Dataset Information

Self-reported and genetically predicted effects of coffee intake on rheumatoid arthritis: Epidemiological studies and Mendelian randomization analysis.

ABSTRACT:

Background and aims

Causal research concerning coffee intake and rheumatoid arthritis (RA) risk is controversial. The objective of this study was to further explore the causal relationship between coffee intake and RA risk.

Methods

The 4,310 participants from NHANES 2003-2006 were included in an epidemiological study to assess the association between coffee intake and RA by weighted multivariate logistic regression. The inverse variance weighted (IVW) method of two-sample Mendelian randomization (MR), employing genetic data from UK Biobank (428,860 cases) of coffee intake and MR-Base platform (14,361 cases and 43,923 controls) of RA, was performed to estimate the causal relationship between coffee intake and RA.

Results

Weighted multivariate logistic regression suggested no significant correlation between coffee intake and RA. Compared to the no-coffee group, the odds ratio for RA in the <1, 1-3, ≥4 cups/day group were 1.297, 1.378, and 1.125 (P = 0.204, 0.098, and 0.698, respectively). In the IVW of MR analysis, there was no causal relationship between coffee intake and RA (OR = 1.47, P = 0.218).

Conclusion

Our study did not support a causal association between coffee intake and RA risk. However, it is necessary to consider valid information on coffee intake, including brewing method, type of coffee, and quantity, in further analysis of coffee intake and RA.

SUBMITTER: Pu B

PROVIDER: S-EPMC9510978 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Publications

Self-reported and genetically predicted effects of coffee intake on rheumatoid arthritis: Epidemiological studies and Mendelian randomization analysis.

Pu Bin B Gu Peng P Zheng ChuRong C Ma LiQiong L Zheng XiaoHui X Zeng ZhanPeng Z

Frontiers in nutrition 20220912

<h4>Background and aims</h4>Causal research concerning coffee intake and rheumatoid arthritis (RA) risk is controversial. The objective of this study was to further explore the causal relationship between coffee intake and RA risk.<h4>Methods</h4>The 4,310 participants from NHANES 2003-2006 were included in an epidemiological study to assess the association between coffee intake and RA by weighted multivariate logistic regression. The inverse variance weighted (IVW) method of two-sample Mendelia ...[more]

PMID: 36172525

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Project description:BackgroundPast studies have demonstrated that patients diagnosed with rheumatoid arthritis (RA) often exhibit abnormal levels of lipids. Furthermore, certain lipid-modifying medications have shown effectiveness in alleviating clinical symptoms associated with RA. However, the current understanding of the causal relationship between lipids, lipid-modifying medications, and the risk of developing RA remains inconclusive. This study employed Mendelian randomization (MR) to investigate the causal connection between lipids, lipid-modifying drugs, and the occurrence of RA.MethodsWe obtained genetic variation for lipid traits and drug targets related to lipid modification from three sources: the Global Lipids Genetics Consortium (GLGC), UK Biobank, and Nightingale Health 2020. The genetic data for RA were acquired from two comprehensive meta-analyses and the R8 of FINNGEN, respectively. These variants were employed in drug-target MR analyses to establish a causal relationship between genetically predicted lipid-modifying drug targets and the risk of RA. For suggestive lipid-modified drug targets, we conducted Summary-data-based Mendelian Randomization (SMR) analyses and using expression quantitative trait loci (eQTL) data in relevant tissues. In addition, we performed co-localization analyses to assess genetic confounders.ResultsOur analysis revealed no significant causal relationship between lipid and RA. We observed that the genetically predicted 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) -mediated low density lipoprotein cholesterol (LDL-C) (OR 0.704; 95% CI 0.56, 0.89; P = 3.43×10-3), Apolipoprotein C-III (APOC3) -mediated triglyceride (TG) (OR 0.844; 95% CI 0.77, 0.92; P = 1.50×10-4) and low density lipoprotein receptor (LDLR) -mediated LDL-C (OR 0.835; 95% CI 0.73, 0.95; P = 8.81×10-3) were significantly associated with a lowered risk of RA. while Apolipoprotein B-100 (APOB) -mediated LDL-C (OR 1.212; 95%CI 1.05,1.40; P = 9.66×10-3) was significantly associated with an increased risk of RA.ConclusionsOur study did not find any supporting evidence to suggest that lipids are a risk factor for RA. However, we observed significant associations between HMGCR, APOC3, LDLR, and APOB with the risk of RA.

Project description:BackgroundThe associations between vegetable intake and cardiovascular diseases have been demonstrated in observational studies, but less sufficiently in randomized trials. Mendelian randomization has been considered a promising alternative in causal inference. The separate effects of cooked and raw vegetable intake remain unclear. This study aimed to investigate the associations between cooked and raw vegetable intake with cardiovascular outcomes using MR.MethodsWe identified 15 and 28 genetic variants statistically and biologically associated with cooked and raw vegetable intake, respectively, from previous genome-wide association studies, which were used as instrumental variables to estimate associations with coronary heart disease (CHD), stroke, heart failure (HF), and atrial fibrillation (AF). The independent effects of genetically predicted cooked and raw vegetable intake were examined using multivariable MR analysis. We performed one-sample and two-sample MR analyses and combined their results using meta-analysis. Bonferroni correction was applied for multiple comparisons. We performed two-sample MR analysis for cardiometabolic risk factors (serum lipids, blood pressure, body mass index, and glycemic traits) to explore the potential mechanisms.ResultsIn the MR meta-analysis of 1.2 million participants, we found null evidence for associations between genetically predicted cooked and raw vegetable intake with CHD, HF, or AF. Raw vegetable intake was nominally associated with stroke (odds ratio [95% confidence interval] 0.82 [0.69-0.98] per 1 daily serving increase, p = 0.03), but this association did not pass the corrected significance level. We found consistently null evidence for associations with serum lipids, blood pressure, body mass index, or glycemic traits.ConclusionsWe found null evidence for associations between genetically predicted vegetable intake with CHD, AF, HF, or cardiometabolic risk factors in this MR study. Raw vegetable intake may reduce risk of stroke, but this warrants more research. True associations between vegetable intake and CVDs cannot be completely ruled out, and future investigations are required for causal inference in nutritional research.

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Dataset Information

Self-reported and genetically predicted effects of coffee intake on rheumatoid arthritis: Epidemiological studies and Mendelian randomization analysis.

Background and aims

Methods

Results

Conclusion

Publications

Self-reported and genetically predicted effects of coffee intake on rheumatoid arthritis: Epidemiological studies and Mendelian randomization analysis.

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