In mice, vitamin D doesn’t turn on a key germ-fighting gene the way it does in humans—so even when the vitamin D signal is present or missing, the gene stays quiet. This means mice and humans respond differently to vitamin D when it comes to fighting infections.

20

Pro

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Against

Evidence from Studies

Supporting (1)

20

Community contributions welcome

20

Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up‐regulated in myeloid cells by 1,25‐dihydroxyvitamin D3

Cross-Sectional Study

Human & Animal & In Vitro

2005 Jul

In humans, vitamin D turns on a gene that helps fight germs, but in mice, it doesn’t — because mice lack the genetic switch that lets vitamin D do that. This study proves the difference is real and built into their DNA.

Contradicting (0)

0

Community contributions welcome

No contradicting evidence found

Gold Standard Evidence Needed

According to GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this specific claim, ordered from strongest to weakest evidence.

Source Study

Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up‐regulated in myeloid cells by 1,25‐dihydroxyvitamin D3

Score: 20

DOI: 10.1096/fj.04-3284com

Similar Assertions

Vitamin D activates a gene in certain human immune cells that helps fight off germs, and this happens because vitamin D directly attaches to a specific spot on the gene to turn it on.

20

0

76%

Humans and other primates have a special genetic switch that lets vitamin D boost their immune system, but mice, rats, and dogs don’t have this switch—so vitamin D works differently in them.

20

0

73%