Body mass index,abdominal fatness,fat mass and the risk of atrial fibrillation: a systematic review and dose–response meta-analysis of prospective studies

Different adiposity measures have been associated with increased risk of atrial fibrillation, however, results have previously only been summarized for BMI. We therefore conducted a systematic review and meta-analysis of prospective studies to clarify the association between different adiposity measures and risk of atrial fibrillation. PubMed and Embase databases were searched up to October 24th 2016. Summary relative risks (RRs) were calculated using random effects models. Twenty-nine unique prospective studies (32 publications) were included. Twenty-five studies (83,006 cases, 2,405,381 participants) were included in the analysis of BMI and atrial fibrillation. The summary RR was 1.28 (95% confidence interval: 1.20–1.38, I² = 97%) per 5 unit increment in BMI, 1.18 (95% CI: 1.12–1.25, I² = 73%, n = 5) and 1.32 (95% CI: 1.16–1.51, I² = 91%, n = 3) per 10 cm increase in waist and hip circumference, respectively, 1.09 (95% CI: 1.02–1.16, I² = 44%, n = 4) per 0.1 unit increase in waist-to-hip ratio, 1.09 (95% CI: 1.02–1.16, I² = 94%, n = 4) per 5 kg increase in fat mass, 1.10 (95% CI: 0.92–1.33, I² = 90%, n = 3) per 10% increase in fat percentage, 1.10 (95% CI: 1.08–1.13, I² = 74%, n = 10) per 5 kg increase in weight, and 1.08 (95% CI: 0.97–1.19, I² = 86%, n = 2) per 5% increase in weight gain. The association between BMI and atrial fibrillation was nonlinear, p _nonlinearity < 0.0001, with a stronger association at higher BMI levels, however, increased risk was observed even at a BMI of 22–24 compared to 20. In conclusion, general and abdominal adiposity and higher body fat mass increase the risk of atrial fibrillation.     

Body mass index,abdominal fatness,and the risk of sudden cardiac death: a systematic review and dose–response meta-analysis of prospective studies

Although overweight and obesity are established risk factors for some types of heart disease including ischemic heart disease, heart failure and atrial fibrillation, less is known about the association between adiposity and sudden cardiac death. We conducted a systematic review and meta-analysis of prospective studies to clarify the association between adiposity and risk of sudden cardiac death. PubMed and Embase databases were searched up to July 20th 2017. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models. The summary RR was 1.16 (95% CI 1.05–1.28, I² = 68%, n = 14) per 5 unit increment in BMI, and 1.82 (95% CI 1.61–2.07, I² = 0%, n = 3) per 0.1 unit increase in waist-to-hip ratio, and 1.03 (95% CI 0.93–1.15, I² = 0%, n = 2) per 10 cm increase in waist circumference. The heterogeneity in the analysis of BMI and sudden cardiac death persisted across most subgroup analyses. The association was stronger among studies with longer follow-up compared to short follow-up and was observed in the European and American studies, but not in the Asian studies. There was a J-shaped association between BMI and sudden cardiac death and the lowest risk was observed in the normal weight range, however, the increased risk with a low BMI was attenuated among studies with a longer duration of follow-up. This meta-analysis suggest an increased risk of sudden cardiac death with increasing BMI and waist-to-hip ratio, however, further studies with stratification for smoking status are needed of waist circumference, weight changes and adiposity at younger ages.     

Physical activity and the risk of heart failure: a systematic review and dose–response meta-analysis of prospective studies

European Journal of Epidemiology - Although physical activity is an established protective factor for cardiovascular diseases such as ischemic heart disease and stroke, less is known with regard to...     

Alcohol consumption and dementia risk: a dose–response meta-analysis of prospective studies

It is widely believed that light-to-moderate alcohol intake may protect against dementia while excessive drinking may instead increase the risk. Nonetheless, these findings need cautious interpretations due to varying methodologies and lack of standard definition, which hindered our transferring into preventative practice. The objective of this study is to investigate the potential dose–response association between alcohol consumption and risk of dementia. A systematic search was conducted in electronic databases to identify relevant studies. Risk estimates were combined using a random-effect model. Eleven studies with 73,330 participants and 4586 cases for all-cause dementia (ACD), five studies with 52,715 participants and 1267 cases for Alzheimer’s dementia (AD) and four studies with 49,535 participants and 542 cases for vascular dementia were included. We observed a nonlinear association between alcohol consumption and ACD risk (p _nonlinearity < 0.05). The alcohol dose associated with lower risk of dementia was confined to at most 12.5 g/day, with the risk hitting bottom (RR ≈ 0.9) at roughly 6 g/day. Of note, the ACD risk seemed to be elevated (≈10%) when the dose surpasses certain levels: 23 drinks/week or 38 g/day. For the alcohol type, recommendation for wine is prioritized. The subgroup analysis further indicated that the effect of alcohol may be greater in younger adults (<60 years old) with regard to fighting against dementia. Modest alcohol consumption (≤12.5 g/day) is associated with a reduced risk of dementia with 6 g/day of alcohol conferring a lower risk than other levels while excessive drinking (≥38 g/day) may instead elevate the risk.     

