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1.
Artigo em Inglês | MEDLINE | ID: mdl-32238406

RESUMO

BACKGROUND: Although vitamin D inhibits breast tumor growth in experiments, the findings from population-based studies remain inconclusive. Our goals were to investigate the association between pre-diagnostic plasma 25-hydroxyvitamin D [25(OH)D] and breast cancer recurrence in the Nurses' Health Studies (NHS) and to explore the molecular underpinnings. METHODS: Plasma 25(OH)D was measured with a high-affinity-protein-binding-assay/a radioimmunoassay. We profiled transcriptome-wide-gene-expression in breast tumors using microarrays. Hazard ratios (HRs) of breast cancer recurrence were estimated from covariate-adjusted-Cox-regressions. We examined differential gene expression in association with 25(OH)D. We derived a gene expression score for 25(OH)D, and assessed associations between the score and cancer recurrence. RESULTS: Although 25(OH)D was not associated with breast cancer recurrence overall (HR=0.97; 95% confidence interval (CI): 0.88-1.08), the association varied by estrogen-receptor (ER) status (p-for-interaction=0.005). Importantly, among ER-positive stage I-to-III cancers, every 5ng/ml increase in 25(OH)D was associated with a 13% lower risk of recurrence (HR=0.87; 95%-CI: 0.76-0.99). A null association was observed for ER-negative cancers. Pathway analysis identified multiple gene-sets (proliferation, migration, and inflammation) that were significantly down-regulated in ER-positive tumors of women with high 25(OH)D (≥30ng/ml), compared to those with low levels. 25(OH)D score derived was marginally associated with reduced risk of recurrence in ER-positive diseases in NHS, however, no association was noted in the replication dataset. CONCLUSIONS: Our findings support an intriguing line of research to better understand the mechanisms underlying the role of vitamin D in breast tumor progression, particularly for the ER-positive subtype. IMPACT: Vitamin D may present a personal-level secondary-prevention strategy for breast cancer.

2.
Eur J Epidemiol ; 2020 Mar 17.
Artigo em Inglês | MEDLINE | ID: mdl-32185575

RESUMO

Adherence to healthful dietary patterns is associated with lower body mass index (BMI) in adults; however, whether maternal diet quality during peripregnancy is related to a lower overweight risk in the offspring remains to be elucidated. We investigated the associations between the Alternate Healthy Eating Index (AHEI), Alternate Mediterranean Diet (aMED) and Dietary Approach to Stop Hypertension (DASH) during peripregnancy and offspring weight outcomes in a study including 2729 mother-child pairs from the Nurses' Health Study II and offspring cohort Growing Up Today Study II. Children, 12-14 years at baseline were 21-23 years at the last follow-up. Overweight or obesity was defined according to International Obesity Task Force (< 18 years) and World-Health-Organization guidelines (18 + years). Maternal dietary patterns were calculated from food frequency questionnaires. Log-binomial models were used to estimate relative risks (RR) and 95% confidence intervals. In models adjusted for sex, gestational age at delivery and maternal total energy intake, greater maternal adherence to aMED and DASH, but not AHEI, was associated with lower overweight risk in the offspring (RRQ5 vs Q1 = 0.82 [0.70-0.97] for aMED and 0.86 [0.72-1.04] for DASH, P for trend < 0.05 for both). After additional adjustment for maternal pre-pregnancy lifestyle factors and socio-demographic characteristic, none of the diet quality scores were significantly associated with offspring overweight risk. Maternal pre-pregnancy BMI did not modify any of these associations. In this population of generally well-nourished women, maternal healthful dietary patterns during the period surrounding pregnancy were not independently associated with offspring overweight risk at ages 12-23 years.

