Thiamine, also known as thiamin or vitamin B1, is one the of B vitamins. Thiamine helps to turn food into energy to keep the nervous system healthy.
Because thiamine and the thiamine–using enzymes are present in all cells of the body, it would be plausible that inadequate thiamine affects all organ systems; however, the cells of the nervous system and heart seem particularly sensitive to the effects of thiamine deficiency.
Nerve damage
Among the most well-known side effects of prolonged, severe thiamine deficiency (beriberi) is damage to the nerves, also known as neuropathy. In fact, neuropathy from thiamine deficiency was among the first deficiency syndrome identified in humans ( 2 ).
In its early stage, thiamin deficiency can cause weight loss and anorexia, confusion, short-term memory loss, and other mental signs and symptoms; muscle weakness; and cardiovascular symptoms (such as an enlarged heart) [7].
In general, neurological symptoms of thiamine deficiency include confusion, psychomotor retardation, lack of insight, impaired retentive memory and cognitive function, confabulation, ataxia, and the loss of vibration and position sense.21, 24 If thiamine is not present in sufficient quantity for the CNS, sensitive ...
Thiamine plays a crucial role for normal cardiac function, since severe thiamine deficiency leads to congestive heart failure (wet beriberi). Consequently, patients undergoing diuretic treatment might have compromised heart function.
Thiamin plays a key role in the maintenance of brain function. Thiamin diphosphate is cofactor for several enzymes involved in glucose metabolism whereas thiamin triphosphate has distinct properties at the neuronal membrane. Thiamin metabolism in the brain is compartmented between neurons and neighbouring glial cells.
Risk Factors for Thiamine Deficiency
Alcoholism. Gastric bypass surgery. Genetic beriberi (inability to absorb thiamine)
Secondary function: Nerve and other supporting cells (such as glial cells) of the nervous system require thiamine. nervous system is particularly sensitive to thiamine deficiency, because of its dependence on oxidative metabolism.
(Beriberi; Vitamin B1 Deficiency)
At first, people have vague symptoms such as fatigue and irritability, but a severe deficiency (beriberi) can affect the nerves, muscles, heart, and brain.
Thiamine pyrophosphate, a thiamine derivative, is essential to the citric acid cycle and thiamine deficiency can result in impaired aerobic respiration and cellular energy production. Thiamine also plays an important role in the pentose phosphate pathway and other key metabolic processes.
Summary: High doses of thiamine -- vitamin B1 -- can reverse the onset of early diabetic kidney disease, according to new research.
If sufficiently prolonged and severe, thiamine deficiency results in brain cell death. Possible mechanisms involved include compromised cerebral energy metabolism and focal accumulation of lactate, both of which could result from decreased activities of alpha KGDH.
Thiamin (vitamin B-1) helps the body generate energy from nutrients. Also known as thiamine, thiamin is necessary for the growth, development and function of cells.
Alcohol decreases the absorption of dietary thiamine by at least 50 percent and can damage the lining of the intestinal tract, resulting in more malabsorption. Cut out caffeine. Coffee and tea, although less damaging to the intestinal tract, can wreak havoc on thiamine absorption.
Early signs of thiamine deficiency include peripheral neuropathies in adults and adolescents and fussiness and irritability in infants. Weakness, nystagmus, ophthalmoplegia, ataxia, and cognitive impairment accompany progression of the disease. Infants may be noted to have a lack of tone.
Thiamin deficiency (causing beriberi) is most common among people subsisting on white rice or highly refined carbohydrates in countries with high rates of food insecurity and among people with alcohol use disorder. Symptoms include diffuse polyneuropathy, high-output heart failure, and Wernicke-Korsakoff syndrome.
Conclusion/interpretation: High dose thiamine supplementation may have beneficial effects on the blood pressure of individuals with hyperglycemia at early stages, and may have a role in the prevention of further vascular complications.
Second, alcoholics may develop a thiamine deficit because of impaired thiamine absorption from the intestine (Hoyumpa 1980). Alcohol damages the lining of the intestine and directly inhibits the transport mechanism that is responsible for thiamine absorption in the intestinal tract (Gastaldi et al. 1989).
As thiamine deficiency progresses, extreme loss of muscle mass can be observed. Early reports of the phenomenon particularly indicate severe wasting of the gastrocnemii. Adults demonstrate considerable weakness related to muscle loss and peripheral neuropathy.
Thiamine deficiency is also responsible for Wernicke's encephalopathy and Korsakoff's syndrome.
Toxicity. It is unlikely to reach a toxic level of thiamin from food sources alone. In the setting of very high intakes, the body will absorb less of the nutrient and flush out any excess amount through the urine.
This discovery of the potent anti-steatotic effect of thiamine may prove clinically useful in managing fatty liver-related disorders.
Severe thiamine deficiency can cause cognitive impairment (Wernicke's encephalopathy), peripheral neuropathy (“dry beriberi”), or heart failure (cardiac, or “wet beriberi”). Cardiac beriberi occurs as a result of decreased cardiac function from impaired cellular metabolism.