Vitamin D Nutrition in the Rabbit

New research is challenging long-held assumptions about vitamin D nutrition in rabbits and the safety of current supplementation practices. This paper explores the evidence and highlights important questions that remain unanswered.

Calcinosis risk defines upper limits, and practical implications for sun-cured hay-based diets.

Abstract

Vitamin D nutrition is generally assumed to be well understood. However, current vitamin D levels included in leading brands of pet rabbit food (800 to 1,000 IU/kg) put rabbits at plausible risk of calcifying soft tissues (calcinosis), including the aorta of the heart. Yet recent research assessing the requirements for dietary vitamin D in pet rabbits is not considering the risk of calcinosis or the unnecessary addition of animal sourced vitamin D3 in hay-containing formulas that already provide hay-based vitamin D.

Outline:

1. Introduction to Vitamin D Nutrition

2. Calcinosis Risk - The Upper Limit

3. Deficiency Risk - How Much Vitamin D do Rabbits Need?

4. Vitamin D2 or D3, What’s the Difference?

5. Closing Statements and Next Steps

Introduction to Vitamin D Nutrition

While most mammals require vitamin D for active calcium absorption, rabbits can absorb a substantial proportion of dietary calcium passively, so circulating calcium tends to track dietary calcium intake more than in many other mammals [1]. Vitamin D (calcitriol) and parathyroid hormone (PTH) still participate in mineral homeostasis, particularly phosphate absorption and renal handling of calcium and phosphate [2, 3]. When vitamin D is not detectable in the blood due to a deficient diet, and combined with low dietary phosphorus, it can result in rickets [4]. If phosphorus is adequate, increased PTH compensates for vitamin D deficiency in some rabbits, while others can still partially show histologic signs of bone disease [5].

Calcinosis Risk – The Upper Limit

The circulating availability of the active form of vitamin D (1,25-dihydroxyvitamin D; calcitriol) is tightly regulated. Enzymes control both activation and degradation of vitamin D to maintain calcitriol within a narrow physiological range [3]. Despite this regulation, excessive exposure to vitamin D, particularly vitamin D3 (cholecalciferol), can still drive toxicity, in part because very high circulating concentrations of precursor metabolites (especially 25-hydroxyvitamin D) can contribute to inappropriate vitamin D receptor signaling [6,7]. In rabbits, vitamin D intoxication can cause soft-tissue mineralization (calcinosis), including vascular/aortic mineralization, and is fatal at high intakes [8–11].

Based on historical pathology reports, the current dietary recommendation of 800 to 1,000 IU vitamin D per kg of complete diet (which should be adjusted for calorie and protein density) may be a chronic excess that puts some rabbits at risk of calcinosis, especially older rabbits exposed long-term [11]. This is because when dietary consumption of vitamin D chronically exceeds the capacity of normal catabolic pathways then two things can happen simultaneously.

1. Excess circulating precursor metabolites (e.g., 25-hydroxyvitamin D) can still weakly bond to and over-activate vitamin D receptors [6, 7]. Over time, this can promote soft-tissue mineralization, including vascular/aortic mineralization [8–11].

2. Vitamin D is fat-soluble and can be sequestered in adipose tissue; this can contribute to a long half-life [7, 8]. These pools of storage have slow turnover and over-time can build up and contribute to persistently high circulating levels of vitamin D that overwhelm catabolic processes thereby increasing the risk of calcinosis (including aortic mineralization) [6–11].

Direct evidence linking ‘within-recommendation’ dietary vitamin D to calcinosis is limited. Most research on calcinosis was based on overdosing with either calcium, vitamin D or both. They discovered that rabbits are ultra-sensitive to vitamin D, even at low to moderate levels of calcium, when compared to other mammals. One controlled feeding study in adult rabbits reported vascular/aortic mineralization after 19 weeks on diets with vitamin D held constant at ~750 IU/kg, at all calcium levels. The presence of calcinosis in adult rabbits at the lowest dietary calcium level (0.8%) provides a snapshot of mechanistic plausibility based on a more current understanding of known vitamin D biology [10]. Furthermore they identified an age effect with adult rabbits being more sensitive to vitamin D and prone to calcinosis than young rabbits. Long-duration reports identified aorta calcification in 41.4% of rabbits (12 out of 29 analyzed) aged 2 years or older on a diet with 1,000 IU/kg of vitamin D3 (Ca and P at recommended levels) [11, 12].

The current dietary recommendation of 800 to 1,000 IU vitamin D3 per kg of diet commonly used in pet rabbit food made by leading brands may be too high because signs of toxicity and calcinosis still show up over time in adult rabbits. However, some research to the contrary identified that this dietary level may not be sufficient in young rabbits based on hormone responses and bone density. This evidence is presented below.

Deficiency Risk - How Much Vitamin D do Rabbits Need?

