Table 5.
# | Authors | Type | Findings | Has Effect |
---|---|---|---|---|
1 | Eyster [141] | In vivo | Equol did not impact atherosclerotic lesions. Similar responses of genes to both equol and estradiol might reflect that equol served as a natural selective estrogen receptor modulator in the arteries. Equol modulated the expression of 10 genes in the atherosclerosis model that estradiol did not. | No |
2 | Zhang [123] | In vivo | Equol intervention reduced atherosclerotic lesions in the aorta in high-fat-diet treated apolipoprotein E-deficient mice. Plasma lipid analysis showed that equol intervention reduced triglycerides, TC, and LDL-C and increased HDL-C. | Yes |
3 | Ahuja [142] | Human | In multivariable models, the odds ratio for the presence of CAC in equol producers compared with the equol in non-producers was 0.10 (95 % confidence interval: 0.01, 0.90, p < 0.04). However, serum ISFs were not related to CAC. | Yes |
4 | Zuo [143] | Human | An 8.8-year prospective study including 2572 subjects (40 to 75 years old) found that ISFs and equol were associated with reduced progression of carotid intima-media thickness. Path analyses indicated that the association of serum equol with atherosclerosis was mediated by increased SHBG and decreased blood pressure but not lipids. | Yes |
5 | Zhang [30] | Human | Urinary levels of ISFs and other metabolites of ISFs were not associated with incident CHD, while urinary equol was significantly associated with CHD. The adjusted odds ratios (95% confidence intervals) for CHD across increasing quartiles of equol levels in women were 1 (reference), 0.61 (0.32, 1.15), 0.51 (0.26, 0.98), and 0.46 (0.24, 0.89) (p = 0.02 for trend). | Yes |
Abbreviations: apoE, apolipoprotein E; cIMT, carotid intima–media thickness; HDL, high-density lipoprotein; LDL, low-density lipoprotein; SBG, systolic blood pressure; SHBG, sex hormone-binding globulin; TC, total cholesterol; CAC, coronary artery calcium; SHBG, sex hormone-binding globulin; CHD, coronary heart disease.