Is It True That Cows Need Supplemental Vitamin B12?

But how truthful is this claim? Is it completely false, or is there some element of truth to it? 

There’s only one way to find out!

If one were to ask whether cows need Vitamin B12 at all and deliberately leave out the word “supplement” from the question, the very easy and short answer would be yes, they sure do. Now, let me get into the longer answer.

Vitamin B12, as a water-soluble vitamin, is important for metabolizing nucleic acids as well as fats and carbohydrates. Primarily it plays a role in purine and pyrimidine synthesis, transfer of methyl groups, and protein formation from amino acids. Other general functions of B12 are in the promotion of red blood cell synthesis and in maintaining the integrity of the nervous system. Vitamin B12 also helps in the synthesis and formation of methionine, one of the essential amino acids, as an important cofactor. Plus, the vitamin contributes to the normal formation and utilization of folic acid (vitamin B9). Vitamin B12 is stored in the liver where it’s slowly released and used by the body, being continually replenished, over time.

This vitamin is produced in the presence of the mineral element Cobalt (Co). They are basically synergistic: one cannot exist without the other. Any deficiencies that occur as a result of vitamin B12 (also called cobalamin) insufficiencies in the diet are only secondary to a more serious cobalt deficiency. In other words, while deficiency symptoms of cobalamin and cobalt are the same, a deficiency in cobalamin is a direct result of a deficiency in cobalt; never vice versa. 

Therefore, where cows need vitamin B12 is where they need cobalt. There is a notable exception to this rule where vitamin B12 alone can show deficiencies in livestock, as I will explain below. 

Cobalt is required in a ruminant’s diet for the synthesis of cobalamin. This mineral is an important part of the structure and properties of cobalamin, plus it’s the primary mineral that aids rumen microorganisms–largely bacteria–in synthesizing cobalamin, as well as their growth.

As a result, rumen microbes rely on a dietary source of cobalt so that they can basically “make” Vitamin B12 for the cow. This is a much different case for most non-ruminants (or monogastrics) where cobalt is of much less importance for their dietary needs than cobalamin, as I’ll show you soon.

Rumen microbes rely on something called the “intrinsic factor“, a glycoprotein that is derived from the degradation of non-protein nitrogen sources (such as urea or ammonia) or other proteins, so that cobalamin can be absorbed. Without the intrinsic factor, ruminants can experience vitamin B12 deficiency. Most cobalamin absorption occurs in the first part of the bovine small intestine (the duodenum).

The presence of a lot of Co in the diet can cause rumen microbes to create more vitamin B12 analogs than cobalamin, the former of which are utterly useless to the bovine. Cobalamin is the only molecule that has the biological activity necessary for absorption, out of several other analogs that rumen microbes are capable of synthesizing.

Therefore, cobalt is the very reason why ruminants don’t normally need a dietary (nor supplemental) source of vitamin B12.

Who said that B12 and Cobalt serve different purposes? As already mentioned, cobalt is required by ruminants for the production of B12. If a ruminant is denied sufficient Co, then she will also be denied her equally necessary B12.

Unfortunately, cattle–as is the case with most ruminants–are not the most efficient users of cobalt:

• On average, between 3 to 13% of dietary cobalt is converted into cobalamin;
• Only 1 to 3% of the vitamin B12 synthesized in the rumen is absorbed in the small intestine.

Fortunately, though, most cobalt gets recycled back into the rumen to be caught by rumen microbes to make more vitamin B12 for the ruminant bovine. 

​One thing that is inarguable is that no ruminant can make its own vitamin B12: all ruminants need microbes in their rumens to synthesize cobalamin for them. As a matter of fact, no living organism in the taxonomic Kingdom Animalia is capable of synthesizing cobalamin.

If an animal doesn’t have their own special workforce to synthesize cobalamin for them (as is the case with all ruminants, as well as pseudo-ruminants and hind-gut fermentors like horses, zebras, and donkeys), then it must be supplied directly in their diet. This is true for all other animals, from birds to pigs, from frogs to humans.

