In this new study, Dr. Catherine Gallerani and colleagues at Vanderbilt University were interested in examining the temporal comorbidity of depression, anxiety, conduct disorder, and substance abuse during adolescence. Specifically, depression during this time period is usually comorbid with other conditions, such as anxiety and substance abuse. Some researchers have examined the temporal relation in the onset of these disorders (what precedes what) which can provide information about which disorders increase the risk for other disorders (this follows the hypothesis that the disorders are separate entities and one makes you more likely to have another), as well which disorder signals an early phase of another disorder (this follows a prodromal view suggesting that some of these disorders may be phases of one another in that, for example, symptoms of anxiety may be an early phase of depression). In the current study, the authors wanted to examine two specific issues: how does the temporal relation between these conditions differ for boys and girls, and whether they differ between adolescents at low or high familial-risk for depression.

The study included 240 adolescents (54% female).  185 had a parent with a history of depression and 55 had parents with no history of psychiatric disorders. These children underwent psychiatric evaluations annually for 5-6 years from 6th to 12th grade.

The results:

1. As expected, children of parents with a history of depression were significantly more likely to develop depression during the study period than children at low-risk for psychopathology. In fact, at-risk children were 12 times more likely to develop depression than their low-risk peers. These at risk children were also more likely to develop anxiety (4 times), conduct disorder (11 times), and substance use disorder (6 times).

2.The temporal relation between the different conditions was affected by the sex of the child. Specifically:

2.A. There was no temporal relation between anxiety and depression for girls. However, for boys, anxiety symptoms more than doubled the risk of developing depression in the future even after controlling for familial risk. That is, across at-risk and low-risk boys, having anxiety predicted the later onset of depression.

2.B. A different pattern was observed for the association between substance abuse and depression. Substance  abuse increased the risk for developing depression by 300% among girls but not among boys. Furthermore, the odds that anxiety predicted depression among was 13 times greater for girls than for boys.

Now, what do we mean when we say “increased risk”? Does this mean that anxiety or substance use causes depression? Are we talking about true ‘mechanistic risk’ as when we say that not wearing a seat belt during a car accident increases the risk that you will be seriously injured? Not quite. In the case of the seat belt, we know the mechanism of risk. We know that not using the seat belt makes you more likely to fly through the windshield and get injured. However, in the case of the temporal association between these disorders, “increased risk” is actually a statistical term we use to refer to the possibility of observing an event in the data. For example, when looking at girls, observing a substance use disorder in the data makes us 3 times more likely that we will observe a diagnosis of depression in the same girl in the future. The data themselves do not address the possible mechanisms behind such increased risk, so we don’t quite know why the presence of one (substance use) increases the possibility of seeing the other (depression). One possibility is that indeed one causes the other - so that for example, being anxious makes you ruminate more, which in turn makes you more likely to be depressed. The other possibility is that both are symptoms of a single process, in that being anxious is simply an early symptom - or early phase - of the depression process.

Regardless of the mechanism at play however, the results are pretty compelling showing different temporal associations between these disorders and depression for boys and girls. The results suggest that we should be particularly attentive to symptoms of anxiety among boys, as these signal an increased possibility for future depression. In contrast, substance abuse among girls seems to be highly associated with future depression onset, and thus we should monitor girls that are found to abuse substances during early adolescence.

Gallerani, C., Garber, J., & Martin, N. (2009). The temporal relation between depression and comorbid psychopathology in adolescents at varied risk for depression Journal of Child Psychology and Psychiatry DOI: 10.1111/j.1469-7610.2009.02155.x

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In the latest issue of the journal of the American Academy of Pediatrics there is a new epidemiological examination of the association between prematurity and autism that highlights the point I was making to my students. There are a number of studies that have found a link between prematurity and autism, in that premature babies are at greater risk for developing autism than full term babies. However, other studies have failed to replicate such findings. What could explain such discrepancy? One possibility is that it is not about being premature that increases the risk for autism, but instead such increased risk is due to complications and other factors associated with prematurity. If these variables have not been controlled similarly across studies then you will find studies providing conflicting results due to unknown, or uncontrolled, characteristics of the sample.

