We hardly even think about vitamin D anymore. It’s one of those vitamins we routinely add to feeds, an inscrutable listing of international units (IUs) on the feed tag. And as for our children, we simply irradiate the milk.
And really, as a livestock producer, when was the last time you saw a case of rickets? Sure, nutritionists annually warn producers about rickets in animals housed indoors for months, as sometimes occurs with some horses and orphan lambs, but the lack of vitamin D is an anomaly, right? I thought so too, until recently, when I reviewed some new research about this vitamin. I found things that really made me sit up and think.
First, we should cover the basics about vitamin D.
We get this fat-soluble vitamin from two different sources – animals and plants. The animal source is a precursor molecule in skin epidermis called “7-dehydrocholesterol.” Ultraviolet light changes this molecule to “cholecalciferol” (vitamin D3), which is then carried by the bloodstream to the liver.
In plants, a corresponding ultraviolet light process creates a different molecule called “ergocalciferol” (vitamin D2). This compound is ingested in the feed, absorbed through the gut wall and then transported to the liver. In both cases, liver enzymes add a hydroxyl group to form “25-hydroxycholecalciferol” (25D). This 25D molecule then moves to the kidney, where another enzyme transforms it to “1,25-dihydroxycholecalciferol” (1,25D), which is the true active form of the vitamin D. It’s this 1,25D molecule that acts as an on-off switch in cells throughout the body to regulate calcium balance, thus controlling a cascade of calcium-related processes such as calcium absorption from the digestive tract, bone formation, milk production, milk fever and so on.
To continue our classic description, textbooks always list the main deficiency of vitamin D as “rickets” – the bone deformation syndrome of children. Also “osteomalacia,” which is rickets in adults. And also, to some extent, “osteoporosis,” a long-term problem of reduced bone density in older adults. Livestock can experience similar calcium-related bone disorders, as well as an additional syndrome of “milk fever” in cattle, which occurs when the onset of lactation drastically reduces blood calcium levels. A similar disorder in sheep, called “hypocalcemia,” occurs in late pregnancy or early lactation in twin-bearing ewes. All these syndromes, however, are still related to calcium balance.
We measure vitamin D in IUs. One microgram of D3 equals 40 IUs. For humans, the National Institutes of Health (NIH) recommends a daily dose of 400 IUs for adults 51 to 70 years old, slightly higher for elderly adults and slightly lower for younger adults and children. Let’s remember: Vitamin D has always been known as the “anti-rachitic factor,” and the official NIH recommendations are designed to prevent rickets and other bone-related disorders, human or animal.
Livestock producers rely on sunshine to provide D3 to their animals or on sun-cured hay to provide D2, or they simply add D3 to mineral mixtures or other supplements. In the human world, not many foods naturally contain high levels of vitamin D, so we irradiate milk to fortify it with vitamin D, or take pills containing D3, or run around in the sunshine without sunscreen, or drink a tablespoon of cod liver oil every day (ugh). Your grandmother may not have been a biochemist, but she was right about one thing: Cod liver oil really is good for you. It’s one of the few human foods that naturally contains lots of vitamin D3.
Usually, that’s the end of the story. But recent medical research has completely revised our understanding of vitamin D. From my perspective, this compound is far more critical than we ever dreamed. Here are some reasons.
For starters, even though it will always be known as a “vitamin,” vitamin D is really more than a vitamin. Typically, vitamins are small molecules that act as cofactors in larger molecules – vitamins become parts of large proteins like enzymes to make these enzymes work properly and catalyze the same reaction over and over again. For example, vitamin K fits like a jigsaw piece into certain blood-clotting enzymes to assist with their carboxylation reactions. Similarly, vitamin B12 is incorporated into three different enzymes to facilitate the transfer of hydrogen ions or methyl groups.
