There are still a number of reasons why a person living in an industrialized country might still develop one of these diseases, or as is probably much more common, shows some of the signs of deficiency but the deficiency is not severe enough to lead to the full presentation of the disease and is therefore not recognized. Deficiencies can result from eating primarily processed foods that have the calories we need but very little nutrition, from eating food (even organic food) that was grown in nutrient-depleted soil or given feed that was grown that way, and by eating foods that have been engineered or bred for traits such as shelf-stability and low cost but that contain much less nutrition to begin with. Additionally, people who follow restricted diets, such as people who are vegan or vegetarian, who need to avoid foods due to allergies and sensitivities, who focus on raw and or locally-grown foods, people living in poverty or for other reasons have limited access to healthy food, or for any other reason eat a limited range of foods may need to be particularly aware of their nutrient intake. Lastly, everyone's body is somewhat different in how it metabolizes various foods and nutrients. Our bodies use enzymes and various biochemical pathways to transform what we eat into what we need in our bodies and some people have enzymes and pathways that function very differently.
Handb Clin Neurol. 2010;95:435-44
"The vitamine doctrine: Although diseases resulting from vitamin deficiencies have been known for millennia, such disorders were generally attributed to toxic or infectious causes until the "vitamin doctrine" was developed in the early 20th century. In the late-19th century, a physiologically complete diet was believed to require only sufficient proteins, carbohydrates, fats, inorganic salts, and water. From 1880-1912, Lunin, Pekelharing, and Hopkins found that animals fed purified mixtures of known food components failed to grow or even lost weight and died, unless the diet was supplemented with small amounts of milk, suggesting that "accessory food factors" are required in trace amounts for normal growth. By this time, Funk suggested that deficiencies of trace dietary factors, which he labeled "vitamines" on the mistaken notion that they were "vital amines," were responsible for such diseases as beriberi, scurvy, rickets, and pellagra.
Vitamin A deficiency eye disease: Night blindness was recognized by the ancient Egyptians and Greeks, and many authorities from Galen onward advocated liver as a curative. Outbreaks of night blindness were linked to nutritional causes in the 18th and 19th centuries... During World War I, Bloch conducted a controlled clinical trial of different diets among malnourished Danish children with night blindness and keratomalacia and concluded that whole milk, butter, and cod-liver oil contain a fat-soluble substance that protects against xerophthalmia... 1925 Fridericia and Holm directly linked vitamin A to night blindness in animal experiments using rats, and in 1929 Holm demonstrated the presence of vitamin A in retinal tissue. In the 1930s, Moore, Karrer, Wald, and others established the provitamin role of beta-carotene.
Although the availability of vitamin A through food fortification and medicinal supplements virtually eliminated ocular vitamin A deficiency from developed countries by the second half of the 20th century, vitamin A deficiency remains a serious problem in developing countries as indicated by global surveys beginning in the 1960s. Millions of children were shown to be vitamin A deficient, with resultant blindness, increased susceptibility to infection, and increased childhood mortality. Beginning in the 1960s, intervention trials showed that vitamin A deficiency disorders could be prevented in developing countries with periodic vitamin A dosing, and in the 1980s and 1990s, large randomized, double-blind, placebo-controlled clinical trials demonstrated the marked efficacy of vitamin A supplementation in reducing childhood mortality."
Chapter 30: historical aspects of the major neurological vitamin deficiency disorders: the water-soluble B vitamins.
Handb Clin Neurol. 2010;95:445-76.
"This historical review addresses major neurological disorders associated with deficiencies of water-soluble B vitamins: beriberi, Wernicke-Korsakoff syndrome, pellagra, neural tube defects, and subacute combined degeneration of the spinal cord.
Wernicke-Korsakoff syndrome: In the late 1870s, Wernicke identified a clinicopathological condition with ophthalmoparesis, nystagmus, ataxia, and encephalopathy, associated with punctate hemorrhages symmetrically arranged in the grey matter around the third and fourth ventricles and the aqueduct of Sylvius. In the late 1880s, Korsakoff described a spectrum of cognitive disorders, including a confabulatory amnestic state following an agitated delirium, occurring in conjunction with peripheral polyneuropathy. Beginning around 1900, investigators recognized the close relationship between Korsakoff's psychosis, delirium tremens, and Wernicke's encephalopathy, but not until several decades later were Wernicke's encephalopathy, Korsakoff's psychosis, and beriberi all linked to the deficiency of a specific dietary factor, i.e. thiamin.
