Roger Seheult
MedCram Videos
Roger Seheult is a physician, educator, and co-founder of MedCram Videos who has treated patients during the COVID-19 pandemic. His published research includes cost-effectiveness evaluations of vilobelimab for mechanically ventilated COVID-19 patients. Additionally, his work has examined the physiological effects of prophylactic bosentan on pulmonary artery pressure and exercise capacity at high altitude.
49 claims checked on air: 3 context 3 contradicted 2 overstated 33 supported 8 unverified 5 flagged
What they said on air - supported
The FDA granted emergency use authorization for convalescent plasma for COVID-19 based on studies that lacked control groups.
"So, for instance, convalescent plasma was approved using emergency use authorization through the FDA. There was no controls in that study." (said at 0:07:45)
The claim is supported. In August 2020, the US FDA issued an Emergency Use Authorization (EUA) for COVID-19 convalescent plasma based primarily on data from the national Expanded Access Program (EAP) registry coordinated by the Mayo Clinic. The EAP was an open-label, pragmatic registry that did not include an untreated or placebo control group; its efficacy signals were derived from internal dose-response comparisons (evaluating outcomes between recipients of high-, medium-, and low-antibody titer plasma) rather than a randomized control arm.
- supports: Convalescent Plasma Antibody Levels and the Risk of Death from Covid-19. (The New England journal of medicine 2021) · cited 554x in the literature
"Of the 3082 patients included in this analysis, death within 30 days after plasma transfusion occurred in 115 of 515 patients (22.3%) in the high-titer group, 549 of 2006 patients (27.4%) in the medium-titer group, and 166 of 561 patients (29.6%) in the low-titer group." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Access to and safety of COVID-19 convalescent plasma in the United States Expanded Access … (PLoS medicine 2021) · cited 65x in the literature
"This registry study was limited by the observational and pragmatic study design that did not include a control or comparator group; thus, the data should not be used to infer definitive treatment effects." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Convalescent Plasma and the US Expanded Access Program: A Personal Narrative. (Current topics in microbiology and immunology 2025) · cited 3x in the literature
"By mid-summer of 2020, strong evidence was produced showing that high-titer CCP given early in the course of hospitalization could lower mortality by as much as a third (Joyner et al. in N Engl J Med 384:1015-1027, 2021; Senefeld et al. in PLoS Med 18, 2021a). These data were used by the FDA in its August decision to grant Emergency Use Authorization for CCP use in hospitals." (abstract, passage verified)
pubmedfull study (doi)
The UK RECOVERY trial showed that dexamethasone provided no clear benefit to COVID-19 patients not requiring oxygen, but reduced mortality most substantially in patients on mechanical ventilators.
"That was a UK RECOVERY trial that came out, showed without a doubt that steroids improve—well, what they found was that patients who were not on oxygen, so in other words early in the course of the disease, did not benefit from steroids. It was equivocal. Whereas those that were the sickest patients on the ventilator requiring high doses of oxygen seemed to be the ones that benefited the most from dexamethasone or steroids." (said at 0:09:50)
The UK RECOVERY trial (a randomized controlled trial of 6,425 hospitalized COVID-19 patients) evaluated 6 mg daily dexamethasone versus usual care and found that mortality reduction varied substantially by baseline respiratory support. In patients receiving invasive mechanical ventilation, dexamethasone produced the greatest mortality reduction (28-day mortality: 29.3% vs. 41.4%; rate ratio 0.64, 95% CI 0.51–0.81). In patients receiving oxygen without mechanical ventilation, there was also a benefit (23.3% vs. 26.2%; rate ratio 0.82, 95% CI 0.72–0.94). However, in patients receiving no respiratory support at randomization, dexamethasone showed no benefit and was statistically equivocal/trended toward harm (17.8% vs. 14.0%; rate ratio 1.19, 95% CI 0.92–1.55).
- supports: Dexamethasone in Hospitalized Patients with Covid-19. (The New England journal of medicine 2021) · cited 10160x in the literature
"In the dexamethasone group, the incidence of death was lower than that in the usual care group among patients receiving invasive mechanical ventilation (29.3% vs. 41.4%; rate ratio, 0.64; 95% CI, 0.51 to 0.81) and among those receiving oxygen without invasive mechanical ventilation (23.3% vs. 26.2%; rate ratio, 0.82; 95% CI, 0.72 to 0.94) but not among those who were receiving no respiratory support at randomization (17.8% vs. 14.0%; rate ratio, 1.19; 95% CI, 0.92 to 1.55)." (abstract, results, passage verified)
pubmedfull study (doi)
Remdesivir demonstrated greater efficacy early in the course of COVID-19 compared to late-stage disease in patients on mechanical ventilators.
"Remdesivir was much more efficacious early in the course of disease and not so much so for those patients on the ventilator." (said at 0:10:51)
The claim is well-supported by randomized controlled trials evaluating remdesivir across different disease severities in COVID-19 patients. In the PINETREE trial (Gottlieb et al., 2022, PMID: 34937145), early administration of remdesivir in symptomatic outpatients reduced the risk of hospitalization or death by 87% compared to placebo. In contrast, in major inpatient trials like the ACTT-1 trial (Beigel et al., 2020, PMID: 32445440) and the WHO Solidarity trial (Hongchao et al., 2021, PMID: 33264556), remdesivir demonstrated significant benefits in time to recovery among patients receiving low-flow oxygen or not on oxygen, but showed little to no clinical efficacy or mortality benefit in patients who were already on mechanical ventilation or ECMO.
