Atherosclerotic Process

Background: What Is Atherosclerosis?

Atherosclerosis begins with endothelial dysfunction—damage to the inner lining of blood vessels—triggered by factors such as oxidative stress, chronic inflammation, and dyslipidemia. Over time, this damage allows lipids, immune cells, and other substances to accumulate within the arterial wall, forming plaques.

Clinical Manifestations: Signs and Symptoms by Arterial Territory

The symptoms of atherosclerosis depend on the vascular bed affected. In many cases, early stages are clinically silent. As the disease progresses, symptom onset typically correlates with significant arterial narrowing or ischemia.

Coronary Arteries:

• Angina (chest pain or pressure with exertion)
• Shortness of breath
  
• Acute myocardial infarction (heart attack)

Cerebral Arteries:

• Transient ischemic attacks (TIAs)
  
• Stroke (ischemic)
  
• Cognitive decline or vascular dementia in chronic cases

Peripheral Arteries:

• Claudication (leg pain with walking)
  
• Cold extremities or numbness
  
• Delayed wound healing or ulceration in advanced disease

Recognition of these patterns allows for targeted assessment and prevention of potentially disabling or fatal events.

Laboratory Evaluation and Biomarkers

A functional assessment of the atherosclerotic process incorporates both conventional and advanced biomarkers. These markers help identify patients at risk, guide personalized interventions, and track progress over time.

Standard Cardiovascular Biomarkers:

• Lipid Panel:
  
  • LDL-C (Low-Density Lipoprotein Cholesterol)
    
  • HDL-C (High-Density Lipoprotein Cholesterol)
    
  • Triglycerides
    
• C-Reactive Protein (hs-CRP)
  
• Fasting Glucose and Insulin: Assesses glycemic control and insulin sensitivity
  
• Hemoglobin A1c: Reflects average blood glucose over three months

Functional and Advanced Biomarkers:

• Atherogenic Index of Plasma (AIP): Log(triglycerides/HDL-C)
  
• Oxidized LDL (oxLDL): More atherogenic than native LDL
  
• Lipoprotein(a) [Lp(a)]: Genetically determined particle associated with plaque formation
  
• Homocysteine: Promotes oxidative stress and endothelial injury
  
• Fibrinogen and D-dimer: Markers of coagulation and thrombotic risk

These tools offer deeper insight into the biological processes driving atherosclerosis and inform more precise treatment strategies.

Root Causes and Contributing Factors

Atherosclerosis is driven by a combination of modifiable and non-modifiable factors. Functional medicine emphasizes identifying and modifying upstream influences that accelerate plaque formation.

1. Chronic Inflammation
   
   • Triggers immune activation and endothelial dysfunction
     
   • Measured by hs-CRP and interleukin-6 (IL-6)
     
2. Dyslipidemia
   
   • Elevated LDL, low HDL, and high triglycerides
     
   • Small dense LDL particles are particularly atherogenic
     
3. Oxidative Stress
   
   • Imbalance between reactive oxygen species (ROS) and antioxidant defenses
     
4. Insulin Resistance and Metabolic Syndrome
   
   • High insulin and glucose levels stimulate hepatic lipogenesis
     
   • Associated with elevated triglycerides and reduced HDL
     
   • Promotes inflammation and vascular remodeling
     
5. Hypertension
   
   • Elevated pressure damages arterial walls
     
6. Lifestyle Influences
   
   • Sedentary behavior, poor dietary habits, tobacco use, and excessive alcohol intake
     
7. Genetic Predisposition
   
   • Family history of early cardiovascular disease or elevated Lp(a)

Understanding the interplay between these variables is essential in constructing a personalized, prevention-focused care plan.

Interfering Factors in Testing and Diagnosis

Several variables can influence cardiovascular biomarker interpretation and must be considered during assessment:

• Acute Illness or Injury: Temporarily elevates CRP and inflammatory markers
  
• Recent Dietary Intake: Triglycerides may rise postprandially; fasting samples are more accurate
  
• Medications and Supplements:
  
  • Statins lower LDL and may affect CRP
    
  • Niacin and omega-3 fatty acids influence lipid subfractions
    
  • High-dose biotin can interfere with immunoassay-based lab tests
    
• Hormonal Shifts: Estrogen status influences lipid profiles

Clinicians must evaluate lab findings in the context of timing, clinical status, and patient history.

Medications That Influence the Atherosclerotic Process

While lifestyle intervention is foundational, pharmacologic agents may be necessary:

Medications That May Improve Risk Profile:

• Statins: Lower LDL and exert anti-inflammatory effects
  
• ACE Inhibitors/ARBs: Lower blood pressure and reduce vascular remodeling
  
• Aspirin (low-dose): May reduce thrombotic events in high-risk patients
  
• Metformin: Improves insulin sensitivity and may reduce cardiovascular events in diabetes
  
• PCSK9 Inhibitors: For patients with genetic dyslipidemia not responsive to statins

Medications That May Worsen Risk Profile:

• Corticosteroids: Elevate glucose and triglyceride levels
  
• Second-generation antipsychotics: Associated with weight gain and dyslipidemia
  
• Hormone therapies: Certain forms may adversely affect cardiovascular risk markers

Medication decisions should balance benefits with metabolic impacts and be reviewed regularly.

Functional Medicine Approach at Intercoastal Health

Our goal is to identify early vascular dysfunction and reverse risk factors before irreversible damage occurs. A personalized, biomarker-guided treatment plan allows for sustainable improvements in cardiovascular health.

Core Strategies Include:

• Anti-Inflammatory Nutrition: Omega-3 fats, fiber, phytonutrients, whole foods; reduce processed foods, sugars, and trans fats
  
• Lipid Optimization: Target particle size, oxidation status, and ratios; supplementation (plant sterols, niacin, red yeast rice)
  
• Insulin and Glucose Regulation: Intermittent fasting, carbohydrate periodization, nutrients (chromium, magnesium, berberine)
  
• Oxidative Stress Reduction: Mitochondrial support (CoQ10, NAC, alpha-lipoic acid), moderate physical activity
  
• Stress Management and Sleep Hygiene: HRV training, relaxation techniques, treat sleep apnea
  
• Ongoing Biomarker Monitoring: Regular lipid panels, CRP, and insulin assessments; adjust interventions based on response

This individualized framework supports vascular resilience and reduces the likelihood of acute cardiovascular events.