JSS or VIT for CSE

Vitamin B12 - biofactor for nerve functions, blood formation and cell division

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vitamin B12 (Cobalamin) is a water-soluble vitamin and cannot be produced by the human organism itself. Humans have to consume the biofactor through their diet, whereby the supply is largely only possible through foods of animal origin. Most people in Germany have enough vitamin B.12 supplied, however, around 8% of men and even 26% of women take less vitamin B.12 through food as recommended by the German Nutrition Society. Pregnant women, vegans, senior citizens and people with gastrointestinal diseases and taking certain drugs are among the risk groups for a B vitamin12-Defect. In the case of insufficient intake through food, impaired absorption and increased need, as well as with vitamin B.12Deficiency diseases is a B vitamin12-Supplementation makes sense.

Supply recommendations and supply situation

According to the recommendations of the German Nutrition Society (DGE)1 the appropriate daily intake is the following amounts of the biofactor vitamin B.12:

babyRecommended intake
0 to under 4 months0.5 µg / day
4 to less than 12 months1.4 µg / day
children 
1 to under 4 years1.5 µg / day
4 to under 7 years2.0 µg / day
7 to under 10 years2.5 µg / day
10 to under 13 years3.5 µg / day
13 to under 15 years4.0 µg / day
Teenagers and adults 
15 to 65 years and older4.0 µg / day
Pregnant women4.5 µg / day
Breastfeeding5.5 µg / day

The estimated value for the intake was increased by the DGE in 2019 from 3.0 to 4.0 µg / day for adults.

According to the National Consumption Study II (NVSII, 2008)2 is the mean daily intake of vitamin B.12 in men at 5.8 µg / day and in women at 4.0 µg / day and thus above the recommendations of the DGE. Nevertheless, 8% of men and 26% of women do not achieve the recommended daily intake. In the case of young women between 14 and 24 years of age, it is even 33% who have less vitamin B.12 as recommended by the DGE. Since the vitamin B12-Supply is largely only possible with food of animal origin, vegetarians and especially vegans are at risk of taking in too little of the biofactor. People with gastrointestinal diseases also belong to the risk groups of a vitamin B.12- Deficiency. In addition, older people often suffer from a vitamin B.12- Undersupply, mostly caused by resorption disorders. According to the result of the Augsburg KORA-Age study, around a third of people over 65 years of age are from vitamin B.12- Undersupply affected. The risk increases with age: among 85 to 93 year olds it is 37.6%3.

These causes can lead to a vitamin B12 deficiency

There are many reasons for a deficiency in the biofactor. The undersupply can be caused by insufficient dietary intake, especially with a vegan or strictly vegetarian diet. Vegans are more likely to develop a B vitamin12-A deficiency, while lacto-ovo-vegetarians who also eat eggs and dairy products have fewer B vitamins12- Undersupply is coming4. Vitamin B should be taken regularly in both risk groups12-Blood levels are checked.

Vitamin B is essential during pregnancy and breastfeeding12-Requirement increased. Therefore, vegans and vegetarians are at greater risk of getting a vitamin B.12-Develop a shortage and pass it on to the child. A vitamin B.12Deficiencies during pregnancy can have severe neurological or haematological consequences for the infant, which is why regular blood level controls are recommended - even during breastfeeding.

Last but not least, alcohol abuse and smoking can lead to a deficiency of the biofactor.

A vitamin B.12Deficiency can also be caused by malabsorption in intestinal diseases (Crohn's disease, celiac disease), intestinal surgery or intestinal resections, as there is not enough vitamin B.12 is absorbed through the intestine. A deficiency of the transport protein intrinsic factor (see below), caused by chronic gastritis, after partial gastric resection or in type A gastritis (an autoimmune disease of the stomach), also leads to a decreased vitamin B.12-Admission.

A vitamin B.12- Deficiency, especially in older people, is also often triggered by drugs5. Stomach acid blockers (antacids, proton pump inhibitors and H.2Antagonists) unfavorable to vitamin B.12- affect blood levels. A study showed that the risk of vitamin B12- 65% deficiency due to long-term use of proton pump inhibitors, in H2-Blocking increased by 25%6.

Even diabetics who take metformin can convert into a vitamin B.12- Lack advised. Studies have shown that vitamin B12- Deficiency in diabetics taking metformin is three times higher than in diabetics who do not take metformin7,8. The vitamin B12-Utake and availability can also be reduced by methotrexate, phenobarbital, colchicine, colestyramine, contraceptives, methyldopa and anti-epileptic drugs.