- supports: Remdesivir for the Treatment of Covid-19 - Final Report. (The New England journal of medicine 2020) · cited 7759x in the literature
"Those who received remdesivir had a median recovery time of 10 days (95% confidence interval [CI], 9 to 11), as compared with 15 days (95% CI, 13 to 18) among those who received placebo (rate ratio for recovery, 1.29; 95% CI, 1.12 to 1.49; P<0.001, by a log-rank test)." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Repurposed Antiviral Drugs for Covid-19 - Interim WHO Solidarity Trial Results. (The New England journal of medicine 2021) · cited 2630x in the literature
"These remdesivir, hydroxychloroquine, lopinavir, and interferon regimens had little or no effect on hospitalized patients with Covid-19, as indicated by overall mortality, initiation of ventilation, and duration of hospital stay." (abstract, conclusions, passage verified)
pubmedfull study (doi) - supports: Early Remdesivir to Prevent Progression to Severe Covid-19 in Outpatients. (The New England journal of medicine 2022) · cited 1288x in the literature
"Among nonhospitalized patients who were at high risk for Covid-19 progression, a 3-day course of remdesivir had an acceptable safety profile and resulted in an 87% lower risk of hospitalization or death than placebo." (abstract, conclusions, passage verified)
pubmedfull study (doi)
Commercial airplanes exchange cabin air roughly tenfold per hour and pass the air through HEPA filters to capture viral particles.
"Well, you may not know this, but they do they do air changes like tenfold every hour and all of that air is going through HEPA filters and so the virus gets trapped." (said at 0:15:59)
Commercial aircraft environmental control systems maintain high air exchange rates (typically 15 to 30 air changes per hour, or every 2 to 4 minutes) and route recirculated air through High-Efficiency Particulate Air (HEPA) filters designed to trap viral aerosols and other airborne particulates. Experimental and computational modeling studies confirm that cabin ventilation and filtration rapidly clear respiratory particles (removing particles 5 to 12 times faster than standard commercial indoor spaces), although localized, close-proximity exposure between passengers within the same row can still occur prior to filtration.
Vitamin D has a steroid structure similar to cortisol, testosterone, estrogen, and progesterone, allowing it to enter the cell nucleus and regulate gene transcription.
"if you look at the structure of vitamin D, it is very similar to the structure of cortisol, of the structure of testosterone, of estrogen, of progesterone. And what do we know about all of these other steroid hormones? They go directly into the nucleus of the cell where they affect transcription of protein factors." (said at 0:19:10)
The claim is supported by biochemical and molecular biology literature. Vitamin D (a secosteroid, derived from steroids with a broken B-ring) shares a core steroid ring structure with classical steroid hormones such as cortisol, testosterone, estrogen, and progesterone. Like these steroid hormones, its biologically active form (1α,25-dihydroxyvitamin D3 or calcitriol) acts via a nuclear receptor (the vitamin D receptor, VDR), which belongs to the nuclear receptor superfamily. Upon binding its ligand, the receptor acts as a nuclear transcription factor to regulate target gene transcription.
- supports: Vitamin D and Its Receptor from a Structural Perspective. (Nutrients 2022) · cited 77x in the literature
"The activities of 1α,25-dihydroxyvitamin D3, 1,25D 3 , are mediated via its binding to the vitamin D receptor (VDR), a ligand-dependent transcription factor that belongs to the nuclear receptor superfamily." (abstract, passage verified)
pubmedfull study (doi) - supports: Genomic signaling of vitamin D. (Steroids 2023) · cited 43x in the literature
"The activation of VDR by 1,25(OH) 2 D 3 is the core mechanism of genomic signaling of vitamin D 3 , which results in the modulation of the epigenome at thousands of promoter and enhancer regions as well as finally in the activation or repression of hundreds of target gene transcription." (abstract, passage verified)
pubmedfull study (doi) - supports: Calcifediol: Mechanisms of Action. (Nutrients 2023) · cited 18x in the literature
"Due to its essential role in calcium and phosphate homeostasis, the secosteroid hormone calcitriol has received growing attention over the last few years. Calcitriol, like other steroid hormones, may function through both genomic and non-genomic mechanisms. In the traditional function, the interaction between the biologically active form of vitamin D and the vitamin D receptor (VDR) affects the transcription of thousands of genes" (abstract, passage verified)
pubmedfull study (doi)
Immune cells express vitamin D receptors.
"They they found vitamin D receptors in the immune cells." (said at 0:22:44)
The claim is supported. It is well-established in immunology and endocrinology that cells across both the innate and adaptive immune systems express the vitamin D receptor (VDR), allowing vitamin D signaling to modulate immune cell activation, differentiation, and inflammatory responses.
Older adults have a higher susceptibility to vitamin D deficiency because aging skin becomes less efficient at producing vitamin D from sunlight.
"The older you are, the more apt you are to get vitamin D deficiencies because your skin is not as effective at turning uh at making vitamin D." (said at 0:23:04)
Published experimental and physiological research demonstrates that aging significantly reduces the skin's capacity to synthesize vitamin D. Human skin samples across different age groups (ages 8–92) show an age-dependent reduction in epidermal 7-dehydrocholesterol concentrations, leading to a greater than twofold decrease in cutaneous previtamin D3 production under ultraviolet irradiation in older individuals compared to younger individuals.
- supports: Aging decreases the capacity of human skin to produce vitamin D3. (The Journal of clinical investigation 1985) · cited 1449x in the literature
"A comparison of the amount of previtamin D3 produced in the skin from the 8- and 18-yr-old subjects with the amount produced in the skin from the 77- and 82-yr-old subjects revealed that aging can decrease by greater than twofold the capacity of the skin to produce previtamin D3." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Vitamin D, Calcium, Parathyroid Hormone, and Sex Steroids in Bone Health and Effects of Ag… (Journal of osteoporosis 2020) · cited 130x in the literature
"In the elderly, various changes in the calcium and vitamin D metabolism, such as decrease in the production of vitamin D, decrease in dietary vitamin D, decreased renal production, increased production of excretory products, decrease in the level of VDR, and decreased calcium absorption by the intestines, can lead to bone loss." (abstract, passage verified)
pubmedfull study (doi)
A study of 191,000 patients published in PLOS ONE found that SARS-CoV-2 positivity rates increased as circulating 25-hydroxyvitamin D levels fell below 50 ng/mL across all races, genders, geographies, and age groups.
