Everywhere I turn people are posting articles about how to NOT TO GET the COVID-19 coronavirus. Most if not all are using huge extrapolations citing correlation and in-vitro studies. In-vitro studies don’t prove much. I can pour gasoline in a petri dish of cancer cells and it will kill the cancer cells. But drinking gasoline will just kill you and may not kill the cancer cells in you. And correlation studies just show a relationship to the virus and not causality. I could easily create the correlation between water exposure and coronavirus. “people who contracted COVID-19 all took showers ergo showers cause COVID-19”.

Silly, right? But this is what many correlation studies do. They don’t show what causes coronavirus. The best that correlation studies can do is give you some ideas for more precise studies to see if causality occurs.

Like hitting the target but not a bull’s eye. And in-vitro studies are pretty much the same. They can give you something to look for, but more rigorous studies need to be done to see if the same thing happens in the living human body. The data points produced by correlation and in-vitro must be put to the test and reproduce the same results numerous times before they can be taken seriously.

But there are a few good studies that – when you connect the dots – look very promising. First let’s identify a couple facts.

• COVID-19 is a reverse transcribed virus like HIV and EBOLA. This means the virus takes advantage of reverse transcriptase which is an enzyme that replicates DNA. The virus makes the DNA in the cell turn into a factory with the sole purpose of replicating the virus. Therefore, these viruses spread within the body so fast. They overwhelm the body and the patient has a very short window of living.

• It’s predicted that this virus is most likely seasonal. What makes “season” or warmer weather so effective at halting these viruses? I will submit it’s the sun and not just warmer temperatures. I will defend this point later.

• There are people in our population who get the virus but don’t develop any symptoms. A spokesperson for the CDC recently stated this and that its those with weak immune systems who are most at danger of dying from the COVID-19 virus. What’s special about those people who get infected but don’t get sick? And are they the link between “travel”related contraction and “community” related contraction where there appears to be no link to travel?

The NIH did a study on the country of Brazil and virus spread. Brazil is about as big as the USA, but it has a very unique characteristic. The northern part of the continent is right at the equator and the further south you go, you get further and further away from the equator. The study in the sources below is called “Seasonal dynamics of influenza in Brazil: the latitude effect”. What they learned was the further south you go in Brazil the higher the virus occurrence and spread. This is very significant because viruses usually occur and spread in the areas of dense populations like the big cities and less so in the rural areas. But the exact opposite is true in Brazil. Viruses occur more often and spread with greater success in the southern less populated portions of the continent. And the big cities in the north see fewer outbreaks. Hmm.

So, we know that more sun exposure leads to higher levels of Vitamin D3. But could Vitamin D3 really be at work here?

A known downstream metabolite of D3 is a peptide called LL37. LL37 is a naturally occurring peptide tasked with the heavy lifting of protecting us against pathogens, fungi and viruses. LL37 has been shown in well done scientific studies to protect against the common seasonal flu. It’s called a human Cathelicidin. In one study they tested LL37 against seasonal H3N2 strain and the mouse adapted H1N1 strain, PR-8. What was discovered was “Unexpectedly, LL37 had markedly reduced activity against Cal09 using several cell types and assays of antiviral activity. A mutant viral strain containing just the hemagglutinin (HA) of 2009 pandemic H1N1 was inhibited by LL37”. This is very promising. But wait, it gets better.

COVID-19 is a retrovirus like HIV that tricks the cell into becoming a factory to produce overwhelming copies of the virus by encoding the DNA. It’s not as easy to deal with as common seasonal viruses or even H1N1.

A study done by the Karolinska University Hospital in Stockholm in Sweden showed that LL37 stopped the replication of the HIV virus. HIV is a retrovirus just like COVID-19, but this was just an in-vitro study. In 2014 a group of scientists at Emory University School of Medicine set out to look at the role of Vitamin D3’s metabolite 25-OH-D and LL37 status in HIV patients. They took 36 patients with HIV and 31 healthy controls and compared their levels of LL37 and the upstream precursor 25-OH-D.

