Offspring Of Control Parents Research Articles

Dim light melatonin patterns in unaffected offspring of parents with bipolar disorder: A case-control high-risk study

BackgroundCircadian dysregulation has long been thought to be a key component in the pathophysiology of bipolar disorder (BD). However, it remains unclear whether this dysregulation constitutes a risk factor, manifestation, or consequence of BD. This study aimed to compare dim light melatonin secretion patterns between unaffected offspring of parents with BD (OBD) and offspring of control parents (OCP). MethodsThis case-control study included unaffected OBD (mean age 14.0 years; male 50.0 %) and age- and sex-matched OCP (mean age 13.0 years; male: 43.5 %). Seventeen saliva samples were collected in dim light conditions. Dim light melatonin onset (DLMO), phase angles, and area under the curve (AUC) were calculated. Results185 saliva samples from 12 OBD (n = 12) and 741 from OCP (n = 46) were collected. Unaffected OBD had a significant lower nocturnal melatonin level (14.8 ± 4.6 vs. 20.3 ± 11.7 pg/mL) and a smaller melatonin AUC within two hours after DLMO (35.5 ± 11.3 vs. 44.6 ± 18.1 pg/mL) but a significant larger phase angle between DLMO and sleep onset (2.2 ± 1.0 vs. 1.4 ± 1.2 h) than OCP. There was no significant between-group difference in DLMO. The graphic illustrations showed a considerably flattened melatonin secretion in unaffected OBD. LimitationsThe main limitations include lack of 24-h dim melatonin secretion measurement, large age range of participants, and small sample size. ConclusionsThese findings suggest that unaffected OBD already presented with circadian rhythm dysregulations. Future investigations are needed to clarify the role of abnormal melatonin secretion in the onset of BD.

Do Children of Patients with Bipolar Disorder have a Worse Perception of Sleep Quality?

IntroductionThe offspring of bipolar parents (BO) is a high-risk population for inheriting the bipolar disorder (BD) and other early clinical manifestations, such as sleep disturbances. ObjectiveTo compare the presence of psychiatric disorders and sleep disturbances of BO versus offspring of control parents (OCP). MethodsA cross-sectional analytical study was conducted that compared BO versus OCP. The participants were assessed using valid tools to determine the presence of psychiatric symptoms or disorders. The “Sleep Evaluation Questionnaire” and “School Sleep Habits Survey” were used to determine sleep characteristics and associated factors. Sleep records (7-21 days) were also obtained by using an actigraphy watch. ResultsA sample of 42 participants (18 BO and 24 OCP) was recruited. Differences were found in the presentation of the psychiatric disorder. The BO group showed a higher frequency of major depression disorder (MDD; P = .04) and Disruptive Mood Dysregulation Disorder (DMDD; P = .04). The OCP group showed a higher frequency of Attention Deficit and Hyperactivity Disorder (ADHD; P = .65), and Separation Anxiety Disorder (SAD; P = .46). Differences were also found in sleep by using subjective measurements. Compared to the OCP group, BO had a worse perception of quality of sleep (P = .02), a higher frequency of nightmares (P = .01), a shorter total sleep time, and a higher sleep latency. Nevertheless, no differences were found between groups in the actigraphy measurements. ConclusionsThe BO group had a higher frequency of Mood Disorders, and at the same time a higher number of sleep disturbances in the subjective measurements. It is possible that there is an association between mood symptoms, sleep disturbances, and coffee intake. No differences were found in the sleep profile by using actigraphy.

¿Los hijos de pacientes con trastorno bipolar tienen una peor percepción de la calidad de sueño?

