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Meta-Analysis
. 2016 Jan 7;2016(1):CD011472.
doi: 10.1002/14651858.CD011472.pub2.

Dietary fibre for the primary prevention of cardiovascular disease

Louise Hartley  1 , Michael D May, Emma Loveman, Jill L Colquitt, Karen Rees
Affiliations
Meta-Analysis

Dietary fibre for the primary prevention of cardiovascular disease

Louise Hartley et al. Cochrane Database Syst Rev. .

Abstract

Background: The prevention of cardiovascular disease (CVD) is a key public health priority. A number of dietary factors have been associated with modifying CVD risk factors. One such factor is dietary fibre which may have a beneficial association with CVD risk factors. There is a need to review the current evidence from randomised controlled trials (RCTs) in this area.

Objectives: The primary objective of this systematic review was to determine the effectiveness of dietary fibre for the primary prevention of CVD.

Search methods: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library, Ovid MEDLINE (1946 to January 2015), Ovid EMBASE (1947 to January 2015) and Science Citation Index Expanded (1970 to January 2015) as well as two clinical trial registers in January 2015. We also checked reference lists of relevant articles. No language restrictions were applied.

Selection criteria: We selected RCTs that assessed the effects of dietary fibre compared with no intervention or a minimal intervention on CVD and related risk factors. Participants included adults who are at risk of CVD or those from the general population.

Data collection and analysis: Two authors independently selected studies, extracted data and assessed risk of bias; a third author checked any differences. A different author checked analyses.

Main results: We included 23 RCTs (1513 participants randomised) examining the effect of dietary fibre. The risk of bias was unclear for most studies and studies had small sample sizes. Few studies had an intervention duration of longer than 12 weeks. There was a wide variety of fibre sources used, with little similarity between groups in the choice of intervention.None of the studies reported on mortality (total or cardiovascular) or cardiovascular events. Results on lipids suggest there is a significant beneficial effect of increased fibre on total cholesterol levels (17 trials (20 comparisons), 1067 participants randomised, mean difference -0.23 mmol/L, 95% CI -0.40 to -0.06), and LDL cholesterol levels (mean difference -0.14 mmol/L, 95% CI -0.22 to -0.06) but not on triglyceride levels (mean difference 0.00 mmol/L, 95% CI -0.04 to 0.05), and there was a very small but statistically significant decrease rather than increase in HDL levels with increased fibre intake (mean difference -0.03 mmol/L, 95% CI -0.06 to -0.01). Fewer studies (10 trials, 661 participants randomised) reported blood pressure outcomes where there is a significant effect of increased fibre consumption on diastolic blood pressure (mean difference -1.77 mmHg, 95% CI -2.61 to -0.92) whilst there is a reduction in systolic blood pressure with fibre but this does not reach statistical significance (mean difference -1.92 mmHg, 95% CI -4.02 to 0.19). There did not appear to be any subgroup effects by the nature of the type of intervention (fibre supplements or provision of foods/advice to increase fibre consumption) or the type of fibre (soluble/insoluble) although the number of studies contributing to each subgroup were small. All analyses need to be viewed with caution given the risks of bias observed for total cholesterol and the statistical heterogeneity observed for systolic blood pressure. Adverse events, where reported, appeared to mostly reflect mild to moderate gastrointestinal side-effects and these were generally reported more in the fibre intervention groups than the control groups.

Authors' conclusions: Studies were short term and therefore did not report on our primary outcomes, CVD clinical events. The pooled analyses for CVD risk factors suggest reductions in total cholesterol and LDL cholesterol with increased fibre intake, and reductions in diastolic blood pressure. There were no obvious effects of subgroup analyses by type of intervention or fibre type but the number of studies included in each of these analyses were small. Risk of bias was unclear in the majority of studies and high for some quality domains so results need to be interpreted cautiously. There is a need for longer term, well-conducted RCTs to determine the effects of fibre type (soluble versus insoluble) and administration (supplements versus foods) on CVD events and risk factors for the primary prevention of CVD.

PubMed Disclaimer

Conflict of interest statement

LH ‐ None

MM ‐ My work in the pharmaceutical industry as a Regulatory Affairs Consultant is not related in any way to this review. I was not involved in development, design or any review of efficacy of drug products. My work is based only in chemistry manufacturing and controls to ensure quality of established drug products for license changes.

EL ‐ None

JC ‐ None

KR ‐ None

Figures

1
1
Study flow diagram.
2
2
Risk of bias summary: review authors' judgements about each risk of bias item for each included study.
3
3
Risk of bias graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.
4
4
Funnel plot of comparison: 1 Fibre versus control, outcome: 1.1 Total Cholesterol mmol/L change.
1.1
1.1. Analysis
Comparison 1 Fibre versus control, Outcome 1 Total Cholesterol mmol/L change.
1.2
1.2. Analysis
Comparison 1 Fibre versus control, Outcome 2 HDL Cholesterol mmol/L change.
1.3
1.3. Analysis
Comparison 1 Fibre versus control, Outcome 3 LDL Cholesterol mmol/L change.
1.4
1.4. Analysis
Comparison 1 Fibre versus control, Outcome 4 Triglycerides mmol/L change.
1.5
1.5. Analysis
Comparison 1 Fibre versus control, Outcome 5 Systolic blood pressure (mmHg) change.
1.6
1.6. Analysis
Comparison 1 Fibre versus control, Outcome 6 Diastolic blood pressure (mmHg) change.
2.1
2.1. Analysis
Comparison 2 Subgroup analyses, Outcome 1 Total cholesterol mmol/L change.
2.2
2.2. Analysis
Comparison 2 Subgroup analyses, Outcome 2 HDL Cholesterol mmol/L change.
2.3
2.3. Analysis
Comparison 2 Subgroup analyses, Outcome 3 LDL Cholesterol mmol/L change.
2.4
2.4. Analysis
Comparison 2 Subgroup analyses, Outcome 4 Triglycerides mmol/L change.
2.5
2.5. Analysis
Comparison 2 Subgroup analyses, Outcome 5 Systolic blood pressure (mmHg) change.
2.6
2.6. Analysis
Comparison 2 Subgroup analyses, Outcome 6 Diastolic blood pressure (mmHg) change.
2.7
2.7. Analysis
Comparison 2 Subgroup analyses, Outcome 7 Total cholesterol mmol/L change.
2.8
2.8. Analysis
Comparison 2 Subgroup analyses, Outcome 8 HDL Cholesterol mmol/L change.
2.9
2.9. Analysis
Comparison 2 Subgroup analyses, Outcome 9 LDL Cholesterol mmol/L change.
2.10
2.10. Analysis
Comparison 2 Subgroup analyses, Outcome 10 Triglycerides mmol/L change.
2.11
2.11. Analysis
Comparison 2 Subgroup analyses, Outcome 11 Systolic blood pressure (mmHg) change.
2.12
2.12. Analysis
Comparison 2 Subgroup analyses, Outcome 12 Diastolic blood pressure (mmHg) change.
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