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EDITORIALS: Keith Hawton A national target for reducing suicide BMJ 1998; 317: 156-157 [Full text]

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Richard Lucas   (22 July 1998)

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Biba R Stanton   (27 July 1998)

Reducing Suicide in Older People

M Abas   (28 August 1998)

Rising youth suicide rates are a delayed effect of falling infant mortality

Thomas J P Verberne   (28 June 1999)

Rising youth suicide rates are partly an effect of pubertal age advancement

Thomas J P Verberne   (5 April 2000)

Untitled 22 July 1998
Richard Lucas Send response to journal: Re: this article	I would like to express appreciation for the excellent and clear editorial by Professor Hawton on the subject of reducing suicide (B.M.J. 18/7/98). While setting targets with measurable aims, such as early detection of depression, is laudable; assessing suicidal risk is complex, with no one answer. As professor Hawton points out "virtually every psychiatric disorder carries a raised risk of suicide", and this will remain so, even if new clinical targets are set. Given such circumstances, Professor Hawton argues that "further developments in mental health must be introduced in ways that encourage clinical creativity and competence without adding to the stifling sense of medicolegal liability that affects many clinicians in psychiatry today." With this latter concern in mind, last year the Association for Psychoanalytic Psychotherapy in the NHS (APP) formed a general psychiatry section. The aim was to create a forum for NHS staff to discuss their clinical concerns rather than stifle them. On the 27th November, at the Tavistock Clinic, London, the APP in conjunction with the Royal College of Psychiatrists, are holding a conference on "Suicide inquiries and how to survive them". The aim of the conference is to examine the current culture of inquiry, to which Professor Hawton has referred, and provide for discussion clinical experiences from doctors and nurses, who have been at the receiving end of such inquiries. Anyone interested in receiving further information on the conference or the activities of the APP are most welcome to contact the APP Conference Administrator (Tel/Fax 0181 582 1922). Yours sincerely, Dr. Richard Lucas. Chairman - APP General Psychiatry Section.
Untitled 27 July 1998
Biba R Stanton, Medical student Send response to journal: Re: this article	Editor, Our Healthier Nation1 proposes suicide rates as the only target for mental health strategy. Keith Hawton2 argues in favour of this policy, emphasising the importance of a target for which data is available. However, targets should not only be measurable but must highlight priority areas in which effective interventions are available. It is unquestionable that the prevention of suicide is intrinsically desirable. Nevertheless, suicide is a relatively rare outcome of psychiatric illness, and cannot be assumed to reflect wider aspects of mental health. There is a danger that, in focusing attention on suicide, resources may be diverted away from areas of equal or greater importance. Furthermore, the use of a rare event as an indicator for mental health may downgrade the importance of mental health issues in health promotion strategy3. There is no convincing evidence for the efficacy of any public health or clinical intervention in the prevention of suicide4. In contrast, there are many other interventions of known efficacy which are currently under-used or under-resourced (e.g. family interventions for schizophrenia). As such, a particular focus on suicide prevention cannot be compatible with evidence based health care. At a local level, the small number of suicides makes changes over time difficult to interpret. Moreover, the effect of national socioeconomic processes is likely to mask any change brought about by local prevention strategies5. Although morbidity is more complex to define and quantify than suicide, methods of measurement are available and routinely used. I would strongly argue for the inclusion of a measure of morbidity alongside suicide rates as a target in Our Healthier Nation. It is only through doing so that wider aspects of mental health will be addressed and that resources will be focused on the most effective interventions. Biba R. Stanton Medical student University of Newcastle-Upon-Tyne NE1 7RU 1 Secretary of State for Health. Our Healthier Nation: a contract for health. London: HMSO, 1998. 2 Hawton K. A national target for reducing suicide. BMJ 1998;317:157-8. 3 McCarthy J, Davidson I. Suicide as an indicator of mental health. BMJ 1994;309:58. 4 Gunnell D, Frankel S. Prevention of Suicide: aspirations and evidence. BMJ 1994;308:1227-33. 5 Gunnell D, Peters TJ, Kammerling RM, Brooks J. Relation between parasuicide, suicide, psychiatric admissions and socioeconomic deprivation. BMJ 1995;311:226-30.