For most of these animals, consuming other animals is the primary way of getting sufficient cobalamin. Animals that are largely herbivorous but still classify as non-ruminants rely on another method of getting sufficient vitamin B12 that they cannot get from their plant-centric diet, which is coprophagia or eating their own poop. Lagomorphs (those in the rabbit family), most rodents, and to a lesser extent nonhuman great apes like gorillas and chimpanzees, all engage in coprophagy which helps them get essential nutrients they couldn’t get with the rest of their diet. Certainly, with these species, the vitamin B12-synthesizing microbes live too far down their digestive tract for these animals to be able to absorb cobalamin without having to resort to coprophagia (Soave & Brand, 1991).

There’s a fourth “supporting argument” that goes along with that quote above which states that vitamin B12 comes from bacteria in the soil. A proceeding argument to that, which I’ll cover later when I get to talking about supplementation, is that cows somehow get such bacteria in their stomachs by eating the dirt as they graze… or something to that effect.

Undoubtedly, the former supporting argument is most certainly not wrong. There are innumerable types and species of bacteria that live in the soil, several of which do indeed synthesize cobalamin from the minute quantities of mineral cobalt found in the soil profiles. Scientists still aren’t exactly sure why such bacteria produce vitamin B12 when it’s exceedingly rare for plants or fungi (as in the fungal fruiting bodies which are mushrooms) to use, let alone require, such a vitamin; the best term that’s used for vitamin B12-producing bacteria that are found with such plants and fungi is concomitant–naturally accompanying or associated with. However, according to some recent findings by MIT biologists as reported by Trafton (2007), they suspect that:

Livestock that are Co-deficient show signs of loss of appetite, reduced growth, loss in weight, and eventually anemia, emaciation, and death. The same symptoms show up with a cobalamin deficiency.

Cobalt deficiency will undeniably lead to a B12 deficiency. For adult ruminants, B12 deficiency almost always runs secondary to a cobalt deficiency, with a notable exception, which I’ll discuss soon.

Cobalt deficiency in cattle happens primarily due to the soil. No, that doesn’t mean that cattle aren’t eating enough dirt to get their cobalt needs met, as I’ll discuss soon; instead, it has far more to do with the cobalt mineral levels in the very plants that cattle eat. 

Different species of plants take up different mineral levels from the soil. Cobalt, for instance, is taken up the greatest by legumes such as alfalfa (Medicago sativa) and clover (Trifolium spp.), and much less by grasses. Legume forages tend to take up twice the amount of cobalt than grasses, particularly in locations where cobalt is abundant. But it’s a different story in locations where cobalt is commonly deficient: legumes and grasses bear the same amounts as each other. 

Cattle and sheep need between 0.07 to 0.015 mg/kg of Co in their diet per day to be healthy. Any forage that contains less than 0.04 to 0.07 mg/kg of cobalt is a cause for concern. Any forage that runs at or below those numbers means that ruminants need to be supplemented with cobalt. More on that later. 

The location most certainly does play a big impact on whether a domesticated ruminant, localized by fences in addition to the concept of ownership and neighbourly trusts, can get enough cobalt in their forage or not. Areas that are known for their cobalt-deficient soils include Western Canada, parts of Australia, New Zealand, Brazil, Norway, and parts of the eastern United States (such as Wisconsin, Michigan, Massachusetts, Pennsylvania, New Hampshire, New York, and even Florida). 

You’re probably wondering this very question: Even if cows have enough cobalt in their diet, can they still run into B12 deficiency problems and if so, how? 

The answer to that is no.

Dietary cobalt is still the top deciding factor in whether livestock are able to get enough vitamin B12 or not. There has been a lot of studies done on this, and all of them have found that as long as cattle were getting enough cobalt–or rather, having their dietary cobalt requirement met–in their diet, regardless of what they were being fed, their rumen microbes were able to synthesize enough cobalamin to meet that animal’s needs. 

I’ve put emphasis on the, “what [livestock] were being fed,” because of what some people have “observed” based on simplistic differences of being forage-fed versus grain-fed. Such people have made the assertion that grain-fed livestock was more likely to get B12-deficient because such a diet, “would make animals have a lower rate of B12 production.”

In other words, there is a belief out there that grain-fed cattle are not producing enough vitamin B12 in their rumen regardless if they’re getting sufficient cobalt in their diet. I’m getting ahead of myself when I begin to mention that this very argument is an attempt to support the reason why vitamin B12 is regularly supplemented to livestock that are kept on a high-concentrate diet. As I’ve said before, more on that in a bit. 

