CHAPTER 7
Coding Errors
This disease, so frequently attending all long voyages, and so particularly destructive to us, is surely the most singular and unaccountable of any that afflicts the human body.
The complete instruction manual for building and operating a human is contained within the genome – the sequence of DNA in our cells. This genome consists of some 3 billion base pairs – the letters of the genetic code – arranged over 23 pairs of chromosomes, like information arranged in the separate volumes of an encyclopaedia. 1 This full DNA complement is held within every one of our cells, except for those with no nucleus, such as red blood cells, and sperms and eggs, which contain only one set of chromosomes. Every time a cell in our body divides, allowing us to grow or maintain our organs or heal a wound, the complete complement of genetic information is copied. This replication process is not 100 per cent perfect, however, and DNA can also become damaged (such as by radiation or certain chemicals). Errors, or mutations, are thereby introduced into the genetic code. The DNA alphabet consists of four letters – A, G, C and T (abbreviations of the bases adenine, guanine, cytosine, and thymine) – and mutations are often due to one of these genetic letters becoming replaced with a different one, like a spelling mistake.
One of the most infamous literary typos in recent years appeared in the historical fiction novel The Queen’s Governess by Karen Harper. The protagonist has been abruptly woken after a night of passion: ‘In the weak light of dawn, I tugged on the gown and sleeves I’d discarded like a wonton last night to fall into John’s arms.’ The intended word, presumably, was ‘wanton’, an archaic term for a promiscuous woman, rather than a kind of Chinese dumpling. The substitution of a single letter has completely changed the meaning of the word. In biology, a mutation in the genetic code can change one of the building blocks of a protein, reducing that protein’s functionality or inactivating it completely.
Overall, the molecular machinery within our cells preserves the DNA code extremely faithfully. We possess hundreds of dedicated proteins for not only replicating DNA, but also proofreading the copies and repairing damage as it occurs. This means that the probability of any letter in the DNA code mutating is less than one in 10 million. But multiplied over the enormous number of base pairs we possess in our whole DNA complement, this error rate still equates to between 100 and 200 mutations arising in the genome of an individual that are passed on to the next generation.2
Most of these mutations have little to no effect on the individual. They strike somewhere within the huge expanses of the human genome that don’t actually code for any proteins (99 per cent of our genome is non-coding). Or, if a mutation does arise in a gene, the substituted nucleotide may not affect the functioning of the protein that is manufactured using the instructions. But every now and then, a mutation has a deleterious effect. The affected protein stops working properly, and the individual suffers a congenital genetic condition. Albinism, for example, is caused by a mutation that blocks the production of melanin. Huntington’s and Tay-Sachs diseases are both relatively common disorders also caused by mutations to a single gene.
We saw in Chapter 1 how genetics altered the history of the Habsburg dynasty; we’ll now discover how a spontaneous genetic mutation that arose in an English queen came to impact some of the most powerful royal families in Europe, and thus the fate of the continent.
THE CURSE OF THE COBURGS
Queen Victoria had nine children, all of whom survived to adulthood, and forty-odd grandchildren. The queen was convinced that royal intermarriages were the best means to ensure lasting peace in Europe, and her strategic matchmaking meant that by the end of the nineteenth century, her grandson, the future George V, was related by blood or marriage to practically every other royal family in Europe.3 Victoria’s children and grandchildren became the kings, queens, emperors and empresses of Germany, Prussia, Spain, Greece, Romania, Norway and Russia, as well as important dukes and duchesses elsewhere. Victoria has therefore been called the ‘grandmother of Europe’.
Her youngest son, Prince Leopold, born in 1853, was a delicate, fragile child. He suffered joint pain, and the slightest bumps and scratches would cause him huge bruising and a great deal of bleeding. He was permanently fretted over by royal physicians but survived to marry and have two children of his own. But at the age of thirty, he slipped down a staircase,4 bumped his head and died of a cerebral haemorrhage.5 Leopold’s poor health may have been taken to be an unfortunate, isolated illness, but disturbingly, a similar trend was emerging among Victoria’s other male descendants. People began whispering about the ‘curse of the Coburgs’. Leopold, often unkindly referred to as the ‘Bleeder Prince’, was a harbinger of a calamity that was to strike royal families across Europe.
Today, the curse of the Coburgs is known as haemophilia.
Haemophilia is caused by a genetic mutation that reduces clotting factors in the blood. These factors help to plug open wounds with a tangled mat of fibrous proteins – a blood clot. If a haemophiliac suffers a cut or a broken blood vessel, the blood will flow for much longer before a clot becomes established – sometimes for days. Even a modest gash can lead to significant blood loss, and a gentle bump can rupture subcutaneous vessels that continue seeping into the surrounding tissue to create a large, painful bruise or even a bulging haematoma. Such internal bleeding is especially dangerous as a surgeon can only attempt to intervene by creating another open wound.6 Haemophiliacs also have an increased risk of bleeding into joints and the brain.7, 8
These clotting factor genes are stored in the DNA on the X-chromosome. Females receive two X-chromosomes from their parents, so even if they inherit one copy of a defective clotting factor gene, they should have a second, normal copy that can compensate and trigger healthy clotting. They are carriers of the mutation but don’t generally suffer from the disorder. Males, however, have XY sex chromosomes and so an inherited mutation on the X chromosome is not masked by another working copy. A female haemophiliac would have to inherit a double copy of the faulty gene: her mother would need to be a carrier and her father also a haemophiliac – a statistical rarity compounded by the unlikelihood of a haemophiliac surviving to reproductive age. Thus it is almost exclusively males that are born with haemophilia, which they inherit via the X chromosome from their mother – genetically speaking, it is known as a sex-linked recessive disease.
Queen Victoria was distressed by the appearance of this disease among her descendants but protested that it did not originate from her side of the family. Indeed, none of her siblings or ancestors suffered from this strange, debilitating malady, but then neither too did the family of her husband, Prince Albert. As haemophilia was previously unknown in Victoria’s family tree, it appears that a spontaneous mutation of the blood clotting gene occurred in either her father’s sperm or her mother’s egg before her conception.9
Two of Victoria’s five daughters, Princesses Alice and Beatrice, also inherited the faulty gene and became carriers of the disease. And then their daughters married into the royal houses of Spain and Russia and bore sons – heirs to two important thrones – with haemophilia.10 In total, over twenty members of European royal families inherited the condition from Victoria.11 The marriage arrangements that the queen had taken such pride in had come to spread a debilitating, and often lethal, genetic disorder across Europe’s royal dynasties. Ironically, however, although the mutation responsible arose within Queen Victoria, the British monarchy was spared as the line of succession passed through Edward VII, who had not inherited the faulty gene – winning a 50/50 genetic coin toss in receiving the unaffected X-chromosome from his mother.
