5 Needs context
The ACE2 gene is located on the X chromosome and escapes X-inactivation, leading to higher ACE2 levels in women.
"ACE2, the gene, is located on the X chromosome, and women have two X chromosomes. Most of the time, in one of those X chromosomes, the gene's inactivated, but there are genes that escape that, and ACE2 is one of those. And so women have much higher levels of ACE2." (said at 0:33:51)
The ACE2 gene is located on the X chromosome (Xp22.2) and has been documented to escape X-chromosome inactivation (XCI) in specific cell types, such as alveolar type 2 lung cells, potentially leading to sex-biased tissue expression. However, stating broadly that this causes women to have 'much higher levels of ACE2' requires significant context: XCI escape is often tissue- and cell-type-specific, and circulating plasma ACE2 concentrations in humans are frequently reported to be higher in males than in females or heavily dependent on age, disease status, and sex hormone regulation.
- context: Gender susceptibility to COVID-19: a review of the putative role of sex hormones and X chr… (Journal of endocrinological investigation 2021) · cited 125x in the literature
"On one hand, ACE2 expression could be increased in women, either by estrogens or constitutively by X chromosome inactivation escape or by reduced methylation, providing a larger reservoir of ACE2 to maintain the fundamental equilibrium of RAS regulatory axis." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Unusual X chromosome inactivation maintenance in female alveolar type 2 cells is correlate… (Stem cell reports 2023) · cited 16x in the literature
"We demonstrate that about 68% of expressed X-linked genes in mouse AT2s, including Ace2, escape XCI. There are genome-wide expression differences between male and female AT2s, likely influencing both lung physiology and pathophysiologic responses." (abstract, results, passage verified)
pubmedfull study (doi)
A University of Chicago study found that African-Americans in Chicago need to spend six times as long in the sun as Caucasians to synthesize the same amount of vitamin D.
"there's a there was a study that came out of the University of Chicago a few years ago that found African-Americans in Chicago have to stay in the sun six times as long as a Caucasian to make the same amount of vitamin D in the skin." (said at 0:45:48)
The speaker misattributes the institution and generalizes a highly preliminary observation. The classic finding that deeply pigmented skin requires approximately six times more ultraviolet radiation (UVR) exposure than lightly pigmented skin to produce equivalent circulating vitamin D concentrations originates from seminal experimental work by Clemens, Adams, Henderson, and Holick published in The Lancet (1982), not a University of Chicago study. In that study, heavily pigmented individuals did not significantly increase serum vitamin D after a standard minimal erythemal dose (MED) of UVR, but re-exposing one Black subject to a UVR dose six times larger produced circulating vitamin D concentrations similar to Caucasians. While melanin acts as a natural sunblock and significantly reduces cutaneous vitamin D3 synthesis per unit of UVR time/intensity, this specific 'six-fold' quantitative figure derives from a small experimental comparison in very few subjects (n=5 total; single-subject dose escalation) rather than a population epidemiological study of Chicago residents.
Aspirin was discovered in 1899 by the German company Bayer.
"Aspirin had just been discovered in 1899 uh by the German company Bayer." (said at 1:23:33)
The year 1899 marks when the German company Bayer registered the trademark "Aspirin" and launched the drug commercially, rather than its chemical discovery. The compound, acetylsalicylic acid, was first synthesized in 1853 by French chemist Charles Frédéric Gerhardt, and pure acetylsalicylic acid was synthesized at Bayer's laboratories on August 10, 1897.
- context: One hundred years of aspirin (Medical History 1999) · cited 32x in the literature
"Acetylsalicylic acid was synthesized by Gerhardt in 1853... on 10 August 1897 he synthesized acetylsalicylic acid... On 23 January 1899 they decided to give this substance the brand name of Aspirin and finally, on 6 March 1899, this was registered at the Kaiserlichen Patentsamt Berlin." (abstract)
openalexfull study (doi) - context: The discovery of aspirin: a reappraisal (BMJ 2000) · cited 246x in the literature
"Hoffmann, a chemist in the pharmaceutical laboratory of the German dye manufacturer Friedrich Bayer & Co in Elberfeld, consulted the chemical literature and came across the synthesis of acetylsalicylic acid and then prepared the first sample of pure acetylsalicylic acid on 10 August 1897. This was marketed in 1899 under the registered trademark of Aspirin." (abstract, passage verified)
openalexfull study (doi)
Vasoconstriction caused by cold exposure triggers demargination of leukocytes into the circulation.
