Hypervitaminosis A#Sources of toxicity

Symptoms may include:

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• Changes in consciousness
• Decreased appetite
• Dizziness
• Vision changes, double vision (in young children)
• Drowsiness
• Headache
• Irritability
• Nausea
• Vomiting

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Signs

• Poor weight gain (in infants and children)
• Skin and hair changes
• Cracking at corners of the mouth
• Hair loss (alopecia)
• Higher sensitivity to sunlight
• Swelling of lips (cheilitis)
• Dryness of lips, mouth, eyes, and inside the nose
• Skin peeling, itching
• Yellow discoloration of the skin (aurantiasis cutis)
• Abnormal softening of the skull bone (craniotabes in infants and children)
• Blurred vision{{Citation |last1=Olson |first1=Jazmine M. |title=Vitamin A Toxicity |date=2023 |url=https://www.ncbi.nlm.nih.gov/books/NBK532916/ |work=StatPearls |access-date=2023-12-18 |place=Treasure Island, Florida (US) |publisher=StatPearls Publishing |pmid=30422511 |last2=Ameer |first2=Muhammad Atif |last3=Goyal |first3=Amandeep}}
• Bone pain or swelling
• Bulging fontanelle (in infants)
• Gastric mucosal calcinosis{{cite journal | vauthors = Gorospe M, Fadare O | title = Gastric mucosal calcinosis: clinicopathologic considerations | journal = Advances in Anatomic Pathology | volume = 14 | issue = 3 | pages = 224–228 | date = May 2007 | pmid = 17452819 | doi = 10.1097/PAP.0b013e31805048ea | s2cid = 45905601 | url = https://zenodo.org/record/1234899 }}
• Heart valve calcification{{cite journal | vauthors = Huk DJ, Hammond HL, Kegechika H, Lincoln J | title = Increased dietary intake of vitamin A promotes aortic valve calcification in vivo | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 33 | issue = 2 | pages = 285–293 | date = February 2013 | pmid = 23202364 | pmc = 3557503 | doi = 10.1161/ATVBAHA.112.300388 }}
• Hypercalcemia
• Increased intracranial pressure manifesting as cerebral edema, papilledema, and headache (may be referred to as idiopathic intracranial hypertension){{cite journal |last1=Libien |first1=J. |last2=Kupersmith |first2=M. J. |last3=Blaner |first3=W. |last4=McDermott |first4=M. P. |last5=Gao |first5=S. |last6=Liu |first6=Y. |last7=Corbett |first7=J. |last8=Wall |first8=M. |last9=NORDIC Idiopathic Intracranial Hypertension Study Group |date=2017-01-15 |title=Role of vitamin A metabolism in IIH: Results from the idiopathic intracranial hypertension treatment trial |journal=Journal of the Neurological Sciences |volume=372 |pages=78–84 |doi=10.1016/j.jns.2016.11.014 |issn=1878-5883 |pmc=5290478 |pmid=28017254}}{{cite journal | vauthors = Wall M | title = Idiopathic intracranial hypertension (pseudotumor cerebri) | journal = Current Neurology and Neuroscience Reports | url = https://link.springer.com/10.1007/s11910-008-0015-0 | volume = 8 | issue = 2 | pages = 87–93 | date = March 2008 | pmid = 18460275 | doi = 10.1007/s11910-008-0015-0 | s2cid = 17285706 }}
• Liver damage{{cite journal | vauthors = Castaño G, Etchart C, Sookoian S | title = Vitamin A toxicity in a physical culturist patient: a case report and review of the literature | journal = Annals of Hepatology | volume = 5 | issue = 4 | pages = 293–395 | year = 2006 | doi = 10.1016/S1665-2681(19)31992-1 | pmid = 17151585 | doi-access = free }}{{cite journal | vauthors = Minuk GY, Kelly JK, Hwang WS | title = Vitamin A hepatotoxicity in multiple family members | journal = Hepatology | volume = 8 | issue = 2 | pages = 272–275 | year = 1988 | pmid = 3356407 | doi = 10.1002/hep.1840080214 | s2cid = 6632550 }}{{cite journal | vauthors = Levine PH, Delgado Y, Theise ND, West AB | title = Stellate-cell lipidosis in liver biopsy specimens. Recognition and significance | journal = American Journal of Clinical Pathology | volume = 119 | issue = 2 | pages = 254–258 | date = February 2003 | pmid = 12579996 | doi = 10.1309/6DKC-03C4-GAAE-N2DK | doi-access = free }}{{cite journal | vauthors = Tholen W, Paquet KJ, Rohner HG, Albrecht M | title = [Cirrhosis of the liver and esophageal bleeding after chronic vitamin A intoxication |id=(author's translation)] | journal = Leber, Magen, Darm | volume = 10 | issue = 4 | pages = 