HoldsUp

Richard Horowitz

Richard Horowitz is a physician specializing in the diagnosis and treatment of Lyme disease, tick-borne coinfections, and chronic illness. His published research primarily focuses on treatment protocols for chronic Lyme disease and post-treatment Lyme disease syndrome, particularly evaluated through dapsone combination therapy regimens and the Multiple Systemic Infectious Disease Syndrome (MSIDS) model. Additionally, his work includes studies on diagnostic assays for babesiosis and clinical reports on therapies for COVID-19.

47 claims checked on air: 5 context 1 contradicted 8 overstated 19 supported 14 unverified

What they said on air - supported

6 citing their own research

0:10:54supportedhighUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:12:28supportedhighUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:24:10supportedvery lowtheir own paperUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:24:38supportedvery lowUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:24:39supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:26:32supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:29:34supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:30:05supportedlowUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:33:06supportedlowUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:34:07supportedlowUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:35:39supportedvery lowtheir own paperUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:36:55supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:39:14supportedlowUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:40:15supportedvery lowUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

0:49:23supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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%.

0:54:56supportedlowtheir own paperUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

1:02:14supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

1:09:06supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

1:16:23supportedmoderateUndiagnosed Infections Are Silently Causing Chronic Disease!

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.

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