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Did Blood Cause Henry VIII’s Madness and Reproductive Woes?

Did Blood Cause Henry VIII’s Madness and Reproductive Woes?



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The life of England’s King Henry VIII is a royal paradox. A lusty womanizer who married six times and canoodled with countless ladies-in-waiting in an era before reliable birth control, he only fathered four children who survived infancy. Handsome, vigorous and relatively benevolent in the early years of his reign, he ballooned into an ailing 300-pound tyrant whose capriciousness and paranoia sent many heads rolling—including those of two of his wives, Anne Boleyn and Catherine Howard.

A new study chalks these mystifying contradictions up to two related biological factors. Writing in “The Historical Journal,” bioarchaeologist Catrina Banks Whitley and anthropologist Kyra Kramer argue that Henry’s blood group may have doomed the Tudor monarch to a lifetime of desperately seeking—in the arms of one woman after another—a male heir, a pursuit that famously led him to break with the Roman Catholic Church in the 1530s. A disorder that affects members of his suspected blood group, meanwhile, may explain his midlife physical and psychological deterioration.

The researchers suggest that Henry’s blood carried the rare Kell antigen—a protein that triggers immune responses—while that of his sexual partners did not, making them poor reproductive matches. In a first pregnancy, a Kell-positive man and a Kell-negative woman can have a healthy Kell-positive baby together. In subsequent pregnancies, however, the antibodies the mother produced during the first pregnancy can cross the placenta and attack a Kell-positive fetus, causing a late-term miscarriage, stillbirth or rapid neonatal death.

While an exact number is hard to determine, it is believed that Henry’s sexual encounters with his various wives and mistresses resulted in at least 11 and possibly more than 13 pregnancies. Records indicate that only four of these yielded healthy babies: the future Mary I, born to Henry’s first wife, Catherine of Aragon, after six children were stillborn or died shortly after birth; Henry FitzRoy, the king’s only child with his teenage mistress Bessie Blount; the future Elizabeth I, the first child born to Anne Boleyn, who went on to suffer several miscarriages before her date with the chopping block; and the future Edward VI, Henry’s son by his third wife, Jane Seymour, who died before the couple could try for a second.

The survival of the three firstborn children—Henry FitzRoy, Elizabeth and Edward—is consistent with the Kell-positive reproductive pattern. As for Catherine of Aragon, the researchers note, “it is possible that some cases of Kell sensitization affect even the first pregnancy.” And Mary may have survived because she inherited the recessive Kell gene from Henry, making her impervious to her mother’s antibodies.

After scanning higher branches of Henry’s family tree for evidence of the Kell antigen and its accompanying reproductive troubles, Whitley and Kramer believe they have traced it back to Jacquetta of Luxembourg, the king’s maternal great-grandmother. “The pattern of reproductive failure among Jacquetta’s male descendants, while the females were generally reproductively successful, suggests the genetic presence of the Kell phenotype within the family,” the authors explain.

The historian David Starkey has written of “two Henrys, the one old, the other young.” The young Henry was handsome, spry and generous, a devoted ruler who loved sports, music and Catherine of Aragon; the old Henry binged on rich foods, undermined his country’s stability to marry his mistress and launched a brutal campaign to eliminate foes both real and imagined. Beginning in middle age, the king also suffered leg pain that made walking nearly impossible.

Whitley and Kramer argue that McLeod syndrome, a genetic disorder that only affects Kell-positive individuals, could account for this drastic change. The disease weakens muscles, causes dementia-like cognitive impairment and typically sets in between the ages of 30 and 40. Other experts have attributed Henry VIII’s apparent mental instability to syphilis and theorized that osteomyelitis, a chronic bone infection, caused his mobility problems. For Whitley and Kramer, McLeod syndrome could explain many of the symptoms the king experienced later in life.

So is time to absolve Henry VIII of his bloodthirsty reputation and cut him some slack as a Kell-positive McLeod syndrome sufferer? If Whitley and Kramer have anything to do with it, we may finally get a definitive answer: They are in the process of asking England’s reigning monarch, Queen Elizabeth, for permission to exhume her distant relative and perform DNA tests on his hair and bones.


How Henry VIII’s Failing Health Affected His Life and Reign

Henry VIII ruled for 37 years, a period that saw him establish England on the world stage. But his reign was also marked by tumult, including his break with the Catholic Church, drastic changes to English religious and political life, profligate spending and an exceedingly troubled personal life that saw several wives cast aside. But how much of this can be chalked up to the injuries and ill-health Henry suffered throughout his life and does medicine help us solve the riddle of this troubled king?


Did syphilis cause Henry VIII's madness and reproductive woes?

Why did Henry VIII have so many wives and mistresses yet so few children? What caused the Tudor monarch's descent into mental instability and physical agony in the second half of his life? A rare blood group and a genetic disorder associated with it may provide clues, a new study suggests. read more

Henry VIII did not die from syphilis. He may have had six wives, as well as a mistress to prove he could sire a male, but he was not promiscuous like Charles II and his relations were. What killed him was septicemia and the results of concussion caused by sporting injuries. read more

The disease weakens muscles, causes dementia-like cognitive impairment and typically sets in between the ages of 30 and 40. Other experts have attributed Henry VIII’s apparent mental instability to syphilis and theorized that osteomyelitis, a chronic bone infection, caused his mobility problems. read more

Henry’s poor reproductive record has led some people to suggest that Henry may have had syphilis. Tudor doctors knew this disease well and called it ‘the great pox’. The Tudor cure for the disease was a six week treatment with mercury where the patient was usually confined to bed. read more

If Henry VIII had syphilis as early as 1509 when he married Catherine (or from early in their marriage), his syphilis would likely have been latent (no visible symptoms) by the time Paracelsus first used mercury as a treatment. read more


Did Blood Cause Henry VIII’s Madness and Reproductive Woes? - HISTORY

Henry VIII, King of England and founder of the Anglican Church, was basically the Brad Pitt of his day when he was younger. Charming, attractive and even kind, for a member of the Royal family. Yet he is most remembered for being gluttonous, impaired and executing wives.

Research conducted by bioarchaeologist Catrina Banks Whitley while a graduate student at Southern Methodist University and anthropologist Kyra Kramer, leads them to speculate that the numerous miscarriages suffered by Henry's wives could be explained if the king's blood carried the Kell antigen. A Kell negative woman who has multiple pregnancies with a Kell positive man can produce a healthy, Kell positive child in a first pregnancy but the antibodies she produces during that first pregnancy will cross the placenta and attack a Kell positive fetus in subsequent pregnancies.

As they write in The Historical Journal, the pattern of Kell blood group incompatibility is consistent with the pregnancies of Henry's first two wives, Katherine of Aragon and Anne Boleyn. If Henry also suffered from McLeod syndrome, a genetic disorder specific to the Kell blood group, it would finally provide an explanation for his shift in both physical form and personality from a strong, athletic, generous individual in his first 40 years to the monstrous paranoiac he would become, virtually immobilized by massive weight gain and leg ailments.

"It is our assertion that we have identified the causal medical condition underlying Henry's reproductive problems and psychological deterioration," write Whitley and Kramer.

Henry married six women, two of whom he famously executed, and broke England's ties with the Catholic Church – all in pursuit of a marital union that would produce a male heir. Historians have long debated theories of illness and injury that might explain the physical deterioration and frightening, tyrannical behavior that he began to display after his 40th birthday. Less attention has been given to the unsuccessful pregnancies of his wives in an age of primitive medical care and poor nutrition and hygiene, and authors Whitley and Kramer argue against the persistent theory that syphilis may have been a factor.

