© by Elizabeth Lee Vliet MD and Kathy Kresnik
Many of my patients and our readers already know a great deal about the benefits of Omega 3 fatty acids in fish oils to reduce heart disease risk, improve brain health, reduce inflammatory joint pain, and improve eyesight. We have summarized these amazing health benefits in my earlier Health Tip. During Heart Month, I wanted to refocus on the emerging science on inflammation and the crucial role of fish oils as another natural strategy to reduce inflammation and therefore reduce risk of heart attacks, strokes, and small vessel disease that can lead to other vascular problems like erectile dysfunction and Reynaud’s. Estrogen loss in menopausal women and testosterone loss in aging men, plus the spike protein damage of the COVID shots, all combine to accelerate inflammation and damage to heart, brain and blood vessels. Menopausal status is recognized as a significant factor increasing cardiovascular disease risk in women, primarily due to the reduction of estrogen’s anti-inflammatory role and protective effects on vascular, lipid, and metabolic function.
In today’s Health Tip, I also explain the inflammatory markers you can track. This is another way to help YOU be more proactive in your health and get the tests you need that your doctor may not routinely check. Many are tests you can order yourself on line, so you don’t even need a physician to give you permission! Then I’ll explain effective strategies YOU can choose to implement to lower inflammation and your overall risk for heart disease. With the known spike protein and lipid nanoparticle damage from the COVID shots ADDING massively to the inflammatory burden on the body, it is even more critical to understand and take action to reduce inflammation in your body to reduce cardiovascular disease and preserve brain function.
Since the late 1990s inflammation has been widely recognized as an important and independent risk factor for cardiovascular disease. The explicit hypothesis that atherosclerosis is an inflammatory disease was prominently articulated by Russell Ross in 1999, which is often cited as the modern turning point in framing inflammation as central to atherogenesis (process by which atherosclerotic plaques (atheromas) form) and its complications.
But even to this day, with all we now know, most doctors and public health agencies still FAIL to include inflammation among the “primary 8” traditional risk factors in standard public‑facing checklists:
- High blood pressure (hypertension) – Chronically elevated blood pressure damages the endothelium and accelerates atherosclerosis, making careful management essential for heart health.
- High atherogenic cholesterol / dyslipidemia – Elevated levels of LDL and non-HDL cholesterol, often accompanied by low HDL and high triglycerides, significantly increase risk.
- Cigarette smoking / tobacco exposure – Both active smoking and regular exposure to secondhand smoke contribute to vascular injury and heightened risk.
- Diabetes mellitus (and significant hyperglycemia) – Type 1 and type 2 diabetes are powerful, independent drivers of atherosclerotic cardiovascular disease (ASCVD) risk.
- Obesity, particularly central/visceral adiposity – Excess body fat, especially around the abdomen, is strongly linked to insulin resistance, hypertension, dyslipidemia, and chronic inflammation.
- Physical inactivity / sedentary lifestyle – Low cardiorespiratory fitness is an independent risk factor, and regular physical activity is crucial for prevention as well as psychological stress and poor sleep.
- Unhealthy diet / unhealthful nutrition – Diets high in saturated and trans fats, refined carbohydrates, sodium, and ultra-processed foods (and low in fruits, vegetables, and fiber) promote atherosclerosis.
- Family history / genetic susceptibility for premature cardiovascular disease – A history of early myocardial infarction or sudden cardiac death in first-degree relatives signals higher risk.
ALL of these factors, except family history, are modifiable if YOU make the right choices that should be a focus of any personal health plan. But in more up-to-date medical practices, physicians will also focus on chronic inflammation as an explicit risk factor and track inflammatory markers to help guide patients to individualized heart disease prevention strategies.
The Role of Inflammation: Emerging Understandings
Inflammation is finally being acknowledged as a critical and independent risk factor for cardiovascular disease. Major cardiovascular organizations now describe inflammation as a driver of atherosclerosis and a modifiable risk pathway. Recent large epidemiologic studies and meta-analyses have demonstrated that higher levels of inflammatory biomarkers—including high-sensitivity C-reactive protein ( hs-CRP ), interleukin-6 (IL-6), fibrinogen, and galectin-3—independently predict cardiovascular events, even after accounting for traditional risk factors.
The 2025 American College of Cardiology scientific statement on inflammation and heart disease stated that ”residual inflammation, measured with high-sensitivity C-reactive protein ( hs-CRP ) remains strongly predictive of recurrent events, even in statin-treated patients. Similarly, elevated hs-CRP in apparently healthy individuals identifies a higher-risk group in whom statin therapy significantly reduces the risk of first major CVD events even if LDL-cholesterol is normal.” And that “the evidence linking inflammation with atherosclerotic CVD is no longer exploratory but is compelling and clinically actionable”.
