There is increasing evidence that childhood Attention-Deficit Hyperactivity Disorder (ADHD) elevates the risk of later Bipolar Spectrum Disorder (BD). However, it remains unclear whether different trajectories of ADHD symptoms confer differential risk for BD.

Data from the Avon Longitudinal Study of Parents and Children were available from 7811 children at age 8 years, 7435 at 10, 6798 at 13, and 1217 at 21–23 years. ADHD symptoms were assessed at 8, 10, and 13 years with the Development and Well-Being Assessment. Clinically significant hypomanic symptoms (CSHS) at 21–23 years were assessed using the Hypomania Symptom Checklist (HCL-32). Group trajectories of ADHD and its subtypes were estimated using latent class growth analysis. The prospective associations between different ADHD trajectories and CSHS were tested using logistic regression analysis.

Persistently high, increasing, remitting, and persistently low ADHD symptom trajectories were identified for the three ADHD-related categories. Individuals with persistently high and increasing levels of ADHD symptoms had increased odds of CSHS compared to persistently low class. Sensitivity analyses validated these results. In separate analyses, persistently high levels of hyperactivity and inattentive, and increasing levels of inattentive symptoms were also independently associated with CSHS.

Young people with a longitudinal pattern of high and increasing ADHD symptoms are at higher risk for developing CSHS in young adulthood compared to individuals with low symptom patterns. These two trajectories in childhood and adolescence may represent distinct phenotypic risk profiles for subsequently developing BD and be clinically significant targets for prevention and treatment of BD.

There is ongoing debate on the nosological position of bipolar disorder (BD) and borderline personality disorder (BPD). Identifying the unique and shared risks, developmental pathways, and symptoms in emerging BD and BPD could help the field refine aetiological hypotheses and improve the prediction of the onset of these disorders. This study aimed to: (a) systematically synthesise the available evidence from systematic reviews (SRs) and meta-analyses (MAs) concerning environmental, psychosocial, biological, and clinical factors leading to the emergence of BD and BPD; (b) identify the main differences and common features between the two disorders to characterise their complex interplay and, (c) highlight remaining evidence gaps.

Data sources were; PubMed, PsychINFO, Embase, Cochrane, CINAHL, Medline, ISI Web of Science. Overlap of included SRs/MAs was assessed using the corrected covered area process. The methodological quality of each included SR and MA was assessed using the AMSTAR.

22 SRs and MAs involving 249 prospective studies met eligibility criteria. Results demonstrated that family history of psychopathology, affective instability, attention deficit hyperactivity disorder, anxiety disorders, depression, sleep disturbances, substance abuse, psychotic symptoms, suicidality, childhood adversity and temperament were common predisposing factors across both disorders. There are also distinct factors specific to emerging BD or BPD.

Prospective studies are required to increase our understanding of the development of BD and BPD onset and their complex interplay by concurrently examining multiple measures in BD and BPD at-risk populations.

There is still an ongoing debate on the nosological position of Bipolar Disorder (BD) and Borderline Personality Disorder (BPD). Identifying the unique and shared risks and developmental pathways in emerging BD and BPD could help the field refine aetiological hypotheses of these disorders. The study aims were to systematically synthesise the available evidence from systematic reviews and meta-analyses concerning environmental, psychosocial, biological, and clinical factors leading to the emergence of BD and BPD to identify the main differences and common characteristics between the two disorders to characterise their complex interplay whilst highlighting remaining evidence gaps.

A literature search was conducted PubMed, PsychINFO, EMBASE, Cochrane, CINAHL, MEDLINE, and ISI Web of Science as the data sources. 19 systematic reviews and meta-analyses involving 217 prospective studies met eligibility criteria.

Results demonstrated that family history of psychopathology, affective instability, attention deficit hyperactivity disorder, anxiety disorders, depression, sleep disturbances, substance abuse, psychotic symptoms, suicidality, childhood adversity and temperament dimensions were common predisposing factors across both disorders. There are also many distinct variables that could be found early in the course of both disorders. Most of the factors should be considered as a general, nonspecific precursor signs and symptoms of both BPD and BD, apart from subsyndromal depression, subsyndromal hypomania, cyclothymia disorder, psychotic symptoms, age at onset of major depression and frequency and loading of affective symptoms.

Although the findings of this review may lead to support the view of BD and BPD as two distinct disorders, there is not sufficient data to either indicate that BD and BPD are separate nosological entities or that BPD should be considered as an extension of BD disorders. Future research is required to increase our understanding of the aetiology of BD and BPD onset and their complex interplay by conducting prospective studies which concurrently examine multiple measures including biological, environmental, psychosocial and clinical factors in BD and BPD at-risk populations. Large, multilevel data sets will enable deep phenotyping and distinguish pathophysiological pathways.