In the study published in Pediatrics, a Swedish team of researchers examined a population sample of 1,216 individuals with a autism spectrum diagnosis and over 6,000 non affected peers. These groups were similar in sex distribution, age, and most importantly: birth hospital. This is key, because it theoretically eliminates the possibility that any differences found between the groups are due to differences in the health services received during birth.  The authors first compared the risk for autism spectrum disorders associated with prematurity, and then examined whether specific neonatal complication factors could explain the observed risk.

Main finding:

1. Being born at or before 31 weeks of gestation doubled the risk for developing an autism disorder  when compared to full term infants.
2. Being born between 32 and 36 weeks of gestation increased the risk for an autism disorder by 55%.

However:

After adjusting (controlling) for neonatal complications and related factors, being born prematurely - even before 32 week gestation - DID NOT increase the risk of developing autism. That is, prematurity itself was not associated with autism once we take into account specific complications that are common among premature infants.

So what are the neonatal factors associated with autism risk?

While controlling for all neonatal and related factors:

1. Low weight for gestational age was a risk factor for autism. Specifically, being small for gestational age increased the risk for developing autism by 86%.
2. Having congenital malformations increased the risk by 106%
3. Having intra-cranial bleeding, edema, or seizures increased the risk by 206%
4. Having Hypoglycemia increased the risk for ASD by 120%

The following neonatal factors were NOT associated with an increased risk for autism: Jaundice, respiratory distress, infections, head and neck injuries during delivery, apgar score, being a twin, or being large for gestational age.

The results are consistent with other findings suggesting that “weight for gestational age” and related complications are more informative when estimating the probability of future neurodevelopmental disorders than simply being premature. This may also help explain why many premature babies don’t show any lasting effects, even when they are born severely premature (<32 weeks), while others have significant developmental complications  (autism, ADHD, learning disabilities) even when they are born only a few weeks premature.

Buchmayer, S., Johansson, S., Johansson, A., Hultman, C., Sparen, P., & Cnattingius, S. (2009). Can Association Between Preterm Birth and Autism be Explained by Maternal or Neonatal Morbidity? PEDIATRICS, 124 (5) DOI: 10.1542/peds.2008-3582

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The authors of the Journal of Child Psychology and Psychiatry study examined participants from two independent longitudinal studies of ADHD. The first study started in the 1980s and included 140 6-to-17 year-old boys with ADHD, 206 siblings, 280 parents, and 120 non-ADHD peers. These kids were assessed for up to 10 years after the initiation of the study. The second study started in 1993 and included 140 6-to-17 year-old girls, 183 siblings, 274 parents, and 122 non-ADHD peers. These girls were followed for up to 5 years. The final sample for the study included 143 ADHD girls and 147 ADHD boys. Both groups were on average approximately 11 years old at the time of the first assessment. However boys were significantly older (mean age 19) at the time of the last followup compared to the girls (mean age 16).

The ADHD diagnoses were obtained via a 3-step procedure that included a comprehensive psychiatric interview. This greatly limits the possibility that some of the ADHD cases included in the study were misdiagnoses. An similar assessment of ADHD symptoms and co-morbid conditions were conducted during the follow up period.

The Results:

1. As you can see from the graphic below, the authors found that ADHD symptoms decline with age in a non-linear fashion. Specifically, the decline in symptoms accelerates with age.

2. As also noted in the graphic below, girls had significantly more ADHD symptoms than boys across all developmental periods. While in the graphic it looks like this difference was more pronounced during early childhood, the statistical analysis conducted indicated that the sex difference in ADHD symptoms was consistent (the same) at all ages.

