Search results and characteristics of studies
From the systematic search, eight studies met the inclusion criteria and were included in the meta-analysis (Fig. 1). The included studies comprised five randomized controlled trials (RCTs) and three crossover trials, conducted across diverse populations: healthy individuals (n = 3), overweight/obese adults (n = 2), male smokers (n = 1), and patients with chronic conditions such as coronary artery disease (CAD) (n = 1) and hyperlipidemia (n = 1). Almond supplementation dosages ranged from 5 g/day to 168 g/day, with intervention durations spanning four to 24 weeks (Table 1).
Meta-analysis results
GPx
The random-effects model (Fig. 2) revealed no significant effect of almond supplementation on GPx levels (WMD = 13.04, 95% CI: −10.14, 36.23; p = 0.270). High heterogeneity was observed (I² = 96%, τ² = 373.63).
Meta-analysis effect of almond supplementation on GPx levels.
MDA
The random-effects model (Fig. 3) showed no significant effect of almond supplementation on MDA (WMD = −0.11, 95% CI: −0.26, 0.04; p = 0.141), with moderate heterogeneity (I² = 42.8%, τ² = 0.0131). The analysis was subgrouped by study design, and supplementation dosage. In terms of supplementation dosage, the results showed the almost complete lack of heterogeneity in bout groups suggesting a source of heterogeneity. Supplementation doses < 60 g/day (WMD = −0.03, 95% CI: −0.11, 0.04; p = 0.372, I² = 0%) showed no effect, whereas doses > 60 g/day significantly reduced MDA levels (WMD = −0.46, 95% CI: −0.75, −0.17; p = 0.002, I² = 0%), suggesting that supplementation dosage is key factor to reaching the propriate result.
Meta-analysis effect of almond supplementation on MDA levels.
SOD
Almond supplementation significantly increased SOD levels (Fig. 4) (WMD = 2.02, 95% CI: 0.52, 3.52; p = 0.008), with high heterogeneity (I² = 92%, τ² = 1.83). While subgroup by dosage: Doses < 60 g/day (WMD = 0.87, 95% CI: −1.09, 2.83; p = 0.385, I² = 85%) and > 60 g/day (WMD = 7.96, 95% CI: −5.46, 21.39; p = 0.245, I² = 95%) showed no significant differences.
Meta-analysis effect of almond supplementation on SOD levels.
UA
The random-effects model (Fig. 5) indicated a significant reduction in UA levels (WMD = −0.64, 95% CI: −1.12, −0.16; p = 0.009), with moderate heterogeneity (I² = 55%, τ² = 0.099).
Meta-analysis effect of almond supplementation on UA levels.
8-hydroxy-2’-deoxyguanosine (8OHdG)
The fixed-effects model (Fig. 6) revealed a significant reduction in 8OHdG levels (WMD = −5.83, 95% CI: −7.38, −4.29; p < 0.001), with no observed heterogeneity (I² = 0%).
Meta-analysis effect of almond supplementation on 8-Hydroxy-2’-deoxyguanosine (8OHdG) levels.
Publication bias and sensitivity analysis
Publication bias was assessed using funnel plot, Egger’s test revealing no publication bias. Sensitivity analyses demonstrated that exclusion15 study did not significantly alter the pooled effect sizes, suggesting the robustness of the results.
Quality assessment of included studies
The methodological quality of the included studies was assessed using the Cochrane Risk of Bias Tool 2.0 (Fig. 7). Most studies (n = 6) demonstrated low risk of bias in key domains such as random sequence generation and selective reporting. However, three studies (Jamshed et al.16; Li et al.17; Jia et al.15 had unclear risk due to insufficient reporting of allocation concealment and blinding procedures. One study (Schincaglia et al.18 was rated as high risk for incomplete outcome data due to significant attrition (> 20% dropout rate). Overall, the included studies were of moderate to high quality, with adequate randomization and low risk of selective reporting, though improved transparency in blinding and allocation concealment is needed in future trials.
Summary of risk of bias in included studies.