Many of the articles on the web are polarised against or in favour of white tigers. This article aims to present researched, complete and unbiased information on the breeding of white tigers and the problems resulting from inbreeding. Contrary to popular belief, inbreeding does not inevitably result in deformity. It is inbreeding of genetically unsound animals that results in deformity and health issues. Information has been drawn from as many sources as possible, particularly from scientific or research publications. Family trees showing the inter-relatedness of individual tigers mentioned here are available on the other white tiger pages on this website.


When a white tiger is mated to an orange tiger that carries the white gene, the expected ratio of white-to-orange offspring is 50/50 (this is an average across a number of litters). However, some of the family trees show a skewed ratio where white offspring consistently outnumber orange offspring. For example, Tony-Kesari matings produced 80% white cubs rather than the expected 50%. Ramana-Kesari matings produced 75% white cubs instead of the expected 25%. There are several possibilities:

Fever coat. There are records of cubs that are born white (or very pale orange) but later change to a normal orange colour. This phenomenon is known as “fever coat” and is due to conditions in the womb preventing melanin from being properly deposited in the hairs of the foetus. It is well documented in domestic cats and has been observed in captive jaguars and leopards. It most often occurs when the mother is ill or stressed – which is likely to be the case in some captive tigers – and is related to the temperature in the womb. Why so few reports of white cubs changing colour? If the cubs were born sickly and died before their first moult then they would have been recorded as “white tigers.” This would contribute to the disproportionate number of "white" cubs born to heterozygous parents, and also to the idea that "white" cubs had a disproportionately high mortality rate.

Relative Birth Weights. According to Desai and Malhotra (1992), un average white tigers are slightly larger and heavier than orange tigers and this disparity begins at birth. The average length and weight of a white tiger cub at birth is 53 cm and 1.37 kg respectively, compared to 50 cm length and 1.25 kg for an orange coloured tiger cub (they did not break this down further to look at orange tigers that carried the white gene). An adult white tiger weighs 120 to 130 kg compared to 105 to 120 kg for an adult orange tiger. (The White Tiger, JH Desai and AK Malhotra, 1992).

If the colour ratio really is skewed in favour of the white colour, white tigers (and golden tigers, which also have the gene) should outnumbered orange tigers in the wild. According to Brigadier General R. G. Burton (The Book Of The Tiger, 1933) "A writer in the 'Oriental Sporting Magazine' for 1833 states that there is certainly a white and he believes a black variety of the Tiger. In recent years white Tigers have been found in increasing numbers in one locality, whether they are true albinos or merely deficient in pigmentation. It would be interesting if a local race of this type were established. White tigers grow larger and apparently faster than their orange relatives and this may also be the case in heterozygous orange (orange-carrying-white) tigers. Such differences might begin in the womb. It is possible that the white colour is a side-effect of a gene that influences size and growth. If larger size and faster growth is beneficial, this would keep the white gene in the gene pool in spite of the reduced camouflage (since most prey species do not see in technicolour, being black-and-white rather than orange-and-white does not put white tigers at a disadvantage). It may be the case that white tigers are less likely to reach adulthood in the wild, but the gene may benefit heterozygous orange tigers. In captivity, many golden tigers display lumbar and pelvic girdle issues (some of which may be due to their increaased size putting a strain on the hip joints), but this is likely to result from inbreeding to selectively produce white and golden cubs.


According to Dan Laughlin (who was once convicted for stealing white tiger cubs) 80% of white tigers die from birth defects associated with the inbreeding necessary to cause a white coat. This is a fallacious figure. The American Zoological Association SSP claim a 35% tiger cub mortality rate in captivity (bitrth to 12 months old). An analysis of Bengal tigers listed in International studbooks and zoo inventories support this,whith white tigers, heterozygous tigers and orange (non-carrier) tigers having almost the same figure, meaning that white tigers do not have higher cub mortality than their orange brethren.

Cub mortality has many causes. Inexperienced or stressed mothers may injure, neglect or kill their cubs. The mother’s health and diet affect the cubs’ health. The presence of other tigers nearby (e.g. in circuses), or lack of privacy are stress factors. Disease, perhaps contracted while being handled, is another killer - many cubs were handled from a far too young age. Feline infectious enteritis (sometimes called "cholera"), from domestic cats, also affected tigers, although routine vaccination has greatly decreased the incidence of this disease. Inbreeding depression affects the immune system, making animals less resilient, and can cause hidden physiological abnormalities as well as visible abnormalities. Transporting young animals cubs to other facilities or TV studios is another stressor. Handling cubs from an early age made them tamer, so many were taken from their mothers and hand-reared. Mothers may kill or reject their cubs after the cubs have been handled. A big contributor was simply the fact that white tiger cubs were a photogenic novelty, and this led to excessive handling and excessive breeding (breeding the females too often) to quickly increase their numbers and meet demand. The quickest way to increase numbers was to breed white tigers together, regardless of how closely related they were, and that was what happened in the 1970s. One white Bengal tiger died of heat stroke in his travelling box at a railway station in India.

