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A Mind-Body Perspective of Major Depressive Disorder Rakesh Jain, MD, MPH R/D Clinical Research, Inc. Lake Jackson, Texas, USA Texas Tech Health Sciences.

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Presentation on theme: "A Mind-Body Perspective of Major Depressive Disorder Rakesh Jain, MD, MPH R/D Clinical Research, Inc. Lake Jackson, Texas, USA Texas Tech Health Sciences."— Presentation transcript:

1 A Mind-Body Perspective of Major Depressive Disorder Rakesh Jain, MD, MPH R/D Clinical Research, Inc. Lake Jackson, Texas, USA Texas Tech Health Sciences Center – Permian Basin Midland, Texas, USA 1

2 Let’s Not Underestimate Our Enemy: Depression is THE Leading Cause of Disability *DALYs represent total number of years lost to illness, disability, or premature death within a given population. They are calculated by adding number of years of life lost to number of years lived with disability for a certain disease or disorder. National Institute of Mental Health. http://www.nimh.nih.gov/statistics/2LIDD.shtml. Accessed June 6, 2011. 2

3 Why is Treatment of Depression so Important? MDD UK Population Annual mortality risk (%) by age groups and diagnoses of mental illness, compared to England and Wales population in 2008 Life expectancy was reduced by 10.6 years for males and 7.2 years in females with MDD compared with UK population Chang CK,et al. PLoS One. 2011;6:e19590. 3

4 A Clinician’s Integrative View of “Mind-Body” Disruptions in Psychiatric Mood Disorders Pain Neuropsychological impairment Neurodegeneration Mood disorders Sleep disorders Osteoporosis Obesity, insulin, and lipid abnormalities Coronary artery disease Substance misuse Inflammation Adapted from Goldstein BI, et al. J Clin Psychiatry. 2009;70(8):1078-1090. Adapted from Szelényi J, Vizi ES. Ann N Y Acad Sci. 2007;1113:311-324. 4

5 Childhood Adversity Represents a Risk for Adulthood Disease Major depression (panel 1): z=4.94, P<.001. High-sensitivity C-reactive protein (hsCRP) level  3 mg/L (panel 2): z=3.24, P=.001. Clustering of metabolic risk markers (panel 3): z=4.58, P<.001.  1 age-related disease risks (panel 4): z=5.66, P<.001. 32-year prospective study. Panel 1: Major Depression Panel 2: hsCRP >3 mg/L Panel 3: Clustering of Metabolic Risk Markers Panel 4: ≥1 Disease Risk Number of Adverse Childhood Experiences % of Study Members With the Condition ≥2 (n=98) 70 60 50 40 30 20 10 0 0 (n=502) 1 (n=253) Adapted from Danese A, et al. Arch Pediatr Adolesc Med. 2009;163(12):1135-1143. 5

6 Association of Depression and Anxiety With Chronic Physical Conditions World Mental Health Survey (N=42,249) P<.05 for all comparisons vs persons with neither depression nor anxiety Depression and anxiety Depression Anxiety *Data show odds ratio with 95% confidence intervals (CI). HTN=hypertension. Scott KM, et al. J Affect Disord. 2007;103(1-3):113-120. 6

7 Depression Decreased Long-term Survival After Myocardial Infarction (MI) Days Postdischarge After MI Long-Term Survival After MI in Relation to Beck Depression Inventory (BDI) Score During Hospitalization Cardiac Death-Free Survival (%) BDI <5 BDI 5 to 9 BDI 10 to 18 BDI ≥19 100 90 80 70 60 0365730109514601825 N=896 Adapted from Lespérance F, et al. Circulation. 2002;105(9):1049-1053. 7

8 Depression and MI: Importance of Depression and its Optimum Treatment Event Rate: Non-responders = 25.6 % Untreated controls = 11.2 % Responders = 7.4 % Data derived from MIND-IT study, participants had post-MI depression MI = myocardial infarction. de Jonge P, et al. Am J Psychiatry. 2007;164:1371-1378. 8

9 MDD was Associated With Progression of Atherosclerosis 3-Year Change in Carotid IMT (mm) BDI-II Total Score P for Linear Trend=.003 N=324 0-1 0.02 0.04 0.06 0.08 0.10 0.12 0.14 0.16 2-45-19 0.00 IMT=intima-media thickness; BDI-II=Beck Depression Inventory II. Adapted from Stewart JC, et al. Arch Gen Psychiatry. 2007;64(2):225-233. 9

