Hypervitaminosis A: Difference between revisions
Reverted good faith edits by 180.94.93.5 (talk): Out of place and broken formatting. (TW) |
→Pathophysiology: Betacarotene can cause carotenosis, a benign condition |
||
| Line 31: | Line 31: | ||
==Pathophysiology== |
==Pathophysiology== |
||
Hypervitaminosis A occurs when the maximum limit for liver stores of [[retinoid]]s is exceeded. The excess vitamin A enters the circulation causing systemic toxicity. [[Betacarotene]], a [[Precursor (chemistry)|precursor]] of vitamin A, is selectively converted into retinoids, so it does not cause toxicity |
Hypervitaminosis A occurs when the maximum limit for liver stores of [[retinoid]]s is exceeded. The excess vitamin A enters the circulation causing systemic toxicity. [[Betacarotene]], a [[Precursor (chemistry)|precursor]] form of vitamin A typical of vegetable sources such as carrots, is selectively converted into retinoids, so it does not cause toxicity; |
||
however, overconsumption can cause [[carotenosis]], a benign condition in which the skin turns orange. |
|||
Although hypervitaminosis A can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed, most cases of vitamin A toxicity result from an excess intake of vitamin A in the form of [[vitamin supplements]]. Toxic symptoms can also arise after consuming very large amounts of preformed vitamin A over a short period of time. (See [[Polar-bear]] liver below.) The U.S. [[Institute of Medicine]] says that the Lowest Observed Adverse Effect Level (LOAEL) for vitamin A, when taken over an extended period of time is 21,600 [[International unit|IU]].<ref>Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium and Zinc. National Academies Press http://books.nap.edu/books/0309072794/html/82.html</ref> Most [[multivitamins]] contain vitamin A doses below 10,000 IU, therefore multi-vitamins are unlikely to cause vitamin A toxicity when taken at their recommended dosages. But in high doses, its [[central nervous system]] toxicity can be enhanced by its [[lipid solubility]] because it is readily transported across the [[blood brain barrier]] and concentrated in the [[brain]].{{Citation needed|date=January 2011}} |
Although hypervitaminosis A can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed, most cases of vitamin A toxicity result from an excess intake of vitamin A in the form of [[vitamin supplements]]. Toxic symptoms can also arise after consuming very large amounts of preformed vitamin A over a short period of time. (See [[Polar-bear]] liver below.) The U.S. [[Institute of Medicine]] says that the Lowest Observed Adverse Effect Level (LOAEL) for vitamin A, when taken over an extended period of time is 21,600 [[International unit|IU]].<ref>Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium and Zinc. National Academies Press http://books.nap.edu/books/0309072794/html/82.html</ref> Most [[multivitamins]] contain vitamin A doses below 10,000 IU, therefore multi-vitamins are unlikely to cause vitamin A toxicity when taken at their recommended dosages. But in high doses, its [[central nervous system]] toxicity can be enhanced by its [[lipid solubility]] because it is readily transported across the [[blood brain barrier]] and concentrated in the [[brain]].{{Citation needed|date=January 2011}} |
||
Revision as of 22:49, 2 December 2011
| Hypervitaminosis A | |
|---|---|
| Specialty | Endocrinology  |
Hypervitaminosis A refers to the effects of excessive vitamin A (specifically retinoid) intake.
Presentation
Effects include
- Birth defects
- Liver problems
- Reduced bone mineral density that may result in osteoporosis
- Coarse bone growths
- Skin discoloration
- Hair loss
- Excessive skin dryness/peeling (desquamation)
- Angular cheilitis
- Intracranial hypertension (see Idiopathic intracranial hypertension[1])
Signs
Signs of acute toxicity include nausea and vomiting, headache, dizziness, blurred vision, and loss of muscular coordination.
Pathophysiology
Hypervitaminosis A occurs when the maximum limit for liver stores of retinoids is exceeded. The excess vitamin A enters the circulation causing systemic toxicity. Betacarotene, a precursor form of vitamin A typical of vegetable sources such as carrots, is selectively converted into retinoids, so it does not cause toxicity; however, overconsumption can cause carotenosis, a benign condition in which the skin turns orange.
