I am not a health care professional, but a mother who brought my
babies into my bed a couple of decades ago when it appeared that that was
the best way for me to get enough rest to be able to care for them. I have
read with interest the recent meta-analysis by Carpenter et al. concluding
that bed-sharing increases the risk of SIDS even in the case of breast-
feeding, non-smoking mothers. [1]
I am not a health care professional, but a mother who brought my
babies into my bed a couple of decades ago when it appeared that that was
the best way for me to get enough rest to be able to care for them. I have
read with interest the recent meta-analysis by Carpenter et al. concluding
that bed-sharing increases the risk of SIDS even in the case of breast-
feeding, non-smoking mothers. [1]
I thank Drs. Renz-Polster and De Bock for pointing out in their June
10 letter the importance of distinguishing between routine, planned bed-
sharing and bed-sharing which may occur as a spur-of-the-moment deviation
from the routine. For parents who want to know if they endanger their
babies by establishing the bed-sharing habit from birth, a study which
does not make this distinction is of limited practical use.
I have a further concern about the present analysis which has not
been mentioned by the other letter-writers. In the section of the article
intended to give an "overview of the absolute risks and increases in risk
associated with bed sharing," the authors chose to focus on a "typical
cohabiting white mother aged 26-30 having a second normal weight baby with
birth weight between 2.5 and 3.5 kg," which they characterize as "the most
common situation of a mother completing her family." They utilized, in
other words, a weight categorization which includes the lower end of
normal birth weights, where SIDS rates are higher, but excludes the entire
upper end of the normal range, from 3.5-4.0 kg, where SIDS rates are
extremely low. Of course all groupings of this sort are essentially
arbitrary, but if a one-kilogram span was desired, then the range of 3.0-
4.0 kg would include far more babies than the one that was used. Among the
control groups in this meta-analysis - which ought to better represent the
general populations than the cases of SIDS - fully 50.1% of the babies had
birth weights over 3.5 kg. It is possible that this percentage drops to
less than half under the specific conditions of race, age, living
situation and birth order cited above, but even so it is clear that the
3.0-4.0 kg category would be more representative than the 2.5-3.5 kg
highlighted as "most common."
The many parents - myself among them - whose babies were born
weighing over 3.5 kg would have to look at the online supplement to the
article to find predicted rates of SIDS in room-sharing versus bed-sharing
conditions. It turns out that for "cohabiting white women age 30+ with 1st
baby birth weight > 3500g," the expected rate of SIDS for breast-fed
infants sleeping supine and sharing a room with parents who are not
smoking or intoxicated is 11 out of a million. For bed-sharing infants the
expected rate is 31 out of a million.[2] In other words, my husband and I
were theoretically running an additional risk of 1 in 50,000 by bed-
sharing. That happens to be, according to the BMJ, the same as the risk of
dying while playing soccer - something we also allowed our children to do.
[3]
Elizabeth Bernstein
Bisbee, Arizona, United States
REFERENCES
1. Carpenter R, McGarvey C, Mitchell EA et al. Bed sharing when
parents do not smoke: is there a risk of SIDS? An individual level
analysis of five major case-control studies. BMJ Open
2013;3:e002299.doi:10.1136/bmjopen-2012-002299.
Brinsden and colleagues1 describe the decrease in the salt content of
bread sold in the UK. They see this as evidence of success for the policy
of voluntary agreements with the food industry. In actuality, a careful
assessment of the facts and figures given in their paper reveals the
failure of the policy.
Between 2001 and 2011 salt intake by adults in the UK fell by about
15%, i.e., from 9.5 to 8.1 g/day. The t...
Brinsden and colleagues1 describe the decrease in the salt content of
bread sold in the UK. They see this as evidence of success for the policy
of voluntary agreements with the food industry. In actuality, a careful
assessment of the facts and figures given in their paper reveals the
failure of the policy.
Between 2001 and 2011 salt intake by adults in the UK fell by about
15%, i.e., from 9.5 to 8.1 g/day. The target is 6 g/day which means that
at the current rate of progress, this will not be achieved until around
2026. To make matters worse, this target is probably set too high. The
2010 version of Dietary Guidelines for Americans recommends that sodium
intake for adults should not exceed 2300 mg (5.9 g salt) per day.2
However, for the half of the population who are aged over 50 years or at
risk, they recommend that a more appropriate upper limit is 1500 mg (3.8 g
salt) per day (USDA). The only practical way to achieve a target of 3.8
g/day of salt for half of all adults is to strive for that target for all
adults.
The paper by Brinsden et al.1 makes the point that the UK has
achieved more success in this area than any other country. In the final
sentence of the paper the authors state: "Governments
around the world now need to follow the UK's lead ..." If other countries
followed that advice, it would probably take them until around 2025 to
2040 (depending on where they are now) to achieve a target salt intake for
adults of 5.9 g/day, or until well beyond 2050 to achieve a target of 3.8
g/day.
Fortunately, there is an alternative strategy. Governments in many
countries have banned various toxic substances, including lead in petrol,
smoking in many indoor public places, and (in some jurisdictions) the
presence of trans-fatty acids in foods. There is no reason to believe that
what works for these substances will not work equally well for salt. If
governments mandated a salt reduction, the targets could be achieved
within a few years at minimal cost. There is probably no other policy that
could have such an enormous beneficial impact on public health, so
quickly, and at so little cost.
1. Brinsden HC, He FJ, Jenner KH, MacGregor G. Surveys of the salt
content in UK bread: progress made and further reductions possible. BMJ
Open 2013;3:e002936.
2. U.S. Department of Agriculture. Diet Guidelines, 2010.
http://www.cnpp.usda.gov/DGAs2010-PolicyDocument.htm (accessed 16 June
2013).
Abstract Alpha-linolenic acid (ALA) consumption has been linked to
risk of prostate cancer theoretically, but the findings were conflicting
from observational studies. Results from recent meta-analysis suggested a
small risk, moderate protective and no effect of alpha-linolenic acid
consumption on prostate cancer risk. However, the relationship, if exists,
between alpha-linolenic acid consumption and prostate cancer ris...
Abstract Alpha-linolenic acid (ALA) consumption has been linked to
risk of prostate cancer theoretically, but the findings were conflicting
from observational studies. Results from recent meta-analysis suggested a
small risk, moderate protective and no effect of alpha-linolenic acid
consumption on prostate cancer risk. However, the relationship, if exists,
between alpha-linolenic acid consumption and prostate cancer risk is
unclear. Thus, the dose-response relationship was assessed by restricted
cubic spline model and multivariate random-effect meta-regression. The
results suggested that a significant association was found between alpha-
linolenic acid consumption and decreased risk of prostate cancer among
subjects consuming 0.2-1.3g of alpha-linolenic acid per day. A potential
nonlinear relationship should be assessed before assuming a linear
relationship.
We read with great interest the article by Carleton et al. [1] titled
''Case-control and prospective studies of dietary alpha-linolenic acid
intake and prostate cancer risk: a meta-analysis.'' The study failed to
confirm an association between dietary ALA intake and prostate cancer
risk. However, the findings were inconsistent with the prior meta-analysis
by Simon et al. [2] and Carayol et al. [3] indicating a small increased
risk and weak protective association between dietary ALA intake and
prostate, respectively. This is a very important investigation considering
the widespread consumption of alpha-linolenic acid and high incidence of
prostate cancer. Thus, it is meaningful regarding the exploration of the
causes and control of prostate cancer. However, we would like to draw
attention to the type of dose-response analysis between alpha-linolenic
acid consumption and risk of prostate cancer, because, Simon et al.,
Carayol et al. and Carleton et al. [1-3]assumed a linear dose relationship
without performing a formal test and the dose relationship was not
assessed in the meta-analysis, and linear associations in epidemiologic
research can rarely be assumed a priori [4]. Besides, categories of alpha-
linolenic acid consumption per day differed between studies, which might
complicate the interpretation of the pooled results across study
populations with different categories. In this respect, a dose-response
meta-analysis provides a solution to the problem, from which a summary
risk estimate can be derived for a standardized increase and specific
exposure values considering alpha-linolenic acid consumption per day.
Studies included in this dose-response analysis must provide the
following information: the number of cases and participants, and odds
ratio (OR for case-control studies) and relative risk (RR for cohort
studies) estimates with 95 % confidence intervals (CIs) for each category
of alpha-linolenic acid consumption were extracted. We extracted the OR or
RR (95 % CI) that reflected the greatest degree of control for potential
confounders. The median or mean alpha-linolenic acid consumption for each
category was assigned to each corresponding OR for every study. If the
upper boundary of the highest category was not provided, we assumed that
the boundary had the same amplitude as the adjacent category. Detailed
information of the included publications is shown in the Table 1 (for case
- control studies) and Table 2 (for cohort studies).
A two-stage random-effects dose-response meta-analysis was performed
taking into account the between-study heterogeneity proposed by Orsini et
al. [5] to compute the trend from the correlated log OR or RR estimates
across categories of alpha-linolenic acid consumption per day. Briefly, a
restricted cubic spline model, with four knots at the 5th, 35th, 65th, and
95th percentiles [6] of the alpha-linolenic acid consumption per day, was
estimated using generalized least-square regression taking into account
the correlation within each set of published ORs or RR [7]. Then we
combined the study-specific estimates using the restricted maximum
likelihood method in a multivariate random-effects meta-analysis [8]. A P
value for nonlinearity was calculated using the method proposed by
Greenland and Longnecker [9]. All statistical analyses were performed with
STATA, version 10.0 (Stata Corporation, College Station, Texas, USA). All
reported probabilities (p values) were two-sided, with p< 0.05
considered statistically significant.
Dose-response analysis of case-control studies
For case-control studies, data from 6 publications [10-15] with 6
studies were used. A nonlinear relationship was found of alpha-linolenic
acid consumption with risk of prostate cancer (P for nonlinearity=
0.0027), and the ORs (95 % CI) of prostate cancer was 0.89 (0.79-1.00),
0.91 (0.78-1.07), 1.25 (1.02-1.54), 1.52 (1.24-1.88), and 1.74 (1.29-2.35)
for 0.4, 1.0, 1.6, 2.1, and 2.5 grams per day (Fig. 1).
