Eating Animal Livers Causes DEATH & Disease Via Vitamin A Toxicity

Eating Animal Livers Causes DEATH & Disease Via Vitamin A Toxicity

Goals of Presentation
Utterly and completely dispel the myth & outright lie that Vitamin A toxicity is impossible from eating liver.

Show that both humans and animals get sick and even DIE from Vitamin A toxicity from eating liver.

Show that Vitamin A toxicity can absolutely happen from eating liver just ONCE.

Show that the liver is toxic to consume from any animal.

Case studies and links provided for all assertions in this presentation (see video info below).

Definitions to Know

Cirrhosis - scarring/fibrosis of the liver.

Desquamation - skin peeling (off).

Dysentery - severe diarrhea with the presence of blood and mucus in the feces.

Coprophagia - eating feces. 

Echolalia - meaningless repetition of another person's spoken words

Bullae - large rounded blisters

Aurantiasis cutis - aka carotenoderma, yellowing or orangish tint to skin

Bear Liver Killing Rat In Study

The vitamin A content and toxicity of bear and seal liver

“It has long been known among Eskimos and arctic-travellers that the ingestion of polar bear liver by men and dogs causes severe illness. It has also been reported that the liver of a certain seal (Phoca barbata) is poisonous, although opinion on this point is less unanimous. 

The very high content of Vitamin A in the liver suggested that it might give rise to hypervitaminosis A if eaten in more than small amounts.

The ingestion of excessive amounts of bear liver by rats led in one instance to fatal hypervitaminosis A.”

Beef Liver Causing Vitamin A Toxicity In A Cat

Hypervitaminosis A-induced hepatic fibrosis in a cat.

"CLINICAL SUMMARY: We report the first case of hepatic stellate cell lipidosis and hepatic fibrosis in a domestic cat that had been fed a diet based on raw beef liver. 

The necropsy findings of chronic liver disease coupled with osteopathology supported the diagnosis of hypervitaminosis A.

As in human hepatology, if there is dietary evidence to support increased intake of vitamin A, then hypervitaminosis A should be considered in the differential diagnosis of chronic liver disease in cats."

Pork Liver Causing Vitamin A Toxicity In A Cat

Hypervitaminosis A in the cat: a case report and review of the literature.

"A case of hypervitaminosis A with secondary entrapment and compression of the left brachial plexus nerve roots is described. A 9-year-old male castrated domestic shorthair, fed a home-made diet based on raw pork liver, was submitted for examination for a left forelimb lameness that evolved to paralysis over a 2-month period. Clinical examination revealed a flaccid paralysis and atrophy of all left forelimb muscles. An ipsilateral Horner's syndrome was also noted. Radiological examination of the cervical and thoracic spine showed massive new bone formation at the ventral aspect of the second cervical to sixth thoracic vertebra. The diagnosis of hypervitaminosis A was made, based on the clinical and radiographic findings, as well as the determination of serum vitamin A concentration, which was 630 microg/dl, three times above the upper normal limit for this species. Despite the unfavourable initial prognosis, the cat progressively regained function of the affected limb approximately 6 months after the diet was changed to a commercial canned food."

Sheep Liver Causing Vitamin A Toxisity In Kittens

Severe retardation of growth with retention and displacement of incisors in young cats fed a diet of raw sheep liver high in vitamin A.

More Liver Causing Vitamin A Toxicity In A Cat

Hypervitaminosis A in a cat.

"A 10-year-old cat that was kept on a diet consisting largely of raw liver was evaluated because of lethargy, partial anorexia, and weight loss of several months' duration. The cat's head and neck were rigidly extended, and a hard mass was palpable in the ventral cervical region. Cervical and thoracic radiography revealed proliferative bony lesions of the cervical and thoracic vertebrae as well as of the sternum and costal cartilages. Serum vitamin A concentration was 4 times normal. For reasons unrelated to hypervitaminosis A, euthanasia and necropsy were performed 6 months after evaluation. The skull and the cervical and first few thoracic vertebrae were rigidly fused, and the vertebral architecture was altered by deposition of new bone. The sternum and costal cartilages were similarly affected. The historical, physical, radiographic, laboratory, and postmortem findings were consistent with the diagnosis of hypervitaminosis A. On the basis of findings in this cat, hypervitaminosis A should be suspected in any sick cat fed a diet consisting partly or completely of raw liver."

The Oldest Suspected Case Of Vitamin A Toxicity

The paleopathology of the liver.

“Our oldest evidence relating the liver to disease is indirect, a probable case of hypervitaminosis A in an early human fossil owing to the ingestion of excessive amounts of animal liver. The skeleton of a Homo erectus, recovered from a site in Kenya, East Africa and dated to 1.5 million years B.P., showed periosteal bone deposition involving the long bones and skull. Thin sections prepared from the fossilized bone revealed the periosteal new bone to be coarse-woven with enlarged, randomly placed lacunae. The same gross and histologic pattern is seen in modern patients with chronic hypervitaminosis A, invariably owing to misguided self medication.

