22 Supported by research
The C6 ELISA test checks for three strains of Borrelia: Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii.
"The C6 ELISA checks for three strains: Borrelia burgdorferi, afzelii, garinii from Europe." (said at 0:10:54)
The C6 ELISA utilizes a synthetic 26-mer peptide corresponding to invariable region 6 (IR6) of the VlsE surface lipoprotein. This region is highly conserved across the three main pathogenic genospecies of the Borrelia burgdorferi sensu lato complex responsible for Lyme disease in North America and Europe: Borrelia burgdorferi sensu stricto, Borrelia afzelii, and Borrelia garinii. Consequently, the C6 ELISA detects antibody responses induced by all three species.
- supports: Antigenic conservation of an immunodominant invariable region of the VlsE lipoprotein amon… (The Journal of infectious diseases 2000) · cited 89x in the literature
"Lyme disease is caused by genetically divergent spirochetes, including 3 pathogenic genospecies: Borrelia burgdorferi sensu stricto, B. garinii, and B. afzelii. Serodiagnosis is complicated by this genetic diversity. A synthetic peptide (C(6)), based on the 26-mer invariable region (IR(6)) of the variable surface antigen of B. burgdorferi (VlsE), was used as ELISA antigen, to test serum samples collected from mice experimentally infected with the 3 genospecies and from European patients with Lyme disease. Regardless of the infecting strains, mice produced a strong antibody response to C(6), which indicates that IR(6) is antigenically conserved among the pathogenic genospecies." (abstract, passage verified)
pubmedfull study (doi) - supports: Diagnosis of lyme borreliosis in europe. (Vector borne and zoonotic diseases (Larchmont, N.Y.) 2003) · cited 119x in the literature
"In Europe, Lyme borreliosis is caused by at least three species, B. burgdorferi sensu stricto, B. afzelii and B. garinii. Thus microbiological diagnosis in European patients must consider the heterogeneity of Lyme disease borreliae for development of diagnostic tools such as PCR primers and diagnostic antigens." (abstract, passage verified)
pubmedfull study (doi)
Urolithin A is a postbiotic that supports mitophagy to renew cellular mitochondria.
"Mitopure contains urolithin A, a clinically studied postbiotic that supports mitophagy, which is your body's natural process for renewing mitochondria." (said at 0:13:26)
Urolithin A is a postbiotic compound produced by gut microbiota from dietary ellagitannins and ellagic acid. Multiple randomized controlled trials and preclinical studies have demonstrated that oral urolithin A (including the proprietary formulation Mitopure) activates mitophagy—the selective autophagy pathway that clears damaged mitochondria and facilitates mitochondrial renewal—and modulates biomarkers of mitochondrial health and muscle function in humans.
Richard Horowitz published the first article in world medical literature on glutathione's efficacy in COVID-19 in April 2020.
"I wrote the first article in the world literature in COVID-19 in April 2020 on glutathione and how it helps with COVID." (said at 0:24:10)
Richard I. Horowitz and colleagues published a two-patient case report titled 'Efficacy of glutathione therapy in relieving dyspnea associated with COVID-19 pneumonia: A report of 2 cases' in Respiratory Medicine Case Reports in April 2020. This was the first published article in the medical literature evaluating clinical treatment with oral and intravenous glutathione in patients with COVID-19 pneumonia. However, because this publication is an uncontrolled case report of only two patients, it provides very low certainty clinical evidence regarding the true therapeutic efficacy of glutathione in COVID-19.
N-acetylcysteine (NAC) inhibits von Willebrand factor to prevent microclots.
"And I also didn't know that NAC was blocking von Willebrand factor, so they weren't getting microclots and dying from it." (said at 0:24:39)
Preclinical and translational studies demonstrate that N-acetylcysteine (NAC) cleaves disulfide bonds in ultra-large von Willebrand factor (VWF) multimers, thereby reducing multimer size, disrupting VWF-mediated platelet aggregation, and inhibiting or dissolving microvascular thrombi.
