title: A substitution model of dietary manipulation is an effective means of optimising lipid profile, reducing C-reactive protein and increasing insulin-like growth factor-1.
abstract: There are two key methods in which fat intake may be manipulated; the 'substitution model' and the 'reduction model'. However insufficient information is known about the mechanisms of dietary fat reduction in individuals who have successfully reduced their fat intake, to be clear as to which strategy offers the greatest chance of success. Our objective was to ascertain the most effective dietary intervention for improving cardiovascular risk profile. Eighty female volunteers (high fat consumers) were recruited. Each subject was randomly allocated into one of the following groups. Substitution of high-fat foods was made with reduced-fat products, by the reduction of high-fat foods, by a combination of substitution and reduction strategies, or no advice was given. Each intervention lasted 3 months. Anthropometric measures and fasting blood samples were taken at baseline and follow-up. The substitution intervention resulted in weight loss (mean -1.4 (95 % CI -2.4, -0.2) kg) and reduced percentage body fat (mean -1.3 (95% CI -2.0, -0.5)%). There was no significant weight change with the other interventions. Fasting triacylglycerols (-0.2 (SEM 0.07) mm; P=0.04), cholesterol and C-reactive protein (CRP) levels (0.8 (SEM 0.2) mg/l; P=0.04) fell with the substitution intervention, but not with the other interventions. Insulin-like growth factor-1 increased with both substitution and reduction (P=0.02). There was no significant change in fasting insulin or glucose with any intervention. The substitution model of dietary intervention is effective even over a relatively short interval of time in reducing fasting total cholesterol, triacylglycerols and CRP. Although the group size for the present study was small and involved females only, it has significant implications for population intervention strategies.
authors.affiliation: Department of Diabetes and Endocrinology, Salford Royal Hospitals NHS Trust, Hope Hospital, Salford M6 8HD, UK. aheald@fs1.ho.man.ac.uk
authors.forename: Adrian H
authors.initials: AH
authors.lastname: Heald
authors.forename: Cheryl
authors.initials: C
authors.lastname: Golding
authors.forename: Reena
authors.initials: R
authors.lastname: Sharma
authors.forename: Kirk
authors.initials: K
authors.lastname: Siddals
authors.forename: Sara
authors.initials: S
authors.lastname: Kirk
authors.forename: Clare
authors.initials: C
authors.lastname: Lawton
authors.forename: Simon
authors.initials: S
authors.lastname: Anderson
authors.forename: J
authors.initials: J
authors.lastname: Martin Gibson
authors.forename: Janet E
authors.initials: JE
authors.lastname: Cade
mesh_terms: D000273:Adipose Tissue / Q000502:physiology; D000328:Adult; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D004041:Dietary Fats / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D008055:Lipids / Q000097:blood*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss / Q000502:physiology
chemical_list: D004041:Dietary Fats; D008055:Lipids; D014280:Triglycerides; D007334:Insulin-Like Growth Factor I; D002097:C-Reactive Protein; D002784:Cholesterol