The B Vitamins – An Overview

The B Vitamins – An Overview

Vitamin B1 (Thiamine)

According to Lonsdale, D. (2006), thiamine (Vitamin B1) plays an essential role in the metabolism of glucose, amino acids, and fats, acting as a cofactor for several enzymes (Lonsdale, 2006). Additionally, a study by Zastre, J. A., Hanberry, B. S., & Sweet, R. L. (2014) highlights that enzymes, including those dependent on thiamine diphosphate, are critical for cellular function and growth (Zastre et al., 2014). An overview of intestinal absorption of water-soluble vitamins, including thiamine, is presented in a study by Said, H. M. (2011), which emphasises the importance of a continuous supply of thiamine to maintain optimal levels in the body (Said, 2011).

Research by Kroes, M. C., & Aparicio, C. L. (2002) has drawn attention to the gut's ability to synthesise certain vitamins, although the exact significance of thiamine deficiency is not yet fully understood (Kroes & Aparicio, 2002). Furthermore, Thurnham, D. I., & Northrop-Clewes, C. A. (2012) note that measuring thiamine levels can be challenging, with enzymes such as transketolases and urine tests being more reliable indicators of thiamine deficiency (Thurnham & Northrop-Clewes, 2012).

Thiamine Deficiency

People with severe gastrointestinal issues and alcoholics may develop a condition known as Wernicke-Korsakoff Syndrome (WKS), which can be manifested by thiamine deficiency. Groups at an increased risk of thiamine deficiency:

Vitamin B2 (Riboflavin)

Riboflavin (Vitamin B2) is crucial for the production of important coenzymes like FAD and FMN, which are necessary for cellular energy production and growth (Lonsdale, 2006). Furthermore, a study by Powers, H. J. (2003) highlights the importance of riboflavin in the conversion of other vitamins such as B3 and B6, underscoring its multifaceted significance for bodily functions (Powers, 2003).

Research by O'Callaghan, A. M., & Williams, J. H. (1993) underscores riboflavin's important role in maintaining normal homocysteine levels, emphasising its significance in counteracting the harmful effects of elevated homocysteine levels (O'Callaghan & Williams, 1993). Moreover, a study by Reed, A. M., & Nijhout, H. F. (2012) stresses the importance of regular riboflavin intake due to its limited storage capacity in the body and its sensitivity to UV light (Reed & Nijhout, 2012).

Finally, another study by Yamauchi, M., & Kurosawa, S. (1985) highlights the importance of using appropriate methods to measure riboflavin status, particularly considering the need for alternative tests for individuals with glucose-6-phosphate dehydrogenase deficiency (Yamauchi & Kurosawa, 1985).

Riboflavin Deficiency

Groups at increased risk for riboflavin deficiency:

  • Vegetarians (especially those who exercise intensively)
  • Pregnant or breastfeeding women who do not eat animal products
  • Vegans
  • People with Brown-Vialetto-Van-Laere Syndrome (BVVL), a genetic disorder affecting the nervous system.
  • Alcoholics
  • The elderly

Vitamin B3 (Niacin or Nicotinic Acid)

According to Jacob, R. A. (1990), Vitamin B3 (Niacin) plays a significant role in the body and participates in a variety of chemical reactions, including energy production. Niacin is essential for the formation of the coenzymes NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate), which are central to cellular processes (Jacob, 1990).

Bender, D. A. (1989) explores niacin metabolism and highlights its role as a precursor to antioxidants (Bender, 1989).

Elvehjem, C. A., Madden, R. J., & Strong, F. M. (1938) describe the discovery and identification of the anti-blacktongue factor, which was later found to be niacin (Elvehjem et al., 1938).

Hoffer, A., & Osmond, H. (1954) also discuss the discovery of niacin and its importance in nutrition (Hoffer & Osmond, 1954).

These studies provide a scientific background and deeper understanding of the biochemical significance of Vitamin B3 (Niacin) in the body's various processes.