The most catastrophic effects of Victoria’s deadly mutation were felt by the royal houses of Spain and Russia.
King Alfonso XIII of Spain unwittingly made one of the most catastrophic decisions of his reign when he married Victoria Eugenie of Battenberg, Princess Beatrice’s daughter. Despite her good health, Victoria Eugenie was a carrier of haemophilia. The Spanish Embassy in London warned Alfonso of the risk that she harboured the debilitating ‘royal disease’ – indeed, two of the young princess’s three brothers were afflicted with haemophilia – but at the time it was impossible to check, and the royal pedigree of the princess offered a great deal of prestige. Alfonso pushed aside any concerns and married Victoria Eugenie in the spring of 1906.12
A son was born to them the following year, named Alfonso after his father, but on the occasion of his circumcision it was discovered that the crown prince did indeed have haemophilia. Their second child, Jaime, was spared the blood disorder but at a young age developed mastoiditis – an infection within the skull – and became deaf and mute. A healthy son, Juan, was finally born in 1913. In all, Alfonso XIII and Victoria Eugenie had seven children together: two haemophiliac sons, one deaf and mute son, two daughters who were possible carriers, one stillborn baby and just one healthy son. The heir apparent, Prince Alfonso, was bedridden for long periods at a time with severe haematomas triggered by minor injuries, and he largely remained out of the public eye. Many considered that the royal blood of Spain had been tainted by the British princess.13
Political crisis in Spain led to a coup d’etat in 1923 and then a dictatorship – consented to by the king – under General Primo de Rivera, who ruled the country until his resignation was forced in 1930. At this point, the king had become hugely unpopular and believed that he could only save the monarchy by abdicating in favour of his eldest son and heir, Alfonso. But public opinion rode against succession of the haemophiliac prince or his deaf and mute brother, Jaime, both of whom were regarded as unfit for the burden of the crown. Had the king had the courage, he might have proclaimed his healthy son, Juan, as his successor and so changed the course of events that were to unfold.
In the municipal elections of April 1931, monarchist political parties won only a tiny overall majority and suffered decisive defeats in many of the largest cities, which were seen as votes against the monarchy. King Alfonso and his family went into voluntary exile as the Second Spanish Republic was declared, and within two years the two eldest princes had both renounced their dynastic claims to the defunct throne.14 While republican sentiment in Spain was strong, and the monarchy increasingly unpopular, the ‘curse of the Coburgs’ had further undermined the monarchy. (Although, this was not the end of the Spanish kingdom: General Franco reinstated the monarchy in 1947 and nominated his successor in 1975 as Juan Carlos I, Alfonso’s grandson.)
RUSSIA
Queen Victoria’s second daughter, Alice, married Louis IV, Grand Duke of Hesse-Darmstadt. They produced two sons, one of whom died of haemophilia as a toddler.15 Their youngest surviving daughter, Princess Alix, met Nicholas Alexandrovich Romanov, the heir to the Russian Empire, in Coburg at the wedding of her brother and their mutual cousin. Nicholas proposed, and they were wed in 1894, three weeks after the death of his father and his ascension to the throne. Alix was received into the Russian Orthodox Church and took the name Alexandra Feodorovna. The risk of her acting as a carrier of the royal disease was known, but by this point, the affliction was so prevalent among European dynasties that it was accepted as something of an occupational hazard.16fn1
The primary duty of a tsarina was to produce a male heir to the throne, but Alexandra’s first four children were all girls. In August 1904, she finally bore a long-awaited prince, Alexei. The painful truth soon became apparent, however, that the little tsesarevich suffered from haemophilia, transmitted down the female line from his great-grandmother Queen Victoria. Alexandra coddled the young boy, lest he should fall and suffer internal bleeding that could so easily prove fatal. A sailor was detailed to accompany Alexei wherever he went to catch him if he stumbled and to carry him when he was unable to walk, as occurred frequently. Alexandra consulted numerous physicians, but treatment for haemophilia was far beyond the medical science of the time, and she became convinced that only a miracle could save her only son and heir to the Russian Empire. She became increasingly withdrawn and turned to prayer for his salvation.
It was in these desperate circumstances, in the summer of 1907, that a fraught Alexandra was introduced to a healer, the enigmatic Grigori Yefimovich. He is better known to history as Rasputin. The name probably derived from rasputnyi, meaning ‘dissolute’,18 and he certainly lived up to it, developing a reputation for debauchery, drunkenness, coarse language and licentious indulgence. He dressed in a peasant blouse and baggy trousers, with greasy black hair that reached his shoulders and a long, unkempt beard – in short, he had the appearance of a dishevelled vagrant. But to contemporaries, Rasputin’s most arresting feature was the penetrating intensity of his ice-blue eyes.19 He presented himself as a mystic and a holy manfn2 with an aura of spiritual authority, and he was supposedly gifted with extraordinary powers of clairvoyance and healing. While we might call him a charlatan, he seemed to genuinely believe in his own abilities.
What’s more, Rasputin seemed to have a preternatural ability to soothe and calm the frequently distressed and sometimes hysterical Alexei. Alexandra persuaded herself that he was also able to ease the prince’s physical pain and stop his internal bleeding. Perhaps there was some truth in this beyond the wishful thinking of a desperate mother. Rasputin was known to use hypnotism, and by stupefying his patient, the reduction in stress and lowering of blood pressure and heart rate could conceivably have had a beneficial influence.21 Whether Rasputin actually had any genuine effect on the tsesarevich’s medical condition was a moot point: the empress believed he could help, and that was all that mattered. As Alexandra’s dependence on him grew, Rasputin became an ever more frequent presence at the Romanov court.
In October 1912, the ten-year-old tsesarevich suffered a particularly bad bout of internal bleeding after accompanying his mother on a jolting carriage ride. The court physicians were powerless to treat a large haematoma swelling in his groin, and the prince was given the last sacraments. The desperate Alexandra sent a telegram to Rasputin, who was at his home in western Siberia. He wired back with the prophetic message, ‘The Little One will not die. Do not allow the doctors to bother him too much.’22 Within hours, the prince’s condition began to improve.