- supports: N-Acetyl Cysteine Prevents Arterial Thrombosis in a Dose-Dependent Manner In Vitro and in … (Arteriosclerosis, thrombosis, and vascular biology 2024) · cited 9x in the literature
"Instead, we propose using N-acetyl cysteine (NAC) to act against the protein VWF (von Willebrand factor), and not platelets, to prevent arterial thrombi from forming." (abstract, background, passage verified)
pubmedfull study (doi) - supports: N-ACETYLCYSTEINE REDUCES VON WILLEBRAND FACTOR MULTIMER SIZE AND IMPROVES RENAL MICROVASCU… (Shock (Augusta, Ga.) 2025) · cited 2x in the literature
"NAC improves renal MBF, possibly by reducing VWF multimer size and reducing microthrombus burden." (abstract, conclusions, passage verified)
pubmedfull study (doi) - supports: N-acetylcysteine in Thrombotic Thrombocytopenic Purpura: A Systematic Review. (Cureus 2026)
"N-acetylcysteine (NAC) has been explored as an adjunctive therapy because of its ability to reduce disulfide bonds within von Willebrand factor multimers." (abstract, introduction, passage verified)
pubmedfull study (doi)
Sleep deprivation increases levels of the inflammatory cytokine interleukin-6 (IL-6).
"when you don't sleep, IL-6, interleukin-6, is high, it's driving inflammation." (said at 0:26:32)
Published meta-analyses support the claim that sleep loss and sleep disturbances are associated with elevated levels of the pro-inflammatory cytokine interleukin-6 (IL-6). In observational studies, sleep disturbance is significantly associated with higher systemic IL-6 levels. In experimental human trials, sustained partial sleep deprivation (e.g., restriction to approximately 4.5 hours per night for three or more consecutive nights) significantly increases circulating IL-6, although a single acute night of total or partial deprivation may not produce a significant change.
- supports: Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis… (Biological psychiatry 2016) · cited 2059x in the literature
"A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = .05-.19) and IL-6 (ES .20; 95% CI = .08-.31)." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Effects of Experimental Sleep Deprivation on Peripheral Inflammation: An Updated Meta-Anal… (Journal of sleep research 2026) · cited 20x in the literature
"Compared to normal sleep, multiple nights of experimental partial sleep deprivation (sleep duration reduced to ~4.30 h for 3+ nights) were associated with a significant increase of interleukin-6 [IL-6, k = 5, d = 0.42, [95% CI = 0.11 to 0.73], p < 0.01] and C-reactive protein [CRP, k = 5, d = 0.76, [95% CI = 0.09 to 1.43], p = 0.03] in blood. A single night of total or partial sleep deprivation was not associated with changes in inflammation." (abstract, results, passage verified)
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A case report of two multiple sclerosis patients treated with ibogaine documented a 70% reduction in brain white matter lesions.
"In one study, they they looked at MS and they looked at the white matter lesions, which was inflammation in the brain before and after ibogaine and their and their symptom profile. And they were there were only two cases in the report, but they both had like a 70% reduction in white matter lesions" (said at 0:28:03)
A 2025 case report (PMID 39981248) described two multiple sclerosis patients treated with ibogaine, documenting marked lesion shrinkage, decreased apparent diffusion coefficient (ADC) values indicative of reduced inflammation and remyelination, and clinical symptom improvements. Because this evidence comes from an uncontrolled two-patient case report, it represents very low certainty evidence that cannot establish causal efficacy, safety, or generalizability.
The NIH stated that 42% of individuals over age 55 will develop dementia.
"We're in the middle of an Alzheimer's epidemic where the NIH said that 42% of people over 55 years old are now going to become demented." (said at 0:29:34)
A 2025 prospective cohort study of 15,043 individuals published in Nature Medicine (funded by the NIH) evaluated lifetime dementia risk from age 55 to 95 years while accounting for mortality as a competing risk. The authors found that the lifetime risk of developing dementia after age 55 was 42% (95% CI: 41–43%), closely matching the claim.
SARS-CoV-2 viral replication requires a reduction in cellular glutathione levels.
"I didn't know at the time that the virus needs to lower glutathione to replicate." (said at 0:24:38)
In vitro mechanistic studies indicate that SARS-CoV-2 infection promotes a pro-oxidant intracellular environment by depleting reduced glutathione (GSH), which facilitates viral replication. In cell culture models (such as Vero E6, Calu-3, and A549 cells), viral infection markedly reduces cellular GSH, while restoring intracellular glutathione balance or administering thiol donors significantly suppresses viral replication and inflammation. Furthermore, molecular studies demonstrate that glutathionylation of the SARS-CoV-2 main protease (Mpro) inhibits its dimerization and enzymatic activity, showing that higher glutathione levels directly impair replication mechanisms. However, because this evidence is derived exclusively from in vitro and molecular models, the clinical certainty is very low.
