Heart Disease and Diabetes: What Are We Trying to Prevent?

As a functional medicine physician, one of the most common scenarios I see in my practice is a patient sitting across from me, holding a copy of their recent lab work. They’re confused, and frankly, a little frustrated. “My doctor said everything is ‘normal’ but I just don’t feel right. I’m tired, I’m gaining weight around my middle, and I have a strong family history of heart disease. Am I missing something?” This moment of confusion isn’t a personal failure; it’s a signal that the system we rely on isn’t built for early insight.

The answer is almost always yes. The conventional model of care is excellent at identifying and treating disease once it has been diagnosed. But conditions like Type 2 diabetes and heart disease don’t simply appear overnight. They are the end result of long, parallel processes—one rooted in vascular biology, the other in metabolic regulation—that often unfold quietly for decades before they intersect in a clinically visible way.

This article is about shifting our focus. Instead of waiting for a diagnosis, we need to look upstream and ask a more powerful question: What are we actually trying to redirect? The answer isn’t just a heart attack or a high blood sugar reading. It is the underlying processes that drive cardiometabolic risk in the first place—arterial injury and atherogenic exposure on one hand, and insulin resistance and chronic metabolic strain on the other. Understanding where these processes begin, how they differ, and how they ultimately converge allows us to intervene earlier and more effectively, long before disease becomes inevitable.

Why Heart Disease and Diabetes Begin Long Before Diagnosis

The most profound shift in understanding chronic disease is recognizing that it is a process, not an event. Cardiovascular disease and Type 2 diabetes develop along different paths, but over time they frequently interact and amplify one another. Cardiovascular disease begins in the artery wall itself, driven by lifelong exposure to atherogenic lipoprotein particles and by the health—or vulnerability—of the vascular endothelium. Metabolic disease, by contrast, begins with energy handling: how the body responds to insulin, stores fuel, and adapts to excess.

This is a critical gap in preventive medicine. Individuals at risk are often exposed to “suboptimal metabolism over years before they present with clinical symptoms” (De Ferranti et al., 2023). In practical terms, this means years of missed opportunity. By the time traditional risk factors like high cholesterol or high blood sugar cross the diagnostic line, the underlying dysfunction is already well-entrenched. Insulin resistance, a key driver of this dysfunction, is thought to precede the development of Type 2 diabetes by as much as 10 to 15 years (Freeman et al., 2023). This long latency period is not a waiting game; it is our greatest window of opportunity for true heart disease prevention.

How Cardiometabolic Disease Develops Over Time

Think of your metabolic health like the plumbing in your house. A major burst pipe (like a heart attack) is an obvious crisis. But the real damage often starts as a slow, hidden leak inside the walls—a gradual buildup of pressure and corrosion. The challenge is that leaks or slow drips don’t announce themselves like a burst pipe. This is how cardiometabolic disease develops. It begins with subtle shifts in how your body processes energy.

A landmark 2022 study in the Journal of the American College of Cardiology found that a staggering 93.2% of U.S. adults have suboptimal cardiometabolic health (O’Hearn et al., 2022). This reflects how widespread these early dysfunctions have become. Insulin resistance creates a vicious cycle in which cells respond poorly to insulin, prompting the pancreas to secrete more. This state of chronic hyperinsulinemia worsens cellular resistance and drives fat storage, inflammation, and abnormal lipid patterns.

Why “Normal” Labs Can Still Signal Future Risk

This brings us back to the “normal” lab report. Reference ranges were never designed for early prevention. Standard reference ranges are typically calculated from the average values of a broad population—a population that, as we’ve seen, is largely metabolically unhealthy. A “normal” result simply means you fall within the average range of a generally unwell population.

Because cardiovascular and metabolic diseases begin long before diagnostic thresholds are crossed, early risk often hides in patterns rather than absolutes. Someone can have early atherosclerotic changes with normal glucose levels, or profound insulin resistance with cholesterol numbers that appear acceptable. Without understanding the distinct pathways involved, these early signals are easy to miss.