Reducing Suicide in Older People 28 August 1998
M Abas Send response to journal: Re: Reducing Suicide in Older People	Dear Sir, While we welcome Hawtons editorial, emphasising the importance of continuing to set national targets to reduce the rate of suicide1, we were surprised by the choice of groups that were selected as being particularly at risk of suicide and therefore requiring special attention. We agree that the rise in the rate of suicide in young men, both nationally and internationally, is of considerable concern. However suicide rates in men over 75 are still the highest of any demographic group. Although it is difficult to accurately predict future changes in rates of suicide, evidence from birth cohort analyses suggest that rates of suicide in older people will increase2. Targeted approaches for reducing suicide in older people would include optimising management of pain and disability and reducing handicap and social isolation. Older people who deliberately harm themselves are even more likely to die by suicide than younger people who deliberately self harm3. Casualty and primary care staff should therefore be particularly alert to older people in this category. Self poisoning is the most commonly used method for suicide in older people. Limiting the availability of analgesics and other medication in those known to be at risk of self harm is therefore a central concern. Finally we agree with Hawton that the Samaritans should continue to receive support. For the first time contacts with people over 60 now make up 8% of calls to the Samaritans, comprising one new call every 15 minutes in the UK4. In Singapore, the Samaritans offer a toll-free telephone line for distressed elderly and the effectiveness of this service, although difficult to show, is being monitored. M Abas Lecturer M J Crawford Research Fellow Section of old age psychiatry, Institute of Psychiatry, London, SE5 8AF. References 1 Hawton K. A national target for reducing suicide. BMJ, 1998; 317: 156-157. 2 Shah A. and De T. Suicide and the elderly. Int J Psych in Clinical Practice, 1998; 2: 3-17. 3 Cattell H. and Jolley D.J. 100 cases of suicide in elderly people. BJPsych, 1995; 166: 451-457. 4 Abas M.A. Depression and suicide in older people. Int J Geriatric Psych, 1995; 10: 707-710. 5 Ko S.M. and Kua E.H. Ethnicity and elderly suicide in Singapore. Int Psychogeriatrics, 1995; 7: 309-317.
Rising youth suicide rates are a delayed effect of falling infant mortality 28 June 1999
Thomas J P Verberne, Clinical psychologist, retired Send response to journal: Re: Rising youth suicide rates are a delayed effect of falling infant mortality	Investigations of significant rises in youth suicide rates found, in each successive birth cohort, a higher suicide rate than in the previous cohort, at the same age. (1, 2) The effect was not restricted to the 15- 24-age-group, but appeared to affect also the ages beyond 24. The proportion of suicides in a given cohort appeared to be a property of that cohort. No satisfactory explanation for the cohort effect was found. It is here proposed that the youth (15-24-year-olds) suicide rate and the infant survival rate (the converse of the infant mortality rate) fluctuate in much the same way because suicide-vulnerability is an inherited vulnerability which is associated with other vulnerabilities. More than 90% of completed suicides in all age groups are associated with psychiatric disorders. (3) Completed suicide has been linked with other dysfunctions and disabilities, including respiratory distress at birth, (4) poor childhood and adolescent physical development, tics, aggression, conduct problems, high emotional instability. (5) Completed suicide was found to share important risk factors with other causes of premature death. (5) Family, (6) twin, (7) adoption, (8) biochemical (9) and nuclear biological (10, 11) studies suggest that genetic influences are an important part of the etiology of suicide. Vulnerability to suicide is