Re: Cobalt deficiency vs. B12 deficiency
Another article about cobalt/B12:
http://www.dcnutrition.com/Minerals/...ecordNumber=68
Some excerpts:
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Ruminants (i.e.-cows, sheep, goats, deer, antelopes, giraffe, etc.) can use elemental cobalt, however, the microbes fermenting and digesting plant material in their first stomach (rumen) convert elemental cobalt into vitamin B12 which the animal can use.
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Intrinsic factor is a mucoprotein enzyme known as Castle's intrinsic factor and is part of normal stomach secretions.
If a person has hypochlorhydria (low stomach acid - usually a NaCl deficiency) the intrinsic factor will not work and B12/cobalt is not absorbed - this is why doctors frequently give B12 shots to older people on salt restricted diets. Sublingual (under the tongue) and oral spray B12 is available; plant derived cobalt is very bioavailable, however, because of low salt diets and cobalt depleted soils, vegetarians frequently have B12 deficiencies.
The B12 intrinsic factor complex is primarily absorbed in the terminal small intestine or ileum; calcium is required for the B12 to cross from the intestine into the bloodstream as well as an active participation by intestinal cells.
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There is an enterohepatic (Intestine direct to the liver) circulation of B12 that recycles B12 from bile and other intestinal secretions which explains why B12 deficiency in vegans may not appear for five to ten years.
The maximum storage level of B12 is 2 mg, which is slowly released to the bone marrow as needed. Excess intake of B12 is shed in the urine i.e. contributing the notion of "expensive urine".
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The discovery of the essentiality of cobalt came from observing a fatal disease ("bush sickness") in cattle and sheep from Australia and New Zealand; it was observed that "bush sickness" could be successfully treated and prevented by cobalt supplements.
Bush sickness was characterized by emaciation (unsupplemented vegans), dull stare, listless, starved look, pale mucus membranes, anorexia (loss of appetite), anemia microcytic/hypochromic) and general unthriftiness.
In humans, a failure to absorb B12/Cobalt results in deficiency disease. This can result from a surgical removal of parts of the stomach (eliminates areas of intrinsic factor production), or surgical removal of the ileum portion of the small bowel, small intestinal diverticula, parasites (tapeworm), celiac disease (allergies to wheat gluten and cows milk albumen) and other malabsorption diseases. Pernicious anemia and demyelination of the spinal cord and large nerve trunks are classic for B12/Cobalt deficiency.
Less than 0.07 ppm cobalt in the soil results in cobalt deficiency in animals and people who eat crops grown from those soils; 0.11 ppm cobalt in the soil prevents and cures Cobalt deficiency.
The RDA for B12/Cobalt is 3 to 4 mcg per day. We prefer expensive urine and like 250 to 400 mcg per day, especially while preparing for pregnancy and nursing (remember a baby being nursed by a deficient mother has their deficiency extended over a long period of time and may result in serious permanent nerve damage).
Cobalt excess in man (20 to 30 mg/day) may create erythropoiesis (increase in RBC production) with increased production of the hormone erythropoieten from the kidney. Cobalt is also a necessary co-factor for the production of thyroid hormone.
Cobalt is a trace mineral nutrient for bacteria. Its only established role in animals is as a component of vitamin B12. Animals like ruminants (cows) that depend on bacteria for vitamin B12 require inorganic cobalt as a nutrient. Only microorganisms are capable of incorporating cobalt into vitamin B12.
The body cannot use unattached cobalt and cobalt supplements are therefore ineffective. Though cobalt has a low order of toxicity, overdosing with cobalt could lead to goiter and over-production of red blood cells in susceptible individuals.
Low concentrations of cobalt salts were once added to beer as an antifoaming agent. However, cobalt was incriminated in several epidemics of cardiac failure among beer drinkers. The typical American diet provides low levels of cobalt. Green leafy vegetables are the richest source, while dairy products and refined grain products are among the lowest. For example, spinach provides 0.4 to 0.6 mcg per gram, and white flour contains 0.003 mcg per gram. The oral intake of cobalt necessary to produce toxicity is many times greater than can be obtained by normal consumption of foods and beverages.
Cobalt Physiology
The only known function of Co is its participation in metabolism as a component of vitamin B12; thus the signs of Co deficiency are in reality signs of a shortage of the vitamin.
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Though the most important tasks of vitamin B12 concern metabolism of nucleic acids and proteins, it also functions in (1) purine and pyrimidine synthesis; (2) transfer of methyl groups; (3) formation of proteins from amino acids; and (4) carbohydrate and fat metabolism (McDowell, 1989). Vitamin B12 promotes red blood cell synthesis and maintains nervous system integrity, which are functions noticeably affected in a deficiency.
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Overall synthesis of protein is impaired in vitamin B12-deficient animals. Wagle et al. (1958) demonstrated that rats and baby pigs deprived of vitamin B12 were less able to incorporate serine, methionine, phenylalanine, and glucose into liver proteins. Impairment of protein synthesis may be the principal reason for the growth depression frequently observed in these animals (Friesecke, 1980).
Re: Cobalt deficiency vs. B12 deficiency
This threads seems to need to be split in two... but before I do that, here some more info:
Green, leafy vegetables contain 20-60 mcg cobalt per 100g.
