What is vitamin B1 (thiamine)?

Thiamine, which is also known as vitamin B1, is an essential micronutrient, which is required for metabolism, enzymatic processes and conduction of nerve signals. All living organisms use thiamine, but it can be made only in bacteria, fungi and plants. In humans, gastrointestinal microbiota also produces thiamine, but not enough for the organism functioning. Thus, we, as well as other animals must obtain vitamin B1 from the diet.

Thiamine deficiency

Deficiency of thiamine can affect the cardiovascular, nervous and immune systems. A severe and chronic form is known as beriberi. Wet beriberi affects cardiovascular system resulting in tachycardia, high arterial and venous pressures, leg swelling. Dry beriberi affects nervous system resulting in impairment of sensory, motor and reflex functions and altered mental status. Worldwide thiamine deficiency is most widely reported in populations where primary food source are polished rice and grains. In Western countries, it most commonly affects people suffering from alcoholism or chronic illness. Thiamine deficiency in patients with alcohol use disorder often lead to Kosakoff syndrome, a chronic disease with severe memory loss and learning problems.

Food sources of thiamine

It is very easy to add foods rich with thiamine to the diet. Food sources of thiamine include beef, pork, eggs, liver, nuts, oats, oranges, seeds, legumes and yeast. Such foods as rice, pasta, breads, cereals and flour are often fortified with vitamin B1 as the processing involved in creating these products removes thiamine. Thiamine supplements and medications are available on market to treat or prevent thiamine deficiency. Remarkably, B1 is well tolerated and has almost no side effects.

Bioavailable analogues of Thiamine

Analogues of vitamin B1, such as benfotiamine or dibenzoyl thiamine, have improved bioavailability, due to their higher lipid solubility, which facilitate permeation in cell membranes. As a result, they provide higher levels of thiamine in muscle, brain and liver. This can be the reason of their higher effectiveness.

Thiamine as medication

Thiamine was the first of the water-soluble vitamins to be discovered, and since early 20th century it was extensively studied. Most commonly thiamine supplementation is used to treat syndromes associated with severe thiamine deficiency and during pregnancy and lactating due to increased need for this vitamin. Rapid recovery can occur within hours if thiamine is given intravenously. If concentrated thiamine supplements are not available, diets rich with thiamine will also lead to recovery, though at a slower rate.

New properties of thiamine

Recently, other important roles of thiamine including the regulation of oxidative stress were discovered [1]. As emotional stress is associated with oxidative stress in the brain, it was hypothesized that thiamine can counteract negative effects of the stress. And indeed, in studies on mice thiamine precluded negative changes in mood and emotionality, as well as neuroinflammation and oxidative stress caused by stress [2,3]. It also ameliorated cellular proliferation and neurogenesis in the hippocampus under stress conditions. In agreement with animal studies, vitamin B1 was also able to ameliorate symptoms of major depressive disorder in patients [4] or work stress-related mood swings [5].

Thus, thiamine was shown as a promising treatment for the depressive-like changes and excessive aggression, caused by stress. Hopefully, new studies on thiamine will be conducted in the nearest future to show novel properties of this vitamin.

 

References

[1]      L. Bettendorff, P. Wins, Biological functions of thiamine derivatives: Focus on non-coenzyme roles, OA Biochem. 1 (2013).

[2]      N. Markova, N. Bazhenova, D.C. Anthony, J. Vignisse, A. Svistunov, K.-P. Lesch, L. Bettendorff, T. Strekalova, Thiamine and benfotiamine improve cognition and ameliorate GSK-3β-associated stress-induced behaviours in mice, Prog. Neuro-Psychopharmacology Biol. Psychiatry. 75 (2017) 148–156.

[3]      A. Gorlova, D. Pavlov, D.C. Anthony, E.D. Ponomarev, M. Sambon, A. Proshin, I. Shafarevich, D. Babaevskaya, K.-P. Lesсh, L. Bettendorff, T. Strekalova, Thiamine and benfotiamine counteract ultrasound-induced aggression, normalize AMPA receptor expression and plasticity markers, and reduce oxidative stress in mice, Neuropharmacology. (2019).

