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      The cardiac and haemostatic effects of dietary hempseed

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      1 , 2 , 1 ,
      Nutrition & Metabolism
      BioMed Central

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          Abstract

          Despite its use in our diet for hundreds of years, hempseed has surprisingly little research published on its physiological effects. This may have been in the past because the psychotropic properties wrongly attributed to hemp would complicate any conclusions obtained through its study. Hemp has a botanical relationship to drug/medicinal varieties of Cannabis. However, hempseed no longer contains psychotropic action and instead may provide significant health benefits. Hempseed has an excellent content of omega-3 and omega-6 fatty acids. These compounds have beneficial effects on our cardiovascular health. Recent studies, mostly in animals, have examined the effects of these fatty acids and dietary hempseed itself on platelet aggregation, ischemic heart disease and other aspects of our cardiovascular health. The purpose of this article is to review the latest developments in this rapidly emerging research field with a focus on the cardiac and vascular effects of dietary hempseed.

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          Most cited references32

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          Hempseed as a nutritional resource: An overview

          J Callaway (2004)
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            Nitric oxide and pathogenic mechanisms involved in the development of vascular diseases.

            Nitric oxide (NO) is a pivotal signaling messenger in the cardiovascular system. NO participates in regulatory functions including control of hemostasis, fibrinolysis, platelet and leukocyte interactions with the arterial wall, regulation of vascular tone, proliferation of vascular smooth muscle cells, and homeostasis of blood pressure. Diminished NO bioavailability and abnormalities in NO-dependent signaling are among central factors of vascular disease, although it is unclear whether this is a cause of, or result of endothelial dysfunction or both pathogenic events. Disturbances in NO bioavailability have been linked to cause endothelial dysfunction, leading to increased susceptibility to atherosclerotic lesion progression, hypertension, hypercholesterolemia, diabetes mellitus, thrombosis and stroke.
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              Conversion of alpha-linolenic acid in humans is influenced by the absolute amounts of alpha-linolenic acid and linoleic acid in the diet and not by their ratio.

              Human in vivo data on dietary determinants of alpha-linolenic acid (ALA; 18:3n-3) metabolism are scarce. We examined whether intakes of ALA or linoleic acid (LA; 18:2n-6) or their ratio influences ALA metabolism. During 4 wk, 29 subjects received a control diet (7% of energy from LA, 0.4% of energy from ALA, ALA-to-LA ratio = 1:19). For the next 6 wk, a control diet, a low-LA diet (3% of energy from LA, 0.4% of energy from ALA, ratio = 1:7), or a high-ALA diet (7% of energy from LA, 1.1% of energy from ALA, ratio = 1:7) was consumed. Ten days before the end of each dietary period, [U-13C]ALA was administered orally for 9 d. ALA oxidation was determined from breath. Conversion was estimated by using compartmental modeling of [13C]- and [12C]n-3 fatty acid concentrations in fasting plasma phospholipids. Compared with the control group, ALA incorporation into phospholipids increased by 3.6% in the low-LA group (P = 0.012) and decreased by 8.0% in the high-ALA group (P < 0.001). In absolute amounts, it increased by 34.3 mg (P = 0.020) in the low-LA group but hardly changed in the high-ALA group. Nearly all ALA from the plasma phospholipid pool was converted into eicosapentaenoic acid. Conversion of eicosapentaenoic acid into docosapentaenoic acid and docosahexaenoic acid hardly changed in the 3 groups and was <0.1% of dietary ALA. In absolute amounts, it was unchanged in the low-LA group, but increased from 0.7 to 1.9 mg (P = 0.001) in the high-ALA group. ALA oxidation was unchanged by the dietary interventions. The amounts of ALA and LA in the diet, but not their ratio, determine ALA conversion.
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                Author and article information

                Journal
                Nutr Metab (Lond)
                Nutrition & Metabolism
                BioMed Central
                1743-7075
                2010
                21 April 2010
                : 7
                : 32
                Affiliations
                [1 ]Department of Physiology, University of Manitoba and Institute of Cardiovascular Sciences, St Boniface Hospital Research Centre, 351 Tache Avenue, Winnipeg, Manitoba, R2H 2A6, Canada
                [2 ]Cardiovascular Research Division, V.I. Lenin Universitary Hospital, s/n Lenin Avenue, Holguin, 80100, Cuba
                Article
                1743-7075-7-32
                10.1186/1743-7075-7-32
                2868018
                20409317
                32458758-f926-4429-abc9-84fa88308d65
                Copyright ©2010 Rodriguez-Leyva and Pierce; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 September 2009
                : 21 April 2010
                Categories
                Review

                Nutrition & Dietetics
                Nutrition & Dietetics

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