Developmental course of ADHD

3. The authors also found a sex difference in the developmental progression of co-morbid conditions. Specifically, while in childhood ADHD in boys and girls were associated with the same co-morbid conditions (Mood Disorders, Disruptive Behavior Disorders, and Anxiety), during adolescence ADHD was no longer associated with anxiety for boys. In contrast, girls continued to show high co-morbidity between ADHD and anxiety in adolescence.

Psychiatric Co-morbidity of ADHD

The good news is that ADHD symptoms appear to decrease with age, and that this decline accelerates as children get older. However, the news are not as good for girls. The study shows that symptoms in girls appear to be more severe than in boys, and that for girls there are more co-morbid conditions during adolescence than for boys. While this may suggest that ADHD is more severe in girls than in boys, we should keep in mind that the results of any study is highly dependent on the sample used, and more importantly the way participants were recruited. For example, boys and girls in this study came from two independent samples, and unknown methodological differences between these samples could be driving some of the results. In addition all of the participants with ADHD were initially included after getting a clinical diagnosis for ADHD by a referral source, which was later confirmed by the study’s own clinician (details on how the recruitment took place were not provided). Therefore, it is possible that these findings reflect sex differences in the initial clinical identification of ADHD by the kid’s clinicians. Specifically, it is possible that girls who were diagnosed and subsequently entered the study simply did so because of experiencing more severe symptoms. While indeed there are some methodological limitations, this is one of the only studies who have provided comprehensive empirical data that help us understand the differences between boys and girls in the progression of ADHD symptoms and co-morbid conditions during childhood and adolescence.

The reference: Monuteaux, M., Mick, E., Faraone, S., & Biederman, J. (2009). The influence of sex on the course and psychiatric correlates of ADHD from childhood to adolescence: A longitudinal study Journal of Child Psychology and Psychiatry DOI: 10.1111/j.1469-7610.2009.02152.x

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This morning I read a study published in a recent issue of the prestigious Archives of General Psychiatry that can help us clarify this issue. The study examined data from the 1981 Finish Birth Cohort study. The study included 5,813 children born in Finland in 1981 and contained data on psychiatric symptoms at age 8, history of bullying at age 8 (from teacher, parents, and self reports), and psychiatric outcomes (hospital treatment,  psychiatric medication use, etc) at age 13 to 24. The authors of the present report were interested in examining whether bullying behaviors at age 8 predicted psychiatric outcomes in adolescents and young adulthood after controlling for psychiatric symptoms at age 8.

Children were classified into 4 groups based on their bullying behavior at age 8, namely: 1) those who were never victims or bullies; 2) those who were bullies only; 3) those who were victims only; 4) those who were both victims and bullies.

The Results:

1. Among females, being a victim (but not a bully) was associated with a significant increase in the risk for later psychiatric hospitalization and psychiatric medication use. Most importantly however, this association was significant even after controlling for the girls’ psychiatric symptoms at age 8. That is, the association between being a victim of bullying and negative psychiatric outcomes could not be accounted for by the presence of psychiatric symptoms in middle childhood.

2. Among males, being a victim (whether alone or when the child is also a bully) was associated with a significant increase in the risk for later psychiatric hospitalization. Further, being both a victim and a bully was associated with an increase in the risk for later psychiatric medication use. However, when the authors controlled for psychiatric symptoms at age 8, being a victim of bullying no longer predicted psychiatric hospitalizations or medication use.

In sum, this study suggests that bullying may play a role in the development of psychiatric problems during adolescence and young adulthood, but only among females. In contrast, being a victim of bullying among males may reflect concurrent psychiatric problems that may place the boys at a higher risk for being victims. Therefore, it is possible that among boys, it is not being a victim of bullying that predicts later psychopathology, but it is the reasons behind why these kids become victims in the first place (for example underlying anxiety, depression, or pre-psychotic symptoms) that signal the eventual emergence of more severe psychiatric difficulties. There is a clear implication for parents and providers. The data suggest that when confronted with a boy who is the victim of bullying we should be attuned to, and if necessary address,  the possible symptoms that may have placed the boy at a greater risk for becoming the victim of bullying.