Niacin Deficiency

If the body receives insufficient niacin, it can convert the amino acid tryptophan into niacin. Approximately 1 mg of niacin can be made from 67 mg of L-tryptophan. The issue arises when too little tryptophan is converted into 5-HTP, and thus also the mood-enhancing hormone serotonin and the sleep hormone melatonin. Therefore, it is highly unhealthy to have a niacin deficiency when suffering from conditions related to serotonin deficiency such as low mood or issues related to melatonin deficiency like sleep problems.

Excessive doses of niacin in the form of nicotinic acid, but not nicotinamide, are associated with expanded capillaries and the so-called "niacin flush," which makes the skin red and sometimes itchy. This is typically a transient symptom. Groups at increased risk for niacin deficiency:

  • People with eating disorders
  • People who are overweight or obese
  • People with gastrointestinal issues that impair absorption
  • People with Crohn’s disease or ulcerative colitis
  • People undergoing dialysis
  • Alcoholics

Vitamin B6 (Pyridoxine)

Vitamin B6, consisting of pyridoxine, pyridoxal, and pyridoxamine, is one of the water-soluble B vitamins and plays a crucial role in several metabolic processes in the body. After Vitamin B6 is absorbed in the jejunum, part of the small intestine, it is converted to the active coenzyme form pyridoxal 5'-phosphate (PLP) in the liver (also in the intestine) and then binds to albumin in the blood serum. It is then transported to various peripheral tissues in the body. Vitamin B6 is also converted into the active coenzyme form pyridoxamine 5’ phosphate (PMP).

Leklem (1990) and McCormick (2006) have explored the significance of Vitamin B6 in protein metabolism and the metabolism of carbohydrates and fats (Leklem, 1990; McCormick, 2006).

According to Shane (1989), Vitamin B6 is essential for cognitive development and maintaining normal homocysteine levels (Shane, 1989). Avram and Vorhees (2002) emphasised Vitamin B6’s role in the immune system and haemoglobin production (Avram & Vorhees, 2002).

These research studies provide a deeper understanding of Vitamin B6’s critical role in the production of neurotransmitters, gluconeogenesis (the process by which glucose is made from compounds the cell cannot use for energy), glycogenolysis (the breakdown of glycogen stored in the liver and muscles to glucose), and immunity, as well as its importance for maintaining normal homocysteine levels and cognitive development. Furthermore, they contribute to the overall picture of Vitamin B6’s comprehensive role in the body’s biochemistry and physiology. Vitamin B6 is also required to form haemoglobin.

Vitamin B6 is measured through blood tests or urine. The most common method is to measure pyridoxal 5'-phosphate in blood plasma.

Pyridoxine Deficiency

Vitamin B6 deficiency is often associated with folic acid (folate) and Vitamin B12 deficiencies. Children with Vitamin B6 deficiency may become irritable, sensitive to sound, and experience seizures, among other symptoms.

Pregnancy, PMS, and Vitamin B6

Research has shown that supplementation with Vitamin B6 may potentially reduce symptoms related to premenstrual syndrome (PMS). A randomised placebo-controlled double-blind study by Brush, M. G., and Perry, J. B. (1976) on 630 patients showed that Vitamin B6 intake led to a significant reduction in PMS symptoms such as mood swings, irritability, forgetfulness, and bloating.

During the early months of pregnancy, a significant percentage of pregnant women, between 50 and 80 percent, experience nausea. Two randomised placebo-controlled studies led by Vutyavanich, T., Wongtra-ngan, S., and Ruangsri, R. (1995) showed that supplementation with 30–75 mg of pyridoxine per day led to a significant reduction in nausea. However, more studies are needed in this area to draw definitive conclusions. According to Chelmow, D., Ruehli, M. S., Huang, E., and Berlin, M. (2015), the American Congress of Obstetrics and Gynecology (ACOG) recommends supplementation of 10–25 mg of Vitamin B6 three times per day to treat nausea during pregnancy.

Folate (Folic Acid)

Folate, one of the water-soluble B vitamins, acts as an essential coenzyme for the formation of nucleic acids DNA and RNA and for the metabolism of amino acids (Scott, 2003). According to Smith and Refsum (2016), folate is also linked to cognitive function and may affect the risk of cognitive decline. Furthermore, Durga, Verhoef, and Anteunis (2007) demonstrated the effects of folic acid supplementation on hearing in older adults.