3.
Int J Cancer ; 2020 Feb 03.
Artigo em Inglês | MEDLINE | ID: mdl-32012248

RESUMO

Early-adulthood body size is strongly inversely associated with risk of premenopausal breast cancer. It is unclear whether subsequent changes in weight affect risk. We pooled individual-level data from 17 prospective studies to investigate the association of weight change with premenopausal breast cancer risk, considering strata of initial weight, timing of weight change, other breast cancer risk factors and breast cancer subtype. Hazard ratios (HR) and 95% confidence intervals (CI) were obtained using Cox regression. Among 628,463 women, 10,886 were diagnosed with breast cancer before menopause. Models adjusted for initial weight at ages 18-24 years and other breast cancer risk factors showed that weight gain from ages 18-24 to 35-44 or to 45-54 years was inversely associated with breast cancer overall (e.g., HR per 5 kg to ages 45-54: 0.96, 95% CI: 0.95-0.98) and with oestrogen-receptor(ER)-positive breast cancer (HR per 5 kg to ages 45-54: 0.96, 95% CI: 0.94-0.98). Weight gain from ages 25-34 was inversely associated with ER-positive breast cancer only and weight gain from ages 35-44 was not associated with risk. None of these weight gains were associated with ER-negative breast cancer. Weight loss was not consistently associated with overall or ER-specific risk after adjusting for initial weight. Weight increase from early-adulthood to ages 45-54 years is associated with a reduced premenopausal breast cancer risk independently of early-adulthood weight. Biological explanations are needed to account for these two separate factors.

4.
Cancer Res ; 80(6): 1357-1367, 2020 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-31969373

RESUMO

Ovarian cancer has few known risk factors, hampering identification of high-risk women. We assessed the association of prediagnostic plasma metabolites (N = 420) with risk of epithelial ovarian cancer, including both borderline and invasive tumors. A total of 252 cases and 252 matched controls from the Nurses' Health Studies were included. Multivariable logistic regression was used to estimate ORs and 95% confidence intervals (CI), comparing the 90th-10th percentile in metabolite levels, using the permutation-based Westfall and Young approach to account for testing multiple correlated hypotheses. Weighted gene coexpression network analysis (WGCNA; n = 10 metabolite modules) and metabolite set enrichment analysis (n = 23 metabolite classes) were also evaluated. An increase in pseudouridine levels from the 10th to the 90th percentile was associated with a 2.5-fold increased risk of overall ovarian cancer (OR = 2.56; 95% CI, 1.48-4.45; P = 0.001/adjusted P = 0.15); a similar risk estimate was observed for serous/poorly differentiated tumors (n = 176 cases; comparable OR = 2.38; 95% CI, 1.33-4.32; P = 0.004/adjusted P = 0.55). For nonserous tumors (n = 34 cases), pseudouridine and C36:2 phosphatidylcholine plasmalogen had the strongest statistical associations (OR = 9.84; 95% CI, 2.89-37.82; P < 0.001/adjusted P = 0.07; and OR = 0.11; 95% CI, 0.03-0.35; P < 0.001/adjusted P = 0.06, respectively). Five WGCNA modules and 9 classes were associated with risk overall at FDR ≤ 0.20. Triacylglycerols (TAG) showed heterogeneity by tumor aggressiveness (case-only heterogeneity P < 0.0001). The TAG association with risk overall and serous tumors differed by acyl carbon content and saturation. In summary, this study suggests that pseudouridine may be a novel risk factor for ovarian cancer and that TAGs may also be important, particularly for rapidly fatal tumors, with associations differing by structural features. SIGNIFICANCE: Pseudouridine represents a potential novel risk factor for ovarian cancer and triglycerides may be important particularly in rapidly fatal ovarian tumors.

