Does Saturated Fat Really Raise Cholesterol and Cause Heart Disease?
Does Saturated Fat Really Raise Cholesterol and Cause Heart Disease?
TL;DR
Cholesterol doesn't cause heart disease. Oxidized cholesterol from inflammation does. PUFAs oxidize LDL particles, creating arterial damage. Saturated fat raises cholesterol slightly but makes it large, fluffy, and protective. Small, dense oxidized LDL (from PUFAs and inflammation) causes atherosclerosis. Eat saturated fat, eliminate PUFAs, inflammation drops, heart disease risk plummets.
Your doctor called.
Your cholesterol is high. Total cholesterol: 250. LDL: 160.
She wants you on statins. Cut the butter. Eat more vegetable oil.
You've been following SugarSaint. Eating butter, eggs, meat. You feel incredible.
Now you're scared. Is the saturated fat killing you?
No. The test doesn't measure what you think it measures.
Cholesterol is like a firefighter at a fire. Blaming cholesterol for heart disease is like blaming firefighters for burning buildings.
What Cholesterol Actually Does
Cholesterol is essential. You die without it.
What cholesterol does:
- Makes cell membranes (every cell needs it)
- Produces hormones (testosterone, estrogen, progesterone, cortisol)
- Makes bile acids (digest fats)
- Synthesizes vitamin D (from sun exposure)
- Repairs damaged tissue (cholesterol accumulates at injury sites)
Your liver makes 80% of your cholesterol. Food contributes 20%. If you eat less, your body makes more.
Why cholesterol goes to arteries: To repair damage. The damage comes from inflammation and oxidative stress. PUFAs cause both.
The Real Cause of Heart Disease
Heart disease (atherosclerosis) is arterial damage.
The actual process:
- Artery walls get damaged (from inflammation, oxidative stress, high blood pressure)
- LDL particles enter the damaged area to repair it
- If LDL is oxidized (from PUFAs), it can't leave
- Oxidized LDL triggers immune response
- Macrophages eat oxidized LDL
- Macrophages become foam cells
- Foam cells accumulate (plaque forms)
- Artery narrows
- Plaque ruptures
- Blood clot forms
- Heart attack or stroke
The problem isn't cholesterol. It's oxidized cholesterol and arterial inflammation.
What causes oxidation and inflammation?
- PUFAs (seed oils)
- High blood sugar from insulin resistance (caused by PUFAs)
- Smoking
- Chronic stress
- Poor sleep
- Sedentary lifestyle (but not overtraining)
Saturated fat doesn't cause any of these.
What Standard Cholesterol Tests Actually Measure
Total cholesterol: Sum of LDL + HDL + VLDL. Mostly meaningless. Tells you nothing about particle size or oxidation.
LDL (low-density lipoprotein): Called "bad" cholesterol. Except it's not cholesterol—it's a protein that transports cholesterol. And it's not inherently bad.
HDL (high-density lipoprotein): Called "good" cholesterol. Transports cholesterol back to liver. Higher is generally better.
Triglycerides: Fat in blood. High triglycerides indicate poor glucose metabolism and insulin resistance (from PUFAs). Should be below 100, ideally below 70.
What they DON'T measure:
- LDL particle size (large vs. small)
- LDL particle number
- Oxidized LDL
- Inflammation (hs-CRP)
- Insulin resistance (fasting insulin)
These matter more than total cholesterol.
Large vs. Small LDL Particles
Not all LDL is the same.
Large, fluffy LDL (Pattern A):
- Big particles
- Don't penetrate artery walls easily
- Don't oxidize easily
- Protective
- Associated with saturated fat intake
Small, dense LDL (Pattern B):
- Tiny particles
- Penetrate artery walls
- Oxidize easily
- Cause atherosclerosis
- Associated with high carb + PUFA intake, insulin resistance
Saturated fat increases large LDL. This is good. It's protective.
PUFAs and high insulin increase small LDL. This is bad. This causes heart disease.
Standard cholesterol tests don't distinguish between these. Your doctor sees "high LDL" and panics. She doesn't know if it's large (good) or small (bad).
Better Tests to Request
Advanced lipid panel:
- LDL particle number (LDL-P)
- LDL particle size
- ApoB (protein on LDL particles, correlates with particle number)
- Lp(a) (genetic risk factor)
Inflammation markers:
- hs-CRP (high-sensitivity C-reactive protein) - should be below 1.0, ideally below 0.5
- Homocysteine - marker of inflammation and B vitamin status
Metabolic markers:
- Fasting insulin - should be below 5, ideally below 3
- HbA1c - should be below 5.5%
- Triglycerides - should be below 100
Calcium score (CT scan):
- Measures actual arterial calcification
- Score of 0 = no plaque
- Best indicator of actual heart disease risk
These reveal your actual risk. Total cholesterol doesn't.
