Sesame (Sesamum indicum L., family Pedaliaceae), also known as sesamum, gingelly, til, goma, ajonjoli, and benniseed, is an annual plant (Figure 1). The seeds are purported to be one of the oldest oilseeds used by humans. The seed colors of this plant vary considerably including white, yellow, gray, brown, and black, depending on the variety and strain of S indicum. Black sesame seeds and white sesame seeds are the most available worldwide. Although the chemical differences among the various colored sesame seeds are not well characterized, it has been reported that the contents of indole-3-carboxylic acid, hesperidin, 2-methoxycinnamic acid, vitamin B2, and hyoscyamine are significantly higher in black seeds compared with white seeds. However, at least for sesame lignans, seed color and content of these bioactives are unrelated.1,2 Although apparently originating in Africa and India, this plant is currently cultivated in diverse regions worldwide from semiarid tropics to temperate areas, and India, China, Tanzania, Sudan, and Myanmar are considered the major producers. Because of the high content of oil, sesame seed is called the queen of oilseeds. Its major use is the production of a notably oxidative rancidity-resistant oil. This oil has numerous uses such as a solvent, a hydrophobic vehicle for drug delivery, and a skin softener, and in the preparation of soaps and margarines.2–7 In cosmetics, it can function as a binder, emulsifier, and viscosity-increasing agent.8 As an edible seed oil, it has many routine and diverse uses in food preparation. It has widespread use globally in salads, and in Asia, the seed and oil are routinely used in cooking. Some Europeans substitute it for olive oil in cooking. The dehulled seed is included in the preparation of numerous food products, condiments, and confectionaries, imparting a distinctive savory, nutty, roasted flavor. For example, besides being sprinkled on the surface of breads, sesame seeds are incorporated into pastries, cakes, and crackers. A sesame-based milk alternative is marketed as well. International culinary applications include, for example, mixing the seed with sugar or honey to make candies in Asia and in the Middle East. In India, sesame is also known as til. Til ke laddu, a traditional sweet enjoyed during the Sankranti spring festival, is a small, rounded product made with dry roasted til, clarified butter (ghee), roasted and crushed peanuts, unrefined cane sugar (jaggery), and cardamom. Shirini konjedi is a Persian sesame brittle. Also in the Middle East, tahini, a butter or paste, is made from ground roasted seeds. This tahini paste can enrich other regional dishes. For example, hummus bi tahini is made with tahini, lemons, and chickpeas and may be additionally flavored with such seasonings as garlic, onion, cumin, or paprika. Baba ghanoush is a dip traditionally prepared from eggplant, tahini, garlic, lemon juice, olive oil, salt, and pepper. The soft, fudgelike confection halva/halvah, popular in the Balkans and Middle East, is a combination of tahini, sugar, salt, and vanilla. Sfouf, also called yellow cake or curcuma cake, is a popular Lebanese snack made with semolina, tahini, aniseed, turmeric, sugar, and pine nuts or almonds. Sesame is a component of the spice mixture zahtar (oregano, thyme, sumac, toasted sesame seed) in the Middle East. The Chinese version of sesame paste, zhi ma jiang, uses heavily roasted hulled raw seeds often blended with peanut, to create a denser, strong-flavored product. Chinese black sesame buns are made from leavened, steamed dough filled with a mix of toasted black sesame seeds, toasted peanuts, lard or butter, sugar, and salt. Goma dofu is a sesame-containing Japanese custard. In Japan, sesame is part of the spice blend, shichimi togarashi (chili pepper flakes, orange peel, sesame seed, ginger, seaweed), and is in the sesame salt, gomasio. Sesame oilseed meal, the by-product from oil extraction, is an ingredient for poultry, fish, and livestock feed. Because of its high protein content, it has garnered increasing attention as a functional food ingredient for human consumption.9–12
The approximate composition of sesame seeds is 20% to 25% protein, 45% to 60% fat, and 3% to 14% carbohydrates. γ-Tocopherol is the major tocopherol in seeds, and ß-sitosterol is the principal sterol in the oil. Besides the presence of antioxidant phytochemicals, the sesame seeds also contain lignans that are of interest for potential health benefits due in part to their conversion by intestinal bacteria to biologically active enterolignans, enterodiol, and enterolactone.13 In the Middle East, sesame consumption is higher than in North America. Studies evaluating the relationship of total lignan intake to disease risk in this region are inconsistent.14–18 The major lignans, unique to sesame, are sesamin and sesamolin (Figure 2). The amounts of sesame lignans depend on plant variety, strain, and geographical factors, and vary from 1500- to 4200-mg/kg seeds for sesamin and from 620 to 3590 mg/kg for sesamolin. Sesamol, sesaminol, sesamolinol, and pinoresinol are lignans present in lesser amounts. Sesamol is nearly undetectable in unroasted, raw seeds. However, during heat processing of sesame seeds and oils and the acidic decoloration (bleaching) of sesame oil, sesamolin is converted to sesamol and sesaminol. Bleaching also leads to the epimerization of sesamin to episesamin.