5.
Cancer Epidemiol Biomarkers Prev ; 29(3): 599-605, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31932411

RESUMO

BACKGROUND: The link between modifiable breast cancer risk factors and tumor genomic alterations remains largely unexplored. We evaluated the association of prediagnostic body mass index (BMI), cigarette smoking, and alcohol consumption with somatic copy number variation (SCNV), total somatic mutation burden (TSMB), seven single base substitution (SBS) signatures (SBS1, SBS2, SBS3, SBS5, SBS13, SBS29, and SBS30), and nine driver mutations (CDH1, GATA3, KMT2C, MAP2K4, MAP3K1, NCOR1, PIK3CA, RUNX1, and TP53) in a subset of The Cancer Genome Atlas (TCGA). METHODS: Clinical and genomic data were retrieved from the TCGA database. Risk factor information was collected from four TCGA sites (n = 219 women), including BMI (1 year before diagnosis), cigarette smoking (smokers/nonsmokers), and alcohol consumption (current drinkers/nondrinkers). Multivariable regression analyses were conducted in all tumors and stratified according to estrogen receptor (ER) status. RESULTS: Increasing BMI was associated with increasing SCNV in all women (P = 0.039) and among women with ER- tumors (P = 0.031). Smokers had higher SCNV and TSMB versus nonsmokers (P < 0.05 all women). Alcohol drinkers had higher SCNV versus nondrinkers (P < 0.05 all women and among women with ER+ tumors). SBS3 (defective homologous recombination-based repair) was exclusively found in alcohol drinkers with ER- disease. GATA3 mutation was more likely to occur in women with higher BMI. No association was significant after multiple testing correction. CONCLUSIONS: This study provides preliminary evidence that BMI, cigarette smoking, and alcohol consumption can influence breast tumor biology, in particular, DNA alterations. IMPACT: This study demonstrates a link between modifiable breast cancer risk factors and tumor genomic alterations.

6.
Nat Commun ; 11(1): 312, 2020 01 16.
Artigo em Inglês | MEDLINE | ID: mdl-31949161

RESUMO

Identifying the underlying genetic drivers of the heritability of breast cancer prognosis remains elusive. We adapt a network-based approach to handle underpowered complex datasets to provide new insights into the potential function of germline variants in breast cancer prognosis. This network-based analysis studies ~7.3 million variants in 84,457 breast cancer patients in relation to breast cancer survival and confirms the results on 12,381 independent patients. Aggregating the prognostic effects of genetic variants across multiple genes, we identify four gene modules associated with survival in estrogen receptor (ER)-negative and one in ER-positive disease. The modules show biological enrichment for cancer-related processes such as G-alpha signaling, circadian clock, angiogenesis, and Rho-GTPases in apoptosis.

7.
Cancer Epidemiol Biomarkers Prev ; 29(2): 343-351, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31826913

RESUMO

BACKGROUND: The V measure captures grayscale intensity variation on a mammogram and is positively associated with breast cancer risk, independent of percent mammographic density (PMD), an established marker of breast cancer risk. We examined whether anthropometrics are associated with V, independent of PMD. METHODS: The analysis included 1,700 premenopausal and 1,947 postmenopausal women without breast cancer within the Nurses' Health Study (NHS) and NHSII. Participants recalled their body fatness at ages 5, 10, and 20 years using a 9-level pictogram (level 1: most lean) and reported weight at age 18 years, current adult weight, and adult height. V was estimated by calculating standard deviation of pixels on screening mammograms. Linear mixed models were used to estimate beta coefficients (ß) and 95% confidence intervals (CI) for the relationships between anthropometric measures and V, adjusting for confounders and PMD. RESULTS: V and PMD were positively correlated (Spearman r = 0.60). Higher average body fatness at ages 5 to 10 years (level ≥ 4.5 vs. 1) was significantly associated with lower V in premenopausal (ß = -0.32; 95% CI, -0.48 to -0.16) and postmenopausal (ß = -0.24; 95% CI, -0.37 to -0.10) women, independent of current body mass index (BMI) and PMD. Similar inverse associations were observed with average body fatness at ages 10 to 20 years and BMI at age 18 years. Current BMI was inversely associated with V, but the associations were largely attenuated after adjustment for PMD. Height was not associated with V. CONCLUSIONS: Our data suggest that early-life body fatness may reflect lifelong impact on breast tissue architecture beyond breast density. However, further studies are needed to confirm the results. IMPACT: This study highlights strong inverse associations of early-life adiposity with mammographic image intensity variation.

