy-induced early menopause.
9 a for subsequent malignancies and the age at menopause.
10 ts except MTX-FA increased the risk of early menopause.
11 GRS1 for age at menarche and GRS2 for age at menopause.
12 ted in pregnancy and one who presented after menopause.
13 noate (PFOA) have been associated with early menopause.
14 remenopausal at baseline and reached natural menopause.
15 gly increased the risk both before and after menopause.
16 hat are unmasked by loss of estradiol during menopause.
17 ve identified 27 loci associated with age at menopause.
18 at were in some cases aggravated by surgical menopause.
19 pear to have higher PFC concentrations after menopause.
20 gnificantly lower risk the second year after menopause.
21 he incidence of hypertension increases after menopause.
22  previously been investigated in relation to menopause.
23 apacity, known as the ovarian reserve, until menopause.
24  is high in low-estrogen conditions, such as menopause.
25 rmone therapy use, smoking status, or age at menopause.
26 inguish the effect of age from the effect of menopause.
27 nt bone loss and weight gain associated with menopause.
28  younger than 50 years who have had surgical menopause.
29 s) follow-up and exclude women with surgical menopause.
30  and a potential determinant of the onset of menopause.
31 the changes observed up to and after natural menopause.
32 derlie glucose and lipid abnormalities after menopause.
33 of the type of lifestyle led by women around menopause.
34 P < 0.001) were associated with older age at menopause.
35 breast cancer experiencing treatment-induced menopause.
36 communities in a rat model that mimics human menopause.
37  woman's reproductive lifespan, resulting in menopause.
38 ce arteries were attenuated by aging and the menopause.
39 nce subjective executive difficulties during menopause.
40 the increased cardiovascular risk of earlier menopause.
41 subgroups or by timing of intervention after menopause.
42 destly associated with a lower risk of early menopause.
43 nd FEV1, is accelerated in women who undergo menopause.
44 s and how they may be altered with aging and menopause.
45 aused by a withdrawal effect of oestrogen at menopause.
46 y and secondary amenorrhoea as well as early menopause.
47 focusing on behaviors that are modifiable at menopause.
48 n and did not have breast cancer or surgical menopause.
49 omen who experience premature or early-onset menopause.
50  in the aging process, as they transition to menopause.
51  parity, lower PCOS risk, and earlier age at menopause.
52 pausal women was shown for increasing age at menopause (0.98; 0.96-0.99 [67,434 unique participants;
53 pression revealed similar results for age at menopause (0.98; 0.96-1.00 [48,894 unique participants;
54 uctive helping could in principle select for menopause [1, 2, 5], but the magnitude of these benefits
55 se 43.7 +/- 8.6 years), women with premature menopause (29.3%) were younger at enrollment (P < 0.001)
56               Among the participants (age at menopause 43.7 +/- 8.6 years), women with premature meno
57 on with increasing (2-year increment) age at menopause (52,736 unique participants; 3 studies); sensi
58 ppears insufficient to explain the timing of menopause [6-8].
59     By 2008, 1,769 women had reached natural menopause, 77 women had a hysterectomy with ovarian cons
60          Risk factors that are modifiable at menopause account for more than one-third of postmenopau
61                The associations of premature menopause (age at menopause of <40 years) and time from
62 age at menopause of <40 years) and time from menopause (age at study enrollment - age at menopause, y
63  occurring before adulthood in 11,781 cases (menopause aged under 45) and 173,641 controls (menopause
64 r these conditions that can be attributed to menopause alone is uncertain.
65 n populations may explain the variability in menopause among different ethnic groups; (5) discuss how
66 e analyzed PFOA in relation to self-reported menopause among women (n = 9,192) 30-65 years old and in
67 ohexane sulfonate (PFHxS) and age at natural menopause among women 20-65 years of age in NHANES (Nati
68 aluation or validated instruments, by age at menopause and duration of the reproductive period.
69 ies evaluating the effect of age at onset of menopause and duration since onset of menopause on inter
70 nalling could inhibit hot flushes during the menopause and during treatment for sex-steroid dependent
71                                              Menopause and eGFR were significantly associated with me
72 iated with MHT in women experiencing natural menopause and for late age at natural menopause warrant
73 e risk include HDP for ischemic stroke, late menopause and gestational hypertension for hemorrhagic s
74  ovarian failure, reducing the risk of early menopause and improving prospects for fertility.
75 gy which overlaps variation in normal age at menopause and is at least partly explained by the additi
76 ogenous estrogens, expressed as older age at menopause and longer reproductive period, is associated
77 en (>55 years of age) and thus may be due to menopause and loss of circulating estrogens.