This evidence establishes inflammation as both a causal and predictive risk factor in atherosclerotic disease. Inflammation should be an added therapeutic target. Elevated inflammatory markers should prompt quick action with anti-inflammatory strategies, even when LDL cholesterol is not dramatically elevated. As you can see in the graph below, the higher your inflammation as measured by hs-CRP , the higher your risk of future cardiovascular events.
Inflammation Effects on the Heart
Inflammation is central to atherosclerosis, plaque instability, and heart failure progression, and affects the heart in several specific ways:
- In atherosclerosis, LDL buildup and immune cell recruitment trigger an inflammatory response. Cytokines such as IL‑1, IL‑6, and TNF‑α lead to a foam cell formation, plaque growth, and thinning of the fibrous cap which increases risk of rupture and thrombosis.
- Systemic inflammatory mediators contribute to endothelial dysfunction, increase oxidative stress, and activate pro‑thrombotic pathways which can lead to blood clots and thereby increase risk of coronary and vascular events.
- In heart failure, elevated hs-CRP and IL‑6 are consistently associated with incident of heart failure and worse outcomes and genetic and clinical data support a causal role of IL‑6 signaling in heart failure and coronary artery development.
If your hs-CRP and IL-6 are higher than normal, you have a greater chance of having a heart attack, stroke, or heart failure—even when your cholesterol is under control. People with heart problems or heart failure tend to do worse if these levels are high. This is why it is important to check your inflammation levels at least annually. Here are some of the tests you can ask your doctor to do, and many are tests you can order on-line yourself if your doctor doesn’t do them.
Inflammation Markers Explained
Inflammation can be reflected in many different blood markers, from broad acute‑phase reactants to more specific cytokines and cell‑based indices. Core routine inflammatory markers are the ones most commonly ordered in general practice and hospitals. These include:
- C‑reactive protein (CRP, including high sensitive CRP – hs-CRP) is a liver‑derived acute‑phase protein that rises quickly with systemic inflammation (infection, tissue injury, many inflammatory diseases like arthritis and others) and falls rapidly as inflammation resolves. CRP is a non-specific inflammatory marker and will rise for many reasons. But it is commonly used as a marker of the low‑grade inflammation in blood vessels that is a surrogate for cardiovascular risk.
For cardiovascular risk, a healthy hs-CRP is generally considered to be below 1 mg/L and ideally closer to the lower end of that range (0.2-0.7 mg/L). hs-CRP higher than 3.0 mg/L is considered high and reflects chronic low-grade inflammation that is used as a marker of heart disease risk, even though there can be other causes of hs-CRP higher than 3.0. If hs-CRP is higher than 10 mg/L, it usually suggests presence of an infection or an acute inflammatory process. It should be repeated two weeks after recovery before being used as a cardiovascular risk indicator. Elevated hs-CRP levels should be repeated at least two weeks apart and the average score used for making risk and intervention decisions.
For assessing risk of cardiovascular disease and/or metabolic syndrome, panels that combine hs-CRP and IL-6 markers to assess vascular inflammation offer a more comprehensive evaluation of cardiovascular risk beyond standard lipid panels of cholesterol, LDLs, HDLs, etc.
- Erythrocyte sedimentation rate (ESR) is an indirect marker of plasma acute‑phase proteins via red cell aggregation. ESR changes more slowly than CRP and is influenced by anemia, age, and other factors and isn’t as widely used for CVD risk.
- Plasma viscosity (PV) – Reflects blood protein content/viscosity; often used similarly to ESR and can be sensitive for conditions like rheumatoid arthritis.
- Procalcitonin (PCT) – Pro‑hormone that rises with systemic bacterial infection; used especially for pneumonia and sepsis and to guide antibiotics.
Other acute‑phase proteins that are established inflammatory markers, even though doctors don’t order these tests as often include:
- Serum amyloid A (SAA) – Acute‑phase protein that can rise markedly in acute inflammation and infection.
- D-dimer – a marker of the presence of break-down fragments of micro (or macro) blood clots. May be elevated after COVID shots, in viral or bacterial infections, pulmonary emboli, deep vein thrombosis, strokes and heart attacks. When elevated, it indicates the presence of micro blood clots that can progress to major clots that can cause heart attacks, strokes or sudden death.
- Fibrinogen – Coagulation factor and acute‑phase reactant; high levels are seen in blood clots, systemic inflammation, and heart disease risk.
