Skip to main content

Main menu

  • Home
  • Issues
    • Issue in progress
    • Issues by date
  • Sections
    • Editorial
    • Review
    • Research
    • Commentary
    • Psychopharmacology for the Clinician
    • Letters to the Editor
  • Topic Collections
  • Instructions for Authors
    • Overview for authors
    • Submission checklist
    • Editorial policies
    • Publication fees
    • Submit a manuscript
    • Dr. Francis Wayne Quan Memorial Prize
    • Open access
  • Alerts
    • Email alerts
    • RSS
  • About
    • General information
    • Staff
    • Editorial Board
    • Contact
  • CMAJ JOURNALS
    • CMAJ
    • CMAJ Open
    • CJS
    • JAMC

User menu

Search

  • Advanced search
JPN
  • CMAJ JOURNALS
    • CMAJ
    • CMAJ Open
    • CJS
    • JAMC
JPN

Advanced Search

  • Home
  • Issues
    • Issue in progress
    • Issues by date
  • Sections
    • Editorial
    • Review
    • Research
    • Commentary
    • Psychopharmacology for the Clinician
    • Letters to the Editor
  • Topic Collections
  • Instructions for Authors
    • Overview for authors
    • Submission checklist
    • Editorial policies
    • Publication fees
    • Submit a manuscript
    • Dr. Francis Wayne Quan Memorial Prize
    • Open access
  • Alerts
    • Email alerts
    • RSS
  • About
    • General information
    • Staff
    • Editorial Board
    • Contact
  • Subscribe to our alerts
  • RSS feeds
  • Follow JPN on Twitter
Editorial

Biologic effects of mindfulness meditation: growing insights into neurobiologic aspects of the prevention of depression

Simon N. Young
J Psychiatry Neurosci March 01, 2011 36 (2) 75-77; DOI: https://doi.org/10.1503/jpn.110010
Simon N. Young
Coeditor-in-Chief, , and the Department of Psychiatry, McGill University, Montréal, Que
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: [email protected]
  • Article
  • Responses
  • Metrics
  • PDF
Loading

A recent paper in the Archives of General Psychiatry confirms that mindfulness-based cognitive therapy (MBCT) “offers protection against relapse/recurrence on a par with that of maintenance antidepressant pharmacotherapy.”1 It is a tribute to the accumulated wisdom of humankind that a traditional Buddhist meditation practice going back 2500 years, which was originally designed in part to deal with the problem of human suffering, has been successfully adapted to prevent the relapse of depression in the modern era. Buddhist meditation techniques were originally adapted by Jon Kabat-Zinn, founding executive director of the Center for Mindfulness in Medicine, Health Care, and Society at the University of Massachusetts Medical School (www.umassmed.edu/Content.aspx?id=43102), for mindfulness-based stress reduction (MBSR). Reviews of MBSR studies suggest that it decreases depression, anxiety and psychologic distress in people with chronic somatic diseases2 and that it reduces stress, ruminative thinking and trait anxiety in healthy people.3 Mindfulness-based cognitive therapy is similar to MBSR and is designed to change some of the cognitions that are associated with depression.4

Mindfulness has been described as “paying attention in a particular way: on purpose, in the present moment, and non-judgementally.”5 In contrast to traditional cognitive behavioural therapy in which dysfunctional thoughts are targeted, the objective of MBCT is to help individuals learn, at times, to become aware of thoughts, feelings and bodily sensations rather than trying to modify them or acting on them. A core skill learned in MBCT is how to recognize and disengage from self-perpetuating patterns of ruminative, negative thought through sustained attention and attention-switching exercises. This self-regulation of attention is thought to help recovered depressed individuals shift attention away from the rumination about dysfunctional cognitions, which may be reactivated during transient mood lowering, and thus allows them to process depression-related information differently.4 Dysfunctional cognitions, such as “If I do not do as well as other people in a particular task it means I am inferior,” “My value as a person depends on what others think of me,” or “It is important that everyone likes me,”6 are risk factors for depression in adults7–9 and children.10,11 Mindfulness-based cognitive therapy targets the ruminative thinking by enhancing awareness and monitoring of thoughts. This suggests that MBCT might not only decrease relapse in depression but also prevent the onset of the first episode of depression in susceptible people. As Insel and Scolnick12 have pointed out, “the great public health success stories of the past century are largely stories of prevention.” Insights into both psychologic and biologic factors that are associated with the prevention of depression should help in the long run to develop better strategies for prevention. I describe some of the biologic factors associated with dysfunctional cognitions and what is known about the biologic effects of MBCT. Finally, I suggest some possible research directions that may provide more information on the systems that MBCT influences when preventing the onset of depression.

