Tag Archives: saturated fat

An Egg a day keeps the doctor away

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When I recommend to my patients that they should eat eggs and vegetables for breakfast rather than breakfast cereals (which have high sugar content and nasty gut inflaming gluten proteins) they often ask “well what about my cholesterol ?”. I tell them that eggs are a health food and that they do not need to worry about their cholesterol.

I first read about the man who ate 25 eggs per day for 15 years here.

Health Correlator: The man who ate 25 eggs per day: What does this case really tell us?

He was 88 years old when some cholesterol fearing physicians studied his plasma lipids (HDL, LDL, triglycerides etc.) and other aspects of his health (blood pressure, weight, etc.) and discovered that he was very healthy at the ripe age of 88.

Normal Plasma Cholesterol in an 88-Year-Old Man Who Eats 25 Eggs a Day — NEJM

This article was published in 1991 and the authors concluded that this man was exceptional in lacking adverse health consequences from eating 25 fat and cholesterol laden eggs every day for 15 years. Since that time, many studies on the health effects of eggs have demonstrated that they are in fact a health food and do not increase cardiovascular risk. In fact they provide a nutrient dense assortment of important vitamins, minerals, fat, and protein. Perhaps most importantly they are very high in choline, an important nutrient which is not hard to come by. Eggs and liver provide an abundance of choline.

Choline is widely used in the human body for many important functions. These include:

  • building block for an important neuro-transmitter called acetyl-choline (you cannot live without it)
  • essential component of the phospholipids that form the outer membrane of all living cells
  • chemical precursor to betaine which is essential to health, particularly for eyesight
  • methyl metabolism (methylation is an essential physiologic chemical process in our body)
  • protects against fatty liver disease

You can read more about the importance of choline here:

Choline – Wikipedia, the free encyclopedia

Regular egg consumption has been demonstrated to improve insulin sensitivity and cardiovascular risk profiles in healthy individuals and in individuals with metabolic syndrome as demonstrated here:

Whole egg consumption improves lipoprotein profil… [Metabolism. 2013] – PubMed – NCBI

Daily egg consumption with modest carbohydrate restriction in that study resulted in:

  • improved insulin sensitivity (good)
  • reduction in oxidized LDL (very good, oxidized LDL is the major instigator for atherosclerosis)
  • reduced triglycerides (high triglycerides are a marker for metabolic syndrome, precursor to diabetes, heart attack and stroke)
  • reduction in other blood lipid markers for cardiovascular risk (apoE, apoC-III, large VLDL, total IDL, small LDL and medium LDL)
  • increase in the size of HDL and LDL particles (reduction in cardiovascular risk)

They concluded that:

“Atherogenic dyslipidemia improved for all individuals”

In adults with metabolic syndrome (hypertension, insulin resistance, obesity, high triglycerides) three whole eggs per day with moderate carbohydrate restriction resulted in:

  • reduced waist size
  • reduced % body fat
  • reduction in inflammation as measured by plasma tumor necrosis factor alpha and serum amyloid

The authors concluded that:

“on a moderate carbohydrate background diet, accompanied by weight loss, the inclusion of whole eggs improves inflammation to a greater extent than yolk-free egg substitute in those with MetS.”

Effects of carbohydrate restriction a… [J Clin Lipidol. 2013 Sep-Oct] – PubMed – NCBI

In yet another study:

Daily intake of 3 whole eggs, as part of a CRD, increased both plasma and lipoprotein lutein and zeaxanthin. Egg yolk may represent an important food source to improve plasma carotenoid status in a population at high risk for cardiovascular disease and type 2 diabetes.

See for yourself:

Egg intake improves carotenoid status by increasi… [Food Funct. 2013] – PubMed – NCBI

In another study:

Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations (lutein and zeazanthin) in older adults with low macular pigment taking cholesterol-lowering statins.

“Lutein and zeaxanthin may reduce the risk of dry, age-related macular degeneration because of their photo-oxidative role as macular pigment.”

