Benquo

Elevated temperature directly impairs pathogen replication.

Bacteria really do grow slower at 39°C 102°F than at 37°C 98.6°F.

No survivable amount of glycine changes that biochemistry.

But the degree and duration of fever may be substantially modulated by glycine status because many of the things fever accomplishes systemically, immune cell function, inflammation control, tissue protection, are things glycine accomplishes through targeted molecular mechanisms.

This leads to a testable prediction.

People with high glycine and glutathione status should mount lower fevers for equivalent infections while maintaining equivalent or better outcomes.

I am not aware of anyone having studied this directly because nobody frames the question this way.

But the mechanistic pieces are all published.

Some are well established, glycine's role in glutathione synthesis, macrophage chloride channels, others more preliminary, the ECM infection study.

They are just sitting in different literatures, sleep biology, amino acid metabolism, innate immunology, pyroptosis research, and nobody has connected them.

Heading Glycine's cooling effect via the SCN is unrelated to its immune benefits.

Remember the NMDA temperature pathway from the beginning of this essay, the one that made me notice the coincidence?

It turns out to be a red herring as a link between sleep and immunity.

The sleep pathway, glycine acting on NMDA receptors in the SCN to cool the core, and the immune pathway, glycine acting on chloride channels on macrophages to prevent pyroptosis, are completely independent.

They involve different receptors, different cell types, and different organ systems.

So when I noticed that glycine lowers temperature and that sick people need more glycine, I was right that they were connected, but for none of the reasons I initially thought.

The NMDA pathway had nothing to do with it.

I had a true belief, glycine, temperature, and illness are linked, that happened to be true, but my justification, because NMDA receptors and thermoregulation, was wrong.

In rabbit experiments, glycine injected directly into the brain's fluid-filled cavities reduced fever caused by two different triggers.

Substances released by white blood cells during infection, leukocytic pyrogen, and prostaglandin E2, which is the specific molecule the brain's thermostat uses to raise the temperature setpoint during illness.