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A Possible Cause of SIDS is Found in SIDS Data of Carpenter et al., BMJO 2013, Figure 1 and Table 1
SIDS is characterized and diagnosed by exclusion, especially when expert pediatric pathologists, trained forensic investigators, and learned epidemiologists are unable to find a sufficient cause of infant death at autopsy, at the scene, or in the data, respectively. Therefore the cause of SIDS may be invisible or immeasurable. Furthermore, SIDS is characterized by the fact that in every such case that the parents had no premonition that their infant was at imminent risk of death and "there was a complete absence of prodromal symptoms or any departure from the normal sufficient to justify the parent in seeking medical advice (1)." Therefore, most authors now look at risk factors that are not causes of death (prone sleep position, maternal smoking, etc.) However, they overlook three possible causal factors that alone might be insufficient to cause SIDS, but may act simultaneously in order to do so, that appear in this paper, as follows:
1) An unknown X-linked recessive allele for SIDS susceptibility with frequency q = 2/3, in Hardy-Weinberg-Equilibrium (HWE), that predicts the 50% male excess of SIDS for equal numbers of males and females at risk. The XY male is at risk with q = 2/3 and the XX female is at risk with q x q = 4/9, a 50% male excess. Given a nominal 5% male excess birth rate the expected male fraction is 0.612 for 60 x 1.05 males per 40 females (2). Table 1 reports 898 male and 578 female SIDS, for male fraction = 0.613;
2) Physiological anemia (3) causing the lognormal-type age distribution of SIDS in their Figure 1 that is its most unique characteristic. Unfortunately, "cases and controls over 1 year of age were excluded", which is like 'throwing the baby out with the bathwater.' The upper 1-year limit for SIDS is an artifact of the perception that SIDS over 1 year may include more false positives, so they should not be included in research studies.(4) Physiological anemia occurs when fetal hemoglobin (HbF) decays rapidly after birth while adult hemoglobin (HbA) slowly begins to replace the HbF. The term infant has its lifetime maximal total Hb at birth and it rapidly falls to their lifetime minimal Hb at or about 2-months of life, and then it follows a slow increase until a new equilibrium Hb concentration is established [we neglect here the different binding strengths of oxygen molecules to HbF and HbA, and pre-term Hb relations]. We estimated 19 as the missing number over 1-year that the authors excluded, by fitting an exponential decay curve to the numbers of SIDS from 8 weeks to 52 weeks in Figure 1 and extrapolating it to 178 weeks as determined previously as the upper limit for SIDS.(5) We then fit these weekly data (w) by the Johnson SB transformation that y = Log[(w + 1.343)/(178 - w)] where y = mu + sigma z, and mu = -1.025, sigma = 0.3, w is age in weeks, and z is a standard normal deviate. We interpret this Figure 1 as the number of the most anemic genetically susceptible infants whose total mix of Hb = HbF + HbA falls below some critical threshold, and therefore cannot survive a respiratory infection (see below) that reduces blood oxygenation in the lungs sufficiently to create an acute anoxic encephalopathy resulting in neuronal death. Hemoglobin concentration cannot be measured accurately at autopsy because of the gravitational settling of red blood cells during hemostasis leading to lividity so it is missing in virtually all SIDS autopsy studies (6); and
3. A prodromal respiratory infection (PRI) contracted from a family member that begins to fulminate shortly before or after the infant is placed for its final sleep. Farber (7) reported such a case where a baby was cared for by a nurse because the mother had a severe sore throat at the time. After a 2 p.m. uneventful feeding by the nurse, the baby was found dead 1.5 hours later, "lying on his back. There was no evidence of bedclothes, pillow or any other object over his face." We propose that the only thing that could have changed from the immediately previous sleep condition, sufficiently to cause death and be unnoticed, had to be a PRI that began to fulminate and cause fatal anoxic encephalopathy "before an important or appreciable amount of lung parenchyma has been involved." The author's Table 1 can provide no data on a potentially fatal respiratory infection presence in the SIDS cases, because, if such visible evidence existed at autopsy, the diagnosis by definition would not be SIDS. However, these data in Table 1 cast a visible shadow of a fulminating PRI. The authors list the SIDS and Control Live-Birth-Order (LBO) as shown below. We assume that Cohabiting Family Members (CFM) = 2 adults + (LBO - 1) Siblings = LBO + 1. We then assume that the probability of not carrying a communicable respiratory infection (CRI) (symptomatic or asymptomatic) is P so the probability of at least one CFM carrying a CRI is 1 - P^(CFM). Setting P = 0.92 by least squares gives the Model values shown. We previously fit U.S. LBO and SIDS data with P = 0.90 (8). Note that a plot of SIDS Fraction or SIDS Model vs CFM goes to the origin (0, 0) that implies that there are no SIDS cases here that are independent of CFM.
