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|Year : 2013
: 55 | Issue : 7 | Page
|Positive therapeutic and neurotropic effects of yoga in depression: A comparative study
GH Naveen1, J Thirthalli1, MG Rao1, S Varambally1, R Christopher2, BN Gangadhar1
1 Department of Psychiatry, Advanced Centre for Yoga, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India
2 Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India
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|Date of Web Publication||8-Aug-2013|
| Abstract|| |
Context: Therapeutic effect of yoga in depression is recognized. Neuroplastic effects of antidepressant therapies are inferred by elevations in brain-derived neurotrophic factor (BDNF). Role of yoga in both these effects has not been studied.
Materials and Methods: Non-suicidal, consecutive out-patients of depression were offered yoga either alone or with antidepressants. The depression severity was rated on Hamilton Depression Rating Scale (HDRS) before and at 3 months. Serum BDNF levels were measured at the same time points. Repeated-measures analysis of variance was performed to look at change across groups with respect to HDRS scores and BDNF levels over 3 months of follow-up. Relationship between change in serum BDNF levels and change in HDRS scores was assessed using the Pearson's correlation coefficient.
Results: Both yoga groups were better than drugs-only group with respect to reduction in HDRS scores. Serum BDNF rose in the total sample in the 3-month period. This was not, however, different across treatment groups. There was a significant positive correlation between fall in HDRS and rise in serum BDNF levels in yoga-only group (r=0.702; P=0.001), but not in those receiving yoga and antidepressants or antidepressants-alone.
Conclusions: Neuroplastic mechanisms may be related to the therapeutic mechanisms of yoga in depression.
Keywords: Antidepressant, brain-derived neurotrophic factor, depression, neuroplasticity, yoga
|How to cite this article:|
Naveen G H, Thirthalli J, Rao M G, Varambally S, Christopher R, Gangadhar B N. Positive therapeutic and neurotropic effects of yoga in depression: A comparative study. Indian J Psychiatry 2013;55, Suppl S3:400-4
|How to cite this URL:|
Naveen G H, Thirthalli J, Rao M G, Varambally S, Christopher R, Gangadhar B N. Positive therapeutic and neurotropic effects of yoga in depression: A comparative study. Indian J Psychiatry [serial online] 2013 [cited 2016 May 2];55, Suppl S3:400-4. Available from: http://www.indianjpsychiatry.org/text.asp?2013/55/7/400/116313
| Introduction|| |
There has been a consistent, on-going search into the biological basis of depression. While the monoamine hypothesis has often been implicated in the pathophysiology of depression. , decreased neuroplasticity in the hippocampus has recently gained importance as a likely factor in the pathogenesis of depression.  This may also explain the relationship between stress and depression. 
Brain-derived neurotrophic factor (BDNF) is a key modulator of neuroplastic changes and has been implicated in the pathophysiology of depression  through the stress pathway. , Decreased serum BDNF levels were observed in drug free patients with depression in comparison with the healthy controls , and serum BDNF level has been shown to increase with antidepressant treatment. ,, A recent study showed serum BDNF levels were significantly correlated with hippocampal volume in moderately depressed patients.  Hence, abnormal neuroplasticity has been proposed as an important pathophysiological mechanism underlying depression. 
For less severe depression, antidepressant therapy or psychotherapy or complementary and alternative systems of medicine treatment could be used as a first line treatment.  Reviews endorse a role for yoga in depression. , Most of the studies have used only a few yoga practices for treating depression either breathing exercises or different Āsanā practices or only meditation. ,, In this study, we have used a generic yoga module developed from traditional texts and validated by the yoga experts as a treatment for depression (Naveen et al., in this issue). Yoga has been shown to have a significant effect on brain neurotransmitters such as gamma-Aminobutyric acid, indicating its potential usefulness in treating depression and anxiety disorders.  Further, yoga therapy can improve cognitive functions, which is one of the indicators of neuroplasticity. ,
We examined in patients with depression the therapeutic effects of yoga as well as its effects on serum BDNF. We also examined the relationship between the antidepressant and neurotropic effects (rise in BDNF) with yoga and medications.