Blood group incompatibility between Henry VIII and his six wives could have driven the Tudor king's reproductive woes, and a genetic condition related to his blood group could finally provide an explanation for his dramatic physical and mental changes at mid-life. Credit: tudorhistory.org

A Kell positive father frequently is the cause behind the inability of his partner to bear a healthy infant after the first Kell negative pregnancy, which the authors note is precisely the circumstance experienced with women who had multiple pregnancies by Henry. The majority of individuals within the Kell blood group are Kell negative, so it is the rare Kell positive father that creates reproductive problems.

Further supporting the Kell theory, descriptions of Henry in mid-to-late life indicate he suffered many of the physical and cognitive symptoms associated with McLeod syndrome – a medical condition that can occur in members of the Kell positive blood group.

By middle age, the King suffered from chronic leg ulcers, fueling longstanding historical speculation that he suffered from type II diabetes. The ulcers also could have been caused by osteomyelitis, a chronic bone infection that would have made walking extremely painful. In the last years of his life, Henry's mobility had deteriorated to the point that he was carried about in a chair with poles. That immobility is consistent with a known McLeod syndrome case in which a patient began to notice weakness in his right leg when he was 37, and atrophy in both his legs by age 47, the report notes.

Whitley and Kramer argue that the Tudor king could have been suffering from medical conditions such as these in combination with McLeod syndrome, aggravated by his obesity. Records do not indicate whether Henry displayed other physical signs of McLeod syndrome, such as sustained muscle contractions (tics, cramps or spasms) or an abnormal increase in muscle activity such as twitching or hyperactivity. But the dramatic changes in his personality provide stronger evidence that Henry had McLeod syndrome, the authors point out: His mental and emotional instability increased in the dozen years before death to an extent that some have labeled his behavior psychotic.

McLeod syndrome resembles Huntington's disease, which affects muscle coordination and causes cognitive disorder. McLeod symptoms usually begin to develop when an individual is between 30 and 40 years old, often resulting in damage to the heart muscle, muscular disease, psychiatric abnormality and motor nerve damage. Henry VIII experienced most, if not all, of these symptoms, the authors found.

Fetal mortality is the Kell legacy, not infertility

Henry was nearly 18 when he married 23-year-old Catherine of Aragon. Their first daughter, a girl, was stillborn. Their second child, a boy, lived only 52 days. Four other confirmed pregnancies followed during the marriage but three of the offspring were either stillborn or died shortly after birth. Their only surviving child was Mary, who would eventually be crowned the fourth Monarch in the Tudor dynasty.

The precise number of miscarriages endured by Henry's reproductive partners is difficult to determine, especially when various mistresses are factored in, but the king's partners had a total of at least 11 and possibly 13 or more pregnancies. Only four of the eleven known pregnancies survived infancy. Whitley and Kramer call the high rate of spontaneous late-term abortion, stillbirth, or rapid neonatal death suffered by Henry's first two queens "an atypical reproductive pattern" because, even in an age of high child mortality, most women carried their pregnancies to term, and their infants usually lived long enough to be christened.

The authors explain that if a Kell positive father impregnates a Kell negative mother, each pregnancy has a 50-50 chance of being Kell positive. The first pregnancy typically carries to term and produces a healthy infant, even if the infant is Kell positive and the mother is Kell negative. But the mother's subsequent Kell positive pregnancies are at risk because the mother's antibodies will attack the Kell positive fetus as a foreign body. Any baby that is Kell negative will not be attacked by the mother's antibodies and will carry to term if otherwise healthy.

"Although the fact that Henry and Katherine of Aragon's firstborn did not survive is somewhat atypical, it is possible that some cases of Kell sensitization affect even the first pregnancy," the report notes. The survival of Mary, the fifth pregnancy for Katherine of Aragon, fits the Kell scenario if Mary inherited the recessive Kell gene from Henry, resulting in a healthy infant. Anne Boleyn's pregnancies were a textbook example of Kell alloimmunization with a healthy first child and subsequent late-term miscarriages. Jane Seymour had only one child before her death, but that healthy firstborn also is consistent with a Kell positive father.

Several of Henry's male maternal relatives followed the Kell positive reproductive pattern.

"We have traced the possible transmission of the Kell positive gene from Jacquetta of Luxembourg, the king's maternal great-grandmother," the report explains. "The pattern of reproductive failure among Jacquetta's male descendants, while the females were generally reproductively successful, suggests the genetic presence of the Kell phenotype within the family."


The honest truth about these trendy diets

Posted On April 29, 2020 15:47:05

This time of year, the subject of dieting is very popular with the promise of quick weight loss, but it’s important to carefully choose your weight-loss strategy. Doing so can help you can drop unwanted pounds safely and successfully — and boost your performance. The below info was provided by Ms. Carolyn Zisman, a nutritionist working at the Human Performance Resource Center.

Low-carb diets

Diets that are typically very low in carbs (less than five percent of calories or 50 grams daily) and high in fat (70–80 percent) can put you into ketosis. This means your body is producing ketones, which uses stored fat (instead of carbs) for energy. Aside from glucose from carbs, ketones from fat are the only fuel your brain can use. You might lose more weight on a moderate-protein, high-fat diet than a typical low-fat one.

(U.S. Navy photo by Mass Communication Specialist 1st Class Todd A. Schaffer)

Additionally, you can lower some risks for heart disease and type two diabetes. These diets also eliminate sugars and sweeteners, and they help you increase your intake of vegetables, omega three-rich seafood, nuts, and seeds. However, keto-type diets eliminate all grains, pastas, breads, beans, starchy vegetables, and nearly all fruit, which are critical sources of fiber, vitamins, and minerals. Carb restriction also might lead to underfueling, hunger, fatigue, depression, irritability, constipation, headaches, and “brain fog,” which can affect your performance. Ketosis might make it harder to meet the extreme physical and mental challenges of your duties, too.

Keto-type diets are also tough to maintain because there are carbs in nearly all foods, including fruits, vegetables, legumes (beans, lentils, and peanuts), dairy products, and grains. Since your body needs to sustain ketosis for weight loss, it might be especially hard in environments with limited food options.

“Caveman” diets

High-protein, moderate-fat diets focus on foods that your hunter-gatherer ancestors ate, including fruits, vegetables, lean meats, fish, nuts and seeds. They’re also high in fiber and low in sodium and refined sugars. In addition, they’re generally healthy and not too hard to follow — whether you’re at home, the mess hall, or eating out.

Since these diets rely heavily on fresh food, it sometimes can take longer to plan meals. Fish and grass-fed meat can be expensive, too. Caveman-type diets also exclude entire food groups—such as whole grains, dairy, and legumes—and increase your risk for nutrient deficiencies. Also, there’s no difference in a high-protein, low-carb diet vs. a reduced-calorie diet for weight loss.

Vietnamese chefs teach Sailors assigned to the aircraft carrier USS Carl Vinson (CVN 70) how to prepare local dishes.

(U.S. Navy photo by Mass Communication Specialist 2nd Class Tom Tonthat)

Carbs are your body’s preferred fuel source, and limiting them can lower your performance. While a low-carb diet is easier to do because you can eat carb-rich, starchy vegetables such as potatoes or squash, there might be times when this isn’t practical, especially if you’re on a mission with MREs or limited produce.

Intermittent fasting

Intermittent fasting (IF) essentially involves skipping meals for partial or full days (12–24 hours), severely restricting calories for several days in a row, or eating under 500 calories on two non-consecutive days.

While some research from animal studies shows that restricted eating might benefit longevity, there’s no evidence that it affects longevity in humans. However, those diagnosed with type two diabetes might be able to manage their blood sugar with IF. Fasting also can be effective with an average weight loss of 7–11 pounds over 10 weeks.

Still, IF can be hard for someone who needs to eat every few hours to sustain energy for physical and mental performance. Some will overeat on non-fasting days, so IF isn’t recommended for those with disordered eating or type one diabetes — or if you take medications that require food.

Weight loss comes down to energy balance: Eat less or move more to burn extra calories. In terms of performance, you need to eat more often to ensure you’re always sufficiently fueled, so fasting can be a challenge.

