Scurvy: Causes, Symptoms and Treatments - Medical News Today Scurvy: Causes, Symptoms and Treatments Written by Peter Crosta M.A. 4 36 Scurvy is a disease caused by a diet that lacks vitamin C (ascorbic acid). Patients develop anemia , debility, exhaustion, edema (swelling) in some parts of the body, and sometimes ulceration of the gums and loss of teeth. The name scurvy comes from the Latin scorbutus. We have known about the disease in humans since ancient Greek and Egyptian times. Scurvy commonly is associated with sailors in the 16th to 18th centuries who navigated long voyages without enough vitamin C and frequently perished from the condition. Modern cases of scurvy are extremely rare. Humans cannot synthesize vitamin C, which is necessary for the production of collagen and iron absorption. We have to obtain it from external sources, i.e. from fruits and vegetables, or some foods which are fortified with vitamin C in order to prevent the vitamin C deficiency known as scurvy. Vitamin C deficiency is especially dangerous for the fetus (developing baby in the womb).

Researchers from the University of Copenhagen reported in the journal PLOS ONE that pregnant women with a vitamin C deficiency can have babies whose brain did not develop properly . What causes scurvy? The primary cause of scurvy is insufficient intake of vitamin C (ascorbic acid). This may be due to ignorance, famine, anorexia , restrictive diets (due to allergies, food fads, etc.), or difficulty orally ingesting foods. Historically, scurvy was the result of long sea voyages where sailors did not bring along enough foods with vitamin C. Who gets scurvy? Though scurvy is a very rare disease, it still occurs in some patients - usually elderly people, alcoholics, or those that live on a diet devoid of fresh fruits and vegetables. Similarly, infants or children who are on special or poor diets for any number of economic or social reasons may be prone to scurvy. Symptoms of scurvy Scurvy symptoms may begin with appetite loss, poor weight gain, diarrhea , rapid breathing, fever , irritability, tenderness and discomfort in legs, swelling over long bones, bleeding (hemorrhaging), and feelings of paralysis.

As the disease progresses, a scurvy victim may present bleeding of the gums, loosened teeth, petechial hemorrhage of the skin and mucous membranes (a tiny pinpoint red mark), bleeding in the eye, proptopsis of the eyeball (protruding eye), constochondral beading (beading of the cartilage between joints), hyperkeratosis (a skin disorder), corkscrew hair, and sicca syndrome (an automimmune disease affecting connective tissue). Infants with scurvy will become apprehensive, anxious, and progressively irritable. They often will assume the frog leg posture for comfort when struck with pseudoparalysis. It is common for infants with scurvy to present subperiosteal hemorrhage, a specific bleeding that occurs at the lower ends of the long bones. Diagnosis of scurvy Physicians initially will conduct a physical exam, looking for symptoms described above. Actual vitamin C levels can be obtained by using laboratory tests that analyze serum ascorbic acid levels (or white blood cell ascorbic acid concentration). Sometimes, radiological procedures are ordered for diagnostic purposes and to see what damage scurvy has already done.

Treatments for scurvy Scurvy is treated by providing the patient with vitamin C, administered either orally or via injection. Orange juice usually functions as an effective dietary remedy, but specific vitamin supplements are also known to be effective. How can scurvy be prevented? Scurvy can be prevented by consuming enough vitamin C, either in the diet or as a supplement. Foods that contain vitamin C include: Oranges, lemons, kiwi fruit and strawberries are all excellent natural sources of vitamin C. Oranges BBC - History - British History in depth: Captain Cook and the Scourge of Scurvy Captain Cook and the Scourge of Scurvy By Jonathan Lamb Last updated 2011-02-17 Scurvy was the scourge of the Royal Navy for decades, and Captain Cook is widely credited with conquering it. But how much of his reputation is deserved, and how much is due to luck? Jonathan Lamb investigates. On this page Print this page The emergence of scurvy Scurvy did not emerge as a problem for maritime explorers until vessels started penetrating the Indian and the Pacific Oceans.

Vasco da Gama lost two thirds of his crew to the disease while making his way to India in 1499. In 1520 Magellan lost more than 80 per cent while crossing the Pacific. Two voyages made by Pedro de Quiros early in the 17th century resulted in huge mortality from a sickness Sir Richard Hawkins called, after his venture into the South Seas, 'the plague of the Sea, and the Spoyle of Mariners'. ... Magellan lost more than 80 per cent of his crew while crossing the Pacific. Scurvy came to public notice in Britain after Commodore George Anson led a squadron into the Pacific in the 1740s to raid Spanish shipping. He lost all but one of his six ships, and two thirds of the crews he shipped (700 survived out of an original complement of 2000), most of them to scurvy. Their symptoms were vividly described by Richard Walter, the chaplain who wrote up the official account of the voyage.

Here were descriptions of its ghastly traces: skin black as ink, ulcers, difficult respiration, rictus of the limbs, teeth falling out and, perhaps most revolting of all, a strange plethora of gum tissue sprouting out of the mouth, which immediately rotted and lent the victim's breath an abominable odour. There were strange sensory and psychological effects too. Scurvy seems to have disarmed the sensory inhibitors that keep taste, smell and hearing under control and stop us from feeling too much. When sufferers got hold of the fruit they had been craving they swallowed it (said Walter) 'with emotions of the most voluptuous luxury'. The sound of a gunshot was enough to kill a man in the last stages of scurvy, while the smell of blossoms from the shore could cause him to cry out in agony. This susceptibility of the senses was accompanied by a disposition to cry at the slightest disappointment, and to yearn hopelessly and passionately for home. Now we know that scurvy was a cocktail of vitamin deficiencies, mainly of C and B, sometimes compounded by an overdose of A from eating seals' livers.

Altogether these produced a breakdown in the cellular structure of the body, evident in the putrescence of the flesh and bones of sufferers, together with night blindness and personality disorders associated with pellagra. In the 18th century no one knew what caused scurvy, whose symptoms were so various it was sometimes mistaken for asthma, leprosy, syphilis, dysentery and madness. Top Prevention Physicians speculated that it was owing to a salt diet, to a lack of oxygen in the body, to fat skimmed from the ships' boiling pans, to bad air, to thickening of the blood, to sugar, to melancholy; but no one knew for certain. People were aware that once victims were on shore they could be recovered by eating scurvy grass, wild celery, wood sorrel, nasturtiums, brooklime, Kerguelen cabbage (Pringlea antiscorbutica), cabbage trees and other esculent plants growing on the shores of distant islands. Fruit and palm wine were also esteemed to be fine remedies, and since 1753, when James Lind published A Treatise of the Scurvy, there was experimental proof that citrus had a rapid beneficial effect.

Captain Cook's voyage around New Zealand and the east coast of Australia © Once on shore it was a superstition among sailors that the smell and the touch of the earth gave the surest cure. One of Anson's crew had his shipmates cut out a turf and put his mouth into the hole. Vitus Bering, the Danish navigator, died of scurvy half buried in the ground. No one had a remedy for scurvy at sea - however; the best on offer was a battery of prophylactic measures, including portable soup (a preparation of dried vegetables), malt, sauerkraut, concentrated fruit juice (rob), vinegar, mustard, molasses and beans. These were aimed at repelling any sign of scurvy from the outset, since it was impossible to control it, once it had gained a footing, other than by going ashore. ... it was impossible to control scurvy, once it had gained a footing, other than by going ashore ... All the British voyages of the Pacific undertaken in the 1760s - by Byron, Wallis, Carteret and Cook - were used to test these prophylactics.

