Vitamin nutrition: What do they really need? (Proceedings)
Everyone knows about vitamins, right?
Vitamins through the rumen
Everyone knows about vitamins, right? We need them; we buy them; we feed them; and then our animals become healthy and happy. Well, maybe or maybe not. Our animals are not humans. They're ruminants or alpacas or horses, and their peculiar digestive anatomies mean that we often worry about things that we don't need to worry about, and we may miss things that we should worry about. So let's engage in some straight talk about feeding vitamins to livestock and see where it leads.
From my nutritional perspective, there are three fundamental categories of vitamins — fat-soluble vitamins, water-soluble vitamins, and vitamin C. The practical questions are relatively simple. Should we include these vitamins in diets? If so, when? If not, why not? We'll discuss these categories in reverse order.
Important note: we are talking here primarily about ruminants — sheep, goats, cattle, deer, elk, giraffes, bison, musk-oxen, etc. These all have a rumen, complete with a few zillion rumen microbes that are quite capable of manufacturing certain compounds that the host animal can later absorb into its own blood. We're also talking about those rumen-like animals called camelids — alpacas, llamas, camels, and such — which chew cud and boast a rumen with the said rumen attributes, but do not have cloven-hooves or a fore-stomach compartment called the omasum. Weird, but it works. And we are also talking about horses, which most definitely do not have a rumen. But horses do have a huge large intestine which effectively plays the corresponding role of a rumen — it contains rumen bugs that manufacture useful compounds which the horse can absorb into its bloodstream.
Now to vitamin C. Properly called ascorbic acid, it's the well-known antioxidant found in citrus fruits. It's also the scurvy vitamin, the reason why the British navy inventoried citrus fruits on their sailing ships, why British seamen are forever designated as limeys. But vitamin C is actually a small molecule derived from glucose using the enzyme L-gulonolactone oxidase which most animals possess. Only a few species lack this enzyme — humans, some higher primates, some fruit-eating bats, guinea pigs, and the red-vented bulbul bird. An exquisitely select club to be sure — they all require vitamin C in their diet. But ruminants are not in this club. Ruminants possess this critical enzyme and happily manufacture their own vitamin C. Therefore, we don't need to feed vitamin C to our livestock. Not unless you are trying to raise a herd of chimpanzees.
Next are the water-soluble vitamins. These are the famous B-vitamins. Whoa! — I can almost hear folks exclaim, "you mean B-complex"? Well, without getting too complex, that terminology actually refers to a commercial injection containing a cocktail of many different B-vitamin compounds. There is no single "B-complex" vitamin. The B-vitamins are actually a group of eight unrelated compounds: thiamin, riboflavin, niacin, biotin, folic acid, B6 (also known as pyridoxine), pantothenic acid, and B12. All are soluble in water, and all are needed daily by our livestock.
Here's the good news: rumen microbes can make all these B-vitamins. That is, during the fermentation process, the rumen bacteria synthesize these molecules, which then can be absorbed by the host animal and used for its own metabolism. Which means that, under normal conditions, we don't need to add B-vitamins to ruminant diets. Based on solid research over the past 80 years, we think that a healthy population of rumen microbes make enough B-vitamins to supply the needs of the host sheep or cow or musk-ox. This principle also applies to camelids, and, as far as we know, generally to horses.
With one exception: vitamin B12. This molecule is a bit of a nutritional oddity. Rumen bacteria are actually quite capable of making it, but they need a critical component first. This component is the element cobalt. The formal chemical name for vitamin B12 is cobalamin. The "cobal" indicates that the molecule contains cobalt, which means that the microbes require enough cobalt to manufacture B12. And this is how we meet the requirements for vitamin B12 — we include cobalt in our ruminant trace mineral mixtures to provide it to the rumen microbes. We don't need to add pre-formed B12 to our ruminant diets or TM mixtures. In regions of where plant cobalt levels are low, we can include 40 ppm cobalt or so in our TM mixtures and stop worrying about it. This is not the only nutritional strategy for B12. In some countries, farmers effectively approach this problem by applying cobalt to pastures in their fertilizers or by using slow-release cobalt boluses, but these techniques are not done in North America.
I would add a practical caution — rumen microbes function well when they function well. Any syndrome that impairs rumen function, like acidosis, or any severe stress or disease that reduces feed intake may greatly alter microbial activity and thus reduce B-vitamin synthesis. Also, some toxic plants contain compounds that specifically target certain rumen vitamin pathways, like bracken fern thiaminase which may destroy rumen thiamin before it can be absorbed by the animal. Under normal, steady-state conditions, the rumen cranks out B-vitamins without problem. Under other conditions, all bets are off. Call a nutritionist.
