The topics of each of the five reviews which follow has an historic section (‘Past’) which varies quite widely according to the history and type of vitamin or specific diets involved. ‘Present’ considers current knowledge of each subject, and ‘Future’ the opportunities for new ideas and developments. The overall support of Phil Fischer, co-editor-in-chief, in compiling this issue and as co-author of the article on thiamine deficiency is much appreciated.
There is no introduction to ‘Past’ as we trust that readers will enjoy perusing this brief section in full!
It is hoped that the historical section will continue to be of value to readers for many years, even though ideas in the present and future might have moved on.
Casey Johnson and Tom Thacher have contributed an in-depth overview of vitamin D: immune function, inflammation, infections and auto-immunity.
Vitamin D plays an active role beyond mineral metabolism and skeletal health, including regulation of the immune system. Vitamin D deficiency is widely prevalent, and observational studies link low vitamin D status to a risk of infections and auto-immune disorders. Their review details vitamin D signalling interactions with the immune system and provides experimental and clinical evidence evaluating vitamin D status, vitamin D supplementation and host susceptibility to infections, inflammation and auto-immunity.
Several observational studies have evaluated potential associations between vitamin status and the incidence and severity of respiratory tract infections. A recent meta-analysis of eight studies with 15,207 participants found that a deficiency of vitamin D might be related to longer duration of acute respiratory infections, but demonstrated mixed results for the incidence.
Self-reported viral respiratory tract infections were twice as likely in vitamin D-deficient participants than in those with optimal vitamin D status. However, other studies lacked demonstrable evidence of a link between vitamin D status and the incidence of viral upper respiratory infections and influenza or influenza-like illness.
A meta-analysis of seven randomised controlled trials (RCTs) and 1527 patients demonstrated no improvement in those receiving vitamin D supplements as an adjuvant therapy for childhood community-acquired pneumonia.
There is evidence that vitamin D supplementation protects against acute respiratory infections, especially in children and those who are vitamin D-deficient; however, the effect appears to be small.
Severe coronavirus 2019 (COVID-19) results from a vigorous and unrestrained immune response to the SARS-COV-2 virus. The clinical manifestations and pathophysiology of severe COVID-19 and acute respiratory distress syndrome are similar and related to the release of pro-inflammatory cytokines. In the context of COVID-19, vitamin D has a potentially favourable effect on cytokine production, the macrophage system and the risk of infection. Optimal vitamin D status may partly protect against SARS-COV-2 infection and promote viral clearance.
Vitamin D deficiency is highly prevalent in patients with mycobacterium tuberculosis (Mtb), and vitamin D signalling may bolster host immunity against it. A meta-analysis of 1787 patients demonstrated an increased proportion of sputum, smear and culture conversions in treating Mtb along with vitamin D supplementation, and therefore vitamin D supplementation can be considered as a combination therapy in appropriate patients with pulmonary Mtb infection.
A meta-analysis of observational studies including 1007 patients and 829 controls found significantly lower mean 25(OH)D levels in patients with multiple sclerosis (MS) and concluded that low vitamin D levels were associated with an increased risk of MS. Several randomised controlled trials (RCTs) have evaluated the potential benefits of vitamin D supplementation for MS; however, the results have largely shown no benefit.
A meta-analysis of 16 observational studies including 10,605 participants identified an inverse relationship between 25(OH)D concentrations and the risk of type 1 diabetes for every 10 nmol/L increase in serum 25(OH)D concentrations. However, the relationship was non-linear with no evidence of further benefit with 25(OH)D concentrations >90 nmol/L.
A meta-analysis of 18 RCTs found that vitamin D supplements in patients with inflammatory bowel disease (IBD) controlled the relapse rate, without significantly affecting inflammatory markers; however, other meta-analyses found no relationship between vitamin D and the clinical course of IBD.
In a meta-analysis of three observational trials, vitamin D supplementation decreased anti-double-stranded DNA antibody positivity in patients with systemic lupus erythematosus, but a meta-analysis of RCTs found that vitamin D supplements conferred no benefit on overall disease activity.
