Atherosclerotic Plaque and Infection Part Two by Jeffrey Dach MD
Back in 2019, I received a telephone call from the president of ICIM, Dr. Eric Born who was impressed with my book, entitled, Heart Book (2018) and invited me to speak at the ICIM meeting (International College of Integrative Medicine) in Philadelphia. Around this same time, I met Stephen Fry MD, a pathologist in Arizona, who informed me that atherosclerotic plaque contains polymicrobial biofilm infected with multiple organisms. I was honored to speak at the ICIM meeting. From the podium, I recognized Dr. Stephen Fry in attendance and I publicly praised his research on polymicrobial biofilm in atherosclerotic plaques.
Header Image: Histopathology of atheroscleroisis in a coronary artery with 45-50% stenosis. Mikael Häggström, M.D. Link to image on Wikimedia Commons.
Dr. Thomas Levy
Also speaking at the 2019 ICIM meeting was the legendary Dr. Thomas Levy, who gave a great talk on dental infection seeding atherosclerotic plaques with oral microbes. Dr. Levy urged all practitioners to order dental X-rays in patients with coronary artery disease to find underlying dental infections. Indeed, modern imaging with scanning electron microscopy of vascular wall biopsies shows the typical rod-shaped and spherical-shaped microorganisms entangled in a mesh-like network compatible with infected biofilm (see image descriptions below). More of this topic is available from Dr. Levy’s 2017 book, Hidden Epidemic.
Benefits of the Plant-Based Diet Dr. Joel Kahn
Another speaker at the meeting was cardiologist, Joel Kahn, MD, who spoke about the plant-based diet. He also discussed metabolic endotoxemia (“leaky gut”) as another source of origin for seeding infection into the atherosclerotic plaque, thus contributing to heart disease. Both Joel Kahn and Kirk Hamilton mentioned the 2017 article by Dr. Esselstyn, who conducted a plant-based diet study of almost 200 patients with significant coronary artery disease. Dr. Esselstyn writes that during four years of follow-up, 99.4% of adherent participants avoided major cardiac events, and angina improved or resolved in 93%. Both Kirk Hamilton and Stephen Fry speculate that the efficacy of the plant-based diet may be due in part to antimicrobial properties of plants (one example being garlic). Dr. Stephen Fry’s pathology lab has identified soil fungal organisms in atherosclerotic plaque specimens. Dr. Fry notes that plants root in the soil and are exposed to soil fungi; over centuries, they have developed resistance to soil fungi for their own survival. For more on this topic see: Plant Based Diet Benefits for Coronary Artery Disease
Infection-Based Model of Atherogenesis with Polymicrobial Biofilm
50 Carotid Arteries
In 2000, Dr. Violet Haraszthy examined atherosclerotic plaque from 50 human carotid endarterectomy specimens using 16s ribosome PCR (16S rDNA) looking for periodontal pathogens using Polymerase Chain Reaction (PCR) They found bacterial 16S rDNA in 72% of specimens and at least one target periodontal pathogen in 44% of atheromas, with multiple species (including Bacteroides forsythus, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Prevotella intermedia) often co-detected in the same plaque. This early study provided strong evidence for polymicrobial colonization of atherosclerotic plaques by oral bacteria. Note: 16s rDNA is the DNA in bacteria which codes for ribosomes, the molecular machines that make proteins in the bacteria. Note: The PCR test was invented by Kary Mullis in 1983, who received the Nobel Prize in Chemistry in 1993. (1)
38 Patients with Coronary Artery Disease
Bacterial DNA was detected in all CHD patients but not in controls or unaffected arteries
In 2006, Dr. Stephan Ott systematically analyzed 16S rDNA signatures in atherosclerotic tissue from 38 patients with coronary heart disease (CHD) using clone libraries, denaturing gradient gel electrophoresis, and fluorescence in situ hybridization (FISH). Bacterial DNA was detected in all CHD patients but not in controls or unaffected arteries. They identified a high bacterial diversity of >50 different species (including Staphylococcus, Proteus, Klebsiella, and Streptococcus species) in >1,500 clones, with a mean diversity score of 12.33 per atheroma. Chlamydia species were detected in over half the patients. This landmark study demonstrated that diverse bacterial colonization, rather than a single pathogen, is common in atherosclerotic lesions. (2)
In 2011, Dr. Omry Koren compared oral, gut, and plaque microbiota in patients with atherosclerosis using 16S rRNA sequencing and quantitative PCR (qPCR). They found bacterial DNA in atherosclerotic plaques, with oral and gut bacteria correlating with disease markers. Specific taxa such as Chryseomonas, Veillonella, and Streptococcus were prominent in plaques, supporting the idea that bacteria from distant sites (oral cavity and gut) can colonize and persist in atheromas as part of polymicrobial communities. (3)
In 2017, Drs. Jeremy Ellis and Stephen Fry) examined explanted vascular filters and atheroma debris from patients and provided evidence for polymicrobial communities, including both prokaryotic and eukaryotic microbes. Their molecular assays detected diverse bacterial and fungal signatures, supporting the presence of complex polymicrobial biofilms in vascular debris and atheromas. (4)
Meta-Analysis of 44 Studies
In 2022, Iman Razeghian-Jahromi et al. conducted a meta-analysis of 44 studies investigating the prevalence of microorganisms in atherosclerotic plaques of coronary arteries in patients with coronary artery disease. Bacterial DNA was commonly detected, with the highest prevalences for Prevotella intermedia (47.6%), Aggregatibacter actinomycetemcomitans (46.2%), Tannerella forsythia (43.7%), Campylobacter rectus (43.0%), Porphyromonas gingivalis (42.6%), and Chlamydia pneumoniae (42.8%). This large-scale analysis confirms that multiple periodontal and other pathogens frequently coexist in coronary plaques and may play a significant role in atherosclerosis development. (5)
Periodontal Bacteria
In 2023, Dr. Xiaofei Huang reviewed the roles of periodontal bacteria in atherosclerosis. He found pathogens in plaques such as Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Fusobacterium nucleatum. These micro-organisms cause endothelial barrier disruption, immune system activation, facilitation of monocyte adhesion and aggregation, and promote foam cell formation. The review emphasizes polymicrobial infection as driver of atherosclerotic plaque progression and destabilization. (6)
Scanning Electron Microscopy of Atherosclerotic Plaque Specimens
In 2014, Dr. Zahra Armingohar used scanning electron microscopy (SEM) and molecular biology methods to study atherosclerotic plaque and aneurysmal wall biopsies taken from patients with and without periodontitis. Bacterial DNA was detected in 95% of vascular biopsies, with higher load and diversity in periodontitis patients. SEM revealed rod- and coccus-shaped bacteria coaggregated in micro-colonies entangled in a meshwork of delicate fibers, with evidence of active division, indicating polymicrobial infected biofilm. (7)
