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Ioanna Tzoulaki - One of the best experts on this subject based on the ideXlab platform.

  • early exposure to social disadvantages and later life body mass index beyond Genetic Predisposition in three generations of finnish birth cohorts
    BMC Public Health, 2020
    Co-Authors: Estelle Lowry, Nina Rautio, Niko Wasenius, Tom Bond, Jari Lahti, Ioanna Tzoulaki
    Abstract:

    The study aimed to explore the association between early life and life-course exposure to social disadvantage and later life body mass index (BMI) accounting for Genetic Predisposition and maternal BMI. We studied participants of Helsinki Birth Cohort Study born in 1934–1944 (HBCS1934–1944, n = 1277) and Northern Finland Birth Cohorts born in 1966 and 1986 (NFBC1966, n = 5807, NFBC1986, n = 6717). Factor analysis produced scores of social disadvantage based on social and economic elements in early life and adulthood/over the life course, and was categorized as high, intermediate and low. BMI was measured at 62 years in HBCS1934–1944, at 46 years in NFBC1966 and at 16 years in NFBC1986. Multivariable linear regression analysis was used to explore associations between social disadvantages and BMI after adjustments for polygenic risk score for BMI (PRS BMI), maternal BMI and sex. The association between exposure to high early social disadvantage and increased later life BMI persisted after adjustments (β = 0.79, 95% CI, 0.33, 1.25, p < 0.001) in NFBC1966. In NFBC1986 this association was attenuated by PRS BMI (p = 0.181), and in HBCS1934–1944 there was no association between high early social disadvantage and increased later life BMI (β 0.22, 95% CI –0.91,1.35, p = 0.700). In HBCS1934–1944 and NFBC1966, participants who had reduced their exposure to social disadvantage during the life-course had lower later life BMI than those who had increased their exposure (β − 1.34, [− 2.37,-0.31], p = 0.011; β − 0.46, [− 0.89,-0.03], p = 0.038, respectively). High social disadvantage in early life appears to be associated with higher BMI in later life. Reducing exposure to social disadvantage during the life-course may be a potential pathway for obesity reduction.

Tiange Wang - One of the best experts on this subject based on the ideXlab platform.

  • habitual coffee consumption and Genetic Predisposition to obesity gene diet interaction analyses in three us prospective studies
    BMC Medicine, 2017
    Co-Authors: Tao Huang, Yan Zheng, Tiange Wang, Jae H Kang, Majken K Jensen, Janey L Wiggs, Louis R Pasquale, Charles S Fuchs
    Abstract:

    Abstract Background Whether habitual coffee consumption interacts with the Genetic Predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. Methods We analyzed the interactions between Genetic Predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The Genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. Results The Genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS ( P interaction  = 0.023) and NHS ( P interaction  = 0.039); similar results were replicated in the WHI ( P interaction  = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m 2 for coffee consumption of   3 cup(s)/day, respectively ( P interaction P interaction  = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m 2 across tertiles of the Genetic risk score. Conclusions Higher coffee consumption might attenuate the Genetic associations with BMI and obesity risk, and individuals with greater Genetic Predisposition to obesity appeared to have lower BMI associated with higher coffee consumption.

  • habitual coffee consumption and Genetic Predisposition to obesity gene diet interaction analyses in three us prospective studies
    BMC Medicine, 2017
    Co-Authors: Tao Huang, Yan Zheng, Tiange Wang, Jae H Kang, Majken K Jensen, Janey L Wiggs, Louis R Pasquale, Charles S Fuchs
    Abstract:

    Whether habitual coffee consumption interacts with the Genetic Predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. We analyzed the interactions between Genetic Predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The Genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. The Genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS (P interaction  = 0.023) and NHS (P interaction  = 0.039); similar results were replicated in the WHI (P interaction  = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m2 for coffee consumption of   3 cup(s)/day, respectively (P interaction  < 0.001). Such interaction was partly due to slightly higher BMI with higher coffee consumption among participants at lower Genetic risk and slightly lower BMI with higher coffee consumption among those at higher Genetic risk. Each increment of 10-risk allele was associated with 78% (95% confidence interval (CI), 59–99%), 48% (95% CI, 36–62%), and 43% (95% CI, 28–59%) increased risk for obesity across these subgroups of coffee consumption (P interaction  = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m2 across tertiles of the Genetic risk score. Higher coffee consumption might attenuate the Genetic associations with BMI and obesity risk, and individuals with greater Genetic Predisposition to obesity appeared to have lower BMI associated with higher coffee consumption.

