DHA is not essential. Agreed as deficiency diseases are not evident. However, does that mean that a dietary intake sufficient to maintain a RBC concentration (and availability to other cells/organs) is not beneficial? 2/n https://twitter.com/mimcburney/status/1381276253651664896">https://twitter.com/mimcburne...

Consider vitamin D. Until 2011, DRI was set to obtain 25(OH)D levels to prevent deficiency (rickets) when they were updated to ‘maintain skeletal health’. 3/n

Based on 25(OH)D concentrations vs bone mineral density, time-to-stand, walk speed, it became obvious higher 25(OH)D levels (>50 nmol/L) were beneficial 4/n

Thus the DRI was increased to levels where 97.5% of the population should have 25(OH)D >50 nmol/L. This DRI is to optimize health (cellular structure/function) NOT deficiency 5/n

Similarly, although DHA deficiency has not been demonstrated, does that mean most https://abs.twimg.com/emoji/v2/... draggable="false" alt="🇺🇸" title="Flagge der Vereinigten Staaten" aria-label="Emoji: Flagge der Vereinigten Staaten"> and https://abs.twimg.com/emoji/v2/... draggable="false" alt="🇨🇦" title="Flagge von Kanada" aria-label="Emoji: Flagge von Kanada"> wouldn’t benefit from higher RBC EPA+DHA levels? 6/n

We need more data correlating nutritional status, in this case RBC EPA+DHA, with outcomes to answer this question. As nutrition scientists, our role is to test hypotheses and interpret the observations. The answer will become evident.....