If you think saturated fats are unhealthy, you should read “Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review.”

Introduction. I’ll just pull out some quotations that give the highlights. (All quotations are from this paper.) First, from the abstract:

The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke.

But what about the effect of saturated fat on LDL (low-density lipoprotein)? The key thing to know here, which not everyone knows is LDL particle number is the right test for heart disease and stroke danger, not the more commonly given test for the quantity of cholesterol in LDL particles. For the LDL particle numbers, which are the right measure to predict disease risk, saturated fat doesn’t have an adverse effect. Continuing in the abstract, this is how the authors of the paper above explain that:

Although SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which are much less strongly related to CVD risk.

A little lower down, here is a summary statement about the effects of saturated fats on the hard outcomes of disease and mortality:

Some meta-analyses find no evidence that reduction in saturated fat consumption may reduce CVD incidence or mortality (3–6), whereas others report a significant—albeit mild—beneficial effect (7,8). 

Where the Idea that Saturated Fat is Bad Came From. In assessing the scientific evidence that saturated fats are unhealthy, one should be aware that this became the “status quo” notion back in the 1950s, long before there was solid scientific evidence one way or another. Ideational inertia since then has given the idea that saturated fats are unhealthy an unfair advantage:

In the 1950s, with the increase in coronary heart disease (CHD) in Western countries, research on nutrition and health focused on a range of “diet-heart” hypotheses. These included the putative harmful effects of dietary fats (particularly saturated fat) and the lower risk associated with the Mediterranean diet to explain why individuals in the United States, Northern Europe, and the United Kingdom were more prone to CHD. In contrast, those in European countries around the Mediterranean had a lower risk. These ideas were fueled by ecologic studies such as the Seven Countries Study.

Evidence on the Effects of Saturated Fat. What do better studies indicate? I have added bullets to separate distinct passages answering this question:

• A few large and well-designed prospective cohort studies, which used validated questionnaires to assess diet and recorded endpoints in a systematic manner, were initiated recently. They demonstrated that replacement of fat with carbohydrate was not associated with lower risk of CHD [coronary heart disease], and may even be associated with increased total mortality (29–31). Furthermore, a number of systematic reviews of cohort studies have shown no significant association between saturated fat intake and coronary artery disease or mortality, and some even suggested a lower risk of stroke with higher consumption of saturated fat (3,6,32,33). 

• … biomarkers of very long-chain SFA (20:0, 22:0, 24:0) were not associated with total CHD (associations for fatal and nonfatal CHD were similar), and if anything, levels in plasma or serum (but not phospholipids) may be inversely associated with CHD (34).

• … increased consumption of all types of fat (saturated, monounsaturated, and polyunsaturated) was associated with lower risk of death and had a neutral association with CVD. By contrast, a diet high in carbohydrate was associated with higher risk of death but not with risk of CVD.

• … the quintile with the highest saturated fat intake (about ∼14% of total daily calories) had lower risk of stroke, consistent with the results from meta-analyses of previous cohort studies (36).

• … the substitution of polyunsaturated for saturated fat was associated with higher CVD risk.

• The PREDIMED (Prevención con Dieta Mediterránea) trial compared a standard low-fat diet with a Mediterranean diet supplemented with nuts or olive oil. Despite an increase in total fat intake by 4.5% of total energy (including slightly higher saturated fat consumption), major cardiovascular events and death were significantly reduced compared with the control group (40).

• Although there was also a positive relation of saturated fat intake with all-cause mortality, this became significant only with intakes well above average consumption (37).

The Key Test to See If It is Safe or Not for You to Consume a Lot of Saturated Fat. Let me comment on the immediately previous bullet point. I am very high on Peter Attia and highly recommend his podcast The Drive. Overall, his views are very similar to mine, and when I discover his views differ, I start modifying mine toward his, believing him to know more than I do. (However, I still have some useful role in the diet-and-health-education ecosystem, since his podcast is often at a considerably more technical level than my posts on diet and health.) In relation to saturated fat, I take seriously Peter Attia’s sense from his clinical experience that when people go on a diet so high in fat that one can stay in ketogenesis even without fasting, that doing that with a lot of saturated fat leads to a seriously elevated LDL cholesterol particle number for a subgroup of about 5% to 20% of patients. Note how limited this danger is: it is for a very large amount of saturated fat, and still only affects a minority of individuals, though given that kind of diet for those individuals it is a serious concern. The bottom line there is that anyone who is going on a diet primarily focusing on saturated fat should make sure to twist their doctor’s arm so they can get an LDL particle number test to see if they are one of those who can tolerate quite a large amount of saturated fat without ill effects or if a large amount of saturated fat is a problem for them. To emphasize again: elevated LDL cholesterol quantity doesn’t by itself mean you should worry. It just means that you really, really need that LDL cholesterol particle number test to know if you are OK with that very-high-saturated-fat diet or not. (Note: everything I said in this paragraph is just repeating what I thought I heard from Peter Attia. I have no other independent knowledge of this issue.)