Although hypervitaminosis A can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed, most cases of vitamin A toxicity result from an excess intake of vitamin A in the form of vitamin supplements. Toxic symptoms can also arise after consuming very large amounts of preformed vitamin A over a short period of time. (See Polar-bear liver below.) The U.S. Institute of Medicine says that the Lowest Observed Adverse Effect Level (LOAEL) for vitamin A, when taken over an extended period of time is 21,600 IU.[2] Most multivitamins contain vitamin A doses below 10,000 IU, therefore multi-vitamins are unlikely to cause vitamin A toxicity when taken at their recommended dosages. But in high doses, its central nervous system toxicity can be enhanced by its lipid solubility because it is readily transported across the blood brain barrier and concentrated in the brain.[citation needed]
Vitamin A causes cells to swell with fluid; too much vitamin A causes them to rupture in hyposmotic environments, hence the toxicity. Toxicity has been shown to be mitigated through vitamin E (tocopherol), cholesterol, zinc, taurine, and calcium.[3] Cholesterol has been shown to prevent retinol induced golgi fragmentation.[4]
Recommended supplement limits
The U.S. Institute of Medicine has established Daily Tolerable Upper Levels (UL) of intake for vitamin A from supplements that apply to healthy populations, in order to help prevent the risk of vitamin A toxicity. These levels for preformed vitamin A in micrograms (µg) and International Units (IU) are
- 0–3 years: 600 µg or 2000 IU
- 4–8 years: 900 µg or 3000 IU
- 9–13 years: 1700 µg or 5665 IU
- 14–18 years: 2800 µg or 9335 IU
- 19+ years: 3000 µg or 10,000 IU
The dose over and above the RDA is among the narrowest of the vitamins and minerals. Possible pregnancy, liver disease, high alcohol consumption, and smoking are indications for close monitoring and limitation of vitamin A administration. However, vitamin A has also been repeatedly tested and used therapeutically over several decades in larger amounts. For example, a total dosage of 100,000 - 400,000 IU has been given for treatment of severe pediatric measles, in areas where vitamin A deficiency may be present, in order to reduce childhood mortality.[5][6]
Toxicity from eating liver
The liver of certain animals — including the polar bear, seal, walrus,[7] and husky — is unsafe to eat because it is extraordinarily high in vitamin A. This danger has long been known to the Inuit and has been recognized by 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.[8] In 1913, Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned (and Mertz died) from eating the liver of their sled dogs during the Far Eastern Party.[9]
Vitamin A itself was not discovered until 1917.
Pathological changes consistent with hypervitaminosis A have been seen in bones of Homo erectus, and have also been attributed to consumption of carnivore liver.[10]
The livers of many other animals have lower levels of vitamin A and are commonly eaten.
See also
References
- ^ Wall M (2008). "Idiopathic intracranial hypertension (pseudotumor cerebri)". Curr Neurol Neurosci Rep. 8 (2): 87–93. doi:10.1007/s11910-008-0015-0. PMID 18460275.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium and Zinc. National Academies Press http://books.nap.edu/books/0309072794/html/82.html
- ^ Pasantes-Morales H, Wright CE, Gaull GE (1984). "Protective effect of taurine, zinc and tocopherol on retinol-induced damage in human lymphoblastoid cells". The Journal of Nutrition. 114 (12): 2256–61. PMID 6502269.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Sarkanen JR, Nykky J, Siikanen J, Selinummi J, Ylikomi T, Jalonen TO (2007). "Cholesterol supports the retinoic acid-induced synaptic vesicle formation in differentiating human SH-SY5Y neuroblastoma cells". Journal of Neurochemistry. 102 (6): 1941–52. doi:10.1111/j.1471-4159.2007.04676.x. PMID 17540009.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Hussey GD, Klein M (1990). "A randomized, controlled trial of vitamin A in children with severe measles". N. Engl. J. Med. 323 (3): 160–4. doi:10.1056/NEJM199007193230304. PMID 2194128.
- ^ Ellison JB (1932). "Intensive vitamin therapy in measles". Br Medical J. ii (3745): 708–11. doi:10.1136/bmj.2.3745.708.
- ^ "Walrus, liver, raw (Alaska Native)". Mealographer. Retrieved 2010-03-25.
- ^ Paul Lips (2003). "Hypervitaminosis A and fractures". N Engl J Med. 348 (4): 1927–8. doi:10.1056/NEJMe020167. PMID 12540650.
- ^ Student BMJ Man's best friend?
- ^ Walker A, Zimmerman MR, Leakey RE (1982). "A possible case of hypervitaminosis A in Homo erectus". Nature. 296 (5854): 248–50. doi:10.1038/296248a0. PMID 7038513.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link)
External links
- Facts about Vitamin A and Carotenoids, from the National Institutes of Health's Office of Dietary Supplements.