Dose-response analysis of cohort studies
For cohort studies, data from 5 publications [16-20] with 5 studies
were used. The departure from nonlinear relationship was not significant
(P for nonlinearity = 0.7488), and the RRs (95 % CI) of prostate cancer
was 0.97 (0.94-1.00), 0.96 (0.93-0.99), 0.95 (0.87-1.04), 0.95 (0.86-
1.05), and 0.94 (0.84-1.06) for 1.0, 1.3, 1.7, 2.0, and 2.3 grams per day
(Fig. 2).
Dose-response analysis of all observational studies
For case-control and cohort studies, data from 11 publications [10-
20] with 11 studies were used. A nonlinear relationship was found of alpha
-linolenic acid consumption with risk of prostate cancer (P for
nonlinearity= 0.0132), and the ORs (95 % CI) of prostate cancer was 0.93
(0.89-0.98), 0.88 (0.81-0.96), 0.87 (0.80-0.95), 0.91 (0.85-0.97), 0.98
(0.91-1.06), 1.00 (0.92-1.09), and 1.00 (0.91-1.10) for 0.4, 0.7, 1.0,
1.3, 1.7, 2.0, and 2.3 grams per day (Fig. 3).
Overall, a significant association was found between alpha-linolenic
acid consumption and decreased risk of prostate cancer among subjects
consuming 0.2-1.3 grams of alpha-linolenic acid per day. Besides,
consuming 1.0 gram of alpha-linolenic acid per day can bring us the
strongest protective effect of prostate cancer risk. A potential nonlinear
relationship should be assessed before assuming a linear relationship,
which is not always the case in epidemiologic research and more studies
are required to confirm this relationship.
All above mentioned 2 tables and 3 figures can be provided if they
were needed.
Acknowledgments None.
References
1. Carleton AJ, Sievenpiper JL, de Souza R, McKeown-Eyssen G, Jenkins
DJ. Case-control and prospective studies of dietary alpha-linolenic acid
intake and prostate cancer risk: a meta-analysis. BMJ open 2013;3(5) doi:
10.1136/bmjopen-2012-002280[published Online First: Epub Date]|.
2. Simon JA, Chen Y-H, Bent S. The relation of alpha-linolenic acid
to the risk of prostate cancer: a systematic review and meta-analysis. The
American journal of clinical nutrition 2009;89(5):1558S-64S
3. Carayol M, Grosclaude P, Delpierre C. Prospective studies of
dietary alpha-linolenic acid intake and prostate cancer risk: a meta-
analysis. Cancer Causes & Control 2010;21(3):347-55
4. Desquilbet L, Mariotti F. Dose-response analyses using restricted
cubic spline functions in public health research. Statistics in medicine
2010;29(9):1037-57 doi: 10.1002/sim.3841[published Online First: Epub
Date]|.
5. Orsini N, Li R, Wolk A, Khudyakov P, Spiegelman D. Meta-analysis
for linear and nonlinear dose-response relations: examples, an evaluation
of approximations, and software. American journal of epidemiology
2012;175(1):66-73 doi: 10.1093/aje/kwr265[published Online First: Epub
Date]|.
6. Durrleman S, Simon R. Flexible regression models with cubic
splines. Statistics in medicine 1989;8(5):551-61
7. Orsini N, Bellocco R, Greenland S. Generalized least squares for
trend estimation of summarized dose-response data. Stata Journal
2006;6(1):40-57
8. Jackson D, White IR, Thompson SG. Extending DerSimonian and
Laird's methodology to perform multivariate random effects meta-analyses.
Statistics in medicine 2010;29(12):1282-97 doi: 10.1002/sim.3602[published
Online First: Epub Date]|.
9. Greenland S, Longnecker MP. Methods for trend estimation from
summarized dose-response data, with applications to meta-analysis.
American journal of epidemiology 1992;135(11):1301-9
10. Andersson SO, Wolk A, Bergstrom R, et al. Energy, nutrient intake
and prostate cancer risk: a population-based case-control study in Sweden.
International journal of cancer. Journal international du cancer
1996;68(6):716-22 doi: 10.1002/(sici)1097-0215(19961211)68:6<716::aid-
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11. De Stefani E, Deneo-Pellegrini H, Boffetta P, Ronco A,
Mendilaharsu M. Alpha-linolenic acid and risk of prostate cancer: a case-
control study in Uruguay. Cancer epidemiology, biomarkers & prevention
: a publication of the American Association for Cancer Research,
cosponsored by the American Society of Preventive Oncology 2000;9(3):335-8
12. Ramon JM, Bou R, Romea S, et al. Dietary fat intake and prostate
cancer risk: a case-control study in Spain. Cancer causes & control :
CCC 2000;11(8):679-85
13. Hedelin M, Chang ET, Wiklund F, et al. Association of frequent
consumption of fatty fish with prostate cancer risk is modified by COX-2
polymorphism. International journal of cancer. Journal international du
cancer 2007;120(2):398-405 doi: 10.1002/ijc.22319[published Online First:
Epub Date]|.
14. Fradet V, Cheng I, Casey G, Witte JS. Dietary omega-3 fatty
acids, cyclooxygenase-2 genetic variation, and aggressive prostate cancer
risk. Clinical cancer research : an official journal of the American
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0432.ccr-08-2503[published Online First: Epub Date]|.
15. Williams CD, Whitley BM, Hoyo C, et al. A high ratio of dietary n
-6/n-3 polyunsaturated fatty acids is associated with increased risk of
prostate cancer. Nutrition research (New York, N.Y.) 2011;31(1):1-8 doi:
10.1016/j.nutres.2011.01.002[published Online First: Epub Date]|.
16. Giovannucci E, Rimm EB, Colditz GA, et al. A prospective study of
dietary fat and risk of prostate cancer. Journal of the National Cancer
Institute 1993;85(19):1571-9
17. Schuurman AG, van den Brandt PA, Dorant E, Brants HA, Goldbohm
RA. Association of energy and fat intake with prostate carcinoma risk:
results from The Netherlands Cohort Study. Cancer 1999;86(6):1019-27
18. Koralek DO, Peters U, Andriole G, et al. A prospective study of
dietary alpha-linolenic acid and the risk of prostate cancer (United
States). Cancer Causes & Control 2006;17(6):783-91
19. Park SY, Murphy SP, Wilkens LR, Henderson BE, Kolonel LN. Fat and
meat intake and prostate cancer risk: the multiethnic cohort study.
International journal of cancer. Journal international du cancer
2007;121(6):1339-45 doi: 10.1002/ijc.22805[published Online First: Epub
Date]|.
20. Wallstrom P, Bjartell A, Gullberg B, Olsson H, Wirfalt E. A
prospective study on dietary fat and incidence of prostate cancer (Malmo,
Sweden). Cancer causes & control : CCC 2007;18(10):1107-21 doi:
10.1007/s10552-007-9050-4[published Online First: Epub Date]|.
Roger Byard, Professor of Pathology, The University of Adelaide, SA,
Australia; John Hunsaker, Forensic Pathologist, University of Kentucky,
Frankfort, Ky, United States.
Dear Sir,
We read with interest the recent analysis of five large case-control
studies involving sudden infant death syndrome (SIDS) with respect to bed
sharing [1]. Our concern is that the possibility of accidental suffocation
was n...
Roger Byard, Professor of Pathology, The University of Adelaide, SA,
Australia; John Hunsaker, Forensic Pathologist, University of Kentucky,
Frankfort, Ky, United States.
Dear Sir,
We read with interest the recent analysis of five large case-control
studies involving sudden infant death syndrome (SIDS) with respect to bed
sharing [1]. Our concern is that the possibility of accidental suffocation
was not addressed. While we would certainly agree with the authors that
"certifying such deaths under headings other than SIDS does nothing to
minimize the tragedy", it may help us to recognise and better understand
different lethal mechanisms. For example, the different sex ratio in
infants found dead alone (2:1) compared to a shared sleeping situation
(1:1) suggests that these groups may not be the same [2]. The current
analysis is not alone in "lumping" all shared sleeping deaths under the
rubric of SIDS as a meta-analysis by Venneman et al in 2012 did exactly
the same [3]. In previous years any infant who died in a cot was labelled
a "cot death". While we came to understand the error of this approach, it
now seems that any infant who dies in a parental bed is being labelled as
SIDS. How does this approach help us recognise the possibility that some
of these deaths may be due to accidental asphyxia [4]? Surely the
increased risk of infant death if a parent has consumed alcohol has more
to do with diminished parental arousal with overlaying, than having an
effect on an infant's intrinsic homeostatic mechanisms?
As in many investigations of infant fatalities, the analysis of
sudden unexpected deaths in infancy associated with bed sharing entails a
broad, complex differential matrix prior to reaching a final decision on
causality. As an example specifically relevant to this discussion, in a
case of an infant found deceased in a standard adult bed with one or more
adults, there may well be other compelling information, investigative
omission, or physical evidence that concerns the forensic pathologist to
such a degree that he/she is suspicious of a type of death that cannot be
determined by either the information available or the autopsy findings.
That is, the contribution of bed sharing is uncertain, irrespective of the
role of parental smoking or substance abuse.
One of the great success stories in SIDS in recent years has been the
realisation that this is a heterogeneous group of infant deaths composed
of a number of distinct (although possibly inter-related) subsets. By
identifying subsets we have been able to show that some of these deaths
have been due to a range of conditions including accidental asphyxia,
inflicted injury, metabolic disturbances, infections and cardiac
channelopathies [5]. Unfortunately, John Emery's concern that SIDS may be
used as a "convenient diagnostic dustbin" [6] if all deaths are grouped
together is perhaps again being realised.