LBO = 1, SIDS = 407, Control = 1836, SIDS Fraction = 0.181, Model = 0.152;
LBO = 2, SIDS = 491, Control = 1566, SIDS Fraction = 0.239, Model = 0.219;
LBO = 3, SIDS = 280, Control = 748, SIDS Fraction = 0.272, Model = 0.280;
LBO = 4, SIDS = 149, Control = 304, SIDS Fraction = 0.329, Model = 0.337;
LBO = 5+, SIDS = 122, Control = 200,SIDS Fraction = 0.379, Model = 0.390.
In summary, SIDS may occur from these three causal factors (genetic susceptibility, physiological anemia, PRI) acting simultaneously that are a function of chance, age and CFM, respectively. There is no explanation we can find in the medical literature , other than an X-linkage in HWE, for a constant male fraction that is different from that of the male birth fraction. There is no explanation other than the maximum hemoglobin at birth for the virtual absence of SIDS immediately after live birth that is the most risky time for all other causes of infant death, the peak SIDS rate at or about the total Hb nadir, followed by an exponential decrease in SIDS rate as the infant's total HbA increases. We know of no other invisible cause of a sudden and unexpected infant death than a fulminating PRI that leaves no visible trace for the pathologist at autopsy or under the microscope in a genetically-susceptible physiologically-anemic infant.
1. Davison WH. Accidental Infant Suffocation. Br Med J. 1945;2(4416):251-2.
2. Mage DT, Donner EM. A genetic basis for the sudden infant death syndrome sex ratio. Med Hypotheses 1997;48:137-42.
3. O'Brien RT, Pearson HA. Physiologic anemia of the newborn infant. J Pediat 1971;79:132-8.
4. Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol. 1991;11(5):677-84.
5. Mage DT. A probability model for the age distribution of SIDS. J Sudden Infant Death Syndrome and Infant Mortality 1996;1(1):13-31.
6. Poets CF, Samuels MP, Wardrop CA, et al. Reduced haemoglobin levels in infants presenting with apparent life-threatening events--a retrospective investigation. Acta Paediatr. 1992;81(4):319-21.
7. Farber S. Fulminating streptococcus infections in infancy as a cause of sudden death. NEJM 1934;211:154-9.
8.Mage DT, Donner M, A unifying theory for SIDS. Int J Pediat 2009; 2009:368270
Conflict of Interest:
Evaluation of a tobacco prevention programme
We read with interest the study titled "Evaluation of a tobacco prevention programme among teenagers in Sweden".  This study makes a great contribution to the tobacco prevention programs. However we would like to bring out few points.
As the investigators had assigned the intervention (exposure), this study cannot be considered a cohort study and it does not have to qualities to be called a randomized controlled trial. Therefore, this study design may be most appropriately called a Quasi-experimental design with non-equivalent comparison.  We appraised the article based on the TREND checklist , which was primarily designed for reporting nonrandomized evaluations of behavioural and public health interventions. The article did not comply with many items in this checklist but we highlight a few important concerns here.
Complete details regarding the intervention such as the actual content of intervention, deliverer, delivery method, information on unit of delivery, number of sessions delivered and length of each session, the setting were not provided. Primary outcomes of the study were not clearly defined, in that they have measured only the prevalence of tobacco use rather than comparing the reduction in the prevalence of tobacco use. This would have also taken care of baseline variations (such as differences in the living conditions) between the comparison groups. Also, the authors have mentioned that the prevalence of smoking in the study area has decreased in the last 10 years; so to rule out any secular trend in the prevalence of smoking in this area and to attribute the change in smoking to the intervention an Interrupted Time Series Analysis  could have been performed.
