MOOD DISORDERS

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36 Mood Disorders control. The pharmacologic trials were also small, mostly under 100 patients enrolled. The small numbers of patients enrolled in both psychotherapy and pharmacologic efficacy trials limits the generalizability of the findings. Study N (completers), Lustman et al., 1997b Lustman et al., 2000 diabetes type, mean age Intervention conditions, follow-up (FU) N=28, type 2-50% nortriptyline vs 49-49,2ys placebo,FU- 9 ws N=54,type 2- 56% fluoxetine vs 45-47ys Paile-Hyvärinen et N=13, type al., 2003 2-100%, 61-62ys placebo, FU- 8 ws paroxetine vs placebo, FU- 4ws Xue et al., 2004 N=48, type 2-85%, paroxetine vs Gülseren et al., 2005 Lustman et al., 2006 21-65ys N=23, type 2- 100%, 58ys N=152, type 2- 65%, N/A Paile-Hyvärinen et N=49, type 2- al., 2007 100%, 59ys placebo fluoxetine vs paroxetine sertraline (flexible doses) vs placebo paroxetine vs placebo Outcome assessment (depression, diabetes Effect size Depression: BDI (p=0.03), DM: HbA1c, Depression: Δ n.s., no outcome reported Depression: HAMD (p
Scale Groups SSRI´s/SNRI´s N Mean Beck Anxiety Inventory - baseline SSRI/SNRI 38/36 23,29/ 24,14 Beck Anxiety Inventory - final SSRI/SNRI 38/36 15,18*/16,50* Zung Depression Inventory- SDS- baseline Zung Depression inventory – final SSRI/ SNRI 38/36 67,26/ 66,83 SSRI/SNRI 38/36 49,39*/ 52,44* I MADRS baseline SSRI/SNRI 38/36 37,21/ 36,89 MADRS final 1 SSRI/SNRI 38/ 36 16,95*/ 17,89* BMI baseline SSRI/SNRI 38/ 36 25,54/ 26,76 BMI final SSRI/SNRI 38/ 36 26,22/ 27,1 * the mean difference is significant at the,05 level Table 5. Score in some scales Depression and Glucose Metabolism (Diabetes Mellitus) http://dx.doi.org/10.5772/53467 In both groups dominated by women (three times) – 27/9 (SSRI´s group); 28/10 (SNRI´s group) and on the other hand, less presumptive SNRI medication type were deployed glob‐ ally in patients with a higher mean age (SNRI´s = 52,7/28-73/; SSRI´s = 41,7 /20-64/). There was an improvement in the scales in both groups: MADRS, Beck Anxiety Inventory, Zung Depression Scale (s. f., table 5). Similar, the results in study Songar et al. (1993) indicate that some relations exist between anxiety and the worsening of metabolic control (mainly in HbA1c). The HDL cholesterol values have improved after six months antidepressive treat‐ ment in both groups (1.31 vs 1.4 /SNRI´s/ 1.38 vs 1.5 /SSRI´s/), which corresponds to the data Svačina et al. (2006) and Hardy et al. (2007). These findings are particularly important be‐ cause from this one that is most closely connected with cardiovascular risks play mainly LDL and HDL components. The triglycerides values have improved statistical significant af‐ ter six months SSRI treatment vs SNRI treatment (Mann-Whitney U=496,000 Asymp. Sig. (2tailed)=0.042 = p≤0.05), which correlates with the monitoring Flechtner-Mors (2008) also in SSRI preparations, which is important from the point of view that higher levels of triglycer‐ ides are considered primary in the aetiology of disorders that are related to oxidative stress and increased levels of LDL. As we expected, HbA1c improved in the SNRI´s (5.55 vs 5.24, n. s.) and SSRI´s group (5.23 vs 5.18, n. s.) which corresponds with the results of several pharmacological studies (Lustman et al., 1997b, 2006; Gülseren et al., 2005). On the other hand can not draw definite causal conclusions regarding the limitations on file size and es‐ pecially the length of the monitoring itself. We confirmed the hypothesis that SSRI´s and SNRI´s do not deteriorate metabolic parameters – HDL, LDL, triglycerides, HbA1c, BMI, even HbA1c will be decrease (n. s.), HDL will be increase (n. s.), triglycerides were im‐ 37
Page 1 and 2: MOOD DISORDERS Edited by Neşe Koca
Page 3: free online editions of InTech Book
Page 6 and 7: VI Contents Chapter 8 Mood Disorder
Page 9 and 10: Chapter 1 Murine Models for Develop
Page 11 and 12: Murine Models for Developping an In
Page 31 and 32: Chapter 2 Depression and Glucose Me
Page 33 and 34: 2.2. Clinical symptoms Depression i
Page 35 and 36: al., 2011, in a group of more than
Page 37 and 38: Depression and Glucose Metabolism (
Page 39 and 40: psychosocial factors which associat
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Page 55 and 56: Depression: Classification, Culture
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86 Mood Disorders and correctly und
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88 Mood Disorders Therapist: “Ima
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90 Mood Disorders 1. Analysis of be
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92 Mood Disorders [7] Wittchen, H.-
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94 Mood Disorders [36] Hollon, S.D.
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96 Mood Disorders [68] Yorbik, O.,
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98 Mood Disorders [103] Lindsley, D
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Mitochondrial Functions in Mood Dis
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Genetic defects or stress can cause
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Figure 2. Representation of process
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ain. Normally the H 2O 2 is then in
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ADP level State 1 Low State 2 High
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2.3.2. Uncoupling proteins Uncoupli
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Complex IV inhibitors KCN and sodiu
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pathogenesis of axonal degeneration
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3.3. Inflammatory and neurodegenera
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plete data exist on the effect of p
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4.3. Effects of mood stabilizers on
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Antidepressant Biological model Aff
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Mood stabilizer Biological model Af
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Long-Term Adaptive Changes Induced
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5-HT 1B/1D (-) SERT 5-HT 1A (-) [5-
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postsynaptic 5-HT 1A receptors in t
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3.3. Neurotrophins modulation by 5-
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BDNF levels before treatment, and a
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References Long-Term Adaptive Chang
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Biological Markers and Genetic Fact
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Collectively, serotonin receptor, T
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imaging and genetics have been emer
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198 Mood Disorders pressed. Already
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200 Mood Disorders cy may takes its
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202 Mood Disorders of the developin
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204 Mood Disorders 2.2.1. Touch and
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206 Mood Disorders found by Jung et
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208 Mood Disorders mize the risk of
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210 Mood Disorders [20] Misri S, Ko
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212 Mood Disorders [49] Melley M, C
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214 Mood Disorders [78] Rahman A, I
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216 Mood Disorders [106] Taylor A,
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218 Mood Disorders [134] Esquivel-S
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Cognitive Functions in Euthymic Bip
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4. Discussion 4.1. Cognitive functi
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poor functional outcome. Executive
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References Cognitive Functions in E
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242 Mood Disorders Figure 1. 2. Fat
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244 Mood Disorders 3.1. The role of
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246 Mood Disorders dylserine is syn
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248 Mood Disorders and 42 (Aβ 42)
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250 Mood Disorders about omega-3 fa
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252 Mood Disorders First, DHA compe
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254 Mood Disorders tained from the
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256 Mood Disorders [11] Salem, N.,
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258 Mood Disorders bind to retinoid
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260 Mood Disorders [67] Yao, J. K.,
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Chapter 11 Neuronal Insulin Recepto
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Neuronal Insulin Receptor Signaling
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involved in the various cognitive a
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