Wallis carried malt, sauerkraut, 'vinegar and mustard without limitation', 30 hundredweight of portable soup, and 180 Magellan jackets to protect the men against cold and damp. Under the direction of the 'Sick and Hurt and Victualling Boards of the Admiralty', Cook was supplied likewise with 40 bushels of malt, 1000lb of portable soup, vinegar, mustard, wheat, together with 'proper Quantities of sauer Kraut and Rob'. Like Wallis, Cook paid strict attention to airing and drying the lower decks, and keeping his men warm and well slept. Top Scurvy takes its toll Cook had five cases of scurvy reported by his surgeon and no deaths from it. Wallis's men were dogged by the disease, three dying of it, and he himself appears to have been suffering from it when he came across Tahiti. Byron reports the 'dreadful havock' made among his crew by the disease, while Carteret records 31 men dead of scurvy, and his ship for the most part of his voyage a hospital.

In his next two voyages Cook's good management, or luck, persisted, and no deaths from scurvy were reported. Since then he has been hailed as the conqueror of the sea's great plague. William Bowles wrote in his poem The Spirit of Discovery (1804): Smile, glowing Health! For now no more the wasted seaman sinks, With haggard eye and feeble frame diseased; No more with tortured longings for the sight Of fields and hillocks green, madly he calls. ... Cook was in no doubt that the principal cause of the health of his crews was owing to regular doses of malt ... Recently Christopher Lawrence has called Cook's regimen 'a representation and an endorsement of 18th-century social order'. For his own part, Cook was in no doubt that the principal cause of the health of his crews was owing to regular doses of malt, and woe betide the sailor who refused it!

In a paper delivered to the Royal Society he said of malt, 'This is without doubt one of the best antiscorbutic [effective against scurvy] sea-medicines yet found out; and if given in time will, with proper attention to other things, I am persuaded, prevent the scurvy from making any great progress for a considerable time'. There were dissenting voices about this at the time, as there still are today. Gilbert Blane and Thomas Beddoes, highly esteemed authorities on scurvy in the 18th century, rightly doubted that there was any antiscorbutic virtue in malt. Thomas Trotter, another expert, thought sauerkraut and portable soup were 'mere placebo'. They stated what Lind had already experimentally deduced - that fresh vegetables and citrus juice are the only substantial sources of vitamin C. But although 'rob' was carried on board Cook's ships, it had been boiled to reduce it, and in the process all its vitamin C (ascorbic acid) had been lost.

Top Cook's men suffer It turns out that Cook's prohibition against the fat from the boiling pans was the only truly antiscorbutic measure he took, for hot salt fat coming into contact with copper acquired a substance that irritates the gut and prevents its absorption of vitamins. James Watt has pointed this out in several articles, together with the plausible conjecture that an infestation of worms caused a similar effect in Cook's own body, precipitating a deficiency of vitamin B that might have been responsible for his odd behaviour in Hawaii shortly before his death. There is no doubt that many people suffered from scurvy on Cook's ships. There is no doubt that many people suffered from scurvy on Cook's ships. On the second voyage William Wales, the astronomer, and Johann Reinhold Forster, the naturalist, both give descriptions of their symptoms, chiefly their growing melancholy and sense of isolation. On the first, Joseph Banks records that once the Endeavour was in the Arafura Sea everyone - except Cook, Solander and himself - were suffering from homesickness, 'the longing for home which the Physicians ...

esteem a disease under the name of Nostalgia.' Thomas Trotter was to characterise the symptoms 20 years later as 'scorbutic Nostalgia', a condition to which Banks himself soon succumbed, when he thought of the explorer William Dampier in these same seas, and confessed, 'this thought made home recur to my mind stronger than it had done throughout the whole voyage'. When they landed at Savu, Banks reported that there were many people sick on board. The deaths at Batavia of Tupaia, the priest from the island of Raiatea, and Charles Green, the astronomer, have usually been ascribed to the dysentery that killed 30 of the Endeavour's crew at the end of the voyage.

Beaglehole suggests, however, that it was not dysentery that put an end to Tupaia's life and Cook himself was adamant that his death was owing to 'the long want of a vegetable diet which he had all his life before been used to, and brought upon him all the disorders attending a sea life.' As for Green, 'he had long been in a bad state of hilth, which he took no care to repair but on the contrary lived in such a manner as greatly promoted the disorders he had had long upon him'. Top Cook's record Cook was referring to the fact that Tupaia refused malt, portable soup and all the other remedies against scurvy, and that Green's addiction to drink was precipitating scorbutic symptoms. However, Tupaia, Green and a crew member named Hicks had been diagnosed at Batavia as the three people suffering from complaints 'occasioned by long continuance at sea', which makes it look as if perhaps Cook's record is not as clean in this respect as has sometimes been thought, and he did lose two of his men to scurvy.

Captain Bligh's Bounty was also afflicted by scurvy © That was not his reputation, however, and based on his example no commander wanted scurvy on his ship. When James Morrison reported that scurvy appeared on the Bounty on the run between the Cape of Good Hope and Tahiti, Captain Bligh wrote in the margin of his manuscript 'Captain Bligh never had a symptom of Scurvy in any ship he commanded', and Vancouver was dismayed when he found it on his vessel, Discovery, while he was mapping the north east coastline of America: 'To my utter astonishment and surprise, I was given to understand from Mr Menzies that the sea scurvy had made its appearance amongst some of the crew.' Clearly it was greeted with the same shock and incredulity as headlice today. In naval logs of the later 18th century, scurvy is scarcely mentioned, fluxes and cholera being far the most common complaints. But Leonard Gillespie, a naval surgeon, had it reported to him that scurvy was still common on the India station, and that in 1781 HMS Egmont lost a third of her crew to the disease, on a return journey from Jamaica.

Thus it has always been hard to say anything authoritative about scurvy, or to trust the testimony of its victims, who are afflicted by emotions so powerful that they lose the virtue of dispassionate neutrality that has been understood to distinguish the minds of explorers and navigators during the Enlightenment. Hence William Wales's terse yet strangely querulous entry in his Resolution journal: 'Brewed Wort [malt] for some of the People who began to have symptoms of the Scurvy. I suppose I shall be believed when I say that I am unhappy in being one of them'. About scurvy so much is to be supposed, so little known for sure. 4 Diseases Caused by a Lack of Essential Vitamins and Minerals | Mental Floss 4 Diseases Caused by a Lack of Essential Vitamins and Minerals Retronaut.com Like us on Facebook Companies pushing products with added vitamins and minerals can fool people into thinking that they’re eating a “healthy” food when they’re not—but it’s not like those vitamins and minerals are there for no reason. For much of human history, diseases of nutrient deficiency were the norm, and in some parts of the world, they still persist.