Perhaps the arrival of Rasputin’s telegraph had simply been a case of good timing. Alexei had already been haemorrhaging for several days, and his body may simply have been able to begin healing itself by that point. Perhaps Rasputin’s insistence on keeping the doctors away actually did have a positive effect: the gaggle of physicians fretting around his bed may have been doing more harm than good, constantly prodding the swollen haematoma to check its progression.23 Furthermore, they were likely to have treated him with aspirin for pain relief, and unbeknown to them at the time, the medicine’s side-effect of thinning the blood would only have exacerbated the bleeding.24 Whatever the reason, soon after receipt of the prophetic telegraph, the tsesarevich began making a miraculous recovery. Alexei’s health was the future of the Romanov dynasty, and Rasputin had become indispensable in the eyes of the tsarina.
With the eruption of the First World War in July 1914, Tsar Nicholas II found himself dragged into a continent-engulfing war against his cousin-in-law, Kaiser Wilhelm II of Germany, who was himself fighting his own cousin, King George V. Queen Victoria’s grand plan of ensuring peace in Europe through an intertwined web of related royals had failed.
Over the first year of the Great War, Nicholas lost some four million of his subjects.25 In September 1915, after the disastrous early defeats, Nicholas travelled to the front to personally take supreme command of the Russian forces. He knew little about military matters, however, and the army continued to flounder. In his absence, Alexandra assumed control of domestic affairs from the imperial palace in Petrograd (St Petersburg). She devoted most of her energies to influencing politics and making recommendations for government appointments. It was not only those within the imperial court but also ministers and commanders of the armed forces who rose or fell depending on her favour. And whispering in her ear was the ever-present Rasputin, using her as a vehicle to further his own power.26 Alexandra urged her husband to follow the advice of ‘Our Friend’, as she referred to Rasputin, on state matters, and Nicholas often acquiesced.27 In the seventeen months of the tsarina’s rule, until February 1917, Russia had four prime ministers, five Ministers of the Interior, three Foreign Ministers, three War Ministers, three Ministers of Transport and four Ministers of Agriculture. Competent officials were removed from post and replaced by obedient supporters, and the government’s ability to function was undermined as officials rarely stayed in office long enough to master the demands of their post, all of which contributed to political instability and domestic turmoil.28
As Rasputin’s influence within the Romanov court grew, so too did the rumours of his misdemeanours. Lurid stories about his drunken orgies and sexual exploits circulated widely. Worst of all was the widespread rumour, which Rasputin only encouraged, that the tsarina herself was among his lovers.29 Alexandra’s close connection with Rasputin became increasingly damaging and undermined the reputation of the royal court among the Russian people. Support for the Romanov dynasty was being eaten away from the inside. Nicholas’s supporters urged him to cut all ties with this toxic man; but he wouldn’t hear it. Nicholas was aware of the whisperings, but he would not remove Rasputin so long as his wife believed that he, and only he, could keep their son alive.30 ‘Better one Rasputin than ten fits of hysterics every day,’ he is reported to have exclaimed in an unguarded moment.31
Alexei’s condition was kept a secret from the Russian people. Whenever he was suffering a bout of bleeding and missed a public appearance, the Romanovs issued an excuse, but no one believed them, and increasingly outlandish rumours circulated about his absences. Honesty about the heir’s haemophilia would have prompted questions over his ability to rule and the dynastic succession, but maintaining the wall of secrecy was even more damaging. Alexandra’s shy and introverted disposition came across as cold and arrogant, and the official reticence on Alexei’s affliction only made the situation worse, undermining the nation’s respect for the empress and thus too the tsar and the crown.32
By the autumn of 1916, the tsar and his wife had become intensely unpopular among all classes of Russian society.33 The public were scandalised by Rasputin’s behaviour and apparent leverage over the tsarina. This was poisoning the monarchy’s relations not only with the Russian people, but also with the traditional pillars of the state: the aristocracy, the government, the Church and the army.34 By assuming command himself, the tsar was increasingly seen as personally responsible for the military defeats, and the flawed decision to take over was blamed on the influence of Alexandra and Rasputin. Some even muttered that Nicholas and his German wife were conspiring with the enemy.35 Continued, grave losses at the front combined with food and fuel shortages at home, exacerbated by incompetent officials, turned the Russian people against the imperial family. The press, released from censorship after the 1905 Revolution, began to write openly of Rasputin as a sinister force within the palace who had the ear of the tsarina and used his influence to pull the strings like a puppet master. In the Russian parliament – the Duma – too, leftist politicians hinted at dark forces near the throne in their speeches.36 As revolutionary sentiments bubbled, it mattered not what was true but what the people thought was true.
Tensions rose until, in December 1916, a plot was hatched by two members of the royal family and an ardent monarchist politician to end the insidious, corrupting influence of Rasputin once and for all. The mystic was lured to Yusupov Palace in Petrograd, where the conspirators poisoned him with cyanide, shot him twice in the chest and twice in the head, beat him with a candlestick, then finally, for good measure, pushed him beneath the ice covering the Moika River, where he drowned.37 They hoped that with the ‘Mad Monk’ gone, the tsar could be persuaded to listen to sense, to relinquish command of the Russian forces to an experienced general, rule the nation in cooperation with the Duma and so save the monarchy.38 But it was too late; the grave damage had already been done.
Within two months of Rasputin’s murder, the Russian people’s exhaustion from the war and long-running discontent with the tsar’s rule erupted into mass protests and violent clashes with the police in Petrograd. It seemed that revolution now was a patriotic act to save Russia. For the rising Bolsheviks, Rasputin had been symptomatic of the broader corruption of the autocratic regime, and his murder by the nobility was seen as an attempt to hold on to power over the proletariat.
Both the Duma and the revolutionary Soviets tried to convince Nicholas to abdicate, allow Alexei to succeed as a constitutional monarch under the regency of his uncle Grand Duke Michael, and take the rest of the royal family into exile. But the tsar would not be parted from his haemophiliac son and declared he would only abdicate in favour of Michael. Whereas the people may have been satisfied with a twelve-year-old boy succeeding as tsar under the tutelage of the elected Duma, they would not accept a simple replacement with another imperial autocrat.39 Michael delegated rule to the provisional government, and Nicholas and his family were placed under house arrest. A republic was declared in September 1917, but ongoing turmoil led to the October Revolution, during which the radical Bolsheviks seized power. The Romanovs were later moved to a house in the Urals, and in the early hours of 17 July 1918, Nicholas and Alexandra and their children, as well as the tsar’s doctor and three servants, were executed by a Bolshevik firing squad. The Romanov dynasty had been extinguished.