Sesame has a long history of use in traditional medicines. Black sesame seeds can be more expensive than other seeds because of the belief in Chinese traditional medicine that they have more health benefits.1 Global applications of sesame-based folk medicines include treatment of hemorrhoids, wounds, asthma, blurred vision, abdominal pain and ulcers, alopecia, toothaches and gum disease, migraine, menstrual irregularities, and inadequate lactation, to name a few. More recently, experimental studies provide preliminary evidence of sesame's antioxidant and anti-inflammatory properties, as well as its potential benefits toward atherosclerosis, cancer, diabetes, hypertension, microbial infections, pain, and wound healing. Furthermore, sesame lignans are marketed in supplemental form for their antioxidant, nutritional, and other purported health benefits.2,3,5,6,9,12,19–22 The current narrative summarizes human studies evaluating sesame seeds, oil, and extracts for alleviating the signs and symptoms of diverse human disorders, and provides suggestions for future research.
For evidence on the potential health benefits of foods and plant constituents, data were gathered from cell culture experiments, animal studies, and human clinical trials. Human studies are particularly important in determining public health recommendations, especially randomized controlled trials that test well-characterized treatments applying appropriate study designs and statistical analyses. With this in mind, a search of the PubMed and Science Direct databases was conducted using terms including S indicum, sesame, sesamin, sesamol, sesamolin, gingelly, arpeh, and benniseed. Full reports of English-language publications and English-language abstracts of foreign-language articles from peer-reviewed journals were the primary sources of information. Although the quality of identified studies varied considerably, all relevant, published investigations were included in this overview so that the totality and diversity of information can be described, and issues for future research can be identified. Additional studies were gleaned from these sources. Studies of sesame as a component in multi-ingredient preparations were not included in this overview.
Absorption, Metabolism, and Distribution of Sesame Constituents
International data on the intake of lignans from plants in general and from sesame in particular in different countries are limited. Individual lignan intakes in several Western countries and Middle East locations were reported.14–16,18,23 In South Korea, the total intake of sesame lignans by men was determined to be 18.4 mg/d and that by women was 13.3 mg/d. The contribution to total sesame lignan intake from sesame seeds was 23%, and that from sesame oil was 77%.24 In Lebanon, sfouf cake was determined to possess one of the highest concentrations of sesame protein with per-occasion consumption in children varying from 78 to 103 mg.25
Little is known about the metabolism and disposition of ingested sesame and its lignan constituents in humans. Such data are important, because any potential contributions of sesame in improving health are impacted by how much is consumed and the ultimate amount and form of its individual bioactive components in target tissues. This information also helps in discerning any negative effects of sesame constituents and their metabolites to various organs.
In a study26 in Finland, individuals (n = 4) were provided a single dose of sesame from whole, crushed, nonroasted seeds (50 g, 3.73-mg lignans/g) after consuming a low-lignan diet for 1 week. The main lignans present in the seeds were sesamin, pinoresinol, and lariciresinol, with the latter 2 at levels only 7.5% and 1.6%, respectively, of that for sesamin. These nonroasted seeds contained no sesamolin or sesamolinol. The time of peak plasma concentrations (tmax) for sesamin and pinoresinol were 1 and 1.1 hours, respectively, with maximum plasma concentrations (Cmax) of 105 and 209 nmol/L, respectively. The plasma elimination half-life values for the ingested lignans were short, less than 6 hours. The major plasma enterolignan metabolites were enterodiol and enterolactone, which were detected at mean concentrations of approximately 720 and 580 nmol/L, respectively, at 24 hours. This suggests that sesame seeds are an important source of sesamin that can efficiently be converted to these enterolignans. In a small Swedish human trial,27 urine metabolites were quantified after consumption of a single dose of a sesame oil–containing muffin (180-mg sesamin, 71-mg sesamolin) by healthy volunteers (n = 6) following a low-lignan diet for 1 week. After 48 hours, the major urine metabolite was a sesamin monocatechol at levels of 22% to 39% of the ingested sesamin amount. No sesamin or sesamolin was detected in the urine, and only small amounts of enterolactone were present. No sesamolin metabolite was found in the urine, which the authors suggested was due to decomposition of sesamolin under the acidic conditions of the stomach. For a Japanese trial with 24 volunteers,28 the plasma concentrations of sesame lignans were evaluated after oral intake of 50-mg sesamin and episesamin (sesamin/episesamin = 1/1). Both sesamin and episesamin were absorbed with Cmax at 5 hours of 2.7 and 19.0 ng/mL, respectively. After repeated oral dosing for 28 days, plasma concentrations of sesamin and episesamin reached steady state levels by 7 days, which were approximately 1.0 and 5.0 ng/mL, respectively. At 5 hours, the unidentified main metabolites of sesamin and episesamin reached a Cmax of 187 and 87.7 ng/mL, respectively. No adverse events were recorded after ingestion of this test sample.
