Hiding in Plain Sight: Modern Thiamine Deficiency
Abstract
:1. Introduction
2. Thiamine Deficiency Definitions and Testing
2.1. Symptoms
2.2. Testing
3. The RDA, Food Fortification and Thiamine Sufficiency
4. Thiamine Deficiency in the General Population
4.1. Obesity
4.2. Diabetes
4.3. Pregnancy
4.4. Psychiatry
4.5. Elderly
4.6. Neurocognitive and Neuromotor Diseases
4.7. In Hospitalized Patients
5. What Makes Thiamine So Important
5.1. Thiamine Dependent Enzymes
5.1.1. Transketolase
5.1.2. Pyruvate Dehydrogenase Complex
5.1.3. 2-Hydroxyacyl-CoA Lyase
5.1.4. Branched Chain Keto-Acid Dehydrogenase
5.1.5. Alpha-Ketoglutarate Dehydrogenase Complex
5.1.6. Thiamine-Influenced Enzymes
6. Thiamine Consumption, Uptake, Activation, and Excretion
6.1. Consumption
6.2. Uptake
- SLC19A1: folate transporter, but also, transports thiamine mono- and di- phospho derivatives [95].
- SLC22A1 (OCT1): organic cation transporter 1, primary hepatic thiamine transporter [97].
- SLC25A19 (MTPP-1): mitochondrial thiamine pyrophosphate carrier [98].
- SLC44A4 (hTPPT/TPPT-1): absorption of microbiota-generated thiamine pyrophosphate in the large intestine [101].
6.3. Activation
6.4. Storage and Elimination
7. Factors Affecting Thiamine Availability and Demand
7.1. High Carbohydrate Diets
7.2. Food Chemicals
7.3. Alcohol, Tobacco, Coffee and Tea Consumption
7.4. Medications and Environmental Exposures
8. Conclusions
Author Contributions
Funding
Data Availability Statement
Conflicts of Interest
Abbreviations
References
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In Vivo | |
---|---|
Study | Outcome |
Effect of thiamine repletion on cardiac fibrosis and protein O-glycosylation in diabetic cardiomyopathy [138]. | In STZ induced diabetic rats, thiamine reduced or reversed hyperglycemia related activation of secondary glucose pathways (polyol/sorbitol, hexosamine, diacylglycerol/PKC, AGE) via upregulation of the PDC enzyme; improved cardiac contractility, reduced cardiac fibrosis and expression of mRNA associated proteins (thrombospondin, fibroconnection, plasminogen activator inhibitor 1, and connective tissue growth factor); and prevented obesity in the overfed arm of the experiment. |
Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine [139]. | High-dose thiamine and benfotiamine therapy increased TKT and PDC activity in STZ induced diabetic rats, increasing ribose-5-phostphate and reduced microalbuminuria and proteinuria by 70–80%. PKC, AGE and oxidative stress were reduced significantly. |
Vitamin B1 analog benfotiamine prevents diabetes-induced diastolic dysfunction and heart failure through Akt/Pim-1–mediated survival pathway [140]. | Benfotiamine prevented hyperglycemia induced diastolic dysfunction and heart failure by several mechanisms in STZ induced diabetic rats |
Powerful beneficial effects of benfotiamine on cognitive impairment and beta-amyloid deposition in amyloid precursor protein/presenilin-1 transgenic mice [141]. | Benfotiamine improved spatial memory, amyloid precursor protein/presenilin-1, reduced amyloid plaques and tau levels dose dependently after 8 weeks of treatment in mouse model. |
In Vivo | |
Effect of thiamine administration on metabolic profile, cytokines and inflammatory markers in drug-naïve patients with type 2 diabetes [142]. | A total of 150 mg thiamine daily significantly reduced blood glucose within a month, in randomized, placebo control trial of 24 drug naïve T2D diabetics |
Effect of high dose thiamine therapy on risk factors in type 2 diabetics [68]. | A 3 month, randomized, placebo controlled trial of 50 T2D patients, given 100 mg 3x thiamine per day. Thiamine significantly improved micro albuminuria, glycated hemoglobin, while decreasing PKC levels. |
The effect of benfotiamine in the therapy of diabetic polyneuropathy [143]. | After 45 days of benfotiamine and vitamin B6 supplementation, 19/22 patients saw statically significant reductions in pain, symptom scores, neurophysiological and biological markers of diabetic neuropathy |
Metabolic benefits of six-month thiamine supplementation in patients with and without diabetes mellitus type 2 [144]. | Six month randomized trial, 60 T2D with medication controlled blood sugar and 26 age- and BMI-matched controls. A total of 100 mg thiamine daily, significantly corrected lipid profiles and creatinine levels. |
Thiamine deficiency and cardiovascular disorders [145]. | One time administration of 100 mg IV thiamine, improved endothelium-dependent vasodilatation in 10 patients with TD2 during an acute glucose tolerance test. |
Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study [146]. | A total of 200 mg/day of thiamine for 1 week in 6 patients with HF receiving diuretics improved left ventricular ejection fraction (LVEF) in four of the patients from 24% to 37%. |
Thiamine supplementation in symptomatic chronic heart failure: a randomized, double-blind, placebo-controlled, cross-over pilot study [147]. | A total of 300 mg/day oral thiamine improved LVEF significantly in HF patients on diuretics. |
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Marrs, C.; Lonsdale, D. Hiding in Plain Sight: Modern Thiamine Deficiency. Cells 2021, 10, 2595. https://doi.org/10.3390/cells10102595
Marrs C, Lonsdale D. Hiding in Plain Sight: Modern Thiamine Deficiency. Cells. 2021; 10(10):2595. https://doi.org/10.3390/cells10102595
Chicago/Turabian StyleMarrs, Chandler, and Derrick Lonsdale. 2021. "Hiding in Plain Sight: Modern Thiamine Deficiency" Cells 10, no. 10: 2595. https://doi.org/10.3390/cells10102595
APA StyleMarrs, C., & Lonsdale, D. (2021). Hiding in Plain Sight: Modern Thiamine Deficiency. Cells, 10(10), 2595. https://doi.org/10.3390/cells10102595