Electronic Letters to:
|
|
eLetters: Electronic letters published:
-
![[Read eLetter]](/icons/misc/sectionDOWN.gif)
Paediatric Bipolar Disorder: A Way Forward
- Aditya N Sharma, AS Le Couteur, Dasha Nicholls, Phillip Graham, Richard Lynn and I. N. Ferrier (27 February 2008)
-
This could be due to higher testosterone in the U.S.
- James M. Howard (27 February 2008)
|
|
|||
|
Aditya N Sharma, Academic SpR and Clinical Lecturer in Child and Adolescent Psychiatry Newcastle University, AS Le Couteur, Dasha Nicholls, Phillip Graham, Richard Lynn and I. N. Ferrier
Send letter to journal:
a.n.sharma{at}ncl.ac.uk Aditya N Sharma, et al.
|
To The Editor British Journal of Psychiatry In their article ‘Incidence of childhood-onset bipolar illness in the USA and Europe’ Post et al(Post, Luckenbaugh, Leverich, et al, 2008) report on the epidemiology of childhood and adolescent onset bipolar disorder in USA and Europe (Netherlands and Germany). This is a very important study that has helped focus our attention to a diagnosis that is under-recognised. The study reports that the onset of bipolar disorder before the age of 19 years was seen in 61% of the US sample compared with only 30% of the sample from Europe. The authors utilised self-reporting and data from the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID)(First, Spitzer, Gibbon, et al, 1996) which correlated well (r=0.80) to establish onset of disorder. However, as the authors themselves state that ‘retrospective assessments of age at onset of illness by SCID interview or self-report (although highly correlated) are both subject to errors in judgement and recall, and are probably more difficult for early episodes’. In addition, the authors do not report whether the patients were euthymic at the time of the self-report. The mood state of the patients at time of interview may also affect recall. The authors themselves state that the limitations of using retrospective techniques mean that the rates reported are unlikely to reflect true incidence of bipolar disorder in childhood and adolescence. Explanations for the reported differing rates of disorder in the two populations include recruitment bias and differing healthcare availability as highlighted by the authors, but there are other factors that may also be relevant. For instance, we know little about clinical practice at the time when these patients were children /adolescents. Perhaps the differences in the reported rates says more about awareness and clinical diagnostic practice of child and adolescent psychiatrists at the time that these adults were young people living in Europe. It would have been helpful to know for example whether these adults were seen in Child and Adolescent Mental Health Services as children and adolescents at all and if so how their difficulties were understood. For example did any of these adults receive, in childhood, a diagnostic formulation that included bipolar disorder or not? There are difficulties in interpreting the results of this study and we would agree with the authors that what is needed is a well designed prospective study comparing prevalence in North America and Europe. The UK Royal College of Paediatrics and Child Health (RCPCH) have the well established British Paediatric Surveillance Unit (BPSU) (Hall & Glickman, 1988) that investigates the epidemiology of rare childhood disorders using a clinician based surveillance methodology (http://bpsu.inopsu.com). For child and adolescent mental health (CAMH) disorders an equivalent surveillance system is in development, namely the Child and Adolescent Psychiatry Surveillance System (CAPSS). This initiative has been supported by the UK Mental Health Research Network (UK MHRN). Our group is pleased to announce that one of the first CAPSS Surveillance survey focusing only on child and adolescent mental health clinicians will be a prospective epidemiological study of Paediatric Bipolar Disorder covering the UK and Ireland. This kind of surveillance methodology is well established as a means of determining incidence rates of rare disorder, and also enables exploration of differences in clinical management. The findings from this study will enable us to compare current UK and US (Moreno, Gonzalo, Blanco, et al, 2007) clinical practice, and lead onto a prospective study of childhood onset bipolar disorder. References: First, M. B., Spitzer, R. L., Gibbon, M., et al (1996) Structured Clinical Interview for DSM-IV Axis I Disorders-Patient Edition (Research Version, 2/96 final): Biometrics Research Department, NY State Psychiatric Institute. Hall, S. M. & Glickman, M. (1988) The British Paediatric Surveillance Unit. Archives of Diseases in Childhood, 63, 344-346. Moreno, C., Gonzalo, L., Blanco, C., et al (2007) National Trends in the Outpatient Diagnosis and Treatment of Bipolar Disorder in Youth. Archives of General Psychiatry, 64, 1032-1039. Post, R. M., Luckenbaugh, D., Leverich, G. S., et al (2008) Incidence of childhood-onset bipolar illness in the USA and Europe. British Journal of Psychiatry, 192, 150-151. |
|||
|
|
|||
|
James M. Howard, Biologist independent
Send letter to journal:
jmhoward{at}anthropogeny.com James M. Howard
|
It is my hypothesis that the "secular trend," the increase in size and earlier puberty in children, is caused by an increase in the percentage of individuals of higher testosterone with time within the population. I suggest this is driven by an increase in percentage of women of higher testosterone within the population with time. This appears to be world-wide but will be higher in some countries than others. I suggest this increase in testosterone is causing the ongoing increase in obesity, diabetes, etc. that is being noticed at this time. That is, excessive maternal testosterone may be affecting fetal development with subsequent increases in the percentage of negative outcomes later in life. It is also my hypothesis that bipolar disorder is caused by an endogenous addiction to testosterone which is easier to demonstrate in women (http://www.anthropogeny.com/Bipolar%20Disorder.htm ). Since bipolar disorder has recently been reported to be rapidly increasing, I suggest BD may also be a result of the negative effects of the latter stages of the secular trend, along with obesity, diabetes, etc. The U.S. may be the site of the most egregious impact of the secular trend's increase in testosterone. This may explain why bipolar disorder is more prevalent in the U.S. (This may also explain why the first-rate medical education and delivery system of the U.S. is unable to reduce the consequences of excessive maternal testosterone that are used to "measure" medical system effectiveness. The U.S. medical system is being overwhelmed, not inadequate.) |
|||