Introduction: Beyond the Cholesterol Myth
You’ve likely heard that high cholesterol—especially LDL, the “bad” kind—spells doom for your heart. It’s a story rooted in the lipid hypothesis: eating fat raises LDL, clogging arteries and inviting heart disease. But what if that’s not the full picture?
Dr. Paul Mason and Professor Tim Noakes challenge this narrative. Mason, a physician, argues your standard cholesterol test reveals your true health status through tools like the triglyceride-to-HDL ratio. Noakes, a National Research Foundation A1-rated scientist and emeritus professor at the University of Cape Town with over 750 publications, calls the cholesterol theory “at best tenuous, at worst wrong,” pointing to insulin resistance from high-carb diets—not cholesterol—as the real driver of heart disease, a stance he’s championed for decades.
Together, they urge a rethink—forget the old scare tactics and use your numbers to uncover what’s really going on.
Measuring Your Triglyceride-to-HDL-to-LDL Ratio
Your cholesterol test isn’t just about total LDL—it’s a window into deeper risks. The triglyceride-to-HDL ratio, paired with LDL insights, reveals whether your LDL is healthy or a hidden threat. Here’s how to calculate it, tailored to your region’s units, and what it means for your heart health.
Step 1: Get Your Numbers
Request a standard lipid panel from your doctor, which includes triglycerides, HDL (high-density lipoprotein), and LDL (low-density lipoprotein). These are reported in mmol/L (millimoles per liter) or mg/dL (milligrams per deciliter), depending on your country. Check your lab report or ask your healthcare provider for these values.
Step 2: Calculate the Triglyceride-to-HDL Ratio
Divide your triglyceride level by your HDL level. The result varies by unit system—here’s how it breaks down, with an example featuring Jane, a 45-year-old woman worried about her health risks:
Canadian Results (mmol/L)
Units used in Canada, Australia, UK, and most of Europe.
Example: Jane’s lipid panel in Canada shows:
Triglycerides: 1.5 mmol/L
HDL: 1.5 mmol/L
LDL: 3.4 mmol/L (approx. 130 mg/dL)
Ratio = 1.5 ÷ 1.5 = 1.0
Interpretation:
Below 0.9: Suggests healthy, large, buoyant LDL—low risk to heart, brain, and organs.
Above 0.9: Indicates a higher chance of small, dense LDL—damaged particles that can form clots, threatening any organ, including heart and brain. Jane’s 1.0 is borderline, hinting at potential trouble if it worsens.
Triglycerides Alone: Below 0.8 mmol/L predicts low small dense LDL risk; above 2.8 mmol/L flags danger—Jane’s 1.5 is moderate but worth watching.
US Results (mg/dL)
Units used in the United States, parts of Latin America, and some Middle Eastern countries.
Example: After moving to the US, Jane’s diet shifts to more processed carbs, and her new test shows:
Triglycerides: 133 mg/dL
HDL: 58 mg/dL
LDL: 130 mg/dL
Ratio = 133 ÷ 58 = 2.3
Why It Worsened: Jane’s higher triglycerides (up from Canada’s equivalent) and steady HDL reflect a jump in small, dense LDL risk—likely from increased sugar and carbs in the US, stressing her system.
Interpretation:
Below 2.0: Suggests healthy LDL—low risk.
Above 2.0: Signals small, dense LDL risk—Jane’s 2.3 shows damage that could clog arteries to her heart, brain, or other organs via blood clots.
Triglycerides Alone: Below 70 mg/dL predicts low risk (near zero at <40 mg/dL); above 250 mg/dL is high risk—Jane’s 133 mg/dL is mid-range but trending toward trouble.
Step 3: Check LDL Context
Jane’s LDL of 130 mg/dL (3.4 mmol/L) might alarm traditional doctors in both countries, but it’s the ratio that matters. A high triglyceride-to-HDL ratio with this LDL suggests small, dense particles—risky despite “normal” levels—while a low ratio points to harmless, large LDL. LDL alone doesn’t tell the whole story; it’s included here to show how it fits with the ratio.
Why It Matters
Studies show this ratio is more indicative than total LDL in predicting heart disease. Jane’s borderline Canadian ratio (1.0) grew to an elevated US ratio (2.3) after her move, signaling damaged LDL that raises risks not just to her heart but also her brain and other organs—blood clots from these particles can shut down any system. Triglycerides over 2.8 mmol/L (250 mg/dL) or HDL below 1.3 mmol/L (52 mg/dL) amplify this warning, making the ratio a practical tool to assess your real status.
Why LDL Isn’t the Villain You Think
The lipid hypothesis blames LDL for artery plaques, but evidence flips the script. A review of 19 studies with over 68,000 people found those with the highest LDL lived longest—16 studies linked higher LDL to a 50% lower death risk, even excluding heart disease patients. LDL isn’t a death sentence; it’s a complex lipoprotein—fat, cholesterol, and protein—made by your liver to deliver lipids to tissues. It starts as VLDL, shrinks to IDL, then LDL, recycling back to the liver. Blaming it for heart disease is like blaming a delivery truck for traffic jams—correlation, not causation.
The Real Culprit: Damaged LDL
Not all LDL is equal. Healthy LDL (large, buoyant) doesn’t harm you—studies show no heart risk increase with higher levels. But when LDL’s protein (ApoB100) gets damaged, it can’t return to the liver, piling up as small, dense particles. These rogue particles, not total LDL, drive heart disease:
A 15-year study of 28,000 women found high LDL particle counts doubled heart risk 2.5 times, while LDL volume didn’t predict anything.
