(This post was updated 11/29/2022)
Why is death from coronary heart disease declining in the US at the same time that obesity and diabetes rates are climbing?
Two editorials recently published in The Lancet show the widely varying opinions on the optimal diet for controlling obesity , diabetes and coronary heart disease that experts on nutrition, diabetes and heart disease hold.
The first paper contains what I would consider the saturated fat “traditionalist” viewpoint. This is a modification of the misguided concept that was foisted on the American public in the 1980s and resulted in the widespread consumption of industrially produced trans-fats and high sugar junk food that was considered heart healthy.
The traditionalists have shifted from condemning all fats to vilifying only saturated and trans fats. They would like to explain at least part of the reduction in coronary heart mortality as due to lower saturated fat consumption and the accompanying lowering of LDL (“bad”) cholesterol.
The SFA traditionalists fortunately are in decline and more and more in the last five years, prominent thinkers, researchers and scientists working on the connection between diet and the heart believe saturated fats are neutral but sugar and refined carbohydrates are harmful in the diet.
Darius Mozzafarian, a highly respected cardiologist and epidemiologist, who is dean of the School of Nutrition Science and Policy at Tufts, wrote the second editorial and is what I would term a saturated fatty acid (SFA) progressive.
He makes the following points which are extremely import
ant to understand and which I have covered in previous posts. I’ve included his supporting references which can be accessed here.
Fat Doesn’t Make You Fat, Refined Starches And Sugar Do
Foods rich in refined starches and sugars—not fats—seem to be the primary culprits for weight gain and, in turn, risk of type 2 diabetes. To blame dietary fats, or even all calories, is incorrectAlthough any calorie is energetically equivalent for short-term weight loss, a food's long-term obesogenicity (love this word!) is modified by its complex effects on satiety, glucose–insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure Thus, foods rich in rapidly digestible, low-fibre carbohydrates promote long-term weight gain, whereas fruits, non-starchy vegetables, nuts, yoghurt, fish, and whole grains reduce long-term weight gain.(1, 2, 3)Overall, increases in refined starches, sugars, and other ultraprocessed foods; advances in food industry marketing; decreasing physical activity and increasing urbanisation in developing nations; and possibly maternal–fetal influences and reduced sleep may be the main drivers of obesity and diabetes worldwide
There Are Many Different Kinds of Saturated Fats With Markedly Different Health Effects: It Makes No Sense to Lump Them All Together
SFAs are heterogeneous, ranging from six to 24 carbon atoms and having dissimilar biology. For example, palmitic acid (16:0) exhibits in vitro adverse metabolic effects, whereas medium-chain (6:0–12:0), odd-chain (15:0, 17:0), and very-long-chain (20:0–24:0) SFAs might have metabolic benefits.4 This biological and metabolic diversity belies the wisdom of grouping of SFAs based on a single common chemical characteristic—the absence of double bonds. Even for any single SFA, physiological effects are complex: eg, compared with carbohydrate, 16:0 raises blood LDL cholesterol, while simultaneously raising HDL cholesterol, reducing triglyceride-rich lipoproteins and remnants, and having no appreciable effect on apolipoprotein B, 5 the most salient LDL-related characteristic. Based on triglyceride-lowering effects, 16:0 could also reduce apolipoprotein CIII, an important modifier of cardiovascular effects of LDL and HDL cholesterol. SFAs also reduce concentrations of lipoprotein(a) ,(6) an independent risk factor for coronary heart disease."
