The Cholesterol Paradox, Part 2

This is part of a series of posts where I share and dissect information about cholesterol, the science behind cholesterol, and common fallacies surrounding cholesterol. Most of these posts are going to be short… where I just share bits of information that I’ve archived or that I’ve recently found, and some thoughts surrounding them. For Part I of this series, click here.

For this post, I want to reflect on a quote from Metabolic Regulation: A Human Perspective by 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. As mentioned in this video by Dr. Peter Attia, cholesterol synthesis and transport in the body is a highly regulated process and is not that influenced by the cholesterol that we eat in food. And any cholesterol that is indeed present blood is carefully controlled by the cholesterol transport system. But keep in mind it’s not the presence of cholesterol in the blood that matters, it’s the amount and type of that cholesterol that matters (specifically the size and number of LDL particles are what matters, but we will dive into that in another post). Cholesterol is vital, and cells need cholesterol to function (cholesterol is actually part of the structural makeup of cells). “Cholesterol” in the blood only becomes “dangerous” if the LDL, which is a protein/cholesterol complex, increases in number, and decreases in particle size.

As Keith states, the way cholesterol is processed from our diet significantly contrasts with that of glucose (sugar). When we eat a typical meal, which usually contains large amounts of sugar and/or carbohydrate (which breaks down into sugar), our blood glucose levels rise and insulin is released in order to control this. It is well known that elevated blood sugar and/or chronically elevated insulin lead to a variety of health problems including diabetes, cancer, heart disease, and chronic inflammatory disease. In light of this, we should most likely be concerned with the amount of sugar/carbohydrate that we consume as opposed to the cholesterol that we consume.

Keep in mind that cholesterol is not the same as fat, and as Keith mentions above, the quality, type and amount of fat that we consume influences the cholesterol levels in our body. But more importantly, and what he doesn’t mention in that particular quote, is that dietary fat only becomes a “concern” if it is consumed in the presence of sugar and/or carbohydrate: when dietary fat is consumed along with sugar/carbohydrate, fat is preferntially stored and the sugar is preferentially “burned”, this being due to the fact that elevated blood sugar and insulin lead to a switching of a cells fuel preference… leading to sugar burning and fat storing, and eventually a dysregulated fat metabolism (as opposed to normal/healthy fat metabolism). This sustained reliance of cells on sugar consumption and fat storage is what leads to problems (via sustained elevation of insulin and eventual development of insulin resistance). In this case, the fat isn’t what causes the issue, it is the “sugar” that causes a cascade of issues (this is why populations consuming “Western” diets of high carb and high fat have higher rates of disease incidence).

There is plenty evidence that shows that dietary fat is not the enemy we once thought, and I’ll conclude this post with some links supporting this:

Notes regarding Pulmonary Hypertension:

  • I strongly believe that metabolic and dietary interventions can improve health conditions and heal individuals with health issues. But, while it is evident from the above links that high fat/low carb diets (like ketogenic diets) are healthy and show promise for cancer, it is NOT evident that this is healthy for Pulmonary Hypertension. I do suspect that low carb only diets (meaning diets low in carb but no elevation in fat content) are healthy for PH, since any dietary intervention that lowers blood glucose and insulin improves health outcomes. And since PH patients typically show insulin resistance and cellular dependence on glycolysis (in pulmonary vasculature) this is further evidence that low carb dietary interventions could be beneficial. However, PH patients have a dysregulated fat metabolism as well, and in light of this, a high fat/low carb diet could be a potential problem. I personally don’t suspect this to be the case, but there is more research to be done… If anything, if ketogenic diets do prove to be unhealthy, I believe the reason for this is only that PH patients can’t process “fat” in the same way that normal individuals do. However, the byproduct of fat metabolism, ketones, could still be very beneficial and there may be a way to bypass fat metabolism but still get the benefits of fat by taking exogenous ketones. I’ll write more about this later…

NOTE: Nothing in this post is written or intended to be medical advice. These are my own thoughts and opinions based on my research. I am not a doctor. I am merely a scientist with a passion for Pulmonary Hypertension.


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