Oxidative stress is present in chronic obstructive pulmonary disease (COPD); however, the effect of increased dietary antioxidants on reducing COPD risk remains unclear. The aim of this study was to investigate the association of the composite dietary antioxidant index (CDAI) with COPD in adults. This study conducted a cross-sectional investigation using data from the National Health and Nutrition Examination Survey (NHANES) spanning from 2015 to March 2020 to explore the association between CDAI and COPD in adults. This study included 9295 participants. Three logistic regression models (crude model, partially adjusted model and fully adjusted model) and restricted cubic spline (RCS) curves were utilised to assess the association between CDAI levels and COPD risk. Subsequently, a two-sample Mendelian randomisation (MR) was employed to analyse the causal impact of antioxidant levels within CDAI on the occurrence of COPD. CDAI levels were inversely associated with COPD after adjusting for confounders (OR = 0·97, 95 % CI 0·95, 1·00), and the association was linear (P < 0·001), and the results of the RCS showed that CDAI was linearly correlated with COPD occurrence (P < 0·001). MR analysis revealed a causal relationship between vitamin C and COPD occurrence (OR = 0·99, 95 % CI 0·98, 1·00, P < 0·05). Our study indicates that dietary sources of antioxidants may reduce the risk of COPD occurrence, and the results of the MR analysis further show that vitamin C is causally associated with a reduced risk of COPD occurrence. However, further exploration is needed to understand how antioxidants prevent COPD.

The course of COVID-19 is highly variable, with genetics playing a significant role. Through large-scale genetic association studies, a link between single nucleotide polymorphisms and disease susceptibility and severity was established. However, individual single nucleotide polymorphisms identified thus far have shown modest effects, indicating a polygenic nature of this trait, and individually have limited predictive performance. To address this limitation, we investigated the performance of a polygenic risk score model in the context of COVID-19 severity in a Russian population. A genome-wide polygenic risk score model including information from over a million common single nucleotide polymorphisms was developed using summary statistics from the COVID-19 Host Genetics Initiative consortium. Low-coverage sequencing (5x) was performed for ~1000 participants, and polygenic risk score values were calculated for each individual. A multivariate logistic regression model was used to analyse the association between polygenic risk score and COVID-19 outcomes. We found that individuals in the top 10% of the polygenic risk score distribution had a markedly elevated risk of severe COVID-19, with adjusted odds ratio of 2.9 (95% confidence interval: 1.8–4.6, p-value = 4e-06), and more than four times higher risk of mortality from COVID-19 (adjusted odds ratio = 4.3, p-value = 2e-05). This study highlights the potential of polygenic risk score as a valuable tool for identifying individuals at increased risk of severe COVID-19 based on their genetic profile.

Although dietary factors have been examined as potential risk factors for liver cancer, the evidence is still inconclusive. Using a diet-wide association analysis, our research evaluated the associations of 126 foods and nutrients on the risk of liver cancer in a Chinese population. We obtained the diet consumption of 72,680 women in the Shanghai Women’s Health Study using baseline dietary questionnaires. The association between each food and nutrient and liver cancer risk was quantified by Cox regression model. A false discovery rate of 0.05 was used to determine the foods and nutrients which need to be verified. Totally 256 incident liver cancer cases were identified in 1,267,391 person-years during the follow-up duration. At the statistical significance level (P ≤ 0.05), higher intakes of cooked wheaten foods, pear, grape and copper were inversely associated with liver cancer risk, while spinach, leafy vegetables, eggplant and carrots showed the positive associations. After considering multiple comparisons, no dietary variable was associated with liver cancer risk. Similar findings were seen in the stratification, secondary and sensitivity analyses. Our findings observed no significant association between dietary factors and liver cancer risk after considering multiple comparisons in Chinese women. More evidence is needed to explore the associations between diet and female liver cancer occurrence.