- supports: SARS-CoV2 infection impairs the metabolism and redox function of cellular glutathione. (Redox biology 2021) · cited 89x in the literature
"Viral infections sustain their replication cycle promoting a pro-oxidant environment in the host cell. In this context, specific alterations of the levels and homeostatic function of the tripeptide glutathione have been reported to play a causal role in the pro-oxidant and cytopathic effects (CPE) of the virus. In this study, these aspects were investigated for the first time in SARS-CoV2-infected Vero E6 cells, a reliable and well-characterized in vitro model of this infection. SARS-CoV2 markedly decreased the levels of cellular thiols, essentially lowering the reduced form of glutathione (GSH)." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Regulation of the Dimerization and Activity of SARS-CoV-2 Main Protease through Reversible… (mBio 2021) · cited 33x in the literature
"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent for coronavirus disease 2019 (COVID-19), encodes two proteases required for replication... We show M pro is susceptible to glutathionylation, leading to inhibition of dimerization and activity." (abstract, results)
pubmedfull study (doi) - supports: Redox-sensitive factors as targets of thiol compounds to hinder SARS-CoV-2 replication and… (Antimicrobial agents and chemotherapy 2026)
"It also alters the host antioxidant response, causing oxidative stress that supports viral replication and cytokine overproduction. This study investigated key pathogenic effectors in Calu-3 and A549-ACE2/TMPRSS2 cells infected with SARS-CoV-2 variants, focusing on replication kinetics, cellular redox state, and inflammatory cytokine profile. A dramatic redox alteration in terms of glutathione (GSH) and Cysteine (Cys) was observed at 48 h p.i., along with a strong pro-inflammatory cytokine response" (abstract, results, passage verified)
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Gliotoxins produced by mold have immunosuppressive properties.
"and they get mold toxins with gliotoxins on top of it, which are immunosuppressive." (said at 0:12:28)
Gliotoxin, a sulfur-containing epipolythiodioxopiperazine (ETP) secondary metabolite produced by fungal species such as Aspergillus fumigatus and Trichoderma, is well-established in the toxicological and microbiological literature as a potent immunosuppressive agent. It impairs host immunity through multiple mechanisms, including inhibition of NF-κB signaling, inhibition of macrophage activation and phagocytosis, generation of reactive oxygen species, and induction of apoptosis in host immune cells.
- supports: Gliotoxin--bane or boon? (Environmental microbiology 2016) · cited 128x in the literature
"Furthermore, GT is long known as an immunosuppressive agent and also reported to have anti-tumour properties. However, recent publications suggest that GT is a virulence determinant of the human pathogen Aspergillus fumigatus." (abstract, passage verified)
pubmedfull study (doi) - supports: Preparations for Invasion: Modulation of Host Lung Immunity During Pulmonary Aspergillosis… (Frontiers in immunology 2018) · cited 69x in the literature
"Among the different secondary metabolites produced by Aspergillus spp. Gliotoxin (GT) is the best known and better characterized virulence factor. It is able to generate reactive oxygen species (ROS) due to the disulfide bridge present in its structure. It also presents immunosuppressive activity related with its ability to kill mammalian cells and/or inactivate critical immune signaling pathways like NFkB." (abstract, passage verified)
pubmedfull study (doi) - supports: The Toxic Mechanism of Gliotoxins and Biosynthetic Strategies for Toxicity Prevention. (International journal of molecular sciences 2021) · cited 36x in the literature
"Gliotoxins show cytotoxic effects via the suppression the function of macrophage immune function, inflammation, antiangiogenesis, DNA damage by ROS production, peroxide damage by the inhibition of various enzymes, and apoptosis through different signal pathways." (abstract, passage verified)
pubmedfull study (doi)
Autopsy studies of Alzheimer's patients reveal biofilms, amyloid, and phosphorylated tau in the brain.
"they looked at autopsy studies of Alzheimer's patients and they would find biofilms, amyloid, and phosphorylated tau in the brains." (said at 0:30:05)
Autopsy studies evaluating the microbial hypothesis of Alzheimer's disease have reported finding bacterial biofilm markers co-localizing with classic neuropathological hallmarks, including amyloid-beta and phosphorylated tau (p-Tau). For example, post-mortem immunohistochemical analysis of Alzheimer's disease brain tissue identified Borrelia burgdorferi aggregates positive for the biofilm marker alginate co-localized with amyloid and phospho-tau markers. Amyloid-beta and hyperphosphorylated tau are standard pathological hallmarks of Alzheimer's disease, while evidence for bacterial biofilms in AD brain tissue comes from preliminary, small-sample autopsy studies.