Louis R Pasquale - One of the best experts on this subject based on the ideXlab platform.

  • habitual coffee consumption and Genetic Predisposition to obesity gene diet interaction analyses in three us prospective studies
    BMC Medicine, 2017
    Co-Authors: Tao Huang, Yan Zheng, Tiange Wang, Jae H Kang, Majken K Jensen, Janey L Wiggs, Louis R Pasquale, Charles S Fuchs
    Abstract:

    Abstract Background Whether habitual coffee consumption interacts with the Genetic Predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. Methods We analyzed the interactions between Genetic Predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The Genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. Results The Genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS ( P interaction  = 0.023) and NHS ( P interaction  = 0.039); similar results were replicated in the WHI ( P interaction  = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m 2 for coffee consumption of   3 cup(s)/day, respectively ( P interaction P interaction  = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m 2 across tertiles of the Genetic risk score. Conclusions Higher coffee consumption might attenuate the Genetic associations with BMI and obesity risk, and individuals with greater Genetic Predisposition to obesity appeared to have lower BMI associated with higher coffee consumption.

  • habitual coffee consumption and Genetic Predisposition to obesity gene diet interaction analyses in three us prospective studies
    BMC Medicine, 2017
    Co-Authors: Tao Huang, Yan Zheng, Tiange Wang, Jae H Kang, Majken K Jensen, Janey L Wiggs, Louis R Pasquale, Charles S Fuchs
    Abstract:

    Whether habitual coffee consumption interacts with the Genetic Predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. We analyzed the interactions between Genetic Predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The Genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. The Genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS (P interaction  = 0.023) and NHS (P interaction  = 0.039); similar results were replicated in the WHI (P interaction  = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m2 for coffee consumption of   3 cup(s)/day, respectively (P interaction  < 0.001). Such interaction was partly due to slightly higher BMI with higher coffee consumption among participants at lower Genetic risk and slightly lower BMI with higher coffee consumption among those at higher Genetic risk. Each increment of 10-risk allele was associated with 78% (95% confidence interval (CI), 59–99%), 48% (95% CI, 36–62%), and 43% (95% CI, 28–59%) increased risk for obesity across these subgroups of coffee consumption (P interaction  = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m2 across tertiles of the Genetic risk score. Higher coffee consumption might attenuate the Genetic associations with BMI and obesity risk, and individuals with greater Genetic Predisposition to obesity appeared to have lower BMI associated with higher coffee consumption.

  • television watching leisure time physical activity and the Genetic Predisposition in relation to body mass index in women and men
    Circulation, 2012
    Co-Authors: Andrea K Chomistek, Jae H Kang, Louis R Pasquale, Gary C Curhan, Walter C Willett, Eric B Rimm
    Abstract:

    Background—Previous studies on gene-lifestyle interaction and obesity have focused mostly on the FTO gene and physical activity, whereas little attention has been paid to sedentary behavior as indicated by television (TV) watching. Methods and Results—We analyzed interactions between TV watching, leisure time physical activity, and Genetic Predisposition in relation to body mass index (BMI) in 7740 women and 4564 men from 2 prospective cohorts: The Nurses' Health Study and the Health Professionals Follow-up Study. Data on physical activity and TV watching were collected 2 years before assessment of BMI. A weighted Genetic risk score was calculated on the basis of 32 established BMI-associated variants. In both women and men, the Genetic associations with BMI strengthened with increased hours of TV watching. An increment of 10 points in the weighted Genetic risk score was associated with 0.8 (SE, 0.4), 0.8 (SE, 0.2), 1.4 (SE, 0.2), 1.5 (SE, 0.2), and 3.4 (SE, 1.0) kg/m2 higher BMI across the 5 categories o...

Liming Liang - One of the best experts on this subject based on the ideXlab platform.