Prior observational studies have reported the potential protective effect of n-3 fatty acids on the prognosis of acute pancreatitis (AP). However, the causal impact of n-3 fatty acids on AP is unclear. We aimed to investigate further the association of n-3 fatty acids with AP. We performed a meta-analysis and Mendelian randomisation (MR) to explore the association between n-3 fatty acids and the prognosis of AP from clinical observation and genetics perspectives, respectively. Nine randomised controlled trials were included in this study. The result meta-analysis showed that complementary therapy of n-3 fatty acids significantly decreased mortality (Relative Risk (RR): 0·30; 95 % CI 0·14, 0·65, P < 0·05) and infectious complications in AP (RR: 0·45; 95 % CI 0·27, 0·77, P < 0·05). Compared with the control groups, the hospital stays (MD: −1·02; 95 % CI −1·85, −0·20, P < 0·05) in AP patients with n-3 fatty acids treatment were statistically reduced. However, the ICU stay (MD: −0·49; 95 % CI −1·29, −0·31, P > 0·05) between control groups and AP patients with n-3 fatty acids treatment was insignificant. Utilising genetic susceptibility analysis in the MR approach, the MR showed n-3 fatty acids have a significant causal effect on the AP risk (OR, 0·887; 95 % CI 0·797, 0·986, P = 0·027, fixed-effect; OR, 0·887; 95 % CI 0·792, 0·993, P = 0·037, random-effect). n-3 fatty acids complementary therapy may improve the prognosis of AP. Furthermore, genetically predicted serum levels of n-3 fatty acids can significantly lower AP risk.

Rheumatoid arthritis (RA) is a prevalent autoimmune disease, and there is growing evidence suggesting a potential correlation between dietary factors and the pathogenesis of this condition. In order to investigate the causal relationship between diet and RA, we conducted a two-sample Mendelian randomisation (MR) analysis to examine the causal associations between twenty-two dietary factors and RA. Summary data from genome-wide association studies (GWAS) of RA were obtained from large GWAS meta-analyses. GWAS summary data for twenty-two dietary factors were obtained from UK Biobank. Random-effects inverse variance weighted was used as the primary method for assessing causality, and analyses of heterogeneity and horizontal pleiotropy were performed to ensure the accuracy of the results. Research indicates a negative genetic causal relationship between cereal intake (OR = 0·64, 95 % CI: 0·41, 0·99, P = 0·048) and oily fish intake (OR = 0·70, 95 % CI: 0·52, 0·95, P = 0·020) with the risk of RA. Other dietary factors were not causally related to RA. Sensitivity analysis shows that our results are reliable. This study provides genetic evidence suggesting that cereal intake and oily fish intake are protective factors for RA, indicating that RA patients and individuals at high risk should make appropriate dietary adjustments.

This study aimed to investigate the association between n-3 PUFA and lung function. First, a cross-sectional study was conducted based on the National Health and Nutrition Examination Survey (NHANES) 2007–2012 data. n-3 PUFA intake was obtained from 24-h dietary recalls. A multivariable linear regression model was used to assess the observational associations of n-3 PUFA intake with lung function. Subsequently, a two-sample Mendelian randomisation (MR) was performed to estimate the potential causal effect of n-3 PUFA on lung function. Genetic instrumental variables were extracted from published genome-wide association studies. Summary statistics about n-3 PUFA was from UK Biobank. Inverse variance weighted was the primary analysis approach. The observational study did not demonstrate a significant association between n-3 PUFA intake and most lung function measures; however, a notable exception was observed with significant findings in the highest quartile for forced vital capacity (FVC) and % predicted FVC. The MR results also showed no causal effect of circulating n-3 PUFA concentration on lung function (forced expiratory volume in one second (FEV1), β = 0·01301, se = 0·01932, P = 0·5006; FVC, β = −0·001894, se = 0·01704, P = 0·9115; FEV1:FVC, β = 0·03118, se = 0·01743, P = 0·07359). These findings indicate the need for further investigation into the impact of higher n-3 PUFA consumption on lung health.