Strategic collaboration and future studies
To achieve the highest quality evidence with adequate power, new, well designed trials undertaken across several sites and latitudes with large, diverse populations and over long periods of intervention and follow-up are required. Currently, the American Academy of Pediatrics recommends universal vitamin D supplementation during early childhood, which creates an ethical dilemma for providing a true placebo arm in this age group.
Elizabeth Keating, Casey Johnson, Kristin Cardiel Nunez and Philip Fischer have written a comprehensive review of thiamine deficiency disorders in women and children.
Thiamine (vitamin B1) is available in common foods such as rice bran, and is necessary for normal cardiovascular, neurological and metabolic processes. Thiamine deficiency is common in parts of Asia and Africa and also in the Pacific Islands and South America. The diagnosis is based on clinical suspicion. It occurs in infants with heart failure, in all age groups with encephalopathy and in older children and adults with peripheral neuropathy. While the disease has existed for hundreds or thousands of years, the advent of the rice mill made the problem much worse. In Southern and South-East Asian cultures, rice has been a food staple for generations, and, traditionally, the grain was separated from the bran and seed-coat layers by hand-milling before cooking. Machine milling was much more efficient and enabled more thorough extraction of the vitamin-rich outer grain layers, quickly replacing hand-milling in most communities. In societies subsisting on polished white rice (machine-milled) in whom, until then, thiamine deficiency had been a problem only intermittently, thiamine deficiency disorders (TDD) became commonplace.
Humans cannot synthesise thiamine endogenously and therefore rely on dietary intake to meet their metabolic requirements. Rich dietary sources include unrefined cereal and legume grains, meat, yeast and nuts. Diets associated with thiamine deficiency primarily include subsistence diets of polished rice and cassava. Exclusively breastfed infants of thiamine-deficient mothers are at greatest risk as they are fully dependent on the transfer of maternal thiamine through breast-milk, and maternal transfer depends on the mother’s thiamine status.
Thiamine deficiency is common, especially in parts of South-East Asia, including Cambodia, Laos, Myanmar, Bhutan and parts of India. Women and children, especially children in the first year of life, are particularly at risk. In several African nations, there is dietary insufficiency of thiamine in about a third of the population, and clinical cases of TDD have been reported, and similarly in South America.
Infantile TDD occurs most commonly between the ages of 1 and 7 months and can present with signs and symptoms of heart failure, including oedema, hepatomegaly, respiratory distress and cardiogenic shock. Cognitive and neurological symptoms include decreased levels of consciousness, nystagmus, convulsions and anorexia. If untreated, it can cause rapid decline and death. The mortality rate of untreated infantile TDD is close to 100%. TDD in older children, adolescents and women commonly presents with encephalopathy, ataxia, nystagmus and peripheral neuropathy. In high-income countries, most cases of TDD are in older children and adolescents, most commonly owing to eating disorders, diabetes, obesity and excessive consumption of sweetened drinks, bariatric surgery and cancer.
Clinical intervention with parenteral thiamine in confirmed or probable cases of TDD has been reported in Brazil, Cambodia, The Gambia, India, Laos, Nigeria and Thailand.
The majority of studies report complete clinical recovery after thiamine injection. In infants presenting with cardiovascular manifestations of TDD, the response to thiamine is rapid with resolution of shock, irritability and tachycardia, and recovery within hours of receiving thiamine.
In Newfoundland, Canada, thiamine fortification was commenced in 1944, soon after thiamine was first isolated. Only 6 years after the fortification programme began, TDD disappeared. Foods fortified with thiamine in the past include wheat and maize flour, margarine, rice cereal, rice, ready-to-eat meals, fish sauce and salt. In China, government regulations were imposed on milling practices to ensure that bran extraction did not exceed 92% in rice or 81% in wheat, and the result was almost complete elimination of TDD in areas where previously it had been prevalent.
In South-East Asia, the estimated prevalence of inadequate thiamine intake decreased from 75% in 1961 to 30% in 2001.
