How to prevent heart disease: cholesterol truths

Dr. Mary Pardee

Cardiovascular disease remains the leading cause of mortality worldwide, with atherosclerotic cardiovascular disease (ASCVD) being one of the primary culprits.

Despite the overwhelming evidence on the role of cholesterol in heart disease, misinformation persists, particularly on social media. To set the record straight, I had the privilege of speaking with Dr. Alo, a board certified cardiologist.

About Dr. Alo

Dr. Alo is a board-certified cardiologist, certified personal trainer, and a passionate advocate for eradicating heart disease and promoting longevity. He practices obesity medicine and specializes in advanced lipids, dedicating his career to debunking myths and providing evidence-based insights to help people take control of their heart health.

What Is ASCVD and Why Should We Care?

ASCVD refers to the buildup of atherosclerotic plaque in the arteries, leading to conditions such as heart attacks, strokes, and peripheral artery disease. Dr. Alo explained the process in simple terms:

"If you have high LDL cholesterol, it gets into your artery walls and starts to build up, forming plaque. Over time, this can lead to blockages, increasing the risk of heart attacks and strokes. This is not debatable in the medical community." - Dr. Alo

He emphasized that ASCVD is largely preventable, citing research demonstrating that lowering LDL cholesterol reduces the incidence of heart disease (Ference et al., 2017).

Can ASCVD Be Entirely Prevented?

Dr. Alo highlighted studies on individuals with hypo-beta lipoproteinemia, a genetic condition where LDL cholesterol levels remain extremely low (5–15 mg/dL).

"These individuals never develop atherosclerosis, no matter what they do. That tells us something very important—if we can keep LDL low, we can essentially prevent ASCVD." -Dr. Alo

The Role of LDL-c and ApoB in ASCVD

ApoB is a key marker for ASCVD risk. Unlike LDL-C, which measures cholesterol concentration, ApoB measures the total number of lipoproteins capable of causing plaque formation.

"If your ApoB is below 60 mg/dL, you're probably not laying down new plaque. The lower, the better," Dr. Alo explained.

A landmark study, the PESA trial, found that subclinical atherosclerosis begins even at LDL-C levels considered "normal" with is 100 mg/dL (Fernández-Friera et al., 2017).

Lowering LDL-C and ApoB: Diet vs. Medication

Dr. Alo underscored that dietary changes, particularly reducing saturated fat intake, have the biggest impact on LDL levels.

"Cutting saturated fat is the single biggest lever for lowering LDL [from a lifestyle perspective]. It can reduce LDL by 5–60%, depending on your starting diet." - Dr. Alo

Other lifestyle interventions, such as increasing fiber intake, can have a modest effect (~1–7% reduction in LDL). However, he noted that exercise, while crucial for overall health, does not significantly lower LDL.

For those with high cholesterol despite lifestyle changes, medications like statins, ezetimibe, and PCSK9 inhibitors are crucial.

"Every single study where LDL was lowered, whether through diet, exercise, or medication, showed improved outcomes. There is no study showing that lowering LDL is harmful." - Dr. Alo

Addressing Common Myths About Statins

Statins remain the most effective and well-studied class of cholesterol-lowering drugs, yet myths persist. Dr. Alo debunked several common misconceptions:

Statins cause insulin resistance.

"Statins may slightly increase A1C in prediabetic individuals (~0.1% rise), but the cardiovascular benefits far outweigh this minor effect." - Dr. Alo

To think of the risk benefit ratio for this example let's take a healthy 35 year old male who has a HbA1C of 5.2% and LDL-c of 145 mg/dL. Putting him on 20 mg of crestor MAY increase his HbA1C to 5.3%

Statins reduce vitamin D and testosterone.

"They don't. These concerns have been studied extensively, and no deficiencies occur. Hormone production is maintained even at very low LDL levels." - Dr. Alo

(If you want to explore any of these, listen to the full interview above).

Statins only add 4 days to your life.

"This claim comes from a flawed study that projected lifespan based on short-term trials. In reality, taking a statin long-term can add 5–15 years to your life."

A study in the British Medical Journal analyzed short-term statin trials, many of which used weaker statins and followed patients for only 2–6 years. They extrapolated limited data to calculate an average survival gain of just 4 days.

However, more comprehensive studies, like the WOSCOPS trial, showed that men who took statins for 5 years had a 13% reduction in all-cause mortality and a 21% reduction in cardiovascular mortality over a 20-year follow-up. The benefit of statins compounds over time, meaning that individuals who take statins consistently for decades will see a significant extension of both lifespan and healthspan (Ford et al., 2016).

The benefits of statins accumulate over time, significantly reducing cardiovascular risk with continued use.