Roger Byard MD, John Hunsaker MD
Conflict of Interest: None
References
1. Carpenter R, McGarvey C, Mitchell EA, et al. Bed sharing when
parents do not smoke: is there a risk of SIDS? An individual level
analysis of five major case-control studies. BMJ Open 2013;3:e002299.
2. Byard RW, Elliott J, Vink R. Infant gender, cosleeping and sudden
death. J Paediatr Child Health 2012;48:517-9.
3. Vennemann MM, Hense H-W, Bajanowski T, Blair PS, Complojer C, Moon
RY, Kiechl-Kohlendorfer U. Bed sharing and the risk of sudden infant death
syndrome: can we resolve the debate? J Pediatr 2012;160:44-8.
4. Byard RW. The triple risk model for shared sleeping. J Paediatr
Child Health 2012;48:947-8.
5. Byard RW. Sudden Death in the Young. 3rd ed. Cambridge, UK,
Cambridge University Press, 2010.
6. Emery JL. Is sudden infant death syndrome a diagnosis? Or is it
just a diagnostic dustbin? Brit Med J 1989;299:1240.
The paper published in your journal by Carpenter et al [1], claims to
resolve uncertainties associated with bedsharing and SIDS. We believe
however, it does little other than fuel further confusion in the minds of
parents and the health professionals charged with providing them with
information and support.
As outlined in other letters the authors chose to use a selection of
older studies...
The paper published in your journal by Carpenter et al [1], claims to
resolve uncertainties associated with bedsharing and SIDS. We believe
however, it does little other than fuel further confusion in the minds of
parents and the health professionals charged with providing them with
information and support.
As outlined in other letters the authors chose to use a selection of
older studies (data collected between 1987 and 2003) in their analysis
that contained incomplete data on key variables such as alcohol, substance
and medication use. Whereas a 2009 British study by Blair et al. [2] did
collect data on smoking, alcohol, prescribed and illegal drugs in the 24
hours prior to death. These researchers did not find an increased risk
for bedsharing and SIDS when these variables and other hazardous
cosleeping arrangements, such as sofa and chair cosleeping were excluded.
Instead they found that the number of babies bedsharing in the SIDS group
(6%) was actually lower than in the control group where there were no
deaths (10%).
It is also problematic that the older studies analysed by Carpenter
et al. also used variable definitions for SIDS and for bedsharing and did
not report breastfeeding data except in a few studies where only
initiation data was collected. The lack of detail on how the breastfeeding
data in Carpenter et al's analysis was obtained and what operational
definitions were used for exclusive, partial and initiation of
breastfeeding were not made available. Due to the known impact
breastfeeding has on the prevention of SIDS [3] the lack of detail in this
area places significant limitations on the study's findings.
Additionally the author's explanation of the saving of health costs
associated with the reduction in bedsharing in relation to its effects on
successful breastfeeding completely overlooks the very broad range of
morbidities and mortalities that breastfeeding protects against across the
lifespan. Likewise there is no acknowledgement when quoting unpublished
data from the Netherlands, where there are active campaigns against
bedsharing, that there is a strong likelihood that parents would not
disclose their bedsharing activities due to fear of censure, resulting in
significant potential for under reporting of bedsharing.
Furthermore there is an unhelpful emphasis on the comparably small
risk for SIDS they have calculated from their analysis in relation to
bedsharing. This potentially leads the novice reader, media and health
consumer to conclude these results, and the author's subsequent finding
that bedsharing should never be undertaken in any circumstance, are
irrefutable. In reality, the significant limitations imposed by the study
design make such a conclusion most inappropriate. Even the attempt to
soften this conclusion by the authors saying they do not suggest babies
shouldn't breastfeed in bed, only that they shouldn't fall asleep in bed,
shows significant lack of insight into the realities and pressures of
night time parenting.
Removing the option of bedsharing as a commonly used night-time
parenting strategy is likely to have significant effects on the wellbeing
of parents. It is also likely to impact negatively on successful
breastfeeding, a factor associated with reduced infant mortality and
morbidity, and may create a riskier sleep environment for some babies,
when parents fall asleep on sofas or armchairs while trying to follow the
authors' advice of 'never bedsharing'. The lack of acknowledgement of
these important issues in the authors' discussion, overlooks important
health promotion opportunities.
Consequently, we are most concerned by the message this paper sends
to the general community. Mothers have already indicated in previous
research [4] that advice against any form of bedsharing doesn't ring true
for them and those who do decide to bedshare would not now disclose their
intentions to health professionals. Such a response to the blanket advice
against any bedsharing shuts down communication channels with parents and
removes the opportunity for health professionals to have open discussions
regarding safe sleeping options. Health professionals have also reported
policies requiring them to advise against any bedsharing did not allow
them to accept and respond to the realities of people's lives and
negotiate low risk alternatives that were appropriate to their individual
situations (4). As health professionals were then unable to meet parent's
needs in this respect this created feelings of personal conflict and moral
tension in having to comply with such policies.
Evidence based practice has been defined as the integration of best
research evidence, clinical expertise and patient values [5]. The authors
have proposed a risk elimination approach to the complex issue of
bedsharing in this paper, which is not evidence based and will not be
effective in reducing infant deaths for three key reasons: 1) current
evidence is not reflected for low risk families; 2) bedsharing is a valued
cultural practice in many communities including those of low and high
risk; and 3) the practicalities of where mothers feed their babies at
night needs serious consideration so that we do not introduce
recommendations that actually increase risk for babies.
A consistent national risk minimisation approach to co-sleeping, in
which the values and circumstances of families is integrated into the
informed decision making process [6], is the only responsible and ethical
approach to address this issue [7], and is required if we are going to
succeed in further reducing sudden infant deaths associated with shared
sleeping environments.
We are extremely disappointed with the conclusions reached by the
authors of this study and the potentially negative impact it may have on
safe sleeping, successful breastfeeding, parent wellbeing and open
communication between health professionals and parents.
1. Carpenter R, McGarvey C, Mitchell EA, Tappin DM, Vennemann MM,
Smuk M, Carpenter JR. 2013, Bed sharing when parents do not smoke: is
there a risk of SIDS? An individual level analysis of five major case-
control studies. BMJ Open 2013;3:5 e002299 doi:10.1136/bmjopen-2012-
002299.
2. Blair PS, Sidebotham P, Evason-Coombe C, Edmonds M, Heckstall-
Smith, EMA, Fleming, P 2009: Hazardous cosleeping environments and risk
factors amenable to change: case-control study of SIDS in south west
England. BMJ 339(Oct13 1): b3666-b3666. doi: 10.1136/bmj.b3666
3. Hauck F, Tanabe K 2008, International trends in sudden infant
death syndrome: stabilization of rates requires further action. Pediatrics
122(3): 660-666.
4. Dodd J 2012, Evaluation of the Department of Health Western
Australia Operational Directive Statewide Co-Sleeping/Bed-Sharing Policy
for WA Health Hospitals and Health Services Collaboration for Applied
Research and Evaluation: Telethon Institute for Child Health Research
under contract with the Department of Health, Western Australia.
5. Sackett, D. (2000) Evidence-based medicine: how to practice and
teach EBM, Volume 2. London: Churchill Livingstone.
6. Young, J., Watson, K., Ellis, L., Raven, L. 2012, Responding to
the evidence: Breastfeed baby if you can - the sixth public health
recommendation to reduce the risk of sudden unexpected death in infancy.
Breastfeeding Review 20(1): 7-15.
7. Fetherston, C., Leach, J. 2012. Analysis of the ethical issues in
the breastfeeding and bedsharing debate. Breastfeeding review 20(3): 7-
17.
This publication [1] is confusing to parents and physicians because it draws far reaching conclusions from unconvincing data.
METHODOLOGICAL PROBLEMS
In our opinion, the validity of this analysis is threatened by selection bias, imputation bias and presentation bias. We think that the conclusions drawn from this study are not generalizable and that many current issues pert...
This publication [1] is confusing to parents and physicians because it draws far reaching conclusions from unconvincing data.
METHODOLOGICAL PROBLEMS
In our opinion, the validity of this analysis is threatened by selection bias, imputation bias and presentation bias. We think that the conclusions drawn from this study are not generalizable and that many current issues pertaining to SIDS epidemiology have not been adequately addressed.
Old data sets The authors perform a secondary analysis of 5 previously published datasets from 1987 through 2003 from different parts of the world. It remains unclear by which criteria these studies have been selected and why the authors have chosen to include exactly these 5 studies and leave out other datasets from the same time period (a priori inclusion criteria are neither described in the paper nor in the supplementary data).
Sleep environments and habits have considerably changed since the time when most cases re-analyzed in this study have been recorded.[2] Public campaigns have resulted in a safer sleeping environment and the use of babybays (sidecar cribs) has changed the practice of bed-sharing profoundly. It is therefore questionable if the results of this study can be generalized to today's situation and questions of young families.
Problematic selection of control groups and adjustment The weaknesses of some of the older studies now re-analyzed by Carpenter et al have not been done away with by lumping the datasets together. In 3 of the 5 studies now combined the controls born at the same maternity ward have not been selected randomly or by a predefined protocol, which may explain the wide discrepancies between cases and controls for important characteristics like marital status or maternal age in Carpenter's current publication (table 1). These discrepancies indicate that the control sample has not been drawn from the same source population as the cases - which in a case-control design of a condition like SIDS with its much higher prevalence in lower socioeconomic strata may introduce substantial bias.[3] Unfortunately, direct measures of socioeconomic status like household income or educational background do not seem to have been part of the original data sources of Carpenter's study. So, as a matter of fact, this study of a condition that is clearly more prevalent in disadvantaged social settings remains unadjusted for any direct measures of socioeconomic status. This may explain some of the surprising findings in table 1, according to which for instance - after multivariate adjustment - a mother in her late twenties is at nearly double the risk of losing her baby to SIDS than a mother aged over 30 years.
