The Treacherous Quest for Healthy Fats
Whether you’re reading consumer or scientific literature these days, healthy fats are a hot topic. The problem is that you’ll run into the quite a bit of conflicting information. The history is tortured. And unfortunately, even as science resolves some issues, others keep cropping up.
For nearly 30 years, nutrition guidelines emphasized low-fat and low cholesterol diets. The 2015 guidelines finally discarded that advice Another issue that’s settled is trans fats. They were banned from from the food supply in 2015 by FDA. Food companies have until 2018 to eliminate them entirely.
So now, we face lingering arguments about saturated fats and omega-6 fatty acids.
Nina Teicholz and others have been stoking controversy about saturated fats over the last few years. She’s created quite a successful brand for herself with The Big Fat Surprise, a best-seller since 2014. Despite all the hubbub, the evidence is pretty clear. Simply cutting saturated fats is not beneficial, because excess sugar and refined carbs tend to replace those calories in free-living people. But replacing saturated fats with healthful unsaturated fats does have a health benefit.
Unfortunately, advice to favor unsaturated fats opens another can of worms – omega-6 fatty acids. These are unsaturated fats in vegetable oils like corn and soybean oil. They are essential fats, meaning your body can’t make them, so you need them in your diet.
But some people worry that we’re eating too much of omega-6 fats. Artemis Simopoulos is high on that list. She’s been selling a sensational diet book on this subject since 1999. She has produced a steady stream of publications in the scientific literature as well. In 2016, she published this paper, suggesting that an excess of omega-6 fatty acids raises the risk of obesity.
However, consensus is elusive on omega-6 fats. The American Heart Association says that cutting omega-6 fatty acids from present levels of consumption would likely do more harm than good for heart health. The Cochrane Collaboration says the evidence is insufficient. In the midst of all this confusion, our good friend and registered dietitian Susan Burke March offers sound advice:
It’s much more important where your fats come from than knowing your ratio of omega-6 and omega-3. In a typical American diet, people consume plenty of omega-6 fats in commodities like chips, crackers, fast food, and deep fried foods. But they don’t eat a lot of foods rich in omega-3s, like salmon, nuts, seeds, and olives. An overload of poor quality, fried foods can contribute to inflammation.
In other words, pay attention to the quality of the food you’re eating over time. An excess of cheap, greasy food will not enhance your health. If you want a template for a better dietary pattern, you can hardly do better than the Mediterranean diet. It offers plenty of healthful fats and good foods, without so much dietary dogma.
Olive Grove, painting by Vincent van Gogh
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February 10, 2017
February 10, 2017 at 10:30 am, David Brown said:
I suspect the healthy fats debate could be resolved if more attention were paid to the arachidonic content of the food supply. Fats are not the only source of fat in the diet. Cell membranes of lean meats contain the 20-carbon chain omega-6 arachidonic acid and the 20-carbon chain omega-3 eicosapentaenoic acid. The body utilizes these fatty acids to make endocannabinoids. When we consume lean protein we consume these fatty acids. Plant proteins do not have these fatty acids associated with them. Why is this important? Excerpt:
Arachidonic acid (AA) in the diet can be efficiently absorbed and incorporated into tissue membranes, resulting in an increased production of thromboxane A2 by platelets and increased ex vivo platelet aggregability. Results from previous studies have shown that AA is concentrated in the membrane phospholipids of lean meats. However, the concentration of AA in the visible fat portion of meats also may be significant despite being ignored in most studies. The aim of this study was to accurately quantitate the AA content of visible fat and the lean portion of beef, lamb, pork, chicken, duck, and turkey. The visible fat of meat contained a significant quantity of AA, ranging from 20 to 180 mg/100 g fat, whereas the AA content of the lean portion of meat was lower, ranging from 30 to 99 mg/100 g lean meat. Beef and lamb meats contained lower levels of AA in both the visible fat and lean portion than that from the other species. (Note that sheep and cattle, being ruminant animals, biohydrogenate unsaturated fatty acids in linoleic acid-rich feed to saturated fats. Consequently, the arachidonic content of beef, mutton, and dairy is fairly low. http://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-5-97
We’re often admonished to eat lean meats other than beef because they contain less saturated fat.
The highest level of AA in lean meat was in duck (99 mg/100 g), whereas pork fat had the highest concentration for the visible fats (180 mg/100 g). The lean portions of beef and lamb contained the higher levels of n-3 polyunsaturated fatty acids (PUFA) compared with white meats which were high in AA and low in n-3 PUFA. The present data indicate that the visible meat fat can make a contribution to dietary intake of AA, particularly for consumers with high intakes of fat from pork or poultry meat. https://www.ncbi.nlm.nih.gov/pubmed/9590632
Feeding livestock grains rather than allowing them to forage for themselves has distorted the fatty acid profile of animal foods of all sorts.
