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* Graduate Program of Nutrition, Department of Human Development and Family Studies, National Taiwan Normal University, Taipei, 106, Taiwan; Department of Obstetrics and Gynecology, Taiwan Adventist Hospital, Taipei, 105, Taiwan; and ** Department of Obstetrics and Gynecology, Taipei City Hospital-Yang Ming Branch, Taipei 111, Taiwan
2 To whom correspondence should be addressed. E-mail: t10005{at}ntnu.edu.tw.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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- and 
-tocopherol to TC increased significantly by 18 and 73%, respectively. All of these variables differed significantly between the 2 treatments. Serum sex hormone–binding globulin and urinary 2-hydroxyestrone (n = 8) increased significantly by 15 and 72%, respectively, after sesame treatment, and these concentrations tended to differ (P = 0.065 and P = 0.090, respectively) from those after the placebo treatment. These results suggest that sesame ingestion benefits postmenopausal women by improving blood lipids, antioxidant status, and possibly sex hormone status.
KEY WORDS: • sesame seed • blood lipids • -tocopherol • sex hormones • postmenopausal women
Roasted sesame seed is a popular food in Taiwan and other Asian countries for its unique flavor and folkloric beliefs in its antiaging effects; results from animal studies have provided some scientific evidence for this (1). Sesame is usually consumed as a semiliquid paste, confectionery, or stuffing in desserts. Oil (50%) expelled from roasted sesame seeds is commonly used as cooking oil and is a traditional medicinal food for Taiwanese women after delivery. Up to 1.5% of the weight of sesame seed or oil is made up of lignans (1), the majority of which are sesamin and sesamolin (1). The level of lignans in sesame is even higher than in flaxseed, which was previously considered the richest source of lignans (2). Flaxseed lignans, isoflavones, and coumestans, have generally been categorized as the 3 major groups of phytoestrogens (3). Enterolactone (ENL)3 and enterodiol, converted from flaxseed lignans by intestinal microflora, are considered the agents responsible for estrogenic activity (4). It was reported recently that sesame lignans are also metabolized efficiently to ENL (5). Therefore, we were interested in investigating the estrogenic potential of sesame.
High contents of lignans and -tocopherol make sesame oil an extremely stable, naturally occurring, edible oil. After ingestion, hepatic metabolites of sesamin, some catechol compounds, have strong radical scavenging activity (6). Sesamin also enhances the retention of -tocopherol, which usually has very low bioavailability (7), by inhibiting its metabolism (8). The synergistic interaction of lignans and tocopherol reduces oxidative stress in animals fed defatted sesame flour (9) or sesame oil (10), but does not affect healthy young women (11).
The high content of dietary fiber and linoleic acid in the sesame seed underlie its capacity to lower plasma cholesterol (12,13). Moreover, sesamin inhibits intestinal absorption of cholesterol and reduces the activity of acyl-CoA:cholesterol acyltransferase and 3-hydroxy-3-methylglutaryl CoA reductase in rats (14). Sesamin, at a rather low dose (65 mg/d, or approximately equivalent to consuming 13 g of sesame seed), lowers plasma cholesterol in subjects with hypercholesterolemia (15) but sesame oil containing 100 mg sesamin does not affect blood lipids in normocholesterolemic young women (11).
Women, after menopause, face undesirable conditions associated with decline of estrogens. One is a greater risk of silent myocardial infarction than in men (16). The prevalence of hypercholesterolemia (>6.21 mmol/L) is higher in women than men in the 45–64 y age group (24 vs. 12%) among Taiwanese (17). Furthermore, LDL peroxidation, associated with the risk of atherosclerosis, increases with aging (18). Therefore, this study was designed to evaluate whether sesame can be a source of phytoestrogens and promote the cardiovascular health of menopausal women. We measured changes in sex hormones, blood lipids, and antioxidant status after its ingestion.
