50 Documented Cases of Poisoning after the Ingestion of Fish, Chicken, and Beef Liver

by Oct 27, 2023BLOG, ENGLISH0 comments

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People who regularly eat liver as part of the carnivore diet often argue that there is no proof that the ingestion of liver could be dangerous, apart from polar bear livers.

The evidence in the medical literature shows that this is not correct.

There are 50 cases of documented poisonings (most likely due to vitamin A but it could also be due to copper) from different types of livers: fish, chicken, and beef.

There are also several documented cases of hypervitaminosis A from the consumption of shark liver. I decided to leave those out, since they don’t seem to be relevant to most people who pursue a carnivore or ketogenic diet.

I also excluded one documented case of hypervitaminosis A in a boy who was eating chicken livers and was taking vitamin A supplements, since the vitamin A intake from the supplements was considerably higher than the one from the chicken livers.

If I had taken into account those cases as well, the total would have been around 54 known cases.

The below list largely builds but also expands on Dr. Garrett Smith’s post on X: https://x.com/NutriDetect/status/1521607494170152961?s=20

The list can be also found in the Muscle Meat Carnivore group on Facebook: https://www.facebook.com/groups/728766289024712/permalink/733036865264321/

List of 50 Documented Cases of Hypervitaminosis A after the Consumption of Various Types of Livers:


Case #1 (FISH LIVER): “A 23-month-old Chinese girl presented to the emergency department with vomiting, irritability, sore eyes and a red, peeling rash on the face. She had consumed four pieces of fish liver the night before. Her grandfather, who also ate the fish liver, had similar symptoms.”

Case #2 (FISH LIVER): “An 11-year-old Chinese boy presented with a 2-day history of abdominal pain, vomiting, headache, a red, peeling rash over his body, blistering on his fingers and tongue and perioral tingling. He and his family had eaten fish livers 8 h prior to the onset of symptoms.”

Case #3 (FISH LIVER): “A 14-year-old Chinese boy presented with a 12-h history of vomiting, severe headache and sore red eyes after ingestion of 8–10 pieces of Polyprion oxygeneios (Hapuka) fish liver. His mother and sibling also had similar symptoms after ingestion of the same fish livers. He was also taking a regular vitamin supplement that contained vitamin A.”

Source of the above 3 cases:

Rebecca M Hayman, Stuart R Dalziel, Acute Vitamin A Toxicity: a Report of Three Paediatric Casese, Journal of Paediatrics and Child Health (48), 2012,  https://onlinelibrary.wiley.com/doi/10.1111/j.1440-1754.2011.02122.x

Case #4, #5, #6 (FISH LIVER): “In December 2007, three patients (two males 41 and 13 years of age and one woman 39 years of age) of the same family ate the liver and muscle of a large fish (about 20 kg) in Keelung, North Taiwan. Three to 4 hours after ingestion, the symptoms appeared as headache, nausea, vomiting, fever, vertigo, and visual disorientation, followed by peeling of the skin after 1 week. The 41-year-old man suffered serious peeling of the skin that took more than 3 months to heal.”


Deng-Fwu Hwang et al, Species Identification and Vitamin A Level in Lutjanid Fish Implicated in Vitamin A Poisoning, Journal of Food Protection, 1 April 2010, Pages 769-773


Case #7 to #17 (11 patients) (FISH LIVER): “Eleven patients (five men, six women) aged from 15 to 45 years were studied at the medical unit of the General Hospital, Colombo, Sri Lanka. The patients belonged to three different families and were taken ill after a meal that included the liver curry of the fish Istiophorus gladius (sailfish, Sinhala: Talapath). The quantity of the fish eaten was about 113 g (4 oz) each. All patients complained of headache and drowsiness, the headache being severe and constant occurring within five to eight hours of the meal; one patient experienced nausea and five vomiting; blurring of vision and redness of eyes without diplopia was present in six cases; and a superficial peeling dermatitis was noted in nine of the patients in the face, neck, and back of chest”,

“The clinical findings in our patients are comparable to those found after ingesting the liver of polar bear or seal, which also contain large amounts of vitamin A.”