A Japanese study showed those with the most small dense LDL faced 5x the heart disease odds.
Triglycerides above 2.8 mmol/L (250 mg/dL) or HDL below 1.3 mmol/L (52 mg/dL) hint at this damage—your ratio tells the tale.
Diet Myths: Fat and Cholesterol Don’t Raise LDL
Forget the old advice to ditch butter and eggs. Studies bust the myth:
Patients ate 35 eggs daily (7000 mg cholesterol) for a month—LDL stayed normal.
Coconut oil (94% saturated fat) lowered LDL, while butter (66% saturated) raised it—saturated fat’s effect isn’t simple.
High-carb, high-sugar diets do more harm—spiking triglycerides and small dense LDL—than saturated fats ever could. Glycated hemoglobin (HbA1c), a marker of unused sugar sticking to proteins, damages arteries over time, raising heart risk more than dietary cholesterol. This explains why diabetics, with often elevated HbA1c, face a 5x higher heart disease risk—sugar, not fat, is the bigger threat.
LDL rises not from dietary fat but from liver production (VLDL) or poor recycling—factors like insulin resistance and high blood sugar, not your steak, drive it.
Hidden Drivers of High LDL
High LDL isn’t always benign—it can signal trouble:
Insulin Resistance: Boosts VLDL production, raising LDL—linked to high dairy intake in studies, though less severe than sugary Western diets.
B12 Deficiency: Increases cholesterol synthesis, pushing LDL up—standard tests miss many cases due to outdated ranges.
Inflammation: Proteins like tumor necrosis factor-alpha (from inflammation) overproduce VLDL, spiking LDL up to 9x normal in animal studies.
Triglyceride Spikes: Beyond carbs/alcohol, underactive thyroid, kidney disease, diabetes, hemochromatosis, or drugs (beta-blockers, corticosteroids) elevate them.
Seed Oils & Plant Sterols: Diets high in refined seed oils (e.g., soybean, corn) contain pseudo-plant cholesterol (phytosterols) that block the liver’s uptake of oxidized LDL, leaving it in circulation to damage the cardiovascular system.
Check these if your LDL or ratio looks off—don’t just blame cholesterol.
Putting It All Together
Your cholesterol test isn’t a death warrant—it’s a tool. Total LDL might not kill you; in fact, it’s often tied to longevity. But damaged, small dense LDL—flagged by a high triglyceride-to-HDL ratio—raises real red flags. Forget the fat phobia—dietary cholesterol in the form of saturated fat isn't the culprit. Instead, watch for insulin resistance, B12 gaps, or inflammation. Use your numbers to dig deeper, and you’ll uncover your real heart health status—not the outdated myth.
Research reveals a striking fact: 75% of heart attack victims have “normal” cholesterol levels—likely meaning total cholesterol, not the triglyceride-to-HDL ratio. Even with good numbers and ratios, other factors—elevated homocysteine, B1 deficiency, or blood clotting issues—can silently threaten your arteries. If you’re over 40 and notice any signs or symptoms of heart disease, normal results might not tell the whole story. Ask us about arterial cleansing—a proactive step to safeguard your cardiovascular health.
Contact us to create a custom formula tailored to your specific needs. We provide cleanses & detoxes carefully designed to address your unique health challenges. We have natural formulas to address nutritional gaps, environmental exposure, or chronic stress, we can help you get to the root cause and rebuild your vitality. Let us support you in restoring your health and resilience.
References
Ravnskov, U., et al. (2016). “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review.” BMJ Open. DOI:10.1136/bmjopen-2015-010401.
Sacks, F. M., et al. (2018). “Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with cardiovascular events in women.” JAMA Cardiology. DOI:10.1001/jamacardio.2018.0894.
Nakajima, K., et al. (2011). “Small dense LDL cholesterol is a predictor of coronary artery disease in a Japanese population.” Atherosclerosis. DOI:10.1016/j.atherosclerosis.2011.05.034.
Hoogeveen, R. C., et al. (2021). “LDL subfractions and coronary artery disease risk in the Multi-Ethnic Study of Atherosclerosis.” Journal of Lipid Research. DOI:10.1194/jlr.P120001151.
Fernandez, M. L. (2006). “Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations.” Journal of Nutrition. DOI:10.1093/jn/136.1.11.
Volek, J. S., et al. (1997). “Comparison of a very low-carbohydrate and low-fat diet on fasting lipids.” Journal of Nutrition.
Selvin, E., et al. (2004). “Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults.” New England Journal of Medicine. DOI:10.1056/NEJMoa040217.
Willett, W. C., et al. (1992). “Intake of trans fatty acids and risk of coronary heart disease among women.” The Lancet. DOI:10.1016/0140-6736(92)90868-P.
DiNicolantonio, J. J., et al. (2018). “Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis.” Open Heart. DOI:10.1136/openhrt-2018-000898.
Noakes, T. D., & Sboros, M. (2017). Lore of Nutrition: Challenging Conventional Dietary Beliefs. Penguin Random House South Africa.
Sachdeva, A., et al. (2009). “Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines.” American Heart Journal. DOI:10.1016/j.ahj.2008.08.010.