Free Radicals (Oxidative Stress): Prevention

To prevent oxidative stress, particular attention must be paid to reducing risk factors.

Modifiable risk factors, that is, those that can be influenced.

  • Diet low in vital nutrients (few cereal products, less than 5 servings of vegetables and fruits (400-800 g/day), little milk and dairy products, less than one to two fish per week, etc).
  • Malnutrition and malnutrition including over- and undernutrition.
  • Smoking the substances inhaled in a single puff from a cigarette, form 1015 free radicals in the lungs a hundred times more than we ourselves have body cells. When detoxifying the tar inhaled at the same time, an additional 1014 free radicals are formed.
  • UV rays for example sunlight, solarium
  • Extreme physical labor
  • Competitive and high-performance sports

Treatable diseases

Environmental stress, intoxications

  • Occupational contact with carcinogens
  • Liver damage from, for example, hydrogen tetrachloride poisoning, ethanol, etc.

As far as possible avoid or reduce medication

What are the protective mechanisms against oxidative stress?

The cells of the body are not defenseless against the attacks of free radicals. So-called antioxidants see Vital Substance Therapy intercept the free radicals and defuse them even before they can damage the cells. Antioxidants are chemical or biological substances that are able to neutralize the potential effect of free radicals. Some antioxidants, e.g. the enzymes superoxide dismutase and catalase, are endogenous, i.e. they are normal components of the body, while others (e.g. vitamins C and E) are exogenous and must be supplied in sufficient quantities every day through the diet. However, a reduced mode of action of such a system is partly responsible for an absolute or relative inefficiency of the antioxidant defense system.

Etiology Examples
Reduced AO intake Hypovitaminosis, unbalanced diet
Reduced AO absorption Malabsorption: celiac disease, Crohn’s disease, ulcerative colitis, etc.
Reduced AO bioavailability Impaired uptake and transport carriers wgn, e.g., aging or biochemical individuality
Enzymatic AO deficit Genetic and/or iatrogenic factors
Abnormally increased AO uptake Abnormally increased production of oxidative species (e.g., smoking)
Medication/drug abuse Microsomal overload
Diseases See above under “Treatable diseases”
AO=antioxidants