Even into the 20th century, conditions caused by a lack of certain vitamins or minerals were endemic to North America and Europe. Artificially added nutrients may not make a food “healthy,” but they do stave off several debilitating, and sometimes fatal, diseases of malnutrition. Here are a few of those maladies. 1. Scurvy Courtesy of The Diseases of Infancy and Childhood The disease of pirates: the grey-death. Scurvy is caused by a lack of vitamin C, whose chemical name, ascorbic acid, is derived from the Latin term for scurvy, scorbutus. Even though the disease was known since ancient times (described by Hippocrates around 400 BCE), it was not a scourge to those who were largely land-bound. Even though its causes were unknown, many cultures realized that eating certain herbs could reverse the symptoms, and as long as there was access to fresh food, it was generally kept under control. Scurvy didn’t become a significant problem until the Age of Discovery (beginning in the 15th century), when people at sea were not able to access that much-needed fresh food for months at a time.

Preserved meats and carbohydrates contained no vitamin C, and unlike most animals, the human body is not able to create vitamin C on its own. The early symptoms of scurvy include spongy gums, pain in the joints, and blood spots appearing under the skin. As the disease progressed, the teeth would become loose, extreme halitosis (bad breath) would develop, the afflicted would become too weak to walk or work, be in too much pain to eat, and would die “mid-sentence,” often from a burst blood vessel. Many of the early explorers lost great numbers of men to scurvy : Vasco de Gama lost 116 out of 170 men in 1499, and in 1520, Magellan lost 208 out of 230. A few deaths were attributable to other causes, but the vast majority were due to scurvy.

Courtesy of TaussMarine.com Despite not being able to pinpoint the exact cause of scurvy, in the 18th century, Naval physician James Lind was able to prove , in what’s considered to be the first controlled scientific experiment, that scurvy could be prevented (and cured) by incorporating citrus fruits such as limes and oranges into the diet of sailors. Although his findings weren’t widely accepted at first, the British Navy eventually began issuing standard rations of lemon juice, and later, limes, to their sailors—which gave rise to the term “limey” in reference to the British. These days, scurvy is an extremely rare condition, almost exclusively caused by someone eating a completely unvaried diet . In most cases, high levels of oral supplementation of vitamin C are enough to reverse the condition in a matter of weeks, and death by scurvy is almost unheard of. 2. Rickets Courtesy of Blatner.com This condition is brought on by a lack of vitamin D, which causes the body to be unable to absorb or deposit calcium. Less commonly, it can also be caused by a lack of calcium or phosphorus, but vitamin D deficiency is by far the most common cause.

Unlike vitamin C, the human body is able to produce vitamin D, but only if it has the metabolic precursors available to it. When the skin is exposed to ultraviolet light (such as from the sun), cholesterol in the skin reacts and forms cholecalciferol, which is then processed in the liver and kidneys to create the active form of vitamin D. Even with a nominally healthy diet, without enough sun exposure, the body can’t produce the vitamin D precursors on its own. This is actually re-emerging as a health concern among some increasingly-indoor groups of people, and is one of the few hypovitaminosis (lack of vitamin) conditions not considered to be a “disease of the past.” Luckily, when the deficiency is recognized, cholecalciferol can be directly taken as a vitamin supplement or acquired from eating organ meats and oils, such as cod liver oil, allowing the body to resume producing vitamin D. Rickets is a condition of children, as the deficiency’s most severe effects are on developing bones; in adults, “bone-softening,” or osteomalacia, can be caused by the same vitamin deficiency.

But in adults, it both takes significantly longer to develop and tends to cause tip-off signs that something is wrong before bone warping sets in, such as extreme pain in the bones, and unexplained muscle weakness. In children, especially those that don’t or can’t receive regular check-ups, deformity and debilitation by the deficiency is often only noticed after significant damage has been done to their developing skeletons. The most telling symptoms of rickets are at the epiphyses (growth plates) of bones: The body is unable to lengthen bones by depositing calcium, and ends up with bones that flare outward in a “cupping” appearance. This leads to costochondral swelling, or what’s known as the “rachitic rosary” along the ribcage of the child, as well as widened wrists and “thick” joints. Before widened wrists or rachitic rosary appears, the softening of the skull bones can lead to “Caput Quadratum”—a square-headed appearance, and often the first sign of skeletal growth problems. If left untreated, rickets also can cause an extremely curved back, stunted growth, and frequent fractures—all of which can lead to permanent and debilitating deformity. 3.

Beriberi Courtesy of Wikimedia Commons This condition is largely confined to Asia, especially in countries where boiled rice is a staple. The Sinhalese term “beri-beri” means, “I cannot, I cannot,” and derives from the inability to perform even the simplest of tasks once the polyneuritis (nerve inflammation) caused by the deficiency of vitamin B1 (thiamine) has permanently damaged the neurons, when the condition has progressed to the end-stage. Although beriberi was known to exist in rice-eating countries several centuries back , its prevalence boomed with the introduction of steam-driven rice-polishing mills from Europe. The superior taste of the milled white rice led many locals to abandon the local (unpolished) brown rice, and in doing so, abandon their primary source of thiamine. From the 1860s to the turn of the 20th century, people whose plant consumption was limited to the polished white rice would often come down with weakness, pain, weight loss, difficulty walking, and emotional disturbances. Beriberi became one of the leading causes of mortality in the region.

In the 1880s, a doctor named Christiaan Eijkman began researching the causes of this epidemic at a laboratory in the Dutch East Indies (now Jakarta, Indonesia), and initially believed that the condition was caused by a bacterial infection. However, after years of study, he came to the conclusion that “white rice is poisonous.” He discovered this by feeding a group of chickens solely white rice, and another group unpolished brown rice. The chickens that ate the white rice came down with beriberi-like symptoms, while the others stayed healthy. Eijkman also discovered that when the chickens fed white rice were subsequently fed brown rice, they recovered from their illness! Later dietary testing on prisoners confirmed his results. Even though he didn’t know the cause of the condition, Eijkman proved that white rice was the culprit, and shared the 1929 Nobel Prize in Medicine for his discovery. Beriberi is occasionally seen in the modern world, but its primary cause is chronic alcoholism —the poor diets of some chronic alcoholics, combined with the decreased absorption of what thiamine is consumed, leads to symptoms that unfortunately are sometimes left undiagnosed until it’s too late.

Recently, beriberi was also seen in Haitian prisons , when the prison system began buying imported polished rice from the United States, and stopped feeding their inmates the local brown rice. 4. Pellagra Courtesy of Open Library What causes blistering of the skin in the sun, pale skin, a craving for raw meat, blood dripping from the mouth, aggression, and insanity? If you answered “vampirism,” you’re close—the myth of the vampire may have its roots in the condition known as “pellagra.” Pellagra is caused by a lack of vitamin B3 (niacin). First identified and commonly diagnosed in the Asturian Empire (now Northern Spain), it was originally called “Asturian leprosy.” However, the condition was seen throughout Europe, the Middle East, and North Africa, wherever a large percentage of food energy was derived from corn, and fresh meat was not available. The area of highest prevalence was Northern Italy, where Francesco Frapoli of Milan called it “pelle agra,” meaning “sour skin.” It was initially believed that either the corn itself, or some insect associated with corn, was causing pellagra.