[4]      A. Ghaleiha, H. Davari, L. Jahangard, M. Haghighi, M. Ahmadpanah, M.A. Seifrabie, H. Bajoghli, E. Holsboer-Trachsler, S. Brand, Adjuvant thiamine improved standard treatment in patients with major depressive disorder: results from a randomized, double-blind, and placebo-controlled clinical trial, Eur. Arch. Psychiatry Clin. Neurosci. 266 (2016) 695–702.

[5]      C. Stough, A. Scholey, J. Lloyd, J. Spong, S. Myers, L.A. Downey, The effect of 90 day administration of a high dose vitamin B-complex on work stress, Hum. Psychopharmacol. Clin. Exp. 26 (2011) 470–476.

 

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Recently I had a great chance to participate in the 19th WPA World Congress of Psychiatry which took place in Lisbon 21-24 of August 2019. Such an international scientific event summarizes recent findings and sets a trend for future research.

The effect of lifestyle on mental health was one of the topics discussed at the conference. Focusing on nutritional impact in psychiatry I will review here some of the studies – research done in animal models or patients and literature reviews – which were presented at the Congress.

All the poster presentations can be viewed on the conference website https://2019.wcp-congress.com/.

Dietary patterns and mental health

  1. Sanchez-Villegas and colleagues from Spain1 presented research on the Mediterranean diet’s effects in patients recovered from depressive disorders. They found that adherence to Mediterranean diet supplemented with extra-virgin olive oil led to the improvement of depressive symptoms. This new study supports previous reports about positive effects of traditional dietary patterns compared to so-called “Western diet”, and this topic was nicely reviewed in the poster presentation of M. Jesus and colleagues (Portugal)2.

I presented a poster3 on a study done in a mouse model of Western diet feeding. We found that genetic deficiency of serotonin transporter exacerbates metabolic alterations and such behavioural consequences of the Western diet as depressive-like behaviour and cognitive impairment. In human, carriers of a genetic variant that reduces serotonin transporter expression are known to be more susceptible to emotionality-related disorders and prone to obesity and diabetes.

Vitamin D and Mental Health

Nutritional psychiatry was traditionally focused on the effects of vitamins and micronutrients on mental health. Several presentations at this conference were dedicated to the role of vitamin D in mental disorders.

Scientists from Egypt (T. Okasha and colleagues)4 showed their results on the correlation between serum level of vitamin D and two psychiatric disorders: schizophrenia and depression. They found lower serum vitamin D levels in the patients with schizophrenia or depression compared to healthy volunteers. These findings indicate a role of vitamin D in the development of psychiatric disorders.

However, the team from Denmark (J. Hansen and colleagues)5 did not find any effect of 3 months vitamin D supplementation on depression symptoms in patients with major depression. The contrariety of the studies on vitamin D benefits in mental health was presented on the review poster by R. Avelar and colleagues (Portugal)6.

Microbiome and Mental Health

There is increasing evidence that microbiota-gut-brain axis influences behaviour and mental health. N. Watanabe and colleagues (Japan)7 presented the results of a study on germfree and commensal microbiota-associated mice. They found increased aggression and impaired brain serotonin metabolism in germfree mice.

  1. Dias and colleagues (Portugal)8 performed a literature review on this topic exploring possible effects of microbiome and probiotics in mental disorder development. The most robust evidence was found for the association of microbiome alterations and depression/anxiety. Up to date literature is lacking replicated findings on proving positive effects of probiotics in mental disorders treatment.

Diabetes Type 2 and Mental Disorders

Risk factors for type 2 diabetes include diet and lifestyle habits. It is getting more obvious that there is an association between type 2 diabetes and the development of mental disorders.

  1. Mhalla and colleagues (Tunisia)9 reported a study done on patients with type 2 diabetes. They found a high prevalence of depression in women with type 2 diabetes. Also, depression in these patients was associated with poorer glycemic control.

