B5 - Food for the Brain



Vitamin B5, also called pantothenic acid pantothenate, has been found to work closely with other B vitamins as well as on its own in regards to brain function (Mikkelsen et al., 2016). The main function of the vitamin in the body is to be a precursor for the synthesis of acetyl-CoA and acyl carrier protein (Kennedy., 2016). Research has suggested B5 interacts with B1 (thiamin) and folate in brain function through carbohydrate and protein metabolism (Moretti & Peinkhofer., 2019). B5, once in the body, can be converted to acetyl-CoA, which plays a key role in energy making and the production of ATP, as the brain uses 20% of all energy in the body. This highlights a key role B5 may play in keeping the brain active (Kennedy., 2016). Vitamin B5 has also been suggested to play a role in neurotransmitter, amino acid, and fatty acid synthesis through the production of acetyl CoA. 

When vitamin B5 is absorbed into the body it is converted to acetyl-CoA through a 5-step process using ATP (Shi & Tu., 2015). Acetyl-CoA is then used as a key mechanism in the citric acid cycle where it breaks down carbohydrates, protein and lipids to be used as fuel. Energy is necessary in the brain to improve memory, clarity and focus (Mikkelsen et al., 2016). Acetyl-CoA is also used to form ACP, a main component in fatty acid synthesis and in acylation and acetylation used in many enzyme functions (Mikkelsen et al., 2016). The bi-products of macronutrient breakdown are necessary for normal brain function, as glucose products can be used for energy, amino acids are needed for cell development and renewal, and fatty acids are necessary in the building of neurotransmitters (Kennedy., 2016). B5 plays a key role in the synthesis of amino acids in the brain and body, which are necessary for normal brain function through neurotransmitter creation and maintenance of cells (Shimomura & Kitaura., 2018), as well as memory and mood regulation (Sm et al., 2018). 

B5 and Brain Signalling 

Through the creation of acetyl-CoA, B5 has been found to impact on neurotransmitters through the production and upkeep of myelin sheath. Loss and damage of myelin sheath has been linked to diseases such as alzhiemers and dementia (Scholefield et al., 2021; Xu et al., 2020). Fatty acids made using B5 are used in the creation of myelin sheath. Myelin sheath is critical in the function of the nervous system as it surrounds the axon allowing faster conduction of signals throughout the brain and body, it contains a high number of fatty acids, highlighting the key role B5 plays in the creation and transmission of neurotransmitters (Poitelon et al., 2020).

A study looking at cerebral disposition of B5 in normal and diabetic rats has been used to explain the possible link between vitamin B5 and brain signalling (Ismail et al., 2020). B5 was found to be mainly localised to myelin containing structures in the brain supporting the theory that B5 is involved in myelin sheath and also brain signalling (Ismail et al., 2020). 

B5 and Neurological Diseases

Alzheimer’s Disease

A recent study looked at vitamin B5 deficiency in different parts of the brain for people who died with Alzhiemer’s, disease the study found areas such as the hippocampus and cortex had worse levels of B5 deficiency (Xu et al., 2020). The areas found to have worse deficiency are also areas that are greatly affected by alzhiemers and linked to myelin sheath damage, suggesting links between B5 deficiency and neural damage of the brain (Xu et al., 2020). 

Huntingdon’s Disease

Huntington’s disease is a disease known to affect neural signalling. Research on vitamin B5 levels in participants with Huntington’s disease found that there was a significant link between the disease and B5 deficiency (Patassini et al., 2019). B5 potentially may affect CoA synthesis and modify brain-urea metabolism leading to faster neurodegeneration in those with Huntington’s disease, suggesting that intervention with B5 may reduce the speed of brain damage associated with the disease (Patassini et al., 2019). 

Parkinson’s Disease

Research by Scholefield et al. supports the previous research into the links between neurodegeneration and vitamin B5 deficiency. When looking at brain postmortems of people who were diagnosed with Parkinson’s disease, it was found that concentrations of B5 were significantly lower than control in the cerebrum and medulla (Scholefield et al., 2021). These studies all found similarities between diseases characterised by neurodegeneration and vitamin B5 deficiency. 