The identification of an ‘adequate’ vitamin D status in pet rabbits has been approached by analyzing the relationship between serum 25-hydroxyvitamin D (25(OH)D) and parathyroid hormone (PTH), and by examining cortical bone density in relation to 25(OH)D. In a cross sectional study of pet rabbits with varied diets of unknown dietary vitamin D levels, segmented regression suggested a PTH breakpoint at a serum level of ~17 ng/mL and a cortical bone density breakpoint at a serum level of ~19 ng/mL [14]. These serum levels identify where the possible deficiency risk occurs. Because diets were not standardized, and the data used to calculate the breakpoint were highly variable, these serum levels should be interpreted as approximate population level thresholds rather than precise individual cut-offs. For example, many pet rabbits in the study had much lower serum vitamin D levels without a PTH response.

Two experimental studies provide limited insight into how dietary vitamin D levels affect serum vitamin D levels in rabbits, but neither assessed aortic or other soft-tissue calcification and were short term studies (2 weeks to 4 weeks) in young rabbits.

In a controlled study of young rabbits (6 weeks old) fed timothy hay (ad libitum) plus a pelleted diet (1 cup/day; vitamin D at 1,100 IU/kg pellets), serum 25-hydroxyvitamin D remained at ~12 ng/mL over the 14 days [15].

The second study had similar limitations of using young rabbits for a short duration. They started with 5 week-old rabbits that received hay and pellets with D3 added at 3,200 IU/kg until 15 weeks of age. Then they discontinued pellets and only fed hay. The study and data collection started at 27 weeks of age and continued for 4 more weeks on the diet of either the control hay (cut and then artificially dried indoors to minimize vitamin D2, measured at 888 IU /kg) or the UVB treated hay (measured vitamin D2 at 2424 IU/kg). The rabbits fed the control hay had a serum value of total vitamin D around 32 ng/mL near the end of the study while the rabbits fed the UV treated hay had a serum value of total vitamin D near 55 ng/mL [16]. As a side note, this finding identifies that vitamin D2 from hay can be a meaningful contributor to total vitamin D status. This is important because leading brands are adding animal sourced vitamin D3 to pet rabbit food while blind to the amount of vitamin D2 already in the hay in the formula.

In young growing rabbits, published evidence suggests that soft-tissue mineralization risk emerges at dietary vitamin D levels several-fold above common recommended concentrations for adult rabbits. A controlled study reported that extra-osseous calcification could not be provoked in young rabbits within ~14 weeks even with vitamin D levels at 5,000 IU/kg, whereas it occurred in some adult rabbits within 19 weeks withvitamin D levels at 750 IU/kg [10]. These findings imply that young rabbits may have a higher toxicity threshold for vitamin D than adult rabbits. This is one reason why the assessment of the deficiency risk in young rabbits in these two studies doesn’t address the deficiency risk in adult rabbits, especially when considering the long-term risk of calcinosis.

Vitamin D2 or D3, What’s the Difference?

Vitamin D3 (cholecalciferol) is typically derived from animal sources and is the form commonly used for pet-food fortification [8]. In humans, vitamin D3 generally raises and maintains circulating 25(OH)D concentrations more effectively than vitamin D2, and 25(OH)D3 has a longer half-life than 25(OH)D2 [17–19]. Sustained high circulating 25(OH)D is a key mechanistic feature of vitamin D toxicity [6, 7].

Vitamin D2 (ergocalciferol) is a plant/fungal-origin form of vitamin D that can occur naturally in sun-cured forages via UVB exposure converting ergosterol to ergocalciferol [16]. Experimental work shows that UVB-irradiated hay can substantially increase rabbit serum 25(OH)D2 and total vitamin D concentrations, highlighting that vitamin D intake from hay can be meaningful we should consider whether vitamin D toxicity is a greater risk than deficiency [16, 20]. Both vitamin D2 and vitamin D3 can be metabolized to the active hormone (calcitriol), although their pharmacokinetics differ [3, 8]. In humans, vitamin D2 is generally less potent/shorter-acting than vitamin D3, and 25(OH)D2 has a shorter half-life than 25(OH)D3—features that may reduce (but do not eliminate) overdose risk [17–19].

Closing Statements and Next Steps

Considering the points of research outlined above, it is likely nutritional nonsense to add vitamin D3 to sun-cured hay-based diets for rabbits. This conflicts with FEDIAF (European Pet Food Industry Federation) current recommendations of vitamin D at 800-1000 IU/kg of diet with the safe upper limit set at 2,000 IU/kg. Further research should be done to compare the long-term calcinosis risk in rabbits being fed vitamin D3 at these levels and at lower levels, versus D2 from sun-cured hay at matched levels. This study should also include analysis of total serum vitamin D levels, PTH response, and cortical bone density. If a 24 month controlled trial at 800–1000 IU/kg of vitamin D shows no difference in vascular/kidney mineralization compared with a lower vitamin D group (~ 300 IU/kg, while Ca/P controlled), that would argue against meaningful chronic risk at this level. This research is needed to determine the safe upper limit of supplementing with animal sourced vitamin D3 or vegan D2 versus relying solely on sun-cured hay-based vitamin D2 which is more variable.

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