This paper is a welcome addition to attempts to explain the effects of the increased deaths in 2015 and beyond. Based on a 25-year career in NHS analysis and demand forecasting may I point out that these recurring periods of higher deaths and medical admissions are always accompanied by higher delayed discharges. Observations such as the association between delayed discharges and deaths/medical admissions have, unfortunately, never been published, however, the curious association between increased deaths and medical admissions has been published. Rather than cite over 100 studies the reader is advised to go to a list of publications at http://www.hcaf.biz/2010/Publications_Full.pdf where multiple aspects of cause and effect and possible causes have been explored.
Time lags are evident, with unexplained increased deaths always lagging unexplained increased emergency admissions, and lags between males and females evident in very small area geographies. Admissions for particular diagnoses rise while others fall during these curious events. Casemix severity may well be affected.
While it is clear that austerity has only exacerbated the impact of the current event on delayed discharges, as noted by the authors, I would be reluctant to say which trends are cause and effect, and which trends arise from association rather than causation.
The clear message is that far more research is required by both...
This paper is a welcome addition to attempts to explain the effects of the increased deaths in 2015 and beyond. Based on a 25-year career in NHS analysis and demand forecasting may I point out that these recurring periods of higher deaths and medical admissions are always accompanied by higher delayed discharges. Observations such as the association between delayed discharges and deaths/medical admissions have, unfortunately, never been published, however, the curious association between increased deaths and medical admissions has been published. Rather than cite over 100 studies the reader is advised to go to a list of publications at http://www.hcaf.biz/2010/Publications_Full.pdf where multiple aspects of cause and effect and possible causes have been explored.
Time lags are evident, with unexplained increased deaths always lagging unexplained increased emergency admissions, and lags between males and females evident in very small area geographies. Admissions for particular diagnoses rise while others fall during these curious events. Casemix severity may well be affected.
While it is clear that austerity has only exacerbated the impact of the current event on delayed discharges, as noted by the authors, I would be reluctant to say which trends are cause and effect, and which trends arise from association rather than causation.
The clear message is that far more research is required by both doctors, medical researchers, epidemiologists, and geographers. Hopefully in due time, a clearer picture will emerge.
We thank Timaeus and Scott for drawing readers' attention to our interpretation(1) of their data which differs from their own(2) (rapid response 28/7/2017). We are glad to explain our thinking especially as the issues go beyond their data and to the concepts and the UK quantitative evidence. We agree that in their paper after adjustment for three socio-economic and an area of residence variables the mortality rate ratios are lower in South Asian groups than in the White group.(2) The explanation for our different interpretation is that we placed emphasis on their model adjusting mortality for age, sex and period while they emphasised the results of models further adjusting for socio-economic status and residence.(2)
Generally the ‘healthy migrant effect’ is considered as unexpected and hence a paradox because immigrant populations sometimes have better health, most usually mortality, despite their socio-economic and other disadvantages.(3, 4) It is not generally understood as an effect that arises after adjustments for socio-economic and other related factors. In Timaeus and Scott’s model 1 the rate ratios for Indian, Pakistani and Bangladeshi populations born abroad and participating in the Longitudinal Study in England and Wales are shown in their table 5 and were 0.91, 0.95 and 1.01 with the 95% confidence intervals all including the reference value of 1. In model 1, the point estimates of the rate ratios for the same ethnic groups born in the UK were simil...
We thank Timaeus and Scott for drawing readers' attention to our interpretation(1) of their data which differs from their own(2) (rapid response 28/7/2017). We are glad to explain our thinking especially as the issues go beyond their data and to the concepts and the UK quantitative evidence. We agree that in their paper after adjustment for three socio-economic and an area of residence variables the mortality rate ratios are lower in South Asian groups than in the White group.(2) The explanation for our different interpretation is that we placed emphasis on their model adjusting mortality for age, sex and period while they emphasised the results of models further adjusting for socio-economic status and residence.(2)
Generally the ‘healthy migrant effect’ is considered as unexpected and hence a paradox because immigrant populations sometimes have better health, most usually mortality, despite their socio-economic and other disadvantages.(3, 4) It is not generally understood as an effect that arises after adjustments for socio-economic and other related factors. In Timaeus and Scott’s model 1 the rate ratios for Indian, Pakistani and Bangladeshi populations born abroad and participating in the Longitudinal Study in England and Wales are shown in their table 5 and were 0.91, 0.95 and 1.01 with the 95% confidence intervals all including the reference value of 1. In model 1, the point estimates of the rate ratios for the same ethnic groups born in the UK were similar to the above for Indian (0.88) and Pakistani (0.99) populations but much lower for Bangladeshis (0.55, with wide confidence intervals).
The interpretation of results following adjustment for socio-economic variables across different ethnic groups is difficult as reflected in a literature with contrary and unexpected findings,(5, 6) stimulating conceptual and methodological explorations.(7) Timaeus and Scott have, in addition to three socio-economic variables, also included one relating to residence in Metropolitan and non-metropolitan areas. Adjustments made little difference to the rate ratio for Indians (0.88), but reduced it for Pakistani (0.78) and Bangladeshi (0.59) populations born abroad (model 2, table 5). It is not straightforward to interpret the data, especially without examining the associations between each variable and the outcome by ethnic group as Fischbacher et al explain.(7)
Given the lack of good evidence for a healthy migrant effect in South Asian/Indian Subcontinent populations in England and Wales, (5, 8-10) though it was clear cut in Scotland, (11, 12) we interpreted Timaeus and Scott's paper as providing little evidence in favour of one. An alternative interpretation that we now offer on further reflection would have been somewhat closer to the authors’ own interpretation i.e. in Indian, Pakistani and Bangladeshi populations there was little evidence of a healthy migrant effect in age and sex adjusted data though adjustment for four additional factors indicated that it may have been suppressed by unfavourable socio-economic circumstances and living in certain kinds of areas.