So what's left? The fat-soluble vitamins: A, D, E, and K. These are unrelated to each other, so we'll treat them individually. With one exception, animals can't make them. The exception is — you guessed it — vitamin D. When exposed to ultraviolet light, specialized enzymes in the skin will transform cholesterol into a vitamin D precursor called cholecalciferol. The blood then transports this compound to the liver and kidneys, where it is ultimately converted to the active form of vitamin D called 1,25-dihydroxycholecalciferol. A similar precursor can be found in bleached hay. The bottom line is that if our livestock roam outdoors in the sunlight for a reasonable period each day, they won't suffer from vitamin D deficiency. Of course, some animals don't see much sunlight, like orphan lambs, orphan calves, barn-housed horses, and confined dairy cows. Then we need to add vitamin D to their diets.
What about vitamin K? Usually this is not a problem because vitamin K is common in forages. Also, some rumen microbes can synthesize it in reasonable amounts. Either way, animals usually receive enough vitamin K to satisfy their requirements, so we don't worry about it. Unless our animals consume some really unusual feeds that contain antagonists of vitamin K, like moldy sweetclover hay (Melilotus alba and M. officinalis), certain sulfa drugs, or Warfarin rat poison. But that is a story for another time.
For vitamin E ... well, historically, we thought that vitamin E was used by livestock in ways similar to selenium, and that green forages contained enough vitamin E to satisfy most requirements. But we are learning that we probably underestimated vitamin E requirements, especially for high-producing animals, animals under stress, animals grazing mature forages, and confined animals fed high-grain diets. So now we are increasing the requirements and routinely adding extra vitamin E to some diets and TM mixtures.
Finally, vitamin A. Fresh green forages usually contain lots of vitamin A (really its precursor, the carotenoids). But deficiencies can occur in confined animals or animals grazing bleached, drought-stricken pastures, etc. Also, hay that has been stored for a year or longer probably contains no vitamin A or vitamin E activity. These vitamins oxidize over time and lose their potency, even if the hay remains green. But unlike other vitamins, vitamin A is stored in the liver, and when animals come off an extended period of grazing green pasture, their livers contain 3+ months of vitamin A in reserve. In many cases, this reserve quietly gets them through a deficient period. But if not, we can always make sure that the TM mixture contains vitamin A, and as a last resort, inject livestock with a single megadose of A and D.
Vitamin A, however, is the only vitamin that we need to worry about toxicosis, at least in theory. For example, if a 150 lb ewe requires 3,648 IU of vitamin A, a toxic dose would be more than 409,000 IU. This is generally hard to reach. But ... but ... remember that vitamin A is fat-soluble and accumulated in livers. Well, fish oils and seal livers contain lots of vitamin A. What eats fish and seals? Polar bears. And polar bear livers contain toxic amounts of vitamin A. The Eskimos knew this. They avoided eating those livers. So if your local feedstore advertises a sale price on ground polar bear liver, don't buy it.
History versus today
Let's imagine, for a moment, that we are nutritional scientists conducting research on critical factors in feeds. As researchers, we are particularly interested in something called "Factor X". We don't know much about Factor X — which is why we are working on it — but we do know that animals do not suffer from a Horrid Syndrome when they receive feeds that contain Factor X.
Now, because this is a magazine article and not a scientific laboratory, let's peak under the hood. Unlike the real world, where scientists work in the dark to shed light on their topics, as readers we can access all the information about Factor X. And in the amazingly complex world of biochemical systems, it turns out that Factor X is intimately involved in many metabolic pathways. With our all-knowing reader perspective, we see that Factor X interacts with Pathways A, B, C, D, E and F.
Now let's switch back to our laboratory, where we are just scientists rather than all-knowing readers. As scientists, we are just beginning to get some glimmers about Factor X — that it seems to be an essential dietary factor that prevents the Horrid Syndrome. Finally, after years of painstaking laboratory work, we discover compelling evidence that Factor X is actually involved with Pathway A. After more experimentation, we successfully outline the detailed biochemistry of Pathway A, and now we can see clearly how Factor X influences it. And there's more — we learn that animals will suffer from the Horrid Syndrome when Pathway A doesn't work properly. By adding Factor X to the diet, we can prevent the Horrid Syndrome. Our goal is in sight: we now feverishly direct our research to determine the best dietary levels of Factor X to support Pathway A and prevent the Horrid Syndrome.
After a few years, the scientific community fully accepts Factor X as a required nutrient. Official government documents dutifully list the recommended levels of Factor X that will prevent the Horrid Syndrome. Our laboratory continues its work on Factor X to flesh out the details of its chemistry and structure. The Horrid Syndrome has been conquered. People are overjoyed. We are given worldwide accolades; we receive tenure at a prestigious university; and there is talk of a Nobel Prize.
