The richest sources of naturally occurring thiamine are meat (especially pork), whole grains, yeast, and legumes. Fortified foods are also a good source. To prevent widespread deficiencies, it is recommended that the target population should consume a fortified food daily. This is generally easily achieved, as food staples such as rice or wheat flour are often fortified with thiamine. Mandatory fortification levels range from 1.5–11 mg per kg of wheat flour [3]. There is no known tolerable upper intake level and no known toxicity for thiamine; however, using the lowest effective dose is recommended [1,3].

The richest sources of naturally occurring thiamine are meat (especially pork), whole grains, yeast, and legumes. Fortified foods are also a good source. To prevent widespread deficiencies, it is recommended that the target population should consume a fortified food daily. This is generally easily achieved, as food staples such as rice or wheat flour are often fortified with thiamine. Mandatory fortification levels range from 1.5–11 mg per kg of wheat flour [3]. There is no known tolerable upper intake level and no known toxicity for thiamine; however, using the lowest effective dose is recommended [1,3].

As noted, foods that contain tannins can inactivate thiamine in the body, thereby putting an individual at risk for deficiency [2[. Tannins are found in tea, coffee, legumes (e.g., chickpeas, pinto beans), and berries (e.g., strawberries, raspberries) [1; 4]. Foods high in caffeine, theobromine, and theophylline, including coffee, tea and chocolate, can also inactivate thiamine in the body [2]. Thiamine status may also be compromised by betel nuts, ferns, African silkworm larvae, and thiaminase-containing fish [3].

Major food sources for riboflavin include organ meats, poultry, fish, eggs, and dairy products such as milk and cheese. Grain products and fortified cereals are additional sources [1]. Certain vegetables such as spinach and beans can also provide riboflavin [7].

Riboflavin deficiency may be associated with the development of cataracts due to the impaired regeneration of reduced glutathione in the lens. Glutathione exists in high concentrations in the reduced form and protects the lens from oxidative damage [8].

Niacin deficiency can result in pellagra, a disease characterized by dermatitis, diarrhea, dementia, and even death. The dementia presents similar to schizophrenia, with hallucinations and delusions, and responds within hours of beginning niacin therapy. The dermatitis results from sun exposure, which suggests a defect in DNA repair [9].

Cerebral pantothenate deficiency is a metabolic defect in those with Huntington disease that could possibly impair the synthesis of CoA by neurons, stimulate polyol-pathway activity, impede glycolysis and tricarboxylic acid activity, and alter brain-urea metabolism. However, it is not known whether the metabolic changes in pantothenic acid deficiency themselves cause brain damage, or whether the metabolic problems occur at later states in the pathogenic process and are not involved in neurodegeneration [15]. Treatment involves oral supplementation with high doses of pantothenic acid to replenish the depleted levels in the brain.

Vitamin B6 intake may be inversely related to the progression of diabetes. Vitamin B6 may improve the activity of plasma insulin, thereby decreasing blood glucose. Vitamin B6 also lowers postprandial blood glucose levels after the ingestion of sucrose and starch by inhibiting the activity of small-intestinal α-glucosidases. It is unclear whether diabetes decreases PLP levels or whether low PLP levels trigger diabetes [16].

Folate is critical for the development of the fetal nervous system and protects against neural tube defects, especially spina bifida [19]. The neural tube forms by 28 days after conception, so supplementation prior to and immediately after conception is vital. The U.S. Public Health Service recommends that all individuals capable of becoming pregnant take 400 mcg of folic acid per day to prevent birth defects [21].

In humans, the liver can store 4–5 mg of vitamin B12. This amount is sufficient to meet requirements for four to five years. Clinical features of deficiency are evident by five years and include fatigue, shortness of breath, and heart palpitations [23]. Deficiency may also lead to neurological manifestations, including numbness and tingling in the extremities (worse in lower extremities), gait disturbance, and cognitive changes, including memory loss and dementia. Individuals may also have a sore tongue, loss of appetite, constipation, and flatulence [1]. Megaloblastic anemia is a potential hematological effect [23].

The causes of vitamin B12 deficiency are numerous and include pernicious anemia, gastric disease, chronic atrophic gastritis, pancreatic disease, pancreatectomy, resection of the ileum, bacterial overgrowth, or HIV infection. Malnutrition, vegetarianism, or vegan diet may also lead to deficiency [23].