More information about sesame bioavailability and lignan metabolism is available from animal models. Collectively, the experiments in rats indicate that, after oral dosing, sesamin is converted by rapid first-pass metabolism in the liver to hydroxylated monocatechol and dicatechol metabolites by cytochromes (CYP) P450 and to their subsequent methylated forms by catechol-O-methyltransferase. These transformations occur in humans as well. Several CYPs can catalyze this conversion of sesamin and episesamin, with CYP2C9 being the main isoform in human liver microsomes.29,30 Sulfate conjugation (by sulfotransferases) and glucuronide conjugation (by uridine diphosphate-glucuronyl transferases) are the next steps in metabolism of these intermediates, which are then distributed in the plasma to numerous tissues in the body including the brain, with highest amounts detected in the liver and kidney. In humans, conjugation reactions occur in the intestinal epithelium and liver, with glucuronide conjugates predominating in the plasma.31 In a more recent pharmacokinetic study in rats,32 100–mg/kg body weight sesamin was orally administered. Blood was sampled up to 24 hours post dosing and liver was harvested 1 hour post dosing in a portion of the animals. In the liver, monocatechol and methylated monocatechol metabolites were detected, and sulfate conjugates were the major products of sesamin metabolism. The level of sesamin-catechol-3-sulfate was detected at 10-fold greater levels than that of sesamin. In addition, only sulfate conjugates were detected in the plasma, with the Cmax values of 2 sulfate conjugates registered at levels 5- to 10-fold higher than that of sesamin suggesting that, in rats, sesamin is rapidly metabolized to sulfate conjugates by the enzyme sulfotransferase. The apparent absorption of sesamin was 54%, with excretion in the urine and feces as metabolite forms. It should be emphasized that, in addition to the parent sesamin molecule, several metabolites of sesamin also possess appreciable biological activity.29,33–36 In light of reported plasma levels of metabolite conjugates, and on the basis of novel hypotheses for other sulfate and glucuronide conjugates,37,38 sesame metabolite conjugates may actually be an effective means of in vivo metabolite transport to target tissues where parent molecules are regenerated after cellular uptake. This warrants further substantiation.
Sesamolin and sesamol are also converted to catechol metabolites, and sulfate and glucuronide conjugates after ingestion.39–45 Absorption of sesamol was determined to be 35% to 46% via multiple sites of absorption.40,41
As far as formation of enterolignans in rats is concerned, sesamin can be converted to enterodiol and enterolactone by gut microbiota with subsequent metabolism to hydroxylated metabolites in the liver and intestinal epithelium. The levels of enterodiol and enterolactone in plasma of rats fed sesame are influenced not only by the amount of lignans ingested but also by the form of sesame-based diet consumed. For example, after rats were fed 1 dose of either sesame- or tahini-containing diets, enterodiol and enterolactone concentrations were higher in plasma from the tahini group, compared with levels in the sesame group.46 This differential effect of the 2 diets was lost after extended feeding. This underscores the need to further evaluate how diverse diets and food matrices may affect sesame disposition and modulate enterodiol and enterolactone formation.
Sesame Intake and Tocopherol Status
In 4 trials, the effect of sesame intake on the status of γ-tocopherol in humans was evaluated. In young women (n = 11) provided buns with 22.5-g sesame oil per day and 9.5-mg γ-tocopherol per day for 4 weeks, compared with baseline, serum γ-tocopherol levels increased but α-tocopherol did not.47 Similar outcomes were reported in an investigation48 in which γ-tocopherol– and sesame seed powder–containing muffins (10.8-g sesame seed) were fed to healthy volunteers (n = 9) for 3 days. Compared with baselines, consumption of sesame was associated with a significant increase in γ-tocopherol level, a decrease in plasma ß-tocopherol, and no changes in plasma α- and δ-tocopherols. In 2 studies,49,50 volunteers (n = 16) were fed 1 dose of sesame oil– and γ-tocopherol–containing muffins (136-mg sesamin and sesamolin). After 48 to 72 hours, compared with baseline, there was a significant decrease in urinary excretion of γ-carboxymethylhydroxychroman (γ-CEHC), which are metabolites of γ-tocopherol. Of interest from one of the studies,50 sesame oil consumption, compared with baseline, resulted in a decrease in plasma area under the curve and Cmax for γ-CEHC in men but not in women, although in both genders, urinary γ-CEHC decreased with sesame intake. The reason for this difference was not discussed.
In rats orally administered sesamin or sesame seed, significant increases were observed not only in plasma levels of γ-tocopherol but also in other tissues such as the liver and lung. Much smaller changes in plasma α-tocopherol levels were observed. Consistent with increased tissue levels of γ-tocopherol was a corresponding decrease in urinary excretion of γ-CEHC, a relationship that also was observed in humans.51–54 Elevation of plasma γ-tocopherol levels was considered to be due to inhibition of further CYP3A-based metabolism of γ-tocopherol by sesamin.55 Sesamin ingestion also affected the disposition of n-3 fatty acids. Specifically, in rats consuming sesamin along with oil containing eicosapentaenoic acid, there was a significant decrease in liver content of eicosapentaenoic acid without influencing lymphatic absorption. No similar effect of sesamin intake was observed for n-6 and n-9 fatty acids. The reason for this sesamin-associated drop in liver n-3 fatty acid content is not known, although the authors suggest that sesamin may be affecting ∆5-desaturase activity. Taken together, these findings suggest that sesame seed intake can potentially lead to elevated plasma γ-tocopherol concentrations likely resulting in greater circulating antioxidant activity, to changes in relative tissue levels of other tocopherols, and to altered n-3 fatty acid status.