Biofilm Evidence in Atherosclerotic Plaques
In 2014, Dr. Bernard Lanter examined carotid arterial plaques from 15 patients and detected 16S rRNA bacterial genes in all samples. Density gradient gel electrophoresis showed polymicrobial colonization with 10–18 distinct bacterial species per sample. Using peptide nucleic acid fluorescence in situ hybridization (PNA-FISH) with an eubacterium-specific probe, they visualized bacteria forming biofilm deposits within the plaques, mostly proximal to the internal elastic lamina and associated with fibrous tissue. Pseudomonas species were identified in several plaques. This study provided direct microscopic evidence of biofilm architecture in human atherosclerotic plaques and suggested that biofilm dispersion triggered by norepinephrine could contribute to plaque instability and rupture. Note: norepinephrine is released by the autonomic nervous system, and its release is inhibited by Beta Blocker drug, propranolol. (8)
Analysis of 63 Studies
In 2016, Dr. Jyoti Chhibber-Goel performed a comprehensive analysis of 63 studies involving 1,791 patients and confirmed the presence of 23 oral commensal bacteria within atherosclerotic plaques. Dr. Chhibber-Goel found plaque-associated bacteria forming biofilm structures, such as “corncob-like” formations involving Fusobacterium nucleatum and Streptococcus species, consistent with polymicrobial communities that may persist and drive chronic inflammation after migrating into the plaque via the bloodstream. (9)
121 Sudden Death Victims
In 2025, Dr. Pekka Karhunen analyzed coronary plaques from 121 sudden-death victims, and endarterectomy samples from 96 surgical patients using real-time quantitative PCR, and immunohistochemistry. Oral viridans group streptococcal DNA was the most common, detected in approximately 42% of both coronary plaques and endarterectomies. Immunohistochemistry showed viridans streptococci colonizing the lipid core and wall of atheromas as biofilm-like structures that evaded detection by macrophages of the innate immune system. The cells within the plaque stained CD68-negative, meaning they were not macrophages. In ruptured or symptomatic atherosclerotic plaques, dispersed bacteria from the biofilm infiltrated the fibrous cap, triggered pattern-recognition receptors, and co-localized with adaptive immune responses. Toll Receptor 2 (TLR2) was the most activated pathway which recognized the bacterial antigen. Viridans streptococcal immunopositivity correlated with severe atherosclerosis and death from coronary heart disease or myocardial infarction. This study provides compelling evidence that latent chronic bacterial biofilms in plaques can evade immune detection, contribute to inflammation, and promote plaque rupture leading to myocardial infarction. (10)
16S and 23S Ribosome DNA Found in Atheromas Using FISH Supporting PolyMicrobial Biofilm
In 2015, Dr. Bernard Lanter used fluorescent in-situ hybridization (FISH) for 16S and 23S rRNA genes on carotid artery specimens, identifying bacterial signatures (including P. acnes) localized within diseased atheroma tissue but absent in healthy controls. Dr. Lanters two studies in 2014 and 2015, and Dr. Pekka Karhunen’s 2025 study of sudden death victims all support polymicrobial biofilm rather than isolated single microorganisms within atherosclerotic plaques. (10) (16)
Not Yet Accepted by Mainstream Medicine
More than 100 years ago, early pathologists suspected atherosclerosis was caused by infection. After all these years, modern molecular and imaging techniques such as 16S rDNA sequencing and FISH confirm that early pathologists were quite correct. Large meta-analyses confirming high prevalence of multiple micro-organisms within atherosclerotic plaque forming biofilm with high polymicrobial diversity. Imaging techniques such as Scanning Electron Microscopy (SEM) and Flourescent In-situ Hybidization (FISH) gives directly visualization and confirms atherosclerotic plaque as polymicrobial infected biofilms. These microbial biofilm communities originating from oral and gut bacteria contribute to chronic inflammation, plaque progression, and instability and exhibit immune evasion and dispersion. While still not accepted by mainstream medicine, the consistent evidence across highly cited studies strongly supports an infection/biofilm component in atherogenesis, and raises serious questions about the cholesterol theory of coronary artery disease.
Despite the accumulating molecular and imaging evidence, mainstream cardiology has yet to accept the infection theory, or polymicrobial biofilm infection theory, as a primary driver of coronary artery disease. In 2015, Drs. Lee Ann Campbell and Michael Rosenfeld reviewed the evidence linking infection to atherosclerosis development. Although epidemiological, pathological, and experimental data support infection as a contributing risk factor for chronic inflammation, large randomized antibiotic intervention trials in the 2000s failed to reduce cardiovascular events or mortality, leading them to be skepticism of the infected biofilm hypothesis. However, one would not expect antibiotics to work for biofilm. Antibiotics are known to be notoriously ineffective for infected biofilm at the following sites:chronic sinusitis, cystic fibrosis lung disease, chronic non-healing wounds, and catheter associated urinary tract infections. (11) (17-19)
Antibiotics Fail Against Bacterial Biofilm
Biofilms are structured communities of bacteria embedded in a protective extracellular matrix. This biofilm matrix, combined with reduced bacterial metabolic activity and other protective mechanisms, creates resistance to antibiotics requiring ten to a thousand fold higher concentration of antibiotics than for free-floating bacteria. This leads to persistence of infection despite antibiotic treatment. Bacteria in biofilms attached to surfaces or tissues form protected communities that resist host immune defenses and antibiotics leading to chronic, persistent infections that are difficult to eradicate as described in 1999 by Dr. Costerton and in 2001 by Dr. Stweart. (20-21)
Biofilms in Chronic Sinusitis
In 2005, Dr. Jose Sanclement used electron microscopy to study surgical speciments finding bacterial biofilms in 80% (24/30) of Chronic Rhino-Sinusitis (CRS) patients versus 0% in controls. Biofilms showed characteristic 3D structure, glycocalyx/matrix, and water channels. The presence of these protected communities in CRS mucosa helps explain why infections are recalcitrant and why antibiotics often provide only temporary relief before relapse as described by Dr Jose Sanclement in 2005. (22)
Artifact or Contamination?