Different forms of meditation have been compared with various control interventions, some of which did not have similar intensity. As a result, the exact component of meditation that produces a beneficial effect is not clear, although the targeting of dysfunctional cognitions is probably the most plausible mechanism. In the rest of this editorial, different forms of meditation are assumed to have similar effects.

The idea that serotonin is related to the control of mood persists, and a small portion of the literature relates serotonin function to dysfunctional attitudes. In one of the first studies of this type, dysfunctional attitudes decreased in healthy participants when they were treated with the serotonin-releasing drug fenfluramine.13 In depressed patients, one of the more common abnormalities reported using positron emission tomography (PET) is an increase in serotonin 2A (5-HT2A) binding potential. In depressed patients, high 5-HT2A binding potential in the cortex was positively associated with dysfunctional attitudes, and the mean value was higher in those exhibiting extremely dysfunctional attitudes than in controls.13 In recovered depressed patients, there was also a positive correlation between 5-HT2A binding potential and dysfunctional attitudes.14 No difference in regional serotonin transporter binding potential was found between participants with major depression and healthy participants. However, in brain regions containing mainly serotonergic nerve terminals, the binding potential was significantly higher in depressed patients with highly negativistic dysfunctional attitudes. There was also a strong association between the serotonin transporter binding potential and dysfunctional attitudes in depressed patients.15 Treatment of depressed patients with fluoxetine decreases dysfunctional attitudes.16 Finally, the mood lowering of recovered depressed patients on medications in response to acute tryptophan depletion was related to their cognitive reactivity,17 a measure of the extent to which dysfunctional attitudes appear when mood is low.

The biologic factors associated with mindfulness meditation have been studied using a variety of different methods. As discussed in recent reviews,18,19 changes in brain function during meditation have been documented using electrophysiology, single photon emission computed tomography, PET and functional magnetic resonance imaging. Results differ somewhat, possibly owing to the use of different forms of meditation, but in general show increased signals in brain regions related to affect regulation and attentional control, with increased release of dopamine. Long-term brain changes are of greater interest to MBCT as a preventive strategy. Several studies have compared brain morphology of experienced meditators with matched controls, and findings include increased cortical thickness along with reduced age-related cortical thinning.18 However, these results could be owing to pre-existing differences in those who choose to meditate and those who do not choose to do so. Two recent studies have overcome this problem by looking at brain morphology before and after an 8-week meditation program. The first study found increases in grey matter in the left hippocampus, the posterior cingulate cortex, the temporo-parietal junction and the cerebellum in those who did MBSR relative to wait-list controls.20 The second study looked at MBSR in stressed but otherwise healthy individuals. Reductions in stress correlated positively with decreases in right basolateral amygdala grey matter density.21

Changes in the brain owing to mindfulness meditation could be a direct effect on the brain or could be mediated in whole or in part by an indirect mechanism. Reduced stress could decrease glucocorticoid levels and modulate the immune system (e.g., cytokines), both of which could feed back to alter the brain. A recent review concluded that there is accumulating evidence that plasma and salivary cortisol can be reduced by MBSR.22 Several studies have looked at immune parameters. In patients with cancer, MBSR tended to return cytokine levels and natural killer cell activities toward normal levels.23,24 In healthy people, meditation increased the antibody titer to influenza vaccine,25 lowered the stress-induced increase in interleukin-626 and decreased C-reactive protein.27

Research on the biologic effects of meditation is relatively new, and there is scope for more work. For example, no studies have yet looked at the effect of meditation on serotonin function. Mindfulness-based cognitive therapy is designed in part to decrease dysfunctional attitudes, which are related to 5-HT2A binding potential. Would MBCT alter 5-HT2A receptor function? As mentioned, in recovered depressed patients on medication, the lowering of mood after acute tryptophan depletion was related to their cognitive re-activity (the extent to which they developed dysfunctional attitudes when their mood was lowered).17 If MBCT decreases dysfunctional attitudes, would it also decrease the lowering of mood in response to acute tryptophan depletion?