10 Relationship Between Obesity, Metabolic Syndrome, and Depression Association between metabolic syndrome (MetS) and depression in each body mass index (BMI) category. Graph displays odds ratio (OR) for depression after adjustment for age, gender, prior cardiovascular disease, employment status, marital status, smoking status, dietary score, and physical activity. Obesity was defined as BMI ≥30 and overweight status as a BMI between 25 and 30 kg/m 2 Odds Ratio - Depression Skilton MR, et al. Biol Psychiatry. 2007;62(11):1251-1257. 10

11 Adipose Tissue: a Potent Source of Inflammation One more reason for Optimum Weight Management Shelton RC, Miller AH. Prog Neurobiol. 2010.91: 275-299. 11

12 MDD, Adiposity, and Inflammatory Markers 50 MDD patients compared with 50 healthy matched controls Miller GE et al. Am J of Cardiol. 2002;90(12):1279-1283. 12

13 Neuroendocrine, Autonomic, and Immune Dysregulation in MDD CRH = corticotropin-releasing hormone; NF-κB = nuclear factor kappa B; ACTH = adrenocorticotropic hormone. Miller AH, et al. Biol Psychiatry. 2009;65(9):732-741. Reprinted with permission from Elsevier Limited. 13

14 Inflammatory Cytokine Levels Were Associated With Symptom Severity in Patients With MDD Comparison of 5 Patients With MDD and 5 Matched Healthy Controls R 2 =0.4058 P=.05 Daily Mean VAS Score (mm) A. Concentration 00.51.01.52.02.5 0 20 40 60 80 100 120 B. Guilt 00.51.01.52.02.5 0 20 40 60 80 100 120 R 2 =0.6711 P=.004* C. Sadness 00.51.01.52.02.5 0 20 40 60 80 100 120 R 2 =0.5139 P=.02 D. Self-Esteem Daily Mean VAS Score (mm) 00.51.0 1.5 2.02.5 0 20 40 60 80 100 120 R 2 =0.735 P=.002* Daily Mean Log IL-6 (pg/mL) E. Suicidal Thoughts 00.51.01.52.02.5 0 20 40 60 80 100 120 R 2 =0.7785 P=.0007* Daily Mean Log IL-6 (pg/mL) F. Tiredness 00.51.01.52.02.5 0 20 40 60 80 100 120 R 2 =0.566 P=.02 Daily Mean Log IL-6 (pg/mL) *Correlations of IL-6 with guilt, self-esteem, and suicidal thoughts remained significant after Bonferroni correction; VAS=Visual Analog Scale. Adapted from Alesci S, et al. J Clin Endocrinol Metab. 2005;90(5):2522-2530. 14

15 Gene transcription cascades Neurotrophins Systems Circuitry Neuronal Circuitry Intra-cellular Pathways Monoamine neurotransmitter- level view “The King is Dead – Long Live the King”: Beyond the Monoamine Hypothesis of Depression Marsden WN. Med Hypotheses. 2011.77:508-528. 15

16 Macro- and Microscopic Structures Involved in Mood Disorders Schloesser RJ, et al. Neuropsychopharmacology. 2008;33:110-133. 16

17 Examining the Neurotrophic Hypothesis of Depression NormalTreatment Depression Berton O, Nestler EJ. Nat Rev Neurosci.2006;7:137-151. 17

18 Glia-Neuron Interaction May Influence Neurotrophic Factors 5-HT=serotonin; BDNF=brain-derived neurotrophic factor; CNS=central nervous system; GLU=glutamate; IDO=indoleamine 2,3 dioxygenase; IFN=interferon; IL=interleukin; NMDA=N-methyl-D-aspartate; QUIN=quinolinic acid; RNS=reactive nitrogen species; ROS=reactive oxygen species; TNF=tumor necrosis factor; TRP=tryptophan. Miller AH, et al. Biol Psychiatry. 2009;65(9):732-741. Reprinted with permission from Elsevier Limited. 18

19 Neurotransmitter–Receptor–Intracellular –Gene Transcription Interactions Racagni G, et al. World J Biol Psychiatry. 2011;12:574-587. 19

20 Circuitry in Depression: Examining Two Models An amygdala-centric circuit largely inspired by structural brain imaging and postmortem studies Another circuit model generated with a greater emphasis on functional imaging results Krishnan V, Nestler RJ. Am J Psychiatry. 2010;167(11):1305-1320. 20