probably a disorder in its own right. (6, 9, 12) On the assumption that suicide vulnerability is under significant genetic control, the inherent stability of inherited characters would ensure stability of the proportion of the suicide-vulnerable within successive cohorts, at the time of conception. However, the proportion of suicide-vulnerable individuals in each birth cohort would vary with, amongst other things, the effectiveness of perinatal and infant care, as expressed, e.g., in the infant mortality rate. It is assumed that an infant's survival chances during the first year of life will tend to be inversely related to the number of that infant's vulnerabilities. When infant mortality is high, the relatively small number of deaths of infants with an above average number of inherited vulnerabilities will contribute little to the total number of infant deaths, the majority of which are contributed by the deaths of infants not thus affected. But once a majority of infants with average and below average numbers of vulnerabilities are surviving, infants with an above average number of vulnerabilities, will start to progressively increase their proportion amongst the survivors. This would be because such infants have a wider margin for improvement in their survival rate. Specifically, the survival rate of suicide-vulnerable infants relative to the overall rate is expected to increase until the curve of survival rates becomes asymptotic. As suicide vulnerability is rarely expressed before puberty, (13) there will be a time lag of at least 10 years between the birth of suicide -vulnerable individuals in a given birth cohort and the first completed suicides within that cohort. Thus, with a few provisos, the infant survival rates of 15 to 24 years earlier will determine the suicide rates within the 15-24-years age group. Figure 1 shows the relation between Australian male infant survival rates, in the period 1938-1996 and Australian male youth suicide rates, in the period 1960-1996. As hypothesized, the survival curve is closely shadowed by the suicide curve. It can be shown that other hitherto puzzling aspects of suicide rates are resolved if the working hypothesis is adopted that vulnerability to suicide is an inherited disorder which tends to be associated with other vulnerabilties impairing the affected individual's survival chances. References 1. Murphy GE, Wetzel RD. Suicide risk by birth cohort in the U.S., 1949-1974. Arch Gen Psychiatry 1980; 37: 519-523. 2. Goldney RD, Katsikitis M. Cohort analysis of suicide rates in Australia. Arch Gen Psychiatry 1983; 40: 71-74. 3. Mo cicki EK. Identification of suicide risk factors using epidemiological studies. Psychiatr Clin North Am 1997; 20: 499-517. 4. Salk L, Lipsitt LP, Sturner WQ, et al. Relationship of maternal and perinatal conditions to eventual adolescent suicide. Lancet 1985; i: 624-627. 5. Neeleman J, Wessely S, Wadsworth M. Predictors of suicide, accidental death, and premature natural death in a general-population birth cohort. Lancet 1998; 351: 93-97. 6. Brent DA, Bridge J, Johnson BA, Connolly J. Suicidal behavior runs in families. A controlled family study of adolescent suicide victims. Arch Gen Psychiatry 1996; 53: 1145-1152. 7. Roy A, Segal NL, Sarchiapone M. Attempted suicide among living co -twins of twin suicide victims. Am J Psychiatry 1995; 152: 1075-1076. 8. Wender PH, Kety SS, Rosenthal D, et al. Psychiatric disorders in the biological and adoptive families of adopted individuals with affective disorder. Arch Gen Psychiatry 1986; 43: 923-929. 9. Gross-Isseroff R, Biegon A, Voet H, Weizman A. The suicide brain: a review of postmortem receptor/transporter binding studies. Neurosci Behav Rev 1998; 22: 653- 661. 10. Bures C, Courtet Ph., Leboyer M, et al. Association between suicide attempts and the tryptophane hydroxylase (TPH) gene [abstract]. Am J Hum Genet 1997; 61 (suppl.): A270. 11. Nielsen DA, Virkkunen M, Lappalainen J, et al. A tryptophan hydroxylase gene marker for suicidality and alcoholism. Arch Gen Psychiatry 1998; 55: 593-602 12. Mann JJ, Underwood MD, Arango V. Postmortem studies of suicide victims. In: Watson SJ, editor. Biology of schizophrenia and affective disease. Washington DC: American Psychiatric Press; 1996, 197-220. 13. Jain SK. Trends in mortality by causes of death in Australia, the states and territories during 1971-92, and in statistical divisions and sub-divisions during 1991-92. Canberra ACT: Joint publication of the National Centre for Epidemiology & Population Health and the Australian Bureau of Statistics, 1994. 