- Email: [email protected]
“New” practice of bedsharing and risk of SIDS
CORRESPONDENCE
“New” practice of bedsharing and risk of SIDS Sir—In commenting on the paper by R G Carpenter and co-workers,1 David Tappin and colleagues (Mar 20, p 994)2 claim parent-infant bedsharing to be a “new practice”, and urge caution in “tampering with our own culturally derived infant care practices”. But what are these practices? If we are urged to venerate our “own” culturally derived infant-care practices, then we should surely be rejecting the cultural changes in UK infant care imported over the past century. The “scientific” baby-care of American John B Watson, who advocated avoidance of physical contact and affection with infants, and New Zealander Frederick Truby King, who encouraged mothers to sleep their babies in quiet darkened rooms and limit physical comfort lest the baby become “spoiled”, changed infant care dramatically and swept aside our biologically and culturally evolved practices. Before the 20th century, UK mothers slept with their babies as a matter of course, as do mothers throughout the world who have not been influenced by recently invented traditions, as did human and prehuman mothers for many millennia previously. Human-infant physiology evolved in such a context (as evidenced by the constant motherinfant physical contact of the great apes), resulting in infants who require close physical contact with a caregiver, day and night, to regulate their temperature, breathing, and other vital functions.3 100 years of rapidly changing infant-care fashions cannot alter several million years of evolutionarily derived infant physiology. Sleep contact is both a culturally and biologically evolved behaviour for human mothers and infants—the view that it is a recent invention is peculiarly myopic. That mother-infant sleep contact is a biologically normal human behaviour does not mean it is inherently safe. As with many aspects of daily life from preparing food to crossing the road, it is the context and manner in which these activities are conducted that make them safe or unsafe. Few sudden infant death syndrome (SIDS) epidemiological studies are sufficiently sophisticated or have enough power to differentiate between different types of bedsharing, which occurs for various reasons and
1558
can be practised in many ways,4 some being safe and some not (eg, cosleeping on a sofa, in overcrowded housing conditions, with intoxicated parents, etc). In an ongoing longitudinal study of infant feeding and sleeping in the northeast of England, we have seen that 70% of breastfeeding mothers repeatedly bedshared with their infant throughout the first 12 weeks, confirming our previously reported finding that 72% of breastfeeding mothers and infants bedshare for some part of the night in the first 3 months of life.5 In their letter, Tappin and colleagues2 report that 4% of younger SIDS infants (five of 123) were found in bed with a non-smoking parent. Even if the 3% of similar bedsharing controls (seven of 263) was not underreported, it is difficult to understand how they can associate such a high degree of risk with this practice. *Helen L Ball, Peter S Blair, Martin P Ward-Platt *Department of Anthropology, University of Durham, Durham DH1 3HN, UK (HLB); Division of Child Health, University of Bristol, Bristol, UK (PSB); and Newcastle Neonatal Service, Royal Victoria Infirmary, Newcastle upon Tyne, UK (MPWP) (e-mail: [email protected]) 1
2
3
4
5
Carpenter RG, Irgens LM, Blair PS, et al. Sudden unexplained infant death in 20 regions in Europe: case control study. Lancet 2004; 363: 185–91. Tappin D, Brooke H, Ecob R. Bedsharing and sudden infant death syndrome (SIDS) in Scotland, UK. Lancet 2004; 363: 994. Trevathan WR, McKenna JJ. Evolutionary environments of human birth and infancy: insights to apply to contemporary life. Child Environ 1994; 11: 88–104. Ball HL. Reasons to bed-share: why parents sleep with their infants. J Reprod Inf Psychol 2002; 20: 207–22. Ball HL. Breastfeeding, bed-sharing and infant sleep. Birth 2003; 30: 181–88.