9.
Am J Epidemiol ; 2019 Dec 17.
Artigo em Inglês | MEDLINE | ID: mdl-31845729

RESUMO

Reproductive events, such as ovulation, trigger an inflammatory cascade. Few studies have examined their long-term influence on inflammatory profiles. We included 3,393 premenopausal and 3,915 postmenopausal women with intact ovaries/uterus from the Nurses' Health Studies, and estimated lifetime ovulatory years (LOY) as age at menopause (age at blood collection for premenopausal women) minus age at menarche, years of oral contraceptive (OC) use, and one year per pregnancy. After adjusting for other inflammation-related factors (e.g., BMI, exercise, diet, etc.), every 5-year increase in LOY was associated with lower C-reactive protein (CRP) in premenopausal (-11.5%; 95% CI: -15.0, -8.0; p<0.0001) and postmenopausal women (-7.2%; 95% CI: -10.0, -4.3; p<0.0001). Older age at menopause (p=0.007), earlier menarche (p=0.007), and shorter duration of OC use (p=0.002) were associated with lower CRP levels in postmenopausal women, whereas only OC duration was positively associated in premenopausal women (p<0.0001). LOY was modestly inversely associated with interleukin-6 only in postmenopausal women (p=0.04). Notably, the associations of CRP with LOY were similar in magnitude compared to those with exercise and a healthy diet, although weaker than that with BMI. Although many reproductive events induce acute inflammation, increased LOY was associated with lower chronic systemic inflammation even after menopause.

10.
J Natl Cancer Inst ; 2019 Dec 13.
Artigo em Inglês | MEDLINE | ID: mdl-31845728

RESUMO

BACKGROUND: Excess body weight is an established cause of postmenopausal breast cancer, but it is unknown if weight loss reduces risk. METHODS: Associations between weight change and risk of breast cancer were examined among women aged ≥50 years in the Pooling Project of Prospective Studies of Diet and Cancer. In 10 cohorts, weight assessed on three surveys was used to examine weight change patterns over approximately 10 years (Interval 1 median= 5.2 years; Interval 2 median = 4.0 years). Sustained weight loss was defined as ≥ 2kg lost in Interval 1 that was not regained in Interval 2. Among 180,885 women, 6,930 invasive breast cancers were identified during follow-up. RESULTS: Compared with women with stable weight (± 2kg), women with sustained weight loss had a lower risk of breast cancer. This risk reduction was linear and specific to women not using postmenopausal hormones (>2-4.5kg lost: Hazard Ratio (HR)= 0.82, 95% confidence interval (CI): 0.70-0.96; >4.5-<9kg lost: HR = 0.75, 95% CI: 0.63-0.90; ≥9kg lost: HR = 0.68, 95% CI: 0.50-0.93). Women who lost ≥9kg and gained some (but not all) of it back were also at a lower risk of breast cancer. Other patterns of weight loss and gain over the two intervals had a similar risk of breast cancer to women with stable weight. CONCLUSIONS: These results suggest that sustained weight loss, even modest amounts, is associated with lower breast cancer risk for women aged ≥50 years. Breast cancer prevention may be a strong weight loss motivator for the two-thirds of American women who are overweight or obese.