There was a higher level of cub mortality (stillbirths and early deaths) in the 1970’s due to intensive inbreeding among Mohan and Begum’ descendants resulting in inbreeding depression. At that time the cubs were novelties and were often handled or exhibited while very young, stressing them and their mothers. Early on, female offspring were sometimes back-crossed to Mohan to produce white cubs (known in livestock breeding as “fixing” a trait). When this was realised, a programme of outcrossing was pursued and early mortality decreased. At least this was the case in Indian zoos. In the USA, there was a similar situation due to the demand for white tigers as a public attraction (inbreeding continued in privately owned white tigers bred for the pet trade). In the 1980s, outcrossing to the Orissa line and the introduction of new foundation tigers improved cub survival rates. Continuing to bring in new blood, plus better animal husbandry, mimics the natural situation, where tigers have large ranges and a wider choice of mates, and reduces cub mortality to a similar level to that in wild tigers.

According to the Times of India report (8th July 2000) Nandankanan zoo had produced 300 tiger cubs - 177 orange and 123 white - since 1967, but few had survived, possibly because of weakening genes, though it did not back this up with numbers, ages or causes of death. 300 cubs over 33 years = 9.1 cubs per year average. Nandankanan Zoo decreased its early mortality rate by not publicly exhibiting tigers until they reached 12 months old. Based on captive Bengal tigers that reached breeding age (about 4 years old), studbook data shows that their average lifespan is almost 13 years, with white tigers and heterozygous tigers often outliving those lacking the white gene. Wild caught tigers lived slightly longer, based on estimated ages, but they had already won the “survival of the fittest” battle before capture. Both white and orange captive tigers have been recorded as reaching their 20s.

In “Inbreeding in white tigers” (Proc. Indian Acad. Sci.. Vol. 88 B, Part I, Number 5, October 1979, pp. 311-323), A K Roychoudhury and K S Sankhala documented the causes of death of white tiger cubs up until 1979. At the time, demand for white tigers meant there was much inbreeding to produce white cubs. The researchers noted weak eyes and shortened legs (Rewati in Washington DC), neck twisting of some white cubs (Delhi), lack of development of kidneys in Salim in Bristol, arching of the backbone of Arun in Calcutta and stillbirths in Delhi and Washington DC. They also noted apparent poor fertility, presumed to be in white tiger males. Although inbreeding is suspected to contribute to early mortality, all these defects and diseases might be ascribed to environmental rather than genetic causes. This is a summary of their data.

Delhi Zoological Park, New Delhi
The main causes of early mortality in Delhi have been pneumonia, trauma of the abdomen, congestion of the lungs, feline enteritis and negligence of the mother.

Raja x Rani (siblings). 20 white cubs in 7 litters. 13 deaths of which 4 were accidental.
Litter 1: Rukko was mauled by her inexperienced mother.
Litter 2: 2 cubs died within a day due to careless handling and neglect by their mother.
Litter 3; Ravi died due to sunstroke.
The remaining nine deaths were non-accidental: 2 were stillborn, 5 died at an early age. Bahadur, litter 4, died of congested lungs. Jagru, litter 5, died of lumber paralysis.

Raja x Radha (his mother). 9 cubs in 2 litters.
Litter 1: All 5 cubs died of pneumonia within seven months of birth.
Litter 2: 2 cubs died of starvation shortly after birth.

Rani x Dalip (her son) and produced one white female cub who died of Parkimouse syndrome and pneumonia within nine days after birth (I cannot find a description of Parkimouse).

Hari x Ashima (born to Rani and Raja in separate litters), had a single stillborn white male at the time of that article. Current studbook is incorrect about the death-date and paternity of their litters, putting Jim as the sire). Hari x Ashima were also seen to mate on multiple occasions without pregnancy resulting.

Mohan x Sukeshi (his grand-daughter) produced 5 litters of two cubs each. Only 2 survived.
Litter 1: 2 cubs died due to maternal neglect.
Litter 3: Gautam died accidentally.
Litter 5: Virat - aged 8 - died after a prolonged illness.
The remaining four deaths including one stillborn are considered to be non-accidental.

Gautam x Homa (son and daughter of Sukeshi x Mohan) had two white male cubs in one litter but both died of pernicious anaemia shortly after their birth.