78 the individual risk factors, such as ages at menopause and menarche.
79 riectomized-osteoporosis rats were used as a menopause and menopause-osteoporosis model, respectively
80 ped by transitional periods such as puberty, menopause and pregnancy, while daily fluctuations in mic
81 seen in young women appears to be lost after menopause and probably contributes to the increased bloo
82 conjecture that in previous studies, earlier menopause and reduced kidney function are the causes rat
83  these effects vary by regimen, time between menopause and study initiation, and prior use of HT.
84       We assessed the associations of age at menopause and time from menopause with fibrosis severity
85 ertain unique concerns, such as dealing with menopause and with aging.
86 en women between 50 and 54 years at onset of menopause and women younger than 50 years at onset; ther
87 oss-sectional) that assessed age at onset of menopause and/or time since onset of menopause as exposu
88 ctional studies; reported on age at onset of menopause and/or time since onset of menopause as exposu
89 py who were recruited into early (<6 y after menopause) and late (10+ y after menopause) groups.
90                Both estrogen loss, caused by menopause, and aging have inflammatory consequences.
91                               Aging, natural menopause, and cancer treatments such as surgical oophor
92 ted to a modifying effect of age, time since menopause, and HT formulation.
93  being premenopausal, having an older age at menopause, and never taking HRT, both in cases and contr
94 and age at first and last live birth, age at menopause, and postmenopausal hormone use.
95 ed to assess the association between gender, menopause, and severity of liver fibrosis.
96  investigate the association between gender, menopause, and the severity of liver fibrosis in patient
97 ementia observed in women following surgical menopause, and they provide increased support that early
98 n) and ovariectomized (induction of surgical menopause) animals that show reduced Runx2 and enhanced
99 P2L locus are associated with age at natural menopause (ANM).
100 ing variation associated with age at natural menopause (ANM).
101 rations, other dairy constituents, and early menopause are warranted.
102  the early cessation of female reproduction (menopause), are argued to be evidence that humans are 'c
103 ductive features, e.g., ages at menarche and menopause, are found to be associated with endometrial c
104          Age and physiologic status, such as menopause, are risk factors for breast cancer.
105 hazard ratios (HRs) for the onset of natural menopause as a function of age and serum PFC levels, and
106 iously associated with normal age at natural menopause as a quantitative trait (QT) were also associa
107                                              Menopause as a result of ovarian follicle depletion is t
108 nset of menopause and/or time since onset of menopause as exposures as well as risk of cardiovascular
109 nset of menopause and/or time since onset of menopause as exposures; and assessed associations with r
110 in life and to cause a delay in the onset of menopause as measured by the number of primordial follic
111  pool of primordial follicles from age 20 to menopause as reported in the biological literature.
112 hytoestrogen-rich soy is known to ameliorate menopause-associated obesity and metabolic dysfunction f
113                                              Menopause at age 40 or more years compared with prematur
114  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
115 metabolic consequences of ageing, gender and menopause at the population level.
116  Among women who were less than 6 years past menopause at the time of randomization, the mean CIMT in
117   Among women who were 10 or more years past menopause at the time of randomization, the rates of CIM
118 ed IDFS in those who were over 5 years since menopause at trial entry (n=1041; HR 0.77, 95% CI 0.63-0
119 rience the cessation of reproductive cycles, menopause, at approximately 50 y of age after a fertilit
120 ons of recent models [5] of the evolution of menopause based on kinship dynamics.
121 on-years, 2041 women reported having natural menopause before the age of 45 y.
122 ial model included menopausal status, age at menopause, BMI, smoking, oral contraceptive use, MHT use
123 the therapy is initiated temporally close to menopause but not when it is initiated later.
124 n therapy was initiated within 6 years after menopause but not when it was initiated 10 or more years
125 s has been associated with the transition to menopause, but the risk of depressive symptoms in the ea
126 ffects of estradiol may vary with time since menopause, but this prediction has not been assessed dir
127 of the variation in both age at menarche and menopause, but to date the known genes explain <15% of t
128 nt of fecal incontinence (FI) in women after menopause by altering neuromuscular continence mechanism
129      Here, we used a mouse model of surgical menopause by ovariectomy and demonstrate a protective ro
130 : As many as 10% of women experience natural menopause by the age of 45 years.
131                                   In theory, menopause can evolve via inclusive fitness benefits [5,
132 Declines in endogenous estrogen levels after menopause can lead to systemic bone loss, including loss
133 ic, child, and biomedical (e.g., medication, menopause, CGG repeats) factors.
