Study reinforces link between obesity, high-fat meals and heart disease

February 17, 2011, University of California - Davis

The effect of a high-fat meal on blood vessel walls can vary among individuals depending on factors such as their waist size and triglyceride levels, suggests new research at UC Davis.

The new research reinforces the link between belly fat, inflammation and thickening of the arterial linings that can lead to heart disease and strokes.

Triglycerides are types of fat molecules, commonly associated with "," known to increase risk of inflammation of the endothelium, the layer of cells that lines arteries.

"The new study shows that eating a common fast food meal can affect inflammatory responses in the blood vessels," said Anthony Passerini, assistant professor of biomedical engineering at UC Davis, who led the project.

"Our techniques allowed us to measure the inflammatory potential of an individual's lipids outside of the body and to correlate that with easily measured characteristics that could be used to help better understand a person's risk for vascular disease," Passerini said.

Passerini collaborated with Scott Simon, professor of biomedical engineering at UC Davis, to develop cell culture models to mimic the properties of blood vessels. They wanted to learn how triglyceride levels can cause endothelial inflammation, and find a way to assess an individual's inflammatory potential.

They recruited 61 volunteers with high and normal fasting triglyceride levels and a range of waist sizes, then measured levels of triglyceride particles in their blood after they ate a typical fast food breakfast from a major fast food franchise: two breakfast sandwiches, hash browns and orange juice.

Passerini's team found that after eating the high-fat meal, the size of a type of a particle called triglyceride-rich (TGRL) varied directly with the individual's waist size and preexisting blood triglyceride level. These particles can bind to the , triggering inflammation and an immune response that brings to repair the damage. Over time, this leads to atherosclerosis.

The researchers tested whether TGRL particles from the volunteers' blood could cause cultured endothelial cells in the laboratory to express markers for inflammation.

There was a mixed response: individuals with both a waist size over 32 inches (not terribly large by most standards) and high triglyceride levels had large lipoprotein particles that bound easily to the endothelial cells and caused inflammation in response to an immune chemical "trigger."

The TGRLs only caused inflammation when exposed to this immune molecule, which suggests that people with existing low-grade inflammation may be more susceptible to endothelial dysfunction related to triglyceride "spikes" that occur after eating high-fat meals, Passerini said.

In people who are predisposed, repeated episodes of inflammation could lead to atherosclerosis. Passerini's lab is continuing to investigate how abdominal obesity, high and inflammation can lead to atherosclerosis.

More information: The findings are published online in the journal American Journal of Physiology - Heart and Circulatory Physiology.

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not rated yet Feb 18, 2011
Highly questionable conclusions. Seems a target driven study. One wanted to find a link, so one was found.

If indeed this link exists why oh why does the obesity paradox exist?

In itself the obesity paradox is already proof positive that the thesis Fat is bad doesn't hold. First resolve that, explain away the paradox. I suggest the most obvious method:
It's a paradox because the underlying thesis is wrong. Change the thesis to reflect the facts and the paradox disappears.

Once that has been done, one will discover that whilst obesity may in itself carry extra risks for certain ailments, it diminishes them for others. With in the endbalance an overall positive effect on life expectancy for the medium obese.

Saves billions of wasted research money, and lets the profession focus on actually curing the ailments themselves rather then preventing one and thereby causing others.

1 / 5 (3) Feb 18, 2011
Was it high fat and low carb? Doubt it.
not rated yet Feb 18, 2011
Was it high fat and low carb? Doubt it.
So when you use Q-Tips do you often find cobwebs in your ears?
1 / 5 (3) Feb 18, 2011
"two breakfast sandwiches, hash browns and orange juice."
So the sugar and starch were not considered as having any impact?

"after eating the high-fat meal, "
AND high sugar/starch meal.

"nsulin facilitates entry of glucose into adipocytes, and within those cells, glucose can be used to synthesize glycerol. This glycerol, along with the fatty acids delivered from the liver, are used to synthesize triglyceride within the adipocyte. By these mechanisms, insulin is involved in further accumulation of triglyceride in fat cells. "
1 / 5 (3) Feb 18, 2011
Egg McMuffin: fat: 12 g, carbs: 30 g, protein: 18g.
Hashbrown: fat: 9g, carbs: 15 g, protein: 1 g.
OJ: small: carbs (sugar) 30 g.

So for this study, if this was the food used, the total fat was 33g, carbs: 105, and protein, 37 g.

The protein and carbohydrates had no impact upon the results?
1 / 5 (3) Feb 19, 2011
18.8%, by weight, of the meal was fat. This is high fat? 60% is carbohydrates which stimulates an insulin response.
How did the 'study' account for carbohydrates?
not rated yet Feb 19, 2011
18.8%, by weight, of the meal was fat. This is high fat?
Yes it is.
60% is carbohydrates which stimulates an insulin response.
And what link does insulin have with heart disease?
How did the 'study' account for carbohydrates?
Why don't you read the paper and find out.


Take a look at the guy who's taking pot shots at an article about fat.
1 / 5 (3) Feb 19, 2011
"High levels of insulin in the blood may be a silent heart-disease risk factor for 25 percent of the trim and otherwise healthy people worldwide."
"There are several signs of insulin resistance or high insulin levels, including obesity, high blood sugar levels, high triglycerides, high low-density lipoprotein, low high-density lipoprotein and high blood pressure; these can put stress on cardiovascular function and increase your risk of heart disease.
In addition to a low-carbohydrate diet,...."

Read more: Why High Insulin Causes Heart Disease | http:/
So the 60% carbohydrates, which stimulate insulin production, played no roll in the experiment?

The paper is not freely available.
2 / 5 (4) Feb 21, 2011
From the author:
"We did not compare different meals for the study. Nor do we dispute
the possibility that the carbohydrates contribute in some meaningful
way, though we did not specifically attempt to dissect out the effect
of high fat vs. high carbs. It seems this will spark some debate over
what is responsible for our findings, but in some sense it misses the

The point the author wanted to make is to blame a high fat diet, but has no supporting research that isolates the 'high fat' as the culprit.

Sloppy research, sloppy conclusions. UC Davis and this site promotes this propaganda.

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