The toxicity of polar bear liver to humans is a consequence of the animal’s Arctic existence and its specialized diet. The liver of Ursus maritimus contains exceptionally high concentrations of Vitamin A, specifically in the form of retinol, a fat-soluble nutrient. Unlike most animals, the polar bear possesses a biological mechanism that allows it to accumulate and store this vitamin far exceeding safe levels for human consumption. Ingesting even a small quantity of this organ can lead to a condition known as acute hypervitaminosis A, a form of poisoning that causes severe, sudden illness and can be fatal. This phenomenon has long been recognized in the Arctic.
Why Polar Bears Store Excessive Vitamin A
The extreme accumulation of Vitamin A in the polar bear’s liver is directly linked to its position as a top predator in the marine Arctic food web. Polar bears feed almost exclusively on marine mammals, primarily ringed and bearded seals, which themselves have high concentrations of the vitamin. Seals acquire this high retinol content through their diet of fish, which in turn consume smaller organisms that concentrate Vitamin A precursors from marine algae and phytoplankton, a process called bioaccumulation.
Vitamin A is a fat-soluble molecule, meaning it cannot be easily excreted through urine and must be stored in the body’s fatty tissues. The liver is the main storage organ for this nutrient in mammals, and in the polar bear, the concentration is pushed to an extreme level. Scientific analysis of polar bear liver has found concentrations ranging from 13,000 to 18,000 International Units (IU) of Vitamin A per gram of wet tissue. Considering the daily recommended intake for a human adult is around 3,000 IU, this concentration is toxic in very small amounts.
The polar bear has evolved specialized hepatic stellate cells that can safely store these massive amounts of Vitamin A without suffering internal toxicity. This hyperaccumulation capacity is likely an evolutionary adaptation that helps the bear manage the high-retinol intake from its seal-heavy diet. The ability to store large reserves of this vitamin may also be beneficial for the bear during long periods of fasting.
Human Health Effects of Acute Poisoning
Consuming polar bear liver delivers a massive dose of retinol that overwhelms the human body’s ability to metabolize and safely store the nutrient, leading to acute hypervitaminosis A. Symptoms typically begin quickly, within a few hours of ingestion, because the excess retinol is released directly into the bloodstream. An early and pronounced symptom is a severe, crushing headache, often accompanied by vertigo and intense nausea and vomiting.
As the poisoning progresses, the affected person may experience drowsiness, dizziness, and extreme irritability. The circulating, unbound retinol begins to damage cell membranes throughout the body, acting almost like a detergent. This cellular damage can lead to blurred vision, pain in the bones, and a noticeable enlargement of the liver.
The most distinctive physical sign of severe toxicity is desquamation, or the widespread peeling of skin. This shedding can affect the entire body, beginning around the mouth and progressing to the face, torso, and limbs. In the most severe cases, the massive cellular disruption can cause liver damage, hemorrhage, coma, and ultimately death.
Historical Discovery and Avoidance
The toxicity of polar bear liver was known to the indigenous peoples of the Arctic long before it was formally recognized by Western science. Traditional knowledge within groups like the Inuit advised against consuming the liver of the polar bear and other Arctic top predators. This avoidance was a survival strategy based on centuries of practical observation.
The first well-documented instance of poisoning in European accounts occurred during the 16th century. In 1596, the Dutch explorer Willem Barents and his crew were stranded near Novaya Zemlya and consumed the liver of a polar bear for sustenance. The surviving crew members documented severe illness, noting that the skin of the sick men peeled off from head to foot.
Accounts from later expeditions, such as that of American explorer Elisha Kane in the 1850s, also recorded instances of acute illness after consuming the liver, eventually linking the symptoms to the toxic organ. Formal scientific confirmation that the cause was an overabundance of Vitamin A was established in the 1940s through chemical and biological analysis. These historical incidents provided the medical community with clear case studies of acute hypervitaminosis A.