It was a tragic ending to the Russian imperial family. We have seen how in Spain Prince Alfonso’s haemophilia called into question his ability to succeed his father, weakening the monarchy in the years leading up to the establishment of a republic. The tsesarevich’s affliction arguably had even more devastating consequences. The distraught tsarina was so desperate to believe that Rasputin could heal her son and heir to the empire, and Nicholas II too reluctant to remove him from the royal court, that the standing of the imperial family was damaged beyond repair. Rasputin’s influence on state affairs, combined with unfounded rumours of an affair with Alexandra and collusion with the German enemy, eroded support for the government in Church and army, and fuelled public discontent until it eventually broke out in anti-monarchist rebellion. The gruelling war and food and fuel shortages stoked civil unrest, which made the Bolsheviks promising peace and bread so popular, but the consequences of royal haemophilia played a significant role too. After the October Revolution, the leader of the provisional government, Alexander Kerensky, concluded, ‘Without Rasputin there would have been no Lenin.’40
And we could add that without a single chance genetic mutation originating with Queen Victoria almost exactly a century earlier, there would have been no Rasputin.
SCURVY
While a mutation inherited from Queen Victoria affected many of the royal families of Europe throughout the nineteenth and twentieth centuries, another genetic defect is present in all of humanity. A gene inactivated early in our primate evolutionary history manifests itself as the debilitating, and eventually fatal, condition known as scurvy.
Scurvy has been known throughout history, striking peasants during famines or armies during sieges. The ancient Egyptians recorded symptoms consistent with scurvy,41 as did the Greek physician Hippocrates in the fifth century BC. The Crusaders suffered from scurvy, particularly when they were observing the restricted diet of Lent.42 But the period in history when the affliction really reared its bleeding-gummed head was during the Age of Sail. From the end of the fifteenth century, advances in ship construction and navigation enabled mariners to undertake longer voyages across open ocean. This meant that hundreds of men were crammed into ships and spent many weeks, often months, away from land, with limited provisions.
The first recorded outbreak of scurvy at sea occurred during Vasco de Gama’s discovery of the passage to India via the southern tip of Africa. Struggling against the monsoon winds on their return trip across the Indian Ocean in 1498, de Gama and his crew spent three months continuously at sea. The disease unfolded in a characteristic, horrifying way. The sailors started feeling weakened and lethargic, with aching joints and bruising easily. Their hands and feet began to swell, then their legs, arms and necks, with their skin taking on a patchy, purple discolouration. Their gums became grotesquely swollen and bled, their teeth loosened and fell out, and their breath stank of putrescence. Fresh wounds failed to heal and became infected, and sailors who had sustained injuries years before watched in horror as the old wounds opened up again. The healed joins of previously broken bones also dissolved, the fracture spontaneously reappearing as if it had never fused. In the final stages of the disease, sailors suffered hallucinations or blindness, before eventually succumbing to it under great pain, their end often delivered by a catastrophic haemorrhage around the heart or brain. Of 170 crew members on de Gama’s voyage, 116 perished, mainly of scurvy, and those who survived were in a dire state of health.43
For three centuries after this pivotal voyage, scurvy remained the greatly feared spectre that relentlessly stalked sailors at sea. Those that didn’t succumb to it were lucky. Christopher Columbus and his crew were largely spared the ravages of scurvy because their journey to the Americas in 1492 took only 36 days, with the trade winds behind them the whole way. Magellan’s first circumnavigation of the globe in 1519–1522 was less fortuitous: he lost 208 out of 230 sailors, again mostly to scurvy.44 And this dreaded disease befell not just the history-making voyages we know today but every other long marine passage that didn’t carry reliable countermeasures. It was the scourge of merchant ships plying the oceanic trade routes and of naval vessels duelling for control of the world’s seas. Scurvy struck terror into the hearts of sailors through the chilling inevitability with which it appeared after only a few weeks away from land.
Throughout the great majority of the Age of Sail, a captain on a long voyage could expect to lose from a third to more than half of his crew to slow and agonising death by scurvy. Sir Richard Hawkins, an English explorer and privateer, described the malady in the early seventeenth century as ‘the plague of the sea, and the spoyle of mariners’.45 Over the three centuries of the Age of Exploration, between 1500 and 1800, it has been estimated that scurvy killed over two million sailors – accounting for more deaths at sea than storms and shipwrecks, naval battles and all other diseases put together.46
During the eighteenth century, at the height of the European power struggle for dominance at sea, the length of time that a navy could keep its sailors healthy and its warships combat-effective was a crucial factor in protecting trade routes, defending overseas colonies and ports and safeguarding against enemy invasion. The first sea power to learn how to effectively combat the debilitating effects of the disease would gain a decisive naval advantage, even if only in the short term.
We now know that scurvy wasn’t caused by the often cramped and squalid conditions below deck on a sailing ship, nor by some feature of the open ocean itself, as had been supposed. Scurvy is a deficiency disease, caused by the absence of a specific ingredient in the sailors’ diet. Their rations were restricted to foodstuffs that preserved well, largely salted meat or fish and cereal grains that were consumed as ship’s biscuits or ‘hardtack’.47 Fresh fruit and vegetables were a luxury available only when making landfall. So, while sailors received a sufficient calorie intake to sustain their energy at sea, their diet lacked some crucial component required for the healthy functioning of the body.
A healthy human diet contains a balance of three key macronutrients: carbohydrates, fat and protein. We break these down during digestion and metabolism to supply the chemical energy that powers our body’s activities and provide all the molecular building blocks from which we construct our cells. But we also need small amounts of other vital substances known as micronutrients. Minerals are inorganic compounds – mostly containing metals – that enable key processes in the body. Salt, for example, offers both the sodium needed by our nerves and muscles and the chlorine that is used for maintaining the water balance inside our cells and for making (hydrochloric) stomach acid. We also need calcium for building bones and teeth, iron for carrying oxygen around in our bloodstream, phosphorus and sulphur for synthesising other crucial components of our cells and smaller amounts of other metals such as copper, cobalt, iodine and zinc. These vital elements within minerals cannot be biochemically synthesised by living organisms – they ultimately derive from the soil and water taken up by the plants and animals we eat.