As fire had not yet been put to use, the soft liver would have been the only easily eaten part of animal kills. Carnivore liver contains toxic levels of vitamin A, and it may well have taken some period of time before early humans learned to avoid carnivore liver.”

Polar Bear Liver

Hypervitaminosis A and fractures.

“The toxicity of certain foods that contain high amounts of vitamin A has been recognized for centuries.

The 1597 diary of Gerrit de Veer, which he wrote while taking refuge in the winter in Nova Zembla during an attempt to reach Indonesia by the northern passage, states that he and his men became gravely ill after eating polar-bear liver. They feared for their lives but ultimately recovered. De Veer’s diary also notes widespread and striking desquamation during recovery.”

Sled Dog Liver

Xavier Mertz (6 October 1882 – 8 January 1913) was a Swiss explorer, mountaineer and skier, from Basel. He took part in the Far Eastern Party, a 1912–1913 component of the Australasian Antarctic Expedition, which claimed his life.

On 14 December, the party were more than 311 miles (501 km) from the Cape Denison hut. As Mertz skied ahead, singing songs from his student days, Ninnis, the largest sledge and the strongest dog team were lost when they broke through the snow lid of a crevasse. Together with the death of their companion, Mawson and Mertz were now severely compromised; on the remaining sledge they had just ten days' worth of food, and no food for the dogs. They immediately turned back west, gradually using the six remaining dogs to supplement their food supply; they ate all parts of the animals, including their livers.

A 1969 study by Sir John Cleland and R. V. Southcott of the University of Adelaide concluded that the symptoms Mawson described—hair, skin and weight loss, depression, dysentery and persistent skin infections—indicated the men had suffered hypervitaminosis A, an excessive intake of vitamin A. Vitamin A is found in unusually high quantities in the livers of Greenland Dogs, of which both Mertz and Mawson consumed large amounts; indeed, as Mertz's condition deteriorated, Mawson may have given him more of the liver to eat, believing it to be more easily digested.”

Fish Liver (Arctic)

Social and transcultural aspects of psychiatry

“Piblokto or Arctic hysteria appears in Eskimo societies. Seen mostly in Eskimo women, symptoms include screaming, uncontrolled wild behaviour, depression, coprophagia, insensitivity to extreme cold (such as running around in the snow naked) and echolalia. It has been suggested that it may be linked to vitamin A toxicity as the Eskimo diet provides rich sources of vitamin A such as liver of arctic fish.

Pibloktoq (hysteria) and Inuit nutrition: possible implication of hypervitaminosis A.

Experimental and clinical studies of nonhumans and humans reveal somatic and behavioral effects of hypervitaminosis A which closely parallel many of the symptoms reported for Western patients diagnosed as hysterical and Inuit sufferers of pibloktoq. Eskimo nutrition provides abundant sources of vitamin A and lays the probable basis in some individuals for hypervitaminosis A through ingestion of livers, kidneys, and fat of arctic fish and mammals, where the vitamin often is stored in poisonous quantities.

Fish Liver #1 (Grouper)

Acute fish liver intoxication: report of three cases. 

“We observed an episode of acute fish liver intoxication in which 3 men 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

Symptomatologically, the clinical pictures of these patients were comparable to acute hypervitaminosis A or retinoid intoxication. The average vitamin A content in the grouper (C. boenak) is high enough to cause acute vitamin A intoxication.”

Fish Liver #2

Acute vitamin A toxicity: A report of three paediatric cases

“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.”

Fish Liver #3

“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.”

Fish Liver #4 (Hapuka)

“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.”

Fish Liver #5 (Shark)

Ingestion of shark liver associated with pseudotumor cerebri due to acute hypervitaminosis A.

“A 25-year-old previously well housewife was transferred from a peripheral coastal hospital to our department with a history of persistent headache, vomiting, and diplopia developing over a period of one week following ingestion of a meal of cooked shark liver. All the other family members too who had partaken of this meal developed those symptoms thus necessitating admission to the local hospital but had recovered with symptomatic treatment within a few days.”

Fish Liver #6 (Reef Fish)

Vitamin A intoxication from reef fish liver consumption in Bermuda.

“We report three historical cases of severe vitamin A intoxication in anglers who had consumed reef fish liver caught in Bermuda. The subsequent analyses of 35 fish livers from seven different fish species revealed that very high concentrations of vitamin A exist in tropical fish liver, even in noncarnivorous fish species. Large variations in concentrations were observed between specimens and between species. The angling population and (especially) pregnant women should be advised of this potential health threat.

Chicken Liver #1

Chronic vitamin A intoxication in infants fed 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.”

Chicken Liver #2

Severe hypervitaminosis A in siblings: Evidence of variable tolerance to retinol intake

“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 2 1/2 years, accompanied by lymphadenopathy, leg pain, and nausea. Limp, vomiting, and fever ensued, and papilledema was noted. 

Diet included chicken liver spread two to three times a week, but did not differ from that of the parents or the healthy sister. Radiographs revealed splayed cranial sutures, but long bones were normal. A cranial CT scan revealed mild nonobstructive hydrocephalus

By age 3 1/2 years, hepatomegaly, splenomegaly, and ascites were present, as were nausea, vomiting, bone pain and tenderness, lethargy, and otorrhea. By age 3 4/12 years, alopecia; a shiny, erythematous, exfoliative rash; and pleural effusion developed.”

