Literature search and study characteristics

The detailed procedures of the article search and screening were presented in Fig. 1. Briefly, the search strategy retrieved 110,704 papers: 33,131 from Pubmed, 72,398 from Embase and 5175 from Cochrane library. After removing 21,411 duplicate articles, 89,293 articles were assessed. Among them, 89,114 articles were excluded after reviewing abstracts and titles, leaving 179 articles for full-text review. Of these, 136 papers were excluded due to: no results provided the association between dietary fat/fat subclasses and cardiovascular disease, duplicate publications, case-control studies, and only investigated fat from breakfast. In total, 43 publications [14, 15, 17, 18, 24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62] (63 studies, since 19 studies reported results for more than one study) that presented risk estimates for dietary total fat or major fat subclasses intake and CVDs risk were identified. The main characters of these studies are presented in Additional file 1: Table S1.

Fig. 1 Search, screening and selection process of prospective cohort studies of dietary total fat and major fat subclasses and risk of cardiovascular disease Full size image

Total fat intake and risk of CVDs

Forty-five studies reported the relationship between total dietary fat intake and CVDs risk (CVDs incidence and mortality). Highest versus lowest levels of total dietary fat were not associated with the CVDs risk [0.97(0.93–1.01), I2 = 54.0%; Fig. 2]. Sensitivity analysis showed that no individual study had an excessive influence on the pooled effect. There was evidence of significant heterogeneity (I2 = 54.0%), which was further explored in meta-regression. All covariates investigated in the meta-regression provided a poor explanation of the heterogeneity. In addition, the analysis was repeated stratified according to each covariate. The results were consistent with that observed in meta-regression.

Fig. 2 Forest plots of cardiovascular disease for the highest versus lowest categories of dietary total fat intake Full size image

Subgroup analysis

As shown in Table 1, non-significant associations of total dietary fat intake with cardiovascular risk were detected in the subgroup analysis conducted by geographical location (Americas, Europe, or Asia); follow-up duration (< 10 years or ≥ 10 years); And whether the results were adjusted for age, sex, physical activity, energy intake, alcohol, smoking, or body mass index.

Table 1 Subgroup analysis of dietary total fat and major fat subclasses and risk of cardiovascular disease Full size table

Publication bias

Egger test showed no evidence of significant publication bias for this meta-analysis with cardiovascular risk and total fat intake (t = − 1.01, P = 0.319).

Trans fatty acids intake and risk of CVDs

Twenty-four studies reported the effect of dietary TFA intake on CVDs risk. Highest versus lowest levels of dietary TFA were associated with increased risk of CVDs [1.14(1.08–1.21), I2 = 26.1%; Fig. 3a]. Sensitivity analysis showed that no individual study had an excessive influence on the pooled effect.

Fig. 3 Forest plots of cardiovascular disease for the highest versus lowest categories of dietary trans fatty acids (a), saturated fatty acids (a), monounsaturated fatty acids (b), and polyunsaturated fatty acids intake (b) Full size image

Subgroup analysis

In subgroup analysis, the positive association between dietary trans fatty acids intake and CVDs risk were observed in most studies except those were not adjusted for smoking and body mass index, and studies adjusted for sex (Table 1).

Publication bias

Egger test showed no evidence of significant publication bias for this meta-analysis with cardiovascular risk and TFA intake (t = − 1.00, P = 0.330).

Saturated fatty acids intake and risk of CVDs

Fifty-six studies reported the association between dietary SFA intake and CVDs risk. Highest versus lowest levels of dietary SFA were not associated with the risk of CVDs [0.97(0.93–1.02), I2 = 56.8%; Fig. 3a]. Sensitivity analysis showed that no individual study had an excessive influence on the pooled effect. There was evidence of significant heterogeneity (I2 = 56.8%), which was further explored in meta-regression. All covariates investigated in the meta-regression provided a poor explanation of the heterogeneity. In addition, the analysis was repeated stratified according to each covariate. The results were consistent with that observed in meta-regression.

Subgroup analysis

As shown in Table 1, a significant inverse association was observed in Asia population [0.84(0.73–0.97), I2 = 42.3%] but not American and European population. No significant associations were found for subgroups by follow-up duration (< 10 years or ≥ 10 years), or whether the results were adjusted for age, sex, physical activity, energy intake, alcohol, smoking, or body mass index (P > 0.05).