193–197 | date = August 1980 | pmid = 6969836 }}{{cite journal | vauthors = Jorens PG, Michielsen PP, Pelckmans PA, Fevery J, Desmet VJ, Geubel AP, Rahier J, Van Maercke YM | title = Vitamin A abuse: development of cirrhosis despite cessation of vitamin A. A six-year clinical and histopathologic follow-up | journal = Liver | volume = 12 | issue = 6 | pages = 381–386 | date = December 1992 | pmid = 1470008 | doi = 10.1111/j.1600-0676.1992.tb00592.x }}{{cite journal | vauthors = Babb RR, Kieraldo JH | title = Cirrhosis due to hypervitaminosis A | journal = The Western Journal of Medicine | volume = 128 | issue = 3 | pages = 244–246 | date = March 1978 | pmid = 636413 | pmc = 1238074 }}{{cite journal | vauthors = Erickson JM, Mawson AR | title = Possible role of endogenous retinoid (Vitamin A) toxicity in the pathophysiology of primary biliary cirrhosis | journal = Journal of Theoretical Biology | volume = 206 | issue = 1 | pages = 47–54 | date = September 2000 | pmid = 10968936 | doi = 10.1006/jtbi.2000.2102 | bibcode = 2000JThBi.206...47E }}{{cite journal | vauthors = Singh M, Singh VN | title = Fatty liver in hypervitaminosis A: synthesis and release of hepatic triglycerides | journal = The American Journal of Physiology | volume = 234 | issue = 5 | pages = E511–514 | date = May 1978 | pmid = 645903 | url = http://ajpendo.physiology.org/cgi/pmidlookup?view=reprint&pmid=645903 | doi = 10.1152/ajpendo.1978.234.5.E511 }}{{cite journal | vauthors = Nollevaux MC, Guiot Y, Horsmans Y, Leclercq I, Rahier J, Geubel AP, Sempoux C | title = Hypervitaminosis A-induced liver fibrosis: stellate cell activation and daily dose consumption | journal = Liver International | volume = 26 | issue = 2 | pages = 182–186 | date = March 2006 | pmid = 16448456 | doi = 10.1111/j.1478-3231.2005.01207.x | s2cid = 41658180 }}
• Premature epiphyseal closure{{cite journal | vauthors = Cho DY, Frey RA, Guffy MM, Leipold HW | title = Hypervitaminosis A in the dog | journal = American Journal of Veterinary Research | volume = 36 | issue = 11 | pages = 1597–1603 | date = November 1975 | pmid = 1190603 }}{{cite journal | vauthors = Kodaka T, Takaki H, Soeta S, Mori R, Naito Y | title = Local disappearance of epiphyseal growth plates in rats with hypervitaminosis A | journal = The Journal of Veterinary Medical Science | volume = 60 | issue = 7 | pages = 815–821 | date = July 1998 | pmid = 9713809 | doi = 10.1292/jvms.60.815 | doi-access = free }}{{cite journal | vauthors = Soeta S, Mori R, Kodaka T, Naito Y, Taniguchi K | title = Immunohistochemical observations on the initial disorders of the epiphyseal growth plate in rats induced by high dose of vitamin A | journal = The Journal of Veterinary Medical Science | volume = 61 | issue = 3 | pages = 233–238 | date = March 1999 | pmid = 10331194 | doi = 10.1292/jvms.61.233 | doi-access = free }}{{cite journal | vauthors = Soeta S, Mori R, Kodaka T, Naito Y, Taniguchi K | title = Histological disorders related to the focal disappearance of the epiphyseal growth plate in rats induced by high dose of vitamin A | journal = The Journal of Veterinary Medical Science | volume = 62 | issue = 3 | pages = 293–299 | date = March 2000 | pmid = 10770602 | doi = 10.1292/jvms.62.293 | doi-access = free }}{{cite journal | vauthors = Rothenberg AB, Berdon WE, Woodard JC, Cowles RA | title = Hypervitaminosis A-induced premature closure of epiphyses (physeal obliteration) in humans and calves (hyena disease): a historical review of the human and veterinary literature | journal = Pediatric Radiology | volume = 37 | issue = 12 | pages = 1264–1267 | date = December 2007 | pmid = 17909784 | doi = 10.1007/s00247-007-0604-0 | s2cid = 34194762 }}
• Spontaneous fracture{{cite journal | vauthors = Wick JY | title = Spontaneous fracture: multiple causes | journal = The Consultant Pharmacist | volume = 24 | issue = 2 | pages = 100–102, 105–108, 110–112 | date = February 2009 | pmid = 19275452 | doi = 10.4140/TCP.n.2009.100 }}
• Uremic pruritus{{cite journal | vauthors = Corić-Martinović V, Basić-Jukić N | title = [Uremic pruritus] | journal = Acta Medica Croatica | volume = 62 | pages = 32–36 | year = 2008 | issue = Suppl 1 | pmid = 18578330 }}

