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So many studies show that saturated fat, particularly palmitic acid, is inflammatory.
This paper shows that it is context-dependent and it's not palmitic acid that is inflammatory, but rather the carriers or solvents that they use along with the saturated fat.
https://www.physiology.org/doi/full/10.1152/ajpendo.00187.2018
"Using a lower-inflammation BSA source and no ethanol, ∼24-h sodium palmitate treatment (≤600 µM) failed to trigger RAW264.7 TNFα release and, in fact, significantly dampened BSA-induced inflammation by >50%. In C2C12 myotubes, only high palmitate concentrations (500–600 µM) elicited IL-6 secretion (>2.5-fold increase). Acute palmitate (200 or 500 µM) treatment did not activate MAP kinase pathways above that of fresh BSA-containing media alone in either cell type. These results highlight the importance of experimental conditions in studies exploring SFA inflammation effects. The limited (or even anti-inflammatory) effects of palmitate that we observed indicate that immunomodulatory effects of SFAs are context-specific."
This paper shows that it is context-dependent and it's not palmitic acid that is inflammatory, but rather the carriers or solvents that they use along with the saturated fat.
https://www.physiology.org/doi/full/10.1152/ajpendo.00187.2018
"Using a lower-inflammation BSA source and no ethanol, ∼24-h sodium palmitate treatment (≤600 µM) failed to trigger RAW264.7 TNFα release and, in fact, significantly dampened BSA-induced inflammation by >50%. In C2C12 myotubes, only high palmitate concentrations (500–600 µM) elicited IL-6 secretion (>2.5-fold increase). Acute palmitate (200 or 500 µM) treatment did not activate MAP kinase pathways above that of fresh BSA-containing media alone in either cell type. These results highlight the importance of experimental conditions in studies exploring SFA inflammation effects. The limited (or even anti-inflammatory) effects of palmitate that we observed indicate that immunomodulatory effects of SFAs are context-specific."
