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Review
. 2023 Feb 14:67.
doi: 10.29219/fnr.v67.8961. eCollection 2023.

Nuts and seeds consumption and risk of cardiovascular disease, type 2 diabetes and their risk factors: a systematic review and meta-analysis

Erik Kristoffer Arnesen  1 , Birna Thorisdottir  2 , Linnea Bärebring  3 , Fredrik Söderlund  4 , Bright I Nwaru  5 , Ulrike Spielau  6   7 , Jutta Dierkes  6   7   8 , Alfons Ramel  9 , Christel Lamberg-Allardt  10 , Agneta Åkesson  4
Affiliations
Review

Nuts and seeds consumption and risk of cardiovascular disease, type 2 diabetes and their risk factors: a systematic review and meta-analysis

Erik Kristoffer Arnesen et al. Food Nutr Res. .

Abstract

Objectives: We aimed to systematically review studies and evaluate the strength of the evidence on nuts/seeds consumption and cardiometabolic diseases and their risk factors among adults.

Methods: A protocol was pre-registered in PROSPERO (CRD42021270554). We searched MEDLINE, Embase, Cochrane Central Register of Controlled Trials and Scopus up to September 20, 2021 for prospective cohort studies and ≥12-week randomized controlled trials (RCTs). Main outcomes were cardiovascular disease (CVD), coronary heart disease (CHD), stroke and type 2 diabetes (T2D), secondary total-/low density lipoprotein (LDL)-cholesterol, blood pressure and glycaemic markers. Data extraction and risk of bias (RoB) assessments (using RoB 2.0 and RoB-NObS) were performed in duplicate. Effect sizes were pooled using random-effects meta-analyses and expressed as relative risk (RR) or weighted mean differences with 95% confidence intervals (CI); heterogeneity quantified as I 2. One-stage dose-response analyses assessed the linear and non-linear associations with CVD, CHD, stroke and T2D. The strength of evidence was classified per the World Cancer Research Fund criteria.

Results: After screening 23,244 references, we included 42 papers from cohort studies (28 unique cohorts, 1,890,573 participants) and 18 RCTs (2,266 participants). In the cohorts, mainly populations with low consumption, high versus low total nuts/seeds consumption was inversely associated with total CVD (RR 0.81; 95% CI 0.75, 0.86; I 2 = 67%), CVD mortality (0.77; 0.72, 0.82; I 2 = 59.3%), CHD (0.82; 0.76, 0.89; I 2 = 64%), CHD mortality (0.75; 0.65, 0.87; I 2 = 66.9%) and non-fatal CHD (0.85; 0.75, 0.96; I 2 = 62.2%). According to the non-linear dose-response analyses, consumption of 30 g/day of total nuts/seeds was associated with RRs of similar magnitude. For stroke and T2D the summary RR for high versus low intake was 0.91 (95% CI 0.85, 0.97; I 2 = 24.8%) and 0.95 (0.75, 1.21; I 2 = 82.2%). Intake of nuts (median ~50 g/day) lowered total (-0.15 mmol/L; -0.22, -0.08; I 2 = 31.2%) and LDL-cholesterol (-0.13 mmol/L; -0.21, -0.05; I 2 = 68.6%), but not blood pressure. Findings on fasting glucose, HbA1c and insulin resistance were conflicting. The results were robust to sensitivity and subgroup analyses. We rated the associations between nuts/seeds and both CVD and CHD as probable. There was limited but suggestive evidence for no association with stroke. No conclusion could be made for T2D.

Conclusion: There is a probable relationship between consumption of nuts/seeds and lower risk of CVD, mostly driven by CHD, possibly in part through effects on blood lipids. More research on stroke and T2D may affect the conclusions. The evidence of specific nuts should be further investigated.

Keywords: atherosclerosis; cardiovascular disease; diabetes mellitus type 2; meta-analysis; nuts; systematic review.

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Conflict of interest statement

The authors declare no potential conflicts of interest. Partial funding was received from the Nordic Council of Ministers and governmental food and health authorities of Norway, Finland, Sweden, Denmark, and Iceland.

Figures

Fig. 1
Fig. 1
Study selection flowchart. Source: Page et al. (32). *Some had more than 1 reason for exclusion.
Fig. 2
Fig. 2
Summary risk of bias per domain in cohort studies.
Fig. 3
Fig. 3
Summary risk of bias per domain in randomized controlled trials. Top: parallell studies, bottom: crossover studies.
Fig. 4
Fig. 4
Summary forest plot of pooled relative risk estimates for associations between high versus low total nuts/seeds consumption and risk of cardiometabolic disease. Meta-analyses were performed with random-effects restricted maximum likelihood models. I2 = heterogeneity (%).
Fig. 5
Fig. 5
Linear (red, dashed line) and non-linear dose-response (black lines with confidence intervals) association between total nuts and seeds consumption and risk of total cardiovascular disease (panel A; 16 studies) and cardiovascular disease mortaltiy (panel B; 15 studies) in cohort studies, with 0 g/day as reference. Circles show the effect estimates for each level of intake in the individual studies, weighted by the inverse of the standard errors. Vertical axes are log scaled.
Fig. 6
Fig. 6
Linear (red, dashed line) and non-linear dose-response (black lines with confidence intervals) association between total nuts and seeds consumption and risk of total coronary heart disase (panel A; 14 studies), coronary heart disease mortality (panel B; 9 studies) and nonfatal coronary heart disase (panel C; 6 studies) in cohort studies, with 0 g/day as reference. Circles show the effect estimates for each level of intake in the individual studies, weighted by the inverse of the standard errors. Vertical axes are log scaled.
Fig. 7
Fig. 7
Linear (red, dashed line) and non-linear dose-response (black lines with confidence intervals) association between total nuts and seeds consumption and risk of total stroke (panel A; 11 studies), ischaemic stroke (panel B; 8 studies) and stroke mortality (panel C; 6 studies) in cohort studies, with 0 g/day as reference. Circles show the effect estimates for each level of intake in the individual studies, weighted by the inverse of the standard errors. Vertical axes are log scaled.
Fig. 8
Fig. 8
Linear (red, dashed line) and non-linear dose-response (black lines with confidence intervals) association between total nuts and seeds consumption and risk of type 2 diabetes in cohort studies (five studies), with 0 g/day as reference. Circles show the effect estimates for each level of intake in the individual studies, weighted by the inverse of the standard errors. Vertical axis is log scaled.
Fig. 9
Fig. 9
Associations of nuts versus meat consumption and cardiometablic endpoints from substitution models in cohort studies.
Fig. 10
Fig. 10
Forest plots of the effects of nut consumption on total cholesterol (A) and LDL-cholesterol (B) in randomized controlled trials, sorted by type of nut intervention. Effect sizes are weighted mean differences with 95% confidence intervals, in mmol/L. Analyses were performed with random-effects restricted maximum likelihood models.
Fig. 11
Fig. 11
Forest plots of the effects of nut consumption on systolic (A) and diastolic (B) blood pressure in randomized controlled trials, sorted by type of nut intervention. Effect sizes are weighted mean differences with 95% confidence intervals, in mmHg. Analyses were performed with random-effects restricted maximum likelihood models.
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