This study appears to be the first to reveal the possible antihypertensive effects of black sesame meal in participants with prehypertension. The results demonstrated that after matching for age, BMI and BP, 4-week daily administration of 2.52 g black sesame meal caused a significant reduction in SBP, by an average of 8.2 mmHg.
Interestingly, the INTERSALT study revealed that a reduction of 2 to 3 mmHg of SBP was associated with a 4% decrease in mortality from CVD in the USA and UK [22
] and a 6.4% decrease in mortality from cerebral vascular disease in Japan [1
]. Based on these longer term studies, if the present reduction in BP with sesame meal (8.2 mmHg) was sustained in the long term, this could reduce the risk of CVD and stroke by 16.4% and 26.2% respectively. This study shows that the ingestion of black sesame meal may have a potential effect on reduction in mortality from CVD and stroke.
Although no previous study has directly investigated the effect of black sesame meal on BP, many studies have reported the potential antihypertensive effect of sesame's contents (i.e. lignan and vitamin E) in humans and rats [8
]. However, this is inconsistent with many other previous studies which reported different results [12
]. Some previous studies have reported that supplementation of either alpha-tocopherol alone or mixed with gamma-tocopherol increased [12
] or did not change [13
] BP in diabetic or treated hypertensive patients [14
]. This may be attributed to an interference of alpha-tocopherol and the antihypertensive drug taken by some subjects in previous studies; whereas subjects in this study were healthy and did not take any antihypertensive drug. Moreover, the dose of vitamin E in those previous studies may have been so high that it caused increased or unchanged effects on BP.
A possible mechanism responsible for the antihypertensive effect of black sesame meal in this study may be an improved balance between relaxing and contracting factors in the endothelium of blood vessels. In this study, black sesame meal may have enhanced the relaxing factor, resulting in improved endothelium-dependent vasorelaxation in the pre-hypertensive participants relating to oxidative stress. The antihypertensive effect of sesamin, in mildly hypertensive humans was supported by a previous study [9
]. The authors reported that the ingestion of 60 g of sesamin per day for 4 weeks decreased SBP by an average of 3.5 mmHg, and DBP by 1.9 mmHg [9
]. Moreover, the increased plasma vitamin E in this study may be due to the increased vitamin E or the inhibition of catabolism of vitamin E. In addition, bioavailability of vitamin E may be increased by interactions between sesame lignan and tocopherols [24
]. The accumulation of vitamin E acts by detoxifying the hydroxyl and proxy radicals, leading to reduced lipid peroxidation, or by reducing excess tissue aldehydes [11
]. This is supported by many previous studies, in which supplementation of either vitamin E or sesamin and sesamolin demonstrated that these antioxidants inhibit lipid peroxidation [3
]. The antioxidant effect is likely to contribute to the decreased endothelial dysfunction from free radicals [26
], resulting in an increase in the vasorelaxing factor, nitric oxide (NO) [27
However, a mechanism that is not relevant to oxidative stress cannot be ruled out. This was supported by a study by Ward et al. (2004) which failed to show a link between oxidative stress and BP [28
]. It was shown that gamma-tocopherol supplementation increased protein expression of nitric oxide synthase [29
], which stimulates vasorelaxation. Moreover, the potential effect of vitamin E on membrane fluidity is likely to be another mechanism of antihypertension. In vitro study, vitamin E was shown to preserve endothelial cell (EC) migration in oxidized low-density lipoprotein cells (oxLDL) and restore the endothelial monolayer after injury by inhibiting changes in membrane integrity caused by oxLDL [30
]. A previous study in rats demonstrated that antihypertensive rats had lower BP than normotensive rats due to reduced membrane fluidity after ingestion of vitamin E 3 d/week for 3 weeks [31
]. These non-antioxidant properties of vitamin E could be important in the prevention of atherosclerosis, resulting in a reduction in BP in humans. Sesamin supplementation also induced NO and inhibited endothelin-1 production by EC [32
]. These findings indicate an improved ability of the endothelium to relax. In addition, a recent study has shown that sesamin inhibited some CYP450 enzymes and the production of 20-hydroxyeicosatetraenoic acid (20-HETE), which might influence BP independently of any effects on oxidative stress [33
]. Moreover, sesamin increased Ca2+
antagonistic vasorelaxing activity [34
]. It should be emphasized in this discussion that these hypotheses are only on the basis of the decrease in MDA and increased vitamin E, because other possible mechanisms were not measured.
A limitation of this study is a lack of data on endothelium-dependent vasorelaxation determined by NO and other antioxidants such as vitamin C. Moreover, the potential effect of vitamin E on membrane fluidity and the ability of sesame lignans to inhibit 20-HETE synthesis in human renal and liver microsomes were not investigated by this study. Thus, further investigation of these variables explaining the mechanisms of black sesame meal on prevention of hypertension is needed. Importantly, having no discernible side effects from the ingestion of black sesame meal throughout this study implies that it may be safe as a nutritional supplement for health promotion.