- Ferritin – Iron‑storage protein that also behaves as an acute‑phase reactant; elevated in many inflammatory and infectious states independent of the status of your iron stores.
- Haptoglobin, mannose‑binding lectin (MBL) – Additional acute‑phase proteins that typically increase with inflammation.
- Negative acute‑phase proteins which drop with inflammation: albumin, transferrin, transthyretin (prealbumin).
Cytokines and signaling markers reflect immunologic signals and are mainly used in research or specialized clinical contexts.
- Pro‑inflammatory cytokines:
- Interleukin‑6 (IL‑6) – Central mediator of acute‑phase response, stimulates CRP production; elevated in many acute and chronic inflammatory states and in cardiovascular risk studies.
- Tumor necrosis factor‑alpha (TNF‑α), IL‑1β, IL‑8, interferon‑gamma (IFN‑γ) have various roles in driving leukocyte activation, fever, and systemic inflammation.
- Anti‑inflammatory/immune‑modulating cytokines: IL‑10 and others are sometimes measured to assess immune competence and balance.
Cell‑based and composite indices: Standard Complete Blood Count (CBC) is a routine laboratory test that is usually ordered as part of every annual physical that can be repurposed as inflammation markers.
- Neutrophil‑to‑lymphocyte ratio (NLR) – Calculated from a CBC; elevated ratio is associated with systemic inflammation and adverse outcomes in multiple conditions.
- Platelet count – Thrombocytosis can accompany chronic inflammation and some malignancies.
- Red cell distribution width (RDW) – Higher RDW correlates with chronic inflammation and worse prognosis in several diseases.
- Other ratios sometimes used in studies: platelet‑to‑lymphocyte ratio (PLR), lymphocyte‑to‑monocyte ratio (LMR), atherogenic index of plasma (AIP) as an inflammation‑linked cardiometabolic risk measure.
Many of the above tests may not be relevant for most people, but I wanted you to see we actually have many ways to check for inflammation in the body, which we can use to guide treatment and lifestyle changes.
Anti-Inflammatory Medication and Lifestyle Change Strategies
Drug trials show that directly dampening vascular inflammation in high-risk patients can reduce major events by roughly 20–30% beyond optimal lipid management. If you are in this category, your physician and/or cardiologist should discuss medication strategies with you.
What about the effectiveness of reducing heart disease risk using lifestyle changes to reduce your systemic inflammation? Here are some interesting statistics on strategies that can used with prescription medications for high-risk individuals. These can serve as preventive “medicine” for lower risk and healthy individuals wanting to reduce later risk of disease.
- Lifestyle interventions (diet, exercise, weight loss, stress management) that improve metabolic health typically lower hs-CRP and IL‑6 and are associated with better cardiovascular outcomes in group and interventional studies.
- Multicomponent lifestyle programs (Mediterranean/plant‑forward diets, increased activity, smoking cessation, weight loss) have produced ~30% reductions in hs-CRP over one year and were accompanied by improvements in blood pressure, lipids, insulin resistance, and clinical risk scores.
- Inflammation reduction: In patients with or at high risk for atherosclerotic cardiovascular disease (ASCVD), targeting a low‑inflammation profile (e.g., hs-CRP <2 mg/L) with aggressive LDL lowering yielded better outcomes than treating lipids alone.
Lifestyle changes reduce both systemic inflammation and the classic heart disease risk factors, so we cannot attribute the benefit solely to reducing inflammation. It really isn’t possible to say it is either-or. BOTH classic heart disease risk factors AND inflammation can be significantly improved through lifestyle and natural solutions and together, these changes show documented benefit to decrease future heart disease.
Anti-Inflammatory Supplements
The single supplement that consistently tops the list with the strongest evidence is omega-3 fatty acids EPA and DHA most commonly found in fish oil. We now have extensive human data showing that Omega 3 fatty acid (fish oil) supplements are a natural approach to reducing inflammation and heart disease risk, demonstrated objectively by reductions in markers like CRP, IL‑6, and TNF‑α, when used as adjuncts to dietary changes, weight loss, improving sleep, and increasing exercise.
Multiple research clinical trials and meta‑analyses show that fish‑oil–derived omega‑3s reduce hs-CRP and other inflammatory markers, particularly at doses ≥1–1.5 g/day combined EPA+DHA, in patients with elevated inflammation or cardiometabolic risk. A dose–response meta‑analysis showed that 1200 mg/day EPA+DHA significantly lowered CRP in cardiometabolic patients, and a 3.6 g/day regimen reduced CRP by roughly 23% over 6 months in high‑CRP adults.
How to Choose the Best Fish Oil
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