Childbirth Pain and Post-Partum Depression: Does Labor Epidural Analgesia Decrease This Risk?

Post-partum depression (PPD) is a common complication of pregnancy worldwide with a prevalence as high as 15% in some countries. Pain has been identified as a risk factor for major depression; however, the relationship between labor-related pain and PPD is less understood. This article sought out to examine the relationship between pain and PPD, examining whether there is a correlation that reducing pain through epidural analgesia can lower the risk for PPD. A PubMed database search was performed using the keywords "post-partum depression" and "labor epidural". Multiple articles including 2 meta-analyses were evaluated for the association between post-partum depression and epidural analgesia for labor. Although there is evidence supporting labor epidural analgesia reducing PPD, many studies including the meta-analyses did not uphold the hypothesis. More well-designed studies on this topic need to be investigated in order to substantiate the current evidence in the literature.

Short duration of marriage at conception as an independent risk factor for schizophrenia.

Short duration of marriage (DoM) is a risk factor for preeclampsia that is also related to the risk for schizophrenia. This analysis examined the risk for schizophrenia associated with DoM and its independence from parental psychiatric disorders, parental ages and fathers' age at marriage. METHOD: Relative Risks (RR) for schizophrenia were estimated using continuous and stratified Cox proportional hazards models in the 90,079 offspring from the prospective population-based Jerusalem birth cohort study (1964-1976). Schizophrenia diagnos in offspring and parental diagnoses of schizophrenia or other psychiatric conditions were identified by cross-linkage to Israel's psychiatric case registry. DoM and paternal age at marriage were abstracted from birth certificates. RESULTS: In the full model, RR for schizophrenia decreased for each 5 years DoM: 0.83 (0.75-0.95), ptrend = 0.0015. Stratified analyses showed the greatest RR risk for DoM <2 years: 1.53 (1.11-1.66) with lesser risk for 2-4 years DoM: 1.38 (1.05-1.81) compared to more DOM of 10+ years. DoM effects were independent from parental psychiatric diagnoses (RRs = 2-6, p~0.00001), paternal age (1.34: p = 0.0001 /5 years- including fathers of 25-34 years). The apparent risk related to later fathers' age at marriage (1.27: p < 0.0001) was eliminated in after accounting for DoM and later paternal age. CONCLUSIONS: Offspring born to couples married for less than 3 years, across all paternal ages, harbored a small increased risk for schizophrenia, which was independent of parental psychiatric disorders and paternal age. Fathers who married late had particularly short DoM, which, along with paternal age, completely explained the risks related to later paternal age at marriage. Further studies are needed to replicate these results and examine if pathogenic pathways include prenatal immune activation.

Parental age effects on odor sensitivity in healthy subjects and schizophrenia patients.

A schizophrenia phenotype for paternal and maternal age effects on illness risk could benefit etiological research. As odor sensitivity is associated with variability in symptoms and cognition in schizophrenia, we examined if it was related to parental ages in patients and healthy controls. We tested Leukocyte Telomere Length (LTL) as an explanatory factor, as LTL is associated with paternal age and schizophrenia risk. Seventy-five DSM-IV patients and 46 controls were assessed for detection of PEA, WAIS-III for cognition, and LTL, assessed by qPCR. In healthy controls, but not schizophrenia patients, decreasing sensitivity was monotonically related to advancing parental ages, particularly in sons. The relationships between parental aging and odor sensitivity differed significantly for patients and controls (Fisher's R to Z: χ(2) = 6.95, P = 0.009). The groups also differed in the association of odor sensitivity with cognition; lesser sensitivity robustly predicted cognitive impairments in patients (<0.001), but these were unassociated in controls. LTL was unrelated to odor sensitivity and did not explain the association of lesser sensitivity with cognitive deficits.Parental aging predicted less sensitive detection in healthy subjects but not in schizophrenia patients. In patients, decreased odor sensitivity strongly predicted cognitive deficits, whereas more sensitive acuity was associated with older parents. These data support separate risk pathways for schizophrenia. A parental age-related pathway may produce psychosis without impairing cognition and odor sensitivity. Diminished odor sensitivity may furthermore be useful as a biomarker for research and treatment studies in schizophrenia. © 2015 Wiley Periodicals, Inc.

Paternal age and mental health of offspring.

The influence of paternal age on the risk for sporadic forms of Mendelian disorders is well known, but a burgeoning recent literature demonstrates, in addition, a paternal age effect for complex neuropsychiatric conditions, including schizophrenia, autism, bipolar disorder, and even for learning potential, expressed as intelligence. Mental illness is costly to patients, their family, and the public health system, accounting for the largest portion of disability costs in our economy. The delayed onset of neuropsychiatric conditions and lack of physical manifestations at birth are common frequencies in the population that have obscured the recognition that a portion of the risks for mental conditions is associated with paternal age. Identification of these risk pathways may be leveraged for knowledge about mental function and for future screening tests. However, only a small minority of at-risk offspring are likely to have such a psychiatric or learning disorder attributable to paternal age, including the children of older fathers.