If you’re a regular reader of this site, then you know that I don’t agree with the nutritional establishment in everything. Among other things, I think it’s a mistake to advice people to eat a lot of cereal grains. That said, I don’t think the nutritional establishment is completely off course. I do support many of the dietary recommendations that are put forth by government-led agencies. For example, I think the recommendation to stay away from processed and energy-dense foods is a good one. Also, perhaps surprising to some, I support the recommendation to limit the consumption of saturated fat.
I almost feel like I can hear people’s reaction to that last statement… “What? He can’t be serious, can he? Hasn’t he read the latest research – the research that vindicates saturated fat?”. Far from everybody will react this way; however, some, perhaps yourself included, undoubtedly will. What I would urge those people to do is to take the time to read through my articles on saturated fat with an open mind. If they do, they may find that they get a better, more well-informed, and balanced perspective on everything that has to do with saturated lipids.
Contrary to what the quote above would imply, I have kept up with the latest research on saturated fat. Not only that, but I have digged into earlier studies and review papers, as well as examined the evolutionary evidence and looked into the biological mechanisms pertaining to the link between saturated fat consumption and human health. I don’t claim to know everything about saturated fat; however, I do feel I have a pretty good understanding of the role this type of nutrient, which is at the center of a lot of dietary controversy, plays in the human diet and how much of it it’s wise to consume.
The recent opinion piece on saturated fat in the British Journal of Sports Medicine misses the mark
Very recently, three cardiologists published an editorial on saturated fat in the British Journal of Sports Medicine (BJSM). In that article, they make the case that it’s time to revise the dietary recommendation to limit the consumption of saturated fat. They also make other statements regarding the link between diet (as well as exercise) and human health; however, in today’s article I thought I’d focus exclusively on saturated fat. (Note: I do agree with some of their statements and recommendations, such as the one to advice people to be more physically active).
The authors argue that the scientific evidence shows that saturated fat is, in the grand scheme of things, benign. A high intake of saturated fat is not going to increase your risk of developing heart disease, stroke, type-2 diabetes, and the like, according to them. In support of this statement, they cite recent meta-analyses that have looked into the relationship between saturated fat consumption and chronic disease risk.
Aseem Malhotra, Rita F. Redberg, and Pascal Meier, the authors of the editorial, are particularly enthusiastic about one recent paper, which they refer to as a landmark systematic review and meta-analysis. That comprehensive meta-analysis and systematic review looked into the effects that saturated fat consumption has on a variety of chronic disease outcomes and found that there was no association between the intake of saturated fat and all-cause cause mortality or the risk of cardiovascular disease, coronary heart disease, ischemic stroke, or type 2 diabetes (1).
The authors also cite other studies in support of this idea; however, I get the impression that they consider the above study to be their crown jewel. I simply can’t understand why they would. Yes, it’s a really big meta-analysis that brings together the results of a lot of studies; however, it doesn’t provide causal evidence as to the link between saturated fat consumption and chronic disease risk, seeing as all of the data are gathered from observational studies. In my opinion, it’s a big stretch to say that it’s a landmark systematic review and meta-analysis.
I’m not the only one who thinks Malhotra et al. overestimate and misinterpret the evidence they present. For example, Alan Hughes, a Professor at University College London, had the following to say about the editorial published in the BJSM:
This editorial is muddled and adds to confusion on a contentious topic. The authors present no really new evidence, misrepresent some existing evidence, and fail to adequately acknowledge the limitations in the evidence that they use to support their point of view. (2)
The problem with observational studies
As everyone who’s taken a course in statistics know, one should be very cautious about drawing causal conclusions from observational studies, in large part because they are extremely prone to confounding. It’s very difficult to adequately control for confounders in observational research. This is particularly true if you’re studying something as intricate as the relationship between diet and health.
You don’t have to be a genius or have a PhD in statistics to understand why this is the case; all you need is a basic understanding of how we humans live. People obviously don’t eat pure fats, carbohydrates, vitamins, or proteins; they eat nutrients as part of food. Two people could have an identical intake of saturated fat, as measured in % of total calories; however, that doesn’t necessarily mean that their diets are identical. They could be different in many respects. For example, one of the diets may be high in fruits and vegetables, whereas the other could be completely devoid of these plant foods.
Not only that, but the two people may live in different environments and adhere to different lifestyles. Perhaps one of them smokes regularly, lives in a mold-infested home, and rarely exercises, whereas the other leads an active, healthy lifestyle. All of these things could obviously affect their risk of developing chronic disease.
