There are good reasons to pay attention to antioxidant nutrition today. Airborne particles, ozone, cigarette smoke, occupational exposures, persistent hyperglycaemia, obesity, poor sleep and chronic inflammation can all increase oxidant production. Human studies have linked ozone and particulate exposure with changes in lipid oxidation markers and antioxidant enzyme activity.

The question of whether we need more antioxidants than people did in the past cannot be reduced to a number. We cannot collect a blood sample from someone who lived a thousand years ago and run it through the same laboratory. The past was not clean either. Indoor biomass smoke, infection, food insecurity, mould, hard physical labour and intense sun exposure created different burdens. A modern city resident has a different exposure profile, not necessarily a greater burden in every domain.

Oxidation is part of biology

The body produces reactive oxygen species during energy production, immune defence and exercise. At appropriate levels they also act as signalling molecules and help drive adaptation. The problem is persistent imbalance, when production exceeds repair and protective capacity.

Protection does not depend on a single vitamin. Glutathione, glutathione peroxidases, superoxide dismutases, catalase, thioredoxin, DNA repair systems and food-derived compounds work as a network. That network requires protein, selenium, zinc, copper, manganese, vitamins and plant compounds. A poor diet with an antioxidant capsule does not provide the same foundation.

Modern oxidative burdens are real for many people

Cigarette smoke delivers oxidants and drives inflammation. Ozone is itself a powerful oxidant. Fine particles can trigger inflammatory responses in the lungs and circulation. Sustained high blood glucose increases glycation and reactive oxygen production. A liver dealing with alcohol, excess energy, medication or occupational exposure also depends on intact defence and clearance pathways.

This gives many people a stronger reason to care about nutrient density and to eat a generous range of vegetables. It does not prove that everyone needs a supplement, and it certainly does not show that larger doses always provide more protection.

Carotenoids: food and colour, not just beta-carotene in a capsule

Carotenoids are a broad family that includes beta-carotene, alpha-carotene, lutein, zeaxanthin and lycopene. They arrive in foods alongside many other compounds, and their concentrations vary with cultivar, light, maturity, storage and cooking.

The distinction between food and supplements is especially important here. In CARET, beta-carotene plus retinol given to smokers and asbestos-exposed workers increased lung cancer incidence by 28% and mortality by 17%, leading to early termination of the trial. That does not make carrots dangerous. It shows that a pharmacological dose of an isolated compound can behave very differently from a food containing a natural mixture of carotenoids.

Selenium, the liver, the brain and mercury

Selenium is incorporated into selenoproteins involved in redox control, thyroid hormone metabolism and cell protection. Animal research shows that the brain retains selenium during low intake, underlining its biological importance. The liver uses selenium-dependent enzymes as part of a much wider defence system.

Mercury has a high affinity for selenium. Laboratory and animal studies show that it can bind to the active sites of selenium-dependent enzymes, including thioredoxin reductases and glutathione peroxidases, inhibit their activity and reduce the selenium available for building replacement selenoproteins. This can increase oxidative strain and narrow the nutritional margin of safety, especially when selenium intake or status is already low, but the mechanism alone does not prove that every exposed person needs a supplement.

The liver is central to this process. It converts dietary forms of selenium into substrates used for selenoprotein synthesis and produces selenoprotein P, which carries selenium to other tissues. A controlled trial found mild functional deficiency in some patients with moderate or severe cirrhosis, and the response depended on the form of selenium given. This cannot be generalised to everyone whose liver is under strain. Liver disease, diet and mercury exposure may change selenium handling and narrow the margin of safety.

This does not mean that selenium simply clears mercury. Binding may reduce some forms of toxicity, but it can also alter the distribution and clearance of both elements. Human findings are inconsistent, so exposure alone cannot determine the right supplemental dose.

Low selenium status deserves attention. Supplementation can improve particular biomarkers when intake is inadequate. In selenium-replete adults, however, a year-long intervention raised body selenium without increasing GPX3 activity or selenoprotein P. In another trial, 200 micrograms per day over several years was associated with more type 2 diabetes, a secondary outcome in that study. In SELECT, selenium did not prevent prostate cancer, while high-dose vitamin E increased risk by 17%.

Mercury exposure and liver disease can make an adequate selenium supply more important and narrow the margin of safety, especially when selenium status is already low. The evidence does not establish a higher dietary requirement for every exposed person. Identify and reduce the exposure, assess diet, liver status and selenium status, and only then decide whether supplementation is justified and at what dose.

More vegetables, not a race for capsules

A diet rich in varied vegetables, legumes, herbs, nuts, seeds, adequate protein and appropriate fats supplies the building blocks for endogenous defence as well as thousands of compounds that do not fit neatly under the antioxidant label. More vegetable volume within a balanced diet is particularly sensible for someone who eats few plants or lives with significant environmental or metabolic stress.

Reducing the exposure may matter more than adding a nutrient. Smoking cessation, ventilation, mould remediation, lower alcohol intake, glucose control, sleep and appropriate physical activity reduce the source of the burden. It makes little sense to continue a major exposure and expect a supplement to cancel it.

Practical conclusion

Many people face meaningful modern sources of oxidative stress, which strengthens the case for a nutrient-dense diet and a wide variety of vegetables. Evidence does not support one high dose of antioxidants or selenium for everyone. Food, correction of a demonstrated gap and exposure reduction are a better foundation than random supplementation.

Research and sources