Cleansing or detoxification

“Detox” diets — also called “cleanses” or “flushes” — claim to help remove toxins from your body, leading to weight loss. Cleanses includes diets, supplements, drinks, laxatives, enemas, or a combination of these strategies.

Non-laxative cleanses or juice fasts can jump-start quick weight loss, but you still need to follow up with a proper approach that is realistic and sustainable. Since your calorie intake is very low on these particular days, it also can affect your physical performance.

Fort Monroe’s Staff Sgt. Joshua Spiess prepares a head of garlic while competing for the Armed Forces Chef of the Year.

Detox-related weight loss is often only temporary and likely results from water loss. You also might gain weight when you resume normal eating. Extreme low-calorie diets can lower your body’s basal metabolic rate (the number of calories needed to perform basic, life-sustaining functions) as it struggles to preserve energy. Detox diets, which often require some fasting and severely limit protein, also can cause fatigue. They can result in vitamin, mineral, and other essential nutrient deficiencies in the long term, too. And the jury’s still out on whether detox diets actually remove toxins from your body. Depending on the ingredients used, detox diets also can cause cramping, bloating, diarrhea, nausea, vomiting, and dehydration, so they aren’t recommended for healthy and safe weight loss.

What’s the best way to lose weight and keep it off?

Quick weight loss (more than two pounds per week) can backfire in terms of health and weight maintenance. If you eat too little, your body might use muscle for fuel, instead of carbs (primary fuel) or fat (secondary fuel). Muscle burns more calories than stored fat, so losing muscle can actually slow your metabolism and ultimately make it harder to lose weight and keep it off.

The best approach is one that provides enough fuel — fruit, vegetables, whole grains, low-fat dairy, lean meat, fish, eggs, nuts, and healthy fats — to perform your duties and preserve muscle. Read HPRC’s “Warfighter Nutrition Guide” for tips to maintain your overall health and body weight.

For safe weight loss, make sure you are not causing harm and still have enough physical and mental strength to perform well. Work with your healthcare provider or a registered dietitian to create a healthy eating plan. You also want to make lifestyle changes that include exercise, so you can stay in warrior-athlete shape.

More on We are the Mighty

MIGHTY TRENDING

1 D. Starkey, Henry: virtuous prince (London, 2008), p. 3.

2 C. Erickson, Great Harry: the extravagant life of Henry VIII (New York, NY, 1980), p. 10.

3 H. Jung, ‘McLeod syndrome: a clinical review’, in Adrian Danek, ed., Neuroacanthocytosis syndromes (New York, NY, 2004), pp. 45–53, at p. 45.

4 K. Lindsey, Divorced, beheaded, survived: a feminist reinterpretation of the wives of Henry VIII (Reading, MA, 1995), p. 135.

5 D. Starkey, Six wives: the queens of Henry VIII (New York, NY, 2003), pp. 628–9.

6 Starkey, Henry: virtuous prince, p. 308.

8 Starkey, Six wives, p. 274.

9 L. B. Smith, Henry VIII: the mask of royalty (Chicago, IL, 1982), p. 128.

10 Starkey, Six wives, p. 274.

14 S. Lipscomb, 1536: the year that changed Henry VIII (Oxford, 2009), pp. 66–7 E. Ives, The life and death of Anne Boleyn (Oxford, 2004), pp. 191–2.

15 Keynes , M. , ‘The personality and health of Henry VIII (1491–1547) ’, Journal of Medical Biography , 13 , ( 2005 ), pp. 174 –83Google Scholar , at p. 180.

16 D. Starkey, The reign of Henry VIII: personalities and politics (London, 1985).

17 M. L. Powell and D. C. Cook, ‘Treponematosis: inquiries into the nature of a protean disease’, in M. L. Powell and D. C. Cook, eds., The myth of syphilis: the natural history of treponematosis in North America (Gainesville, FL, 2005), pp. 9–62, at pp. 24–30.

18 Agbaje , I. , ‘Increased concentrations of the oxidative DNA adduct 7,8-dihydro-8-oxo-2-deoxyguanosine in the germ line of men with type 1 diabetes ’, Reproductive BioMedicine Online , 16 , ( 2008 ), pp. 401 –9CrossRefGoogle ScholarPubMed .

19 Murphy , C. , ‘Second opinions: history winds up in the waiting room ’, The Atlantic , 287 , ( 2001 ), pp. 16 – 18 Google Scholar .

20 R. Hutchinson, The last days of Henry VIII: conspiracy, treason and heresy at the court of the dying tyrant (London, 2005), pp. 205–10.

21 Ives, Life and death, p. 190.

22 Erickson, Great Harry, p. 304.

23 Starkey, Six wives, pp. 123, 161 A. Fraser, The wives of Henry VIII (New York, NY, 1992), p. 136.

25 Santiago , J. C. et al., ‘ Current clinical management of anti-Kell alloimmunization in pregnancy ’, European Journal of Obstetrics and Gynecology and Reproductive Biology , 136 , ( 2008 ), pp. 151 –4CrossRefGoogle ScholarPubMed Baichoo , V. and Bruce-Tagoe , A. , ‘ Recurrent hydrops fetalis due to Kell allo-immunization ’, Annals of Saudi Medicine , 20 , ( 2000 ), pp. 415 –16CrossRefGoogle ScholarPubMed M. E. Caine and E. Mueller-Heubach, ‘Kell sensitization in pregnancy’, American Journal of Obstetrics and Gynecology, Jan. (1986), pp. 85–90 Bowman , J. M. et al., ‘ Maternal kell blood group alloimmunization ’, Obstetrics and Gynecology , 79 , ( 1992 ), pp. 239 –44Google ScholarPubMed Mayne , K. et al., ‘ The significance of anti-Kell sensitization in pregnancy ’, Clinical and Laboratory Hematology , 12 , ( 1990 ), pp. 379 –85CrossRefGoogle ScholarPubMed Marsh , W. L. , and Redman , C. M. , ‘ The Kell blood group system: a review ’, Transfusion , 30 , ( 1990 ), pp. 158 –67CrossRefGoogle ScholarPubMed Berkowitz , R. L. et al., ‘ Death in utero due to Kell sensitization without excessive elevation of the Delta OD 450 value in amniotic fluid ’, Obstetrics and Gynecology , 60 , ( 1982 ), pp. 746 –9Google Scholar Goh , J. T. et al., ‘ Anti-Kell in pregnancy and hydrops fetalis ’, Aust NZ Journal of Obstetrical Gynaecology , 33 , ( 1993 ), pp. 210 –11Google ScholarPubMed .

26 Dhodapkar , K. and Blei , F. , ‘Treatment of hemolytic disease of the newborn caused by anti-Kell antibody with recombinant erythropoietin ’, Journal of Pediatric Hematology/Oncology , 23 , ( 2001 ), pp. 69 – 70 CrossRefGoogle ScholarPubMed , at p. 69.

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Blood group anomaly could explain Tudor king’s reproductive problems and tyrannical behavior

Blood group incompatibility between Henry VIII and his wives could have driven the Tudor king’s reproductive woes, and a genetic condition related to his suspected blood group could also explain Henry’s dramatic mid-life transformation into a physically and mentally-impaired tyrant who executed two of his wives.

Research conducted by bioarchaeologist Catrina Banks Whitley while she was a graduate student at SMU and anthropologist Kyra Kramer shows that the numerous miscarriages suffered by Henry’s wives could be explained if the king’s blood carried the Kell antigen. A Kell-negative woman who has multiple pregnancies with a Kell-positive man can produce a healthy, Kell-positive child in a first pregnancy But the antibodies she produces during that first pregnancy will cross the placenta and attack a Kell-positive fetus in subsequent pregnancies.

