Mood lability among offspring of parents with bipolar disorder and community controls

Abstract

Objectives Early identification of bipolar disorder (BP) symptomatology is crucial for improving the prognosis of this illness. Increased mood lability has been reported in BP. However, mood lability is ubiquitous across psychiatric disorders and may be a marker of severe psychopathology and not specific to BP. To clarify this issue, this study examined the prevalence of mood lability and its components in offspring of BP parents and offspring of community control parents recruited through the Pittsburgh Bipolar Offspring Study. Methods Forty-one school-age BP offspring of 38 BP parents, 257 healthy or non-BP offspring of 174 BP parents, and 192 offspring of 117 control parents completed a scale that was developed to evaluate mood lability in youth, i.e., the Children’s Affective Lability Scale (CALS). Results A factor analysis of the parental CALS, and in part the child CALS, revealed Irritability, Mania, and Anxiety/Depression factors, with most of the variance explained by the Irritability factor. After adjusting for confounding factors (e.g., parental and offspring non-BP psychopathology), BP offspring of BP parents showed the highest parental and child total and factor scores, followed by the non-BP offspring of BP parents, and then the offspring of the controls. Conclusions Mood lability overall and mania-like, anxious/depressed, and particularly irritability symptoms may be a prodromal phenotype of BP among offspring of parents with BP. Prospective studies are warranted to clarify whether these symptoms will predict the development of BP and/or other psychopathology. If confirmed, these symptoms may become a target of treatment and biological studies before BP develops.

Descripción de perfiles psicopatológicos y neurocognitivos de hijos de pacientes con trastorno bipolar tipo I dentro un programa de intervencion multimodal: PRISMA

“…Estos síntomas estaban presentes incluso desde la etapa escolar. En cuanto a las manifestaciones subumbrales o prodró-micas de síntomas afectivos de inicio temprano, nuestros hallazgos son congruentes con lo reportado en estudios previos [36][37][38] . Algunos autores mencionan que el riesgo elevado de trastornos del ánimo es atribuible a las subformas más leves, que incluyen ciclotimia y distimia o trastornos depresivos menores, pese a tener un padre con una forma grave y recurrente de TB.…”

“…También se han reportado tasas elevadas de trastornos de ánimo (diferentes del TB), trastornos de ansiedad y trastornos disruptivos 33 . Un estudio prospectivo, realizado en una población Amish con un seguimiento de 16 años 5 , identificó síntomas subsindromales de manía 9 años antes del inicio del TB claramente manifiesto; entre los más frecuentemente observados se encontraron dificultades en la concentración, alteraciones en la psicomotricidad, ansiedad, insomnio, labilidad emocional y comportamientos grandiosos y audaces; los primeros tres también se evidenciaron en nuestro estudio 5,[36][37][38][39][40][41][42] .…”

Further Evidence of a Cohort Effect in Bipolar Disorder

“…30 Thus, behaviorally based epigenetic effects related to parental illness, stressors, or substances of abuse could be supplemented by germ cell conveyance of vulnerability from the previous generation. Such a contributing germ cell epigenetic mechanism has not been previously discussed or postulated as a possible contributor to the cohort effect, but such a possibility deserves further exploration, particularly since multiple illnesses, including substance abuse, also show cohort effects 6,7 and contribute to vulnerability to bipolar disorder.…”

CACNA1C rs1006737 genotype and bipolar disorder: Focus on intermediate phenotypes and cardiovascular comorbidity

“…There is no known cause of BD, however there is substantial evidence that BD is associated with structural and functional neuroanatomic features, as well as peripheral markers of inflammation, oxidative stress, and neurotrophic factors (Berk et al, 2011;Frey et al, 2013). Despite the fact that the high degree of heritability of BD has been recognized for decades (Berk et al, 2011), only recently have molecular genetic studies provided compelling replicated evidence that specific genotypes confer risk for BD (Birmaher et al, 2009(Birmaher et al, , 2013. In 2008, two genome-wide association studies found significant associations between BD and a single nucleotide polymorphism (SNP) on the calcium channel, voltage dependent, L type, alpha 1C subunit gene (CACNA1C), rs1006737 Sklar et al, 2008).…”