scholarly journals Association of serum 25-hydroxyvitamin D concentrations with risk of dementia among individuals with type 2 diabetes: A cohort study in the UK Biobank

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.

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>


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Xiao ◽  
Jingyi Lv ◽  
Shiyu Wang ◽  
Yang Zhou ◽  
Lunwen Chen ◽  
...  

Abstract Background Vitamin D deficiency has been associated with type 2 diabetes (T2D) and metabolic syndrome (MS) and its components. However, it is unclear whether a low concentration of vitamin D is the cause or consequence of these health conditions. Thus, this study aimed to evaluate the association of vitamin D concentrations and its genetic risk scores (GRSs) with MS and its component diseases, such as T2D, in middle-aged and elderly participants from rural eastern China. Methods A subset of 2393 middle-aged and elderly individuals were selected from 70,458 participants of the Nantong Chronic Diseases Study of 2017–2018 in China. We used two 25-hydroxyvitamin D (25[OH]D) synthesis single-nucleotide polymorphisms (SNPs) (DHCR7-rs12785878 and CYP2R1-rs10741657) and two 25(OH) D metabolism SNPs (GC-rs2282679 and CYP24A1-rs6013897) for creating GRSs, which were used as instrumental variables to assess the effect of genetically lowered 25(OH) D concentrations on MS and T2D based on the Wald ratio. F statistics were used to validate that the four SNPs genetically determined 25(OH) D concentrations. Results Compared to vitamin D sufficient individuals, individuals with vitamin D insufficiency had an odds ratio (OR [95% confidence interval {CI}]) of MS of 1.30 (1.06–1.61) and of T2D of 1.32 (1.08–1.64), individuals with vitamin D deficiency had an ORs (95% CI) of MS of 1.50 (1.24–1.79) and of T2D of 1.47 (1.12–1.80), and those with vitamin D severe deficiency had an ORs (95% CI) of MS of 1.52 (1.29–1.85) and of T2D of 1.54 (1.27–1.85). Mendelian randomization analysis showed a 25-nmol/L decrease in genetically instrumented serum 25(OH) D concentrations using the two synthesis SNPs (DHCR7 and CYP2R1 genes) associated with the risk of T2D and abnormal diastolic blood pressure (DBP) with ORs of 1.10 (95%CI: 1.02–1.45) for T2D and 1.14 (95%CI: 1.03–1.43) for DBP. Conclusions This one sample Mendelian randomization analysis shows genetic evidence for a causal role of lower 25(OH) D concentrations in promoting of T2D and abnormal DBP in middle-aged and elderly participants from rural China.


2019 ◽  
Vol 89 (5-6) ◽  
pp. 285-292
Author(s):  
Kaustubh Bora ◽  
Alice Abraham Ruram

Abstract. Background: Although inadequate vitamin D and altered parathyroid hormone (PTH) are implicated in deranged glucose metabolism and risk of future diabetes, their role in regulating glucose homeostasis in established cases of diabetes is unclear. We aimed to (i) evaluate vitamin D status, and (ii) determine if vitamin D and PTH were associated with parameters of glucose homeostasis in type 2 diabetes (T2D) patients from Meghalaya, India. Methods: We determined 25-hydroxyvitamin D (25-OH-D) and PTH concentrations in 251 T2D patients (not on insulin), and examined their associations with the following parameters of glucose homeostasis: fasting blood sugar (FBS), post-prandial blood sugar (PPBS), glycated hemoglobin (HbA1c), fasting insulin (FI), homeostasis model assessments of insulin resistance (HOMA-IR) and β-cell function (HOMA-β). Results: None of the patients had adequate vitamin D (mean 25-OH-D = 19.3 ng/mL); 47.8% patients were deficient (25-OH-D < 20 ng/mL), while 52.2% were insufficient (25-OH-D < 30 ng/mL) vitamin D. Significant ( P < 0.05) univariate associations were observed between: 25-OH-D and FI ( r = 0.14); 25-OH-D and HOMA-β ( r = 0.13); PTH and FI ( r = −0.18), and PTH and HOMA-β ( r = −0.11). However these associations disappeared after controlling for potential confounders. The 25-OH-D and PTH levels were not associated with any of the tested parameters of glucose homeostasis. Conclusion: There was widespread prevalence of vitamin D deficiency/insufficiency in our sample T2D patients. However, neither vitamin D nor PTH appeared to play a major role in influencing glucose homeostasis in this present selection of T2D cases.


2015 ◽  
Vol 100 (4) ◽  
pp. E591-E595 ◽  
Author(s):  
Mercedes Clemente-Postigo ◽  
Araceli Muñoz-Garach ◽  
Marta Serrano ◽  
Lourdes Garrido-Sánchez ◽  
M. Rosa Bernal-López ◽  
...  