Physical activity and the risk of gestational diabetes mellitus: a systematic review and dose–response meta-analysis of epidemiological studies

Physical activity has been inconsistently associated with risk of gestational diabetes mellitus in epidemiological studies, and questions remain about the strength and shape of the dose–response relationship between the two. We therefore conducted a systematic review and meta-analysis of cohort studies and randomized trials on physical activity and gestational diabetes mellitus. PubMed, Embase and Ovid databases were searched for cohort studies, and randomized controlled trials of physical activity and risk of gestational diabetes mellitus, up to August 5th 2015. Summary relative risks (RRs) were estimated using a random effects model. Twenty-five studies (26 publications) were included. For total physical activity the summary RR for high versus low activity was 0.62 (95 % CI 0.41–0.94, I² = 0 %, n = 4) before pregnancy, and 0.66 (95 % CI 0.36–1.21, I² = 0 %, n = 3) during pregnancy. For leisure-time physical activity the respective summary RRs for high versus low activity was 0.78 (95 % CI 0.61–1.00, I² = 47 %, n = 8) before pregnancy, and it was 0.80 (95 % CI 0.64–1.00, I² = 17 %, n = 17) during pregnancy. The summary RR for pre-pregnancy activity was 0.70 (95 % CI 0.49–1.01, I² = 72.6 %, n = 3) per increment of 5 h/week and for activity during pregnancy was 0.98 (95 % CI 0.87–1.09, I² = 0 %, n = 3) per 5 h/week. There was evidence of a nonlinear association between physical activity before pregnancy and the risk of gestational diabetes mellitus, p_nonlinearity = 0.005, with a slightly steeper association at lower levels of activity although further reductions in risk were observed up to 10 h/week. There was also evidence of nonlinearity for physical activity in early pregnancy, p_nonlinearity = 0.008, with no further reduction in risk above 8 h/week. There was some indication of inverse associations between walking (before and during pregnancy) and vigorous activity (before pregnancy) and the risk of gestational diabetes mellitus. This meta-analysis suggests that there is a significant inverse association between physical activity before pregnancy and in early pregnancy and the risk of gestational diabetes mellitus. Further studies are needed to clarify the association between specific types and intensities of activity and gestational diabetes mellitus.     

Coffee consumption and risk of pancreatic cancer: a systematic review and dose–response meta-analysis

The association between coffee consumption and pancreatic cancer risk has been extensively studied; however, there is no consistent conclusion. Therefore, this meta-analysis study sought to evaluate dose–response relationship between them. A search was conducted using the PubMed and Web of Science databases. Thirteen high-quality cohort studies were identified, involving in 959,992 study participants and 3831 pancreatic cancer cases. Comparing the highest with lowest categories of coffee intake, the pooled relative risk (RR) was 1.08 (95% CI 0.94–1.25). For dose–response analysis, no evidence of a nonlinear dose–response association between coffee consumption and pancreatic cancer (p for nonlinearity =0.171) was found. The risk of pancreatic cancer was increased by 5.87% (RR =1.06, 95% CI 1.05–1.07) with the increment of one cup/day. Coffee consumption was identified to be related with the increasing risk of pancreatic cancer in a dose–response manner. Nevertheless, further mechanistic studies are needed to clarify the concerned issues.     

Egg consumption and risk of GI neoplasms: dose–response meta-analysis and systematic review

Purpose

Previous epidemiological studies on egg consumption and the risk of gastrointestinal (GI) neoplasms suggest a positive association; however, data are limited and the evidence remains controversial. This study aims to investigate and quantify the potential dose–response relationship with an evaluation of cancer site-specific differences.

Methods

Relevant studies were identified after the literature search via electronic databases until January 2014. Subgroup analysis for serving portions was performed using two standardized classification methods: (1) less than 3, or 3 or more eggs per week; (2) less than 3, 3–5, or more than 5 eggs per week. Method two excludes studies that only reported consumption frequency. Pooled adjusted odds ratios (ORs) comparing highest and lowest categories of dietary pattern scores were calculated using a random-effects model.

