Vitamin B1 — a deficiency that mimics neurosis and fatigue?

Aim of the study: Dementia is a syndrome characterized by progressive cognitive impairment that interferes with independent function in daily activities. Symptoms of dementia depend on its cause and vary greatly between individuals. There is extensive evidence supporting a relationship between diet and cognitive functions.

Results: Folic acid supplementation proved to have better outcomes on cognitive tests than their respective control groups. The combined supplementation of folic acid and vitamin B12 showed some discrepancies between studies. Thiamine as supplementation did not only prove to have a positive impact on cognitive performance when given alone but also when given in combination with folic acid. Regarding vitamin D supplementation, the results observed were not so encouraging. A concomitant supplementation of low-dose vitamin E and vitamin C was also not associated with an improvement of cognitive function. The findings of this systematic review suggest that supplementation of B Complex vitamins, especially folic acid, may have a positive effect on delaying and preventing the risk of cognitive decline. Ascorbic acid and a high dose of vitamin E, when given separately, also showed positive effects on cognitive performance, but there is not sufficient evidence to support their use.

Aim of the study: Approximately 5.7 million Americans carry the diagnosis of systolic heart failure (HF), a major health care burden. HF is a known manifestation of thiamine deficiency (TD). HF patients are at unique risk for developing TD, which may contribute to further altered cardiac function and symptoms.

Results: We performed a systematic review of the literature and a meta-analysis to evaluate the prevalence of TD in HF patients, risk factors for and mechanisms of development of TD in HF population, and outcomes of thiamine supplementation in HF patients. We found 54 studies that met our selection criteria, 9 of which were suitable for meta-analysis. TD is more common in HF patients than control subjects (odds ratio 2.53, 95% confidence interval 1.65-3.87). Diuretic use, changes in dietary habits, and altered thiamine absorption and metabolism were identified as possible mechanisms of TD in HF patients. Small observational studies and randomized control trials suggest that thiamine supplementation in HF population may improve ejection fraction and reduce symptoms. Thiamine deficiency is more prevalent in the HF population, and its supplementation may be beneficial. The therapeutic role of thiamine in HF warrants further study.

Aim of the study: Despite the targeting of traditional risk factors for cardiovascular disease, disease burden has not been completely eliminated. Thiamine is an essential cofactor in carbohydrate metabolism and individuals with diabetes are thiamine deficient.

Results: The pathophysiology of recognised complications of thiamine deficiency is similar to that underlying atherosclerosis and the metabolic syndrome, namely oxidative stress, inflammation and endothelial dysfunction. This review examines the mechanisms by which thiamine deficiency occurs in individuals with diabetes, how this deficiency leads to hyperglycaemic-induced damage, and the effect of thiamine replacement on vascular disease, endothelial function and oxidative stress. Thiamine administration can prevent the formation of harmful by-products of glucose metabolism, reduce oxidative stress and improve endothelial function. The potential benefit of long-term replacement in those with diabetes is not yet known but may reduce cardiovascular risk and angiopathic complications.

Aim of the study: The rapid improvement in the clinical manifestations of thiamine deficiency with thiamine supplementation is well known. To study this process in more detail, we rendered rats thiamine deficient either by dietary deprivation alone (DD) or, in addition, by daily pyrithiamine administration (DD + PT).

Results: We observed the cerebral metabolic and histological responses of these rats after 1 or 7 days of thiamine supplementation both prior to and at the onset of clinical sequelae. The cerebral metabolic response to thiamine deficiency and replenishment was determined with the [14C]deoxyglucose technique for measurement of local cerebral glucose utilization (LCGU). Our results indicate that thiamine replenishment reverses the LCGU changes resulting from thiamine deprivation of short duration. However, prolonged thiamine deprivation may result in LCGU changes that are not completely reversible by thiamine replenishment, before the appearance of the clinical or histological consequences of thiamine deficiency.

Aim of the study: A 64-year-old man living alone with markedly unbalanced dietary habits presented to the prior hospital with distal sensory disturbances and weakness in all four extremities. After admission, he experienced a rapid progression of lower limb weakness, rendering him unable to walk, for which he was subsequently transferred to our department.