The Effects of Dietary Saturated Fats Depend on Complex Interactions With The Other Ingredients in Food
Dietary SFAs are also obtained from diverse foods, including cheese, grain-based desserts, dairy desserts, chicken, processed meats, unprocessed red meat, milk, yoghurt, butter, vegetable oils, and nuts. Each food has, in addition to SFAs, many other ingredients and characteristics that modify the health effects of that food and perhaps even its fats. Judging the long-term health effects of foods or diets based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations. Endogenous metabolism of SFAs provide further caution against oversimplified inference: for example, 14:0 and 16:0 in blood and tissues, where they are most relevant, are often synthesised endogenously from dietary carbohydrate and correlate more with intake of dietary starches and sugars than with intake of meats and dairy.(4)
Dietary Saturated Fat Should Not Be a Target for Health Promotion
"These complexities clarify why total dietary SFA intake has little health effect or relevance as a target. Judging a food or an individual's diet as harmful because it contains more SFAs, or beneficial because it contains less, is intrinsically flawed. A wealth of high-quality cohort data show largely neutral cardiovascular and metabolic effects of overall SFA intake.7 Among meats, those highest in processing and sodium, rather than SFAs, are most strongly linked to coronary heart disease.7Conversely, higher intake of all red meats, irrespective of SFA content, increases risk of weight gain and type 2 diabetes; the risk of the latter may be linked to the iron content of meats.2, 8 Cheese, a leading source of SFAs, is actually linked to no difference in or reduced risk of coronary heart disease and type 2 diabetes.9, 10 Notably, based on correlations of SFA-rich food with other unhealthy lifestyle factors, residual confounding in these cohorts would lead to upward bias, causing overestimation of harms, not neutral effects or benefits. To summarise, these lines of evidence—no influence on apolipoprotein B, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources—provide powerful and consistent evidence for absence of appreciable harms of SFAs."
Dietary Saturated Fats May Raise LDL cholesterol But This Is Not Important: Overall Effects On Obesity and Atherosclerosis Are What Matters
"a common mistake made by SFA traditionalists is to consider only slices of data—for example, effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trends; and expedient nutrient contrasts. Reductions in blood cholesterol concentrations in Western countries are invoked, yet without systematic quantification of whether such declines are explained by changes in dietary SFAs. For example, whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France.11Changes in dietary fats11 simply cannot explain most of the reductions in blood cholesterol in Western countries—even less so in view of the increasing prevalence of obesity. Medication use also can explain only a small part of the observed global trends in blood cholesterol and blood pressure. Whether decreases in these parameters are caused by changes in fetal nutrition, the microbiome, or other unknown pathways remains unclear, thus highlighting a crucial and greatly underappreciated area for further investigation."
Dietary Saturated Fats Are Neutral For Coronary heart Disease Risk
Finally, SFA traditionalists often compare the effects of SFAs only with those of vegetable polyunsaturated fats, one of the healthiest macronutrients. Total SFAs, carbohydrate, protein, and monounsaturated fat each seem to be relatively neutral for coronary heart disease risk, likely due to the biological heterogeneity of nutrients and foods within these macronutrient categories.7Comparisons of any of these broad macronutrient categories with healthy vegetable fats would show harm,12 so why isolate SFAs? Indeed, compared with refined carbohydrates, SFAs seem to be beneficial.7 The overall evidence suggests that total SFAs are mostly neutral for health—neither a major nutrient of concern, nor a health-promoting priority for increased intake.
Focusing On Reducing Saturated Fats Leads To Unhealthy Dietary Choices
I’ve written about this a lot. The most baffling aspect of this is the promotion of low or non-fat dairy.
There is no evidence that low fat dairy products are healthier than full fat dairy products.
Non-fat yogurt filled with sugar should be considered a dessert, not a healthy food.
"Continued focus on modifying intake of SFAs as a single group is misleading—for instance, US schools ban whole milk but allow sugar-sweetened skim milk; industry promotes low-fat foods filled with refined grains and sugars; and policy makers censure healthy nut-rich snacks because of SFA content.13 "
It is extremely hard to change most people’s opinions on dietary fat.
My patients have been hearing the SFA traditionalist dogma for decades and thus it has become entrenched in their minds.
When I present to them the new progressive and science-based approach to fat and saturated fat some find it so mind boggling that they become skeptical of the skeptical cardiologist!
Hopefully, in the next few years, the progressive SFA recommendations will become the norm and maybe , some day in the not too distant future, the inexplicable recommendations for low-fat or non fat dairy will disappear.
As more data accumulates we may become SFA enthusiasts!
For another viewpoint (?from an SFA enthusiast) and a detailed description of both editorials see Axel Sigurdsson’s excellent post here.
1 thought on “Are All Saturated Fatty Acids Bad? Traditionalists versus Progressives”
These matters may finally get sorted as more scientists become interested in essential fatty acid research. http://www.fatsoflife.com/pufa-august-2015/a-balanced-approach-to-omega-3-benefits/