"And this was published by uh it was published in PLOS ONE, the journal, uh an article titled "SARS-CoV-2 Positivity Rates Associated with Circulating 25-Hydroxyvitamin D Levels." ... And what they found was that as your levels as your levels started to drop below 50 nanograms per milliliter, we started to see an increase in SARS-CoV-2 positivity rate. And it didn't matter based on race, gender, geography, or age." (said at 0:24:08)
A retrospective observational study of 191,779 patients across the United States published in PLOS ONE (Kaufman et al., 2020) evaluated circulating 25-hydroxyvitamin D [25(OH)D] levels in relation to SARS-CoV-2 test positivity. The authors reported that SARS-CoV-2 positivity was inversely related to 25(OH)D levels, decreasing continuously as levels rose toward 50-55 ng/mL (5.9% positivity at ≥55 ng/mL vs 12.5% at <20 ng/mL). This inverse relationship persisted after multivariable adjustment across all evaluated age groups, sexes, racial/ethnic census proportions, and geographic latitudes. Because this was a retrospective cross-sectional laboratory analysis, it shows an epidemiological association rather than proven causality.
- supports: SARS-CoV-2 positivity rates associated with circulating 25-hydroxyvitamin D levels. (PloS one 2020) · cited 396x in the literature
"A total of 191,779 patients were included (median age, 54 years [interquartile range 40.4-64.7]; 68% female. The SARS-CoV-2 positivity rate was 9.3% (95% C.I. 9.2-9.5%) and the mean seasonally adjusted 25(OH)D was 31.7 (SD 11.7). The SARS-CoV-2 positivity rate was higher in the 39,190 patients with "deficient" 25(OH)D values (<20 ng/mL) (12.5%, 95% C.I. 12.2-12.8%) than in the 27,870 patients with "adequate" values (30-34 ng/mL) (8.1%, 95% C.I. 7.8-8.4%) and the 12,321 patients with values ≥55 ng/mL (5.9%, 95% C.I. 5.5-6.4%)... SARS-CoV-2 positivity is strongly and inversely associated with circulating 25(OH)D levels, a relationship that persists across latitudes, races/ethnicities, both sexes, and age ranges." (abstract, results and conclusions, passage verified)
pubmedfull study (doi)
Circulating 25-hydroxyvitamin D is converted into active 1,25-dihydroxyvitamin D not only in the kidneys but also locally within white blood cells.
"And then it gets converted into 1,25-dihydroxyvitamin D in the kidneys for metabolism or in the white blood cells where they need it there." (said at 0:24:38)
The claim accurately reflects established human biochemistry and immunology. While the kidneys are the primary site of systemic endocrine conversion of circulating 25-hydroxyvitamin D into active 1,25-dihydroxyvitamin D via the enzyme CYP27B1 (1α-hydroxylase), white blood cells—predominantly monocytes, macrophages, and dendritic cells—also express CYP27B1. In response to immune stimuli (such as interferon-gamma or pathogen-associated molecular patterns), these immune cells convert 25-hydroxyvitamin D locally into 1,25-dihydroxyvitamin D to mediate autocrine, intracrine, and paracrine immune functions.
- supports: Immune regulation of 25-hydroxyvitamin D-1alpha-hydroxylase in human monocytic THP1 cells:… (The Journal of clinical endocrinology and metabolism 2006) · cited 78x in the literature
"25-Hydroxyvitamin D can be activated to 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] by the rate-limiting enzyme 1alpha-hydroxylase in cells of the immune system under control of immune stimuli, such as interferon-gamma (IFNgamma)." (abstract, introduction, passage verified)
pubmedfull study (doi) - supports: Vitamin D and the immune system: new perspectives on an old theme. (Endocrinology and metabolism clinics of North America 2010) · cited 525x in the literature
"Crucially, these effects seem to be mediated via localized autocrine or paracrine synthesis of 1,25(OH)(2)D(3) from precursor 25-hydroxyvitamin D(3), the main circulating metabolite of vitamin D." (abstract, passage verified)
pubmedfull study (doi) - supports: Regulation of the extrarenal CYP27B1-hydroxylase. (The Journal of steroid biochemistry and molecular biology 2014) · cited 179x in the literature
"Special emphasis is placed on soluble factors (i.e., cytokines) in the local microenvironment of these human diseases that coordinate amplification and feedback inhibition of the macrophage CYP27B1-hydroxylase." (abstract, passage verified)
pubmedfull study (doi)
Observational studies show that COVID-19 patients with vitamin D deficiency had higher rates of hospitalization, mechanical ventilation, and mortality.
"We see people being admitted to the hospital had lower rates than those that had similar symptoms but were not SARS-CoV-2 positive. ... they showed that there was a difference in mortality, that there was a difference in which ones went on to need ventilators." (said at 0:25:40)
Multiple systematic reviews and meta-analyses of observational studies confirm that vitamin D deficiency is consistently associated with increased risk of hospitalization, severe disease requiring intensive care or mechanical ventilation, and higher mortality in patients with COVID-19. For example, a meta-analysis of 54 observational studies including over 1.4 million individuals found that vitamin D deficiency was associated with significantly higher odds of COVID-19 hospitalization, ICU admission, and death. Because these findings come from observational studies, the certainty of evidence for causation is low due to potential residual confounding (e.g., advanced age, obesity, underlying chronic illness, and reverse causation where acute inflammation lowers serum 25-hydroxyvitamin D levels). However, the claim specifically asserts what observational studies show, which is accurate.
