Discover more from Entelechy with Matt Neilsen
Saturated Fat, Animal Foods, and the Lipid Hypothesis
When asked about religion and politics, Mark Twain is rumored to have said, “I am quite sure now that often, very often, in matters concerning religion and politics a man's reasoning powers are not above the monkey's.” In recent years, a third topic appears to be competing for the dubious honor of “things-you-don’t-bring-up-at-dinner-parties”: diet. The Internet wars waged over diet are quite spectacular, with each side arming themselves with the latest cherry-picked data to hurl at their opponents. Discussions about diet have taken on the ideological fervor of the Salem Witch Trials. Disagree with the consensus opinion, and you will quickly be labeled a heretic and burned at the stake!
There are hundreds of dietary dogmas, but for the purposes of this article we will examine just one of them: “Saturated fat is bad for you.” We will first examine some of the evidence in favor of the argument, which includes topics like the Lipid Hypothesis and epidemiology studies. Then, we will look at evidence that argues saturated fat actually supports human health, which will include evidence from more epidemiology studies, anthropology/archaeology, and metabolism. Finally, we will synthesize the arguments into a general framework and provide practical recommendations.
The Lipid Hypothesis
In order to understand the arguments against saturated fat, it is critical to understand what is known as the “Lipid Hypothesis”. The Lipid Hypothesis is the observation that saturated fat tends to increase a lipoprotein in the blood called low-density lipoprotein, or LDL.
Many people are familiar with the term LDL because it is often referred to as the “bad cholesterol”. This same type of language is used on the American Heart Association website where they say that saturated fat can raise cholesterol levels, worsen lipid profiles, and that “decades of sound science has proven it can raise your “bad” cholesterol and put you at higher risk for heart disease”. High LDL levels have been strongly correlated with an increased incidence of atherosclerotic cardiovascular disease, as demonstrated in the Framingham Heart Study. Medline Plus, a service of the National Library of Medicine, also claims that saturated fats are unhealthy and can lead to heart disease.
Conversely, it has been known for many years that monounsaturated and polyunsaturated fats tend to decrease LDL levels, at least in the short-term. This is why organizations like the US Department of Health and Human Services recommend replacing saturated fats in the diet with unsaturated fats, especially polyunsaturated fats.
The second line of evidence against saturated fat comes from the observation that increased animal food consumption is correlated with increased cancer risk in Western populations. The World Health Organization says that animal consumption is correlated with increased cancer risk. The International Agency for Research on Cancer – a subset of the World Health Organization – stated in 2015 that red meat consumption (both processed and unprocessed) is “probably carcinogenic” and is in the same category as smoking cigarettes and exposure to asbestos. The World Cancer Research Fund has stated that increased consumption of animal foods will increase the incidence of numerous cancers. Since animal-based sources of food – particularly meat, dairy, and eggs – are rich sources of saturated fats, this appears to provide another line of evidence that saturated fats ought to be reduced in the human diet.
Given the strength of the evidence against saturated fat, why is there controversy about the role of saturated fat in the diet?
The reason for the controversy is that there is a lot of contradictory evidence concerning the role of LDL in the diet and the link between animal-food consumption and health outcomes. For example, LDL appears problematic primarily in the context of metabolic dysfunction (i.e. insulin insensitivity). We discussed the Framingham Heart Study earlier which demonstrated a relationship between LDL levels and heart disease. However, when the data are stratified by HDL, the risk of high LDL largely vanishes. Since HDL is a reasonable proxy for insulin sensitivity/metabolic function, it seems to indicate that the underlying metabolic health of the person is just as important – and perhaps even more so – as absolute LDL levels.
More recent meta-analyses do not find a correlation between saturated fat intake and heart disease. LDL may actually be protective against mortality in some situations, leading to what’s known as the “LDL Paradox”, and appears to be protective to those over age 60. Additionally, recent meta-analyses (2019) call into question whether meat consumption is causal in heart disease.
The picture becomes even muddier when looking at cohort studies done on non-Western populations. For example, a 2013 meta-analysis of prospective cohort studies with nearly 300,000 subjects in Asian populations indicated the exact opposite of research in Western countries. In Asia, animal consumption was correlated with lower rates of cardiovascular disease and cancer. This phenomenon is likely a result of “Healthy User Bias”, which we will discuss in the recommendations section.
Anthropology & Archaeology
Another line of evidence that muddies the saturated fat waters comes from the fields of anthropology and archaeology. Throughout the natural world, animals appear to thrive when they consume diets that are consistent with their evolutionary past. Yet evidence from anthropology and archaeology indicates that humans evolved as high-level carnivores. In other words, humans ate a lot of saturated fat throughout their evolutionary past. Delta 15 nitrogen levels indicate Homo neandertalensis was a high-trophic carnivore. Stable isotope studies using strontium, nitrogen, sulfur, and carbon indicate Homo sapiens was also a high-trophic carnivore, even higher than Homo neandertalensis and other known carnivores like lions & hyenas.