Does the LDL-to-HDL Ratio Matter?

One common myth in cholesterol management is that the ratio of LDL to HDL matters more than absolute LDL levels. However, research clearly shows that the primary driver of ASCVD is LDL and ApoB levels alone, regardless of the HDL number.

"LDL is the primary factor in plaque formation, not the ratio. Some people naturally have high HDL, but that does not protect them from ASCVD if their LDL remains high," Dr. Alo explained.

In fact, HDL is highly variable among individuals, influenced by genetics, sex, and lifestyle. While low HDL can be a marker of metabolic dysfunction, raising it through interventions has not been shown to reduce ASCVD risk. Studies confirm that the best predictor of cardiovascular disease is absolute LDL-c and ApoB levels—not the LDL-to-HDL ratio (Ference et al., 2017).

Lean Mass Hyper-Responders

One of the most debated topics online is whether young, fit individuals with high LDL (often referred to as "lean mass hyper-responders") should worry.

Dr. Alo cited multiple studies, including the CARDIA and PESA trials, showing that even in "metabolically healthy" individuals, high LDL predicts early atherosclerosis.

PESA trial data demonstrate that individuals with LDL-c levels of 50 mg/dL or lower had no detectable atherosclerosis, reinforcing the importance of LDL reduction in preventing plaque buildup.

The higher the LDL-c was, the greater the percentage of subjects who had atherosclerosis.

"A high LDL is like rolling the dice with your health. You might be okay, but the odds are not in your favor. The longer it's elevated, the higher your risk."- Dr. Mary

Lipoprotein(a): The Less Discussed Risk Factor

Lipoprotein(a) is a genetically determined marker significantly increasing cardiovascular risk.

"If Lp(a) is elevated, the goal is to get LDL as low as possible—ideally below 40 mg/dL. PCSK9 inhibitors can reduce Lp(a) by ~28%, but we await outcome data to confirm benefits."

What Else Can We Do for Longevity?

Are there other evidence-based longevity strategies for those already optimizing cholesterol, diet, and exercise?

"Honestly, not much. There’s no strong data that things like red light therapy, saunas, or cold plunges extend lifespan. The best bet remains diet, exercise, and keeping cholesterol in check."- Dr. Alo

Conclusion: The Evidence is Clear

The science on cholesterol and ASCVD is conclusive—high LDL and ApoB drive atherosclerosis, and lowering them extends life. While diet plays a role, medications are often necessary to achieve optimal levels if you wish to prevent ASCVD.

As Dr. Alo put it:

"Every study we have shows that the lower your LDL, the longer and healthier you live."

Dr. Alo Instagram: @dr.alo

If you live in California, schedule a complimentary consultation to discuss advanced lipid testing and heart health optimization with Dr. Mary here.

References

• Ference, B. A., Ginsberg, H. N., Graham, I., et al. (2017). Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. European Heart Journal, 38(32), 2459-2472. https://doi.org/10.1093/eurheartj/ehx144

• Fernández-Friera, L., Fuster, V., López-Melgar, B., et al. (2017). Normal LDL-cholesterol levels are associated with subclinical atherosclerosis in the absence of risk factors. Journal of the American College of Cardiology, 70(24), 2979-2991. https://doi.org/10.1016/j.jacc.2017.10.024

• Ford, I., Murray, H., Packard, C. J., et al. (2016). Long-term follow-up of the West of Scotland Coronary Prevention Study. Circulation, 133(11), 1073-1080. https://doi.org/10.1161/CIRCULATIONAHA.115.019014

• Friedman, G. D., Cutter, G. R., Donahue, R. P., Hughes, G. H., Hulley, S. B., Jacobs, D. R., Liu, K., & Savage, P. J. (1988). CARDIA: Study design, recruitment, and some characteristics of the examined subjects. Journal of Clinical Epidemiology, 41(11), 1105–1116. https://doi.org/10.1016/0895-4356(88)90080-7

• Fernández-Friera, L., Peñalvo, J. L., Fernández-Ortiz, A., Ibáñez, B., López-Melgar, B., Laclaustra, M., Oliva, B., Mocoroa, A., Mendiguren, J., Martínez de Vega, V., García, L., Molina, J., Sánchez-González, J., Guzmán, G., Alonso-Farto, J. C., Guallar, E., Civeira, F., Sillesen, H., Pocock, S., … Fuster, V. (2015). Prevalence, vascular distribution, and multiterritorial extent of subclinical atherosclerosis in a middle-aged cohort: The PESA (Progression of Early Subclinical Atherosclerosis) study. Circulation, 131(24), 2104–2113. https://doi.org/10.1161/CIRCULATIONAHA.114.014310

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