Potential Health Benefits of Sesame in Human Trials
Relatively more information is available regarding the impact of plant lignans on health compared with sesame lignans. Consumption of plant lignans in general has the potential to decrease risk of cardiovascular disease.23 For other diseases, such as, for example, breast cancer, the relationship of dietary lignans to risk requires further clarification especially in light of the lower amounts of lignans typically consumed in many countries and the possibly different effects depending on the disease.56–59
Blood Glucose and Lipid Regulation
The effect of sesame seed extracts in particular on blood glucose and lipid regulation in several health disorders is summarized in Table 1. When all trials are considered together, considerable heterogeneity is apparent and several methodological shortcomings were noticeable. Most of the studies identified were small, with 81% evaluating 40 subjects or less. Duration of sesame administration was short with 78% of the trials continuing for 60 days or less. Furthermore, some studies lacked statistical comparisons between the separate outcomes of the control and treatment groups, and blinding in studies was inconsistent. Amounts of sesame given to participants also varied substantially. Moreover, sesame samples varied considerably in the form and manner that they were administered to participants. Specifically, sesame was provided as unground seeds,61,90 seed powder,48,60,66,68,74,86,88 oil incorporated into vegetable soup,70 oil dispensed to individuals for inclusion in foods,77 oil dispensed individually to patients for exclusive use as cooking oil,80 bulk quantities of oil provided to households for use as the only edible oil in food preparation and cooking,69,71,75,76,78,79 and sesame-containing food bars.61 These differences in treatment methods are important to acknowledge, because they may alter the bioavailability of bioactives present in sesame products.
TABLE 1 -
Effect of Sesame on Cardiovascular Disease (CVD) and Diabetes (T2DM) Risk Factors
||Main CVD/T2DM Outcomes
||10.8 g/d (n = 9); 3 d
||*NE: TC, TG, HDL, LDL
||NE: MDA, plasma carotenoids
|50 g/d (n = 24); 5 wk, postmenopausal ♀
||*↓LDL, ↓TC, ↑BW, ↑% body fat
NE: HDL, TG
|↓TBARS, ↑Vit E, ↑γ-tocopherol, ↓DHEAS, ↓SHBG, ↑U-2OH-E1
NE: estrone, estradiol, FSH
||25 g/d (n = 16); 4 wk, postmenopausal ♀
NE: TC, TG, LDL, HDL
||30 g/d (n = 70); 9 wk
||*↓Muscle mass, ↓WC, ↓HC, ↑% body fat, ↓ICO, ↓BAI
NE: BW, BMI, % visceral fat
|22.5 g/d (n = 11); 4 wk, ♀
||*NE: TC, TG, LDL, HDL
||64.8 mg/d (n = 6), placebo (n = 6); 4 wk, ♂
||#↓TC, ↓LDL, ↓ApoB
NE: TG, HDL
||50 g (n = 20); 4 h postprandial, ♂
||*↓FBG, ↓DBP, ↑TG, ↓pulse rate, ↑FMD,
NE: TC, LDL, HDL, SBP, PWV
NE: ICAM-1, VCAM-1, E-sel, FRAP
||25 g/d (n = 33), placebo (n = 33); 5 wk
||#NE: BW, TC, LDL, HDL, TG, BP, HR
||↑Urinary excretion of mammalian lignans, enterolactone, enterodiol
NE: IL-6, TNF-α, CRP, F2-isoP
||30 g/d (n = 68); 9 wk
||*↓SI, ↓HOMA-IR, ↑HOMA-%S, ↓HOMA-%B, ↑QUICKI
NE: TC, TG, LDL, HDL, ApoB, Apo-A1, L(p)a, VAI, SBP, DBP, FBG, stroke risk, MI risk, CVD risk
NE: creatinine, ALP, AST, GGT
||2.52 g/d (n = 15); 4 wk
|↓MDA, ↑Vit E
||35 g/d (n = 17-50); 45-60 d
||*↓TG, ↓BW, ↓BMI, ↑↓SBP, ↑↓DBP
NE: TC, HDL, LDL
|↓TBARS, ↑TAC, ↑SOD, ↑CAT, ↑GSH, ↑ß-carotene, ↓Na+, ↑K+
NE: TNF-α, CRP, MDA
|35-40 g/d (n = 356), controls (n = 40); 60 d
||#↓TC, ↓TG, ↓LDL, ↑HDL, ↓SBP, ↓DBP
||↓TBARS, ↑SOD, ↑GPx, ↑CAT, ↑GSH, ↑Vit C, ↑Vit E, ↑ß-carotene
|35 g/d (n = 14);
NE: SBP, DBP
|NE: blood ICAM, blood ADMA
||60 mg/d (n = 12), placebo (n = 13); 4 wk
||28 g/d (n = 20), controls (n = 16); 6 wk
NE: TC, LDL, WC, SBP, DBP, FBG
||35 g/d (n = 40); 45 d
||*↓TC, ↓TG, ↓LDL, ↓FBG, ↓HbA1c, ↓BW, ↓BMI, ↓SBP, ↓DBP
|↑SOD, ↑CAT, ↑Vit E, ↑Vit C, ↑ß-carotene, ↑GSH
|36 g/d (n = 18), glibenclamide (n = 18); 60 d
||Sesame: *↓FBG, ↓HbA1c, ↓TC, ↓LDL, ↓TG, ↑HDL
Glibenclamide: *↓FBG, ↓HbA1c,
NE: TC, LDL, TG, HDL
|Sesame: ↑SOD, ↑GPx, ↑CAT, ↑GSH, ↑Vit C, ↑Vit E, ↑ß-carotene
Glibenclamide: ↑SOD, ↑GPx, ↑CAT
NE: Vit C, Vit E, GSH, ß-carotene
|30 mL/d (n = 23), soybean oil controls (n = 23); 90 d
||#↓FBG, ↓HbA1c, ↑SI
NE: BW, BMI, RBC, WBC, Hct, Hb, albumin, globulin
|↑GPx, ↑SOD, ↑CAT, ↓TBARS, ↓ALP, ↓ALT, ↓AST, ↓CK, ↓Fe, ↓Zn, ↓Na+
NE: K+, Ca++