Mainstream medicine has an opposing viewpoint. Detection of bacterial DNA and biofilm-like structures via sensitive molecular methods such as 16S rRNA PCR and FISH is frequently interpreted by mainstream medicine as merely artifact arising from contamination or environmental bacteria. Another opposing view is these findings represent secondary colonization of damaged plaques by bacteria engulfed and transported by macrophages, rather than evidence of primary active polymicrobial infection driving plaque initiation, progression, or rupture. I would reply that secondary colonization probably does occur, and is supportive rather than dismissive of the role of infected biofilms. These two ideas were noted as a possible explanations in 2006 by Dr. Stephan Ott and in 2016, Dr. Elena Ziganshina. These opposing perspectives are used by mainstream cardiology in order to maintain and prop up the cholesterol paradigm and continue to treat patients with statins and other lipid-lowering therapies , instead of anti-inflammatory and antimicrobial strategies directed at biofilms. (2) (12)
Aged Garlic AntiMicrobial Properties
Numerous randomized, double-blind, placebo-controlled trials led by Dr. Matthew Budoff beginning in 2004 and continuing through later studies in 2006, 2013, and 2020, show that aged garlic extract has antimicrobial properties that significantly slows the progression of coronary artery calcium (CAC) scores and reduces vulnerable low-attenuation plaque in patients with atherosclerosis, including those on statin therapy or with diabetes. Garlic is effective even though conventional antibiotics fail in similar settings. Biofilms are notoriously resistant to standard antibiotics because their protective extracellular matrix prevents penetration of the antibiotic allowing the bacteria to persist in a dormant state. The biofilm matrix acts as a barrier and protects micro-organisms from both immune clearance and antimicrobial agents. Natural compounds in garlic, allicin and other organosulfur molecules, exert antimicrobial effects through alternative mechanisms, such as disruption of biofilm formation, modulation of inflammation, or direct antimicrobial activity that overcomes antibiotic resistance. Mainstream cardiology views the presence of bacterial DNA within the atherosclerotic plaque as artifact and points to the failure of antibiotic clinicl trials, thus protecting the cholesterol theory and statin drug paradigm. Dr. Budoff’s numerous clinical trials using garlic for calcium score shows natural antimicrobials like garlic are effective for reducing progresion of calcium score, a marker of atherosclerotic plaque burden, while synthetic antibiotics fail to eradicate biofilm-protected micro-organisms, and have no effect on calium score. (13-15) (23-25)
Plant-Derived Antimicrobials Effective Against Bacterial Biofilms
The medical evidence for plant-derived antimicrobials is strongest for oral/periodontal pathogen models in which biofilm is disrupted using mechanisms such as quorum-sensing disruption, EPS reduction, and bacterial cell membrane damage. There are very few human clinical studies on using natural antimicrobials on atherosclerotic plaque biofilms. Most are in vitro or in vivo animal studies.
Note: EPS = Extracellular Polymeric Substances, the sticky, gel-like sticky biofilm matrix that bacteria produce and secrete around themselves. (Fleming, 2010) (27)
Note: GTFs are bacterial enzymes that polymerize sucrose into extracellular glucans,water-insoluble and soluble polysaccharides that are critical for biofilm formation. (Bowen, 2011) (28)
Note: Quorum sensing: bacteria communicate and coordinate group behaviors allowing the colony to act as a single multicellular organism. (Bowen, 2011) (29)
Garlic Organosulfurs (Aged Garlic, Allicin, Ajoene, Diallyl Disulfide)
Garlic has anti-biofilm properties by disrupting quorum sensing, inhibiting biofilm formation, and eradicating biofilms in various bacteria species, especially effective for oral pathogens as described in 2026 by Dr. Qumsani. For more, see the Chapter 8. Coronary Calcium Score, Benefits of Aged Garlic . (26)
Natural Substances with Antimicrobial Effects
In 2024, Dr. Roberto Arrigoni reviews the antimicrobial effects of natural compounds, writing:
Polyphenols like quercetin, curcumin, epigallocatechin gallate (EGCG), lanthypeptides (microbisporicin, cynnamin, and avermipeptin), and alkaloids (berberine and coptisin) are representative of natural products with antimicrobial activity...Curcumin, a polyphenolic compound, is a product derived from the stem of curcuma, with a broad spectrum of antibacterial activities against both Gram-negative and Gram-positive bacteria. Quite interestingly, curcumin possesses synergistic or additive antibacterial activity in combination with a series of antibiotics, such as polymyxin B, tetracycline, ciprofloxacin, colistin, and other natural adjuvants, i.e., berberine and epigallocatechin gallate (EGCG). Furthermore, curcumin has been demonstrated to inhibit biofilm formation, exerting antimicrobial effects against P. gingivalis. At the same time, curcumin exhibits anti-inflammatory activity, reducing levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-alpha while increasing the release of the anti-inflammatory cytokine, IL-10. (30)
The Apo-E Mouse Model of Atherosclerosis
The Apo-E knockout mouse is genetically modified to have hypercholesterolemia and accelerated atherosclerosis. This animal model is popular in research circles to study the effect of a drug or natural substance against the atherosclerotic process. A second genetic modification sometimes added to the mouse. This is the knock out of the LDL receptor, which makes the atherosclerosis worse, and even more advanced. (31-32)
Curcumin (from Turmeric) Animal studies, Anti-Biofilm and Anti-Inflammatory Effects
Curcumin has excellent anti-inflammatory effects via NF-Kb inhibition which reduces heart attacks and major cardiovascular events (MACE) in animal models, rabbits and APO-E mouse, and in human studies. Curcumin (from turmeric) has well-documented anti-inflammatory effects that include inhibition of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), a central transcription factor driving pro-inflammatory cytokine production, adhesion molecule expression, and atherosclerosis progression. This mechanism is supported by extensive in vitro, animal, and some human data. Multiple studies in ApoE-/- (apolipoprotein E knockout) mice and rabbits show reduced atherosclerotic plaque/lesion formation (a key precursor to heart attacks and major adverse cardiovascular events, or MACE). Human evidence includes reductions in post-CABG myocardial infarction (MI/heart attacks), inflammatory markers, and short-term MACE-related outcomes in small clinical trials. In the APO-E mouse model, curcumin inhibits biofilm formation, reduces EPS production, disrupts quorum sensing, and shows activity against oral pathogens and other bacteria. Efficacy is often enhanced in with nano-formulations.
