scholarly journals Baseline vitamin D status, sleep patterns, and the risk of incident type 2 diabetes in data from the UK Biobank study

2020 ◽  
Author(s):  
Mengying Wang ◽  
Tao Zhou ◽  
Xiang Li ◽  
Hao Ma ◽  
Zhaoxia Liang ◽  
...  

<b>Background: </b>Circulating vitamin D concentrations have been associated with the risk of type 2 diabetes (T2D), but the results are inconsistent. Emerging evidence suggests that vitamin D metabolism is linked to sleep behaviors. We investigated the prospective association between serum 25-hydroxyvitamin D (25OHD) and the risk of incident T2D, and whether such association was modified by sleep behaviors. <p><b>Research design and methods: </b>The study included 350 211 individuals free of diabetes in the UK Biobank. Serum 25OHD (nmol/L) concentrations were measured. Five sleep behaviors including sleep duration, insomnia, snoring, chronotype, and daytime sleepiness were included to generate overall sleep patterns, defined by healthy sleep scores. We also calculated genetic risk scores of sleep patterns.<b> </b></p> <p><b>Results:</b> During a median follow-up of 8.1 years, we documented 6940 incident T2D cases. We found that serum 25OHD were significantly associated with a lower risk of incident T2D, and the multivariate adjusted hazard ratio (HR; 95% confidence interval [CI]) for per 10 nmol/L increase was 0.88 (0.87-0.90). We found a significant interaction between 25OHD and overall sleep patterns on the risk of incident T2D (<i>P</i> for interaction=0.002). The inverse association between high 25OHD and T2D was more prominent among participants with healthier sleep patterns. Among the individual sleep behaviors, daytime sleepiness showed the strongest interaction with 25OHD (<i>P</i> for interaction=0.0006). The reduced HR of T2D associated with high 25OHD appeared to be more evident among participants with no frequent daytime sleepiness compared with those with excessive daytime sleepiness. The genetic variations of the sleep patterns did not modify the relation between 25OHD and T2D. </p> <p><b>Conclusions: </b>Our study indicates that higher serum 25OHD concentrations are associated with a lower risk of incident T2D; and such relations are modified by overall sleep patterns, with daytime sleepiness being the major contributor. </p>

2020 ◽  
Author(s):  
Mengying Wang ◽  
Tao Zhou ◽  
Xiang Li ◽  
Hao Ma ◽  
Zhaoxia Liang ◽  
...  

<b>Background: </b>Circulating vitamin D concentrations have been associated with the risk of type 2 diabetes (T2D), but the results are inconsistent. Emerging evidence suggests that vitamin D metabolism is linked to sleep behaviors. We investigated the prospective association between serum 25-hydroxyvitamin D (25OHD) and the risk of incident T2D, and whether such association was modified by sleep behaviors. <p><b>Research design and methods: </b>The study included 350 211 individuals free of diabetes in the UK Biobank. Serum 25OHD (nmol/L) concentrations were measured. Five sleep behaviors including sleep duration, insomnia, snoring, chronotype, and daytime sleepiness were included to generate overall sleep patterns, defined by healthy sleep scores. We also calculated genetic risk scores of sleep patterns.<b> </b></p> <p><b>Results:</b> During a median follow-up of 8.1 years, we documented 6940 incident T2D cases. We found that serum 25OHD were significantly associated with a lower risk of incident T2D, and the multivariate adjusted hazard ratio (HR; 95% confidence interval [CI]) for per 10 nmol/L increase was 0.88 (0.87-0.90). We found a significant interaction between 25OHD and overall sleep patterns on the risk of incident T2D (<i>P</i> for interaction=0.002). The inverse association between high 25OHD and T2D was more prominent among participants with healthier sleep patterns. Among the individual sleep behaviors, daytime sleepiness showed the strongest interaction with 25OHD (<i>P</i> for interaction=0.0006). The reduced HR of T2D associated with high 25OHD appeared to be more evident among participants with no frequent daytime sleepiness compared with those with excessive daytime sleepiness. The genetic variations of the sleep patterns did not modify the relation between 25OHD and T2D. </p> <p><b>Conclusions: </b>Our study indicates that higher serum 25OHD concentrations are associated with a lower risk of incident T2D; and such relations are modified by overall sleep patterns, with daytime sleepiness being the major contributor. </p>


PLoS Medicine ◽  
2022 ◽  
Vol 19 (1) ◽  
pp. e1003906
Author(s):  
Tingting Geng ◽  
Qi Lu ◽  
Zhenzhen Wan ◽  
Jingyu Guo ◽  
Liegang Liu ◽  
...  