- supports: Association of vitamin D deficiency with COVID-19 infection severity: Systematic review an… (Clinical endocrinology 2022) · cited 111x in the literature
"Vitamin D deficiency was associated with significantly higher mortality (odds ratio [OR]: 2.47, 95% confidence interval [CI]: 1.50-4.05; 12 studies; hazard ratio [HR]: 4.11, 95% CI: 2.40-7.04; 3 studies), higher rates of hospital admissions (OR: 2.18, 95% CI: 1.48-3.21; 3 studies) and longer hospital stays (0.52 days; 95% CI: 0.25-0.80; 2 studies) as compared to nonvitamin D deficient status." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Vitamin D Status and SARS-CoV-2 Infection and COVID-19 Clinical Outcomes. (Frontiers in public health 2021) · cited 163x in the literature
"Severe deficiency, deficiency and insufficiency of vitamin D were all associated with ICU admission (odds ratio [OR], 95% confidence intervals [95%CIs]: 2.63, 1.45-4.77; 2.16, 1.43-3.26; 2.83, 1.74-4.61, respectively), mortality (OR, 95%CIs: 2.60, 1.93-3.49; 1.84, 1.26-2.69; 4.15, 1.76-9.77, respectively), SARS-CoV-2 infection (OR, 95%CIs: 1.68, 1.32-2.13; 1.83, 1.43-2.33; 1.49, 1.16-1.91, respectively) and COVID-19 hospitalization (OR, 95%CIs 2.51, 1.63-3.85; 2.38, 1.56-3.63; 1.82, 1.43-2.33)." (abstract, findings, passage verified)
pubmedfull study (doi) - supports: The role of vitamin D in outcomes of critical care in COVID-19 patients: evidence from an … (Public health nutrition 2024) · cited 21x in the literature
"Overall, vitamin D status is a critical factor influencing the mortality rate, disease severity, admission to intensive care unit and being detached from mechanical ventilation." (abstract, conclusions, passage verified)
pubmedfull study (doi)
ACE2 balances angiotensin II and angiotensin-(1-7), reducing pro-oxidative products and increasing antioxidant products.
"The other aspect of angiotensin or ACE2, I should say, is that it gets rid of pro-oxidative products and it increases antioxidant products. So, for instance, angiotensin II and angiotensin-(1-7), those are in balance, and ACE2 tries to keep those in balance." (said at 0:34:54)
The renin-angiotensin system comprises two counter-regulatory arms: the classical ACE/Angiotensin II/AT1R axis (which promotes vasoconstriction, inflammation, and reactive oxygen species generation via NADPH oxidases) and the protective ACE2/Angiotensin-(1-7)/Mas receptor axis. ACE2 directly cleaves Angiotensin II to form Angiotensin-(1-7), thereby depleting the pro-oxidative peptide and generating a counter-regulatory peptide that stimulates antioxidant defense pathways.
In a Spanish randomized controlled trial led by Marta Castillo, 2% of patients treated with calcifediol were admitted to the ICU compared to 50% in the placebo group.
"It was Marta Castillo who published, she was the lead author on this one out of Spain... And what they found was in the calcifediol group there was only 2% that went to the intensive care unit, whereas in the placebo group 50% of those went to the intensive care unit." (said at 0:36:40)
In a 2020 pilot randomized clinical trial conducted in Córdoba, Spain, led by Marta Entrenas Castillo, 76 hospitalized COVID-19 patients receiving standard care were randomized 2:1 to receive calcifediol or no calcifediol. In the calcifediol group, 1 of 50 patients (2%) required ICU admission, compared to 13 of 26 patients (50%) in the control group (untreated with calcifediol). The control group received best available therapy without an active placebo.
Window glass blocks almost all UVB radiation while allowing UVA radiation to pass through.
"You go behind a piece of glass, there's there's almost no UVB at all. The only thing that's coming through is UVA, which is, you know, nasty ultraviolet radiation." (said at 0:47:11)
Standard window glass absorbs virtually all ultraviolet B (UVB) radiation while allowing significant amounts of ultraviolet A (UVA) radiation to pass through. Reviews and optical measurements confirm that ordinary architectural and non-laminated vehicle glass blocks almost all UVB but transmits a substantial portion of UVA, with transmission depending on thickness, tinting, and laminates.
- supports: Implication for photosensitive patients of ultraviolet A exposure in vehicles. (The British journal of dermatology 2004) · cited 42x in the literature
"Window glass blocks all UVB but not all UVA." (abstract, background, passage verified)
pubmedfull study (doi) - supports: Photoprotection by window glass, automobile glass, and sunglasses. (Journal of the American Academy of Dermatology 2006) · cited 194x in the literature
"It has been known for some time that window glass filters out UVB and transmits UVA and visible light." (abstract, passage verified)
pubmedfull study (doi) - supports: Photoprotection: clothing and glass. (Dermatologic clinics 2014) · cited 26x in the literature
"In general, all types of glass block UV-B. For UV-A, the degree of transmission depends on the type, thickness, and color of the glass." (abstract, passage verified)
pubmedfull study (doi)
An observational study of over 191,000 individuals found that SARS-CoV-2 positivity rates began to increase as circulating vitamin D levels dropped below 50 ng/mL.
"those studies that we talked about earlier where they took looked at 191,000 people that SARS-CoV-2 rates started to go up once levels dropped below 50." (said at 0:48:55)
A retrospective observational study by Kaufman et al. (2020) analyzed 191,779 patients across all 50 US states and found that SARS-CoV-2 positivity rates were inversely associated with circulating 25-hydroxyvitamin D levels. Test positivity declined continuously as circulating vitamin D levels increased up to approximately 50–55 ng/mL (positivity was 12.5% for <20 ng/mL, 8.1% for 30–34 ng/mL, and 5.9% for ≥55 ng/mL), meaning positivity rates increased as levels fell below that range. Because this is a retrospective observational study, it demonstrates an association rather than proven causality.