What they found was counter intuitive. While both the healthy controls and HIV infected patients had similar levels of LL37, the 25-OH-D levels were far lower in HIV patients. The conclusion of the study was that the relationship between Vitamin D and LL37 was more indicative of HIV status than just LL37 alone. Those with HIV had far lower levels of 25-OH-D but similar levels of LL37 than healthy controls putting the spotlight back on the primary metabolite of Vitamin D3 – 25-OH-D.

This has led many who want to be protected against retrovirus like HIV, and now COVID-19, to begin injecting the LL37 peptide. But we need more evidence to make sure this is what’s protecting against viral replication. Let’s look closer.

Taking a D3 supplement works at raising both 25-OH-D and LL37 alike. Is there any effect we may be missing?

A study done by Harvard Medical School looked at the relationship between vitamin D3 supplementation, 25-OH-D and LL37 in a critically ill group of people. Thirty patients in the intensive care unit for sepsis were given either a placebo (10 patients) a bolus dose of 200,000IU vitamin D3 (10 patients) or a bolus does of 400,000IU of vitamin D3 within 24 hours of onset of sepsis or septic shock. Blood samples were taken at baseline before any D3 was administered, then again at 1, 3, 5- and 7-day intervals. The median 25-OH-D levels were 17ng/mL before supplementation. Peak levels were achieved by day 5. Bioavailable 25-OH-D levels were as follows. In the placebo group the median rise was 8%, in the 200,000IU group median rise was 45% and in the 400,000IU group the median rise was 96% with the highest rise of 136% in several subjects in the 400,000IU group.

The change in LL37 was affected by available 25-OH-D as well with a median rise of 30% in the 400,000IU group. What is completely unexpected was the placebo group had a higher rise in LL37 than the 200,000IU group of 17% and 4% respectively. Taken along with the study done by Emory University School of Medicine, the magic may not be LL37 but available 25-OH-D.

Wow, that was a long way around to the conclusion that while supplementing with Vitamin D3 may raise LL37 levels, the real magic of suppressing retro-viral replication and the potential as therapeutic treatment and prophylactic against getting infected looks like bio-available 25-OH-D itself. Good news is taking a daily high dose of a quality D3 supplement should have you covered either way.

As far as dosing goes, many are afraid to take Vitamin D3 because it’s a fat-soluble vitamin. Darker skinned people, like myself, must take more as we evolved with higher sun exposure and have more circulating 25-OH-D Binding protein, so we need higher doses than fair skinned people to achieve higher levels of bio-available 25-OH-D. I personally take 20,000IU a day during the winter months and get out in the sun almost daily during the summer. As a point of reference, when you take the family to the beach for the weekend and spend a few days basking in the sun, your body will make will over 200,000IU of D3 in your skin, this is the best way to get your D3! But having your bioavailable 25-OH-D levels tested is quick and easy. Many walk-in labs like Any Lab Test Now allow you to order your own blood test. Get your bioavailable 25-OH-D levels tested today.  Start supplementing, have it tested again in a couple weeks to find your best personal dose. Having bioavailable 25-OH-D between 50ng/dL and 80ng/dL is considered ideal by most authorities.

Sources

Effect of Cholecalciferol Supplementation on Vitamin D Status and Cathelicidin Levels in Sepsis: A Randomized, Placebo-Controlled Trial

https://pubmed.ncbi.nlm.nih.gov/26086941

Seasonal dynamics of influenza in Brazil: the latitude effect

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6307116

The Antimicrobial Peptide LL-37 Inhibits HIV-1 Replication

https://pubmed.ncbi.nlm.nih.gov/17627504

Antiviral Activity of the Human Cathelicidin, LL-37, and Derived peptides on Seasonal and Pandemic Influenza A Viruses

https://pubmed.ncbi.nlm.nih.gov/25909853

LL-37 Concentrations and the Relationship to Vitamin D, Immune Status, and Inflammation in HIV-Infected Children and Young Adults

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077005

Effect of Cholecalciferol Supplementation on Vitamin D Status and Cathelicidin Levels in Sepsis: A Randomized, Placebo-Controlled Trial

https://pubmed.ncbi.nlm.nih.gov/26086941

Seasonal dynamics of influenza in Brazil: the latitude effect

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6307116

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Carl Lanore is the host of the Super Human Radio podcast, the longest running health, fitness & anti-aging podcast in the world in its 15^th year of continuous production. Learn more at http://superhumanradio.net