This belief was reinforced when much of France eliminated corn as a food staple and virtually eradicated the condition. Between the era that corn was introduced to Europe (the early 16th century) and the late 19th century, pellagra was found almost everywhere that poor people subsisted on cornmeal and little else. Around the turn of the 20th century, people began to notice that despite subsisting on just as much corn as poor Europeans, poor Mesoamerican natives didn’t come down with the condition. It was eventually discovered that this was because the traditional processing of corn in the Americas involved “ nixtamalization ,” in which the kernels were soaked in limewater before hulling them. The alkali solution freed up the niacin that was present in the grain, but previously inaccessible. Despite the extensive work of Dr. Joseph Goldberger in the 1910s and 1920s , which proved that pellagra wasn’t caused by a germ but by a dietary deficiency, the condition was occurring in epidemic proportions in the rural Southern US until the 1940s.

Today, pellagra is most common in the poorest regions of the world, especially places that rely upon food aid programmes. Some countries still ship unfortified cornmeal rather than corn masa (nixtamalized corn) or fortified cornmeal to developing countries or to their own impoverished populations. China, parts of Africa, Indonesia, and North Korea all have endemic pellagra among their lowest classes. ******* The discovery of important vitamins and how to produce them has been so significant to human health that many of those who were integral to the discoveries have been awarded the Nobel Prize in Medicine; more than 10 Nobel Prizes have been divided among almost 20 eminent scientists for the discovery or isolation of vitamins A, B1, B12, C, D, E, and K. Over the second half of the 20th century, after the beginning of widespread supplementation to everyday food items, the incidences of the conditions covered here went down dramatically across much of the world. Of course, the minerals essential to the human body play similarly important roles in maintaining health. However, humans have not historically had a widespread significant problem acquiring these nutrients, as most plants absorb many minerals from the soil.

With the increased processing of our food throughout the 20th century, however, some of these minerals have been lost, and have had to be re-added to the average Western diet through supplementation. In the rest of the world, displacement due to war, and unfortified food from aid programmes, has left survivors with enough calories, but not enough nutrients. Supplementation of assistance food and local fortification of salt and flour is beginning to help give displaced people (especially displaced children) a new chance at life without these and other nutritional diseases. In the developed world, you won’t be the healthiest bloke on the block if you eat nothing but breakfast cereal and cartons of juice—but the food industry has ensured that you at least won’t die of malnutrition. Even people with healthy diets benefit from the supplementation of vitamins and minerals in common foodstuffs, and adding the nutrients costs next to nothing. Doctors and nutritionists still agree that the healthiest way to acquire your necessary vitamins and minerals is by eating a balanced diet and spending time outdoors each day, but in the course of modern life, that’s not always possible, and if people are going to eat poorly either way, we may as well keep them from dropping dead of scurvy!

What is Scurvy? Vitamin C Deficiency, Sailors and Symptoms [Medical History, Science Education] - YouTube What is Scurvy? Vitamin C Deficiency, Sailors and Symptoms [Medical History, Science Education] Want to watch this again later? Sign in to add this video to a playlist. Need to report the video? Sign in to report inappropriate content. The interactive transcript could not be loaded. Loading... Rating is available when the video has been rented. This feature is not available right now. Please try again later. Uploaded on Jun 9, 2010 a funny poem about scurvy and life at sea for sailors in the 18th Century Category Lack of Vitamin C causes a reawakening of scurvy cases in the UK Lack of Vitamin C causes a reawakening of scurvy cases in the UK Share Article ChemistDirect examines the seeming rise of vitamin C deficiency in the UK and discusses the link between this and low income families. Increased Vitamin C intake can help prevent Scurvy Scurvy was the scourge of pirates and sailors in the 18th century, and it occurs only if people do not eat enough Vitamin C.

It is shocking that a disease from that time would rise again in the 21st century. (PRWEB UK) 5 July 2013 Recent reports of scurvy cases in the UK clearly indicate that vitamin C deficiency may be more prevalent than is generally assumed. In England, between 2004 and 2005, 61 children were admitted to the hospital with scurvy, but by 2007 and 2008, the figures rose to 94. Worse yet, there has been a rise of more than 50% during the last 3 years. Stephen O’Brien, the Conservative Health spokesman, who stated these figures said: “Scurvy was the scourge of pirates and sailors in the 18th century, and it occurs only if people do not eat enough Vitamin C. It is shocking that a disease from that time would rise again in the 21st century.” A survey of Low Income Diet and Nutrition a couple years back took valid plasma vitamin C measurements in 433 men and 876 women.

The outcome was that an estimated 25% of the men and 16% of the women in the low-income/materially deprived population had plasma vitamin C concentrations that were indicative of deficiency, and a further fifth of the population had levels in the depleted range. Reporting low-dietary vitamin C intake, not taking vitamin supplements, and smoking were all predictors of extreme low vitamin C levels. Public Health UK stated after the survey that: “Health professionals need to be aware that poor vitamin C status is relatively common among adults living on a low income in the UK.” But should a poor vitamin C status among adults and families living on low income be considered normality? Glyn and Julie Seabridge, parents of eight-year-old Dylan Seabridge who allegedly died from scurvy 18 months ago, from West Wales wait to find out. Both parents are currently facing trial at Swansea Crown Court, charged with the neglect and ill treatment of their son. Their indicated intention of pleading not guilty to the charge has been received with a mixture of feelings from the UK public, some of whom scorn the parents for the abuse of their son, and others who express their sympathy for the growing plight of poverty among low income families in the UK.

The question remains: Could the boy’s life have been spared by something as simple as an increase in vitamin C intake? A dietitian from Rhondda Valley, Sioned Quirke, expressed her surprise and concern regarding the case by stating: “Rickets and scurvy seem to be coming back. When I was training 10 years ago we were told about these diseases as ‘past conditions’. The difference between now and then is that scurvy and rickets conditions nowadays are out of choice. People tend to complain that fruit and vegetables are not affordable, when in fact they are.” Dr. Mark Temple, of the British Medical Association's public health committee, stated that food standards in the UK are worse now than they were during wartime rations. On an average, each person in Britain is eating 8 lb 13 oz (approx 4 kg) less fruit and vegetables a year than in 2007--a drop of 3%.

Food experts at the Dutch bank Rabobank even state that on an average, Britons eat 12 oz (346 g) of fruit and vegetables each day, which is well below the 14.1 oz (400 g) that is recommended by the World Health Organisation. An increase of fruit and vegetable intake as well as vitamin C supplements must be seen before things get any worse. The World Health Organization (WHO) admits that while it is not possible to relate daily servings of fruits and vegetables to an exact amount of Vitamin C , each individual’s dietary goal should be 400g of Vitamin C daily in order to meet the 1970’s Food and Agriculture Organization of the United Nations guidelines for lowering the risk of chronic disease. The WHO goal has been roughly translated into the recommendation of 5 portions of fruit and vegetables per day. References: What causes Scurvy? What causes Scurvy? Main Image: Scurvy occurs due to Vitamin C deficiency. Scurvy is derived from the Latin term "scorbutus". Scurvy has existed in ancient Greek and Egyptian times. Between the 16th to 18th centuries, scurvy was widely prevalent amongst the sailors.

They went for long voyages and did not get foods enriched with Vitamin C. In this 21st century, scurvy has become rare in modern societies. Due to scurvy, the body fails to synthesize vitamin C, which is vital for the production of collagen and for the absorption of iron. Scurvy can be fatal if not treated. Patients need to obtain vitamin C from external sources like citrus fruits. Regular consumption of fruits, vegetables or diets fortified with vitamin C helps to prevent scurvy. Content What Causes Scurvy? Scurvy is rare in contemporary time. However, it still prevails in third world countries. The disease is especially seen in elderly people, alcoholics, people on chemotherapy, and those with anorexia or poor gastrointestinal conditions. Scurvy can occur in infants or children suffering from severe malnutrition. Vitamin C deficiency leads to scurvy. Moreover, this may be occur due to nutritional ignorance, famine, restrictive diets (due to allergies, or food fads), and eating disorders (anorexia or bulimia). What Are the Symptoms of Scurvy?

