Debunking Fat & Cholesterol Myths

Cholesterol-and-Fat-1

For decades, fat and cholesterol have been demonized as culprits for cardiovascular disease and obesity albeit for no good reason as there is no good scientific evidence to support these claims. Only recently has the mainstream science and nutrition community started to recognize that fat isn’t the issue. Instead, as researchers are finding, an increased risk of cardiovascular disease and obesity is more closely linked to the consumption of processed foods, higher intake of carbohydrates, as well as poor lifestyle choices. Let’s take a closer look!

Fat & Cholesterol – What Are They Exactly?

When talking about fat and cholesterol, we tend to lump the two together and think of them interchangeably. However, fat and cholesterol are very different. Fat is a macronutrient. Macronutrients are the nutrients we need in high amounts in our diets. They provide energy, often displayed in the form of “calories” on food labels. Fats are hydrocarbons, meaning they contain hydrogen and carbon components. The hydrocarbon chains that fats are comprised of determine their function and help differentiate between the supposed “good” and “bad” kinds of fats, unsaturated and saturated fat, respectively. The difference between saturated and unsaturated fats has to do with the difference in saturation of hydrogen atoms. Unsaturated fats contain a double bond, meaning they have fewer hydrogen atoms attached to the carbon atoms.1 Saturated fats contain no double bonds.

Cholesterol, on the other hand, is an organic sterol, which is a waxy, lipid substance. 25% comes from our diet, and the liver makes the other 75%.2 Cholesterol, unlike fat, does not provide energy to the body. There are two types of cholesterol, LDL, and HDL. LDL, or low-density lipoproteins, are often referred to as the “bad” cholesterol. HDL, or high-density lipoproteins, is considered to be the “good” cholesterol. HDL is considered “good” because it helps clear excess LDL from the bloodstream, sending it back to the liver to be broken down and excreted. As a side note, it is important to understand that LDL and HDL are not actually “cholesterol”. They are the proteins in the body that carry around cholesterol.

Despite the common belief that we should eliminate fat and cholesterol from our diets, we need to consume these in our diets for regular functioning and body processes. Fats protect your organs, provide energy, aid in hormone production, and help in the absorption of fat-soluble vitamins, such as vitamin A and K. Cholesterol is responsible for the production of sex hormones, building certain tissues throughout the body, and helping in the production of bile in the liver.3 It is also necessary for vitamin synthesis, cellular integrity and hormone synthesis. In fact, certain diseases, such as Smith-Lemli-Opitz Syndrome, where cholesterol cannot be synthesized properly leads to serious issues such as autism and reduced muscle.

Dietary Saturated Fat – Why the bad rap?

In the 20th century, heart disease became an epidemic amongst the American population. Statistics showed that it was the number 1 cause of death. Researchers made a correlation between the high consumption of saturated fat and heart disease because saturated fats were found, in the short-term, to be associated with increased total cholesterol. The problem(s)? There was no solid scientific evidence to back up these claims. The studies and evidence presented were based on animal trials and general assumptions. Experiments were never well controlled in these studies, and researchers never accounted for confounding factors. There was also no evidence from human studies to back up this saturated fat/heart disease hypothesis.

More specifically, researchers also failed to recognize that total “cholesterol” is a flawed marker of heart disease, because total cholesterol includes both “bad” LDL cholesterol, and “good” HDL cholesterol.

What researchers actually found is that, in the short term, saturated fat increases both HDL and LDL cholesterol, and HDL is associated with a lower risk of heart disease.

In reality, there is no such thing as “good” or “bad” cholesterol. You need both HDL and LDL for proper physiological function (LDL is good, and actually helps bring cholesterol into the cells and helps to maintain cellular fluidity). The only time cholesterol is “bad” is when it ends up in the wrong places. Under the influence of inflammation and other factors, this can result in plaque buildup in arterial walls, causing blockages and wreaking havoc on the cardiovascular system. More importantly, it turns out that the type of cholesterol that increases the risk of developing arterial plaques is small sized, dense, LDL particles, in high numbers. The reason for this is that smaller sized LDL particles have a higher chance of being absorbed in the arterial wall becoming oxidized, which is a critical step in the development of atherosclerosis. Larger LDL particles are less susceptible to arterial wall penetration and oxidation. Furthermore, the larger the number of these smaller particles, the higher the chances of these processes occurring.