Author(s):  
Medityas Winda Krissinta ◽  
M.I. Diah Pramudianti ◽  
Dian Ariningrum

Background: Type 2 diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia. Metabolic syndrome (MS) is a complex metabolic disorder like hyperglycemia, obesity, dyslipidemia, and hypertension. Vitamin D controls genes associated with regulation of insulin and renin production. The aim of this study was to analyze the relation between total levels of 25-hydroxyvitamin D [25(OH)D] and the incidence of MS in  type 2 DM patients.Methods: This case control study was conducted from October to November 2018 in Dr Moewardi Hospital Surakarta in 84 people with type 2 diabetes mellitus. All subjects were 34-75 years old. The research data were analyzed with a 2x2 test table to determine the odd ratio (OR) of each study variable, then multivariate analysis with logistic regression then continued.Results: The mean total level of 25(OH)D is 18.01 ± 6.10 ng/dl. Bivariate and multivariate OR analysis showed that poor glycemic control with the incidence of MS (OR: 11.154; 95% Cl: 3.933-31.631; p = 0.001); female sex (OR : 1.788; 95% Cl: 0.750-4.261; p = 0.188); age < 50 year (OR: 1.644; 95% Cl: 0.614-4.404; p = 0.321); and  total  25(OH)D deficiency (OR: 1.250; 95% Cl: 0.317-2.022; p = 0.637).Conclusion: total 25(OH)D level is not associated with the incidence of MS in the type 2 DM patients. Further study was needed using by healthy group control to explain the role of vitamin D in type 2 DMKeywords: type 2 DM, metabolic syndrome, 25(OH)D


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2889
Author(s):  
Adriana Florinela Cӑtoi ◽  
Mihaela Iancu ◽  
Alina Elena Pârvu ◽  
Andra Diana Cecan ◽  
Cristina Bidian ◽  
...  

Vitamin D deficiency is highly prevalent in patients with overweight/obesity and type 2 diabetes (T2DM). Herein, we investigated the relationship between vitamin D status and overweight/obesity status, insulin resistance (IR), systemic inflammation as well as oxidative stress (OS). Anthropometric and laboratory assessments of 25-hydroxyvitamin D (25(OH)D) and glycemic, pro-inflammatory and OS biomarkers were performed in a sample of 47 patients with T2DM who were divided into categories based on overweight and degree of obesity. The main findings were: the overweight/obesity status correlated negatively with the degree of serum 25(OH)D deficiency (ρ = −0.27) with a trend towards statistical significance (p = 0.069); the homeostasis model assessment of insulin resistance (HOMA-IR) was significantly different (p = 0.024) in patients with 25(OH)D deficiency, as was total oxidant status (TOS) and oxidative stress index (OSI) in patients with severe serum 25(OH)D deficiency as compared to those with 25(OH)D over 20 ng/mL (TOS: p = 0.007, OSI: p = 0.008); and 25(OH)D had a negative indirect effect on TOS by body mass index (BMI), but BMI was not a significant mediator of the studied relationship. In a setting of overweight and increasing degree of obesity, patients with T2DM did not display decreasing values of 25(OH)D. Subjects with the lowest values of 25(OH)D presented the highest values of BMI. Patients with 25(OH)D deficiency were more insulin resistant and showed increased OS but no elevated systemic inflammation. The negative effect of 25(OH)D on TOS did not seem to involve BMI as a mediator.


2011 ◽  
Vol 81 (5) ◽  
pp. 317-327 ◽  
Author(s):  
Moira S. Hutchinson ◽  
Yngve Figenschau ◽  
Bjørg Almås ◽  
Inger Njølstad ◽  
Rolf Jorde

The relationships between vitamin D concentrations, hyperglycemia, and insulin resistance remain uncertain. During 2008 - 2010, an oral glucose tolerance test was performed in 3520 subjects from Tromsø, Norway. Serum 25-hydroxyvitamin D [25(OH)D] was measured in 1193 subjects with normal glucose tolerance, in 304 with isolated impaired fasting glucose, in 254 with isolated impaired glucose tolerance, in 139 with a combination of the two, and in 194 subjects with type 2 diabetes. Serum 25(OH)D did not differ between subjects with isolated impaired fasting glucose or impaired glucose tolerance, but was lower in all groups of deranged glucose metabolism as compared with normal subjects. These differences could not be explained by differences in intakes of vitamin D from cod liver oil or other supplements and remained statistically significant after adjustment for gender, age, body mass index, physical activity score, and month of examination. When the cohort was divided according to serum 25(OH)D quartiles, there was an improvement in all measures of glucose metabolism (fasting and 2-hour plasma glucose, serum insulin, HbA1c) and estimates of insulin resistance (QUICKI , HOMA-IR, ISI0.120) with increasing serum 25(OH)D quartile. However, interventional studies are needed to prove a causal relationship between vitamin D and glucose metabolism.


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