Initial symptoms include sudden weight loss, loss of appetite, irritability, rapid breathing, diarrhea, discomfort in legs, bleeding or hemorrhage, swelling, and paralytic feelings. In progressive stage, gum bleeding, loosening of teeth, petechial hemorrhage, bleeding in the eyes, constochondral bleeding, hyperkeratosis (skin disorder), and sicca syndrome (autoimmune connective tissue disorder) may occur. Scurvy is also called as "Barlow's Disease". Affected babies become irritated and assume frog leg posture when struck with pseudoparalysis. Subperiosteal hemorrhage may also occur. How is Scurvy Treated? Usually doctors perform physical examination along with blood tests. Ascorbate level in the body is determined. Interventional radiologic procedures are used to diagnose "bone mineral density." Vitamin C supplements are prescribed, or injected. Daily intake of vitamin C helps in rapid recovery. How to Prevent Scurvy? Regular consumption of fruits and vegetables helps to prevent scurvy. Particularly good sources include citrus fruits such as lemons, oranges, and grapefruit.

Kiwi fruit, red and green peppers, brussels sprouts, strawberries, broccoli, tomato, cantaloupe, potato, cauliflower, and cabbage are also packed with vitamin C. One can also take vitamin C supplements. What Is the Recommended Intake for Vitamin C? The Recommended Intake for Vitamin C can vary on health factors. Pregnant and lactating women need higher doses of Vitamin C. Children (1 to 8 years): 15 to 25 mg/day Children and teenaged kids: 65mg to 90mg/day Adults: 75mg to 90 mg/day External References Scurvy - The Canadian Encyclopedia Science & Medicine Scurvy Scurvy is a disease caused by a dietary deficiency of vitamin C (ascorbic acid). The disease has occurred with regular frequency throughout human history and prehistory in populations lacking fresh foods, especially vegetables and meat. Scurvy Scurvy is a disease caused by a dietary deficiency of vitamin C (ascorbic acid). The disease has occurred with regular frequency throughout human history and prehistory in populations lacking fresh foods, especially vegetables and meat.

Deficiency in vitamin C may accompany wars and famine, but it is most commonly associated with post-Renaissance European exploration , particularly ocean voyages. Vitamin C was first isolated in 1928 by the Hungarian scientist Albert Szent-Györgyi, and synthesized by a Swiss group in 1933. It is important in maintaining the healthy condition of the body's mesenchyma, specifically connective tissues (which bind together and support body structures), osteoid (the organic part of bone) and dentin (the bone-like portion of teeth). Deficiency of the vitamin causes a breakdown in the binding function of these tissues, producing a series of characteristic signs and symptoms: weakness, lethargy, irritability, anemia, purple spongy gums which bleed freely, loosening teeth, the reopening of healed scars (including refracturing of bone) and hemorrhaging in the mucous membranes and skin. In severe cases the mortality rate is high. Scurvy was a serious problem throughout the whole period of exploration and settlement in Canada.

In 1535 Jacques Cartier's voyage to the New World brought him to the present location of Québec City ( Stadacona ) where he and his men spent the winter. Signs of scurvy soon appeared among the crew. By Feb 1536 only 10 of the 110 men on the expedition were in good health. Also, Cartier noted that many people in the local native population succumbed to the disease before the end of 1535. Many of Cartier's men were saved by drinking a native concoction of ground coniferous needles and bark (called "anneda," probably white cedar) boiled in water. In 1542 a party of 200 French under Roberval wintered near Cartier's earlier camp. During that winter about 50 died of the disease, and it appears they did not employ the cure that had saved Cartier's men. Subsequent explorations and settlements in the New World met regularly with the catastrophic effects of scurvy during long and cold winters and food shortages. During the 18th century scurvy caused more losses in the British navy than were suffered in enemy action.

A surgeon with the Royal Navy, James Lind, conducted an extensive controlled experiment on the effects of diet on sailors with scurvy, and the results were published in 1753 in the landmark book A Treatise of the Scurvy. Lind recommended the use of citrus fruits in treating and preventing scurvy during ocean voyages, advice which was not heeded by the Royal Navy until 1795. Scurvy was a major problem on nearly all of the 19th-century polar expeditions, and the tragic loss of John Franklin 's third arctic expedition in 1847 has been partly attributed to the disease. Though foods known to be antiscorbutic (anti-scurvy) were carried by these expeditions, the effectiveness diminished over a period of months as the vitamin C oxidized, leaving the explorers without protection. Many armies during WWI also suffered very severe outbreaks; by WWII the problem of scurvy was monitored closely and all but eliminated. In Canada the years 1945-65 were marked by outbreaks of scurvy in bottle-fed infants given evaporated milk (then lacking in vitamin C).

Today scurvy is rare and is usually related to poor attention to diet, or to diets heavily weighted towards a single food low in vitamin C. Scurvy - Symptoms, Causes, Treatment Scurvy Scurvy Although scurvy is more a deficiency disease than one of the haemopoietic system, it has two points of resemblance: marked capillary bleeding and progressive anemia. Scurvy is due to a prolonged deficiency of vitamin C in the diet and takes about 4 to 8 months to develop clinical signs. Habitation in an unhealthy surrounding predisposes. Vitamin C is required for the activity of prolyl hydroxylase, which is responsible for the extensive hydroxylation of prolines in collagens. Deficiencies in proline hydroxylation interfere with the assembly of the procollagen triple-helix, resulting in degradation of the collagen. An understanding of the cause and remedy for scurvy grew out of the experience of British sailors in the 18th century. It occupies an interesting place in the history of the world when English sailors became progressively ill after long voyages at sea.

It was only with the observation that the consumption of fruit helped to ward off the devastating effects of scurvy did the sailors begin to transport limes with them. Scurvy has been known since ancient times, but the discovery of the link between the dietary deficiency of ascorbic acid and scurvy has dramatically reduced its incidence over the past half-century. Sporadic reports of scurvy still occur, primarily in elderly, isolated individuals with alcoholism. The incidence of scurvy in the pediatric population is very uncommon, and it is usually seen in children with severely restricted diets attributable to psychiatric or developmental problems. The condition is characterized by perifollicular petechiae and bruising, gingival inflammation and bleeding, and, in children, bone disease. Scurvy was in some ways a more serious, certainly a more widespread problem. Relatively few men actually died of scurvy except on very long ocean passages, but it effectively limited the time a squadron could stay at sea, and thus directly affected the efficiency of the Service. No strategy of blockade, or any other which depended on keeping squadrons at sea for long periods, was possible in the face of endemic scurvy. The difficulty was to find a cure.