The present thrust in reducing the risk of TDD is supplementation. Thiamine-deficient mothers are at greatest risk, and routine preventive supplementation of pregnant and lactating women may be warranted. However, it has been estimated that only 0.05–0.35% of oral single-dose thiamine is secreted in breast-milk and available to the breastfed infant; it might be better to supplement the mother at higher doses closer to the recommended daily intake, and for longer to ensure that the breastfed infant is receiving the thiamine it needs. A complicating factor is that some populations commonly consume fermented fish, betel nuts and fermented tea leaves, all of which contain anti-thiamine compounds which inhibit the absorption and bio-availability of thiamine, exacerbating deficiency, even when there is an adequate intake of thiamine.
Laura M. Kinlin and Michael Weinstein have written an in-depth historical review of scurvy and the current position in middle- and low-income counties and high-income countries.
Although scurvy has existed since antiquity, for centuries it was a medical mystery, eluding understanding while claiming millions of lives. It continues to exist, including in children and young people. It is often mistaken for other conditions (e.g. haematological malignancy and osteo-articular infections), even when there are clinically compatible signs and symptoms and when the diet is deficient in vitamin C.
A terrible affliction
‘Their gums were rotten even to the very roots of their very teeth, and their cheeks hard and swollen, the teeth were loose neere ready to fall out …… ’. This description of scurvy in 1596 by William Clowes, the English sea surgeon, captures some of the most prominent clinical manifestations of scurvy.
Affected infants may adopt the ‘pithed frog’ position with the hips, knees and legs abducted. Untreated scurvy can be fatal.
In humans, vitamin C is an essential nutrient which must be obtained from the diet. Important sources include citrus fruit, potatoes, spinach, strawberries, cauliflower and broccoli. Breast-milk is an adequate source for infants as long as it is not heated or pasteurised. An inadequate intake of vitamin C can result rapidly in scurvy (within 1–3 months). Specific radiological findings include a white line at the ends of the metaphyses (the Fraenkel sign), healing fractures at the periphery of the zone of calcification (Pelkan spurs) and increased density outlining the epiphyses (Wimberger ring). A suggested corrective vitamin C dose is 100 mg three times daily for 1 week, then 100 mg daily until full recovery).
Antiquity to the Middle Ages
Thought to be one of the oldest diseases in human history, scurvy has probably existed since the discovery of agriculture. The ability to grow and store grain led to the movement of populations into temperate regions with long winters, and the consequent reliance on vitamin C-poor foods over prolonged periods when crops could not be grown probably heralded the advent of scurvy.
Throughout the ages, there are numerous references to a disease resembling scurvy. Dating to approximately 1500 BC in ancient Egypt, the Ebers papyrus appears to depict symptoms of severe vitamin C deficiency, specifically bleeding gums and petechial haemorrhages. Hippocrates’ ‘ileos ematitis’ is generally accepted to be a credible description of scurvy.
Hirsch, after analysis of the work of ancient authors, concludes that it is only Hippocrates who reported a disease ‘which can be unequivocally regarded as scurvy’. In contrast, Wilson, in his dissertation on treatment before the 19th century, found ‘slender evidence’ of descriptions of scurvy. He asserted that conditions during early civilisation would not have predisposed to the development of scurvy. Relatively mild winters meant that there was ready and consistent access to fruit and edible plants. Voyages at sea were not long and sailors therefore did not lack vitamin C.
By the Middle Ages, conditions were substantially more conducive to the development of vitamin C deficiency. Amongst the Crusaders who had little access to green vegetables, scurvy is thought to have been relatively prevalent; it is convincingly described in numerous documents which chronicle the Crusades.
Scurvy is also believed to have been endemic in the Middle Ages in Northern Europe during the late winter because of a paucity of foods rich in vitamin C. Salted fish and meat were mainstays of the typical diet with no access to vegetables; potatoes were not introduced into Europe until later.
An epidemic during the Age of Sail
While scurvy was relatively common during the Middle Ages, the Age of Sail brought an epidemic from the late 15th to the mid-19th century. Prolonged voyages with inadequate supplies of fresh food created conditions in which scurvy flourished. Claiming more than two million lives, the disease was responsible for more deaths at sea than combat, storms or infectious diseases combined. Numerous cures were found but their significance was not understood; they were not widely implemented and/or not sustained: ‘One of the strangest things is that people kept figuring out cures and then forgetting them’.
