Two interesting studies:
"BACKGROUND: High-glycemic index diets have been linked to greater risk of cardiovascular disease and type 2 diabetes.
Postprandial glycemia within the normal range may promote oxidative stress and inflammatory processes underlying the development of disease. OBJECTIVE: We explored acute differences in the activation of the inflammatory marker nuclear factor-kappaB after consumption of 2 carbohydrate meals matched for macronutrient and micronutrient composition but differing in glycemic index. DESIGN: After an overnight fast, 10 young, lean healthy subjects were fed in random order 3 meals providing 50 g of available carbohydrate as glucose, white bread, or pasta. Venous blood samples were collected at 0, 1, 2, and 3 h, and nuclear proteins were extracted from mononuclear cells. Changes in nuclear factor-kappaB-p65 proteins were detected by Western blotting. Acute changes in other markers of oxidative stress (nitrotyrosine and soluble intercellular adhesion molecule-1) were also assessed. RESULTS:
The maximum increase in nuclear factor-kappaB activation was similar after the bread meal [mean (+/-SEM) area under the curve: 69 +/- 16% optical density x h]
and the glucose challenge (75 +/- 9% optical density x h),
but was 3 times higher than after the pasta meal (23 +/- 5% optical density x h) (P < 0.05). Similarly, changes in nitrotyrosine, but not soluble intercellular adhesion molecule-1, were higher after glucose and bread than after pasta (P = 0.01 at 2 h). CONCLUSIONS:
The findings suggest that high-normal physiologic increases in blood glucose after meals aggravate inflammatory processes in lean, young adults. This mechanism may help to explain relations between carbohydrates, glycemic index, and the risk of chronic disease."http://www.ncbi.nlm....pubmed/18469238"Abstract
The aim was to study the effect of a standardized oral fat load (OFL) on different inflammatory parameters in a large sample of adult healthy subjects (n = 286) of both sexes. The fat load was given between 08:00 and 09:00 h after a 12-h fast. Blood samples were drawn before and 3, 6, 9, and 12 h after the OFL. All patients underwent a measurement of body mass index (BMI), blood glucose (BG), systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (Tg), soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin), and tumor necrosis factor-α (TNF-α). Fasting plasma glucose (FPG) increase was +3.26% at 3 h, +4.35% at 6 h, +1.09% at 9 h while FPG decrease was −1.09% at 12 h. High-density lipoprotein cholesterol increase was +2.08% at 3 h, and at 12 h during OFL study; a significant HDL-C decrease was present in subjects after 6 h (−4.17%;
P < 0.05 vs 0). A significant Tg change was observed after 6 h (+70.37%;
P < 0.01 vs 0) and 9 h (+58.33%;
P < 0.05 vs 0) respectively, and the increase was +22.22% at 3 h and +18.52% at 12 h. Total cholesterol increase was +0.52% after 3 h, +1.04% after 6 h, while after 12 h the decrease was −0.52%. Low-density lipoprotein cholesterol increase was +1.64% after 6 h with a decrease of −0.82% at 9 and 12 h. A significant sICAM-1, hsCRP, and sE-selectin variation was observed after 6 and 9 h, while a significant sVCAM-1 change occurred after 3, 6, and 9 h. Soluble ICAM-1 increase was +20.58% at 3 h, +34.10% at 6 h (
P < 0.05 vs 0) +25.94% at 9 h (
P < 0.01 vs 0), and +19.14% at 12 h; sVCAM-1 increase was +13.97% (
P < 0.05 vs 0) at 3 h, +18.55% at 6 h (
P < 0.01 vs 0), +12.02% at 9 h (
P < 0.05 vs 0), and +8.70% at 12 h. High-sensitivity CRP increase was +36.36% at 3 h, +90.91% at 6 h (
P < 0.01 vs 0), +63.64% at 9 h (
P < 0.05 vs 0), and +36.36% at 12 h. Soluble E-selectin increase was +27.11% at 3 h, +51.90% at 6 h (
P < 0.05 vs 0), +45.19% at 9 h (
P < 0.01 vs 0), and +20.12% at 12 h. Interleukin-6 increase was +61.11% at 3 h (
P < 0.05 vs 0), +83.33% at 6 h (
P < 0.001 vs 0), +55.56% at 9 h (
P < 0.01 vs 0), and +22.22% at 12 h. Tumor necrosis factor-α increase was +42.86% at 3 h (
P < 0.05 vs 0), +71.43% at 6 h (
P < 0.01 vs 0), (+50.00% at 9 h (
P < 0.05 vs 0), and +28.57% at 12 h
. We observed that the OFL induces a complex and massive systemic inflammatory response that includes IL-6, TNF-α, hsCRP, and cell adhesion molecules, even before Tg significantly rises."http://www.springerl...8n32355687p665/So yes, carbohydrates cause a postprandial inflammation, but so does fat.
Edited by Blue, 21 October 2009 - 04:01 PM.