Aquacobalamin is one of the B12 vitamins. As such, it participates in the synthesis of amino acids. Deficiency of aquacobalamin and other cobalamins can lead to severe disorders that may include irreversible neurological damage.
What is aquacobalamin?
Aquacobalamin or aquocobalamin belongs to the vitamin B12 group, which are also known as cobalamins in biology. The term cobalamins is derived from the central cobalt atom around which the other atoms of the molecule are grouped. Aquacobalamin is the vitamin B12a. The other two cobalamins are called hydroxycobalamin (vitamin B12b) and nitritocobalamin (vitamin B12c). However, nutritional science also refers to another cobalamin, cyanocobalamin, as vitamin B12. The different use of the terms is often confusing for patients, especially since the different B12 vitamins have different effects and interact at the same time. As early as the 1920s, physicians discovered the importance of the liver in the treatment of pernicious anemia. Later, science was able to identify this form of anemia as a consequence of cobalamin deficiency. Because vitamin B12 is stored in the liver, it contains particularly high concentrations of the substance. For this reason, doctors often still recommend including liver in the diet for B12 deficiency.
Function, effect and tasks
A chemical reaction turns aquacobalamin into a nitrosyl complex. This is of great importance for numerous biological processes. The complex is formed from a reaction of aquacobalamin with nitrite in water solutions. In many biological processes, aquacobalamin does not act alone, but in combination with the other vitamins of the B12 group. Cobalamins play an important role in the nervous system in particular; a deficiency of vitamin B12 can therefore lead to irreversible neurological damage. Cell division and blood formation also depend on aquacobalamin. The liver stores cobalamins, thereby enabling continuous availability of the vital vitamin. Due to this storage, a deficiency of vitamin B12 does not have to be immediately reflected in the blood count. The liver can absorb about 2000 – 5000 µg of vitamin B12. Medicine does not differentiate between the various cobalamins; aquacobalamin is included in this value, as are the other variants. Overdosage is rare and usually occurs when patients take additional supplements. Intravenous administration of vitamin B12 in particular can lead to overdose. It may result in acne and local allergic reactions. However, therapeutic treatment sometimes necessitates intravenous administration of cobalamins, for example, to treat severe vitamin B12 deficiency.
Formation, occurrence, properties, and optimal levels
Aquacobalamin and other B12 vitamins are predominantly found in animal foods. However, recent studies indicate that the concentration of vitamin B12 is very low, especially in products from conventional animal husbandry. The reason for this is the poor nutrition of animals in industrial factory farming, which is primarily aimed at rapid growth. Certain bacteria can also produce vitamin B12 outside animal bodies. However, especially in the synthesis of cobalamins during lactic acid fermentation, it is controversial to what extent the composition of the end products is sufficient for the human body. The correct composition of the various vitamins of the B12 group is also doubtful. For aquacobalamin, i.e. vitamin B12a, no explicit standard values exist. For all B12 vitamins, nutritional science indicates a daily requirement of 3 µg for adults, which is relatively low compared to the guideline values for other vitamins. The human body cannot synthesize cobalamins on its own and therefore relies on ingesting them through food. Other foods, such as B12-enriched toothpaste, can also help meet daily requirements.
Diseases and disorders
Deficiency of vitamin B12 can cause various medical conditions. One of these is funicular myelosis. This is a disease of the nervous system that belongs to the demyelinating diseases. Funicular myelosis manifests itself in neurological symptoms, which mainly affect motor function and physiological perception. Demyelination of the nerve cells triggers these deficits.In the normal state, a myelin cell surrounds the nerve cells. This forms around the axon and insulates it from the outside; in this way, it ensures the electrical conductivity of the neuron. In demyelinating diseases, which include multiple sclerosis, this insulating layer degenerates, impairing the transmission of electrical signals. As a result, the nervous system receives incomplete information and produces incorrect or absent responses. Another potential consequence of cobalamin deficiency is pernicious anemia or Biermer’s disease. It may also precede funicular myelosis. Pernicious anemia is a form of anemia that is fatal without treatment. The first signs are pallor, fatigue, dizziness and circulatory problems. In advanced stages, the skin may turn yellow – a result of increased concentrations of bilirubin. Bilirubin is a breakdown product of the red blood pigment hemoglobin. Other symptoms include an inflamed tongue and gastrointestinal discomfort. In addition, pernicious anemia leads to neurological symptoms that include tingling in the hands and feet, numbness, and motor disorders such as paralysis, unsteady gait, and coordination problems. Another form of anemia, megaloblastic anemia, may also occur as a result of a deficiency of vitamin B12, including aquacobalamin, and cause a disturbance in folic acid metabolism. Furthermore, metabolic disorders may develop in the form of methylmalonate aciduria or homocystinuria. Cobalamin deficiency also potentially affects the immune system-not only through indirect effects but also directly through hypersegmented white blood cells.