| Materials and Methods|| |
The study subjects came from yet another larger study comparing clinical effects of yoga-only with either medication-only or a combination.  A three-group, single blind comparative trial design was used in this study. Depressive disorder patients attending out-patient services with a score of 11 or more on Hamilton Depression Rating Scale (HDRS) and score of 2 or less on the suicide item of HDRS  were recruited after screening by the researcher Naveen GH and a psychiatry resident (Mukund G. Rao. Patients were aged between 18 and 55 years. A psychiatrist made clinical diagnosis of depressive disorder using the mini international neuropsychiatric interview (MINI);  a psychiatry resident trainee also reached a Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) diagnosis of depressive disorder in these patients.  Out of the 137 patients, 101 were medication-naïve and 36 were medication-free for at least 1 month. Patients with mental retardation, substance abuse disorders (except nicotine and caffeine), organic disorders such as dementia, epilepsy or cerebrovascular accidents, history suggestive of psychosis or bipolar disorder, or having suicidal risk or catatonia were excluded from the study. None had received yoga as treatment before. Patients did not have any indications for electroconvulsive therapy (i.e., catatonia/severe depression). Written informed consent to take part in the study was obtained. The study was approved by the Institutional Ethics Committee. The option of yoga therapy, either alone or in combination with medication or medication alone, was offered to patients. There were three naturalistic groups of patients: Medication-alone (n=78); yoga therapy-alone (n=23) and medications + yoga therapy (n=36). The duration of the follow up was 12 weeks.
Yoga therapy module
The construction and description of the yoga module is described separately elsewhere.  The module is available on request with the authors.
The participants of the yoga + antidepressant therapy and yoga therapy-alone groups were requested to come daily for a period of 10 days to the National Institute of Mental Health and Neurosciences, where a yoga professional taught them the yoga practices. Each session of training/practice lasted 1 hour. The participants were then asked to come to perform yoga in the yoga therapy center once a week for the next 2 weeks. The subjects were instructed to continue yoga at home thereafter, but attend one booster training session in the yoga therapy center at the end of the next 2 months. Home practices were monitored by a family member. They were also instructed to maintain a register to document the duration of each day's yoga at home.
During 3 months of the study period, the patients on antidepressant medications received consultation with their respective psychiatry consultants. The antidepressant type and dose were chosen by these consultants. This treatment remained unchanged in nearly all patients. Antidepressants administered were escitalopram (10-15 mg/day), fluoxetine (20-40 mg/day), duloxetine (60 mg/day), sertraline (50-100 mg/day), amitriptyline (25-100 mg/day) and mirtazapine (7.5-15 mg/day).
The researcher had a telephonic conversation with all the subjects at different time points during the 3 months of treatment to encourage compliance to medication/yoga practice.
A rater trained in psychiatry for 18 months and blind to the group status of the patients (psychiatry resident) rated the severity of depression using the HDRS and clinical global impression (CGI) (baseline and 3 months thereafter). 
Assessment of neurotrophin levels (At baseline and at 12 weeks): Venous blood was sampled between 8:30 am and 11 am before breakfast at baseline and 12 weeks thereafter. The sample was allowed to clot and the serum was separated within 30 min. Coded serum samples were stored at −80°C. The BDNF assay was performed in batches within a period of 3 months from the beginning of the sample collections. Analysis was performed with the help of biochemist using the enzyme-linked immunosorbent assay with commercial kits (Ray Biotech Inc.,Wembley, Middlesex, UK) according to the manufacturer's instructions. The intra- and inter-assay coefficient of variations was 1.34% and 4.34%, respectively.
The sample for statistical analysis consisted of only those who had both clinical (HDRS and CGI) and BDNF data at baseline and after 3 months (12 weeks). The demographic and baseline clinical profile were compared between three groups using Chi-square test and analysis of variance. Two-way repeated-measures analysis of variance (RMANOVA) was used to examine the change in HDRS, CGI and BDNF over two assessments. Pearson's correlation coefficient was computed to examine the relations between fall in HDRS (pre - post) and rise in BDNF (post - pre). For significance, alpha was fixed at P<0.05.
| Results|| |
Only 62 patients were available for assessments at the time points required for this study (yoga-alone=19; yoga with medications=22; only medications=21). The three groups were not different with respect to baseline socio-demographic details, illness and other parameters except education; patients choosing yoga had higher education [Table 1].
