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Sesame Seeds:  our new ‘flax seed’

Jacob Schor, ND, FABNO

August 6, 2010


Few people eat flax seeds because they love their flavor, they eat flax seeds because they are supposed to be good for you.  Sesame seeds, on the other hand, taste good.  Imagine what humus made with mashed flax seeds would taste like.  Sesame seeds win out over flax seeds when it comes to taste.  It now seems that sesame seeds also compete with flax seeds at providing health benefit.


When it comes to lignin content, flax seeds are the clear winner.  A Dutch analysis tells us that flax seeds contain 301,120 mcg/100 gm while sesame seeds only contain 39,348 mcg/100 gm.    While it might seem that flax wins this competition as sesame seeds contain only about 13% of the lignans by weight as flax, there are several considerations that argue that they may have equal effect.


First, lignans, in both sesame and flax seeds, are converted by gut bacteria into phyotestrogenic chemicals that are active in the blood.  When these phytoestrogens levels are measured, both seeds have equivalent effect at raising serum levels.   Even if in the lab flax looks better, in animals the benefit looks equal.

Second, actual lignan content may not matter that much as both seeds easily supply more than enough lignans to maximize benefit.  Both seeds supply lignans in such overabundance that it probably doesn’t really matter.  In McCann’s June 2010 paper that found a correlation between high lignan content in the diet and improved survival among breast cancer patients, their definition of a high lignan diet was eating more than 319 mcg per day.   Thus according to their data, eating 0.1 gram of flax seed per day made a significant difference.  Even if a woman needed to eat ten times as much sesame seed to get an effect equivalent to flax, eating even one gram per day is easy to do.  It is easier to eat sesame streets than flax seeds.  Patients do not complain about sesame seeds being a bulking laxative like they do about flax.  Sesame tastes good.  Sesame is a food, flax a nutrient.


Third, our knowledge of sesame’s health benefits is growing.  Sesame is valued for both its anti-inflammatory action and it’s anticancer action.  Let’s look at some recent papers and see how we might interpret them clinically:


Sesamin, a chemical isolated from sesame seeds, changes the way white blood cells are drawn to chemoattractants, reducing the production of the cytokines involved in infection, inflammation and cancer.

Sesamin decreases the damaging effect that oxidized blood lipids have on endothelial function.   Thus they may have value in atherosclerosis and cardiovascular disease.   Indeed, in animal models sesame extracts actually prevent lipid oxidation normally triggered by various chemical oxidizing agents.  

Sesame also protects brain neurons as seen in rat brain reperfusion experiments in which blood flow is cut off and then restored.   If a similar effect occurred in the human brain, this form of protection is what we would desire to bring to our stroke patients.

Epidemiological and clinical trials suggest sesame may have a mild effect at lowering blood pressure, enough to drop numbers by a few points.   Yet these findings are not unanimous.  A 2009 clinical trial in which obese or overweight men and women were feed about an ounce of sesame seeds/day for five weeks raised urinary excretion of the mammalian lignans by approximately 8-fold (P<0.001) but, “…did not produce significant changes in blood indices of cardiovascular disease risk…”  Blood lipids and blood pressure did not change, nor did markers of systemic inflammation (C-reactive protein, interleukin-6, tumor necrosis factor-alpha) or lipid peroxidation.

A number of published studies suggest sesame may have anti cancer effect.  Most of these are in vitro or rodent studies.  We still lack the human trials that we would prefer to reference.  Thus we must look at this information cautiously, favorable though it might appear. 

In a May 2010 paper, researchers from MD Anderson described some of the mechanisms by which sesame acts to prevent or inhibit cancer.  Testing the sesame extract, sesamin, they found that it inhibited a range of different types of cancer cells including leukemia, multiple myeloma, and colon, prostate, breast, pancreas and lung cancers.  Sesamin enhanced tumor necrosis factor alpha’s action at inducing apoptosis.  This action was linked to a suppression of production of certain chemicals linked to cell survival (Bcl-2 and survivin), proliferation (cyclin D1), inflammation (cyclooxygenase-2), invasion (matrix metalloproteinase-9) and angiogenesis (vascular endothelial growth factor).  Sesamin downregulated NF-kappaB, a factor normally stimulated by various inflammatory and carcinogenic triggers. 

I’ve focused on NF-kappaB in past reviews that suggest that lowering this chemical increases gemcitabine’s action against pancreatic cancer:

Two months later in July 2010, researchers from the National Institutes of Health reported that sesamin inhibits the ability of macrophages to make vascular endothelial growth factor (VEGF) and thus limits angiogenesis, that is growth of new vessels to deliver blood to cancer tumors.

Other studies suggest that sesame protects agains development of colon cancer and will inhibit skin cancer.     

A clinical trial published in February 2010, tells us that oral sesame oil was useful in treating small bowel obstruction caused by adhesions.   Other studies suggest a similar possible effect against leukemia and lymphoma cells.    

A 2007 paper suggests we consider using sesame oil to protect the kidneys during cisplatin treatment. 