An increased intake of cobalt increases B12 concentration, improves survival rate and increases growth rate in lambs grazing cobalt-deficient pastures.
And here's a study which suggests that animals on a corn- or barley-based diets deficient in Cobalt adversely affects their vitamin B12 status... and that supplemental Cobalt also decreased their MMA levels, meaning that the cobalt/B12 was active. This doesn't, of course, necessarily mean that we'd see the same results in a similar study on humans.
Also, the effect of the Cobalt supplementation was stronger in the animals not on the barley based diet. Maybe this is because barley grass already/apparently contain good B12 levels, which at last should be bioavailable and active for non-human animals?
Re: Cobalt deficiency vs. B12 deficiency
Oh my ... This cobalt theory makes SO much sense... How come nobody mentions cobalt when talking about B12 ? After reading all this and more here and there I feel like we're on to something here.. It's soil that's depleted in cobalt and without it, we can't synthesize vit b12, so taking vit b12 supplements seems pretty absurd since our body needs cobalt in the first place.
Also, i had heard that swimming in lake waters one day would be giving me enough b12 for 2 weeks at a time (for the water one gulps in while swimming) and i now discover there's cobalt in lake waters.. Also, there's cobalt in feces, and organic veggies are often grown in soil spread with manure.. again, more cobalt rather than more vit. b12... anyway, i'll keep reading but this is very interesting..
Re: Cobalt deficiency vs. B12 deficiency
Hi vegetarian_cat, I believe the reduced of the good bacteria needed to synthesize B12 more of a problem than lack of Cobalt as such - but this is pure speculation. The general reduction of natural nutrients in soil and the way we treat water could possibly represent a problem for both Cobalt and B12.
Re: Cobalt deficiency vs. B12 deficiency
Comparison of the dietary cobalt intake in three different Australian diets (2004)
"Differences in the dietary intake of cobalt were assessed for vegans, lacto-ovo-vegetarian and non-vegetarian Australians using food intake logs, and daily or average trend recall over three months. A significant decrease in cobalt intake was observed for the lacto-ovo-vegetarian population compared with the intake in vegans and omnivores. There is no RDI for cobalt, however, the cobalt intake of Australians was similar to that reported in other countries. Microflora above the terminal ileum have been shown to produce significant amounts of biologically available vitamin B12. This study was unable to demonstrate a correlation between elemental cobalt intake and serum vitamin B12 concentrations in humans, as has been shown in vitro."
Re: Cobalt deficiency vs. B12 deficiency
From Changes in serum concentrations of methylmalonic acid and vitamin B12 in cobalt-supplemented ewes and their lambs on two cobalt-deficient properties.
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Supplementation of the ewe with a cobalt bullet appeared to protect the growth performance of the lamb for 90 days and influence the subsequent serum vitamin B12 response in the lamb to vitamin B12 supplementation.
CLINICAL SIGNIFICANCE:Supplementing ewes with cobalt bullets in late pregnancy can improve the vitamin B12 status of their lambs, and modify their response to vitamin B12 supplementation.
This is about sheep, and not humans, but still: could this suggest that consuming more cobalt rich food (some green vegetables like broccoli and spinach, oats, some nuts etc) would affect our B12 status positively?
More about cobalt levels in food here:
http://www.thecdi.com/cdi/images/doc...ood_Feb_06.pdf
Re: Cobalt deficiency vs. B12 deficiency
Reduction of plasma homocysteine and serum methylmalonate concentrations in apparently healthy elderly subjects after treatment with folic acid, vitamin B12 and vitamin B6: a randomised trial.
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Suboptimal vitamin status is an important cause of elevated P-tHcys and S-MMA in apparently healthy elderly subjects. Oral B-vitamin therapy is an effective and convenient way to normalise P-tHcys and S-MMA.
In other words: this study suggests that taking folic acid, B12 and B9 does normalize homocysteine and MMA levels. Hcy and MMA levels are both considered useful markers for the activity in B12 (from food or supplements).
Re: Cobalt deficiency vs. B12 deficiency
Age-related hearing loss, methylmalonic acid, and vitamin B12 status in older adults. (PMID 18032219)
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Abstract
Hearing loss has been associated with poor vitamin B12 status in some, but not all studies. This study examined a possible relationship between age-related hearing loss and poor B12 status in 93 older adults using different indices of B12 status. Hearing loss was defined as pure-tone average threshold > 25 decibel hearing level. Participants with methylmalonic acid (MMA) > 271 nmol/L at baseline received 1,000 g/d, and those with MMA < or = 271 nmol/L were randomly assigned to receive 0, 25, or 100 microg/d of B12. In a series of logistic regression analyses, compared with participants with normal hearing, those with impaired hearing had a significantly higher serum mean MMA concentrations in the best and the worst ears and a higher prevalence of elevated MMA (> 271 nmol/L) in the worst ear only. Thus, elevated MMA concentration may be associated with hearing loss in older adults. However, short-term B12 supplementation was unrelated to improvements in hearing status in B12-deficient individuals.
Could the fact that hearing loss is only associated with poor B12 status in some studies - combined with that conclusion that "elevated MMA concentration may be associated with hearing loss in older adult" possibly indicate that, at least for some medical conditions, it's not the B12 level itself that's important, but the MMA level? MMA levels can be influenced in various ways - not only with B12 supplementation.