Category Archives: Cholesterol

Time Magazine: “Eat Butter”

TimeMagEatButterThe cover of Time Magazine’s next issue is going to say “Eat Butter.” The associated cover story by Bryan Walsh is entitled “Ending The War On Fat.” I haven’t read the article, so I don’t know what he bases his claims on. But I have read thousands of studies in my lifetime, and “eat butter” is not my conclusion. My cover story would read “Don’t Eat Butter.”

Here’s the video that accompanied Time’s story. It’s emceed by Walsh. It’s going to tell you that everything you’ve been led to believe about fat is wrong.  It’s wrong.
http://c.brightcove.com/services/viewer/federated_f9?isVid=1&isUI=1

Dr. McDougall addressed Time’s upcoming story here. Marion Nestle addressed it here. (Nestle says saturated fat consumption is down, and so are deaths from heart disease.)

There is an abundance of research that implicates consumption of saturated fat in the development of heart disease. I am curious how Walsh will present this. McDougall says that one particular study, paid for by the National Dairy Council, is often cited to justify the “eat butter” proclamation:

Meta-Analysis Of Prospective Cohort Studies Evaluating The Association Of Saturated Fat With Cardiovascular Disease, American Journal of Clinical Nutrition, March 2010

However, that study was taken to task, not least of which by the renowned Dr. Stamler, in the very same issue where the study was published:

Diet-Heart: A Problematic Revisit, Jeremiah Stamler, American Journal of Clinical Nutrition, March 2010

Stamler infers that the authors’ intent was not to clarify the association between fat and heart disease, but to inject doubt.

“… the authors seem to be dissociating themselves from prevailing national and international dietary recommendations to the general population for primordial, primary, and secondary prevention of CHD/CVD and the established major metabolic risk factors. But they are not explicit. Is that their intent?

What are those prevailing recommendations?

“Specifically, do they disagree with the merits of heart-healthy fare on the basis of DASH-, OmniHeart-, Mediterranean-, East Asian–type eating patterns, which emphasize vegetables, fruit, whole grains, legumes/seeds/nuts, fat-free/low-fat dairy products, fish/shellfish, lean poultry, egg whites, seed oils in moderation, alcohol (if desired) in moderation, and portion size/calorie controlled and deemphasize red and processed meats, cheeses, ice cream, egg yolks, cookies/pastries/pies/cakes/other sweets/sweetened beverages, snacks, and salt/commercial foods with added salt. Estimated nutrient composition of this fare is as follows: total fat ≈20–25% of kcal, SFA 6–7%, MUFA 7–9%, PUFA 7–9%, cholesterol <100 mg/1000 kcal, total protein 18–25%, vegetable protein 9–12%, carbohydrate 55–60% (mostly complex), fiber 30–35 g/d, 50–65 mmol Na/d (2900–3770 mg NaCl/d), mineral/vitamin intake high (6). A vast array of concordant multidisciplinary research evidence is the sound foundation for these recommendations.”

Nothing has changed. Don’t eat butter.

Animal Fat Is A Natural Reservoir For Environmental Pollutants

BaconFat3With all the debate about weather fat in the diet is good or bad, one morsel getting lost in the discussion is that animal fat is a natural reservoir for environmental pollutants. Persistent Organic Pollutants (POPs) are largely hydrophobic, meaning they don’t dissolve well in water but they dissolve easily in fat. They also bioaccumulate, meaning they are found in higher, more concentrated amounts in animals higher in the food chain (such as tuna, salmon, fish-eating fowl, and farmed animals fed fish meal and other animal products), and, of course, ourselves:

“POPs are lipophilic chemicals that can pass through biological phospholipid membranes and bio-accumulate in fatty rich tissues of humans.”

Consumption of fat and cholesterol has been repeatedly linked to weight gain, arterial plaque buildup, blood glucose abnormalities, even cancer progression. Could it be the chemicals dissolved in that animal fat that are contributing to these ailments? Yes, says researcher Jerome Ruzzin from the University of Bergen in Norway:

Public Health Concern Behind The Exposure To Persistent Organic Pollutants And The Risk Of Metabolic Diseases, BMC Public Health, April 2012

There is now solid evidence demonstrating the contribution of POPs, at environmental levels, to metabolic disorders. Thus, human exposure to POPs might have, for decades, been sufficient and enough to participate to the epidemics of obesity and type 2 diabetes.”

“The general population is exposed to sufficient POPs, both in term of concentration and diversity, to induce metabolic disorders. This situation should attract the greatest attention from the public health and governmental authorities.”

No mincing of words there!

What are POPs?

