Thursday, January 17, 2008

Big Macs and Whoppers: Spikes in after-meal glucose and lipid levels lead to inflammation and CVD

January 16, 2008 Michael O'Riordan

Kansas City, MO - The modern-day diet of Big Macs and Domino's Pizza, especially when combined with a sedentary lifestyle, is an obvious cardiovascular risk factor, but new research suggests that one aspect making these diets so deadly is the exaggerated after-meal increase in glucose and lipids that leads to inflammation and eventually atherosclerosis [1].

In a state-of-the-art paper published in the January 14, 2008 issue of the Journal of the American College of Cardiology, lead author Dr James O'Keefe (Cardiovascular Consultants, Kansas City, MO) and colleagues say that these after-meal spikes in glucose and lipid levels, a state known as postprandial dysmetabolism, induces immediate oxidative stress and leads to atherogenic changes.

"The risk factors that we have come to understand in cardiovascular disease, such as hypertension, high cholesterol levels, and diabetes, in fact have their genesis in the acute toxic effects of the modern-day overprocessed foods that make up too much of our diets," O'Keefe told heartwire. Understanding the postprandial effects of a highly processed, calorie-dense, nutrient-depleted diet is "key to understanding, preventing, and treating coronary disease and many other related conditions such as hypertension, diabetes, dyslipidemia, and Alzheimer's disease," he said.

All sorts of immediate acute changes after a Big Mac

In an interview with heartwire, O'Keefe said that a maladaptive, modern diet is often an underlying cause of chronic inflammation, an important consideration now that systemic inflammation is routinely recognized as a mediator of coronary artery disease.

"Inflammation, however, is often thought of as a nebulous concept," said O'Keefe. "We might think that some people have inflammation, such as those with diabetes or those with abdominal obesity, while others do not. What has not gotten a lot of attention is that some people have inflammation because they are eating the wrong foods."

When individuals hit up their local Burger King—home of the Whopper—the excessive consumption of calorie-dense, nutrient-free food causes a surge in blood glucose and triglyceride levels. As a result of the meal, glucose and free fatty acids immediately overwhelm the body's ability to handle the surge, resulting in a flooding of the Kreb's cycle and the production of superoxide anions. The postprandial production of these free radicals acutely triggers atherogenic changes, such as "increases in LDL oxidation, sympathetic tone, vasoconstriction, and thrombogenicity," explained O'Keefe. Higher C-reactive protein (CRP) and other inflammatory markers confirm the postprandial spikes in inflammation with highly processed foods.

Whole foods, on the other hand, such as those high in fiber and low on the glycemic index, including whole grains, legumes, vegetables, and fruits, have been shown to markedly blunt the after-meal increase in glucose, triglycerides, and inflammation, said O'Keefe. Lean protein, vinegar, fish oil, tea, and cinnamon have also been shown to positively affect postprandial dysmetabolism.

"With a lot of these foods, and various types of diets such as the traditional hunter-gatherer or the Mediterranean diet, the most powerful effect they have is their ability to blunt spikes in postprandial glucose and triglyceride levels," said O'Keefe. "When we start thinking about what type of foods are good for us, it's actually pretty easy. We need to figure out what effect it has on postprandial glucose and triglyceride levels."


With a lot of these foods, and various types of diets such as the traditional hunter-gather or the Mediterranean diet, the most powerful effect they have is their ability to blunt spikes in postprandial glucose and triglyceride levels.



O'Keefe also highlighted the consumption of alcohol and its postprandial effects. Light to moderate alcohol consumption has shown a biphasic, dose-dependent effect on adverse health outcomes, including coronary disease, stroke, dementia, and all-cause mortality. Although alcohol is known to increase HDL-cholesterol levels, O'Keefe believes the effect of alcohol on postprandial glucose levels is the most likely mechanism of benefit. One to two drinks in healthy nondiabetic individuals can significantly lower postprandial glucose and insulin levels, and as the group notes in their paper, alcohol intake and postprandial glucose follow the same J-shaped relationship seen between alcohol and systemic inflammation, as well as alcohol and adverse cardiovascular events.

O'Keefe noted that there are various approaches to combating inflammation but said such traditional "shortcuts," including the consumption of antioxidants such as vitamin E, are not effective enough. The oxidative stress engendered by the postprandial surge in glucose levels simply overwhelms any benefit the supplements might provide. Moreover, a high-fiber, low-glycemic-index-based diet provides enough antioxidants, all without the surge in inflammation brought on by processed foods.

While even endocrinologists abandoned the measurement of postprandial glucose levels 10 years ago, they are starting to begin to measure it again, said O'Keefe. There is no standard test meal for measuring postprandial triglyceride levels, but guidelines might emerge in the future, he noted.

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