- supports: SARS-CoV-2 positivity rates associated with circulating 25-hydroxyvitamin D levels. (PloS one 2020) · cited 396x in the literature
"A total of 191,779 patients were included (median age, 54 years [interquartile range 40.4-64.7]; 68% female. The SARS-CoV-2 positivity rate was 9.3% (95% C.I. 9.2-9.5%) and the mean seasonally adjusted 25(OH)D was 31.7 (SD 11.7). The SARS-CoV-2 positivity rate was higher in the 39,190 patients with "deficient" 25(OH)D values (<20 ng/mL) (12.5%, 95% C.I. 12.2-12.8%) than in the 27,870 patients with "adequate" values (30-34 ng/mL) (8.1%, 95% C.I. 7.8-8.4%) and the 12,321 patients with values ≥55 ng/mL (5.9%, 95% C.I. 5.5-6.4%)." (abstract, results, passage verified)
pubmedfull study (doi)
A study of 20,000 patients in the Mayo Clinic database taking vitamin D doses up to 55,000 IU/day identified only one case of hypercalcemia, in an individual with serum levels between 200–300 ng/mL.
"there was a study where this, uh, this Polish scientist looked at the Mayo Clinic's database and they looked at 20,000 people... One person had hypercalcemia out of those 20,000, and they had ranges—people supplementing anywhere from 0 to 55,000 units a day—and, uh, really just one person. And that person's vitamin D level, if I recall correctly, was up in the, the 200-300 range. That's nanograms per milliliter." (said at 0:50:30)
A 10-year retrospective population-based study using the Rochester Epidemiology Project database (Mayo Clinic) evaluated 20,308 serum 25-hydroxyvitamin D [25(OH)D] measurements between 2002 and 2011. While 1,714 individuals had 25(OH)D levels exceeding 50 ng/mL and four had hypercalcemia temporally associated with elevated levels, chart review revealed only one individual with true acute clinical vitamin D toxicity and hypercalcemia directly attributable to vitamin D, occurring at a serum 25(OH)D concentration of 364 ng/mL.
Vitamin D supplementation has a non-linear dose-response where the first 1,000 IU increases serum 25(OH)D by 4.8–5 ng/mL, while at higher doses (15,000–30,000 IU) each 1,000 IU increases levels by approximately a tenth of that rate.
"What we notice actually is that the first thousand units that you supplement causes an increase of about 4.8 to 5, uh, nanograms per milliliter. Whereas when you get up to about 15, 20, 30,000, that, uh, each additional thousand goes up by about a tenth of that. So it's a, it's a nonlinear relationship." (said at 0:51:40)
The relationship between oral vitamin D intake and circulating serum 25-hydroxyvitamin D [25(OH)D] concentrations is well established to be non-linear (curvilinear). Clinical and observational dose-response investigations demonstrate that at low baseline inputs, an initial daily intake of 1,000 IU typically raises serum 25(OH)D by approximately 4.8 to 5 ng/mL (roughly 12 nmol/L). At much higher daily doses (such as 15,000 to 30,000 IU/day), the rate of increase flattens markedly due to saturation of hepatic 25-hydroxylase and upregulation of 24-hydroxylase catabolic pathways, resulting in an incremental rise per 1,000 IU that is roughly one-tenth of the initial slope (approximately 0.5 ng/mL per 1,000 IU).
The SHADE randomized controlled trial in India showed that COVID-19 patients given 60,000 IU/day of vitamin D for 7 days had higher SARS-CoV-2 PCR negativity rates at day 21 (roughly 60% vs 20%) and significantly lower fibrinogen levels.
"based on the SHADE study. This is another randomized controlled trial that came out of India. Um, and it showed basically when they supplemented patients in the hospital with 60,000 units a day for 7 days that there was an improvement by day 21 in the number of COVID-negative patients on testing... it was like 60 versus 20% at week three were negative by, by just supplementing with vitamin D. The other thing that they looked at was fibrinogen, which was a, a marker of inflammation that was significantly lower as well." (said at 0:53:45)
The SHADE randomized, placebo-controlled trial conducted in India (Rastogi et al., 2022) evaluated 40 asymptomatic or mildly symptomatic, vitamin D-deficient SARS-CoV-2-positive participants randomized to receive 60,000 IU/day of oral cholecalciferol for 7 days (n=16) or placebo (n=24). By day 21, 62.5% (10/16) in the vitamin D group compared to 20.8% (5/24) in the control group achieved viral clearance (SARS-CoV-2 RNA negativity, p=0.018). Furthermore, serum fibrinogen levels decreased significantly in the intervention group compared to controls (p=0.007). The certainty of evidence for this specific finding is low due to serious imprecision from the small sample size (n=40).
A French study of nursing home residents hospitalized with COVID-19 found significantly better clinical outcomes in patients who had received an 80,000 IU vitamin D dose within the preceding 30 days compared to those who received it over 30 days prior.
"there was a great study that looked at that in France. Um, you know, apparently the practice was that every nursing home patient would get 80,000 international units of vitamin D every 3 months... when they sorted them to those that had gotten it within the last 30 days to those that had gotten it past 30 days, there was a statistically significant, clinically significant difference between those that had gotten it recently and those that have gotten it more than a month out." (said at 0:56:46)
A quasi-experimental study conducted in a French nursing home (Annweiler et al., 2020) evaluated 66 elderly residents with COVID-19. Participants who had received bolus vitamin D3 supplementation during the acute infection or in the preceding month (often standard 80,000 IU boluses given periodically) experienced significantly higher survival (82.5% vs. 44.4%, adjusted HR = 0.11, p = 0.003) and lower disease severity on the Ordinal Scale for Clinical Improvement compared to those who had not received recent supplementation. The certainty of evidence is low due to the small sample size (n=66, with only 9 comparator patients) and non-randomized, quasi-experimental design.
Aging reduces cutaneous vitamin D synthesis capacity by two to four times compared to youth.
