Table 1.

What can alter levels of oxidative damage levels in humans or other animals?

Obesity (humans, rodents)

Hyperglycaemia (humans, rodents)

High plasma low‐density lipoprotein cholesterol (humans, rodents)

High‐cholesterol diet (rabbits and rats; probably not humans)

Zinc intake (rabbits, some other animals; human data inconclusive)

Body iron levels (rabbits, rats, mice, maybe humans)

Certain foods (humans, e.g. dark soy sauce, tomato; rodents)*

Diabetes (in some human studies, not others)†, but probably not the metabolic syndrome

Intake of polyunsaturated fatty acids‡ (docosahexaenoic acid, possibly eicosapentaenoic acid, humans)

^*It is essential to carry out appropriate controls in testing effects of foods, because the consumption of any food (antioxidant or not) can sometimes alter levels of certain biomarkers.

^†May depend on how well glucose and lipids have been normalized in the diabetic cohorts studied, or on the degree of obesity, because hyperglycaemia, hyperlipidaemia and obesity can all increase F₂‐isoprostane levels, i.e. it may not be diabetes per se but its sequelae or predisposing factors that cause the oxidative stress (at least as revealed by studies of F₂‐isoprostanes).

^‡Despite the propensity of polyunsaturated fatty acids to oxidize in vitro, growing evidence suggests that they minimize oxidative damage in vivo. This table is adapted from references [4] and [44] with permission. For full details and references, please see [4,44].