134 through January 1, 2015) using the key terms menopause, climacteric, reproductive period, depression,
135 hat has been previously shown to mimic human menopause compared to sham-operated (SHM) intact control
136 es greater overall and 8 times greater after menopause compared with women with no depression history
137 ty associated with premature and early-onset menopause could be an important factor affecting risk of
138 ew that grandmother effects alone select for menopause coupled with long post-reproductive lifespan.
139         Alterations in hormone levels during menopause decrease bone density and may worsen oral heal
140        The risk of depressive symptoms after menopause decreased by 35% for each unit (SD) increase b
141                                        Early menopause, defined as the cessation of ovarian function
142 tment for weight, height, physical activity, menopause duration, calcium intake, and the interaction
143  using CAL (dependent variable), adjusted by menopause, education, and family income, demonstrated an
144                                        Early menopause (EM) affects up to 10% of the female populatio
145                            Similarly, age at menopause, endometriosis, and tubal ligation were only a
146 e is reduced by maturation and atresia until menopause ensues.
147 hormones over the lifespan (e.g. puberty and menopause), exogenous sex hormones (e.g. hormonal contra
148  first live birth, menopausal status, age at menopause, family history of breast or ovarian cancer, b
149 Risk factors include obesity, male sex, age, menopause, fluid retention, adenotonsillar hypertrophy,
150  1.54, 2.17, and 1.30, respectively), age at menopause (for ages 49-51 and >/=52 years vs. </=48 year
151 g 25 years of follow-up, 1,045 women reached menopause (for NM, n = 588; for HOC, n = 304; and for HB
152 (<6 y after menopause) and late (10+ y after menopause) groups.
153                The genitourinary syndrome of menopause has a negative impact on quality of life of po
154  the natural final menstrual period (FMP) or menopause has been associated with numerous health outco
155  women, ovarian hormone loss associated with menopause has been related to cognitive decline.
156 r an average of 5.4 years of HT during early menopause has longer term protective effects on global c
157        Few modifiable risk factors for early menopause have been identified, but emerging data sugges
158 entially modifiable factors affecting age at menopause have not been examined longitudinally in large
159 maturely via bilateral ovariectomy (surgical menopause) have a significantly increased risk for cogni
160  BCC was associated with late age at natural menopause (hazard ratio [HR] for >/= 55 years v 50 to 54
161  ovarian hormone loss, memory type examined, menopause history, and hormone receptor status.
162  or disease outcomes in the context of their menopause history.
163 ancer, oral contraceptive pill use, surgical menopause, hormone replacement therapy, statins, acetami
164 gest a positive association between PFCs and menopause; however, at least part of the association may
165 borderline significantly lower risk of early menopause (HR: 0.87; 95% CI: 0.76, 1.00; P-trend = 0.03)
166 parity, age at first and last births, age at menopause, hysterectomy, oophorectomy, hormone therapy u
167 e metastases and, for women with established menopause, improved disease outcomes.
168 al loci significantly associated with age at menopause in African Americans.
169 ve shown decreased pregnancy rates and early menopause in female cancer survivors; however, infertili
170                          Time since onset of menopause in relation to risk of developing intermediate
171 esynaptic boutons are altered with aging and menopause in rhesus monkeys (Macaca mulatta) and that th
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  group divided by age 50, the average age at menopause in the U.S. (P = 0.08): ACOR and 95% CI of hav
175 tween alcohol intake and BMD in women around menopause in the United Kingdom and to determine whether
176 size the challenge in determining definitive menopause in women with chemotherapy-induced amenorrhea.
177 ound detrimental effects of E2 therapy after menopause, including increased stroke risk and dementia.
178 incidence of sarcoidosis decreased as age at menopause increased (P-trend = 0.03).
179 ing, but decreased by over 50% with surgical menopause induced by ovariectomy in aged monkeys.
180                                      Because menopause is accompanied by marked alterations in hypoth
181                                              Menopause is an important physiological stage in women's
182  Observational studies have shown that early menopause is associated with adverse cardiovascular dise
183                                              Menopause is associated with bone loss and enhanced visc
184                                   RATIONALE: Menopause is associated with changes in sex hormones, wh
185               The loss of hormone cycling at menopause is associated with cognitive decline and demen
186 Furthermore, genetic susceptibility to later menopause is associated with higher PCOS risk (P=1.6 x 1
187                        Hormone therapy after menopause is controversial.
188  years, and the average US woman who reaches menopause is expected to live another 30 years.