Variable interpretations of data are sometimes genuine and sometimes mistakes; ours is in the former category. On this theme, Timaeus and Scott stated women born in the West Africa had lower all-cause mortality than those born in England and Wales in Wild et al’s work. But the SMR was 121(9) They also said that immigrants to England and Wales from most places of origin have lower all-cause mortality than the UK born population-that is not true for many groups, particularly those from the Indian subcontinent.(5, 9, 10, 13)
Timaeus and Scott say that UK-born minority ethnic populations do not have lower mortality than UK born Whites(2) but, as shown above, for the South Asian groups the point estimates of the rate ratios were similar to those for South Asians born abroad, and in the case of Bangladeshis were considerably lower. (That the confidence intervals straddled the reference value is surely a reflection of the smaller numbers of outcomes.)
We welcome this debate, which will hopefully stimulate further work, especially on linked mortality data sets, which are producing results(1, 2, 12, 14) which are somewhat different, especially in South Asians, from those in cross-sectional analysis of unlinked mortality and population size data.(5, 9, 10, 13) The totality of the evidence merits careful examination, possibly with reanalysis for better comparison, to judge whether there is truly a healthy migrant effect in South Asians in the UK.
1. Hayes L, White M, McNally RJQ, Unwin N, Tran A, Bhopal R. Do cardiometabolic, behavioural and socioeconomic factors explain the ‘healthy migrant effect’ in the UK? Linked mortality follow-up of South Asians compared with white Europeans in the Newcastle Heart Project. Journal of Epidemiology and Community Health. 2017.
2. Scott AP, Timaeus IM. Mortality differentials 1991-2005 by self-reported ethnicity: findings from the ONS Longitudinal Study. J Epidemiol Community Health. 2013;67(9):743-50.
3. Roura M. Unravelling migrants' health paradoxes: a transdisciplinary research agenda. J Epidemiol Community Health. 2017;71(9):870-3.
4. Bhopal RS. Migration, Ethnicity, Race and Health in Multicultural Societies. 2 ed. Oxford: Oxford University Press; 2014.
5. Marmot MG, Adelstein AM, Bulusu L. Immigrant mortality in England and Wales 1970 -78. Causes of death by country of birth. London: HMSO; 1984.
6. Harding S, Balarajan R. Longitudinal study of socio-economic differences in mortality among South Asian and West Indian migrants. EthnHealth. 2001;6:121-8.
7. Fischbacher CM, Cezard G, Bhopal RS, Pearce J, Bansal N. Measures of socioeconomic position are not consistently associated with ethnic differences in cardiovascular disease in Scotland: methods from the Scottish Health and Ethnicity Linkage Study (SHELS). International Journal of Epidemiology. 2014;43(1):129-39.
8. Balarajan R, Bulusu L, Adelstein AM, Shukla V. Patterns of mortality among migrants to England and Wales from the Indian subcontinent. BMedJ. 1984;289:1185-7.
9. Wild SH, Fischbacher C, Brock A, Griffiths C, Bhopal R. Mortality from all causes and circulatory disease by country of birth in England and Wales 2001-2003. J Public Health (Oxf). 2007;29(2):191-8.
10. Balarajan R, Bulusu L. Mortality among immigrants in England and Wales, 1979 - 83. In: Britton M, editor. Mortality and Geography: A review in the mid 1980's. London: HMSO; 1990. p. 103-21.
11. Fischbacher C, Steiner M, Bhopal R, Chalmers J, Jamieson J, Knowles D, et al. Variations in all cause and cardiovascular mortality by country of birth in Scotland, 1997-2003. Scottish Medical Journal. 2007;52(4):5-10.
12. Gruer L, Cezard G, Clark E, Douglas A, Steiner M, Millard A, et al. Life expectancy of different ethnic groups using death records linked to population census data for 4.62 million people in Scotland. Journal of Epidemiology and Community Health. 2016;70:1251-4.
13. Wild S, McKeigue P. Cross sectional analysis of mortality by country of birth in England and Wales, 1970-92. BMJ. 1997;314(7082):705-10.
14. Wallace M, Hill K. Mortality Among Immigrants in England and Wales: A Longitudinal Study. 2014.
To the Editor:
Jackson et al (1) demonstrate that head injuries sustained from 0 to 7 years predict higher rates of arrest and conduct problems in young adults. We would like to highlight however, that their findings suggest that head injury of a certain type is specifically linked to juvenile offence.
A careful examination of their work reveals a trend towards very early occurrence of head trauma that results in serious brain damage. The severity and age distribution of their dataset do not match those reported on overall (i.e. accidental and not accidental) pediatric head trauma. The British national enquiry (2) on overall pediatric head injury reports that 19% of injured children were younger than a year and that 21% of them had a Glasgow score below 15. Conversely, Jackson et al (1) show that 31% of head traumas occurred in the first year of life and that 38% of them resulted in loss of consciousness. An abundance of literature shows that, compared to children with accidental head trauma, abused children are more often < 1 year of age and hospitalized longer (3). Serious pediatric head injury in very young children is caused by inflicted trauma in a substantial number of cases. Brain hemorrhages are also markedly more common in abusive head injuries; this complication has been reported in 8-10% of children in the accident group (4), meanwhile Jackson et al (1) report the same in 18% of their subjects. Taken together, these data point at a large number...
