Psychiatric Times.
No. 5
Clinical
From Chaos to Consilience
Using the New Mind-Body Science to Improve the Diagnosis and Treatment of Major Depression
By
Charles L. Raison, MD, Rakesh Jain, MD, MPH,
Vladimir Maletic, MD, and Jon W. Draud, MD, MS
A PDF of this article will be provided on request; please contact Dr Charles Raison at
craison@emory.edu
The concept of a mind-body neurobiological approach to depression will be explored in detail at "Treating The Whole Patient: The Mind-Body Connection." This new meeting will be held November 1-2, 2009 in conjunction with the US Psychiatric and Mental Health Congress, which will be held in Las Vegas on November 2-5, 2009. For information about that conference and to register, please call (800) 447-4474 or visit
www.psychcongress.com |
April 24, 2009
As we’ll discuss in the next 2 parts of this series, understanding these disruptions in danger/adaptation pathways in brain and body is at the heart of what the new science offers. It presents new ways of thinking about how we diagnose, treat, and make prognoses about many of the world’s most vexing behavioral disturbances—which are the primary requirements we ask of any scientifically based disease state.
“So, what’s in it for me?”
If you are a busy practicing physician, you may be asking yourself: “Interesting stuff…but what’s in it for me? How might I benefit from this new mind–body neurobiology? How does it help me be a better clinician?”
This is, of course, an eminently important issue. Our first response is that because the era of looking at depression as a mind–brain–body disease has finally arrived, we practicing clinicians need to be ready for it. Whether we are psychiatrists or primary care physicians, we need to be ready because it will change how we diagnose and treat a range of psychiatric conditions. These changes will likely be reflected—at least to some degree—in the next edition of DSM. We believe the change will be all for the good. We will be able to make diagnoses more efficiently, completely, and realistically, and this will markedly improve our treatment outcomes, as we’ll discuss in part 3.
While parts 2 and 3 of our series will address key treatment implications of the new science, the central point we are trying to make here is that diagnostic yields will improve if we alter our thinking about depression as a primarily mind or mind–brain disorder to a symptom complex that is activated by abnormalities in the whole person: mind, brain, body, and spirit (although we make no claims toward any special understanding of the spiritual realm!).
Increased recognition of the bodily symptoms of depression means we will less often miss the disorder or undertreat patients who present with primarily physical complaints. Indeed, our acknowledgment of the paramount importance of mind and body symptoms in depression will lead us to watch for the resolution in both symptom domains before we declare an individual’s depression to be in remission. Similarly, we will recognize that the treatment of symptoms such as anxiety and pain—which are not currently on the DSM “short list” for depression—is as essential as the treatment of any other symptoms if we are to help our patients achieve optimal long–term outcomes. Finally, the recognition that depression is intimately linked to the risk factors from which it arises provides a strong rationale for developing preventive strategies that are likely to benefit society in general and our patients in particular.
There is of course much else to discuss together. We invite you to continue this dialogue with us in the upcoming parts 2 and 3 of this series of articles.
Dr Raison is assistant professor and clinical director of the Mind–Body Program in the department of psychiatry and behavioral sciences at Emory University School of Medicine in Atlanta. Dr Raison is paid by CME LLC to provide/present this information. The opinions expressed are those of Dr Raison/CME LLC and do not necessarily reflect the views of Emory University or Emory Healthcare. Dr Raison’s participation in this activity does not constitute or imply endorsement by Emory University or Emory Healthcare. Dr Raison is on speakers’ bureaus for Lilly and Wyeth and serves on advisory boards for Lilly and Wyeth. He receives research support from Centocor.
Dr Maletic is clinical professor in the department of neuropsychiatry and behavioral sciences at the University of South Carolina School of Medicine in Columbia. He is on speakers’ bureaus for Lilly, Takeda, and Novartis, and serves on advisory boards for Lilly and Takeda.
Dr Draud is medical director of psychiatry and addiction medicine at Baptist Hospital in Nashville and at Middle Tennessee Medical Center in Murphreesboro. He is on speakers’ bureaus and serves as a consultant for Lilly, Pfizer, Cephalon, Forest, Takeda, AstraZeneca, and Sanofi–Aventis.
Dr Jain is director of adult and child psychopharmacology research at R/D Clinical Research, Inc, in Lake Jackson, Tex. He is on speakers’ bureaus for Jazz, Lilly, Pfizer, Takeda, and Shire; he serves as a consultant for Addrenex, Impax, Lilly, Shire, Takeda, and Pfizer.
References
1. Miller AH, Maletic V, Raison CL. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression.
Biol Psychiatry. 2009;65:732–741.
