Saturated fat and cholesterol are trying to kill you. Eating them will clog your arteries and lead you to an early grave. If you want to live a longer life, don’t eat anything that contains saturated fat or cholesterol, as with it, you are essentially poisoning yourself!

This message has been echoed across the West for the past 40 years. But does it have the scientific backing implied from its sheer prevalence? Well, fortunately for us all, it does not.

Starting at the very beginning, it is important we understand the risks being pushed upon us. Primarily, people claim that cholesterol and saturated fat will cause heart disease through the clogging of our arteries. But this claim is rather overstated. For instance, cholesterol, a type of dietary fat, is a waxy substance that is the structural component of cell membranes and the precursor to various steroid hormones, vitamin D and bile acids (used to digest dietary fats). About 80% of our body’s cholesterol is produced from within the liver and intestines, while only 20% comes from dietary sources. Because cholesterol cannot dissolve in blood, it must be transported to the liver for removal. As a result, our body produces particles called lipoproteins to enable our fatty substances to be transported through the bloodstream to cells.

Lipoproteins, a lipid and protein, have various types, but the most famous are high-density lipoprotein (HDL) and low-density lipoprotein (LDL) which have been individually labelled as “good” and “bad” for public simplification.

Whereas in reality, they just have different roles. For example, LDL carries cholesterol from the liver to tissues like a delivery truck. HDL instead picks up excess cholesterol from tissues and returns them back to the liver for excretion. Here is where it gets interesting. If you were to consume more cholesterol, then your body would create less. Essentially, if your cholesterol was 30% from diet, you would not have 110%. Instead, your liver would produce the remaining 70% and your levels would stay within the same range. Similarly, this rule applies for eating under the 20% margin.

Cholesterol has been associated with cardiovascular disease (CVD) for decades, but for an odd reason. This connection was first discovered in epidemiological studies where populations with higher blood cholesterol had more heart attacks. However, it turns out that this was not a direct culprit, but instead a vital correlation. Modern research has indicated that a chronically skewed ratio of lipoproteins, mainly LDL, has a direct effect on fatty plaques in the arteries. For instance, when LDL particles, which carry cholesterol, are high, they can readily infiltrate the inner artery linings. This retained LDL can become oxidised, triggering a process that turns them into fatty streaks and enabling clogs.

Interestingly, LDL’s relationship within metabolically healthy individuals is slightly different. For example, when we mention those on the carnivore diet (mainly animal products) or high-protein omnivores, the original assumption becomes faded. Current evidence shows that these people were extremely low risk, but elevated LDL proved to still be the biggest risk factor, not cholesterol.

But where does saturated fat fit into all this? Well, to break through some of the misconceptions first. No, saturated fat does not contain cholesterol or vice versa. Yes, we need saturated fat within our diet to govern distinct metabolic functions (cell membrane structure, gene transcription and protein modification, for example). Saturated fat and cholesterol are not the same substance, in fact, they are completely different in the way they are structured and in the way they work.

However, saturated fat intake influences blood cholesterol more than dietary cholesterol does. Now, I understand how odd that sounds. But if you were to consume high-cholesterol, low-saturated fat foods (eggs, shrimp, liver), your LDL does not rise. On the other hand, eating a high saturated fat diet has been found to increase your LDL, which we now know is a causation of CVD. Although this is the case, historical dietary guidelines focused on reducing saturated fat and cholesterol, presumably because they often coexist in food. For example, cutting down fatty meats will reduce saturated fat and cholesterol.

Dietary saturated fatty acids can increase LDL indirectly through the downregulation of LDL receptors’ expression. In other words, the more saturated fatty acids in your blood, the less suppression of LDL in the liver, so more of this low-density lipoprotein is created. However, the critical questions are whether this rise in LDL is transient or sustained? And how much saturated fat would we need to increase LDL to dangerous levels?