The thing is, such a statement is only based on speculation, not facts. However, it is partly correct. 

Studies have shown that high-concentrate diets do certainly reduce the amount of cobalamin that gets synthesized in the rumen. However, this reduction is caused by several factors; not this super-oversimplified notion that being grain-fed is solely to blame for reduced ruminal cobalamin production.

Two major factors that I’ve found have a lot to do with an increased requirement for cobalt than “usual” for forage-fed livestock; the first factor is purely environmental, where conditions such as heavy rains, soil conditions (which can be influenced by fertilizer applications such as lime which will decrease Co availability in the pasture stand), stage of maturity of the forage plants, plant species (as discussed above), and climate can reduce forage-cobalt concentration and availability to the grazing animal. Secondly, forage diets encourage higher production of B12 analogs that are often antagonistic to the kind of cobalamin that the animal needs. However, with all the research that I’ve been digging through and books I’ve been reading, all of them clearly state that it’s not so much the analogs that are the problem but rather the question of whether these animals are getting enough cobalt in their diet. Period, end of story. 

Therefore, cattle that become B12-deficient aren’t just B12-deficient because their rumens aren’t synthesizing enough vitamin B12! No, it’s primarily because those animals are receiving insufficient amounts of cobalt in their diet. (Or, as I’ll discuss below, certain conditions create stores of vitamin B12 to be used up quicker than what’s normally used.) As I’ve mentioned above, the cobalt content of the diet is the primary limiting factor for ruminal microbial synthesis of vitamin B12 (NASEM, 2016).

But what about this notable exception that I hinted at above? Well, it’s about these baby calves… 

Here’s something that you may not know: Ruminants are not born with a fully-formed reticulorumen. Instead, they are born with the same digestive system as a typical non-ruminant. The rumen in a newborn calf and lamb is barely the size of a pea, whereas the abomasum (their true stomach) is as big and fully functional as any dog’s or human’s stomach. The rumen (as well as the reticulum and omasum) becomes fully formed by the time the calf is three months (12 weeks) old, and when a lamb is around two months (50 to 60 days) old.

As such, just like with most any non-ruminant (except those coprophagic animals I mentioned above), baby calves and baby lambs (any newborn ruminant animal, from bison to deer) need to get their vitamin B12 directly from a source that already has enough vitamin B12 in it. Feeding them cobalt only will cause them to get B12-deficient. Their dietary need for cobalt doesn’t matter until their rumen is nearly mature.

So, where do baby calves and baby lambs get their vitamin B12? They get it directly from their mother’s milk. Milk is an excellent source of vitamin B12. If these young animals can’t get their own mother’s milk as a B12 source, then there must be enough B12 supplied in the milk replacer formula. Either way, vitamin B12 for these young animals needs to come from an animal protein source.

But what happens when they get B12 deficient? That’s where they need a direct source of vitamin B12. If the situation is dire, an injection of Vitamin B12 is sure to help reverse the symptoms of a life-threatening deficiency than feeding it to an animal that simply won’t eat (since loss of appetite is a symptom of B12-deficiency).

Speaking of supplementing livestock… 

For adult ruminants, the answer is very simple: A blue salt block.

I told you there was a reason I added that photo above! 

This blue salt block is sold at most farm supply stores that are situated in well-known cobalt-deficient areas of the world, such as where I live and grew up (in Western Canada). 

This blue block is basically an iodized cobalt salt block. That’s right: it contains trace minerals Iodine, Cobalt, and Salt (NaCl). 

If you’re someone who’s not so worried about feeding other important trace minerals (such as Iron, Manganese, Zinc, Copper, Selenium, and Molybdenum), then simply throwing out a blue salt block is all that needs to be done to supplement cattle and sheep so that their rumen microbes can make enough vitamin B12. 

I’ve heard this argument expressed far too much. Here’s the original quote for this claim:

I’ll first admit that this quote just irked me for some reason… Hmm, wonder why. I’ve got a few more things to say about the source and where this came from, but not here; later.

This particular quote, and hence the often-reiterated arguments that try to undermine the fact that ruminants are very capable of not relying on much in the way of outside sources of Vitamin B12 like we are, is one of the reasons I wrote this blog post in the first place.