2. Anand P, Thomas SG, Kunnumakkara AB, et al. Biological activities of curcumin and its analogues (Congeners) made by man and Mother Nature.
Biochem Pharmacol. 2008;76:1590–1611.
3. Bradley RG, Binder EB, Epstein MP, et al. Influence of child abuse on adult depression: moderation by the corticotropin–releasing hormone receptor gene.
Arch Gen Psychiatry. 2008;65:190–200.
4. Otte C, McCaffery J, Ali S, Whooley MA. Association of a serotonin transporter polymorphism (5–HTTLPR) with depression, perceived stress, and norepinephrine in patients with coronary disease: the Heart and Soul Study.
Am J Psychiatry. 2007;164:1379–1384.
5. Maletic V, Raison CL. At the crossroads of mind and body: focus on the neurobiology of depression, fibromyalgia, and neuropathic pain.
Front Biosci. In press.
6. Skala JA, Freedland KE, Carney RM. Coronary heart disease and depression: a review of recent mechanistic research.
Can J Psychiatry. 2006;51:738–745.
7. Szuster–Ciesielska A, Slotwinska M, Stachura A, et al. Accelerated apoptosis of blood leukocytes and oxidative stress in blood of patients with major depression.
Prog Neuropsychopharmacol Biol Psychiatry. 2008;32:686–694.
8. Frodl TS, Koutsouleris N, Bottlender R, et al. Depression–related variation in brain morphology over 3 years: effects of stress?
Arch Gen Psychiatry. 2008; 65:1156–1165.
9. Kendler KS, Gardner CO Jr. Boundaries of major depression: an evaluation of
DSM–IV criteria.
Am J Psychiatry. 1998;155:172–177.
10. McGlinchey JB, Zimmerman M. Examining a dimensional representation of depression and anxiety disorders’ comorbidity in psychiatric outpatients with item response modeling.
J Abnorm Psychol. 2007; 116:464–474.
11. Hudson JI, Mangweth B, Pope HG Jr, et al. Family study of affective spectrum disorder.
Arch Gen Psychiatry. 2003;60:170–177.
12. Raison CL, Lin JM, Reeves WC. Association of peripheral inflammatory markers with chronic fatigue in a population–based sample.
Brain Behav Immun. 2009;23:327–337.
13. Kessler RC, Berglund P, Demler O, et al; National Comorbidity Survey Replication. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS–R).
JAMA. 2003;289:3095–3105.
14. Hasin DS, Goodwin RD, Stinson FS, Grant BF. Epidemiology of major depressive disorder: results from the National Epidemiologic Survey on Alcoholism and Related Conditions.
Arch Gen Psychiatry. 2005;62:1097–1106.
15. Stone EA, Lin Y, Quartermain D. A final common pathway for depression? Progress toward a general conceptual framework.
Neurosci Biobehav Rev. 2008;32:508–524.
16. Meyer–Lindenberg A, Weinberger DR. Intermediate phenotypes and genetic mechanisms of psychiatric disorders.
Nat Rev Neurosci. 2006;7:818–827.
17. Caspi A, Sugden K, Moffitt TE, et al. Influence of life stress on depression: moderation by a polymorphism in the 5–HTT gene.
Science. 2003;301:386–389.
18. Johnson SL, Cuellar AK, Ruggero C, et al. Life events as predictors of mania and depression in bipolar I disorder.
J Abnorm Psychol. 2008;117:268–277.
19. Pezawas L, Meyer–Lindenberg A, Goldman AL, et al. Evidence of biologic epistasis between BDNF and SLC6A4 and implications for depression.
Mol Psychiatry. 2008;13:709–716.
20. Dennett DD.
Darwin’s Dangerous Idea: Evolution and the Meanings of Life. New York: Simon & Schuster; 1995.
21. Wang H, Moser M, Schiltenwolf M, Buchner M. Circulating cytokine levels compared to pain in patients with fibromyalgia—a prospective longitudinal study over 6 months.
J Rheumatol. 2008;35:1366–1370.
22. Pitsavos C, Panagiotakos DB, Papageorgiou C, et al. Anxiety in relation to inflammation and coagulation markers, among healthy adults: the ATTICA study.
Atherosclerosis. 2006;185:320–326.
23. Irwin MR, Wang M, Ribeiro D, et al. Sleep loss activates cellular inflammatory signaling.
Biol Psychiatry. 2008;64:538–540.
24. Akiskal HS, Akiskal KK. In search of Aristotle: temperament, human nature, melancholia, creativity and eminence.
J Affect Disord. 2007;100:1–6.
25. Jamison KR.
Touched With Fire: Manic–Depressive Illness and the Artistic Temperament. New York: Free Press; 1993.