Vegan For Life
by Jack Norris, RD &
Ginny Messina, MPH, RD
Are Intestinal Bacteria a Reliable Source of B12?
Summary: Given that many otherwise healthy vegans develop B12 deficiency when not supplementing their diets with B12, intestinal bacteria cannot be relied upon to prevent B12 deficiency in vegans.
- Bacteria in the Large Intestine
- Bacteria in the Small Intestine
- Iranian Villagers
Are raw foodists or people who eat fermented foods exceptions? No. See the section Raw Foodist Vegans.
It has long been assumed that B12 is produced by bacteria in the large intestine (aka the colon), but since B12 is produced below the ileum (where B12 is absorbed), it is not available for absorption. This theory is reinforced by the fact that many species of totally or primarily vegetarian animals eat their feces. Eating feces allows them to obtain B12 on their diets of plant foods.
The best evidence I have found for this theory is reported by Herbert (1). He reports a study in the 1950s in England where vegan volunteers with B12 deficiency (as shown by megaloblastic anemia) were fed B12 extractions made from their own stools and it cured their deficiency. He said it proves that the colon bacteria of vegans produce enough B12 to cure a deficiency, but that the B12 produced by the bacteria in the colon is excreted rather than absorbed. This appears to be convincing evidence.
However, the study Herbert cites as the source, "Callender ST, Spray GH. Latent pernicious anemia. Br J Haematol. 1962;8:230-40," does not mention this experiment.
There is another study by Callender and Spray that sounds like it could be the one Herbert is describing, "Preparation of hematopoietically active extracts from faeces. Lancet 1951(June 30):1391-2." This study was not performed on vegans, but rather on people with pernicious anemia who cannot properly absorb B12. The B12 was isolated from the stool samples and given to the subjects intravenously. Because these people were ingesting B12, the B12 in their stool could have been from the B12 they were eating.
On the other hand, according to Lactobacillus lactis Dorner and Lactobacillus leichmannii assays, there were substantial amounts of B12 analogue found in the feces (e.g., 5 µg per 10 ml (2 teaspoons)). This seems like too much to have been provided by only the diet and enterohepatic circulation. Apparently, some of this B12 analogue was active, and there was enough to counteract any inactive B12 analogue in their stools. Thus, this study provides good evidence that there is active B12 produced by bacteria in the colon of at least some humans.
A variable to consider is that there are over 400-500 species of bacteria in the average human's colon and these bacteria have not all been delineated. It is plausible that some humans have B12-producing bacteria in significant amounts while other humans do not. Some bacteria in the digestive tract absorb B12 for their own use, further complicating this situation.
Allen and Stabler found that more than 98% of B12 analogue in the human stool is inactive (2). This was in people who had a consistent intake of vitamin B12. They determined that 81% of nonabsorbed, ingested B12 was destroyed or degraded into inactive analogue. This may or may not be the case in people with much lower, or no, vitamin B12 intakes.
B12 deficiency has been found with relatively high frequency among vegetarian Indian immigrants in England, while it is supposedly uncommon among native Indians with identical dietary patterns (3, 4). Healthy Indian subjects have a more extensive amount of bacteria in their small intestine than people in the West (3).
Albert et al. (3) (1980) measured B12 production of bacteria in the small intestines of people in India using a Euglena gracilis Z assay. Results were confirmed by an Ochromonas malhamensis assay, which is thought to be specific for active B12. They determined that some active B12 was produced by members of the bacteria genera Klebsiella and Pseudomonas. Further confirmation using chromatography and bioautography showed a molecule with similar properties to cyanocobalamin. Albert et al. speculated that when Indians migrate to the West, their digestive tracts become like those characteristic of people in Western countries: with little or no bacteria in their upper small intestines. An article in Nutrition Reviews (5) (1980) suggested some alternative causes of Indian immigrants to Britain having more B12 deficiency than Indian natives:
- In India, water is contaminated with various bacteria, including those from human and animal feces.
- The practice of defecating in open fields and lack of proper sewage.
- The mode of toilet hygiene where water is used instead of toilet paper.
|Table 1. B12 Status of a Group of Indians age 27-554|
|Number||Average serum B12||serum B12 < 203||MMA > .26 µmol/l||HCY > 15 µmol/l|
|A - Tended to eat only small amounts of animal products | B - 1 person was vegan | C - A low folate status could have contributed to the high HCY levels7 | HCY - homocysteine | MMA - methyl malonic acid|
Halstead et al. (8) reported that some Iranian villagers with very little animal product intake (dairy once a week, meat once a month) had normal B12 levels. None had megaloblastic anemia. Their average B12 level was 411 pg/ml which was quite high considering their diet. The authors speculated this could be because their diets, which were very low in protein, allowed for B12-producing bacteria to ascend into the ileum where the B12 could be absorbed. They also speculated that because they lived among their farm animals and their living areas were littered with feces, they picked up enough B12 through contamination.
Halstead et al.'s 1960 report was in contrast to Wokes et al.'s 1955 report (9) in which numerous British vegans were found to have neurological symptoms of B12 deficiency.
It is possible that some vegans can ward of overt vitamin B12 deficiency, and even mild B12 deficiency, through B12 production by bacteria in the small intestine. However, this is an unusual condition, especially in Western countries, and should not be relied upon, including by raw foodists.
2. Allen RH, Stabler SP. Identification and quantitation of cobalamin and cobalamin analogues in human feces. Am J Clin Nutr. 2008 May;87(5):1324-35.
4. Refsum H, Yajnik CS, Gadkari M, Schneede J, Vollset SE, Orning L, Guttormsen AB, Joglekar A, Sayyad MG, Ulvik A, Ueland PM. Hyperhomocysteinemia and elevated methylmalonic acid indicate a high prevalence of cobalamin deficiency in Asian Indians. Am J Clin Nutr. 2001 Aug;74(2):233-41.
6. Sarode R, Garewal G, Marwaha N, Marwaha RK, Varma S, Ghosh K, Mohanty D, Das KC. Pancytopenia in nutritional megaloblastic anaemia. A study from north-west India. Trop Geogr Med. 1989 Oct;41(4):331-6.
8. Halsted JA, Carroll J, Dehghani A, Loghmani M, Prasad A. Serum vitamin B12 concentration in dietary deficiency. Am J Clin Nutr. 1960 May-Jun;8:374-6.
9. Wokes F, Badenoch J, Sinclair HM. Human dietary deficiency of vitamin B12. Am J Clin Nutr. 1955 Sep-Oct;3(5):375-82.