Postpartum Depression in Kinshasa (DR Congo): Prevalence and Risk Factors.

Postpartum depression in Kinshasa (DR Congo): prevalence and risk factors.

Filed under: Depression Treatment

Med Sante Trop. 2013 Feb 7;
Imbula Essam B, Okitundu Luwa EA, Mampunza Ma-Miezi S

Objective. To identify the frequency, risk factors, and clinical forms of postpartum depression (PPD) in Kinshasa. Methods. In a cross-sectional study in well-baby clinics in Kinshasa in 2009, 120 mothers of 61 boys and 59 girls aged 1-10 months agreed to participate in the study. Their mean age was 28.4 ± 12.2 years. The Edinburgh Postnatal Depression Scale, the Goldberg Scales of Anxiety and Depression and the DSM-IV Criteria were used to detect PPD. Results. The numbers and percentage (95% CI) of women with PPD was 61/120, 50.8% (41.9-59.7) according to the Edinburgh scale and 53/120, 44.2% (35.3-3.1) according to the Goldberg scale. The DSM-IV criteria confirmed clinical forms with a frequency of 31/120, 25.8% (18.0-36.6); 22 (70.6%) of these had anxiety according to the Goldberg Scale (p<0.001). In the bivariate analysis, PPD defined by DSM IV was more common in mothers whose child was in poor health (11/25, 44.0% (p<0.002)), who were especially young (<20 years) 8/12, 66.7% (p = 0.044), who had felt no happiness on learning she was pregnant (23/74, 31.1% (p = 0.096)), who practiced non-exclusive breastfeeding the first 6 months (5/12, 41.7% (p>0.05)), or who belonged to an evangelical Protestant church (20/65, 30.8% (p>0.05)). Conclusion. In this study, PPD was common, and anxiety the predominant clinical form. The risk factors reported indicated the role of psychosocial stress in PPD. PPD is a public health problem often overlooked in primary health care.
HubMed – depression

 

Comparison of phenelzine and geometric isomers of its active metabolite, ?-phenylethylidenehydrazine, on rat brain levels of amino acids, biogenic amine neurotransmitters and methylamine.

Filed under: Depression Treatment

J Neural Transm. 2013 Feb 8;
Matveychuk D, Nunes E, Ullah N, Velázquez-Martinez CA, Mackenzie EM, Baker GB

Phenelzine is a monoamine oxidase (MAO) inhibitor used in treatment of depression and anxiety disorders. It also elevates brain levels of ?-aminobutyric acid (GABA) and inhibits primary amine oxidase (PrAO), an enzyme whose activity and/or expression has been reported to be increased in diabetes mellitus, Alzheimer’s disease and cardiovascular disorders. Phenelzine is not only an inhibitor of, but also a substrate for, MAO and it has been suggested that an active metabolite, namely ?-phenylethylidenehydrazine (PEH), is responsible for phenelzine’s effects on amino acids. PEH is also a strong inhibitor of PrAO but has weak effects on MAO. PEH has a double bond and can thus exist as (E)- and (Z)-geometric isomers, but to date the two isomers have not been compared with regard to their neurochemical effects. We have investigated the effects of phenelzine, (E)- and (Z)-PEH on rat whole brain levels of amino acids, biogenic amine neurotransmitters and methylamine (an endogenous substrate of PrAO). Under the conditions used in the study, (E)- and (Z)-PEH appear to be equivalent in their neurochemical properties. Both PEH isomers and phenelzine produced marked increases in rat brain levels of GABA and alanine while decreasing brain levels of glutamine. Phenelzine increased brain levels of biogenic amine neurotransmitters (noradrenaline, dopamine and serotonin), whereas neither PEH isomer altered levels of these neurotransmitters to a considerable extent. All three drugs significantly increased rat brain levels of methylamine, with (E)- and (Z)-PEH causing a greater increase than phenelzine. These results are discussed in relation to the possible therapeutic applications of these drugs.
HubMed – depression

 

Downregulation of Serotonergic Gene Expression in the Raphe Nuclei of the Midbrain Under Chronic Social Defeat Stress in Male Mice.

Filed under: Depression Treatment

Mol Neurobiol. 2013 Feb 8;
Boyarskikh UA, Bondar NP, Filipenko ML, Kudryavtseva NN

There is ample experimental evidence supporting the hypothesis that the brain serotonergic system is involved in the control of chronic social defeat stress (CSDS), depression, and anxiety. The study aimed to analyze mRNA levels of the serotonergic genes in the raphe nuclei of midbrain that may be associated with chronic social defeats consistently shown by male mice in special experimental settings. The serotonergic genes were the Tph2, Sert, Maoa, and Htr1a. The Bdnf and Creb genes were also studied. The experimental groups were composed of male mice with experience of defeats in 21 daily encounters and male mice with the same track record of defeats followed by a no-defeat period without agonistic interactions (relative rest for 14 days). It has been shown that mRNA levels of the Tph2, Maoa, Sert, Htr1a, Bdnf, and Creb genes in the raphe nuclei of defeated mice are decreased as compared with the controls. The expression of the serotonergic genes as well as the Creb gene is not restored to the control level after the 2 weeks of relative rest. mRNA levels of Bdnf gene are not recovered to the control levels, although some upregulation was observed in rested losers. CSDS experience inducing the development of mixed anxiety/depression-like state in male mice downregulates the expression of serotonergic genes associated with the synthesis, inactivation, and reception of serotonin. The Bdnf and Creb genes in the midbrain raphe nuclei are also downregulated under CSDS. Period of relative rest is not enough for most serotonergic genes to recover expression to the control levels.
HubMed – depression

 


 

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