Diet-by-Gene Interactions. Further down in the article, the authors discuss diet-by-gene interactions. Let me advise that genetics is moving so fast in improved methods and larger sample sizes that anything said about these genetics is likely to be contradicted and outclassed by results coming five years from now.

Particular Foods. Then comes a useful discussion of evidence about health risk from particular foods. Again, I’ll add bullets to distinguish passages:

• … despite its high content of SFAs [saturated fatty acids], dairy fat does not promote atherogenesis (89). The ability of adult humans to digest the sugar unique to milk, lactose, evolved separately numerous times (90,91), demonstrating unequivocally that the ancestors of many modern humans required continuous dairy consumption for survival to reproductive age. Bovine (92), goat (93), and sheep (94) domestication started around the same time, about 10,000 years ago, coinciding with the emergence of lactase persistence (i.e., the ability to digest lactose). The saturated fat of the meat of these species was likely a major contributor to human diets, along with fruit oils—where available—such as olive, avocado, and palm, all low in polyunsaturated fat, with the latter also being high in saturated fat. Coconut fat would have been the only abundant lipid-rich seed, and that too is highly saturated. … These historical facts demonstrate that saturated fats were an abundant, key part of the ancient human diet.

• By the 1970s, many experimental studies in animal models were conducted with dietary coconut oil of unspecified origin, which reliably caused dramatic increases in hepatic and blood cholesterol in rodents; this was taken as evidence that dietary SFAs are inherently atherogenic (95,96). However, coconut oils of the era were usually highly processed and often fully hydrogenated. Recent gentle preparation methods yield “virgin” coconut oils (97) that do not raise LDL cholesterol compared with customary diets and have similar effects compared with olive oil in humans (98). Studies in rodents demonstrated that while highly processed (“refined-bleached-deodorized”) coconut oil raises serum cholesterol, virgin coconut oil does not (99,100).

• Human studies that assume all foods high in saturated fats are similarly atherogenic come, in many cases, from an era prior to the recognition of process contaminants.

• Dark chocolate contains stearic acid (C18:0), which has a neutral effect on CVD risk. However, chocolate contains other nutrients that may be more important for CVD and type 2 diabetes than its SFA content. Experimental and observational studies suggest that dark chocolate has multiple beneficial health effects, including potential antioxidative, antihypertensive, anti-inflammatory, antiatherogenic, and antithrombotic properties, as well as preventive effects against CVD and type 2 diabetes (118–120).

• Although intake of processed meat has been associated with increased risk of CHD, intake of unprocessed red meat is not, which indicates that the SFA content of meat is unlikely to be responsible for this association (121).

• The dietary recommendation to reduce intake of SFAs without considering specific fatty acids and food sources is not aligned with the current evidence base. As such, it may distract from other more effective food-based recommendations, and may also cause a reduction in the intake of nutrient-dense foods (e.g., dairy, unprocessed meat) that may help decrease not only the risk of CVD, type 2 diabetes, and other noncommunicable diseases, but also malnutrition, deficiency diseases, and frailty, particularly among “at-risk” groups. Furthermore, based on several decades of experience, a focus on total SFAs has had the unintended effect of misleadingly guiding governments, consumers, and industry toward foods low in SFAs but rich in refined starch and sugar. 

Conclusion: Overall, the main drift of the article is to recommend unprocessed food—without worrying much about whether that unprocessed food is rich in saturated fat or not.

Conversely, avoid food that that says it is “low in saturated fat” or simply “low-fat” that comes from a package or can with a complex nutritional label, because it is likely to be highly processed. And if you think it is innocent despite being highly processed, read the ingredient list carefully and with high probability you will see there is a lot of sugar in it, not to mention other additives.

The kind of label you would want as an indication of food quality is something like “unprocessed.” But foods that are genuinely unprocessed often are not required to have a label at all! Another way to think of the distinction between processed and unprocessed food (not original with me) is to realize that unprocessed food, because it tends to have a shorter shelf-life, is often around the periphery of the grocery store, closer to the loading dock or the back room. Processed food is often in the middle of the grocery store. The only staples I get from the center of the grocery store are (a) chocolate (see “Intense Dark Chocolate: A Review”) and (b) flavored sparkling water (see “In Praise of Flavored Sparkling Water”).

For annotated links to other posts on diet and health, see:

• Miles Kimball on Diet and Health: A Reader's Guide