Homa x Tippu (son of Rani x Raja), produced four cubs in two litters and all of them died of unknown causes within a few days after their birth. Homa x Tippu were seen to mate on multiple occasions without pregnancy occurring.
When Homa was mated to Moti, a coloured tiger unrelated to the white tigers, she produced four cubs, of which one was stillborn. Another male cub died within 24 hr of his birth due to starvation as the mother was not producing sufficient milk.
Dalip x Sukeshi and Dalip x Homa were seen to mate on several occasions without resulting in pregnancy. Before Virat’s death, he mated with Chameli several times but no pregnancy resulted.
The male white tigers appeared unable to fertilise the female white tigers when the females were in oestrus. Roychoudhury and Sankhala believed that subsequent matings and conceptions proved the males had fertility issues, but overlooked the possibility that oestrus females might have failed to ovulate or were in “false oestrus.” Feline ovulation occurs after mating, hence the females need to mate more than once to ensure fertilisation.

Calcutta Zoological Garden, Calcutta
The majority of deaths in the Calcutta Zoo have been due to feline enteritis but a few died of trypanosomiasis, In addition, Arun had abnormal arching of the backbone.

Radha’s second litter comprised two males, Neeladri and Himadri, and orange female, Malini, tht founded the line of white tigers in Calcutta.
Malini x Neeladri produced 7 litters comprising 14 cubs of which 7 were white.
Litter 3; male cub euthanized due to gangrene.
Litter 4: female cub (Kiranmala) was killed by her brother, Barun.

Chandni (white tigress from Malini x Neeladri first litter litter) was mated to Himadri (her uncle) and she produced 20 white cubs in 6 litters.
Litter 1: all died - not nursed by their mother.
Litter 2: all died - not nursed by their mother.
Litter 3: 3 cubs died -not nursed by their mother.

Ravi x Sashi (son and daughter of Malini and Neeladri) produced 3 white and 10 orange cubs in 3 litters. All died of unknown causes within 5 days after birth.

Arun and Rupa in Calcutta were kept in the same enclosure for some time but they did not produce any offspring.

National Zoological Park, Washington DC, USA

Mohini x Samson (her uncle)
Litter 1: Rajkumar (white), Ramana (orange) and Ramani (orange). All contracted an acute form of feline distemper. Only Ramana survived.
Litter 2: 2 orange cubs, one was stillborn.

Mohini x Ramana (her son)
Litter 1: Male died shortly after birth – he had shortened tendons in his forelegs which prevented “kneading action” hence he could not nurse. Female Rewati survived. She had crossed eyes and short legs.
Litter 2: 5 cubs. 3 were crushed to death while Mohini was giving birth the stillborn 5th cub. The 3 that died were believed to have been too weak to survive even if the accident had not occurred. Surviving cub, Moni, died at 16 months old due to neurological issues (possibly caused during birth or when siblings were crushed).
When Mohini’s daughter Kesari was mated to a normal coloured male, named Poona, she had a litter of six normal coloured cubs of which only one female named Marvin survived. Four of the cubs died from a viral (unspecified) type of pneumonia. The cause of death of the fifth cub was not diagnosed. All of them died within four months of their birth.

Bristol Zoo, Bristol, England

Champak x Chameli (son and daughter of Mohan x Radha) and Mohan produced 3 litters comprising 14 cubs.
Litter 1: 4 cubs all died within 10 days of birth.
Litter 2: one cub died and was eaten by mother.
Litter 3: 2 cubs died in infancy.
Champak, Akbar, Sarala, Shusmita and Seeta all died from loss of appetite and swelling of the abdomen.
Sumati x Akbar produced one white male named Salim, whose kidney was not properly developed. He was put to sleep before he was two years old.
When Chameli was mated to Champak, Shusmita to Akbar and Nirmala to Roop, all of them miscarried twice at about 42 days. Sumati was mated to both Akbar and Roop, she aborted three times.

Circus Tigers

It is almost impossible to work out the mortality rate of white circus tigers because the records are often not available. Robert Baudy, Julius von Uhl and Josip Marcan all bred white tigers starting in the 1960s. Baudy had a ruthless approach to destroying any animal that was not productive or was defective at birth, but there are no publicly available records relating to his tigers.

Von Uhls' tiger cubs were often born while the circus was travelling and were generally removed from the mother for hand-rearing. At a few months of age, the cubs were doing publicity events. He bred a number of litters from Raja and Sheba II (both heterozygotes). Some appear to be singleton litters. In other cases only one cub survived. In many cases they were lost to follow-up. Out of a litter of 6 in May/June 1975, including 3 white cubs, only heterozygote Obie is known to have reached adulthood. Two white and one orange cub were born in June 1976, the 2 white cubs were both deformed and were destroyed in infancy. Of three white cubs born in June 1977, it appears than none survived beyond 6 months (Scarlett O’Hara). Two white cubs (Manju and Bill Atma) were born to Raja and Sheba II while at Henry Doorly Zoo in November 1981, only one survived infancy.