  • association of obesity and its Genetic Predisposition with the risk of severe covid 19 analysis of population based cohort data
    Metabolism-clinical and Experimental, 2020
    Co-Authors: Zhaozhong Zhu, Kohei Hasegawa, Michimasa Fujiogi, Carlos A Camargo, Liming Liang
    Abstract:

    Abstract Objective We aimed to examine the associations of obesity-related traits (body mass index [BMI], central obesity) and their Genetic Predisposition with the risk of developing severe COVID-19 in a population-based data. Research design and methods We analyzed data from 489,769 adults enrolled in the UK Biobank—a population-based cohort study. The exposures of interest are BMI categories and central obesity (e.g., larger waist circumference). Using genome-wide genotyping data, we also computed polygenic risk scores (PRSs) that represent an individual's overall Genetic risk for each obesity trait. The outcome was severe COVID-19, defined by hospitalization for laboratory-confirmed COVID-19. Results Of 489,769 individuals, 33% were normal weight (BMI, 18.5–24.9 kg/m2), 43% overweight (25.0–29.9 kg/m2), and 24% obese (≥30.0 kg/m2). The UK Biobank identified 641 patients with severe COVID-19. Compared to adults with normal weight, those with a higher BMI had a dose-response increases in the risk of severe COVID-19, with the following adjusted ORs: for 25.0–29.9 kg/m2, 1.40 (95%CI 1.14–1.73; P = 0.002); for 30.0–34.9 kg/m2, 1.73 (95%CI 1.36–2.20; P  Conclusions In this large population-based cohort, individuals with more-severe obesity, central obesity, or Genetic Predisposition for obesity are at higher risk of developing severe-COVID-19.

  • Genetic Predisposition to dyslipidemia and type 2 diabetes risk in two prospective cohorts
    Diabetes, 2012
    Co-Authors: Liming Liang, Alessandro Doria
    Abstract:

    Dyslipidemia has been associated with type 2 diabetes, but it remains unclear whether dyslipidemia plays a causal role in type 2 diabetes. We aimed to examine the association between the Genetic Predisposition to dyslipdemia and type 2 diabetes risk. The current study included 2,447 patients with type 2 diabetes and 3,052 control participants of European ancestry from the Nurses’ Health Study and the Health Professionals Follow-up Study. Genetic Predisposition to dyslipidemia was estimated by three genotype scores of lipids (LDL cholesterol, HDL cholesterol, and triglycerides) on the basis of the established loci for blood lipids. Linear relation analysis indicated that the HDL cholesterol and triglyceride genotype scores, but not the LDL cholesterol genotype score, were linearly related to elevated type 2 diabetes risk. Each point of the HDL cholesterol and triglyceride genotype scores was associated with a 3% (odds ratio [OR] 1.03 [95% CI 1.01–1.04]) and a 2% (1.02 [1.00–1.04]) increased risk of developing type 2 diabetes, respectively. The ORs were 1.39 (1.17–1.65) and 1.19 (1.01–1.41) for type 2 diabetes by comparing extreme quartiles of the HDL cholesterol genotype score and triglyceride genotype score, respectively. In conclusion, Genetic Predisposition to low HDL cholesterol or high triglycerides is related to elevated type 2 diabetes risk.

Yan Zheng - One of the best experts on this subject based on the ideXlab platform.

  • habitual use of fish oil supplements Genetic Predisposition and risk of fractures a large population based study
    The American Journal of Clinical Nutrition, 2021
    Co-Authors: Zhendong Mei, Guochong Chen, Chenhao Lin, Zhonghan Sun, Chenglin Liu, Xin Geng, Changzheng Yuan, Yan Zheng
    Abstract:

    BACKGROUND Epidemiologic studies have suggested an inverse association between circulating concentrations of long-chain ω-3 PUFAs and fracture risk. However, whether supplementation of long-chain ω-3 PUFA (i.e. fish oil) is associated with fracture risk, and whether the association is modified by Genetic Predisposition to fracture risk remain unclear. OBJECTIVES To evaluate the associations of habitual fish oil supplement use with fracture risk, and to explore the potential effect modification by Genetic Predisposition. METHODS This study included 492,713 participants from the UK Biobank who completed a questionnaire on habitual fish oil supplement use between 2006 and 2010. HRs and 95% CIs for fractures were estimated from multivariable Cox proportional hazards models. A weighted fracture-Genetic risk score (GRS) was derived from 14 validated single nucleotide polymorphisms. RESULTS During a median follow-up of 8.1 y, 12,070 incident fractures occurred among participants free of fracture at baseline (n = 441,756). Compared with nonuse, habitual use of fish oil supplements was associated with a lower risk of total fractures (HR = 0.93; 95% CI: 0.89, 0.97), hip fractures (HR = 0.83; 95% CI: 0.75, 0.92), and vertebrae fractures (HR = 0.85; 95% CI: 0.72, 0.99). The inverse association for total fractures was more pronounced among participants having a higher fracture-GRS than among those with a lower fracture-GRS (P-interaction <0.001). Among participants with a history of fracture at baseline (n = 50,957), fish oil use was associated with a lower risk of total recurrent fractures (HR = 0.88; 95% CI: 0.82, 0.96) and vertebrae recurrent fractures (HR = 0.64; 95% CI: 0.46, 0.88) but not with hip fracture recurrence. CONCLUSIONS Our findings suggest that habitual fish oil supplement use is associated with lower risks of both incident and recurrent fractures. The inverse associations of fish oil use with total fractures appeared to be more pronounced among individuals at higher Genetic risk of fractures than those with lower Genetic risk.

