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Free radicals are generated during inflammatory processes, radiotherapy, and smoking, and during the course of a wide range of diseases. They may cause uncontrolled damage of multiple cellular components, the most sensitive of which are unsaturated lipids, proteins and DNA and they also disrupt the normal replication process. They have been implicated as a cause of a wide range of diseases, including malignant, acute inflammatory and traumatic diseases, cardiovascular disease, neurodegenerative conditions such as Alzheimer's disease, senile macular degeneration, and cataract. The defence against uncontrolled damage by free radicals is provided by antioxidant enzymes (e.g. catalase, superoxide dismutase) and antioxidants, which may be endogenous (e.g. glutathione) or exogenous (e.g. vitamins C and E, carotenoids). A possible causal link between antioxidant and cardiovascular disease has emerged from epidemiological studies although several RCTs have not confirmed this.

Epidemiological studies

Dietary intake

A high intake of fruits and vegetables has been linked to reduced risk of heart disease, cerebrovascular disease and total cardiovascular morbidity and mortality.
A high intake of nuts (rich in vitamin E) and dietary components, e.g. red wine, onions, apples (rich in flavonoids), which are strong scavengers of free radicals, have also been linked to reduced risk of cardiovascular disease.
The seasonal variation in cardiovascular disease, which is higher in winter, has been related to decreased intake of fresh fruit and vegetables.
The decline in cardiovascular disease in the USA since the 1950s has been associated with a simultaneous increase in the intake of fresh fruit and vegetables.

Status of antioxidant nutrients.

The level of antioxidant nutrients in the circulation, has been reported to be inversely related to cardiovascular morbidity and mortality, extent of atherosclerosis assessed by ultrasound, and clinical signs of ischaemic heart disease. The tissue content of lycopene, a marker of vegetable intake, has been reported to be low in patients with myocardial infarction.

Antioxidants, especially vitamin E, have been shown to prevent the initiation and progression of atherosclerotic disease in animals. They also reduce the oxidation of low-density lipoprotein (LDL) in the arterial wall in vitro. Oxidation of LDL is an initial event in the atherosclerotic process.