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Optimal ApoB: Insights for Cardiovascular Health and Longevity

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While cholesterol has long been in the spotlight for heart health, there's a lesser-known yet crucial player: Apolipoprotein B (ApoB). This key component of lipoproteins plays a significant role in cardiovascular disease risk.

At Superpower, we've delved deep into the research to establish an optimal range for ApoB that's more stringent than conventional standards. Our approach is proactive, focusing on prevention rather than just diagnosis. By identifying and managing ApoB levels early, we aim to reduce cardiovascular risk before it becomes a clinical concern.

Key Points

  • "Normal" Isn't Optimal: Conventional ApoB ranges may allow silent progression of heart disease. Lower ApoB levels are crucial for optimal cardiovascular health.
  • The Cumulative Impact: Even ApoB levels considered "desirable" by traditional standards can contribute to plaque buildup over time, underscoring the importance of early detection and long-term management.
  • Redefining Healthy Levels: Research supports a lower ApoB range to significantly reduce the risk of cardiovascular events.
    • Conventional Range: less than 80 mg/dL
    • Optimal Range: less than 80 mg/dL

What is ApoB?

Apolipoprotein B, or ApoB, is a crucial protein in the body's lipid transport system. Each ApoB molecule attaches to a package of fats, forming a lipoprotein - essentially creating a molecular "vehicle" for transporting lipids through the bloodstream. This function makes ApoB an integral part of several lipoprotein types, including Low-Density Lipoprotein (LDL), Very Low-Density Lipoprotein (VLDL), and Lipoprotein(a) (Lp(a)).

ApoB plays two important roles in how our body handles fats. First, it helps package fats into transportable units, like a container that keeps things organized. Second, it acts like a key that allows these fat packages to enter our cells. Because of these roles, ApoB is directly involved in the processes that can lead to the buildup of fatty deposits in our arteries, a condition known as atherosclerosis.

The unique feature of ApoB is its one-to-one relationship with potentially artery-clogging lipoprotein particles, each containing exactly one ApoB molecule. This makes ApoB an accurate measure of the total number of harmful lipid-carrying particles in the bloodstream than traditional lipid panels provide.

Why should anyone care about ApoB?

ApoB levels provide a more accurate assessment of cardiovascular risk than traditional cholesterol measurements.

Think of ApoB as the driver of the vehicles that transport cholesterol. While knowing your cholesterol level is like knowing how much cargo is being transported, measuring ApoB tells you how many vehicles are on the road. More vehicles mean more potential for traffic jams in your arteries, regardless of how much cargo each is carrying.

ApoB provides a direct count of the potentially harmful particles in your bloodstream that can lead to heart attacks and strokes. Each ApoB molecule represents one lipoprotein particle capable of penetrating your artery walls, setting the stage for atherosclerosis. The fewer particles you have, the lower the probability of this penetration occurring.

What is the conventional reference range?

The conventional reference range for ApoB is typically:

  • Desirable: Less than 100 mg/dL
  • Borderline High: 100-129 mg/dL
  • High: 130 mg/dL or higher

These ranges are set to identify high-risk individuals rather than preventing disease or optimize health. They may not be ideal for early detection or proactive cardiovascular management.

What is the Superpower Optimal Range for ApoB?

At Superpower, we recommend a more stringent optimal range for ApoB:

  • Superpower Optimal Range: Less than 80 mg/dL

Our range is based on population studies and clinical research that have shown decreased cardiovascular risk at these lower levels.

Why is the Conventional Range for ApoB Problematic?

The conventional ApoB range is problematic because it is reactive rather than preventive. It allows for higher levels of ApoB-containing particles than may be optimal for long-term health.

ApoB levels below 100 mg/dL, deemed "desirable," can still allow silent progression of atherosclerosis. This range fails to consider the cumulative impact of long-term exposure to ApoB levels that contribute to plaque buildup over time.

Additionally, the current range doesn't account for individual variability in cardiovascular disease risk factors such as genetics, lifestyle, and other health conditions. Using a one-size-fits-all approach and only raising concerns when ApoB levels exceed 100 mg/dL can lead to missed opportunities for early intervention.

Research supports these concerns.

Standard ApoB cutoffs underestimate cardiovascular risk, especially in individuals with metabolic syndrome or diabetes, who may need lower ApoB targets [1,2]. Even "normal" ApoB levels were associated with subclinical atherosclerosis in young adults, suggesting current guidelines may not be stringent enough to prevent early cardiovascular disease [3,4].

Supporting Evidence from Research Studies

We have conducted an extensive review of published research to establish our Superpower Optimal Range for ApoB of less than 80 mg/dL. This range is rooted in robust scientific evidence and offers significant benefits for cardiovascular, metabolic, and overall health.

Lower ApoB levels have been consistently linked to enhanced cardiovascular protection. Studies have demonstrated that ApoB is a superior marker for cardiovascular risk assessment, outperforming traditional lipid measures [5, 6]. Intriguingly, this lower range aligns with our evolutionary past; hunter-gatherer populations, known for low cardiovascular disease rates, typically shows ApoB levels below 80 mg/dL [7-9].