We now know that major changes have taken place in the food supply over the last 100 years, when food technology and modern agriculture led to enormous production of vegetable oils high in ω-6 fatty acids, and changed animal feeds from grass to grains, thus increasing the amount of ω-6 fatty acids at the level of LA (from oils) and arachidonic acid (AA) (from meat, eggs, dairy). This led to very high amounts of ω-6 fatty acids in the food supply for the first time in the history of human beings. Traditionally, animals grazed. Grass contains ALA (ω-3), whereas grains, corn and soya (which are now fed to animals) are high in LA (ω-6). This imbalance in the amount of ω-6 and ω-3 fatty acids is a new phenomenon that was never a part of human evolution. Human beings evolved on a diet that had equal amounts of ω-6 and ω-3 fatty acids. This balanced ratio of ω-6 to ω-3 is critical to human development during pregnancy and lactation, in the prevention of chronic diseases and in their management. The typical Western diet now provides an ω-6 to ω-3 ratio of around 16:1. High dietary intake of ω-6 fatty acids as occurs today leads to increases in white adipose tissue and chronic inflammation, which are the ‘hallmarks of obesity’. http://openheart.bmj.com/content/3/2/e000385.full
The American Heart Association argues that linoleic acid lowers cholesterol and is thus important for reducing heart attack risk. The research cited also shows that very high intakes of linoleic acid are associated with slightly lower heart disease mortality. What hasn’t been tested in humans is what would happen if linoleic acid intake were lowered to preindustrial levels of 1% of energy or less. Experiments with mice yield these results.
Dietary intake of linoleic acid (LNA, 18:2n-6) has increased dramatically during the 20th century and is associated with greater prevalence of obesity. The endocannabinoid system is involved in regulation of energy balance and a sustained hyperactivity of the endocannabinoid system may contribute to obesity. Arachidonic acid (ARA, 20:4n-6) is the precursor for 2-AG and anandamide (AEA), and we sought to determine if low fat diets (LFD) could be made obesogenic by increasing the endocannabinoid precursor pool of ARA, causing excessive endocannabinoid signaling leading to weight gain and a metabolic profile associated with obesity. Mice (C57BL/6j, 6 weeks of age) were fed 1 en% LNA and 8 en% LNA in low fat (12.5 en%) and medium fat diets (MFD, 35 en%) for 16 weeks. We found that increasing dietary LNA from 1 to 8 en% in LFD and MFD significantly increased ARA in phospholipids (ARA–PL), elevated 2-AG and AEA in liver, elevated plasma leptin, and resulted in larger adipocytes and more macrophage infiltration in adipose tissue. In LFD, dietary LNA of 8 en% increased feed efficiency and caused greater weight gain than in an isocaloric reduction to 1 en% LNA. Increasing dietary LNA from 1 to 8 en% elevates liver endocannabinoid levels and increases the risk of developing obesity. Thus a high dietary content of LNA (8 en%) increases the adipogenic properties of a low fat diet. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3889814/
Rat experiments indicate that balancing omega-3/6 intake is important.
Dietary intake studies have shown that the fat intake of the U.S. diet averages a PUFA balance of ~ 9.5% . In the present study the diet PUFA balance ranged from 1 to 86% and was found to elicit the greatest response on both membrane lipid and triglyceride fatty acid composition. If the current results in rats also apply to humans, an average PUFA balance of 9.5% in the modern human diet is of considerable concern, as it indicates there are huge numbers of people consuming a diet with a very low and likely inadequate PUFA balance without knowing it. http://www.sciencedirect.com/science/article/pii/S0005273612000156
The Center for Science in the Public Interest (CSPI), a vegetarian activist group, is especially vehement about limiting saturated fat intake. Interestingly, T. Colin Campbell (also an anti-animal food enthusiast) sees things in a different light.
I propose that this argument for or against saturated fat should have been moot from the very beginning of this research. Here’s why. The original hypothesis that dietary fat, especially saturated fat, is chiefly responsible for heart disease began with laboratory studies over a century ago and the findings are, at best, uncertain. Much more impressive evidence also was published to show that the early stages of heart disease, atherosclerosis, and its predictive serum cholesterol marker, were increased much more by dietary protein than by dietary fat, especially the protein in animal-based foods. Later, around 1940, more of the same evidence favoring protein was published. The animal protein, casein, was shown to be five times more effective in raising cholesterol in experimental rabbits than the plant protein, soy. In a human study, replacing dietary protein (mostly animal based) with soy protein lowered serum cholesterol much more effectively than lowering dietary fat. http://nutritionstudies.org/fallacious-faulty-foolish-discussion-about-saturated-fat/
Campbell’s argument ignores an important difference between animal and plant cell membranes. Plants do not contain arachidonic acid. The proteins are identical.
February 10, 2017 at 11:03 am, Ted said:
Thanks, David, for providing much food for thought. Or maybe thought for food.