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B12

  • Serum Vitamin B12 in Children

    Dietary vitamin B12 intake was inadequate in 43% in an extremely impoverished indigenous population of Panamanian children aged 12 to 60 months.

    These children were poorer, had less frequent diarrhea, and obtained a higher percentage of their energy from carbohydrate than children with adequate intake. Energy intake positively predicted dietary vitamin B12 intake. In contrast, serum vitamin B12 concentrations were normal in all but 3% of the children. Serum vitamin B12 was positively associated with weekly servings of fruit, corn-based food, and name (a traditional starchy food), but not with animal-source foods. Finally, serum vitamin B12 was not associated with Ascaris intensity but was lowered with increasing frequency of diarrhea.

    Although inadequate dietary intake of vitamin B12 was common, most serum values were normal. Nevertheless, diarrheal disease emerged as a negative predictor of serum vitamin B12 concentration.

  • Vitamin B12 Levels in Long-Term Vegans

    Serum vitamin B12, serum folate and red blood cell folate levels were examined among 36 strict vegans of 5-35 years' duration.

    Vitamin B12 levels among the vegans were generally lower than in a control population. Most of the vegans had vitamin B12 values less than 200 pg/ml

    None of the vegans had any hematologic evidence of vitamin B12 deficiency, however four of them had neurologic complaints. Long-standing vegans should be monitored for vitamin B12 levels.

    Red blood cell folate levels were normal but serum folate levels among the vegans were higher than among the controls. 

  • B12 Oral Supplements and Cognitive Function

    Vitamin B-12 status did not change significantly after treatment in the placebo group with daily supplementation with high doses of oral vitamin B-12 alone or in combination with folic acid.

    Oral vitamin B-12 supplementation corrected mild vitamin B-12 deficiency.

    Vitamin B-12 + folic acid supplementation increased red blood cell folate concentrations and decreased total homocysteine concentrations by 36%.

    Improvement in memory function was greater in the placebo group than in the group who received vitamin B-12 alone. Neither supplementation with vitamin B-12 alone nor that in combination with folic acid was accompanied by any improvement in other cognitive domains.

  • Research Needed for B12 and Neurodegenerative Disease

    Having established the association of vitamin B12 insufficiency with neurodegenerative disease, the challenge is to discern the direction, if any, of causation.

    Most neurological impairments present a slow, progressive course (Josephs et al., 2009) and vitamin B12 levels may take a number of years to deplete (Herbert, 1988). Studies investigating causation would need to continue over an extended period of time.

    Low serum vitamin B12 levels may play a role in the pathogenesis of neurodegenerative disease; however, it is equally plausible that neurological impairment may lead to poor nutrition and hence to inadequate dietary intake. Also, any association may simply be coincident or the factors predisposing patients for neurodegenerative disease may simply also expose the patient to a higher risk of vitamin B12 deficiency, for example, poor nutrition. Further intervention studies in large samples followed over an extended period of time are required. This will allow for further investigation of the role, if any, of vitamin B12 in the onset or progression of neurodegenerative disease, as well as the latent period of effect of vitamin B12 insufficiency before cognitive deficits are evident.

  • Risk Factors for Vitamin B12 Deficiency

    Those experiencing pernicious anemia (an auto-immune reaction to either the parietal cells or intrinsic factor) go on to develop vitamin B12 deficiency through malabsorption if untreated. Deficiency could develop within 1–3 years in those experiencing malabsorption. 

    Patients having surgical alteration of the distal ileum, Crohn’s disease, and using metformin are also at an increased riskfor malabsorption.

    Herbert (1994) estimates that deficiency could take as long as 20–30 years to develop in persons having normal absorption/reabsorption and suddenly ceasing to include substantial amounts of vitamin B12 in their diet during adulthood. This is due to the large amount of vitamin B12 that can be stored in the body and recycled through enterohepatic reabsorption. 

    The prevalence of vitamin B12 deficiency increases with age and is associated with a number of conditions and treatments.

    The main causes of vitamin B12 deficiency are

    • poor dietary intake (as in vegetarianism),
    • poor absorption (occurring in achlorhydria, pernicious anemia, Helicobacter pylori (H. pylori) infection, Crohn’s disease, and metformin use),
    • poor distribution (genetic predisposition for aberrant proteins that are inefficient in transport or cellular uptake of vitamin B12).
  • Vitamin B12 Cobalamin

    Vitamin B12, also called cobalamin, is a water-soluble vitamin that has a key role in the normal functioning of the brain and nervous system, and the formation of red blood cells. It is involved in the metabolism of every cell of the human body, especially affecting DNA synthesis, fatty acid and amino acid metabolism.

