Interactions between infant care practices and physiological development in Asian infants

doi:10.1016/0378-3782(94)90210-0

Early Human Development

Volume 38, Issue 3, 15 September 1994, Pages 181-186

https://doi.org/10.1016/0378-3782(94)90210-0 Get rights and content

Abstract

Asian infants are less likely to suffer cot death despite apparently higher prevalence of some risk factors. This paper compares the development of night time body temperature patterns in a small sample of Asian babies with the pattern already established for white infants, where babies who develop an adult-like night time temperature pattern later than usual share characteristics with victims of SIDS. The Asian infants had similar body temperature patterns to whites, but tended to develop the adult-like pattern later, not earlier as might have been expected. More Asian infants than white in our sample slept in the parental bed, and, before the adult-like body temperature patterns appeared, co-sleeping infants had higher body temperatures than those in their own cots. Asian infants slept in significantly warmer rooms than whites, but under similar amounts of bedding. These studies do not therefore reveal any physiological difference between Asians and whites which might account for low vulnerability to cot death, indeed, if anything the reverse.

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Cited by (23)

The influence of bed-sharing on infant physiology, breastfeeding and behaviour: A systematic review
2019, Sleep Medicine Reviews
Citation Excerpt :
All studies, except the latter, had an adaptation night before data were collected. Another four papers reported on longitudinal physiological or video data [50–53]. Others related biochemical measures of cortisol reactivity [54–57], melatonin rhythms [58] and nicotine exposure [59] to sleep location.
This review aimed to better understand the underlying physiology of the risks and benefits of bed-sharing. Eight databases were searched using terms relating to adult–infant/baby, bed-sharing/co-sleeping combined with outcome terms for physiology, sleep, cardiovascular, respiratory, temperature and behaviour. Of 836 papers identified, 59 papers representing 48 cohorts met inclusion criteria. Objective data using various methodologies were available in 27 papers and subjective data in 32 papers. Diverse measures were reported using variable definitions of bed-sharing. Identified physiological and behavioural differences between bed-sharing and cot-sleeping included increased behavioural arousals, warmer in-bed temperatures and increased breastfeeding duration in bedshare infants as well as differences in infant overnight sleep architecture, cardiorespiratory control and cortisol responses to stress.
We concluded that many differences are context-specific, and dependent on the subjective view of the parents and their cultural values. Objective risk arises if the infant is unable to mount an appropriate physiological or behavioural response to their micro-environment. More studies in the bed-sharing setting are needed to identify infant risk, the potential benefits of a safer environment, and how bed-sharing interacts with infant care practices other than sleep.
Parent-child bed-sharing: The good, the bad, and the burden of evidence
2017, Sleep Medicine Reviews
Citation Excerpt :
Bed-sharing parents also looked at or touched their infants more often than parents of cot-sleeping infants [177]. Physiologically, bed-sharing infants have been reported to have higher baseline body temperatures [183,184], a greater increase in temperature after sleep onset [85], higher axillary temperatures during non-rapid-eye-movement-sleep (REM) [185], and generally warmer thermal conditions (including more bedding [186] and face-covering events) than solitary sleepers [85]. In contrast, Ball [187] found no differences in temperature between bed-sharing and solitary sleeping infants, and no evidence of lowered oxygen saturation in bed-sharing infants [182].
The practice of parent and child sharing a sleeping surface, or ‘bed-sharing’, is one of the most controversial topics in parenting research. The lay literature has popularized and polarized this debate, offering on one hand claims of dangers, and on the other, of benefits – both physical and psychological – associated with bed-sharing. To address the scientific evidence behind such claims, we systematically reviewed 659 published papers (peer-reviewed, editorial pieces, and commentaries) on the topic of parent-child bed-sharing. Our review offers a narrative walkthrough of the many subdomains of bed-sharing research, including its many correlates (e.g., socioeconomic and cultural factors) and purported risks or outcomes (e.g., sudden infant death syndrome, sleep problems). We found general design limitations and a lack of convincing evidence in the literature, which preclude making strong generalizations. A heat-map based on 98 eligible studies aids the reader to visualize world-wide prevalence in bed-sharing and highlights the need for further research in societies where bed-sharing is the norm. We urge for multiple subfields – anthropology, psychology/psychiatry, and pediatrics – to come together with the aim of understanding infant sleep and how nightly proximity to the parents influences children's social, emotional, and physical development.