Vasco da Gama’s expedition from Portugal to India in 1497 was one of the first sea voyages to be affected by scurvy — more than half of the crew died of it. da Gama noted that oranges received from local traders were an effective treatment; however, the importance of citrus fruit in preventing and treating the disease was not widely recognised until much later.
In 1601, James Lancaster, an English merchant and privateer, led a pioneering expedition to the Spice Islands. He recognised the benefits of lemon juice for preventing scurvy, knowledge that might have come from his exposure to Portuguese merchants who had been using lemon juice on shorter expeditions as early as the mid-16th century. The crew of one of Lancaster’s ships regularly received lemon juice while those on the other three ships who did not were frequently affected by scurvy. After leading his ships into port mid-voyage to obtain fresh fruit, Lancaster had his crews squeeze thousands of lemons to make barrels of the important ‘lemon water’. By the early 17th century, lemon juice was regularly taken to prevent and cure scurvy at sea.
Over the course of the 17th century, citrus fruit was used less frequently at sea. It was hypothesised that decline in the use of lemon juice and lemon water was multi-factorial: lemons were expensive and sometimes difficult to obtain, ships’ crews were reluctant to drink the bitter juice, and preventive medicine as a concept seemed to be falling out of favour. By the 18th century, the ‘use of lemon juice was all but forgotten’. Voyages at sea became longer and scurvy became more problematic than ever before.
In 1734, the Dutch physician Johan Backstrom coined the term 'anti-scorbutic', referring to fresh vegetables, and he was the first to suggest that scurvy was a disease of deficiency. His explanations aligned with mariners’ observations but were dismissed.
Then in 1740 came one of the worst medical disasters at sea of all time. More than 2000 crew left Portsmouth, UK for a circumnavigation of the globe led by George Anson, the Royal Navy officer, and only 200 survived; most of the deaths were caused by scurvy. The tragedy inspired a golden age of scurvy research in England.
James Lind, a naval surgeon, published a treatise on scurvy in 1753 and dedicated it to Anson. He described one of the first clinical trials in history: 12 sailors with scurvy were assigned to six different treatments, including oranges and lemons. Except for the fruit which was taken for 6 days, the treatments were administered for 14 days. Those who received oranges and lemons recovered fully.
Lind is now widely credited with discovering the cure for scurvy (although this was really a rediscovery). Lind himself, however, seems to have failed to recognise the significance of his observations.
Many Royal Navy authorities were unconvinced by Lind’s work, and wort of malt (fermented barley malt) was suggested as a treatment as it was inexpensive and easily stored.
When James Cook began a series of voyages in 1768, he was tasked with investigating various possible treatments for scurvy, including wort of malt and lemon rob (lemon juice that has been thickened or concentrated by evaporation). There were no deaths from scurvy in his crews, but how this was achieved is not clear.
Wort of malt was adopted subsequently and was used extensively by the Royal Navy at the expense of an effective cure for scurvy and costing many sailors their lives. Nevertheless, there remained advocates for citrus fruit, one of whom was Gilbert Blane, the Scottish physician and Royal Navy medical officer. Blane was aware of Ling’s work on scurvy, collected data on the disease and concluded that lemon and orange juice was effective. He quietly ignored naval authorities’ instructions and stopped using malt wort. When his initial appeal to distribute lemon juice widely to Royal Navy mariners was dismissed, he provided lemon juice to the West Indies fleet and demonstrated a substantial reduction in morbidity and mortality related to scurvy. Blane subsequently convinced the Royal Navy to offer lemon juice routinely to all its sailors. This change came into effect in 1795, more than 40 years after Lind published his work and 1 year after his death.
By the beginning of the 19th century, the Royal Navy was using more than 50,000 gallons of lemon juice annually. British sailors quickly became healthier which translated into military success. Their ability to remain at sea for long periods of time without succumbing to scurvy has been credited with the successful blockade of the English channel over 20 years, preventing Napoleon from invading England.