Unknown author, Clinical curio: acute vitamin A toxicity from ingesting fish liver curry, British Medical Journal, volume 287, September 1983


Case #18: (FISH LIVER, Halibut Liver Oil): “(…) a 3 year old boy of Jewish parentage, had appeared well up to the fall of 1938, when he was about 18 months old. At that time his appetite diminished and he seemed to be disinclined to play. Six months later (May 1939) he had a severe attack of tonsillitis, for which he was given sulfanilamide for two days. Two months after this, July 26, 1939, he had a tonsillectomy followed by hemorrhage, after which he received three transfusion. A blood count done after the hemorrhage showed severe anemia and 2,900 white cells per cubic millimeter, of which 44 per cent were neutrophils. The patient’s liver and spleen were found to be enlarged, and clubbing of the fingers was noted. At this time he lost much of his hair, and that which grew back was sparse, dry and coarse.”

”(…) When the patient entered the hospital in March 1940, his hair was sparse, dry and rather coarse, and eyebrows and fine hair over the body was lacking. The fingers and toes were slightly clubbed. He was pale and sallow, but there was no increase in pigmentation and no jaundice and the scleras were clear.”

“Roentgenograms of the chest and skull showed no abnormalities, but those of the limbs revealed considerable irregularity in corticol structure. In the phalanges and metacarpals the cortex was extremely thin and the medullary cavities appears to be “vacuolated.” “

“On questioning the mother, it was learned that beginning at 2 to 3 months of age the child had received a teaspoonful of halibut liver oil a day (about 240,000 U.S.P. units of vitamin A) up to the present time. Moreover, he had on occasion drunk the oil directly from the bottle in undetermined amounts.”

Interesting: “Whether or not it is justifiable to label as “abnormal” a liking for an article of food which most people would not eat by choice, there is no doubt that the child’s liking for halibut liver oil was a factor in the case which is reported. It is interesting that this desire for the oil was replaced by a desire for butter and carrots after the administration of the oil was discontinued, and that as the patient improved clinically he lost all such desires.


Hugh W. Josephs, MD, Hypervitaminosis A and Carotenemia, American Journal of Diseases of Children, January 1944,  https://jamanetwork.com/journals/jamapediatrics/article-abstract/1179829

Case #19 (PERCOMORPH LIVER OIL, a blend of natural fish liver oils): “(…) a white girl 3 years of age, was admitted Aug. 24, 1948 to the pediatric service of Syracuse Memorial Hospital with anorexia, tenderness of the extremities, low grade fever, weakness, pronounced irritability and severe generalized pruritus and scratching, especially severe in the lower extremities; symptoms were of two weeks’ duration. The child felt that she could not walk properly and described a sensation of “walking on stones”. She cried whenever the mother attempted to pick her up. Her past history included frequent infections of the upper part of the respiratory tract but no childhood diseases.”

“On questioning the mother, it was learned that the patient had been receiving approximately 400,000 to 500,000 units of vitamin A and 60,000 to 70,000 units of vitamin D daily in the form of perdomorph liver oil since 14 months of age, a period of almost two years.”


Tyree C. Wyatt, MD, et al, HYPERVITAMINOSIS A, Report of a Case, Journal of the American Medical Association (JAMA), September 1950,


Case #20 (PERCOMORPH LIVER OIL and COD LIVER OIL): “(…) a 23-month old infant, was admitted to Babies’ and Children’s Hospital, Cleveland on Dec. 22, 1944. The complaint was soreness and swollen legs.”

“(…) He was irritable and anorexic. (…) In addition, he had anorexia, constipation and pruritus, and he was restless and irritable.”

“He got from 1 to 2 teaspoons (from about 4 to 8 cc.) of cod liver oil daily from the age of 2 weeks.”

“The skin of the face was erythematous, and there was roughening of the epidermis over the right leg; the lips were dry and cracked, and there was bleeding at the corners of the mouth. The hair was coarse, dry and sparse. There were a few non-tender, discrete, movable shot-sized lymph nodes in the anterior, cervical and supraclavicular spaces.”

“His mother was requestioned about the vitamins she gave her son, and this time she admitted giving the following: (1) a preparation of vitamin complex, 2 teaspoons daily; (2) 1 dicalcium phosphate capsule daily; (3) grains (325 mg.) of saccharated ferrous carbonate twice daily ; (4) 50 mg. ascorbic acid daily, and (5) percomorph liver oil with viosterol (Mead), 1 teaspoon daily from the newborn period until October 1944 and then 2 teaspoons daily until the time of admission. His symptoms began shortly after the vitamins had been increased. The last preparation noted had not been given during each hospital stay, and each time he got better. It was learned that the patient was abnormally fond of butter, which he would eat by the teaspoonful.”