There was a significant drop in depression scores over time across all groups ([Table 2]; RMANOVA occasion effect: F=271.7; df=1, 59; P<0.001); patients receiving yoga therapy had greater improvement than those receiving medications only (group effect: F=5.7; df=2, 59; P=0.005; group X occasion interaction effect: F=6.2; df=2, 59; P=0.004). CGI severity score showed similar results (occasion effect: F=369.6; df=1, 59; P<0.001; group effect: F=12.4; df=2, 59; P<0.001; group X occasion effect: F=10.5; df=2, 59; P<0.001). With respect to serum BDNF levels, the occasion effect (F=4.5; df=1, 59; P=0.039) and group effect (F=4.1; df=2, 59; P=0.02) were significant; group X occasion effect was, however, not significant (F=0.14; df=2, 59; P=0.87).
|Table 2: Outcome variables at baseline and at 3-months across the three groups|
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In the total sample, drop in HDRS and rise in BDNF were not correlated (r=0.1, P=0.5). The correlation was not significant in medication only (r=−0.15; P=0.5) as well as in medication plus yoga (r=−0.11; P=0.62) groups. However, in the yoga-only group, there was a high correlation between the decline in HDRS and rise in BDNF levels (r=0.7, P=0.001).
| Discussion|| |
Our study showed that there was a significant reduction in HDRS scores at follow-up in patients with depression in all three groups. Patients receiving yoga with or without anti-depressants had a greater reduction in depression scores than antidepressant alone. A previous study had reported Sudarshan Kriya Yoga to have equivalent antidepressant efficacy to imipramine.  The remission rate in our study was 59.9% and previous studies have shown rates ranging from 23.52% to 100%. ,,,,,,, There was a significant increase in BDNF levels at follow-up as indicated by significant within subject occasion effect. However, there was no occasion X group interaction, suggesting that the change in BDNF was not different across the three groups.
In the entire group, there was no correlation between change in BDNF levels and that in HDRS scores. This is consistent with studies, ,,, which have examined this issue earlier. There was a significant positive correlation between change (reduction) in HDRS and change (rise) in serum BDNF levels in yoga-only group (r=0.7; P=0.001). This was not so in those receiving antidepressants (either with or without yoga). Antidepressant medications may have a direct influence on serum BDNF levels, ,,, thus confounding the relationship between change in depression score and that in BDNF levels. This confound was absent in yoga-only group. It may be noted that dose and type of antidepressant were not controlled. It is possible that the finding of such a correlation in the yoga-only group could be related to the absence of the medication confound. Yoga may have different biological mechanisms that operate on both antidepressant and BDNF elevation pathways. Stress reduction mechanisms, by way of quieting the hypothalamic-pituitary-adrenal (HPA) axis, may be particularly relevant to the effect of yoga in reducing depression. This is a first study, which looked at the changes in serum BDNF levels after yoga.
We used a yoga-therapy module rigorously validated for use in patients with depression. Patients with suicidal risk were not recruited due to ethical reasons. None of the patients except two received any other form of intervention that could have altered the depression outcome, such as supportive therapy/cognitive behavior therapy. The raters being blind to the allocation status of the patients avoided any possible bias in the assessments. We used a standardized diagnostic tool, the MINI  to diagnose depressive disorder. Further, antidepressant drugs and dosages used in this study are according to the standard treatment algorithms.  Assessment of serum BDNF level was performed by a biochemist who was blind to the treatment status of the patients. Standard procedure was followed to collect and store the serum samples. It is known that BDNF being a small peptide is sensitive to climatic changes; BDNF concentrations are also related to platelet BDNF release. 
