13 replies to this topic

[TheFountain]

I'm surprised nobody shared this here. Oh wait, no i'm not....





Link Between Obesity, High-Fat Meals and Heart Disease Reinforced by New Study

ScienceDaily (Feb. 17, 2011) — 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 "bad cholesterol," 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 lipoprotein (TGRL) varied directly with the individual's waist size and preexisting blood triglyceride level. These particles can bind to the endothelium, triggering inflammation and an immune response that brings white blood cells 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 triglyceride levels and inflammation can lead to atherosclerosis.
The findings are published online in the American Journal of Physiology -- Heart and Circulatory Physiology. The other authors of the paper, all at the UC Davis Department of Biomedical Engineering, are: graduate student Ying Wang, staff researcher John Schulze, clinical coordinator Nadine Raymond, and undergraduates Tyler Tomita and Kayan Tam. The work was funded by grants from the National Institutes of Health and a fellowship from the Howard Hughes Medical Institute to Wang.

http://www.scienceda...10217151445.htm

[TheFountain]

And before anybody starts making brilliant little observations about there being carbs in hash browns and orange juice, the meals seemed equally dense in fat. usually hash browns are deep fried, which adds a substantial amount of fat, and the breakfast sandwiches tend to be equally high in fat and carbs. So erring on the side of caution is advised.

Personally, I do not do well on high fat, low carb diets. I always gain weight from them, especially around the waist. I also do not seem to react well to bleached grain products however whole grains do not seem to hurt me in moderate consumption, but indiscriminate fat consumption of more than about 50-70 grams a day tops always leads to the same result. More belly fat! And that's regardless of the kind of fat consumed. But as a rule I have learned to minimize saturated fat, despite what all the brilliant paleo bloggers claim about it, based mostly on animal studies and guess work.

Human studies are where it's at!

Edited by TheFountain, 13 December 2011 - 12:40 PM.

[arska]

IMHO, these studies should take into account the omega6:omega3 ratio of the meal. The highly refined seed oils are rich in omega6, which excess promotes variety of cellular level metabolic problems.

There is also this interesting article by Dr. Stephanie Seneff of MIT,in which she considers that the dietary content of sulphur might play a big role in metabolic syndrome:

Another way to compensate for defective glucose metabolism in the muscle cells is to gain weight. Fat cells must now convert glucose into fat and release it into the blood stream as triglycerides, to fuel the muscle cells. In the context of a low fat diet, sulfur deficiency becomes that much worse a problem. Sulfur deficiency interferes with glucose metabolism, so it's a much healthier choice to simply avoid glucose sources (carbohydrates) in the diet; i.e. to adopt a very low-carb diet. Then the fat in the diet can supply the muscles with fuel, and the fat cells are not burdened with having to store up so much reserve fat.

→ source (external link)

[niner]

Thanks for bringing this up, TheFountain. I think you are misinterpreting it, but thanks nonetheless, because it raises an important point. The following is background from medscape.

Question
What is the significance of postprandial triglyceride levels compared with fasting triglyceride levels?

Response from Vera Bittner, MD, MSPH
Professor of Medicine, Section Head, Preventive Cardiology, University of Alabama at Birmingham, Birmingham, Alabama
In 1979, Zilversmit^[1] proposed that atherogenesis was a postprandial phenomenon. Ingestion of a fatty meal results in the production of triglyceride-rich lipoproteins (chylomicrons and, secondarily, very-low-density lipoproteins), particles which are then metabolized to atherogenic remnants. Humans spend most of their time in a postprandial state, not in a fasting state, and their arteries are thus exposed to postprandial plasma most of the time. One would thus surmise that postprandial lipid values would correlate better with prognosis than fasting values.
This has indeed been shown in recent epidemiologic studies. Bansal and colleagues^[2] analyzed the prognostic value of fasting and nonfasting triglyceride levels in a cohort of 26,509 healthy women enrolled in the Women's Health Study. After 11.4 years of follow-up, nonfasting, but not fasting, triglycerides in the upper tertile of the distribution were associated with an almost 2-fold increase in cardiovascular disease even after adjustment for age, blood pressure, smoking, use of hormone therapy, total and high-density lipoprotein cholesterol, diabetes mellitus, body mass index, and high-sensitivity C-reactive protein.^[2] In another study published in the same issue of the Journal of the American Medical Association, authors from Denmark similarly concluded that nonfasting triglyceride levels were predictive of myocardial infarction, ischemic heart disease, and death in men and women.^[3]
What are the practical implications of this observation? "Lipid tolerance testing" (analogous to glucose tolerance testing) has been suggested by some, but this is not practical for most practitioners and to date we have no data to suggest that treatment strategies should be altered based on such testing. It is important, however, not to dismiss triglyceride elevations in individuals who forget to fast for their regular blood draw. Such an elevation should prompt discussion with the patient about the link between such triglyceride elevations and insulin resistance, future cardiovascular disease, and the importance of lifestyle modifications (quality and quantity of food, weight management, physical activity).^[4-9]
Current treatment guideline recommendations are based on fasting lipoprotein measurements.^[4] Low-density lipoprotein cholesterol remains the primary target of therapy for patients with borderline fasting hypertriglyceridemia (150-199 mg/dL). For fasting triglyceride levels between 200 and 499 mg/dL, non-high-density lipoprotein cholesterol becomes a secondary target of therapy. If fasting triglyceride levels are very high (≥ 500 mg/dL), prevention of acute pancreatitis is the primary goal, and triglyceride-lowering drugs (fibrates, nicotinic acid, fish oil) become first-line therapy in these patients.