Consumption of 2 and 4 egg yolks/d for 5 wk i… [Am J Clin Nutr. 2009] – PubMed – NCBI

Studies of the benefits of high-cholesterol egg consumption have  been so convincing that even the American Heart Association has removed advice to avoid eggs.

“…there have been a number of epidemiological studies that did not support a relationship between cholesterol intake and cardiovascular disease. Further, a number of recent clinical trials that looked at the effects of long-term egg consumption (as a vehicle for dietary cholesterol) reported no negative impact on various indices of cardiovascular health and disease”

Exploring the factors that affect blood cholesterol… [Adv Nutr. 2012] – PubMed – NCBI

From an evolutionary medicine point of view, eggs and ample dietary cholesterol have been around a long time in the human diet.

“Paleoanthropologists suggest that dietary cholesterol has been in the human diet for millions of years (7–10). Sources included eggs, bone marrow, and organ meats. Stone Age intake of cholesterol is uncertain, but it may well have exceeded current dietary recommendations.

 There are many important biological roles for cholesterol that span the spectrum from cell membrane structure to steroid hormone synthesis, bile acid synthesis, and others. The vital role of cholesterol in human metabolism and the well-established place of dietary cholesterol in the native human diet provide a robust theoretical challenge to the view that dietary cholesterol poses a threat to human health.

 More important still are prospective, population-based studies that, when similarly scrupulous about variation in other dietary components, find no association between cholesterol intake in general, or egg intake in particular, and the risk of CVD (13).”

Exploring the factors that affect blood cholesterol… [Adv Nutr. 2012] – PubMed – NCBI

Here are more links to discover that eggs are a health food.

Egg consumption and endothelial function: a randomized controlled crossover trial.

Endothelial function testing as a biomarker of vascular disease.

Daily egg consumption in hyperlipidemic adults–effects on endothelial function and cardiovascular risk.

Endothelial function testing as a biomarker of vascular disease.

Daily egg consumption in hyperlipidemic adults–effects on endothelial function and cardiovascular risk.

High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification.

Plasma LDL and HDL characteristics and carotenoid content are positively influenced by egg consumption in an elderly population.

Eggs distinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet.

Significance of small dense low-density lipoprotein-cholesterol concentrations in relation to the severity of coronary heart diseases.

Rethinking dietary cholesterol. [Curr Opin Clin Nutr Metab Care. 2012] – PubMed – NCBI

Endothelial function is the term used to describe how well the arteries can expand and contract to meet the needs of blood flow. It is considered an important tool for assessing cardiovascular risk and it is impaired in metabolic syndrome, diabetes and in patients with coronary artery disease. Compromise of endothelial function is part of the process of atherosclerosis and heart attacks.

“There is thus a case to be made that endothelial function is potentially a summative measure of overall cardiac risk status and at least a valuable addition to standard risk measures (45). The ever-expanding footprint of research in this area in the cardiology literature attests to its importance.”

Despite (or because of) their high fat and cholesterol content, eggs have not been found to have any negative effects on endothelial function.

Rethinking dietary cholesterol. [Curr Opin Clin Nutr Metab Care. 2012] – PubMed – NCBI

So far since launching this blog a few weeks ago we have discovered that saturated fat and cholesterol containing foods are not the villains portrayed by the media, doctors and professional organizations that give us nutritional advice.

We have reviewed evidence that added sugar, sweetened beverages, refined carbohydrates (especially flour foods), trans-fats, and excessive polyunsaturated omega six fats from processed “vegetable oil” are the culprits with regards to obesity, diabetes, heart attack and stroke. These culprit components of the modern Western diet were definitely absent from the diets of our paleolithic ancestors. We have not evolved to tolerate them. These modern manufactured and processed “foods” represent an unhealthy deviation from our evolutionary past.

There is so much more to discuss. In the spirit of more work ahead during this 50th anniversary week of John F Kennedy’s assassination. I will close with a quote from JFK’s favorite poet and friend, Robert Frost.

“I have promises to keep, / And miles to go before I sleep, / And miles to go before I sleep.”