"when you just like we know when you take a cold shower that vasoconstriction causes demargination of leukocytes and that causes the amount of leukocytes in solution if you will or in the in the vasculature to go through find the viral particles and report to their lymph nodes" (said at 1:32:23)
Acute cold exposure (such as cold-water immersion or cold ambient air) triggers sympathetic nervous system activation, resulting in surges of catecholamines (norepinephrine and epinephrine) and cortisol that cause a transient mobilization (demargination) and increase in circulating leukocytes and granulocytes. However, this demargination is primarily mediated by catecholamine signaling and hemodynamic shear forces acting on vascular endothelial adhesion molecules, rather than peripheral vasoconstriction itself directly dislodging white blood cells. Furthermore, while circulating immune cell counts transiently rise following cold stress, clinical evidence does not demonstrate that taking a cold shower meaningfully enhances antiviral surveillance or active viral clearance in lymph nodes.
- supports: Immune changes in humans during cold exposure: effects of prior heating and exercise. (Journal of applied physiology (Bethesda, Md. : 1985) 1999) · cited 163x in the literature
"Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Residual effects of short-term whole-body cold-water immersion on the cytokine profile, wh… (International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group 2021) · cited 52x in the literature
"CWI also induced the marked release of the stress hormones Epi, NE, and cortisol. The change in IL-6 concentration after CWI was delayed and TNF-α production was decreased, but IL-1β was not affected within 48 h after CWI. A delayed increase in neutrophil percentage and decrease in lymphocyte percentage occurred after CWI." (abstract, results, passage verified)
pubmedfull study (doi)
N-acetylcysteine (NAC) functions as an antioxidant and recycles the glutathione peroxidase system to mitigate oxidative stress.
"NAC is a great antioxidant. It's packed with antioxidants and it it's recycles that the the glutathione peroxidase system which is helpful in dealing with oxidative stress." (said at 1:54:40)
N-acetylcysteine (NAC) functions as an antioxidant and precursor for intracellular glutathione (GSH) synthesis, helping cells counteract oxidative stress. However, the claim's description of its mechanism needs qualification: NAC is a single amino acid derivative (a cysteine prodrug) rather than something "packed with antioxidants," and it does not directly recycle the glutathione peroxidase enzyme. Glutathione peroxidase utilizes reduced glutathione (GSH) to detoxify peroxides, producing glutathione disulfide (GSSG), which is subsequently reduced back to GSH by glutathione reductase. NAC supports this system by supplying cysteine to replenish GSH pools rather than directly recycling the peroxidase system.
- supports: The Multifaceted Therapeutic Role of N-Acetylcysteine (NAC) in Disorders Characterized by … (Current neuropharmacology 2021) · cited 284x in the literature
"The sulfhydryl-containing tripeptide glutathione (GSH), which is synthesized and maintained at high concentrations in all cells, is one of the mechanisms by which cells protect themselves from oxidative stress." (abstract, passage verified)
pubmedfull study (doi) - context: The mechanism of action of N-acetylcysteine (NAC): The emerging role of H 2 S and sulfane … (Pharmacology & therapeutics 2021) · cited 468x in the literature
"Conventionally, it is assumed that NAC acts as (i) a reductant of disulfide bonds, (ii) a scavenger of reactive oxygen species and/or (iii) a precursor for glutathione biosynthesis." (abstract, passage verified)
pubmedfull study (doi) - context: N-acetylcysteine Pharmacology and Applications in Rare Diseases-Repurposing an Old Antioxi… (Antioxidants (Basel, Switzerland) 2023) · cited 94x in the literature
"N-acetylcysteine (NAC), a precursor of cysteine and, thereby, glutathione (GSH), acts as an antioxidant through a variety of mechanisms, including oxidant scavenging, GSH replenishment, antioxidant signaling, etc." (abstract, 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.