Hawthorn Circus tigers Frosty (white) and Bengali (heterozygous orange) produced 8 known cubs between 1978 and 1982 – 6 white, 2 heterozygous orange –all did within a few weeks. A year after Bengali’s last litter with Frosty, Bengali and Saber II (heterozygote) produced 3 white cubs, one died before one year and 2 survived to breed. It would be easy to suggest that Frosty transmitted genetic defects, but there are many other variables: Bengali was more experienced, the locations where the cubs were born, the skill of the hand-rearers etc.


Some people argue that a founder has to be wild-caught. Others argue that it is any unrelated strain. I have over 30 years experience in cat genetics, including monitoring (and sometimes advising on) the development of new breeds from foundation animals.

A foundation animal is the root of the family tree. It is an animal that has made a large input into the gene pool at the start of a breeding programme so that its genes (and mutations) are over-represented in the gene pool – something known as the “founder effect.” The original founders of any breed or variety may be related to each other – parent-offspring or sibling-sibling matings are not uncommon – and display or carry the desirable mutation. That mutation becomes a fixed or common trait in the descendants. All animals in the breed or variety can trace their lineage, however indirectly, to one of the foundation animals, often through multiple lines of descent.

An unrelated outcross is not a foundation animal unless it is used so extensively that its genes become over-represented in the gene pool. If that is the case, it starts a new foundation line and the previous lines are the original foundation lines. Most outcrosses are used in a limited way to keep the gene pool healthy and cannot be considered founders, they are just contributors of healthy genes. If they display or carry the same sought-after mutation (from a very distant relationship to other foundation animals or from a compatible spontaneous mutation) they may be used to found new breeding lines that are then crossed with animals from the original breeding lines.

The problem with white tigers is that circuses (and smaller zoos linked to circuses) did not always document the ancestry of their normal colour tigers, only starting to keep detailed records when selectively breeding white tigers. Orange circus tigers came from various sources including orange offspring from early white tiger breeding, both in the USA and India, the buyers being unaware of their linke to white tigers. Many were traded via animal exchanges and intermediaries whose records no longer exist.


Sara Iverson has produced a genealogy showing the two white tiger bloodlines converging in America, with Mohan and Begum on one side and Como Zoo's brother-sister pair of wild caught Amur tigers on the other. Iverson's chart illustrates the critical junctures where the bloodlines intersect, first with Kesari and Tony at Cincinnati Zoo and later Ranjit and Obie in Omaha, like marriages between royal houses. According to "Tigers Of The World", the Indian subspecies was, at one time, represented in North America by five individuals, all siblings highly inbred for white coloration with co-efficients of 0.406. All of this means white tigers have been greatly inbred.

It is not true that infant mortality in white tigers is 80%. This urban legend seems to have originated with opponents of white tigers. Poor husbandry, stressed mothers and feline infectious enteritis (for which a vaccine is now available) played a large part in white tiger cub mortality.

White tigers show a problem called inbreeding depression - continued inbreeding to fix a particular trait (the white colour) shows up other deleterious genes in the population. As a result, white tigers are prone to being cross-eyed and have other problems as noted later. Andy Goldfarb, tiger trainer who worked at MarineWorld in Vallejo, has said that when stressed or confused all white tigers cross their eyes. Inbreeding depression can be overcome by crossing white tigers to unrelated orange tigers; although the offspring will all be orange, they can be bred back to the white parent to produce white cubs. White tigers are now found in numerous zoos, not so much for conservation purposes (since they are essentially "man-made" and most are mongrels of Bengal and Amur tigers), but because they are a hit with the public. Contrary to the claims of zoos, white tigers are not a separate "endangered species"; they are colour morphs of orange tiger which have been bred in the same way domestic cat varieties have been perpetuated. White tigers are often larger than normal Bengal tigers.

The rising number of unusual tigers reported in Similipal suggests that inbreeding is causing recessive genes to surface in that location. Inbreeding in zoos is causing other recessive genes to show up; not just colour variations, but also physical deformities. However, some of the deformities historically associated with white tiger cubs were due to being raised on a concrete floor in an old-fashioned zoo or in a circus wagon. This had a detrimental effect on their forelegs. It might have affected white tigers disproportionately because of their faster growth and heavier weight compared to orange tiger cubs.