21 Inflammation and Depression: the Brain-Body Link Capuron L, Miller AH. Pharmacol Ther. 2011;130:226-238. 21

22 Depression and Inflammation: What is the link ? Induction of indoleamine 2,3-dioxygenase (IDO) by IF and some PICs is associated with depleted plasma tryptophan, which may interfere with brain 5- HT synthesis, and increased production of anxiogenic and depressogenic tryptophan catabolites (such as kynurinate, and quinolinic acid) All abovementioned factors cause neuroprogression, that is a combination of neurodegeneration, neuronal apoptosis, and lowered neurogenesis and neuroplasticity. Stroke, AD, HD, PD, MS Psychological stress IFNy, IL-2, IL-1β, TNFα, IL-6 Microglial activation Neuroinflammation IFNy, IL-2, IL-1β, TNFα, IL-6 Peripheral CMI activation and inflammation CVD; COPD; RA; SLE; IBD; HIV Diabetes; Metabolic syndrome Postpartum period; Hemodialysis IFNα-immunotherapy; Predisposing factors: immune and inflammatory genes Lowered levels of peptidases (DPP IV and PEP) Melancholic symptoms Anxiety Fatigue and somatic symptoms SERT 5-HT L-tryptophan IDO TRYCATs IDO L-tryptophan Leonard B, Maes M. Neurosci Biobehav Rev. 2012;36:764-785. 22

23 A “Tripartite” Model of Mind-Body Link: Inflammatory, Autonomic, and HHPA Axis Abnormalities Jain R, et al. Curr Diab Rep. 2011;11:275-284. 23

24 The Multi-channel Connections Between Mind and Body in Inflammatory Signaling Capuron L, Miller AH. Pharmacol Ther. 2011;130:226-238. 24

25 What Are the Treatment Implications of This Emerging Mind-Body Neurobiology? Footnote goes here 25

26 Depressed mood Decreased interest or pleasure Significant appetite or weight change Fatigue Insomnia or hypersomnia Psychomotor disturbances Worthlessness/guilt Impaired concentration Thoughts of death/suicide A Clinician’s View Of Major Depression: 16 out of 9 Symptoms! (All are Important to the Clinician) Irritability Brooding Pain Tearfulness Anxiety or phobias Obsessive rumination Excessive worry over physical health Excessive worry over physical health Associated symptoms DSM-IV diagnostic criteria APA. DSM-IV-TR. 2000:352,356. 26

27 Which Interventions to Pick for Optimally Treating this Mind-Body Condition – Depression ? Footnote goes here 27

28 Survival Time Since End of Treatment (Months) Continued medication (n=28) Placebo (n=21) Prior behavioral activation (n=27) Prior cognitive therapy (n=30) Cognitive Therapy and Behavioral Activation Were Advantageous in Delaying Relapse Participants were initially assigned to 16 weeks of antidepressant treatment (n=100), cognitive therapy (n=45), and behavioral activation (n=43); treatment responders on antidepressants were randomized to continue with medication or placebo; relapse was defined as HAM-D score of  14; recurrence was defined with same criteria during second year of follow-up Adapted from Dobson KS, et al. J Consult Clin Psychol. 2008;76(3):468-477. 28

29 Impact of Cognitive Therapy on Amygdala and Prefrontal (Dorsolateral PFC) Activity in MDD 12 Weeks of Cognitive Therapy 0.15 0.10 0.05 0.00 -0.05 24681012 Time (Seconds) BOLD Signal (% Change) Time (Seconds) BOLD Signal (% Change) 0.30 0.15 0.10 0.05 24681012 14 16 18 0.00 0.20 0.25 Pre Post Control a. Emotionalb. Cognitive Is it you? UGLY Put the digits in numerical order 7 4 3 1 5 Patients with depression (n=9) Controls (n=24) Adapted from DeRubeis RJ, et al. Nat Rev Neurosci. 2008;9(10):788-796. Reprinted with permission from Macmillan Publishers Ltd. 29

30 CBT and Inflammation: Symptoms and Neurobiological Marker Improvement CRP=C-reactive protein; CABG=coronary artery bypass graft. Doering LV et.al. Altern Ther Health Med. 2007;13(3):18-21. 30

31 Psychotherapy and Receptor Changes: Is this even possible? This is first direct demonstration of a specific neurotransmitter mechanism involved in neurobiology of psychotherapy. Increased serotonin 5-HT1A receptor binding in multiple cortical regions following psychotherapy in patients with MDD Significant increase in 5-HT1A density in PSY group compared to FLU group in frontal, temporal, and parietal cortex (angular gyrus, medial prefrontal cortex, orbitofrontal cortex) Short-term psychodynamic psychotherapy (PSY, n=8) or fluoxetine (FLU, 20 mg/d, increased up to 40 mg/d if needed, n=15) for 16 weeks Karlsson H, et al. Psychol Med. 2010;40:523-528. 31