14. Australian Bureau of Statistics. Suicides, Australia 1961-1981 (including historical series 1881-1981). Canberra ACT: Commonwealth of Australia, 1983. 15. Australian Bureau of Statistics. Causes of death, Australia, 1955-1996. Canberra ACT: Commonwealth of Australia, 1956-1997. 16. Australian Bureau of Statistics. Causes of infant and child deaths, Australia, 1982-1996. Canberra ACT: Commonwealth of Australia, 1998. 17. Australian Bureau of Statistics. Deaths, Australia, 1959-1996. Canberra ACT: Commonwealth of Australia, 1967- 1997. 18. Australian Bureau of Statistics. Suicides, Australia 1982-1992. Canberra ACT: Commonwealth of Australia, 1994. Figure 1 Australian male infant survival rates per 1,000 of live births (period 1938-1996) and Australian male youth (15-24) age-specific suicide rates per 100,000 of population (period 1960-1996). The suicide data points correspond, on the vertical axis, with the infant survival data points of 20 years earlier. Data source: Australian Bureau of Statistics (14-18).
Rising youth suicide rates are partly an effect of pubertal age advancement 5 April 2000
Thomas J P Verberne, Clinical Neuropsychologist (ret.) Send response to journal: Re: Rising youth suicide rates are partly an effect of pubertal age advancement	Solomon and Hellon, investigating all deaths by suicide registered in Alberta, Canada between 1951 and 1977, for which age and gender were available, found that “once a cohort entered the 15-19-year-old age range with a high rate of suicide, the rate for that cohort remained consistently high as it aged” (1, p. 511). The cohort effect was also observed in data from the U.S. (2), and Australia (3). In attempts at explaining the effect, a secular trend to suicide at younger ages was considered but rejected (2). In fact, in industrialized countries, a secular trend towards earlier puberty has been well documented (4, 5). Consistent with this trend, U.S. data showed a doubling of the suicide rate between 1950 and 1979 for boys aged 10-14 (from .05 per 100,000 to 1.1 per 100,000 of population) (6). In the same period, the rate of girls in the same age group quintupled (from 0.1 per 100,000 to 0.5 per 100,000 of population) (6). Australian data showed very similar rises, for the same age and sex groups, for the period 1965 to 1985 (7). In considering these findings, it should be kept in mind that the secular trend toward pubertal age advancement (PAA) has only a limited effect on the youth suicide rate. There are two interrelated reasons for this. One, there is no evidence of PAA of more than two years, even over a period of a century, or more (4). Two, the S-shaped curve, plotting suicide frequency as a function of age, is a characteristic growth curve: near-zero frequencies below the age of 14, then rapidly rising but relatively low frequencies up to the age of 20, then a slowing down in the rate of increase when the curve reaches average adult values. Thus, a drop in pubertal age affects only the rates on the lower part of the curve, where the number of suicides at each age is low and thus contributes relatively little to the pooled suicide rate of all 15-24-year -olds. The PAA effect is estimated to account for around 8 per cent of the total variance of the changes in the U.S. youth suicide rate reported by Murphy and Wetzel (2). Thus, the major part of these changes was probably due to the falling U.S. infant mortality rate (8). References 1. Solomon MI, Hellon CP. Suicide and age in Alberta, Canada, 1951 to 1977: a cohort analysis. Arch Gen Psychiatry 1980; 37: 511-513. 2. Murphy GE, Wetzel RD. Suicide risk by birth cohort in the U.S., 1949-1974. Arch Gen Psychiatry 1980; 37: 519-523. 3. Goldney RD, Katsikitis M. Cohort analysis of suicide rates in Australia. Arch Gen Psychiatry 1983; 40: 71-74. 4. Eveleth PB, Tanner JM. Worldwide variation in human growth. 2nd ed. Cambridge: Cambridge University Press, 1990. 5. Tanner JM. Trend towards earlier menarche in London, Oslo, Copenhagen, The Netherlands and Hungary. Nature 1973; 243: 95-96. 6. Eisenberg L. The epidemiology of suicides in adolescents. Pediatr Ann 1984; 13: 47-54. 7. Kosky R. Is suicidal behaviour increasing among Australian youth? Med J Aust 1987; 147: 164-166. 8. Verberne TJP. Rising youth suicide rates are a delayed effect of falling infant mortality. eBMJ [28 June, 1999].