Posted on 05/19/2021 7:21:02 PM PDT by nickcarraway
Having low blood levels of vitamin D may not increase a person's risk for severe COVID-19, a study published Wednesday by JAMA Network Open found.
People with extremely low levels of vitamin D in their blood were not more likely to test positive for antibodies to the coronavirus, the data showed. The presence of antibodies -- cells made by the immune system -- suggests past infection.
Those with moderately low levels of the vitamin also did not have a higher risk for testing positive for coronavirus antibodies, the researchers said.
"We found no evidence for an independent association between low levels of vitamin D" and testing positive for COVID-19 antibodies, wrote researchers from Quest Diagnostics, a national chain of medical testing laboratories.
"These findings do not support the hypothesis that vitamin D plays a role in susceptibility to ... infection," they said.
Vitamin D is considered to be an important nutrient for immune health, according to the Harvard T.H. Chan School of Public Health.
Earlier studies have suggested that having low levels of the nutrient could indicate poor immune system health and raise the risk for severe COVID-19.
This risk is particularly acute in Black people, who historically have lower levels of vitamin D than those in other racial and ethnic groups, studies show.
Data indicate that Black people also are at increased risk for infection and severe COVID-19.
More than 40% of adults in the United States are considered to be deficient in vitamin D, including roughly 80% of Black people, according to the recent estimates.
For this study, the Quest Diagnostics researchers tested more than 18,000 adults ages 37 to 56 in the United States for coronavirus antibodies.
All 18,000 adults had available information on prepandemic blood vitamin D levels in their medical records, the researchers said.
About one in four had extremely low levels of the nutrient in the blood before the pandemic, while another 60% had moderately low levels.
Among the study participants, 900, or 5%, tested positive for antibodies suggesting past COVID-19 infection.
Participants with extremely low levels of vitamin D were 4% more likely to test positive for coronavirus antibodies.
Those with moderately low levels, however, actually were 7% less likely to test positive, the researchers said.
"Individuals [positive for COVID-19 antibodies] did have lower vitamin D levels than [negative] individuals, both before and during the pandemic," the researchers wrote.
"However, low levels of vitamin D were not associated with [positivity] after adjusting for" other factors, they said.
*** researchers can find anything they are paid to find.***
That’s the way it’s been for a long, long time. It’s part of the reason I left the field 35 years ago.
Same here, been religious with it for 20+ years, not a single cold or flu. Up until that point,I always got Maddog colds my whole life, every year.
Low THC levels increase risk last I heard.
Lies
What about people with high levels of vitamin D3 along with zinc? How did they fare against Covid-19? They did not mention that.
What does this establish? It isn't going to stop a germ from getting in you - it's about how bad the infection will be / how it affects you - severity symptoms, how long it lasts, etc.
Low vitamin D levels can make you more susceptible to blood clots / thrombosis - one of the things COVID19 infections can cause. That was the whole basis for emphasizing the need to not be vitamin D deficient when this whole thing started...not whether or not you have antibodies.
In other words - we all must take the experimental vaccines to be safe, no matter one’s age or health risks. Vax the kids they say.
“ Though I don’t think high levels of D make one “bullet proof” against covid. This is just one study, and not very convincing IMO.”
That’s what I thought about the study indicating high THC levels offer protection but I’m not taking any chances. It’s working so far.
“Having low blood levels of vitamin D may not increase a person’s risk for severe COVID-19, a study published Wednesday by JAMA Network Open found.”
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“May”. One of the classic weasel words like “might” or “could”.
It is entirely believable. It just doesn’t mean anything. It is a completely meaningless study.
This is an incredibly meaningless article. Having high levels of vitamin D isn’t going to keep a virus from getting inside of you - it could affect how well your immune system responds as well as the severity of other symptoms. Antibodies would be present either way.
“Generally, whatever mainstream media tells me what is to be in my best interest, I take the opposite approach.”
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Very good observation/recommendation.
Me too.
It’s strange that it was published by JAMA. I would think the Chan School authors would first submit this to the New England Journal. Maybe they did.
???
Liberal propaganda. Just like the hydrochloroquine lies they peddaled.
🙃
(Meaning....in upside-down world :)
When the Chicom Cooties hit me, it was very minor. One of the reasons was I was outside alot and took plenty of Vitamin D.
Researchers have found that people are likely to believe just about anything if it is preceded by the phrase “researchers have found”.
CC
Yep dead on Mrs. Z. 30 years of D3, Zinc and magnesium with calcium. Not a cold, flu or anything.
Vitamin D treatment improves your ability to fight off lung infection.
But Vitamin D also increases the expression of ACE2 receptors.
And ACE2 receptors are what Covid spike proteins bind to in order to infect you.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657015/
In our study, 25OHD supplementation was not associated with the severity of COVID-19. On the other hand, a trend toward a 2-fold higher mortality in users was found.
Vitamin D could boost mucosal defenses and protect against infections, and it has been suggested to down-regulate the inflammatory burden contributing to acute respiratory distress syndrome and lung injury, the main cause of death in COVID-19 patients.
Enhanced ACE2 expression is considered a protective factor in acute lung injury. Vitamin D increases the expression of ACE2, and this may apply not only to airway epithelium but also to other organs and monocyte-derived macrophages.
However, ACE2 is the binding site of SARS-CoV-2, and increased ACE2 expression may result in enhanced viral homing and organ damage, as well as in an aberrant innate immune response with hyperactivation of macrophages —perhaps at least in patients with high complication, such as those admitted in our outbreak area.
Our data may appear in contrast with recent literature suggesting that higher serum 25OHD is associated with more favorable COVID-19 outcomes, with lower progression of respiratory illness and to critical illness, as well as lower mortality rates, although no association has been also reported.
However, disease-related inflammation may negatively affect 25OHD metabolism, particularly that of its binding protein, resulting in reduced circulating levels and assessment bias.
It is with this background that we decided to evaluate the association between supplementation rather than serum levels and outcome. Nonetheless, we evaluated serum 25OHD in a subgroup of consecutive patients, demonstrating that supplementation results in substantially higher and adequate circulating levels.
Therefore, although the potential utility of vitamin D in the prevention of respiratory-tract infections is more substantial, its benefits in COVID-19 (prevention and management) still need to be clarified by appropriate intervention trials.
In conclusion, 25OHD supplementation was not associated with hospitalization but appeared to be a risk factor for higher in-hospital mortality in COVID-19.
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