ORCID Profile
0000-0002-7883-0341
Current Organisation
Sun Yat-Sen University
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Publisher: Wiley
Date: 06-02-2023
DOI: 10.1002/OBY.23669
Abstract: Sleep apnea and snoring have been associated with type 2 diabetes, with BMI playing a role in the pathway, but the directions of causality are unclear. This study examined the causal associations of sleep apnea and snoring with type 2 diabetes while assessing the role of BMI using multiple genetic methods. Five genetic methods were used: two‐s le bidirectional univariable Mendelian randomization (MR) inverse variance‐weighted (MR‐IVW) multivariable MR‐IVW network MR and latent causal variable method. Compared with univariable MR‐IVW, the odds ratio (95% CI) of type 2 diabetes for genetically predicted sleep apnea and snoring using the largest genome‐wide association study decreased dramatically, from 1.61 (95% CI: 1.16‐2.23) to 1.08 (95% CI: 0.59‐1.97) and from 1.98 (95% CI: 1.25‐3.13) to 1.09 (95% CI: 0.64‐1.86) after adjustment for BMI. Network MR showed that BMI accounts for 67% and 62% of the total effect of sleep apnea and snoring on type 2 diabetes, respectively. The latent causal variable suggested that sleep apnea and snoring have no direct causal effect on type 2 diabetes. These results first suggest that the associations of sleep apnea and snoring with type 2 diabetes were mainly driven by BMI. The possible indirect effects of sleep apnea and snoring on type 2 diabetes through BMI cannot be ruled out.
Publisher: Frontiers Media SA
Date: 18-08-2022
Abstract: Previous observational studies have found that lower levels of circulating polyunsaturated fatty acids (PUFAs) were associated with a higher risk of sleep apnea (SA). However, the causality of the association remains unclear. We used the two-s le Mendelian randomization (MR) study to assess the causal association of omega-3 and omega-6 fatty acids with SA. Single-nucleotide polymorphisms (SNPs) predicting the plasma level of PUFAs at the suggestive genome-wide significance level ( p & 5 × 10 –6 ) were selected as instrumental variables (IVs) from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) ( n = ∼8,000) Consortium. For outcomes, the summary-level statistics of SA were obtained from the latest genome-wide association study (GWAS), which combined five cohorts with a total number of 25,008 SA cases and 172,050 snoring cases (total = 523,366). We found no association of α-linolenic acid (ALA) [odds ratio (OR) = 1.09 per% changed, 95% confidence interval (CI) 0.67–1.78], eicosapentaenoic acid (EPA) (OR = 0.94, 95% CI 0.88–1.01), docosapentaenoic acid (DPA) (OR = 0.95, 95% CI 0.88–1.02), and docosahexaenoic acid (DHA) (OR = 0.99, 95% CI 0.96–1.02) with the risk of SA using inverse-variance weighted (IVW) method. Moreover, for omega-6 PUFAs, no association between linoleic acid (LA) (OR = 0.98, 95% CI 0.96–1.01), arachidonic acid (AA) (1.00, 95% CI 0.99–1.01), and adrenic acid (AdrA) (0.93, 95% CI 0.71–1.21) with the risk of SA was found. Similarly, no associations of PUFAs with SA were found in single-locus MR analysis. In the current study, we first found that there is no genetic evidence to support the causal role of omega-3 and omega-6 PUFAs in the risk of SA. From a public health perspective, our findings refute the notion that consumption of foods rich in PUFAs or the use of PUFAs supplementation can reduce the risk of SA.
Publisher: Oxford University Press (OUP)
Date: 05-01-2023
Abstract: Previously, observational studies have identified associations between sleep apnea (SA) and cardiovascular diseases (CVDs), whereas whether the associations are causal remain unclear. We used the bi-directional, two-s le Mendelian randomization (MR) study to assess the existence and direction of the causal relationship between SA or snoring and CVDs. Multivariable MR (MVMR) was used to assess the direct effect of SA on CVDs after adjusting for body mass index (BMI). Single-nucleotide polymorphisms (SNPs) associated with SA and snoring were obtained from the latest genome-wide association study, which combined five cohorts with a total number of 25 008 SA cases and 172 050 snoring cases (total = 523 366). Among the analytic s le of 523 366 in iduals (25 008 SA cases and 172 050 snoring cases), and after correcting for multiple testing, inverse-variance weighted (IVW) showed that SA and snoring increased the risk of hypertension [odds ratio (OR) = 1.03, 95% CI 1.02–1.05 and 1.05, 1.03–1.07], and coronary artery disease (CAD) (1.41,1.19–1.67 and 1.61,1.26–2.07) with all false-discovery rate (FDR) & 0.05, but such associations were decreased dramatically after adjusting for BMI using MVMR-IVW (0.06 & FDRBMI adjusted & 0.20). SA and snoring were not associated with atrial fibrillation (AF), heart failure (HF), or stroke. The presence of hypertension may increase the risk of SA (1.53, 1.04–2.25), but this association did not pass multiple comparisons (FDR & 0.05). Our results suggest that SA and snoring increased the risk of hypertension and CAD, and these associations may partly be driven by BMI. Conversely, no evidence of CVDs causally influencing SA or snoring was found.
No related grants have been discovered for JIAO WANG.