John A. Toomey, MD, and Russell A. Morissette, MD, Hypervitaminosis A, American Journal of Diseases of Children, 1947,


Case #21, #22, #23 (REEF FISH LIVER): “Three historical cases of fish poisoning among anglers were recorded in the 1970s in Bermuda. All episodes occurred after the consumption of fish liver from fish captured near Challenger Bank, Bermuda. The clinical presentations of these patients were similar to those of retinoid intoxication. These Bermudian anglers experienced intense headache, myalgia, progressive desquamation, generalized aching pain, and superficial vesicles and bullae of the skin. Sequelae for some included hair loss and diffuse peeling of the skin on the palms and soles, as well as a partial pigmentation loss. Symptoms began after ingestion of a meal of reef fish liver from (specifically) Challenger Bank, a submerged seamount, 12 mi offshore from Bermuda, the cone of which is roughly 200 ft (61 m) below the surface.”


E. Deweilly, et al, Vitamin A Intoxication from Reef Fish Liver Consumption in Bermuda, Journal of Food Protection, September 2011,


Case #24, #25, #26 (FISH LIVER, Grouper Fish): “We observed an episode of acute fish liver intoxication in which 3 man experienced dizziness, headache, blurred vision, nausea, vomiting, fever, and desquamation after ingesting the liver of the grouper fish Cephalopholis boenak (C. boenak). One of the patients had full-blown symptoms and presented with a high fever, headache, dizziness, generalized aching pain, and superficial vesicles and bullae of the skin. The treatment was mainly supportive. In the follow-up period, he subsequently developed hair loss and diffuse peeling of the skin on his palms and soles.”


Y K Chiu et al, Acute fish liver intoxication: report of three cases, September 1999,


Case #27 (FISH LIVER, Ocean Perch): “We report a case of a 27-year-old man presenting with chief complaints of flushing, headache, nausea, and joint pain. He had consumed 800 g of grilled ocean perch liver the day before and had experienced numbness shortly after. Although physical examination revealed only facial flushing, we suspected acute vitamin A intoxication due to his diet history. On day 2 after ingestion, his serum retinol levels were elevated at 1577 ng/mL, which confirmed vitamin A intoxication. He returned for follow-up on day 4 after ingestion, by which time his presenting symptoms had improved, but he had developed desquamation of his facial skin.”

“Desquamation and cheilitis subsequently occur 2–7 days after ingestion (3,4,6,7). In our case, the patient presented with typical signs and symptoms with headache, flushing, desquamation, cheilitis, and nausea.”

IMPORTANT: “The levels of serum retinol, a potentially toxic form of vitamin A, are generally not elevated, even after the ingestion of a large amount of food rich in vitamin A.”


Yosuke Homma MD et al, A Case Report of Acute Vitamin A Intoxication due to Ocean Perch Liver Ingestion, Journal of Emergency Medicine, July 2015, 


Case #28 and #29, (FISH LIVER, crowned amberjack), translated from French with Google Translate:  “A 45-year-old man and his 42-year-old wife (…) purchased from a boat based at Grau-du-Roi an exceptional piece: an adult crowned amberjack (Seriola dumerili) weighing more than 40 kg captured watches in the Mediterranean.”

“Having the habit of consuming monkfish liver, he decided to reserve for himself the piece that cannot be put up for sale. This offal was divided into two parts and eaten simply pan-fried the same day at noon for the patient and eight p.m. for his wife. Both people specified that the taste of this unusual dish was of rare finesse. After 10 hours., at the beginning of the night, the patient started having headaches that increased in intensity quickly. After 14 hours, he first vomited, then quickly non-productive. His wife then in turn had the same symptoms with disabling helmet headaches, then more heavy vomiting. The next morning, after 20 hours for the husband, the 2 patients had moderately pruritic bilateral palmar erythrosis.”

“The clinical examination found in the 2 subjects a major skin dryness with peeling at the level of 4 limbs and head, rotating dizziness, palpation painful muscle masses, asthenia in the patient who most often remained lying down. Faced with the unusual evolution of this food poisoning, the center anti-poison was consulted and hypervitaminosis A was mentioned by ingestion of large carnivorous fish liver.”

“Despite the absence of retinoid dosage in our patients, the history, the chronology of events and the table collective clinic characteristic of hypervitaminosis A (headache, dizziness, vomiting, myalgia, blurred vision, erythrosis, xeroderma then desquamation) allow us to discuss the diagnosis of fish liver poisoning carnivores rich in retinoids.”