Pellagra and niacin: Pellagra was unknown prior to the introduction of maize into Europe from the New World. In the 18th century, Casàl and Frapolli described the clinical features of pellagra in Europe, and linked it with poverty and subsistence on nutritionally marginal corn-based diets. In the United States, pellagra became epidemic among poor Southerners in the early 20th century, in part because of economically-driven reliance on monotonous, nutritionally inadequate diets, combined with new manufacturing methods that removed vitamins from processed grain... (D)uring the depression, the collapse of cotton as an economically viable crop facilitated crop diversification, which contributed to an abrupt decline in pellagra mortality in the early 1930s... (V)itamin fortification of foodstuffs during World War II ultimately eradicated endemic pellagra in the United States.
Neural tube defects and folate: Folate deficiency was initially recognized clinically as a macrocytic anemia in the 1920s, and only clearly separated from pernicious anemia by the mid-20th century. When folic acid was isolated and synthesized in the 1940s, it was shown to correct the macrocytic anemia associated with pernicious anemia, while the neurological manifestations progressed. In the 1950s and 1960s,.. Beginning in the 1960s, folate deficiency was increasingly recognized as the major cause of preventable neural tube defects. In the early 1990s well-designed randomized trials established that folate supplementation could prevent neural tube defects. Trial data, collectively indicating that periconceptual folate administration reduces both the occurrence and recurrence risks of neural tube defects by at least 70%, helped establish governmental recommendations concerning folic acid intake and health policy concerning vitamin fortification of foodstuffs... Recent studies have established genetic predispositions for neural tube defects, including both infant and maternal gene polymorphisms for enzymes involved in folate-dependent homocysteine metabolism, which help explain how the genotype of the mother, the genotype of the unborn child, and environmental factors (e.g. folate intake) can all impact on the risk of neural tube defects.
Subacute combined degeneration and B(12) deficiency: Pernicious anemia was recognized clinically in the mid-19th century by Addison, but the most important neurological manifestation - subacute combined degeneration of the spinal cord - was not recognized clinically and linked with pernicious anemia until the end of the 19th century... In the 1920s, Minot and Murphy showed that large quantities of ingested liver could be used to effectively treat pernicious anemia, and specifically could improve or prevent progression of neurological manifestations, and could extend life expectancy beyond 2 years. Beginning in the late 1920s, Castle demonstrated that a substance elaborated by the gastric mucosa ("intrinsic factor") was essential for the absorption of a dietary factor ("extrinsic factor," later shown to be vitamin B(12)) needed to prevent pernicious anemia. Over two decades, from the late 1920s until the late 1940s, increasingly potent liver extracts were manufactured that could be given either intramuscularly or intravenously. In 1947, vitamin B(12) was isolated by Folkers and colleagues, and nearly simultaneously by Smith. Shortly thereafter the therapeutic efficacy of vitamin B(12) on subacute combined degeneration was demonstrated by West and Reisner and others. By 1955, Hodgkin determined the molecular structure of cyanocobalamin using computer-assisted x-ray crystallography, allowing complete chemical synthesis of vitamin B(12) in 1960 by an international consortium. Beginning in the late 1950s, the absorption and biochemistry of vitamin B(12) were elaborated, and several lines of evidence converged to support an autoimmune basis for pernicious anemia.
More on These Diseases:
Pellagra (from Medscape)
"Pellagra is defined by the systemic disease resulting from niacin deficiency, and it is characterized by diarrhea, dermatitis, dementia, and death, which usually appear in this order. GI tract symptoms always precede dermatitis, or, according to Rille, "Pellagra begins in the stomach"."
Wernicke-Korsakoff Syndrome (from Medscape)
Acute thiamine deficiency leads to mitochondrial dysfunction and therefore oxidative toxicity in areas of the brain starting with areas with the highest metabolic activity. The exact mechanism of neuronal cell death remains to be elucidated.
Additional findings include increased astrocyte lactate and edema, increased extracellular glutamate concentrations, increased nitric oxide from endothelial cell dysfunction, deoxyribonucleic acid (DNA) fragmentation in neurons, free radical production and increase in cytokines, and breakdown of the blood-brain barrier.
The amnestic component is related to damage in the diencephalon, including the medial thalamus, and connections with the medial temporal lobes and amygdala. The slow and incomplete recovery of memory deficits suggests that amnesia is related to irreversible structural damage.
Mortality may be secondary to infections and hepatic failure, but some deaths are directly attributable to irreversible defects of severe and prolonged thiamine deficiency (eg, coma)."
An original discovery: selenium deficiency and Keshan disease (an endemic heart disease).
Rickets (from Mayo Clinic)
"Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Vitamin D promotes the absorption of calcium and phosphorus from the gastrointestinal tract. A deficiency of vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.
Symptoms include delayed growth, pain in the spine, pelvis, and legs; and muscle weakness. In children it can skeletal bone malformations such as bowed legs, thickened wrists and ankles, and breastbone projection."