- supports: Borrelia burgdorferi Co-Localizing with Amyloid Markers in Alzheimer's Disease Brain Tissu… (Journal of Alzheimer's disease : JAD 2022) · cited 37x in the literature
"Positive Borrelia structures were evaluated for co-localization with biofilm and AD markers such as amyloid and phospho-tau (p-Tau) using immunohistochemical methods. The results showed the presence of B. burgdorferi antigen and DNA in patients with AD pathology and among those, one of them was previously diagnosed with Lyme disease. Interestingly, a significant number of Borrelia-positive aggregates with a known biofilm marker, alginate, were found along with the spirochetal structures. Our immunohistochemical data also showed that Borrelia-positive aggregates co-localized with amyloid and phospho-tau markers." (abstract, methods and results, passage verified)
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Johns Hopkins researchers discovered that Lyme disease bacteria form biofilm persisters similar to tuberculosis and leprosy.
"about 10 years ago, Johns Hopkins researchers found out that Lyme was a specific type of a bacteria called a biofilm persister bacteria, like tuberculosis and leprosy." (said at 0:33:06)
Starting around 2014-2015, researchers at Johns Hopkins Bloomberg School of Public Health (led by Dr. Ying Zhang, who previously studied persister mechanisms in Mycobacterium tuberculosis) published a series of studies showing that Borrelia burgdorferi in stationary phase forms antibiotic-tolerant persister cells and biofilm-like microcolonies in vitro and in animal models. The researchers screened drug libraries to identify agents active against these dormant forms, drawing direct parallels to persistent infection paradigms such as tuberculosis. While persister and biofilm formation represents a phenotypic state rather than a separate taxonomic class of bacteria, and the clinical significance of these forms in human Post-Treatment Lyme Disease Syndrome (PTLDS) remains an active area of investigation based largely on preclinical evidence, the attribution to Johns Hopkins researchers and the timing accurately reflect the published literature.
Dapsone penetrates the brain and inhibits NLRP3 inflammasomes.
"I looked at dapsone, and it was, all right, it gets great penetration into the brain... number two, it blocks NLRP3 inflammasomes in the brain." (said at 0:34:07)
Published literature confirms both components of the claim. Pharmacokinetic studies in humans demonstrate that dapsone crosses the blood-brain barrier and penetrates into cerebrospinal fluid (CSF). Preclinical mechanistic and animal studies show that dapsone acts as an inflammasome competitor and inhibits NLRP3 inflammasome activation and downstream neuroinflammatory signaling (such as IL-1β and IL-18) in the brain.
According to BMJ Global Health, one in seven people worldwide has been exposed to Lyme disease.
"where BMJ Global Health said one out of seven people in the world have now been exposed to Lyme, right?" (said at 0:36:55)
A 2022 systematic review and meta-analysis published in BMJ Global Health (Dong et al., pooling 89 studies comprising 158,287 participants) estimated the global seroprevalence of Borrelia burgdorferi sensu lato at 14.5% (95% CI 12.8% to 16.3%), which corresponds to approximately one in seven individuals having serological evidence of exposure.
Hydroxychloroquine (Plaquenil) alkalizes the intracellular compartment, enhances antibiotic efficacy, and targets cystic forms of Borrelia burgdorferi.
"And the reason for Plaquenil, by the way, is it alkalizes the intracellular compartment so these antibiotics are more effective, helps with the autoimmune manifestations, um even hits the cystic forms of Lyme" (said at 0:39:14)
The speaker's claims accurately reflect published hypotheses and in vitro findings, though evidence is limited primarily to in vitro models and observational clinical data. Hydroxychloroquine is a weak base (lysosomotropic agent) that concentrates in acidic intracellular compartments (such as endosomes and lysosomes) and elevates their pH toward neutrality. Studies evaluating Lyme disease therapy (e.g., Donta, 2003) noted that macrolide antibiotics lose efficacy at acidic pH, and adding hydroxychloroquine alkalinizes these compartments to enhance antibiotic effectiveness. Additionally, an in vitro study by Brorson et al. (2002) demonstrated that hydroxychloroquine has direct bactericidal activity against cystic forms of Borrelia burgdorferi and disrupts/ruptures cystic structures. However, certainty is low because clinical evidence supporting this regimen comes primarily from uncontrolled observational cohorts and in vitro experiments rather than rigorous randomized controlled trials.