Guillaume Ardigier et al, Intoxication par ingestion de foie de sériole de Méditerranée: tableau clinique d’une hypervitaminose A, Poisoning after ingestion of Mediterranean greater amberjack liver: Hypervitaminosis A clinical feature, La Presse Medicale, July 2010,


Case #30 to #40, 11 cases, (FISH LIVER, Halibut): “Eleven fishermen developed symptoms of acute vitamin A poisoning 5 hours after eating from 20 to 300 g of fried halibut liver, containing approximately 2-30 million units of vitamin A. The liver came from an unusually large halibut with a length of 2 m, which had been caught in the North Atlantic.”

“The men complained of dull heavy headaches, dizzyness and nausea; 4 men vomited. The next day all men appeared to have redness and desquamation of the skin. All but one sailor felt better. Appetites were normal. When the home port, Scheveningen, was reached several members of the crew visited their family doctors to show their red, peeling skin. All were able to sail again a few days later.”


J. P. Nater and H. M. G. Doeglas, Halibut Liver Poisoning in 11 Fishermen, Acta Dermato-Venereologica, 1970,


Case #41 and #42, (CHICKEN LIVER): “Twin female infants were fed 120 gm of chicken liver homogenate daily for four months. They developed irritability, vomiting, and bulging anterior fontanelles. Computed tomograms of the brain revealed enlarged ventricles in both infants and dilated subarachnoid spaces in one. Plasma vitamin A concentrations were elevated. After all sources of vitamin A intake were stopped, the infants recovered without sequelae.”


C. Patrick Mahoney, Chronic Vitamin A Intoxication in Infants Fed Chicken Liver, American Academy of Pediatrics, 1980,


Case #43 and #44 (CHICKEN LIVER) ONE DEATH: “Patient 1. This white boy was born to unrelated parents of European Jewish extraction. His first 6 months of life were complicated by poor growth and persistent otitis media. Myringotomy tubes were placed, and bilateral mastoidectomies were eventually performed. He was otherwise healthy until age 3 years, when he complained of severe leg pain. Radiographs demonstrated periosteal new bone formation on both tibias, both femurs, and the right radius. Increased intracranial pressure and splayed cranial sutures and hypercalcemia (11.2 mg/dL, 2.8 mmol/L) were present. In the following year, otitis recurred and symptoms of increased intracranial pressure (headache, nausea, vomiting, and papilledema) continued, necessitating placement of a ventrieulo- peritoneal shunt. An erythematous, exfoliative rash, alopecia totalis, liver disease, and ascites ensued. He died of renal failure associated with severe coagulopathy, pneumonia, and sepsis. Vitamin supplements had not been given on a daily basis, but multivitamins containing 2500 IU (750 REq) vitamin A had been occasionally used during the first 9 months of life. A 10-day course of a multivitamin containing 450 IU (137 REq) vitamin A had been given in the second Year. Chicken liver spread, consisting of approximately 25 g chicken liver fried in fat, was ingested two to three times a week. Dietary intake, however, did not differ from that of the parents or a healthy older sister.”

“Patient 2. The younger brother of patient 1 had recurrent exudative otitis beginning at 5 months of age, requiring myringotomies and intermittent antibiotic therapy. Otitis media characterized by a profuse black exudate recurred at age 289years, accompanied by lymphadenopathy, leg pain, and nausea. Limp, vomiting, and fever ensued, and papilledema was noted. Vitamin supplements containing 2500 IU (750 REq) vitamin A had been administered daily during the first few months of life. Diet included chicken liver spread two to three times a week, but did not differ from that of the parents or the healthy sister. Radio- graphs revealed splayed cranial sutures, but long bones were normal. A cranial CT scan revealed mild nonobstructive hydrocephalus.”

“Therefore, one chicken liver spread sandwich could contain as much as 10,500 IU (3380 REq) vitamin A, and the daily intake of vitamin A might have totaled 15,000 IU (4550 REq), including milk and multivitamin supplementation.”