The protective mechanism of lower ApoB is multifaceted. Fewer ApoB-containing lipoproteins in the bloodstream reduce the chance of these particles penetrating and becoming trapped in arterial walls, a key step in atherosclerosis development [5, 10]. This process also minimizes inflammation, as retained particles undergo modifications that trigger inflammatory responses [11, 12]. By reducing the particle load, we decrease the fuel available for both modifications and inflammation, further protecting arterial health.

Lower ApoB levels also demonstrate a synergistic relationship with other aspects of metabolic health. Research has shown strong associations between ApoB, insulin resistance, and other components of metabolic syndrome, suggesting that targeting ApoB could have benefits beyond cardiovascular protection [13].

Long-term studies further support the benefits of lower ApoB. Research has shown that individuals with lifelong lower ApoB levels have a reduced risk of heart disease[14], while those with ApoB below 65 mg/dL experienced significantly fewer heart-related issues[15, 16]. Even in younger populations, conventionally "normal" ApoB levels were associated with subclinical atherosclerosis, emphasizing the potential benefits of lower targets across all age groups [3, 17].

Importantly, the advantages of lower ApoB extend beyond prevention. Studies have demonstrated that reducing ApoB levels in patients already on statin therapy led to further decreases in heart attacks and is positively associated with lower mortality from all causes, highlighting its role in managing residual risk even in treated patients [18].

This body of evidence underscores the profound impact of maintaining lower ApoB levels on cardiovascular health, metabolic synergy, and inflammation reduction, supporting the proposed optimal range as a key strategy for both prevention and management of cardiovascular disease.

The Key Takeaway

At Superpower, our focus is on prevention rather than cure.

Elevated ApoB levels are a significant risk factor for cardiovascular disease, cognitive decline, and other health issues. Conventional reference ranges are too permissive, allowing for silent progression of atherosclerosis and other complications.

By aiming for an optimal ApoB range of less than 80 mg/dL, we prioritize early intervention and proactive health management, supported by the latest clinical research.

References

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  2. Cole, Justine et al. “Use of Apolipoprotein B in the Era of Precision Medicine: Time for a Paradigm Change?.” Journal of clinical medicine vol. 12,17 5737. 3 Sep. 2023, doi:10.3390/jcm12175737
  3. Wilkins, John T et al. “Analysis of apoB Concentrations Across Early Adulthood and Predictors for Rates of Change Using CARDIA Study Data.” Journal of lipid research vol. 63,12 (2022): 100299. doi:10.1016/j.jlr.2022.100299
  4. Cantey, Eric P, and John T Wilkins. “Discordance between lipoprotein particle number and cholesterol content: an update.” Current opinion in endocrinology, diabetes, and obesity vol. 25,2 (2018): 130-136. doi:10.1097/MED.0000000000000389
  5. Sniderman, Allan D et al. “Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review.” JAMA cardiology vol. 4,12 (2019): 1287-1295. doi:10.1001/jamacardio.2019.3780
  6. Pencina, Michael J et al. “Apolipoprotein B improves risk assessment of future coronary heart disease in the Framingham Heart Study beyond LDL-C and non-HDL-C.” European journal of preventive cardiologyvol. 22,10 (2015): 1321-7. doi:10.1177/2047487315569411
  7. Cordain, L et al. “Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.” The American journal of clinical nutrition vol. 71,3 (2000): 682-92. doi:10.1093/ajcn/71.3.682
  8. Walker, A R. “Are health and ill-health lessons from hunter-gatherers currently relevant?.” The American journal of clinical nutrition vol. 73,2 (2001): 353-6. doi:10.1093/ajcn/73.2.353
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  10. Borén, Jan, and Kevin Jon Williams. “The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity.” Current opinion in lipidology vol. 27,5 (2016): 473-83. doi:10.1097/MOL.0000000000000330
  11. Gisterå, Anton, and Göran K Hansson. “The immunology of atherosclerosis.” Nature reviews. Nephrology vol. 13,6 (2017): 368-380. doi:10.1038/nrneph.2017.51
  12. Rocha, Viviane Zorzanelli et al. “Insights into the Role of Inflammation in the Management of Atherosclerosis.” Journal of inflammation researchvol. 16 2223-2239. 24 May. 2023, doi:10.2147/JIR.S276982
  13. Taskinen, Marja-Riitta et al. “Dietary Fructose and the Metabolic Syndrome.” Nutrients vol. 11,9 1987. 22 Aug. 2019, doi:10.3390/nu11091987
  14. Ference, Brian A et al. “Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease.” JAMAvol. 321,4 (2019): 364-373. doi:10.1001/jama.2018.20045
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  16. Behbodikhah, Jennifer et al. “Apolipoprotein B and Cardiovascular Disease: Biomarker and Potential Therapeutic Target.” Metabolites vol. 11,10 690. 8 Oct. 2021, doi:10.3390/metabo11100690
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