The Reference: Sourander, A., Ronning, J., Brunstein-Klomek, A., Gyllenberg, D., Kumpulainen, K., Niemela, S., Helenius, H., Sillanmaki, L., Ristkari, T., Tamminen, T., Moilanen, I., Piha, J., & Almqvist, F. (2009). Childhood Bullying Behavior and Later Psychiatric Hospital and Psychopharmacologic Treatment: Findings From the Finnish 1981 Birth Cohort Study Archives of General Psychiatry, 66 (9), 1005-1012 DOI: 10.1001/archgenpsychiatry.2009.122

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I thought it would be appropriate to start the month with some thoughts about the new Autism prevalence study that was just published in Pediatrics and which hit the news cycle this morning.

In sum, the study found that the prevalence of parent-reported rates of autism was higher than previous estimates. Specifically, they found that 1.1% of all children aged 3 to 17 had autism (1 in 91) as compared to previous estimates of approximately 1 in 150.

Does this suggest an increase in autism rates between 2003 and 2007? Maybe, in that the finding is consistent with the possibility that autism rates are increasing. However, there are a number of issues that must be taken into account, especially the methodological differences between this study and the CDC study that reported prevalence rates for 2002.

For a more detailed explanation of the CDC report from where the 1 in 150 rate comes from read my previous post on the topic: Autism rates in the USA: where did the 1 in 150 number came from?

How was the current study conducted?
The study include an analysis of the 2007 National Survey of Children’s Health (NSCH). The NSCH consists of a random and representative telephone survey of parents of 78,037 children. Each family provided data on a single child, so that if a family had more than one child, only one of the children was selected as the target child for interview purposes. During the interview the parents were asked whether “they had ever been told by a doctor or other health care provider that their child had ‘autism, Asperger’s disorder, pervasive developmental disorder, or other autism spectrum disorder.’ “ If the parent said yes, then they were asked whether the child currently had autism or another ASD.

They found a prevalence of 110 cases of current ASDs per 10,000 children, or 1 in 91 children. As expected rates were 4 times higher in boys than in girls.

There are two key differences between this study and the previous CDC report:

1. Unlike the CDC report, this study was nation-wide and included all US regions. In contrast, the CDC report was based on autism rates observed in only 15 states. Therefore, the current report appears to be more representative of the US population than the previous study.
2. The current study was based on parental reports during a phone survey with no corroboration of the diagnoses endorsed by the parents. That is, we assume that parents are correct when asked… does your child current have Autism or ASD? The authors could not verify the veracity of these parental reports through review of medical or educational records. In contrast, the CDC report was based on a review of medical and educational records, and documented diagnoses were doubled checked by trained clinicians to make sure that there was sufficient evidence for each diagnosis. Therefore, the CDC study was much more conservative in estimating autism rates because diagnoses were obtained from medical and educational records rather than from parental reports.

Clearly, neither the CDC nor the current Pediatric study is near perfect, and they provide only a rough estimation of autism cases in the US. Unfortunately, the very significant differences in methodology between these two studies make it impossible to determine with certainty whether the new rate of 1 in 91 reflects a true increase in autism or is simply a byproduct of different estimation procedures not used in previous studies.

The reference: Michael D. Kogan, PhD,a Stephen J. Blumberg,, PhD,b Laura A. Schieve, PhD,c Coleen A. Boyle, PhD,c, James M. Perrin, MD,, Reem M. Ghandour, DrPH,, Gopal K. Singh, PhD,, Bonnie B. Strickland, PhD,, Edwin Trevathan, MD, MPH,, & Peter C. van Dyck, MD, MPH (2009). Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children in the US, 2007 Pediatrics, 124 (4) : 10.1542/peds.2009-1522

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Last week the Journal of Clinical Psychiatry published one of our studies that examined age and gender differences in the presentation of clinical depression among children and adolescents. The study was part of a large NIMH-funded Program Project on child depression led by my collaborator and recent mentor Maria Kovacs. For those who may not be familiar with Dr. Kovacs’ work, she is one of the world leaders in child depression research. She has been studying childhood onset depression for several decades and is the creator of the Child Depression Inventory - one of the most used child assessment instruments in the world.