Thyroxine adherence in primary hypothyroidism Sir—Physicians who read Caroline Roberts and Paul Ladenson’s Seminar on hypothyroidism (Mar 6, p 793),1 particularly those in primary care, might feel that the ambulatory approach to primary hypothyroidism is largely cut and dried: we have an established safe, cheap, effective, oncedaily, lifelong replacement therapy (identical to the natural hormone) to offer our patients; we can precisely monitor treatment with routinely available ultra-sensitive thyrotropin assays; we can even be awed by the major advances in molecular and genomic research that expands on the
negative hormonal feedback loop that is the pathophysiological basis for our clinical management. Such complacency would be misplaced. We continue to flounder against one of the oldest observations made in clinical practice—ie, that no matter how sound the science, our patients do not take their medication as prescribed,2 particularly when that medication is for a chronic disorder. Using a previously validated questionnaire,3 I asked 327 patients with primary hypothyroidism about any difficulties they had in taking their Such an prescribed thyroxine.4 approach is relatively good (specificity 87%) at ruling-in non-adherence.2 Patients who admit to non-compliance are generally non-compliant. Their self-reported non-adherence with thyroxine was 22%.4 The true prevalence of non-adherence with thyroxine will be much higher. Such questioning has a low sensitivity (55%) for ruling-out non-adherence.2 The issue of patients’ compliance with thyroxine merited only one sentence in the eight-page Seminar.1 None of the 164 references cited in the review related to the reluctance of patients to take thyroxine (or how this could be effectively addressed). Many references related to the molecular or genomic basis of primary hypothyroidism. I suspect that this balance might accurately reflect that in the medical literature. Something has gone seriously awry with the focus of medical research. The effectiveness of thyroxine for this disorder was shown some 113 years ago.1 Compared with the number of patients with chronic disorders that could benefit from higher levels of adherence with drugs of established effectiveness, how many patients stand to benefit from a greater understanding of the molecular genetic basis of this common condition? Mike Crilly Department of Public Health, University of Aberdeen Medical School, Polwarth Building at Foresterhill, Aberdeen AB25 2ZD, UK (e-mail: [email protected]) 1
2
3
4
Roberts CG, Ladenson PW. Hypothyroidism. Lancet 2004; 363: 793–803. Stephenson BJ, Rowe BH, Haynes RB, Macharia WM, Leon G. The rational clinical examination: is this patient taking the treatment as prescribed? JAMA 1993; 269: 2779–81. Morisky DE, Green LW, Levine DM. Concurrent and predictive validity of a selfreported measure of medication adherence. Med Care 1986; 24: 67–74. Crilly MA. Thyroxine adherence study: a randomised controlled clinical trial in primary care. Manchester: University of Manchester, 2003 (MD thesis).
THE LANCET • Vol 363 • May 8, 2004 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet publishing Group.
“New” practice of bedsharing and risk of SIDS Sir—In commenting on the paper by R G Carpenter and co-workers,1 David Tappin and colleagues (Mar 20, p 994)2 claim parent-infant bedsharing to be a “new practice”, and urge caution in “tampering with our own culturally derived infant care practices”. But what are these practices? If we are urged to venerate our “own” culturally derived infant-care practices, then we should surely be rejecting the cultural changes in UK infant care imported over the past century. The “scientific” baby-care of American John B Watson, who advocated avoidance of physical contact and affection with infants, and New Zealander Frederick Truby King, who encouraged mothers to sleep their babies in quiet darkened rooms and limit physical comfort lest the baby become “spoiled”, changed infant care dramatically and swept aside our biologically and culturally evolved practices. Before the 20th century, UK mothers slept with their babies as a matter of course, as do mothers throughout the world who have not been influenced by recently invented traditions, as did human and prehuman mothers for many millennia previously. Human-infant physiology evolved in such a context (as evidenced by the constant motherinfant physical contact of the great apes), resulting in infants who require close physical contact with a caregiver, day and night, to regulate their temperature, breathing, and other vital functions.3 100 years of rapidly changing infant-care fashions cannot alter several million years of evolutionarily derived infant physiology. Sleep contact is both a culturally and biologically evolved behaviour for human mothers and infants—the view that it is a recent invention is peculiarly myopic. That mother-infant sleep contact is a biologically normal human behaviour does not mean it is inherently safe. As with many aspects of daily life from preparing food to crossing the road, it is the context and manner in which these activities are conducted that make them safe or unsafe. Few sudden infant death syndrome (SIDS) epidemiological studies are sufficiently sophisticated or have enough power to differentiate between different types of bedsharing, which occurs for various reasons and