In one final twist in the circuitous history of scurvy in the Age of Sail, the Royal Navy began using limes from the West Indies in the mid-19th century. The replacement of lemons was significant because limes contain substantially less vitamin C, and the vitamin content is further reduced by oxidation as it was pumped through copper pipes. Scurvy was prevented less effectively, and confidence in the value of citrus juice diminished; however, the impact of these changes were mitigated by faster travel at sea owing to steam power, a better quality of food for sailors and their more robust stores of vitamin C at the outset of their voyages.
Land scurvy
Lessons learned at sea did not lead to prevention of scurvy on land. Although it became increasingly rare in sailors during the 19th century, it still occurred in, amongst others, prisoners, explorers and soldiers.
One of the outbreaks on land in the 19th century was around 1823 at the National Penitentiary in Millbank, London. A change in diet was suspected, but other factors (e.g. cold, over-working and depression) were thought to have contributed. In 1840, William Baly, a physician at the prison and lecturer on forensic medicine, noted that those with scurvy had no potatoes in their diet and he recommended that they be added to prison diets. The importance of potatoes in preventing scurvy was again demonstrated during the Great Potato Famine (1845–1852) when blighted potato crops in successive harvests led to the re-emergence of scurvy in Europe, particularly in Ireland.
During the Gold Rush (1848–1850), more than 100,000 people travelled to northern California, often a journey of many months. It is estimated that more than 10,000 died of scurvy.
Similar outbreaks occurred in the Crimean war (1853–1856), the American civil war (1861–1965) and during the siege of Paris during the Franco-Prussian war (1870–1871).
Scurvy was a major problem in explorations of the Arctic in the 19th and early 20th centuries when expeditions lasted months to years and fresh food was lacking. The consumption of fresh seal meat, in particular, was recognised as an effective means of prevention.
Infantile scurvy
Scurvy in young children is rarely described before the end of the 19th century. This probably reflects its low incidence in the very young owing to prolonged breast-feeding (common during the 17th and 18th centuries) and the use of potato as a weaning food (adopted during the 18th century).
Infantile scurvy, a term used for scurvy in those up to 3 years of age, emerged in the later 19th century with changes to common feeding practices: use of heated milk and the introduction of manufactured proprietary infant foods. The heating of milk resulted in an overall decline in infant mortality as bacterial contamination of raw milk frequently caused severe illness in the very young; however, the process also led to the destruction of vitamin C. Proprietary infant foods were flour-based, lacking vitamin C and of overall poor nutritional quality. Families of higher socio-economic status relied on breast-feeding and relatively inexpensive weaning foods. Early cases of scurvy therefore occurred primarily amongst the affluent.
Discovery of vitamin C
At the beginning of the 20th century, it was generally understood that scurvy was caused by an essential element missing from the diet. Work by Axel Holist and Theodor Frølich between 1907 and 1912 was critical in identifying vitamin C.
In 1928, Albert Szent-Györgyi isolated a compound he called hexuronic acid from the adrenal cortex. Although he had identified the elusive anti-scorbutic substance, he did not recognise it as such.
In 1932, Charles Glen-King and his team were the first to isolate and test the active substance in lemon juice in guinea pig assays and identified that it was the hexuronic acid which Szent-Györgyi had detected. The compound was renamed ascorbic acid in recognition of its action against scurvy (anti-scorbutic) and it also became known as vitamin C.
In 1933, the molecular structure of vitamin C was determined by a British team and a Swiss team working independently; a method of commercial synthesis followed, allowing vitamin C to become a practical, inexpensive and readily available food additive.
Not gone, but forgotten
During the later 20th century, scurvy became increasingly rare, largely owing to developments in food processing and better understanding of the disease. However, scurvy is far from being eradicated and it continues to occur worldwide in a variety of populations.
In adults, modern scurvy has been reported in the elderly and in institutionalised individuals with a wide variety of others disorders.
Outbreaks have occurred in refugee populations with limited access to fresh fruit and vegetables, most notably in Ethiopia, Kenya, Somalia and Sudan.
