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COBALAMIN (B12) IN FOCUSNEEDS®
Cobalamin, also known as vitamin B12, cannot be manufactured by humans and is obtained exclusively from the diet. Cobalamin is an enzyme cofactor for enzymes in energy metabolism and methylation/folate metabolism. Cobalamin has critical functions in the nervous system, including in the synthesis of myelin, and in the formation of red blood cells. Cobalamin deficiency is common, especially in individuals with vegan-like diets, gastrointestinal conditions, and/or autoimmune disease. Deficiency can result in anemia, functional symptoms (fatigue, weakness, lightheadedness), or neurological features (numbness or tingling, problems walking, psychosis, behavioral changes), which may be irreversible. Cobalamin is often used in the treatment of brain disorders like autism. It is also used to treat elevated levels of blood homocysteine, and as a general “energy” supplement. The form of cobalamin used in most nutritional supplements is cyanocobalamin, although other forms are preferred due to the lack of need to detoxify the cyanide component. Premium variants of B12 include adenosylcobalamin and hydroxycobalamin, which have more-direct action on enzymes. Side effects are rare at usual doses used in oral supplementation.
Cobalamin, also known as vitamin B12 or simply as B12, is one of the eight B-complex vitamins. Cobalamin cannot be manufactured by humans and is thus a true vitamin, obtained exclusively from the diet.
Methylcobalamin and 5-deoxyadenosylcobalamin are the active forms of cobalamin used in human enzymes. The form of cobalamin used in most nutritional supplements is cyanocobalamin but is not preferred due to the need to detoxify the cyanide component, however small. Premium forms of B12 include adenosylcobalamin and hydroxycobalamin, which are more-easily converted to the active forms used by the body’s enzymes. These are the forms present in FocusNeeds®.
Cobalamin is an enzyme cofactor for only two human enzymes, yet they are in critical pathways: energy metabolism and methylation/folate metabolism. Among many other functions, some of the more critical requirements for cobalamin are in DNA synthesis, the function of the nervous system, including via the synthesis of myelin (white matter), and in the formation of red blood cells.
Cobalamin deficiency is common, especially in individuals with diets poor in animal products, gastrointestinal conditions, and/or autoimmune disease. Deficiency might first present as a megaloblastic (large red blood cells) anemia. Functional symptoms are common, including fatigue, weakness, lightheadedness, constipation, diarrhea, loss of appetite, heart palpitations, or shortness of breath. Neurological features are also common, and may in part be irreversible, including numbness or tingling, problems walking, loss of vision or taste, anxiety, depression, mania, psychosis, memory loss, or behavioral changes.
Multiple studies support the role of cobalamin in the treatment of autism and related brain disorders. Cobalamin, often along with folate and pyridoxine, is sometimes used to treat elevated levels of blood homocysteine, which is a risk factor for cardiovascular disease. Although extensively studied in the related condition of autism, in ADD/ADHD the supplementation of cobalamin has not been well studied. Lower vitamin B12 levels were found in several studies in individuals with autism and with ADHD, and a meta-analysis of studies revealed the same (PMID 35034564). Its use to improve cognitive function and dementia have not been substantiated. Cobalamin is a common ingredient in “energy drinks”.
Cobalamin is water-soluble and excessive amounts are excreted by the kidneys, so toxicity is unlikely. Far higher dosages are frequently provided by injection in children with autism. Side effects are rare at usual doses used in oral supplementation.
Laboratory testing can reveal the presence of a deficiency of this nutrient, but this test often fails to reveal deficiencies that are mild. The preferred test is to measure blood methylmalonate and homocysteine levels, which are elevated even in mild cobalamin deficiency. Decreased brain and/or spinal cord myelination is another sign of potential cobalamin deficiency.
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