Vitamin E deficiency does not occur primarily as a result of inadequate dietary intake, because adequate amounts of vitamin E are present in a mixed diet. Vitamin E deficiency usually develops as a result of congenital or acquired disease. In the foreground are diseases with fat malassimilation, as is the case, for example, in sprue, short bowel syndrome, cystic fibrosis, and A-beta lipoproteinemia. Fat assimilation disorders are characterized by a lack of utilization of dietary fatty acids or fat-soluble vitamins due to a lack of enzymatic cleavage in the intestine (maldigestion) or due to absorption defects (malabsorption). In the case of suboptimal vitamin E supply or marginal deficiencies, the known pathological consequences of oxidative stress due to an inadequate antioxidant defense system only become apparent after a longer period of time. Oxidative stress is associated with the pathogenesis of
- Tumor diseases
- Atherosclerosis respectively coronary heart disease (CHD)
- Cataract (cataract)
- Neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease.
- Disease-related sequelae such as reperfusion injury to the heart.
Acute symptoms are seen exclusively in very severe vitamin E deficiency states. Since vitamin E is mobilized in malnutrition from the large stores in the depot fat over long periods in minor amounts, it takes adults with filled depots about 1-2 years until clinical symptoms are observed. Typical signs of vitamin E deficiency
- Shortening of the lifetime of erythrocytes (red blood cells) and increased hemolysis tendency increased degradation or disintegration of erythrocytes due to destruction of the cell membrane.
- Influencing the activity (both increase and decrease) of numerous enzymes, especially membrane enzymes according to the latest findings are so far 147 different enzymes and enzyme systems known to be influenced by a vitamin E deficiency
Increase in lipid peroxidation in the blood and tissues.
The main biological function of vitamin E is as a lipid-soluble antioxidant to prevent the destruction of polyunsaturated fatty acids (for example, linoleic, arachidonic, docosahexaenoic acids) by lipid peroxidation processes in tissues, cells, cell organelles, and artificial systems, thus protecting membrane lipids, lipoproteins, and depot lipids. In case of insufficient vitamin E reserves in the body, lipid peroxidation in blood and tissues increases. On the basis of measurements, increased lipid peroxidation products, such as malonaldehyde, hydroperoxy fatty acids, fluorescent products, ethane and pentane, could be detected in individuals with low vitamin E plasma concentrations. As a result of the insufficient antioxidant protection system and the increase in lipid peroxidation products in plasma due to vitamin E deficiency, the oxidative stress in the body increases, increasing the risk of developing radical-related diseases. Neuromuscular disorders
- Myopathies Disease of muscle cells due to inflammation of muscle tissue, muscle weakness and increase in plasma creatine kinase, with increased urinary creatine excretion indicating muscle membrane damage.
- Neuropathies disease of the peripheral nervous system, neurological disorders, disorders in neuromuscular information transmission with disturbances of depth sensitivity, areflexia failure of intrinsic reflexes , ataxia disorders of coordination of movements and balance regulation concerning the movements of the eyes, muscles involved in the act of speech and voice, muscles of the head, neck, trunk, extremities , encephalopathy pathological changes of the brain.
Deficiencies in premature infants
Premature infants have very low vitamin E stores and immature intestinal absorption of lipophilic substances. In addition, the need is increased at this stage due to growth and development. Finally, manifest deficiency symptoms are particularly common in preterm infants, such as.
- Reduced half-life of erythrocytes (red blood cells) with hemolytic anemia Deficiency of erythrocytes as a result of increased degradation or decay of erythrocytes.
- Bronchopulmonary dysplasia (chronic lung disease, whereby premature infants must be artificially ventilated for a prolonged period of time due to a condition known as respiratory distress syndrome, while requiring supplemental oxygenation) because pulmonary surfactant (the surface-active substance lining the respiratory system of the lungs) is composed of lipids and proteins, it is defenselessly exposed to oxidative attack in the presence of vitamin E deficiency and is unable to perform its function adequately
- Vascular disorders ventricular hemorrhage and intracranial hemorrhage (cerebral hemorrhage), respectively
- Retrolental fibroplasia Damage to the optic nerve and retina with opacities in the vitreous area.