I’ll be extremely blunt here: That quote is not truthful. As you all can already see, I’ve done an extensive amount of research in writing about this topic and have supplied numerous references to back up what I’ve been discussing here. It has also helped me a great deal to have the practical knowledge and experience of watching how cattle and “other grass-eating animals” graze, how pasture management works, among many other things.

With that, the author of this quote is making a dangerously erroneous–not to mention asinine–assumption that all pastures are severely overgrazed with so much bare soil in between plants, and grasses so poorly anchored in the soil that they’re easily pulled up by grazing herbivores, that it’s not even funny. 

Such an “observation” couldn’t be further from the truth. In my experience and travels, it’s very, very rare to find such pasture conditions; the only exception I can think of is in areas of arid environments where land is severely understocked–or rested for far too long–and livestock are poorly managed such that they are allowed to overgraze and be far too spread out to have any kind of necessary trampling, hoof-impact on the dead plant material that is not breaking down.

Most pastures, at least those that I’ve seen in my travels, have more than enough plant material–both dead and living–covering the soil surface and thereby prevent much in the way of opportunity for cattle to eat any soil. But this is on cattle pastures. Sheep and horse pastures can be even more severely-overgrazed where plants are literally chomped right down to the soil with their roots exposed. 

As you can rightly guess, overgrazing is a sign of a management problem, no matter what kind of livestock we’re talking about.

It’s rather laughable to even think that it’s a common occurrence for cattle to pull up plants by the roots as they graze! Honestly, they’re not pigs. Pasture plants are more-often-than-not so well-rooted and well-anchored that a grazing cow or sheep or horse is incapable of pulling them up: a good thing because I’ve yet to meet a cow, horse, or sheep, or goat, who likes to eat a plant, roots and all.

Do you want to know what’s better than a sheep, cow, or horse at pulling up plants? I do: it’s a plow.

The only time I have seen cattle “deliberately” (more like accidentally as they never intended to do it; they just wanna eat) pulling up plants when trying to graze is when those plants were very shallow-rooted annuals trying to make a go of it in some very bare-soil feedlot; or some quackgrass was doing its best to spread out its shallow rhizomes in some seemingly prime-opportunity real estate, minus the cattle. These “grass-eating animals” are just interested in eating the green stuff; I’ve seen them almost-violently bob their heads up and down when they bring up a clump with their mouths, just so that they can sever the green leaves away from the bottom half of the plant and eat those instead. They don’t give a damn about the roots, let alone the soil attached. Again, they’re not pigs!

Regardless, and in following the “logic” of the quote above, if cattle aren’t able to eat the soil between plants, how do they get their B12 and how do they get the bacteria in the rumen to get B12?

If you were paying attention, I’ve already mentioned above that cattle don’t need direct sources of vitamin B12. All they need is enough cobalt in their diet. I also have already discussed that cattle can readily get enough cobalt in their diet just by eating plants (as in, obviously, the leaves and stems, not the roots). Plants are more than capable of uptaking minerals into their cells, which then gets consumed by the herbivore. Ruminants grazing in cobalt-sufficient areas will get plenty of cobalt on pastures with a plant species mixture that contains both grasses and legumes like clovers or alfalfa.

And about those areas where the soil doesn’t provide enough cobalt to be uptaken by the plants that the animals eat? As mentioned, a salt block that contains cobalt solves that problem. Simple.

Secondly, cattle don’t need to eat soil to get–and keep–bacteria in their rumens. They would have gotten such necessary bacteria when they were young–just when their rumen was reaching maturity–from a variety of sources; their diet that they’ve maintained throughout their entire life has supported the continued existence of such bacteria in their gut. (Guess what, bacteria can also be found on the surfaces of leaves… gosh, who knew!)

Whoever came up with the idea that cows need to eat dirt to get bacteria into their gut needs to give their head a shake and go do some reading!

Therefore, NO, pastured cattle do NOT need to eat dirt to get their vitamin B12 (or cobalt).

This brings me to a question about cases where cattle do and will eat soil.

Soil-eating is just one symptom of a mineral deficiency disorder called pica. Cattle with pica will also chew on bones, chew on wood, drink urine, eat other small animals (if they’re that desperate), and try to eat other foreign objects they normally wouldn’t eat. Cattle are not the only ones who can get pica–most all other animals that feel so form of mineral deficiency craving that isn’t met by their normal diet may get it. Animals with pica are often deficient in phosphorus, sodium, cobalt, copper, even magnesium, calcium, and iodine. Pica can also be a sign that animals aren’t getting enough fibre in their diet, or there is a more serious underlying problem like a brain disorder (Rogers, 2001). Pica can also be a behavioural problem, particularly in intensively confined animals. 