IntroductionThe offspring of bipolar parents (BO) is a high-risk population for inheriting the bipolar disorder (BD) and other early clinical manifestations, such as sleep disturbances. ObjectiveTo compare the presence of psychiatric disorders and sleep disturbances of BO versus offspring of control parents (OCP). MethodsA cross-sectional analytical study was conducted that compared BO versus OCP. The participants were assessed using valid tools to determine the presence of psychiatric symptoms or disorders. The “Sleep Evaluation Questionnaire” and “School Sleep Habits Survey” were used to determine sleep characteristics and associated factors. Sleep records (7-21 days) were also obtained by using an actigraphy watch. ResultsA sample of 42 participants (18 BO and 24 OCP) was recruited. Differences were found in the presentation of the psychiatric disorder. The BO group showed a higher frequency of major depression disorder (MDD; P=.04) and Disruptive Mood Dysregulation Disorder (DMDD; P=.04). The OCP group showed a higher frequency of Attention Deficit and Hyperactivity Disorder (ADHD; P=.65), and Separation Anxiety Disorder (SAD; P=.46). Differences were also found in sleep by using subjective measurements. Compared to the OCP group, BO had a worse perception of quality of sleep (P=.02), a higher frequency of nightmares (P=.01), a shorter total sleep time, and a higher sleep latency. Nevertheless, no differences were found between groups in the actigraphy measurements. ConclusionsThe BO group had a higher frequency of Mood Disorders, and at the same time a higher number of sleep disturbances in the subjective measurements. It is possible that there is an association between mood symptoms, sleep disturbances, and coffee intake. No differences were found in the sleep profile by using actigraphy.

Intergenerational Effects of Sevoflurane in Young Adult Rats

Sevoflurane administered to neonatal rats induces neurobehavioral abnormalities and epigenetic reprogramming of their germ cells; the latter can pass adverse effects of sevoflurane to future offspring. As germ cells are susceptible to reprogramming by environmental factors across the lifespan, the authors hypothesized that sevoflurane administered to adult rats could induce neurobehavioral abnormalities in future offspring, but not in the exposed rats themselves. Sprague-Dawley rats were anesthetized with 2.1% sevoflurane for 3 h every other day between postnatal days 56 and 60. Twenty-five days later, exposed rats and nonexposed controls were mated to produce offspring. Adult male but not female offspring of exposed parents of either sex exhibited deficiencies in elevated plus maze (mean ± SD, offspring of both exposed parents vs. offspring of control parents, 35 ± 12 vs. 15 ± 15 s, P < 0.001) and prepulse inhibition of acoustic startle (offspring of both exposed parents vs. offspring of control parents, 46.504 ± 13.448 vs. 25.838 ± 22.866%, P = 0.009), and increased methylation and reduced expression of the potassium ion-chloride ion cotransporter KCC2 gene (Kcc2) in the hypothalamus. Kcc2 was also hypermethylated in sperm and ovary of the exposed rats. Surprisingly, exposed male rats also exhibited long-term abnormalities in functioning of the hypothalamic-pituitary-gonadal and -adrenal axes, reduced expression of hypothalamic and hippocampal Kcc2, and deficiencies in elevated plus maze (sevoflurane vs. control, 40 ± 24 vs. 25 ± 12 s, P = 0.038) and prepulse inhibition of startle (sevoflurane vs. control, 39.905 ± 21.507 vs. 29.193 ± 24.263%, P < 0.050). Adult sevoflurane exposure affects brain development in male offspring by epigenetically reprogramming both parental germ cells, while it induces neuroendocrine and behavioral abnormalities only in exposed males. Sex steroids may be required for mediation of the adverse effects of adult sevoflurane in exposed males.

Preliminary investigation of the relationships between sleep duration, reward circuitry function, and mood dysregulation in youth offspring of parents with bipolar disorder