Non-random allocation to treatment groups is a major limitation of this study. The three groups were not different with respect to baseline socio-demographic details, illness and other parameters. Hence, the possibility of bias due to baseline differences is small. Nevertheless, we cannot rule out the possibility of differences in unmeasured variables influencing the outcome measures. The dropout rate from the study is substantial (close to 50%). This is not surprising as patients were not severely depressed; yoga practice too has several barriers leading to attrition.  A few other limitations are worth mentioning. This study had a single-blind design where the rater was blind to the treatment status of the patients, but the latter were aware about their treatments. Hence, we cannot rule out the possibility of awareness about the treatment having an influence on the outcome. Theoretically, use of "placebo-yoga" could have resulted in unbiased assessment of the outcome measures. However, "placebo-yoga" is not possible because, the general public is aware of yoga techniques in India. Hence, placebo-arm and double-blind design pose a challenge in yoga research.  Further, attrition rate was about 35.76%. This is a problem associated with such studies in depression: Dropout percentages in earlier studies have ranged from 13% to 55%. ,,,,,
The interactions of BDNF with serotonergic systems, HPA axis and other biological markers have been extensively studied. , An important issue is whether serum BDNF levels are related to brain BDNF levels. It may be noted that BDNF crosses blood brain barrier and hence serum BDNF reliably reflects brain BDNF concentrations.  Pre-clinical studies in rats have shown a positive correlation between serum and cortical levels.  Future studies could look to explore the relation between serum BDNF levels and cerebrospinal fluid BDNF levels in patients with depression. Association between BDNF levels and volumetric changes in the hippocampus may be worth exploring as it is evident that patients with depression have decreased hippocampus volume. 
Though significant statistically, the magnitude of BDNF change detected in this sample was small. Furthermore, the differences obtained in therapeutic effects by the interventions were not seen in the BDNF responses. This leads to a suspicion if the two are related at all. The only argument in this favor comes from the observed direct correlation of antidepressant effects and BDNF elevating effects in the yoga-alone group. This calls for more research. Alternative tropic mechanisms such as changes in the vascular endothelial growth factor levels , in the serum deserve examination.
In summary, yoga alone produced substantial antidepressant effects that correlated with the elevation serum BDNF levels. The findings argue for a neuroplastic mechanism of antidepressant action for yoga. The limitations of the study weaken this argument and point the need to investigate other tropic mechanisms.
| Acknowledgments|| |
We thank Mr. Sushrutha and Mr. Bhagath of Swami Vivekananda Yoga Anusandhana Samsthana for their help with transliteration.
| References|| |
|1.||Ruhé HG, Mason NS, Schene AH. Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: A meta-analysis of monoamine depletion studies. Mol Psychiatry 2007;12:331-59. |
|2.||Leonard BE. Evidence for a biochemical lesion in depression. J Clin Psychiatry 2000;61 Suppl 6:12-7. |
|3.||Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27. |
|4.||Calabrese F, Molteni R, Racagni G, Riva MA. Neuronal plasticity: A link between stress and mood disorders. Psychoneuroendocrinology 2009;34 Suppl 1:S208-16. |
|5.||Allen SJ, Dawbarn D. Clinical relevance of the neurotrophins and their receptors. Clin Sci (Lond) 2006;110:175-91. |
|6.||Beyer JL, Krishnan KR. Volumetric brain imaging findings in mood disorders. Bipolar Disord 2002;4:89-104. |
|7.||Schmidt HD, Duman RS. The role of neurotrophic factors in adult hippocampal neurogenesis, antidepressant treatments and animal models of depressive-like behavior. Behav Pharmacol 2007;18:391-418. |