|30 g/d (n = 93); 9 wk
||*↓SI, ↓HOMA-IR, ↓HOMA-%B, ↑HOMA-%S, ↑QUICKI, ↑BW, ↑BMI, ↓WHR, ↑visceral fat (%), ↓WC, ↓ICO
NE: FBG, % muscle mass, % body fat, BAI, HC
|NE: GGT, AST, ALP
|30 g/d (n = 25); 45 d
||*↓FBG, ↓TC, ↓LDL, ↓HbA1c
NE: TG, HDL
||200 mg/d (n = 24), placebo (n = 24); 8 wk
NE: BMI, WC, % body fat, SI, HOMA-IR, BAI
NE: IL-6, CRP, adiponectin
|8.7 mg/d; 8 wk
||*↓TC, ↓LDL, ↑SI
NE: TG, HDL
||30 g/d (n = 20); 6 wk
||*NE: FBG, SI, HOMA-IR, anthropometric measures
|Defatted seed flour
||30 g/d (n = 14); 60 d, ♀
NE: FBG, HbA1c
||50 g/d (n = 24); 6wk
||*NE: BMI, BW, WC, TC, TG, LDL, HDL, AIP
||30 mL/d (n = 24); 8 wk
||*↓FBG, ↓HOMA-IR, ↓TC, ↓TG, ↓BP
NE: HDL, SI
||40 g/d (n = 21); 4 wk
||*↓LDL, ↓TC, ↓LDLox, ↓LDLTBARS
NE: BW, BMI, TG, HDL
||60 g/d (n = 24); 1 mo
NE: TC, HDL, BW
||40 g/d (n = 19); 60 d
NE: HDL, TG
|↓TBARS, ↑SOD, ↑GPx
||4.5 g/d (n = 15); 2 mo
||*NE: TC, TG, LDL, HDL
||200 mg/d (n = 22), placebo (n = 22); 6 wk, ♀
NE: TC, LDL, TG, SBP, DBP, WC, BAI
Abbreviations: ADMA, asymmetric dimethylarginine; AIP, adiposity index of plasma; ALP, alkaline phosphatase; ALT, alanine aminotransferase; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; AST, aspartate aminotransferase; BAI, body adiposity index; BMI, body mass index; BP, blood pressure; BW, body weight; CAT, catalase; CK, creatine kinase; CRP, C-reactive protein; DBP, diastolic blood pressure; DHEAS, dehydroepiandrosterone sulfate; E-sel, E-selectin; F2-isoP, F2-isoprostane; FBG, fasting blood glucose; FMD, flow-mediated dilation; FRAP, ferric-reducing ability of plasma; FSH, follicle-stimulating hormone; GGT, gamma-glutamyl transferase; GPx, glutathione peroxidase; GSH, reduced glutathione; Hb, hemoglobin; HbA1c, glycated hemoglobin A1c; HC, hip circumference; Hct, hematocrit; HDL, high-density lipoprotein; HR, heart rate; HOMA-IR, homeostasis model assessment for insulin resistance; HOMA-%B, homeostasis model assessment for ß-cell function; HOMA-%S, homeostasis model assessment for insulin sensitivity; ICAM, intracellular adhesion molecules; ICO, index of central obesity; IL-6, interleukin 6; 8-iso-PG-F2α, urinary 8-iso-prostaglandin F2α; LDL, low-density lipoprotein; LDLTBARS, low-density lipoprotein–associated TBARS; LDLOX, oxidized low-density lipoprotein; L(p)a, L(p)a cholesterol; MDA, malondialdehyde; MetS, metabolic syndrome; MI, myocardial infarction; NE, no effect; n-6FA, n6-polyunsaturated fatty acids; PWV, carotid-femoral pulse wave velocity; QUICKI, quantitative insulin sensitivity check index; RBC, red blood cell; SBP, systolic blood pressure; SHBG, serum hormone-binding globulin; SI, serum insulin; SOD, superoxide dismutase; TAC, total antioxidant capacity; TBARS, thiobarbituric acid reactive substances; TC, total cholesterol; TG, serum triglycerides; TNF-α, tumor necrosis factor α; U-2OH-E1, urinary 2-hydroxy estrone; VAI, visceral adiposity index; VCAM, vascular cell adhesion molecule-1; Vit, vitamin; WBC, white blood cells; WC, waist circumference; WHR, waist-to-height ratio.
Symbols: ♀, only female participants; ♂, only male participants; *, treatment compared with baseline; #, treatment compared with placebo control; ↑, increase; ↓, decrease; ↑↓, inconsistent.
In healthy subjects, no consistent effects on blood glucose levels, lipid profiles, and anthropometric measures were observed among participants provided sesame seed, oil, flour, or sesamin.47,48,60,61,63,85 Similar inconsistencies in these outcomes were observed for hypercholesterolemic/hyperlipidemic, overweight, and hypertensive subjects.66–68,70–72,88–90 Furthermore, in hypertensive individuals, overall effects on blood pressure were inconsistent. Despite the methodological weaknesses noted, trials administering sesame oil showed evidence of a trend toward correcting aberrant blood glucose and hemoglobin A1c levels in subjects with diabetes and metabolic syndrome.76–79,87 When markers of inflammation were measured in 3 studies,69,70,87 there was no consistent influence of sesame oil consumption. In addition, in those trials that evaluated the impact of ingestion of sesame extracts on anthropometric measures, no consistent effect was reported. Furthermore, no adverse effects from consuming these diverse sesame products were reported.
