Tag Archives: polyunsaturated fat

Obesity Epidemic Requires a Paradigm Shift

The obesity epidemic requires a paradigm shift. Several medical myths stand in the way of taking the most effective steps to safely help patients lose weight. The most important myth relates to saturated fat. Saturated fat consumption does not contribute to cardiovascular disease. This must be understood and accepted by the medical community so that sound advice can be given.

A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.( Am J Clin Nutr. 2010 Mar;91(3):497-9. )

In fact, as early as 2004, Mozaffarian et. al. investigated the influence of diet on atherosclerotic progression in postmenopausal women with quantitative angiography and found that:

In multivariate analyses, a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter (P = 0.001) and less progression of coronary stenosis (P = 0.002) during follow-up. (Am J Clin Nutr. 2004 Nov;80(5):1175-84)

In addition, they further found that:

Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high.

            Polyunsaturated fat intake was positively associated with progression when replacing other fats (P = 0.04)

These findings should come as no surprise given the basic science of atherosclerosis. Oxidized and glycated LDL stimulate macrophages to become foam cells initiating the creation of plaque. Cellular receptors that allow macrophages to ingest oxidized LDL are specific for oxidized LDL. These receptors do not recognize normal LDL to a significant degree.

Holovet et. al. studied the ability of oxidized LDL versus the Global Risk Factor Assessment Score (GRAS) to detect coronary artery disease. GRAS identified coronary artery disease 49% of the time, while oxidized LDL was correct 82% of the time.

In a large prospective study, Meisinger et al found that plasma oxidized LDL was the strongest predictor of CHD events when compared to conventional lipoprotein risk assessment and other risk factors for CHD.

Polyunsaturated fats are easily oxidized, saturated fats are not. It is the polyunsaturated fatty acids (PUFA) in the membrane of LDL particles that become oxidized and then initiate the cascade of inflammatory events leading to atherosclerosis. The major source of these PUFA in the American diet are “vegetable oils” (corn oil, soy oil etc.)  rich in the omega-6 PUFA, linoleic acid.

So why is this important to understand relative to the obesity epidemic? Because the most effective weight loss “diet” is arguably a low carbohydrate/high fat (LCHF) diet. This approach does not require calorie counting. This approach has been demonstrated to spontaneously reduce caloric intake whereas low fat diets require calorie counting and result in persistent hunger.

When compared to low fat calorie restricted diets  the LCHF approach has been equal or superior with respect to weight loss, insulin sensitivity, blood pressure reduction, and lipid profiles whenever these parameters have been measured.

But LCHF has not been embraced by the medical community due to the perceived dangers of saturated fat consumption and a low-fat ideology that lacks legitimate scientific evidence.

Once we dispel the mythology of saturated fat, the safety and efficacy of LCHF will be more readily accepted by physicians, the media and the lay public.

The nutritional villains in our society are highly refined and easily oxidized “vegetable oils” filled with pro-inflammatory omega-6 PUFA (linoleic acid), added sugar (especially HFCS) so prevalent in most processed foods and soft drinks, and the nutrient poor wasted calories of processed flour foods. These three culprits are responsible for our epidemics of obesity, insulin resistance and metabolic syndrome. These three conspire together to generate fatty liver disease, atherosclerotic plaque, and chronic inflammation.

When a LCHF approach is combined with  eating only fresh whole foods and avoiding added sugar, refined flour, and unhealthy  “vegetable oils”, we have the perfect recipe for our obesity epidemic.

The following references provide examples of studies that have demonstrated the efficacy, safety and  usual superiority of the LCHF  approach to weight loss.

Dig Dis Sci. 2007 Feb;52(2):589-93. Epub 2007 Jan 12. The effect of a low-carbohydrate, ketogenic diet on nonalcoholic fatty liver disease: a pilot study. Tendler D, Lin S, Yancy WS Jr, Mavropoulos J, Sylvestre P, Rockey DC Westman EC.

