Henry VIII's Health in a Nutshell (3 page)

Thus, the king fathered a total of at least eleven, and possibly sixteen, pregnancies with four different women. Fertility was obviously not Henry’s problem. It was foetal and neonate mortality that denied him his heirs.
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Several theories have been proffered to explain the extreme foetal and neonate mortality of Henry’s offspring, but these frequently centre on possible ailments experienced by the king’s wives. There are a few postulations regarding Henry’s losses that look at the king’s physiology for answers. The best known of these is the speculation that Henry had syphilis. However, a theory from 2010 regarding Henry’s blood antigens has also been gaining ground in academic and public forums, and unlike the idea that the king had syphilis, it has not been disproven.

The idea that king had syphilis was first postulated by a Victorian physician in 1888
²¹
. Since the Victorians viewed Henry as a rotter, a bounder and a rascal, as well as believing venereal disease to be the due punishment from God for having sex outside the confines of holy matrimony, this hypothesis was more or less accepted as an enjoyably lewd certainty for the next few decades. The theory was soundly and conclusively debunked in 1931 by Frederik Chamberlin, but that didn’t halt the spread of the salacious slander. The premise that Henry was riddled with syphilis was just too delightfully raunchy to refute. Even now, 100 years after it was unmasked as a myth, the idea that the king had this particular sexually transmitted disease keeps re-emerging from the depths of social media.

The fact is that neither Henry nor any of his wives ever showed symptoms of syphilis. Henry lived long enough that the tertiary stage of syphilis, which usually appears within three to ten years of contracting the disease, would have developed. This stage of syphilis is hard to overlook. It results in gaping sores in the lymph node areas, potentially the destruction of the nasal cavity, loss of the front teeth and palate erosion, and granulomatous lesions -- especially on the scalp and tibia. It would be extremely unlikely that syphilis would manifest as sores on Henry’s thighs for twenty-plus years but show no other symptoms. In a court setting wherein Henry was attended at the bath and toilet by courtiers, the physical signs of syphilis would not have been unnoted. More to the point, the physicians of Henry’s time were aware of the nature of the syphilitic symptoms. If they had seen signs of the “Great Pox” on the king, they would have identified his symptoms as such and attempted to treat him accordingly.
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The most common treatment for syphilis by Tudor physicians involved dosing syphilitic patients with massive quantities of mercury, yet Henry was never given mercury
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nor any other putative cure.

Furthermore, it does not solve the mystery of the death of Henry’s neonates and foetuses. Syphilis can only cause miscarriage if the mother has the disease or if the foetus has been exposed during pregnancy. Even then, children with congenital syphilis often survive infancy, in spite of cognitive and physical handicaps. Some people argue that three of his surviving children were the first born in Henry’s new relationship with their mothers, and therefore the women may not have contracted syphilis from him early enough for it to have affected their firstborn children. However, this argument cannot be made in relation to his daughter Mary. If Henry had been syphilitic then Mary Tudor would have almost certainly been affected in light of the fact that she was the fifth born child of his first wife, Katherina of Aragon. If syphilis was to blame as the cause of the many miscarriages preceding Mary’s birth, then her mother would have become infected almost immediately after her marriage to the king. In addition, none of Henry’s four surviving children showed symptoms consistent with congenital syphilis as adults. Although both his sons died in their teens, their health problems more closely resembled tuberculosis than any other known disease at the time. Furthermore, typical manifestations of congenital syphilis include an alteration to the teeth referred to as Hutchinson’s incisors and mulberry molars, as well as rashes and skin infections resembling secondary syphilis occurring within the first few weeks of life
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. None of these ailments or problems was reported in any of Henry’s offspring.

The latest theory that attempts to formulate a reason for Henry’s reproductive disappointments and mental alteration as an older king is the postulation that Henry had a Kell positive blood type, and that he developed the McLeod syndrome as a consequence
²⁵
. Henry’s Kell positive blood type would explain why his sexual partners suffered foetal and neonatal loss, while McLeod’s syndrome would explain why the king became physically weaker and mentally unstable in his later years.