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File:Basel 2012-10-06 Batch Part 4 (16).JPG, a potentially toxic source of vitamin A. Hypervitaminosis A can result from ingestion of too much vitamin A from diet (rare), supplements, or prescription medications.]]

Hypervitaminosis A results from excessive intake of preformed vitamin A. Genetic variations in tolerance to vitamin A intake may occur, so the toxic dose will not be the same for everyone.{{cite journal | vauthors = Carpenter TO, Pettifor JM, Russell RM, Pitha J, Mobarhan S, Ossip MS, Wainer S, Anast CS | title = Severe hypervitaminosis A in siblings: evidence of variable tolerance to retinol intake | journal = The Journal of Pediatrics | volume = 111 | issue = 4 | pages = 507–12 | date = October 1987 | pmid = 3655980 | doi = 10.1016/s0022-3476(87)80109-9 }} Children are particularly sensitive to vitamin A, with daily intakes of 1500 IU/kg body weight reportedly leading to toxicity.

• It is "largely impossible" for provitamin carotenoids, such as beta-carotene, to cause toxicity, as their conversion to retinol is highly regulated. No vitamin A toxicity has ever been reported from ingestion of excessive amounts. Overconsumption of beta-carotene can only cause carotenosis, a harmless and reversible cosmetic condition in which the skin turns orange.
• Preformed vitamin A absorption and storage in the liver occur very efficiently until a pathologic condition develops.{{cite journal | vauthors = Penniston KL, Tanumihardjo SA | title = The acute and chronic toxic effects of vitamin A | journal = The American Journal of Clinical Nutrition | volume = 83 | issue = 2 | pages = 191–201 | date = February 2006 | pmid = 16469975 | url = http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=16469975 | doi = 10.1093/ajcn/83.2.191 | doi-access = free }} When ingested, 70–90% of preformed vitamin A is absorbed.