If MBCT is to be tested for the prevention of the onset of the first episode of depression, and not just relapse, knowledge about how it works will be helpful in selecting participants for such a study. Prevention studies usually last years and involve a large number of participants; they are therefore very expensive. Unfortunately, medicine provides many examples of negative prevention trials. For example, a large trial of β carotene and vitamin A found no benefit after 4 years of treatment and an adverse effect on the incidence of lung cancer and cardiovascular disease in smokers,28 whereas a study lasting 8 years found no beneficial effect of a low-fat diet on coronary heart disease.29 A prevention study with MBCT would not be easy to carry out. The success of such a study might be influenced by how the patients were selected. Participants should have a strong motivation to practise meditation for years and a high risk for depression. People who have never experienced depression but come from a family with a high incidence of depression have a high risk for the illness and, having seen the effects of depression on their family members, would have a good motivation to practise MBCT if there were a chance that it would protect them from the illnes. In addition, if they had above-average levels of dysfunctional cognitions and cognitive reactivity, they might be expected to benefit from MBCT. The biologic measures that might be useful to help select patients must be speculative at this stage, but 1 or more serotonergic measures might be candidates. For a prevention study with a large sample size, simple measures would be important. Platelet serotonin can be measured relatively easily, and in one study, people with high trait anxiety had more dysfunctional attitudes and high platelet serotonin levels than controls with low trait anxiety.30 Furthermore, platelet 5-HT2A receptor binding was positively related to suicidal ideation in depressed patients,31 so the idea that a simple biologic maker for response to MBCT might be discovered is plausible. Increasing knowledge about the neurobiologic effects of MBCT may foster the convergence of the biologic and psychologic aspects of psychiatry and also aid in the design of much needed primary prevention studies in mood disorders.

Footnotes

  • Competing interests: None declared.

