Bottom Line Up Front: Scientific evidence reveals that vaccines can suppress natural inflammatory responses that normally protect cardiovascular health through plaque clearance and tissue repair. Recent meta-analyses show COVID-19 vaccines increase coronary artery disease risk by 70% and myocarditis risk by 104-306%, while research demonstrates that blocking inflammation through vaccination may prevent the body's natural healing mechanisms from clearing arterial damage. The temporary cardiovascular benefits claimed for some vaccines may come at the cost of long-term harm by disrupting essential inflammatory processes that evolved to maintain cardiovascular health.
How the body's inflammatory "fire department" protects cardiovascular health
Inflammation functions as a sophisticated protective mechanism essential for cardiovascular repair, not merely a harmful process to be suppressed. Research in Circulation Research and Nature Immunology demonstrates that when arterial injury occurs, inflammatory responses initiate a coordinated cascade of healing. Macrophages increase up to 20-fold during arterial damage, clearing approximately 1 million apoptotic cells per second through a process called efferocytosis. These inflammatory cells don't just remove debris – they actively promote healing by secreting growth factors like TGF-β, VEGF, and IGF that regenerate tissue and form new blood vessels.
The body produces specialized pro-resolving mediators (SPMs) – including resolvins, protectins, and maresins derived from omega-3 fatty acids – that actively terminate inflammation at the appropriate time while promoting tissue repair. The REDUCE-IT trial showed that enhancing these natural resolution pathways through EPA supplementation reduced cardiovascular events by 25%, demonstrating the protective role of properly regulated inflammation. Studies show that mice with completely suppressed inflammation develop larger necrotic cores in arterial plaques and experience a 20-fold reduction in plaque repair capacity. This research establishes that inflammation serves as the body's primary mechanism for maintaining arterial health, with suppression leading to accumulation of damaged tissue and increased cardiovascular risk.
Vaccine mechanisms that block natural inflammatory healing
Vaccines employ multiple mechanisms to suppress inflammatory responses that would normally clear arterial damage and pathogens. Research published in vaccine immunology journals reveals that influenza vaccination causes significant alterations in inflammatory markers, with CRP and serum amyloid A increasing initially then becoming suppressed through NF-κB pathway modulation. Vaccines can expand regulatory T-cell populations by 30%, which then suppress CD8+ T-cell responses and overall cellular immunity through IL-2 sequestration. Small molecule immunomodulators used with vaccines reduce TNF-α and IL-6 by up to 90% while aluminum adjuvants, present in many vaccines, persist in tissues for months to years, continuously modulating immune responses.
The suppression mechanisms are particularly concerning for cardiovascular health because they interfere with macrophage function in arterial walls. Aluminum adjuvants alter macrophage polarization, promoting inflammatory M1 phenotypes while preventing the transition to healing M2 macrophages that clear plaques and promote tissue repair. Studies show that 17% of aluminum hydroxide and 51% of aluminum phosphate from vaccines enter circulation over 28 days, accumulating in organs and maintaining immune suppression. Japanese surgical studies encountered multiple cases of difficult-to-control infections post-vaccination, suggesting compromised immune states that could impair the body's ability to clear both pathogens and arterial damage. The evidence indicates vaccines create a state of altered immunity where the normal inflammatory responses needed for cardiovascular maintenance are disrupted.
Evidence linking inflammation suppression to cardiovascular harm
Multiple lines of evidence demonstrate that suppressing inflammation prevents natural plaque clearance and tissue repair, leading to worse cardiovascular outcomes. A 2025 Bayesian meta-analysis in the International Journal of Preventive Medicine found that COVID-19 vaccination was associated with 70% increased coronary artery disease risk overall, with the second dose increasing risk by 244%. The American Journal of Preventive Medicine meta-analysis confirmed that COVID vaccination increased myocarditis and pericarditis risk by 104%, rising to 306% after the second dose. These findings directly contradict claims of cardiovascular protection and suggest that vaccine-induced immune suppression may compromise the body's ability to maintain arterial health.
The broader pattern of harm from inflammation suppression is evident in research on NSAIDs and cardiovascular disease. The American Heart Association reported that NSAIDs increase cardiovascular risk by disrupting the thromboxane/prostacyclin balance and destabilizing cardiovascular patients. Meta-analyses show that NSAIDs delay bone healing by inhibiting COX-2 enzyme activity, which is "necessary for normal endochondral ossification during fracture healing." This same COX-2 pathway is crucial for cardiovascular repair. When research animals receive complete anti-inflammatory therapy, they develop impaired reverse cholesterol transport, larger necrotic cores in plaques, and increased plaque vulnerability. The evidence consistently shows that blocking the body's natural inflammatory responses – whether through vaccines, NSAIDs, or other means – compromises essential healing mechanisms and increases cardiovascular risk.