Sesame oils have long been thought to raise platelet counts and we still frequently employ them for this situation in our practice.  Paul Reilly and Mark Gignac have reported their clinical use of sesame oil for this purpose on OncANP’s chat room.  Standard Process that has sold nutritional supplements made from sesame oil to health practitioners specifically to increase platelet levels for the better part of a century.  As well accepted as this use is, we have yet to see any peer reviewed clinical trials supporting these claims.

At this time there is one significant caution to using sesame with cancer patients.  We discourage women from eating sesame when they have breast cancer and are being treated with tamoxifen.  Papers published in 2007 and 2008 looked at breast tumor growth in mice treated with both sesame seeds and tamoxifen.  While flaxseed increases tamoxifen’s inhibition of breast cancer growth, sesame does not. In fact sesame actually decreases tamoxifen’s benefit.  Yet, like flax, sesame increased tamosifen’s bone strengthening benefits.

There are numerous ways that patients can add sesame seeds into their diet. We suggest to our patients that they make and eat foods that have tahini (ground sesame butter) added as an ingredient (humus, baba-ghanoush, tahina etc) or to eat the seeds directly on food.  Many people prefer the taste of slightly ground sesame seeds.  They can be purchased pre-ground but I have found fresh ground to be preferable and have purchased small hand grinders from our local Korean market.  The novelty of using these gadgets seems to have increased sesame consumption in our home.  So also has experimenting with the various types of sesame seeds available.  At the moment, I am trying to use up all the seeds in our grinder as I’ve recently purchased a bag labeled as ‘wild’ sesame seeds that I'm eager to try.




Milder, I. E. J., Arts, I. C. W., Van de Putte, B., Venema, D. P., and Hollman, P. C. H. 2005. Lignan contents of Dutch plant foods: a database including lariciresinol, pinoresinol, secoisolariciresinol, and matairesinol. British Journal of Nutrition, 93:393-402.

Nutr Cancer. 2005;52(2):156-65.

Whole sesame seed is as rich a source of mammalian lignan precursors as whole flaxseed.

Coulman KD, Liu Z, Hum WQ, Michaelides J, Thompson LU.

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.


The mammalian lignans enterolactone and enterodiol, which are produced by the microflora in the colon of humans and animals from precursors in foods, have been suggested to have potential anticancer effects. This study determined the production of mammalian lignans from precursors in food bars containing 25 g unground whole flaxseed (FB), sesame seed (SB), or their combination (FSB; 12.5 g each). In a randomized crossover study, healthy postmenopausal women supplemented their diets with the bars for 4 wk each separated by 4-wk washout periods, and urinary mammalian lignan excretion was measured at baseline and after 4 wk as a marker of mammalian lignan production. Results showed an increase with all treatments (65.1-81.0 mumol/day; P < 0.0001), which did not differ among treatments. Lignan excretion with the whole flaxseed was similar to results of other studies using ground flaxseed. An unidentified lignan metabolite was detected after consumption of SB and FSB but not of FB. Thus, we demonstrated for the first time that 1) precursors from unground whole flaxseed and sesame seed are converted by the bacterial flora in the colon to mammalian lignans and 2) sesame seed, alone and in combination with flaxseed, produces mammalian lignans equivalent to those obtained from flaxseed alone.

PMID: 16201847

J Agric Food Chem. 2009 Jul 22;57(14):6101-6.

Biotransformation of sesaminol triglucoside to mammalian lignans by intestinal microbiota.

Jan KC, Hwang LS, Ho CT.

Graduate Institute of Food Science and Technology, National Taiwan University, Taipei, Taiwan.


Plant lignans occur widely in foods, with flaxseed recognized as their richest source. Some plant lignans can be converted by intestinal microbiota to the mammalian lignans, enterodiol and enterolactone, which may have protective effects against hormone-related diseases such as breast cancer. This study determined whether plant lignans in sesame seed, particularly sesaminol triglucoside (STG), could be metabolized to mammalian lignans. STG is a furofuran lignan with methylenedioxyphenyls. The transformation of furofuran lignans to mammalian lignans by intestinal microbiota involves the hydrolysis of glucoside, demethylenation of a methylene group, oxidation of dibenzylbutanediol to dibenzylbutyrolactone, and reductive cleavage of furofuran rings. STG has methylenedioxyphenyl moieties in their structures that may require additional oxidative demethylenation of the methylenedioxyphenyl ring for conversion to mammalian lignans. However, STG is metabolized, via intestinal microbiota, to a catechol moiety. The major STG metabolite was characterized as 4-[((3R,4R)-5-(6-hydroxybenzo[d][1,3]dioxol-5-yl)-4-(hydroxymethyl)tetrahydrofuran-3-yl)methyl]benzene-1,2-diol using NMR and mass spectrometry, and STG could be converted to enterolactone and enterodiol by rat intestinal microflora.

PMID: 19537732

J Nutr. 2006 Apr;136(4):906-12.

Sesamin is one of the major precursors of mammalian lignans in sesame seed (Sesamum indicum) as observed in vitro and in rats.

Liu Z, Saarinen NM, Thompson LU.

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 3E2, Canada.