Much has been made by medical historians of the work of Dr. James Lind, the great naval physician who first provided experimental proof of the antiscorbutic properties of oranges and lemons, and the Admiralty has been freely castigated for not adopting this remedy at once. In fact Lind's celebrated controlled trial may have occurred by accident, and he does not appear to have appreciated its importance himself, or to have made it very clear to his readers. The value of lemons against scurvy was a commonplace known amongst seafarers for generations, but the fruit was only one of many remedies, good or bad, which neither the naval nor the medical world had any scientific method of sifting. Moreover, lemons were scarce and expensive in northern Europe, and the obvious method of preserving them incidentally destroyed the vitamin. Patients may present with hyperkeratotic papules centered in follicles. Hair may grow in a corkscrew-like pattern and may be associated with hemorrhage, often with minor trauma. In chronic disease, ecchymoses, usually over pressure points such as the shins, may occur. The mouth may show gingival hypertrophy.

Hemorrhage may occur in any mucosal surface including conjunctiva, sublingual, and skin. In addition, hemorrhage in the skeletal muscle, intra-articular sites, and subperiosteal region of the epiphyses of the long bones may occur. What are the causes of scurvy? Fortunately, there was a general understanding among sea officers that scurvy was a dietary disease, caused either by the presence of something harmful in the sailor's diet, or by the absence of something essential, and in either case curable by fresh victuals. Scurvy is due to a prolonged deficiency of vitamin C in the diet and takes about 4 to 8 months to develop clinical signs. Habitation in an unhealthy surrounding predisposes. What are the signs and symptoms of scurvy? In scurvy, the body stores are markedly depleted; plasma concentration is nearly nil and none in the urine. The white blood cells and the platelets normally have a concentration of about thirty times of blood plasma.

The chief deficiency sign is an inability of producing and maintaining the intercellular ground substance as collagen of all fibrous tissues: the matrix of bones, cartilages and dentine and all non-epithelial cement substances especially of vascular endothelium. As a result there is an increased permeability of the capillaries to the red blood corpuscles causing hemorrhages, new bone formation stops but as bone absorption still goes on, the bones become friable at the growing ends, interference with timely collagen formation causes delay in healing of wounds. Some other important symptoms of scurvy are gradual weakening, pale skin, sunken eyes, tender gums, muscle pain, loss of teeth, internal bleeding, and the opening of wounds such as sword cuts that had healed many years before. Exhaustion, fainting, diarrhea, and lung and kidney trouble followed. There is massive periosteal reaction with increase in the distance between tibia and fibula. This deficiency disease usually shows epidermal pallor in the upper part of the epidermis. Psoraisiform hyperplasia with pallor of the lower half of the epidermis. Numerous extravasated rbcs with lymphocytic infiltrate in the upper dermis are also present.

The diagnosis of scurvy is made on clinical and radiographic grounds, and may be supported by finding reduced levels of vitamin C in serum or buffy-coat leukocytes. The response to vitamin C is dramatic. Clinicians should be aware of this potentially fatal but easily curable condition that is still occasionally encountered among children. Is scurvy, an 18th century seafarers' disease, making a comeback? | PhillyVoice Battery of canons on the broad side of a ship. November 22, 2015 Is scurvy, an 18th century seafarers' disease, making a comeback? Researcher finds uptick in Vitamin C deficiency among low-income, mentally ill patients By Michael Tanenbaum PhillyVoice Staff In the United States, the prevalence of nutrient deficiencies is pretty stark: nine out of 10 Americans fell short of key nutrients in their diet in a 2011 study for the National Milk Mustache Campaign. While that proportion is alarming, remedies are plentiful. Pairing vitamins and supplements with a more balanced diet to address a particular nutrient deficiency enables most people to reverse harmful health effects in due time.

Those with fewer resources or a dependable support network are not as fortunate, however, and with an abundance of cheap, low-nutrient food, one disease thought to be a thing of pirate tales could be making a comeback. Eric Churchill, a physician at Baystate Medical Center in Springfield, Massachusetts, first considered the possibility of a modern day scurvy diagnosis in 2009, when a middle-aged man came to his office with bleeding gums, swelling, bruises, and general malaise, Slate reports. Churchill learned that the man, who suffered from mental illness, had subsisted on nothing but bread and cheese for years in an impoverished food desert. Known historically to affect sailors in the 1700's who lacked access to fresh produce, scurvy had largely dropped from medical consciousness until Churchill – visited by multiple patients with critically low vitamin C levels – decided to conduct a 5-year study. In the rare cases that have popped up, the disease has generally been associated with alcoholics, the elderly and severely malnourished children.

Churchill's study of 120 individuals revealed that 29 had vitamin C deficiencies low enough to qualify for a scurvy diagnose, a surprise given the low threshold (Churchill said a handful of McDonald's ketchup packets contain enough vitamin C to stave off scurvy). Extrapolating from the study in Springfield, Churchill realized that the condition, which often surfaces with mysterious symptoms, may be far more common than thought in American cities. What's worse, he said, is that it's going undiagnosed. The Springfield findings are supported by a 2003-2004 CDC study that found 6-8 percent of the U.S. population, primarily males, had deficiencies that qualify as scurvy. Among low-income individuals, the range jumped to 10-17 percent. An epidemiologist at the University of Massachusetts-Amherst said that the lack of attention to scurvy in recent decades is probably attributable to the ease of treatment. Those who have it are in many cases consuming no fruits or vegetables at all. “I think it’s not a sexy topic from a research point of view,” said Elizabeth Bertone-Johnson.

“We've understood what causes [scurvy] for several hundred years and we know how to reverse scurvy. We know how to improve vitamin C deficiency with fruits and vegetables and supplements. So it's old news.” Still, Churchill and his colleagues plan to write up the results of their study and map out scurvy cases to illustrate the effects of the disease among vulnerable populations. Later, he hopes, public health researchers will pick up the cause and pursue further studies that emphasize the consequences of food deserts and the need to offer nutrition education to those at risk. Scurvy: Background, Pathophysiology, Etiology Pathophysiology Overview Background Scurvy is a state of dietary deficiency of vitamin C (ascorbic acid). The human body lacks the ability to synthesize and make vitamin C and therefore depends on exogenous dietary sources to meet vitamin C needs. Consumption of fruits and vegetables or diets fortified with vitamin C is essential to avoid ascorbic acid deficiency. Although scurvy is uncommon, it still occurs and can affect adults and children who have chronic dietary vitamin C deficiency (see the image below). Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia, a characteristic of scurvy.

See 21 Hidden Clues to Diagnosing Nutritional Deficiencies , a Critical Images slideshow, to help identify clues to conditions associated with malnutrition. Next: Pathophysiology Humans, other primates, and guinea pigs are unable to synthesize L-ascorbic acid (vitamin C); therefore, they require it in their diet. [ 1 ] The enzyme, L-gluconolactone oxidase, which would usually catalyze the conversion of L-gluconogammalactone to L-ascorbic acid, is defective due to a mutation or inborn error in carbohydrate metabolism. The total body pool of vitamin C is approximately 1500 mg. The absorbed vitamin is found ubiquitously in body tissues, with the highest concentrations in glandular tissue and the lowest concentrations in muscle and stored fat. Ascorbic acid is metabolized in the liver by oxidation and sulfation. The renal threshold for excretion by the kidney in urine is approximately 1.4 mg/100 mL plasma. Excess amounts of ascorbic acid are excreted unchanged or as metabolites. When body tissue or plasma concentrations of vitamin C are low, excretion of the vitamin is decreased.