Results: Thiamine supplementation resulted in rapid clinical improvement, confirming a diagnosis of vitamin B1 deficiency neuropathy. Although this condition typically follows a subacute course, it can occasionally present acutely, mimicking Guillain-Barré syndrome (GBS), as seen in this case. Our findings suggest that even glucose-free infusions may exacerbate latent vitamin B1 deficiency by increasing metabolic demand through lactate metabolism and enhancing urinary excretion via diuresis. It is essential to consider vitamin B1 deficiency in the differential diagnosis of patients presenting with an acute progressive clinical course resembling GBS.

Aim of the study: Thiamine deficiency is a life-threatening nutritional abnormality observed in the patients with obesity and following bariatric surgery. The aim of the present study is to determine the prevalence of thiamine deficiency prior to and after bariatric procedures.

Results: The baseline prevalence is 7% for thiamine deficiency in bariatric surgery candidates. The prevalence rate of thiamin deficiency increased to 19% and 9% 3 and 6 months after surgery; however, the rate decreased to 6% 1 year after surgery. Due to the higher prevalence of thiamine deficiency in the early post-operative phase, close monitoring during this period is recommended. A similar strategy should be implemented for pregnant women with history of bariatric surgery in their first trimester.

Aim of the study: This review examines both historical and recent evidence to clarify the current understanding of the relationship between B vitamin deficiencies and neuropathies.

Results: Vitamin B1 (thiamine) deficiency can lead to neurological disorders such as beriberi and Wernicke's encephalopathy, conditions with significant prevalence and mortality rates. Vitamin B12 (Cobalamin) is crucial for DNA synthesis, fatty acid metabolism, and myelin production, with its deficiency leading to neuropathies and cognitive disorders. Excess vitamin B6 (pyridoxine), rather than deficiency, appears to be associated with neuropathy. Vitamin B1 and B12 deficiencies are linked to classic neuropathies, while the connection between vitamin B6 deficiency and neuropathy is less clear, though excess B6 is associated with neurotoxicity. Nutritional deficiencies are less common in developed countries but remain significant in developing nations. In developed countries, factors like alcohol consumption, bariatric surgery, and metformin use are increasing these deficiencies in clinical practice.

Aim of the study: Thiamin is a hydrosoluble vitamin that plays a role in several biological processes, mainly in glucose metabolism. There are several risk factors for developing thiamin deficiency, such as malnutrition, refeeding syndrome, gastrointestinal surgery, and alcoholism.

Results: Thiamin deficiency can be diagnosed clinically, and all clinicians should be aware of this disease, especially in patients with risk factors for thiamin deficiency. Thiamin supplementation should be started as early as possible in patients suspected to have thiamin deficiency. Treatment is safe, inexpensive, simple, and life-saving. Diagnosis is confirmed on a positive response to treatment.

Aim of the study: Wernicke's encephalopathy (WE) is a neurological disorder primarily caused by thiamine deficiency, typically presenting with malnutrition, confusion or delirium, oculomotor abnormalities (such as nystagmus or ophthalmoplegia), and ataxia. Although commonly associated with alcoholism, WE is frequently observed in oncology patients but is often under-recognised, leading to inadequate diagnosis and treatment.

Results: Both patients were diagnosed based on clinical presentation and magnetic resonance imaging, which is crucial for detecting neurological deficits. Immediate treatment with intravenous thiamine led to a positive clinical response. Early recognition and treatment of WE in oncology patients is essential, as the neurological deficits are potentially reversible. Intravenous thiamine supplementation, and supportive care, can prevent long-term complications.

Aim of the study: An eight-year-old boy with recurrent abdominal pain, refusal to eat, gagging, and weight loss for five months experienced a sudden clinical deterioration after a gastrointestinal endoscopy with biopsy. Initially misdiagnosed with pancreatitis, he underwent hospitalization, fasting, and parenteral nutrition (PN) for 15 days.

Results: Transferred to a university hospital, abdominal beriberi was suspected, and intravenous thiamine was promptly administered. Symptoms resolved within 24 h. A review of the PN prescribed revealed the absence of thiamine, confirming the diagnosis. Healthcare professionals often associate thiamine deficiency with alcoholic adults presenting Wernicke encephalopathy; however, abdominal beriberi should also be considered in children with acute abdomen, especially when elevated serum lactate indicates impaired cellular metabolism due to thiamine deficiency.