Cola

Cola is high in salicylates from its flavouring base — kola nut, citrus oils and spices — not from the sugar. The diet version is no lower on this axis. Neither study publishes a value for this particular drink.

Regular cola is high in FODMAP from high-fructose corn syrup (excess fructose); sugar-free versions avoid that but may add polyol sweeteners that are also FODMAP.

Cola is sweetened with high-fructose corn syrup in much of the world and with sucrose elsewhere, and the label rarely makes the difference obvious. A can is a large dose either way, drunk fast and without fibre.

Cola's caffeine is widely said to slow DAO - the same claim the coffee entry carries, repeated in nearly every food list on this subject and supported by remarkably little. What the bottle adds is not one mechanism but a stack of elimination-list items: caramel colour, phosphoric acid, often benzoate. The volume is what makes it count - nobody drinks 30 ml of cola, and a caffeinated drink taken by the half-litre is a different exposure from a coffee.

Cola contains no oxalate itself - ion chromatography measures it under 1 mg per litre. The fructose route is closed: on controlled diets of up to a fifth of calories as fructose, urinary oxalate does not move, and liver cells do not convert fructose to oxalate at all. What remains is empirical: drinking a cola raises urinary oxalate in volunteers, and in the large cohorts it is the SUGARED cola, not the diet kind, that tracks with kidney stones. The mechanism is not elucidated — calcium, acidity and magnesium shift together — but the signal is measured, and it belongs to the sugared version alone.

Cola is carbonated water with sugar or sweetener, caramel colour, acid and caffeine. None of those is a protein, and tyramine needs protein, bacteria and time. It is on the scale because caffeinated drinks are reviewed alongside tyramine on some protocols, not because it carries any.