Scurvy occurs after vitamin C has been eliminated from the diet for at least 3 months and when the body pool falls below 350 mg. One study identified a genetic polymorphism of the human plasma protein haptoglobin, Hp 2, that may be an important non-nutritional modifying factor in the pathogenesis of vitamin C deficiency. The Hp 2-2 polymers are less efficient inhibitors of hemoglobin-driven oxidative stress, leading to ascorbic acid depletion. The Hp 2-2 phenotype is present in 35% of whites and 50% of South Asians and East Asians and may help identify patients who are more prone to develop clinically significant vitamin C deficiency. [ 2 ] Vitamin C functionality Vitamin C is required as a redox agent, reducing metal ions in many enzymes and removing free radicals. In this capacity, it protects DNA, protein, and vessel walls from damage caused by free radicals. Vitamin C is functionally most relevant for the triple-helix formation of collagen; a vitamin C deficiency results in impaired collagen synthesis.

The typical pathologic manifestations of vitamin C deficiency, including poor wound healing, are noted in collagen-containing tissues and in organs and tissues such as skin, cartilage, dentine, osteoid, and capillary blood vessels. Pathologic changes in affected children and adults are a function of the rate of growth of the affected tissues; hence, the bone changes are often observed only in infants during periods of rapid bone growth. Defective collagen synthesis leads to defective dentine formation, hemorrhaging into the gums, and loss of teeth. Hemorrhaging is a hallmark feature of scurvy and can occur in any organ. Hair follicles are one of the common sites of cutaneous bleeding. The bony changes occur at the junction between the end of the diaphysis and growth cartilage. Osteoblasts fail to form osteoid (bone matrix), resulting in cessation of endochondral bone formation. Calcification of the growth cartilage at the end of the long bones continues, leading to the thickening of the growth plate. The typical invasion of the growth cartilage by the capillaries does not occur.

Preexisting bone becomes brittle and undergoes resorption at a normal rate, resulting in microscopic fractures of the spicules between the shaft and calcified cartilage. With these fractures, the periosteum becomes loosened, resulting in the classic subperiosteal hemorrhage at the ends of the long bones. Guidelines for the evaluation of fractures in infants and young children have been established. [ 3 ] Intra-articular hemorrhage is rare because the periosteal attachment to the growth plate is very firm. Although the clinical manifestations are unclear, vitamin C is a cofactor in the metabolism of tyrosine and cholesterol and the synthesis of carnitine, neurotransmitters (eg, norepinephrine), peptide hormones, corticosteroids, and aldosterone. Vitamin C also affects hematopoiesis by enhancing the absorption of iron from the small intestine by reducing dietary iron from the ferric form to the ferrous form. This may contribute to the anemia seen with vitamin C deficiency, in which the availability of intracellular iron is reduced. Vitamin C is also necessary to convert folic acid to its active metabolite, folinic acid.

Previous Next: Etiology Scurvy is caused by a prolonged dietary deficiency of vitamin C. Humans obtain 90% of their intake of vitamin C from fruits and vegetables, and cooking these sources decreases vitamin C content 20-40%. The US Food and Drug Administration (FDA) recommends a daily dietary allowance of vitamin C of 75 mg for women and 90 mg for men. The body's pool of vitamin C can be depleted in 1-3 months. Ascorbic acid is prone to oxidation in vivo, and body stores are affected by environmental and lifestyle factors (eg, smoking), biological conditions (eg, inflammation, iron excess), and pathologic conditions (eg, malabsorption) that may alter its oxidation.

Risk factors for vitamin C deficiency include the following: [ 4 ] Babies who are fed only cow's milk during the first year of life Alcoholic individuals [ 1 ] and those who conform to food fads Elderly individuals who eat a tea-and-toast diet; retired people who live alone and those who eat primarily at fast food restaurants Economically disadvantaged persons, who tend to not purchase foods high in vitamin C (eg, green vegetables, citrus fruits) [ 5 ] Refugees who are dependent on external suppliers for their food and have limited access to fresh fruits and vegetables Cigarette smokers: These individuals require an increased intake of vitamin C because of lower vitamin C absorption and increased catabolism Pregnant and lactating women and those with thyrotoxicosis: These individuals require an increased intake of vitamin C because of increased utilization People with anorexia nervosa or anorexia from other diseases such as acquired immunodeficiency syndrome (AIDS) or cancer [ 6 ] People with type 1 diabetes have increased vitamin C requirements, as do those on hemodialysis and peritoneal dialysis [ 7 , 8 ] People with disease of the small intestine such as Crohn, Whipple, and celiac disease, as well as

 after gastric bypass surgery, [ 9 ] because vitamin C is absorbed in the small intestine Individuals with iron overload disorders - These may lead to renal vitamin C wasting Other factors that may lead to vitamin C deficiency include ignorance (eg, boiling of fruit juices), restrictive diets imposed by food allergies, and neurodevelopmental disabilities associated with compromised oral intake of foods.

A case report of vitamin C deficiency in a patient on coumadin raises the possibility of risk in the vitamin K–restricted diet, since overlap exists in foods containing vitamin K and vitamin C. [ 10 ] Recent evidence shows that iron is important in the absorption of vitamin C, and iron deficiency may lower the expression of the sodium-dependent vitamin C transporter in intestinal cells, leading to vitamin C deficiency. [ 11 ] Besides poor diet and anorexia in cancer patients, another mechanism of vitamin C deficiency has been proposed. In a study of cancer patients with adequate daily intake but low serum vitamin C levels, authors proposed increased use of vitamin C possibly to scavenge lipid peroxides or vitamin C sequestration by tumor cells. [ 12 ] Previous Epidemiology United States statistics Data from the National Health and Nutrition Examination Survey (NHANES 2003-2004) that assessed the prevalence of vitamin C deficiency in the United States among a sample of 7277 children and adults (older than age 6 y) found that men aged 20-39 and those older than 60 years had a higher prevalence of deficiency than similarly aged women.

Overall, 8.2 % of men and 6% of women (7.1% overall prevalence) were deficient in vitamin C, which is decreased from the NHANES 1994, which showed 14% of men and 10% of women deficient. [ 13 ] NHANES 2005-2006 showed a lower prevalence of 3.6% of vitamin C deficiency among men and women older than 6 years. [ 14 ] Patients at risk include those with chronic malnutrition, who are elderly or alcoholic, who subsist on diets devoid of fresh fruits and vegetables, and men who live alone (widower scurvy). Infants and children on restrictive diets because of medical, economic, or social reasons are at risk for scurvy. Occurrence of scurvy is uncommon in those younger than 7 months, although infants fed evaporated or condensed milk formulas may develop this disease. If a mother has an adequate diet, breast milk contains sufficient vitamin C for a baby's needs. Commercially available formulas and many prepared fruit juices are fortified with vitamin C.

Other reported cases include people with monotonous or peculiar diets, including patients undergoing dialysis as well as those with cognitive disorders, [ 15 , 16 ] psychiatric illnesses, [ 17 ] malabsorption, inflammatory bowel disease , cancer chemotherapy, Whipple disease , or dyspepsia (those who avoid acidic foods). International statistics The international occurrence of scurvy is unknown. Scurvy is a problem when general malnutrition exists, as in some impoverished, underdeveloped third world countries. Scurvy also occurs in epidemic proportions in international refugee camps and in populations that subsist mainly on cereal grains. A study of nonhospitalized patients in Paris found that 5% of women and 12% of men were deficient [ 18 ] ; in those older than 65 years, this proportion increased to 15% of women and 20% of men.