Interestingly, researchers have found that in the short-term, saturated fat consumption actually helps convert small LDL particles to larger particles.4,5,6 Researchers have actually found that low-carb diets, high in saturated fats, can reduce the risk of heart disease significantly due to the favourable cholesterol profiles obtained following these diets; fewer numbers of small LDL particles, and higher numbers of large LDL and HDL particles.7,8 Low-fat diets do NOT reduce the amount of small LDL particles, and actually, have been shown to result in an unfavorable lipid profile (high small LDL, low HDL, and increase triglycerides).9,10 

There are a few large studies (systemic reviews and meta-analyses) that take an in-depth look into all of the data obtained to date on observational studies and controlled trials about saturated fat and heart disease. Here are there conclusions:

  1. A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.11
  2. Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.12

Perhaps most importantly, a recent scientific study from 2017 explored macronutrients and their relationship to mortality and cardiovascular disease from 18 countries in 5 different continents. They concluded the following:

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”13

Dietary Cholesterol

We’ve already covered why cholesterol is good, and identified that the only time cholesterol is potentially “bad” is when you have an increased number of small-sized LDL particles. Even in these scenarios, this doesn’t mean you will get heart disease, but that you are increasing your risk of heart disease. In fact, cholesterol-lowering therapies do not lower risk of cardiovascular disease.14 Heart disease is a complex phenomenon, and researchers are finding out that it is driven by a variety of factors, including inflammatory and autoimmune factors, as well as genetic and epigenetic factors.

But what about the cholesterol in our diet? Does this impact our cholesterol levels?

It turns out that dietary cholesterol actually has no impact on our blood cholesterol levels. Only a small portion of the cholesterol from our diet actually gets absorbed into the body. Furthermore, when our bodies sense low levels of cholesterol, they ramp up cholesterol synthesis to make up for the lack of cholesterol. In fact, avoidance of dietary cholesterol can result in malnutrition, due to the reduced consumption of healthy foods that also happen to contain cholesterol, and even increased risk of heart attacks.15,16

The most important factors for achieving ffavourableblood cholesterol profiles appear to be of epigenetic origin, and include: 1) decreasing the amount of dietary carbohydrates, 2) elimintation of processed foods, 3) avoidance of inflammatory foods, 4) positive lifestyle choices (like increased exercise frequency).17,18,19,20

Genetics or hereditary factors also play a role in blood cholesterol profiles. The liver is a key player in cholesterol homeostasis and LDL and HDL production, and individuals with genetic conditions that affect the liver are more susceptible to cholesterol issues.21

The Bottom Line

Cholesterol and fat do a whole lot of good for our bodies. Without them, we would have many problems functioning properly. Don’t believe everything you read. Do your research and stay educated about what foods you are putting in your body!

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What Is Cholesterol? A Brief Background & A Few Fun Facts

Cholesterol

Cholesterol is a sterol. A sterol is a naturally occurring unsaturated steroid alcohol. Sterols are typically waxy solids, and they are part of the steroid family.

The diagram for cholesterol is below.

Cholesterol-2

The reason cholesterol is called a steroid “alcohol” is because of the presence of the hydroxyl group (the “OH” group in the diagram, circled in red). This hydroxyl group is one of the main functional groups of cholesterol, and this is the site that determines whether the cholesterol is in its active form, or storage form (the storage form is called “cholesterol ester”).

Sterols are produced by all types of life, including plants, animals, bacteria, and fungi. However, cholesterol, specifically, is unique only to animals. You may have heard of phytosterols, and these are the analogs of “cholesterol” that the plant kingdom makes.

Phytosterols in brief

Our bodies can’t properly absorb phytosterols. In fact, they compete with cholesterol absorption. Phytosterols have actually been used in attempt to “lower” the cholesterol absorbed from our diet because phytosterols displace cholesterol from micelles which are the in the gut (cholesterol micelles are formed when we break down hydrophobic foods in the stomach such as fats and cholesterol). The theory goes that reducing cholesterol from the diet will reduce blood cholesterol levels and reduce risk of developing cardiovascular disease. However, these attempts don’t make much sense in light of the following two key facts:

  1. The amount of cholesterol we get from our diet is significantly less than the amount that is synthesized by our cells. Moreover, if our cells sense low levels of cholesterol, they will ramp up attempts to synthesize more cholesterol.
  2. Cholesterol and lipid-lowering therapies have NO impact on reducing the risk of cardiovascular disease.

Back to cholesterol…

Cholesterol is necessary for life. Without it, we wouldn’t have functioning cells and cellular systems. Cholesterol is one of the main building blocks of our cell membranes. It is vital for carefully controlling cell membrane fluidity, how cells interact with other cells, and how the cell transport nutrients and other compounds from inside and outside. Furthermore, cholesterol is necessary for vitamin synthesis and is the precursor to sex hormones (progesterone, testosterone and estradiol) and bile acids. In short, your body NEEDS cholesterol. It is necessary for life. And it is a good thing.