During the last decade her team has been following an unusually large sample of children and adolescents diagnosed with clinical depression in Hungary. As part of that study, we recently analyzed and published data that allowed us to closely examine how depression is manifested among these children and adolescents. We were particularly interested in examining whether there were specific differences in the presentation of depression between boys and girls, as well as between younger children (as young as 7 years of age) and adolescents.

The study consisted of 559 children with a DSM-based diagnosis of major depression disorder, including 247 depressed girls and 312 depressed boys ranging in age from 7 to 15 (mean age 11). Depression diagnosis was obtained via a semi-structured clinical interview (the Interview Schedule for Children and Adolescents-Diagnostic Version). The results of this interview was then analyzed by two independent psychiatrists and diagnosis was determined using a consensus procedure. This helped us make sure that all children included in the study had a confirmed diagnosis of depression based on standard DSM-IV criteria. We then examined the individual symptoms endorsed during these interviews and attempted to identify different patterns of symptoms across different age groups as well as between boys and girls.

The results:

Below you can see the unadjusted rates of each symptom (% present) for boys and girls across all ages.

Unadjusted Rates (%) of Depressive Symptoms for Girls and Boys With Major Depressive Disorder

There are a few things worth mentioning. First, depressed mood and irritability were the two most common symptoms among these kids, and anhedonia was relatively less frequent (only between 40 and 50% of the sample showed this symptom). This is not consistent with the DSM-IV criteria that indicates that irritability should replace depressed mood in the diagnostic criteria of depression in children. Our analysis suggests that contrary to the DSM-IV assumption, depressed mood is extremely common among depressed children. In contrast, it is anhedonia that is less common in this population. We were also surprised at how common were thoughts of death in this group, which highlights the need for clinicians and educators to assess for suicidal ideation among depressed kids.

Below you can see the results of the changes in odds ratio for age and sex while adjusting for the intercorrelation between symptoms.

Adjusted Multivariate Odds Ratios (95% CI) of Each Symptom Adjusted for Age and Sex via Alternating Logistic Regression

The column of the left tells you how the odds for each symptom changed per year (the odds of being present). The asterisks indicate which symptom significantly changed per year. In sum, depressed mood, hypersomnia, psychomotor retardation, fatigue, and thoughts of death, and suicidal ideation significantly increased from middle childhood to adolescence, while psychomotor agitation significantly decreased per year.

The column on the right tells us how the odds for each symptoms changed by the sex of the child. Specifically,  anhedonia, insomnia, hypersomnia, and somatic complaints were more likely to be seen in females, while psychomotor agitation was more likely to be seen in males.

In sum, this study provides an overview of the symptom presentation of depression among depressed children and adolescents. The study is compelling in that it presents an examination of symptoms among a very large sample of depressed kids. In fact, this is the largest research sample of children with a diagnosis of major depression ever examined for this purpose. The study suggests that, contrary to previous reports, depressed mood is extremely common in this population. The analysis also suggested that the presentation of depression becomes more neurovegetative with age and among females. Neurovegetative symptoms include those that reflect whole-body processes, such as sleep and motor functioning, so clinicians should be particularly attentive to these symptoms. Finally, thoughts of death and suicidal ideation were very common, also highlighting the need for more careful screening of suicidality among depressed children.]

