HoldsUp

FoundMyFitness · 2020-04-14 · Rhonda Patrick (host)

COVID-19 Q&A #1 with Rhonda Patrick, Ph.D.

88 claims checked against research: 5 contradicted 3 overstated 5 needing context 60 supported 15 unverified

5

Contradicted by research

0:26:20Rhonda Patrick (host)contradictedmoderate

According to NHANES data, approximately 70% of the US population has vitamin D insufficiency and 28.9% has vitamin D deficiency.

"According to NHANES data, approximately 70% of the US has what is called vitamin D insufficiency, while a further 28.9% has low enough levels to be called deficient." (said at 0:26:20)

The speaker misinterprets the NHANES epidemiological findings. In an analysis of NHANES 2001–2010 data (n = 26,010 US adults) applying Endocrine Society cutoffs, the prevalence of vitamin D deficiency (<50 nmol/L) was 28.9% and the prevalence of vitamin D insufficiency (50 to <75 nmol/L) was 41.4%. Combined, approximately 70.3% of US adults had non-optimal vitamin D status (<75 nmol/L). The speaker conflated the combined total (~70%) with the rate of insufficiency alone, incorrectly asserting that 70% had insufficiency plus 'a further 28.9%' with deficiency.

0:51:54Rhonda Patrick (host)contradictedmoderate

Sitting in a hot bath submerged from the waist down for one hour increases heat shock protein levels.

"One study found that participants that sat in hot baths from their waist down for 1 hour were able to increase their heat shock protein levels." (said at 0:51:54)

Human trials investigating 1 hour of hot water immersion (at 39°C to 40°C) have failed to demonstrate an increase in heat shock protein (HSP) levels. In a controlled trial evaluating sedentary overweight adults immersed in 39°C water for 1 hour, acute monocyte intracellular HSP72 (iHsp72) expression remained unchanged (P = 0.57), and a 2-week repeated immersion protocol significantly reduced extracellular HSP72 concentrations by 17% compared with controls. Similarly, in individuals with type 2 diabetes undergoing 1-hour hot water immersion sessions at 40°C, repeated passive heating produced no significant change in plasma extracellular HSP70 levels.

1:04:08Rhonda Patrick (host)contradictedlow

Case reports indicate that intravenous vitamin C at doses between 1 to 10 g reduced hemolysis in patients with glucose-6-phosphate dehydrogenase deficiency.

"Other case reports have indicated that when given a dose between 1 to 10 g, intravenous vitamin C actually reduced hemolysis." (said at 1:04:08)

The published medical literature contradicts the claim that intravenous vitamin C at doses between 1 and 10 g reduces hemolysis in glucose-6-phosphate dehydrogenase (G6PD) deficiency. In patients with G6PD deficiency, erythrocytes lack adequate NADPH generation to regenerate reduced glutathione against oxidative stress; intravenous vitamin C acts as a pro-oxidant and is a well-established trigger of acute hemolytic anemia. Systematic reviews of published case reports indicate that vitamin C administration at doses starting as low as 1 g/day induces or exacerbates hemolysis in G6PD-deficient individuals, making G6PD deficiency a known contraindication rather than an indication for vitamin C therapy.

1:05:39Rhonda Patrick (host)contradictedhigh

Common clinical features in COVID-19 patients include low albumin levels, low lymphocyte numbers, low neutrophil numbers, and decreased percentages of CD8-positive T cells.

"A common clinical feature in COVID-19 patients is low albumin levels, low lymphocyte numbers, low neutrophil numbers, and decreased percentage of CD8-positive T cells." (said at 1:05:39)

While hypoalbuminemia (low albumin), lymphopenia (low lymphocyte count), and decreased CD8-positive T cell counts are well-documented clinical features in COVID-19 patients, neutrophil counts are typically normal or elevated (neutrophilia), particularly in severe disease. Systematic reviews and meta-analyses demonstrate that severe COVID-19 is characterized by significantly higher neutrophil counts (and an elevated neutrophil-to-lymphocyte ratio), rather than low neutrophil numbers.

1:10:57Rhonda Patrick (host)contradictedvery low

SARS-CoV-1 activates the NLRP3 inflammasome, triggering NF-κB and a cytokine storm in the lungs.

"SARS-CoV-1, the virus responsible for the original SARS outbreak, activates the NLRP3 inflammasome, triggering NF-κB and a cytokine storm in the lungs." (said at 1:10:57)

SARS-CoV-1 is known to stimulate NF-κB signaling and activate the NLRP3 inflammasome, contributing to the severe inflammatory cytokine storm observed during infection. However, the speaker describes the molecular sequence backwards: NF-κB activation functions as the upstream priming event (Signal 1) driving the transcription of pro-IL-1β and inflammasome components, which are subsequently processed and released upon NLRP3 inflammasome activation (Signal 2), rather than the NLRP3 inflammasome triggering NF-κB.

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.