"depending on your age, you know, you're anywhere between two or four times less likely to make as much as you were when you were younger." (said at 0:58:23)
Classic comparative studies examining human skin samples across different age groups demonstrate an age-dependent decline in epidermal 7-dehydrocholesterol (provitamin D3) concentrations and previtamin D3 production capacity upon ultraviolet exposure. In vitro irradiation of human skin from elderly individuals (aged 77–82 years) compared to young individuals (aged 8–18 years) showed a decrease of greater than twofold in the capacity of skin to synthesize previtamin D3, with literature widely documenting a two- to fourfold reduction (up to ~75%) across the human lifespan.
People who get more sleep prior to vaccination develop a stronger immune response with higher antibody titers, such as to the influenza vaccine.
"We know for a fact that people who get more sleep before they get an immunization have a better immune response with higher antibody titers to, for instance, the flu vaccine." (said at 1:04:11)
Published systematic reviews, meta-analyses, and prospective studies confirm that adequate sleep duration surrounding vaccination is associated with significantly higher antibody titers. A 2023 meta-analysis of studies evaluating sleep and viral vaccinations (including influenza, hepatitis, and SARS-CoV-2) found that objectively measured short sleep duration was associated with a robust reduction in antibody responses (effect size 0.79). Prospective investigations examining specific time windows around influenza vaccination specifically demonstrate that shorter sleep duration in the nights preceding immunization predicts significantly lower antibody titers 1 to 4 months post-vaccination.
- supports: Temporal Links Between Self-Reported Sleep and Antibody Responses to the Influenza Vaccine… (International journal of behavioral medicine 2021) · cited 82x in the literature
"Analyses focused on nightly sleep on the days preceding and after the vaccination revealed that shorter sleep duration on the two nights before the vaccination predicted fewer antibodies 1 and 4 months later." (abstract, results, passage verified)
pubmedfull study (doi) - supports: A meta-analysis of the associations between insufficient sleep duration and antibody respo… (Current biology : CB 2023) · cited 51x in the literature
"Objectively assessed short sleep was associated with a robust decrease in antibody response (total n = 304, ages 18-60; overall ES [95% CI] = 0.79 [0.40, 1.18]). In men, the pooled ES was large (overall ES [95% CI] = 0.93 [0.54, 1.33]), whereas it did not reach significance in women (overall ES [95% CI] = 0.42 [-0.49, 1.32]). These results provide evidence that insufficient sleep duration substantially decreases the response to anti-viral vaccination and suggests that achieving adequate amount of sleep during the days surrounding vaccination may enhance and prolong the humoral response." (abstract, results, passage verified)
pubmedfull study (doi) - supports: A Narrative Review on How Timing Matters: Circadian and Sleep Influences on Influenza Vacc… (Vaccines 2025) · cited 6x in the literature
"Short sleep duration-especially in the two nights preceding vaccination-was associated with reduced antibody levels, while acute sleep deprivation the night after vaccination transiently reduced antibody levels in males." (abstract, results, passage verified)
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In a viral challenge study with rhinovirus, subjects with 7 or more hours of sleep and good sleep efficiency had a five- to sevenfold lower risk of developing a cold compared to those with less sleep.
"they subjected them to rhinovirus and they put it into their nose and they waited to see how many people came down with, uh, with a common cold. And when they looked back and, and saw what their sleep habits were, it was a five- to sevenfold difference if you looked at those people that got 7 or more hours of sleep per night versus those that got less, and, uh, whether or not they had a good sleep efficiency." (said at 1:04:38)
The statement accurately reflects findings from prospective rhinovirus challenge studies. In Cohen et al. (2009), 153 healthy participants were tracked for baseline sleep habits and subsequently quarantined and challenged with rhinovirus: participants with lower sleep efficiency (<92%) were 5.50 times (95% CI, 2.08–14.48) more likely to develop a clinical cold than those with high efficiency (≥98%), and participants sleeping <7 hours were 2.94 times (95% CI, 1.18–7.30) more likely to develop a cold than those sleeping ≥8 hours. In a subsequent actigraphy challenge study by Prather et al. (2015), participants sleeping <5 hours were 4.50 times more likely to develop a cold compared to those sleeping >7 hours.
- supports: Sleep habits and susceptibility to the common cold. (Archives of internal medicine 2009) · cited 608x in the literature
"There was a graded association with average sleep duration: participants with less than 7 hours of sleep were 2.94 times (95% confidence interval [CI], 1.18-7.30) more likely to develop a cold than those with 8 hours or more of sleep. The association with sleep efficiency was also graded: participants with less than 92% efficiency were 5.50 times (95% CI, 2.08-14.48) more likely to develop a cold than those with 98% or more efficiency." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Behaviorally Assessed Sleep and Susceptibility to the Common Cold. (Sleep 2015) · cited 407x in the literature
"Specifically, those sleeping < 5 h (odds ratio [OR] = 4.50, 95% confidence interval [CI], 1.08-18.69) or sleeping between 5 to 6 h (OR = 4.24, 95% CI, 1.08-16.71) were at greater risk of developing the cold compared to those sleeping > 7 h per night" (abstract, results, passage verified)
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Slow-wave sleep occurs primarily at the beginning of the night and is associated with human growth hormone secretion.
"And they are slow-wave sleep, which is right at the beginning of the night. In fact, this is the type of sleep that is associated with growth hormone secretion, especially in children." (said at 1:08:53)
Extensive physiological and clinical evidence confirms that slow-wave sleep (SWS) predominates during the early sleep cycles (the first few hours of the night) and is closely coupled with major pulses of growth hormone (GH) secretion. In humans, the largest and most consistent 24-hour pulse of GH release occurs shortly after sleep onset in association with slow-wave sleep across childhood, adolescence, and adulthood.
SARS-CoV-1, SARS-CoV-2, and MERS suppress the innate immune system early in the course of infection.