​No doubt there are exceptions, and yet another outstanding myth (or two) to bust that comes of this, so let’s get to that next, shall we?

​With deficient cattle, a direct administration of vitamin B12 is given and acts a lot faster to reverse B12-deficiency symptoms than feeding cobalt-mineral. One study mentioned in the DSM article referenced below showed that there was a rapid, overnight improvement in appetite in cobalt-deficient animals. Oral dosing (which typically means the animal has a tube put down its throat so that the important mineral it was lacking can be given to an animal that otherwise wasn’t interested in eating) of cobalt showed that it took seven to 10 days for animals to finally gain a healthy interest in eating again. This may not be the case with sheep, however; oral dosing or direct administration with a needle has found to be equal in righting cobalt deficiencies. 

Therefore, simply increasing the amount of cobalt in a cobalt-deficient bovine’s diet doesn’t cut the mustard because such a form of supplementation acts much too slowly for the animal to get right back on track to start healing itself again. 

Vitamin B12 is “supplemented” to these animals in the form of an injectable. This injectable is injected into the muscle (intramuscular or IM) where it can be quickly taken up in the tissues, and done so once a week until the animals are recommended by a veterinarian to not need them again, particularly when cobalt is already being added to the diet at a rate that an animal needs to remain healthy.

​Vitamin B12 can certainly be fed to cattle, but it’s not the wisest thing to do. Cyanocobalamin, the most common, readily available and stable form of artificial vitamin B12, tends to get largely and extensively destroyed by the rumen microbes so that very little of it, if any, gets utilized in a cow’s body beyond the rumen. This logically makes dietary cobalt the most logical (not to mention cheapest) form to supply cattle as a form of cobalamin supplementation… once again, IF the animals are raised in an area that is well known to have cobalt-deficient soils!

As a result, such people are apt to conclude that, because of this, cows in CAFOs supposedly no longer have the necessary bacteria in their gut to produce cobalamin for them, they become far more reliant on a direct source of vitamin B12 which must be included in the feed ration.

Unfortunately, there is no scientific nor practical, realistic evidence that supports this theory. I have never heard of, nor can see any clear context of how and why confined animal feeding operations would purposefully feed such powerful antibiotics to livestock to the point where rumen microbes become that compromised. It makes no economic sense to perform such practices. 

The only time medically-important antibiotics would be used is if animals are clearly ill from a clearly-diagnosed bacterial infection. Feeding them would not only be counterproductive as they would get destroyed by rumen microbes–and destroy important microbes in the process–but also impractical as their effectiveness for treatment would be moot. That’s why all such antibiotics are injected via needle and syringe under the skin or into the muscle.

That doesn’t mean that all antibiotics aren’t fed, because there certainly are. However, these are not the type of antibiotics most of us are familiar with. In fact, these are antibiotics that aren’t of any importance in human medicine. These are primarily ionophores.

You see, such an aforementioned theory can only make sense if you’re not aware of what ionophores are. But after you understand what ionophores are and do, then maybe you can better understand how such a theory falls flat on its face.

Ionophores are a “special” type of antibiotic that selects certain types of rumen bacteria that help with improving feed efficiency, particularly in finishing cattle. It also selects strongly against other types of rumen microbes so that the other types that are selected for, due to the action of this feed additive, can proliferate in greater numbers. Ionophores such as monensin sodium (Rumensin®) or lasalocid sodium (Bovatech®) aren’t broad-spectrum bacteria-killers like some medically-associated antibiotics can be, if given at high-enough doses.

Do ionophores select against B12-synthesizing bacteria? I haven’t found any evidence that confirms nor negates this, so I’m not at liberty nor am I qualified to even say whether it does or not.

However, there’s another interesting piece of information to ponder. Ionophores, in their strong selection towards certain bacteria, also select for one of three major products of rumen fermentation, namely volatile fatty acids (VFA), with the main VFA selected for being propionate over acetate and butyrate. Some research has found that high levels of propionate (also called propionic acid) have been shown to induce vitamin B12/cobalt deficiency. The mode of action and biochemistry of how that happens is a bit too complicated to share here; my apologies.

