This has been a wild week in terms of COVID-19. States reopening, protests in states that are still closed, and lots of confusion about what to do to manage the spread of COVID-19. Again, my single biggest concern is that abject terror helps no one. What does help is continuing to put the risks in perspective. To do that this morning we’ll look at two past pandemics that you’ve likely never heard about, a new study on Vitamin D, and old research on infections and blood clots.
COVID-19 Is NOT the Flu
The SARS-CoV-2 virus that causes COVID-19 is not the flu. First, it seems to have an infection fatality rate of 3-6X flu. It also had the potential to overwhelm our healthcare systems just like in the 1918 pandemic. Hence, please don’t comment that I am directly comparing COVID-19 to the flu. However, all we have are flu pandemics for comparison at scale.
The Big One: 1918
Pretty much everyone now has heard about the influenza pandemic of 1918 (3). Even with some social distancing, it killed an estimated 675,000 people in the US and 50 million worldwide. It began as a mild flu in an Army base in the spring of 1918 and then was taken by World War I troops to Europe where it mutated (H1N1) and then was brought back home. Almost none of us alive today remembers this event, but there have been flu pandemics in our lifetimes that were very serious, so let’s dig in.
In the winter of 1957, a new influenza A virus began Asia, triggering a pandemic (called the “Asian Flu”). This H2N2 virus came from birds. It was first reported in Singapore and then Hong Kong in the winter and spring of 1957, and then on the east and west coast of the United States in summer 1957.
- Worldwide deaths were 1.1 million
- United States deaths were 116,000
However, the world was a much smaller place back then. So translated to today’s numbers we would see:
- Worldwide deaths would be 3.0 million
- US deaths would be 252,000
The 1968 influenza pandemic was caused by a virus called H3N2 which was a mutation of the original H1N1 flu and the 1957 virus. It was first noted in the US in the early fall of 1968. Like the novel coronavirus, most of the deaths were in people 65 years and older. This virus is now our seasonal flu, but the virus undergoes “antigenic drift”. That means that small mutations in the surface of the virus make it harder for our immune systems to detect.
- Worldwide deaths were 1 million
- United States deaths were 100,000
Translated to today’s numbers:
- Worldwide deaths would be 2.2 million
- US deaths would be 163,000
So have seen serious pandemics like this before. In fact, if you’re in your 60’s to 70’s, you’ve seen two that had more deaths than this one to date.
Flattening the Second Curve
The Well Being Trust and the American Academy of Family Physicians put out a report this week about the number of deaths from alcoholism, drug abuse, and suicide that the United States will experience from the shutdown (4). They peg the mean number of excess deaths caused by social distancing to be about 70,000. If the economic recovery is slow, that number could rise to about 150,000. This doesn’t factor in the number of deaths that will happen from people deferring needed medical care due to the shutdown or being terrified to go to the hospital (5).
Can Vitamin D Help?
I wrote a blog a few weeks ago that reviewed research that Vitamin D levels are related to better immunity and may explain why respiratory viruses don’t impact as many people during the summer (6-10). A new study this week looked at Vitamin D levels and inflammatory markers in hospitalized COVID-19 patients in Germany, South Korea (S. Korea), China (Hubei), Switzerland, Iran, UK, US, France, Spain, Italy (11). Patients with the lowest Vitamin D levels were about 15% more likely to get severe COVID-19 and the nasty cytokine storm that everyone has been discussing. So get outside to make more Vitamin D or take 5,000 U of D3 each day, either way, this study, if it makes it through peer review, could be another arrow in the quill for why being outdoors is so critical to our health.
Blood Clots and the Media
The media these past two weeks have been stoking panic that COVID-19 creates blood clots! They’ve also been claiming that this is unique to this awful disease! Please begin running in the streets (with a mask on) and shrieking loudly or just click on our ads! But is any of this true? Nope.
The concept that blood clots can be caused by infections goes back to a paper on Typhoid fever in 1903! (12) We also know from more recent research that patients with common urinary tract infections are at double the risk of blot clots (13). Canadian doctors also noted major clotting events in some patients who were treated during the 2009 H1N1 pandemic (14). The low platelet counts and lots of small clots (DIC or Disseminated Intravascular Coagulation) which has been observed with COVID-19 has also been reported in other SARS infections (15). Hence, in summary, while the idea of blood clots in patients with infections may seem strange, it’s actually quite common.