Publication bias

Egger test showed no evidence of significant publication bias for this meta-analysis with cardiovascular risk and saturated fatty acids intake (t = − 0.28, P = 0.777).

Monounsaturated fatty acids intake and risk of CVDs

Forty-three studies reported the relationship between dietary MUFA intake and CVDs risk. Highest versus lowest levels of dietary MUFA were not associated with the risk of CVDs risk [0.97(0.93–1.01), I2 = 50.3%; Fig. 3b]. Sensitivity analysis showed that no individual study had an excessive influence on the pooled effect. There was evidence of significant heterogeneity (I2 = 50.3%), which was further explored in meta-regression. All covariates investigated in the meta-regression provided a poor explanation of the heterogeneity. In addition, the analysis was repeated stratified according to each covariate. The results were consistent with that observed in meta-regression.

Subgroup analysis

Non-significant associations of dietary monounsaturated fatty acids intake and cardiovascular risk were detected in the subgroup analysis conducted by geographical location (Americas, Europe, or other), follow-up duration (< 10 years or ≥ 10 years), and whether the results were adjusted for age, sex, physical activity, energy intake, alcohol, smoking, or body mass index (Table 1).

Publication bias

Egger test showed no evidence of significant publication bias for this meta-analysis with cardiovascular risk and monounsaturated fatty acids intake (t = − 1.45, P = 0.154).

Polyunsaturated fatty acids intake and risk of CVDs

Forty-five studies reported the effect of dietary PUFA intake on CVDs risk. Highest versus lowest levels of dietary PUFA were not associated with the risk of cardiovascular disease [0.97(0.93–1.004), I2 = 55.8%; Fig. 3b]. Sensitivity analysis showed that no individual study had an excessive influence on the pooled effect. There was evidence of significant heterogeneity (I2 = 55.8%), which was further explored in meta-regression. All covariates investigated in the meta-regression provided a poor explanation of the heterogeneity. In addition, the analysis was repeated stratified according to each covariate. The results were consistent with that observed in meta-regression.

Subgroup analysis

In subgroup analysis, a significant inverse association was observed in the studies that has been followed up more than 10 years [0.95(0.91–0.99), I2 = 62.4%] (Table 1). No significant associations were found for the other subgroups analysis (P > 0.05).

Publication bias

Egger test showed no evidence of significant publication bias for this meta-analysis with cardiovascular risk and polyunsaturated fatty acids intake (t = − 1.74, P = 0.088).

Dose-response analysis

The dose-response analysis suggested non-significant linear relationship between dietary total fat, SFA, MUFA, and PUFA and CVDs risk [0.99(0.97–1.01), P linearity = 0.164 and 1.01(0.99–1.02), P linearity = 0.848 for an increment of 5% energy and 5 g/day of total dietary fat, respectively; 0.99(0.95–1.04), P linearity = 0.474 and 0.98 (0.95–1.00), P linearity = 0.526 for an increment of 5% energy and 5 g/day of SFA, respectively; 0.96(0.91–1.02), P linearity = 0.471 and 1.00 (0.94–1.06), P linearity = 0.256 for an increment of 5% energy and 5 g/day of MUFA, respectively; 0.92(0.84–1.01), P linearity = 0.757 for an increment of 5% energy of dietary PUFA intake). However, the risk of CVDs increased 16% [1.16(1.07–1.25), P linearity = 0.033], and 4% [1.04(1.01–1.07), P linearity = 0.030] for an increment of 2% energy of dietary TFA intake and 5 g/day dietary PUFA intake, respectively (Figs. 4, 5, Additional file 2: Figure S1, Additional file 3: Figure S2, Additional file 4: Figure S3, Additional file 5: Figure S4, and Additional file 6: Figure S5).

Fig. 4 Dose-response analyses of the linear association between dietary total fat (a), trans fatty acids (b), saturated fatty acids (c), monounsaturated fatty acids (d), and polyunsaturated fatty acids intake (e) and the risk of cardiovascular disease (% energy/day) Full size image