Additionally, we have strong evidence that hominids have been high-level hunters for at least 2 million years, with butchery evidence going back 3.5 million years. We also have many examples of indigenous cultures (prior to Western contact) consuming high amounts of animal products – and therefore saturated fat – with low levels of heart disease (Inuit, Masai, Sami, Hadza, Mongolians). Indigenous Polynesian groups consuming very high saturated fat diets from coconuts show no increase in heart disease. If saturated fat is truly so bad for human health, then why do we have numerous examples of human populations thriving on high saturated fat diets? And why would something that our species evolved to eat for 3.5 million years now be killing us?
The final line of evidence that calls into question saturated fat’s bad reputation has to do with the role that saturated fat plays in our metabolism. Saturated fat plays a critical role in satiety signaling through the generation of molecules called reactive oxygen species (ROS). Reactive oxygen species like superoxide and hydrogen peroxide are used by the cell to determine whether the mitochondria are burning glucose or fat through a process called the Randle cycle. This process is incredibly important because it helps the cell to regulate energy balance. Saturated fat is uniquely good at creating physiologic insulin resistance at the level of the mitochondria, which is important if you want your fat cells to stop growing and instead start using their stored energy for fuel. Interventional mouse studies support the critical role saturated fat plays in telling the cell to halt lipogenesis and begin burning fat for fuel.
It's also worth pointing out that even if you eat a very low-fat diet, your body will still convert the starch you eat into fat through a process called de novo lipogenesis. And guess what type of fat de novo lipogenesis produces? You guessed it: saturated fat.
ROS generation is also necessary for sending the satiety signal to the hypothalamus, which is how your brain knows to down-regulate appetite. Insufficient ROS signaling at the hypothalamus may be a key reason many people never feel satiated on Western diets. Finally, visceral fat and the hypothalamus both have high expressions of LPL (lipoprotein lipase), which has a high affinity for saturated fat. This causes visceral fat to become physiologically insulin resistant (meaning it will not take in more energy) and sends a satiety signal to the hypothalamus (thereby inhibiting further energy intake). Both of these phenomena are crucial for healthy weight gain/loss.
Saturated fat has been a natural part of the human diet for millions of years, and an increasing amount of evidence is painting a new picture about the role of saturated fat in human health. It appears that the correlations in Western populations between saturated fat and heart disease have less to do with saturated fat and more to do with the typical foods consumed with it: refined vegetable oils, refined carbohydrates, and sugar. In other words, the meat in your burger isn’t hurting you, but the highly refined accouterments – the processed bun, sugar-laden sauces, and fries deep-fried in oxidized vegetable oil – may be the culprits behind the epidemic of heart disease in Western civilization.
This is an example of what I referred to earlier as “Healthy User Bias”. In Western society, we have been told that meat and saturated fats are bad for us for nearly 70 years. Consequently, who tends to eat more meat in Western societies: people who think a lot about health, or people who don’t? The answer should be obvious. The types of people who tend to eat meat are also more likely to eat fast food, smoke, not exercise, be of lower socioeconomic status, and engage in other risky behaviors. Unfortunately, epidemiology studies are inherently unable to separate correlation from causation, and so we have an entire industry that may be maligning saturated fat on the basis of bad evidence.
There is a broad range of dietary patterns that have been demonstrated in free-living humans to produce robust health. Remove seed/vegetable oils, remove refined carbohydrates, and remove sugar, and you will solve 90% of the problems. Some people will need to go the extra step of removing specific offending foods that are unique to their biochemistry (wheat, dairy, nightshade vegetables, etc.). If your ancestors from 500 years ago could not recognize the food you are eating, then you would probably be wise to avoid it. Eat whole foods – including nutrient-dense animal foods – and engage in other healthy lifestyle choices (sleep, movement, stress management, etc.).
One last point:
I am critical of the conclusions many medical professionals draw from the Lipid Hypothesis. However, I agree that saturated fat does tend to raise LDL, and LDL is strongly correlated with heart disease in the setting of metabolic dysfunction. If a person refuses to remove the seed oils, refined carbs, and sugar out of their diet, then they may want to consider reducing their intake of saturated fat so as to limit the amount of oxidized LDL (OXLAMs) in circulation. I think this is a poor solution as it doesn't address the underlying issue, but people will be people.
(Actually, if you want to watch a very funny video clip that makes this point better than I ever could in 80 seconds, watch "It's Not About the Nail". I promise you’ll enjoy it.)