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1.
Front Psychol ; 14: 1108093, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37621933

RESUMEN

Background: Studies examining weight change patterns and depression are scarce and report inconsistent findings. This study-aimed to elucidate the association between weight change patterns and the risk of depression in a large, representative sample of US adults. Methods: Data from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 was analyzed. Five weight change groups were categorized: stable normal, weight loss, weight gain, maximum overweight, and stable obesity. Depression was ascertained using the validated Patient Health Questionnaire (PHQ-9) and depression was defined as PHQ score ≥ 10. Results: A total of 17,556 participants were included. Compared with participants who maintained normal weight, stable obesity participants had increased risks of depression across adulthood from age 25 years to 10 years before the survey (OR = 1.61, 95% CI =1.23 to 2.11), in the 10 years period before the survey (OR = 2.15, 95% CI =1.71 to 2.70), and from age 25 years to survey (OR = 1.88, 95% CI =1.44 to 2.44). Weight gain was associated with an increased risk of depression from age 25 years to 10 years before the survey (OR = 1.71, 95% CI = 1.41 to 2.04), in the 10 years period before the survey (OR = 1.73, 95% CI = 1.35 to 2.21), and for the period from age 25 years to survey (OR = 1.83, 95% CI = 1.49 to 2.24). In the stratified analyses, we found statistically significant interactions with sex. Conclusion: Our study suggested that stable obesity and weight gain across adulthood were associated with increased risks of depression.

2.
Saudi J Gastroenterol ; 29(1): 39-46, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-36254930

RESUMEN

Background: Accumulated studies have shown that low expression of 25-hydroxyvitamin D [25(OH)D] was significantly associated with the risk of non-alcoholic fatty liver disease (NAFLD). However, the exact causality is still unknown. The aim of this study was to investigate whether levels of 25(OH)D are associated with risk of NAFLD, using a two-sample Mendelian randomization (MR). Methods: Data from a recent large vitamin D genome-wide association study (GWAS) on 417,580 Europeans were utilized, and the largest published histology-based NAFLD GWAS study (1,483 cases and 17,781 healthy controls) for genetic variants predicted to cause NAFLD were searched. All genetic datasets for the MR analyses were obtained using publicly available summary statistics based on individuals of European ancestry from the MR-Base and NHGRI-EBI GWAS Catalog database. Inverse-variance weighted (IVW) MR approach was used to estimate causal effects in the main analysis, complemented by 4 additional methods to control for pleiotropy. Sensitivity analyses were conducted to verify whether heterogeneity and pleiotropy can bias the MR results. Results: The MR analysis did not provide strong evidence for the causal association of circulating 25(OH)D with NAFLD by IVW method (OR = 0.746, 95%CI 0.517-1.078; P = 0.119). The results were consistent using four other MR methods. Sensitivity analysis using all different analytical approaches yielded similar results. There was no evidence for pleiotropy (MR-Egger intercept: -0.0003758, P = 0.970). The replication process also showed consistent results using IVW method (P = 0.710). Conclusion: This study indicates that serum 25(OH)D levels did not possess an obvious effect on the risk of NAFLD. The associations in previous studies may be due to residual confounding or reverse causation.


Asunto(s)
Enfermedad del Hígado Graso no Alcohólico , Humanos , Enfermedad del Hígado Graso no Alcohólico/epidemiología , Enfermedad del Hígado Graso no Alcohólico/genética , Estudio de Asociación del Genoma Completo , Análisis de la Aleatorización Mendeliana , Polimorfismo de Nucleótido Simple , Vitamina D/genética
3.
Front Nutr ; 9: 993425, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36466397

RESUMEN

Background: Telomere length, which is related to chronic diseases and premature mortality, is influenced by dietary factors. Zinc is known as a dietary antioxidant micronutrient, however, its impact on telomere length remains unclear. Objective: We aimed to examine the potential effect of dietary zinc intake on telomere length among middle-aged and older individuals in the US. Materials and methods: Our study included 3,793 US participants aged 45 years and older from the 1999 to 2002 National Health and Nutrition Examination Survey (NHANES). 24-h dietary recall interviews were employed to evaluate zinc consumption. Leukocyte telomere length was assessed by real-time quantitative polymerase chain reaction (qPCR). We adopted generalized linear models to investigate the effect of dietary zinc intake on telomere length, and subgroup analyses were further applied. We further evaluated the dose-response relationship using restricted cubic spline analysis. Results: Among the 3,793 participants, the average telomere length was 0.926 ± 0.205 (T/S ratio) or 5509.5 ± 494.9 (bp). After adjusting for major confounders, every 5 mg increment in dietary zinc consumption was related to 0.64% (95% CI: 0.17%, 1.10%) longer telomere length. In the subgroup analyses, significant relationships were found in females (Percentage change: 1.11%; 95% CI: 0.48%, 1.75%), obese (Percentage change: 0.88%; 95% CI: 0.26%, 1.50%), and low energy intake individuals (Percentage change: 0.99%; 95% CI: 0.51%, 1.46%). Additionally, we revealed a positive linear relationship between dietary zinc intake and telomere length (P for non-linearity = 0.636). Conclusion: Our study revealed that elevated dietary zinc intake was significantly related to longer telomere length among adults aged 45 years and older in the US. And the association was more pronounced in females, obese, and low energy intake individuals.

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