Free radicals sound like something from a chemistry textbook. They are — but they're also directly relevant to ageing, disease risk, and how your diet affects your cells.
The Chemistry (Simplified)
Atoms bond by sharing electrons in pairs. When a molecule loses an electron and ends up with an unpaired one, it becomes a free radical — highly unstable and reactive.
To stabilise itself, a free radical steals an electron from the nearest available molecule. That molecule then becomes a free radical itself, steals from the next one, and so on — creating a chain reaction of molecular damage.
This process is called oxidative stress when it exceeds the body's ability to neutralise it.
The most biologically significant free radicals are reactive oxygen species (ROS): superoxide (O₂⁻), hydroxyl radical (OH•), and hydrogen peroxide (H₂O₂, which is not technically a radical but generates them).
Where Free Radicals Come From
Normal metabolism: Energy production in the mitochondria (cellular "power plants") generates free radicals as a byproduct. Approximately 1-2% of oxygen used in cellular respiration becomes superoxide. This is unavoidable and normal.
External sources that increase free radical production:
- Smoking: Each puff of cigarette smoke introduces billions of free radicals directly. This is the primary mechanism behind smoking-related cellular damage.
- UV radiation: UV light triggers free radical formation in skin cells — the mechanism behind UV-related skin ageing and skin cancer.
- Air pollution and environmental toxins: Particulate matter and chemical pollutants generate ROS in lung and systemic tissue.
- Chronic stress: Cortisol and stress hormones drive inflammatory signalling that increases ROS production.
- Ultra-processed foods and sugar: Excess sugar promotes oxidative stress through advanced glycation end-products (AGEs) and metabolic inflammation.
- Excessive exercise: Intense exercise transiently increases ROS — this is part of the adaptation signal, but chronic overtraining without recovery increases oxidative damage.
- Alcohol: Alcohol metabolism in the liver produces acetaldehyde and ROS.
What Free Radical Damage Does
Lipid peroxidation: Free radicals attack polyunsaturated fatty acids in cell membranes, degrading membrane integrity and function. Particularly damaging in the brain (which is rich in polyunsaturated fats) and in LDL cholesterol particles (oxidised LDL is the primary driver of arterial plaque).
DNA damage: Free radicals attack DNA directly, causing strand breaks and base modifications. The body has DNA repair mechanisms, but cumulative damage that outpaces repair contributes to mutation accumulation and cancer risk.
Protein oxidation: Proteins oxidised by free radicals lose function or misfold. Oxidised proteins accumulate with age and are implicated in neurodegenerative diseases (Alzheimer's, Parkinson's) — where aggregates of damaged proteins are a hallmark finding.
Mitochondrial damage: The mitochondria both produce and are vulnerable to ROS. Mitochondrial DNA damage reduces energy production efficiency and is a central mechanism of cellular ageing.
The Role of Free Radicals in Ageing
The "free radical theory of ageing" (Harman, 1956) proposed that accumulated oxidative damage over a lifetime drives biological ageing. While the complete theory has been refined — it's now clear ageing is multifactorial and some ROS signalling is beneficial — the evidence that oxidative damage contributes meaningfully to age-related decline is robust.
Key evidence: centenarians consistently show higher antioxidant enzyme activity and lower oxidative stress markers than age-matched controls. Caloric restriction — the most reproducible lifespan extension intervention in animals — consistently reduces oxidative stress markers.
Free Radicals and Inflammation
Free radicals and inflammation are interlinked: oxidative stress activates NF-κB (a master inflammatory signalling molecule), which triggers cytokine production. Inflammation then generates more ROS. This cycle is a central mechanism in cardiovascular disease, metabolic syndrome, and many cancers.
Protection: The Antioxidant System
Antioxidants are the body's defence against free radical damage. They donate electrons to free radicals without becoming unstable themselves, stopping the chain reaction.
The body's endogenous antioxidants (glutathione, superoxide dismutase, catalase) handle most free radical neutralisation. Dietary antioxidants (vitamins C and E, polyphenols, carotenoids) support and extend this system — particularly important when free radical production is elevated.
Practically: The evidence supports reducing free radical sources (not smoking, minimising ultra-processed food, managing chronic stress, using sunscreen) as much as increasing antioxidant intake. Both sides of the equation matter. For brain health specifically, DHA-rich foods and polyphenols have the most evidence for protecting against neuronal oxidative damage.