Bivariate and multivariate analysis (Table 1) showed that there were no significant differences in the prevalence of smoking between the control group, participants, and non-participants at the end of the intervention. But the authors have mentioned that the prevalence of smoking was significantly lower among participants compared with non- participants and the control group by using Test for Trend between 3 groups at the end of intervention (Figure 2). We believed that the impact of this program could have been better estimated using baseline and follow up data and performing a Propensity Score weighted Difference-in- Difference analysis.  These important limitations cast a doubt over the method of analysis and the interpretations arising thereof and they have to be corrected or borne in mind to prevent wrongful conclusions.
1. Hedman L, Andersson M, Stridsman C, Ronmark E. Evaluation of a tobacco prevention programme among teenagers in Sweden. BMJ Open [Internet] 2015;5(5):e007673-e007673. Available from: http://bmjopen.bmj.com/cgi/doi/10.1136/bmjopen-2015-007673
2. U.S. Department of Health and Human Services. Centers for Disease Control and Prevention. Office of the Director. Office of Strategy and Innovation. Introduction to Program Evaluation for Public Health Programs?: A Self-Study Guide. 2011;(October):1-100.
3. Jarlais D, Cynthia L, Crepaz N. Improving the Reporting Quality of Nonrandomized Evaluations of Behavioral and Public Health Interventions: The TREND Statement. Am J Public Health 2004;94(3):361-6.
4. Lagarde M. How to do ( or not to do ) . . . Assessing the impact of a policy change with routine longitudinal data. Health Policy Plan [Internet] 2012;(January 2011):76-83. Available from: http://heapol.oxfordjournals.org/content/27/1/76.full?sid=3e9e83cf-fbcc- 4140-a869-b02f14f3074c
5. Shahidur K, Koolwal G, Samad H. Handbook on Impact Evaluation: Quantitative Methods and Practices. The World bank; 2009.
Conflict of Interest:
Vitamin D and endothelial function
Please be aware that cytomegalovirus (CMV) has a preference for endothelial tissue.
It has been proposed that Vitamin D may be interacting with CMV in the expression of endothelial conditions (1-5).
Also be aware that there may be time-dependant (i.e. year the study was conducted) relationships between the outcome observed in some studies (1-11).
1. Jones R (2013) Could cytomegalovirus be causing widespread outbreaks of chronic poor health. In Hypotheses in Clinical Medicine, pp 37-79, Eds M. Shoja, et al. New York: Nova Science Publishers Inc. Available from: http://www.hcaf.biz/2013/CMV_Read.pdf
2. Jones R (2013) Recurring outbreaks of a subtle condition leading to hospitalization and death. Epidemiology: Open access 4(3): 137.
3. Jones R (2014) A Study of an Unexplained and Large Increase in Respiratory Deaths in England and Wales: Is the Pattern of Diagnoses Consistent with the Potential Involvement of Cytomegalovirus? British Journal of Medicine and Medical Research 4(33): 5179-5192.
4. Jones R (2015) Roles for cytomegalovirus in infection, inflammation and autoimmunity. In Infection and Autoimmunity, 2nd Edition, Eds: N Rose, et al. Elsevier: Amsterdam. Chapter 18, pp 319-357.
5. Jones R (2015) An unexpected increase in adult appendicitis in England (2000/01 to 2012/13): Could cytomegalovirus (CMV) be a risk factor? British Journal of Medicine and Medical Research 5(5): 579-603.
6. Jones R (2015) A previously uncharacterized infectious-like event leading to spatial spread of deaths across England and Wales: Characteristics of the most recent event and a time series for past events. British Journal of Medicine and Medical Research 5(11): 1361- 1380.
7. Jones R, Beauchant S (2015) Spread of a new type of infectious condition across Berkshire in England between June 2011 and March 2013:Effect on medical emergency admissions. British Journal of Medicine and Medical Research 6(1): 126-148.
