Nothing published in preprint* form was interesting enough for me to take a deep dive into, but there were a few studies worth mentioning, and here they are.
One paper suggested that tocilizumab, an inhibitor of interleukin-6 (IL-6), reduces mortality from COVID-19. Whether patients received it, after some basic inclusion criteria, was left to the judgment of the physician, and 77 who received it were compared to 94 who did not. The study wasn't randomized, so it doesn't give us clear evidence of cause-and-effect. Nevertheless, the IL-6 blocker looks promising. Admission to the ICU was over 60% lower in those who received tocilizumab, 10.3% vs 27.6%, and the number requiring ventilation was 0% instead of 13.8%. I previously covered how IL-6 predicted the need for ventilation with stunning accuracy, so it is quite interesting that the rate of needing ventilation was zero on those receiving the IL-6 blocker.
This is interesting because there is some evidence that bovine lactoferrin, taken 100 mg twice a day before meals, cuts IL-6 in half when given to pregnant women suffering from iron deficiency anemia. I'll do a more comprehensive review of lactoferrin in COVID-19 soon.
A small study from Singapore suggested vitamin D, magnesium, and vitamin B12 in combination are helpful for COVID-19. This also was not randomized and does not give clear evidence of cause-and-effect. They started treating patients on April 6 with 1000 IU vitamin D, 150 mg magnesium, and 500 mcg B12. Patients receiving this combination had an 81% lower risk of initiating oxygen therapy (17.6% vs. 61.5%). It appears that the controls were those between January 15 and April 5 who preceded the policy of giving the combination. I don't put much stock in this given that the viral genomics could have shifted over that time, sunshine is greater, weather is different, and so on. However, it is about as promising as the tocilizumab study, which also was not randomized, and it makes the nutrient combination look almost as powerful as the drug.
A German autopsy study suggested that the virus invades neurons within the nose, and uses them as an entryway into the brain. I previously covered in vitro evidence suggesting the virus infected the neurons within the nose. This autopsy study confirms and expands that. 14% of the subjects had blood clots that caused infarctions within the brain, further confirming the importance of blood clotting in this disease. Infection of the central nervous system could explain why loss of taste occurs alongside loss of smell, something harder to explain if only the neurons of the nose get infected (though not impossible to explain, since smell defects could be subjectively mistaken as taste defects).
An in vitro paper found that zinc finger antiviral protein (ZAP), which is stimulated by interferon and dependent on zinc, strongly suppresses replication of SARS-CoV-2, the coronavirus that causes COVID-19. This is one more mechanism by which zinc could be preventative, something I've covered here and here.
That's all for today, though I hope to get my deep dive into lactoferrin out soon.
Stay safe and healthy,
Chris
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I am not a medical doctor and this is not medical advice. I have a PhD in Nutritional Sciences and my expertise is in conducting and interpreting research related to my field. Please consult your physician before doing anything for prevention or treatment of COVID-19, and please seek the help of a physician immediately if you believe you may have COVID-19.
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*Footnotes
* The term “preprint” is often used in these updates. Preprints are studies destined for peer-reviewed journals that have yet to be peer-reviewed. Because COVID-19 is such a rapidly evolving disease and peer-review takes so long, most of the information circulating about the disease comes from preprints.