The Kell antigen system is determined by a group of antigens on the human red blood cells and most individuals are negative for the antibody system. If Henry had a Kell positive blood type and his sexual partner did not, then any Kell positive foetus conceived after the first pregnancy would be attacked by the mother’s antibodies. After giving birth to the first Kell positive infant, or miscarrying a Kell positive foetus at any time during the pregnancy, a small amount of blood from the embryo will have been transferred to the mother. This blood transfer will cause her to experience alloimmunization, and therefore develop anti-Kell antibodies. The mother will now be “allergic” to any Kell positive foetus in her womb, and her subsequent Kell positive pregnancies are at risk because her antibodies will attack the foetus as though it were a dangerous foreign body, such as a virus. Foetuses that are Kell negative will not be attacked by the mother’s antibodies, and will thus carry to term if otherwise healthy. Therefore, being Kell positive is only a reproductive problem if the
father
of the foetus has the Kell antigens, since a mother who is Kell positive will not have an alloimmunization to either Kell positive or Kell negative foetuses.

When a Kell negative mother’s body attacks a Kell positive foetus it usually results in an illness know as haemolytic disease of the new-born (HDN), which is also called foetal erythroblastosis. HDN happens when the mother’s antibodies have destroyed the baby’s red blood cells. In milder cases, this attack on the infant’s red blood cells will just cause anaemia, where there will be too few red blood cells but not to the point where it is fatal, and/or jaundice when the red blood cells break down and produce bilirubin which can turn the baby yellow but usually isn’t a serious problem. During HDN, the baby’s red blood cells are attacked in mass quantities by the mother’s antibodies, which leads to hydrops foetalis, where fluid starts to build up in the abdomen, heart and lungs and which places pressure on the heart. This affects the hearts ability to pump. There can also be autoimmune haemolytic anaemia where so many red blood cells burst that there is insufficient blood plasma. The foetal response to maternal anti-Kell antibodies is the second most common reason for HDN
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. HDN and its complications are incredibly dangerous now and would have been almost uniformly fatal to a new-born in the Tudor era.

Because of the alloimmunization, a Kell negative woman carrying a Kell positive foetus often results in the pregnancy naturally aborting some time after twenty weeks gestation. Some pregnancies do result in infants born between thirty-one to forty weeks, but without modern medical intervention those babies will also usually die within twenty-four hours of birth
²⁷
. This means that a Kell negative woman whose partner is a Kell positive man has an increased risk of suffering from repeated late-term miscarriages, stillbirths and the death of her new-borns shortly after they are delivered
²⁸
. More rarely, infants can have hypo regenerative anaemia, which is basically the manifestation of HDN being delayed, in which case symptoms do not appear until two to six weeks after birth and therefore the baby may not die until it is a month or two old
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. The obstetrical losses suffered by Henry’s first two queens are similar to, and in some cases identical to, documented cases of Kell affected pregnancies
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.

Since most people with the Kell positive blood type can pass either a Kell positive or a Kell negative gene on to their children, every pregnancy fathered by Henry had roughly a fifty/fifty chance of being Kell negative. Any Kell positive foetus conceived after the first birth would have initiated a deadly alloimmunization within the mother’s womb, but a Kell negative foetus would not be attacked by the mother’s antibodies and would have as much chance of survival as any other healthy baby born during this era. This explains why at least one of his children, Mary, survived even though she was not the first-born of Katherina of Aragon. If Mary, the fifth baby born to Henry’s first queen, did not get the Kell positive gene from her father then she would have been safe in the womb, unlike her Kell positive siblings.
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The pregnancies of Henry’s second queen, Anne Boleyn, were a textbook example of a healthy first child and subsequent late-term miscarriages. Any of Anne’s pregnancies conceived after the birth of her daughter, Elizabeth, had unsuccessful outcomes. Henry’s third queen, Jane Seymour, had only one child before her death, but a healthy firstborn is normal with a Kell positive father. The only mistress formally acknowledged to have given Henry a child was Bessie Blount, who produced a healthy firstborn son, but then had no more children by the king.