Researchers try to control for all of these covariates, but as you can imagine, it’s virtually impossible to stay on top of all of these things. The problem is further compounded by the fact that many observational studies, as well as some clinical trials, rely on self-reported data: a type of data that are inherently less accurate than let’s say data acquired via measurements of biological material.
Here’s what the researchers of the “landmark” study mentioned earlier had to say about the risk of confounding in observational studies:
… observational studies cannot provide causal evidence of an effect of saturated or trans fatty acids on the development of health outcomes examined; they can describe only associations. Measurement error is often serious in epidemiologic studies of diet and disease, which can bias such associations towards the null. (1)
Another thing I think it’s important to point out that it’s very difficult to adequately assess the relationship between saturated fat intake and chronic disease incidence, seeing as chronic diseases such as type-2 diabetes and heart disease develop over many years. Let’s say that a hypothetical observational study that lasted 6 years found that people who got between 10-14% of their calories from saturated fat were at no higher risk of developing heart disease than people who got between 6-10% of their calories from saturated fat. Can we draw any conclusions about the link between saturated fat consumption and heart disease risk from this study? No. At least I wouldn’t. Most people don’t eat the same diet their whole lives. Their diets fluctuate. It might be that the diets the people included in this study consumed in the years prior to the start of the study greatly affected their risk of developing heart disease during the study period. Moreover, as previously mentioned, a whole range of other factors may have confounded the saturated fat-health relationship.
All of this is to say that I don’t put much weight on observational studies, particularly in the context of diet-health relationships pertaining to the link between specific nutrients and various health outcomes. There are just too many unknown factors. I don’t find it surprising at all that many observational studies have found that there is no significant association between saturated fat intake and chronic disease risk, given that there are so many possible confounders at play in observational research and that the human diet is composed of many different components.
What does the experimental research show?
What about clinical trials? What do they show? The authors of the opinion piece in the BJSM seem to think that the evidence from experimental studies strongly supports the idea that saturated fat is harmless. This is, as I’ve explained in my previous articles on saturated fat, simply not the case. I’m not going to delve into the research in this area again here; however, what I would like to point out is that Malhotra et al. neglect to mention that several meta-analyses, including one published by Cochrane (3), refute the idea that a high intake of saturated fat doesn’t adversely affect the blood lipid profile or raise chronic disease risk (4, 5). They only cite studies that support their position; they don’t mention any studies that don’t.
I’m not the only one who’ve noticed this. Several other people have as well. For example, Dr. Amitava Banerjee, a senior clinical lecturer in clinical data science and honorary consultant cardiologist at University College London, had the following to say about the research Malhotra et al. cite (and didn’t cite) in their editorial:
Unfortunately the authors have reported evidence simplistically and selectively. They failed to cite a rigorous Cochrane systematic review which concluded that cutting down dietary saturated fat was associated with a 17% reduction in cardiovascular events, including CHD, on the basis of 15 randomised trials. (6)
The fact is that the studies in this area show conflicting results. Some suggest that it’s unwise to eat a lot of saturated fat, whereas others indicate that saturated fat intake is not a good predictor of chronic disease incidence.
I get the impression that a lot of people get so hung up on the statistical procedures and details of these studies that they forget to look at the big picture of things. When we think about it, it isn’t really surprising that the studies in this area show conflicting results. It’s exactly what one would expect, given that the relationship between diet and health is very complex. As mentioned earlier, it’s very difficult to measure how one dietary variable such as saturated fat intake affects chronic disease risk, part of the reason being that you can’t change one variable without also changing another.
For example, let’s say that you run a clinical trial with the purpose of elucidating the relationship between saturated fat intake and the incidence of type-2 diabetes. You split the participants you’ve recruited for the study into two groups and instruct the participants in group A to get 10% of their calories from saturated fat and the participants in group B to get 20% of their calories from saturated fat. You give all of the participants the same instructions regarding what to eat, so as to keep their diets as identical as possible, with the exception that you tell the participants in group B to eat more butter, bacon, and cheese than those in group A, who you instruct to get the majority of their fats from avocados, fish, and nuts.
After the 2 years are over and you’ve assembled all of the data, you find, via your statistical analyses, that the incidence of type-2 diabetes was higher in group B than in group A. While interesting, these results aren’t necessarily reproducible. This is particularly true if they are only barely significant. If you had run the exact same trial again, you might not have found the same results, in part because the participants you would have included in this new study would have had a different diet and medical history than the ones included in the previous experiment.