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MATERIALS AND METHODS |
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Study design. This was a randomized, placebo-controlled crossover study. Subjects were randomized with 1 group receiving 50 g of sesame powder daily and the other 50 g of rice powder for 5 wk. After a 3-wk washout period, the subjects received the alternative powder for another 5 wk. The supplemental amount of 50 g/d was based on that used in flaxseed studies (20). Rice and sesame powders could be distinguished easily by color and flavor, but the subjects were not aware of their health benefit. The subjects were advised to maintain their usual lifestyle, level of physical activity, and dietary habits, except to decrease cooking oil, which was mostly polyunsaturated oil, or starch intake during the 2 supplementation periods to keep their body weight unvaried. They were instructed to keep the powder refrigerated, and to consume it with milk while having breakfast or to spread it on rice in 3 meals. They met technicians to pick up the supplements and had body weight measured each week. The compliance was monitored and ensured by weekly interviews and self-reported daily consumption records. Fasting blood samples and first-morning urine samples were collected on the first morning of each dietary period and the morning following the end of each dietary period. Written informed consent was obtained from each participant before inclusion in the study. The protocol was approved by the Human Experimentation Committee of Taiwan Adventist Hospital, Taipei, Taiwan.
Biochemical analysis.
Plasma, serum, and urine samples were collected as described (21) and stored at –70°C until the end of the study. Samples from the same subject were analyzed sequentially by random order in the same run for each assay. Lipoproteins were isolated from plasma by ultracentrifugation as described (21). Cholesterol (C) and triglycerides (TG) of plasma and lipoproteins were measured by using enzymatic kits (Randox). LDLs were oxidized in vitro and lag time of conjugated diene formation and amounts of LDL thiobarbituric acid reactive substances (TBARS) produced after 1 and 3 h of oxidation were measured (21). Serum - and - tocopherol was determined by HPLC according to the method described by Kaplan et al. (22), and the values were expressed as serum concentrations or relative to plasma cholesterol (23). Serum estradiol, dehydroepiandrosterone sulfate (DHEAS), sex hormone–binding globulin (SHBG), and follicular stimulating hormone (FSH) were measured by enzyme immunoassy (EIA) kits (IBL) and estrone by radioimmunoassay (DSL). Urinary 2-hydroxyestrone (2-OHE1) and 16-hydroxyestrone (16-OHE1) were also measured by EIA kit (Immuna Care). The concentrations were divided by the creatinine concentrations to account for differences arising from variations in urine concentration. Urinary creatinine was determined using a commercial kit (Randox).
The intraassay CV for cholesterol, TG, estrone, estradiol, FSH, DHEAS, and SHBG were 1.9, 2.8, 6.1, 4.2, 9.5, 5.2, and 6.4%, respectively; the interassay CV for them were 1.7, 5.0, 11.1, 5.1, 16.0, 3.9, and 11.4%, respectively. The intraassay CV for 2-OHE1, and 16-OHE1 were 5.5 and 8.6%, respectively, and there were no interassay CV for them because we conducted a single assay.
Other measurements. Sesame lignans were analyzed by HPLC (24) after chloroform:methanol (2:1) extraction. Fatty acid profiles in sesame extract and serum total lipids were analyzed by GC according to the method of Lepage and Roy (25). Percent body fat was measured as described (21).
Statistical methods.
Data are presented as means ± SD. All observed results at the start of the second phase were compared with those at the start of the first phase by a paired, two-tailed t test. When baseline data of the 2 phases did not differ, data from both groups were pooled by sesame or rice treatments (n = 24). Data that were not normally distributed, as analyzed by Kolmogorov-Smirnov test, were transformed prior to analysis (see table footnotes for details). The comparisons among treatments were made by repeated-measures analysis of covariance, and values before each treatment phase served as the covariate. Comparisons within treatments were made by a paired, two-tailed t test. The relations among changes in some outcome variables were assessed using two-tailed Pearson's or Spearman's bivariate correlations. Due to instrumental error while measuring the lag time of copper oxidized LDL on 1 day of the study, samples from 5 subjects were lost, so the number of lag-time measures was reduced to 19. Subjects with data points below the detection range were excluded, so the sample size for estrone and estradiol was 23. Due to budgetary restriction, FSH was measured in 20 of 24 randomly selected subjects, and urinary 2-OHE1 and 16-OHE1 were measured for 8 subjects in the upper tertile of the increased -tocopherol levels after sesame ingestion. Differences were considered significant at P < 0.05. All analyses were conducted using SPSS 11.5.