Last but not least, kidney disease, vitamin B disorders12-Metabolism as well as fish tapeworm infestation and other intestinal parasites a vitamin B.12-Cause shortage.

Facts about the physiology of vitamin B12

vitamin B12 is an umbrella term for different compounds that are active in the human body and have the same basic chemical structure: the so-called cobalamines. The two forms cyano- and hydroxocobalamin, which can be converted into effective forms in the body (methyl- and 5‘-adenosylcobalamin), are used therapeutically.
So far, methylcobalamin has not been used therapeutically, but only in the form of dietary supplements. Even if methylcobalamin is supplied, it is first converted and must be restored to methylcobalamin in the body cells.

Role of cobalamin in the human body
Cobalamin is indispensable for the organism9. So is vitamin B.12 - partly in combination with the biofactor folic acid - involved in DNA synthesis and thus in all growth processes and essential for the renewal and reproduction of body cells. The biofactor is also important for erythropoiesis (formation of red blood cells). With a vitamin B.12- Deficiency can therefore lead to blood formation disorders and anemia. Also has vitamin B.12 an important function for the central nervous system, as it is involved in the formation and regeneration of the myelin sheaths (insulating layer that surrounds nerve fibers).

vitamin B12 is actively and passively absorbed
After ingestion through food, vitamin B is found12 (Cobalamin) into the blood in several steps. In the first step it is bound to the protein haptocorrin (HC), which protects the acid-sensitive cobalamin from the low pH value of the stomach. HC splits off in the duodenum and cobalamin is bound to the intrinsic factor (IF) released from stomach cells. Vitamin B is found in the small intestine12 actively absorbed in the form bound to the IF. The absorption capacity is limited to approx. 1 mg per day. In addition, vitamin B12 but also to a lesser extent passively, via diffusion, and in this way gets into the blood. The IF plays no role in this mechanism and there is no relevant limitation of the resorption capacity. This passive absorption mechanism can be used therapeutically in patients with a lack of IF (e.g. after gastric resection) in order to obtain sufficient vitamin B.12-Ensure absorption. Studies have shown that after oral administration of 1,000 µg vitamin B12 10.5 µg are absorbed via the intestine, of which only 14% via the IF and 86% passively via the diffusion mechanism10. It could also be proven that oral high-dose therapy of 1,000-2,000 µg vitamin B12 is as effective as intramuscular injection in the case of absorption disorders11,12.

What are the consequences of a vitamin B12 deficiency?

vitamin B12 is stored in both the liver and the muscles. Only when the vitamin B12-The memory there is almost empty, clinical complaints occur. Affected is the nervous system (central and peripheral) on the one hand, and the blood-forming system on the other. The symptoms of deficiency can occur completely independently of one another. Because of the slow depletion of the memory, symptoms of a vitamin B appear12- Deficiency often only takes months or years. If the consequences of the deficiency are very advanced, however, they are irreversible, especially in the area of ​​the nervous system.

Unspecific complaints
A vitamin B.12- Deficiency shows itself initially with unspecific physical and psychological symptoms. Affected people are tired, limp and show a weakened immune system. You feel unsteady on your feet and suffer from abnormal sensations in the lower extremities such as tingling, burning and numbness. A vitamin B.12-The deficiency is also evident in the psychological area with sleep and concentration disorders and poor memory. Affected people may appear increasingly confused and have mood swings.

Neurological diseases (funicular myelosis and polyneuropathy)
An unrecognized vitamin B.12Deficiency can lead to serious neurological disorders. In the central nervous system, the degeneration of the posterior cords of the spinal cord (nerve fibers in the spinal cord that pull towards the brain) and the most important motor pathway (pyramidal tract) are the main focus (funicular myelosis); This results in disturbances in deep sensitivity (lack of information from the motor brain centers about the position of the extremities in the joints) and thus an unsteady gait and stance. A typical complaint is also a feeling of constriction or cuffs on the lower legs and ankles. In addition, there are neurological deficits in the peripheral nervous system (polyneuropathy), which manifest themselves with numbness, tingling sensation and painful abnormal sensations in the hands and feet.

Cognitive impairment
Studies show that with a vitamin B12-In the absence of an increased risk of developing dementia13. A deficiency of the biofactor is linked to significantly lower memory performance14 and is one of the most common causes of dementia15. Vascular dementia can be caused by an increased blood level of homocysteine, a vascular damaging amino acid, which can be reduced with vitamin B12 supplements16,17.

depressions
In about 30% of people who suffer from depression, vitamin B was lowered12-Blood levels detected. Especially in seniors with a vitamin B.12Deficiency is observed to increase the risk of developing depression18. Studies have also shown that vitamin B12-Supplementation makes depressed patients more responsive to antidepressants (selective serotonin reuptake inhibitors (SSRIs))19.