32 Physical Exercise and Mental Health Is It Time to Start Prescribing It? 32

33 Neurobiology of Exercise: a Complex Cascade That Also involves Neurotransmitters and Receptors Function Disease Structure Executive Controls Prefrontal and Cingulate Cortex Emotional Controls Amygdala, Prefrontal Cortex External Input Visual Olfactory Acoustic Gustatory Somatosensory ANS and Endocrine Systems DA ↓ Parkinson’s Disease ↑ ROS Alzheimer’s Dementia Schizophrenia Depression Sleep Disorders Obesity Diabetes CVD Immune Disorder IBD, Constipation, Colon Cancer Learning and Memory Immune Control Gastrointestinal Control Muscle Cardiovascular Consequences Metabolic Consequences Liver, WAT, Pancreas Thermal Consequences Behavior Social Sexual Coping Addictive Escape Fight & Flight Stress Sleep Ingestive Motor Controls Motor Cortex Striatum, Brainstem, Cerebellum, Spinal Cord Motivational Controls Reward,Wanting,Selection Hypothalamus, Accumbens, VTA Cognitive Controls Hippocampus, Cortex Neural Primary Afferents “Exercise” Internal Feedback “Consequences of exercise” Humoral Factors CNS Energy Balance Repair Plasticity Protection Neurogenesis Transcription NA, 5-HT,GABA, Glutamate, Glycine BDNF/TrkB ERK/CREB NFKB ANS=autonomic nervous system; BDNF=brain-derived neurotrophic factor; CNS=central nervous system; CREB=cyclic adenosine monophosphate response element-binding protein; CVD=cardiovascular disease; DA=dopamine; ERK=extracellular signal-regulated kinase; 5-HT=5-hydroxytryptamine; GABA=gamma amino butyric acid; IBD=inflammatory bowel disease; NA=noradrenaline; NFκB=nuclear factor of kappaB; ROS=reactive oxygen species; TrkB=tyrosine residue kinase receptor-type 2; VTA=ventral tegmental area; WAT=white adipose tissue. Reprinted by permission from Macmillan Publishers Ltd: Dishman RK et al. Obesity. 2006;14(3):345-356. 33

34 Clinical and Neurobiological Evidence for Exercise and Wellness: Receptors are Involved Here, too! VAS Scores before and after exercise Euphoria and Happiness were significantly different (P<0.05) Reduction in opioid receptor availability after exercise (red is P<0.05) Boecker H et al. Cereb Cortex. 2008;18(11):2523-2531. 34

35 Exercise’s Effects on Hippocampal Cell Proliferation and Neurogenesis Ki 67 positive newly generated cells DCX positive young neuronal cells # p<0.10 *** p<0.001 Van der Borght K, et al. Hippocampus. 2009;19:928-936. 35

36 Physical Exercise: a Modulator of Inflammatory Cytokines Nicklas BJ, et al. J Am Geriatr Soc. 2008;56:2045-2052. 36

37 Effect of Different Types of Exercise Mead GE, et al. Cochrane Database of Syst Rev. 2008 Oct 8;(4):CD004366. 37

38 HAM-D 17 Reduction from Baseline 12 Weeks Duration Low Dose: 7.0-kcal/kg/week energy expenditure PHD: Public Health Dose -17.5-kcal/kg/week energy expenditure Depression and Aerobic Exercising: Emerging Evidence of Efficacy p=0.03 p=0.04 T T T N = 80 Hamilton Rating Scale for Depression - 17 0 4 8 12 16 ControlLow DosePublic Health Dose Dunn AL, et al. Am J Prev Med. 2005;28(1):1-8. 38

39 39

40 Yoga as a Mind-Body Intervention Mean thalamic GABA levels in subjects with Major Depressive Disorder (MDD) and low back pain (LBP) (n=2) compared to normal subjects (n=19) before (Scan 1) and after (Scan 2) a 12-week yoga intervention StressYoga-Based Practices Sympathetic Nervous System (SNS) Parasympathetic Nervous System Hypothalamic-pituitary-adrenal Axis  Hypothalamic-pituitary-adrenal Axis  GABA Activity GABA Activity Streeter CC, et al. Med Hypotheses. 2012;78:571-579. 40