Several meta-analyses were initiated to determine whether sesame consumption significantly affected blood glucose and lipid dysregulation, blood pressure, and body weight. Four meta-analyses were published analyzing the impact of sesame on cardiovascular disease and type 2 diabetes mellitus risk factors.93–96 The duration of interventions was noted to range from approximately 4 to 8 weeks; doses of sesame varied from 2.5 to 50 g/d, and those for sesamin varied from 3.6 to 200 mg/d.96 In meta-analyses by Sohouli et al94 and Yargholi et al,95 both reported that sesame consumption, compared with controls, was associated with a significant decrease in fasting blood glucose (weighted mean difference, −21.3 to −28.2 mg/dL) and in hemoglobin A1c values (weighted mean difference, −0.75% to −1.00%). However, no significant effect of sesame on serum insulin or homeostatic model assessment for insulin resistance was detected. In contrast, Huang et al96 found no significant effect of sesame intake on fasting blood sugars. The basis for this inconsistency is not known but may be due partly to participants' characteristics and the methodological qualities of specific trials selected for inclusion in the analysis. Specifically, the report by Huang et al96 included 16 trials in the analysis, whereas 8 trials were selected for each of the other 2 analyses.94,95 From 1 analysis, no specific source of sesame supplementation was identified as a main contributor to decreasing fasting blood glucose and hemoglobin A1c values.95 All sources of sesame were effective, although this should be confirmed in future studies. Taken together, these findings suggest that sesame seed products favorably influence blood glucose levels without influencing insulin resistance.
Two meta-analyses93,96 examined the influence of sesame feeding on blood lipid profiles. Both were in agreement that sesame intake significantly suppressed serum triglyceride levels, compared with controls. There was no agreement as to whether sesame intake significantly influenced total cholesterol, low-density lipoprotein, and high-density lipoprotein values. In contrast, a recent meta-analysis of randomized controlled trials determined that consumption of sesamin supplements significantly reduced serum total cholesterol and low-density lipoprotein levels but did not affect triglyceride and high-density lipoprotein.97
Two meta-analyses96,98 detected a significant decrease in systolic blood pressure associated with sesame intake, compared with controls, but found no consistent effect on diastolic blood pressure. A similar outcome was observed in the analysis of studies with supplemental sesamin.97 In addition, as reported in 3 meta-analyses,96,97,99 the effect of sesame and sesamin on body weight and body mass index was inconsistent.
Sesame seed powder, oil, and sesamin were evaluated as treatments for diverse conditions and found to have analgesic properties (Table 2). Doses and methods of delivery differed considerably, and numbers of subjects varied from 17 to 60. For arthritic conditions, ingestion of seed powder100,101 or sesamin103 resulted in significant decreases in reported joint pain and tenderness, and improved joint flexibility and mobility of participants. In fact, topical seed oil was associated with similar magnitudes of improvement as those observed for topical administration of the nonsteroidal anti-inflammatory drug diclofenac.102 Three trials measured markers of inflammation.100,101,103 Blood levels of tumor necrosis factor α and cyclooxygenase-2 decreased after treatment with sesamin, whereas C-reactive protein and interleukin-6 levels responded inconsistently for subjects provided seed powder or sesamin. In those trials evaluating the topical administration of sesame oil for subjects with trauma to the extremities or for phlebitis,104–110 a significant suppression of pain was observed, compared with controls. Collectively, these studies suggest that further examination of sesame dose, manner of administration, and treatment duration for the alleviation of different sources of pain is warranted.
TABLE 2 -
Human Studies of Sesame for Pain Management
||Standard treatment + 40 g/d (n = 22); 2 mo
||Versus control (standard treatment, n = 23):
↓knee pain, ↑mobility, ↓IL-6
NE: MDA, TAC, CRP
||Topical oil 5 drops 3×/d (n = 47), topical 1% diclofenac gel 3×/d (n = 47); 4 wk
||Sesame vs baseline:
↓knee joint pain, ↑knee flexion angle, ↓time for 8-m walk
NE: analgesic consumption
Sesame vs diclofenac: similar magnitude of benefits, less use of analgesics compared with sesame oil
|Rheumatoid arthritis ♀
||200 mg/d (n = 22); 6 wk
||Versus placebo (n = 22):
↓swollen joints, ↓joint tenderness, ↓pain severity, ↑physical activity, ↓CRP, ↓COX-2, ↓TNF-α, ↓serum hyaluronidase
NE: serum aggrecanase, IL-1ß, IL-6
|Trauma: upper/lower extremity
||Topical oil 10 drops 2×/d (n = 17); 9 d
||Versus control (topical paraffin oil, n = 18):
NE: frequency of NSAID use
|Standard treatment + 10 drops topical oil 1×/d (n = 60); 10 d
||Versus control (standard treatment, n = 66):
↓pain severity, ↓use of NSAIDs
|Topical oil 10 drops + massage 3×/d (n = 41); 2 d
||Versus control (topical cooking oil + massage, n = 41):
|Phlebitis (chemotherapy induced)
||Topical oil, 10 drops + massage 2×/d (n = 28); 7 d
||Versus control (massage, n = 30):
|Topical oil, 10 drops 2×/d (n = 30); 2 wk
||Versus control (n = 30):
↓pain + erythema + swelling, ↓incidence of phlebitis, delayed occurrence of phlebitis
|Topical oil, 5 drops every 6 h (n = 18); 30 h
||Versus control (topical liquid paraffin, n = 18):
|Topical oil, 10 drops 2×/d (n = 30); 30 d
||Versus control (topical liquid paraffin, n = 30):
↓pain + erythema + swelling, ↓incidence of phlebitis, ↑vein survival time, delayed phlebitis development
Abbreviations: COX-2, cyclooxygenase-2; CRP, C-reactive protein; IL-1ß, interleukin 1ß; IL-6, interleukin 6; MDA, malondialdehyde; NE, no effect; NSAID(s), nonsteroidal anti-inflammatory drug(s); TAC, total antioxidant capacity; TNF-α, tumor necrosis factor α.
