It's widely recognized that vitamin D plays an important role in bone health. Dogs, cats and humans normally acquire their vitamin D through dietary sources. Humans can also synthesize vitamin D with skin exposure to ultraviolet light (sunlight).

In addition to bone health, the role of vitamin D in the preservation of cellular health is well established in humans. Vitamin D is present in many different cells, tissues, and organs such as cardiac cells, immune cells, vascular smooth muscle, and the intestinal cells. Because vitamin D is involved in so many cellular (and genetic) functions, an insufficient level is associated with a variety of diseases including: cardiovascular disease, diabetes, cancer, infectious disease, gastrointestinal disease, and skeletal disease, among other disorders.

Similar to human research, veterinary studies have reported that dogs with insufficient vitamin D are at risk for cardiac and inflammatory bowel disease as well as cancer, and they remain at risk for these diseases for a period of up to 12 months after beginning vitamin D supplementation.

Chronic intestinal disease

Weight loss, vomiting, and diarrhea over the course several weeks with no obvious cause can indicate possible chronic intestinal disease, also known as chronic enteropathy (CE). There are many conditions that fall under the category of chronic enteropathy including:

  • Inflammatory bowel disease
  • Food allergy or intolerance
  • Exocrine pancreatic insufficiency (EPI)
  • Chronic GI parasitism (e.g. Giardia)
  • Bacterial overgrowth  (SIBO)
  • Lymphangiectasia
  • Others

A correlation of vitamin D deficiency with inflammatory bowel disease is well established in humans, and reports confirming a link between vitamin D deficiency in dogs with CE are accumulating. The onset of intestinal inflammation during vitamin D deficiency and alleviation with supplementation is one supportive example.

Other factors associated with the link between vitamin D deficiency and CE include a loss of protein (albumin) through the intestines; the presence of vitamin D receptors on many immune cell types; and the connection between sufficient vitamin D and maintenance of normal intestinal bacteria (GI flora).

Cancer

As mentioned, many cell types have vitamin D receptors and a lack of vitamin D can impair their function. A wealth of data support the connection between low serum vitamin D levels and an increased risk for various cancers in humans, and similar evidence is beginning to accumulate for animals. For example, a laboratory study in mice found that insufficient vitamin D was associated with increased risk for cancer. A recent study of skin mast cell tumors (MCTs), which are most frequently seen in older dogs, particularly Labrador retrievers, found that low levels of vitamin D are associated with MCTs. A study of 335 dogs with cancer found that those with cancer (benign and malignant) had lower levels of vitamin D; a relationship further supported by another study in dogs with tumors in the spleen.

Vitamin D Toxicity 

Vitamin D toxicity (hypervitaminosis D) is much more common than deficiency. Since it is a fat soluble vitamin, excess amounts are stored in the liver and fatty tissues of the body. Rodent poison containing vitamin D3 is often implicated in vitamin D toxicity (as it causes hypercalcemia) in dogs, and is toxic at lower doses when consumed in a bait. An excess of calcium (hypercalcemia) is toxic to all tissues, but its effects are most pronounced in the kidneys, nervous system, and cardiovascular system and can be life-threatening. Oversupplementation of vitamin D during drug treatment of diseases (eg, hypoparathyroidism) or through ingestion of certain plants, antipsoriasis creams, or excessive amounts of vitamin pills / injections can also result in toxicity. If you suspect an overdosage or exposure to excessive amounts of vitamin D contact your veterinarian or pet emergency clinic immediately. Also consult your veterinarian before beginning any vitamin or herbal supplementation regimen in your dog.

In the first study of its kind, researchers determined the range of vitamin D sufficiency in dogs is achieved at blood levels measuring 100 ng/mL and, although not yet validated, suggested that vitamin D toxicity likely occurs at blood levels above 150 ng/mL. They recommended a target range of 100-120 ng/mL for vitamin D sufficiency in dogs, and encouraged further study.

The Future

In spite of what we have learned regarding vitamin D levels and the association with various diseases, it remains unknown as to whether low vitamin D is always causal or the result of the disease. For example, in the case of rats, it is known that restricting vitamin D leads to the development of chronic enteropathy, however low vitamin D levels can also develop due to impaired or poor absorption from diseased intestines. Future studies are needed to further examine the cause and effect of hypovitaminosis D in various diseases.

Based on what we know from research today, it seems appropriate for blood vitamin D levels to be monitored in dogs with chronic enteropathy, and supplementation should be considered in patients with low blood levels. When supplementing a patient with medication to manage low vitamin D levels, periodic monitoring is recommended to measure vitamin D and blood calcium levels - so that dosing patients can be adjusted to avoid toxicity.

Veterinary professionals learn more: Vitamin D Status in Dogs with Chronic Enteropathy and Vitamin D in Healthy Dogs and Dogs with Cancer

 

References

Husbands B. Low stores of 25-hydroxyvitamin D levels and its association with cancer in dogs. VCS presentation, 2013

Merck Veterinary Manual. Hypercalcemia in Dogs and Cats.

Selting KA, Sharp CR, Ringold R, Thamm DH, Backus R. Serum 25-hydroxyvitamin D concentrations in dogs - correlation with health and cancer risk. Vet Comp Oncol. 2014 Jul 8. doi: 10.1111/vco.12101. [Epub ahead of print]

Titmarsh H, Gow AG, Kilpatrick S, et al. Association of vitamin D status and clinical outcome in dogs with a chronic enteropathy. J Vet Intern Med. 2015;29(6):1473-1478.