The Problematic Paradigm of LCL-C, Part 12

Part 12 - The Effects of Diet on LDL-C, As Told By Energy Delivery

Previous - Part 11 - The Effects of Diet on Markers of Cardiovascular and Metabolic Health

In the previous, penultimate section we touched on the ways in which macronutrient distribution affects common markers of cardiometabolic health. One incredibly popular marker still remains, though, and that is of course LDL-C.

There are a couple good reasons to save LDL-C for last. For one, it doesn’t move in a consistent direction with carbohydrate restriction in the way HDL-C, triglycerides, or blood sugar might – how it moves depends on who is restricting carbohydrates. But mostly, we’re discussing it last because this entire series focuses on the shortcomings of the modern cholesterol paradigm, in which LDL-C is the central player.

To be clear, I am not making the claim that nothing in the world aside from energy delivery affects LDL-C levels. For example, plant sterols (essentially the plant version of cholesterol, but not usable in the human body) lower LDL-C to a certain degree. But, as has been explained at length in this series, I am making the claim that energy delivery is the primary driver of LDL cholesterol levels. And furthermore, that this energy system is driven primarily by what you eat.

So…what happens to your LDL-C when you eat more carbs, or, perhaps, what happens when you eat less?

 

Personal Anecdote

Early last month I consumed a fairly prodigious amount of cheese (and more – the reasons why are here, but aren’t important) over the course of a weekend before having my blood drawn the next day. My LDL-C on that morning? 108mg/dl. This was on the heels of some significant fat consumption – a three day average of 192g of saturated fat, some 8 or 9 times more than the USDA recommend the average person eat in a day.

Just 13 days later, another blood draw returned an LDL-C of 180 mg/dl. In the intervening days, I consumed a maximum of 152g of saturated fat and averaged only 83g per day. Clearly, saturated fat consumption didn’t drive the extreme increase in LDL-C, as it is traditionally thought to do. So, what happened?

The important missing information is that the second blood draw came on day 3 of an extended fast, meaning I had literally consumed nothing – zero grams of fat – the two days prior. My LDL-C was elevated for the exact reasons that have been outlined at length in these writings – increasing LDL-C is an unavoidable consequence of utilizing fat for energy.

 

Low-Carb Trials and LDL-C

We don’t need to rely on my stories for evidence though – studies indeed demonstrate that healthy individuals will see a rise in LDL-C during extended fasting.^1,2 Healthy individuals moving to a very low-carbohydrate diet experience the same, just as we would expect.^3–7 Note the use of the word “healthy” here – these are individuals without significant metabolic dysfunction. They neatly fit the profile we’ve described of a metabolically healthy individual with excellent health markers that experience an increase in LDL-C as a consequence of trafficking triglycerides for energy.

But what if they weren’t healthy? Imagine instead a study that enrolled only those with metabolic dysfunction, obesity, and insulin resistance. These individuals might very well already have elevated LDL-C alongside poor markers of metabolic health, a consequence of poor triglyceride utilization, increased return of triglycerides to the liver, and compensatory VLDL production. The traditional cholesterol paradigm would likely be aghast at the suggestion that these individuals consume more fat, with their LDL-C already considered a risk to their health and the increased fat, surely, likely to elevate it even further.

But of course, this is not what happens. As many studies that demonstrated, the common finding in these individuals is indeed lower LDL-C following the transition to a low-carb, high-fat diet.^8–21 Of course, an energy delivery model of lipid metabolism explains clearly why this is the case – reduced blood sugar and insulin levels allow for improved fatty acid utilization, increased triglyceride clearance, reduced triglyceride return to the liver, and the gradual reduction of excess VLDL production. Much like my fasting example above, a traditional paradigm that suggests fat consumption as the prime driver of elevated LDL-C levels simply cannot explain these observations.

(You may notice here that these findings, taken together, suggest that over a long enough time frame an obese individual restricting carbohydrates would experience BOTH an initial decrease in LDL-C and then again increasing LDL-C levels following a return to normal weight and metabolic health. Of course, every other possible marker of health – HDL-C, triglycerides, blood sugar, body fat, blood pressure, etc. – would be much closer to optimal by the end of this journey)

 

Conclusion

If you’ve read the first eleven sections on this topic, nothing written above is surprising or even new. While the traditional paradigm continues to stress carbohydrate consumption in an effort to lower LDL-C, it is overwhelmingly clear that this approach may or may not have the desired effect but will certainly contribute to worsening metabolic health. I’ll end this series with the conclusion from my paper on cholesterol and lipid metabolism:

 

“This paper is absolutely not intended to make the argument that elevated LDL-C via an energy-driven increase in endogenous VLDL production is a metabolic state for which one need necessarily strive. Instead, this particular metabolic presentation is examined at length because it succinctly highlights the failure of the lipid-heart and diet-heart hypotheses that have undermined public health for decades. It is not a metabolic state towards which one needs to strive, but, far more importantly, it is also does not appear to be a metabolic state of which one needs to be afraid. The full body of scientific evidence, massive in both scope and depth, makes this incredibly clear.

What this paper is meant to argue is that the myopic focus on LDL-C and total cholesterol and the demonization of dietary fat must begin receding from medical, nutritional, and public consciousness if chronic health is to improve in western society. It is absolutely meant to highlight the indisputable evidence that every legitimate marker of chronic and cardiometabolic health – HDL-C, triglycerides, modified LDL particles, and others – has been repeatedly and overwhelmingly demonstrated to improve with a decrease in carbohydrate consumption. The understanding that poor triglyceride utilization, driven by insulin resistance and excess carbohydrate consumption, is the primary factor in metabolic dysfunction is crucial to recognizing the failure of conventional guidelines in addressing these risk factors. An energy deliver model of lipid metabolism best explains the available interventional evidence and wide range of lipid observations, existing in stark contrast to the abject catastrophe that is an entrenched paradigm of outdated and anti-scientific dogma pushing unsuspecting persons quickly and aggressively towards dyslipidemia, disease, and death.

The lipid-heart hypothesis has been allowed to survive for so long because the broad relationship between LCL-C and cardiovascular disease will always exist in an insulin resistant population that overconsumes carbohydrates. While the relationship is loosely valid in a diseased population, it should not be considered good enough for the purposes of preventing or especially treating cardiometabolic disease. Instead, the goal in both cases must be to prevent or reverse the underlying insulin resistance and the host of hyperglycemia-induced damages that occur alongside it. Only when this happens, when lipids are fairly viewed as an energy delivery system rather than as a disease state, can cardiovascular, metabolic, and chronic health truly be improved.”

 

 

Key takeaways

• LDL-C is increased when a metabolically healthy person significantly reduces carbohydrate consumption, either through fasting or a low-carb diet
• LDL-C is reduced when a person with poor metabolic health reduces carbohydrates, because previous elevations were driven by metabolic dysfunction rather than fat consumption
• Advocacy for an increase in carbohydrate consumption has variable effects on LDL-C, a marker with little to no independent relationship with cardiovascular disease, while clearly and consistently worsening every other marker of cardiometabolic health

 

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