Apolipoprotein E gene promoter -219G->T polymorphism increases LDL-cholesterol concentrations and susceptibility to oxidation in response to a diet rich in saturated fat.
Level 2 - randomized trial
Individual randomized crossover dietary trial
PubMed 15531693 · doi:10.1093/ajcn/80.5.1404
What was done
Fifty-five healthy men with the APOE 3/3 genotype (7 GG, 38 GT, and 10 TT for the promoter -219G->T polymorphism) completed three 4-week dietary phases. All subjects started with a saturated fatty acid (SFA)-rich diet (38% fat, 20% SFA, 12% MUFA, 47% carbohydrate), followed in a randomized crossover design by either a carbohydrate (CHO)-rich diet (30% fat, <10% SFA, 12% MUFA, 55% CHO) or a monounsaturated fatty acid (MUFA)-rich diet (38% fat, <10% SFA, 22% MUFA, 47% CHO). Plasma lipids, apolipoprotein B, and LDL oxidation lag time were assessed after each diet.
What was found
The abstract reports statistical comparisons (P < 0.05) without absolute values or confidence intervals. Following the SFA diet, TT subjects had significantly shorter LDL oxidation lag times than G allele carriers, and T allele carriers had higher LDL cholesterol and apolipoprotein B concentrations than GG subjects. Switching from the SFA diet to CHO or MUFA diets resulted in a significantly greater increase in lag time in TT subjects compared to GG or GT subjects. Switching from the SFA to the CHO diet also caused a significantly greater reduction in LDL cholesterol and apolipoprotein B in T allele carriers than in GG subjects.
Why it matters
The study shows that the APOE promoter -219G->T polymorphism alters LDL oxidation susceptibility and lipid responses to changes in dietary fat composition.
Limits
The study included only 55 healthy men who were all APOE 3/3 homozygotes, resulting in small genotype subgroups (7 GG, 10 TT). The initial SFA diet was not randomized in sequence. Women were excluded, and no exact numerical values, baseline levels, or effect sizes are provided in the abstract.
Cited by
- supports Saturated fat intake raises atherogenic lipoprotein levels in individuals possessing specific genetic susceptibilities.