Chicken Liver #3 - DEATH

“A 2-year-old boy had signs and symptoms of chronic hypervitaminosis A. A course of increasing severity led to eventual death. A younger brother later had similar clinical features. Chicken liver spread containing up to 420 IU/g vitamin A was the likely source of intoxication

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 ventrieuloperitoneal shunt. An erythematous, exfoliative rash, alopecia totalis, liver disease, and ascites ensued. He died of renal failure associated with severe coagulopathy, pneumonia, and sepsis.”

Beef Liver #1 Cirrhosis (scarring/fibrosis of liver)

Hepatic and dermatologic manifestations of chronic hypervitaminosis A in adults. Report of two cases.

Hepatic cirrhosis developed as a manifestation of vitamin A toxicity in one of the patients; this appears to be the first reported case of chronic hypervitaminosis A in an adult induced by the long-term frequent ingestion of beef liver.”

Beef Liver #2 - Headaches and Obesity

Liver Lover’s Headache: Pseudotumor Cerebri and Vitamin A Intoxication.

“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. 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.

Beef Liver #2 - Headaches and Obesity (cont.)

“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.

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.) Random serum vitamin A levels (normally 30 to 70 mcg/dL) were elevated in four of the five patients (75 mcg/dL, 107 mcg/dL, 121 mcg/dL, and 146 mcg/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.

These observations in adults warrant closer attention to the possibility of habitual ingestion of liver and other dietary sources of vitamin A in patients with PTC. Added scrutiny of the diet is further justified because liver and vegetables rich in vitamin A are often recommended in weight-reducing diets.”

More Organ Meats (Liver) = Worse Sperm Motility

Meat intake in relation to semen quality and reproductive hormone levels among young men in Spain

“The aim of this study was to assess the associations of intake of different types of meat with semen parameters and reproductive hormones in healthy young men. This cross-sectional study included 206 men, 18–23 years, from Southern Spain. 

[...] men who consumed organ meats had significantly lower progressive sperm motility (51·5 v. 42·8 %; P = 0·001) and higher luteinising hormone levels (4·0 v. 4·6 IU/l; P = 0·03) compared with men who did not consume organ meats.

High Vitamin A Veg + Liver + Seaweed = Toxicity

Vitamin A toxicity secondary to excessive intake of yellow-green vegetables, liver and laver.

“We report a case of sudden onset of vitamin A poisoning. A 20-year-old Japanese woman had been eating pumpkin and only a very limited amount of other foods on a daily basis for 2 years. She was overly concerned about weight reduction. Aurantiasis cutis and abnormal liver function tests were noted by her family doctor in 1995 when she was 18 years old. At that time, she stopped eating pumpkin. However, she secretly continued an excessive intake of other beta-carotene-rich vegetables, liver and laver for about 2 years. Two and one-half years after being seen by her family physician, she experienced sudden onset of low-grade fever, limb edema, cheilitis, dry skin, and headache. These symptoms worsened daily. A liver needle biopsy was performed, and it showed a normal portal tract along with fat-laden Ito cells in the space of Disse. A final diagnosis of vitamin A poisoning and hepatic injury secondary to an eating disorder was made. Her symptoms and serum beta-carotene levels returned to normal with successful adjustment of her diet.”

Finland Gov't Warns Against Liver Consumption #1

[Health risks related to high content of vitamin A in liver].

"The Finnish Board of Health has issued recommendations on diminished use of liver and foodstuffs containing liver in order to avoid overdosage of vitamin A and the health risks related thereto. Inter alia [Among other things] pregnant women and children are advised wholly to refrain from the consumption of liver and liver products."

Finland Gov't Warns Against Liver .Consumption #2

Intake of vitamin A from liver foods among Finnish 1-, 3- and 6-year old children - a quantitative risk assessment

“This risk assessment showed that long term liver consumption may expose children to retinoid intakes higher than what is considered safe. The amount of vitamin A obtained from liver-based retinoids, seems to remain below the safe intake from a single portion. With long-term consumption of liver foods however, there is a risk of exceeding upper tolerable intake levels. However, in long term consumption moderate portions of liver foods are still safe as long as they are not consumed too often. The safe portion size and eating frequency depend on the age group and type of liver food. When considering the total daily vitamin A intake from the nutritional point of view, liver consumption has a positive effect. However, the benefits of eating liver can probably be substituted by a well-balanced diet with plenty of vegetables and a reasonable amount of meat without the risk of an excess intake of retinoids.”

In Conclusion...

This should utterly and completely dispelled the myth & outright lie that Vitamin A toxicity is impossible from eating liver. Do not listen to ANYONE who claims otherwise!

I’ve shown that both humans and animals can get sick and even DIE from Vitamin A toxicity from eating liver.

I’ve shown that Vitamin A toxicity can absolutely happen from eating liver just ONCE, and that the liver is toxic to consume from any animal.

I have provided the case studies, aka references, for all the assertions in this presentation in the video info below.