References

  1. ↵
    1. Segal ZV,
    2. Bieling P,
    3. Young T,
    4. et al
    .Antidepressant monotherapy vs sequential pharmacotherapy and mindfulness-based cognitive therapy, or placebo, for relapse prophylaxis in recurrent depression.Arch Gen Psychiatry 2010;67:1256–64.
    OpenUrlCrossRefPubMed
  2. ↵
    1. Bohlmeijer E,
    2. Prenger R,
    3. Taal E,
    4. et al
    .The effects of mindfulness-based stress reduction therapy on mental health of adults with a chronic medical disease: a meta-analysis.J Psychosom Res 2010;68:539–44.
    OpenUrlCrossRefPubMed
  3. ↵
    1. Chiesa A,
    2. Serretti A
    .Mindfulness-based stress reduction for stress management in healthy people: a review and meta-analysis.J Altern Complement Med 2009;15:593–600.
    OpenUrlCrossRefPubMed
  4. ↵
    1. Segal ZV,
    2. Williams JMG,
    3. Teasdale JD
    (2002) Mindfulness-based cognitive therapy for depression — a new approach to preventing relapse (Guilford Press, New York (NY)).
  5. ↵
    1. Kabat-Zinn J
    (1994) Wherever you go, there you are: mindfulness meditation in everyday life (Hyperion, New York (NY)).
  6. ↵
    1. de Graaf LE,
    2. Roelofs J,
    3. Huibers MJ
    .Measuring dysfunctional attitudes in the general population: the dysfunctional attitude scale (form A) revised.Cognit Ther Res 2009;33:345–55.
    OpenUrlCrossRefPubMed
  7. ↵
    1. Church NF,
    2. Brechman-Toussaint ML,
    3. Hine DW
    .Do dysfunctional cognitions mediate the relationship between risk factors and post-natal depression symptomatology?.J Affect Disord 2005;87:65–72.
    OpenUrlCrossRefPubMed
    1. Segal ZV,
    2. Pearson JL,
    3. Thase ME
    .Challenges in preventing relapse in major depression: report of a National Institute of Mental Health Workshop on state of the science of relapse prevention in major depression.J Affect Disord 2003;77:97–108.
    OpenUrlCrossRefPubMed
  8. ↵
    1. Teasdale JD,
    2. Cox SG
    .Dysphoria: self-devaluative and affective components in recovered depressed patients and never depressed controls.Psychol Med 2001;31:1311–6.
    OpenUrlPubMed
  9. ↵
    1. Abela JRZ,
    2. Brozina K,
    3. Haigh EP
    .An examination of the response styles theory of depression in third- and seventh-grade children: a short-term longitudinal study.J Abnorm Child Psychol 2002;30:515–27.
    OpenUrlCrossRefPubMed
  10. ↵
    1. Abela JRZ,
    2. Skitch SA
    .Dysfunctional attitudes, self-esteem, and hassles: cognitive vulnerability to depression in children of affectively ill parents.Behav Res Ther 2007;45:1127–40.
    OpenUrlCrossRefPubMed
  11. ↵
    1. Insel TR,
    2. Scolnick EM
    .Cure therapeutics and strategic prevention: raising the bar for mental health research.Mol Psychiatry 2006;11:11–7.
    OpenUrlCrossRefPubMed
  12. ↵
    1. Meyer JH,
    2. McMain S,
    3. Kennedy SH,
    4. et al
    .Dysfunctional attitudes and 5-HT2 receptors during depression and self-harm.Am J Psychiatry 2003;160:90–9.
    OpenUrlCrossRefPubMed
  13. ↵
    1. Bhagwagar Z,
    2. Hinz R,
    3. Taylor M,
    4. et al
    .Increased 5-HT2A receptor binding in euthymic, medication-free patients recovered from depression: a positron emission study with [11C]MDL 100,907.Am J Psychiatry 2006;163:1580–7.
    OpenUrlCrossRefPubMed
  14. ↵
    1. Meyer JH,
    2. Houle S,
    3. Sagrati S,
    4. et al
    .Brain serotonin transporter binding potential measured with carbon 11-labeled DASB positron emission tomography: effects of major depressive episodes and severity of dysfunctional attitudes.Arch Gen Psychiatry 2004;61:1271–9.
    OpenUrlCrossRefPubMed
  15. ↵
    1. Fava M,
    2. Bless E,
    3. Otto MW,
    4. et al
    .Dysfunctional attitudes in major depression: changes with pharmacotherapy.J Nerv Ment Dis 1994;182:45–9.
    OpenUrlPubMed
  16. ↵
    1. Booij L,
    2. van der Does AJW
    .Cognitive and serotonergic vulnerability to depression: convergent findings.J Abnorm Psychol 2007;116:86–94.
    OpenUrlCrossRefPubMed
  17. ↵
    1. Rubia K
    .The neurobiology of meditation and its clinical effectiveness in psychiatric disorders.Biol Psychol 2009;82:1–11.
    OpenUrlCrossRefPubMed
  18. ↵
    1. Chiesa A,
    2. Serretti A
    .A systematic review of neurobiological and clinical features of mindfulness meditations.Psychol Med 2010;40:1239–52.
    OpenUrlCrossRefPubMed
  19. ↵
    1. Hölzel BK,
    2. Carmody J,
    3. Vangel M,
    4. et al
    .Mindfulness practice leads to increases in regional brain gray matter density.Psychiatry Res 2011;191:36–43.
    OpenUrlCrossRefPubMed
  20. ↵
    1. Hölzel BK,
    2. Carmody J,
    3. Evans KC,
    4. et al
    .Stress reduction correlates with structural changes in the amygdala.Soc Cogn Affect Neurosci 2010;5:11–7.
    OpenUrlCrossRefPubMed
  21. ↵
    1. Matousek RH,
    2. Dobkin PL,
    3. Pruessner J
    .Cortisol as a marker for improvement in mindfulness-based stress reduction.Complement Ther Clin Pract 2010;16:13–9.
    OpenUrlCrossRefPubMed
  22. ↵
    1. Witek-Janusek L,
    2. Albuquerque K,
    3. Chroniak KR,
    4. et al
    .Effect of mindfulness based stress reduction on immune function, quality of life and coping in women newly diagnosed with early stage breast cancer.Brain Behav Immun 2008;22:969–81.
    OpenUrlCrossRefPubMed
  23. ↵
    1. Carlson LE,
    2. Speca M,
    3. Patel KD,
    4. et al
    .Mindfulness-based stress reduction in relation to quality of life, mood, symptoms of stress, and immune parameters in breast and prostate cancer outpatients.Psychosom Med 2003;65:571–81.
    OpenUrlAbstract/FREE Full Text
  24. ↵
    1. Davidson RJ,
    2. Kabat-Zinn J,
    3. Schumacher J,
    4. et al
    .Alterations in brain and immune function produced by mindfulness meditation.Psychosom Med 2003;65:564–70.
    OpenUrlAbstract/FREE Full Text
  25. ↵
    1. Pace TW,
    2. Negi LT,
    3. Adame DD,
    4. et al
    .Effect of compassion meditation on neuroendocrine, innate immune and behavioral responses to psychosocial stress.Psychoneuroendocrinology 2009;34:87–98.
    OpenUrlCrossRefPubMed
  26. ↵
    1. Fang CY,
    2. Reibel DK,
    3. Longacre ML,
    4. et al
    .Enhanced psychosocial well-being following participation in a mindfulness-based stress reduction program is associated with increased natural killer cell activity.J Altern Complement Med 2010;16:531–8.
    OpenUrlCrossRefPubMed
  27. ↵
    1. Omenn GS,
    2. Goodman GE,
    3. Thornquist MD,
    4. et al
    .Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease.N Engl J Med 1996;334:1150–5.
    OpenUrlCrossRefPubMed
  28. ↵
    1. Howard BV,
    2. Van Horn L,
    3. Hsia J,
    4. et al
    .Low-fat dietary pattern and risk of cardiovascular disease: the women’s health initiative randomized controlled dietary modification trial.JAMA 2006;295:655–66.
    OpenUrlCrossRefPubMed
  29. ↵
    1. Davis DD,
    2. Dunlop SR,
    3. Shea P,
    4. et al
    .Biological stress responses in high and low trait anxious students.Biol Psychiatry 1985;20:843–51.
    OpenUrlPubMed
  30. ↵
    1. Lauterbach E,
    2. Brunner J,
    3. Hawellek B,
    4. et al
    .Platelet 5-HT2A receptor binding and tryptophan availability in depression are not associated with recent history of suicide attempts but with personality traits characteristic for suicidal behavior.J Affect Disord 2006;91:57–62.
    OpenUrlPubMed
PreviousNext
Back to top

