Physiological Mechanisms and Life History Trade-Offs in Salmonids Shape In-Tissue Correlations of an Essential Micronutrient.

The lack of a fitness-based theory of micronutrient allocation to specific tissues hinders understanding of the ultimate causes of mass juvenile mortality due to thiamine (vitamin B1) deficiency, which is an emerging threat to marine and coastal ecosystems worldwide. We modeled the optimal allocation of thiamine in salmon to somatic and reproductive tissues to investigate correlations between tissue thiamine levels, adult mortality, juvenile recruitment, and excretion rates that change with thiamine concentration. The model showed a positive correlation between thiamine levels in gonads and muscles, with a slope that increased with time. This was driven by a constrained thiamine input in salmon, but a negative or no correlation was found in scenarios with high thiamine input. These predictions were confirmed by analysis of empirical data from Atlantic salmon (Salmo salar) populations that differ in the occurrence of episodic thiamine deficiency. A positive correlation was indicative of low thiamine input, regardless of how juvenile recruitment and adult survival increased with thiamine concentration. The model output suggests that renal (i.e., kidney) reuptake is fundamental to understanding micronutrient allocation strategies. Measuring correlations between micronutrient concentrations in reproductive and somatic tissues of adults may help to detect early signs of thiamine deficiency before mass mortality of juveniles occurs. This can complement the previously suggested tissue concentrations and food web indicators. Future studies should try to distinguish and quantify the factors that alter the net thiamine input in salmonids and the subsequent allocation to offspring. Particular attention should be given to changes in thiamine uptake from the diet, including intestinal uptake mechanisms and effects of thiaminase activity. Additionally, more information is needed on internal factors that reduce thiamine availability, such as thiamine degradation as an antioxidant during lipid metabolism, and other physiological factors that can potentially increase thiamine loss, including allocation mechanisms and renal processes.