Efecto del aripiprazol en los niveles plasmáticos de prolactina en pacientes diagnosticados de esquizofrenia tratados con risperidona o paliperidona. Factores involucrados.

133 p.La hiperprolactinemia es un efecto secundario del tratamiento con risperidona o paliperidona que puede paliarse de forma eficaz añadiendo aripiprazol al tratamiento. Nuestro objetivo es valorar factores clínicos y demográficos pueden influir en el efecto del aripiprazol. Presentamos un ensayo clínico, realizado en 20 mujeres y 54 hombres con esquizofrenia, en monoterapia con risperidona y/o paliperidona. Se añadieron 5mg/día de aripiprazol, valorando la prolactina sérica y el estado psicopatológico al cabo de 1 y 4 semanas. Inicialmente, el 95% de las mujeres y 92% de los hombres presentaban hiperprolactinemia. Los niveles medios de prolactina (SD) eran mayores en mujeres 110.94ng/ml (54.01) que en hombres 48.11 (28.76), en los más jóvenes y en los que llevaban menos tiempo en tratamiento. El aripiprazol disminuye significativamente la prolactina sérica desde la primera semana y de forma diferente según el sexo. La primera semana disminuye 26.57 ng/ml (42.82) en mujeres y 9.52 (10.56) en hombres; en mujeres hay una diminución adicional de 23.37 ng/ml (49.41) hasta el día final, en hombres es de 1.73 (13.02). En cuanto a las variables intra-sujetos, los niveles son superiores en mujeres que en hombres y en los de menor edad. La dosis de antipsicótico, el tipo de tratamiento o su duración no influyen significativamente. La disminución porcentual de prolactina es mayor en mujeres (mediana=56.8%) que en hombres (23.7%). La hiperprolactinemia se normaliza en 8 individuos, sin embargo, la gravedad asociada disminuye de forma considerable. Aun así, un 61% de mujeres tienen niveles finales clasificados como moderados-graves frente a un 15% de hombres.Se detecta una disminución de la sintomatología positiva y negativa al cabo de un mes, independiente del sexo, aunque inicialmente los hombres estaban más graves que las mujeresAñadir 5mg/dia de aripiprazol es eficaz para disminuir los niveles de prolactina y la gravedad asociada a la hiperprolactinemia; siendo la respuesta diferente según el sexo

Genetics of adult attachment: An updated review of the literature

Attachment style, which has been theorized to be rooted in childhood bonding experiences, influences adult cognitive, emotional and interpersonal functioning. Despite its relationship with early experiences, research indicates that the continuity of attachment style across childhood and adulthood is only partial, being a malleable tendency that is shaped throughout development, with an increasing influence of genetics, as it occurs in other cognitive and behavioral phenotypes. Genetic research indicates that up to 45% of the variability in anxious and 39% in avoidant adult attachment style could be explained by genetic causes, but the precise mechanisms remain unclear. A narrative review is conducted analyzing the existing literature regarding the implication of candidate genes related to oxytocin, dopaminergic pathways, serotonergic pathways and brain-derived neurotrophic factor in adult attachment, with both vulnerability and differential susceptibility approaches, yielding mixed results. We highlight the lack of genome-wide studies and the scarcity of epigenetic investigation. Based on the existing data, we conclude that the genetics of adult attachment is an area that requires further research to clarify its etiological role and that it should be preferably approached as an interaction between nature and nurture

Role of Mitochondrial Complex IV in Age-Dependent Obesity.

Aging is associated with progressive white adipose tissue (WAT) enlargement initiated early in life, but the molecular mechanisms involved remain unknown. Here we show that mitochondrial complex IV (CIV) activity and assembly are already repressed in white adipocytes of middle-aged mice and involve a HIF1A-dependent decline of essential CIV components such as COX5B. At the molecular level, HIF1A binds to the Cox5b proximal promoter and represses its expression. Silencing of Cox5b decreased fatty acid oxidation and promoted intracellular lipid accumulation. Moreover, local in vivo Cox5b silencing in WAT of young mice increased the size of adipocytes, whereas restoration of COX5B expression in aging mice counteracted adipocyte enlargement. An age-dependent reduction in COX5B gene expression was also found in human visceral adipose tissue. Collectively, our findings establish a pivotal role for CIV dysfunction in progressive white adipocyte enlargement during aging, which can be restored to alleviate age-dependent WAT expansion