Outside of India, the white tigers (and possibly the golden tabby tigers) in captivity are hybrid Bengal/Amur tigers and are prone to cross eyes (strabismus: the nerves of the visual pathways are routed to the wrong side of the brain), "star-gazing" (related to nutritional imbalances possibly associated with hand rearing), a weakened immune system and poor tolerance of anaesthesia. Although "star-gazing" is sometimes seen in white tigers, "Tigers Of The World" notes that this is a nervous disorder unconnected with crossed eyes and not specific to white tigers. Parkinson's syndrome has also been associates with white tigers (Rathore and Khera 1981). Vitamin B-1 deficiency resulting in star gazing has been diagnosed in hand-reared big cats.

Zoo vet David Taylor treated two white tigers, purchased from Cincinatti zoo, at a German safari park (they had salmonella poisoning) and found they reacted strangely to the anaesthetic. "The majority of albinos cannot synthesize an enzyme called tyrosinase, which could conceivably alter the way the body handles injectable anaesthetics" according to Taylor in his book "Vet On The Wild Side". At the time (1987), he had been treating 2 young white tigers with salmonella poisoning at Fritz Wurm's Stukenbrock safari park. However white tigers are not albinos, but chinchillas so this statement is erroneous when applied to the tigers.

Strabismus is evidently associated with the white colour, rather than simply to inbreeding, since normal coloured tigers related to the white strains are rarely cross-eyed. Bhim and Sumita were cross-eyed despite being born to unrelated parents; Ranjit, Bharat, Priya and Peela were bred from a brother-sister mating and were not cross-eyed. It is also associated with Bengal/Amur hybrids since only one pure Bengal white tiger has been reported to be cross eyed, this being Mohini's daughter Rewati. Rewati's younger brother, Moni, was normal eyed. Tony, common ancestor of most North American white tigers, is sometimes claimed to be cross eyed as were the Hawthorn Circus's 2 three quarters Amur white tigers, Bagheera and Frosty. According to Cuneo, Tony (who eventually died of cancer) had normal vision and was not cross-eyed. Frosty was cross-eyed. Selective breeding could reduce or eliminate strabismus in white tigers in the same way it has been eliminated from Siamese cats. The effects of inbreeding don't end with crossed eyes. Selective breeding has eliminated crossed eyes in Cuneo's tigers and, out of around 80 tigers, only a few of his oldest white tigers have this defect. Hawthorn Circus has avoided breeding siblings together or parents to offspring as has happened in zoos. The 2 white males they obtained from the Cincinnati zoo in 1976 (bred from Kesari and Tony) were outcrossed to gold tigers. A white male from that litter, Arjun, apparently went insane and should have been destroyed, but instead was retired in Germany and may have been used for breeding.

Many of the white tigers trained at Ringling Circus by Wade Burck's are claimed to be hard of hearing. One, Bagheera, was reported to be stone deaf. According to Cuneo none of the tigers had any hearing deficit otherwise they could not be used in shows. Trainers often mistake obstinacy for deafness! Three of Burck's tigers are cross-eyed. All are neurotic and easily spooked. One, Silver, is mentally retarded from inhaling placental fluids and suffering oxygen starvation at birth. Silver remained comatose for four months and was tube fed. At 5 years old, Silver roars continuously, bangs his head against his cage bars, swats phantom flies and is afraid of everything including whips, music, meat and Burck. Burck himself was mauled by a white tiger called Frosty during a fight between two tigers. Roychoudhury states that Bagheera and Frosty's paternity is unknown (Thornton 1978), though Thornton's 1978 article in The Journal Of Zoology suggested that the registered Amur tiger originally named Genghis and later called Ural had been their mother's preferred partner during "gang matings" in the Hawthorn Circus. (The tigers trained by Burck at Ringling and Hawthorn were owned by Cuneo).

According to Wade Burck, at a certain point everybody started claiming that their white tigers came from an unrelated strain. This may have been prompted by the picture of Frosty in “Sports Illustrated” showing his severely crossed-eyes.


There are no white tigers in the current zoo population that can trace ancestry to only Mohan and Begum. All current white tigers, whether generic or pure Bengal, have been outcrossed to unrelated tigers. There was a lot of past inbreeding, but later generations have been deliberately outcrossed to unrelated tigers or distant relatives. Unfortunately, this is only true of reputable zoos and conscientious private owners. There are still facilities that mate close relatives in order to get white cubs for the exotic pet market. These are not registered in any studbook so statistics about their health and longevity are unavailable. These “tiger mills” want tigers to “breed true” for the white colour and are unconcerned about producing deformed or unsound white tigers.