In children and young people, scurvy has been reported in association with numerous conditions including developmental disability, anorexia nervosa and other food disorders, e.g. an extremely selective diet.
In paediatrics, scurvy is more commonly reported in those with autism spectrum disorders in whom food refusal, limited food repertoire and high-frequency single food intake are common.
In a review of cases of scurvy in a Canadian children’s hospital between 1953 and 1963, only a minority had been correctly diagnosed on admission. The misdiagnosis and extensive investigation in cases of scurvy described over many decades may stem from clinicians’ lack of familiarity with scurvy, or the perception that it is exclusively a disease of the past.
Looking to the future through the lens of the past
Scurvy’s long history is punctuated by serial learning and re-learning of important lessons concerning prevention and cure. The unfortunate result, best appreciated only in retrospect, was missed opportunities for intervention over the course of centuries.
Future preventive efforts should focus on (i) anticipatory guidance and early nutritional intervention, informed by an understanding of scurvy’s epidemiology, with the aim of preventing the disease in those at risk (primary prevention), and (ii) prompt recognition and treatment to minimise morbidity and healthcare costs (secondary prevention). Necessary to these efforts is a better understanding of the epidemiology of ‘modern scurvy’ and dispelling the myth of scurvy as a disease of the past.
The World Health Organization has published strategies for preventing scurvy in emergency settings affecting large groups broadly and in refugee populations specifically. The principal recommendations include the provision of food rations with adequate amounts of vitamin C, provision of food rations sufficient to allow for trading, fortification of relief food, provision of vitamin C supplements and cultivation of fruit and vegetables by refugees (e.g. in home gardens).
Given the prevalence of feeding problems in children and young people with autism spectrum disorders, review of their diets and feeding is an essential component of health surveillance.
Thought to be one of the oldest diseases in history, scurvy continues to exist in the present, particularly in certain at-risk groups.
Jatinder Singh Goraya and Sukhjot Kaur have written an in-depth review of vitamin B12 deficiency in mothers and children and the risk of neuro-regression in infants.
Vitamin B12 (cobalamin) is a water-soluble vitamin which is obtained from foods of animal origin. Following absorption from the ileum with the help of intrinsic factor, it is stored in the liver.
Vitamin B12 deficiency in infants has been recognised since the middle of the 20th century. With few exceptions, it results from maternal vitamin B12 deficiency which can occur when there is a deficient intake of foods of animal origin by vegetarians, in those on strict diets or owing to the cost of such foods. In low- and middle-income countries such as India, religious beliefs and a lack of access to foods rich in vitamin B12 are the most common causes of the deficiency in mothers, and, in high-income countries, pernicious anaemia and vegan diets are the most common causes of a maternal deficiency.
Vitamin B12 deficiency in children is most common during infancy. Almost always, it results from prolonged exclusive breastfeeding by mothers who themselves are deficient. Although common throughout the world, vitamin B12 deficiency in infants caused by a maternal deficiency is particularly prevalent in India and Turkey. Prolonged deficiency of nutritional vitamin B12 in infants is associated with neuro-regression and long-term neurocognitive and language deficits. Infants born to vitamin B12-deficient mothers have suboptimal vitamin B12 stores and, in the absence of appropriate dietary intervention or supplementation, they are at risk of developing vitamin B12 deficiency. Unless proven otherwise, all exclusively breastfed infants of vegetarian mothers should be considered to be vitamin B12-deficient.
Early symptoms and signs of nutritional vitamin B12 deficiency include irritability, anorexia, feeding difficulties, aversion to foods other than breast-milk, spitting of non-breast-milk foods and failure to thrive. Pallor and darkening of the skin, especially the knuckles, may become minimally noticeable. More advanced cases may result in ‘infantile tremor syndrome’. The first indication of a therapeutic response is noticeable by 24–48 hours, but tremor symptoms may persist for 3–4 weeks. Unfortunately, in some cases, neurological recovery, including cognitive, language and motor function, may be incomplete, especially when the diagnosis and treatment of the deficiency are delayed.