To the Editor:
Jackson et al (1) demonstrate that head injuries sustained from 0 to 7 years predict higher rates of arrest and conduct problems in young adults. We would like to highlight however, that their findings suggest that head injury of a certain type is specifically linked to juvenile offence.
A careful examination of their work reveals a trend towards very early occurrence of head trauma that results in serious brain damage. The severity and age distribution of their dataset do not match those reported on overall (i.e. accidental and not accidental) pediatric head trauma. The British national enquiry (2) on overall pediatric head injury reports that 19% of injured children were younger than a year and that 21% of them had a Glasgow score below 15. Conversely, Jackson et al (1) show that 31% of head traumas occurred in the first year of life and that 38% of them resulted in loss of consciousness. An abundance of literature shows that, compared to children with accidental head trauma, abused children are more often < 1 year of age and hospitalized longer (3). Serious pediatric head injury in very young children is caused by inflicted trauma in a substantial number of cases. Brain hemorrhages are also markedly more common in abusive head injuries; this complication has been reported in 8-10% of children in the accident group (4), meanwhile Jackson et al (1) report the same in 18% of their subjects. Taken together, these data point at a large number of inflicted head injury within the sample of Jackson et al. In addition, much of the literature on the sequelae of early abuse shows that individuals who had been maltreated as children are at greater risk for being arrested as juveniles (5). Therefore, we would like to suggest that the well known mechanism that “violence begets violence” is worth to be taken into account for the proven association between pediatric head trauma and later violent delinquency.
REFERENCE
1. Jackson TL, Braun JM, Mello M, et al. The relationship between early childhood head injury and later life criminal behaviour: a longitudinal study. J Epidemiol Community Health 2017;71:800-5. doi: 10.1136/jech-2016-208582.
2. Trefan L, Houston R, Pearson G, et al. Epidemiology of children with head injury: a national overview. Arch Dis Child 2016;101:527-32. doi: 10.1136/archdischild-2015-308424.
3. Niederkrotenthaler T, Xu L, Parks Se, et al. Descriptive factors of abusive head trauma in young children--United States, 2000-2009. Child Abuse Negl 2013;37:446-55.doi: 10.1016/j.chiabu.2013.02.002.
4. Reece M, Sege R. Childhood head injuries: accidental or inflicted? Arch Pediatr Adolesc Med 2000;154:11-15.
5. Lansford JE, Miller-Johnson S, Berlin LJ, et al. Early physical abuse and later violent delinquency: a prospective longitudinal study. Child Maltreat 2007;12:233-45.
This paper makes a number of claims about health in the North relative to the South of England using comparisons of relatively low death rates. When the denominator in such calculations is a very low rate of death, the size of the difference can appear large. However, if we compare the absolute risk of dying, it is relatively close in the North and South and if we were to divide the rate of survival in the South by the rate of survival in the North each year, we would have a very small comparative statistic.
Abstracts and conclusions can easily be taken out of context and authors of papers like this one should be careful to present appropriate information. For example, the conclusion "...1.2 million northern excess deaths under age 75 over five decades.." implies very high potential death rates, a million! But this figure is presented with no population and reflects experience over 50 years. If we divide by 50, we get 24,000 deaths a year. A further weakness is that no measure of population is provided to put this total number of deaths in context. Using a plausible estimate of 20 million, for example, implies excess deaths at a rate of about 1.2 per 1,000 people. I wonder how many residents of the North are planning to migrate South today to reduce their risk of an early death by just over 1 in 1,000. Yes we should be concerned about all differences in health across regions and social groups but by inflating them with misleading divisions of one small num...
This paper makes a number of claims about health in the North relative to the South of England using comparisons of relatively low death rates. When the denominator in such calculations is a very low rate of death, the size of the difference can appear large. However, if we compare the absolute risk of dying, it is relatively close in the North and South and if we were to divide the rate of survival in the South by the rate of survival in the North each year, we would have a very small comparative statistic.
Abstracts and conclusions can easily be taken out of context and authors of papers like this one should be careful to present appropriate information. For example, the conclusion "...1.2 million northern excess deaths under age 75 over five decades.." implies very high potential death rates, a million! But this figure is presented with no population and reflects experience over 50 years. If we divide by 50, we get 24,000 deaths a year. A further weakness is that no measure of population is provided to put this total number of deaths in context. Using a plausible estimate of 20 million, for example, implies excess deaths at a rate of about 1.2 per 1,000 people. I wonder how many residents of the North are planning to migrate South today to reduce their risk of an early death by just over 1 in 1,000. Yes we should be concerned about all differences in health across regions and social groups but by inflating them with misleading divisions of one small number by another, researchers are contributing to the sensationalisation of such differences.