|8.||Aydemir O, Deveci A, Taskin OE, Taneli F, Esen-Danaci A. Serum brain-derived neurotrophic factor level in dysthymia: A comparative study with major depressive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2007;31:1023-6. |
|9.||Karege F, Bondolfi G, Gervasoni N, Schwald M, Aubry JM, Bertschy G. Low brain-derived neurotrophic factor (BDNF) levels in serum of depressed patients probably results from lowered platelet BDNF release unrelated to platelet reactivity. Biol Psychiatry 2005;57:1068-72. |
|10.||Aydemir O, Deveci A, Taneli F. The effect of chronic antidepressant treatment on serum brain-derived neurotrophic factor levels in depressed patients: A preliminary study. Prog Neuropsychopharmacol Biol Psychiatry 2005;29:261-5. |
|11.||Huang TL, Lee CT, Liu YL. Serum brain-derived neurotrophic factor levels in patients with major depression: Effects of antidepressants. J Psychiatr Res 2008;42:521-5. |
|12.||Matrisciano F, Bonaccorso S, Ricciardi A, Scaccianoce S, Panaccione I, Wang L, et al. Changes in BDNF serum levels in patients with major depression disorder (MDD) after 6 months treatment with sertraline, escitalopram, or venlafaxine. J Psychiatr Res 2009;43:247-54. |
|13.||Eker C, Kitis O, Taneli F, Eker OD, Ozan E, Yucel K, et al. Correlation of serum BDNF levels with hippocampal volumes in first episode, medication-free depressed patients. Eur Arch Psychiatry Clin Neurosci 2010;260:527-33. |
|14.||Pittenger C, Duman RS. Stress, depression, and neuroplasticity: A convergence of mechanisms. Neuropsychopharmacology 2008;33:88-109. |
|15.||Greenberg PE, Stiglin LE, Finkelstein SN, Berndt ER. The economic burden of depression in 1990. J Clin Psychiatry 1993;54:405-18. |
|16.||Pilkington K, Kirkwood G, Rampes H, Richardson J. Yoga for depression: The research evidence. J Affect Disord 2005;89:13-24. |
|17.||Uebelacker LA, Epstein-Lubow G, Gaudiano BA, Tremont G, Battle CL, Miller IW. Hatha yoga for depression: Critical review of the evidence for efficacy, plausible mechanisms of action, and directions for future research. J Psychiatr Pract 2010;16:22-33. |
|18.||Janakiramaiah N, Gangadhar BN, Murthy PJ, Harish MG, Subbakrishna DK, Vedamurthachar A. Antidepressant efficacy of Sudarshan Kriya Yoga (SKY) in melancholia: A randomized comparison with electroconvulsive therapy (ECT) and imipramine. J Affect Disord 2000;57:255-9. |
|19.||Shapiro D, Cook IA, Davydov DM, Ottaviani C, Leuchter AF, Abrams M. Yoga as a complementary treatment of depression: Effects of traits and moods on treatment outcome. Evid Based Complement Alternat Med 2007;4:493-502. |
|20.||Sharma VK, Das S, Mondal S, Goswami U, Gandhi A. Effect of Sahaj Yoga on neuro-cognitive functions in patients suffering from major depression. Indian J Physiol Pharmacol 2006;50:375-83. |
|21.||Streeter CC, Jensen JE, Perlmutter RM, Cabral HJ, Tian H, Terhune DB, et al. Yoga Asana sessions increase brain GABA levels: A pilot study. J Altern Complement Med 2007;13:419-26. |
|22.||Manjunath NK, Telles S. Spatial and verbal memory test scores following yoga and fine arts camps for school children. Indian J Physiol Pharmacol 2004;48:353-6. |
|23.||Gangadhar BN, Naveen GH, Rao MG, Thirthalli J, Varambally S. Positive antidepressant effects of generic yoga in depressive out-patients: A comparative study. Indian J Psychiatry 2013;55:S369-73. |
|24.||Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry 1960;23:56-62. |
|25.||Sheehan DV, Lecrubier Y, Sheehan KH, Amorim P, Janavs J, Weiller E, et al. The Mini-International Neuropsychiatric Interview (M.I.N.I.): The development and validation of a structured diagnostic psychiatric interview for DSM-IV and ICD-10. J Clin Psychiatry 1998;59 Suppl 20:22-33. |
|26.||American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4 th ed., (Text Revision). Washington, DC: American Psychiatric Association; 2000. |
|27.||Naveen GH, Rao MG, Vishal V, Thirthalli J, Varambally S, Gangadhar BN. Development and feasibility of yoga therapy module for out-patients with depression in India. Indian J Psychiatry 2013;55:S350-6. |
|28.||Guy W. ECDEU assessment manual for psychopharmacology. National Institute of Mental Health, Rockville (MD); 1976:218-22. |