Moreover, if you had used different sources of fat in the new study, but still kept the same saturated fat intake level in both groups as in the previous trial, this could have affected the results of the research. For example, let’s say that you the second time around instructed the participants in group B to stay away from butter, bacon, and cheese and instead get their saturated fat from coconut, organ meats, and eggs. These latter foods differ in several respects to the former. Among other things, they have a markedly lower saturated fat density and higher nutrient density. Moreover, coconut primarily contains lauric acid, a type of saturated fatty acid that affects the blood lipid profile differently than other saturated fatty acids. (It may actually decrease the ratio of total to HDL cholesterol, as opposed to raising it (4))
I’m not telling you all of this so as to make you confused and dizzy. I’m saying it to show that it’s difficult to assess the relationship between the intake of specific nutrients such as saturated fat and chronic disease risk.
Making sense of the chaos
So, how can we make sense of all of this? The answer to this question is quite simple: We have to look at the totality of the evidence. We can’t simply look at a few meta-analyses and leave it at that. We have to assess the totality of research on saturated fat that’s been done and determine what the weight of the evidence from that research shows. This doesn’t mean that we have to read every single study that has ever been done on saturated fat. It just means that we should strive to collect all of the pieces of the puzzle. We shouldn’t deliberately leave some pieces out just because they don’t fit with the version of the puzzle we want to create. We all have our biases; however, we should try to put those aside and seek the truth.
While important, assessing the results of experimental studies that investigate the link between saturated fat intake and various health outcomes is not sufficient to get us where we want to go. We also have to consider how different foods and nutrients affect our hormone levels, gene expression, and so forth, and perhaps more importantly, we have to examine the evolutionary evidence. This leads us over to one of my main critiques of the opinion piece in the BJSM. The authors don’t mention any of the many studies that have found a link between saturated fat and endotoxemia/chronic inflammation or acknowledge that a high intake of foods such as bacon and cream can contribute to causing a range of health problems.
It’s kind of ironic that Malhotra et al. recognize that chronic inflammation is at the root of coronary artery disease, yet fail to mention that a solid body of research suggests that a high intake of saturated fat can cause inflammation via activation of toll-like receptor 4 (7, 8, 9, 10, 11). Furthermore, Malhotra et al. don’t say anything about the evolutionary evidence pertaining to the role saturated fat played in sculpting the human genetic make-up.
In my opinion, this is a huge oversight. The evolutionary evidence should be the first type of evidence we examine when we set out to investigate the role between diet and health. As I’ve pointed out in my previous articles on saturated fat, contrary to what a lot of people believe, the preagricultural human diets that conditioned the human genetic make-up over millions of years were not high in saturated fat. They certainly weren’t devoid of saturated fat; however, they didn’t contain large quantities of this type of lipid, due in large part to the fact that they didn’t contain butter, bacon, cheese, and other similar foods with a very high concentration of saturated fat.
The bottom line
As a whole, I feel the weight of the evidence clearly shows that it’s unwise and unhealthy to consume a lot of saturated fat (Check out my comprehensive article on saturated fat for a full breakdown of the evidence or this recent post for an overview of the key things you need to know). What I mean by that is not that it’s smart to avoid all foods that contain saturated fat. Absolutely not. Actually, I think most people could benefit from eating more eggs, grass-fed meats, and other similar nutrient-dense whole foods. However, I think it would be a fatal mistake to start telling people that it’s okay to eat a lot of evolutionarily novel high-fat foods such as bacon and other fatty, processed meats and dairy foods such as cheese and cream.
These foods differ in several respects from the aforementioned ones. Among other things, they contain a very high concentration of saturated fat. The concentration of saturated fat found in these foods is supernormal when compared to the concentration found in the foods that were available throughout the vast majority of our genus’ evolutionary history. There’s no evolutionary precedent for the consumption of these types foods. That doesn’t mean we should avoid them like the plague; however, I would argue that it’s a very bad idea to eat a lot of them.
This illustrates one very important thing: it’s better to focus on making good food choices than on achieving a certain intake of a specific nutrient. After all, we eat foods; we don’t eat isolated nutrients. As long as you adhere to prudent, ancestral diet, you don’t really have to think about how much saturated fat you’re taking in, as you will naturally achieve a balanced intake of the various nutrients that you need.
The longstanding advice to limit the consumption of saturated fat makes people more likely to restrict their consumption of fatty meats, cheese, cream, and other similar high-fat foods. I think this is a good thing. That said, the advice may also have caused some damage, in the sense that it may have made people avoid nutrient-dense foods such as eggs and organ meats. Hence, it might be better to instruct people on what types of food choices they should make, as opposed to setting limits on certain nutrients.