The development of the circadian heart rate rhythm (CHR) in Asian infants
2012, Early Human Development
Citation Excerpt :
Between 8 and 12 weeks, the CHR in non-Asian CHIME infants is ubiquitous as was also shown in a previous study from our laboratory and other reports [8,10,13]. By contrast, the CHR in Asian Torajan infants was observed in only one out of three infants; the CHR begins to rise in the Asian Torajan infants between four and six months of age, similar to Petersen and Wailoo's finding [16] of a late appearance of the circadian temperature rhythm in Asian immigrants in Britain. No other comparable cross-cultural studies can be found in the literature that deal with this phenomenon.
To test the hypothesis that term-born Asian infants, at reduced risk to die of Sudden Infant Death Syndrome (SIDS) exhibit a circadian heart rate rhythm (CHR) at a later age than non-Asian term infants.
Repeated overnight heart rate (HR) traces obtained with a battery-operated Polar S810i heart-rate monitor at home in 17 Asian Torajan infants in Indonesia, were compared with those of 52 non-Asian infants monitored as part of the Collaborative Home Infant Monitoring Evaluation (CHIME). HR was determined using a moving window averaging technique. A comparison of median HR during quiet sleep (QS) episodes (identified by minimum HR variability), established the presence of CHR.
Seventy three percent of non-Asian CHIME infants ≤ 7 weeks exhibited CHR compared to 45% of Asian Torajan infants. Between 8 and 12 weeks, 94% of non-Asian CHIME infants exhibited CHR, compared to 33% of Asian Torajan infants (p < 0.001). Forty seven and 56% of Asian Torajan infants exhibited the CHR at the age intervals of 16–20 weeks and 21–25 weeks respectively. Active wakefulness percentages as a function of the entire recording and median QS HR were not significantly different in the two groups.
Despite the fact that Asian Torajan infants were on average a week older than non-Asian CHIME babies, between two and three months of age only one in three exhibited the CHR, compared to virtually all non-Asian CHIME infants. We speculate that the cause of this difference rests in the infants' environment rather than their genetic origin.
Ethnicity, infection and sudden infant death syndrome
2004, FEMS Immunology and Medical Microbiology
Epidemiological studies found the incidence of SIDS among Indigenous groups such as Aboriginal Australians, New Zealand Maoris and Native Americans were significantly higher than those for non-Indigenous groups within the same countries. Among other groups such as Asian families in Britain, the incidence of SIDS has been lower than among groups of European origin. Cultural and childrearing practices as well as socio-economic factors have been proposed to explain the greater risk of SIDS among Indigenous peoples; however, there are no definitive data to account for the differences observed. We addressed the differences among ethnic groups in relation to susceptibility to infection because there is evidence from studies of populations of European origin that infectious agents, particularly toxigenic bacteria might trigger the events leading to SIDS. The risk factors for SIDS parallel those for susceptibility to infections in infants, particularly respiratory tract infections which are also major health problems among Indigenous groups. Many of the risk factors identified in epidemiological studies of SIDS could affect three stages in the infectious process: (1) frequency or density of colonisation by the toxigenic species implicated in SIDS; (2) induction of temperature-sensitive toxins; (3) modulation of the inflammatory responses to infection or toxins. In this review we compare genetic, developmental and environmental risk factors for SIDS in ethnic groups with different incidences of SIDS: low (Asians in Britain); moderate (European/Caucasian); high (Aboriginal Australian). Our findings indicate: (1) the major difference was high levels of exposure to cigarette smoke among infants in the high risk groups; (2) cigarette smoke significantly reduced the anti-inflammatory cytokine interleukin-10 responses which control pro-inflammatory responses implicated in SIDS; (3) the most significant effect of cigarette smoke on reduction of IL-10 responses was observed for donors with a single nucleotide polymorphism for the IL-10 gene that is predominant among both Asian and Aboriginal populations. If genetic makeup were a major factor for susceptibility to SIDS, the incidence of these deaths should be similar for both populations. They are, however, significantly different and most likely reflect differences in maternal smoking which could affect frequency and density of colonisation of infants by potentially pathogenic bacteria and induction and control of inflammatory responses.