The paper citation is Buchan IE, et al.,North-South disparities in English mortality 1965– 2015: longitudinal population study, J Epidemiol Community Health 2017;0:1–9. doi:10.1136/jech-2017-20919
Hayes et al. [1] repeatedly cite a 2013 article by Scott and Timæus [2], also published in this journal, as having ‘not found a healthy migrant effect in South Asians’ and as providing ‘little evidence of a South Asian mortality advantage’. This contradicts our own interpretation of the results that we presented in that paper. We concluded that ‘Immigrants are selected for good health’. Moreover, with specific reference to South Asians, we stated that: ‘adjusted for SES and residence, … Indian, Pakistani, [and] Bangladeshi … immigrants all had lower mortality than UK-born Whites who were living in similar circumstances to them … This suggests that immigrants from the Indian subcontinent … are … selected for health’.
We think it regrettable that Hayes et al. do not indicate to readers of their paper that their interpretation of the results in our paper is almost diametrically opposed to our own. Moreover, they provide no explanation whatsoever of why they came to the view that we had misinterpreted our results.
Our study investigated all-cause mortality at ages 1−79 in 1991−2005 by self-reported ethnicity and country of birth. The data were from the Office for National Statistics Longitudinal Study of England and Wales for the cohort aged 0−64 in 1991. Poisson regression was used to adjust the estimates for metropolitan residence and three indicators of socioeconomic status. In the fully-adjusted model, but not the model that adjusted only for age, sex and per...
Hayes et al. [1] repeatedly cite a 2013 article by Scott and Timæus [2], also published in this journal, as having ‘not found a healthy migrant effect in South Asians’ and as providing ‘little evidence of a South Asian mortality advantage’. This contradicts our own interpretation of the results that we presented in that paper. We concluded that ‘Immigrants are selected for good health’. Moreover, with specific reference to South Asians, we stated that: ‘adjusted for SES and residence, … Indian, Pakistani, [and] Bangladeshi … immigrants all had lower mortality than UK-born Whites who were living in similar circumstances to them … This suggests that immigrants from the Indian subcontinent … are … selected for health’.
We think it regrettable that Hayes et al. do not indicate to readers of their paper that their interpretation of the results in our paper is almost diametrically opposed to our own. Moreover, they provide no explanation whatsoever of why they came to the view that we had misinterpreted our results.
Our study investigated all-cause mortality at ages 1−79 in 1991−2005 by self-reported ethnicity and country of birth. The data were from the Office for National Statistics Longitudinal Study of England and Wales for the cohort aged 0−64 in 1991. Poisson regression was used to adjust the estimates for metropolitan residence and three indicators of socioeconomic status. In the fully-adjusted model, but not the model that adjusted only for age, sex and period, immigrants of every ethnicity other than African and other non-Caribbean Black immigrants had significantly lower mortality than the UK-born White population. Most of our estimates of mortality by ethnic group in the UK-born population had wide confidence intervals. However, the UK-born Black Caribbean population had significantly higher mortality than the White population when we adjusted only for age, sex and period. This association disappeared after we also adjusted for socioeconomic status and place of residence.
Our own interpretation of these results remains that they demonstrate that immigrants to England and Wales, including those from South Asia, are selected for good health. However, the potential reduction in mortality arising from this healthy migrant effect is largely offset by the adverse consequences of the low socioeconomic status of most immigrants compared with the population as a whole (and equally vice versa). Our results provide no evidence to suggest that selection for health in one generation results in a persistent benefit to the mortality of subsequent generations.
References
[1] Hayes L, White M, McNally RJQ, et al. Do cardiometabolic, behavioural and socioeconomic factors explain the ‘healthy migrant effect’ in the UK? Linked mortality follow-up of South Asians compared with white Europeans in the Newcastle Heart Project. Journal of Epidemiology and Community Health 2017. doi:10.1136/jech-2017-209348
[2] Scott AP, Timæus IM. Mortality differentials 1991-2005 by self-reported ethnicity: findings from the ONS Longitudinal Study. Journal of Epidemiology and Community Health 2013; 67:743-50. doi:10.1136/jech-2012-202265
This is an excellent article which serves to highlight the value of Public Health work in economic terms. The findings need to be taken into account as future health and social care systems evolve. For example, in the UK, Sustainability & Transformation Plans (STPs) will only truly be sustainable if they get past paying lip service to Public Health programmes and actually invest in their implementation.
One aspect of the paper that is less helpful, however, is the distinction between 'local' and 'national' Public Health programmes. Such a distinction is arguably unclear and invalid given the fact that many national programmes require effective local implementation in order to be effective. This local implementation includes local investment, local co-design of delivery and local promotion and engagement of stakeholders and residents. In the UK, this work is undertaken by Public Health teams in local authorities in partnership with Clinical Commissioning Groups, Primary Care teams, Pharmacists and the Voluntary Sector. Effective local implementation also relies to some degree on co-design with residents.
To take an example from the list of 'National' interventions, family planning programmes in the UK are usually funded from the local Public Health budget and implemented according to a local strategy. For example, in some areas universal provision is supplemented by outreach services aimed at offering vulnerable women...
This is an excellent article which serves to highlight the value of Public Health work in economic terms. The findings need to be taken into account as future health and social care systems evolve. For example, in the UK, Sustainability & Transformation Plans (STPs) will only truly be sustainable if they get past paying lip service to Public Health programmes and actually invest in their implementation.
One aspect of the paper that is less helpful, however, is the distinction between 'local' and 'national' Public Health programmes. Such a distinction is arguably unclear and invalid given the fact that many national programmes require effective local implementation in order to be effective. This local implementation includes local investment, local co-design of delivery and local promotion and engagement of stakeholders and residents. In the UK, this work is undertaken by Public Health teams in local authorities in partnership with Clinical Commissioning Groups, Primary Care teams, Pharmacists and the Voluntary Sector. Effective local implementation also relies to some degree on co-design with residents.