Peace,

Bob Hansen MD

Saturated Fat vs. Sugar

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Within one week of my post on saturated fat two discussions supporting my position have appeared in peer-reviewed journals. The first discussion can be found here.

Observations: Saturated fat is not the major issue | BMJ

The second can be found here.

Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence

The first article was written by a cardiologist who teaches and practices at Croydon University Hospital in London. He states that advice to reduce saturated fat intake

“has led to the over-medication of millions of people with statins and has diverted our attention from the more egregious risk factor of atherogenic dyslipidaemia”

He states that recent studies “have not supported any significant association between saturated fat intake and risk of CVD”. He discusses sugar and highly refined carbohydrates as the culprit in causing atherogenic (artery plaque forming) dyslipidaemia (abnormal blood lipid profiles).

Here are comments by three Professors about Dr. Malhotra’s article:

David Haslam, Chair of Britain’s National Obesity Forum states the following.

“It’s extremely naive of the public and the medical profession to imagine that a calorie of bread, a calorie of meat and a calorie of alcohol are all dealt in the same way by the amazingly complex systems of the body. The assumption has been made that increased fat in the bloodstream is caused by increased saturated fat in the diet, whereas modern scientific evidence is proving that refined carbohydrates and sugar in particular are actually the culprits.”

Professor Robert Lustig (Pediatric Endocrinologist, UCSF) stated

“Food should confer wellness, not illness. And real food does just that, including saturated fat. But when saturated fat got mixed up with the high sugar added to processed food in the second half of the 20th century, it got a bad name. Which is worse, the saturated fat or the added sugar? The American Heart Association has weighed in – the sugar many times over. Plus added sugar causes all of the diseases associated with metabolic syndrome. Instead of lowering serum cholesterol with statins, which is dubious at best, how about serving up some real food?”

Timothy Noakes (Professor of Exercise and Sports Science, University of Cape Town) states

“Focusing on an elevated blood cholesterol concentration as the exclusive cause of coronary heart disease is unquestionably the worst medical error of our time. After reviewing all the scientific evidence I draw just one conclusion – Never prescribe a statin drug for a loved one.”

Here is the abstract summary of the second article cited above.

“Although early studies showed that saturated fat diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease (CAD), the evidence of dietary saturated fats increasing CAD or causing premature death was weak. Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD and other adverse health effects or at worst are weakly associated in some analyses when other contributing factors may be overlooked. Several recent analyses indicate that SFAs, particularly in dairy products and coconut oil, can improve health. The evidence of ω6 polyunsaturated fatty acids (PUFAs) promoting inflammation and augmenting many diseases continues to grow, whereas ω3 PUFAs seem to counter these adverse effects. The replacement of saturated fats in the diet with carbohydrates, especially sugars, has resulted in increased obesity and its associated health complications. Well-established mechanisms have been proposed for the adverse health effects of some alternative or replacement nutrients, such as simple carbohydrates and PUFAs. The focus on dietary manipulation of serum cholesterol may be moot in view of numerous other factors that increase the risk of heart disease. The adverse health effects that have been associated with saturated fats in the past are most likely due to factors other than SFAs, which are discussed here. This review calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs, for which mechanisms for adverse health effects are lacking.”

Of course both articles produced a stormy debate with letters to the editor from supporters and detractors, but thank God this debate has finally entered mainstream academic discussion.

These two authors have coincidentally introduced the topics of my next two blogs so please stay tuned for discussions of sugar/refined carbohydrates and coconut oil (filled with health promoting and infection fighting medium chain triglycerides)

Go in peace

Bob Hansen MD

Saturated fat, does it matter?

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Recommendations to reduce saturated fat consumption have pervaded our media since the AHA published its first dietary guidelines for the American public in 1961. The AMA at first opposed the recommendations but the AHA pushed on. The guidelines encouraged substitution of polyunsaturates for saturated fat. The guidelines were presented in a two page report with 1/2 page of references. A subsequent independent review of those references revealed that 1/2 of them did not support the recommendations, details, details.