Problematic imputation Alcohol and drug consumption are among the most important risk factors associated with SIDS in bed-sharing infants and are also more prevalent in the social settings in which SIDS most frequently occurs. In an analysis of all SIDS cases in Alaska between 1992 and 2004 for example, 32% of the bed-sharing victims had slept with an adult person impaired by alcohol or drugs during the night of their death [4] - a percentage that underscores that accurate information on this exposure has to be considered crucial for any valid statement on risk attribution to bed-sharing versus room-sharing.
In the source datasets of the study by Carpenter et al data on alcohol and drug consumption are missing for over 60% of the cases (table 1). To fill the gaps the authors resort to imputing the missing data. However, given the large amount of missing data, this strategy may introduce substantial bias.[5] [6] The imputation model as described by the authors in the supplementary online material is based on the assumption that values are missing at random between their datasets. This is almost certainly not the case for alcohol or drug consumption, the patterns of which differ along secular trends and between cultures and socioeconomic strata.[7] [8] In a study that draws cases from countries with widely disparant cultural backgrounds and drinking habits like Ireland and New Zealand it is, in our opinion, not valid to assume equal distribution and determinants for alcohol and drug consumption.
Important exposures missing In spite of its claim to analyze risk factors "in depth as never before" (p 8) this study does not include some important risk factors for SIDS like paternal aclohol and drug use. This is not a trivial shortcoming as alcohol and drug use are one of the few plausible explanations why SIDS cases occur significantly more often on weekends than on week days[9], with an exceptional peak on New Year.[10] The authors do not see this as a threat to the validity of their result and claim in the discussion that paternal alcohol and drug use "does not add further to the risk of SIDS" (above and beyond maternal alcohol and drug use). They base this statement on an analysis from their ECAS study. [11] We remain unconvinced. For one, maternal alcohol and drug use is far from reliably ascertained in this study (see above). Also, it is plainly not conceivable to us why a drugged or drunken father sleeping next to his infant should not pose an additional and independent risk to baby's welfare.
Data on other important risk factors for SIDS, like the quality of the sleep environment or sleeping with a non-caregiver (see below), are also absent.
It could be argued that the less-than-perfect ascertainment or imputation of environmental influences is negligible as "it all dials out somehow between groups". This, however is not true and a serious misconception. Many of the exposures relevant in SIDS "act" primarily through the proximity to the baby and therefore affect bed-sharing infants and room-sharing infants differentially. In SIDS research, an equal influence of missing or unreliable data on subgroups therefore can not be assumed. Any mind altering influence for example (like alcohol or drug use) will have a much greater impact on the risk associated with bed-sharing than on the risk associated with room-sharing. Therefore, the less a study is able to capture exposures which act more effectively on bed-sharing infants than on room-sharing infants, the more risk will be falsely attributed to the bed-sharing cases. We wish the authors had commented on this very relevant issue in their discussion.
No information on intended versus non-intended bed-sharing One of the co-authors, Mechthild Vennemann, has, in her recent meta-analysis of SIDS-cases[12] as well as in the report of her German study (which is also part of the dataset of the current study) [13] brought up an important issue. It is well known that bed-sharing occurs under two fundamentally different circumstances: in some families sharing the bed with the baby is part of the normal, everyday sleep routine (these cases have been called primary, routine or "usual" bed-sharers). Other mothers or families use bed-sharing only on special, exceptional occasions. It has to be assumed that some of the latter cases are associated with a higher a priori or subsequent risk. The baby may have been taken into the family bed because it has been unusually fussy during daytime (which may indicate the onset of an infection), or the mother may not have felt up to getting up at night, therefore taking her baby to bed with her. Some of these maternal choices may represent the influence of mind altering influences like alcohol, drug or medication use.
The differentiation of routine versus non-routine bed-sharing has proven important. In Vennemann's meta-analysis SIDS was twice as likely for non-routine bed-sharers than for primary bedsharers. As a matter of fact, in her dataset primary bed-sharing was not associated with a higher risk of SIDS at all ("Routine bed sharing did not increase the risk of SIDS. However, bed sharing during the last night when bed sharing was not routine increased the risk two-fold."). Given the importance of this ongoing discussion, brought up by one of the study authors herself, it certainly comes as a surprise that this issue is not even mentioned as a limitation of this study.
POTENTIAL MISCLASSIFICATION BIAS
Problematic definition of breastfed cases The authors report breastfed versus bottle-fed cases. However, in their definition of "breastfeeding" they also include cases that are being partially bottle-fed. This is problematic as some of the cases labeled as "breastfed" may indeed not have been breastfed during sleep time but instead may have been in the process of being weaned during the period of their death.
Weaning is not a trivial issue in SIDS research as the peak-incidence of SIDS (with most cases occurring between 2 and 4 months of life) parallels the incidence of weaning especially in the social groups where SIDS is most common. [14] [15] This association asks for explanation and may indeed be causally related if one considers findings from sleep research: sleep regulation is entirely different in bed-sharing babies being breastfed during the night than in babies being bottle-fed at nighttime, with the former babies spending less time in deep sleep and showing higher arousability than the latter. [16] [17] A baby that is being actively weaned and for example not nursing at nighttime may therefore indeed be ridded of the protective dyadic sleep regulation typical for the fully breastfed infant.
The issue of a protective effect of a lighter, more active sleep is being widely discussed in the context of pacifier use, which has been shown to be one of the few protective influences against SIDS [18 ] [19] and which presumably also acts through its influence on sleep regulation - frequent suckling providing for an overall lighter, more active sleep with more arousals. This explanation is also in keeping with the epidemiological evidence that clearly shows a link between the intensity of breastfeeding and SIDS. [20]
Grouping fully breastfed and partially weaned babies together in a study of SIDS therefore is problematic to say the least. Indeed this lumping may be equivalent to lumping together protective factors and risk factors in one exposure - with all the confusing implications when it comes to interpreting the results. And again, as in the case of missing data, this putative misclassification may lead to an exaggerated risk attribution to the bed-sharing cases.
Possible lack of identification of non-caregivers We are also concerned about another potential misclassification. Studies suggest that sleeping with a "non-caregiver" may pose a higher risk of SIDS to the infant than sleeping with a "usual caregiver" (who is usually a parent). In the study by Margaret Blabey of SIDS and bed-sharing, 29% of cases had slept with a non-caregiver (like an aunt, sibling or friend) during the night of their death. [21] It is not clear to us if the cases in the Carpenter study have really been classified along the line of parents versus non-parents, at least there is no mention about any exclusion of cases based on their status as non-parents or non-caregivers.
How easily misclassification or missing data can lead to false risk attribution to bed sharing may be illustrated by the following example: A mother may breastfeed her baby at daytime but bottle-feed at nighttime. As bottle feeding can be delegated, she may, to catch a good night's sleep, ask her partner to feed the baby at night while she sleeps in a seperate bed. Had the baby died during that night while sleeping at the side of the mom's partner, the case would have been classified and analyzed in this study as a breastfed baby dying of SIDS while bed-sharing. Had the partner chosen to drink alcohol in the evening, it would not have been identified as an additional risk.
INADEQUATE DISCUSSION OF ISSUES RELATED TO RISK INTERPRETATION OF BED SHARING
Breastfeeding has a protective effect on SIDS, cutting its risk by about 50%.[22] It also has a protective effect on maternal and child health, including risk reduction for infections, autoimmune disorders, and metabolic disorders. [23] It is well known that bed-sharing facilitates breastfeeding [24] [25] and is associated with higher rates of breastfeeding (as well as a longer duration). [26] [27] Therefore the question if general advice against bed-sharing - as put forward by Carpenter et al - may inadvertently jeopardize the practice and promotion of breastfeeding, is an important one as it may introduce the risk of not being breastfed in the name of avoiding possible risks associated with bed-sharing. [28] [29] The authors deal with this complex issue by referring to secular data from the Netherlands, in which bed-sharing incidence, according to a personal communication to the author, apparently dropped while breastfeeding rates went up. This resorting to ecological associations that have not been examined for causal relationship is unsatisfartory in this debate, and clearly other studies show opposite associations (i.e. decreasing incidence of SIDS in the face of increasing prevalence of bed-sharing) [30] [31], none of which are mentioned or discussed.
Bed-sharing as a lifestyle choice The authors describe bed sharing as easily avoidable. This misses two important points. First, babies do sleep better in proximity with their attachment person, they fuss less, cry less and need less soothing. [32] For many families life with a small baby is a stressful period, as evidenced by the high prevalence of maternal fatigue, depression (peaking at 4 - 12 weeks post partum) and emotional dysregulation on the baby's part (e.g. excessive crying resp. "colics", peaking at 4 - 8 weeks post partum). [33] [34] So, for many parents, it is not easy to relinquish soothing care practices like bed-sharing. [35] [36] Second, it has been suggested that parents anxious about possible hazards of bed-sharing may choose alternative settings for breastfeeding instead, like sofas or armchairs, with the obvious risk of falling asleep in a clearly hazardous sleep environment. [37]
SUMMARY: A MISSED OPPORTUNITY
SIDS and bed sharing have been an interesting topic for scientists from many fields and specialties. Anthropologists point out that human infants have evolved as co-sleepers, i.e. they have, for reasons of thermoregulation and protection from predators, among others, slept with their (nursing) mothers during most of human history. According to this line of scientific enquiry, a baby sleeping solitarily would have been a dead baby until very recently. In fact, the overwhelming majority of human infants who have ever slept on earth have done so in close proximity to a nurturing, protecting and warming mother. [38] [39]
Modern sleep research supports this assumption of an evolved dyadic sleep arrangement by pointing out that the sleep physiology of an infant is clearly geared toward reciprocal regulation: sleep states are co-regulated in a sense that brain activity and sleep stages are synchronized. [40] [41] As part of intuitive interactions during light sleep the co-sleeping baby is frequently being repositioned by the mother and placed face to face in a position facilitating subsequent nursing, i.e. on its side or on its back. [42] [43] [44] Indeed, the observations of widespread supine sleeping in cultures where co-sleeping is part of the traditional cultural practice has been the starting point for questioning the prone position as the safest option for baby sleep in the 1980ies and has given decisive support to the back-to-sleep campaign so successful in preventing SIDS in industrial nations worldwide since the early 1990ies. [45] [46]
So from an ethological perspective it is ever more important to approach the core question in SIDS research with appropriate scientific tools - namely, if the well described risks associated with bed-sharing are a feature of bed-sharing in and of itself or if they stem from potentially avoidable environmental exposures that in some cases go along with bed-sharing.