To take an example from the list of 'National' interventions, family planning programmes in the UK are usually funded from the local Public Health budget and implemented according to a local strategy. For example, in some areas universal provision is supplemented by outreach services aimed at offering vulnerable women long acting contraception that enables them to take more control over their family planning. Another example is childhood vaccination, which while delivered according to a national schedule, relies on local work with schools and primary care to maximise uptake.
Public Health is cost effective. However, we mustn't make the mistake of thinking that nationwide 'one size fits all' programmes can fulfill its potential. Our population's appetite for being 'done unto' is waning fast - and we need to get back to recognising the role of co-design and implementation at a local community level if we are to sustain enthusiasm for Public Health work.
Sirs,
Peckham et al's selective reporting of the findings of the SCHER report
(2011) risks giving readers of your journal a highly misleading
interpretation of data on the fluoride intake of children in areas
supplied with water containing 1 mg/l of fluoride.
Careful analysis of the full detail of the SCHER report (2011) shows
that 6 to 12 year olds will not exceed the recommended upper limit (UL) of
2.5 mg per...
Sirs,
Peckham et al's selective reporting of the findings of the SCHER report
(2011) risks giving readers of your journal a highly misleading
interpretation of data on the fluoride intake of children in areas
supplied with water containing 1 mg/l of fluoride.
Careful analysis of the full detail of the SCHER report (2011) shows
that 6 to 12 year olds will not exceed the recommended upper limit (UL) of
2.5 mg per day even if they are routinely taking fluoride supplements (as
tablets, drops or lozenges), swallowing 10% of their toothpaste, and
consuming around two or three times as much water per day as the European
Food Safety Authority (EFSA) estimates to be likely. It also shows that 1
to 6 year olds are very unlikely to exceed the recommended UL of 1.5 mg of
fluoride per day unless they are routinely taking fluoride supplements,
swallowing around 40% of their toothpaste and possibly also putting more
than the recommended amount of paste on their brush.
SCHER's estimates were based on figures provided by EFSA which, in
its earlier 2005 report, states: "Children aged 1-8 years have fluoride
intakes from food and water well below the UL provided the fluoride
content of their
drinking water is not higher than 1.0 mg/l." It also states: "For
children older than eight years and adults the probability of exceeding
the UL on a normal diet is estimated to be low. However, consumption of
water with a high fluoride content, e.g., more than 2-3 mg/l, predisposes
to exceeding the UL."
The target level in fluoridation schemes in England is 1 mg/l.
The above suggests that Peckham et al have not correctly represented
what SCHER was saying in the body of its report. Further, it should be
borne in mind that medical and dental practitioners in England do not
prescribe fluoride supplements to children in fluoridated areas and that
parents are advised to supervise their children's toothbrushing up to
about the age of seven - in both fluoridated and non-fluoridated areas -
to ensure that they put only a pea-sized amount of toothpaste on the brush
and they do not swallow any after they have finished brushing.
Finally, in the specific context of the Peckham et al hypothesis on
hypothyroidism, it is worth noting SCHER's conclusion that "a systematic
evaluation of human studies does not suggest a potential thyroid effect at
realistic human exposures to fluoride."
Yours sincerely,
Michael A Lennon OBE
Professor Emeritus
University of Sheffield
Dr John F Beal MBE
Hon Senior Lecturer in Dental Public Health
University of Leeds
Conflict of Interest:
Dr John Beal - Vice Chair, British Fluoridation
Prof Michael Lennon - Scientific Advisor, British Fluoridation Society
The World Health Organisation's setting of global viral hepatitis elimination targets, focused on hepatitis B & C, is most welcome1. In their commentary article, Hellard, Sacks-Davis & Doyle describe strategies by which hepatitis C elimination by 2030 can be achieved by a combination of direct acting antiviral drugs against hepatitis C, opioid substitution therapy and needle and syringe programmes...
The World Health Organisation's setting of global viral hepatitis elimination targets, focused on hepatitis B & C, is most welcome1. In their commentary article, Hellard, Sacks-Davis & Doyle describe strategies by which hepatitis C elimination by 2030 can be achieved by a combination of direct acting antiviral drugs against hepatitis C, opioid substitution therapy and needle and syringe programmes 2.
The authors are optimistic of achieving this World Health Organisation hepatitis C virus elimination target. They describe in detail how hepatitis C could be eliminated in persons who inject drugs in Australia with the aforementioned strategies.
Hellard et al focus on persons who inject drugs as the subgroup with the highest prevalence of hepatitis C disease. This is true in other developed countries. However, what is striking about their reflections on hepatitis C elimination in the Australian context is the absence of reference to hepatitis C in men who have sex with men and the potential impact of immigration.
Hepatitis C virus infection in Human Immunodeficiency Virus -infected men who have sex with men has been increasingly recognised in Europe and North America for over a decade. The epidemiology of sexual transmission of hepatitis C has recently been reviewed by Chan et al3.
International migration of persons from high prevalence developing countries to developed countries risks the introduction/ re-introduction of hepatitis C. The complex interplay between immigration and viral hepatitis has recently been reviewed by Sharma et al4.
Countries which aim to achieve the World Health Organisation target of hepatitis C elimination by 2030 need to monitor the evolving epidemiology of hepatitis C in all at-risk groups be they persons who inject drugs, men who have sex with men or immigrants as part of their hepatitis C elimination strategies.
