learn-about-psychology

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Attention-deficit/hyperactivity disorder (ADHD) is highly prevalent among children, but also affects an estimated 2.5% to 4.4% of adults (Stickley, Koyanagi, Ruchkin, & Kamio, 2016). Individuals with ADHD compose 4% to 25.9% of people who complete suicide, “which is frequently higher than the estimated prevalence of suicide (5.29%) worldwide” (Chou, Liu, Hu, & Yen, 2016), making the potential relationship between the disorder and suicidality a topic of investigation. Extensive research exploring ADHD suicidality has focused on the influence of medication use, comorbid mental illness, and inconsistent diagnostic measures on the relationship between ADHD and suicidality. However, research has failed to deeply examine the role of social and societal factors in suicidality among individuals with ADHD.

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Risky Families & 5-HTTLPR

It has been previously proposed that the carriers of two short alleles of the serotonin transporter gene-linked polymorphic region (5-HTTLPR) are at a higher risk for being depressed. Therefore, to confirm this gene-environment interaction, the researchers mentioned in the article studied the association between symptoms of depression, stressful early environment due to family, recent or current adversity/stress, and the 5-HTTLPR gene. 

There were 118 participants in this experiment. The participants’ psychological distress and psychosocial resources were measured using some questionnaires. Moreover, stress in the participants’ early life was measured by Risky Families questionnaire that measures the relation between family stress and mental/physical health consequences. After this, the participants’ DNA samples were collected. Results showed a gene-environment interaction (GxE) does exist between early family stress/current adversity and 5-HTTLPR in terms of depression symptoms. Furthermore, the s/s genotype of the gene is protective against depression symptoms in a supportive early environment but harmful in an early stress or current stress environment. Additionally, family environment did not notably suggest depressive symptomology for participants that were s/l or l/l. However, it should be noted that current adversity or the genotype predict depression symptoms by themselves. 

There were numerous limitations in this study. Firstly, the researchers didn’t look at diagnosed depression, rather, they looked at depression symptoms. This means that the clinical significance of the results is not clear. Secondly, early family stress environment was “relatively modest” in the participants of the study. None of the participants had a diagnosed major mental disorder, therefore, the results show that even moderate family stress may be associated with depression symptoms. Lastly, the sample size that was used was small and this may have hidden some small effects of current stress or 5-HTTLPR on depression symptoms. Therefore, a replication that considers all these factors needs to be conducted.

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Comparative Analysis of Completed Suicide Using High Resolution Brain SPECT Imaging

Studies in the past have implicated that history of depression is a major factor in the risk for suicide. Numerous brain imaging studies have been conducted to find the underlying neurobiological causes of depression. Amen et al (2009) conducted an experiment in which they compared brains of 12 psychiatric patients who committed suicide to brains of non-suicidal patients with depression and healthy subjects. They mainly looked at the groups’ regional cerebral blood flow (rCBF) using statistical parametric mapping. 

Results demonstrated that there was a generally lower rCBF in the overall cortex of the suicidal patients compared to the healthy comparison subjects. There was compromised impulse control and limbic dysregulation. Specifically, there was low activity in Brodmann’s areas 11 and 25. There was also low perfusion in ventral tegmentum, and medial prefrontal cortex and orbital cortex. This was an imperative finding because activity in the amygdala without release of dopamine to medial prefrontal cortex can lead to depressive symptoms. Furthermore, there was a greater deactivation in the posterior cingulate of the depressed patients who committed suicide. This is a significant difference in the brain of a suicidal vs typical depressed but non-suicidal subject. 

However, there were numerous limitations in this study. For instance, one thing that was not controlled for was medications. Some of the severely depressed patients were on medications while their scans were being taken which could have affected their rCBF. Another thing that was not controlled for was season. They tried to randomize assignments into comparison groups to lessen variability due to season. Furthermore, there were issues with the odd heterogeneity of the study group. Studying suicide implies retroactive data attainment and analysis. For instance, the researchers were not able to acquire resting scans of these 12 patients which would have made their data more credible. Moreover, having each ones BDI scores would have controlled for the severity of the symptoms of depression. Therefore, these results show that further research on this topic is necessary.

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