ISPID statement on fear-based prevention strategies

Besides the important goal of preventing perinatal and infant death, ISPID also has the goal of providing education on bereavement and advocating for bereaved parents. ISPID is deeply concerned with recent health promotion campaigns that vilify parents or go too far with symbolism (for example: bed headboards as tombstones, or mothers depicted as meat cleavers or ogres in fairy tales). These over-simplified health campaigns might also mislead the public on the facts surrounding SIDS and its prevention.

We believe that such strategies are unnecessary, can be misleading and are very hurtful to parents who are already in deep pain. We disavow such strategies and encourage those who create campaigns for perinatal or infant death prevention to seriously consider the impact on parents who have had babies die and the extreme fear these might cause those parents with newborn infants.

For the latest evidence-based information on SIDS Prevention, please see ISPID's reduce the risk advice.

ISPID statement on the following research paper:

Walther T, Dietrich N, Langhammer M, Kucia M, Hammon H, Renne U, Siems WE, Metages C. High-protein diet in lactation leads to a Sudden Infant Death-Like Syndrome in mice. Plos One 2011; 6 (3): e17443. doi:10.1371/journal.pone.0017443

This recent article published in the open access journal Plos One reports that in mice, a high protein diet during lactation leads to an increased number of deaths in the offspring. As the offspring were well they have termed this "A Sudden Infant Death-Like Syndrome" and suggested that this may explain the occurrence of SIDS in human infants who are breastfed. However, breastfeeding has been widely reported to reduce the incidence of SIDS and is recommended by most SIDS prevention information as being protective. The authors go on to suggest that pregnant women and breastfeeding mothers should not eat a high protein diet. There are a number of issues raised by this paper which need to be addressed in context.

The group studied female mice which were either fed a control diet of 21% protein or a high protein diet containing 42% protein. After delivery the mice pups were fostered to other mothers who were either fed the control diet or the high protein diet until the pups were weaned. The mothers who ate the high protein diet during pregnancy put on less weight, had smaller litter sizes, their pups weighed less and more of their pups died. After cross fostering the pups fed by the mothers who were on the high protein diet were 8 times more likely to die during this period, even if their own mothers had eaten the control diet during pregnancy. There were no differences in heart rate, blood pressure or heart function between the groups of pups after weaning. This study showed that this doubling in protein in the diet of pregnant mice had significant effects on birth outcomes which resulted in lower birth weight offspring and when the high protein diet was fed to lactating mothers the pups whose mothers had a normal diet whilst pregnant went on to show a significant increase in unexplained death. The study draws parallels with the Sudden Infant Death Syndrome which however may not be relevant.

Firstly, the study was in mice and there is no indication of how the doubling of protein in the mouse diet relates to the human situation. The American Institute of Medicine recommends that in adults 17-21% of daily calorific intake is protein, with no less than 10% and no more than 35%.

Secondly, the findings are also somewhat counter intuitive, as presumably a high protein diet is equated to "improved" nutrition, yet the offspring were much smaller at birth and throughout life, suggesting that other mechanisms may be involved.

Thirdly, the study concludes that the mechanism of increased protein in the diet may explain the deaths of some infants who are breastfed. In numerous large epidemiological studies fewer breastfed infants die than those who were bottle fed and breast feeding is recommended as a risk reduction strategy for SIDS.
Fourthly, it is currently believed that SIDS is multifactorial and that a vulnerable infant, such as one who was born low birth weight, to a smoking mother or prematurely may have an inability to overcome a life threatening situation due to an abnormality in autonomic cardiovascular control. In this study there was no evidence that the mice in the "at risk" group had any abnormalities in heart function.

Thus, although this is an interesting study, it is difficult to extrapolate the findings to the human situation. Further research in infants would be required to support the conclusions of the study and to recommend the findings of not eating a high protein diet during pregnancy and breastfeeding for inclusion in any reducing the SIDS risk campaign.

Mothers should follow their health professionals' advice and eat a balanced diet during pregnancy and breastfeeding and to breast feed their infant if possible, for as long as possible, to reduce the risk of SIDS.

ISPID statement on the following research paper:

Livolsi A, Niederhoffer N, Dali-Youcef N, Rambaud C, Olexa C, Mokni W, Gies JP, Bousquet P. Cardiac muscarinic receptor overexpression in sudden infant death syndrome. Plos One 2010; 5 (3): e9464.

Livolsi, Bousquet and colleagues from Strasbourg have published an excellent piece of research comparing neurotransmitter receptors in the heart between infants who died of SIDS and control infants dying of other causes. They found a statistically significant difference in the levels of a particular receptor (muscarinic receptors) in the SIDS cases. SIDS is generally understood to result from a vulnerable infant at a particular developmental stage being exposed to specific environmental stressors. This research may help to explain why some infants are particularly vulnerable. As the authors point out, further research is needed to see if their results can be replicated elsewhere, to further understand the normal development of neurotransmitter receptors in the heart, and how an overexpression of these receptors might act to increase vulnerability.

The environmental risk factors linked to SIDS, including parental smoking and unsafe sleeping environments have been well documented. Regardless of any underlying causes of infant vulnerability, those risk factors remain. Whilst this study provides a useful step forward in SIDS research, all parents can continue to take steps to minimise the risks of SIDS by following the reduce the risk messages.

ISPID statement on the following research paper:

Duncan JR, Paterson DS, Hoffman JM, Mokler DJ, Borenstein NS, Belliveau RA, Krous HF, Haas EA, Stanley C, Nattie EE, Trachtenberg FL, Kinney HC. Brainstem serotonergic deficiency in Sudden Infant Death Syndrome. JAMA 2010; 303 (5): 430-437.

The findings of this important research paper support what we know from earlier studies about the involvement of serotonin in SIDS: babies who die of SIDS show differences in their medullary serotoninergic system, which controls blood pressure, breathing, temperature regulation and arousal from sleep. We still do not know why these differences occur. Genetics may play a part as well as environmental factors like smoking. At present, a test on serotonin levels can only be conducted after death, so there is no possibility of identifying those at risk.
But parents can help to protect their babies by following the reduce the risk advice.