Plant lignans occur in many foods, with flaxseed presently recognized as the richest source. Some plant lignans can be converted by intestinal microbiota to the mammalian lignans, enterodiol and enterolactone, which may have protective effects against hormone-related diseases such as breast cancer. This study determined whether plant lignans in sesame seed, particularly sesamin, could be metabolized to the mammalian lignans. The total plant lignan concentration in sesame seed (2180 micromol/100 g) was higher than that in flaxseed (820 micromol/100 g). In vitro fermentation with human fecal inoculum showed conversion of sesamin to the mammalian lignans, although at a lower rate (1.1%) compared with that of secoisolariciresinol diglucoside (57.2%). However, when fed to female Sprague-Dawley rats for 10 d, sesamin (15 mg/kg body weight) and a 10% sesame seed diet resulted in greater (P < 0.05) urinary mammalian lignan excretion (3.2 and 11.2 micromol/d, respectively), than the control (< 0.05 micromol/d). We conclude that sesame seed is a rich source of mammalian lignan precursors and sesamin is one of them. From intermediate metabolites of sesamin identified in rat urine by GC-MS, a tentative metabolic pathway of sesamin to mammalian lignans is suggested.

Breast Cancer Res Treat. 2010 Jul;122(1):229-35. Epub 2009 Dec 22.

Dietary lignan intakes in relation to survival among women with breast cancer: the Western New York Exposures and Breast Cancer (WEB) Study.

McCann SE, Thompson LU, Nie J, Dorn J, Trevisan M, Shields PG, Ambrosone CB, Edge SB, Li HF, Kasprzak C, Freudenheim JL.

Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.


Dietary lignan intakes have been associated with reduced breast cancer risks; however, no previous studies have investigated whether lignan intake might be associated with breast cancer survival. We examined the association of dietary lignan intakes with survival in 1122 women with primary, incident, histologically confirmed breast cancer identified between 1996 and 2001, and with vital status determined through December 31, 2006. Diet in the 12-24 months before diagnosis was assessed with an extensive food frequency questionnaire, and potential confounders assessed from an extensive epidemiologic interview and abstracted clinical data. Lignan intake was calculated using published food composition data. Hazard ratios (HR), and 95% confidence intervals (CIs) for dietary lignan intakes with all cause, and breast cancer mortality were estimated using Cox proportional hazards adjusting for age, education, race, total energy intake, tumor stage, and body mass index. Of the 1122 women with complete dietary data, 160 had died by the end of follow-up. Among postmenopausal women only, those in the highest versus lowest quartile of lignan intakes had a statistically significant reduction in the risk of all cause mortality (HR 0.49, 95% CI 0.26-0.91) and a significantly reduced risk of breast cancer mortality (HR 0.29, 95% CI 0.11-0.76). Higher intakes of dried beans (HR 0.61, 95% CI 0.36-1.03), but not fruits, vegetables, or grains, were also weakly associated with overall mortality. In summary, our results suggest that higher lignan intakes may be associated with improved survival among postmenopausal women with breast cancer.

PMID: 20033482

J Nutr. 2010 Feb;140(2):377-81. Epub 2009 Dec 23.

Sesamin inhibits bacterial formylpeptide-induced inflammatory responses in a murine air-pouch model and in THP-1 human monocytes.

Cui Y, Hou X, Chen J, Xie L, Yang L, Le Y.

Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Shanghai, 200031, China.


The reaction of human leukocytes to chemoattractants is an important component of the host immune response and also plays a crucial role in the development of inflammation. Sesamin has been shown to inhibit lipid peroxidation and regulate cytokine production. In this study, we examined the effect of sesamin on inflammatory responses elicited by the bacterial chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF) in vitro and in vivo and explored the mechanisms involved. fMLF is recognized by a human G protein-coupled receptor formyl peptide receptor (FPR) on phagocytic leukocytes. Sesamin at concentrations between 12.5 and 50 micromol/L inhibited fMLF-induced chemotaxis of human monocyte cell line THP-1 differentiated with dibutyryl cyclic AMP (P < 0.01). Similarly, sesamin inhibited FPR-transfected rat basophilic leukemia cell [epitope-tagged human FPR (ETFR) cell] migration toward fMLF (P < 0.01). In fMLF-induced inflammation in a murine air-pouch model, intraperitoneal administration of sesamin (12 mgkg(-1)d(-1) for 2 d) suppressed leukocyte infiltration into the air pouch induced by fMLF [(62.89 +/- 7.93) x 10(4) vs. (19.67 +/- 4.43) x 10(4) cells/air pouch; n = 9; P < 0.001]. Ca(2+) mobilization and mitogen-activated protein kinase extracellular signal-regulated kinase (ERK1/2) activation are involved in fMLF-induced leukocyte migration. Pretreatment of ETFR cells with sesamin inhibited fMLF-induced ERK1/2 phosphorylation in a dose-dependent manner but did not affect fMLF-induced Ca(2+) flux. Electrophoretic mobility shift assay showed that pretreatment of THP-1 cells with sesamin dose dependently inhibited fMLF-induced nuclear factor-kappaB (NF-kappaB) activation. These results suggest that sesamin inhibits leukocyte activation by fMLF through ERK1/2- and NF-kappaB-related signaling pathways and thus is a potential compound for the management of inflammatory diseases.