Sesame extracts were tested in small trials or pilot studies to treat other diverse disorders (Table 3). These preliminary findings may provide a basis for further pursuit of preclinical and additional clinical studies of sesame extracts to treat these diverse conditions.
TABLE 3 -
Human Studies of Sesame for Relief of Diverse Conditions
||1 spray of Nozoil/nostril, 3×/d (n = 40); 20 d
1-3 sprays of Nozoil/nostril, 3×/d (n = 79); 14 d
↓nasal mucus dryness, ↓crust formation, ↓nasal blockage vs control (isotonic NaCl, n = 79):
↓nasal mucus dryness, ↓nasal stuffiness, ↓nasal crustiness
||Soft oil capsule, 3×/d (n = 35); 6 wk
↓total dyspepsia symptom score
|Cough in children
||5 mL at bedtime (n = 53); 3 d
||Versus placebo (starch syrup, n = 54):
NE: cough frequency, cough strength
||0.5 mL/d + 30 μg/wk IFN-ß-1α (n = 54); 6 mo
||Versus control = 30 μg/wk IFN-ß-1α (n = 39):
↑serum IL-10, ↓NO, ↓IFN-γ, ↓TNF-α, ↓lymphocyte proliferation
NE: clinical relapse of disease
|Adhesive small bowel obstruction (SBO)
||150 mL/d adjunct to nasogastric intubation + conventional treatment (n = 31); 6-10 d
||Versus control (conventional treatment, n = 33):
↓time for spontaneous stool passage, ↓length hospitalization, ↓need for corrective relaparotomy
NE: complications and recurrence of SBO after surgery
||30 min/d Ayurvedic forehead oil-dripping treatment (n = 20); 2 wk
||Versus control (warm H2O forehead drip, n = 20):
↑self-reported sleep quality
NE: perception of sleepiness, specific sleep measurements, quality of life, postintervention sleep quality
||0.5 mg/kg bw/d (n = 25); 3 mo
↑sperm count, ↑sperm motility
NE: sperm morphology
|Sport training improvement
||40-g/d powder paste (n = 10); 28 d
||Versus control paste (n = 10):
↓CK, ↓MDA, ↑Vit A, ↑Vit E
NE: LDH, CRP, max aerobic capacity, peak aerobic capacity speed
||Alcohol/water extract from 60-g seed powder
||400-mL tea per day (n = 21); 7 d
↑frequency menstrual bleeding, ↓menstrual delay, ↓use menstrual drugs
NE: blood flow, pain
|Management of early pregnancy loss
||Water extract from 30-g seed powder
||200 mL tea per day (n = 44); 5 d
||Versus control (expectant management, n = 43):
↑ in complete resolution of retained product of conception, ↓vaginal blooding, ↓vaginal pain
|Mild cognitive impairment
||Alcohol/water extract from sesame seed cake
||1.5 g/d (n = 28); 12 wk
||Versus control (n = 30):
↑verbal learning, ↓plasma amyloidß(1-40), ↓plasma amyloidß(1-42)
NE: visual learning, 8-OHdG
Abbreviations: CK, creatine kinase; CRP, C-reactive protein; IFN-ß-1α, interferon-ß1α; IFN-γ, interferon-γ; IL-10, interleukin 10; LDH, lactate dehydrogenase; max, maximum; MDA, malondialdehyde; NaCl, sodium chloride; NE, no effect; NO, nitric oxide; TNF-α, tumor necrosis factor α; Vit, vitamin; 8-OHdG, 8-hydroxy-2'-deoxyguanosine.
Of interest are reports that sesame oil can improve oral health by its use in a traditional Ayurvedic treatment, oil pulling,123–130 and other oral hygiene approaches.131–133 The practice of oil pulling involves swishing an oil around the mouth for a specified time and then spitting out the oil. Its purpose is to remove bacteria and improve oral health.