    No fungi, plants, nor animals (including humans) are capable of producing vitamin B12. Only bacteria and archaea have the enzymes needed for its synthesis. Proved food sources of B12 are animal products (meat, fish, dairy products). Some research states that certain non-animal products possibly can be a natural source of B12 because of bacterial symbiosis.

    B12 is the largest and most structurally complicated vitamin and can be produced industrially only through a bacterial fermentation-synthesis. This synthetic B12 is used to fortify foods and sold as a dietary supplement.

    Vitamin B12 consists of a class of chemically related compounds (vitamers), all of which show pharmacological activity. It contains the biochemically rare element cobalt (chemical symbol Co). The vitamer is produced by bacteria as hydroxocobalamin, but conversion between different forms of the vitamin occurs in the body after consumption

    B12 aids in lowering homocysteine levels and may lower the risk of heart disease. 

    Recommended daily amount: 2.4 mcg

    Example sources: fortified cereals, doenjang and chunggukjang (fermented soybeans), nori (seaweed). 

  • B12 Supplementation Effective Sublingually and Orally

    A dose of 500 µg of cobalamin given either sublingually or orally is effective in correcting cobalamin deficiency

  • Vitamin B12 Deficiency as a Worldwide Problem

    Pernicious anemia is a common cause of megaloblastic anemia throughout the world and especially in persons of European or African descent. Dietary deficiency of vitamin B12 due to vegetarianism is increasing and causes hyperhomocysteinemia.

    The breast-fed infant of a vitamin B12–deficient mother is at risk for severe developmental abnormalities, growth failure, and anemia. Elevated methylmalonic acid and/or total homocysteine are sensitive indicators of vitamin B12–deficient diets and correlate with clinical abnormalities.

    Dietary vitamin B12 deficiency is a severe problem in the Indian subcontinent, Mexico, Central and South America, and selected areas in Africa. Dietary vitamin B12 deficiency is not prevalent in Asia, except in vegetarians. Areas for research include intermittent vitamin B12 supplement dosing and better measurements of the bioavailability of B12 in fermented vegetarian foods and algae.

  • B12 May Be Synthesized by Small Intestine Microflora

    In man, physiological amounts of vitamin are absorbed by the intrinsic factor mediated mechanism exclusively in the ileum, the third portion of the small intestine. Human faeces contain appreciable quantities of vitamin B12 or vitamin B12-like material presumably produced by bacteria in the colon, but this is unavailable to the non-coprophagic individual. However, the human small intestine also often harbours a considerable microflora and this is even more extensive in apparently healthy southern Indian subjects. We now show that at least two groups of organisms in the small bowel, Pseudomonas and Klebsiella sp., may synthesise significant amounts of the vitamin.

Aristotle

Educating the mind without educating the heart is no education at all.

Protein Digestibility-Corrected Amino Acid Score

The protein digestibility-corrected amino acid score (PDCAAS) has been adopted by FAO/WHO as the preferred method for the measurement of the protein value in human nutrition. 

PDCAAS = Amino Acid Score x Digestibility

The method is based on comparison of the concentration of the first limiting essential amino acid in the test protein with the concentration of that amino acid in a reference (scoring) pattern. This scoring pattern is derived from the essential amino acid requirements of the preschool-age child.

Although the principle of the PDCAAS method has been widely accepted, critical questions have been raised in the scientific community:

  1. the validity of the preschool-age child amino acid requirement values (more than 4 times greater than the EAA requirement for an adult),
  2. the validity of correction for fecal instead of ileal digestibility,
  3. the truncation of PDCAAS values to 100%.

The reference scoring pattern was based on studies performed more than 25 years ago on a limited number of 2-year-old children recovering from malnutrition.

According to the current official recommendations, a 2-year old child needs ~ 3x higher essential-to-non-essential amino acid ratio, and needs essential amino acids in different proportions than adult. Methionine/cysteine is the limiting essential amino acids for adults, and for children it is lysine or tryptophan.

The use of fecal digestibility overestimates the nutritional value of a protein because amino acid nitrogen entering the colon is lost for protein synthesis in the body and is, at least in part, excreted in urine as ammonia.

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