Interestingly enough, this got me thinking about carnivores. Unfortunately, we have no long-term CVD studies, but as of right now, there is no evidence that those on an animal-based diet have higher CVD risk. At first glance, this is quite bewildering since their diet consists primarily of saturated fat. Indeed, a common finding within relevant studies is that they have elevated LDL, but since our body can regulate its lipoprotein function, their HDL was also elevated, leading to cholesterol being excreted. Current understanding indicates that these individuals are able to survive without risk due to the improved insulin resistance, lower blood glucose levels, lower triglycerides and reduction in inflammation markers (such as C-reactive Protein). Moreover, the excessive saturated fat does lead to a higher LDL in some cases, but there is no evidence that this has caused clogging of arteries. Now, this may be due to this diet being a relatively new phenomenon without enough time to show dangers, or because something else is in play.

Confusingly, but most interestingly, there are two types of low-density lipoproteins, cholesterol-rich and cholesterol-poor. Current studies indicate that those on low-carbohydrate/ketogenic diets, such as carnivore, have far fewer cholesterol-poor LDL particles compared to high-carbohydrate peers. Importantly, the dense LDL finds it easier to penetrate arterial walls and oxidise, which may be one of the reasons CVD is lacking in carnivores.

However, these individuals and the relevant scientific understanding suggest to us that the LDL rise from saturated fat is transitory and not persistent, especially since LDL levels drop back to baseline after saturated fat consumption drops.

As a result, we should start to consider whether a low-inflammation environment negates elevated LDL. The logic here is that atherosclerosis is fundamentally an inflammatory process since LDL particles must oxidise to provoke plaque formation. In a low-inflammatory environment, there may be less oxidative stress, so lower expression of plaque. The risk of plaque formation within a healthy environment drops a significant amount, however, assuming this risk becomes benign seems to be an overestimate from current genetic studies.

Therefore, current guidelines should declare that someone with high LDL but low CRP (the main inflammation blood marker) will have minimal risk of cardiovascular disease, but not zero risk.

Moreover, the protective factors don’t stop at CRP. We also have a lack of fermenting carbohydrates in the gut, adequate thyroid function, lean body mass and proper liver function to help reduce any inflammation in the body.

Taking someone who fits into this sphere, being an individual who is physically fit, low in body fat and has no inflammatory or genetic condition, how much saturated fat would they have to eat to increase their risk of heart disease? Well, raising someone’s LDL to 130mg/dL (borderline high) would require roughly 30-40g (20-27 eggs) of saturated fat every day for decades. And even then, with effective thyroid hormones, exercise, and a full nutritional profile, you’d likely need 40g+ before meaningful LDL-driven plaque progression.

Unfortunately, we cannot all be the so-called “healthy person”. Many of us live with genetic conditions, obesity, food disorders and lack of physical fitness. Therefore, it becomes vital to reduce the inflammation within our body, not simply reduce our saturated fat intake. In fact, sending the message to people that “reducing your cholesterol and saturated fat could save your life” is not beneficial to those involved. When an individual is at risk of a serious health condition, it is vital they are fully informed about the benefits of lowering bodily inflammation through a clean diet, exercise, reducing body fat, adequate sleep and (if you eat carbs) enough fibre.

However, for those who are not high-risk individuals, saturated fat and cholesterol are something that should not be feared unless you eat 40g+ daily. In fact, if you are metabolically healthy, there is no adequate evidence that eating a diet high in saturated fat and cholesterol is dangerous unless consumption levels reach extreme, and even then, good thyroid function and low CRP would almost negate it.

In conclusion, the long-standing fear around saturated fat and cholesterol is not as clear as most believe. While elevated LDL levels can increase cardiovascular risk, context matters. For the metabolically healthy individuals with low inflammation and good thyroid function, the risks associated with a higher saturated fat and cholesterol diet are minimal, and even then, the amount you would have to consume is unsustainable. Therefore, rather than focusing on reducing these vital nutrients, maintaining a healthy body fat amount, staying physically fit and managing inflammation are far more effective strategies for long-term heart health.