Other essential micronutrients are organic compounds known as vitamins, which, unlike minerals, have been synthesised by organisms. Humans need these specific chemicals to function properly, but we are biochemically incapable of manufacturing them ourselves and so must derive them from our diet. All chemical reactions inside cells are driven by specific enzymes, and if a species evolves with a mutation that has knocked out a metabolic enzyme, it may lose the ability to synthesise a particular chemical product (as well as other compounds derived from it). Different species would therefore define their own list of vitamins differently: while one may need to source a particular organic compound as an essential dietary micronutrient, another might be able to happily create their own. For humans, there are thirteen essential vitamins. These were named alphabetically as they were discovered over the twentieth century, with deletions from the list when it was found that a chemical wasn’t actually required in the diet, and numbers added when scientists realised that some were chemically related to each other: they are vitamins A, B1/2/3/5/6/7/9/12, C, D, E and K. The human biochemical factory is able to synthesise vitamin D using a chemical reaction driven by UV rays in the sunlight hitting the skin. But many people living at higher latitudes cannot synthesise enough this way, so it is still considered a dietary vitamin.
The different vitamins are involved in a range of processes in the body, from assisting the action of enzymes in running vital biochemical reactions in our cells to helping us extract energy or absorb other key nutrients from our diet. If our diet lacks one of these crucial ingredients, our body’s stockpile of it becomes depleted and we develop a deficiency disease.
Humans appear to be more flawed in this way than other animals.48 Whereas most animals can spend their whole life eating just a single type of food without suffering any ill effects – buffalo are very happy munching nothing but grass, for instance – humans must secure an adequate supply of the numerous essential micronutrients from a particularly diverse diet.
Indeed, the very reason we have accumulated these metabolic mutations is because over our evolutionary history we have eaten a wide variety of plants – and more recently also scavenged and then hunted for meat – across a range of different habitats. Any mutation that knocked out a metabolic enzyme may not have had any immediate detrimental effect: the organic molecule it had produced was likely still present in the varied foods we ate, and so the mutation was not removed from the population by natural selection. We accumulated defects in our biochemical factory because they were masked by the varied diet of our primate and then hunter-gatherer ancestors. This means that our ancestors being ecologically gifted with a rich and varied diet created a lasting requirement for such a diet in order to survive.49 When humans developed agriculture, and our diet became focussed on a restricted number of staple cereal crops and cultivated fruit and veg, deficiency diseases started to appear.50fn3
For sailors during the Age of Sail, the vital element lacking in their diet was vitamin C. It is a water-soluble vitamin, which means that the body can store only a limited amount of it (compared to fat-soluble vitamins such as A and D).53 This organic compound is present in sufficient quantities in a balanced diet that includes fresh fruit and veg, but not in the preserved provisions aboard a ship. From the moment they left harbour, the sailors’ limited body stores of vitamin C began to deplete, until after a month or so at sea they began experiencing the effects of its deficiency.54
All animals that suffer from scurvy lack a particular enzyme called L-gulonolactone oxidase, or GULO for short, which performs the final step in the chemical manufacturing pathway for making vitamin C.55 Between 60 and 40 million years ago, our branch of the primate evolutionary tree acquired a mutation in the GULO gene that stopped this important enzyme functioning.56 But this mutation went unnoticed by evolution as our forest-dwelling ancestors had plenty of vegetation and fruit in their natural diet rich in vitamin C. Over time, the GULO code accumulated more and more errors so that today it exists in human DNA as no more than a ghost gene, like an irredeemably rusty component in a car engine.
The main role of vitamin C in the body is to support the synthesis of a long-stranded protein called collagen. Collagen is the most abundant protein in the human body and provides structural strength within connective tissue. Connective tissue serves as the foundation of the skin and gives it its elasticity. It holds our internal organs in place, and it lines blood vessels and nerves. Collagen also makes up tendons and ligaments, gives structure to muscles, serves as the scaffolding of cartilage and bone and is integral to the process of wound healing. In short, if the body stops being able to form and maintain collagen, its very fabric begins to fall apart.
Nearly every other animal species on the planet is able to synthesise its own vitamin C, usually in the liver,57 but humans – as well as other apes, monkeys and tarsiers – have lost this biochemical ability.fn4 It was a chance mutation millions of years ago within a tree-dwelling ancestor that was to have such dire consequences for mariners during the Age of Sail.
THE SEARCH FOR A CURE
One of the worst health disasters at sea was the catastrophe that befell a Royal Navy campaign in the Spanish Pacific, led by Commodore George Anson. In 1739, England and Spain once again descended into open warfare. Before being subsumed into the wider European power struggle of the War of the Austrian Succession, the Anglo-Spanish conflict began over the two age-old rivals’ efforts to dominate trade around Spanish America.fn5 After British successes around the Caribbean early in the war, Commodore Anson was charged with leading a squadron of warships to harry Spanish possessions on the Pacific coast. His mission was to attack vulnerable towns and to capture one of the enormously valuable treasure galleons as it transported silver from the mines in Mexico to the Philippines and then on to China for trade. After a lengthy period of preparation needed for repairing the ships and trying to muster enough men, Anson’s squadron finally set sail in September 1740. But these months of delay, during which the assembled crew had already been living on ship’s rations, meant that Anson’s men were beginning to weaken with malnutrition even before they departed.
After they rounded Cape Horn at the tip of South America and entered the Pacific, Anson’s ships were damaged and scattered during three months of fierce storms; two returned home and another was wrecked off the coast of Chile. But far worse than the raging of the winds were the ravages of scurvy. By the end of April 1741, practically every man aboard Anson’s flagship, the Centurion, was suffering. Forty-three crew members died of the affliction that month, and double that number in May. As the number of men fit and able to work the ship’s rigging rapidly dwindled, the scene below decks became increasingly desperate. The stench was unbearable amid the tightly packed hammocks full of the sick and dying. Corpses were frequently left where they lay, the surviving crewmen too weak to tip them overboard.
The Centurion was able to rejoin the two other remaining ships from the expedition at a pre-arranged rendezvous at the Juan Fernández islands.fn6 Of the roughly 1,200 men who had set sail aboard the three ships ten months before, almost three-quarters had died. Despite now recuperating on dry land, with plenty of fresh crops planted there during previous expeditions, it took three weeks for the continuing deaths from scurvy to stop. After three months of recovery, the remaining ships continued their mission, attacking Spanish shipping and towns along the South American coast. In the summer of 1742, they set sail across the Pacific to China, again losing sailors every day to scurvy, until there was only enough crew for just one ship. Anson now pursued his second objective, sailing the Centurion towards the Philippines in the hunt for a Manila galleon, where in June 1742 they captured such a Spanish treasure ship, laden with over 1.3 million silver coins.