As published in The Historical Journal (Cambridge University Press), the pattern of Kell blood group incompatibility is consistent with the pregnancies of Henry’s first two wives, Katherine of Aragon and Anne Boleyn.


Contents

Lampreys live mostly in coastal and fresh waters and are found in most temperate regions. Some species (e.g. Geotria australis, Petromyzon marinus, and Entosphenus tridentatus) travel significant distances in the open ocean, [10] as evidenced by their lack of reproductive isolation between populations. Other species are found in land-locked lakes. Their larvae (ammocoetes) have a low tolerance for high water temperatures, which may explain why they are not distributed in the tropics.

Lamprey distribution may be adversely affected by overfishing and pollution. In Britain, at the time of the Conquest, lampreys were found as far upstream in the River Thames as Petersham [ citation needed ] . The reduction of pollution in the Thames and River Wear has led to recent sightings in London and Chester-le-Street. [11] [12]

Distribution of lampreys may also be adversely affected by dams and other construction projects due to disruption of migration routes and obstruction of access to spawning grounds. Conversely, the construction of artificial channels has exposed new habitats for colonisation, notably in North America where sea lampreys have become a significant introduced pest in the Great Lakes. Active control programs to control lampreys are undergoing modifications due to concerns of drinking water quality in some areas. [13]

Basic external anatomy of a lamprey

Anatomy Edit

Adults superficially resemble eels in that they have scaleless, elongated bodies, and can range from 13 to 100 cm (5 to 40 inches) in length. Lacking paired fins, adult lampreys have large eyes, one nostril on the top of the head, and seven gill pores on each side of the head.

The brain of the lamprey is divided into the forebrain, diencephalon, midbrain, cerebellum, and medulla. [14]

The heart of the lamprey is anterior to the intestines. It contains the sinus, one atrium, and one ventricle protected by the pericardial cartilages. [14]

The pineal gland, a photosensitive organ regulating melatonin production by capturing light signals through the photoreceptor cell converting them into intercellular signals of the lamprey is located in the midline of its body, for lamprey, the pineal eye is accompanied by the parapineal organ. [15]

The buccal cavity, anterior to the gonads, are responsible to attaching, through suction, to either a stone or their prey. This then allows the tongue to be able to have contact with the stone to rasp algae, or tear at the flesh of their prey to be able to drink their blood. [16]

The pharynx is subdivided the ventral part forming a respiratory tube that is isolated from the mouth by a valve called the velum. This is an adaptation to how the adults feed, by preventing the prey's body fluids from escaping through the gills or interfering with gas exchange, which takes place by pumping water in and out of the gill pouches instead of taking it in through the mouth.

One of the key physical components to the lamprey are the intestines, which are located ventral to the notochord. Intestines aid in osmoregulation by intaking water from its environment and desalinating the water they intake to an iso-osmotic state with respect to blood, and are also responsible for digestion. [17]

Near the gills are the eyes, which are poorly developed and buried under skin in the larvae. The eyes consummate their development during metamorphosis, and are covered by a thin and transparent layer of skin that becomes opaque in preservatives. [18]

Morphology Edit

The unique morphological characteristics of lampreys, such as their cartilaginous skeleton, suggest they are the sister taxon (see cladistics) of all living jawed vertebrates (gnathostomes). They are usually considered the most basal group of the Vertebrata. Instead of true vertebrae, they have a series of cartilaginous structures called arcualia arranged above the notochord. Hagfish, which resemble lampreys, have traditionally been considered the sister taxon of the true vertebrates (lampreys and gnathostomes) [19] but DNA evidence suggests that they are in fact the sister taxon of lampreys. [20]

Studies have shown that lampreys are amongst the most energy-efficient swimmers. Their swimming movements generate low-pressure zones around the body, which pull rather than push their bodies through the water. [21]

Research on sea lampreys has revealed that sexually mature males use a specialized heat-producing tissue in the form of a ridge of fat cells near the anterior dorsal fin to stimulate females. After having attracted a female with pheromones, the heat detected by the female through body contact will encourage spawning. [22]

Due to certain peculiarities in their adaptive immune system, the study of lampreys provides valuable insight into the evolution of vertebrate adaptive immunity. Generated from a somatic recombination of leucine-rich repeat gene segments, lamprey leukocytes express surface variable lymphocyte receptors (VLRs). [23] This convergently evolved characteristic allows them to have lymphocytes that work as the T cells and B cells present in higher vertebrates immune system. [24]

Northern lampreys (Petromyzontidae) have the highest number of chromosomes (164–174) among vertebrates. [25]

Pouched lamprey (Geotria australis) larvae also have a very high tolerance for free iron in their bodies, and have well-developed biochemical systems for detoxification of the large quantities of these metal ions. [26]

Lampreys are the only extant vertebrate to have four eyes. [27] Most lampreys have two additional parietal eyes: a pineal and parapineal one (the exception is members of Mordacia). [28]

Adaptations Edit

Different species of lamprey have many shared physical characteristics. However, the same anatomical structure can serve different functions in the lamprey depending on whether or not it is carnivorous. For example, non-carnivorous species use their teeth to scrape algae from rocks for food, [29] rather than drilling into the flesh of hosts. The mouth and suction capabilities of the lamprey not only allow it to cling to a fish as a parasite, [30] but provide it with limited climbing ability so that it can travel upstream and up ramps or rocks to breed. [31] [30] This ability has been studied in an attempt to better understand how lampreys battle the current and move forward despite only being able to hold onto the rock at a single point. [31] Some scientists are also hoping to design ramps [31] that will optimize the lamprey’s climbing ability, as lampreys are valued as food in the Northwest United States and need to be able to get upstream to reproduce. [30]

The last common ancestor of lampreys appears to have been specialized to feed on the blood and body fluids of other fish after metamorphosis. [32] They attach their mouthparts to the target animal's body, then use three horny plates (laminae) on the tip of their piston-like tongue, one transversely and two longitudinally placed, to scrape through surface tissues until they reach body fluids. [33] The teeth on their oral disc are primarily used to help the animal attach itself to its prey. [34] Made of keratin and other proteins, lamprey teeth have a hollow core to give room for replacement teeth growing under the old ones. [35] Some of the original blood-feeding forms have evolved into species that feed on both blood and flesh, and some who have become specialized to eat flesh and may even invade the internal organs of the host. Tissue feeders can also involve the teeth on the oral disc in the excision of tissue. [36] As a result, the flesh-feeders have smaller buccal glands as they do not require to produce anticoagulant continuously and mechanisms for preventing solid material entering the branchial pouches, which could otherwise potentially clog the gills. [37] A study of the stomach content of some lampreys has shown the remains of intestines, fins and vertebrae from their prey. [38] Although attacks on humans do occur, [39] they will generally not attack humans unless starved. [40] [19]

Carnivorous forms have given rise to the non-carnivorous species that feed on algae, [41] and "giant" individuals amongst the otherwise small American brook lamprey have occasionally been observed, leading to the hypothesis that sometimes individual members of non-carnivorous forms return to the carnivorous lifestyle of their ancestors. [42]

Another important lamprey adaptation is its camouflage. Similarly to many other aquatic species, most lampreys have a dark-colored back, which enables them to blend in with the ground below when seen from above by a predator. Their light-colored undersides allow them to blend in with the bright air and water above them if a predator sees them from below.

Lamprey coloration can also vary according to the region and specific environment in which the species is found. Some species can be distinguished by their unique markings – for example, Geotria australis individuals display two bluish stripes running the length of its body as an adult. [43] These markings can also sometimes be used to determine what stage of the life cycle the lamprey is in G. australis individuals lose these stripes when they approach the reproductive phase and begin to travel upstream. [43] Another example is Petromyzon marinus, which shifts to more of an orange color as it reaches the reproductive stage in its life cycle.