In 2020, Dr. Saeed Mohammadian reviewed all the animal studies on curcumin, finding curcumin inhibits the atherosclerotic activity of the white cell of the immune system called a monocyte, a premature cell form which differentiates into a macrophage, writing:
we show that curcumin can exert antiatherosclerotic effect through inhibiting the atherogenic properties of monocytes, including inflammatory cytokine production, adhesion, and transendothelial migration, as well as intracellular cholesterol accumulation. Note: Monocytes and macrophages are immune cells. The monocyte is a white blood cell formed in the bone marrow that circulates through the bloodstream and infiltrates into arterial plaque.The macrophage is a mature, highly phagocytic form of a monocyte. A circulating monocyte infiltrates into arterial plaque and then transforms into a macrophage which engulfs oxidized low-density cholesterol (ox-LDL). Once the ox-LDL is inside, the macrophage then morphs into a foam cell, a key step in the atherosclerotic process. (33-37)
The ApoE/LDLR Double Knowkout Mouse Model of Atherosclerosis
In 2005, Dr. Olszanecki was first to report the anti-atherogenic effect of low dose of curcumin in the apoE/ LDLR-double knockout mice, an animal model of accelerated atherosclerosis formation. After four months of feeding curcumin to the mice, the formation of atherosclerotic plaque was reduced by almost 50 percent. Remarkably, this was accomplished without any significant change in serum cholesterol or triglycerides. Dr. Olszanecki writes:
Curcumin…premixed with diet, was given for 4 months at a dose of 0.3 mg/ per day/ per mouse. In this model curcumin inhibited atherogenesis, measured both by “en face” method and “cross-section” method (565,867 microm2 vs. 299,201 microm2, p<0,05). Importantly, curcumin influenced neither the concentrations of cholesterol and triglycerides in blood nor animal body weight. To our knowledge, this is the first report that shows the anti-atherogenic effect of low dose of curcumin in fine model of atherosclerosis: gene-targeted apoE/LDLR-double knockout mice. (39-41)
In many animal studies, cytomegalovirus (CMV) infection accelerates atherosclerisis. In 2020, Dr. Ya-li found curcumin effectively inhibited atherosclerosis in Apo-E mice infected with cytomegalovirus (CMV) by intraperitoneal injection of the virus. Dr. Ya-li found curcumin has outstanding anti-viral activity against CMV, writing:
Curcumin inhibits the formation of atherosclerosis in ApoE−/− mice by suppressing cytomegalovirus activity in endothelial cells. (42-44)
Curcumin Anti-Inflammatory Effects in Rabbit Model of Atherosclerosis
Curcumin was found to have anti-atherosclerotic and anti inflammatory effects in cholesterol fed rabbits, an early animal model for atherosclerosis. (45-46)
In 2025, Dr. Rajesh Yadav studied the therapeutic potential and mechanisms of curcumin in prevention of cardiovascular disease, commenting its anti-inflammatory properties through inhibition of the inflammatory master controller, Nuclear Factor kappaB (NF-kB), writing:
This article explores how curcumin reduces atherosclerosis by inhibiting NF-κB and MAPK signaling pathways, reducing oxidative stress, modulating lipid metabolism, and increasing nitric oxide bioavailability. Curcumin has been shown in preclinical studies to reduce aortic lesion area, inhibit pro-inflammatory cytokines, and improve endothelial function, and clinical trials show that it has the potential to improve vascular health in at-risk groups. (47)
Curcumin Antimicrobial Properties
In 2022, Dr. Yaseen Hussain explored the anti-microbial properties of curcumin, finding broad antibacterial, anti-fungal and anti-viral effects, writing:
Curcumin is a bioactive compound that is extracted from Curcuma longa and that is known for its antimicrobial properties…broad spectrum of antibacterial actions against a wide range of bacteria, even those resistant to antibiotics. Curcumin has been shown to be effective against the microorganisms that are responsible for surgical infections and implant-related bone infections, primarily Staphylococcus aureus and Escherichia coli. The efficacy of curcumin against Helicobacter pylori and Mycobacterium tuberculosis, alone or in combination with other classic antibiotics, is one of its most promising antibacterial effects. Curcumin is known to have antifungal action against numerous fungi that are responsible for a variety of infections, including dermatophytosis. Candidemia and candidiasis caused by Candida species have also been reported to be treated using curcumin. Life-threatening diseases and infections caused by viruses can be counteracted by curcumin, recognizing its antiviral potential. In combination therapy with other phytochemicals, curcumin shows synergistic effects, and this approach appears to be suitable for the eradication of antibiotic-resistant microbes and promising for achieving co-loaded antimicrobial pro-regenerative coatings for orthopedic implant biomaterials. Poor water solubility, low bioavailability, and rapid degradation are the main disadvantages of curcumin. The use of nanotechnologies for the delivery of curcumin could increase the prospects for its clinical application, mainly in orthopedics and other surgical scenarios. Curcumin-loaded nanoparticles revealed antimicrobial properties against S. aureus in periprosthetic joint infections. (48-49)
Human Study: Curcumin Reduces MI Associated with CABG
In 2012, Dr. Wongcharoen studied the benefits of curcumin in 121 patients in the hospital undergoing CABG finding antioxidant and anti-inflammatory effects of curcuminoids that may account for their cardioprotective effects. Curcumin reduced the incidence of in-hospital myocardial (MI) infarction after coronary artery bypass operation (CABG) to 13.1%, compared to incidence of 30% in the placebo group. This is a 56% reduction in MI in the curcumin group! Dr. Wongcharoen writes:
We aimed to evaluate whether curcuminoids prevent MI after CABG compared to placebo. The 121 consecutive patients undergoing CABG were randomly allocated to receive placebo or curcuminoids 4 g/day beginning 3 days before the scheduled surgery and continued until 5 days after surgery. The primary end point was incidence of in-hospital MI. The secondary end point was the effect of curcuminoids on C-reactive protein, plasma malondialdehyde, and N-terminal pro-B-type natriuretic peptide levels. Baseline characteristics were comparable between the curcuminoid and placebo groups. Mean age was 61 ± 9 years. On-pump CABG procedures were performed in 51.2% of patients. Incidence of in-hospital MI was decreased from 30.0% in the placebo group to 13.1% in the curcuminoid group (adjusted hazard ratio 0.35, 0.13 to 0.95, p = 0.038). Postoperative C-reactive protein, malondialdehyde, and N-terminal pro-B-type natriuretic peptide levels were also lower in the curcuminoid than in the placebo group. In conclusion, we demonstrated that curcuminoids significantly decreased MI associated with CABG. The antioxidant and anti-inflammatory effects of curcuminoids may account for their cardioprotective effects shown in this study. (50-52)
Curcumin Benefits for CABG Patient Same as Statin Drug
I was astounded to learn the anti-inflammatory benefit of curcumin for the patient undergoing CABG is similar to that obtained using a statin drug as shown in 2017 by Dr. Michael Curtis. Patients undergoing CABG on a statin drug roughly 50% reduction in peri-operative mortality, same as the above curcumin study by Dr. Wongcharoen. In other words, why use a statin drug when the same anti-inflammatory benefits can be obtained with curcumin? For more on this topic, see: Statins Reduce Peri-Operative Mortality, Surely You Must Be Joking.