But vitamin D is a horse of a very different color. Vitamin D is manufactured in one tissue (skin), transported to two other organs for activation (liver and kidney) and then transported to cells all over the body to regulate their actions. Uh, isn’t this exactly the description of a hormone? Yes, vitamin D is indeed a hormone. Its “vitamin” moniker is really just a historical accident. Vitamin D was discovered during the golden age of vitamin advances in the early 20th century. In fact, it was the fourth such molecule found (hence the name “D” – after A, B and C.) To confuse things further, only one B-vitamin (thiamine) had been identified by then.
Upon entering a cell, 1,25D is conveyed to the nucleus, where it combines with a specialized vitamin D receptor (VDR) which then links with another molecule called the retinoid-X receptor (RXR). This vitamin VDR-RXR complex then binds directly to DNA at multiple sites adjacent to various target genes. This act of binding induces the target gene to activate or shut down, depending on the gene. Kind of like a toggle switch.
We now know 1,25D exerts some regulatory control over at least 1,000 different genes. And only a few of these genes are involved in calcium metabolism. The others are involved in some surprising things. For example: Two genes activated by 1,25D code for the production of two small peptides that have powerful antimicrobial action – cathelicidin and defensin-beta-2. In other words, the body can make its own natural antibiotics, which is a very good thing indeed.
Add to this knowledge an extraordinary discovery: Skin cells can create 1,25D from D3 by themselves. In other words, these epidermal cells contain all the necessary enzymes to transform D3 into 1,25D, and thus they avoid the requirement to transport D3 to the liver and kidney first. Why is this important? Current speculation is that such a localized system allows these epidermal cells to respond to a potential infection threat by rapidly increasing the amount of antimicrobial compounds in the skin, which is certainly a useful trait for people trying to stay alive in a fearful microbial world.
Speaking of speculations – tuberculosis (TB) has been a scourge of mankind since the pharaohs. But long before the discovery of antibiotics, doctors knew people suffering from TB seemed to improve when they moved to hot, dry places like Arizona or the Mediterranean. It was the effect of the dry climate, they assumed. But now we have an inkling of a real mechanism for TB control, and it’s related to vitamin D. The higher level of ultraviolet (UV) light in these hot, dry places maximizes the endogenous production of D3, which increases the production of those antimicrobial compounds, which seem to be at least partially effective against the TB bacteria.
Another gene regulated by 1,25D controls the level of cytokines, which are small molecules released by some immune cells during an inflammatory response. The binding of 1,25D to these genes reduces the amount of cytokines secreted by these cells, which seems to reduce the inflammatory response. Here’s the gig: Certain human autoimmune diseases are related to long-term exaggerated inflammatory responses of the immune system. Researchers are currently wondering if 1,25D or its analogues (chemical look-alikes) could be useful in treating or preventing autoimmune diseases like autoimmune diabetes, inflammatory bowel disease and even multiple sclerosis.
And then there is the potential link to cancer – currently a very active field of medical research. Scientists are generating a growing body of evidence that higher doses of vitamin D may reduce the risk of certain types of cancers. A few years ago, the Canadian Cancer Society formally increased its vitamin D recommendations for all adults to 1,000 IU supplementation during the fall and winter months. (Canada’s high latitudes mean it receives only low levels of UV light at that time of year.) This is a complex situation, of course, because exposure to too much sun is clearly a causative factor for some skin cancers.
But how do all these fundamental roles for vitamin D relate to livestock? Well, if we accept the premise that the current vitamin D recommendations for livestock are based only on the avoidance of rickets, then we might consider that we may be missing an entire level of requirements. Who knows what levels of vitamin D are needed for optimal long-term health, not just for avoiding rickets?
Meanwhile, please excuse me. It’s getting near my noon lunchtime. I think I’ll go outside and sit in the sun a while.
Woody Lane is a certified forage and grassland professional with AFGC and teaches forage/grazing and nutrition courses in Oregon. His book, Capturing Sunlight, Book 1: Skills & Ideas for Intensive Grazing, Sustainable Pastures, Healthy Soils, & Grassfed Livestock, is available on Amazon and through his website.