At the time of the 1989 White Tiger Studbook (Dr. A.K. Roychoudhury, a statistician with a genetics background), the entire captive population of tigers carrying white genes was descended from 16 individuals of which eleven were wild born and five were of unknown origin. In addition to the tigers listed in the studbook, A.K. Roychoudhury mentioned one white and two normal coloured (possibly heterozygous) cubs were born to two normal coloured tigers of unknown ancestry (female Kummo, sire's name unknown) of “Asian Circus” on August 1, 1987; these were not recorded in the studbook. All white and heterozygous tigers in zoos today can still trace part of their ancestry to Mohan and Begum, and to the other early foundation tigers were Pradeep, Sikha, and Rani. Early on, 14 more tigers became part of the foundation gene pool. They came from different areas, which has aided genetic diversity. Most current white tigers trace back to a few prolific founders whose genes are now over-represented in the modern captive white tiger gene pool. A foundation animal joins the gene pool when its first offspring is born, and it leaves the gene pool when its last descendant (gene-carrier) dies.

Inbreeding is the mating of close relatives. The opposite, outcrossing, is mating between completely unrelated animals. Inbreeding is used in a limited way in pets and livestock in order to fix a trait. In wild animal collections, genetic diversity is more important than conformity, but inbreeding can occur when opposite sex cubs are housed together too long, or when zoos cannot find a suitable unrelated mate or don’t want to risk transferring an animal to or from another zoo.

In the Orissa lines (descended from Pradeep and Sikha), there is less early inbreeding than in the Rewa line (from Mohan and Begum), with more pairings to distant relatives and to unrelated orange Bengal tigers exchanged with other Indian zoos. Among the Indian tigers, there have been a few close matings, but these are in the minority and a similar level of inbreeding may occur in the wild. It may be a different story for the generic white tigers outside of India, especially those in private hands. In general, severely inbred lines suffer reduced fertility and often die out. Other from early inbred lines became pets or performing animals and were not bred from.

Inbreeding is measured and expressed as the Coefficient of Inbreeding (COI) on a scale of 0 to 1. It is widely used in breeding domestic animals, both pet-stock and farm livestock. A COI of 0 = no inbreeding; a COI of 0.25 = 25% inbreeding (typically brother-sister) and a COI of 0.01 = 1% inbreeding. In livestock and pet breeding, “inbred” refers to severely inbred animals with a high COI.

Because the Orissa white tigers traced back to a wild-born heterozygous orange tiger unrelated to the Rewa white tigers, mating tigers from each line produced non-inbred cubs regardless of the COI of their parents (Debabrata was inbred, Diana was highly inbred).

Sara Elizabeth Carney’s 2013 genetic study on a group of orange and white tigers found an average heterozygosity (genetic variation) score of 76.1% for white tigers and 77.2% for orange. Even though the tigers were all related, and therefore had similar heterozygosity scores, 76% indicates a high level of genetic variation and means they were not inbred. (Sara Elizabeth Carney, “Genetic Diversity of White Tigers and Genetic Factors Related to Coat Color ,” May 2013.)


Captive tigers, particularly the white and stripeless tigers, have genetic variation no longer found in the wild. Some DNA variants, and mitochondrial lineages (non-nuclear DNA inherited only from the mother), have become extinct in the wild, but still exist in captive tigers. When compared to DNA extracted from museum specimens, the genetic diversity is now a fraction of what it used to be. Because of the loss of genetic diversity in the wild, even cross-bred tigers may be genetically valuable for conservation since individual subspecies risk becoming inbred to the point of extinction and need to be outcrossed to other subspecies in order to survive. The problem is, reintroducing white tigers into the wild might simply put them back into the cross-hairs of trophy hunters’ guns.


There has also been interest in white tigers in connection with Chediak-Higashi Syndrome (oculocutaneous albinism). This is similar to albino mutations and has been observed in domestic cats where it causes bluish lightening of the fur colour and is associated with crossed eyes and prolonged bleeding after surgery. Mohini was screened for Chediak-Higashi on arrival at Washington, but was negative. It is not true that Chediak-Higashi Syndrome is widespread in white tigers. It is not known where that urban legend originated. Tests and post mortem examinations have not upheld this claim.

Roychoudhury and Sankhala believed that cleft palates were directly linked to the white gene like crossed eyes. Cleft or malformed palates might explain why some white tigers stick out their tongues. Cleft palates would contriubte to cub mortality.

Other deformities include shortened tendons of the forelegs, abnormal kidneys, arched backbone and twisted neck. Reduced fertility and miscarriages were noted by Sankhala and attributed to inbreeding; to reduce mortality rates, fresh blood from tawny tigers must be introduced into white tiger breeding programmes. Some of the white tigers born to North American lines have "bulldog" faces with a snub nose, jutting jaw, domed head and wide-set eyes with an indentation between the eyes. At New Delhi Zoo, cubs born with arched backs and clubbed feet have had to be euthanased; other defects in the line include crooked spines, sway back and shortened limbs. A white tiger born at the Cincinnati Zoo developed central retinal degeneration at the Milwaukee County Zoo. Ed Maruska noted in "Tigers Of The World", that a couple of white tiger cubs born at Cincinnati Zoo had cataracts. An article published in the children's edition of National Geographic notes that circus people refer (erroneously) to white tigers as "stargazers" due to their strabismus. Following the Mohan/Radha mating, out of 48 subsequent white tiger litters there were 148 cubs. 105 died without reproducing. This represents a high mortality rate among white tigers. However, 33 of those deaths were related to accidents while the remaining 72 deaths may have been due to a combination of genetic anomalies and poor husbandry.