Anson finally returned home via the Indian Ocean, having circumnavigated the globe. After a voyage lasting nearly four years, the expedition had delivered a haul of loot, but its success had come at a staggering human cost. Of the nearly 2,000 men who had set out with Anson, only 188 made it home alive. Just three had been killed during the capture of the Spanish galleon.62
The true tragedy of scurvy at sea was that effective remedies were known from the appearance of the same symptoms within malnourished land-based populations. European and American folk medicine knew how to treat the early signs of the disease by eating cresses and spruce leaves,63 which we now know are rich in vitamin C. Individual sea captains in the sixteenth century also discovered from experience that fresh vegetables and fruit, and especially citrus fruits, could cure scurvy. The Elizabethan explorer and privateer Sir Richard Hawkins noted in 1590 ‘that which I have seene most fruitful is sower [sour] oranges and lemons’.64 But for centuries, navies and merchant ships adopted these remedies haphazardly, unable to preserve the foodstuffs for long periods at sea or failing to understand what the all-important ingredient in the diet was. We now call vitamin C ascorbic acid, because it was the long sought-after ‘antiscorbutic’ agent to prevent scurvy.
The Royal Navy in the eighteenth century was acutely aware of the problems of scurvy and tried to take measures to combat it. The problem was that the Sick and Hurt Board, which made recommendations to the admiralty on how Royal Navy ships should be provisioned, was dominated by classically trained physicians. The medical establishment at the time had a misguided understanding of the causes of scurvy, believing that it was an internal putrefaction of the body caused by poor digestion and the damp environment on ship. They dismissed as mere anecdote the first-hand accounts of sea captains and naval surgeons on which remedies were actually effective in combatting scurvy, as they did not fit with the prevailing theories of disease. Anson’s voyage, for instance, had been provisioned with elixir of vitriol – sulphuric acid mixed with alcohol, sugar and spices – under the false belief that the antiscorbutic effect of citrus fruits was due to their acidity aiding digestion.65
But the appalling loss of life on Anson’s disastrous voyage helped focus medical minds. In 1747, the naval surgeon James Lind compared the efficacy of several treatments that were considered at the time, including cider, vinegar, sulphuric acid and seawater, as well as oranges and lemons, in what is often described as the first controlled clinical trial. He took a group of sailors suffering from scurvy, ensuring that the cases were as similar as possible, and divided them randomly among the different treatment regimes. This systematic experiment demonstrated decisively that scurvy could be successfully treated with dietary supplements of citrus fruit – the sailors assigned to that treatment were able to return to duty within a week. He published his results, but unfortunately his treatise had little impact on naval practice.
The main problem was that although Lind’s trial had shown the efficacy of citrus fruit in treating scurvy, he didn’t appear to fully appreciate its significance: his publication recommended citrus fruit while still espousing a multitude of other, ineffective treatments.66 What’s more, he went on to develop a process for preserving citrus juice for long-term storage aboard ships by heating it to reduce the water content and concentrate the citrus juice, so that 24 oranges or lemons became just 100 millilitres or so of fluid. He claimed, without testing, that this fruit syrup would retain its antiscorbutic potency for years, when in fact heating destroys the vitamin C and makes the remedy ineffective.67
Scurvy continued to ravage not just mariners in the navy, but also those aboard merchant ships, including the slave ships crossing the Atlantic from Africa. Thomas Trotter was a surgeon aboard a slave ship based out of Liverpool in the 1780s, when he discovered that by straining fresh lemon juice and then bottling it under a thin layer of olive oil to help protect it from the air, the antiscorbutic properties of the juice were still effective more than a year later. Trotter, who would become an ardent critic of the slave trade, was convinced that this remedy could save ‘the lives of poor retches who perished’, but the slavers were unwilling to add extra victualling costs to their voyages.68 Yet Trotter continued his campaign, eventually being appointed as the Physician of the Channel Fleet,69 while other advocates of the use of citrus juice rose to influential positions on the Sick and Hurt Board.
It seems tragic that, although Lind’s careful clinical trial had provided all the evidence that should have been needed, it wasn’t for another forty years after the publication of his treatise that the Royal Navy began routinely provisioning its ships with lemon juice. The sea change had come with the reformation of the Sick and Hurt Board by physicians with practical experience of scurvy at sea who persuaded the admiralty to go against the theories held by the medical establishment. Experienced fleet admirals now also insisted on being provided with citrus juice. Rear Admiral Alan Gardner, for example, demanded daily lemon juice rations for his voyage to India in 1793 and arrived after a four-month stint at sea without a trace of scurvy among his crew. When the news reached home, other fleet commanders clamoured to be supplied with the effective antiscorbutic.
Finally, in 1796, the Royal Navy agreed to provision all its warships posted on foreign service with lemon juice, and from 1799, all those in home waters around the British coast received it in their rations as well.70 The effects of this new policy were transformative. Between 1794 and 1813, the sick rate in the Royal Navy dropped from around 25 per cent to 9 per cent.71 Scurvy had effectively vanished from British warships. Before the introduction of lemon juice rations, a ship could operate for only ten weeks before being overrun by scurvy. But after 1799, the Royal Navy was able to keep its squadrons and fleets at sea for four months without resupply of fresh provisions.72
The Royal Navy had finally conquered its greatest foe, granting it a decisive advantage over its rivals which were not yet fully safeguarding their crews. In particular, it meant the admiralty could now keep its crews healthy and its warships at full operational strength for the core component of British military strategy: the naval blockade.fn7
NAVAL BLOCKADE
Many states through history have wielded naval power to further their interests. Since the early modern period, European states have deployed open ocean navies, the relative strengths of which waxed and waned over time in response to geopolitical threats or opportunities. But for the English, and then the British, a standing navy became a crucial force for defending the island against invasion. The Royal Navy, formed in the early sixteenth century, repeatedly clashed with the Spanish, French and Dutch fleets, evolving into a tool for not only safeguarding the homeland but also protecting Britain’s growing maritime economy and overseas colonies.
The paramount role of the Royal Navy had always been to command the English Channel and shield the island against ships arriving from the continent, in particular the northern shores of France, Belgium and the Netherlands. But as England and then Great Britain increased its number of overseas possessions, the marine territory that needed to be defended grew significantly. Merchant shipping returning to Britain from the Caribbean and North America, or further afield from India and South East Asia across the northern Atlantic was funnelled through a key region of sea off the British coast known as the Western Approaches. The colonies themselves also needed protection, and if a rival European fleet was allowed to slip away into the vast expanse of the Atlantic, it could be lost without trace for weeks, until it appeared suddenly over the horizon to attack one of Britain’s overseas colonies. Dedicating a sufficient number of warships to defend each of the valuable colonies, as well as serving convoy duty along the sea routes and protecting the Channel, would be impossibly expensive, and dispersing the available ships too widely would make the navy ineffective in any of its roles.