Results

Thirty-seven case–control and seven cohort studies were included for meta-analysis, which contained a total of 424,867 participants and 18,852 GI neoplasm cases. The combined odds ratio (OR) was calculated to 1.15 (95 % CI 1.09–1.22; p value heterogeneity <0.001), showing only a slight increase in risk. The correlation was stronger for colon cancers 1.29 (95 % CI 1.14–1.46; p value heterogeneity <0.22). Dose–response analysis revealed similar results with stratification methods, and the ORs for an intake of <3 and ≥3 eggs per week were 1.14 (95 % CI 1.07–1.22; p value heterogeneity = 0.38) and 1.25 (95 % CI 1.14–1.38; p value heterogeneity = 0.25), respectively. With method 2, the ORs for an intake of <3, 3–5, and >5 eggs per week were 1.13 (95 % CI 1.06–1.21; p value heterogeneity = 0.25), 1.14 (95 % CI 1.01–1.29; p value heterogeneity = 0.06), and 1.19 (95 % CI 1.01–1.39; p value heterogeneity <0.001), respectively.

Conclusion

This study provides evidence that egg consumption is associated with a positive dose–response association with the development of GI neoplasms.     

Alcohol,alcoholic beverages,and melanoma risk: a systematic literature review and dose–response meta-analysis

Purpose

Several studies in recent years have investigated the relationship between alcohol intake and melanoma risk, with conflicting results. To help clarify this issue, we conducted a literature review and dose–response meta-analysis of studies published until June 30th, 2017, that examined the association between alcohol intake (overall and by beverage type) and melanoma risk.

Methods

We used random effect models with maximum likelihood estimation to calculate summary relative risk (SRR) and 95% confidence intervals (95%CI).

Results

We included 20 independent studies (encompassing 10,555 melanoma cases and over 1.6 million non-cases/controls) published during 1986–2016, of which six had a prospective cohort study design. Adjustment for phenotypic characteristics and sunlight exposure was performed in 11 and nine studies, respectively. Alcohol intake was moderately associated with melanoma risk: the SRR were 1.29 (95% CI 1.14–1.45) for those in the highest vs. lowest category of current alcohol intake, and 1.96 (95% CI 1.02–3.76, I²?=?0%) for cumulative intake. In the dose–response analysis, the increase in risk associated with a 10 g increment in daily alcohol intake was 1.07 (95% CI 1.03–1.11). Risk estimates did not differ by gender, study design and adjustment for confounders; between-studies heterogeneity was acceptable, and there was no evidence of publication bias.

Conclusions

Our findings suggest that alcohol drinking may be moderately associated with increased melanoma risk, although residual confounding and bias cannot be ruled out. Further research is needed to confirm these findings, clarify the role of the different alcohol sources, and investigate the interaction with known melanoma risk factors.

     

Whole grain and refined grain consumption and the risk of type 2 diabetes: a systematic review and dose–response meta-analysis of cohort studies

Several studies have suggested a protective effect of intake of whole grains, but not refined grains on type 2 diabetes risk, but the dose–response relationship between different types of grains and type 2 diabetes has not been established. We conducted a systematic review and meta-analysis of prospective studies of grain intake and type 2 diabetes. We searched the PubMed database for studies of grain intake and risk of type 2 diabetes, up to June 5th, 2013. Summary relative risks were calculated using a random effects model. Sixteen cohort studies were included in the analyses. The summary relative risk per 3 servings per day was 0.68 (95 % CI 0.58–0.81, I² = 82 %, n = 10) for whole grains and 0.95 (95 % CI 0.88–1.04, I² = 53 %, n = 6) for refined grains. A nonlinear association was observed for whole grains, p _nonlinearity < 0.0001, but not for refined grains, p _nonlinearity = 0.10. Inverse associations were observed for subtypes of whole grains including whole grain bread, whole grain cereals, wheat bran and brown rice, but these results were based on few studies, while white rice was associated with increased risk. Our meta-analysis suggests that a high whole grain intake, but not refined grains, is associated with reduced type 2 diabetes risk. However, a positive association with intake of white rice and inverse associations between several specific types of whole grains and type 2 diabetes warrant further investigations. Our results support public health recommendations to replace refined grains with whole grains and suggest that at least two servings of whole grains per day should be consumed to reduce type 2 diabetes risk.     