In this issue

Journal of Psychiatry and Neuroscience: 36 (2)
J Psychiatry Neurosci
Vol. 36, Issue 2
1 Mar 2011
  • Table of Contents
  • Index by author

Article tools

Respond to this article
Print
Download PDF
Article Alerts
To sign up for email alerts or to access your current email alerts, enter your email address below:
Email Article

Thank you for your interest in spreading the word on JPN.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Biologic effects of mindfulness meditation: growing insights into neurobiologic aspects of the prevention of depression
(Your Name) has sent you a message from JPN
(Your Name) thought you would like to see the JPN web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Biologic effects of mindfulness meditation: growing insights into neurobiologic aspects of the prevention of depression
Simon N. Young
J Psychiatry Neurosci Mar 2011, 36 (2) 75-77; DOI: 10.1503/jpn.110010

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
‍ Request Permissions
Share
Biologic effects of mindfulness meditation: growing insights into neurobiologic aspects of the prevention of depression
Simon N. Young
J Psychiatry Neurosci Mar 2011, 36 (2) 75-77; DOI: 10.1503/jpn.110010
Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • No citing articles found.
  • Google Scholar

Similar Articles

Content

  • Current issue
  • Past issues
  • Collections
  • Alerts
  • RSS

Authors & Reviewers

  • Overview for Authors
  • Submit a manuscript
  • Manuscript Submission Checklist

About

  • General Information
  • Staff
  • Editorial Board
  • Contact Us
  • Advertising
  • Reprints
  • Copyright and Permissions
  • Accessibility
  • CMA Civility Standards
CMAJ Group

Copyright 2022, CMA Impact Inc. or its licensors. All rights reserved. ISSN 1180-4882.

All editorial matter in JPN represents the opinions of the authors and not necessarily those of the Canadian Medical Association or its subsidiaries.
To receive any of these resources in an accessible format, please contact us at CMAJ Group, 500-1410 Blair Towers Place, Ottawa ON, K1J 9B9; p: 1-888-855-2555; e: [email protected].
View CMA's Accessibility policy.

Powered by HighWire