Lifecycle Edit

The adults spawn in nests of sand, gravel and pebbles in clear streams, and after hatching from the eggs, young larvae—called ammocoetes—will drift downstream with the current till they reach soft and fine sediment in silt beds, where they will burrow in silt, mud and detritus, taking up an existence as filter feeders, collecting detritus, algae, and microorganisms. [44] The eyes of the larvae are underdeveloped, but are capable of discriminating changes in illuminance. [45] Ammocoetes can grow from 3–4 inches (8–10 cm) to about 8 inches (20 cm). [46] [47] Many species change color during a diurnal cycle, becoming dark at day and pale at night. [48] The skin also has photoreceptors, light sensitive cells, most of them concentrated in the tail, which helps them to stay buried. [49] Lampreys may spend up to eight years as ammocoetes, [50] while species such as the Arctic lamprey may only spend one to two years as larvae, [51] prior to undergoing a metamorphosis which generally lasts 3–4 months, but can vary between species. [52] While metamorphosing, they do not eat. [53]

The rate of water moving across the ammocoetes' feeding apparatus is the lowest recorded in any suspension feeding animal, and they therefore require water rich in nutrients to fulfill their nutritional needs. While the majority of (invertebrate) suspension feeders thrive in waters containing under 1 mg suspended organic solids per litre (<1 mg/l), ammocoetes demand minimum 4 mg/l, with concentrations in their habitats having been measured up to 40 mg/l. [54]

During metamorphosis the lamprey loses both the gallbladder and the biliary tract, [55] and the endostyle turns into a thyroid gland. [56]

Some species, including those that are not carnivorous and do not feed even following metamorphosis, [53] live in freshwater for their entire lifecycle, spawning and dying shortly after metamorphosing. [57] In contrast, many species are anadromous and migrate to the sea, [53] beginning to prey on other animals while still swimming downstream after their metamorphosis provides them with eyes, teeth, and a sucking mouth. [58] [57] Those that are anadromous are carnivorous, feeding on fishes or marine mammals. [10] [59] [60]

Anadromous lampreys spend up to four years in the sea before migrating back to freshwater, where they spawn. Adults create nests (called redds) by moving rocks, and females release thousands of eggs, sometimes up to 100,000. [57] The male, intertwined with the female, fertilizes the eggs simultaneously. Being semelparous, both adults die after the eggs are fertilized. [61]

Taxonomists place lampreys and hagfish in the subphylum Vertebrata of the phylum Chordata, which also includes the invertebrate subphyla Tunicata (sea-squirts) and the fish-like Cephalochordata (lancelets or Amphioxus). Recent molecular and morphological phylogenetic studies place lampreys and hagfish in the superclass Agnatha or Agnathostomata (both meaning without jaws). The other vertebrate superclass is Gnathostomata (jawed mouths) and includes the classes Chondrichthyes (sharks), Osteichthyes (bony fishes), Amphibia, Reptilia, Aves, and Mammalia.

Some researchers have classified lampreys as the sole surviving representatives of the Linnean class Cephalaspidomorphi. [62] Cephalaspidomorpha is sometimes given as a subclass of the Cephalaspidomorphi. Fossil evidence now suggests lampreys and cephalaspids acquired their shared characters by convergent evolution. [63] [64] As such, many newer works, such as the fourth edition of Fishes of the World, classify lampreys in a separate group called Hyperoartia or Petromyzontida, [62] but whether this is actually a clade is disputed. Namely, it has been proposed that the non-lamprey "Hyperoartia" are in fact closer to the jawed vertebrates.

The debate about their systematics notwithstanding, lampreys constitute a single order Petromyzontiformes. Sometimes still seen is the alternative spelling "Petromyzoniformes", based on the argument that the type genus is Petromyzon and not "Petromyzonta" or similar. Throughout most of the 20th century, both names were used indiscriminately, even by the same author in subsequent publications. In the mid-1970s, the ICZN was called upon to fix one name or the other, and after much debate had to resolve the issue by voting. Thus, in 1980, the spelling with a "t" won out, and in 1981, it became official that all higher-level taxa based on Petromyzon have to start with "Petromyzont-".

The following taxonomy is based upon the treatment by FishBase as of April 2012 with phylogeny compiled by Mikko Haaramo. [65] Within the order are 10 living genera in three families. Two of the latter are monotypic at genus level today, and in one of them a single living species is recognized (though it may be a cryptic species complex): [66]

Geotria Gray 1851 (pouched lamprey)

Mordacia Gray 1853 (southern topeyed lampreys)

  • Geotria australisGray 1851 (Pouched lamprey)
  • Mordacia lapicida(Gray 1851) (Chilean lamprey)
  • Mordacia mordax(Richardson 1846) (Australian lamprey)
  • Mordacia praecoxPotter 1968 (Non-parasitic/Australian brook lamprey)
  • Petromyzon marinusLinnaeus 1758 (Sea lamprey)
  • Ichthyomyzon bdellium(Jordan 1885) (Ohio lamprey)
  • Ichthyomyzon castaneusGirard 1858 (Chestnut lamprey)
  • Ichthyomyzon fossorReighard & Cummins 1916 (Northern brook lamprey)
  • Ichthyomyzon gageiHubbs & Trautman 1937 (Southern brook lamprey)
  • Ichthyomyzon greeleyiHubbs & Trautman 1937 (Mountain brook lamprey)
  • Ichthyomyzon unicuspisHubbs & Trautman 1937 (Silver lamprey)
  • Caspiomyzon wagneri(Kessler 1870) Berg 1906 (Caspian lamprey)
  • Caspiomyzon graecus(Renaud & Economidis 2010) (Ionian brook lamprey)
  • Caspiomyzon hellenicus(Vladykov et al. 1982) (Greek lamprey)
  • Tetrapleurodon geminisÁlvarez 1964 (Mexican brook lamprey)
  • Tetrapleurodon spadiceus(Bean 1887) (Mexican lamprey)
  • Entosphenus follettiVladykov & Kott 1976 (Northern California brook lamprey)
  • Entosphenus lethophagus(Hubbs 1971) (Pit-Klamath brook lamprey)
  • Entosphenus macrostomus(Beamish 1982) (Lake lamprey)
  • Entosphenus minimus(Bond & Kan 1973) (Miller Lake lamprey)
  • Entosphenus similisVladykov & Kott 1979 (Klamath river lamprey)
  • Entosphenus tridentatus(Richardson 1836) (Pacific lamprey)
  • Lethenteron alaskenseVladykov & Kott 1978 (Alaskan brook lamprey)
  • Lethenteron appendix(DeKay 1842) (American brook lamprey)
  • Lethenteron camtschaticum(Tilesius 1811) (Arctic lamprey)
  • Lethenteron kessleri(Anikin 1905) (Siberian brook lamprey)
  • Lethenteron ninaeNaseka, Tuniyev & Renaud 2009 (Western Transcaucasian lamprey)
  • Lethenteron reissneri(Dybowski 1869) (Far Eastern brook lamprey)
  • Lethenteron zanandreai(Vladykov 1955) (Lombardy lamprey)
  • Eudontomyzon stankokaramani(Karaman 1974) (Drin brook lamprey)
  • Eudontomyzon morii(Berg 1931) (Korean lamprey)
  • Eudontomyzon danfordiRegan 1911 (Carpathian brook lamprey)
  • Eudontomyzon mariae(Berg 1931) (Ukrainian brook lamprey)
  • Eudontomyzon vladykovi(Oliva & Zanandrea 1959) (Vladykov's lamprey)
  • Lampetra aepyptera(Abbott 1860) (Least brook lamprey)
  • Lampetra alavariensisMateus et al. 2013 (Portuguese lamprey)
  • Lampetra auremensisMateus et al. 2013 (Qurem lamprey)
  • Lampetra ayresi(Günther 1870) (Western river lamprey)
  • Lampetra fluviatilis(Linnaeus 1758) (European river lamprey)
  • Lampetra hubbsi(Vladykov & Kott 1976) (Kern brook lamprey)
  • Lampetra lanceolataKux & Steiner 1972 (Turkish brook lamprey)
  • Lampetra lusitanicaMateus et al. 2013 (lusitanic lamprey)
  • Lampetra pacificaVladykov 1973 (Pacific brook lamprey)
  • Lampetra planeri(Bloch 1784) (European brook lamprey)
  • Lampetra richardsoniVladykov & Follett 1965 (Western brook lamprey)
  • Entosphenus macrostomusDr. Dick Beamish 1980 (Cowichan lake lamprey)