PMID: 20032476

J Agric Food Chem. 2009 Dec 9;57(23):11406-17.

Sesamin mitigates inflammation and oxidative stress in endothelial cells exposed to oxidized low-density lipoprotein.

Lee WJ, Ou HC, Wu CM, Lee IT, Lin SY, Lin LY, Tsai KL, Lee SD, Sheu WH.

Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan.


Sesamin, a lignan from sesame oil, has been shown to have antihypertensive and antioxidative properties. This study examined the effects of sesamin on oxidized low-density lipoprotein (oxLDL)-induced endothelial dysfunction. Oxidative stress was determined by measuring the generation of intracellular reactive oxygen species (ROS) and by measuring the expression levels of superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS). To assess the pro-inflammatory effects of oxLDL, ELISA was used to detect IL-8 expression, endothelin-1 (ET-1) secretion, and nuclear factor-kappaB (NF-kappaB) activation. The expression of adhesion molecules (ICAM-1, VCAM-1, and E-selectin) was examined by flow cytometry. In addition, several apoptotic signaling pathways were also investigated. The data showed that sesamin significantly ameliorated oxLDL-induced ROS generation and SOD-1 inactivation. Sesamin also attenuated the oxLDL-induced activation of NF-kappaB, suggesting that the inhibitory effects of sesamin on IL-8 and ET-1 release, adhesion molecule expression, and the adherence of THP-1 cells were at least partially through the blockade of NF-kappaB activation. Furthermore, sesamin attenuated oxLDL-induced apoptotic features, such as intracellular calcium accumulation and the subsequent collapse of mitochondrial membrane potential, release of cytochrome c, and activation of caspase-3. Results from this study may provide insight into possible molecular mechanisms underlying sesamin's beneficial effects against oxLDL-mediated vascular endothelial dysfunction.

PMID: 19951001 [

Food Chem Toxicol. 2009 Oct;47(10):2507-15. Epub 2009 Jul 14.

Free radical scavenging and antiatherogenic activities of Sesamum indicum seed extracts in chemical and biological model systems.

Visavadiya NP, Soni B, Dalwadi N.

BRD School of Biosciences, Sardar Patel Maidan, Sardar Patel University, Vallabh Vidyanagar 388 120, Gujarat, India.


An emerging consensus underscores the importance of oxidative events in vascular disease including excess production of reactive oxygen/nitrogen species (ROS/RNS), in addition to lipoprotein oxidation. Sesamum indicum has long been used extensively as a traditional food. The aim of present study was to evaluate antioxidant action of aqueous and ethanolic seed extracts from S. indicum using various in vitro ROS/RNS generated chemical and biological models. Results demonstrated that the graded-dose (25-1000 microg/ml) of aqueous and ethanolic extracts markedly scavenged the nitric oxide, superoxide, hydroxyl, 1,1-diphenyl-2-picrylhydrazyl and 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radicals and, showed metal chelating ability as well as reducing capacity in Fe(3+)/ferricyanide complex and ferric reducing antioxidant power assays. In biological models, both extracts were found to inhibit metal-induced lipid peroxidation in mitochondrial fractions, human serum and LDL oxidation models. In lipoprotein kinetics study, both extracts significantly (P<0.05) increased lag phase time along with reduced oxidation rate and conjugated dienes production. Ethanolic extract of S. indicum showed higher amounts of total polyphenol and flavonoid content as compared to their counterpart. The IC(50) values of both extracts were compared with respective antioxidant standards. Overall, ethanolic extract of S. indicum possess strong antioxidant capacity and offering effective protection against LDL oxidation susceptibility.

PMID: 19607871 [PubMed - indexed for MEDLINE]

Planta Med. 2010 Jan;76(1):20-6. Epub 2009 Jul 13.

Neuroprotective effect of defatted sesame seeds extract against in vitro and in vivo ischemic neuronal damage.

Jamarkattel-Pandit N, Pandit NR, Kim MY, Park SH, Kim KS, Choi H, Kim H, Bu Y.

Department of Herbal Pharmacology, College of Oriental Medicine, Kyung Hee University, Seoul, Korea.