How could the Royal Navy deploy its limited ships so as to adequately meet all the strategic demands placed upon it? The solution was the formation of the Western Squadron, a formidable concentration of warships stationed off the south-west coast of Britain. From here, the formation could move to achieve several goals at the same time: screening the entrance to the English Channel to shield against invasion; guarding the vulnerable home stretch of Britain’s sea lanes in the Western Approaches to protect the lifeblood of its maritime economy; and, with periodic patrols down into the Bay of Biscay, preventing a rival power concentrating its naval forces which could threaten Britain’s colonies. Dominance of the coastline and Atlantic waters of the western European promontory – those of the western shores of France and the Iberian Peninsula – became strategically vital in protecting British interests.74
By the 1740s, the Western Squadron had become the navy’s main battle fleet and the lynchpin of Britain’s naval shield.75 It was commanded by Lord Anson after his long, scurvy-plagued campaign in Spanish America, who oversaw much of this growth.76 The key strategy that enabled a single concentration of warships to be effective over such a large area was the implementation of a naval blockade.
It meant that during wartime, an enemy’s principal ports could be sealed by a dominant naval force lying just out at sea, not only curtailing their military threat but also hindering their maritime trade and choking their economy. In ideal circumstances, an impregnable close blockade could be maintained to prevent enemy warships leaving harbour and combining into a strong fleet. But it is difficult to establish a permanent, complete guard over all major enemy ports to prevent their ships slipping away. So, more commonly, a loose blockade was employed, whereby small, manoeuvrable frigates kept a continuous close watch on the harbours. If the enemy ships dared to emerge, the main battle fleet stationed further away was alerted, via a chain of signal ships, and moved in to engage them with a superior force in decisive battle.77
Maintaining an effective blockade for many years at a time was an enormous logistical challenge, with stationed ships needing to be resupplied at sea and regularly relieved by replacement vessels from home ports, but the practice made efficient use of the ships at the admiralty’s disposal.78 As the late-nineteenth-century US naval strategist Alfred Thayer Mahan described it, ‘Whatever the number of ships needed to watch those in an enemy’s port, they are fewer by far than those that will be required to protect the scattered interests imperiled by an enemy’s escape.’79
The Royal Navy was able to achieve command of the seas through this form of passive defence – controlling the waters of Western Europe not by annihilating the enemy’s fleet (although the opportunity to do so would of course have been welcomed) but by confining their ships to harbour. Some ships or squadrons still had to be stationed to protect key strategic points elsewhere, but the principal defence of overseas possessions across the empire was enacted off the coast of Western Europe.
This strategic doctrine faltered, however, when France and Spain joined the War of American Independence. Despite being the largest navy in the world, the Royal Navy was stretched very thin and did not have enough ships to effectively blockade American ports, support its troops along the coast and protect the Caribbean colonies while also containing French and Spanish ships in their home ports. These quickly caused trouble for the British along the North American coast and in the Caribbean. And then there was the navy’s old foe. Scurvy undeniably contributed to the loss of the Thirteen Colonies,80 with British crews debilitated by the disease and the sailors that survived needing to spend long periods of convalescence in naval hospitals. Out of the 175,900 sailors recruited between 1774 and 1780, more than 18,500 died from disease, compared to only 1,243 killed in action. In 1782, at the height of the Revolutionary War, the sick list numbered 23,000 sailors out of a total force of around 100,000.81 While British troops were harried on land by local strains of malaria (as we saw in Chapter 3), scurvy stalked Royal Navy sailors at sea.
By the time of the Napoleonic Wars twenty years later, however, reform of the Sick and Hurt Board had seen the Royal Navy provisioning all its warships with daily rations of lemon juice. With the numbers of crew falling prey to scurvy reduced dramatically, the Western Squadron successfully blockaded the main French naval bases at Le Havre in the English Channel, Brest at the north-western tip of France and Rochefort in the Bay of Biscay. The naval cordon around France was completed by the Mediterranean Squadron, commanded by Nelson between 1803 and 1805, which blockaded the southern coastal port of Toulon. Rochefort was held under a close blockade to keep the warships pinned and unable to leave harbour, whereas Nelson operated a looser blockade of Toulon, hoping to entice Napoleon’s fleet based there to attempt a break for it so that he could force them into action and achieve a decisive victory at sea.
The Spanish fleet, based out of Cadiz, just north-east of the Straits of Gibraltar, and Ferrol, on the north-western tip of the Iberian Peninsula, was now allied with the French, and Napoleon planned to combine the two fleets and wrest control of the English Channel to provide safe passage for an invasion flotilla to land a French army on the southern English coast. French ships successfully evaded the blockade on several occasions but were unable to inflict a decisive victory over the British. The Royal Navy maintained their dominance of the waves, attacking the French at home and abroad at will, while British and allied shipping was free to trade around the world, helping to finance the war effort against imperial France.
But in January 1805, Napoleon’s fleet was able to slip the net of the British blockade at Toulon and join forces with the Spanish at Cadiz. They sailed to the Caribbean, pursued by Nelson, before turning north to pick up the westerly winds to carry them back to Europe. They intended to help break out the Brest fleet from their blockade and then sweep with their large numbers of ships-of-the-line into the English Channel to clear it of British warships. The plan was abandoned after French and Spanish losses at the Battle of Cape Finisterre, however, and the commander of the combined Franco-Iberian fleet, Pierre-Charles Villeneuve, decided to return to Cadiz. When Napoleon gave orders for the allied fleet to put to sea again and sail to Naples, Villeneuve made for the narrow gateway into the Mediterranean, the Strait of Gibraltar. Nelson’s blockading fleet caught and engaged them 40 kilometres down the coast, just off the Cape of Trafalgar, on 21 October 1805.
Despite having spent many months at sea by this point, the men in Nelson’s fleet were virtually free of scurvy.82 The British Mediterranean fleet had suffered only 110 deaths from scurvy (and 141 hospitalisations) out of some 7,000 sailors between August 1803 and August 1805 during the blockade of Toulon. Nelson – who had almost died of scurvy himself in 1780 as a young captain during the American Revolutionary War83 – had ‘spent two years on the Victory, wanting ten days’,84 without once stepping foot onto dry land. In contrast, the French and Spanish ships were rife with scurvy – the Spanish commander at Trafalgar reported that some of his ships were weakened with more than 200 cases of scurvy each,85 around a quarter of the men aboard a ship-of-the-line.