189 omen may suggest that decreased oestrogen at menopause is partially responsible for the gender-relate
190 served association between measured PFOA and menopause is subject to reverse causation for this outco
191                                              Menopause is the transition from reproductive to non-rep
192                               Earlier age at menopause is widely considered to be associated with an
193    We therefore sought to uncover additional menopause loci and investigate the relevance of European
194 ci and investigate the relevance of European menopause loci by performing a GWAS meta-analysis in 651
195 nomenon, we used an animal model of surgical menopause, long-term (10-week) bilateral ovariectomy in
196  sensitive to menstrual cycle changes, while menopause, long-term HRT, and presence of milk in lactat
197 omen were stratified according to time since menopause (&lt;6 years [early postmenopause] or >/=10 years
198                                 Menarche and menopause mark the onset and cessation, respectively, of
199                                       Age at menopause marks the end of a woman's reproductive life a
200                     Bone loss with aging and menopause may be linked to vascular endothelial dysfunct
201 gest that, in addition to lipid alterations, menopause may contribute to future metabolic and cardiov
202      Variations in the hormonal milieu after menopause may influence neural processes concerned with
203 3) highlight which of the symptoms preceding menopause may result from antagonistic co-evolution of M
204 rawal (such as following surgical or natural menopause) may impact the efficacy of progesterone.
205  age of 44.92 [2.81] years), and 12 women in menopause (mean [SD] age, 56.25 [3.19] years).
206 smoking, physical activity, body mass index, menopause, menopausal hormone therapy, and alcohol, brea
207 oup analyses by age, age at menarche, age at menopause, menopausal status, number of pregnancies, bre
208 rt the hypothesis that temporal proximity to menopause modifies the relation between endogenous serum
209 th reproductive age and by 16% compared with menopause (multivariate analysis of variance, group effe
210 cular disease (CVD) before and after natural menopause (NM), hysterectomy with at least 1 ovary conse
211  at menarche, first and last live birth, and menopause; number of live births; hormonal contraceptive
212                                              Menopause occurs at a median age of 51.3 years, and the
213 away during prepubertal and adult life until menopause occurs, and apoptosis has been identified as a
214 ple birth was strongly associated with early menopause (odds ratio = 1.42, confidence interval: 1.11,
215  associations of premature menopause (age at menopause of <40 years) and time from menopause (age at
216 ed and conflicting evidence on the effect of menopause on asthma.
217 set of menopause and duration since onset of menopause on intermediate CVD end points, CVD outcomes,
218   Here we report the effects of age, sex and menopause on serum metabolites in 26,065 individuals of
219  investigated the influence of aging and the menopause on the acute vasodilatory effects of estrogen
220       When examined according to years since menopause onset (<10 years) rather than age group, resul
221            Loss of endogenous E2 in women at menopause or after surgical oopherectomy leads to an inc
222 it can be expected to successfully bridge to menopause or allow for a less-invasive intervention.
223 alcium balance that developed in women after menopause or oophorectomy.
224 ostmenopausal includes patients with natural menopause or that induced by ovarian suppression or abla
225 ncome, nativity, smoking, physical activity, menopause, oral contraceptive use, hormone therapy, and
226 orosis and ovariectomized rats as a model of menopause-osteoporosis and menopause women.
227 teoporosis rats were used as a menopause and menopause-osteoporosis model, respectively.
228 esus macaques, soon after surgically-induced menopause [ovariectomy (OVX)], on tests of memory and at
229 the associations between six loci and age at menopause (P-value < 0.05): AMHR2, RHBLD2, PRIM1, HK3/UM
230 cline in ovarian estradiol production during menopause plays a significant role in shaping memory cir
231 gonadotropin alterations indicative of early menopause, poor oocyte quality, and infertility.
232 nopause aged under 45) and 173,641 controls (menopause/pre-menopausal at >/= 45 years), in models con
233 r regression to determine whether time since menopause predicted serum PFC levels.
234                            Females who enter menopause prematurely via bilateral ovariectomy (surgica
235 life, measured by the Greene Climacteric and Menopause Quality of Life scales.
236 f hypertension, and the greater morbidity in menopause reflects this neglect.