Early Warning Signs That Matter More Than a Diagnosis

Because metabolic dysfunction and vascular injury begin so early, the most meaningful clues are often found in subtle trends rather than diagnoses. These signals are not diseases themselves, but they are powerful invitations to look deeper. Four patterns deserve particular attention:

• Elevated insulin with normal glucose: This is the classic sign of early insulin resistance. Your pancreas is in overdrive, compensating for your cells’ sluggish response to insulin. Your blood sugar looks fine, but the system is under immense strain. This state of hyperinsulinemia is a powerful driver of both weight gain and inflammation.
• Rising waist circumference despite stable weight: Where you store fat matters more than what the scale says. An expanding waistline (generally over 35 inches for women and 40 inches for men) is a strong indicator of increasing visceral fat—the metabolically active, inflammatory fat stored deep within the abdomen around your organs. This is a far more significant warning sign for future cardiometabolic risk than your total BMI.
• Triglycerides creeping up while HDL drifts down: This pattern on a standard lipid panel is a powerful proxy for insulin resistance. A study in The Permanente Journal confirmed that the ratio of triglycerides to HDL cholesterol is a reliable marker of insulin resistance and cardiovascular risk (Bertsch and Merchant, 2015). When your triglycerides are rising and your “good” HDL cholesterol is falling, it’s a clear sign that your body is struggling to manage energy and fats efficiently.
• Elevated hs-CRP with other markers normal: High-sensitivity C-reactive protein (hs-CRP) is a direct measure of inflammation in the body. You can have perfect cholesterol and blood sugar, but if your hs-CRP is chronically elevated, it signals a “fire in the arteries.” This low-grade inflammation is a primary driver of atherosclerotic plaque formation and instability, a risk factor that is completely invisible on a standard lipid panel.

What Actually Drives Cardiovascular and Metabolic Risk

To prevent disease meaningfully, we must distinguish between risk factors and root causes. High blood pressure, dyslipidemia, weight gain, and elevated glucose are not isolated problems. They are downstream expressions of deeper dysfunction in metabolic regulation and vascular health.

Insulin Resistance as a Common Root Cause

Insulin resistance is the central pillar of cardiometabolic disease. When your cells become resistant to insulin’s message, it triggers a cascade of problems. The resulting high insulin levels (hyperinsulinemia) directly contribute to high blood pressure, unhealthy lipid patterns (high triglycerides, low HDL), and fat storage, particularly around the midsection. Furthermore, there is a destructive, reciprocal relationship between insulin resistance and the health of our blood vessels. As researchers in the journal Circulation explained, insulin resistance promotes endothelial dysfunction (the loss of flexibility and proper function of the blood vessel lining), and endothelial dysfunction, in turn, worsens insulin resistance, creating a dangerous feedback loop (Kim et al., 2006).

Chronic Inflammation and Blood Vessel Health

If insulin resistance is the engine of cardiometabolic disease, chronic inflammation is the fire it ignites. It’s not just about cholesterol passively building up in your arteries. The process begins when the delicate lining of the blood vessels (the endothelium) is injured by factors like high blood sugar, oxidized particles, or high blood pressure. This injury triggers an immune response. Immune cells rush to the area, and in a chronic state, this “healing” response goes awry. It promotes the formation of unstable plaque, creating what can be described as a “fire in the arteries” that can eventually lead to plaque rupture and a heart attack or stroke.

Blood Sugar Regulation Beyond A1C

For decades, we have relied on two main tests for blood sugar: fasting glucose and Hemoglobin A1C (a three-month average). While useful for diagnosing diabetes, they are late-stage, lagging indicators of a problem that has been developing for years. They can miss two crucial, earlier signs of trouble.

The first is postprandial hyperglycemia, or dramatic spikes in blood sugar after a meal. Research published in Endocrine Practice has shown that these after-meal spikes are an independent risk factor for cardiovascular disease, even when fasting glucose is normal (Gerich, 2006). The second, as we’ve discussed, is fasting insulin. By measuring fasting insulin, we can directly see if the pancreas is overworking to maintain that “normal” fasting glucose, giving us a much earlier and more sensitive window into metabolic dysfunction.

How to Prevent Heart Disease and Diabetes Before Diagnosis

The knowledge that disease begins years before diagnosis is not a cause for fear, but for empowerment. It gives us a clear directive: to act early, to look deeper, and to build a foundation of health that makes disease less likely to occur in the first place. This is the essence of the functional medicine approach to prevention.

Identifying Risk Years Before Disease Develops

True prevention starts with better assessment. Instead of waiting for conventional markers to become abnormal, we must use more sensitive tools to detect dysfunction early. This means going beyond a standard lipid panel to look at a more comprehensive set of biomarkers.

Key markers include:

• Apolipoprotein B (ApoB): A direct measure of the total number of potentially artery-clogging particles (like LDL). ApoB is a more accurate predictor of risk than LDL cholesterol alone.
• Lipoprotein(a) or Lp(a): A genetic risk factor for heart disease that is independent of lifestyle. Knowing your number is critical.
• Inflammatory Markers: Such as hs-CRP and others that reveal the level of “fire” in your system.
• Fasting Insulin: To assess hidden insulin resistance.