1558
can be practised in many ways,4 some being safe and some not (eg, cosleeping on a sofa, in overcrowded housing conditions, with intoxicated parents, etc). In an ongoing longitudinal study of infant feeding and sleeping in the northeast of England, we have seen that 70% of breastfeeding mothers repeatedly bedshared with their infant throughout the first 12 weeks, confirming our previously reported finding that 72% of breastfeeding mothers and infants bedshare for some part of the night in the first 3 months of life.5 In their letter, Tappin and colleagues2 report that 4% of younger SIDS infants (five of 123) were found in bed with a non-smoking parent. Even if the 3% of similar bedsharing controls (seven of 263) was not underreported, it is difficult to understand how they can associate such a high degree of risk with this practice. *Helen L Ball, Peter S Blair, Martin P Ward-Platt *Department of Anthropology, University of Durham, Durham DH1 3HN, UK (HLB); Division of Child Health, University of Bristol, Bristol, UK (PSB); and Newcastle Neonatal Service, Royal Victoria Infirmary, Newcastle upon Tyne, UK (MPWP) (e-mail: [email protected]) 1
2
3
4
5
Carpenter RG, Irgens LM, Blair PS, et al. Sudden unexplained infant death in 20 regions in Europe: case control study. Lancet 2004; 363: 185–91. Tappin D, Brooke H, Ecob R. Bedsharing and sudden infant death syndrome (SIDS) in Scotland, UK. Lancet 2004; 363: 994. Trevathan WR, McKenna JJ. Evolutionary environments of human birth and infancy: insights to apply to contemporary life. Child Environ 1994; 11: 88–104. Ball HL. Reasons to bed-share: why parents sleep with their infants. J Reprod Inf Psychol 2002; 20: 207–22. Ball HL. Breastfeeding, bed-sharing and infant sleep. Birth 2003; 30: 181–88.
Thyroxine adherence in primary hypothyroidism Sir—Physicians who read Caroline Roberts and Paul Ladenson’s Seminar on hypothyroidism (Mar 6, p 793),1 particularly those in primary care, might feel that the ambulatory approach to primary hypothyroidism is largely cut and dried: we have an established safe, cheap, effective, oncedaily, lifelong replacement therapy (identical to the natural hormone) to offer our patients; we can precisely monitor treatment with routinely available ultra-sensitive thyrotropin assays; we can even be awed by the major advances in molecular and genomic research that expands on the
negative hormonal feedback loop that is the pathophysiological basis for our clinical management. Such complacency would be misplaced. We continue to flounder against one of the oldest observations made in clinical practice—ie, that no matter how sound the science, our patients do not take their medication as prescribed,2 particularly when that medication is for a chronic disorder. Using a previously validated questionnaire,3 I asked 327 patients with primary hypothyroidism about any difficulties they had in taking their Such an prescribed thyroxine.4 approach is relatively good (specificity 87%) at ruling-in non-adherence.2 Patients who admit to non-compliance are generally non-compliant. Their self-reported non-adherence with thyroxine was 22%.4 The true prevalence of non-adherence with thyroxine will be much higher. Such questioning has a low sensitivity (55%) for ruling-out non-adherence.2 The issue of patients’ compliance with thyroxine merited only one sentence in the eight-page Seminar.1 None of the 164 references cited in the review related to the reluctance of patients to take thyroxine (or how this could be effectively addressed). Many references related to the molecular or genomic basis of primary hypothyroidism. I suspect that this balance might accurately reflect that in the medical literature. Something has gone seriously awry with the focus of medical research. The effectiveness of thyroxine for this disorder was shown some 113 years ago.1 Compared with the number of patients with chronic disorders that could benefit from higher levels of adherence with drugs of established effectiveness, how many patients stand to benefit from a greater understanding of the molecular genetic basis of this common condition? Mike Crilly Department of Public Health, University of Aberdeen Medical School, Polwarth Building at Foresterhill, Aberdeen AB25 2ZD, UK (e-mail: [email protected]) 1
2
3
4
Roberts CG, Ladenson PW. Hypothyroidism. Lancet 2004; 363: 793–803. Stephenson BJ, Rowe BH, Haynes RB, Macharia WM, Leon G. The rational clinical examination: is this patient taking the treatment as prescribed? JAMA 1993; 269: 2779–81. Morisky DE, Green LW, Levine DM. Concurrent and predictive validity of a selfreported measure of medication adherence. Med Care 1986; 24: 67–74. Crilly MA. Thyroxine adherence study: a randomised controlled clinical trial in primary care. Manchester: University of Manchester, 2003 (MD thesis).
THE LANCET • Vol 363 • May 8, 2004 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet publishing Group.