“Persistent organic pollutants (POPs), including dioxins, furans, polychlorinated biphenyls (PCBs), and organochlorine pesticides, are chemicals mainly created by industrial activities, either intentionally or as by-products [13]. Because of their ability to resist environmental degradation, these substances are omnipresent in food products, and found all around the world, even in areas where they have never been used like Antarctica [14]. Thus, virtually all humans are daily exposed to POPs.”

What foods contain the most POPs?

“In the general population, exposure to POPs comes primarily from the consumption of animal fat like fatty fish, meat and milk products; the highest POP concentrations being commonly found in fatty fish [15–26].”

Some diseases linked to POPs (from a variety of studies: humans, animals, cell models):

Bio-accumulation of PCBs has been linked to non-alcoholic fatty liver disease (NAFLD) and elevated blood pressure.

Animals exposed to environmental levels of POP mixtures through the intake of non-decontaminated fish oil (obtained from farmed Atlantic salmon) exhibited insulin resistance, glucose intolerance, abdominal obesity and NAFLD [44]. In rats fed decontaminated crude salmon oil, which contained very low levels of POPs, these metabolic disturbances were almost absent.

The presence of POPs in farmed Atlantic salmon fillet was found to accelerate the development of visceral obesity and insulin resistance in mice.

Another important issue is the regulation of organochlorine pesticides, which are chemicals strongly linked to type 2 diabetes [29, 32, 33, 37, 44, 45] as well as breast and prostate cancer [94] and Parkinson disease [95]

It looks like we can’t get away from DDT, even though it was banned here in 1972:

“Not surprisingly, a recent US monitoring study revealed that DDT and its metabolites as well as endosulfan and aldrin, are still largely present in food, and daily consumed by humans.”

Children are at greater risk of exposure:

“Because of their high food intake per kilogram body weight required to maintain whole-body homeostasis and growth, children are likely to be at higher risk for environmental pollutant exposure. Not surprisingly, many scientific studies have highlighted that children are over-exposed to dioxins and dl-PCBs, and exceed the TDI of 2 pg/kg body weight.”

SalmonFillet3Finally, here’s a list of limits set by the European Union:

  • Ruminants: 4.5 pg/g fat
  • Poultry and farmed game: 4.0 pg/g fat
  • Pigs: 1.5 pg/g fat
  • Marine oils: 10 pg/g fat

You can see that the limit for marine oils is double that for fat from land animals. Why? They need to get together on this and create standards that apply across the board, and are based on public health, not commerce. Speaking of salmon, he says that “eating 1 g of fat from a fatty fish fillet could induce an exposure to 70 pg.”

What are Paleos eating? I mean, you can’t be Paleo and vegan at the same time. How do you avoid all these dissolved POPs?

Regulating vehicle emissions, pesticides, and industrial wastes is at odds with economic growth. Which is why I think pollution and its attendant chronic disease load is here to stay.

Eggs, Dietary Cholesterol, And Heart Disease

Dr. Greger is taking on eggs today (again):

So, do eggs and other sources of dietary cholesterol raise the risk for heart disease? Dr. Greger argues they do.

EggsScrambled2As I’ve come to understand, you have to look at the whole diet. For instance, for a given amount of saturated fat eaten, a given amount of dietary cholesterol (eggs) eaten at the same time will raise serum LDL cholesterol higher than if that dietary cholesterol was paired with a polyunsaturated fat, such as corn oil.1

Also, is any of that dietary cholesterol oxidized? Because if it is (and unless you eat it raw and very close in time to the demise of its source, some of it will be) it will contribute to the development of atherosclerosis and heart disease (and to the growth of cancer, as I just wrote). So says Fred Kummerow, a 98-year-old emeritus professor of comparative biosciences at the University of Illinois:

“Oxidized lipids contribute to heart disease both by increasing deposition of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a major contributor to heart attack and sudden death.”

And Professor Kummerow is of a mind that cholesterol is actually good for your heart! (Fortunately, our bodies manufacture all we need.)

Also, fruits and vegetables contain compounds that act as anti-oxidants, slowing further oxidation of consumed fats. You have to look at the whole diet.

You can’t judge well the effect of a single nutrient outside the context of the whole diet. It’s also risky to generalize the effects you may see of a nutrient in a small and perhaps homogeneous group. Nutrients, like dietary cholesterol, act differently in men vs. women, in old vs, young, in healthy vs. diseased (e.g. diabetes).

What is helpful, in my opinion, is to reflect upon the body of evidence. In this case, it looks like their exists a credible body of evidence to support limiting egg (and other dietary cholesterol) consumption.

1 Hypercholesterolemic Effect Of Dietary Cholesterol In Diets Enriched In Polyunsaturated And Saturated Fat, Atherosclerosis, Thrombosis, and Vascular Biology, 1994