Fe-deficiency anaemia is a major public health concern in children under 5 years of age. TMPRSS6 gene, encoding matriptase-2 protein, is implicated in Fe homoeostasis and has been associated with anaemia and Fe status in various populations. The aim of this cross-sectional study was to investigate the associations between the single nucleotide polymorphism (SNP) TMPRSS6 rs855791 and biomarkers of anaemia and Fe deficiency in Brazilian children attending day care centres. A total of 163 children aged 6–42 months were evaluated. Socio-economic, demographic, biochemical, haematological, immunological and genotype data were collected. Multiple logistic and linear regressions with hierarchical selection were used to assess the effects of independent variables on categorised outcomes and blood marker concentrations. Minor allele (T) frequency of rs855791 was 0·399. Each copy of the T allele was associated with a 4·49-fold increased risk of developing anaemia (P = 0·005) and a 4·23-fold increased risk of Fe deficiency assessed by serum soluble transferrin receptor (sTfR) (P < 0·001). The dose of the T allele was associated with an increase of 0·18 mg/l in sTfR concentrations and reductions of 1·41 fl and 0·52 pg in mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH), respectively. In conclusion, the T allele of SNP TMPRSS6 rs855791 was significantly associated with anaemia and Fe deficiency assessed by sTfR in Brazilian children attending day care centres. The effect was dose dependent, with each copy of the T allele being associated with lower MCV and MCH and higher concentrations of sTfR.

Over the years, numerous observational studies have substantiated that various dietary choices have opposing effects on CVD. However, the causal effect has not yet been established. Thus, we conducted a Mendelian randomisation (MR) analysis to reveal the causal impact of dietary habits on CVD. Genetic variants strongly associated with 20 dietary habits were selected from publicly available genome-wide association studies conducted on the UK Biobank cohort (n 449 210). Summary-level data on CVD were obtained from different consortia (n 159 836–977 323). The inverse-variance weighted method (IVW) was the primary outcome, while MR-Egger, weighted median and MR Pleiotropy RESidual Sum and Outlier were used to assess heterogeneity and pleiotropy. We found compelling evidence of a protective causal effect of genetic predisposition towards cheese consumption on myocardial infarction (IVW OR = 0·67; 95 % CI = 0·544, 0·826; P = 1·784 × 10−4) and heart failure (IVW OR = 0·646; 95 % CI = 0·513, 0·814; P = 2·135 × 10−4). Poultry intake was found to be a detrimental factor for hypertension (IVW OR = 4·306; 95 % CI = 2·158, 8·589; P = 3·416 × 10−5), while dried fruit intake was protective against hypertension (IVW OR = 0·473; 95 % CI = 0·348, 0·642; P = 1·683 × 10−6). Importantly, no evidence of pleiotropy was detected. MR estimates provide robust evidence for a causal relationship between genetic predisposition to 20 dietary habits and CVD risk, suggesting that well-planned diets may help prevent and reduce the risk of CVD.

Although previous studies suggested the protective effect of Zn for type 2 diabetes (T2D), the unitary causal effect remains inconclusive. We investigated the causal effect of Zn as a single intervention on glycaemic control for T2D, using a systematic review of randomised controlled trials and two-sample Mendelian randomisation (MR). Four primary outcomes were identified: fasting blood glucose/fasting glucose, HbA1c, homeostatic model assessment for insulin resistance (HOMA-IR) and serum insulin/fasting insulin level. In the systematic review, four databases were searched until June 2021. Studies, in which participants had T2D and intervention did not comprise another co-supplement, were included. Results were synthesised through the random-effects meta-analysis. In the two-sample MR, we used single-nucleotide polymorphisms (SNP) from MR-base, strongly related to Zn supplements, to infer the relationship causally, but not specified T2D. In the systematic review and meta-analysis, fourteen trials were included with overall 897 participants initially. The Zn supplement led to a significant reduction in the post-trial mean of fasting blood glucose (mean difference (MD): −26·52 mg/dl, 95 % CI (−35·13, −17·91)), HbA1c (MD: −0·52 %, 95 % CI: (−0·90, −0·13)) and HOMA-IR (MD: −1·65, 95 % CI (−2·62, −0·68)), compared to the control group. In the two-sample MR, Zn supplement with two SNP reduced the fasting glucose (inverse-variance weighted coefficient: −2·04 mmol/l, 95 % CI (−3·26, −0·83)). From the two methods, Zn supplementation alone may causally improve glycaemic control among T2D patients. The findings are limited by power from the small number of studies and SNP included in the systematic review and two-sample MR analysis, respectively.