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Authors' reply

Published online by Cambridge University Press:  02 January 2018

Jae-Min Kim
Affiliation:
Department of Psychiatry and Depression Clinical Research Centre, Chonnam National University Medical School, Kwangju, Korea
Robert Stewart
Affiliation:
King's College London, Institute of Psychiatry, Section of Epidemiology, London, UK
Sung-Wan Kim
Affiliation:
Department of Psychiatry and Depression Clinical Research Centre, Chonnam National University Medical School, Kwangju, Korea. Email: jsyoon@chonnam.ac.kr
Su-Jin Yang
Affiliation:
Department of Psychiatry and Depression Clinical Research Centre, Chonnam National University Medical School, Kwangju, Korea. Email: jsyoon@chonnam.ac.kr
Il-Seon Shin
Affiliation:
Department of Psychiatry and Depression Clinical Research Centre, Chonnam National University Medical School, Kwangju, Korea. Email: jsyoon@chonnam.ac.kr
Jin-Sang Yoon
Affiliation:
Department of Psychiatry and Depression Clinical Research Centre, Chonnam National University Medical School, Kwangju, Korea. Email: jsyoon@chonnam.ac.kr
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Abstract

Type
Columns
Copyright
Copyright © Royal College of Psychiatrists, 2008 

As Assies & Pouwer appropriately point out, there has been growing evidence for an underlying metabolic link between the key components of one-carbon metabolism and PUFAs both in depression and dementia. Reference Das1 However, we do not fully agree with their recommendation for measuring these factors in combination. Our reasons are as follows. One of the main potential mood stabilising effects of PUFAs in depression is thought to be their dampening action against abnormal intracellular signal transduction by (a) inhibiting G-protein-mediated and phospholipase-C-mediated hydrolysis of crucial membrane phospholipids; Reference Sperling, Benincaso, Knoell, Larkin, Austen and Robinson2 (b) modulating the influx of calcium ions; Reference Honen, Saint and Laver3 and (c) reducing the activity of protein kinase C. Reference Seung Kim, Weeber, Sweatt, Stoll and Marangell4 In addition, PUFA actions are closely related to inflammatory and immune pathways, which are also potentially important in the pathogenesis of depression. Reference Maes and Smith5 Compared with these more established findings, the evidence for relationships between one-carbon metabolism and PUFAs in depression is relatively scant. For these reasons, we cannot recommend measuring PUFAs in the context of one-carbon metabolism at the present time, particularly for clinical purposes. However, we do feel that Assises & Pouwer's suggestions should encourage future animal and clinical studies on these interesting research issues.

References

1 Das, UN. Folic acid and polyunsaturated fatty acids improve cognitive function and prevent depression, dementia, and Alzheimer's disease – but how and why? Prostaglandins Leukot Essent Fatty Acids 2008; 78: 11–9.Google Scholar
2 Sperling, RI, Benincaso, AI, Knoell, CT, Larkin, JK, Austen, KF, Robinson, DR. Dietary omega-3 polyunsaturated fatty acids inhibit phosphoinositide formation and chemotaxis in neutrophils. J Clin Invest 1993; 91: 651–60.Google Scholar
3 Honen, BN, Saint, DA, Laver, DR. Suppression of calcium sparks in rat ventricular myocytes and direct inhibition of sheep cardiac RyR channels by EPA, DHA and oleic acid. J Membr Biol 2003; 196: 95103.Google Scholar
4 Seung Kim, HF, Weeber, EJ, Sweatt, JD, Stoll, AL, Marangell, LB. Inhibitory effects of omega-3 fatty acids on protein kinase C activity in vitro . Mol Psychiatry 2001; 6: 246–8.Google Scholar
5 Maes, M, Smith, RS. Fatty acids, cytokines, and major depression. Biol Psychiatry 1998; 43: 313–4.Google Scholar
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