Dairy foods intake and risk of Parkinson’s disease: a dose–response meta-analysis of prospective cohort studies

Dairy foods have been linked to Parkinson’s disease (PD), and a meta-analysis of prospective cohort studies on dairy foods intake and PD risk was conducted. Eligible studies were identified in a literature search of EMBASE and PubMed up to April 2014. Seven results from prospective studies were included, including 1,083 PD cases among 304,193 subjects. The combined risk of PD for highest vs. lowest level of dairy foods intake was 1.40 (1.20–1.63) overall, 1.66 (1.29–2.14) for men and 1.15 (0.85–1.56) for women. For highest vs. lowest level, the PD risk was 1.45 (1.23–1.73) for milk, 1.26 (0.99–1.60) for cheese, 0.95 (0.76–1.20) for yogurt and 0.76 (0.51–1.13) for butter. The linear dose–response relationship showed that PD risk increased by 17 % [1.17 (1.06–1.30)] for every 200 g/day increment in milk intake (P_{for non-linearity} = 0.22), and 13 % [1.13 (0.91–1.40)] for every 10 g/day increment in cheese intake (P_{for non-linearity} = 0.39). The absolute risk differences were estimated to be 2–4 PD cases per 100,000 person-years for every 200 g/day increment in milk intake, and 1–3 PD cases per 100,000 person-years for every 10 g/day increment in cheese intake. Dairy foods (milk, cheese) might be positively associated with increased risk of PD, especially for men.     

Height and body fatness and colorectal cancer risk: an update of the WCRF–AICR systematic review of published prospective studies

Purpose

There is no published dose–response meta-analysis on the association between height and colorectal cancer risk (CRC) by sex and anatomical sub-site. We conducted a meta-analysis of prospective studies on the association between height and CRC risk with subgroup analysis and updated evidence on the association between body fatness and CRC risk.

Methods

PubMed and several other databases were searched up to November 2016. A random effects model was used to calculate dose–response summary relative risks (RR’s).

Results

47 studies were included in the meta-analyses including 50,936 cases among 7,393,510 participants. The findings support the existing evidence regarding a positive association of height, general and abdominal body fatness and CRC risk. The summary RR were 1.04 [95% (CI)1.02–1.05, I² = 91%] per 5 cm increase in height, 1.02 [95% (CI)1.01–1.02, I² = 0%] per 5 kg increase in weight, 1.06 [95% (CI)1.04–1.07, I² = 83%] per 5 kg/m² increase in BMI, 1.02 [95% (CI)1.02–1.03, I² = 4%] per 10 cm increase in waist circumference, 1.03 [95% (CI)1.01–1.05, I² = 16%] per 0.1 unit increase in waist to hip ratio. The significant association for height and CRC risk was similar in men and women. The significant association for BMI and CRC risk was stronger in men than in women.

Conclusion

The positive association between height and risk of CRC suggests that life factors during childhood and early adulthood might play a role in CRC aetiology. Higher general and abdominal body fatness during adulthood are risk factors of CRC and these associations are stronger in men than in women.

     

Milk and dairy consumption and risk of cardiovascular diseases and all-cause mortality: dose–response meta-analysis of prospective cohort studies

With a growing number of prospective cohort studies, an updated dose–response meta-analysis of milk and dairy products with all-cause mortality, coronary heart disease (CHD) or cardiovascular disease (CVD) have been conducted. PubMed, Embase and Scopus were searched for articles published up to September 2016. Random-effect meta-analyses with summarised dose–response data were performed for total (high-fat/low-fat) dairy, milk, fermented dairy, cheese and yogurt. Non-linear associations were investigated using the spine models and heterogeneity by subgroup analyses. A total of 29 cohort studies were available for meta-analysis, with 938,465 participants and 93,158 mortality, 28,419 CHD and 25,416 CVD cases. No associations were found for total (high-fat/low-fat) dairy, and milk with the health outcomes of mortality, CHD or CVD. Inverse associations were found between total fermented dairy (included sour milk products, cheese or yogurt; per 20 g/day) with mortality (RR 0.98, 95% CI 0.97–0.99; I² = 94.4%) and CVD risk (RR 0.98, 95% CI 0.97–0.99; I² = 87.5%). Further analyses of individual fermented dairy of cheese and yogurt showed cheese to have a 2% lower risk of CVD (RR 0.98, 95% CI 0.95–1.00; I² = 82.6%) per 10 g/day, but not yogurt. All of these marginally inverse associations of totally fermented dairy and cheese were attenuated in sensitivity analyses by removing one large Swedish study. This meta-analysis combining data from 29 prospective cohort studies demonstrated neutral associations between dairy products and cardiovascular and all-cause mortality. For future studies it is important to investigate in more detail how dairy products can be replaced by other foods.     