Sesame (Sesamum indicum L.) is an important oilseed crop that possesses a wide spectrum of pharmacological activities. Many studies have been conducted to investigate its health-promoting effects. Compared to other plant oils, sesame seed oil is highly stable to oxidation and has been demonstrated to have protective effects against ischemia-reperfusion injury in the rat brain. However; the effects of defatted sesame seeds extract (DSE) have not been studied yet. The purpose of this study was to evaluate the protective effect of DSE against ischemia models. For in vitro ischemia, oxygen-glucose deprivation followed by reoxygenation (OGD-R, 4 h OGD followed by 24 h reoxygenation) in HT22 cells was used to investigate the protective effects on cell death and the inhibitory effects on lipid peroxidation. For in vivo ischemia, the middle cerebral artery occlusion (MCAo, 2 h of MCAo followed by 22 h of reperfusion) rat model was used. Twenty-two h after occlusion the rats were assessed for neurobehavioral deficit and infarct volume. DSE (0.1-10 microg/mL) significantly reduced the cell death and inhibited lipid peroxidation induced by OGD-R. DSE (30, 100 and 300 mg/kg, p.o.) given twice at 0 h and 2 h after onset of ischemia reduced brain infarct volume dose-dependently and improved sensory-motor function. The therapeutic time window of DSE (300 mg/kg, p.o.) was 2 h after MCAo in rats. In conclusion, our results show that DSE may be effective in ischemia models by an antioxidative mechanism. Copyright Georg Thieme Verlag KG Stuttgart . New York.

PMID: 19598078

J Nutr Sci Vitaminol (Tokyo). 2009 Feb;55(1):87-91.

Antihypertensive effects of sesamin in humans.

Miyawaki T, Aono H, Toyoda-Ono Y, Maeda H, Kiso Y, Moriyama K.

NTT West Kansai Health Administration Center, 604, Bano-cho, Nakagyo-ku, Kyoto 604-8172, Japan.


Sesamin, one of the lignans contained in sesame, has been considered to have medicinal effects. It has been reported that sesamin suppressed the development of hypertension in rats. In this study, using a double-blind, cross-over, placebo-controlled trial, we investigated the effect of 4-wk administration of sesamin on blood pressure (BP) in mildly hypertensive humans. Twenty-five middle-aged subjects with mild hypertension were divided into two groups, matched by age and body mass index. Twelve subjects were allocated to 4-wk intake of capsules with 60 mg sesamin per day and 13 subjects to 4-wk intake of a placebo (period 1). After a 4-wk washout period, the subjects received the alternative administration for 4 wk (period 2). BP decreased with statistical significance with the administration of sesamin (systolic: 137.6+/-2.2 to 134.1+/-1.7 mmHg, p=0.044, diastolic: 87.7+/-1.3 to 85.8+/-1.0 mmHg, p=0.045), but little changed with the placebo (systolic: 135.0+/-1.8 to 135.1+/-1.7 mmHg, diastolic: 85.9+/-1.2 to 86.6+/-1.2 mmHg). In conclusion, 4-wk administration of 60 mg sesamin significantly decreased BP by an average of 3.5 mmHg systolic BP and 1.9 mmHg diastolic BP. These results suggest that sesamin has an antihypertensive effect in humans. Epidemiological studies suggested that a 2-3 mmHg decrease in BP reduces the rate of cardiovascular diseases; therefore, it is considered that BP reduction achieved by sesamin may be meaningful to prevent cardiovascular diseases.

Nutr Metab Cardiovasc Dis. 2009 Dec;19(11):774-80. Epub 2009 Apr 5.

Sesame supplementation does not improve cardiovascular disease risk markers in overweight men and women.

Wu JH, Hodgson JM, Puddey IB, Belski R, Burke V, Croft KD.

School of Medicine and Pharmacology, University of Western Australia, PO Box X2213 GPO, Perth WA 6847, Australia.


BACKGROUND AND AIMS: Pre-clinical studies suggest that sesame and its lignans induce beneficial changes in risk factors related to cardiovascular disease and increase the bioavailability of mammalian lignans. However, only very few intervention trials have investigated the potential bioactivities of sesame in humans. We aimed to investigate the effects of sesame supplementation in humans on blood lipids, blood pressure, systemic oxidative stress, inflammatory biomarkers and mammalian lignan metabolism. METHODS AND RESULTS: We conducted a randomized, placebo-controlled cross-over intervention trial at a university research centre. Overweight or obese men and women (n=33) consumed 25g/d of sesame ( approximately 50mg/d of sesame lignan) and an iso-caloric placebo matched for macronutrient composition for 5 wks each. Each intervention period was preceded by a 4-wk washout period. Blood lipid profiles, day time ambulatory blood pressure, oxidative stress and inflammatory biomarkers and urinary mammalian lignans were measured before and after each intervention. Results are presented as the effect of sesame supplementation relative to placebo. Urinary excretion of the mammalian lignans, enterolactone and enterodiol, increased by approximately 8-fold (P<0.001). Blood lipids and blood pressure were not altered. In addition, markers of systemic inflammation (C-reactive protein, interleukin-6, tumor necrosis factor-alpha) and lipid peroxidation (F(2)-isoprostanes) were not affected. CONCLUSION: Supplementation with 25g/d of sesame can significantly increase the exposure to mammalian lignans. However, this did not cause any improvement in markers of cardiovascular disease risk in overweight or obese men and women.

PMID: 19346113

Mol Cancer Res. 2010 May;8(5):751-61. Epub 2010 May 11.

Sesamin manifests chemopreventive effects through the suppression of NF-kappaB-regulated cell survival, proliferation, invasion, and angiogenic gene products.

Harikumar KB, Sung B, Tharakan ST, Pandey MK, Joy B, Guha S, Krishnan S, Aggarwal BB.

Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.


Agents that are safe, affordable, and efficacious are urgently needed for the prevention of chronic diseases such as cancer. Sesamin, a lipid-soluble lignan, is one such agent that belongs to a class of phytoestrogens, isolated from sesame (Sesamum indicum), and has been linked with prevention of hyperlipidemia, hypertension, and carcinogenesis through an unknown mechanism. Because the transcription factor NF-kappaB has been associated with inflammation, carcinogenesis, tumor cell survival, proliferation, invasion, and angiogenesis of cancer, we postulated that sesamin might mediate its effect through the modulation of the NF-kappaB pathway. We found that sesamin inhibited the proliferation of a wide variety of tumor cells including leukemia, multiple myeloma, and cancers of the colon, prostate, breast, pancreas, and lung. Sesamin also potentiated tumor necrosis factor-alpha-induced apoptosis and this correlated with the suppression of gene products linked to cell survival (e.g., Bcl-2 and survivin), proliferation (e.g., cyclin D1), inflammation (e.g., cyclooxygenase-2), invasion (e.g., matrix metalloproteinase-9, intercellular adhesion molecule 1), and angiogenesis (e.g., vascular endothelial growth factor). Sesamin downregulated constitutive and inducible NF-kappaB activation induced by various inflammatory stimuli and carcinogens, and inhibited the degradation of IkappaBalpha, the inhibitor of NF-kappaB, through the suppression of phosphorylation of IkappaBalpha and inhibition of activation of IkappaBalpha protein kinase, thus resulting in the suppression of p65 phosphorylation and nuclear translocation, and NF-kappaB-mediated reporter gene transcription. The inhibition of IkappaBalpha protein kinase activation was found to be mediated through the inhibition of TAK1 kinase. Overall, our results showed that sesamin may have potential against cancer and other chronic diseases through the suppression of a pathway linked to the NF-kappaB signaling. (c)2010 AACR.

PMID: 20460401

Inflammation. 2010 Jul 9. [Epub ahead of print]

Sesamin Inhibits Macrophage-Induced Vascular Endothelial Growth Factor and Matrix Metalloproteinase-9 Expression and Proangiogenic Activity in Breast Cancer Cells.

Lee CC, Liu KJ, Wu YC, Lin SJ, Chang CC, Huang TS.

National Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town, Miaoli County, 350, Taiwan, Republic of China.


Sesamin is a sesame component with antihypertensive and antioxidative activities and has recently aroused much interest in studying its potential anticancer application. Macrophage is one of the infiltrating inflammatory cells in solid tumor and may promote tumor progression via enhancement of tumor angiogenesis. In this study, we investigated whether sesamin inhibited macrophage-enhanced proangiogenic activity of breast cancer cell lines MCF-7 and MDA-MB-231. Using vascular endothelial cell capillary tube and network formation assays, both breast cancer cell lines exhibited elevated proangiogenic activities after coculture with macrophages or pretreatment with macrophage-conditioned medium. This elevation of proangiogenic activity was drastically suppressed by sesamin. Vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) induced by macrophages in both cell lines were also inhibited by sesamin. Nuclear levels of HIF-1alpha and NF-kappaB, important transcription factors for VEGF and MMP-9 expression, respectively, were obviously reduced by sesamin. VEGF induction by macrophage in MCF-7 cells was shown to be via ERK, JNK, phosphatidylinositol 3-kinase, and NF-kappaB-mediated pathways. These signaling molecules and additional p38(MAPK) were also involved in macrophage-induced MMP-9 expression. Despite such diverse pathways were induced by macrophage, only Akt and p38(MAPK) activities were potently inhibited by sesamin. Expression of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha were substantially increased and involved in macrophage-induced VEGF and MMP-9 mRNA expression in MCF-7 cells. Sesamin effectively inhibited the expression of these cytokines to avoid the reinforced induction of VEGF and MMP-9. In conclusion, sesamin potently inhibited macrophage-enhanced proangiogenic activity of breast cancer cells via inhibition of VEGF and MMP-9 induction.

PMID: 20617373

Cancer Lett. 2007 Feb 8;246(1-2):63-8. Epub 2006 Mar 6.

Modifying effect of dietary sesaminol glucosides on the formation of azoxymethane-induced premalignant lesions of rat colon.

Sheng H, Hirose Y, Hata K, Zheng Q, Kuno T, Asano N, Yamada Y, Hara A, Osawa T, Mori H.

Department of Tumor Pathology, Graduate School of Medicine, Gifu University Hospital, 1-1 Yanagido, Gifu, Japan.