When folate is consumed, it is converted into the active form 5-methyl-tetrahydrofolate (5-methyl-THF) before entering the bloodstream (Bailey & Gregory, 1999). Its significance in controlling circulating homocysteine levels, an amino acid that can have harmful effects on nerve cells at high levels, has been highlighted by Baggott, Oster, and Tamura (1992). They also point out the importance of measuring folate status by analysing levels in erythrocytes rather than serum.

Since rising homocysteine levels can be caused by several factors, including folate and other B-vitamin deficiencies, a comprehensive assessment of nutritional status is needed to understand the role of folate in the body (Smith & Refsum, 2016).

Folic Acid or Folate Deficiency

Groups at increased risk for folate deficiency:

  • Poor diet
  • Alcoholism
  • Problems with nutrient absorption (gluten intolerance, Crohn’s, Ulcerative Colitis, IBS)
  • Pregnancy (increases folate requirements due to its role in nucleic acid synthesis)
  • People who have undergone stomach surgery

MTHFR and Folate

The MTHFR gene provides instructions for forming an enzyme called MTHFR (methyl-tetrahydrofolate reductase). The MTHFR enzyme, along with folate, is crucial for converting the amino acid homocysteine into methionine, which is necessary for protein formation, antioxidant use, helping the liver manage fat, combating depression and inflammation, detoxifying the body from toxins and heavy metals. Additionally, Vitamin B12 is needed for this process to function optimally (van der Linden et al., 2006).

Unfortunately, up to 30–40% of the population has a defect in the MTHFR gene, which means their ability to convert homocysteine into methionine is impaired. Mutations are more common in families with neural tube defects, suggesting that these individuals may require additional folate (Klerk et al., 2002).

This information indicates that it is important to consider the MTHFR gene and its impact on folate metabolism to understand its potential link to various health outcomes and the need for specific nutrients for people with this genetic defect (Yan et al., 2013). For people with a defect in the MTHFR gene, methylfolate is often recommended instead of folic acid.

Vitamin B12 (Cobalamin)

Vitamin B12 is one of the water-soluble B vitamins. According to Herbert (1988), Vitamin B12 exists in several forms, with methylcobalamin and 5-deoxyadenosylcobalamin being the active forms in the body’s metabolism. All forms contain the mineral cobalt, which is why all forms of Vitamin B12 are called cobalamins.

According to Carmel (2008), Vitamin B12 is required for the formation of red blood cells, nervous system function, DNA synthesis, and the conversion of homocysteine into methionine. Absorption of Vitamin B12 requires a substance known as intrinsic factor, which is produced in the stomach and depends on adequate levels of stomach acid.

According to Sharabi, Cohen, and Sulkes (2003), Vitamin B12 is absorbed at the end of the small intestine, and research has shown that supplementation with 500 micrograms of Vitamin B12 leads to the absorption of about 10 micrograms in healthy individuals.

According to Andrès and Loukili (2004), Vitamin B12 status is usually measured in blood plasma or serum, but according to Stabler (2013), blood levels may not reliably reflect intracellular concentrations.

Vitamin B12 Deficiency

Groups at increased risk for Vitamin B12 deficiency:

  • The elderly, some may need significantly higher doses than normal due to reduced stomach acid
  • People with low stomach acid levels
  • People taking medication to lower stomach acid, such as proton pump inhibitors like Omeprazole and Losec
  • Vegetarians and especially strict vegans
  • People with pernicious anaemia
  • People with gluten intolerance, Crohn's, ulcerative colitis
  • People who have had surgery affecting the stomach or small intestine
  • Breastfed children of women who follow a strict vegetarian or vegan diet. These children may develop a Vitamin B12 deficiency within a few months, and if untreated, it can lead to severe and potentially permanent nerve damage.