Polyunsaturated fat, Saturated fat and the AHA

The present paradigm among physicians and cardiologists presents saturated fat as a disease producing component of animal foods. Dietary recommendations include the reduction of saturated fat and replacement with carbohydrates and/or monounsaturated and polyunsaturated fats. In fact, the American Heart Association (AHA) updated its recommendations to increase the consumption of polyunsaturated fats as a percentage of total caloric intake in January 2009.

This was met by protests from three NIH scientists who had done extensive research in the area of fat consumption and health. Those scientists wrote letters to the editor of Circulation, the scientific journal of the AHA. Those protest letters were not published in print but were published on-line (where only geeks like me would find them,  the vast majority of physicians would never lay eyes on them)

The authors of those letters subsequently produced a brilliant study that involved forensic research. They conducted interviews with principal investigators who directed the studies upon which the AHA had based it’s recommendations. They discovered important data that had been collected but not mentioned in those study publications by painstakingly sleuthing multiple sources. They then produced a meta-analysis of the data from the studies. Their meta-analysis was published in the British Journal of Nutrition Dec 2010.


What they found was astonishing. The AHA had based it’s recommendations on faulty data. A major point of refutation involved  omega 3 fatty acids (fish oil which is arguably cardio- protective) vs omega 6 fatty acids. Both are poly-unsaturated fatty acids (PUFA). The AHA paradigm has been that replacing saturated fat with omega 6 PUFA results in reduction of cholesterol (short term studies) and therefore should reduce heart attacks and stroke. But the studies they used to support their recommendations were not “clean”.

Only three of the nine studies were “pure” omega 6 interventions, which increased omega-6 FA without a concurrent rise in omega-3.

Four of the studies increased both omega 3 and omega 6 PUFA. In one of those four studies the patients were given the equivalent of 16 fish oil capsules per day.

The control diets had an estimated 3% manufactured trans fats in the diet. This unquestionably increases risk of heart attack and creates a confounding factor.

The Omega 6 diets increased the risk of heart disease and death compared to the mixed omega 3 and omega 6 studies. The risk of cardiac death was increased by 28% in the omega 6 diets compared to the mixed diets.

The mixed omega 6 omega 3 diets showed an 8% risk reduction of death from all causes and a 22% risk reduction from cardiac death.

So the AHA had made recommendations that could possibly be harmful and certainly not helpful. Despite this great piece of investigative science, the AHA did not change it’s recommendations.

Since that time Christopher Ramsden and colleagues have published a sequel “to evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death”.


In their summary they stated:

“substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. “

There you have it. The AHA has not withdrawn it’s dietary recommendations to increase n-6 fat despite the compelling evidence to the contrary. This is unfortunately a consistent pattern.

Why would an increase in omega 6 fats and a reduction in saturated fat increase cardiovascular events?

Here is one explanation which is supported by basic science. Omega 6 fats are PUFA (polyunsaturated). PUFA are easily oxidized but saturated fat is not. When PUFA sit in the membrane (outer wall) of LDL particles they become oxidized and the oxidized LDL particle stimulates macrophages (white blood cells) to become foam cells and create plaque in the walls of your arteries. Saturated fats are not easily oxidized. Saturated fats do not contribute to the formation of oxidized LDL.

The AHA encourages us to consume “vegetable oils” (oils made from corn, soy, cottonseed, safflower, etc) instead of saturated fat. The predominant fat in “vegetable oil” is linoleic acid, the major omega 6 fat in the American diet. Linoleic acid is not the hero in this story and saturated fat is not the villain that the AHA portrays it to be.

Having said that, one might ask the following. If PUFA are easily oxidized and omega 3 fats are are also PUFA, then how could omega 3 fats be “cardio-protective” while omega 6 fats are damaging?

Good question. That will be addressed in  future posts.

But before we get to that, there are other data on saturated fats that must be discussed in order to dispel the fear of saturated fat.  That data and discusion will come in the next post.

Go in peace, the post is ended.

Bob Hansen MD