“The patient remained well until 4 months after the infusion, when signs of increased intracranial pressure recurred and a ventriculoperitoneal shunt was placed. A liver biopsy specimen was obtained at this time, revealing features of severe vitamin A overload, including periportal fibrosis, crystalloid mitochondrial inclusions, and disrup- tion of hepatic architecture by numerous lipid-laden, nonparenchymal stellate (Ito) cells.” [This was after around 1.5 years on a low vitamin A diet of less than 300 IU/day. – Paola]

“Our two patients received chicken liver potentially containing large amounts of vitamin A. The ingested amounts would account for a total weekly intake of approximately 60,000 IU vitamin A, or an average daily intake of 5000 to 10,000 IU. These calculations assume that vitamin A content of the consumed liver was consis- tently as great as the maximum measured in raw, random samples. It is possible that livers of even greater vitamin A content were consumed. Nevertheless, the fatal outcome in the older child and the severe protracted course in the younger boy are not consistent with the usual course of vitamin A intoxication. ”

IMPORTANT: “A sister with identical dietary intake was healthy and had normal circulating levels of retinol and retinyl esters, suggesting variable tolerance within the family.”


Thomas O. Carpenter MD, et al, Severe hypervitaminosis A in siblings: evidence of variable tolerance to retinol intake, The Journal of Pediatrics 1987,


Case #45 (BEEF LIVER + Supplements): “Patient 1. A 29-year-old white man originally presented (…)  with a chief complaint of chronic fatigue of five years’ duration.”

“At the time of his presentation in 1979, he complained of lack of energy, anorexia, and decreased muscle strength.”

“Our initial clinical impressions at this time were: (1) malnutrition sec- ondary to anorexia of unclear cause, (2) history of infectious mononucleosis, (3) history of Gilbert’s disease.”

“The biopsy findings of cirrhosis prompted further questioning of the patient about his vitamin A intake. He then disclosed that he had a fondness for beef liver and may have regularly consumed two or three large portions (6 to 8 ounces) per week for the past eight to nine years. This quantity of liver provides an average daily intake of 30,000 to 40,000 IU of preformed vitamin A. In addition, the patient admitted taking a daily multivitamin supplement intermittently, which contained 5,000 IU of vitamin A per tablet.”

“On the basis of these findings, a diagnosis of hepatic cirrhosis secondary to chronic hypervitaminosis A was made.”


Stephen B. Inkeles, MD, et al, Hepatic and Dermatologic Manifestations of Chronic Hypervitaminosis A in Adults, The American Journal of Medicine, 1986,

Report of Two Cases


Case #46 – #50, five cases, (BEEF LIVER): “We wish to draw attention to dietary habits of patients with pseudotumor cerebri (PTC), a syndrome of elevated intracranial pressure that typically occurs in obese young women and is characterized by headache and papilledema. The nature of this condition is usually undiscovered but is associated with a variety of disorders, the most predictable of which is vitamin A intoxication. In fact, pseudotumor cerebri occurs in 30% to 50% of patients with hypervitaminosis A.1,2 This causal relationship prompted us to conduct a dietary survey of approximately 50 patients with idiopathic PTC.”

“Surprisingly, we discovered five patients who ate beef liver at least once or twice a week. Several patients consumed liver at multiple meals during a single day or regularly on luncheon sandwiches; two patients disclosed that they routinely purchased 6 to 24 lb of liver each week. None of the patients were using any of the medications occasionally associated with PTC. With the exception of mild to moderate papilledema, general physical and neurological examination findings were normal. Cranial computed tomographic scans were also normal, and CSF pressure was elevated in each of the four patients who permitted a lumbar puncture. Dietetic estimates of daily vitamin A intake in the five patients were 60,000 IU, 64,000 IU, 70,000 IU, 87,000 IU and 341,000 IU. (Recommended dietary allowance is 4,000 to 5,000 IU/day.) [This has since been lowered – Paola] Random serum vitamin A levels (normally 30 to 70 ug/dl) were elevate in four of the five patients (75 ug/dl, 107 ug/dl, 121 ug/dl, and 146 ug/dl). Two patients were men and three were women. All five patients were mildly to severely obese, and each had habitually ingested liver for several years or more. Skin manifestations of vitamin A intoxication were not observed in any of the patients;, this suggests the possibilty that neural membranes have the lowest level of sensitivity to chronic hypervitaminosis A.”


John B. Selhorst, MD, et al, Liver Lover’s Headache: Pseudotumor Cerebri and Vitamin A Intoxication, Journal of the American Medical Association (JAMA), 1984,


Picture credit:

Home made pate wrapped in bacon from pork and liver on rustic table with knife on plate

Stock Photo ID: 465326053

Copyright: miromiro



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