1. Dietary fat may contribute to insulin resistance. From one review:
"Overall, most animal and cell studies seem to indicate that saturated and trans-unsaturated fatty acids significantly increase insulin resistance."2. Dietary fat contains some of the highest levels of Persistant Organic Pollutants of the foods we eat.
- Skeletal Muscle Lipid Deposition And Insulin Resistance: Effect Of Dietary Fatty Acids And Exercise, American Journal of Clinical Nutrition, 2007
This study found that people with high levels of POPs were 38 times! more likely to have diabetes than those with low levels:3. Dietary fat contributes to inflammation. One way it does so is by increasing absorption of endotoxins, to which we launch an inflammatory response. Chronic inflammation is linked to insulin resistance, diabetes, and other elements of the Metabolic Syndrome. Also, endotoxins by themselves (independent of inflammatory markers) have been linked to diabetes. (Endotoxins are bits of bacterial membrane that are absorbed along with the fat we eat. They're thought to derive, in part, from bacteria that live in the intestines.)
A Strong Dose-Response Relation Between Serum Concentrations Of Persistent Organic Pollutants [POPs] And Diabetes: Results From The National Health And Examination Survey 1999–2002, Diabetes Care, 2006
Here's just one recent study on the topic of endotoxins. This is a hot area right now:
High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects, Diabetes Care, Online December 2011
"Ingestion of a high-fat meal led to a significant rise in endotoxin levels in type 2 diabetic, IGT [impaired glucose tolerance], and obese subjects over the 4-h time period (P < 0.05). These findings also showed that, at 4 h after a meal, type 2 diabetic subjects had higher circulating endotoxin levels (125.4%↑) than NOC [nonobese control] subjects (P < 0.05).And a study that links dietary fat, specifically saturated fat, to inflammation:
These studies have highlighted that exposure to a high-fat meal elevates circulating endotoxin irrespective of metabolic state, as early as 1 h after a meal. However, this increase is substantial in IGT and type 2 diabetic subjects, suggesting that metabolic endotoxinemia is exacerbated after high-fat intake."
Acute And Chronic Saturated Fatty Acid Treatment As A Key Instigator Of The TLR-mediated Inflammatory Response In Human Adipose Tissue, Journal of Nutritional Biochemistry, January 2012
"[Our] data highlights the potential risk of a continued high fat diet on inducing an inflammatory response, as it appears to be more pronounced than the glucose induced response. This would also appear to align with clinical studies that suggest hyperlipidaemia may impact more significantly over time than hyperglycaemia in the pathogenesis of metabolic disease.
This study implicates elevated SFAs [saturated fatty acids] as a key instigator of the inflammatory response."
Saturated fat seems to be the riskiest type.
A low-fat dietary pattern did NOT reduce the risk of diabetes in postmenopausal women.
Avoidance of fat weight gain is probably more important than macronutrient composition in prevention of diabetes. Exercise helps too.
I remember those studies based on the Women's Health Initiative. This one and the cardiovascular disease (CVD) one (http://jama.ama-assn.org/content/295/6/655.long).
The two groups were not that far apart in their eating styles. If you could say that the "low-fat" group received no benefit vis-a-vis diabetes, you could as well say that the "low-carb" group received no benefit. Indeed, some have argued, the low-fat group was not low-fat enough, and the low-carb group was not low-carb enough.
There was a trend toward lower diabetes' risk with the low-fat group. The low-fat group also lost a little more weight than the low-carb group.
(Likewise, there was a trend for lower CVD in the low-fat group, "Trends toward greater reductions in CVD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.")
All of those observations were not as strong as they might have been had the groups been further apart in their eating styles.
I forgot to say, women in these studies eating "low-fat" were eating about 30% of their calories from fat. I think that's a lot of fat.
30%! What kind of a low-fat diet is that? Nutrisystem uses 20%. Ornish says like 10%. No wonder they got diabetes.
@Anon, I've heard it said.
Once again, higher fat intake increases resistance to insulin... drum roll please... BECAUSE THE BODY DOESN'T NEED INSULIN when digesting fat. It's the body's natural response to increased fat intake. Also, saturated fat does NOT increase inflammation (unless that "saturated" fat is lard, which can increase inflammation in mice due to its HIGH OMEGA 6 content).
Bix, check out the Okinawans. They ate MORE fat and animal protein than the traditional Japanese... and lived longer. I understand how incredibly complex nutrition is with all of the conflicting studies, but I think you're set off on the wrong path going low-fat.
Wow.. that saturated fat study was done... IN VITRO! It's worthless! How many paleo people do you know with lots of inflammation? (I sure don't know any. Most have CRP's of .5 or less on SUPER-HIGH saturated fat diets).
In fact, I do find nutrition science complex. I try to stay open to new thinking.
The Okinawans ate more fat and protein than traditional Japanese? That's weird, this study, an extensive investigation of six decades of archived population data, found they ate only about 6% of their diet as fat, only 9% as protein. I'm not saying you're wrong, I'm just trying to understand.
Traditional Okinawan Diet: Sweet Potatoes
I have read that a high-fat meal increases inflammation in numerous studies - animal, human, and test tube.
Here's one in humans:
A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation
Thus, the present model predicts that, in the postprandial phase, increases in endotoxin released from the gut may contribute to increased leukocyte activation, to the release of cytokines such as TNF-α, and, indirectly, to endothelial cell activation. Accordingly, much evidence from other recent studies suggests that inflammatory indicators are indeed increased after a high-fat meal.
Low-grade endotoxemia may contribute to the postprandial inflammatory state and could represent a novel potential contributor to endothelial activation and the development of atherosclerosis.
"What is clear from the research thus far is that dietary fat intake does influence insulin action."
Does dietary fat influence insulin action?
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