title: SFAs do not impair endothelial function and arterial stiffness.
abstract: BACKGROUND
  It is uncertain whether saturated fatty acids (SFAs) impair endothelial function and contribute to arterial stiffening.
  
  
  OBJECTIVE
  We tested the effects of replacing SFAs with monounsaturated fatty acids (MUFAs) or carbohydrates on endothelial function and arterial stiffness.
  
  
  METHODS
  With the use of a parallel-designed randomized controlled trial in 121 insulin-resistant men and women, we measured vascular function after 1 mo of consumption of a high-SFA (HS) diet and after 24 wk after random assignment to the HS diet or diets that contained <10% SFAs and were high in either MUFAs or carbohydrates. The primary outcome was a change in flow-mediated dilation (FMD), and secondary outcomes were changes in carotid to femoral pulse wave velocity (PWV) and plasma 8-isoprostane F2α-III concentrations.
  
  
  RESULTS
  For 112 participants with data available for analysis on the specified outcomes, no significant differences were shown. FMD with the HS reference diet was 6.7 ± 2.2%, and changes (95% CIs) after 6 mo of intervention were +0.3 (-0.4, 1.1), -0.2 (-0.8, 0.5), and -0.1 (-0.6, 0.7) with HS, high-MUFA (HM), and high-carbohydrate (HC) diets, respectively. After consumption of the HS reference diet, the geometric mean (±SD) PWV was 7.67 ± 1.62 m/s, and mean percentages of changes (95% CIs) were -1.0 (-6.2, 4.3) with the HS diet, 2.7 (-1.4, 6.9) with the HM diet, and -1.0 (-5.5, 3.4) with the HC diet. With the HS reference diet, the geometric mean (±SD) plasma 8-isoprostane F2α-III concentration was 176 ± 85 pmol/L, and mean percentage of changes (95% CIs) were 1 (-12, 14) with the HS diet, 6 (-5, 16) with the HM diet, and 4 (-7, 16) with the HC diet.
  
  
  CONCLUSIONS
  The replacement of SFAs with MUFAs or carbohydrates in healthy subjects does not affect vascular function. This trial was registered at Current Controlled Trials (http://www.controlled-trials.com/ISRCTN) as ISRCTN 29111298.
authors: Diabetes and Nutritional Sciences Division, King's College London, London, United Kingdom. tom.sanders@kcl.ac.uk
authors: Thomas A B
authors: TA
authors: Sanders
authors: Fiona J
authors: FJ
authors: Lewis
authors: Louise M
authors: LM
authors: Goff
authors: Philip J
authors: PJ
authors: Chowienczyk
mesh_terms: D000328:Adult; D004032:Diet; D004040:Dietary Carbohydrates / Q000494:pharmacology*; D004041:Dietary Fats / Q000494:pharmacology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005227:Fatty Acids / Q000494:pharmacology*; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D011674:Pulse; D014652:Vascular Diseases / Q000209:etiology; D059289:Vascular Stiffness / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005227:Fatty Acids; D005229:Fatty Acids, Monounsaturated; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost
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