Dietary fiber intake and risk of type 2 diabetes: a dose–response analysis of prospective studies

Observational studies suggest an association between dietary fiber intake and risk of type 2 diabetes, but the results are inconclusive. We conducted a meta-analysis of prospective studies evaluating the associations of dietary fiber intake and risk of type 2 diabetes. Relevant studies were identified by searching EMBASE (from 1974 to April 2013) and PubMed (from 1966 to April 2013). The fixed or random-effect model was selected based on the homogeneity test among studies. In addition, a 2-stage random-effects dose–response meta-analysis was performed. We identified 17 prospective cohort studies of dietary fiber intake and risk of type 2 diabetes involving 19,033 cases and 488,293 participants. The combined RR (95 % CI) of type 2 diabetes for intake of total dietary fiber, cereal fiber, fruit fiber and insoluble fiber was 0.81 (0.73–0.90), 0.77 (0.69–0.85), 0.94 (0.88–0.99) and 0.75 (0.63–0.89), respectively. A nonlinear relationship was found of total dietary fiber intake with risk of type 2 diabetes (P _{for nonlinearity} < 0.01), and the RRs (95 % CI) of type 2 diabetes were 0.98 (0.90–1.06), 0.97 (0.87–1.07), 0.89 (0.80–0.99), 0.76 (0.65–0.88), and 0.66 (0.53–0.82) for 15, 20, 25, 30, and 35 g/day. The departure from nonlinear relationship was not significant (P _{for nonlinearity} = 0.72), and the risk of type 2 diabetes decreased by 6 % (RR 0.94, 95 % CI 0.93–0.96) for 2 g/day increment in cereal fiber intake. Findings from this meta-analysis indicate that the intakes of dietary fiber may be inversely associated with risk of type 2 diabetes.     

Effect of long-term weight gain on the risk of breast cancer across women’s whole adulthood as well as hormone-changed menopause stages: A systematic review and dose–response meta-analysis

Adult weight gain is a good indicator of excess body fatness for breast cancer risk. However, little is known about the effect of weight gain during other special periods in women’s lifetime. A publication search in PubMed and Embase through April 2020 was conducted. A primary meta-analysis comparing the highest and lowest category and a secondary meta-analysis based on dose–response meta-analysis were performed to calculate risk estimates with 95% confidence intervals using a random-effects model. For postmenopausal breast cancer, the relative risk for highest vs. lowest category of adult weight gain and weight gain since menopause were 1.55 and 1.59 (RR = 1.55, 95% CI: 1.40, 1.71; RR = 1.59, 95% CI: 1.23, 2.05). For per 5 kg increase in adult weight gain, the summary RR of postmenopausal breast cancer was 1.08 (RR = 1.08, 95% CI: 1.07, 1.09), which is much stronger in Asian women (RR = 1.34, 95% CI: 1.22, 1.47). There was no significant finding among premenopausal women (RR = 1.00, 95% CI: 0.83, 1.21). Same as adult weight gain, weight gain since menopause might be an equivalent predictor for postmenopausal breast cancer risk. More studies are warranted to confirm the magnitude of this association further.     

Caffeine intake during pregnancy and adverse birth outcomes: a systematic review and dose–response meta-analysis

Caffeine is commonly consumed during pregnancy, crosses the placenta, with fetal serum concentrations similar to the mother’s, but studies of birth outcome show conflicting findings. We systematically searched Medline and Embase for relevant publications. We conducted meta-analysis of dose–response curves for associations between caffeine intake and spontaneous abortion, stillbirth, preterm delivery, low birth weight and small for gestational age (SGA) infants. Meta-analyses included 60 unique publications from 53 cohort and case–control studies. An increment of 100 g caffeine was associated with a 14 % (95 % CI 10–19 %) increase in risk of spontaneous abortion, 19 % (5–35 %) stillbirth, 2 % (?2 to 6 %) preterm delivery, 7 % (1–12 %) low birth weight, and 10 % (95 % CI 6–14 %) SGA. There was substantial heterogeneity in all models, partly explained by adjustment for smoking and previous obstetric history, but not by prospective assessment of caffeine intake. There was evidence of small-study effects such as publication bias. Greater caffeine intake is associated with an increase in spontaneous abortion, stillbirth, low birth weight, and SGA, but not preterm delivery. There is no identifiable threshold below which the associations are not apparent, but the size of the associations are generally modest within the range of usual intake and are potentially explained by bias in study design or publication. There is therefore insufficient evidence to support further reductions in the maximum recommended intake of caffeine, but maintenance of current recommendations is a wise precaution.