We do not think that the study by Carpenter et al adds to answering this question. From a public health standpoint we are instead left with more confusion, as the answer given by Carpenter et al is based on an analysis with several shortcomings, including inadequate imputation, missing or unreliable ascertainment of confounders (like paternal and maternal drug use), missing data on routine versus non-routine bed-sharing as well as misclassification of some exposures (like partial bottle-feeding) - introducing a clear und possibly unidirectional bias in risk-attribution to the bed-sharing cases.
Given these constraints we would have hoped for a more cautionary interpretation. SIDS epidemiology has changed considerably since the times during which the data of this study have been collected, with the SIDS rate in countries like Germany now 89% lower than just 20 years back (down from a high of 1285 cases in 1991 to 147 cases in 2011). [47] In fact two recent analyses of SIDS cases in the post back-to-sleep era show that 99% of cases are now associated with at least 1 risk factor and that the vast majority of cases are now occurring in high risk environments. [48] So instead of making far reaching and statistically tenous claims about the dangers of bed-sharing even for those who do avoid the known risk factors, this study would have served parents and policymakers better by fitting their claims to their modest methodology.
The authors have shown that the vast majority of SIDS cases are related to avoidable environmental exposures: 78% of their SIDS cases were exposed to tobacco smoke, 65 % were not breastfed (and many more may have only partially been breastfed), 43 % were placed on their tummy for sleep and 43% died while sleeping in a separate room from their parents. These data are real and well ascertained. But the recommendations of the authors are directed against any and all bed-sharing in all kinds of circumstances during the first 3 months - which for us, given the source and limitations of their data, represents an overgeneralization. The authors, in our opinion, are advancing an issue to their core message, in which their data are the weakest.
No study so far has convincingly shown that there is a risk of dying for fully breastfed babies sleeping with their non-smoking or non-obtunded mother in a safe environment. We should therefore be more careful with the messages we bring out to the community, as many parents presume that whatever is being published by scientist represents rigorous research. Of course we should inform the public about the risks that can be associated with bed-sharing and that bed sharing needs to be practiced in a safe way. We should warn about the dangers of using mind altering substances or tobacco while co-sleeping with a baby. We should warn about unsafe sleep environments like sofas, armchairs or waterbeds. We should inform families that co-sleeping with a baby may not be fully safe if practiced by a non-caregiver or even a non-breastfeeding mother or the father.
However, we should be careful not to overextend our warnings. We should bear in mind that the decision to share the bed with baby also represents a lifestyle and relational choice. [49] Burdening this choice with warnings derived from less than rigorous data does not serve families. It also does not serve the debate when Carpenter et al, in an attempt to infer a causal relationship between SIDS and bed-sharing per se, refer to the behaviour of piglets, implying that the dangers of bed-sharing may indeed be a mammalian heritage (see their application of Bradford Hill's criteria on page 9): "Sows are normally separated by a bar from piglets to prevent them from being crushed when she turns over, but allowing her piglets to feed." This, to us, is biologistic folklore.
What we find especially disconcerting is the mode and style in which the discussion and the key messages are being put forward to the reader. Most parts of the discussion of this paper read like a discussion of a seminal randomized controlled trial of immense power and homogeneity, while in fact this is a secondary analysis of a convenience sample of mostly old case-control studies from different sociocultural regions of the world with limited adjustment, missing and probably mislabeled data and daring imputation. This is not all the fault of the authors, some of these constraints are inherent to the methodology and data sets that SIDS research, by its very nature, is restricted to. But these restrictions should be ever more of a reason to stay away from inflated claims and generalizations.
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Authors:
Herbert Renz-Polster, MD, Paediatrician, Associated Scientist, Mannheim Institute of Public Health
Freia De Bock, MD, MPH, Paedatrician, Senior Scientist and Project Leader "Child & Health", Mannheim Institute of Public Health
Mannheim Institute of Public Health (MIPH),
Medical Faculty Mannheim, Heidelberg University Social and Preventive Medicine
Ludolf-Krehl-Strasse 7-11
D-68167 Mannheim
www.miph.uni-hd.de
On behalf of the PLP10 study co-authors (1), Ioannis S Patrikios,
George N Loukaides and Mario C Pantzaris, I report our opinion and
response to the e-letter "Omega-3, omega-6 and vitamin treatment for
relapsing-remitting multiple sclerosis" by Oivind Torkildsen. We really
appreciate the comments by Dr Oivind Torkildsen (2) and we thank him for
giving us the chance to clarify more on th...
On behalf of the PLP10 study co-authors (1), Ioannis S Patrikios,
George N Loukaides and Mario C Pantzaris, I report our opinion and
response to the e-letter "Omega-3, omega-6 and vitamin treatment for
relapsing-remitting multiple sclerosis" by Oivind Torkildsen. We really
appreciate the comments by Dr Oivind Torkildsen (2) and we thank him for
giving us the chance to clarify more on the subject. On the other hand we
have to acknowledge that even though we respect his approach and course of
thinking we keep a totally different bio-reasoning on the evaluation of
the PLP10 study results. Moreover, we feel the need to report that all
comparisons that follow are only used for statement clarification purposes
and for no other reason.
We acknowledge that at the time of preparation of the manuscript we
were fully aware of all references mentioned in the e-letter, by Oivind
Torkildsen, including the OFAMS study (2), Bates (3) and the published
review articles (4, 5); but it was not possible for us to discuss all and
everything in this single PLP10 article (1) where the main target was to
report a difficult subject, a clinical study, and with limitations on the
number of references and words. However, the Farinottis' review paper, the
first and major one (Cochrane review, dietary intervention for multiple
sclerosis, 2007) (6), is cited in our work. The Farinottis' 2012 paper (5)
is an update of the previous one (6). Moreover, we believe that the
rational and background information in the introduction, of our paper, is
clear and enough (as a non-review article), with all ingredients that have
been used, very well discussed / explained and referenced.
It was not our intention and/or our purpose to discuss all previous
trials that have been performed testing PUFAs, mainly because we strongly
believe that our intervention is not comparable to any of the formulations
or PUFA supplements that have been used in those trials but instead
totally different; like the quantities/quality/purity of the specific
PUFAs used, ratio of the main ingredients, stereochemistry and molecular
shape, additives like the specific vitamins and especially gamma-
tocopherol. It was our decision to consider as a much more important issue
the explanation and discussion, why the PLP10 formulation had the
potential to probably be effective, as a result of a possible synergy
between the known bio-abilities of each ingredient that has been used;
than to try to discuss what has been previously tested and failed, on PUFA
formulations and trials. In a way, it is our belief that the formulations
are the ones that have been probably failed but not the PUFAs. It is
widely known, accepted and well reported by Mehta (8), as well as by
Farinotti (5, 6), that those studies are overloaded with crucial
methodological limitation such as inappropriate study design, undefined
endpoints, mixed multiple sclerosis (MS) type population, inappropriate
statistics and many others. This is the actual statement by Mehta:
"controlled and noncontrolled trials have produced mixed results regarding
the efficacy of PUFAs in MS; however, these trials have several
limitations that could partially explain the lack of a treatment effect";
also, "finally, relative uncertainty exists in relation to the optimal
dosing of omega-3 and omega-6 PUFAs" (8).
It is well defined (5, 6, 7) that the most probable and major issue
of the puzzle is to elucidate the correct formulation between the specific
PUFAs to be used for a possible efficacy and for conclusive results on the
relation of these specific PUFAs with MS. Mehta reports: "Despite the lack
of definitive evidence that PUFAs can be beneficial in MS, the anti-
inflammatory potential of these agents is intriguing" (8). Although, we
believe that specific antioxidant vitamins have to be co-supplied along
with other specific essential molecules of the omega-6 series, among other
structured molecules, as in PLP10. The scientific plausibility of these
ingredients is recognized out of numerous scientific published reports but
the correct formulation is the missing clue.
Moreover, it is obvious that major issues and novelties that are
discussed in the PLP10 paper have been gone unnoticed. This could be the
reason that someone can fall in the trap and try to compare the PLP10
intervention/formula with other PUFA blends (using different EPA, DHA, GLA
formulations) for MS therapy that have been previously clinically tested.
For example, we believe that it is not scientifically correct to compare
the OFAMS study or any previous PUFA study on MS with the PLP10 study or
draw any conclusions as a result of comparing the two studies. Otherwise
it is like comparing peaches and apples; except if as a result of someone
using EPA, DHA, LA and GLA among others and in different quantity,
quality, ratio, etc., are considered all the same anyway. But then we are
not discussing Biochemistry or bio-metabolism but something else. In that
case let us go years back and remember the Dopamine story. Through
research, Dopamine was reported as a potential biomolecule for efficacy on
Parkinsons' disease. Many studies have been conducted in order to prove
those research findings (of Dopamine as a therapeutic drug on Parkinsons'
disease) without conclusive efficacy until one researcher (George
Constantin Cotzias, L-Dopa treatment) considerably increased the
quantity/dosage of it and the efficacy issue has been resolved.
