Beriberi may also be caused by shortcomings other than inadequate intake - diseases or operations on the digestive tract, alcoholism, dialysis or genetic<unk> es. All those causes mainly affect the central nervous system, and provoke the development of Wernicke's encephalopathy. Wernicke's disease is one of the most prevalent neurological or neuropsychiatric diseases. In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases. Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12.5% or more. Mortality caused by Wernicke's disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries. The number of people with Wernicke's disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases. Genetics Genetic diseases of<unk>  transport are rare but serious.<unk>  responsive megaloblastic anemia syndrome (TRMA) with diabetes mellitus and sensorineural deafness is an autosomal recessive disorder caused by mutations in the gene SLC19A2, a high affinity<unk>  transporter. TRMA patients do not show signs of systemic<unk> , suggesting redundancy in the<unk>  transport system. This has led to the discovery of a second high-affinity<unk>  transporter, SLC19A3. Leigh disease (subacute necrotising encephalomyelopathy) is an inherited disorder that affects mostly infants in the first years of life and is invariably fatal. Pathological similarities between Leigh disease and WE led to the hypothesis that the cause was a defect in<unk>  metabolism. One of the most consistent findings has been an abnormality of the activation of the pyruvate dehydrogenase complex. Mutations in the SLC19A3 gene have been linked to biotin-thiamine responsive basal ganglia disease, which is treated with pharmacological doses of<unk>  and biotin, another B vitamin. Other disorders in which a putative role for<unk>  has been implicated include subacute necrotising encephalomyelopathy, opsoclonus myoclonus syndrome (a paraneoplastic syndrome), and Nigerian seasonal ataxia (or African seasonal ataxia). In addition, several inherited disorders of ThDP-dependent enzymes have been reported, which may respond to<unk>  treatment.
Thiamine deficiency
Fluorine deficiency
Boron deficiency 
Selenium deficiency
Biotin deficiency
Chromium deficiency
Copper deficiency
Magnesium deficiency