• Diet – Liver is high in vitamin A. The liver of certain animals, including the polar bear, bearded seal,{{cite journal | vauthors = Rodahl K, Moore T | title = The vitamin A content and toxicity of bear and seal liver | journal = The Biochemical Journal | volume = 37 | issue = 2 | pages = 166–168 | date = July 1943 | pmid = 16747610 | pmc = 1257872 | doi = 10.1042/bj0370166 }}The Phoca barbata listed on pages 167–168 of the previous reference is now known as [http://eunis.eea.europa.eu/species/11684 Erignathus barbatus] fish and{{cite journal |vauthors=Schmitt C, Domangé B, Torrents R, de Haro L, Simon N |title=Hypervitaminosis A Following the Ingestion of Fish Liver: Report on 3 Cases from the Poison Control Center in Marseille |journal=Wilderness Environ Med |volume=31 |issue=4 |pages=454–456 |date=December 2020 |pmid=32861618 |doi=10.1016/j.wem.2020.06.003 |s2cid=221384282 |url=|doi-access=free }} walrus,{{cite web |date= 2006 |first=Jason |last=Morrison |url=http://www.mealographer.com/food/Walrus/liver-raw-Alaska-Native-35083.html |title=Walrus, liver, raw (Alaska Native) |website=Mealographer |access-date=2010-03-25}} are particularly toxic (see {{slink|Liver (food)#Poisoning}}). It has been estimated that consumption of {{convert|500|g}} of polar bear liver would result in an acute toxic dose for humans.
• Supplements – Dietary supplements can be toxic when taken above recommended dosages.
• Cod liver oil - According to the United States Department of Agriculture, a tablespoon (13.6 grams or 14.8 mL) of cod liver oil contains 4,080 μg of vitamin A.{{cite web |url=https://fdc.nal.usda.gov/food-details/173577/nutrients |title=Fish oil, cod liver |website=U.S. Department of Agriculture |access-date=11 April 2025}} The tolerable upper intake level (UL) is 3000 μg/day for adults, 600 μg/day for children ages 1-3 years and 900 μg/day for children ages 4-8 years, so for all ages, but especially for young children, a tablespoon a day exceeds the UL.

• Acute toxicity occurs over hours or a few days.
• Chronic toxicity results from adult daily intakes greater than 25,000 IU for 6 years or longer and more than 100,000 IU for 6 months or longer.{{cn|date=April 2025}}

Retinol is absorbed and stored in the liver very efficiently until a pathologic condition develops.

When ingested, 70–90% of preformed vitamin A is absorbed. Water-miscible, emulsified and solid forms of vitamin A supplements are more toxic than oil-based supplements.{{cite journal| issn = 0002-9165| volume = 78| issue = 6| pages = 1152–59| last1 = Myhre| first1 = AM|last2=Carlsen |first2=MH |last3=Bøhn |first3=SM |last4=Wold |first4=HL |last5=Laake|first5=P |last6=Blomhoff |first6=R |title = Water-Miscible, Emulsified, and Solid Forms of Retinol Supplements Are More Toxic Than Oil-Based Preparations| journal = Amer J Clin Nutr| date = December 2003| doi = 10.1093/ajcn/78.6.1152| pmid = 14668278| doi-access = free}}

Eighty to ninety percent of the total body reserves of preformed vitamin A are in the liver (with 80–90% of this amount being stored in hepatic stellate cells and the remaining 10–20% being stored in hepatocytes). Fat is another significant storage site, while the lungs and kidneys may also be capable of storage.

Until recently, it was thought that the sole important retinoid delivery pathway to tissues involved retinol bound to retinol-binding protein (RBP4). More recent findings, however, indicate that retinoids can be delivered to tissues through multiple overlapping delivery pathways, involving chylomicrons, very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), retinoic acid bound to albumin, water-soluble β-glucuronides of retinol and retinoic acid, and provitamin A carotenoids.{{cite journal | vauthors = Li Y, Wongsiriroj N, Blaner WS | title = The multifaceted nature of retinoid transport and metabolism | journal = Hepatobiliary Surgery and Nutrition | volume = 3 | issue = 3 | pages = 126–139 | date = June 2014 | pmid = 25019074 | pmc = 4073323 | doi = 10.3978/j.issn.2304-3881.2014.05.04 }}

The range of serum retinol concentrations under normal conditions is 1–3 μmol/L. Elevated amounts of retinyl ester (i.e., >10% of total circulating vitamin A) in the fasting state have been used as markers for chronic hypervitaminosis A in humans. Candidate mechanisms for this increase include decreased hepatic uptake of vitamin A and the leaking of esters into the bloodstream from saturated hepatic stellate cells.