Hellard et al acknowledge the high cost of direct acting antivirals as a barrier to elimination, but point out that prices are likely to fall in future. Despite this, many developing countries will not be able to afford hepatitis C direct acting antivirals on any significant scale. The state of public health in some of the poorest developing countries is unfortunate. I note that according to the World Health Organisation "..1.1 billion people has no access to any type of improved drinking source of water" (sic)5. For resource-poor countries, the chances of achieving hepatitis C elimination by 2030 appear slim.
In conclusion, the goal of hepatitis C elimination by 2030 is possible in developed nations with robust strategies targeting all at-risk groups. Regrettably, there is less room for optimism in the most resource-poor developing countries where simple aspirations like supplying safe drinking water take priority.
References:
1. Global Health Sector Strategy on Viral Hepatitis 2016-2021. World Health Organisation http://www.who.int/hepatitis/strategy2016-2021/ghss-hep/en/ (accessed 2/9/16)
2. Hepatitis C elimination by 2030 through treatment and prevention: think global, act in local networks. J Epidemiol Community Health Published online first 24 June 2016 doi:10.1136/jech-2015-
205454
3. Sexually acquired hepatitis C infection: a review. Chan DPC, Sun HY, Wong HTH & Hung CC. International Journal of Infectious Diseases 2016;49:47-58 http://dx.doi.org/10.1016/j.ijid.2016.05.030
4. Immigration and viral hepatitis. Sharma S et al. Journal of Hepatology 2015;63:515-522
5. World Health Organisation: Water sanitation and health (WSH) http://www.who.int/water_sanitation_health/mdg1/en/ (accessed 1/9/16)
The analysis of data on the prevalence of hypothyroidism in areas
with different concentrations of fluoride in the public drinking water
supplies, by workers at the University of Kent,[1] is interesting but by
no means conclusive. The authors rightly emphasise that their findings do
not prove that fluoridation causes people to develop the condition,but
only that there is a clear correlation. In fact this study raises m...
The analysis of data on the prevalence of hypothyroidism in areas
with different concentrations of fluoride in the public drinking water
supplies, by workers at the University of Kent,[1] is interesting but by
no means conclusive. The authors rightly emphasise that their findings do
not prove that fluoridation causes people to develop the condition,but
only that there is a clear correlation. In fact this study raises more
questions that it actually answers.
Public Health England's Water Fluoridation Health Monitoring Report
for England 2014 [2], so widely cited by supporters of the practice, is in
fact riddled with statistical improprieties. It has become the norm for
the dental public health sector to dismiss all complaints that
fluoridation is harmful to thyroid function, and the 2014 PHE report fails
to mention it at all. This study appears to challenge that position.
In this new study the authors report that there is an at least 30%
greater prevalence of hypothyroidism in areas with more than 0.3mg/l of
fluoride in the public water supplies. However, this limit is not a
threshold; it is merely the dividing point between two out of the three
arbitrarily chosen ranges of fluoride concentration in drinking water. The
apparent 'boundary' between a safe and an unsafe concentration of fluoride
is an experimental artifact, not a representation of what happens in real
life.
So it is only permissible to draw a generalised conclusion from this
study. This is disappointing. Fluoride overdose is now endemic - half of
all children growing up in fluoridated water areas develop at least some
detectable form of dental fluorosis, the only visible biomarker for
incipient fluoride toxicosis. In non-fluoridated areas the prevalence of
this condition is around one quarter.
Clearly, other sources of bioavailable fluoride are already
contributing to this undesirable body-burden. If there is a causative link
between fluoride absorption and thyroid function, then it is reasonable to
propose that all bioavailable fluoride sources may contribute to the
problem. This would imply that that many people may be prone to
hypothyroidism due to the increasing background contamination of our foods
and dental products with fluoride. If so, this might suggest that the
extra fluoride in some water supplies may be pushing more people over the
threshold at which GPs start to notice that more of their patients have
this condition.
Another missed opportunity?
There is one intriguing feature of this study that illustrates what
could be done to clarify our understanding of the medical consequences of
water fluoridation, if only the government would stop prevaricating and
put some real effort into sorting out the whole mess.
This new study compares hypothyroidism prevalence across the country
with data on the average annual fluoride level maintained in drinking
water supplies during 2012. Those of us in the Lake District will be aware
that, although the authors show (correctly) that West Cumbria was not
fluoridated in 2012, in fact the region has been fluoridated since around
1970.
The local water supplier, United Utilities, shut down its
fluoridation activities in 2007 to carry out maintenance, resuming
fluoridation in September 2013. So for six years those people who had been
drinking fully fluoridated water for up to almost forty years had their
access to the 'benefits' of this product interrupted.
Both accidents and anomalies can provide unique opportunities to
examine novel questions that that may never be considered when looking at
generalised data, and this six year halt to fluoridation in West Cumbria
provided just such an opportunity. So it is unfortunatle that the new
study does not reveal whether the risk of hypothyroidism in West Combria
is elevated.
It would have been enormously interesting to learn how prevalent
hypothyroidism was in this area before and during, and is now after, that
fluoride-free interlude. Was the prevalence of the condition elevated
before fluoridation stopped? If so, did it fall, during the hiatus in
supply? And has it increased again since?
Presumably raw data are available to answer these questions, but have
not yet been analysed. It would be fascinating to see whether or not the
prevalence of hypothyroidism changed. The results of such an analysis
might yet provide support for proposing that correlation may reasonably
imply causation and, if so, whether stopping the practice in other
fluoridated areas might bring similar relief to the afflicted.