Sesame, which has been reported to have preventive effects against various disordered conditions, contains small quantities of lignans and several precursors to them such as sesaminol glucosides (SG). The lignans have the potent antioxidative activity and are suggested to have chemopreventive property. In the present study, we evaluated the modulating effect of SG on the development of colon precancerous lesions, aberrant crypt foci (ACF) and beta-catenin-accumulated crypts (BCAC), in the azoxymethane (AOM)-induced short-term model using male F344 rats. Dietary SG (500 ppm) significantly decreased the incidence of AOM-induced ACF when compared to the control (P<0.01). The incidences of AOM-induced BCAC in the SG-treated groups (250 or 500 ppm) were also significantly lower than that of the control group (P<0.01). Interestingly, administration of 500 ppm SG clearly decreased serum triglyceride level and mRNA expression of intestinal fatty acid-binding protein in the colonic mucosa, as compared to the control. These findings indicate that dietary SG inhibits AOM-induced carcinogenesis and suggest SG as a possible chemopreventive agent.

Prostaglandins Leukot Essent Fatty Acids. 1992 Jun;46(2):145-50.

Selective growth inhibition of a human malignant melanoma cell line by sesame oil in vitro.

Smith DE, Salerno JW.

Department of Physiological and Biological Sciences, Maharishi International University, Fairfield, Iowa 52556.


Ayurveda, an ancient and comprehensive system of natural medicine, recommends regular topical application to the skin of sesame oil, above all other oils, as a health-promoting procedure. We examined the effect of sesame oil and several other vegetable oils and their major component fatty acids on the proliferation rate of human normal and malignant melanocytes growing at similar rates in serum-free media. We found that sesame and safflower oils, both of which contain large amounts of linoleate in triglyceride form, selectively inhibited malignant melanoma growth over normal melanocytes whereas coconut, olive and mineral oils, which contain little or no linoleate as triglyceride, did not. These oils were tested at a range of 10-300 micrograms/ml. We found that of the fatty acids tested, only linoleic acid was selectively inhibitory while palmitic and oleic were not. These fatty acids were tested in the range of 3-100 micrograms/ml. These results suggest that certain vegetable oils rich in linoleic acid, such as the sesame oil, recommended for topical use by Ayurveda, may contain selective antineoplastic properties which are similar to those demonstrated for essential polyunsaturated fatty acids and their metabolites. This suggests that whole vegetable oils may have potential clinical usefulness.

PMID: 1502251

Am J Surg. 2010 Feb;199(2):160-5.

Therapeutic value of sesame oil in the treatment of adhesive small bowel obstruction.

Ji ZL, Li JS, Yuan CW, Chen WD, Zhang YN, Ju XT, Tang WH.

Department of General Surgery, Zhong Da Hospital and College of Clinical Medicine, Southeast University, Nanjing, Jiangsu 210009, China.


BACKGROUND: The optimal treatment of partial adhesive small bowel obstruction (SBO) is still controversial. The purpose of this study was to determine the effects of oral administration of sesame oil to the standard of conservative treatment in this disease. METHODS: Sixty-four cases of partial adhesive SBO were retrospectively allocated into either the control group or the intervention group (with sesame oil added), and clinical results were compared. RESULTS: Of the 64 patients, 33 were in the control group and 31 in the intervention group. Significantly fewer patients required surgical intervention in the intervention group than in the control group (4/31 vs 16/33, P = .0029). Less SBO resolution time (24 hour vs 30 hour, P = .0019) and a shorter hospital stay (6 days vs 10 days, P = .0235) were observed in the interventional group. CONCLUSIONS: Our study showed that sesame oil was a safe and effective adjunct to the standard treatment of partial adhesive SBO. Copyright 2010 Elsevier Inc. All rights reserved.

Int J Mol Med. 2001 May;7(5):485-8.

Sesaminol from sesame seed induces apoptosis in human lymphoid leukemia Molt 4B cells.

Miyahara Y, Hibasami H, Katsuzaki H, Imai K, Osawa T, Ina K, Komiya T.

Kuki Sangyo Co., Ltd., Yokkaichi-city, Mie 510-0059, Japan.


The exposure of human lymphoid leukemia Molt 4B cells to sesaminol, a component of sesame oil led to both growth inhibition and the induction of apoptosis. Morphological change showing apoptotic bodies was observed in the cells treated with sesaminol. The fragmentation of DNA by sesaminol to oligonucleosomal-sized fragments that are characteristics of apoptosis was observed to be concentration- and time-dependent. These findings suggest that growth inhibition of Molt 4B cells by sesaminol results from the induction of apoptosis in the cells.

PMID: 11295108

Int J Mol Med. 2001 Apr;7(4):369-71.

Sesamolin from sesame seed inhibits proliferation by inducing apoptosis in human lymphoid leukemia Molt 4B cells.

Miyahara Y, Hibasami H, Katsuzaki H, Imai K, Komiya T.

Kuki Sangyo Co., Ltd., 11 Onoue-cho, Yokkaichi-city, Mie 510-0059, Japan.


The exposure of human lymphoid leukemia Molt 4B cells to sesamolin, a component of sesame seed led to both growth inhibition and the induction of apoptosis. Morphological change showing apoptotic bodies was observed in the cells treated with sesamolin. The fragmentation of DNA by sesamolin to oligonucleosomal-sized fragments that are characteristics of apoptosis was observed to be concentration- and time-dependent. These findings suggest that growth inhibition of Molt 4B cells by sesamolin results from the induction of apoptosis in the cells.

PMID: 11254875

Shock. 2007 Feb;27(2):199-204.