"We've got good evidence now from immunologists that SARS-CoV-1, SARS-CoV-2, and MERS, all three of those, they kind of act the same way in that early on in the disease, they suppress the innate immune system." (said at 1:16:20)
Published immunological and virological research confirms that all three highly pathogenic human coronaviruses—SARS-CoV-1, SARS-CoV-2, and MERS-CoV—employ molecular mechanisms to suppress and evade the host's innate immune response early during infection. Specifically, they utilize viral structural and non-structural proteins to block pattern recognition receptors (such as dsRNA sensors), antagonize MAVS and STING signaling pathways, and blunt early type I and type III interferon (IFN) production and downstream signaling, which delays antiviral defenses and facilitates initial viral replication.
- supports: Control of Innate Immune Activation by Severe Acute Respiratory Syndrome Coronavirus 2 and… (Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 2021) · cited 10x in the literature
"Infection with highly pathogenic human CoVs often results in a severe respiratory disease characterized by a delayed and blunted interferon (IFN) response, accompanied by an excessive production of proinflammatory cytokines. This indicates that CoVs developed effective mechanisms to overcome the host innate immune response and promote viral replication and pathogenesis." (abstract, passage verified)
pubmedfull study (doi) - supports: Insight into the mechanisms of coronaviruses evading host innate immunity. (Biochimica et biophysica acta. Molecular basis of disease 2023) · cited 19x in the literature
"The coronaviruses manage to block, escape, or dampen the innate immune response by antagonizing double-stranded RNA (dsRNA) sensor, mitochondrial antiviral-signaling protein (MAVS) and stimulator of IFN genes (STING) pathways, epigenetic modification, posttranslational modifications, and host mRNA translation." (abstract, passage verified)
pubmedfull study (doi) - supports: Modulation of Host Innate Immune Response by Highly Pathogenic Human Coronaviruses during … (Journal of microbiology and biotechnology 2026)
"The innate immune system plays a pivotal role in the early detection and control of viral infections through mechanisms such as cytoplasmic RNA sensors, Toll-like receptors, interferon signaling, and inflammasome activation. However, these coronaviruses effectively exploit and subvert these processes, suppressing antiviral defenses while amplifying inflammatory cascades." (abstract, passage verified)
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Genetic mutations that abolish interferon secretion were identified exclusively in severe COVID-19 patients and explained a significant proportion of severe cases in a cohort published in Science.
"there's a couple of papers that were published in Science uh about a month or two ago. They could explain 14% of all of the severe cases in their cohort based on two findings. One was a genetic a bunch of genetic mutations that basically left the the subjects hamstrung in terms of secreting and producing interferon... All of those mutations were found only in the severe COVID-19 patients." (said at 1:19:01)
Two companion papers published in Science in September 2020 by the COVID Human Genetic Effort evaluated type I interferon (IFN) impairment in severe COVID-19. Zhang et al. (PMID 32972995) identified loss-of-function inborn errors in 13 genes governing type I IFN immunity in 3.5% (23 of 659) of patients with life-threatening COVID-19 pneumonia, which were functionally deleterious and absent or depleted in asymptomatic/mild controls. Bastard et al. (PMID 32972996) concurrently identified neutralizing autoantibodies against type I IFNs in 10.2% (101 of 987) of patients with life-threatening COVID-19, combining to explain approximately 14% of severe cases across the two findings.
Autoantibodies neutralizing type I interferon were found in approximately 10% of patients with severe COVID-19, and in none of the mild to moderate patients, in a study published in Science.
"The other one that made up about 10% was older patients that had developed antibodies to interferon. So essentially their interferon levels even though they're being produced they were being inactivated. All of these patients that had antibodies against SARS-CoV or against interferon were in the severe, none in the mild to moderate group." (said at 1:20:01)
A landmark study published in Science (Bastard et al., 2020) evaluated patients with SARS-CoV-2 infection and found that at least 101 of 987 patients (~10.2%) with life-threatening COVID-19 pneumonia harbored neutralizing IgG autoantibodies against type I interferons (such as IFN-α and/or IFN-ω). These neutralizing autoantibodies were completely absent in all 663 individuals tested who had asymptomatic or mild SARS-CoV-2 infection.
- supports: Autoantibodies against type I IFNs in patients with life-threatening COVID-19. (Science (New York, N.Y.) 2020) · cited 2875x in the literature
"We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs... These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals." (abstract, results, passage verified)
pubmedfull study (doi)
Penicillin was discovered in 1928.
"and then you have the discovery of penicillin in 1928." (said at 1:30:10)
Historical and scientific literature universally recognizes that Alexander Fleming discovered penicillin in September 1928 at St. Mary's Hospital in London.
The AstraZeneca/Oxford COVID-19 vaccine uses a chimpanzee adenovirus vector to deliver DNA into the nucleus, where it is transcribed into mRNA.
"The other one that's coming out is the AstraZeneca Oxford one is does does very same thing except instead of using mRNA in a little like a a lipid droplet like a butter droplet if you like. It's using a different vector. It's actually using a chimpanzee adenovirus... In this case, the message is not an mRNA. It's actually a DNA. And so, the DNA goes in to the nucleus in in the AstraZeneca Oxford uh uh version where it is transcribed into an mRNA." (said at 1:48:31)
The AstraZeneca/Oxford COVID-19 vaccine (ChAdOx1 nCoV-19 / AZD1222) utilizes a replication-deficient chimpanzee adenovirus vector (derived from isolate Y25) to deliver double-stranded DNA encoding the SARS-CoV-2 spike glycoprotein into the host cell nucleus. Inside the nucleus, the transgene DNA is transcribed by host cellular machinery into mRNA, which is subsequently translated into the spike protein antigen in the cytoplasm.
A flu vaccine administered in Europe around 2009-2010 was found to be associated with an increased risk of narcolepsy, hypothesized to be caused by cross-reactivity against hypocretin-producing neurons.