What Happens When You Eat Saturated Fat
Short-term (weeks):
- Total cholesterol might increase slightly
- LDL might increase slightly
- HDL increases (good)
- Triglycerides drop (good)
- Inflammation markers drop (hs-CRP)
Long-term (months):
- LDL particle size shifts to large, fluffy type
- Insulin sensitivity improves (triglycerides drop further)
- Oxidative stress decreases
- Actual heart disease risk decreases despite higher cholesterol number
Studies show:
- Populations eating high saturated fat (Kitavans, Masai, Tokelauans) have low heart disease
- Saturated fat intake doesn't correlate with heart disease in large studies
- Replacing saturated fat with PUFAs increases heart disease risk in some trials
The cholesterol-heart hypothesis is outdated. Data doesn't support it.
What About Statins
Statins lower cholesterol by blocking liver production.
Benefits:
- Lower LDL (number on paper)
- Small reduction in heart attack risk (mostly in men with existing heart disease)
Downsides:
- Block CoQ10 production (needed for mitochondrial energy)
- Cause muscle pain and weakness in many people
- Cognitive side effects (brain needs cholesterol)
- May increase diabetes risk
- Deplete fat-soluble vitamins
- Don't address root cause (inflammation and oxidation)
Who might benefit:
- Men with existing heart disease
- People with familial hypercholesterolemia (genetic condition)
- High-risk individuals who won't make lifestyle changes
Who probably doesn't benefit:
- Healthy people with slightly elevated cholesterol
- Women (less evidence of benefit)
- People willing to optimize metabolism and eliminate PUFAs
Work with your doctor. Don't stop statins without supervision. But understand they're not fixing the root problem.
How to Actually Reduce Heart Disease Risk
Eliminate PUFAs. Stop eating seed oils. This stops LDL oxidation. This stops arterial inflammation. This is the single most important change.
Eat saturated fats. Butter, coconut oil, ghee, animal fats. These make stable, non-oxidizing LDL particles.
Improve insulin sensitivity. Fix PUFA-induced insulin resistance. Lower blood sugar. Lower triglycerides. This reduces small, dense LDL.
Support thyroid function. Thyroid hormone regulates cholesterol metabolism. Low thyroid = high cholesterol. Fix thyroid, cholesterol often normalizes.
Reduce inflammation. Sleep well. Manage stress. Fix your gut. Track hs-CRP to monitor.
Exercise appropriately. Walking and strength training improve metabolic health. Chronic cardio can worsen things. Find balance.
Don't smoke. Obvious but important. Smoking directly damages arteries.
Most people see improved cardiovascular markers within 3-6 months:
- Triglycerides drop
- HDL rises
- hs-CRP falls below 1.0
- Insulin sensitivity improves
- Blood pressure normalizes
LDL might stay elevated. That's fine if it's large particles and inflammation is low.
FAQ
Q: My doctor says I need statins because my LDL is 180. What do I do? A: Request advanced testing (LDL-P, particle size, hs-CRP, fasting insulin, calcium score). If you have large LDL, low inflammation, and no arterial calcification, your risk is low despite high LDL number. Discuss with your doctor. Consider a second opinion from a lipidologist who understands advanced testing.
Q: Can I eat unlimited saturated fat? A: Eat to satiety. Most people naturally eat 100-150g fat per day on this approach. There's no evidence high saturated fat intake is harmful when PUFAs are eliminated and metabolism is healthy.
Q: What if I have familial hypercholesterolemia (genetic high cholesterol)? A: This is a special case. You genuinely have elevated LDL from birth. You still benefit from eliminating PUFAs (reduces oxidation of that LDL). You might need medication (statins or PCSK9 inhibitors). Work with a knowledgeable cardiologist.
Q: Should I worry about dietary cholesterol from eggs? A: No. Dietary cholesterol has minimal effect on blood cholesterol for most people. Eat eggs. They're nutrient-dense. The yolks contain choline, vitamin A, and healthy fats your body needs.
This isn't medical advice. I'm not your doctor. Work with a qualified healthcare provider for cardiovascular health management.
Want the complete cardiovascular health optimization protocol?
The SugarSaint course includes detailed strategies for reducing actual heart disease risk through PUFA elimination, insulin sensitivity improvement, inflammation reduction, and metabolic optimization.
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