Douglas Cross, CSci, CBiol. FSB.
References
1. Peckham S, Lowery D, Spencer S.(2015) Are fluoride levels in
drinking water associated with hypothyroidism prevalence in England? A
large observational study of GP practice data and fluoride levels in
drinking water. J Epidemiol Community Health 2015;0:1-6.
doi:10.1136/jech-2014-204971
2. Public Health England. Water Fluoridation. Health monitoring
report for England
2014. PHE publications gateway number: 2013547, 2014.
In relation to the reported findings in this study of a correlation
between higher socioeconomic position and incidence of brain tumour,
specifically giloma and acoustic neuroma, among a cohort of Swedish-born
residents, the authors postulate 'completeness of cancer registration' and
'detection bias' as a potential explanation.
This seems unlikely, especially given the progressive nature of brain
tumour pathology...
In relation to the reported findings in this study of a correlation
between higher socioeconomic position and incidence of brain tumour,
specifically giloma and acoustic neuroma, among a cohort of Swedish-born
residents, the authors postulate 'completeness of cancer registration' and
'detection bias' as a potential explanation.
This seems unlikely, especially given the progressive nature of brain
tumour pathology, i.e. socioeconomic background would have little effect
on the eventual likelihood of a patient entering the (taxpayer funded)
medical system, and thus small statistical significance.
In May 2011, the International Agency for Research on Cancer
classified radiofrequency electromagnetic fields - as emitted by mobile
phones - as "possibly carcinogenic to humans" (IARC Group 2B), based on
"limited" epidemiological studies showing an indication of an increased
risk of glioma or acoustic neuroma.
In May 2016, it was reported (http://microwavenews.com/news-
center/ntp-cancer-results) that the US government's recently completed $25
million National Toxicology Program study shows statistically significant
increases in cancer - specifically giloma and malignant schwannoma of the
heart, the latter affecting the same type of cell as acoustic neuroma -
among rats that had been exposed to GSM or CDMA signals for two years.
Is it not the case that those with higher SEP, i.e. professionals as
opposed to manual labourers, would statistically be more likely to have an
increased exposure to microwaves from both cordless and mobile phones,
used as an administrative tool in the workplace (regardless of personal
use outside of these hours).
Mobile phone use in the workplace became widespread during the 1980's
and onwards. The authors of this study looked at a primary diagnosis of
brain tumour among cohort members between 1993 and 2010. Allowing for a
latency period of up to 10 years plus for the development of brain tumour
following carcinogenic exposure, is it not worth exploring this potential
link, rather than the somewhat weaker theory of 'detection bias'.
This paper is a welcome addition to attempts to explain the effects of the increased deaths in 2015 and beyond. Based on a 25-year career in NHS analysis and demand forecasting may I point out that these recurring periods of higher deaths and medical admissions are always accompanied by higher delayed discharges. Observations such as the association between delayed discharges and deaths/medical admissions have, unfortunately, never been published, however, the curious association between increased deaths and medical admissions has been published. Rather than cite over 100 studies the reader is advised to go to a list of publications at http://www.hcaf.biz/2010/Publications_Full.pdf where multiple aspects of cause and effect and possible causes have been explored.
Time lags are evident, with unexplained increased deaths always lagging unexplained increased emergency admissions, and lags between males and females evident in very small area geographies. Admissions for particular diagnoses rise while others fall during these curious events. Casemix severity may well be affected.
While it is clear that austerity has only exacerbated the impact of the current event on delayed discharges, as noted by the authors, I would be reluctant to say which trends are cause and effect, and which trends arise from association rather than causation.
The clear message is that far more research is required by both...
Show MoreWe thank Timaeus and Scott for drawing readers' attention to our interpretation(1) of their data which differs from their own(2) (rapid response 28/7/2017). We are glad to explain our thinking especially as the issues go beyond their data and to the concepts and the UK quantitative evidence. We agree that in their paper after adjustment for three socio-economic and an area of residence variables the mortality rate ratios are lower in South Asian groups than in the White group.(2) The explanation for our different interpretation is that we placed emphasis on their model adjusting mortality for age, sex and period while they emphasised the results of models further adjusting for socio-economic status and residence.(2)
Generally the ‘healthy migrant effect’ is considered as unexpected and hence a paradox because immigrant populations sometimes have better health, most usually mortality, despite their socio-economic and other disadvantages.(3, 4) It is not generally understood as an effect that arises after adjustments for socio-economic and other related factors. In Timaeus and Scott’s model 1 the rate ratios for Indian, Pakistani and Bangladeshi populations born abroad and participating in the Longitudinal Study in England and Wales are shown in their table 5 and were 0.91, 0.95 and 1.01 with the 95% confidence intervals all including the reference value of 1. In model 1, the point estimates of the rate ratios for the same ethnic groups born in the UK were simil...
Show MoreTo the Editor:
Show MoreJackson et al (1) demonstrate that head injuries sustained from 0 to 7 years predict higher rates of arrest and conduct problems in young adults. We would like to highlight however, that their findings suggest that head injury of a certain type is specifically linked to juvenile offence.