In a case series from Thailand that reviewed 28 cases of scurvy in infants and children (10 mo to 9 y and 7 mo; median age, 29 mo) hospitalized over a 7-year period (1995-2002), investigators noted prolonged consumption of heated milk (ultra-high temperature [UHT] milk) and inadequate intake of vegetables and fruits were the risk factors for the development of scurvy. [ 19 ] In tests of plasma vitamin C levels in the low-income/materially deprived population of the United Kingdom, carried out between 2003 and 2005 (433 men; 876 women), the Low Income Diet and Nutrition Survey found evidence of vitamin C deficiency in an estimated 25% of men and 16% of women. [ 5 ] Another 20% of the study population had vitamin C levels in the depleted range. According to the report, predictors of plasma vitamin C levels at or below the depleted range include being male, having a low dietary intake of vitamin C, not taking vitamin supplements, and smoking.

[ 5 ] A study of healthy elderly (age 70-75 y) persons living in Padua, Italy took a baseline and 10-year follow-up dietary history and found vitamin C deficiency rose over the 10-year span, from 3-6% in men and 2.3-4.5% in women, which led the authors to recommend multivitamin supplementation in healthy elderly persons. [ 20 ] Race, sex, and age differences in incidence According to NHANES 2004, non-Hispanic white men (11.8%) (had a slightly increased risk of vitamin C deficiency compared with non-Hispanic black men (8.9%) and Mexican American men (7.7%). [ 13 ] Similarly, the non-Hispanic white women (8.2%) had higher rates of vitamin C deficiency compared with non-Hispanic black women (5%) and Mexican American women (4.2%). Mexican American males and females had a lower risk of vitamin C deficiency probably because the traditional Mexican diet is rich in chilies, tomatoes, and squashes, which are high in vitamin C.

[ 13 ] Some studies show vitamin C deficiency to be more common among men, whereas others show equal distribution among men and women. NHANES 2004 shows slightly higher prevalence for men (8.2%) than for women (6%). NHANES 2007-2008 data showed that among American males older than 20 years, the daily intake was 26 mg higher than for females. In fact, teenage females had the lowest intake, followed by preadolescent females and women in their sixties. [ 21 ] Although scurvy can occur at any age, the incidence of scurvy peaks in children aged 6-12 months who are fed a diet deficient in citrus fruits or vegetables as well as in elderly populations, who sometimes have "tea-and-toast" diets deficient in vitamin C. Scurvy is uncommon in the neonatal period. Previous Next: Prognosis Typically, scurvy carries an excellent prognosis if diagnosed and treated appropriately.

Manifestations of scurvy, including the following, tend to dramatically improve, resolving within weeks, if adequate oral vitamin C is given in daily doses to recoup body stores: Spontaneous bleeding stops within 1 day Muscle and bone pain abate quickly Bleeding and sore gums heal in 2-3 days Ecchymoses heal within 12 days In advanced scurvy, serum bilirubin normalizes in less than 1 week, and anemia is corrected in less than a month. Complications The predominant morbidity associated with this disease is a result of hemorrhage into various tissues and depends on the site of involvement. Subperiosteal hemorrhages cause pain and tenderness, resulting in pseudoparalysis. Loss of function at the site of the hemorrhage and anemia are typical sequelae of the hemorrhages observed in scurvy. Subperiosteal hemorrhage in the tibia and femur causes excruciating pain. Laboratory data suggest that the neonatal brain is particularly susceptible to vitamin C deficiency and that this condition may adversely affect early brain development.

[ 22 ] Until minimal daily requirements of vitamin C were supplied, scurvy plagued prolonged naval voyages and military campaigns as personnel succumbed to its devastating effects. Lethargy, fatigue, and hemorrhagic manifestations of impaired collagen synthesis affecting oral, ophthalmic, musculoskeletal, cardiac, and gastrointestinal structures and functions incapacitated or killed more people than enemy action in many cases. Previous Coauthor(s) Mose July, MD Fellow in Endocrinology, Diabetes and Metabolism, Marshall University School of Medicine Mose July, MD is a member of the following medical societies: American Association of Clinical Endocrinologists , Endocrine Society Disclosure: Nothing to disclose. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape.

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC Additional Contributors Janet J Wong, MD Consulting Dermatologist, Department of Dermatology, University of Connecticut School of Medicine Janet J Wong, MD is a member of the following medical societies: American Academy of Dermatology Disclosure: Nothing to disclose. Van Perry, MD Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio Van Perry, MD is a member of the following medical societies: American Academy of Dermatology Disclosure: Nothing to disclose. Kathryn Schwarzenberger, MD Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care Kathryn Schwarzenberger, MD is a member of the following medical societies: Women's Dermatologic Society , American Contact Dermatitis Society , Medical Dermatology Society , Dermatology Foundation , Alpha Omega Alpha , American Academy of Dermatology Disclosure: Nothing to disclose.

Steven M Schwarz, MD, FAAP, FACN, AGAF Professor of Pediatrics, Children's Hospital at Downstate, State University of New York Downstate Medical Center Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics , American College of Nutrition , American Association for Physician Leadership , New York Academy of Medicine , Gastroenterology Research Group , American Gastroenterological Association , American Pediatric Society , North American Society for Pediatric Gastroenterology, Hepatology and Nutrition , Society for Pediatric Research Disclosure: Nothing to disclose.

Anne Elizabeth Laumann, MBChB, MRCP(UK), FAAD Professor of Dermatology, Chief of General Dermatology, Director of the Collagen Vascular Disorders Clinic, Northwestern University, The Feinberg School of Medicine Anne Elizabeth Laumann, MBChB, MRCP(UK), FAAD is a member of the following medical societies: American Academy of Dermatology , Association of Professors of Dermatology , British Association of Dermatologists , Chicago Dermatological Society , Chicago Medical Society , Illinois Dermatological Society , Illinois State Medical Society , Medical Dermatology Society , Society for Investigative Dermatology , Women's Dermatologic Society Disclosure: Nothing to disclose. Henry Driscoll, MD Farrell Professor of Endocrinology, Chief, Department of Medicine, Section of Endocrinology, Joan C Edwards School of Medicine at Marshall University Henry Driscoll, MD is a member of the following medical societies: American College of Physicians , American Diabetes Association , American Federation for Medical Research , American Medical Association , Endocrine Society , Massachusetts Medical Society , Sigma Xi , West Virginia State Medical Association Disclosure: Nothing to disclose.

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology Disclosure: Nothing to disclose. Julia Sanger Minocha, MD Resident Physician, Department of Medicine, Northwestern University, The Feinberg School of Medicine Julia Sanger Minocha, MD is a member of the following medical societies: Alpha Omega Alpha , American College of Physicians , Phi Beta Kappa Disclosure: Nothing to disclose. Bradley S Buckler, MD Fellow in Neonatal-Perinatal Medicine, Medical College of Georgia Disclosure: Nothing to disclose. Acknowledgements The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Anjali Parish, MD, Kumaravel Rajakumar, MD, and Tarita Thomas, PhD, MBA,to the development and writing of the source articles.

Question: A deficiency of what vitamin causes the curse of sailors of the 18th century, scurvy?
Answer: Vitamin C