It’s a common occurrence that following a challenging (or longer) workout, there’s an immediate...
Author: Dr. Greg Fors, Chief Science Officer, Biospec Nutritionals
Cardiovascular disease is still the #1 cause of death in the United States. In 2023, cardiovascular disease caused 919,032 deaths—about 1 in 3 deaths (roughly one death every ~34 seconds). Heart disease alone accounted for 680,981 deaths. [1,2]
Here’s the part that should make you mad: most people don’t discover they’re “high risk” until after the event. Why? Because the usual “yearly physical” approach often checks a few basic numbers—and misses the real drivers.
The failing model: “Your labs look fine… see you next year.”
Blood pressure and cholesterol medications can be appropriate and sometimes lifesaving—but they rarely address why the disease is progressing. Many people are told they’re “fine” because the paperwork looks better, while the artery wall is still being injured by:
- insulin resistance (often years before diabetes)
- inflammation and oxidative stress (“rusting”)
- genetic clotting/inflammation risk like Lp(a)
- methylation issues and elevated homocysteine
- smoking/toxins and chronic stress physiology
If the current approach were enough, we’d see cardiovascular disease falling in a big way. We don’t. [3]
The cholesterol myth (and the truth)
You’ve been taught a simple story: “High cholesterol causes heart disease.” Real life is more honest—and more hopeful.
Cholesterol is not a toxin
Cholesterol is essential for life: it’s part of every cell membrane; it’s used to make steroid hormones (stress hormones and sex hormones); your brain is cholesterol-rich and tightly regulates its own supply.
So, the real question isn’t “Do you have cholesterol?” The real question is: Why is cholesterol being recruited to an inflamed, injured artery wall?
My “Band-Aid” model (plain English)
When the artery lining (the endothelium) is repeatedly irritated—by high blood pressure, smoking, high glucose/insulin, inflammation, toxins—your body responds. Cholesterol-carrying particles can act like a temporary repair patch. But if the injury continues, that patch gets trapped under the artery lining; over years it becomes plaque.
And when LDL particles become oxidized—what I call “rancid” or “rusted”—they shift from “repair mode” to damage mode, accelerating inflammation and instability.
“Size matters”: why a standard cholesterol panel can miss the real danger
At most yearly physicals your blood lipid panel may include: Total Cholesterol, LDL-C, HDL-C, Triglycerides. Helpful, but incomplete.
Three people can all have LDL-C of 130 mg/dL and have very different risk, because what matters more often is:
- how many LDL particles you have
- how small/dense they are
- how inflamed/oxidized is the environment
Consider asking your doctor to run these tests. Here’s why:
ApoB: the number I don’t ignore
Apolipoprotein B (ApoB) is one of the best reality checks for atherogenic particle burden (how many plaque-forming particles are circulating). Large analyses support ApoB as a stronger risk marker than LDL-C, especially when LDL-C looks “okay” but particle number is high. [4]
You may want to consider a healthy Mediterranean diet, or other evidence-based dietary pattern to lower your ApoB cholesterol marker.* You may also consider adding specific nutraceutical botanicals like red yeast rice and berberine if recommended by your licensed healthcare physician or nutrition specialist.* Both ingredients are supported in meta-analyses for their cardiometabolic benefits.* [6,7]
Important Clinical Note: Use appropriate medical supervision, review medications and interactions, avoid during pregnancy, and monitor liver enzymes (and CK when indicated), especially if symptoms arise.
Lp(a): the “sticky” LDL particle most people never get tested
One particularly dangerous particle is lipoprotein(a)—Lp(a). Think of it as LDL with extra “Velcro”: sticky, pro-inflammatory, and prone to oxidation.
Additionally, it’s important to understand that:
• Lp(a) is largely genetic
• Many standard labs don’t include it
• Niacin extended release and carnitine with exercise has shown to lower Lp(a).* [8,9]
Awareness of your true risk and potential treatment options are key to long-term prevention and improved overall health.
Homocysteine: “sandpaper” on the artery wall
Homocysteine is a functional marker of methylation status—and when elevated, it can behave like chronic irritation to the vascular lining and influence clotting biology. Higher homocysteine levels are associated with significantly higher cardiovascular and all-cause mortality risk in large analyses. [5]
Homocysteine is specifically modifiable by the intake of increased methyl-folate and methylcobalamin (B12) as methylation donors.* Clinical studies support homocysteine reduction with methylfolate-containing supplementation.* [10–12]
The biggest missed driver: early insulin resistance
One of the most dangerous myths is: “If your glucose is normal, you’re fine.”
In many people, glucose can look “normal” for years because the pancreas is pumping out high insulin to keep it down. Unfortunately, insulin resistance begins to occur. Over time, this pattern of insulin resistance drives: belly weight gain, higher blood pressure (which is regularly linked to higher insulin levels), higher triglycerides, lower HDL, and more small/dense LDL particles. This cluster is often called metabolic syndrome—and it is a direct pipeline to cardiovascular disease.