8. Jones R. (2015) Unexpected and Disruptive Changes in Admissions Associated with an Infectious-like Event Experienced at a Hospital in Berkshire, England around May of 2012. British Journal of Medicine and Medical Research 6(1): 56-76.
9. Jones R (2015) Recurring Outbreaks of an Infection Apparently Targeting Immune Function, and Consequent Unprecedented Growth in Medical Admission and Costs in the United Kingdom: A Review. British Journal of Medicine and Medical Research 6(8): 735-770.
10. Jones R (2015) A new type of infectious outbreak? SMU Medical Journal 2(1): 19-25.
11. Jones R (2015) Are emergency admissions contagious? BJHCM 21(5): 227-235.
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Correlation does not equal causality; selective presentation of the literature is beyond doubt
The reply by Rachiotis et al is disappointing. The main issue I raised was on the very selective presentation of the literature, in which the authors do not really respond. The second issue is the causality question.
As I had extensively stated in my response, our previous reports disputed a rise in suicides in Greece before 2010 and clearly reported this increase after 2010 [1-5]. I do not really follow the arguments of Rachiotis et al on this matter which is perfectly clear. The report in increased rates after 2010 was included in a letter and in an international study which is full and difficult to miss . On the contrary, the authors of the paper under discussion have repeatedly suggested the increase in suicide rates had started already since 2007. It is disappointing that Rachiotis et al did not take into consideration especially our international study which was the second to mention an increase of suicides in Greece  and discussed the issue of suicides and economic crisis in the whole of Europe Furthermore, Since they can not explain the problematic temporal relationship between unemployment rise and increase in suicides, they change their argument from 'unemployment' to 'extreme austerity'. The discussion here is on the possible effect of unemployment. And any university student in the field knows that correlation does not imply causality unless specific properties are met.
1. Fountoulakis KN, Koupidis SA, Grammatikopoulos IA, et al. First reliable data suggest a possible increase in suicides in Greece. Bmj 2013;347:f4900 doi: 10.1136/bmj.f4900[published Online First: Epub Date]|.
2. Fountoulakis KN, Koupidis SA, Siamouli M, et al. Suicide, recession, and unemployment. Lancet 2013;381(9868):721-2 doi: 10.1016/S0140-6736(13)60573-5[published Online First: Epub Date]|.
3. Fountoulakis KN, Savopoulos C, Siamouli M, et al. Trends in suicidality amid the economic crisis in Greece. European archives of psychiatry and clinical neuroscience 2013;263(5):441-4 doi: 10.1007/s00406 -012-0385-9[published Online First: Epub Date]|. 4. Fountoulakis KN, Siamouli M, Grammatikopoulos IA, et al. Economic crisis-related increased suicidality in Greece and Italy: a premature overinterpretation. Journal of epidemiology and community health 2013;67(4):379-80 doi: 10.1136/jech-2012-201902[published Online First: Epub Date]|.
5. Fountoulakis KN, Kawohl W, Theodorakis PN, et al. Relationship of suicide rates to economic variables in Europe: 2000-2011. The British journal of psychiatry : the journal of mental science 2014 doi: 10.1192/bjp.bp.114.147454[published Online First: Epub Date]|.
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Psychological counselling and risk stratification over the telephone: human or voice algorithm?
If a psychological screening and risk stratification system that does not require a awkward face to face meeting works, society will benefit from emotion prediction algorithms deployed to the young-who prefer app or phone based assessment and feedback.
I urge the researchers to assess the interposition of technology (like automated voice feedback) to mediate a telephone conversation. This risks disabling, or could augment, our inclination for civil and honest discourse. There is no more natural, direct and transparent interaction than the client calmly and politely elaborating on their distress to start proceedings. The call taker listens attentively, without interruption, and responds with meaningful solutions to the problem.
If there is no satisfactory resolution, referring the call to a senior clinician is advisable. In case of conflict, negotiating the timeline for fixing the complaint and the procedure for external mediation is an advisable last stop on the phone journey. A face to face meeting is held where the telling nuances of facial gestures and body language enhances prospects of a difficult resolution. Without the interference of technology, we are likely to remain well-tuned to our human condition and be mindful of others.