A careful examination of their work reveals a trend towards very early occurrence of head trauma that results in serious brain damage. The severity and age distribution of their dataset do not match those reported on overall (i.e. accidental and not accidental) pediatric head trauma. The British national enquiry (2) on overall pediatric head injury reports that 19% of injured children were younger than a year and that 21% of them had a Glasgow score below 15. Conversely, Jackson et al (1) show that 31% of head traumas occurred in the first year of life and that 38% of them resulted in loss of consciousness. An abundance of literature shows that, compared to children with accidental head trauma, abused children are more often < 1 year of age and hospitalized longer (3). Serious pediatric head injury in very young children is caused by inflicted trauma in a substantial number of cases. Brain hemorrhages are also markedly more common in abusive head injuries; this complication has been reported in 8-10% of children in the accident group (4), meanwhile Jackson et al (1) report the same in 18% of their subjects. Taken together, these data point at a large number...
This paper makes a number of claims about health in the North relative to the South of England using comparisons of relatively low death rates. When the denominator in such calculations is a very low rate of death, the size of the difference can appear large. However, if we compare the absolute risk of dying, it is relatively close in the North and South and if we were to divide the rate of survival in the South by the rate of survival in the North each year, we would have a very small comparative statistic.
Abstracts and conclusions can easily be taken out of context and authors of papers like this one should be careful to present appropriate information. For example, the conclusion "...1.2 million northern excess deaths under age 75 over five decades.." implies very high potential death rates, a million! But this figure is presented with no population and reflects experience over 50 years. If we divide by 50, we get 24,000 deaths a year. A further weakness is that no measure of population is provided to put this total number of deaths in context. Using a plausible estimate of 20 million, for example, implies excess deaths at a rate of about 1.2 per 1,000 people. I wonder how many residents of the North are planning to migrate South today to reduce their risk of an early death by just over 1 in 1,000. Yes we should be concerned about all differences in health across regions and social groups but by inflating them with misleading divisions of one small num...
Show MoreHayes et al. [1] repeatedly cite a 2013 article by Scott and Timæus [2], also published in this journal, as having ‘not found a healthy migrant effect in South Asians’ and as providing ‘little evidence of a South Asian mortality advantage’. This contradicts our own interpretation of the results that we presented in that paper. We concluded that ‘Immigrants are selected for good health’. Moreover, with specific reference to South Asians, we stated that: ‘adjusted for SES and residence, … Indian, Pakistani, [and] Bangladeshi … immigrants all had lower mortality than UK-born Whites who were living in similar circumstances to them … This suggests that immigrants from the Indian subcontinent … are … selected for health’.
We think it regrettable that Hayes et al. do not indicate to readers of their paper that their interpretation of the results in our paper is almost diametrically opposed to our own. Moreover, they provide no explanation whatsoever of why they came to the view that we had misinterpreted our results.
Our study investigated all-cause mortality at ages 1−79 in 1991−2005 by self-reported ethnicity and country of birth. The data were from the Office for National Statistics Longitudinal Study of England and Wales for the cohort aged 0−64 in 1991. Poisson regression was used to adjust the estimates for metropolitan residence and three indicators of socioeconomic status. In the fully-adjusted model, but not the model that adjusted only for age, sex and per...
Show MoreThis is an excellent article which serves to highlight the value of Public Health work in economic terms. The findings need to be taken into account as future health and social care systems evolve. For example, in the UK, Sustainability & Transformation Plans (STPs) will only truly be sustainable if they get past paying lip service to Public Health programmes and actually invest in their implementation.
One aspect of the paper that is less helpful, however, is the distinction between 'local' and 'national' Public Health programmes. Such a distinction is arguably unclear and invalid given the fact that many national programmes require effective local implementation in order to be effective. This local implementation includes local investment, local co-design of delivery and local promotion and engagement of stakeholders and residents. In the UK, this work is undertaken by Public Health teams in local authorities in partnership with Clinical Commissioning Groups, Primary Care teams, Pharmacists and the Voluntary Sector. Effective local implementation also relies to some degree on co-design with residents.
To take an example from the list of 'National' interventions, family planning programmes in the UK are usually funded from the local Public Health budget and implemented according to a local strategy. For example, in some areas universal provision is supplemented by outreach services aimed at offering vulnerable women...
Show MoreSirs, Peckham et al's selective reporting of the findings of the SCHER report (2011) risks giving readers of your journal a highly misleading interpretation of data on the fluoride intake of children in areas supplied with water containing 1 mg/l of fluoride.
Careful analysis of the full detail of the SCHER report (2011) shows that 6 to 12 year olds will not exceed the recommended upper limit (UL) of 2.5 mg per...
The World Health Organisation's setting of global viral hepatitis elimination targets, focused on hepatitis B & C, is most welcome1. In their commentary article, Hellard, Sacks-Davis & Doyle describe strategies by which hepatitis C elimination by 2030 can be achieved by a combination of direct acting antiviral drugs against hepatitis C, opioid substitution therapy and needle and syringe programmes...
The analysis of data on the prevalence of hypothyroidism in areas with different concentrations of fluoride in the public drinking water supplies, by workers at the University of Kent,[1] is interesting but by no means conclusive. The authors rightly emphasise that their findings do not prove that fluoridation causes people to develop the condition,but only that there is a clear correlation. In fact this study raises m...
In relation to the reported findings in this study of a correlation between higher socioeconomic position and incidence of brain tumour, specifically giloma and acoustic neuroma, among a cohort of Swedish-born residents, the authors postulate 'completeness of cancer registration' and 'detection bias' as a potential explanation.
This seems unlikely, especially given the progressive nature of brain tumour pathology...
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