My last blog looked at a meta-analysis of the major studies subsequently published on this topic and found that implementation of that recommendation does not reduce heart attacks or cardiac deaths and in fact there was a trend (not statistically significant) for worse outcomes associated with substituting PUFA (polyunsaturated fatty acids, primarily linoleic acid) for SFA (saturated fatty acids).

Please note that we are talking hard endpoints here, death and heart attack. So much of the literature that consumes this issue only looks at the effect on so called risk factors. When you actually look at the clinical outcomes (death, heart attack, stroke)  there is no benefit demonstrated when saturated fats are reduced.

In 1966 the makers of Mazola Corn Oil and Mazola Margarine sponsored publication of Your Heart Has Nine Lives, a book advocating the substitution of vegetable oils for butter and other “artery clogging” saturated fats.

The history of this campaign to demonize SFA and glorify PUFA is well described in Gary Taubes Good Calories, Bad Calories, as well as in Mary Enig’s essay The Oiling of America. I would encourage you to read both.  The latter is available on line as is Gary Taubes’ famous essay What if its all a big fat lie?

http://www.westonaprice.org/know-your-fats/the-oiling-of-america

In 2010 a highly respected lipid research group published what should have been a wake-up call study for the medical profession.

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

The data included 5 to 23 years follow up on 347,747 subjects. 11,006 developed coronary heart disease or stroke. Intake of saturated fat was not associated with an increased risk of coronary heart disease (CHD), stroke, or  cardiovascular disease (CVD =CHD plus stroke).

“there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

To be clear, association (statistical correlation) does not prove or disprove causation, but if such a large amount of data from prospective studies shows no statistically significant correlation, than a causative theory should be rejected until and unless randomized controlled clinical trials suggest otherwise.

This study should have created a tsunami in the media and in the medical community but it hardly caused a ripple in the pond. Michael Eades explains why in an excellent post here.

http://www.proteinpower.com/drmike/lipid-hypothesis/eat-less-move-die-anyway/

The editors of the journal published a scathing rebuke of the authors but could not find anything wrong with the data and conclusions except that the data refuted their belief system. Busy physicians tend to read the editorials and place more credence in an editorial than in a study that questions or refutes a major thesis.

Lets look at some other studies that considered hard clinical endpoints.

Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial.

The objective of this study was:

“To test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk.”

This study was a randomized controlled trial of 48,835 postmenopausal women aged 50-79 years of diverse backgrounds and ethnicity.

“RESULTS: By year 6, mean fat intake decreased by 8.2% of energy intake in the intervention vs the comparison group, with small decreases in saturated (2.9%), monounsaturated (3.3%), and polyunsaturated (1.5%) fat; increases occurred in intakes of vegetables/fruits (1.1 servings/d) and grains (0.5 serving/d).”

Did this decrease heart attacks or strokes? NO

“The diet had no significant effects on incidence of CHD (hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.90-1.06), stroke (HR, 1.02; 95% CI, 0.90-1.15), or CVD (HR, 0.98; 95% CI, 0.92-1.05).”

Now lets look at a study where women were followed after a heart attack to see if reducing saturated fat helped.

Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr. 2004 Nov;80(5):1175-84.

In this study quantitative coronary angiography was performed at baseline and after mean follow up of 3.1 years. 2243 coronary artery segments in 235 women were studied.

Here is what they found.

  • 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
  • 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 (of coronary atherosclerosis) when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein
  • Monounsaturated and total fat intakes were not associated with progression. (extra virgin olive oil and macadamia nuts are rich in monounsaturated fat)

The P values cited demonstrate unequivocal statistical significance for all of these associations.

So intake of carbohydrate and polyunsaturated fat was positively associated with progression of coronary atherosclerosis. Conversely, saturated fat intake was associated with less progression of coronary stenosis.  Again, I must point out that association does not prove or disprove causation. Nevertheless, there have been no prospective studies that demonstrate an association between saturated fat consumption and cardiovascular events (real clinical endpoints). Here we have data that show a negative association with saturated fat but positive association with carbohydrate and polyunsaturated fat consumption.