The upshot? Again, fomenting panic helps nobody. As I always say, let’s have a heavy heart and a clear mind. This is a bad bug, but looking at exactly what it is, and isn’t, will help us make the best decisions in the difficult pandemic calculus that we’re now facing.
(1) Centers for Disease Control and Prevention. 1957-1958 Pandemic (H2N2 virus). https://www.cdc.gov/flu/pandemic-resources/1957-1958-pandemic.html. Accessed 5/7/20.
(2) Centers for Disease Control and Prevention. 1968 Pandemic (H3N2 virus). https://www.cdc.gov/flu/pandemic-resources/1968-pandemic.html. Accessed 5/7/20.
(3) Centers for Disease Control and Prevention. 1918 Pandemic (H1N1 virus). https://www.cdc.gov/flu/pandemic-resources/1918-pandemic-h1n1.html. Accessed 5/8/20.
(4) The Well Being Trust and the Robert Grahm Center (American Academy of Family Physicians). PROJECTED
DEATHS OF DESPAIR from COVID-19. https://wellbeingtrust.org/wp-content/uploads/2020/05/WBT_Deaths-of-Despair_COVID-19-FINAL-FINAL.pdf Accessed 5/8/20.
(5) Rosenbaum L. The Untold Toll – The Pandemic’s Effects on Patients without Covid-19 [published online ahead of print, 2020 Apr 17]. N Engl J Med. 2020;10.1056/NEJMms2009984. doi:10.1056/NEJMms2009984
(6) Beard JA, Bearden A, Striker R. Vitamin D and the anti-viral state. J Clin Virol. 2011;50(3):194–200. doi:10.1016/j.jcv.2010.12.006
(7) Leary PF, Zamfirova I, Au J, McCracken WH. Effect of Latitude on Vitamin D Levels. J Am Osteopath Assoc. 2017 Jul 1;117(7):433-439. doi: 10.7556/jaoa.2017.089.
(8) Zittermann A, Pilz S, Hoffmann H, März W. Vitamin D and airway infections: a European perspective. Eur J Med Res. 2016;21:14. Published 2016 Mar 24. doi:10.1186/s40001-016-0208-y
(9) Hughes DA, Norton R. Vitamin D and respiratory health. Clin Exp Immunol. 2009;158(1):20–25. doi:10.1111/j.1365-2249.2009.04001.x
(10) Medscape. What is the prevalence of vitamin D deficiency in the US? https://www.medscape.com/answers/128762-54281/what-is-the-prevalence-of-vitamin-d-deficiency-in-the-us Accessed 3/21/20.
(11) Daneshkhah A, et al. The Possible Role of Vitamin D in Suppressing Cytokine Storm and Associated Mortality in COVID-19 Patients. medRxiv 2020.04.08.20058578; doi: https://doi.org/10.1101/2020.04.08.20058578
(12) Wright A, Knap H. US National Library of Medicine. A NOTE ON THE CAUSATION AND TREATMENT OF THROMBOSIS OCCURRING IN CONNECTION WITH TYPHOID FEVER. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2037216/pdf/medcht00006-0149.pdf. Accessed 5/9/20.
(13) Smeeth L, Cook C, Thomas S, Hall AJ, Hubbard R, Vallance P. Risk of deep vein thrombosis and pulmonary embolism after acute infection in a community setting. Lancet. 2006;367(9516):1075‐1079. doi:10.1016/S0140-6736(06)68474-2
(14) Paul E. Bunce, Sasha M. High, Maral Nadjafi, Katherine Stanley, W. Conrad Liles, Michael D. Christian, Pandemic H1N1 Influenza Infection and Vascular Thrombosis, Clinical Infectious Diseases, Volume 52, Issue 2, 15 January 2011, Pages e14–e17, https://doi.org/10.1093/cid/ciq125
(15) Yang M, Ng MH, Li CK. Thrombocytopenia in patients with severe acute respiratory syndrome (review). Hematology. 2005;10(2):101‐105. doi:10.1080/10245330400026170