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Mediterranean‐style dietary pattern is associated with surrogate measures of insulin resistance in the Framingham Offspring Cohort
Author(s) -
Rumawas Marcella E,
McKeown Nicola M,
Rogers Gail,
Dwyer Johanna T,
Meigs James M,
Jacques Paul F
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a6
Subject(s) - insulin resistance , waist , medicine , mediterranean diet , framingham risk score , cohort , abdominal obesity , insulin , endocrinology , offspring , quartile , body mass index , biology , disease , pregnancy , confidence interval , genetics
The traditional Mediterranean diet is associated with a lower risk of cardiovascular diseases (CVD). Improved insulin sensitivity may be one mechanism by which adoption of Mediterranean‐style dietary pattern may reduce CVD risk. A diet score was developed to capture a Mediterranean‐style dietary pattern in the Framingham Offspring Cohort. We examined the relationship between this diet score and insulin resistance markers (fasting & 2‐hr plasma glucose & insulin and the homeostasis model assessment insulin resistance [HOMA‐IR]) in 1238 men & 1505 women without diabetes in the cohort. After adjustment for potential confounding factors, a higher diet score, reflecting greater similarity to Mediterranean‐style dietary pattern, was associated with lower fasting insulin levels (mean 35 vs 32 μU/mL in the lowest vs highest quartiles of diet score; P trend<0.01), 2‐hr insulin (116 vs 98 μU/mL; P trend<0.01), HOMA‐IR (8.4 vs 7.7; P trend<0.01) in subjects with abdominal obesity (waist circumference >108 cm in men or >88 cm in women), but not in those with lesser waist circumferences. No significant association was found between the Mediterranean diet score and fasting and 2‐hr glucose. In individuals with greater abdominal adiposity, greater consistency with a Mediterranean‐style dietary pattern was associated with better insulin sensitivity. Supported by NIH/NHLBI Contract N01‐HC‐25195 & Grant NIA # 5R01‐AG 16495