The role of bacterial toxins in Sudden Infant Death Syndrome (SIDS)
2001, International Journal of Medical Microbiology
There is increasing evidence for the involvement of bacterial toxins in some cases of Sudden Infant Death Syndrome (SIDS), particularly the pyrogenic toxins of Staphylococcus aureus. This had led to the hypothesis that some SIDS deaths are due to induction of inflammatory mediators by infectious agents or their products during a period in which the infant is unable to control these normally protective responses. The genetic, developmental and environmental risk factors identified for SIDS are assessed in relation to frequency or density of mucosal colonisation by toxigenic bacteria and their effects on induction and control of inflammatory responses to the toxins.
Cortisol levels and control of inflammatory responses to toxic shock syndrome toxin-1 (TSST-1): The prevalence of night-time deaths in sudden infant death syndrome (SIDS)
1999, FEMS Immunology and Medical Microbiology
There is evidence that inflammatory responses have been induced in the tissues and body fluids of many SIDS infants. We suggested that some of these deaths are due to uncontrolled inflammatory responses to infectious agents and possibly cigarette smoke. The majority of SIDS deaths occur during the 2–4 month age range when infants have decreasing levels of maternal antibodies to infectious agents. Most deaths occur during the early hours of the morning. Adults are more susceptible to inflammatory responses at night due to lower levels of cortisol associated with circadian rhythm patterns. Infants develop these patterns between the ages of 7 weeks and 4 months, at which time their night-time cortisol levels drop dramatically.
The objective of this study was to use an in vitro model system to assess the effects of different cortisol levels on pro-inflammatory cytokine production in response to the staphylococcal toxic shock syndrome toxin-1 (TSST-1) which has been identified in a significant number of SIDS infants. Levels of cortisol present in infants at night and during the day before and after the development of the circadian rhythm pattern were examined. Human buffy coats (n=9) were stimulated with TSST-1 and responses assessed over 72 hours by a bioassay for tumour necrosis factor-α (TNF-α) and an enzyme linked immunosorbent assay (ELISA) for interleukin-6 (IL-6). Cortisol levels present in an infant at night after development of circadian rhythm (≤5 μg dl⁻¹), did not significantly increase or decrease production of either TNF-α or IL-6. Concentrations of cortisol greater than 5 μg dl⁻¹ usually found in infants during the day or at night prior to the physiological change significantly decreased production of TNF-α at 12 hours and of IL-6 at 12 and 16 hours.
Only cortisol levels greater than 5 μg dl⁻¹ significantly decreased production of the pro-inflammatory cytokines by human buffy coats stimulated with TSST-1. If the switch to the circadian rhythm pattern occurs in an infant when maternal antibodies are still present or after they have developed their own active immunity, the infant could neutralise common viruses, toxins or bacteria; however, if this switch occurs in an infant when antibody levels are low, this could be a window of vulnerability during which infants are at an increased risk of death if uncontrolled inflammatory responses are induced by infectious agents or their products.

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Regulation of breathing and other physiological influencesInteractions between infant care practices and physiological development in Asian infants

Abstract

Sleeping body temperature in 3–4 month old infants

Arch. Dis. Child.

The development of night time temperature rhythms over the first six months of life

Arch. Dis. Child.

Factors affecting the development of night time temperature rhythms

Arch. Dis. Child.

Regulation of breathing and other physiological influences
Interactions between infant care practices and physiological development in Asian infants