11.
Nutrients ; 11(11)2019 Nov 05.
Artigo em Inglês | MEDLINE | ID: mdl-31694190

RESUMO

BACKGROUND: Flavonoids potentially exert anti-cancer effects, as suggested by their chemical structures and supported by animal studies. In observational studies, however, the association between flavonoids and breast cancer, and potential underlying mechanisms, remain unclear. OBJECTIVE: To examine the relationship between flavonoid intake and sex hormone levels using timed blood samples in follicular and luteal phases in the Nurses' Health Study II among premenopausal women. METHODS: Plasma concentrations of estrogens, androgens, progesterone, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), prolactin, and sex hormone-binding globulin (SHBG) were measured in samples collected between 1996 and 1999. Average flavonoid were calculated from semiquantitative food frequency questionnaires collected in 1995 and 1999. We used generalized linear models to calculate geometric mean hormone concentrations across categories of the intake of flavonoids and the subclasses. RESULTS: Total flavonoid intake generally was not associated with the hormones of interest. The only significant association was with DHEAS (p-trend = 0.02), which was 11.1% (95% confidence interval (CI): -18.6%, -3.0%) lower comparing the highest vs. lowest quartile of flavonoid intake. In subclass analyses, the highest (vs. lowest) quartile of flavan-3-ol intake was associated with significantly lower DHEAS concentrations (-11.3% with 95% CI: -18.3%, -3.7%, p-trend = 0.01), and anthocyanin intake was associated with a significant inverse trend for DHEA (-18.0% with 95% CI: -27.9%, -6.7%, p-trend = 0.003). CONCLUSION: Flavonoid intake in this population had limited impact on most plasma sex hormones in premenopausal women. Anthocyanins and flavan-3-ols were associated with lower levels of DHEA and DHEAS.

12.
J Natl Cancer Inst ; 2019 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-31593240

RESUMO

BACKGROUND: Experimental evidence supports a role of lipid dysregulation in ovarian cancer progression. We estimated associations with ovarian cancer risk for circulating levels of four lipid groups, previously hypothesized to be associated with ovarian cancer, measured 3-23 years before diagnosis. METHODS: Analyses were conducted among cases (N = 252) and matched controls (N = 252) from the Nurses' Health Studies. We used logistic regression adjusting for risk factors to investigate associations of lysophosphatidylcholines (LPC), phosphatidylcholines (PC), ceramides (CER), and sphingomyelins (SM) with ovarian cancer risk overall and by histotype. A modified Bonferroni approach (0.05/4=0.0125; 4 lipid groups) and the permutation-based Westfall and Young approach were used to account for testing multiple correlated hypotheses. Odds ratios (OR; 10th -90th percentile) and 95% confidence intervals of ovarian cancer risk were estimated. All statistical tests were two-sided. RESULTS: SM sum was statistically significantly associated with ovarian cancer risk (OR(95%CI)=1.97(1.16-3.32); p-value=0.01/permutation-adjusted-p=0.20). C16:0 SM, C18:0 SM, C16:0 CER were suggestively associated with risk (ORs: 1.95-2.10; p-values: 0.004-0.01/permutation-adjusted-p: 0.08-0.21). SM sum, C16:0 SM, and C16:0 CER had stronger ORs among postmenopausal women (OR range: 2.16-3.22). ORs were similar for serous/poorly differentiated and endometrioid/clear cell tumors, although C18:1 LPC and LPC to PC ratio were suggestively inversely, while C18:0 SM was suggestively positively associated with risk of endometrioid/clear cell tumors. No individual metabolites were associated with risk when using the permutation-based approach. CONCLUSION: Elevated levels of circulating SMs 3-23 years before diagnosis were associated with increased risk of ovarian cancer, regardless of histotype, with stronger associations among postmenopausal women. Further studies are required to validate and understand the role of lipid dysregulation in ovarian carcinogenesis.