Effects include increased bone turnover and altered metabolism of fat-soluble vitamins. More research is needed to fully elucidate the effects.

Retinoic acid suppresses osteoblast activity and stimulates osteoclast formation in vitro, resulting in increased bone resorption and decreased bone formation. It is likely to exert this effect by binding to specific nuclear receptors (members of the retinoic acid receptor or retinoid X receptor nuclear transcription family) which are found in every cell (including osteoblasts and osteoclasts).{{cn|date=July 2022}}

This change in bone turnover is likely to be the reason for numerous effects seen in hypervitaminosis A, such as hypercalcemia and numerous bone changes such as bone loss that potentially leads to osteoporosis, spontaneous bone fractures, altered skeletal development in children, skeletal pain, radiographic changes,{{cite journal | vauthors = Barker ME, Blumsohn A | title = Is vitamin A consumption a risk factor for osteoporotic fracture? | journal = The Proceedings of the Nutrition Society | volume = 62 | issue = 4 | pages = 845–850 | date = November 2003 | pmid = 15018484 | doi = 10.1079/PNS2003306 | doi-access = free }} and bone lesions.{{cite journal | vauthors = Hough S, Avioli LV, Muir H, Gelderblom D, Jenkins G, Kurasi H, Slatopolsky E, Bergfeld MA, Teitelbaum SL | title = Effects of hypervitaminosis A on the bone and mineral metabolism of the rat | journal = Endocrinology | volume = 122 | issue = 6 | pages = 2933–2939 | date = June 1988 | pmid = 3371268 | doi = 10.1210/endo-122-6-2933 }}

Preformed vitamin A is fat-soluble and high levels have been reported to affect the metabolism of the other fat-soluble vitamins D, E, and K.

The toxic effects of preformed vitamin A might be related to altered vitamin D metabolism, concurrent ingestion of substantial amounts of vitamin D, or binding of vitamin A to receptor heterodimers. Antagonistic and synergistic interactions between these two vitamins have been reported, as they relate to skeletal health.

Stimulation of bone resorption by vitamin A has been reported to be independent of its effects on vitamin D.

Preformed vitamin A and retinoids exert several toxic effects regarding the redox environment and mitochondrial function. {{cite journal | vauthors = de Oliveira MR | title = Vitamin A and Retinoids as Mitochondrial Toxicants | journal = Oxidative Medicine and Cellular Longevity | volume = 2015 | pages = 1–13 | year = 2015 | pmid = 26078802 | pmc = 4452429 | doi = 10.1155/2015/140267 | doi-access = free }}

Assessing vitamin A status in persons with sub-toxicity or toxicity is complicated because serum retinol concentrations are not sensitive indicators in this range of liver vitamin A reserves. The range of serum retinol concentrations under normal conditions is 1–3 μmol/L and, because of homeostatic regulation, that range varies little with widely disparate vitamin A intakes.

Retinyl esters can be distinguished from retinol in serum and other tissues and quantified with the use of methods such as high-performance liquid chromatography.

Elevated amounts of retinyl ester (i.e., >10% of total circulating vitamin A) in the fasting state have been used as markers for chronic hypervitaminosis A in humans and monkeys. This increased retinyl ester may be due to decreased hepatic uptake of vitamin A and the leaking of esters into the bloodstream from saturated hepatic stellate cells.

