- Email: [email protected]
Parental neglect during childhood and increased risk of obesity in young adulthood
facilitate presentation of antigens to immunocompetent cells and their activation which could lead to a long-lasting immune response. We are grateful to Mrs C White for reviewing the typescript. References 1
2
3
4 5
Milliner DS, Shinaberger JH, Shuman P, Coburn JW. Inadvertent aluminium administration during plasma exchange due to aluminium contamination of albumin-replacement solutions. N Engl J Med 1985; 312: 165-67. Gupta RK, Relyveld EH, Lindbald EB, Bizzini B, Ben-Efraim S, Gupta CK. Adjuvants-a balance between toxicity and adjuvancy. Vaccine 1993; 11: 293-06. Gluck R, Mischler R, Brantschen S, Just M, Althaus B, Cryz SJ Jr. Immunopotentiating reconstituted influenza virus virosome (IRIV) vaccine delivery system for immunization against hepatitis A. J Clin Invest 1992; 90: 2491-95. Herzenberg LA, Tokuhisa T. Epitope specific regulation. J Exp Med 1982; 155: 1730-40. Etlinger HM, Gillessen D, Lahm HW, Matile H, Schonfeld HJ,
Parental neglect young adulthood
Trzeciak A. Use of prior vaccinations for the development of new vaccines. Science 1990; 249: 423-25. 6 Schutze MP, Deriaud E, Przewlocki G, Le Clerc C. Carrier-induced epitopic suppression is initiated through clonal dominance.J Immunol 1989; 142: 2635-40. 7 André FE, Hepburn A, D’Hondt E. Inactivated candidate vaccines for hepatitis A. Prog Med Virol 1990; 37: 72-95. 8 Ambrosch F, Wiedermann G, André FE, et al. Comparison of HAV antibodies induced by vaccination, passive immunization and natural infection. In: Hollinger FB, Lemon SM, Margolis HS, eds. Viral hepatitis and liver disease. Baltimore: Williams and Wilkins, 1991: 98-100. 9 Anon. Hepatitis A: a vaccine at last. Lancet 1992; 339: 1198-99. 10 André FE, D’Hondt E, Delem A, Safary A. Clinical assessment of safety and efficacy of an inactivated hepatitis A vaccine: rationale and summary of findings. Vaccine 1992; 10 (suppl 1): S160-68. 11 Poovorawan Y, Tieamboonlers A, Chumdermpadetsuk S, Glück R, Cryz SJ. Control of a hepatitis A outbreak by active immunization of high-risk susceptibles. J Infect Dis (in press). 12 Gluck R. Towards a universal IRIV traveller vaccine. Third Conference on International Travel Medicine, April 26-29, 1993. Paris (abstr). International Society of Travel Medicine, Paris, 1993.
during childhood and increased risk of obesity in
Summary
Introduction
The association of various features of family life with obesity in childhood is well established, but less is known about the effect of these influences on the risk of later obesity. In this prospective, population-based study, we examined the influence of parental care in childhood on the risk of obesity in the offspring in young adulthood. In 1974, 1258 pupils aged 9-10 years were randomly selected from the third grade of Copenhagen schools. Information on 987 pupils was obtained from the form teachers on family structure and the perceived support from the parents; school medical services reported on the child’s general hygiene. 756 (86%) of the 881 eligible participants were followed up 10 years later. The influence of family factors in childhood on the risk of obesity (body-mass index >95th centile) in young adulthood was estimated by odds ratios with control for age and body-mass index in 1974, sex, and social background. Family structure (biological or other parents and number of siblings) did not significantly affect the risk of adult obesity. Parental neglect greatly increased the risk in comparison with harmonious support (odds ratio 7·1 [95% Cl 2·6-19·3]). Dirty and neglected children had a much greater risk of adult obesity than averagely groomed children (9·8
Although it is generally accepted that characteristics of family life are closely linked to the development and maintenance of obesity in children,l the extent to which they determine the child’s later propensity to obesity has not been much investigated.2-4 The possible influence of family factors5,6 has been debated for several decades. Bruchmade interesting observations while treating obese
[3·5-28·2]). However, being an only child, receiving overprotective parental support, or being well-groomed had no effect. Parental neglect during childhood predicts a great risk of obesity in young adulthood, independent of age and bodymass index in childhood, sex, and social background. Lancet 1994; 343: 324-27
Institute of Preventive Medicine, Copenhagen Health Services, Kommunehospltalet, DK-1399 Copenhagen (I Lissau PhD, Prof T I A Sørensen Dr Med Sci); and Department of Paediatrics, Rigshospitalet, University of Copenhagen (I Lissau), Denmark
Correspondence to: Dr Inge Lissau 324
children. She described a prototype of a mother of an obese child as ambivalent, exerting overprotection and rejection at the same time. Many obese children were unwanted, only children, or an afterthought. In a cross-sectional study of Copenhagen schoolchildren, Quaade8 could not replicate her findings. In this 10-year follow-up study of a randomly selected cohort of 9-10-year-old children,9-11 we examined the effects of family structure and parents’ care for their offspring’s well-being during childhood on risk of obesity in young adulthood.
Subjects and methods In 1974, a random sample of children, mostly aged 9-10 years, was drawn from the population of pupils attending the third school grade in the Copenhagen municipality.12 The sample comprised 1258 children, 25% of the population. The key professionals at school (the form teacher and the school nurse or doctor) and the parent or guardian answered questionnaires about the child. Complete information from school sources was obtained at the first examination for 987(78%).881 children who were still living on the island of Sjaelland were followed up 10 years later by a mailed questionnaire and a subsequent home visit in 1984-85." The participation rate in follow-up was 86% (756). The 231 children who were not followed up (106 not available for 10-year follow-up and 125 non-respondents) showed, as expected, more school difficulties and health problems, and were of lower social class than
participants." The form teachers’ questionnaire was completed for 1120 children (89%); it included questions on family structure and an assessment of the teacher’s perceived support by the parents of their child (table 1). In Denmark, the form teacher normally has
*With control for body-mass index, age at examination in childhood, sex, and confounder score.