Background Several epidemiological studies have suggested that vitamin D status is associated with risk of dementia in general populations. However, due to the synergistic effect between diabetic pathology and neuroinflammation, and the prothrombotic profile in patients with diabetes, whether vitamin D is associated with risk of dementia among patients with diabetes is unclear. This study aimed to investigate the associations of circulating vitamin D levels with risks of all-cause dementia, Alzheimer disease (AD), and vascular dementia (VD) among adults with type 2 diabetes (T2D). Methods and findings This study included 13,486 individuals (≥60 years) with T2D and free of dementia at recruitment (2006–2010) from the UK Biobank study. Serum 25-hydroxyvitamin D (25[OH]D) concentrations were measured using the chemiluminescent immunoassay method at recruitment. Serum 25(OH)D ≥ 75 nmol/L was considered sufficient, according to the Endocrine Society Clinical Practice Guidelines. Incidence of all-cause dementia, AD, and VD cases was ascertained using electronic health records (EHRs). Each participant’s person-years at risk were calculated from the date of recruitment to the date that dementia was reported, date of death, date of loss to follow-up, or 28 February 2018, whichever occurred first. Among the 13,486 individuals with T2D (mean age, 64.6 years; men, 64.3%), 38.3% had vitamin D ≥ 50 nmol/L and only 9.1% had vitamin D ≥ 75 nmol/L. During a mean follow-up of 8.5 years, we observed 283 cases of all-cause dementia, including 101 AD and 97 VD cases. Restricted cubic spline analysis demonstrated a nonlinear relationship between serum 25(OH)D and risk of all-cause dementia (Pnonlinearity < 0.001) and VD (Pnonlinearity = 0.007), and the nonlinear association reached borderline significance for AD (Pnonlinearity = 0.06), with a threshold at around a serum 25(OH)D value of 50 nmol/L for all the outcomes. Higher serum levels of 25(OH)D were significantly associated with a lower risk of all-cause dementia, AD, and VD. The multivariate hazard ratios and 95% confidence intervals for participants who had serum 25(OH)D ≥ 50 nmol/L, compared with those who were severely deficient (25[OH]D < 25 nmol/L), were 0.41 (0.29–0.60) for all-cause dementia (Ptrend < 0.001), 0.50 (0.27–0.92) for AD (Ptrend = 0.06), and 0.41 (0.22–0.77) for VD (Ptrend = 0.01). The main limitation of the current analysis was the potential underreporting of dementia cases, as the cases were identified via EHRs. Conclusions In this study, we observed that higher concentrations of serum 25(OH)D were significantly associated with a lower risk of all-cause dementia, AD, and VD among individuals with T2D. Our findings, if confirmed by replication, may have relevance for dementia prevention strategies that target improving or maintaining serum vitamin D concentrations among patients with T2D.


Diabetes Care ◽  
2020 ◽  
Vol 43 (11) ◽  
pp. 2776-2784
Author(s):  
Mengying Wang ◽  
Tao Zhou ◽  
Xiang Li ◽  
Hao Ma ◽  
Zhaoxia Liang ◽  
...  

Diabetes Care ◽  
2018 ◽  
Vol 41 (4) ◽  
pp. 762-769 ◽  
Author(s):  
Céline Vetter ◽  
Hassan S. Dashti ◽  
Jacqueline M. Lane ◽  
Simon G. Anderson ◽  
Eva S. Schernhammer ◽  
...  

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim V Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  

Background: Coffee intake has been linked to lower type 2 diabetes (T2D) risk. We hypothesized this may be mediated by coffee’s effects on inflammation. Methods: Using participants from the UK Biobank (UKB n=145370) and Rotterdam Study (RS n=7172) cohorts, we studied associations of coffee intake with incident T2D; longitudinally measured insulin resistance (HOMA IR); serum levels of inflammation markers; and the mediating role of inflammation. Statistical regression models were adjusted for sociodemographic, lifestyle and health factors. Results: The median follow up was 7 (UKB) and 9 (RS) years. An increase of one coffee cup/day was associated with 4-6% lower T2D risk (RS HR=0.94 [95% CI 0.90; 0.98]; UKB HR=0.96 [0.94; 0.98]); lower HOMA IR (RS β=-0.017 [-0.024; -0.010]); with lower C reactive protein (CRP) and higher adiponectin (Figure1). Consumers of filtered coffee had the lowest T2D risk (UKB HR=0.88 [0.83; 0.93]). CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D (Figure 1). Conclusions: We suggest that coffee’s beneficial effects on lower T2D risk are partially mediated by improvements in systemic inflammation.Figure 1. a CRP and a adiponectin refer to the effect of coffee intake on CRP and adiponectin levels. a CRP RS : β=-0.014 (-0.022; -0.005); UKBB a CRP UKB : β=-0.011 (-0.012; -0.009) and RS a adiponectin : β=0.025 (0.007; 0.042). b CRP and b adiponectin refer to the effect of coffee related levels in CRP and adiponectin on incident T2D, independent of coffee. RS b CRP : HR=1.17 (1.04; 1.31); UKB b CRP : HR=1.45 (1.37; 1.54); and b adiponectin : HR=0.58 (0.32; 0.83). c′ refers to coffee’ effect on T2D going directly or via others mediators. UKB c′ independent of CRP : HR=0.96 (0.94; 0.99); RS c′ independent of CRP : HR=0.94 (0.90; 0.99); and RS c′ independent of CRP+adiponectin : HR=0.90 (0.80; 1.01). Coffee related changes in CRP may partially explain the beneficial link between coffee and T2D, mediating a 3.4% (0.6; 4.8, RS) and 9.6% (5.7; 24.4, UKB). Evidence of mediation was also found for adiponectin.


SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A377-A377
Author(s):  
C Vetter ◽  
HS Dashti ◽  
JM Lane ◽  
SG Anderson ◽  
ES Schernhammer ◽  
...  
Keyword(s):  

Diabetes Care ◽  
2018 ◽  
Vol 41 (9) ◽  
pp. 1878-1886 ◽  
Author(s):  
David A. Jenkins ◽  
Jack Bowden ◽  
Heather A. Robinson ◽  
Naveed Sattar ◽  
Ruth J.F. Loos ◽  
...  

2010 ◽  
Vol 64 (3) ◽  
pp. 351-355 ◽  
Author(s):  
A. A. Tahrani ◽  
A. Ball ◽  
L. Shepherd ◽  
A. Rahim ◽  
A. F. Jones ◽  
...  

2016 ◽  
Vol 9 ◽  
pp. CMED.S39427 ◽  
Author(s):  
Fernando Gondim ◽  
Ana Caribé ◽  
Karine Ferreira Vasconcelos ◽  
Alexandre Dantas Segundo ◽  
Francisco Bandeira

Background Vitamin D deficiency has been associated with cardiovascular risk factors, including type 2 diabetes mellitus (T2DM). Evidence shows that patients with low serum 25-hydroxyvitamin D (25OHD) concentrations have a higher risk of developing coronary artery disease. Objective The objective of this study was to assess vitamin D as a predictor of the severity in diabetics with acute coronary syndrome (ACS). Methods A total of 166 patients were diagnosed with ACS. Serum 25OHD concentrations were analyzed, and risk factors for ACS were evaluated. Results Patients diagnosed as having acute myocardial infarction with elevation of the ST segment had a higher rate of 25OHD, <20 ng/mL compared to ≤30 ng/mL (47.8% × 13.4%, P = 0.03). Diabetics with vitamin D deficiency had more multivessel lesions in the coronary angiography than non-diabetics (69% × 31.8%, P = 0.007). After adjustments for confounders, serum 25OHD remained associated with more severe disease. Conclusion Vitamin D deficiency is associated with more severe ACS and is a predictor of more extensive coronary lesions in patients with T2DM.


2020 ◽  
Author(s):  
Ada Admin ◽  
Yann C. Klimentidis ◽  
Amit Arora ◽  
Michelle Newell ◽  
Jin Zhou ◽  
...  

Although hyperlipidemia is traditionally considered a risk factor for type-2 diabetes (T2D), evidence has emerged from statin trials and candidate gene investigations suggesting that lower LDL-C increases T2D risk. We thus sought to more comprehensively examine the phenotypic and genotypic relationships of LDL-C with T2D. Using data from the UK Biobank, we found that levels of circulating LDL-C were negatively associated with T2D prevalence (OR=0.41[0.39, 0.43] per mmol/L unit of LDL-C), despite positive associations of circulating LDL-C with HbA1c and BMI. We then performed the first genome-wide exploration of variants simultaneously associated with lower circulating LDL-C and increased T2D risk, using data on LDL-C from the UK Biobank (n=431,167) and the GLGC consortium (n=188,577), and T2D from the DIAGRAM consortium (n=898,130). We identified 31 loci associated with lower circulating LDL-C and increased T2D, capturing several potential mechanisms. Seven of these loci have previously been identified for this dual phenotype, and 9 have previously been implicated in non-alcoholic fatty liver disease. These findings extend our current understanding of the higher T2D risk among individuals with low circulating LDL-C, and of the underlying mechanisms, including those responsible for the diabetogenic effect of LDL-C-lowering medications.


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