Hypervitaminosis A can be prevented by not ingesting more than the US Institute of Medicine Daily Tolerable Upper Level of intake for Vitamin A. This level is for synthetic and natural retinol ester forms of vitamin A. Carotene forms from dietary sources are not toxic. Possible pregnancy, liver disease, high alcohol consumption, and smoking are indications for close monitoring and limitation of vitamin A administration.{{multiref2|1={{cite journal |last1=Carazo |first1=Alejandro |last2=Macáková |first2=Kateřina |last3=Matoušová |first3=Kateřina |last4=Krčmová |first4=Lenka Kujovská |last5=Protti |first5=Michele |last6=Mladěnka |first6=Přemysl |title=Vitamin A Update: Forms, Sources, Kinetics, Detection, Function, Deficiency, Therapeutic Use and Toxicity |journal=Nutrients |date=18 May 2021 |volume=13 |issue=5 |pages=1703 |doi=10.3390/nu13051703 |doi-access=free|pmid=34069881 |pmc=8157347 |hdl=11585/838659 |hdl-access=free }}|2={{cite web |title=Beta-carotene Information |website=Mount Sinai Health System |url=https://www.mountsinai.org/health-library/supplement/beta-carotene}} }}

• Stopping high vitamin A intake is the standard treatment. Most people fully recover.
• Phosphatidylcholine (in the form of PPC or DLPC), the substrate for lecithin retinol acyltransferase, which converts retinol into retinyl esters (the storage forms of vitamin A).
• Vitamin E may alleviate hypervitaminosis A.{{cite journal | vauthors = McCuaig LW, Motzok I | title = Excessive dietary vitamin E: its alleviation of hypervitaminosis A and lack of toxicity | journal = Poultry Science | volume = 49 | issue = 4 | pages = 1050–1051 | date = July 1970 | pmid = 5485475 | doi = 10.3382/ps.0491050 | doi-access = free }}
• Liver transplantation may be a valid option if no improvement occurs.{{cite journal | vauthors = Cheruvattath R, Orrego M, Gautam M, Byrne T, Alam S, Voltchenok M, Edwin M, Wilkens J, Williams JW, Vargas HE | title = Vitamin A toxicity: when one a day doesn't keep the doctor away | journal = Liver Transplantation | volume = 12 | issue = 12 | pages = 1888–1891 | date = December 2006 | pmid = 17133567 | doi = 10.1002/lt.21007 | s2cid = 32290718 }}

If liver damage has progressed into fibrosis, synthesizing capacity is compromised and supplementation can replenish PC. However, recovery is dependent on removing the causative agent: halting high vitamin A intake.{{cite journal | vauthors = Gundermann KJ, Kuenker A, Kuntz E, Droździk M | title = Activity of essential phospholipids (EPL) from soybean in liver diseases | journal = Pharmacological Reports | volume = 63 | issue = 3 | pages = 643–659 | year = 2011 | pmid = 21857075 | doi = 10.1016/S1734-1140(11)70576-X | s2cid = 4741429 }}{{cite journal | vauthors = Okiyama W, Tanaka N, Nakajima T, Tanaka E, Kiyosawa K, Gonzalez FJ, Aoyama T | title = Polyenephosphatidylcholine prevents alcoholic liver disease in PPARalpha-null mice through attenuation of increases in oxidative stress | journal = Journal of Hepatology | volume = 50 | issue = 6 | pages = 1236–1246 | date = June 2009 | pmid = 19398233 | pmc = 2809859 | doi = 10.1016/j.jhep.2009.01.025 }}{{cite journal | vauthors = Wu J, Zern MA | title = Hepatic stellate cells: a target for the treatment of liver fibrosis | journal = Journal of Gastroenterology | volume = 35 | issue = 9 | pages = 665–672 | year = 2000 | pmid = 11023037 | doi = 10.1007/s005350070045 | s2cid = 40851639 }}{{cite journal | vauthors = Navder KP, Lieber CS | title = Dilinoleoylphosphatidylcholine is responsible for the beneficial effects of polyenylphosphatidylcholine on ethanol-induced mitochondrial injury in rats | journal = Biochemical and Biophysical Research Communications | volume = 291 | issue = 4 | pages = 1109–1112 | date = March 2002 | pmid = 11866479 | doi = 10.1006/bbrc.2002.6557 }}