Not only were Nelson’s crews shielded from the ravaging effects of scurvy, they were also more experienced at seamanship and better drilled in gunnery. Nelson played to these advantages with the unorthodox naval tactic of cutting through the line of enemy warships in two columns – a calculated gamble that paid off and secured the Royal Navy a decisive victory over the French and Spanish fleets.
The superior health of the British sailors, and the boost this gave to the effectiveness of sea power, was undoubtedly a major contributor to Nelson’s fleet prevailing.86 The conquest of scurvy and victory at Trafalgar had assured British naval supremacy, and the Royal Navy continued to dominate the seas until the Second World War. As naval historian Christopher Lloyd put it, ‘Of all the means which defeated Napoleon, lemon juice and the carronade gun [a naval cannon] were the two most important.’87 For almost another decade after the Battle of Trafalgar, the Royal Navy maintained a blockade of the French coast, choking France’s wartime economy. Napoleon’s response was the Continental System, imposing an embargo on British imports across those parts of Europe that were controlled by, or in coalition with, France. But Britain’s control of the oceans meant it was able to divert its trade across the Atlantic to North and South America, and merchants also smuggled copious goods into Spain and Russia. This drove Napoleon to invade both Spain and Russia to enforce the boycott, resulting ultimately in his disastrous defeat and retreat from Moscow in 1812. Of the Grande Armée’s 615,000 men who marched into Russia in 1812, only 110,000 frostbitten and half-starved survivors returned.88
The Royal Navy had finally vanquished one of its most enduring foes, the debilitating and lethal scourge of scurvy, while, for a time at least, it continued to ravage American and continental European sailors, who weren’t provided with lemon juice.89 The British had obtained a crucial strategic advantage, and while the practice of long-term blockade was supported by carefully planned logistics, biologically, their command of the seas was enabled by their effective countermeasures to our defective genome. Before long, however, lemons preserved in seawater came to be adopted by the navies of other nations,90 and from the late 1800s, the advent of steam-powered ships greatly shortened oceanic voyages, which meant that few crews needed to spend months away from port, and the spectre of scurvy at sea receded. But for three and a half centuries, our defunct GULO gene played a pivotal role in the Age of Sail.
CITRUS AND THE RISE OF THE MAFIA
There’s a little known side-story to this. The adoption of lemon juice rations by the Royal Navy created a huge demand for citrus: between 1795 and 1814, the admiralty issued some 7.3 million litres of lemon juice.91 With the British climate not conducive to local production, sweet lemons had to be imported, mostly from around the Mediterranean. The admiralty first sourced its vital supply from Spain, but when the Spanish allied with Napoleon in 1796, it switched to buying Portuguese lemons, and then to those grown in Malta after the capture of the island in 1798.92 Then, from 1803, Nelson turned Sicily into a giant lemon juice factory93 to supply antiscorbutics for the Royal Navy worldwide.94fn8
Rural regions of the island, where the hot climate is ideal for citrus cultivation, have historically suffered from weak governmental control. Neither the Bourbon kings who ruled Sicily from 1735, nor the Savoy dynasty after Italian unification and independence in 1861, had enough political strength to enforce the law, including the rights of private property. The feudal system remained dominant in Sicily until the nineteenth century, with the barons exercising administrative, fiscal and judicial power over their dominions. After the auctioning of feudal lands in 1812, many tenants became landowners but were forced to hire private guards to protect their estates against the rampant brigands. Corruption and intimidation tactics prevailed.
The surge in demand for lemons driven by naval procurement created a commodity boom and injected a huge influx of cash into this unstable situation, greatly exacerbating the problems. It is out of this lawless landscape that the mafia emerged. The combination of high lemon prices, high levels of local rural poverty and a weak rule of law meant the owners of citrus orchards were extremely vulnerable to scrumping. Hundreds of pieces of fruit – representing a huge value on the market – could be stolen off the branches in a single night. With no centralised authority, the plantation owners were forced to turn elsewhere, hiring muscle to provide private security. This soon evolved into the practice of extortion and the threat of violence if the producer refused to pay the protection money. The mafiosi also acted as intermediaries between the rural growers and the international exporters in the harbours, so when a sale had been agreed, a lemon was placed on top of the gate to the grove to indicate that the property was under their protection. Their power only increased as the international demand for lemons snowballed: over just thirteen years between 1837 and 1850, exports rose from 740 barrels of lemon juice per year to over 20,000.98
By the 1870s, the organisation we would recognise as the modern Mafia had emerged, quickly expanding into wider racketeering and extortion and other organised crime. They came to infiltrate the economic and political institutions of the whole of Italy, and then the United States, which saw more than four million Italians, mostly from the impoverished south and Sicily, arrive between 1870 and the First World War.99
VITAMIN D AND A DEFICIENCIES
As a deficiency disease, scurvy afflicted mariners for hundreds of years during the Age of Sail. But other vitamin deficiencies have affected large numbers of people through history. Vitamin D, for example, is synthesised in our skin when it is exposed to the UV rays in sunlight. But in the far northern latitudes, not only do people need to wrap up against the cold, but the sunlight is weaker, and the winters are long and dark – so the human body is unable to produce enough vitamin D for itself. This vitamin is needed to help absorb calcium from our food, and so a deficiency leads to softened bones that become deformed. This manifests as the debilitating disorders of rickets in children and osteomalacia in adults.
Historical documents and skeletal remains indicate that rickets was common in northern parts of the Roman Empire and medieval Europe.100 The indigenous Inuit across northernmost Canada and Greenland, and the Norse in Scandinavia, however, were largely protected as their diet contained sufficient amounts of oily fish such as cod and salmon that are rich in vitamin D.101 And unlike vitamin C, vitamin D is fat-soluble and the body can store a sufficient reserve for months, so they could weather an inconstant supply.
Humans also need to obtain vitamin A from their diet, either in an active form from animals, or as an inactive ‘provitamin’ such as beta-carotene – the red-orange pigment in fruit and veg (including carrots, sweet potatoes, tomatoes and butternut squash) – some of which the body is then able to convert into vitamin A.102 But many people around the world suffer vitamin A deficiency, especially those in developing nations dependent on white (milled) rice as a staple. Vitamin A deficiency affects around one third of children globally and is the leading cause of preventable childhood blindness; it also increases the risk of death from other common illnesses.103 One solution to this widespread problem is the genetic modification of rice crops to produce beta-carotene in the edible parts of the grain, creating ‘Golden Rice’.104 Technology is being used to add genes to one of our most ancient staple crops in order to compensate for biochemical inadequacies in our own make-up.
We’ll turn now from the historical ramifications of defects in our genetic code, to the numerous processing glitches and biases in our psychology.