Understanding Metabolic Resilience and Flexibility

A core goal of prevention is to improve your metabolic flexibility—your body’s ability to efficiently switch between burning carbohydrates and fats for fuel. Think of it like a hybrid engine. A metabolically flexible person can use the carbs from a meal for immediate energy and then seamlessly switch back to burning stored body fat between meals or overnight.

Metabolic inflexibility, a hallmark of insulin resistance, is like having an engine stuck in “sugar-burning mode.” The body struggles to access fat stores, leading to energy crashes, sugar cravings, and difficulty losing weight. We can train our bodies to become more flexible through smart nutrition (managing the type and timing of carbohydrates), regular exercise, and building muscle.

Using Early Markers to Guide Long-Term Prevention

This is where everything comes together. When you combine advanced risk assessment with a focus on building metabolic resilience, you create a truly personalized and proactive prevention plan. Knowing your specific early markers—be it high insulin, inflammation, or a high ApoB particle count—allows you to target your interventions.

Your lab results are no longer just a pass/fail grade; they become a roadmap. This data empowers you to make targeted, sustainable lifestyle changes—not as a punishment, but as a precise strategy to reverse the trajectory of disease and build a more resilient you.

This article is for informational purposes only and does not constitute medical advice. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. 

What You’ll Learn in the Affairs of the Heart Virtual Program 

If you are ready to move beyond the confusion of “normal” lab tests and take a proactive role in your long-term health, I invite you to join our new virtual program, “Affairs of the Heart.” 

This will be a 4-week, 90-minute virtual class focused on cardiovascular and metabolic risk literacy. This program is not about ordering or reviewing individual labs. Instead, the emphasis is on helping you understand what actually drives risk, why cholesterol and glucose alone miss so much, and how markers like insulin, inflammation, ApoB, and particle size fit into a bigger picture. 

The goal is for you to leave informed, confident, and better equipped to navigate the next steps in your health journey. 

Register Now! 

Dates: March 10, 17, 24, and 31.

Where: Virtual Sessions

References 

1. Freeman, A. M., Acevedo, L. A., & Pennings, N. (2023). Insulin Resistance. In StatPearls. StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK507839/ 
2. De Ferranti, S. D., et al. (2023). Next Generation, Modifiable Cardiometabolic Biomarkers: Mitochondrial Adaptation and Metabolic Resilience: A Scientific Statement From the American Heart Association. Circulation, 148(19), 1594–1614. https://doi.org/10.1161/CIR.0000000000001185 
3. O’Hearn, M., et al. (2022). Trends and Disparities in Cardiometabolic Health Among U.S. Adults, 1999-2018. Journal of the American College of Cardiology, 80(2), 138-151. https://pubmed.ncbi.nlm.nih.gov/35798448/
4. Bertsch, R. A., & Merchant, M. A. (2015). Study of the Use of Lipid Panels as a Marker of Insulin Resistance to Determine Cardiovascular Risk. The Permanente Journal, 19(4), 4–10. https://doi.org/10.7812/TPP/14-237 
5. Lebovitz, H. E. (2006). Insulin resistance–a common link between type 2 diabetes and cardiovascular disease. Diabetes, Obesity & Metabolism, 8(3), 237–249. https://doi.org/10.1111/j.1463-1326.2005.00521.x 
6. Kim, J. A., Montagnani, M., Koh, K. K., & Quon, M. J. (2006). Reciprocal relationships between insulin resistance and endothelial dysfunction: molecular and pathophysiological mechanisms. Circulation, 113(15), 1888–1904. https://doi.org/10.1161/CIRCULATIONAHA.105.563213 
7. Mensah, G., Arnold, N., Prabhu, S., et al. (2025). Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement: A Report of the American College of Cardiology. Journal of the American College of Cardiology. https://doi.org/10.1016/j.jacc.2025.08.047 
8. Gerich, J. E. (2006). Postprandial Hyperglycemia and Cardiovascular Disease. Endocrine Practice, 12(Suppl 1), 47-51. https://doi.org/10.4158/EP.12.S1.47 
9. Romero-Cabrera, J. L., Ankeny, J., Fernández-Montero, A., Kales, S. N., & Smith, D. L. (2022). A Systematic Review and Meta-Analysis of Advanced Biomarkers for Predicting Incident Cardiovascular Disease among Asymptomatic Middle-Aged Adults. International Journal of Molecular Sciences, 23(21), 13540. https://doi.org/10.3390/ijms232113540 
10. The Institute for Functional Medicine. (n.d.). Heart Health & Metabolic Function: The Gut Microbiome Influence. Retrieved from http://www.ifm.org/articles/gut-flora-and-cardiometabolic-conditions