"a flu vaccine that was uh it was it was a regular flu vaccine. Was not an mRNA, was not a DNA, was just a regular flu vaccine that was administered uh in Europe a number of years ago. This is back in 2009, 2010. And they did find an increased risk of of narcolepsy in patients that were vaccinated with that type of type of type of vaccine. And the thought process there was is that perhaps there was an immune response that cross-reacted with uh the portion of the brain that produces uh hypocretin which is the the basis for narcolepsy" (said at 1:51:13)
Extensive epidemiological and translational evidence confirms that an influenza vaccine administered in Europe during the 2009–2010 H1N1 pandemic (specifically Pandemrix, an AS03-adjuvanted vaccine) was associated with a significantly increased risk of narcolepsy type 1, predominantly in children and adolescents. Narcolepsy type 1 is characterized by the destruction of hypocretin (orexin)-producing neurons in the lateral hypothalamus, occurring predominantly in individuals carrying the HLA-DQB1*06:02 allele. Mechanistic research supports the hypothesis that the vaccine triggered an autoimmune response that cross-reacted with hypocretin-producing neurons or associated neuronal antigens via molecular mimicry.
- supports: Incidence of narcolepsy in Norwegian children and adolescents after vaccination against H1… (Sleep medicine 2013) · cited 178x in the literature
"The data collected during 3 years following vaccination showed a significantly increased risk for narcolepsy with cataplexy (P<.0001) and reduced CSF hypocretin levels in vaccinated children ages 4-19 years the first year after Pandemrix® vaccination, with a minimum incidence of 10 of 100,000 individuals per year." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Narcolepsy and A(H1N1)pdm09 vaccination: shaping the research on the observed signal. (Human vaccines & immunotherapeutics 2014) · cited 12x in the literature
"Epidemiological data from several European countries suggested an increased risk of the chronic sleep disorder narcolepsy following vaccination with Pandemrix(™), an AS03-adjuvanted, pandemic A(H1N1)pdm09 influenza vaccine. Further research to investigate potential associations between Pandemrix™ vaccination, A(H1N1)pdm09 influenza infection and narcolepsy is required. Narcolepsy is most commonly caused by a reduction or absence of hypocretin produced by hypocretin-secreting neurons in the hypothalamus, and is tightly associated with HLA-II DQB1*06:02." (abstract, passage verified)
pubmedfull study (doi) - supports: Epidemiology and Pathophysiology of Childhood Narcolepsy. (Paediatric respiratory reviews 2018) · cited 59x in the literature
"Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. ... Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix)" (abstract)
pubmedfull study (doi)
A study showed that 60% of patients had myocarditis or heart tissue inflammation one month after COVID-19 infection.
"there's one study that showed that 60% a month out still had uh myocarditis or inflammation of heart tissue." (said at 1:54:36)
A widely cited prospective observational cohort study by Puntmann et al. (2020) evaluated 100 patients recently recovered from COVID-19 using cardiovascular magnetic resonance (CMR) imaging at a median of 71 days (range: 64–92 days) after diagnosis. The study reported evidence of ongoing myocardial inflammation (defined by elevated myocardial native T2) in 60% of patients (60 of 100) and cardiac involvement overall in 78%.
Published studies have documented new-onset psychosis as a rare post-infection complication in previously healthy individuals who contracted COVID-19.
"I've seen studies, one recent study that showed that one rare side effect was psychosis. People actually hearing things and seeing things. Uh It's very rare, but it's certainly something that's well documented in people that have been completely healthy until they came down with the virus." (said at 1:55:15)
The speaker's claim is supported by published literature. A systematic review of published case reports identified 57 cases of new-onset or exacerbated psychosis associated with COVID-19, noting that roughly 69% occurred in patients with no prior psychiatric history, with hallucinations and delusions being the primary manifestations. Additionally, a large retrospective cohort study of 236,379 COVID-19 survivors found a 6-month incidence of psychotic disorder of approximately 1.4%, confirming it as a rare but documented neuropsychiatric sequela.
A Kawasaki disease-like inflammatory illness occurs in children following COVID-19 infection.
"we saw in kids there was this Kawasaki-like illness that was occurring." (said at 1:56:07)
Extensive epidemiological and clinical surveillance confirmed that a hyperinflammatory condition with clinical features overlapping with Kawasaki disease—termed Multisystem Inflammatory Syndrome in Children (MIS-C) or Paediatric Inflammatory Multisystem Syndrome Temporally Associated with SARS-CoV-2 (PIMS-TS)—occurs in pediatric populations following SARS-CoV-2 infection. Systematic reviews and meta-analyses show shared features including prolonged fever, rash, conjunctivitis, mucocutaneous changes, and coronary artery involvement, alongside differences such as an older age distribution, more frequent gastrointestinal symptoms, and myocardial dysfunction.
A study showed that N-acetylcysteine (NAC) supplementation improves symptoms in influenza virus infection.
"I'm also taking NAC, N-acetylcysteine. There's a study that showed that it improves symptoms in the flu virus." (said at 1:58:15)
A landmark randomized, double-blind, placebo-controlled multicenter trial by De Flora et al. (1997) evaluated oral N-acetylcysteine (600 mg twice daily for 6 months) in 262 individuals. While seroconversion rates to influenza A/H1N1 were similar between groups, only 25% of seropositive subjects receiving NAC developed symptomatic illness compared to 79% receiving placebo, alongside significant reductions in symptom severity and duration of bed rest.
Taking more than 40 milligrams of elemental zinc per day can cause copper deficiency.
"zinc uh 40 milligrams, you don't want to take more than 40 milligrams of zinc a day. That's elemental zinc. Otherwise, you can have copper." (said at 1:58:40)
High zinc intake is well established to cause secondary copper deficiency by upregulating intestinal metallothionein, which preferentially binds copper and inhibits its absorption. Dietary reference authorities, including the U.S. Institute of Medicine and FDA, established the Tolerable Upper Intake Level (UL) for elemental zinc in adults at 40 mg per day specifically to prevent zinc-induced disruption of copper status and associated clinical complications such as anemia and neutropenia.
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