and see: Statin Drugs Anti-Inflammatory Effects Reduce Mortality after Cardiac Surgery.(50-52)
Blood Thinning Effects
Perhaps some of the benefits in preventing MI in CABG patients may be due to blood thinning effects of both Curcumin and statins. Both statin drugs and curcumin have demonstrated blood-thinning effects. Both have antithrombotic, antiplatelet and anticoagulant properties. Statins have mild antithrombotic effects via decreased thrombin generation, enhanced fibrinolysis, and inhibition of platelet activation and aggregation. Curcumin (from turmeric) inhibits platelet aggregation via reduced thromboxane formation and calcium signaling, and has some anticoagulant properties. (54-55)
Self Reported Consumption of Curcumin
In 2019, Dr. Maryam Hashemian did a prospective cohort study of 44,000 participants followed 11 years and found the self-reported consumption of curcumin (turmeric) was associated with 10% reduced risk of overall mortality and 9% reduced risk of cardiovascular mortality. (53)
Curcumin and Statins Anti-inflammatory Effects
Perhaps the most convincing study on the anti-inflammatory benefits of statin drugs comes from the 2008 JUPITER Trial by Dr. Paul Ridker, who studied17,802 apparently healthy men and women with normal cholesterol levels, with LDL cholesterol less than 130 mg/dL. However, this group was selected for high inflammatory marker CRP was elevation, meaning high-sensitivity C-reactive protein (hs-CRP) was greater than 2.0 mg/L. The study group was randomized to rosuvastatin 20 mg daily or placebo. Rosuvastatin reduced LDL cholesterol by 50% and hs-CRP by 37%. The primary composite cardiovascular endpoint rate was reduced by 44% (hazard ratio 0.56). Thus showing the anti-inflammatory benefit of statin drugs, despite normal cholesterol levels. Dr. Paul Ridker writes:
in this randomized trial of apparently healthy men and women who did not have hyperlipidemia but did have elevated levels of high-sensitivity C-reactive protein, the rates of a first major cardiovascular event and death from any cause were significantly reduced among the participants who received rosuvastatin as compared with those who received placebo. (98)
This is the primary report of the JUPITER trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin). It randomized 17,802 apparently healthy men and women with LDL cholesterol <130 mg/dL and high-sensitivity C-reactive protein (hs-CRP) ≥2.0 mg/L to rosuvastatin 20 mg daily or placebo. Rosuvastatin reduced LDL cholesterol by 50% and hs-CRP by 37%. The primary composite cardiovascular endpoint rate was reduced by 44% (hazard ratio 0.56). (98)
More Supportive Studies, 2017 Cantos Trial by Dr. Ridker NEJM
In 2017, Dr. Paul M. Ridker did the CANTOS trial, in which10,000 patients with prior myocardial infarction and residual elevated inflammation (high-sensitivity C-reactive protein ≥2 mg/L) were randomized to the anti-inflammatory monoclonal antibody canakinumab (targeting interleukin-1β) at doses of 50, 150, or 300 mg every three months versus placebo, on top of standard care including high-intensity statins. Over a median 3.7 years, the 150 mg dose reduced the primary composite of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death by 15% (hazard ratio 0.85) without any reduction in LDL cholesterol or other lipids; CRP fell substantially in a dose-dependent manner. This directly supports the hypothesis that statins reduce cardiac events partly through anti-inflammatory effects rather than solely via cholesterol lowering: canakinumab achieved event reduction by pure inflammation inhibition (no lipid change), proving residual inflammatory risk drives recurrent events even when lipids are controlled. Because a pure anti-inflammatory intervention works, one would expect natural substances with comparable anti-inflammatory actions (for example plant-derived compounds that dampen the same IL-1β/IL-6/CRP pathway) to confer analogous cardiovascular protection.
In 2018, Dr. Paul M. Ridker did a secondary analysis of CANTOS Trial examining whether the degree of CRP reduction after canakinumab predicted benefit. Patients who achieved on-treatment hsCRP <2 mg/L experienced a 25% reduction in major adverse cardiovascular events and a 31% reduction in both cardiovascular and all-cause mortality, whereas those whose CRP remained ≥2 mg/L showed little or no significant benefit; the relationship held across multiple sensitivity analyses. The magnitude of inflammation reduction, not baseline characteristics or lipid changes, determined outcome improvement. This reinforces that statin benefits arise substantially from their anti-inflammatory actions (statins also lower CRP), because the clinical gains tracked tightly with CRP lowering independent of lipids. Consequently, natural anti-inflammatory agents such as curcumin, capable of producing similar sustained CRP reductions would be expected to yield comparable reductions in cardiac events.
2017, Dr. Paul M. Ridker did an analysis of the same CANTOS cohort, canakinumab produced a dose-dependent reduction in incident lung cancer and lung-cancer mortality (most pronounced at higher doses), alongside the cardiovascular benefits, again without lipid changes. Although focused on cancer, the finding demonstrates that targeting the identical inflammatory pathway produces systemic benefits beyond the vasculature. It further buttresses the statin hypothesis by showing that inflammation reduction alone (the non-lipid component of statin action) is biologically potent; natural substances such as curcumin sharing this anti-inflammatory mechanism could therefore deliver parallel cardiovascular (and potentially broader) protective effects.
Colchicine study
Colchicine is an anti-inflammatory drug commonly used for Gout patients. In 2019, Dr. Jean-Claude Tardif in the COLCOT trial randomized 4,745 patients within 30 days after myocardial infarction to low-dose colchicine (0.5 mg daily, a potent anti-inflammatory agent originally derived from the autumn crocus plant) or placebo, added to optimal medical therapy that included near-universal statin use and followed for 22 months. For the group with added colchicine, the major outcomes of cardiovascular death, resuscitated cardiac arrest, myocardial infarction, stroke, or urgent revascularization for angina fell by 23% (hazard ratio 0.77), driven especially by large reductions in stroke and urgent revascularization. Colchicine has negligible effects on lipids yet meaningfully lowers inflammatory markers; its success on top of statins isolates the incremental value of anti-inflammation. This supports the view that a substantial fraction of statin efficacy stems from anti-inflammatory rather than purely lipid-lowering properties, and it directly illustrates that a natural anti-inflammatory substance such as curcumin can produce cardiovascular benefits comparable in magnitude to those attributed to the non-lipid actions of statins.
2020, Dr. Stefan M. Nidorf: In the LoDoCo2 trial, 5,522 patients with chronic coronary disease (most already on statins and antiplatelet therapy) received low-dose colchicine 0.5 mg daily or placebo. After a median 28.6 months the primary composite of cardiovascular death, spontaneous myocardial infarction, ischemic stroke, or ischemia-driven revascularization was reduced by 31% (hazard ratio 0.69); key secondary composites and individual components such as myocardial infarction and revascularization also improved. Colchicine again acted principally through anti-inflammatory mechanisms (lowering CRP and IL-6) with no meaningful lipid changes. The consistent benefit in a stable population already receiving lipid-lowering therapy strengthens the hypothesis that statin-mediated event reduction is partly anti-inflammatory; because colchicine is itself a natural product, the results supply concrete evidence that natural substances with anti-inflammatory effects can deliver cardiovascular risk reductions of similar clinical importance to the inflammation-related component of statin therapy.