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RESULTS |
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The serum -tocopherol concentration and the ratio of serum - or -tocopherol to plasma TC increased significantly after sesame treatment, but did not change after rice, and the values differed significantly between the 2 treatments (Table 3). The lag time of LDL oxidation did not change after either treatment. The levels of TBARS in LDL that was oxidized for 1 and 3 h decreased significantly after sesame treatment, but not after rice, and the values differed significantly between the 2 treatments (Table 3). The change in -tocopherol did not correlate with the change in LDL lag time or LDL-TBARS, but the change in EPA was positively correlated with the change in LDL-TBARS 3 h (r = 0.57, P = 0.004) after sesame treatment.
Sesame or rice ingestion did not affect serum levels of estrone, estradiol, and FSH (Table 4). Serum DHEAS decreased significantly by 18% and SHBG increased significantly by 15% after the sesame treatment, but they did not change after the rice treatment. The concentrations of DHEAS differed significantly between the 2 treatments, and those of SHBG tended to differ (P = 0.065) (Table 4). Urinary 2-OHE1 excretion in the selected 8 subjects increased significantly by 72% after sesame, and by 29% after rice treatment, but the values did not differ between treatments (P = 0.090). The ratio of urinary 2-OHE1 to 16-OHE1 increased significantly by 47% after sesame treatment, but the values did not differ between treatments.
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DISCUSSION |
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-linolenic acid [18:3 (n-3)] level (50%) in flaxseed oil (20) and a high linoleic acid level (44%) in sesame oil. Although a small but significant increase in serum linoleic acid occurred (Table 2) after sesame ingestion, no correlation was found with the change in plasma-TC or LDL-C levels. Therefore, the increased intake of linoleic acid could not have been a major factor contributing to the decrease of plasma lipids. Other constituents, such as dietary fiber (12) and sesamin (15), may play an essential role. Starch-rich rice powder was not an optimal placebo to identify the component in the oil and dietary fiber-rich sesame seed powder that contributed to the observed changes. However, because stewed rice is a staple food in Taiwan, this placebo could help minimize the psychologic effect of attending a study on the biological endpoints. Rice affected only the level of plasma TG, which increased after supplementation. This might have been due to the increased intake of starch (26).
Antioxidant status.
-Tocopherol did not previously get much attention because of its low biological activity. However, though not consistently observed (27), recent evidence suggests that -tocopherol might be more important than -tocopherol in the prevention of cardiovascular disease (7). The low plasma concentration of -tocopherol is partly due to the discrimination of hepatic cytochrome P450 (CYP) that preferentially metabolizes -tocopherol (28). Sesame lignans were found to have a -tocopherol sparing effect by inhibiting CYP activity (8,29). Our study showed increased serum levels of -tocopherol (Table 3), similar to 2 other trials in humans (11,30). This -tocopherol sparing effect was not observed in flaxseed (31). Flaxseed lignans have even decreased - and -tocopherol levels in rat plasma and liver (32). Rye bran alkylresorcinols are also recently found to be another food component having a -tocopherol sparing effect in rats and HepG2 cells (33), but are less effective than sesamin (33). Therefore, so far, sesame is the most potent food known to effectively improve -tocopherol bioavailability.
The lag time of LDL oxidation was not prolonged despite the antioxidative activities of - and -tocopherols and sesame lignans. Whether sesame lignans and ENL can be incorporated into LDL in vivo has not been investigated. There was no correlation between the changes in -tocopherol levels and the lag time of LDL oxidation after sesame ingestion. A dose-response study indicates that at least 180 mg/d of -tocopherol is needed to prolong the lag time of LDL oxidation ex vivo (34), which is much higher than 12 mg -tocopherol and 1 mg -tocopherol supplied by sesame in this study. Sesame ingestion significantly decreased LDL-TBARS production (Table 3). The discrepancy between the results of the LDL lag time and LDL-TBARS was not unexpected because the former is predominantly determined by LDL-antioxidant contents (35) and the latter by LDL-polyunsaturated fatty acid contents (36). AA (20:4) and EPA (20:5), with more than 3 double bonds, are important precursors of TBARS (36). Our study also showed a positive correlation between changes of EPA and LDL-TBARS 3-h levels after sesame ingestion. The decreased levels of AA and EPA after sesame ingestion might be due to the inhibition of the activity of 
5-desaturase by sesamin (37). On the other hand, flaxseed consumption showed either no antioxidant effects or increased in vivo oxidative stress in humans (38).