Vitamin A toxicity is known to be an ancient phenomenon; fossilized skeletal remains of early humans suggest bone abnormalities may have been caused by hypervitaminosis A, as observed in a fossilised leg bone of an individual of Homo erectus, which bears abnormalities similar to those observed in people suffering from an overdose of Vitamin A in the present day.{{Cite web |date=1974-01-01 |title=KNM-ER 1808 {{!}} The Smithsonian Institution's Human Origins Program |url=http://humanorigins.si.edu/evidence/human-fossils/fossils/knm-er-1808 |access-date=2024-04-09 |website=humanorigins.si.edu |language=en}}{{Cite web |title=Do we know how some early human ancestors died? |url=https://australian.museum/learn/science/human-evolution/how-do-we-know-how-they-died/ |access-date=2024-04-09 |website=The Australian Museum |language=en}}

Vitamin A toxicity has long been known to the Inuit, as they will not eat the liver of polar bears or bearded seals due to them containing dangerous amounts of Vitamin A. It has been known to Europeans since at least 1597 when Gerrit de Veer wrote in his diary that, while taking refuge in the winter in Nova Zemlya, he and his men became severely ill after eating polar bear liver.{{cite journal | vauthors = Lips P | title = Hypervitaminosis A and fractures | journal = The New England Journal of Medicine | volume = 348 | issue = 4 | pages = 347–349 | date = January 2003 | pmid = 12540650 | doi = 10.1056/NEJMe020167 }}

It is claimed that, in 1913, Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned (and Mertz died) from eating the livers of their sled dogs during the Far Eastern Party.{{cite journal |last1=Nataraja |first1=Anjali |title=Man's best friend? |journal=BMJ |date=1 May 2002 |volume=324 |issue=Suppl S5 |url= https://www.bmj.com/content/324/Suppl_S5/0205158 |doi=10.1136/sbmj.0205158 |pages=131–170 |url-access=subscription |department=Student BMJ}} Another study suggests, however, that exhaustion and diet change are more likely to have caused the tragedy.{{cite journal | vauthors = Carrington-Smith D | title = Mawson and Mertz: a re-evaluation of their ill-fated mapping journey during the 1911-1914 Australasian Antarctic Expedition | journal = The Medical Journal of Australia | volume = 183 | issue = 11–12 | pages = 638–641 | year = 2005 | doi = 10.5694/j.1326-5377.2005.tb00064.x | pmid = 16336159 | s2cid = 8430414 | url = https://www.mja.com.au/journal/2005/183/11/mawson-and-mertz-re-evaluation-their-ill-fated-mapping-journey-during-1911-1914 }}

Some Arctic animals demonstrate no signs of hypervitaminosis A despite having 10–20 times the level of vitamin A in their livers as non-Arctic animals. These animals are top predators and include the polar bear, Arctic fox, bearded seal, and glaucous gull. Plasma concentrations are maintained in a non-toxic range despite the high liver content.{{cite journal | vauthors = Senoo H, Imai K, Mezaki Y, Miura M, Morii M, Fujiwara M, Blomhoff R | title = Accumulation of vitamin A in the hepatic stellate cell of arctic top predators | journal = Anatomical Record | volume = 295 | issue = 10 | pages = 1660–68 | date = October 2012 | pmid = 22907891 | doi = 10.1002/ar.22555 | doi-access = free }}

• Vitamin poisoning
• Far Eastern Party
• Retinoic acid syndrome
• Piblokto

{{Reflist}}

{{Medical resources

| ICD10 = {{ICD10|E|67|0|e|65}}

| ICD9 = {{ICD9|278.2}}

| ICDO =

| OMIM =

| DiseasesDB = 13888

| MedlinePlus = 000350

| eMedicineSubj = med

| eMedicineTopic = 2382

}}

• [http://ods.od.nih.gov/factsheets/cc/vita.html#risk Facts about Vitamin A and Carotenoids], from the National Institutes of Health's Office of Dietary Supplements.

{{Poisoning and toxicity}}

Category:Effects of external causes

Category:Hypervitaminosis

Category:Vitamin A