Synapomorphies are certain characteristics that are shared over evolutionary history. Organisms possessing a notochord, dorsal hollow nerve cord, pharyngeal slits, pituitary gland/endostyle, and a post anal tail during the process of their development are considered to be Chordates. Lampreys contain these characteristics that define them as chordates. Lamprey anatomy is very different based on what stage of development they are in. [69] The notochord is derived from the mesoderm and is one of the defining characteristics of a chordate. The notochord provides signaling and mechanical cues to help the organism when swimming. The dorsal nerve cord is another characteristic of lampreys that defines them as chordates. During development this part of the ectoderm rolls creating a hollow tube. This is often why it is referred to as the dorsal "hollow" nerve cord. The third Chordate feature, which are the pharyngeal slits, are openings found between the pharynx or throat. [70] Pharyngeal slits are filter feeding organs that help the movement of water through the mouth and out of these slits when feeing. During the lamprey's larval stage they rely on filter feeding as a mechanism for obtaining their food. [71] Once lampreys reach their adult phase they become parasitic on other fish, and these gill slits become very important in aiding in the respiration of the organism. The final Chordate synapomorphy is the post anal tail which is a muscular tail that extends behind the anus.

Often times adult amphioxus and lamprey larvae are compared by anatomists due to their similarities. Similarities between adult amphioxus and lamprey larvae include a pharynx with pharyngeal slits, a notochord, a dorsal hollow nerve cord and a series of somites that extend anterior to the otic vesicle. [72]

Fossil record Edit

Lamprey fossils are rare because cartilage does not fossilize as readily as bone. The first fossil lampreys were originally found in Early Carboniferous limestones, marine sediments in North America: Mayomyzon pieckoensis and Hardistiella montanensis, from the Mississippian Mazon Creek lagerstätte and the Bear Gulch limestone sequence. None of the fossil lampreys found to date have been longer than 10 cm (3,9 inches), [73] and all the Paleozoic forms have been found in marine deposits. [74]

In the 22 June 2006 issue of Nature, Mee-mann Chang and colleagues reported on a fossil lamprey from the Yixian Formation of Inner Mongolia. The new species, morphologically similar to Carboniferous and other forms, was given the name Mesomyzon mengae ("Meng Qingwen's Mesozoic lamprey").

The exceedingly well-preserved fossil showed a well-developed sucking oral disk, a relatively long branchial apparatus showing a branchial basket, seven gill pouches, gill arches, and even the impressions of gill filaments, and about 80 myomeres of its musculature. Unlike the North American fossils, its habitat was almost certainly fresh water. [75]

Months later, a fossil lamprey even older than the Mazon Creek genera was reported from Witteberg Group rocks near Grahamstown, in the Eastern Cape of South Africa. Dating back 360 Million years, this species, Priscomyzon riniensis, is very similar to lampreys found today. [76] [77] [78]

The lamprey has been extensively studied because its relatively simple brain is thought in many respects to reflect the brain structure of early vertebrate ancestors. Beginning in the 1970s, Sten Grillner and his colleagues at the Karolinska Institute in Stockholm followed on from extensive work on the lamprey started by Carl Rovainen in the 1960s that used the lamprey as a model system to work out the fundamental principles of motor control in vertebrates starting in the spinal cord and working toward the brain. [80]

In a series of studies by Rovainen and his student James Buchanan, the cells that formed the neural circuits within the spinal cord capable of generating the rhythmic motor patterns that underlie swimming were examined. Note that there are still missing details in the network scheme despite claims by Grillner that the network is characterised (Parker 2006, 2010 [81] [82] ). Spinal cord circuits are controlled by specific locomotor areas in the brainstem and midbrain, and these areas are in turn controlled by higher brain structures, including the basal ganglia and tectum.

In a study of the lamprey tectum published in 2007, [83] they found electrical stimulation could elicit eye movements, lateral bending movements, or swimming activity, and the type, amplitude, and direction of movement varied as a function of the location within the tectum that was stimulated. These findings were interpreted as consistent with the idea that the tectum generates goal-directed locomotion in the lamprey.

Lampreys are used as a model organism in biomedical research, where their large reticulospinal axons are used to investigate synaptic transmission. [84] The axons of lamprey are particularly large and allow for microinjection of substances for experimental manipulation.

They are also capable of full functional recovery after complete spinal cord transection. Another trait is the ability to delete several genes from their somatic cell lineages, about 20% of their DNA, which are vital during development of the embryo, but which in humans can cause problems such as cancer later in life, after they have served their purpose. How the genes destined for deletion are targeted is not yet known. [85] [86]

As food Edit

Lampreys have long been used as food for humans. [87] They were highly appreciated by the ancient Romans. During the Middle Ages they were widely eaten by the upper classes throughout Europe, especially during Lent, when eating meat was prohibited, due to their meaty taste and texture. King Henry I of England is claimed to have been so fond of lampreys that he often ate them late into life and poor health against the advice of his physician concerning their richness, and is said to have died from eating "a surfeit of lampreys". Whether or not his lamprey indulgence actually caused his death is unclear. [88]

On 4 March 1953, Queen Elizabeth II's coronation pie was made by the Royal Air Force using lampreys. [89]

In southwestern Europe (Portugal, Spain, and France), Finland and in Latvia (where lamprey is routinely sold in supermarkets), lampreys are a highly prized delicacy. In Finland (county of Nakkila), [90] and Latvia (Carnikava Municipality), the river lamprey is the symbol of the place, found on their coats of arms. In 2015 the lamprey from Carnikava was included in the Protected designation of origin list by the European Commission. [91]

Sea lamprey is the most sought-after species in Portugal and one of only two that can legally bear the commercial name "lamprey" (lampreia): the other one being Lampetra fluviatilis, the European river lamprey, both according to Portaria (Government regulation no. 587/2006, from 22 June). "Arroz de lampreia" or lamprey rice is one of the most important dishes in Portuguese cuisine.

Lampreys are also consumed in Sweden, Russia, Lithuania, Estonia, Japan, and South Korea. [ citation needed ] In Finland, they are commonly eaten grilled or smoked, but also pickled, or in vinegar. [93]

The mucus and serum of several lamprey species, including the Caspian lamprey (Caspiomyzon wagneri), river lampreys (Lampetra fluviatilis and L. planeri), and sea lamprey (Petromyzon marinus), are known to be toxic, and require thorough cleaning before cooking and consumption. [94] [95]

In Britain, lampreys are commonly used as bait, normally as dead bait. Northern pike, perch, and chub all can be caught on lampreys. Frozen lampreys can be bought from most bait and tackle shops.

