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ARS Home Northeast Area Beltsville, Maryland (BHNRC) Beltsville Human Nutrition Research Center Food Components and Health Laboratory Research Publications at this Location





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Title:   Author  item
                                            Baer, Daviditem
                                            GEBAUER, SARAH - University Of Marylanditem
                                            RUSSELL, TRACY - University Of Vermont
  Submitted to: European Journal of Clinical Nutrition
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 2/27/2014
                                    Publication  Date: 4/16/2014
                                    Citation: Baer, D.J., Gebauer, S., Russell, T. 2014. Impact of stearic acid and oleic acid on hemostatic factors in the context of controlled diets consumed by healthy men. European Journal of Clinical Nutrition. 68:1072-1074.Interpretive Summary: Blood clot formation and breakdown is a highly controlled biological process.  Factors that increase blood clotting may increase risk for coronary heart disease.  An increase in blood LDL cholesterol may also increase risk for coronary heart disease.  Evidence suggests that stearic acid, a saturated fatty acid, effects LDL cholesterol differently than other saturated fatty acids – consumption of stearic acid does not increase LDL cholesterol whereas consumption of other saturated fatty acids typically raises LDL cholesterol.  In fact, stearic acid may lower LDL cholesterol and have no effect of HDL cholesterol, thus lowering the ratio of total cholesterol to HDL-C.  Since stearic acid does not raise LDL cholesterol, its use as an alternative for trans fatty acids in foods is possible since stearic acid can provide some of the same functional properties as trans fatty acids without the negative effect on LDL cholesterol.  However, the effect of stearic acid on other markers of cardiovascular disease risk, such as markers of hemostasis, is unclear.  In a randomized crossover study, 50 men consumed 6 controlled diets for 5 weeks each.  The diets contained fat or fatty acids with 8% replaced across diets as follows: carbohydrate (control), stearic acid, oleic acid, trans fatty acids, trans fatty acids and stearic acid combined, and saturated fatty acids (lauric, myristic, and palmitic).  At the end of each treatment, factor VIIc, plasminogen activator inhibitor-1 (PAI-1), and plasmin alpha-2-antiplasmin complex were measured.  There were no differences in these measures when comparing the stearic diet to the carbohydrate control diet (P > 0.05), whereas the oleic acid diet increased factor VIIc and PAI-1 when compared to carbohydrate control (P = 0.05). In conclusion, stearic acid and oleic acid had similar effects on these factors involved in hemostasis in healthy men, within the context of a highly-controlled diet.  These data are of interest to food manufacturers, those involved in establishing food labeling policy, clinicians, dietitians and research scientists interested in heart disease.
                                Technical Abstract: Evidence suggests that stearic acid (STE) differentially affects lipoprotein risk factors compared with other saturated fatty acids (SFA). When compared to cholesterol-raising SFA, STE lowers LDL-cholesterol (LDL-C) and has a neutral effect on HDL-C, thus lowering the ratio of total cholesterol to HDL-C. STE may serve as a viable alternative to TFA due to physical characteristics, as well as neutral or beneficial effects on lipoprotein risk factors compared with other SFA and TFA. The impact of STE on other markers of cardiovascular disease risk, such as markers of hemostasis, is unclear. In a randomized crossover study, 50 men consumed 6 controlled diets for 5 wk each [39% en from fat, 15% en from protein, and 46% en from carbohydrate (CHO)]. Fat or fatty acids (8%) was replaced across diets as follows: STE, Oleic Acid (OL), CHO (control), TFA, TFA/STE (4% of en each), and 12:0 –16:0 SFA. There were no differences in factor VIIc, plasminogen activator inhibitor-1 (PAI-1), and plasmin alpha-2-antiplasmin complex when comparing the OL and STE diets (P > 0.05). There were no differences in these measures when comparing the STE diet to the CHO control diet (P > 0.05), whereas the OL diet increased factor VIIc and PAI-1 when compared to control (P = 0.05). In conclusion, STE and OL similarly affect markers of hemostasis in healthy men, within the context of a highly-controlled diet.


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