The paper being discussed here:

Am J Physiol Heart Circ Physiol. 2011 Mar;300(3):H784-91. Epub 2010 Dec 17.
Endothelial inflammation correlates with subject triglycerides and waist size after a high-fat meal.
Wang YI, Schulze J, Raymond N, Tomita T, Tam K, Simon SI, Passerini AG.

Department of Biomedical Engineering, University of California, Davis, California 95616, USA. agpasserini@ucdavis.edu

A rise in postprandial serum triglycerides (PP-sTG) can potentiate inflammatory responses in vascular endothelial cells (ECs) and thus serves as an independent risk factor for predicting increased cardiovascular morbidity. We examined postprandial triglyceride-rich lipoproteins (PP-TGRLs) in subjects ranging from normal to hypertriglyceridemic for their capacity to alter EC acute inflammatory responses. Cultured human aortic ECs (HAECs) were conditioned with PP-TGRLs isolated from human serum at the peak after a moderately high-fat meal. VLDL particle size increased postprandially and varied directly with the subject's PP-sTG level and waist circumference. PP-TGRL particles bound to HAECs and were internalized via LDL receptor-mediated endocytosis. PP-TGRL alone did not induce an inflammatory response over the range of individuals studied. However, combined with low-dose TNF-α stimulation (0.3 ng/ml), it elicited a net 10-15% increase above cytokine alone in the membrane expression of VCAM-1, ICAM-1, and E-selectin, which was not observed with fasting TGRLs. In contrast to upregulation of ICAM-1 and E-selectin, VCAM-1 transcription and expression varied in direct proportion with individual PP-sTG and waist circumference. The extent of monocyte arrest on inflamed HAECs under shear stress also correlated closely with VCAM-1 expression induced by conditioning with PP-TGRL and TNF-α stimulation. This ex vivo approach provides a quantitative means to assess an individual's inflammatory potential, revealing a greater propensity for endothelial inflammation in hypertriglyceridemic individuals with abdominal obesity.

PMID: 21169396

In brief, this is not the death knell of paleo. It's telling us that a junk food meal that is high in fat, including unhealthy n-6 fats, and also high in carbs and pro-inflammatory AGEs, is bad for fat people and people with high fasting triglycerides. Who fits that description? People who eat crappy carb-loaded diets. It's actually telling us that a paleo diet protects you against the occasional junk food meal, and it explains why the high post prandial trigs that a paleo dieter might experience are not harmful.

[TheFountain]

niner, why must you partake of indiscriminate carb bashing with comments like ' People who eat crappy carb-loaded diets'?

Any number of epidemiology samples tells us that there are plenty of cultures that live 'heart healthy' life styles on very high carb diets.

Sure, avoid bleached carbs. But blanketing statements with carb bashing sentiments that have no bearing on the total picture really harms the knowledge base of the community with fuzzy logic.

As I said, I personally gain weight on high fat, low carb diets. Call me a freak with a weird polymorphism, but I know several people like this. And it's not about inflammatory fats vs non-inflammatory fats, because I tried for 6 months straight to consume a diet of MUFA, SFA with very low carb intake (sub 50 grams) and very minimal omega fats (5 grams a dat tops) and still gained belly and hip fat.

At the least this proves that people should be treated as genetically dissimilar specimens, till a better answer can be layed out and explained.

[niner]

niner, why must you partake of indiscriminate carb bashing with comments like ' People who eat crappy carb-loaded diets'?

I'm not bashing all carbs. I'm bashing crappy junk food diets, which are carb loaded. I'm bashing high GI carbs. And I'm responding to your paleo bashing...

[TheFountain]

I think I am trying to spread some perspective about the 'carbs vs fat' debacle that pervades this forum. Because for some people I think macronutrient rationing is useless. Call it a polymorphism of some strange genetic phenotype or what have you, but from the macroscopic evidence, it seems to me a real phenomenon. I know a lot of people who gain weight easily on high fat, low carb diets, and lose it on the reverse. Just as I am sure you know people who are wheat/gluten sensitive and do poorly on other diets.