A Johns Hopkins study showed that a 6-day combination of rifampin, azithromycin, and methylene blue eradicated Bartonella in cell culture.
"Johns Hopkins again, they published that if you do for 6 days in culture rifampin, Zithromax, and methylene blue, it kills Bart." (said at 0:40:15)
A 2020 in vitro study by researchers at the Johns Hopkins Bloomberg School of Public Health (Zheng et al., BMC Microbiology) evaluated drug combinations against stationary phase and biofilm-forming Bartonella henselae. The researchers found that methylene blue and rifampin were the most active single agents and that two-drug combinations containing azithromycin, rifampin, and methylene blue (such as azithromycin/methylene blue and rifampin/methylene blue) completely eradicated biofilm B. henselae after 6 days of exposure in culture. Because these findings are strictly in vitro, clinical efficacy in humans remains unestablished.
One-third of the global population has non-alcoholic steatohepatitis or fatty liver disease.
"One-third of the world's population has non-alcoholic steatohepatitis or fatty liver." (said at 0:49:23)
Large systematic reviews and meta-analyses estimate that approximately one-third of the global adult population has non-alcoholic fatty liver disease (NAFLD, now often termed metabolic dysfunction-associated steatotic liver disease or MASLD). A 2022 meta-analysis across 72 studies comprising over 1 million individuals found a worldwide pooled prevalence of 32.4% (95% CI: 29.9%–34.9%), with more recent estimates ranging from 30% to 38%.
Approximately 50% of buildings in the United States have water damage.
"and then there's 50% of buildings are water-damaged." (said at 0:56:26)
Large-scale assessments and public health syntheses of indoor environmental quality in the United States (including analyses by the EPA and Lawrence Berkeley National Laboratory) estimate that approximately 47% to 50% of residential buildings have signs of dampness, moisture problems, or water damage.
A culture study conducted with Eva Sapi demonstrated that combining dapsone with doxycycline, rifampin, and azithromycin progressively reduced Borrelia biofilm persister cells.
"So, we found, and I did a study with Eva Sapi from the University of New Haven in culture... every time we added a drug, like when we added doxycycline to dapsone, it lowered the biofilm persisters; we added rifampin to doxy and dapsone, it lowered the biofilm even more. We added Zithromax." (said at 0:35:39)
A 2020 in vitro study co-authored by Richard Horowitz and Eva Sapi evaluated dapsone alone and in combination with doxycycline, rifampin, and azithromycin against Borrelia burgdorferi biofilm forms. The culture study showed that combining dapsone with these intracellular antibiotics significantly decreased biofilm mass, viability, and protective glycosaminoglycan content compared to monotherapies. Because these findings are derived exclusively from in vitro cell culture models, certainty regarding clinical translation to human Lyme disease remains very low.
The Horowitz Multiple Systemic Infectious Disease Syndrome (MSIDS) questionnaire was validated in a study of 1,600 people.
"And the Horowitz MSIDS questionnaire, which is on my website, cangetbetter.com, if you take this questionnaire, it will give you a probability of tick-borne, but also you bring it to your doctor. There's 38 items on there... The beauty of the questionnaire is we validated it in 1,600 people." (said at 0:54:56)
A 2017 validation study by Horowitz and Freeman published in the International Journal of General Medicine evaluated the construct, convergent, and discriminant validity of the Horowitz Multiple Systemic Infectious Disease Syndrome Questionnaire (HMQ). The publication reported empirical evaluation across cohorts totaling over 1,500–1,600 participants (including Study 1 with 537 patients and Study 2 with 999 participants, alongside a third comparison cohort), finding acceptable internal reliability and ability to distinguish self-reported or confirmed Lyme disease patients from healthy controls.
- supports: Empirical validation of the Horowitz Multiple Systemic Infectious Disease Syndrome Questio… (International journal of general medicine 2017) · cited 38x in the literature
"Three studies evaluated such a screening tool, namely the Horowitz Multiple Systemic Infectious Disease Syndrome (MSIDS) Questionnaire. The purpose was to see if the questionnaire could accurately distinguish between Lyme patients and healthy individuals. Study 1 examined the construct validity of the scale examining its factor structure and reliability of the questionnaire among 537 individuals being treated for Lyme disease. Study 2 involved an online sample of 999 participants, who self-identified as either healthy (N=217) or suffering from Lyme now (N=782) who completed the Horowitz MSIDS Questionnaire (HMQ) along with an outdoor activity survey." (abstract, methods, passage verified)
pubmedfull study (doi)
Elevated VEGF levels occur in Long COVID, Bartonella infections, and cancer.
