The science behind the deck

“Phytase already lifted the mineral status and health of the animals we eat.”

Bedford and colleagues have shown across decades of animal research that supplemental phytase raises mineral availability, bone mineralisation and growth in the pigs and poultry raised for food⁸⁹. Selle and Ravindran documented the underlying mechanism, how phytic acid binds minerals and how phytase releases them, in 2010⁶. Close to all commercial monogastric feed now contains phytase, so tens of billions of animal doses stand behind its safety and effect.

Phytic acid locks up iron, zinc, magnesium, calcium, copper and amino acids.

Selle and Ravindran described in 2010 how phytic acid's six negative charges bind the major dietary minerals before the body can absorb them⁶. Kumar and colleagues reviewed the same effect in human nutrition in 2010⁵, and Sandberg showed in 2002 that reducing phytic acid raises mineral bioavailability from legumes⁴. Cowieson and colleagues demonstrated in 2006 that phytic acid also impairs protein and amino-acid digestion⁷.

Crops carry fewer minerals than they used to, and the trend is worsening.

Davis and colleagues found in 2004 that the mineral content of 43 garden crops declined measurably between 1950 and 1999¹¹. Myers and colleagues demonstrated in 2014 that rising atmospheric CO2 lowers the iron, zinc and protein in staple crops¹², and Loladze showed the same year that elevated CO2 shifts the plant ionome and depletes the minerals at the base of human nutrition¹³.

Modern livestock get phytase because their grain-based feed is high in phytic acid.

Selle and Ravindran set out in 2010 how phytase breaks phytic acid apart to release bound nutrients, and why phytase is added to the soy- and grain-based rations fed to modern pigs and poultry⁶. Human digestion supplies almost none of this enzyme.

In humans, supplemental phytase raises mineral absorption. This is the proven core.

Troesch and colleagues showed in 2013 that phytase from Aspergillus niger significantly increased iron and zinc absorption in humans¹. Chondrou and colleagues reported in 2024 that phytase supplementation and dephytinisation improved trace-element bioavailability², and Hurrell and Egli established in 2010 that phytic acid is the principal dietary inhibitor of iron absorption³. This mineral-absorption benefit is the settled, human-proven foundation of everything Goodphyte does.

Iron is the endurance athlete's weak point, and phytic acid is the biggest dietary drag on it.

Hurrell and Egli confirmed phytic acid as the leading inhibitor of dietary iron in 2010³, Troesch and colleagues showed phytase reverses it in 2013¹, and Shaw and colleagues reported in 2025 that lowering phytic acid improved iron status in female runners¹⁴.

The energy and mood effect: mechanism, honestly framed.

Lu (2019) and Kriseldi (2021) showed in animals that deep phytase breakdown releases free inositol, which supports glucose uptake¹⁵¹⁶.

A completed human hypertension pilot is the wedge into the pharma opportunity.

In a registered 14-day human pilot, Svolos and colleagues (2026) dosed the phytase component and found that 8 of 19 completers showed consistent systolic and diastolic blood-pressure reductions, with zero adverse events and stable liver function¹⁹. The honest caveats are a small sample, no placebo and an exploratory subgroup, so a larger placebo-controlled trial is the natural next step. Data available to qualified reviewers under NDA.