Berberine (from Berberis Species, Goldenseal, etc.)
Berberine has significant anti-atherosclerotic, anti-microbial biofilm properties. Berberine destabilizes bacterial membranes, inhibits cell division (FtsZ), and reduces biofilm formation; often synergistic with other agents against resistant bacterial strains. In 2024, Dr. Roberto Arrigoni reviews the antimicrobial and anti-biofilm effects of Berberine, writing:
Berberine…and its antimicrobial properties have intensively been studied. Berberine nanoparticles (BRBNPs) have been demonstrated to be very effective in in vitro assays against both Gram-negative, and Gram-positive bacteria. In addition, BRBNPs [berberine nanoparticles], when complexed with EGC [green tea extract], were very effective against MRSA [methicillin resistant staph aureus] in an in vivo murine model [88]. The above complex can affect the ability of MRSA to create a biofilm, inhibiting agrA-D gene expression. In this respect, nanoparticles based on the combination of berberine with cinnamomic acid can more easily penetrate MDR bacteria, thus decreasing biofilm formation. In the same direction, fusic acid, curcumin, and thymol, respectively, when combined with berberine, synergizes in the inhibition of S. aureus biofilm formation. Berberine has been shown to be very active against K. pneumoniae strains, synergizing with certain antibiotics, i.e., norfloxacin, ciprofloxacin, and doxycycline. Moreover, berberine can restore susceptibility to antibiotics (tigecycline, meropenem, ciprofloxacin, and sulbactam) against multi-drug-resistant A. baumannii. Berberine can destabilize the bacterial cell membrane, intercalating and cleaving the bacterial DNA [96]…Also, berberine is an effective antimicrobial against enterotoxigenic and enteropathogenic E. coli strains in infected animals [99]. …Regarding [Pseudomonas] P. aeruginosa, there is evidence that berberine synergizes with different antibiotics, such as amikacin, azithromycin, and tobramycin, against aminoglycoside-resistant P. aeruginosa strains. It has been reported that berberine can act through blockage of the …efflux pump, reducing biofilm formation. Note: For more on Berberine see: the Chapter on Berberine Antidote for a Modern Epidemic. (30)
Anti-Atherosclerotic Effects of Berberine
In 2022, Dr. Dongdong Jia did a metanalysis of 16 pre-clinical studies using Berberine in ApoE mice, finding berberine treatment of the mice decreases the atherosclerotic plaque area and macrophage content, writing,
Twelve articles (16 studies; 312 ApoE -/- mice) were included…Berberine could significantly decrease plaque area and plaque macrophage content … and change the secretion of inflammatory cytokines …but there were no significant differences in high-density lipoprotein levels and plaque lipid content …The results were robust across a range of sensitivity analyses. Therefore, the results indicate that berberine is a promising drug for the treatment of atherosclerosis through regulating lipid metabolism, inflammation, and plaque composition. (56-62)
Epigallocatechin Gallate (EGCG) (Major Catechin in Green Tea)
EGCG from green tea has anti-atherosclerotic effects by inhibiting foam cell formation. Remember, foam cells are macrophages that ingest oxidized cholesterol, thus appearing “foamy” under the microscope. Green tea extract also has antimicrobial activity and inhibits biofilm formation by inhibiting glucosyltransferases (GTFs), reducing EPS, and disrupting quorum sensing. EGCG shows strong anti-biofilm activity against oral pathogens like S. mutans and P. gingivalis. Note: GTFs are bacterial enzymes that polymerize sucrose into extracellular glucans,water-insoluble and soluble polysaccharides that are critical for biofilm formation. EPS is extracellular polymeric substances which forms the protective, sticky matrix of the biofilm. Quorum sensing: bacteria communicate and coordinate group behaviors allowing the colony to act as a single multicellular organism. (63-66)
EGCG Blocks Foam Cell Formation
In 2023, Dr. Jin-jin Yu studied the effect of EGCG on atherosclerosis in vitro and in vivo ApoE knockout mice finding ECGC inhibited inflammatory signalling, blocked formation of foam cells, and blocked the pathological effects of oxidized LDL, all key drivers of the atherosclerotic process, writing:
This study established in vitro and in vivo models of ox-LDL-induced macrophages and HFD-induced ApoE−/− mice to study the effects of ECG on atherosclerotic lesions. Firstly, the study confirmed that ECG has a therapeutic effect in different stages of atherosclerotic plaques. Subsequently, the results showed that the ox-LDL-induced release of pro-inflammatory mediators and the expression of the related protein CD86 in macrophages were inhibited by ECG. ECG blocked the formation of cellular foam by downregulating the expression of CD36 and LOX-1 proteins, thereby increasing SOD activity and reducing MDA production in cells. ECG also prevented ox-LDL-induced apoptosis, promoted macrophage migration, and increased plaque stability. The results confirmed that ECG attenuated ox-LDL-induced green fluorescence of ROS in macrophages by inhibiting the expression of related proteins in the NF-κB signaling pathway and activating the HO-1/Nrf2 signaling pathway. These results indicated that ECG has anti-oxidative stress and anti-inflammatory potential, and its molecular mechanism may be related to the inhibition of intracellular NF-κB signaling pathway proteins and activation of the HO-1/Nrf2 signaling pathway. ox-LDL= oxidized LDL low density lipoprotein. (67-69)
High Dose EGCG extracts may cause Liver Enzyme Elevation
In 2017, Dr. Zheming Yu did a randomized controlled trial showing elevation of liver enzymes from high dose green tea extract. High-dose EGCG shifts to a pro-oxidant, causing mitochondrial damage, reactive oxygen species (ROS) generation, and glutathione depletion in liver cells, thus causing liver enzyme elevation, most reports are in women, though males may also be involved. This may ocurr with high dose extracts. Drinking green tea, however, appears safe. This revelation tends to reduce any enthusiasm for using green tea extracts in a calcium score protocol. However, when used in moderation and with periodic monitoring of liver function, it should be safe. (99)
Coffee and Caffeine Has Anti-Atherosclerotic Effects