"VEGF we see with Long COVID, but we see it with Bartonella, you'll see with cancer." (said at 1:02:14)
Elevated vascular endothelial growth factor (VEGF/VEGFA) levels and signaling have been documented in Long COVID cohorts, Bartonella infections, and malignant cancers. Proteomic analyses of patients with post-acute sequelae of COVID-19 (Long COVID) demonstrate significant upregulation of circulating VEGFA compared to recovered controls. In Bartonella species infections (such as B. henselae and B. quintana), the bacteria stimulate host cells to secrete VEGF and express factors that activate the VEGF pathway, driving characteristic vasoproliferative lesions (such as bacillary angiomatosis). In oncology, tumor-derived VEGF overexpression is a well-established hallmark that mediates tumor angiogenesis.
- supports: Bartonella quintana variably expressed outer membrane proteins mediate vascular endothelia… (Infection and immunity 2006) · cited 37x in the literature
"Remarkably, only B. quintana strain JK-31 induced secretion of vascular endothelial growth factor (VEGF) from THP-1 and HeLa 229 cells upon infection similar to the secretion induced by B. henselae Marseille" (abstract, results, passage verified)
pubmedfull study (doi) - supports: The Bartonella autotransporter BafA activates the host VEGF pathway to drive angiogenesis. (Nature communications 2020) · cited 41x in the literature
"Pathogenic bacteria of the genus Bartonella can induce vasoproliferative lesions during infection. The underlying mechanisms are unclear, but involve secretion of an unidentified mitogenic factor. Here, we use functional transposon-mutant screening in Bartonella henselae to identify such factor as a pro-angiogenic autotransporter, called BafA." (abstract, results, passage verified)
pubmedfull study (doi) - supports: VEGFA sex-specific signature is associated to long COVID symptom persistence. (BMC medicine 2025) · cited 4x in the literature
"Findings revealed VEGFA overexpression in long COVID patients (effect size 0.322, SE = 0.098, p = 0.0013), along with sex-specific expression patterns and the influence of sex-hormonal status in females, with significant overexpression of circulating VEGFA levels specifically in postmenopausal women" (abstract, results, passage verified)
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Chronic disease accounts for 86 percent of healthcare costs in the United States.
"86% of our health care costs, and 70% is chronic disease." (said at 1:09:06)
The claim is supported by national health surveillance and expenditure data. According to analysis published by the Centers for Disease Control and Prevention (CDC), chronic health conditions account for 86% of total healthcare spending in the United States, alongside being the leading causes of death and disability.
Dietary consumption of xylitol has been linked to an increased risk of strokes and cardiovascular events.
"People, you know, don't realize like if you have cardiovascular risks and you're taking xylitol in your diet, which has now been linked, right, to strokes, right, that and now you have heat stress that you are more at risk for certain strokes than you might have been from the past." (said at 1:16:23)
A 2024 study published in the European Heart Journal (Witkowski et al.) found that elevated circulating levels of xylitol were significantly associated with an increased 3-year risk of incident major adverse cardiovascular events (MACE, which includes myocardial infarction and stroke) in an independent validation cohort of 2,149 patients (adjusted HR 1.57, 95% CI 1.12–2.21). Complementary mechanistic and interventional human studies demonstrated that dietary consumption of xylitol raised plasma levels, heightened platelet reactivity, and enhanced thrombosis potential.
- supports: Xylitol is prothrombotic and associated with cardiovascular risk. (European heart journal 2024) · cited 61x in the literature
"In initial untargeted metabolomics studies (discovery cohort), circulating levels of a polyol tentatively assigned as xylitol were associated with incident (3-year) major adverse cardiovascular event (MACE) risk. Subsequent stable isotope dilution LC-MS/MS analyses (validation cohort) specific for xylitol (and not its structural isomers) confirmed its association with incident MACE risk [third vs. first tertile adjusted hazard ratio (95% confidence interval), 1.57 (1.12-2.21), P < .01]. Complementary mechanistic studies showed xylitol-enhanced multiple indices of platelet reactivity and in vivo thrombosis formation at levels observed in fasting plasma." (abstract, results, passage verified)
pubmedfull study (doi)
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.