|29.||Butler LD, Waelde LC, Hastings TA, Chen XH, Symons B, Marshall J, et al. Meditation with yoga, group therapy with hypnosis, and psychoeducation for long-term depressed mood: A randomized pilot trial. J Clin Psychol 2008;64:806-20. |
|30.||Gonul AS, Akdeniz F, Taneli F, Donat O, Eker C, Vahip S. Effect of treatment on serum brain-derived neurotrophic factor levels in depressed patients. Eur Arch Psychiatry Clin Neurosci 2005;255:381-6. |
|31.||Shimizu E, Hashimoto K, Okamura N, Koike K, Komatsu N, Kumakiri C, et al. Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants. Biol Psychiatry 2003;54:70-5. |
|32.||Yoshimura R, Mitoma M, Sugita A, Hori H, Okamoto T, Umene W, et al. Effects of paroxetine or milnacipran on serum brain-derived neurotrophic factor in depressed patients. Prog Neuropsychopharmacol Biol Psychiatry 2007;31:1034-7. |
|33.||Gervasoni N, Aubry JM, Bondolfi G, Osiek C, Schwald M, Bertschy G, et al. Partial normalization of serum brain-derived neurotrophic factor in remitted patients after a major depressive episode. Neuropsychobiology 2005;51:234-8. |
|34.||Anderson IM, Nutt DJ, Deakin JF. Evidence-based guidelines for treating depressive disorders with antidepressants: A revision of the 1993 British Association for Psychopharmacology guidelines. British Association for Psychopharmacology. J Psychopharmacol 2000;14:3-20. |
|35.||Baspure S, Jagannathan A, Kumar S, Varambally S, Thirthalli J, Venkatasubramanain G, et al. Barriers to yoga therapy as an add-on treatment for schizophrenia in India. Int J Yoga 2012;5:70-3. |
|36.||Gangadhar B, Varambally S. Yoga as therapy in psychiatric disorders: Past, present, and future. Biofeedback 2011;39:60-3. |
|37.||Block W, Träber F, von Widdern O, Metten M, Schild H, Maier W, et al. Proton MR spectroscopy of the hippocampus at 3 T in patients with unipolar major depressive disorder: Correlates and predictors of treatment response. Int J Neuropsychopharmacol 2009;12:415-22. |
|38.||Piccinni A, Marazziti D, Catena M, Domenici L, Del Debbio A, Bianchi C, et al. Plasma and serum brain-derived neurotrophic factor (BDNF) in depressed patients during 1 year of antidepressant treatments. J Affect Disord 2008;105:279-83. |
|39.||Woolery A, Myers H, Sternlieb B, Zeltzer L. A yoga intervention for young adults with elevated symptoms of depression. Altern Ther Health Med 2004;10:60-3. |
|40.||Manji HK, Quiroz JA, Sporn J, Payne JL, Denicoff K, A Gray N, et al. Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for difficult-to-treat depression. Biol Psychiatry 2003;53:707-42. |
|41.||Ren-Patterson RF, Cochran LW, Holmes A, Sherrill S, Huang SJ, Tolliver T, et al. Loss of brain-derived neurotrophic factor gene allele exacerbates brain monoamine deficiencies and increases stress abnormalities of serotonin transporter knockout mice. J Neurosci Res 2005;79:756-71. |
|42.||Pan W, Banks WA, Fasold MB, Bluth J, Kastin AJ. Transport of brain-derived neurotrophic factor across the blood-brain barrier. Neuropharmacology 1998;37:1553-61. |
|43.||Karege F, Perret G, Bondolfi G, Schwald M, Bertschy G, Aubry JM. Decreased serum brain-derived neurotrophic factor levels in major depressed patients. Psychiatry Res 2002;109:143-8. |
|44.||Videbech P, Ravnkilde B. Hippocampal volume and depression: A meta-analysis of MRI studies. Am J Psychiatry 2004;161:1957-66. |
|45.||Halmai Z, Dome P, Dobos J, Gonda X, Szekely A, Sasvari-Szekely M, et al. Peripheral vascular endothelial growth factor level is associated with antidepressant treatment response: Results of a preliminary study. J Affect Disord 2013;144:269-73. |
|46.||Ibrahim L, Duncan W, Luckenbaugh DA, Yuan P, Machado-Vieira R, Zarate CA Jr. Rapid antidepressant changes with sleep deprivation in major depressive disorder are associated with changes in vascular endothelial growth factor (VEGF): A pilot study. Brain Res Bull 2011;86:129-33. |
National Institute of Mental Health and Neurosciences, Bangalore, Karnataka
Source of Support: The research was done under the Advanced Centre for Yoga - Mental Health and Neurosciences, a collaborative centre of NIMHANS and the Morarji Desai Institute of Yoga, New Delhi, Conflict of Interest: None
[Table 1], [Table 2]
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