But in the back of our minds, there is a little nagging voice. What about those other Pathways — B, C, D, E, and F? During the halcyon days of our research, when we were racing to solve the problem of the Horrid Syndrome, we didn't know much about those other pathways, and we had no idea that Factor X was even remotely involved with them. We had concentrated our efforts on the Horrid Syndrome, and preventing it became our overriding goal. Based on this research, the published dietary requirements for Factor X were designed specifically to prevent the Horrid Syndrome.
That little nagging voice returns: What if those other pathways are also critical? What if our dietary recommendations are too low for those pathways, but their deficiency symptoms are more subtle than the Horrid Syndrome? What if we missed something important?
OK, let's leave our quaint little fairy tale. The Horrid Syndrome is just a figment of my overactive imagination. It doesn't really exist.
Or does it?
Let's change the words. For Factor X and the Horrid Syndrome, let's substitute "vitamin D" and "rickets". Or "selenium" and "white muscle disease".
Here is a real-world, non-fairy tale scoop. Rickets was a widespread scourge since the beginning of the industrial revolution in the late 1700s, when people moved from their farms to work in factories in smog-filled cities. By the mid-1800s, doctors had learned that cod liver oil and also sunbathing could prevent rickets, but no one knew why. In the first decades of the 20th century, during the heyday of vitamin discoveries, scientists worked hard to identify the mysterious nutritional factor in cod liver oil with anti-rachitic properties. Anti-rachitic is the scientific term for something that prevents rickets. By the mid-1930s, researchers had discovered two forms of vitamin D: ergocalciferol (D2) and cholecalciferol (D3). By the late 1960s, scientists had worked out the complex metabolic pathway that showed how vitamin D influenced calcium absorption and thus bone health and density. Nutritionists pegged the dietary levels of vitamin D to prevent rickets in children and its analogue in adults, osteomalacia. Similarly, in the livestock world, animal nutritionists set vitamin D requirements to prevent rickets and other calcium-related diseases in livestock. Those dietary requirements have not changed in many years. In fact, the authors of the 2007 NRC reference book on Small Ruminants retained the 1981 vitamin D levels because they couldn't find enough data to justify a change. In other words, what was good enough in 1981 is good enough today.
But recent research in human medicine has overtaken our old knowledge about vitamin D. We've recently learned that vitamin D has a fundamental role in controlling gene expression, which affects such diverse pathways as immune function, inflammatory response, cell growth, and the release of localized antimicrobial compounds in the skin. None of these pathways was understood or even considered when scientists originally worked on the dietary recommendations for vitamin D. Researchers in 1981 did not have our modern technologies to manipulate genes, and they did not know of the existence of thousands of control compounds which we now have characterized in exquisite detail. In human medicine, which may move a tad faster than the livestock industry, the Canadian Cancer Society recently upped its dietary vitamin D recommendations by 150%.
Then there is selenium. For years, our nutritional research was designed to prevent the obvious syndromes of selenium deficiency, such as white muscle disease, exudative diathesis in poultry, and mulberry heart disease in hogs, to name a few. In the U.S. after much regulatory wrangling (because the window between selenium requirements and toxicity is rather narrow, and also because of some 1940s research linking selenium to cancer), federal regulations of 1987 now limit selenium to 0.3 ppm in a total diet for livestock, with similar tight caps in minerals and supplements.
But again, today's scientists have technologies their predecessors never dreamed of twenty years ago. We can now detect things in parts per trillion (that's one millionth of a ppm), and we can manipulate genes and cells in ways that were just science fiction when I was a kid. Recent research has shown that selenium is involved in immune function and possibly cancer prevention. That selenium-based enzymes control thyroid hormone and thus can influence basal metabolic rate. That selenium molecules sequester heavy metals which may influence those toxicities, especially in a contaminated world. But have we recently revised our selenium recommendations for livestock and humans? Are we certain that our current selenium recommendations are sufficient for these functions? Have we carried out extensive nutritional studies to find out? In all cases, the answer is no.
And I've discussed only two nutrients. What about all the other vitamins and minerals?
I suspect that for some of these nutrients, we may be underestimating their true nutritional requirements. We've been spectacularly successful at eliminating their Horrid Syndromes, but what about those B, C, D, E, and F pathways? As we uncover more and more of the total biochemical picture, we may need to adjust our dietary numbers. Yes, it's harder to research subtle metabolic pathways, and it's even harder to quantify nutrient requirements that properly support those pathways. But "harder" does not mean that higher requirements don't exist.
All we need, of course, is a bazillion dollars for research and a centrifuge the size of Kansas. No problem.