Sesame oil attenuates Cisplatin-induced hepatic and renal injuries by inhibiting nitric oxide-associated lipid peroxidation in mice.

Hsu DZ, Chen KT, Lin TH, Li YH, Liu MY.

Department of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan.


Although cisplatin (cis-diamminedichloroplatinum) is an effective drug for the treatment of several solid tumors and has been used therapeutically for decades, several cisplatin-induced side effects have limited its therapeutic dosage in clinical studies. Our aim was to examine the effect of sesame oil on cisplatin-induced hepatic and renal injuries in mice (8-week-old female SPF C57BL/6) given subcutaneous cisplatin (0, 5, 10, or 20 mg/kg). Hepatic and renal functions, lipid peroxidation (LPO) levels, and reactive oxygen free radicals were evaluated 3 days after cisplatin administration, and tumor volumes were recorded 0, 3, 6, and 9 days after cisplatin administration. Sesame oil (i) potently attenuated cisplatin-associated hepatic and renal injuries; (ii) decreased cisplatin-initiated LPO as well as the production of hydroxyl radical, peroxynitrite, and nitrite in blood and tissue; and (iii) did not affect the antitumor capacity exerted by cisplatin in mice with melanoma. We suggest that sesame oil attenuates cisplatin-induced hepatic and renal damage by at least partially inhibiting nitric oxide-associated LPO in mice. Sesame oil might be a new approach for preventing cisplatin-induced multiple organ injury during the treatment of tumors.

PMID: 1722479

Exp Biol Med (Maywood). 2007 Jun;232(6):754-61.

Interaction of sesame seed and tamoxifen on tumor growth and bone health in athymic mice.

Sacco SM, Power KA, Chen J, Ward WE, Thompson LU.

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, 150 College Street, Toronto, ON, Canada.


Some premenopausal breast cancer patients use phytoestrogen-rich soy and flaxseed to alleviate side effects induced by drugs such as tamoxifen (TAM). Lignan-rich flaxseed protects against breast cancer and increases the effectiveness of TAM. This study determined the interactive effects of lignan-rich sesame seed (SS) and TAM on estrogen-responsive MCF-7 breast tumor growth and bone health in ovariectomized athymic mice under premenopausal-simulated conditions. Ovariectomized mice with an estrogen implant and established MCF-7 tumors were treated for 8 weeks as follows: (i) positive control fed basal diet (BD), (ii) SS group fed BD supplemented with 10% ground SS, (iii) TAM group with TAM implant fed BD, (iv) SS + TAM group with TAM implant fed BD supplemented with 10% SS, and (v) negative control fed BD with no estrogen implant. Palpable tumor data, adjusted for body weight, showed that SS does not inhibit MCF-7 tumor growth and tends to negate the tumor inhibitory effect of TAM by increasing cell proliferation and reducing apoptosis. SS alone and combined with TAM enhanced femur biomechanical strength but caused no differences in bone mineral content or bone mineral density in either the femur or lumbar vertebrae. SS is not protective and interacts adversely with TAM in MCF-7 breast tumors but induces beneficial effects on bone both alone and when combined with TAM.

PMID: 17526767

Menopause. 2008 Jan-Feb;15(1):171-9.

Lignan-rich sesame seed negates the tumor-inhibitory effect of tamoxifen but maintains bone health in a postmenopausal athymic mouse model with estrogen-responsive breast tumors.

Sacco SM, Chen J, Power KA, Ward WE, Thompson LU.

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.


OBJECTIVE: Flaxseed, the richest source of mammalian lignan precursors, enhances the tumor growth-inhibitory effect of tamoxifen while exerting no adverse effects on other estrogen-responsive tissues such as bone. Ingestion of sesame seed produces mammalian lignans comparable with flaxseed, but its anticancer potential is unknown. This study determined the interactive effects of sesame seed and tamoxifen on established MCF-7 tumor growth and bone health in ovariectomized athymic mice simulating a postmenopausal condition. DESIGN: Mice with established MCF-7 tumors were treated for 8 weeks with (1) basal diet (negative control), (2) 10% sesame seed, (3) basal diet + tamoxifen implant, (4) 10% sesame seed + tamoxifen implant, or (5) basal diet + estrogen implant (positive control). Weekly palpable tumor size, final tumor weight, cell proliferation, and apoptosis were measured. Bone mineral content, bone mineral density, and biomechanical strength testing were performed on the femur and lumbar vertebrae. RESULTS: Sesame seed induced regression of established tumor size similar to the negative control but tended to negate the tumor-inhibitory effect of tamoxifen, in part by reducing apoptosis. Sesame seed combined with tamoxifen induced higher bone mineral content, bone mineral density, and biomechanical strength in the femur and lumbar vertebrae than either treatment alone. A significant positive relationship was found between final tumor weight and bone strength parameters. CONCLUSIONS: Sesame seed is not protective and negatively interferes with tamoxifen in inducing regression of established MCF-7 tumor size but beneficially interacts with tamoxifen on bone in ovariectomized athymic mice.

PMID: 17545920