A famous example of the results of excessive inbreeding is Kenny Rogers who lived at the Turpentine Creek Wildlife Refuge, Eureka Springs, Arkansas. Kenny was born on 04.04.98 at Bentonville, Arkansas (probably Don Blount's establishment), and had a deformed nose and snaggle teeth which gave him a both fearsome and pitiful appearance. His unshed “baby” canine teeth competed with his adult canine teeth for space in his mouth. Because of the crowded teeth and deformed skull, he could not completely close his mouth and constantly drooled and slobbered. His pug-like nose was pushed into his face, obstructing his breathing. This made him unsaleable and therefore worthless to his breeders. The inbreeding also affected his mental capacities and personality. Kenny was non-aggressive and became very friendly with his keepers. He required surgery in 2007 and 2008 for tumours and died on 28.6.2008, aged 10, due to cancer. He was rescued with Willie, an orange tiger (probably carrying the white gene) with lesser deformities (severe cross eyes), but also unsaleable and who died aged 12.

Kenny’s parents were white tigers Loretta and Conway – these were full-siblings. Loretta was producing cubs that were still-born or short-lived. Willie could not have come from the same pairing as he was orange coloured. Because they no longer produced viable, saleable offspring, the parents were also given to Turpentine Creek Wildlife Refuge. Loretta died aged 23 and Conway died aged 19. Don Blount of Bentonville traded many of his white tigers to Betty Young of Riverglen Feline Conservation Park, West Fork, Arkansas. Don't be fooled by the term "conservation" - Riverglen is a notorious white tiger mill and was the origin of white tiger Jupiter that killed trainer Charles "Chuck" Lizza III and Cat Dancer Joy Holiday (Jupiter was found to be highly inbred despite papers saying he wasn't). By March 2013, Turpentine Creek Wildlife Rescue had rescued the remaining 30 tigers, including white tigers (including George and Chopper, who had an untreated abscess) from Riverglen. Betty Young has since died. Turpentine Creek's other white tigers were siblings Zena and Zeus.

Jack Hanna made the comment in his book about white tigers being prone to physical problems which is why Taj was pulled for hand rearing. She was unable to stand properly on her hind legs and risked becoming deformed or lame on the slick floor of the tiger den. This problem has also been observed by Cuneo. However, some zoos have reported leg problems and juvenile lameness due to over feeding (feeding on muscle meat is another cause; the calcium deficiency affects bone growth). Overfed fed cubs take on the appearance of an English bull dog, though this is reversible if caught early. Some snub nosed white tigers might fall into this category as opposed to having a brachycephaly mutation though tigers the size and shape of bull dogs have been reported in the wild. Many captive tigers, and especially white tigers, die of liver or kidney problems caused by poor diet. On good diets they are long-lived - Sheba III, Bagheera and Frosty's orange mother (not to be confused with Tony's mother, Sheba II), lived to be 26.

In the 1950s, EP Gee noted the wild white tigers of Rewa and adjacent districts were larger than orange tigers, leading sportsmen and naturalists to wonder if it was a separate breed or variety of tiger and whether wild white tigers prefer to mate with white tigers rather than orange ones. By 1959, this could not be answered in the wild due to the lack of white tigers in the wild. He noted that if the gene was a recessive mutant as Haldane advised, then the white tigers were homozygous and a pure-breeding white strain could be perpetuated in captivity at Rewa, but advised against excessive inbreeding as it could lead to deterioration. Gee added "Such a white breed of tiger, if firmly established in India, would, give this country a considerable amount of prestige in the zoological world, as well as provide a fillip for tourism and at a later date a possible economically valuable item of export ‘to foreign countries." This economic viability, not just for India, but also for zoos and circuses would prove genetically disastrous for many of the tigers.

In general, white and golden tigers grow faster than their normal coloured kin. Detailed records from zoos show tht white tigers are born larger and grow faster which could give them an advantage in the wild. Records show that orange tigers that carry the white gene also tend to become larger than average. KS Sankhala wrote "One of the functions of the white gene may have been to keep a size gene in the population in case it is ever needed." My own feeling is that if heterozygous orange tigers grow bigger and have an advantage, this coincidentally kept the white gene in the population (unfortunately trophy hunters generally aimed for the largest tigers, thus depleting the carriers of the white gene).