Depression is an important factor influencing insomnia. H.C. Kim (Republic of Korea)10 found insomnia in one-third of patients with diabetes type 2.

The group from Romania (A. Ciobanu and colleagues)11 created a meta-analysis of the medical literature showing an association of diabetes type 2 with Alzheimer’s disease. They highlighted the role of insulin signaling in cognition and proposed glucose blood level control as a therapeutic approach in Alzheimer’s disease.

 

Thus, a lot of studies were recently done on the role of nutrition in psychiatric disorders development and therapy. However, there is still room for future discoveries!

REFERENCES:
From 19th WPA World Congress of Psychiatry proceedings:

  1. Sanchez-Villegas, B. Cabrera-Suárez, M. Santos Burguete, P. Molero, A. González-Pinto, C. Chiclana, J. Hernández-Fleta. INTERVENTION WITH MEDITERRANEAN DIET IN THE IMPROVEMENT OF DEPRESSIVE SYMPTOMS IN PATIENTS RECOVERED FROM DEPRESSIVE DISORDER. PREDI-DEP TRIAL PRELIMINARY RESULTS;
  2. Jesus, C. Cagigal, T. Silva, V. Martins, C. Silva. DIETARY PATTERNS AND THEIR INFLUENCE IN DEPRESSION;
  3. Veniaminova, A. Gorlova, J. Hebert, D. Radford-Smith, R. Cespuglio, A. Schmitt-Boehrer, K. Lesch, D. Anthony, T. Strekalova. THE ROLE OF GENETIC SEROTONIN TRANSPORTER DEFICIENCY IN CONSEQUENCES OF EXPOSURE TO THE WESTERN DIET: A STUDY IN MICE;
  4. Okasha, W. Sabry, M. Hashim, A. Abdelrahman. VITAMIN D SERUM LEVEL AND ITS CORRELATION WITH MAJOR DEPRESSIVE DISORDER AND SCHIZOPHRENIA;
  5. Hansen, M. Pareek, A. Hvolby, A. Schmedes, T. Toft, E. Dahl, C. Nielsen7, P. Schulz8. VITAMIN D3 SUPPLEMENTATION AND TREATMENT OUTCOMES IN PATIENTS WITH DEPRESSION;
  6. Avelar, D. Guedes, J. Velosa, F. Passos, A. Delgado, A. Corbal Luengo, M. Heitor. VITAMIN D AND MENTAL HEALTH: A BRIEF REVIEW;
  7. Watanabe, K. Mikami, K. Keitaro, F. Akama, Y. Aiba, K. Yamamoto, H. Matsumoto. INFLUENCE OF COMMENSAL MICROBIOTA ON AGGRESSIVE BEHAVIORS;
  8. Dias, I. Figueiredo, F. Ferreira, F. Viegas, C. Cativo, J. Pedro, T. Ferreira, N. Santos, T. Maia. EMOTIONAL GUT: THE RELATION BETWEEN GUT MICROBIOME AND MENTAL HEALTH;
  9. Mhalla, M. Jabeur, H. Mhalla, C. Amrouche, H. Ounaissa, F. Zaafrane3, L. Gaha. DEPRESSION IN ADULTS WITH TYPE 2 DIABETES: PREVALENCE AND ASSOCIATED FACTORS;
  10. Kim. FACTORS RELATED TO INSOMNIA IN TYPE 2 DIABETICS;
  11. A. Ciobanu, L. Catrinescu2, C. Neagu3, I. Dumitru3. THE CONNECTION BETWEEN ALZHEIMER’S DISEASE AND DIABETES

 

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Rates of obesity and metabolic diseases are rapidly growing, and much attention is paid to study the effects of consumed foods on human health. We know already that dietary preferences can be a serious factor of diseases and even a cause of them, in a man. However, we do not know molecular and cellular mechanisms behind these effects. Thus, we do not know how these negative processes can be neutralized or diminished by preventive or curative interventions. As such mechanistic studies are needed.

