Henry VIII’s struggle to father a male heir resulted from a kind of sperm damage commonly found in British men today and linked to his playboy lifestyle, an interdisciplinary study suggests.
The research from a historian and an NHS fertility specialist sheds new light on the succession crisis that changed the course of English history. It draws on recent findings that fragmentation of DNA in sperm, rather than issues with women’s fertility, may be responsible for recurrent miscarriages.
According to the authors, the Tudor king’s medical history should be used to raise awareness of male infertility and reduce stigma.
The researchers said Henry’s actions in disposing of wives who did not produce a son indicated that he blamed the women for his reproductive difficulties — in line with prevailing attitudes of the day. However, the failed pregnancies of successive wives, Henry’s living habits and a comparison with the reproductive success of his courtiers all pointed to semen problems consistent with those identified by co-author Dr Channa Jayasena in living men three years ago.
Writing in The Journal of Interdisciplinary History, Jayasena, consultant in reproductive endocrinology and andrology at Imperial College London, and Dr Valerie Shrimplin, a 16th century specialist, say the causes in Henry’s case may have included obviously unhealthy behaviours such his 5,000-calorie daily diet — but also intensive “high-impact” exercise in early adulthood when he was famed for his love of hunting on horseback and jousting.
“This is best thought of as Domestos, and it basically functions to keep the semen sterile . . . Unfortunately some men may have too much”
Dr Channa Jayasena
Between 1509 and 1536, Henry’s first two wives, Catherine of Aragon and Anne Boleyn, had a total of ten pregnancies with seven miscarriages or neonatal deaths and no surviving sons. Catherine’s surviving daughter was the future Mary I and Anne’s was the future Elizabeth I, but Henry was dissatisfied and determined to father a male heir to safeguard the new Tudor dynasty.
Significantly, Catherine of Aragon’s failure to give birth to a healthy son contributed to Henry’s decision to break with the Roman Catholic church in order to have his marriage annulled and marry the younger Anne Boleyn. Anne’s own miscarriages led in turn to a souring of marital relations that culminated in her execution.
Jane Seymour, Henry’s third wife, died shortly after giving birth to their only child, the future Edward VI, who would die aged 15, and no pregnancies are recorded for his later wives, Anne of Cleves, Katherine Howard or Catherine Parr.
The researchers found that, despite today’s common perception that pregnancy was always very dangerous in this period, Henry’s courtiers suffered far lower rates of loss than the king and his wives. Records indicate that 70 per cent of pregnancies attributed to Henry and his wives resulted in miscarriage or stillbirth. In contrast, 10 per cent of 179 pregnancies recorded for the wives of 31 noblemen of Henry’s court were unsuccessful.
The comparison excluded illegitimate children due to a lack of reliable data, although Henry acknowledged one illegitimate son, Henry FitzRoy.
In 2019, Jayasena and colleagues at Imperial College found that men whose partners suffered repeated miscarriages had twice as much DNA damage to their sperm as a control group. They said the damage may be triggered by molecules known as reactive oxygen species.
Jayasena explained: “This is best thought of as Domestos, and it basically functions to keep the semen sterile. It is made by white blood cells in the semen to stop bacteria munching the sperm. Unfortunately some men may have too much of that and that may in turn kill the sperm and cause DNA fragmentation.”
In their paper, Shrimplin and Jayasena state that Henry’s excessive meat- and carbohydrate-heavy diet, the vigorous sporting sessions of his younger days, and his morbid obesity later, were all risk factors that made it likely he suffered from this type of sperm damage. “Hence, the consistent problems with miscarriage and stillbirth probably originated with him.”
They note that in his youth Henry was a strapping sports enthusiast with a muscular build and 42in chest. By his 30s he had become grossly overweight, with estimates gleaned from his clothing and armour indicating that he eventually attained a waist of 44in, a chest of 58in, and a weight of 28st.
Shrimplin said: “He lived on bread and meat, which is a link to the modern trend, with some men often living on burgers and takeaways and chips.”
The researchers said other factors causing damage to Henry’s sperm may have included genetic predisposition, psychological stress and the effects of sexually transmitted infections.
Jayasena said that if one studied 100 men today, problems arising from DNA fragmentation in sperm would affect “tens” to some extent, with modern risk factors including junk-food diets, use of anabolic steroids and smoking. Reduced sperm function affects around half of couples seeking fertility treatment.
In the study, they write: “Increased recognition of the importance of male infertility to human health deserves increased recognition, diagnosis and treatment to ensure that affected couples receive proper support . . . Maybe the knowledge that Henry VIII, one of the most powerful rulers in European history, was almost certainly affected by this condition, will alleviate the emasculation and social stigma that is still attached to male infertility.”
Jayasena said a spotlight on the issue could bring wider benefits for men’s health. “If we can identify men who are having critical problems with their fertility in their 30s and 40s then I think these will be the same guys who, if we don’t intervene now, will present to coronary care units or have a stroke in their 70s or 80s, so this is the public health message as well.”
A study by US researchers in 2011 suggested that Henry’s reproductive difficulties may have arisen from Henry being positive for the so-called Kell blood group. If his wives were Kell negative, each marriage could have produced one healthy Kell-positive baby, while subsequent Kell-positive foetuses would have died and Kell-negative foetuses would have survived. The theory could fit the pattern of his wives’ pregnancies.
Jayasena said: “What we present is an alternative possibility, so it clearly doesn’t disprove the other one and neither does the other one disprove ours. And it’s possible of course in medicine and life that two factors can combine and synergise to produce a bad outcome.”