The reference:

Ildikó Baji, Nestor L. Lopez-Duran, Maria Kovacs, Charles J. George, László Mayer, Krisztina Kapornai, Enikő Kiss, Julia Gádoros, & Ágnes Vetró (2009). Age and Sex Analyses of Somatic Complaints and Symptom Presentation of Childhood Depression in a Hungarian Clinical Sample J Clin Psychiatry

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In an article to be published in the Journal of Autism and Developmental Disorders, Dr. Kimberly Baker and a team from the University of South Carolina report the findings from a very interesting study on the perception of spoken emotions by typically developing children and kids with high functioning autism and Aspergers’s disorder. The authors were interested in expanding our understanding the way children with HFA and Asperger’s process spoken emotions. The study included a combined group of 19 kids with HFA or Asperger’s (labeled High Functioning Forms of Autism, or HFFA) and 19 typically developing children. Both groups included 13 males and 6 females. The range in age from 10 to 14 years, with a mean age of 12 in both groups. All participants were right handed.

The study used 4 nonsense passages that were narrated to display four emotions: Anger, Happy, Sadness, and neutral. These passages were presented using a Dichotic Listening Task. In this task, two passages containing two different emotions were presented simultaneously to the right or left ear. For example, the happy passage was presented to the right ear while the sad passage was presented to the left ear.  The children then had to select the emotions included in both passages using a multiple-choice sheet.

The results:

1. There was no difference between the autism and typically developing groups in the proportion of correct responses identifying emotions. See the figure below.
2. There was no difference between the groups in the way the cerebral hemisphere processed the emotions
3. When combining both groups,  sadness was processed better when presented to the left ear (processed by the right hemisphere). However, there was no hemisphere difference in the processing of anger or happiness.

HFA vs. Typically developing kids in the recognition of spoken emotions

Definitely the most critical limitation of this study is the sample size. The number of participants in each group (19) makes it very difficult to find statistically significant differences between the groups even when the differences actually exist. However, looking at the graphic above we can see that the HFFA group actually scored better (albeit not statistically significantly better) that then typically developing group when the emotion was presented to the left ear, and a bit worse when the emotion was presented to the right ear. The patterns for each emotion were also mixed, with the HFFA scoring better for some emotions (Anger, Neutral) and worse for others (Happy, Sadness). Therefore, there was no clear pattern or tendency in the results that would suggest that the lack of significant findings would be mostly due to limitations in the sample size. The authors stated that these findings are consistent with other recent examinations of emotion recognition deficits in autism that suggest that such deficits are more related to general cognitive deficits rather than the presence of autism.

The reference:

Baker, K., Montgomery, A., & Abramson, R. (2009). Brief Report: Perception and Lateralization of Spoken Emotion by Youths with High-Functioning Forms of Autism Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-009-0841-1

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1. In this new study the author first presented 4 issues that remain unresolved from previous research linking maternal obesity and ADHD
2. Since obesity is associated with distress, is it possible that it is the distress during pregnancy that increases the risk for ADHD rather than the obesity?
3. It is possible that maternal obesity and child ADHD are simply related to a common genetic factor. In such a case, it would be the genetic factor, and not the obesity that increases the risk for ADHD
4. Maternal obesity is associated with small birth weight due to fetal growth restrictions, and some studies have linked small birth size to ADHD, possibly through its effects on emotional regulation. Thus, is small birth size the possible link between maternal obesity and ADHD?
5. Maternal obesity is also associated with childhood obesity. Is it possible then than the increased risk for ADHD is due to childhood obesity?

To begin to tackle these issues, the author examined a cohort of women who were pregnant in Sweden from 1999 to 2000. The cohort for this analysis included 1,714 mother-child dyads who were evaluated when the child was 5 years of age. The Body Mass Index of the mothers was obtained during pregnancy and divided into 4 groups: underweight (15–19.99), normal weight (20–24.99),  overweight (25–29.99), and obese (+30). ADHD symptoms and emotionality  at age 5 were assessed via a questionnaires completed by both mothers and teachers. A number of covariates (or potentially explanatory factors) were also measured including maternal stress during pregnancy (divorce, financial problems, etc), socio-economic   status, smoking, the child’s own weight, and depression.