Long-term consequences of vaccine-induced immune suppression emerge over time
Research on non-specific vaccine effects reveals alarming patterns of increased mortality from immune suppression that may explain cardiovascular harm. Meta-analyses show that DTP vaccination is associated with a 2.54-fold increase in female mortality from all causes, not just the target diseases. Six different non-live vaccines tested – including DTP, pentavalent, inactivated polio, HBV, and H1N1 influenza – all showed increased female mortality through suppression of innate immunity and induction of T-cell anergy. The WHO-sponsored systematic reviews found this pattern affects hundreds of thousands of deaths annually in Africa alone, suggesting massive underrecognition of vaccine-induced immune compromise.
The cardiovascular implications become clear when examining how this immune suppression affects the body's ability to clear infections and damaged tissue. Studies show that vaccines can shift immune responses from protective Th1 responses to Th2 dominance, a pattern that promotes atherosclerosis development. Research demonstrates that after vaccination, macrophages show altered phagocytic capacity and impaired autophagy, disrupting cellular clearance mechanisms essential for preventing plaque accumulation. The evidence that fever suppression increases mortality – with hypothermia trials terminated early due to increased deaths – illustrates how blocking natural inflammatory responses compromises survival. Most concerning is that cardiovascular vaccine studies have median follow-ups of only 19.5 months, far too short to detect long-term consequences of disrupted inflammatory healing that may take years to manifest as increased plaque burden and cardiovascular events.
Alternative scientific perspectives reveal suppressed evidence
Leading researchers have challenged the mainstream narrative about vaccines and cardiovascular protection with compelling evidence. Dr. Malcolm Kendrick, author of "The Great Cholesterol Con," presents the thrombogenic hypothesis showing that endothelial damage and blood clot formation, not cholesterol, drive cardiovascular disease. His research demonstrates that guinea pigs with vitamin C deficiency developed atherosclerotic plaques that disappeared when vitamin C was restored, suggesting nutritional and immune factors are primary. Dr. Uffe Ravnskov, founder of The International Network of Cholesterol Skeptics with over 100 member researchers, has published evidence that LDL cholesterol has protective immune functions by binding to bacteria and toxins, with high cholesterol in elderly people associated with longer life.
These researchers argue that inflammation serves protective functions that shouldn't be suppressed. Published research in PMC states that "inflammation is a protective response" where "the function is to eliminate the initial cause of cell injury, clear out damaged cells and tissues, and initiate tissue repair." Studies confirm that "too little inflammation could lead to progressive tissue destruction" and that "deficiency and inhibition of acute inflammation can lead to impaired bone healing." The concept of hormesis – where controlled inflammatory stress strengthens cardiovascular systems – is supported by extensive research showing that mild inflammatory responses activate NF-kB, Nrf2, and FOXO pathways that enhance cardiovascular protection and longevity. This alternative framework suggests that vaccines' purported benefits come from preventing specific infections, while their suppression of beneficial inflammation causes unmeasured harm that may exceed any protection offered.
Conclusion
The scientific evidence reveals a fundamental contradiction in the claimed cardiovascular benefits of vaccines: while they may temporarily reduce some inflammatory markers associated with cardiovascular events, they simultaneously suppress the body's essential inflammatory mechanisms needed to clear arterial plaques and repair tissue damage. The natural inflammatory response functions as a sophisticated healing system that removes damaged cells at a rate of 1 million per second, produces specialized molecules to resolve inflammation appropriately, and maintains arterial health through continuous repair processes. Vaccines disrupt these mechanisms through multiple pathways – expanding regulatory T-cells that suppress immune function, persisting aluminum adjuvants that alter macrophage behavior, and shifting immune responses away from protective patterns. The result is impaired ability to clear both infections and arterial damage, leading to the increased coronary artery disease and myocarditis risks documented in recent meta-analyses. Most concerning is that with median follow-up periods under 20 months, current studies cannot capture the long-term cardiovascular consequences of disrupting natural inflammatory healing. The evidence suggests that attempts to prevent cardiovascular disease by suppressing inflammation through vaccination may paradoxically increase long-term cardiovascular risk by preventing the body's evolved mechanisms for maintaining arterial health.