As pests Edit

Sea lampreys have become a major pest in the North American Great Lakes. It is generally believed that they gained access to the lakes via canals during the early 20th century, [96] [97] but this theory is controversial. [98] They are considered an invasive species, have no natural enemies in the lakes, and prey on many species of commercial value, such as lake trout. [96]

Lampreys are now found mostly in the streams that feed the lakes, and controlled with special barriers to prevent the upstream movement of adults, or by the application of toxicants called lampricides, which are harmless to most other aquatic species however, these programs are complicated and expensive, and do not eradicate the lampreys from the lakes, but merely keep them in check. [99]

New programs are being developed, including the use of chemically sterilized male lampreys in a method akin to the sterile insect technique. [100] Finally, pheromones critical to lamprey migratory behaviour have been isolated, their chemical structures determined, and their impact on lamprey behaviour studied, in the laboratory and in the wild, and active efforts are underway to chemically source and to address regulatory considerations that might allow this strategy to proceed. [101] [102] [103]

Control of sea lampreys in the Great Lakes is conducted by the U.S. Fish and Wildlife Service and the Canadian Department of Fisheries and Oceans, and is coordinated by the Great Lakes Fishery Commission. [104] Lake Champlain, bordered by New York, Vermont, and Quebec, and New York's Finger Lakes are also home to high populations of sea lampreys that warrant control. [105] Lake Champlain's lamprey control program is managed by the New York State Department of Environmental Conservation, the Vermont Department of Fish and Wildlife, and the U.S. Fish and Wildlife Service. [105] New York's Finger Lakes sea lamprey control program is managed solely by the New York State Department of Environmental Conservation. [105]

In folklore Edit

In folklore, lampreys are called "nine-eyed eels". The name is derived from the seven external gill slits that, along with one nostril and one eye, line each side of a lamprey's head section. Likewise, the German word for lamprey is Neunauge, which means "nine-eye", [106] and in Japanese they are called yatsume-unagi (八つ目鰻, "eight-eyed eels"), which excludes the nostril from the count. In British folklore, the monster known as the Lambton Worm may have been based on a lamprey, since it is described as an eel-like creature with nine eyes. [ citation needed ]

In literature Edit

Vedius Pollio kept a pool of lampreys into which slaves who incurred his displeasure would be thrown as food. [107] On one occasion, Vedius was punished by Augustus for attempting to do so in his presence:

. one of his slaves had broken a crystal cup. Vedius ordered him to be seized and then put to death, but in an unusual way. He ordered him to be thrown to the huge lampreys which he had in his fish pond. Who would not think he did this for display? Yet it was out of cruelty. The boy slipped from the captor's hands and fled to Augustus' feet asking nothing else other than a different way to die – he did not want to be eaten. Augustus was moved by the novelty of the cruelty and ordered him to be released, all the crystal cups to be broken before his eyes, and the fish pond to be filled in.

This incident was incorporated into the plot of the 2003 novel Pompeii by Robert Harris in the incident of Ampliatus feeding a slave to his lampreys.

Lucius Licinius Crassus was mocked by Gnaeus Domitius Ahenobarbus (cos. 54 BC) for weeping over the death of his pet lamprey:

So, when Domitius said to Crassus the orator, Did not you weep for the death of the lamprey you kept in your fish pond? – Did not you, said Crassus to him again, bury three wives without ever shedding a tear? – Plutarch, On the Intelligence of Animals, 976a [109]

This story is also found in Aelian (Various Histories VII, 4) and Macrobius (Saturnalia III.15.3). It is included by Hugo von Hofmannsthal in the Chandos Letter:

And in my mind I compare myself from time to time with the orator Crassus, of whom it is reported that he grew so excessively enamoured of a tame lamprey – a dumb, apathetic, red-eyed fish in his ornamental pond – that it became the talk of the town and when one day in the Senate Domitius reproached him for having shed tears over the death of this fish, attempting thereby to make him appear a fool, Crassus answered, "Thus have I done over the death of my fish as you have over the death of neither your first nor your second wife."

I know not how oft this Crassus with his lamprey enters my mind as a mirrored image of my Self, reflected across the abyss of centuries.

In George R. R. Martin's novel series, A Song of Ice and Fire, Lord Wyman Manderly is mockingly called "Lord Lamprey" by his enemies in reference to his rumored affinity to lamprey pie and his striking obesity. [111]

Kurt Vonnegut, in his late short story "The Big Space Fuck", posits a future America so heavily polluted – "Everything had turned to shit and beer cans", in his words – that the Great Lakes have been infested with a species of massive, man-eating ambulatory lampreys. [112]


Solving the puzzle of Henry VIII

Could blood group anomaly explain Tudor king's reproductive problems and tyrannical behavior?

Southern Methodist University

IMAGE: Blood group incompatibility between Henry VIII and his six wives could have driven the Tudor king's reproductive woes, and a genetic condition related to his blood group could finally provide. view more

DALLAS (SMU) - Blood group incompatibility between Henry VIII and his wives could have driven the Tudor king's reproductive woes, and a genetic condition related to his suspected blood group could also explain Henry's dramatic mid-life transformation into a physically and mentally-impaired tyrant who executed two of his wives.

Research conducted by bioarchaeologist Catrina Banks Whitley while she was a graduate student at SMU (Southern Methodist University) and anthropologist Kyra Kramer shows that the numerous miscarriages suffered by Henry's wives could be explained if the king's blood carried the Kell antigen. A Kell negative woman who has multiple pregnancies with a Kell positive man can produce a healthy, Kell positive child in a first pregnancy But the antibodies she produces during that first pregnancy will cross the placenta and attack a Kell positive fetus in subsequent pregnancies.

As published in The Historical Journal (Cambridge University Press), the pattern of Kell blood group incompatibility is consistent with the pregnancies of Henry's first two wives, Katherine of Aragon and Anne Boleyn. If Henry also suffered from McLeod syndrome, a genetic disorder specific to the Kell blood group, it would finally provide an explanation for his shift in both physical form and personality from a strong, athletic, generous individual in his first 40 years to the monstrous paranoiac he would become, virtually immobilized by massive weight gain and leg ailments.

"It is our assertion that we have identified the causal medical condition underlying Henry's reproductive problems and psychological deterioration," write Whitley and Kramer.

Henry married six women, two of whom he famously executed, and broke England's ties with the Catholic Church - all in pursuit of a marital union that would produce a male heir. Historians have long debated theories of illness and injury that might explain the physical deterioration and frightening, tyrannical behavior that he began to display after his 40th birthday. Less attention has been given to the unsuccessful pregnancies of his wives in an age of primitive medical care and poor nutrition and hygiene, and authors Whitley and Kramer argue against the persistent theory that syphilis may have been a factor.

A Kell positive father frequently is the cause behind the inability of his partner to bear a healthy infant after the first Kell negative pregnancy, which the authors note is precisely the circumstance experienced with women who had multiple pregnancies by Henry. The majority of individuals within the Kell blood group are Kell negative, so it is the rare Kell positive father that creates reproductive problems.

Further supporting the Kell theory, descriptions of Henry in mid-to-late life indicate he suffered many of the physical and cognitive symptoms associated with McLeod syndrome - a medical condition that can occur in members of the Kell positive blood group.

By middle age, the King suffered from chronic leg ulcers, fueling longstanding historical speculation that he suffered from type II diabetes. The ulcers also could have been caused by osteomyelitis, a chronic bone infection that would have made walking extremely painful. In the last years of his life, Henry's mobility had deteriorated to the point that he was carried about in a chair with poles. That immobility is consistent with a known McLeod syndrome case in which a patient began to notice weakness in his right leg when he was 37, and atrophy in both his legs by age 47, the report notes.

Whitley and Kramer argue that the Tudor king could have been suffering from medical conditions such as these in combination with McLeod syndrome, aggravated by his obesity. Records do not indicate whether Henry displayed other physical signs of McLeod syndrome, such as sustained muscle contractions (tics, cramps or spasms) or an abnormal increase in muscle activity such as twitching or hyperactivity. But the dramatic changes in his personality provide stronger evidence that Henry had McLeod syndrome, the authors point out: His mental and emotional instability increased in the dozen years before death to an extent that some have labeled his behavior psychotic.

McLeod syndrome resembles Huntington's disease, which affects muscle coordination and causes cognitive disorder. McLeod symptoms usually begin to develop when an individual is between 30 and 40 years old, often resulting in damage to the heart muscle, muscular disease, psychiatric abnormality and motor nerve damage. Henry VIII experienced most, if not all, of these symptoms, the authors found.

