I think we should not worry about this.
I 've reread the recent paper in Nature carefully again and its stated clearly that immediate C16 intake influence neither C16 levels in the blood nor the fusion state.
C16 graph.png 187.32KB
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This figure is not shown in the article itself, its in a supplemental material pdf so I cut it out. Authors rationalize it by stating that C16 levels in the blood are buffered and controlled. It doesn't go up after a C16 meal and even doesn't fall after 2 days low-fat diet.
Unlike the C18:0 drink, the C16:0 drink did not induce mitochondrial fusion (Supplementary Fig. 6b). C16:0 ingestion also did not increase C16:0-TAG levels in blood (Supplementary Fig. 6c). This suggests that serum C16:0-TAG levels are more buffered than C18:0-TAG levels, in agreement with the fact that C16:0-TAG levels also do not drop after 2 days of a low-fat diet (Fig. 2d).
in this light, I am not even sure that C16 intake is a factor at all in its blood levels or is it just a function of a liver function (just like blood sugar levels). Need to look further into this topic.
So...C16 is irrelevant in this setting, we could move on)