Coffee and caffeine consumption have multipe anti-atherosclerotic effects including blocking oxidation of LDL (low-density lipoprotein), suppressing hepatic PCSK9, upregulating the antioxidant enzyme (paraoxonase-1 PON-1), and improving macrophage cholesterol efflux. While coffee as a whole beverage significantly blocks foam cell development, it does so via a collaborative of various phenolic acids, chlorogenic, caffeic, and ferulic acids, that directly inhibit formation of foam cells. The caffeine component of coffee prevents atherosclerotic plaque progression by protecting vascular smooth muscle cells and acting on LDL receptor clearance. In other words, caffeine has a dual-action. It optimizes systemic lipid clearance at the hepatic level to prevent lipid entry into the artery wall, while simultaneously controlling the cellular behavior of smooth muscle cells lining the interior of blood vessels, thus preventing atherosclerotic plaque progression and narrowing of the lumen of blood vessels. If you are a coffee adict like I am, this is a good thing for prevention of cardiovascular disease. (70-75)
In 2010, Dr. Uto-Kondo proved that consuming a single cup of coffee caused a 40% increase in promoting cholesterol efflux from human monocyte-derived macrophages, effectively preventing them from storing lipids and transforming into dangerous foam cells. (70)
In 2024, Dr. Zhou studied natural alkaloids and caffeine found in coffee to test their direct impact on macrophage foam cell formation in vitro. Dr. Zhou confirmed that caffeine directly mitigates lipid droplet storage and blocks macrophage foam cell formation, explaining the cardioprotective effects of coffeel. (71)
Caffeine Upstream Protection via PCSK9 & SREBP2 Suppression
In 2022, Dr. Richard C Le discovered that caffeine blocks the activation of the transcription factor SREBP2, which suppresses the expression and secretion of PCSK9, which drastically increases the liver’s ability to clear circulating LDL cholesterol before it can penetrate the arterial walls, undergo oxidation, and recruit macrophages to form foam cells. Note: there is an entire class of new cholestreol lowering drugs called PCSK9 inhibitors. For more on this see: Evolucomab, Are You Joking Me? (72)
Macrophages turn into foam cells when they absorb oxidized LDL. This is a key step in the atherosclerotic process. In 2007, Dr. Natella found that drinking coffee safely incorporates strong antioxidants into human LDL particles. This creates massive resistance to LDL oxidation, blocking formation of foam cells in the intima. (73) (75)
Prevention of Plaque Area and Smooth Muscle Proliferation
In 2013, Dr. Divani studied in vivo and in vitro animal models demonstrated that chronic treatment with caffeine significantly reduces atherosclerotic plaque area in hyperlipidemic settings. It establishes that caffeine stops the migration and destructive proliferation of vascular smooth muscle cells (VSMCs) that typically gather around foam cells during early fatty-streak stabilization. (74)
Benefits of Green Tea (Pressurized Hot Water Extract GPHWE)
In terms of prevention of atherosclerotic disease, you might be surprised to know that in animal studies, green tea extract has results comparable to those achieved with the statin drug, Simvastatin. (76)
Traditional green tea is a simple infusion (steeping), while GPHWE is a concentrated extract optimized for maximum bioactive recovery. Hot water (100 °C) under pressure (15 psi) for 15 min,
In 2025, Dr. Rahni Hossain studied mechanisms of a green tea extract in the prevention of atherosclerosis, finding results comparable with the statin drug, simvastatin, writing:
Rich in catechins and flavonoids, green tea pressurized hot water extract (GPHWE) demonstrated potent antioxidant activity … In vitro, GPHWE protected …macrophages from oxidized LDL (Ox-LDL)-induced cytotoxicity and apoptosis by mitigating oxidative stress and enhancing cell survival. Animal studies using mice fed a high-fat diet (HFD) revealed notable improvements in lipid profiles, including decreases in total cholesterol, LDL, the atherosclerosis index (AI), the coronary risk index (CRI), and triglycerides, as well as lower levels of malondialdehyde (MDA), an indicator of oxidative stress. These results were comparable to those achieved with Simvastatin. Molecular docking studies indicated … the mechanisms of GPHWE involve antioxidant properties, regulation of lipids, and stabilization of plaques…. This comprehensive approach positions GPHWE as a promising natural remedy for preventing atherosclerosis and reducing cardiovascular risk….The in vivo results indicate that GPHWE is effective at modulating lipid metabolism and reducing the risk of atherosclerosis, with effects similar to Simvastatin. ..In summary, this research establishes a solid foundation for advancing GPHWE as a sustainable and effective strategy for cardiovascular disease prevention. (76-77)
EGCG Enhances Nitric Oxide
In 2025, Dr. Reza Eshraghi studied the cardioprotective and antihypertensive effects of EGCG, finding that EGCG induced vasorelaxation primarily through enhancing nitric oxide (NO). (78)
Benefits of EGCG in Abdominal Aortic Aneurysm (AAA).
There is no FDA‐approved, safe, and effective medication available for this AAA, and the only accepted management is surgery or some type of invasive endovascular intervention.
Preclinical animal studies using EGCG in 2006 by Dr. Ro reported significant improvement in AAA diameter and dilation between rats treated with AneuMastat (EGCG) and congtrol rats. Untreated mice had a significantly larger aorta diameter at sacrifice relative to their starting size (768 vs. 532 µm, p = 0.001). Additionally, no significant increase in aorta size was seen within treated or Sham mouses (550 vs. 580 µm and 478 vs. 477 µm). Aneumastat is a polyphenol‐rich EGCG. Another study by Dr. Tyrie studied aneumastat as a preventive medication for AAA, reporting significant decrease in the prevalence of AAA in mice taking aneumastat (EGCG). (79)
EGCG Anti-Inflammatory Effects
In 2020, Dr. Reddy studied the inhibitory effect of EGCG on NF‐κB activation in ECs (endothelial cells). HCAECs (enothelial cells) were stimulated with TNF‐alpha for an hour and treated with EGCG at the specific concentrations. The results showed that ECGG effectively suppressed NF‐κB transcriptional activity in TNF‐alpha stimulated HCAECs (endothelial cells) [100]. (80)
EGCG Decreases Plaque Formation in ApoE mice
In 2018, Dr. Wang found EGCG decreases atherosclerotic plaque formation in mice by increasing anti‐inflammatory cytokine and interleukin‐10 levels and reducing pro‐inflammatory cytokine, IL‐6 and TNF‐α levels. Furthermore, EGCG modulated high‐fat‐induced dyslipidemia. (81-82)
Where to Buy High-Quality Green Tea Extracts (Closest Alternatives)
You can easily buy concentrated, standardized green tea extracts that deliver high levels of the same key bioactives (polyphenols and EGCG). Many use water-based or optimized extraction methods and are available in capsule or powder form.
Search for “green tea extract EGCG” or “standardized green tea extract.” from Thorne, Pure Encapsulations, or Zhou Nutrition.
Look for standardized to 95%+ polyphenols and/or 50%+ EGCG (or higher). Decaffeinated options if you want to avoid caffeine.