Again, a low carb healthy diet, and the use of botanicals such as berberine and cinnamon extracts can help to improve insulin resistance.* Human evidence supports improvements in glycemic control and insulin resistance measures with specific botanical ingredients. [13–16]
The “10-Test” Cardiovascular Risk Workup I Recommend
If you want your true risk—not just your paper risk—these are markers I commonly recommend (and that many functional and preventive clinicians can order):
- Fasting glucose + fasting insulin (early insulin resistance)
- Hemoglobin A1c (trend toward prediabetes)
- Triglycerides (often an early insulin-resistance alarm)
- Total cholesterol / HDL / LDL + key ratios (context matters)
- Homocysteine (methylation + vascular injury risk)
- ApoB (atherogenic particle burden) [4]
- Lp(a) (genetic “sticky LDL” risk)
- Oxidized LDL (are particles “rusting” and turning inflammatory?)
- Lp-PLA2 activity (vascular-specific inflammation; plaque vulnerability signal)
- Omega-3 Index (cell-membrane inflammation balance) There are additional tools depending on your history (family risk, symptoms, calcium score, etc.).
There are additional tools depending on your history (family risk, symptoms, calcium score, etc.). The point is: we can stop guessing.
If any of this sounds like you, it’s time to look deeper
Consider advanced risk testing if you have:
-
family history of early heart disease or stroke
-
belly weight gain, rising blood pressure, rising triglycerides
-
“normal cholesterol” but worsening health trends
-
prediabetes, fatty liver, metabolic syndrome
-
plaque/calcification despite “good labs”
-
brain fog, fatigue, chronic inflammation, chronic pain
The takeaway (and my challenge to you)
Cardiovascular disease is rarely sudden. It’s usually a slow process—and that’s good news because it means you have time to intervene.
But intervention starts with truth: better testing → better clarity → better choices → better outcomes.
If you’re ready to stop relying on a basic annual panel and start measuring what actually drives risk, talk with your clinician about a cardiometabolic + advanced cardiovascular risk evaluation.
Educational content only; not medical advice. Do not stop or change medications without first discussing with your prescribing clinician.
*This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
References
[1] Centers for Disease Control and Prevention. Heart Disease Facts. (accessed Feb 1, 2026). URL: https://www.cdc.gov/heart-disease/data-research/facts-stats/index.html
[2] Centers for Disease Control and Prevention. FastStats: Leading Causes of Death. (accessed Feb 1, 2026). URL: https://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm
[3] American Heart Association. Heart disease remains leading cause of death as key health risk factors continue to rise. News release (accessed Feb 1, 2026). URL: https://newsroom.heart.org/news/heart-disease-r emains-leading-cause-of-death-as-key-health-risk-factors-continue-to-rise
[4] Marston NA, et al. Apolipoprotein B and Cardiovascular Risk. Circulation/AHA (accessed Feb 1, 2026). DOI/URL: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.124.068885
[5] Fan R, et al. Association of Plasma Homocysteine With All-Cause and Cardiovascular Mortality: Meta-analysis. (accessed Feb 1, 2026). URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC4288948/
[6] Li P, et al. Red Yeast Rice for Hyperlipidemia: A Meta-Analysis of randomized trials. 2022. URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC8802088/
[7] Ju J, et al. Efficacy and safety of berberine for dyslipidaemias: systematic review and meta-analysis. 2018. URL: https://pubmed.ncbi.nlm.nih.gov/30466986/
[8] Sahebkar A, et al. Effect of extended-release niacin on plasma lipoprotein(a): systematic review and meta-analysis. 2016. URL: https://pubmed.ncbi.nlm.nih.gov/27733255/
[9] Serban MC, et al. Impact of L-carnitine on plasma lipoprotein(a) concentrations: systematic review and meta-analysis. 2016. URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC4709689/
[10] Venn BJ, et al. Randomized trial comparing L-methylfolate vs folic acid for lowering homocysteine. 2003. URL: https://www.sciencedirect.com/science/article/pii/S0002916523056629
[11] Schmidl D, et al. Methylfolate-containing supplement reduced homocysteine in patients with diabetes (pilot study). 2020. URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC7190578/
[12] Pokushalov E, et al. Methylfolate + methylcobalamin (with cofactors) reduced homocysteine. 2024. URL: https://www.mdpi.com/2072-6643/16/11/1550
[13] Ye Y, et al. Berberine and insulin resistance: systematic review/meta-analysis. 2021. URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC8107691/
[14] Guo J, et al. Berberine improved insulin resistance including HOMA-IR: meta-analysis. 2021. URL: https://onlinelibrary.wiley.com/doi/10.1155/2021/2074610
[15] Zarezadeh M, et al. Cinnamon supplementation and insulin resistance: review/meta-analysis evidence. 2023. URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC10268424/
[16] Wang JG, et al. Cinnamon extract improved insulin sensitivity: randomized placebo-controlled trial (pilot). 2007. URL: https://www.sciencedirect.com/science/article/pii/S0015028206045559