Sex hormone status.
To our knowledge, this is the first study to evaluate the estrogenic effect of sesame. The estrogenic effects of flaxseed lignans in postmenopausal women include decreasing plasma levels of estrone sulfate and estradiol (39) and switching estrogen metabolism from 16-hydroxylation to a less carcinogenic pathway (2-hydroxylation) (40,41). Our study did not show decreased serum estrogens by sesame. Instead, a significant decrease in serum DHEAS level after sesame ingestion was found. Estrogen treatment also decreased plasma DHEAS level in postmenopausal women (42) and monkeys (43), probably by binding to estrogen receptors in adrenocortical cells. Soy flour, a food source of phytoestrogens, decreased serum androgen concentration in men (44). DHEAS is a precursor of androgens. Serum DHEAS levels decline with age and DHEA/DHEAS replacement has been claimed as "a fountain of youth" (45). But some evidence indicates adverse effects of DHEAS on breast cancer and cardiovascular diseases, especially in postmenopausal women (46,47), suggesting sesame ingestion might provide some protection.
Most studies show that a high level of SHBG is associated with decreased risks of breast cancer (48) and cardiovascular disease (49) possibly by decreasing free estradiol and free androgen concentrations. Several studies in women who consumed soy isoflavones found an increase in serum SHBG (50,51). ENL stimulates SHBG syntheses in hepatocytes (52) and plasma SHBG levels were positively correlated with urinary lignan excretion (52). These observations might help support our finding that serum SHBG concentration tended to increase with sesame treatment (Table 4). In contrast, flaxseed ingestion has not been found to increase plasma SHBG concentration (39,41,53).
Two major estrogen metabolites are 2-OHE1 and 16-OHE1. The former is not estrogenic, whereas the latter is estrogenic and genotoxic (54). The increased ratio of 2-OHE1 to 16-OHE1 has been shown to decrease breast cancer risk in some (55) but not all (56) studies. The enzyme involved in the 16-hydroxylation of estrone, CYP3A4 (57), was also reported to be the enzyme inhibited by sesame lignans that increases the bioavailability of -tocopherol (8,28,29). Based on these published results, and due to budgetary limitation, estrogen metabolites were measured in only 8 subjects of the upper tertile of increased serum -tocopherol levels obtained by sesame treatment, but a parallel decrease in 16-OHE1 was not observed in this study (Table 4). Instead, our observation actually supports a later finding that CYP3A4 is indeed not the main enzyme in the metabolism of -tocopherol (58). On the other hand, as with flaxseed, sesame ingestion increased 2-OHE1 and the ratio of 2-OHE1 to 16-OHE1 (40,41), but a larger sample size is needed to confirm these effects. It is interesting that when data of other variables from these 8 subjects were analyzed, all the statistical results were the same as when data from all subjects were analyzed except that their SHBG levels differed significantly between rice and sesame treatments (P = 0.027). Therefore, we speculate that sesame might have the potential to increase the level of serum SHBG in certain subjects.
Sesame seeds, at a dose of 50 g/d for 5 wk, significantly decreases blood DHEAS, TC, LDL-C concentrations, the ratio of LDL-C to HDL-C, and in vitro production of LDL-TBARS, and significantly improves and -tocopherol status. Sesame ingestion tends to increase plasma SHBG (P = 0.065) and might have beneficial effects on urinary 2-OHE1 excretion, but this needs further confirmation. Based on the variables tested, we conclude that sesame seed may benefit postmenopausal women and the effects are at least comparable with those found in flaxseed. Moreover, unlike flaxseed oil, which is devoid of lignans, sesame seeds or oil can be easily incorporated into a healthy normal diet as a rich source of lignans or phytoestrogens.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: AA, arachidonic acid; C, cholesterol; CYP, cytochrome P450; DHEAS, dehydroepiandrosterone sulfate; ENL, enterolactone; EPA, eicosapentaenoic acid; FSH, follicular stimulating hormone; OHE1, hydroxyestrone; SHBG, serum sex hormone binding globulin; TBARS, thiobarbituric acid reactive substances; TC, total cholesterol, TG, triglyceride.
Manuscript received 17 October 2005. Initial review completed 4 December 2005. Revision accepted 13 February 2006.
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