Inflammation After Eating a Mixed Meal

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 7 No. 2 • April 2004

If the law says that . . . a [government] board or authority may do what it pleases, anything that board or authority does is legal—but its actions are certainly not subject to the Rule of Law. By giving the government unlimited powers, the most arbitrary rule can be made legal; and in this way a democracy may set up the most complete despotism imaginable.

The conflict is thus not, as it has often been misconceived in nineteenth-century discussions, one between liberty and law. As John Locke had already made clear, there can be no liberty without law. The conflict is between different kinds of law—law so different that it should hardly be called by the same name: one is the law of the Rule of Law, general principles laid down beforehand, the ‘rules of the game’ which enable individuals to foresee how the coercive apparatus of the state will be used, or what he and his fellow-citizens will be allowed to do, or made to do, in stated circumstances. The other kind of law gives in effect the authority power to do what it thinks fit to do. Thus the Rule of Law could clearly not be preserved in a democracy that undertook to decide every conflict of interests not according to rules previously laid down but ‘on its merits.’

— F. A. Hayek, The Road to Serfdom (1944)

Inflammation After Eating a Mixed Meal: Eating May Be Hazardous to Your Health

A new study1 found inflammatory effects in nine normal-weight subjects after eating a 910-calorie mixed meal. The subjects were nondiabetic, aged 29–38 years, and of normal weight. The subjects’ gender(s) was not provided.

The mixed meal consisted of 910 calories from egg-muffin and sausage-muffin sandwiches and two hash-browns, with 81 grams of carbohydrate, 51 grams of fat, and 32 grams of protein, eaten over 15 minutes. The control subjects were given 300 ml of water in a fasted state in place of the mixed meal.

This is a high-carbohydrate, high-fat, and (the way we see it) not very appetizing meal. The purpose of the study, however, was not to test for a good or bad diet but to see whether “. . . the intake of a 900-calorie mixed meal induces an increase in ROS [reactive oxygen species] generation by leukocytes and an inflammatory response at the cellular level.” The results confirmed the hypothesis.

Plasma glucose concentrations were not changed significantly after the meal, but plasma insulin concentrations increased significantly at 1 hour after the meal and remained elevated at 2 and 3 hours. Plasma triacylglycerol (triglycerides) were increased significantly at 2 and 3 hours following the meal. Nuclear NF-kappaB in mononuclear cells was statistically significantly increased after the meal, probably due to the inhibited expression of I-kappaB, the protein that maintains NF-kappaB in the cytosol of cells, preventing it from moving into the nucleus. The I-kappaB expression was decreased by the induction of IKK-alpha and IKK-beta, which phosphorylate I-kappaB and cause its degradation.

C-reactive protein, an inflammatory substance associated with cardiovascular disease risk, was significantly increased after the meal. The authors note that proinflammatory stimuli, such as endotoxin and cytokines (such as tumor necrosis factor-alpha), induce an increase in intranuclear NF-kappaB and a decrease in I-kappaB.

NADPH oxidase is a major source of superoxide radicals; the p47phox subunit of this enzyme in the mononuclear cell homogenates was increased significantly at 1 hour and remained elevated for 3 hours after the meal. All nine subjects showed increased ROS (reactive oxygen species) generation by mononuclear cells after meal intake. None of these proinflammatory changes occurred in the control subjects getting water.

The authors note that these proinflammatory effects last for about 3 hours after the intake of the meal. Since people may eat again only a few hours after a meal, it is possible that chronic overeating may result in a nearly continuous state of inflammation. These effects may explain (at least in part) the reason for the reduced postischemic brachial artery vasodilation after eating a meal (especially a high-fat meal). Earlier studies have shown that taking vitamins E and C before a meal prevents this abnormality. As the authors note, these effects of ordinary eating in nonobese individuals need to be studied further, because obesity is associated with an increase in oxidative stress and an increase in plasma concentrations of proinflammatory mediators, such as tumor necrosis factor-alpha, interleukin-6, and C-reactive protein. It almost (but not quite) makes you wish you didn’t need to eat.

This study underscores the need to take antioxidants just before or with a meal. We hypothesize that a possible explanation for inflammatory reactions after eating food is that for most of human history, the food eaten was much dirtier (contained far more bacteria, parasites, and viruses) than our food today. Thus, having an inflammatory reaction after eating food that would be protective against infection makes sense. Using Third World countries as a model, the likelihood is great that infectious disease will be the #1 killer before you reach reproductive age (except in areas where there is ongoing warfare). The inflammation following food consumption also provides an explanation, at least in part, for why eating less (as in caloric restriction) has healthful benefits.

  1. Aljada et al. Increase in intranuclear nuclear factor kappaB and decrease in inhibitor kappaB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect. Am J Clin Nutr 79:682-90 (2004).

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