Still, that doesn’t quite answer the question of whether ionophores select against B12-synthesizing bacteria. At this point, it may be safe to assume that they do, but in an entirely different way than we might expect. I hope more research is done in the future in this area to answer this question.

Therefore, it’s plausible that the use of ionophores may have a to play in not directly supplementing cattle vitamin B12, but rather in their “higher-than-normal” dietary cobalt requirement to stave off deficiency risk. However, it’s highly unlikely that antibiotics themselves are to blame for having to supplement vitamin B12 to cattle. 

Chalk it up to far too many misconceptions flying around, and an inability to fully understand the gravity (and complexity) of bovine nutrition and ruminant digestive physiology. Unfortunately, many will point fingers at such information that I’ve provided and denounce it as “meat industry propaganda” or “meat industry lies and cover-ups,” creating a whole rather amusingly trivial conspiracy theory that is only a sad attempt at justifying their unwillingness to learn from the true experts out there. Instead, they’d rather find out from heavily biased anti-farming, anti-livestock sources to confirm their bias, and use those as their “proof” that they, how should I put it, “did their own research.”

I digress. However, this largely explains why there is this prevailing belief that all livestock are supplemented–you may see it called being “fortified”–with B12 prior to slaughter so that the “evil meat industry” can claim that meat is a natural source of vitamin B12. (Except that meat is a perfectly natural source of vitamin B12; as we all know, there are mountains and decades of evidence and research that supports this undeniable fact.)

My primary suspicion, though, is that an article posted in the Baltimore Post-Examiner by this Dr. Jennifer Rooke back in 2013 is primarily to blame. Many anti-meat critics have unquestionably used this article as their “source” for supporting their claim that most all livestock are supplemented with vitamin B12. Or rather, as Dr. Rooke put it, that (bolding is mine):

This is the same source that claimed that heavy antibiotic use in livestock is responsible for killing gut bacteria in farm animals.

It’s also the same source that tells that, “pesticides often kill B12 producing bacteria and insects in soil.” Again, where is the evidence that supports this claim? I don’t think I have to do any Googling to find out that there is none. Quite frankly, we still don’t know fully how pesticides affect other living organisms, including bacteria. Pesticides have been created with a mode of action that directly kills targeted weeds, insects, and certain types of fungi. We do know that pesticides also indirectly and unintentionally kill other living organisms. But the fact that these chemicals directly or “often kill” soil-borne B12-producing bacteria? Where’s the proof??

Again, I digress.

I believe another reason–without ripping Rooke’s “informative” article to shreds even more–that people may believe that vitamin B12 is fed to livestock is in the wording: Livestock.

“Livestock” is usually referring to cattle, but I think there’s some serious confusion about the term because it’s often also used to encapsulate other farm animals like pigs and domestic fowl (chickens).

Here’s the thing: If we looked at the production of pigs and chickens only on CAFOs, we can now clearly see how such a statement that Rooke mentioned may in fact be true. Pigs and chickens must get vitamin B12 directly supplemented in their diets because they don’t have the same kind of digestive tract that a cow does to convert cobalt into cobalamin. Instead, these porcine and avian monogastrics must get their vitamin B12 from dietary sources, such as animal products; if they are not supplied sufficient animal products in their diet, then B12 must also be supplemented in their diet. 

A third and final reason for the misconception is the inherent misunderstanding of feeding vitamins by and large to ruminants in a confined feeding situation, no matter if this is in a feedlot where a bunch of steers are being finished, in a typical confinement dairy operation, or in a drylot where a beef cow herd is being overwintered on stored feed. When the urbanized meat-questioning Average Jane gets wind of cattle needing to be fed vitamins in their feed, her mind may automatically make her assume that these animals are being fed vitamin B12 supplements. I can’t blame her for being ignorant, but if she turns that thought into a belief, that’s where she can get herself into hot water.