The OFAMS and PLP10 studies in reality are experimenting on two
completely different PUFA "cocktail" formulations and through two
completely different study designs. The OFAMS daily dose of the EPA (1350
mg) was almost in double the ratio compared to the DHA (850 mg) (a very
low dosage, in our opinion anyway); that means EPA: DHA, 2:1 wt/wt and
without any other ingredient in the supplements, but only those two
specific omega-3 PUFAs. Moreover, an immediate effect (within the first 6
months on intervention) was expected since the study design included a
single endpoint at 6 months, changing then to the addition of interferon;
and this six month- period is reported as an evaluation for monotherapy
(2). In our opinion this is an extremely short period for an efficacy
indication as a result of an orally consumed PUFA formulation. All of
these parameters are contradicting to our study philosophy and the
therapeutic approach. Our philosophy was primarily focusing on the
evaluation of the involved biochemical network of events that are probably
simultaneously participating (contributing) in the pathogenesis. The
holistic, systems medicine approach, as we have been discussing it. Our
formula has been prepared to contain exactly the opposite ratio of those
specific ingredients (EPA: DHA, 1: 3 wt/wt) than the ratio of those
ingredients in the OFAMS study; 6 times more than the total daily quantity
of the EPA + DHA used in the OFAMS study, in 1:1 wt/wt ratio of the total
omega-3 to the total omega-6 content within the PLP10 formulation in
contrast to the OFAMS study supplements; not to discuss the additional
ingredients of the PLP10 formulation (2, 1). All of these specificities
concerning the PLP10 formulation have been used for a specific purpose and
have been based on a biochemical rational; believing, as explained in the
article and in the supplementary data, on the potential manipulative
abilities by each one of those ingredients on the involved network of bio-
mechanisms and factors in the MS pathology(from the dietary factors, the
genes involved, the immunological and pro/anti-inflammatory mediators up
to the triggering of the reparatory mechanisms).
It is true that the intervention A which included all PUFAs and other
specific fatty acids, as in PLP10 (intervention B), had no any significant
efficacy but the same is true for the intervention C that included only
gamma-tocopherol but no vitamin E (alpha-tocopherol). The primary
evaluation of this specific observation is the reason behind the
conclusion that this significant positive efficacy of PLP10, on both the
annual relapse rate and disability progression, might be the result of a
synergistic effect of all ingredients within the PLP10 "cocktail" formula
on the total network of events in the pathophysiology of MS. It is our
strong belief that most (if not all) of the previous studies on the PUFAs
are associated with several important limitations. Moreover, crucial
parameters that are concerning and related to the biochemistry of the
essential PUFA supplements that are consumed orally (in relation to the
bioavailability, ratio, quantities, quality, purity, chronotherapy, etc)
are missing or ignored by the protocols and the designs of the previous
studies.
It is a frowned upon for anyone to report conclusively that the EPA,
DHA and/or LA and GLA cannot support/affect and or manipulate specific
anti-inflammatory /reparative biomechanisms in neurodegenerative type of
diseases in general and specifically MS when the data and results were
collected out of studies associated with so many important limitations.
The "problem" with the OFAMS study, in our opinion, is clearly the
formulation [the ingredients used (focused only on omega-3 PUFA), dosage
(minimal) and ratio (EPA in excess compared to DHA)]. Furthermore, we
believe that the OFAMS study was not properly designed for a nutritional
supplement formulation and it was associated with limitations regarding
the chronotherapy, endpoint assignment and study length parameters (i.e.
specific omega-6 PUFAs were missing as well as antioxidants and the study
included an endpoint with an efficacy expectation in a very short time
after the first dose of treatment). According to our overview for the
pathophysiology of the disease, in relation to the aforementioned
ingredients (within the supplements used in the OFAMS study), someone
would probably expect increased inflammation activity as a result of such
interventions, since increased quantities of free radicals would result
from the additionally consumed PUFA without normalization of the
antioxidants within the organism; especially in a body that is most
probably suffering by significant antioxidant deficiency (8) and mostly
within the first six months on treatment where the PUFA content begin to
be normalized, thus forcing probably the excess release of arachidonic
acid (inflammation initiator) from the cellular membranes.
Considerably high number of in vivo, in vitro and ex vivo published
data are reporting strong positive results on all of the individual
ingredients within the PLP10 formulation in relation to the biomechanisms
involved in MS and the related anti-inflammatory, protective and
reparative mechanisms. For example, Calder published several excellent
papers (as well as review papers) (9, 10), Van Miteren (8), Lippi (11) and
many others like Gallai (12), Endres (13), Gil ? (14) etc. To our
knowledge, our intervention is novel and the only one that is containing
such a blend of PUFAs and other specific fatty acids along with specific
antioxidants, specifically including gamma-tocopherol and in such high
dosage.
As a conclusion we strongly believe that the unexpected strong
efficacy of PLP10 most probably is due to the synergistic effect of all
ingredients within the intervention and not only due to vitamins. Once
again, more conclusive results will be available upon completion of the
present, phase III, large size, multicenter, double-blind, randomized,
placebo-controlled, "MINERAL" clinical study that is in progress and is
aiming to answer, hopefully, most of the aforementioned issues.
References
1 Pantzaris MC, Loukaides GN, Ntzani EE, Patrikios IS. A novel oral
nutraceutical formula of omega-3 and omega-6 fatty acids with vitamins
(PLP10) in relapsing remitting multiple sclerosis: a randomised, double-
blind, placebo-controlled proof-of-concept clinical trial. BMJ Open. 2013;
3 (4).
3 Bates D, Cartlidge NE, French JM, et al. A double-blind controlled
trial of long chain n-3 polyunsaturated fatty acids in the treatment of
multiple sclerosis. J Neurol Neurosurg Psychiatry. 1989; 52 : 18-22.
4 Geldern G, Mowry EM. The influence of nutitional factors on the
prognosis of multiple sclerosis. Nature Reviews Neurology. 2012; 8, 678-
689
5 Farinotti M, Vacchi L, Simi S, Di Pietrantonj C, Brait L, Filippini
G.Dietary interventions for multiple sclerosis. Cochrane Database Syst
Rev. 2012; 12: CD004192.
6 Farinotti M, Simi S, Di Pietrantonj C, et al. Dietary interventions
for multiple sclerosis (Review). Cochrane Database Syst Rev
2007(1)CD004192.
7 Mehta LR, Dworkin RH, Schwid SR. Polyunsaturated fatty acids and
their potential therapeutic role in multiple sclerosis. Nat Clin Pract
Neurol 2009;5:82-92.
8 Van Meeteren ME, Teunissen CE, Dijkstra CD, et al. Antioxidants and
polyunsaturated fatty acids in multiple sclerosis. Eur J Clin Nutr
2005;59:1347-61.
9 Calder PC. n?3 Polyunsaturated fatty acids, inflammation, and
inflammatory diseases. Am J Clin Nutr 2006;83:S1505-19.
10 Calder P. Polyunsaturated fatty acids, inflammatory processes and
inflammatory bowel diseases Mol. Nutr Food Res 2008;52:885-97
11 Riccio P. The molecular basis of nutritional intervention in
multiple sclerosis: a narrative review. Complement Ther Med 2011;19:228-
37.
12 Gallai V et al. (1995) Cytokine secretion and eicosanoid
production in the peripheral blood mononuclear cells of MS patients
undergoing dietary supplementation with n-3 polyunsaturated fatty acids. J
Neuroimmunol 56: 143-153
13 Endres S et al. (1989) The effect of dietary supplementation with
n-3 polyunsaturated fatty acids on the synthesis of interleukin-1 and
tumor necrosis factor by mononuclear cells. N Engl J Med 320:265-271
14 Gil A. Polyunsaturated fatty acids and inflammatory diseases.
Biomed Pharmacother 2002;56:388-96.
Cardiovascular risk study was carried by Heinonnen et al to establish
an association between sedentary lifestyle and cardiovascular risk in
young adults.
Although due to its cross sectional design, it cannot be extrapolated to
address the causality of findings. Nevertheless, it is indeed a good piece
of research wherein all confounders except television viewing, which is a
growing practice, are accounted for.
However, thi...
Cardiovascular risk study was carried by Heinonnen et al to establish
an association between sedentary lifestyle and cardiovascular risk in
young adults.
Although due to its cross sectional design, it cannot be extrapolated to
address the causality of findings. Nevertheless, it is indeed a good piece
of research wherein all confounders except television viewing, which is a
growing practice, are accounted for.
However, this study did not take in to consideration the health status of
an individual, which could have been easily incorporated using a
questionnaire. Also, simple blood pressure and heart rate measurements
along with the biochemical tests to assess the present cardiovascular
profile of an individual, would have given this study a complete justice.
Infact, Roger Sodjinou et al demonstrated high prevalence of hypertension
in sedentary workers, even though previously diagnosed hypertensives were
excluded from the study 1.An emerging body of evidence consistently
suggests that excessive sedentary behavior, may be linked to increased
risk for obesity 2,dyslipidemia 3 and impaired glucose metabolism4.The
change in lifestyle not only improves glucose tolerance but also reduces
the magnitude of several other cardiovascular risk factors5.
Ekelund et al suggested physical activity as a strong predictor of
metabolic status and insulin resistance6. Thus, association between
fasting blood glucose and sedentary time will reinforce the above
mentioned hypothesis.
Last but not the least; adolescent group could have been included in the
study, due to high prevalence of future risk of cardiovascular morbidity
and mortality in these individuals7. According to a recent study by Regan
et al, engagement in excessive sedentary work represents a health risk for
adolescents8.It is thus required to target them to inculcate healthy
lifestyle.
This study indeed opens avenue for future investigators to look upon the
above mentioned factors for devising a better approach for preventing
cardiovascular diseases.