41 Mindfulness Based Cognitive Therapy (MBCT) Footnote goes here 41

42 Walking Down the Street On the other side of the street you see somebody you know. You smile and wave. The person does not wave back and keeps walking. You're walking down the street. 42

43 Non- awareness Old patterns intrude Wish for things to be different Rumination Depression Memory bias Poor problem solving Mindlessness and Vulnerability to Depression 43

44 Low mood Old patterns intrude Wish for things to be different Mindful awareness Freedom to choose not to “go there” Safe “platform” Calm Connected Creative Mindfulness and Prevention of Relapse into Depression 44

45 Volumetric Changes Over 8 Weeks of Mindfulness Based Therapy – Focus on Amygdala Stressed but otherwise healthy individuals (N 1⁄4 26) participated in 8- week mindfulness-based stress reduction intervention Holzel BK, et al. SCAN. 2010;5:11-17. 45

46 Volumetric Changes in Hippocampus With 8 Weeks of Mindfulness Based Therapy 16 healthy, meditation-naïve participants were obtained before and after they underwent 8-week program. Changes in gray matter concentration were investigated using voxel-based morphometry, and compared with waiting list control group of 17 individuals. Holzel BK, el al. Psychiatry Res. 2011;191:36-43. 46

47 ANS and Inflammatory Responses, Stress, and Meditation 50 healthy women (mean age=41.32, range=30–65), 25 novices and 25 experts, were exposed to each of the conditions (yoga, movement control, and passive-video control) during three separate visits. Kiecolt-Glaser JK et al. Psychosom Med. 2010;72:113-121. 47

48 Mindfulness Based Cognitive Therapy (MBCT) – Promising New Therapy M-ADM = Medication (anti-depressant continuation) MBCT= Mindfulness based CT Pla+Clin = Placebo plus clinical management Segal Z, et al. Arch Gen Psychiatry. 2010;67(12):1256-1264. 48

49 Neurobiological Driven Rationale: Combination May be the Gold Standard Therapy in Depression Limbic Hyperactivity Limbic Hyperactivity Dorsal Cortex Emotional/ Cognitive Dysregulation Dorsal Cortex Emotional/ Cognitive Dysregulation Pleasure Circuit Dampening Pharmacotherapy Cognitive-Behavioral Therapy Positive Activity Interventions Pharmacotherapy + Cognitive-Behavioral Therapy + Positive Activity Interventions Pharmacotherapy + Cognitive-Behavioral Therapy + Positive Activity Interventions Layous K, et al. J Altern Complement Med. 2011;17:675-683. 49

50 Complete and Several Types of Incomplete States of Mental Health Incomplete mental illness Complete mental health Incomplete mental health Complete mental illness High subjective well-being symptoms Low subjective well-being symptoms Low mental illness symptoms High mental illness symptoms Struggling Flourishing Languishing Floundering Slade M. BMC Health Serv Res. 2010;10:26. 50

51 Pharmacological Interventions in Depression 51

52 Functional Connectivity Across the “Big Three” Monoamine Systems: Serotonin, Norepinephrine, and Dopamine Kennedy SH, et al. J Affect Dis. 2011;132 (Suppl 1):S21-S23. 52

53 Atypical and Other Augmentations with Antidepressants: What is the Receptor-based Biological Rationale for these Augmentation Strategies? Mathew SJ, et al. Neuropsychopharmacology. 2008;33:20080-2092. 53

54 BDNF Levels After 8 Weeks of Antidepressant Treatment 2 HAM-D: 23.2 HAM-D: 8.2 N=10 p=.007 p<.001* N=28 N=18 *Value is for difference between baseline and follow-up in treated samples. BDNF Levels After 12 Weeks of Antidepressant Treatment 1 0 25 30 35 40 45 0 5 10 15 20 12 30 40 50 10 20 BaselineFollow-UpControls Patients sBDNF Levels (ng/dL) BDNF (ng/dL) Antidepressant Treatment May Normalize BDNF Levels 1. Aydemir O, et al. Prog Neuropsychopharm Biol Psych. 2005;29(2):261-265. 2. Gonul AS, et al. Eur Arch Psychiatry Clin Neurosci. 2005;255(6):381-386. 54

55 Relationship Between Change in BDNF Levels, Duration of Treatment, and Treatment Response in MDD Patients r = 0.65 p=0.02 r = 0.52 p=0.01 Meta-regression based on 10 case control and 13 clinical trial studies assessing 1504 subjects Change in BDNF – Effect Size Brunoni AR, et al. Int J Neuropsychopharmacology. 2008;11(8):1169-1180. 55