Will the underlying vitamin B12-If the deficiency is recognized and corrected in time, some damage is reversible If the disease progresses, however, the nerve damage is irreparable.

Megaloblastic anemia
A long-lasting vitamin B.12Deficiency leads to changes in the blood count in the form of megaloblastic anemia. Megaloblastic anemia is a specific form of anemia in which the DNA synthesis of the blood-forming cells in the bone marrow is disturbed. There are developmental disorders of the erythrocytes (red blood cells) with too few but much larger erythrocytes because cell division is disturbed, but not cell growth. Since this means that less oxygen is transported in the blood, megaloblastic anemia manifests itself symptomatically as weakness, fatigue, dizziness and pale skin and mucous membranes. The combination of megaloblastic anemia with the above symptoms of the nervous system as a result of an IF deficiency or antibody-related IF inactivation is historically referred to as pernicious anemia or pernicious anemia.


Warning: megaloblastic anemia cannot only be caused by a vitamin B.12-, but can also be triggered by a folic acid deficiency, which is why both biofactors must be checked if there is any suspicion. Folic acid supplementation alone with the presence of vitamin B at the same time12-Deficiency would be vitamin B12- aggravate dependent neurological disorders.

These foods contain vitamin B12

Good vitamin B.12-Suppliers are meat and meat products, especially offal, sausage products, eggs, fish and crustaceans as well as milk and dairy products. However, vitamin B are12-Derivatives sensitive to light and heat, so that frying, boiling and especially repeated heating in the microwave can lead to a loss of the biofactor of up to 30%. The vitamin B12-Losses can be reduced to around 10% by careful preparation of the food.
Food of plant origin does not contribute to vitamin B.12Supply at.

Can vitamin B12 be overdosed?

vitamin B12 cannot be overdosed with oral intake, as only a limited amount is absorbed and an excess of the water-soluble vitamin is excreted again.
In the past it was observed that the vitamin B12-Levels may be increased in some cancers. The connection has been partially confirmed, but no conclusive findings are yet available. In fact, however, recent research suggests that certain types of cancer may be the B12Values ​​could increase20.

To note

The diagnosis of the vitamin B12 status solely by measuring the total vitamin B.12 in the blood is often not clearly possible with a single laboratory parameter21. At blood levels below 200 ng / L there is a heavy vitamin B.12- Deficiency, however, very likely. Only with a total cobalamin level above 400 ng / l can there be a sufficient probability of sufficient vitamin B.12-Supply can be assumed. At values ​​between 200 and 400 ng / l, differentiation is possible with the help of the measurement of the "active" vitamin B.12 (Holotranscobalamin (Holo-TC)) makes sense. The determination of metabolic compounds that are found in vitamin B.12- Deficiency in the tissue cells, give the most reliable information about the actual B vitamin12Activity in the cells. The compounds that can be used for this purpose are methylmalonic acid (MMA) or homocysteine, but measuring them is more complex than determining blood levels. If you want to get the greatest possible information with a single laboratory value, the Holo-TC value is the best option, which is the earliest parameter of a vitamin B at a value below 35 pmol / l12Represents deficiency; the “gray area” is between 36 and 55 pmol / l. With renal insufficiency, all laboratory parameters can be unreliable, so a treatment attempt with vitamin B12 is indexed.