  • habitual coffee consumption and Genetic Predisposition to obesity gene diet interaction analyses in three us prospective studies
    BMC Medicine, 2017
    Co-Authors: Tao Huang, Yan Zheng, Tiange Wang, Jae H Kang, Majken K Jensen, Janey L Wiggs, Louis R Pasquale, Charles S Fuchs
    Abstract:

    Whether habitual coffee consumption interacts with the Genetic Predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. We analyzed the interactions between Genetic Predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The Genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. The Genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS (P interaction  = 0.023) and NHS (P interaction  = 0.039); similar results were replicated in the WHI (P interaction  = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m2 for coffee consumption of   3 cup(s)/day, respectively (P interaction  < 0.001). Such interaction was partly due to slightly higher BMI with higher coffee consumption among participants at lower Genetic risk and slightly lower BMI with higher coffee consumption among those at higher Genetic risk. Each increment of 10-risk allele was associated with 78% (95% confidence interval (CI), 59–99%), 48% (95% CI, 36–62%), and 43% (95% CI, 28–59%) increased risk for obesity across these subgroups of coffee consumption (P interaction  = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m2 across tertiles of the Genetic risk score. Higher coffee consumption might attenuate the Genetic associations with BMI and obesity risk, and individuals with greater Genetic Predisposition to obesity appeared to have lower BMI associated with higher coffee consumption.

  • habitual coffee consumption and Genetic Predisposition to obesity gene diet interaction analyses in three us prospective studies
    BMC Medicine, 2017
    Co-Authors: Tao Huang, Yan Zheng, Tiange Wang, Jae H Kang, Majken K Jensen, Janey L Wiggs, Louis R Pasquale, Charles S Fuchs
    Abstract:

    Abstract Background Whether habitual coffee consumption interacts with the Genetic Predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. Methods We analyzed the interactions between Genetic Predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The Genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. Results The Genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS ( P interaction  = 0.023) and NHS ( P interaction  = 0.039); similar results were replicated in the WHI ( P interaction  = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m 2 for coffee consumption of   3 cup(s)/day, respectively ( P interaction P interaction  = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m 2 across tertiles of the Genetic risk score. Conclusions Higher coffee consumption might attenuate the Genetic associations with BMI and obesity risk, and individuals with greater Genetic Predisposition to obesity appeared to have lower BMI associated with higher coffee consumption.

  • Genetic Predisposition to central obesity and risk of type 2 diabetes two independent cohort studies
    Diabetes Care, 2015
    Co-Authors: Tao Huang, Yan Zheng, Sylvia H Ley, Joann E Manson
    Abstract:

    OBJECTIVE Abdominal obesity is a major risk factor for type 2 diabetes (T2D). We aimed to examine the association between the Genetic Predisposition to central obesity, assessed by the waist-to-hip ratio (WHR) Genetic score, and T2D risk. RESEARCH DESIGN AND METHODS The current study included 2,591 participants with T2D and 3,052 participants without T2D of European ancestry from the Nurses’ Health Study (NHS) and the Health Professionals Follow-up Study (HPFS). Genetic Predisposition to central obesity was estimated using a Genetic score based on 14 established loci for the WHR. RESULTS We found that the central obesity Genetic score was linearly related to higher T2D risk. Results were similar in the NHS (women) and HPFS (men). In combined results, each point of the central obesity Genetic score was associated with an odds ratio (OR) of 1.04 (95% CI 1.01–1.07) for developing T2D, and the OR was 1.24 (1.03–1.45) when comparing extreme quartiles of the Genetic score after multivariate adjustment. CONCLUSIONS The data indicate that Genetic Predisposition to central obesity is associated with higher T2D risk. This association is mediated by central obesity.