13.
Cancer Epidemiol Biomarkers Prev ; 28(11): 1845-1852, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31387969

RESUMO

BACKGROUND: Regular aspirin use may lower ovarian cancer risk by blocking the cyclooxygenase enzymes, resulting in lower expression of prostaglandins, including prostaglandin E2 (PGE2). We evaluated whether higher prediagnosis PGE-M (a urinary biomarker of PGE2) was associated with increased ovarian cancer risk in three prospective cohorts. METHODS: We conducted a case-control study nested in the Nurses' Health Study (NHS), NHSII, and Shanghai Women's Health Study. Our analyses included 304 cases of epithelial ovarian cancer diagnosed from 1996 to 2015 and 600 matched controls. We measured urinary PGE-M using LC/MS with normalization to creatinine. Measures from each study were recalibrated to a common standard. We estimated ORs and 95% confidence intervals (CI) using conditional logistic regression, with PGE-M levels modeled in quartiles. Multivariable models were adjusted for ovarian cancer risk factors. RESULTS: There was no evidence of an association between urinary PGE-M levels and ovarian cancer risk for women with PGE-M levels in the top versus bottom quartile (OR = 0.80; 95% CI, 0.51-1.27; P trend = 0.37). We did not observe heterogeneity by histotype (P = 0.53), and there was no evidence of effect modification by body mass index (P interaction = 0.82), aspirin use (P interaction = 0.59), or smoking (P interaction = 0.14). CONCLUSIONS: Prediagnosis urinary PGE-M levels were not significantly associated with ovarian cancer risk. Larger sample sizes are needed to consider a more modest association and to evaluate associations for specific tumor subtypes. IMPACT: Systemic prostaglandin levels do not appear strongly associated with ovarian cancer risk. Future research into aspirin use and ovarian cancer risk should consider local prostaglandins and prostaglandin-independent mechanisms.

14.
Am J Epidemiol ; 188(11): 1932-1943, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31364705

RESUMO

We identified plasma metabolites associated with habitual physical activity among 5,197 US participants from the Nurses' Health Study (NHS), Nurses' Health Study II (NHS II), and the Health Professionals Follow-up Study (HPFS). Physical activity was assessed every 2-4 years via self-report questionnaires. Blood was collected in the NHS in 1989-1990, in NHS II during 1996-1999, and in the HPFS during 1993-1995. Metabolic profiling was conducted by liquid chromatography-mass spectrometry. Our study included 337 known metabolites, with 256 of them classified as lipids. We corrected for multiple testing by controlling the tail probability of the proportion of false positives (TPPFP) and accounted for correlated tests using bootstrapping. Physical activity was significantly associated with 20 metabolites after correction for multiple testing (TPPFP < 0.05), and positive associations were found for most of the metabolites, including 2 amino acids (citrulline and glycine), 4 cholesteryl esters (C18:2, C18:1, C16:0, C18:3), 8 phosphocholines (PCs) (C36:4 PC-A, C34:3 PC plasmalogen, C36:3 PC plasmalogen, C34:2 PC plasmalogen, C36:2 PC) and lysophosphatidylcholines (C18:2, C20:5, C18:1), and 3 phosphatidylethanolamines (PEs) (C38:3 PE plasmalogen) and lysophosphatidylethanolamines (C18:2, C18:1). We independently replicated the 20 metabolites among 2,305 women in the Women's Health Initiative using 1993 data, and half of the metabolites were replicated. Our study may help identify biomarkers of physical activity and provide insight into biological mechanisms underlying the beneficial effect of being physically active on cardiometabolic health.

15.
Metabolites ; 9(7)2019 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-31319517

RESUMO

The application of metabolomics technology to epidemiological studies is emerging as a new approach to elucidate disease etiology and for biomarker discovery. However, analysis of metabolomics data is complex and there is an urgent need for the standardization of analysis workflow and reporting of study findings. To inform the development of such guidelines, we conducted a survey of 47 cohort representatives from the Consortium of Metabolomics Studies (COMETS) to gain insights into the current strategies and procedures used for analyzing metabolomics data in epidemiological studies worldwide. The results indicated a variety of applied analytical strategies, from biospecimen and data pre-processing and quality control to statistical analysis and reporting of study findings. These strategies included methods commonly used within the metabolomics community and applied in epidemiological research, as well as novel approaches to pre-processing pipelines and data analysis. To help with these discrepancies, we propose use of open-source initiatives such as the online web-based tool COMETS Analytics, which includes helpful tools to guide analytical workflow and the standardized reporting of findings from metabolomics analyses within epidemiological studies. Ultimately, this will improve the quality of statistical analyses, research findings, and study reproducibility.