In fact, lack of cholesterol can cause malnutrition. Furthermore, individuals with Smith-Lemli-Opitz syndrome have genetic mutations that prevent them from properly synthesizing cholesterol, and this can lead to mental disabilities and skeletal muscle issues

Overall, there is no such thing as good or bad cholesterol. Cholesterol wrongfully gets a bad rap for being a culprit of atherosclerosis and cardiovascular disease because it is present in atherosclerotic plaques. However, cholesterol itself is not to blame. To date, evidence does NOT support a link between dietary cholesterol and cardiovascular disease.

The only time cholesterol is “bad” is when it ends up in a place where it doesn’t belong, like an artery wall, during periods of inflammation. When this occurs, it can initiate the process of atherosclerosis. This is not the normal fate of cholesterol, however. Atherosclerosis only occurs in states of inflammation where cholesterol ends up in the wrong places.

How and why does cholesterol end up in the wrong places? In short, metabolism and epigenetics play a big role. However, this will be discussed in detail in a later post. In the meantime, stay tuned!

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Why Eating or Avoiding Dietary Cholesterol Has No Effect on Blood Cholesterol Levels

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Avoiding Cholesterol

Cholesterol synthesis and metabolism are tightly regulated within the human body. It turns out that when the cell senses low levels of cholesterol, our body initiates cholesterol synthesis (via the SREBP system) as well as processes to enhance the uptake of cholesterol. Thus, avoiding dietary cholesterol in an attempt to lower blood cholesterol levels doesn’t make much sense in light of this ability of our body to regulate cholesterol synthesis. Any attempt to lower cholesterol in the body would be counteracted by the body ramping up cholesterol production and uptake.

Eating Cholesterol

This is a quote from Metabolic Regulation: A Human Perspective by biochemist Keith N. Frayn (my emphasis added):

Perhaps surprisingly, the amount of cholesterol in the diet is not a major factor affecting the blood cholesterol concentration. The amount of cholesterol we eat is not large in comparison with the body pool: we eat less than 1g per day whereas the amount of cholesterol in the body is more like 140g, of which about 8g is present in the plasma. Contrast this with glucose, where we eat several “plasma’s-worth” in a single meal. And cholesterol is not rapidly absorbed like glucose: it enters the plasma slowly, even more so than triacylglycerol. Further, cholesterol intake leads to cholesterol entering cells, which effectively suppresses cholesterol synthesis. The blood cholesterol concentration is related far more closely to the dietary intake of particular fatty acids, especially the ratio of saturated to polyunsaturated fatty acids.” 

So, the cholesterol that we eat pales in comparison to that stored in our bodies. Again, cholesterol synthesis and transport in the body is a highly regulated process. As mentioned in this video by Dr. Peter Attia, cholesterol levels in the body are not that influenced by the cholesterol in our diet, since a majority of the cholesterol from our diet is in the form of cholesterol ester, which is the storage form of cholesterol which doesn’t get absorbed by our gut. The unesterified active version of cholesterol in our diet does get absorbed. And again, the amount of active absorbable cholesterol in the diet is very small in comparison to the amount stored and synthesized by our bodies; on a daily basis, we typically get ~300-500mg of cholesterol from our diet, whereas we synthesize ~800-1,200mg of cholesterol in our cells per day.

As Dr. Attia suggests in the video, the total store of cholesterol in the body is akin to a giant swimming pool, and there are two very small hoses that contribute to, and control, the swimming pool levels: an internal hose (cholesterol synthesis) and an external hose (cholesterol input from diet). Anything in biology that resembles this situation, with a large store of something with two very small contributing inputs, suggests that the system is highly regulated and that what is moving the “cholesterol needle” isn’t the small inputs (diet and internal synthesis) but something else…

Bottom Line

Avoiding cholesterol, or eating cholesterol, does not have a profound impact on blood cholesterol levels. Any cholesterol that is indeed present blood is carefully controlled by the cholesterol transport system. Furthermore, cholesterol isn’t “bad”, and avoidance of dietary cholesterol can be problematic. In fact, genetic deficiencies in cholesterol synthesis pathways can lead to conditions that can cause mental disabilities and skeletal muscle problems.

Cholesterol is vital, and cells need cholesterol to function (cholesterol is actually part of the structural makeup of cells). It’s not the presence of cholesterol in the blood that matters, it’s the type, amount, and size of that cholesterol that matters. “Cholesterol” in the blood only becomes “dangerous” if the LDL, which is a protein/cholesterol complex, increases in number, and decreases in particle size.

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NOTE: Nothing in this post is written or intended to be medical advice or to replace medical advice. We are not doctors. We are merely individuals with a passion for health, fitness, nutrition, and scientific research.