237 nonhuman primates are vulnerable to age- and menopause- related decline in working memory, a cognitiv
238 s, are suggested to have positive effects on menopause-related adiposity and cardiovascular disease r
239 nonhuman primates are vulnerable to age- and menopause-related decline in working memory, a cognitive
240                                              Menopause results from loss of ovarian function and mark
241    Classic life-history theory predicts that menopause should not occur because there should be no se
242 dex, height, age at menarche, parity, age at menopause, smoking, alcohol and family history of BC) an
243 or prevention has limited negative impact on menopause-specific and health-related QOL in healthy pos
244                                              Menopause-specific and health-related QOL were assessed
245               Conclusion Negative changes in menopause-specific QOL influence a woman's decision to s
246 in any MENQOL domain or, especially, overall menopause-specific QOL, was associated with early treatm
247 stics and clinically meaningful worsening in menopause-specific quality of life (QOL) with treatment
248 -related QOL were assessed by using the four Menopause-Specific Quality of Life Questionnaire (MENQOL
249 ating exemestane, participants completed the Menopause-Specific Quality of Life Questionnaire (MENQOL
250 vestigated the association between worsening menopause-specific quality of life, baseline participant
251 pplement use, energy intake, and, for women, menopause status and estrogen use.
252          Among 3,204 women aged 40-55 years, menopause status associates additionally with glycine an
253            In meta-analysis of 10,083 women, menopause status associates with amino acids glutamine,
254 sociation of SHBG with T2D did not change by menopause status, whereas the associations of ESH and T2
255 women with higher levels of PFCs had earlier menopause than did women with the lowest PFC levels.
256 d) had a significant 17% lower risk of early menopause than women with the lowest intake [quintile me
257  experienced depressive symptoms approaching menopause, the risk of depressive symptoms declined afte
258      Additionally, during the 10 years after menopause, the risk of stroke roughly doubles in women.
259                                              Menopause timing has a substantial impact on infertility
260 ed to examine the relation of age at natural menopause to lifestyle and anthropometric factors.
261  the aging process, as women transition into menopause, to identify neuronal and cognitive changes th
262 the etiology of depression with onset in the menopause transition ("perimenopausal depression") invol
263  who had no history of depression before the menopause transition had a low risk of depressive sympto
264 ich the changing hormonal environment of the menopause transition may interact with the psychosocial
265  of premenopausal women followed through the menopause transition, and prospective cohort studies of
266 ptoms increases two- to threefold during the menopause transition.
267 eport difficulties in this domain during the menopause transition.
268 ounseling, infertility, abortion, lactation, menopause treatment, and endometrial cancer.
269 levels increased for the first 7 years after menopause (trend test, p < 0.0001), providing further ev
270 fication by age, body mass index, time since menopause, use of hormone replacement therapy, use of ca
271  ovariectomized (OVX) mice, a model of human menopause, using co-expression network analysis.
272 atural menopause and for late age at natural menopause warrant further investigation.
273 age 40 or more years compared with premature menopause was associated with a 50% decreased risk for d
274                               Younger age at menopause was associated with a higher risk of DCIS but
275 , and hormone replacement therapy, premature menopause was associated with an increased likelihood of
276              A novel association with age at menopause was detected for a variant rs1800932 in the mi
277 nterval 1.3-2.7, P = 0.001), while time from menopause was directly associated with an increased like
278                 The cumulative risk of early menopause was low after MTX-FA but was substantial after
279 , hormonal use, diabetes and age at menarche/menopause was obtained for all individuals.
280 rate of hysterectomy, and time since natural menopause was positively associated with serum PFCs.
281 ea (which has been associated with premature menopause) was associated with a significantly lower ris
282  and (2) self-reported information on age at menopause were analyzed.
283         Impaired kidney function and earlier menopause were associated with perfluorooctanoic acid (P
284 ve cohort study of 6040 women with a natural menopause were followed up at 3-y intervals over 9 y.
285                      Cases of incident early menopause were identified from all participants who were
286  menarche, parity, breastfeeding, and age at menopause, were not associated with pancreatic cancer ri
287 reproductive duration [time from menarche to menopause]) were self-reported at study baseline in 1993
288 ssociation between multiple births and early menopause, which connects events pre-birth, when the ooc
289                                A hallmark of menopause, which follows the decline in the ovarian prod
290  of vitamin D and calcium and incident early menopause while accounting for potential confounding fac
291 ore severe fibrosis compared to women before menopause, while postmenopausal women have a similar sev
292 n at higher risk for depression due to early menopause who could benefit from psychiatric interventio
293 most increased among women reporting natural menopause who used MHT for 10 or more years versus women
294                 The potential association of menopause with carotid intima-media thickness as well as
295         We analysed the association of early menopause with events occurring before adulthood in 11,7
296 sociations of age at menopause and time from menopause with fibrosis severity in postmenopausal women
297 ats as a model of menopause-osteoporosis and menopause women.
298  menopause (age at study enrollment - age at menopause, years) with fibrosis severity (stage 0-4) wer
299 onal associations were assessed for eGFR and menopause (yes/no).
300  were compared between women who experienced menopause younger than 45 years and women 45 years or ol

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