Jean-Pierre Chouraqui has written a comprehensive review of vegetarian diets and diets which restrict animal-source foods during childhood in high-income countries.
Increasing numbers of people in the West are restricting their intake of meat and other animal products for reasons relating to health or ethics. In many Asian countries, these restrictions are already common for cultural, religious or socio-economic reasons. Children’s diets are largely determined by their parents, leading to a parallel increase in the prevalence of vegetarian diets in childhood. The review assesses current data on vegetarian diets in children from birth to 18 years. In general, the more restrictive the diet and the younger the child, the greater the risk of nutritional deficiency. Of particular concern are pregnant and nursing women, infants and young children. Vegan and macrobiotic diets should be discouraged in pregnant and lactating mothers and in young children. Those on such diets should pay careful attention to ensuring nutritional adequacy, blood monitoring and appropriate supplementation.
Vegetarian diets (VGD), i.e. the more or less total avoidance of foods of animal origin, are increasingly popular in western countries, especially in young adults and adolescents, and the prevalence of those on a vegan diet (VND) has increased by 350% in the past decade.
In Asia, VGD have been part of the cultural and religious tradition for thousands of years. The regular consumption of a meatless diet in India occurred around the beginning of the 1st millennium BCE and was mentioned in Greece in the middle of the millennium. After disappearing in Europe in late antiquity, vegetarianism re-emerged during the Renaissance and gradually became more widespread from the 19th century. Humans are omnivores by nature, and animal-source foods have always been part of the human diet.
Because of their requirements for growth and neurocognitive and psychomotor development, infants, children and adolescents are at particular risk of an inadequate nutritional intake. Weaning is a crucial period (4–6 months of age) when infants are introduced to solids with the gradual introduction of new foods, textures and tastes, together with gradual reduction of milk intake until they finally acquire their family’s dietary pattern. Children’s eating behaviour depends on their parents who purchase the food, set an example and will usually want their children to eat as they do.
Vegetarianism encompasses various dietary patterns according to the degree of exclusion of animal-source foods (ASF). The most common VGD is lacto-ovo-vegetarian (LOVD) which excludes meat, fish and seafood but includes dairy produce, eggs and honey, together with a wide variety of plant-source foods. The strictest VGD is veganism which excludes all ASF.
There are various reasons why people adopt a VGD, including religious, ethical, environmental, health and socio-economic status. Worldwide, many people object to eating flesh out of respect for animal rights; for example, all the Dharmic religions founded in India (Hinduism, Jainism, Buddhism and Sikhism) restrict intake of ASF. Most adult Indians (80%) restrict to some extent the amount of meat they consume, and up to 40% are vegetarian. For them, the consumption of dairy produce is encouraged and cows are sacred. However, VGD is not mandatory, except for Jains, 92% of whom are vegetarian and some of whom are vegan. Most Sikhs adopt a lacto-vegetarian diet and also many Buddhists, especially those practising Mahayana Buddhism, as in China, Japan, Korea and Vietnam. In Judaism and Islam, a few adhere to some form of restriction of animal produce and any meat consumed must be kosher or halal.
In industrialised countries, the most common reasons for adopting a VGD include concern about animal welfare, environmental issues and health. Those with anorexia nervosa often adopt a VGD or VND in an attempt to avoid gaining weight or to hide a restricted food intake.
In western countries, food choices, especially vegetarianism, have become a way in which people express their ideals and identities, allowing them to connect with communities, e.g. vegan climate activists who share a similar dietary pattern, beliefs and values. The UK has the highest number of vegans of all ages with a four-fold increase over the past 5 years.
Milk and dairy produce, which are consumed only by omnivores and those following an LOVD, contain 18 of 22 essential nutrients including calcium (a major source), phosphorus, magnesium, zinc, iodine, potassium and vitamins A, B2 and B12.
Guidelines for VGN and particularly VND require a well planned diet which includes a wide variety of foods including grains, legumes, vegetables, fruit, protein, iron, calcium, zinc, n-3 fatty acids and B12. If these are lacking in the diet, supplementation should be considered.