For those of us living in industrialized nations, it is assumed that we get a reasonably adequate amount of the nutrients that our bodies need. This assumption seems based on several things, including the practice of fortification of foods such as adding vitamin D to milk, calcium to orange juice, and B vitamins to wheat flour. It is also assumed that people living in the first world have access to a range of nutritious foods and can afford to eat a balanced diet. While there is some truth in these assumptions, and we don't see high levels of many nutrient-deficiency driven diseases in most developed countries, These assumptions can also give a false sense of security. One of the reasons that some foods are fortified is that much of the nutrition is lost during the processing stage and some of those nutrients are added back in (usually not in the same form that they occurred in in the unprocessed food). White wheat flour is a good example of this.
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.
Blindness and Other Vision Problems - including night blindness and other vision problems can result from vitamin A deficiency. B12 deficiency can cause blurry or disturbed vision (from optic neuropathy caused by damage to the optic nerve).
Abnormal Bone Growth - when caused by vitamin D deficiency is called Rickets, which causes bones to grow soft or thickened, leading to skeletal deformities such as bowed legs as well as pain. More on 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 lead to skeletal bone malformations such
as bowed legs, thickened wrists and ankles, and breastbone projection."
Neural tube defects - including cleft lip, cleft palate
Poor Immune Function - can be caused by vitamin A deficiency
Pellagra
"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.
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.
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.
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. "Thiamine appears to have a role in axonal conduction, particularly in acetylcholinergic and serotoninergic neurons. A reduction in the function of these enzymes leads to diffuse impairment in the metabolism of glucose in key regions of the brain, resulting in impaired cellular energy metabolism.
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)."