However, not all white tigers end up larger than their normal-coloured kin, again possibly a result of inbreeding depression and deleterious genes meeting up. One of Alan Gold's troop of performing white tigers included an abnormally small white tiger bred from Hawthorn Circus white tigers; it was possibly one of Taj and Ika's cubs born at the Columbus Zoo.

Sankhala also observed that white tigers are whiter in Rewa and this was related to the temperature. This sounds similar to temperature-dependent albinism in Siamese cats and contributed to early beliefs that the gene involved was a form of albinism. However, white tigers are chinchilla, not albino. The chinchilla gene (colour inhibitor gene) restricts the normal colour to the outer third or quarter of the hair. The longer the fur the more colour there is, hence more heavily furred Bengal/Amur hybrids in cooler climes look darker than the shorter furred white Bengal tigers in India.


In short, white tigers simply should not be selectively bred. They once occurred naturally in the wild and bred with orange tigers as part of a healthy and diverse gene pool. Breeding tigers purely for colour (to attract the public) meant that unhealthy animals were used in breeding (these would have died out in the wild due to competition with healthier animals and would not have passed on their genes). If white tigers had been allowed to crop up at a natural ratio in zoo stock then there would not be an outcry about inbreeding and health issues. The same problems occur in domestic livestock whenever they are bred for appearance and not for health. For example, Persian cats and Pug dogs have flat faces that lead to breathing problems. Blue-eyed white cats tend to be deaf. When a small pool of white tigers were inbred for colour, it created a genetic bottleneck and allowed deleterious genes to become widespread. White tigers have their place in the species (white tigers and white gene carriers may have genes for faster growth).

The white tigers in the USA are not purebred Bengal tigers, having been crossed to the Amur tiger, and the mongrelised tigers were bred purely as a public attraction. In domestic livestock, 5+ generations of backcrossing to purebred animals means the descendants from an outcross are considered pure, but in zoos they are still considered genetically contaminated. A possible common-sense solution is to import heterozygous orange Bengal tigers from India and to not use white offspring in breeding, but to use their orange heterozygous siblings. This would keep the white gene in the gene pool (with any benefits it might confer), while preventing selective breeding for the white colour. Unfortunately, the general public (and those who own exotic “pets”) remains in love with the white tiger and this drives selective breeding for white at the expense of their health.

Transcription errors in the studbook make them appear less inbred – a transcription error of a death date means Jim is erroneously shown as siring white cubs that were actually produced by Hari x Ashima (siblings).

F1 cross of Bengal and Amur tiger: 50% Bengal/50% Amur
F2 backcross to Bengal tiger: 75% Bengal/25% Amur
F3 backcross to Bengal tiger: 87.5% Bengal/12.5% Amur
F4 backcross to Bengal tiger: 93.75% Bengal genes
F5 backcross to Bengal tiger: 96.9% Bengal genes
F6 backcross to Bengal tiger: 98.5% Bengal genes
F7 backcross to Bengal tiger: 99.25% Bengal genes
F8 backcross to Bengal tiger: 99.6% Bengal genes
F9 backcross to Bengal tiger: 99.8% Bengal genes
F10 backcross to Bengal tiger: 99.9% Bengal genes


Textual content is licensed under the GFDL.

For more information on the genetics of colour and pattern:
Robinson's Genetics for Cat Breeders & Veterinarians 4th Ed (the current version)
Genetics for Cat Breeders, 3rd Ed by Roy Robinson (earlier version showing some of the historical misunderstandings)
Cat Genetics by A C Jude (1950s cat genetics text; demonstrates the early confusion that chinchilla was a form of albinism)

Pant, M. M. & Dhariyal, I. D. (1979) : White tiger progeny, its economic potentialities. Indian Forester. Special issue on 1st International Symposium on tiger. New Delhi, 22nd-24th Feb. pp. 52-58.
Rathore, B. S. & Khera, S. S. (1979): Mortality in tigers in India. Paper presented in 1st International Symposium on tiger. New Delhi.
Roychoudhury, a. K. & Sankala, S. K. (1979) : Inbreeding in white tigers. Proc. Indian Acad, Sci. 8SB: 311-313.
Roychoudhury, A. K. (1980) : Is there any lethal gene in the tiger of Rewa? Curr. Sci. 49: 518-520.
Saharia, V. B. (1979) : Population dynamics in captive tigers. Wildlife News letter 7: 36-40.

For more information on genetics, inheritance and gene pools see:
The Pros and Cons of Inbreeding
The Pros and Cons of Cloning