The results:

1. 37% of the mothers were classified as either overweight or obese (28% overweight and 10% obese)
2. Obese mothers were significantly more depressed than the mothers in any of the other weight categories
3. Children of obese mothers had significantly more symptoms of inattention but not hyperactivity when these symptoms were reported by the teachers. Specifically, maternal obesity was associated with a 2-fold increase in risk of teacher-rated inattention symptoms when compared to the children of normal-weight mothers. This association remained stable after controlling for the possible explanatory factors.
4. Maternal Obesity was also associated with an increased risk for negative emotion regulation difficulties as indicated by a teacher-reported emotionality questionnaire.
5. Maternal Obesity was not associated with any symptom when the symptoms were reported by the mother.

A couple of things were surprising. First, the results of the teacher-reported inattention problems were strong, which was of note given that no association was found between obesity and hyperactivity. This discrepancy between inattention and hyperactivity actually points towards a clear link between obesity and adhd (at least inattentive type). That is, since obesity was associated with inattention but not hyperactivity, it is unlikely that the original findings reflected simply an association between obesity and more general behavioral problems in childhood. Instead, the link seems to be specific to one aspect of ADHD. Second, the lack of association between obesity and maternal reported symptoms continues a pattern of findings I have previously discussed (see  for example this article on the effects of multiple daycare arrangements) that suggests that there are some limitations in the nature of maternal reports of the child behavior. In my experience working on several large scale family-based longitudinal studies, fathers and teachers reports of kids’ behaviors tend to agree with each other, but these reports do not always agree with the mother’s. It seems that mothers often see, or report, different behavioral tendencies in their children when compared to what teachers see (or report).

In sum, the study provides additional evidence linking maternal obesity to inattention problems in early childhood. This study expands previous findings by also showing that such a link can not be fully explained by a number of potential factors, such as maternal stress, depression, and socio-economic status. However, please also note that this study did not actually assessed for the presence of ADHD. That is, these kids did not undergo the comprehensive evaluation needed for an accurate diagnosis of ADHD. Instead, the study assessed ADHD-related symptoms as reported by teachers and parents. It would be interesting to see if obesity is associated with true ADHD diagnoses in this population.

The reference: Rodriguez, A. (2009). Maternal pre-pregnancy obesity and risk for inattention and negative emotionality in children Journal of Child Psychology and Psychiatry DOI: 10.1111/j.1469-7610.2009.02133.x

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The study included 306 preschool children (age 3 to 5) recruited from community sources in the St. Louis area. However, this is not a normative community sample, as the recruitment strategy was designed to recruit children at risk for depression and other psychiatric disorders (for example due to a family history of depression). This is a common and appropriate recruitment technique when the objective of the study is to examine the disease process rather than to provide normative or epidemiological information about the condition.  The participating children and their parents underwent a series assessments upon entry to the study (baseline) and then 12 (wave 1) and 24 (wave 2) months later.

The results

1. At baseline 25% (N=75) children met diagnostic criteria for major depression disorder, 26% (N=79) met criteria for other psychiatric disorder, and 47% ( N= 146) did not meet criteria for any psychiatric disorder.
2. At baseline, there was a significant difference in age among the groups, with depressed kids being more likely to be older than the kids in the other psychiatric diagnostic group. There were no gender differences between the depressed kids and the other groups.
3. At baseline, the depressed kids were more likely to have experienced more traumatic events than the non-depressed kids.
4. Below you can see the analysis of the longitudinal progression of MDD compared to other disorders.  Looking only at the top section of the draw, compared to kids without any psychiatric disorder at base line, kids with MDD were 11 times more likely to have MDD vs No disorder at follow up. Similarly, kids with MDD were 7 times more likely than kids with no disorder to have MDD vs. Psychiatric disorder at follow up. Finally kids with MDD were not more likely than the no disorder group to have another psychiatric disorder vs. no disorder. A Similar interpretation can be applied to the other two draws.