The logic has always been that substituting PUFA for SFA reduces cholesterol levels (short term studies) and therefore it should reduce heart attacks and strokes. But if you search the medical literature you find that the overwhelming body of data shows no reduction in hard clinical outcomes by reducing saturated fat, in fact just the opposite is true as in the two Ramsden studies cited in my previous post.

Uffe Ravnskov has pointed out that the proponents of the dietary  saturated fat-cholesterol theory often times misrepresent the data from published studies and cite those studies in support of the theory when in fact the data actually refute the theory. (as was the case for the AHA’s first dietary recommendations demonizing saturated fat in 1961) Uffe’s letters to the editor have been a nuisance to the proponents of that theory for decades.

An exhaustive review of the literature by Ravnskov was published in 1996. The summary deserves a complete quotation here.

J Clin Epidemiol. 1998 Jun;51(6):443-60.

The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.

Source

uffe.ravnskov@swipnet.se

Abstract

A fat diet, rich in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA), is said to be an important cause of atherosclerosis and cardiovascular diseases (CVD). The evidence for this hypothesis was sought by reviewing studies of the direct link between dietary fats and atherosclerotic vascular disease in human beings. The review included ecological, dynamic population, cross-sectional, cohort, and case-control studies, as well as controlled, randomized trials of the effect of fat reduction alone. The positive ecological correlations between national intakes of total fat (TF) and SFA and cardiovascular mortality found in earlier studies were absent or negative in the larger, more recent studies. Secular trends of national fat consumption and mortality from coronary heart disease (CHD) in 18-35 countries (four studies) during different time periods diverged from each other as often as they coincided. In cross-sectional studies of CHD and atherosclerosis, one group of studies (Bantu people vs. Caucasians) were supportive; six groups of studies (West Indians vs. Americans, Japanese, and Japanese migrants vs. Americans, Yemenite Jews vs. Yemenite migrants; Seminole and Pima Indians vs. Americans, Seven Countries) gave partly supportive, partly contradictive results; in seven groups of studies (Navajo Indians vs. Americans; pure vegetarians vs. lacto-ovo-vegetarians and non-vegetarians, Masai people vs. Americans, Asiatic Indians vs. non-Indians, north vs. south Indians, Indian migrants vs. British residents, Geographic Study of Atherosclerosis) the findings were contradictory. Among 21 cohort studies of CHD including 28 cohorts, CHD patients had eaten significantly more SFA in three cohorts and significantly less in one cohort than had CHD-free individuals; in 22 cohorts no significant difference was noted. In three cohorts, CHD patients had eaten significantly more PUFA, in 24 cohorts no significant difference was noted. In three of four cohort studies of atherosclerosis, the vascular changes were unassociated with SFA or PUFA; in one study they were inversely related to TF. No significant differences in fat intake were noted in six case-control studies of CVD patients and CVD-free controls; and neither total or CHD mortality were lowered in a meta-analysis of nine controlled, randomized dietary trials with substantial reductions of dietary fats, in six trials combined with addition of PUFA. The harmful effect of dietary SFA and the protective effect of dietary PUFA on atherosclerosis and CVD are questioned.

That was published in 1998, since then the evidence remains as Uffe described it 15 years ago. More studies show no relationship between saturated fat consumption and cardiovascular death, heart attack, or stroke.

Finally, multiple autopsy studies around the world have been conducted to investigate an association between diet and atherosclerosis. None of these studies have demonstrated a positive association between degree of atherosclerosis and saturated fat intake.

Yet the AHA continues to recommend lower levels of saturated fat consumption while showing little concern for the problem of sugar and refined carbohydrates.

In my next post I will discuss why sugar and refined carbohydrates are major players in the physiology of atherosclerosis. Future posts will address the China Study, Forks Over Knives, the Ornish Diet and related topics. Additionally I will discuss why an egg a day keeps the doctor away.

Go in peace.

Bob Hansen MD.

Polyunsaturated fat, Saturated fat and the AHA

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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.

http://www.ncbi.nlm.nih.gov/pubmed/21118617

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”.

http://www.ncbi.nlm.nih.gov/pubmed/23386268

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