The fact is, these vitamin supplements that cattle are receiving in their diet while being housed in the barn or on a dirt lot do not include vitamin B12. These vitamin supplements are vitamins A and E. Vitamin A and E are important nutrients that are commonly found in green, fresh forage. However, they denature and become completely inaccessible to the animal when that fresh green forage dries in the sun and is baled up as hay, or when it is put into an anaerobic environment where it ferments and becomes silage. Vitamin A is important for vision and bone, plus reproduction. Vitamin E is closely tied with the mineral Selenium, both which are important for muscle development. Vitamin A especially is important to include as an artificial supplement to cattle that are on stored-feed diets. Grazing animals, however, do not need such a supplement.

So, Is it True that Cows need Supplemental Vitamin B12?

Where do ruminants get enough cobalt? It’s not by eating dirt, that’s just ridiculous. Ruminants get it by eating plants. Plants uptake a lot of nutrients into their cells including minerals such as cobalt. When plants get eaten by the cow, they get broken down by the rumen microbes, which then take the nutrients for themselves and fermentation byproducts for the cow to use. The cobalt “found” in the plant tissues is used by rumen bacteria to produce cobalamin (vitamin B12).

What if plants don’t have enough cobalt? That’s much to do with location. Thus, if a ruminant is raised in a location where cobalt is deficient in the soil, then they need to rely on a dietary source of cobalt, such as the classic blue salt block.

There are only two exceptions where cobalt is not enough and vitamin B12 must be given directly: One is when a bovine is very young: less than three months of age. Young calves do not have a fully functional rumen until that age, so they need a dietary source of B12 instead. If they cannot get it from their mother’s milk, and if the feed and milk replacer isn’t enough either, then supplementary B12 is required to prevent deficiency. The second exception is when a bovine is apparently very sick from either a gut disorder that may have wreaked havoc on their rumen microbial communities (like what acidosis can do) or are suffering from serious cobalt/B12 deficiency; in such a case a “booster shot” of vitamin B12 is necessary to set that animal in order. Injection works much quicker than if the animal were simply given a higher amount of cobalt mineral in their diet.

Otherwise, healthy ruminants–even those who are raised on “factory farms” (or rather, CAFOs)–only require cobalt mineral in order to get their vitamin B12, and in order to thrive. The presumption that cows need B12 supplements is based on misinformation and may I say serious confusion in the difference between the digestive system of a pig (or human) versus a cow. There’s a very good reason why cows are hailed as the prized grass-eating herbivores of the farming world, and pigs are not! 

DSM. Vitamin B12 – Ruminants – Compendium. DSM in Animal Nutrition & Health. https://www.dsm.com/anh/en_US/products/vitamins/vitamin-nutrition-compendium/ruminants/vitamin-b12.html

Ensminger, M.E. & C.E. Olentine Jr. 1978. Feeds & Nutrition-Complete, First Edition. Clovis, CA. The Ensminger Publishing Company

National Academies of Sciences, Engineering, and Medicine. 2016. Nutrient Requirements for Beef Cattle, Eighth Revised Edition. Washington, DC: The National Academies Press, doi: 10.17226/19014

National Academy of Sciences. 2001. Nutrient Requirements of Dairy Cattle, Seventh Revised Edition. Washington, DC: National Academy Press, ISBN 0-309-06997-1

Minson, D.J. 1990. Forage in Ruminant Nutrition. San Diego, CA: Academic Press Inc., ISBM 0-12-498310-3

Reddit r/Vegan Discussion. 2018 February. RE: “The B12 in meat is from supplements given to the cows….so why not just take the supplement directly” Link HERE. 

Soave, O. & C.D. Brand. 1991. Coprophagy in animals: a review. Cornell Veterinarian, 81:357-364.  
https://www.ncbi.nlm.nih.gov/pubmed/1954740 

Rogers, P. 2001. Pica (depraved appetite) & Slurry/Urine drinking in Cattle. Grange Research Centre, Dunsany, Ireland. http://homepage.eircom.net/~progers/picaurin.htm 

Rooke, J. 2013 October. Do Carnivores need Vitamin B12 Supplements? Baltimore Post-Examiner. 
https://baltimorepostexaminer.com/carnivores-need-vitamin-b12-supplements/2013/10/30

Trafton, A. 2007 March. MIT biologists solve vitamin puzzle. MIT News, Massachusetts Institute of Technology. http://news.mit.edu/2007/b12  

Watanabe, F. & T. Bito. 2017. Vitamin B12 sources and microbial interaction. Experimental Biology & Medicine, 243(2): 148-158. doi: 10.1177/1535370217746612