BackgroundAltered reward circuitry function is observed in individuals with bipolar disorder (BD) and their unaffected offspring (OBP). While OBP are at elevated risk for BD, modifiable risk factors that may exacerbate neural vulnerabilities in OBP remain under-characterized. As sleep loss is strongly linked to mania in BD, this study tested associations between sleep duration, reward circuitry function, and mood dysregulation in OBP. MethodsTwo groups of youth unaffected with BD (9–17yr) completed a number-guessing fMRI reward paradigm: 25 OBP and 21 age-sex-IQ-matched offspring of control parents with non-BD psychopathology (OCP), to differentiate risk for BD from risk for psychopathology more broadly. Regressions tested effects of group status, self-reported past-week sleep duration, and their interaction on neural activity and bilateral ventral striatum (VS) functional connectivity to win>control. Correlations with parent-reported mood dysregulation were assessed. ResultsGroup effects were observed for right posterior insula activity (OCP>OBP) and VS-left posterior insula connectivity (OBP>OCP). Group⁎sleep duration interactions were observed for left dorsal anterior-mid-cingulate (daMCC) activity and VS-left anterior insula/ventrolateral prefrontal cortex (VLPFC) connectivity. Specifically, sleep duration and daMCC activity were positively related in OBP, but negatively related in OCP and sleep duration and VS-left anterior insula/VLPFC connectivity were negatively related in OBP, but positively in OCP. Additionally, increased VS-left posterior insula connectivity and VS-left anterior insula/VLPFC connectivity were associated with greater mood dysregulation in OBP only. LimitationsCross-sectional design and small sample size. ConclusionsAltered reward-related VS-insula connectivity could represent a neural pathway underpinning mood dysregulation in OBP, and may be modulated by shortened sleep duration.

Evolution of Resistance in Potamopyrgus antipodarum

Host-parasite interactions are believed to exert strong selection in natural communities. Most notably, parasites should select for increased resistance in hosts, while hosts should select for increased infectivity in parasites (Koskella &amp; Lively, 2007; Koskella, Vergara, &amp; Lively, 2011; Lohse, Guiterrez, &amp; Kaltz, 2006). Under this coevolutionary process, can host populations evolve resistance to their rapidly evolving parasite populations? This experiment was designed to determine if hosts rapidly adapt to resist parasites that are themselves under selection to infect their hosts. The New Zealand freshwater snail, Potamopyrgus antipodarum, is naturally infected by the trematode Microphallus. Microphallus is a castrating parasite and is thus likely to impose strong selection on its snail host (Hechinger, 2012). Snails and parasites were collected from a natural lake in summer 2013. These hosts constitute the parental generation of the experiment: they were either exposed to parasite eggs (Exposed) or not exposed (Control). Parental snails matured and reproduced over the course of a year. Their offspring were then exposed to parasites collected from the same lake in summer 2014. These parasites would have had one to a few additional generations of evolution relative to 2013 parasites. After parasite development (~3 months), the offspring were dissected to determine infection status and thereby their resistance to infection. The offspring of Control parents had a significantly higher mean infection rate (35%: less resistant) than the offspring of Exposed parents (30%: more resistant). This result indicates that increased resistance to parasitism evolved in a single host generation. Our finding provides evidence that a host population can rapidly evolve resistance to a parasite population that is itself rapidly co-evolving to infect its host. We predict that the evolution of host resistance would be far greater after multiple generations of parasite selection, and this could be the subject of future study.

Parental Legacy in Insects: Variation of Transgenerational Immune Priming during Offspring Development

In insects, a parental immune challenge can prepare and enhance offspring immune activity. Previous studies of such transgenerational immune priming (TGIP) mainly focused on a single offspring life stage. However, different developmental stages may be exposed to different risks and show different susceptibility to parental immune priming. Here we addressed the question (i) whether TGIP effects on the immunity of Manduca sexta offspring vary among the different developmental offspring stages. We differentiated between unchallenged and immunochallenged offspring; for the latter type of offspring, we further investigated (ii) whether TGIP has an impact on the time that enhanced immune levels persist after offspring immune challenge. Finally, we determined (iii) whether TGIP effects on offspring performance depend on the offspring stage. Our results show that TGIP effects on phenoloxidase (PO) activity, but not on antibacterial activity, vary among unchallenged offspring stages. In contrast, TGIP effects on PO and antibacterial activity did not vary among immunochallenged offspring stages. The persistence of enhanced immune levels in immunochallenged offspring was dependent on the parental immune state. Antibacterial (but not PO) activity in offspring of immunochallenged parents decreased over five days after pupal immune challenge, whereas no significant change over time was detectable in offspring of control parents. Finally, TGIP effects on the developmental time of unchallenged offspring varied among stages; young larvae of immunochallenged parents developed faster and gained more weight than larvae of control parents. However, offspring females of immunochallenged parents laid fewer eggs than females derived from control parents. These findings suggest that the benefits which the offspring gains from TGIP during juvenile development are paid by the adults with reduced reproductive power. Our study shows that TGIP effects vary among offspring stages and depend on the type of immunity (PO or antibacterial activity) as well as the time past offspring immune challenge.

