The baseline levels of serum lipid parameters are similar to those obtained in other groups of healthy postmenopausal women (Kreijkamp-Kaspers, et al., 2004; Welty, Lee, Lew, & Zhou, 2007). In the current study serum lipids values for TC, LDL-c, HDL-c and TAG are as follows: 5.68 r 0.165 mmol/L, 3.57 r 0.136 mmol/L, 1.65 r 0.066 mmol/L, and 0.966 r 1.08 mmol/L. These values are similar to reports by a comparable to another study of healthy postmenopausal women for TC, LDL-c, HDL-c and TAG: 5.91 r 1.01 mmol/L, 3.70 r 0.83 mmol/L, 1.50 r 0.39 mmol/L and 3.32 r 2.51 mmol/L (Welty et al., 2007). TAG and higher HDL-C were slightly lower in this study group compared to these previous studies, and may indicate a comparatively ‘healthy’ lipid profile in terms of CVD risk (Wu et al., 2006).
In the current study isoflavones did not have a hypo-cholesterolemic effect. There were no changes in TC, LDL-c or TAG. This contrasts with results from Clerici et al. (2007) that isoflavone-enriched pasta reduced both serum TC and LDL-c by 7.3% and 8.6% respectively over a 4-week intervention. Equol producers (n=20) in the group exhibited a similar decrease in serum TC but a larger decrease in serum LDL-c than non-equol producers (Clerici et al., 2007); serum equol was 25.5 r 4 ng/ml in equol producers, which is considerably higher than the equol producers of the current study. The hyper-cholesterolemic sample population recruited by Clerici et al. (2007) may exhibit greater response to isoflavone supplementation (and serum equol) than normolipidemic populations.
In agreement with the results of this study, lipid parameters were not improved after one year of isoflavone supplementation (99 mg/day aglycone) in healthy postmenopausal women (Kreijkamp-Kaspers et al., 2004), nor in the equol producer subgroup (n=60). However, Kreijkamp-Kaspers et al. (2004) did not measure the final serum equol levels and cannot adequately account for the effect of equol production. In another study of postmenopausal women lipid parameters did not respond to isoflavones even when analysing the equol producers (n=117) separately (Hall et al., 2006).
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The current study reported a synergistic effect between kiwifruit consumption and isoflavone supplementation exclusively in equol producers; serum HDL-c increased by 9.5% following the kiwifruit/isoflavone treatment. Equol producers receiving isoflavone treatment alone had no change in serum HDL-c, whereas non-equol producers experienced a decline in serum HDL-c across both treatments (-5.0% in the isoflavone and -4.6% in the kiwifruit/isoflavone treatment). No other interventions have reported similar findings relative to equol production. Although serum HDL-c decreased in non-equol producers, HDL-c was significantly higher at baseline and decreased to a level equivalent to the equol producers after each treatment.
Potter et al. (1998) reported an increase in serum HDL-c in postmenopausal women receiving 56 mg isoflavone per day for 24 months; it is not known whether equol production modulated this effect, as serum equol was not measured. A study by Wu et al. (2006) found a significant increase in serum HDL-c following 6-month isoflavone supplementation in conjunction with walking, but this effect was significant for walking independently of isoflavone intake.
The findings of this study suggest that some bioactive component/s of green kiwifruit may act in synergy with equol, due to the fact serum HDL-c dropped in non-equol producers consuming kiwifruit. Serum HDL-c is inversely associated with risk of CVD development; this relationship has been partially attributed to the action of sequestering detrimental oxidised-LDL-c (Navab, Reddy, Van Lenten, & Fogelman, 2011). Regular long-term supplementation of isoflavones and kiwifruit in postmenopausal equol producing women may reduce the risk of CVD development. The physiological mechanism underlying this benefit in equol producers is unclear but there are several possibilities that require further research. It is not currently known how HDL-c synthesis is affected by ER-E agonist activity. Equol’s antioxidant qualities may reduce systemic inflammation: an inflammatory environment is detrimental to the anti-atherogenic role of HDL-c (Navab et al., 2011) and a study by Nishide et al. (2013) found a reduction in inflammatory cytokine expression in the bone marrow cells of Ovx mice treated with equol. Moreover, equol and the carotenoid lutein, which is present in kiwifruit, have been shown to act synergistically in their inhibition of
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osteoclastogenesis (Tadaishi et al., 2011). It is possible, although not estimated in this study that a combination of antioxidants, from equol and lutein, decreased systemic inflammation during the kiwifruit and isoflavone treatment and this was associated with the increase in serum HDL-c. However, research is this area is limited and further studies are warranted to measure the correlation between serum equol, carotenoids and lipids in postmenopausal women supplemented with isoflavones.
HDL-c is also affected by particular dietary factors and nutrients. Specific foods, such as, oatmeal, legumes, and walnuts have been shown to increase HDL-c (Welty et al., 2007). Polyunsaturated fatty acids (PUFA) can increase HDL-c while trans-fatty acids tend to decrease HDL-c. (Mensink, Zock, Kester, & Katan, 2003). A high intake of low glycaemic carbohydrates can lead to a decrease HDL-c (Mensink et al., 2003). It is unclear whether intake of these dietary factors differed between study groups or over the intervention period, as they were not reported in this study. However, the changes in serum HDL-c seen here are consistent across the group according to equol production, which is directly related to isoflavone intake, and it is not likely that other dietary components had a major effect on this parameter.