Biotin

Biotin, also known as Vitamin B7 or Vitamin H, is an important member of the water-soluble B vitamin group. According to Said et al. (1998), biotin functions as a cofactor for several key enzymes necessary for proper metabolism in the body. Its role also extends to gene regulation, which is highlighted in studies by Zempleni et al. (2008), pointing to its participation in epigenetic mechanisms and cellular signalling.

According to Mock (2012), biotin is also particularly important for fetal growth and development during pregnancy. Adequate levels of biotin in the mother’s body are essential to support optimal embryonic development and to minimise the risk of developmental anomalies. Furthermore, Trüeb (2016) notes that biotin deficiency can lead to negative consequences for hair, skin, and nails, highlighting its importance for maintaining healthy skin and hair function.

Research by Patil et al. (2017) highlights that biotin also has the potential to affect glucose metabolism and insulin resistance, suggesting its role in managing glucose levels.

Biotin Deficiency

Avidin, a protein found in substantial amounts in raw egg whites, binds to biotin in the small intestine and prevents its absorption. People who consume raw egg whites over time risk biotin deficiency and may need biotin supplementation. Groups at increased risk for biotin deficiency:

  • Long-term consumption of raw egg whites
  • Smokers
  • Pregnant women (Rapidly dividing cells in the fetus require biotin, increasing the demand for biotin during pregnancy. Research shows many pregnant women develop marginal or subclinical biotin deficiency during pregnancy.)
  • Certain liver disorders
  • People taking anticonvulsant medications

Vitamin B5 (Pantothenic Acid)

Pantothenic acid, also known as Vitamin B5, is an important part of the B vitamin family and serves as a crucial precursor for the synthesis of coenzyme A, which is necessary for various biochemical reactions in the body. Coenzyme A plays a vital role in transporting fatty acids to the mitochondria, as well as in the production of important hormones and lipids (Gropper & Smith, 2013).

Its derivative, pantethine, has been shown to have cholesterol-lowering properties and is used in certain contexts to help regulate cholesterol levels in the body (Evans & Emanuel, 2002).

These studies offer insight into the significant role that pantothenic acid plays in the body’s biochemical processes and its potential health benefits, highlighting its relevance in therapeutic contexts and for overall health (Wagner & Blau, 1991).

Pantothenic Acid Deficiency

Some groups of people are at greater risk of developing pantothenic acid deficiency. These groups may include individuals with severe malnutrition, chronic alcoholics, people with digestive issues that reduce nutrient absorption, and people with certain hereditary diseases that affect the metabolism of pantothenic acid.

Pantothenic Acid Deficiency

Some groups of people are at greater risk of developing pantothenic acid deficiency. These groups may include individuals with severe malnutrition, chronic alcoholics, people with digestive issues that reduce nutrient absorption, and people with certain hereditary diseases that affect the metabolism of pantothenic acid.

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Scientific references and sources

Show reference

Referenser Tiamin B1 (Tiamin)

Lonsdale, D. (2006). Evidence-based complementary and alternative medicine, 3(1), 49-59.

Zastre, J. A., Hanberry, B. S., & Sweet, R. L. (2014). Essays in biochemistry, 59, 1-41.

Said, H. M. (2011). Biochemical Journal, 437(3), 357-372.

Kroes, M. C., & Aparicio, C. L. (2002). Journal of Nutritional & Environmental Medicine, 12(2), 107-118.

Thurnham, D. I., & Northrop-Clewes, C. A. (2012). Nestlé Nutrition Institute Workshop Series, 70, 1-12.

Referenser Vitamin B2 (Riboflavin) 

Lonsdale, D. (2006). Evidence-based complementary and alternative medicine, 3(1), 49-59.

Powers, H. J. (2003).  The American Journal of Clinical Nutrition, 77(6), 1352-1360.

O'Callaghan, A. M., & Williams, J. H. (1993). British Journal of Nutrition, 69(3), 541-550.

Reed, A. M., & Nijhout, H. F. (2012). Disease Models & Mechanisms, 5(1), 1-8.

Yamauchi, M., & Kurosawa, S. (1985). Journal of Chromatography B: Biomedical Sciences and Applications, 342, 111-118.

Referenser Niacin

Jacob, R. A. (1990). Niacin. In Vitamins (pp. 87-122). Academic Press.