There is limited information from human trials supporting specific mechanisms of action of sesame in mediating physiological responses. A meta-analysis evaluating the influence of sesame intake on inflammatory biomarkers134 concluded that sesame consumption was associated with a significant decrease in serum levels of interleukin 6, but not for C-reactive protein and tumor necrosis factor α. There is evidence in humans that sesame oil may suppress oxidative stress (thiobarbituric acid reactive substances, malondialdehyde), elevate antioxidant defense markers (total antioxidant capacity, superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase), and enhance levels of the nutrients vitamin E, vitamin C, and beta carotene.69–71,75,77,87 Other potential mechanisms observed from animal trials have been reviewed2,3,12,135–142 and include exhibiting estrogenic and antiestrogenic properties, inhibiting neurological damage and neurodegeneration, lowering levels of proinflammatory markers and cytokines, suppressing fatty acid synthesis and cholesterol synthesis and absorption, maintaining cholesterol homeostasis, promoting fatty acid oxidation, altering immunomodulatory and anti-inflammation signaling networks, and modifying endothelium-dependent vasodilatory and vasorelaxation responses.
Sesame is considered generally recognized as safe for human consumption by the US Food and Drug Administration for inclusion in food consistent with its intended use as a natural seasoning or flavoring (21 CFR 182.0). Furthermore, sesame oil, as an indirect additive, is approved for incorporation into coatings that interface with food during manufacturing, packaging, and transporting (21 CFR 175.300). A toxicological and clinical assessment of sesame determined it to be safe for numerous cosmetic applications.8
Some limited adverse events after use of sesame131,143,144 were reported. However, a significant issue regarding sesame is its allergenicity in children and adults, with varying prevalence worldwide. There is some evidence, although limited, that sesame allergy is more prevalent in the Middle East than in Western countries.25,145–147 Several sesame constituents were identified as potential human allergens.148 The forms of sesame eaten, for example, as whole seeds or in tahini, may affect the magnitude of the allergic response.149,150 Nonetheless, one report suggested that an oral dose of 1-g sesame protein (approximately 4-g tahini paste, 1 teaspoon) will cause objective symptoms in more than 90% of sesame-allergic individuals.150 Although its prevalence in North America is low,151 it can produce serious immediate and delayed hypersensitivity in sensitive individuals. Precautionary allergen avoidance is recommended to minimize this.2,8,145,151–153 Labeling of sesame presence in food products is mandatory in the European Union. Although food labeling regulations in the United States currently do not recognize sesame as a priority allergen to be routinely included in food labels, there are efforts to change this.154,155
There is some evidence from preclinical experiments that sesame constituents may have the potential to interact with drugs by affecting the activity of several CYP enzymes involved in their metabolism. Specifically, sesamin is an inhibitor of CYP2C9, which is a CYP isoform that metabolizes anticlotting, diabetic, and nonsteroidal anti-inflammatory drugs.29,30 Preclinical studies by Yasuda et al156 suggest that no serious effect on CYP2C9-dependent drug metabolism would be expected at doses of sesamin typically ingested by humans. Similarly, the clinical investigation of Tomimori et al28 concluded that no clinically significant effect on CYP2C9 was apparent after repeated ingestion of 50-mg sesamin per day for 28 days and that sesamin would be safe and tolerable in healthy subjects at typical levels encountered in supplements. However, 2 recent preclinical reports evaluating the CYP2C9-dependent 7-hydroxylation of warfarin157,158 provide conflicting conclusions as to whether likely blood levels resulting from oral intake of sesamin have the potential to affect warfarin metabolism by human liver enzymes. The potential for interactions of sesamin with drugs metabolized by CYP2C9 in humans is not well characterized and warrants additional monitoring. Furthermore, there is evidence that sesamin can inhibit the activities of cytochrome P450 3A4 and cytochrome P450 4F2.12,55,159–161 Inhibition of CYP3A4 is associated with increased plasma concentrations of γ-tocopherol. CYP3A4 also participates in the metabolism of a wide variety of substrates including retinoic acid, bile acid, testosterone, estrogen, cholesterol, dietary chemicals, and environmental toxins, as well as drugs such as acetaminophen, codeine, and cyclosporin A and the novel heart rate-lowering agent, ivabradine. CYP4F2 catalyzes the ω-oxidation of the n-6 fatty acid arachidonic acid and the proinflammatory agent leukotriene B as well as the metabolism of vitamins E and K1. The potential interactions of sesamin with CYP3A4- and CYP4F2-dependent substrate metabolism as well as with drug conjugation reactions in humans are not well characterized and deserve further evaluation. This issue is important to clarify because commercial sesamin supplements are currently readily available with recommended daily doses of up to 200 to 250 mg/d, whereas other sesame seed products for human consumption provide little information on the amounts of bioactives present.
There is initial evidence that sesame intake may improve blood glucose regulation, but less consistent is the evidence for its capacity to improve lipid dysregulation and hypertension. Additional larger, well-designed randomized controlled trials are needed that evaluate multiple doses and intervention durations for different sources of sesame (eg, whole seeds, powdered seeds, oil, specific constituents) and that also address potential mechanisms of action. In addition, on the basis of preliminary results, human studies are warranted that examine sesame's possible analgesic effects for participants with different sources of pain. The inadequate standardization of doses among trials needs to be improved by more consistent reporting of sample composition. Measuring blood levels of select metabolites can provide more insights into sesame bioavailability and participants' compliance. Routinely reporting analyses of diets is important so that the effect of subjects' diets on treatment outcomes can be better characterized. Furthermore, whether the administration of sesame at typical culinary doses can provide consistent benefits deserves clarification. Although the results of some studies seem promising, they are too preliminary to recommend the use of sesame products and supplements for customary use in improving health or treating disorders.
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