Why We Got Saturated Fat Wrong

How LDL-C Focus Misled Us—and Why Carbs Matter More

For 50 years, we have been taught a simple story: Eating saturated fat raises your LDL cholesterol, and high LDL causes heart disease.

Therefore—so the logic goes—foods like eggs, red meat, butter, and full-fat dairy must be harmful.

This idea shaped dietary guidelines, food policy, and public fear. But today, the science tells a very different story—one that’s more interesting, more hopeful, and far more accurate.

The Real Problem: We Focused on LDL-C Instead of Metabolism

LDL cholesterol (“bad cholesterol”) became the center of cardiovascular prevention beginning in the 1960s. But as a growing number of researchers now show, including the American Heart Association itself, LDL-C was a poor marker for evaluating dietary risk.

Two recent comprehensive reviews—one by Nina Teicholz and another by Astrup and colleagues in the Journal of the American College of Cardiology—make the same point:

The saturated-fat–LDL story was built on weak evidence.When better trials were finally done, reducing saturated fat did NOT reduce heart disease.

Even more surprising: whole foods rich in saturated fat (full-fat dairy, cheese, yogurt, unprocessed meat, dark chocolate) consistently show neutral or beneficial effects on heart disease and diabetes risk.

So why did LDL-C lead us astray?

Because LDL-C changes tell us almost nothing about the quality of LDL particles, the metabolic environment in which they circulate, or the inflammatory signals that make them harmful.

As the new evidence shows, the body’s internal metabolic state—not dietary saturated fat—is what determines LDL behavior.

And nothing influences that metabolic state more strongly than carbohydrates, insulin signalling, and energy overload.

The Breakthrough Study: Carbohydrates, Not Saturated Fat, Raise Blood Saturated Fat

One of the most striking pieces of evidence comes from a controlled feeding study by Volk et al. (PLoS ONE). Sixteen adults with metabolic syndrome were fed diets ranging from very-low-carb to high-carb, while saturated fat intake moved in the opposite direction.

Here’s what they found:

1. Eating more saturated fat did NOT increase saturated fat in the blood.

When saturated fat intake nearly doubled—from 46 to 84 grams per day—blood saturated fats did not increase.

2. But when participants ate more carbohydrate, their blood saturated fats rose.

As carbs increased from 47 to 346 grams per day, the body produced more saturated fat internally through a process called de novo lipogenesis.

The biomarker that tracked this shift was palmitoleic acid, which rose steadily as carbohydrate intake increased—and is strongly associated with:

• insulin resistance

• inflammation

• type 2 diabetes

• metabolic syndrome

• cardiovascular disease

In other words:

Carbohydrates—not saturated fat—drive the production and accumulation of harmful saturated fats in the bloodstream.

This turns the old narrative on its head.

How Did We Get It So Backwards?

Because for decades, we looked at LDL-C as if it were a simple gauge of dietary risk. The logic was: saturated fat raises LDL-C → therefore saturated fat is harmful.

But now we know:

1. LDL-C is not the strongest predictor of heart disease.

ApoB particle number, inflammation, and insulin resistance explain far more risk.

2. Saturated fat changes LDL-C mostly by increasing large, buoyant LDL particles, which are far less harmful than the small, dense particles produced during carbohydrate overload.

3. The foods highest in saturated fat are often nutritionally dense, anti-inflammatory, and metabolically stabilizing when eaten as whole foods.

Meanwhile, diets high in refined carbohydrates raise insulin, increase liver fat production, elevate circulating saturated fats, and drive the inflammatory state that makes LDL particles dangerous.

It’s Time to Shift the Question

Instead of asking:

“How much saturated fat did you eat?”

We should be asking:

“Why is the body producing so much internal saturated fat?”

“Is excess carbohydrate overwhelming the liver?”

“Is there metabolic inflammation or energy imbalance?”

This shift isn’t theoretical—it is already reflected in modern cardiometabolic research, which increasingly recognizes:

• carbohydrate intolerance

• insulin resistance

• mitochondrial overload

• inflammatory stress

as the real engines behind cardiovascular disease.

Saturated fat is not the villain we once imagined. In the right metabolic context—especially when carbohydrate intake is controlled—saturated fat is simply one of the body’s many energy substrates.

The New Takeaway for the Public

Here’s the simplest way to say it:

Your blood saturated fat is influenced far more by what your body makes from excess carbohydrates than by the saturated fat you eat.

And:

LDL-C alone is an outdated lens for evaluating diet and heart disease.Metabolic health matters more.

This doesn’t mean everyone should eat unlimited saturated fat. Context always matters. But the science is now clear:

It’s time to stop fearing saturated fat—and start paying attention to carbohydrates, insulin, and metabolic inflammation.

This is not just a correction of dietary dogma.

It’s an opportunity to rebuild public health on stronger, more accurate science.

Teicholz, N. (2023). A short history of saturated fat: The making and unmaking of a scientific consensus. Journal of Lipid Research, 64(11), 100392. https://doi.org/10.1016/j.jlr.2023.100392

Astrup, A., Magkos, F., Bier, D. M., Brenna, J. T., de Oliveira Otto, M. C., Hill, J. O., King, J. C., Mente, A., Ordovas, J. M., Volek, J. S., Yusuf, S., & Krauss, R. M. (2020). Saturated fats and health: A reassessment and proposal for food-based recommendations. Journal of the American College of Cardiology, 76(7), 844–857. https://doi.org/10.1016/j.jacc.2020.05.077

Volk, B. M., Kunces, L. J., Freidenreich, D. J., Kupchak, B. R., Saenz, C., Artistizabal, J. C., Fernandez, M. L., Bruno, R. S., Maresh, C. M., Kraemer, W. J., Phinney, S. D., & Volek, J. S. (2014). Effects of step-wise increases in dietary carbohydrate on circulating saturated fatty acids and palmitoleic acid in adults with metabolic syndrome. PLOS ONE, 9(11), e113605. https://doi.org/10.1371/journal.pone.0113605