Problems in pregnancy due to a Kell positive foetus are uncommon, but men with Kell positive blood are not necessarily rare. An American study that took place between 1993 and 1995 found that 22% of the women surveyed with a positive antibody screen had antibodies that would attack a foetus will the Kell positive blood type
³²
. In England approximately 9% of the population has a blood type positive for the Kell antigen
³³
. Nevertheless, the small percentage of Kell positive people means that 91% of Henry’s potential queens were Kell negative. Such numbers suggest that the frequency of this blood group in England is common enough that it would be a reasonable explanation for Henry’s reproductive problems.

While the theory that Henry VIII was Kell positive is based primarily on the fact that the reproductive patterns of his partners are consistent with that of a Kell positive father, there is nevertheless at least one other source that provides evidence for the theory: Henry’s family tree. In family trees carrying the Kell positive gene the daughters are able to reproduce successfully but male lines tend to die out. This is precisely what occurred in the offspring of Henry’s maternal great-grandmother, Jacquetta Woodville.

Jacquetta of Luxembourg came to England to marry royalty but fell in love with and married Richard Woodville, a mere earl, after she was widowed. It was all very scandalous at the time. She and Richard had fourteen children, and all but one of them lived to adulthood. Her daughters were all able to reproduce, but Jacquetta’s sons were mostly childless. Henry VIII’s mother was one of Jacquetta’s granddaughters, and Henry’s maternal cousins descended from his Woodville grandmother had similar reproductive troubles to his own.

In their 2013 article in the
Journal of Royal College of Physicians of Edinburgh
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, doctors Stride and Lopes-Floro argued that the reproductive patterns of Jacquetta’s sons are:

[C]learly relevant in establishing whether she could have been a carrier of the Kell positive gene. As previously noted, K/k homozygosity is rare, and it is more probable that Jacquetta could have been a K/k heterozygote, such that her offspring had a 50% chance of inheriting the immunogenic K allele. If this is correct we would expect to find that a review of her Kell positive male children would have not more than a single healthy child. Lewis Woodville, the first son, born in 1438, appears from limited information to have died age 12 in 1451 without issue. Anthony Woodville, the second son, born in 1442, played a leading role in the events of the time; he was an excellent jouster, and fought in the battles of Towton and Barnet. Though twice married he never had any children. John Woodville, the third son, born in 1445, was married to Catherine Neville, the Dowager Duchess of Norfolk, a marriage of political expediency perhaps to advance the power of the Woodville family. She was at least 65 years old, he was 19 or 20, yet she outlived him, as John was executed in 1469. Unsurprisingly there were no children. Lionel Woodville, the fourth son, born in 1447, went into the church, becoming Bishop of Salisbury. There is no evidence of marriage or offspring, beyond improbable rumours that he fathered Stephen Gardiner, subsequent Bishop of Winchester. Lionel is recorded as being the first person to receive an honorary university degree, in this case from Oxford. Richard Woodville, the fifth son, officially did not marry, and had no children. Richard adopted a low profile and tried to avoid taking sides in the War of the Roses. There are unconfirmed rumours that he married secretly and had one son, who was raised under a different name to avoid the violent deaths of many of his relatives. Edward Woodville, the sixth son, born in 1455, appears never to have married and had no known children. Thomas Woodville, the seventh son, is documented as marrying Ann Holland, but history does not record any offspring. Thus of seven sons, four clearly had no children, and the other three had no documented offspring. Only Anthony and Thomas had documented marriages, but no children; Lewis died young; John married a postmenopausal woman; and Lionel, Richard and Edward never married. This does not confirm or refute Kell blood group positivity, but it supports the above deduction that Jacquetta was the most likely source of this condition if it is causative. As such, Jacquetta’s genes may well have been the curse preventing Henry VIII’s attempts to produce healthy male heirs.