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  1. www.dge.de/wissenschaft/referenzwerte/vitamin-b12/
  2. Max Rubner Institute (MRI): National Consumption Study II. Results report, part 2. Karlsruhe, 2008. www.mri.bund.de/fileadmin/MRI/Institute/EV/NVSII_Abschlussbericht_Teil_2.pdf, pp. 123-124
  3. Conzade R, Koenig W, Heier M et al .: Prevalence and Predictors of Subclinical Micronutrient Deficiency in German Older Adults: Results from the Population-Based KORA-Age Study. Nutrients 2017, 9 (12): 1276 DOI.org/10.3390/nu9121276. www.mdpi.com/2072-6643/9/12/1276/xml
  4. Herrmann W, Schorr H, Obeid R, Geisel J: Vitamin B12 status. Particularly holotranscobalamin II and methylmalonic acid concentrations and Hyperhomocysteinemia in vegetarians. Am J Clin Nutr 2003, 78: 131-136 www.ncbi.nlm.nih.gov/pubmed/12816782
  5. Gröber U, Schmidt J, Kisters K: Important drug-micronutrient interactions: A selection for clinical practice. Critical Reviews in Food Science and Nutrition. doi.org/10.1080/10408398.2018.1522613
  6. Lam JR, Schneider JL, Zhao W, Corley DA: Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA. 2013 Dec, 310 (22): 2435-42 DOI: 10.1001 / jama.2013.280490 www.ncbi.nlm.nih.gov/pubmed/24327038
  7. De Groot-Kamphuis DM, van Dijk PR, Groenier KH et al .: Vitamin B12 deficiency and the lack of its consequences in type 2 diabetes patients using metformin. Neth J Med 2013 Sep, 71 (7): 386-390 www.ncbi.nlm.nih.gov/pubmed/24038568
  8. Damião CP, Rodrigues AO, Pinheiro MFMC et al .: Prevalence of vitamin B12 deficiency in type 2 diabetic patients using metformin: a cross-sectional study. Sao Paulo Med J 2016 June 03, ISSN 1516-318 dx.doi.org/10.1590/1516-3180.2015.01382111
  9. Pietrzik K, Golly I, Loew D: Handbuch der Vitamins, 1st edition, Urban & Fischer, 2008
  10. Biesalski HK, Bischoff S, Pirlich M, Weimann A (eds.): Nutritional medicine. According to the nutritional medicine curriculum of the German Medical Association, 5th edition, Stuttgart: Thieme, 2018
  11. Bolaman Z et al .: Oral versus intramuscular cobalamin treatment in megaloblastic anemia: A single-center, prospective, randomized, open-label study. Clinical Therapeutics 2003, 25 (12) DOI: doi.org/10.1016/S0149-2918(03)90096-8. www.clinicaltherapeutics.com/article/S0149-2918(03)90096-8/abstract
  12. Vidal-Alaball JV, Butler CC, Cannings-John R et al .: Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency. Cochrane Database.Syst Rev 2005 Jul, 20 (3): CD004655 www.ncbi.nlm.nih.gov/pubmed/16034940
  13. Chen H, Liu S, Ji L et al .: Associations between Alzheimer's disease and blood homocysteine, vitamin B12 and folate: a case-control study. Curr Alzheimer Res 2015, 12 (1): 88-94 www.ncbi.nlm.nih.gov/pubmed/25523421
  14. Köbe T, Witte AV, Schnelle A et al .: Vitamin B12 concentration, memory performance and hippocampal structure in patients with mild cognitive impairment. Am J Clin Nutr 2016 Apr, 103 (4): 1045-54 DOI: 10.3945 / ajcn.115.116970. Epub 2016 Feb 24
  15. Djukic M, Wedekind D, Franz A, Gremke M, Nau R: Frequency of dementia syndromes with a potentially treatable cause in geriatric in-patients: analysis of a 1-year interval. Eur Arch Psychiatry Clin Neurosci 2015 Aug, 265 (5): 429-438 DOI: 10.1007 / s00406-015-0583-3. Epub 2015 Feb 26. www.ncbi.nlm.nih.gov/pubmed/25716929
  16. Wolters M, Ströhle A, Hahn A: Qualified nutritional advice in the pharmacy. Part 3: New Findings on Vitamin D and B12. Dtsch Apoth Ztg 2005, 145: 221-228
  17. Gröber U, Kisters K, Schmidt J: Neuroenhancement with Vitamin B12 - underestimated neurological significance. Nutrients 2013, 5: 5031-5045
  18. Tiemeier H et al .: Vitamin B12, folate and homocysteine ​​in depression: the Rotterdam Study. Am J Psychiatry 2002, 159: 2009-2101
  19. Syed EU, Mohammad Wasay M, Awan S: Vitamin B12 Supplementation in Treating Major Depressive Disorder: A Randomized Controlled Trial. Open Neurol J 2013, 7: 44-48 DOI: 10.2174 / 1874205X01307010044 www.ncbi.nlm.nih.gov/pmc/articles/PMC3856388/
  20. Arend et al .: Elevated vitamin B12 levels and cancer risk in UK primary care: a THIN database cohort study. American Association for Cancer Research (Online) 2019 January, 14
  21. Reiners K: vitamin diseases. In: Hoffmann GF, Grau AJ (Hrsg): Metabolic diseases in neurology. Stuttgart: Thieme, 2004: 163-176 www.thieme-connect.de/products/ebooks/book/10.1055/b-002-11387