Bender, D. A. (1989). Niacin metabolism. Nutrition and Biochemistry of Niacin, 19-34.

Elvehjem, C. A., Madden, R. J., & Strong, F. M. (1938). The isolation and identification of the anti-blacktongue factor. Journal of the American Chemical Society, 60(12), 2734-2735.

Hoffer, A., & Osmond, H. (1954). The discovery of niacin. The Canadian Journal of Chemical Engineering, 32(12), 178-179.

Referenser Vitamin B6 (Pyridoxin)

Leklem, J. E. (1990). The Journal of nutrition, 120(11), 1503-1507.

McCormick, D. B. (2006). Physiological Reviews, 86(4), 897-922.

Shane, B. (1989). Nutrition Reviews, 47(6), 196-204.

Avram, D., & Vorhees, C. V. (2002). National Toxi. Program technical report series, 500, 7-20.

Brush, M. G., & Perry, J. B. (1976). The British journal of clinical practice, 30(6), 193-196.

Vutyavanich, T., Wongtra-ngan, S., & Ruangsri, R. (1995). American Journal of Obstet. & Gynec., 173(3), 881-884.

Chelmow, D., Ruehli, M. S., Huang, E., & Berlin, M. (2015).Obstet. & Gynec., 126(3), e12-e24.

Referenser Folat (folsyra)

Smith, A. D., & Refsum, H. (2016). Annu Rev Nutr, 36, 211-39.

Durga, J., Verhoef, P., & Anteunis, L. J. (2007). Ann Intern Med, 146(1), 1-9.

Scott, J. M. (2003). Proceedings of the Nutrition Society, 62(3), 441-444.

Bailey, L. B., & Gregory, J. F. (1999). The Journal of Nutrition, 129(4), 779-782.

Baggott, J. E., Oster, R. A., & Tamura, T. (1992). C. Epidemiology and Prevention Biomarkers, 1(6), 439-446.

van der Linden, I. J., Afman, L. A., Heil, S. G., Blom, H. J., & den Heijer, M. (2006). European journal of medical genetics, 49(4), 288-295.

Klerk, M., Verhoef, P., Clarke, R., Blom, H. J., Kok, F. J., & Schouten, E. G. (2002). JAMA, 288(16), 2023-2031.

Yan, L., Zhao, L., Long, Y., Zou, P., Ji, G., Gu, A., ... & Wang, X. (2013). Genetics and molecular research: GMR, 12(4), 5376-5386.

Referenser Vitamin B12

Herbert, V. (1988). The American journal of clinical nutrition, 48(3), 852-858.

Carmel, R. (2008). The American journal of clinical nutrition, 88(3), 757-758.

Andrès, E., & Loukili, N. H. (2004). CMAJ: Canadian Medical Association Journal, 171(3), 251-259.

Stabler, S. P. (2013). New England Journal of Medicine, 368(2), 149-160.

Sharabi, A., Cohen, E., & Sulkes, J. (2003). British journal of clinical pharmacology, 56(6), 635-638.

Referenser Biotin

Said, H. M. (1998). The American Journal of Clinical Nutrition, 68(2), 225-228.

Zempleni, J., Wijeratne, S. S. K., Hassan, Y. I., & Biotin, M. (2008). Journal of Nutritional Biochemistry, 19(4), 279-285.

Mock, D. M. (2012). The Journal of Nutrition, 142(1), 7-10.

Trüeb, R. M. (2016). International Journal of Trich. 8(2), 73.

Patil, V. S., Mali, R. S., Biyani, K. R., & Patil, A. G. (2017). International Journal of D. in Developing Countries, 37(4), 433-436.

Kapoor, A., Mehta, K. P., & Kapoor, A. (2009). The Egyptian Journal of Neur., Psy. and Neuros., 46(3), 717-721.

Referenser Vitamin B5 (Pantotensyra)

Gropper, S. S., & Smith, J. L. (2013). Advanced nutrition and human metabolism. Cengage Learning.

Evans, A. A., & Emanuel, R. (2002). Nutrition Research, 22(8), 843-857.