This email is from Rhonda Patrick at Found My Fitness.
This is very important information. The upshot here is optimizing vitamin D status from the sun and supplementation is not a very important things to do for your overall health but surprise but how.Vitamin D might be ultimately proven to be a crucial factor in reducing susceptibility to lung injury due to COVID-19, the primary killing complication associated with COVID-19.
Tomorrow, I'll share with you critical strategies to assess and optimize your vitamin D metabolism..
HINT: It isn't going to Walmart and grabbing the 1000 pills of Vitamin D2 for $3!
Strap on your thinking caps as it's a bit sciencey but that's what makes Rhonda's posts so interesting and trusting.
What mediates the COVID-19 lung complication?
An enzyme called ACE2.
If that enzyme sounds familiar, it's because ACE2 (short for angiotensin converting enzyme 2) plays a critical role in infection from SARS-CoV-2 – the virus that causes COVID-19.
If you watch one video this week about COVID-19 and it's not the Q&A posted four days ago, which was the first of a multi-part series, found here, then I hope it's this one:
Here's an important 20-minute clip...
The effect of vitamin D on susceptibility to COVID-19-associated lung injury.
Let's back up a bit, though, and I'll fill you in on a little background on vitamin D.
The first thing to know about vitamin D is that it is NOT just a vitamin. It's a steroid hormone. Underscoring its importance: it actually regulates more than 5% of the protein-encoding genome!
Somewhat alarmingly, this is actually another way of saying that possibly as much as 70% of people, which is the percentage of people in the United States that have a vitamin D status that the Endocrine Society refers to insufficient, may be experiencing at least partial dysregulation in up to 5% of their protein-encoding genome!
At the very least, it's almost certainly the case among the 30% that fully qualifies as vitamin D deficient are.
You can obtain small quantities of vitamin D in food, but your primary source is a stepwise process that starts in your skin following exposure to ultraviolet light and continues in your liver and kidneys, where the vitamin's active form is made.
Since ultraviolet light is required for vitamin D synthesis, reduced exposure to the sun or having dark-colored skin impairs vitamin D production. Older adults, whose skin isn't as efficient at producing vitamin D, and obese people, whose excess fat stores sequester the vitamin, are also more likely to be deficient.
RESPIRATORY TRACT INFECTIONS
A ton of evidence suggests that vitamin D is protective against respiratory tract infections. Data from 25 randomized controlled trials from around the world demonstrate that vitamin D supplementation reduced the risk of acute respiratory infection by more than 50 percent, especially in people with low baseline vitamin D levels.
Where does ACE2 fit in?
SARS-CoV-2 virus enters human cells via the ACE2 receptor. Viral particles bind to the ACE2 receptor and together they travel into the cell. These viral particles can bind to a large number of ACE2 molecules, sequestering them from the cell surface and decreasing ACE2. This has been shown to happen with the virus that caused the original SARS outbreak, SARS-CoV-1, which also binds to the ACE2 receptor.
The accompanying loss of ACE2 function can cause serious health consequences due to ACE2's participation in key physiological processes.
Here's where vitamin D deficiency comes in...
Vitamin D deficiency leads to overexpression of renin (an enzyme produced in the kidneys) and subsequent activation of the renin-angiotensin system, a critical regulator of blood pressure, inflammation, and body fluid homeostasis. Loss of ACE2 function in the setting of SARS-CoV-2 infection upsets the balance of this critical system, promoting neutrophil infiltration, excessive inflammation, and lung injury. If lung injury progresses to hypoxia, the kidneys release renin, setting up a vicious cycle for decreasing ACE2.
In turn, lower levels of ACE2 promote more damage, culminating in acute respiratory distress syndrome, or ARDS. a severe form of acute lung injury that occurs in as many as 17 percent of all COVID-19 cases and can lead to respiratory failure and death.
But vitamin D acts as an endocrine repressor of the renin-angiotensin system by downregulating the expression of renin, the rate-limiting enzyme of the renin-angiotensin cascade, and rescuing lung function.
A preclinical model of acute lung injury showed that administration of vitamin D provided protection against lung injury by increasing ACE2 levels and decreasing renin production.
Here's the kicker: The acute lung injury led to a decrease in ACE2, driving even worse lung injury. Vitamin D supplementation increased ACE2 receptor levels, but only in conditions of acute lung injury where ACE2 levels decreased. When vitamin D was given to control animals, it didn't increase ACE2 levels. This means that vitamin D normalizes ACE2 levels in situations only where it is decreased.
Many aspects of modern life are at odds with our natural production of vitamin D. We wear clothes. We wear sunscreen. We might work inside all day – or be under stay-at-home orders. Supplemental vitamin D might be a viable means to increase our vitamin D to sufficient levels and potentially reduce the risk of complications associated with COVID-19.
Practical take-home? Let's talk about the tolerable upper intake of vitamin D.
The Nutrition board of the Institute of Medicine conservatively set the tolerable upper intake of vitamin D at a level of around 4,000 IU/day including safe for pregnant and lactating women, which suggests that it is generally thought that, at that dose, toxicity is extremely unlikely.
This is good to know because while that dose is on the upper end by the standard of tolerable upper intake, it has been demonstrated across multiple studies to improve vitamin D blood status in otherwise deficient individuals.
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In good health now more than ever,