16.
Cancer Causes Control ; 30(9): 943-953, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31264139

RESUMO

PURPOSE: Epidemiologic evidence supports an association between high mammographic density and increased breast cancer risk yet etiologic mechanisms remain largely unknown. Mixed evidence exists as to whether circulating lipid levels influence mammographic density and breast cancer risk. Therefore, we examined these associations in the Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII), two large prospective cohorts with information on PMD and circulating lipid measures, long follow-up, and breast cancer risk factor and outcome data. METHODS: We conducted a nested case-control study among women in the NHS and NHSII. Percent mammographic density (PMD) was measured using Cumulus software, a computer-assisted method, on digitized film mammograms. Cross-sectional associations between circulating lipids [total cholesterol (n = 1,502), high-density lipoprotein (HDL-C; n = 579), and triglycerides (n = 655)] and PMD were evaluated among controls. All analyses were stratified by menopausal status at time of mammogram. Relative risks for breast cancer by lipid and PMD measures were estimated among postmenopausal women in the full nested case-control study (cases/controls for cholesterol, HDL-C, and triglycerides were 937/975, 416/449, and 506/537, respectively). RESULTS: There were no significant associations between circulating lipid levels and PMD among healthy women, irrespective of menopausal status. The association between PMD and breast cancer risk among postmenopausal women was not modified by circulating lipid levels (p interaction = 0.83, 0.80, and 0.34 for total cholesterol, HDL-C, and triglycerides, respectively). CONCLUSION: Overall, no association was observed between lipid levels and PMD, and there was no evidence that lipid levels modified the association between PMD and breast cancer risk.


Assuntos
Densidade da Mama , Neoplasias da Mama/epidemiologia , Lipídeos/sangue , Adulto , Mama/diagnóstico por imagem , Neoplasias da Mama/diagnóstico , Estudos de Casos e Controles , Feminino , Humanos , Mamografia , Pessoa de Meia-Idade , Enfermeiras e Enfermeiros , Pós-Menopausa , Risco
17.
Am J Epidemiol ; 188(6): 991-1012, 2019 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-31155658

RESUMO

The Consortium of Metabolomics Studies (COMETS) was established in 2014 to facilitate large-scale collaborative research on the human metabolome and its relationship with disease etiology, diagnosis, and prognosis. COMETS comprises 47 cohorts from Asia, Europe, North America, and South America that together include more than 136,000 participants with blood metabolomics data on samples collected from 1985 to 2017. Metabolomics data were provided by 17 different platforms, with the most frequently used labs being Metabolon, Inc. (14 cohorts), the Broad Institute (15 cohorts), and Nightingale Health (11 cohorts). Participants have been followed for a median of 23 years for health outcomes including death, cancer, cardiovascular disease, diabetes, and others; many of the studies are ongoing. Available exposure-related data include common clinical measurements and behavioral factors, as well as genome-wide genotype data. Two feasibility studies were conducted to evaluate the comparability of metabolomics platforms used by COMETS cohorts. The first study showed that the overlap between any 2 different laboratories ranged from 6 to 121 metabolites at 5 leading laboratories. The second study showed that the median Spearman correlation comparing 111 overlapping metabolites captured by Metabolon and the Broad Institute was 0.79 (interquartile range, 0.56-0.89).


Assuntos
Epidemiologia/organização & administração , Saúde Global , Metabolômica/organização & administração , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores , Índice de Massa Corporal , Criança , Métodos Epidemiológicos , Feminino , Comportamentos Relacionados com a Saúde , Testes Hematológicos , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Fatores Socioeconômicos , Adulto Jovem
18.
Curr Nutr Rep ; 8(3): 202, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31197622

RESUMO

The original version of this article was revised: "The article was published with errors on text as the author's corrections were misinterpreted."