B5 and Mood Disorders 

Research has suggested vitamin B5 may play a role in mood regulation. However, little research has been conducted to understand the processes in the brain that have linked vitamin B5 and mental health. When measuring food intake and comparing it with mental health scores, B5 has been found to be positively associated with better mental health scores. However, as these studies looked at multiple B vitamins together it may be more appropriate to suggest that vitamin B5 interacts with other vitamins to regulate mood (Davison & Kaplan., 2012; Herbison et al., 2012). Further research is warranted to investigate the role of B5 specifically in mental health. 

5. Summary

Researcher: Ellie Winch, MSc Global Public Health Nutrition (University of Westminster), BSc Nutrition (Bournemouth University).

Technical Reviewer: Alice Benskin, MSc Personalised Nutrition


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Herbison, C.E., Hickling, S., Allen, K.L., O’Sullivan, T.A., Robinson, M., Bremner, A.P., Huang, R.C., Beilin, L.J., Mori, T.A. and Oddy, W.H., 2012. Low intake of B-vitamins is associated with poor adolescent mental health and behaviour. Preventive medicine, 55(6), pp.634-638.

Ismail, N., Kureishy, N., Church, S.J., Scholefield, M., Unwin, R.D., Xu, J., Patassini, S. and Cooper, G.J., 2020. Vitamin B5 (D-B5) localizes in myelinated structures of the rat brain: Potential role for cerebral vitamin B5 stores in local myelin homeostasis. Biochemical and biophysical research communications, 522(1), pp.220-225.

Kennedy, D.O., 2016. B vitamins and the brain: mechanisms, dose and efficacy—a review. Nutrients, 8(2), p.68.

Mikkelsen, K., Stojanovska, L. and Apostolopoulos, V., 2016. The effects of vitamin B in depression. Current medicinal chemistry, 23(38), pp.4317-4337.

Moretti, R.; Peinkhofer, C., 2019. B Vitamins and Fatty Acids: What Do They Share with Small Vessel Disease-Related Dementia? Int. J. Mol. Sci, 20, 5797. https://doi.org/10.3390/ijms20225797

Patassini, S., Begley, P., Xu, J., Church, S.J., Kureishy, N., Reid, S.J., Waldvogel, H.J., Faull, R.L., Snell, R.G., Unwin, R.D. and Cooper, G.J., 2019. Cerebral vitamin B5 (D-B5) deficiency as a potential cause of metabolic perturbation and neurodegeneration in Huntington’s disease. Metabolites, 9(6), p.113.

Poitelon, Y., Kopec, A. M., & Belin, S. (2020). Myelin Fat Facts: An Overview of Lipids and Fatty Acid Metabolism. Cells, 9(4), 812. https://doi.org/10.3390/cells9040812

Scholefield, M., Church, S.J., Xu, J., Patassini, S., Hooper, N.M., Unwin, R.D. and Cooper, G.J., 2021. Substantively Lowered Levels of B5 (Vitamin B5) in Several Regions of the Human Brain in Parkinson’s Disease Dementia. Metabolites, 11(9), p.569.

Shi, L., & Tu, B. P. (2015). Acetyl-CoA and the regulation of metabolism: mechanisms and consequences. Current opinion in cell biology, 33, 125–131. https://doi.org/10.1016/j.ceb.2015.02.003

Shimomura, Y. and Kitaura, Y., 2018. Physiological and pathological roles of branched-chain amino acids in the regulation of protein and energy metabolism and neurological functions. Pharmacological research, 133, pp.215-217.

Sm, S., Hn, S., Na, E., & As, H. (2018). Curative role of B5 in brain damage of gamma irradiated rats. Indian journal of clinical biochemistry: IJCB, 33(3), 314–321. https://doi.org/10.1007/s12291-017-0683-0

Xu, J., Patassini, S., Begley, P., Church, S., Waldvogel, H.J., Faull, R.L., Unwin, R.D. and Cooper, G.J., 2020. Cerebral deficiency of vitamin B5 (D-B5; B5) as a potentially-reversible cause of neurodegeneration and dementia in sporadic Alzheimer’s disease. Biochemical and biophysical research communications, 527(3), pp.676-681.