5. The researchers also examined the predictors of depression at follow up. Four factors were significant predictors of MDD at follow up:  having MDD at baseline (increased odds of 264%), having a family history of an affective disorder, having disruptive disorder at baseline, and having family income levels below $20,000.
6. Below you can also see the trajectory of MDD based on different severity at baseline. Severe MDD appears to follow a chronic trajectory. Those with less severe MDD follow two trajectories: a recovery, and a recovery-relapse trajectory. The authors could not identify any factors that would help us predict the  trajectories (e.g., chronic vs. recover) among kids with MDD.

There are two critical findings presented in this study. One is that MDD in preschool is highly stable and predictive of future MDD, specially when baseline MDD is severe (more than 50% of the kids with initial MDD continued to have MDD at follow up). Thus, it does not appear that MDD in preschool is a developmental transitional phase. Second, MDD appears to be a risk factor uniquely for MDD. That is, unlike more general ‘internalizing symptoms,’ which are predictive of a number of different disorders, the presence of MDD in preschool does not seem to be an indicator of future ‘general’ psychopathology, but instead it is mostly an indicator of future MDD. This suggests that the MDD diagnosis obtained at this age truly reflects a somewhat homogeneous disease process that is in place and is not simply a reflection of a non-specific dysregulation of emotion that could precede a number of conditions.

Luby, J., Si, X., Belden, A., Tandon, M., & Spitznagel, E. (2009). Preschool Depression: Homotypic Continuity and Course Over 24 Months Archives of General Psychiatry, 66 (8), 897-905 DOI: 10.1001/archgenpsychiatry.2009.97

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In the latest issue of Pediatrics, a British team of researchers presented a cohort study of 219 survivors of extreme prematurity. The authors examined the cognitive and clinical profile of these kids at age 6 and 11, and compared them to  a group of 153 typically developing peers. The children completed a series of neurocognitive tasks, including the Kaufman-Assessment Battery for Children, a full pediatric evaluation to assess for the presence of cerebral palsy, motor functioning, and sensory impairment.

The results:

1. Mean composite cognitive functioning scores were significantly lower in the preterm kids compared to their peers  (score of 83.7  vs. 104.1). This effect did not appear to be explained by socio-economic status of the families.
2. Among typically developing peers, there was no difference in cognitive functioning between boys and girls. However, among the preterm children, boys had significantly lower cognitive scores than girls (by 8 points).
3. When categorizing the impairment into 4 levels (severe, moderate, mild, no impairment), serious impairment (severe or moderate) was observed in 40% of preterm kids but only 1.3% of their typically developing peers. A gender effect was also observed. Serious impairment was seen in 50% of preterm boys but only 31% of preterm girls.
4. Cerebral palsy was also twice as common among boys (25%) than girls (11%).
5. Finally, as you can see in the graphic below, the rates of disabilities from age 6 to 11 did not change much. However, there appears to be a slight decrease in the rate of severe disability with a comparable increase in the rate of moderate disability.

Rates of disability among preterm children

In sum, the rates of serious cognitive deficits among preterm children are around 50%, indicating that despite advances in care, prematurity continues to lead to significant cognitive impairment. However, the rates of impairment among girls were significantly lower than among boys. Although it seems surprising that boys were more susceptible to the effects of prematurity than girls, other studies have reported similar findings. In fact, premature boys have lower survival rates than girls, suggesting that differences in the sex differentiation process before birth (such as exposure to androgens) may place boys at higher risk. Are there any neonatal endocrinologists in house who could shed some light on why exposure to androgens before birth may lead to greater susceptibility to developmental insults?

The reference:

Johnson, S., Fawke, J., Hennessy, E., Rowell, V., Thomas, S., Wolke, D., & Marlow, N. (2009). Neurodevelopmental Disability Through 11 Years of Age in Children Born Before 26 Weeks of Gestation PEDIATRICS, 124 (2) DOI: 10.1542/peds.2008-3743

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