FETAL MORTALITY, NOT INFERTILITY IS THE KELL LEGACY

Henry was nearly 18 when he married 23-year-old Catherine of Aragon. Their first daughter, a girl, was stillborn. Their second child, a boy, lived only 52 days. Four other confirmed pregnancies followed during the marriage but three of the offspring were either stillborn or died shortly after birth. Their only surviving child was Mary, who would eventually be crowned the fourth Monarch in the Tudor dynasty.

The precise number of miscarriages endured by Henry's reproductive partners is difficult to determine, especially when various mistresses are factored in, but the king's partners had a total of at least 11 and possibly 13 or more pregnancies. Only four of the eleven known pregnancies survived infancy. Whitley and Kramer call the high rate of spontaneous late-term abortion, stillbirth, or rapid neonatal death suffered by Henry's first two queens "an atypical reproductive pattern" because, even in an age of high child mortality, most women carried their pregnancies to term, and their infants usually lived long enough to be christened.

The authors explain that if a Kell positive father impregnates a Kell negative mother, each pregnancy has a 50-50 chance of being Kell positive. The first pregnancy typically carries to term and produces a healthy infant, even if the infant is Kell positive and the mother is Kell negative. But the mother's subsequent Kell positive pregnancies are at risk because the mother's antibodies will attack the Kell positive fetus as a foreign body. Any baby that is Kell negative will not be attacked by the mother's antibodies and will carry to term if otherwise healthy.

"Although the fact that Henry and Katherine of Aragon's firstborn did not survive is somewhat atypical, it is possible that some cases of Kell sensitization affect even the first pregnancy," the report notes. The survival of Mary, the fifth pregnancy for Katherine of Aragon, fits the Kell scenario if Mary inherited the recessive Kell gene from Henry, resulting in a healthy infant. Anne Boleyn's pregnancies were a textbook example of Kell alloimmunization with a healthy first child and subsequent late-term miscarriages. Jane Seymour had only one child before her death, but that healthy firstborn also is consistent with a Kell positive father.

Several of Henry's male maternal relatives followed the Kell positive reproductive pattern.

"We have traced the possible transmission of the Kell positive gene from Jacquetta of Luxembourg, the king's maternal great-grandmother," the report explains. "The pattern of reproductive failure among Jacquetta's male descendants, while the females were generally reproductively successful, suggests the genetic presence of the Kell phenotype within the family."

Catrina Banks Whitley is a research associate in the Office of Archaeological Studies at the Museum of New Mexico. Anthropologist Kyra Kramer is an independent researcher.

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Cursed Royal Blood

A portrait of Henry VIII by German artist Hans Holbein the Younger

Photo by Toby Melville/Reuters

“There are so many women in the world, so many fresh and young and virtuous women, so many good and kind women. Why have I been cursed with women who destroy the children in their own wombs?”

So complains Hilary Mantel’s fictional version of Henry VIII—and Sunday marks the date, 477 years ago, when Anne Boleyn paid the price for his lament.

Boleyn was the second of Henry’s six wives. Though Henry broke with the Catholic Church to marry Boleyn, he had her executed on May 19, 1536, three years after she became his wife. He was frustrated with her and her inability to have a male child—something that four of Henry’s other five wives also failed to do.

Reading Mantel’s enthralling novel Bring Up the Bodies, which documents the souring of the marriage through the lens of Henry’s adviser Thomas Cromwell, I couldn’t help wondering how this situation—indeed, the course of history—might have turned out differently if the 16 th -century English court had access to modern medicine.

Clearly, Henry could conceive healthy children. Most historians accept that the future king Edward VI and the future queens Mary I and Elizabeth I were Henry’s legitimate children by Jane Seymour, Katherine of Aragon, and Anne Boleyn, respectively. Along with a son by his mistress, Bessie Blount, then, Henry had four surviving children from at least 11 known pregnancies. Henry’s wives were clearly fertile, yet they suffered repeated miscarriages.

Possible explanations for the cause of Henry’s woes—speculation, for instance, that he might have had syphilis or diabetes—haven’t solved the mystery of why he had such trouble begetting healthy kids. But the fact that his many wives all suffered miscarriages implicates Henry as the culprit, says Kenneth Moise, a maternal-fetal medicine doctor and co-director of the Texas Fetal Center in Houston.

“With that many women who have that many losses, there’s something he’s doing wrong,” Moise says.

In 2010 freelance academic Kyra Kramer suggested what that something might be: a certain form of a protein that sprouts from the surface of all of our blood cells. This protein—the Kell protein—comes in dozens of versions that, by themselves, are totally harmless. But if we’re exposed to blood from someone with a different Kell protein than our own, our body can see the different Kell protein as a foreign invader and send antibodies—the human version of guided missiles—to seek and destroy the invader. This is more likely to happen when the invading protein is one rare version of the Kell protein, the variety that scientists call the “K antigen,” or “big K.” Ninety-one percent of Caucasians have one of the “little k” versions of the Kell protein, and only 9 percent have the big K version.

If a woman without the big K antigen conceives a baby who has it, she’ll be exposed to big K when she gives birth to that baby. Her immune system will whip up anti-K antibodies she’ll carry them forever after in her body. If she then conceives another child with the big K antigen, her anti-K antibodies will cross the placenta and attack the baby’s own blood cells, with fatal consequences: The oxygen-deprived baby will almost certainly die.

In a paper in the Historical Journal, Kramer and her co-author, Catrina Banks Whitley, proposed that Henry might have carried the big K antigen, while his wives did not. If Henry’s babies inherited the big K antigen, the first of them born to any of his wives could be born healthy. But these pregnancies would sensitize their mothers to the big K antigen, and they’d miscarry any later babies who had it.

It’s a neat theory. But Moise notes one possible hole in it: Queen Mary. She wasn’t Katherine of Aragon’s first child Katherine’s previous four children all died in the womb or soon after birth. If Henry did carry the big K antigen, he likely passed it on to one of Katherine’s first four babies, and Katherine would have developed antibodies to it, devastating her later pregnancies. Mary never would have been born.

If Henry had one copy of the gene for big K antigen and one copy of a gene for a little k antigen—if he was what geneticists call a heterozygote—Mary could have inherited the benign little k version and survived. But if Henry was a heterozygote, each of his babies had only a 50-50 chance of inheriting the troublesome big K antigen from him, so you’d expect half of his children to have survived. At most, one-third of them lived.

Kramer, however, who has written a book about her theory, points out that “genetics is a bit like dice … probabilities are not ironclad rules.” She herself has three daughters, though most men, including her husband, have a 50-50 chance of passing on a male chromosome.

Exhuming Henry and testing his genes would be the only way to prove whether Kramer is right, but no one has been willing to pay for that project yet.

If Henry and his wives were alive today, they might not have had to suffer the heartbreak of so many lost babies. We now test all pregnant women for Kell and other blood type antibodies early in pregnancy. If a woman carries antibodies to K antigen, doctors can test her fetus for anemia and transfuse her baby with blood free of big K. Between 92 and 95 percent of big K-antigen babies who receive these intrauterine transfusions survive, Moise says. Before 1963, when the first intrauterine transfusion was performed, all of these babies died.

Had more of Henry’s children lived, he might have secured an heir while still a young man, sparing his kingdom the distraction of his marital exploits and his break with the church.

As for Henry’s marriages and Anne Boleyn’s life—who knows it’s unclear whether Henry’s tendency to grow tired of his wives had to do with their reproductive misfortunes or his tyrannical temper. Medicine can save a life, but it might not be able to appease the whims of a king.


Watch the video: Μήπως έχεις κλίση να γίνεις μοναχός; - Πατήρ Αθανάσιος Μυτιληναίος (August 2022).