These studies can be in principle carried out in vitro or in vivo. Food consumption and consumed nutrients affects both the brain and a periphery. Another words, these processes are systemic and involve a lot of interplay mechanisms. Consequently, in vitro approach has very limited potential to achieve research goal with studies on diets. For example, the use of a tissue from peripheral organs or brain, cell cultures or even mini-organs would not help to understand systemic mechanism.

With in vivo approach, human studies cannot help to understand the mechanisms and they exclude any interventions. The remaining solution then is the use of animal models – of course, in compliance with the three R’s principle1 (reduction, refinement, replacement). “Replacement” defines the choice of the object: to use the lowest phylogenetic ordered animal possible, when it’s impossible to use in vitro methodology or a non-animal model, to address a given scientific question.

The most commonly used animal in nutritional research is a mouse. Are mice perfect organisms to model dietary-induced disorders?

Like us, humans, mice are omnivore mammals, and almost all the genes in mice share functions with the genes in humans. In comparison to other mammals, mice have small size of the body (3000 times smaller than a human), and genetically identical mice (like human monozygotic twins) are available for experimental use. Basal metabolic rate per gram of body weight is 7 times greater in mice than in humans which speeds up the development of diet-induced disease. Because of the rapid generation and short life cycle (about 2 years) mice are used to study the effects of maternal diet in the offspring and model diet role in aging processes. Mice display complex behaviours, including social interactions, cognitive functions and emotionality, that are similar to human features.

The use of mice in nutritional research offers a unique tool: possibility to study the role of a given gene using genetic modification. Generation of mutant mice is well established in comparison with other mammalian species. Many genetically modified mouse models were developed over the years, including knockout mice in which genetic material is deleted, mice carrying additional genetic material or “humanized” models expressing human genes.

Numerous mouse models were generated to use in nutrition research. Probably the most popular model in diet research is diet-induced obesity model (DIO model)2 in which animal is fed high-fat or high-density diets – to mimic the most common cause of obesity in humans. Changes seen in DIO mice are remarkably consistent with those seen in obese patients. DIO mice are used to investigate mechanisms of obesity development and novel medication screening.

Another prominent example of a model in nutrition research is the ob/ob mouse3. Due to a mutation in hormone leptin these mice display severe obesity, insulin resistance and dyslipidemia. Studies performed on this model revealed new aspects of hypothalamus role in human energy metabolism.

Mouse model plays its role in development of anti-obesity and anti-diabetic medication. Information about the receptors and hormones that regulate food intake and energy balance can be used to choose a target for a new drug. For example, mice lacking serotonin 5-HT2C receptor were found to exhibit mild obesity and type 2 diabetes4, suggesting the role of this receptor in regulation of food intake. Recently appetite reducing drug (lorcaserin), 5-HT2C receptor agonist, was developed.

However, there are certain limitations in translating discoveries from mouse models to humans in nutrition research. There are clear differences in feeding patterns, nutrient metabolism and hormone control between humans and mice. In case those aspects are key features of the study, another available model could be used.

No model is perfectly mimicking all aspects of human disease. It is likely that better new models will be developed in the nearest future to study the human conditions not adequately replicated in mouse models. But for now, mouse model is a useful tool in studying dietary-induced diseases and it plays an important role in translational research and advancement of human health.

REFERENCES

  1. Tannenbaum, J. & Bennett, B. T. Russell and Burch’s 3Rs then and now: the need for clarity in definition and purpose. J. Am. Assoc. Lab. Anim. Sci. 54, 120–32 (2015).
  2. Hariri, N. & Thibault, L. High-fat diet-induced obesity in animal models. Nutr. Res. Rev. 23, 270–299 (2010).
  3. Ingalls, A. M., Dickie, M. M. & Snell, G. D. Obese, a new mutation in the house mouse. J. Hered. 41, 317–318 (1950).
  4. Tecott, L. H. et al. Eating disorder and epilepsy in mice lacking 5-HT2C serotonin receptors. Nature 374, 542–546 (1995).
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