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Occurrence and impact of negative behavior, including domestic violence and abuse, in men attending UK primary care health clinics: a cross-sectional survey
I have read with deeper interest the Occurrence and impact of negative behavior, including domestic violence and abuse, in men attending UK primary care health clinics: a cross-sectional survey. The study has great contribution to behavior change modifiers in UK. The study on domestic violence on heterosexual partners is timely. The methods applied for this study were best suited for England and other developed countries. The nature of our society in Kenya which is greatly embedded on culture would less likely produce the same results. The age in question of 18 years still is na?ve. The type of vices they are involved in are different as compared to the UK i.e. unauthorized liquor drinking and others are wasted in bhang (cannabis sativa). Although the study was on males it would be interesting to do a replica on females who also experience domestic violence and abuse. This would present a platform for the comparison of the varied experiences.
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role of male involvement in safe birth outcome
Dear Editor, This paper is an interesting article, which addresses the role of traditional birth attendants in supporting the maternal, newborn and child health care. Pakistan has made a significant progress in training the traditional birth attendant to incorporate them into assisting of safe delivery through deploying them to the health facility to assist in deliveries. Based on the study findings in the paper, the study focus was based on one gender rather than involving both genders, other studies have shown that male partner participation has contributed to uptake of skilled delivery, a study by Judith Mange et al (2013) showed that male have the key decision making role at home and often control the finances of the house. Therefore, it would be my wish if both partners were involved to give a greater outcome to the study. It would be important if the authors also included the local authority, family members to form part of the referral system in order to reduce deaths that occur as a results of pregnancy. By Celestine Okang'
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Re: Associations between source of information about sex and sexual health outcomes in Britain: findings from the third National Survey of Sexual Attitudes and Lifestyles
Dear editor Addressing issues of sexuality among young people at this point is timely. Many studies have attributed inadequate sexual information among young people to their inability to make informed sexual choices which results into negative sexual outcomes including sexual transmitted diseases and unintended pregnancies.
The authors in this study attribute sources of information to transformational change among young people in developed countries. The study also showed that, implementing sexual education in schools enable adolescents to make informed choices on sexual matters. This study suggested that schools and parents are the main source of sexual and reproductive health information to youths. While this is true in developed countries, studies done in LMICs show different results in that, in LMICs, schools have well designed and elaborate sexual education curriculum, but with inadequate implementation, enforcement of educational guidelines and un-examinable curriculums. In addition, majority of parents are shy to openly discuss sexual matters with their Adolescents - owing to socio- cultural backgrounds. The study could have made comparisons in LMICs and see the outcome of such findings. On methodology, this study used cross-sectional design; further research on this topic in LMICs can employ qualitative design to explore associations between source of information and sexual health outcomes among young people this is due to socio- cultural factors. By Faith Chesire
Conflict of Interest:
DATA COLLECTION LIMITATION TO THE RESPONDENTThe idea of community involvement is relevant and ideal since it is recommended as one of the elements of primary health care which would then lead to the achievement of health care for all. This study has presented interesting findings which are good for the general health care system however, being that this was a qualitative study, the participants should have been given more time to express their understanding of over diagnosis and this could have given room for probes which could have produce more information for the study's conclusion. This is a very good study and it's recommendations are very good and should be taken up by the relevant persons.
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Comments on the referenced article
Dear Editor, Ref: Article: Predictors of skilled attendance at delivery among antenatal clinic attendants in Ghana: a cross-sectional study of population data - Amoakoh Coleman M, Ansah EK, Agyepong IA, et al
It is interesting to learn about the identified demographic, maternal, community and contextual predictors of skilled attendance at delivery among women who attend ANC at least once during their pregnancy in Ghana.
Characteristics of the study population on Table 2 could have been separated into the categories studied for ease of understanding, reference and also to guide the discussion.
The author indicates that women who are less likely to have skilled attendance at delivery can be identified during antenatal care using data using their socio economic and socio demographic data, and can be targeted with interventions to improve skilled attendance at delivery. Are there any of such existing interventions around the world and how effective have they been? Would such interventions be sustainable in the study area considering the economic constraints faced in developing countries?
Thank you, Liz Otieno
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