19.
Eur J Epidemiol ; 34(7): 625-635, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31081539

RESUMO

We investigated the relationship between maternal history of nightshift work before and shift work during pregnancy and offspring risk of depression and anxiety, among mothers participating in the Nurses Health Study II and in their offspring enrolled in the Growing Up Today Study 2 between 2004 and 2013. Case definitions were based on offspring self-reports of physician/clinician-diagnosed depression and/or anxiety, regular antidepressant use and depressive symptoms assessed using the Center for Epidemiologic Studies Depression Scale. Multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using generalized estimating equation models. We found no associations between maternal nightshift work before pregnancy or during pregnancy and offspring mental health disorders (e.g., nightshift work before pregnancy: depression (based on physician/clinician diagnosis): ORever nightwork = 1.14; 95% CI, 0.88-1.47; either depression or anxiety: ORever nightwork = 0.93; 95% CI, 0.81-1.08; nightshift work during pregnancy: depression: ORever nightwork = 1.14; 95% CI, 0.68-1.94; depression or anxiety: ORever nightwork =1.17; 95% CI, 0.70-1.98) and no dose-response relationship with longer history of nightshift work (all PTrend >0.10). Stratifying by maternal chronotype revealed a higher risk of depression for offspring whose mothers worked nightshifts before pregnancy and reported being definite morning chronotypes (a proxy for circadian strain) (ORever nightwork = 1.95; 95% CI, 1.17, 3.24 vs. ORever nightwork = 0.93; 95% CI, 0.68, 1.28 for any other chronotype; PInteraction = 0.03). Further studies replicating our findings and refined understanding regarding the interplay of nightshift work and chronotype and its potential influences on offspring mental health are needed.


Assuntos
Crianças Adultas/psicologia , Ansiedade/epidemiologia , Transtornos Cronobiológicos , Depressão/epidemiologia , Mães/psicologia , Jornada de Trabalho em Turnos/efeitos adversos , Adolescente , Adulto , Ansiedade/fisiopatologia , Depressão/fisiopatologia , Feminino , Humanos , Masculino , Gravidez , Fatores de Risco , Adulto Jovem
20.
J Nutr ; 149(7): 1215-1221, 2019 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-31095304

RESUMO

BACKGROUND: Intake of nuts has been inversely associated with risk of type 2 diabetes and cardiovascular disease, partly through inducing a healthy lipid profile. How nut intake may affect lipid metabolites remains unclear. OBJECTIVE: The aim of this study was to identify the plasma lipid metabolites associated with habitual nut consumption in US men and women. METHODS: We analyzed cross-sectional data from 1099 participants in the Nurses' Health Study (NHS), NHS II, and Health Professionals Follow-up Study. Metabolic profiling was conducted on plasma by LC-mass spectrometry. Nut intake was estimated from food-frequency questionnaires. We included 144 known lipid metabolites that had CVs ≤25%. Multivariate linear regression was used to assess the associations of nut consumption with individual plasma lipid metabolites. RESULTS: We identified 17 lipid metabolites that were significantly associated with nut intake, based on a 1 serving (28 g)/d increment in multivariate models [false discovery rate (FDR) P value <0.05]. Among these species, 8 were positively associated with nut intake [C24:0 sphingomyelin (SM), C36:3 phosphatidylcholine (PC) plasmalogen-A, C36:2 PC plasmalogen, C24:0 ceramide, C36:1 PC plasmalogen, C22:0 SM, C34:1 PC plasmalogen, and C36:2 phosphatidylethanolamine plasmalogen], with changes in relative metabolite level (expressed in number of SDs on the log scale) ranging from 0.36 to 0.46 for 1 serving/d of nuts. The other 9 metabolites were inversely associated with nut intake with changes in relative metabolite level ranging from -0.34 to -0.44. In stratified analysis, 3 metabolites were positively associated with both peanuts and peanut butter (C24:0 SM, C24:0 ceramide, and C22:0 SM), whereas 6 metabolites were inversely associated with other nuts (FDR P value <0.05). CONCLUSIONS: A panel of lipid metabolites was associated with intake of nuts, which may provide insight into biological mechanisms underlying associations between nuts and cardiometabolic health. Metabolites that were positively associated with intake of nuts may be helpful in identifying potential biomarkers of nut intake.

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