Third-party tested for purity (heavy metals are a concern with some tea extracts). Enhanced absorption versions (e.g., phytosome form). Popular reputable options (widely available):
Zhou Nutrition Green Tea Extract. Zenwise Green Tea Extract
Nature’s Nutrition or similar high-EGCG formulas (often 98% polyphenols / 45–50% EGCG). Pure Encapsulations or Thorne Green Tea Phytosome (better bioavailability)
Bulk powder from PureBulk for custom dosing
Check the label — Look for the exact standardization (e.g., “standardized to 50% EGCG” or “98% polyphenols”).
Dose: Typical effective range in studies is 250–500 mg extract per day (providing ~100–200+ mg EGCG).
Quercetin (Flavonoid in Onions, Apples, Berries, etc.)
Quercetin interferes with quorum sensing and reduces biofilm formation in various bacteria, including peri-odontal bacterial species found in the oral cavity. (83)
Additional Compounds (Commonly Grouped as Natural Biofilm Disruptors Effective Against Oral/Periodontal Biofilms Relevant to Vascular Disease)
Resveratrol (from Grapes, Berries)
Modulates quorum sensing and reduces biofilm formation. (84)
Manuka Honey / Methylglyoxal (MGO)
Manuka honey disrupts biofilm matrix and inhibits formation, especially in oral and wound pathogens. Manuka honey’s MGO component disrupts biofilm formation. (85-86)
Oregano Oil / Carvacrol disrupts bacterial membranes and has strong anti-biofilm effects against Gram-positive and oral bacteria. (87)
Cranberry Proanthocyanidins (PACs) have anti-adhesion and anti-biofilm activity in oral pathogens which prevents initial attachment). Cranberry PACs are among the best-studied natural anti-adhesion agents. These compounds are frequently discussed together in reviews on natural anti-biofilm agents because they target similar pathways, ie. quorum sensing, EPS, disruption of bacterial membranes, relevant to polymicrobial biofilms in vascular disease.(88-89)
Proteolytic Enzymes and Biofilm
The three widely available proteolytic enzymes are serrapeptidase, nattokinase and lumbrokinase. Proteolytic enzymes the protein components in biofilms, the fibrin, amyloids, and adhesins in the extracellular polymeric substance (EPS), the matrix of bacterial biofilms. Thus these enzymes inhibit biofilm formation, reduce biomass of the biofilm, and disperse established biofilms. This makes the bacteria embedded in the biofilm more vulnerable to antibiotics and the immune system. Synergy of proteolytic enzymes with antibiotics is well-supported in at least one key nattokinase study in 2018 by Dr. S. Hogan, with improved killing in mature biofilms involving medical device related infections. Combinations with natural antimicrobials such as garlic, oregano, curcumin, etc. have not yet been studied. However, the matrix-disrupting action of proteolytic enzymes suggests enhances penetration and efficacy of other antimicrobial agents. This is a common principle in biofilm research. For more on Proteolytic Enzymes, see the Chapter on Fibrinolytic and Proteolytic Enzymes, Medical Use.
Nattokinase (90-93)
Serrapeptidase (94-96)
Lumbrokinase
Lumbrokinase has potent fibrinolytic/proteolytic activity, targeting fibrin in the biofilm matrix. Lumbrokinase is commonly used in chronic infection protocols, such as chronic Lyme disease. In 2023, Dr. Wang found that Lumbrokinase has anti-biofilm effects even at low concentrations, e.g., 1 µg/mL. Lumbrokinase inhibited Staph. aureus biofilm formation with a 68% reduction in a biomaterial model, thus supporting antibiofilm potential. (97)
Conclusion: Although not yet accepted by mainstream cardiology, the evidence supporting the infection theory of atherosclerosis as polymicrobial biofilm is firmly established in the medical literature. It is also clear that the major benefit of statin drugs relates to antimicrobial and anti-inflammatory effects. It is also my opinion that these same antimicrobial and anti-inflammatory benefits can be obtained equally with natural substances listed here, such as aged garlic, curcumin, vitamin K, Tocotrienol vitamin E, nattokinase and berberine etc. This is a superior plan, since we are avoiding the toxic effects of statin drugs on muscle and brain. Remember, statins are derived from poison mushrooms, and remain a potent poison to the mammalian cell. When we look at the data on slowing progression of calcium score, we find that aged garlic and other natural substances are superior to statin drugs. The addition of proteolytic enzymes to our calcium score protocol creates a more powerful effect because of their anti-biofilm and anti-thrombotic effects, both of which play a major role in the pathogenesis of cardiovascular disease.
Heart Book: How to Keep Your Heart Healthy by Jeffrey Dach MD
My new book is available on Amazon:
Link to Kindle Version
Link to Paperback Version
Heart Book is a journey through the confusing maze of literature on coronary artery disease, the number-one killer in America. With his years of practice in vascular radiology, Dr. Dach has the background, credentials, and experience to transform your understanding of heart disease. The old medical paradigms have been upended, yet mainstream cardiology clings to these tired dogmas as if nothing has changed. Be prepared to be shocked, amazed, provoked, and gratified as this book empowers you to take control of your own heart health.
Articles with Related Interest:
The Failure of Cholesterol Lowering Drugs
Coronary Artery Disease: Questions and Answers
Does Cholesterol Cause Coronary Artery Disease ?
Calcium Score Determines Who to Treat with Statin Drug
Calcium Score Diabetes and Statin Drugs
Plant Based Diet, Health Benefits for Coronary Artery Disease
LDL-Cholesterol Does Not Cause Coronary Artery Disease
Low Level Endotoxemia, Depression, Endocrinopathy and Coronary Artery Disease
Fibrinolytic Enzymes, Nattokinase, Lumbrokinase Prevent and Reverse Atherosckerosis
Reverse Heart Disease with Coronary Calcium Score
Low Level Endotoxemia LPS Theory of Coronary Artery Disease
Calcium Score Paradigm Shift in Cardiology
Coronary Calcium Score Benefits of Aged Garlic
The Art of the Curb Side Cholesterol Consult
Cholesterol and Atherosclerosis:Autopsy Studies Show No Correlation
Statin Denialism Internet Cult with Deadly Consequences
Defending the Cholesterol Hypothesis in the Elderly
Does High Cholesterol Cause Heart Disease ?
Familial Hypercholesterolemia and Statin Drugs
Donating Blood Prevents Heart Disease
Does Cholesterol Cause Heart Disease ? Part two
Atherosclerotic Plaque as Infected Biofilm on Electron Microscopy
Coronary Calcium Score Paradigm Shift Podcast
Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663
my web site: https://drjeffreydachmd.com/
my personal blog: www.jeffreydachmd.com
Bioidentical Hormones 101 Second Edition
Menopausal Hormone Replacement, Health Benefits
Natural Thyroid Toolkit by Jeffrey Dach MD
Cracking Cancer Toolkit ebook
Cracking Cancer Toolkit print version
Heart Book by Jeffrey Dach MD
==========================================
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