[TheFountain]

Oh and people do like to bash the carb portion of junk foods, but they seem to be forgetting that a lot of these junk foods are equally high in fat.

[The Immortalist]

niner, why must you partake of indiscriminate carb bashing with comments like ' People who eat crappy carb-loaded diets'?

Any number of epidemiology samples tells us that there are plenty of cultures that live 'heart healthy' life styles on very high carb diets.

He said "Crappy carb-loaded diets" not "healthy carb-loaded diets". The people who are heart healthy on high carb diets don't eat the shit that western cultures do.

As I said, I personally gain weight on high fat, low carb diets.

You were obviously not counting your calories meticulously enough. I went on a diet that was only 20g of carbs a day with a moderate amount of protein and the rest mostly sat fat and Monounsaturated fat for an entire month and I did not gain a single pound nor gain any extra fat around my waist. I was also eating the same amount of calories I usually do.

Edited by The Immortalist, 13 December 2011 - 08:55 PM.

[Mind]

Everyone has a diet that works well for them. Fountain, you eat more (healthy) carbs than most around here and you are healthy. That's great. Some people have good success with a higher (healthy) lipid diet. That is fine as well.

I am glad you post studies to help everyone evaluate their diet. As Niner points out, this study is unfortunately seriously deficient in an attempt to tease out affects of fat in diets.

[TheFountain]

You were obviously not counting your calories meticulously enough. I went on a diet that was only 20g of carbs a day with a moderate amount of protein and the rest mostly sat fat and Monounsaturated fat for an entire month and I did not gain a single pound nor gain any extra fat around my waist. I was also eating the same amount of calories I usually do.

Oh, I didn't count calories? I'll have you know that I was consuming the same amount of calories in fat that I now consume in carbs.

And besides, according to Duke, calories don't matter.

http://www.longecity...674#entry370674

[The Immortalist]

You were obviously not counting your calories meticulously enough. I went on a diet that was only 20g of carbs a day with a moderate amount of protein and the rest mostly sat fat and Monounsaturated fat for an entire month and I did not gain a single pound nor gain any extra fat around my waist. I was also eating the same amount of calories I usually do.

Oh, I didn't count calories? I'll have you know that I was consuming the same amount of calories in fat that I now consume in carbs.

And besides, according to Duke, calories don't matter.

http://www.longecity...674#entry370674

No, you are not gaining weight eating the same amount of calories because if you were you would be a human fusion reactor. You should go to NASA and be studied if this is truly the case. It’s not.

All jokes aside I would really like to believe you the fountain.
Have you considered increased water retention as the culprit of you gaining weight while on a high fat diet?

[TheFountain]

You were obviously not counting your calories meticulously enough. I went on a diet that was only 20g of carbs a day with a moderate amount of protein and the rest mostly sat fat and Monounsaturated fat for an entire month and I did not gain a single pound nor gain any extra fat around my waist. I was also eating the same amount of calories I usually do.

Oh, I didn't count calories? I'll have you know that I was consuming the same amount of calories in fat that I now consume in carbs.

And besides, according to Duke, calories don't matter.

http://www.longecity...674#entry370674

No, you are not gaining weight eating the same amount of calories because if you were you would be a human fusion reactor. You should go to NASA and be studied if this is truly the case. It’s not.

All jokes aside I would really like to believe you the fountain.
Have you considered increased water retention as the culprit of you gaining weight while on a high fat diet?

No, my body just does not react well to a lot of fat! Why is that so difficult to believe? There is no evidence that insulin in healthy individuals is the driver of weight gain.

[Esoparagon]

But was it high carb and high fat or just high fat meals with low carbs? It's really not significant. See. This is what Taubes is talking about when he talks about how it's hard to good meaningful science.

This was a study on eating fast food junk food. It's not a study on the effects of eating high fat low carb.

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.

.

This says nothing about a high fat low carb diet. Those foods are all high carb too. The sandwich has lots of glucose in the bread. Orange juice is like an infusion of glucose to the blood stream. Hash browns are crumbed potatoes.

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

This is an example of the establishment trying to find evidence for their pre-conceived conclusions. They label the food choices high fat when they are actually high fat and high carbohydrate foods. There's a big difference. In addition how do they know that the effect on the triglycerides was related to the fat in the meal and not in fact the glucose? Or some other factor?

It also doesn't say anything about the effects of fat in the absence of carbs. It also doesn't show the effects on high fat low carb meals on people who have been eatnig that way for a substantial amount of time. This study really shows a link - a correlation - between fast food junk food, obesity and heart disease in the general public with either normal or high fasting triglyceride levels.

The difficulty with health research is that there are a lot of variables so it's hard to do good science. The second problem is that it corrupt to the brim with government money and political agendas.

Edited by Esoparagon, 09 January 2012 - 02:31 AM.