56 How Norepinephrine Interacts With Serotonin: Role of Receptors Stahl SM. Essential Psychopharmacology: Neuroscientific Basis and Practical Applications; 2000:254. 56

57 Bio-Psycho-Social Interactions in Depression Occur at the Cellular and Sub-cellular Level Mathew SJ, et al. Neuropsychopharmacology. 2008;33:20080-2092. 57

58 Relationship Between H1 and M1 Antagonism: Using Anti-psychotics as a Proxy to Examine This Issue Matsui-Sakata A, et al. Drug Metab Pharmacokinet. 2005;20(5):368-378. 58

59 Footnote goe here Why is Achieving Sustained Remission So Important in Major Depression? 59

60 Kupfer DJ, Frank E. Am J Psychiatry. 1987;144(1):86-88. The Kupfer Curve: the Life Story of Depression ResponseRemissionRecovery RelapseRecurrenceRelapse “Normalcy” Symptoms Syndrome Treatment Phases Progression to disorder Work with your doctor to avoid relapse and recurrence AcuteMaintenanceContinuation 60

61 What Is Remission? It Depends on Whom You Ask A Researcher’s Definition A Clinician’s Definition A Patient’s Definition What is the score on rating instrument? What is the score on rating instrument? Are the symptoms gone? Am I functioning well? Do I feel optimistic and self-confident? Are the symptoms gone? Am I functioning well? Do I feel optimistic and self-confident? Zimmerman M et al. Am J Psychiatry. 2006.163(1):148-150. 61

62 Remission’s Importance: Its Impact on Patient’s Lives Impacts Physical Functioning 1,2 Impacts Social Functioning 1,2 Impacts Children’s Mental Well-being 3 Impacts Occupational Functioning 1,2 Impacts Marital Functioning 4 Increased relapse risk; faster relapse 5,6 1. Sobocki P et al. Int J Clin Pract. 2006;60(7):791-798. 2. Keller MB. JAMA. 2003;289(23):3152-3160. 3. Weissman MM et al. JAMA. 2006;295(12):1389-1398. 4. Bromberger JT et al. J Nerv Ment Dis. 1994;182(1):40-44. 5. Thase M et al. Am J Psychiatry. 992;149(8):1046-1052. 6. Judd LL et al. J Affect Disord. 1998;50(2-3):97-108. 62

63 STAR*D Reveals its Secrets: the Dangers of Residual Symptoms Residual Symptoms: Sleep disturbance Sad mood Appetite/weight change Concentration Outlook Suicidal ideation Involvement Energy/fatigue Psychomotor Increasing number of symptom domains leads to increased risk of relapse (x 2 [5]=17.7155, P=0.0033) Overall 40% relapse rate 0 domains 1 domain 2 domains 3 domains 4 domains 5 domains 1.00 0.75 0.50 0.25 0.00 0102030405060 QIDS Relapse Time (Weeks) Cumulative Probability of Relapse Residual Symptom Domains QIDS=16-item Quick Inventory of Depressive Symptomatology. Nierenberg AA et al. Psychol Med. 2010;40(1):41–50. 63

64 What Does a Prospective Study Reveal About Differences Between Nonremitters and Remitters? Statistically smaller areas in nonremitted patients were: anterior cingulum, hippocampus, amygdala, DL-PFC, and DM-PFC 3-year follow-up study (38 patients, 30 controls) Gray matter density decline in nonremitted patients vs remitted patients DL-PFC, dorsolateral prefrontal cortex DM-PFC, dorsomedial prefrontal cortex Frodl TS et al. Arch Gen Psychiatry. 2008;65(10):1156-1165. 64

65 Remission Rates with SSRIs vs SNRIs Debate: What is the Latest? SNRI remission rates were 5.7% higher A meta-analysis of head-to-head SSRIs vs. SNRIs trials Remission as the outcome measured Odds Ratio IV, Random, 95% CI 12 Favors SNRIs 0.20.5 5 Favors SSRIs 600 300 400200 1.5 1 0.5 0 -0.5 -1.5 100 500 Number of Patients in Each Trial (N) In (odds ratio) Machado M et al. J Clin Pharm Ther. 2010;35(2):177-188. 65

66 In Conclusion… Depression is truly a Mind-Body Disorder Evidence supporting this concept is strong Utilizing this Mind-Body approach to understanding and treating Depression will lead to improved outcomes for patients 66


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