References:
1.Roger Sodjinou , Victoire Agueh , Benjamin Fayomi and H?l?ne Delisle
Obesity and cardio-metabolic risk factors in urban adults of Benin:
Relationship with socio-economic status, urbanisation, and lifestyle
patterns BMC Public Health 2008, 8:84
2.Jakes RW, Day NE, Khaw KT, Luben R, Oakes S, et al. (2003) Television
viewing and low participation in vigorous recreation are independently
associated with obesity and markers of cardiovascular disease risk:
EPICNor folk population-based study. Eur J Clin Nutr 57: 1089-1096
3.Thorp AA, Healy GN, Owen N, Salmon J, Ball K, et al. (2010) Deleterious
associations of sitting time and television viewing time with
cardiometabolic risk biomarkers: Australian Diabetes, Obesity and
Lifestyle (AusDiab) study 2004-2005. Diabetes Care 33: 327-334
4.Healy GN, Dunstan DW, Salmon J, Shaw JE, Zimmet PZ, et al. (2008)
Television time and continuous metabolic risk in physically active adults.
Med Sci Sports Exerc 40: 639-645.
5.Eriksson J, Lindstrom J, Valle T, et al. Prevention of type II diabetes
in subjects with impaired glucose tolerance: the Diabetes Prevention Study
(DPS) in Finland: study design and 1-year interim report on the
feasibility of the lifestyle intervention programme. Diabetologia
1999;42:793-801
6.Ekelund U, Brage S, Griffin SJ, Wareham NJ, ProActive UKResearch Group
(2009) Objectively measured moderate- and vigorous-intensity physical
activity but not sedentary time predicts insulin resistance in high-risk
individuals. Diabetes Care 32:1081-1086
7.Physical Activity and Health: A Report of the Surgeon General. Atlanta,
Ga: US Department of Health and Human Services, Centers for Disease
Control and Prevention, National Center for Chronic Disease Prevention and
Health Promotion; 1996
8.Regan ?, Heary C. Patterns of sedentary behaviours in Irish female
adolescents. . J Adolesc.2013 Apr;36(2):269-78
In their paper1 Carpenter et al. conclude that bed-sharing of infants
under 3 months with their parents even when the latter did not smoke and
had no other risk factors the adjusted odds ratio for SIDS was 5.1 (2.3 to
11.4). This risk was greatly increased when the parents smoked, took
alcohol or drugs. These findings are not surprising and confirm that co-
sleeping is particularly dangerous for babies under three months of...
In their paper1 Carpenter et al. conclude that bed-sharing of infants
under 3 months with their parents even when the latter did not smoke and
had no other risk factors the adjusted odds ratio for SIDS was 5.1 (2.3 to
11.4). This risk was greatly increased when the parents smoked, took
alcohol or drugs. These findings are not surprising and confirm that co-
sleeping is particularly dangerous for babies under three months of age.
The main message is that co-sleeping (with or without other risk factors
such as alcohol, other drugs or smoking) should never occur, but it is OK
to breast feed in the parental bed and then to put the baby to sleep "face
up" in its own cot (with clean linen) in the same room as the parent(s).
The study pre-supposes that accidental smothering is the reason for these
deaths while providing no autopsy evidence to that effect. The paper does
not discuss the role of bacterial infection and only briefly alludes to it
peripherally in terms of thermal stress (overheating) and the release of
lethal toxins. It has been our view, that the theory of respiratory
compromise due to smothering may account for only a very small minority of
cases. The parental bed or sofa represents a dangerous sleeping surface,
as both of these are heavily contaminated with bacteria such as
Escherichia coli and Staphylococcus aureus which are equipped with a
variety of lethal toxins. A baby sleeping in such a contaminated
environment could inhale or ingest shed skin cells covered in these
bacteria. A genetically susceptible baby is at risk in the co-sleeping
situation. This risk is further increased with every additional risk
factor.
Infection has long been recognised as a risk factor for SIDS as shown
by symptoms and signs of respiratory and/or gastrointestinal infection in
the days preceding SIDS death.2 Infection of normally sterile sites with
major bacterial pathogens in SIDS has been independently described by two
research groups.3,4 This finding could represent the 'footprint' of a
bacteraemic episode prior to death.5,6 Bloodstream infection is a
profound inducer of hypoxaemia; the mechanism of which is not fully
understood, however, the cytokine storm almost certainly plays a major
role7 and the hypoxaemia the storm produces seems to precede the final
demise in monitored SIDS cases. In addition, it is plausible that the
findings of Vargas et al.8 in relation to Pneumocystis lung
colonization/infection, with increased mucus production, could contribute
to hypoxaemia.
Not only is infection (via sepsis or toxaemia) an inducer of
hypoxaemia, it is also a key thermogenesis inducer and is usually
overlooked by SIDS researchers married to linking prone sleep to
respiratory physiology. On the other hand, supportive evidence for
plausible links between prone sleep position and infection have been
proposed based on bacterial colonization and toxin induction with raised
nasopharyngeal temperatures prone,9,10 and bacterial contamination of the
sleeping surface promoting colonization of the infant's nasopharynx and
gut.9-11 From studies in a neonatal ward conducted many years ago, it has
long been known that organisms, such as E. coli are shed into the air and
onto surrounding furniture by infants and their care-givers and that these
bacteria can then colonize other infants and sometimes cause serious
infection.12 Furthermore, as skin scales decorated with Staphylococcus
aureus, and coliform (e.g. Escherichia coli) bacteria are shed in
"dangerous sleeping environments" (parental bed, sofa, etc.) it is not
unreasonable to conjecture that prone babies will inhale or ingest these
bacteria and thereby provide the first step in a pathway leading to SIDS
via the so-called "Common Bacterial Hypothesis of SIDS"13 or via toxigenic
effects of these bacteria,5,6,14-24 Hypotheses of pathogenesis fail to
adequately link all the known risk factors for SIDS into a holistic, all-
encompassing hypothesis. Respiratory and brainstem and cardiac hypotheses
compete to explain hypoxemia in the progression to SIDS and therefore do
not satisfy a complete pathogenetic mechanism.
A microbiological basis needs to be considered as the key for the
epidemiological risk factors and the physiological findings provide a
plausible explanation for SIDS.
Conflict of Interest: The authors have no conflicts of interest to
disclose.
Word count: 804 (excluding abstract and references)
Contributors' Statement:
Paul N. Goldwater: Professor Goldwater drafted the initial manuscript and
approved the manuscript as submitted.
Karl A. Bettelheim: Dr Bettelheim conceptualized the article and reviewed
and revised the manuscript and approved the manuscript as submitted.
REFERENCES
1. Carpenter R, McGarvey C, Mitchell EA, Tappin DM, Vennemann MM, Smuk M,
Carpenter JR Bed sharing when parents do not smoke: is there a risk of
SIDS? An individual level analysis of five major case-control studies. BMJ
Open Access Research, May 21, 2013.
2. Hoffman HJ, Damus K, Hillman L, Krongrad E: Risk factors for SIDS.
Results of the National Institute of Child Health and Human Development
SIDS Cooperative Epidemiological Study. Ann N Y Acad Sci. 1988; 533: 13-
30.
3. Weber MA, Klein NJ, Hartley JC, Lock PE, Malone M, Sebire NJ:
Infection and sudden unexpected death in infancy: a systematic
retrospective case review. Lancet 2008; 371: 1848-1853.
4. Goldwater PN: Sterile site infection at autopsy in sudden
unexpected deaths in infancy. Arch Dis Child. 2009;94(4):303-7. Epub 2008
Sep 15.
5. Goldwater PN. A perspective on SIDS pathogenesis. The hypotheses:
plausibility and evidence. BMC Medicine 2011;9:64.
http://www.biomedcentral.com/1741-7015/9/64.
6. Highet AR, Berry AM, Goldwater PN. Novel hypothesis for
unexplained sudden unexpected death in infancy (SUDI) Arch Dis Child 2009;
94:841-843.
7. Hotchkiss RS, Karl IE. The pathophysiology and treatment of
sepsis. New Engl J Med. 2003; 348(2): 138-150.
8. Vargas SL, Ponce CA, Gallo F, Felipe Astorga J, Bustamante R,
Chab? M, Durand-Joly I, Iturra P, Miller RF, Moukthar Aliouat EI, Dei-Cas
E. Near universal prevalence of Pneumocystis and associated increase in
mucus in the lungs of infants with sudden unexpected death. Clin Infect
Dis 2013; 56: 171179.
9. Blackwell CC, Gordon AE, James VS, MacKenzie DA, Mogensen-Buchanan
M, El Ahmer OR, Al Madani OM, T?r? K, Csuk?s Z, S?tonyi P, Weir DM,
Busuttil A. The role of bacterial toxins in sudden infant death syndrome
(SIDS). Int J Med Microbiol 2002; 291:561-570.
10. Molony N, Blackwell CC, Busuttil A. The effect of prone posture
on nasal temperature in children in relation to induction of
staphylococcal toxins implicated in Sudden Infant Death Syndrome FEMS
Immunol. Med. Microbiol. 1999; 25: 109-114.
11. Goldwater PN. Sudden infant death syndrome: A critical review of
approaches to research Arch Dis Child 2003, 88:1095-1100
12. O'Farrell SM, Lennox-King SMJ, Bettelheim KA, Shaw EJ, Shooter,
RA. Escherichia coli in a maternity ward. Infection 1976, 4:146-152.
13. Morris JA. The common bacterial toxins hypothesis of sudden
infant death syndrome. FEMS Immunol Med Microbiol 1999; 25:11-17.
14. Bettelheim KA, Dwyer BW, Smith DL, Goldwater PN, Bourne, AJ.
Toxigenic Escherichia coli associated with sudden infant death syndrome.
Med J Aust. 1989; 151:538.
15. Bettelheim, KA, Goldwater, PN, Dwyer, BW, Bourne, AJ & Smith,
DL. Toxigenic Escherichia coli associated with Sudden Infant Death
Syndrome. Scand J Infect Dis.1990; 22:467-476.
16. Bettelheim, KA, Smith, H, Goldwater, PN, Morris, JA, Murrell,
TGC, Sweet, C, Weaver, SA. Sleeping position and cot deaths Lancet 1991;
338:192.
17. Bettelheim KA, Chang BJ, Elliott SJ, Gunzburg ST, Pearce, JL.
Virulence factors associated with strains of Escherichia coli from cases
of sudden infant death syndrome (SIDS). Comp Immunol Microbiol Infect Dis.