Dimensional psychopathology in offspring of parents with bipolar disorder

To compare the dimensional psychopathology in offspring of parents with bipolar disorder (BP) with offspring of community control parents as assessed by the Child Behavior Checklist (CBCL). Offspring of parents with BP, who were healthy or had non-BP disorders (any psychiatric disorder other than BP; n = 319) or who had bipolar spectrum disorders (n = 35), and offspring of community controls (n = 235) ages 6-18 years were compared using the CBCL, the CBCL-Dysregulation Profile (CBCL-DP), and a sum of the CBCL items associated with mood lability. The results were adjusted for multiple comparisons and for any significant between-group demographic and clinical differences in both biological parents and offspring. With few exceptions, several CBCL (e.g., Total, Internalizing, and Aggression Problems), CBCL-DP, and mood lability scores in non-BP offspring of parents with BP were significantly higher than in offspring of control parents. In addition, both groups of offspring showed significantly lower scores in most scales when compared with offspring of parents with BP who had already developed BP. Similar results were obtained when analyzing the rates of subjects with CBCL T-scores that were two standard deviations or higher above the mean. Even before developing BP, offspring of parents with BP had more severe and higher rates of dimensional psychopathology than offspring of control parents. Prospective follow-up studies in non-BP offspring of parents with BP are warranted to evaluate whether these dimensional profiles are prodromal manifestations of mood or other disorders, and can predict those who are at higher risk to develop BP.

Lifetime Psychiatric Disorders in School-aged Offspring of Parents With Bipolar Disorder

Whether offspring of parents with bipolar disorder (BP) are at specifically high risk to develop BP and other psychiatric disorders has not been adequately studied. To evaluate lifetime prevalence and specificity of psychiatric disorders in offspring of parents with BP-I and BP-II. Offspring aged 6 to 18 years who have parents with BP and community control subjects were interviewed with standardized instruments. All research staff except the statistician were blind to parental diagnoses. Parents with BP were recruited primarily through advertisement and outpatient clinics. Control parents were ascertained by random-digit dialing and were group matched for age, sex, and neighborhood to parents with BP. Three hundred eighty-eight offspring of 233 parents with BP and 251 offspring of 143 demographically matched control parents. Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) Axis I disorders. Adjusting for demographic factors, living with 1 vs both biological parents, both biological parents' non-BP psychopathology, and within-family correlations, offspring of parents with BP showed high risk for BP spectrum disorders (odds ratio [OR] = 13.4; 95% confidence interval [CI], 2.9-61.6) and any mood (OR = 5.2; 95% CI, 2.3-11.4), anxiety (OR = 2.3; 95% CI, 1.3-4.0), and Axis I (OR = 2.2; 95% CI, 1.5-3.3) disorders. Offspring of parents with BP with high socioeconomic status showed more disruptive behavior disorders and any Axis I disorders than offspring of control parents with high socioeconomic status. Families in which both parents had BP had more offspring with BP than families with only 1 parent with BP (OR = 3.6; 95% CI, 1.1-12.2). More than 75.0% of offspring who developed BP had their first mood episode before age 12 years, with most of these episodes meeting criteria for BP not otherwise specified and, to a lesser degree, major depression. Offspring of parents with BP are at high risk for psychiatric disorders and specifically for early-onset BP spectrum disorders. These findings further support the familiality and validity of BP in youth and indicate a need for early identification and treatment.

Multivariate comparison of adolescent offspring of substance abuse parents: Community and treatment samples

Adolescent offspring of substance abuse parents (SA+) were compared on the scales of the Drug Use Screening Inventory to offspring of control parents (SA-). Neither clinical nor community samples of SA+ subjects were different from controls. These findings indicate that parental substance abuse does not necessarily impart maladjustment to their offspring.