Vitamin A is an essential fat-soluble micronutrient that is vital to maintaining healthy skin, gastrointestinal function, reproduction, and robust immunity. Vitamin A is obtained preformed in the diet or produced from plant-based precursors, primarily beta-carotene. Insufficiency of vitamin A is associated with infections, inflammation, skin disorders, compromised growth, and gastrointestinal complications. Excess vitamin A can be toxic and contribute to liver damage, bone disorders, hyperlipidemia, and temporary hypothyroidism.
Standard Range: 38.00 – 98.00 ug/dL (1.33 – 3.42 umol/L
The Optimal DX Range: 57.00 – 66.00 ug/dL (1.99 – 2.30 umol/L)
Low vitamin A is associated with susceptibility to infection, night blindness, Bitot’s spots, altered growth (Sommer 2008), anemia, inflammation, skin disorders, malnutrition, decreased DHA synthesis, cancerous and precancerous conditions, potential disruption of the gut microbiome, and impaired digestion, absorption, and secretory IgA transport (Wiseman 2017).
High vitamin A is associated with excess intake (dietary and pharmaceutical), birth defects, headaches, nausea, vomiting, liver damage, pancreatitis, transient hypothyroidism, hypertriglyceridemia, hypercholesterolemia, elevated transaminases, bone resorption and hypercalcemia, skin irritation, dryness, and peeling, and compromised bone integrity (Olson 2022). Excess carotenoid intake can cause red orange discoloration of the skin though it may not correlate with elevated serum retinol levels.
Vitamin A occurs in the diet primarily as retinol (animal-based) or as a carotenoid precursor (plant-based) that is converted to vitamin A. Retinol can be converted to other forms including retinals and retinoic acids in the body where they are involved in a wide range of metabolic activities. These include vision, immunity, reproduction, cell differentiation, embryonic development, growth, skin integrity, and wound healing, especially in the inflammatory stages (Polcz 2019).
Vitamin A is important to preserving mucosal and epithelial integrity which directly affects immune competence and gastrointestinal function. A significant amount of vitamin A can be lost in the urine during pathogen challenge, perpetuating a vicious cycle of infection and malnutrition (Huang 2018).
Serum levels of retinol may not decrease until body stores begin to decline, therefore a persistent reduction in serum levels should be promptly assessed and addressed. A decrease in circulating retinol can occur during protein deficiency as well, due to decreased production of retinol binding protein (RBP), its primary carrier in circulation (de Pee 2002). Infections can reduce production of RBP, decreasing availability to tissues. Vitamin A is also transported by prealbumin, a major plasma protein that transports thyroxine (T4) (Pagana 2021).
It should be noted that conversion of plant-based carotenoids to retinol may be inefficient. It takes at least 12 molecules or more of beta-carotene to produce 1 molecule of vitamin A (Sommer 2008). Also, a number of ethnic differences and genetic polymorphisms can reduce the amount of beta-carotene effectively converted to vitamin A. Conversion may be reduced by up to 59% (Lietz 2012).
Food sources of animal-based vitamin A include liver, chicken, beef, eggs, fish, milk, cheese, butter, and fortified breakfast cereals. Plant-based sources include leafy greens, carrots, sweet potatoes, and other orange and yellow vegetables. The plant-based precursor is less likely to cause toxicity. Vitamin A toxicity, which can occur with topical or oral supplements, is associated with birth defects, headaches, nausea, vomiting, pancreatitis, transient hypothyroidism, hypertriglyceridemia, hypercholesterolemia, skin irritation, dryness, and peeling (Olson 2022).
Vitamin A insufficiency can significantly compromise immunity, skin integrity, and eye health, and promote excess inflammation. Provision of vitamin A can restore tissue integrity, restore antibody response, and reduce intestinal inflammation. Frank deficiency is recognized at a serum retinol level below 19.6 ug/dL (0.7 umol/L) though a level below 29.4 ng/dL (1.05 umol/L) is of concern in pregnancy (Wiseman 2017). Sustaining optimal levels of serum retinol can insure maintenance of vital body stores and functions.
de Pee, Saskia, and Omar Dary. “Biochemical indicators of vitamin A deficiency: serum retinol and serum retinol binding protein.” The Journal of nutrition vol. 132,9 Suppl (2002): 2895S-2901S. doi:10.1093/jn/132.9.2895S
Huang, Zhiyi et al. “Role of Vitamin A in the Immune System.” Journal of clinical medicine vol. 7,9 258. 6 Sep. 2018, doi:10.3390/jcm7090258
Lietz, Georg et al. “Single nucleotide polymorphisms upstream from the β-carotene 15,15'-monoxygenase gene influence provitamin A conversion efficiency in female volunteers.” The Journal of nutrition vol. 142,1 (2012): 161S-5S. doi:10.3945/jn.111.140756
Olson, Jazmine M., et al. “Vitamin A Toxicity.” StatPearls, StatPearls Publishing, 11 July 2022.
Pagana, Kathleen Deska, et al. Mosby's Diagnostic and Laboratory Test Reference. 15th ed., Mosby, 2021.
Polcz, Monica E, and Adrian Barbul. “The Role of Vitamin A in Wound Healing.” Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition vol. 34,5 (2019): 695-700. doi:10.1002/ncp.10376
Sommer, Alfred. “Vitamin a deficiency and clinical disease: an historical overview.” The Journal of nutrition vol. 138,10 (2008): 1835-9. doi:10.1093/jn/138.10.1835
Wiseman, Elina Manusevich et al. “The vicious cycle of vitamin a deficiency: A review.” Critical reviews in food science and nutrition vol. 57,17 (2017): 3703-3714. doi:10.1080/10408398.2016.1160362