1995; 18:179-188.
18. Bettelheim KA, Luke RKJ, Johnston N, Pearce JL, Goldwater, PN. A
Possible Murine Model for Investigation of Pathogenesis of Sudden Infant
Death Syndrome Curr Microbiol 2012, 64:276-282.
19. Goldwater, PN, Bettelheim, KA. Curliated Escherichia coli,
soluble curlin and the sudden infant death syndrome (SIDS): J Med
Microbiol 2002; 51:1009-1012.
20. Highet, AR, Goldwater PN. Staphylococcal enterotoxin genes are
common in Staphylococcus aureus intestinal flora in Sudden Infant Death
Syndrome (SIDS) and live comparison infants. FEMS Immunol Med Microbiol.
2009; 57:151-155.
21. Pearce JL, Luke RKJ, Bettelheim KA. Sudden infant death syndrome:
What questions should we ask? FEMS Immunol Med Microbiol 1999; 25:7-10.
22. Pearce JL, Luke RKJ, Bettelheim KA. Extraintestinal Escherichia
coli isolations from SIDS cases and other cases of sudden death in
Victoria, Australia FEMS Immunol Med Microbiol 1999; 25:137-144.
23. Pearce JL, Luke RKJ, Bettelheim KA. Infection and food: a factor
in sudden infant death syndrome? FEMS Immunol Med Microbiol 2004; 42:66-
75.
24. Pearce JL, Bettelheim KA, Luke RKJ, Goldwater, PN. Serotypes of
Escherichia coli in Sudden Infant Death Syndrome. J Appl Microbiol 2010;
108:731-735.
Charlotte K Russell -
Research Associate, Department of Anthropology, Durham University
Helen L Ball -
Professor of Anthropology, Department of Anthropology, Durham University;
Director of the Parent-Infant Sleep Lab
Dear Editor,
This publication analyses SIDS-risks associated with bed-sharing
under different circumstances using data from five historical SIDS
studies. Unlike previous analyse...
Charlotte K Russell -
Research Associate, Department of Anthropology, Durham University
Helen L Ball -
Professor of Anthropology, Department of Anthropology, Durham University;
Director of the Parent-Infant Sleep Lab
Dear Editor,
This publication analyses SIDS-risks associated with bed-sharing
under different circumstances using data from five historical SIDS
studies. Unlike previous analyses of these data, this analysis includes
data on feeding type. It promises, at last, to enable those of us working
with parents and the staff who support them to be able to answer
complicated but commonly asked questions about SIDS, and allow parents to
make informed decisions about any potential risk associated with their
personal and cultural infant care beliefs and behaviours.
Because this analysis is based on old data, however, it can only
inform us as to the risks as they existed 15-26 years ago: knowledge both
of bed-sharing behaviour and safety issues not considered here have
advanced considerably in the intervening period. The authors present
analysis of a dataset in which 'safer' bed-sharing is considered as
distinct from bed-sharing in conjunction with known hazards (that is,
breastfeeding infants bed-sharing in the absence of smoking, alcohol,
drugs and sofa-sharing). Babies were categorized as bed-sharing if they
were found dead in the parental bed, or woke up in the parental bed in the
morning following the 'index night' (deviating from the original analyses
which used many different definitions for 'bed-sharing'). This definition
under-estimates the number of 'control' babies who bed-shared as some
infants bed-share for a portion of the night and are placed in a cot
following the last feed, so would not wake up in the parents' bed (and
would be classed here as 'room-sharers'), however babies who die would not
be returned to the cot. 'Accidental' (and consequently unplanned) bed-
sharing is therefore also likely to be overrepresented in the SIDS group
(Ball 2012). Both factors would inflate the risk associated with bed-
sharing.
The authors predict a SIDS-rate of approximately 1 per 10,000 babies
for room-sharers, and 2 per 10,000 babies for bed-sharers. The current
rate of SIDS in UK is 1/3000, or 3.4/10,000, which means that both sleep
locations for breastfed infants of non-smoking parents in the absence of
alcohol experience very few SIDS deaths. It is curious, therefore, that
the authors focus attention only to this small difference in predicted
SIDS rates for breastfed babies of non-smoking parents who bed-share
compared to room-sharing-while ignoring the hugely inflated risks
associated with hazardous bed-sharing environments. It appears as though
the authors choose to target breastfeeding mothers in this way as they are
a sub-group with strong opinions about the benefits of bed-sharing, even
though the infants of these mothers contribute negligibly to UK SIDS
rates.
The recommendations of the authors that parents are advised to
'simply avoid bedsharing' indicates a worrying lack of cultural awareness
or sensitivity to childrearing beliefs of different groups of parents on
the part of these SIDS researchers. Such a recommendation does not allow
parents, especially those whose infants are at low risk for SIDS (healthy
term births, breastfed, not exposed to parental smoking or alcohol
consumption), to make an informed choice to bed-share or not. While single
message recommendations may have been appropriate and effective in
previous campaigns targeting simple infant care practices such as supine
vs. prone sleep position, they are inappropriate and ineffective for
addressing infant care issues involving relational behaviours and cultural
beliefs (Ball and Volpe 2012). Closing down all discussion of the reasons
why parents might bed-share with their infant by issuing a dogmatic
recommendation inhibits health professionals from raising the topic,
causes parents to lie about their behavior, and stifles the provision of
information about hazardous sleeping environments and the degrees of risk
involved (Fetherston and Leach, 2013).
We argue that SIDS is not the only issue that must be taken into
consideration when considering parent-infant bed-sharing, and that risk
minimization, involving parent education and facilitating informed choice,
is a more logical and ethical approach to the bed-sharing issue, than one
focusing on risk elimination.
References:
Ball, H. L. (2012). Sleeping with the baby. IBFAN Breastfeeding
Briefs, No. 53, September 2012.
Ball, H. L., & Volpe, L. E. (2013). Sudden Infant Death Syndrome
(SIDS) risk reduction and infant sleep location - moving the discussion
forward. Social Science & Medicine, 79, 84-91.
Fetherston C.M., & Leach, J.S. (2012) Analysis of the ethical
issues in the breastfeeding and bedsharing debate. Breastfeeding Review,
20(3): 7-17.
Conflict of Interest:
Ball and Russell run the Infant Sleep Information Source (ISIS), an online source of infant sleep research information for parents and health professionals (www.isisonline.org.uk). They do so as part of their academic outreach activities and do not receive any income from the project.
To the editor,
I am not a health care professional, but a mother who brought my babies into my bed a couple of decades ago when it appeared that that was the best way for me to get enough rest to be able to care for them. I have read with interest the recent meta-analysis by Carpenter et al. concluding that bed-sharing increases the risk of SIDS even in the case of breast- feeding, non-smoking mothers. [1]
...Brinsden and colleagues1 describe the decrease in the salt content of bread sold in the UK. They see this as evidence of success for the policy of voluntary agreements with the food industry. In actuality, a careful assessment of the facts and figures given in their paper reveals the failure of the policy.
Between 2001 and 2011 salt intake by adults in the UK fell by about 15%, i.e., from 9.5 to 8.1 g/day. The t...
Abstract Alpha-linolenic acid (ALA) consumption has been linked to risk of prostate cancer theoretically, but the findings were conflicting from observational studies. Results from recent meta-analysis suggested a small risk, moderate protective and no effect of alpha-linolenic acid consumption on prostate cancer risk. However, the relationship, if exists, between alpha-linolenic acid consumption and prostate cancer ris...
Roger Byard, Professor of Pathology, The University of Adelaide, SA, Australia; John Hunsaker, Forensic Pathologist, University of Kentucky, Frankfort, Ky, United States.
Dear Sir,
We read with interest the recent analysis of five large case-control studies involving sudden infant death syndrome (SIDS) with respect to bed sharing [1]. Our concern is that the possibility of accidental suffocation was n...
Dear Editor,
The paper published in your journal by Carpenter et al [1], claims to resolve uncertainties associated with bedsharing and SIDS. We believe however, it does little other than fuel further confusion in the minds of parents and the health professionals charged with providing them with information and support.
As outlined in other letters the authors chose to use a selection of older studies...
Dear Editor,
This publication [1] is confusing to parents and physicians because it draws far reaching conclusions from unconvincing data.
METHODOLOGICAL PROBLEMS
In our opinion, the validity of this analysis is threatened by selection bias, imputation bias and presentation bias. We think that the conclusions drawn from this study are not generalizable and that many current issues pert...
Response by the authors:
On behalf of the PLP10 study co-authors (1), Ioannis S Patrikios, George N Loukaides and Mario C Pantzaris, I report our opinion and response to the e-letter "Omega-3, omega-6 and vitamin treatment for relapsing-remitting multiple sclerosis" by Oivind Torkildsen. We really appreciate the comments by Dr Oivind Torkildsen (2) and we thank him for giving us the chance to clarify more on th...
Cardiovascular risk study was carried by Heinonnen et al to establish an association between sedentary lifestyle and cardiovascular risk in young adults. Although due to its cross sectional design, it cannot be extrapolated to address the causality of findings. Nevertheless, it is indeed a good piece of research wherein all confounders except television viewing, which is a growing practice, are accounted for. However, thi...
In their paper1 Carpenter et al. conclude that bed-sharing of infants under 3 months with their parents even when the latter did not smoke and had no other risk factors the adjusted odds ratio for SIDS was 5.1 (2.3 to 11.4). This risk was greatly increased when the parents smoked, took alcohol or drugs. These findings are not surprising and confirm that co- sleeping is particularly dangerous for babies under three months of...
Charlotte K Russell - Research Associate, Department of Anthropology, Durham University
Helen L Ball - Professor of Anthropology, Department of Anthropology, Durham University; Director of the Parent-Infant Sleep Lab
Dear Editor,
This publication analyses SIDS-risks associated with bed-sharing under different circumstances using data from five historical SIDS studies. Unlike previous analyse...
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