Table 2: Likelihood of obesity In young adulthood In relation to family factors estimation 14 with
Table 1: Prevalence of obesity In childhood and young adulthood In relation to family factors In childhood
daily contact with the pupils and teaches them at least one major subject, usually for several years. He or she is the person mainly responsible for contact with parents and coordination of class work. 97% (247) of the form teachers had known the participating pupil for
least 6 months.12 The school medical service (59 school nurses, 16 school medical officers) at the same time, but independently, answered a questionnaire (for 1100 children [87%]) about the general hygiene of the child (table 1) and reported the height and weight. The reported height (without shoes, to the nearest cm) and weight (naked or in light underwear, to the nearest kg) were those recorded at the latest examination.12 The age of the child (in months) at the time of measurement was recorded for all but 11 qf the participants. In 1984-85, the participants (aged 20-21 years) were re-examined. Height and weight were obtained by the questionnaire.9 Body-mass index (weight/height2) was used to define degree of overweight (90th centile) and obesity (95th centile). Limits of overweight for male participants were 18.7 kg/m2 at age 9-10 and 25.9 kgfm2 at age 20-21; the limits for females were 18.9 kg/m2 and 24-2 kg/m2, respectively. The corresponding cut-offs for obesity were 20-2 kg/m2 and 26-9 kgfm2 for male participants and 20-1 1 kgfm2 and 26-3 kg/m2 for females. It has been shown previously that obesity in young adults is related to parental social factors.9,13 The mother or guardian reported by mailed questionnaire (for 887 children [71 %]) on her own and the father’s school education and on householder’s occupation. We defined low education as 7 years of primary school, middle as 9 years of school (leaving with a general certificate, ordinary level), and high as 10-12 years (leaving with secondary school certificate of education or general certificate of education, advanced level). Occupational status was classified low for unskilled manual workers and pensioners; middle for lower-level salaried employed, non-academic self-employed, and skilled manual workers; and high for those with academic university degrees, managing directors, factory owners, and upper-level salaried employed. Quality of housing was classified according to the Commission of Dwellings in areas with poor and good houses (known by postal code for all 1258 children).12 We controlled for the possible confounding effect of these four social variables by a confounder score, as well as by the four variables separately.99 Overweight and obesity were used as dependent variables. The main analysis comprised two steps. In the first step, prevalence of overweight and obesity in young adulthood was calculated in relation to family factors in childhood. In the second step, we carried out logistic regression analysis by maximum likelihood
body-mass index and age at examination in the social confounder score as covariates. and childhood,15 sex, CI for odds ratios were calculated from the standard errors of 95% the coefficients. The social confounder score for each individual was made by a separate logistic regression analysis with overweight as the dependent variable, and the four social factors as independent nominal scale variables; a value of zero was assigned to missing information. Thus, the confounder score is a single continuous variable that brings together information on the four social variables.
at
Results The prevalence of obesity in childhood and young adulthood in relation to the family factors in childhood is shown in table 1. Other results are based on the prospective analysis of obesity in young adulthood while controlling for body-mass index in childhood. Family structure in childhood had no significant effect on the likelihood of obesity in young adulthood when bodymass index and age at examination in childhood, sex, and the social confounder score were included as covariates
(table 2). By contrast, parental support as perceived by the form teacher had a highly significant effect on the child’s risk of obesity in young adulthood (table 2). Children receiving no support had a significantly higher risk than those raised with harmonious parental support. Overprotective support tended to increase the risk of obesity, but the effect was not significant. General hygiene in childhood also had a highly significant effect on the risk of obesity in young adulthood. In comparison with averagely groomed children, those considered dirty and neglected were 9 8 times more likely to be obese in young adulthood. The analysis was repeated in several other ways, with essentially the same results. We analysed the risk of being overweight rather than obese (body-mass index above the 90th centile), the risk of becoming obese or overweight excluding the children already obese (36) or overweight (76) in childhood, and the risk of being or of becoming obese or overweight with control for the four social variables separately and together (instead of using the confounder score) in the multivariate analysis.
Discussion
parental care for the offspring’s well-being has a highly significant association with obesity in young adulthood: parental neglect during childhood predicts a Lack of
325
greatly increased risk of obesity in young adulthood. Neither overprotective parental support nor family structure was significantly associated with the risk. Johnston3concluded after reviewing work published up to 1985, "Despite 45 years of concentrated research, our ignorance about childhood obesity is amazing. There are plenty of correlations and risk ratios, but few in depth prospective data allow us to disaggregate a condition that has been a complex and heterogeneous collection of causes".3This statement still seems to be valid. Our results are difficult to compare with those of other studies addressing this problem because of differences in design (cross-sectional or prospective), setting (general or clinic population), sample selection (random or non-random), age group, definition of obesity, control of confounding, and assessment of family factors. The advantages and limitations of our study have been discussed,9,lO but the main point is that the temporal sequence between assessment of family factors and obesity is established. The assessment of the family factors was based on limited information from a mailed questionnaire. The reliability was checked,12 but the questionnaire was not directly validated. However, the information was collected many years before the assessment of obesity in young adulthood. We believe that no other key professionals know as much about the parents and the family homes as the form teachers. In view of the reservations, it is surprising that parental neglect was such a strong predictor of prospective obesity. The strength of the association suggests that the questions used elicit information on a very important component of the psychosocial influence on obesity. For screening of individuals at risk it is an obvious advantage that the risk factors can be easily investigated. It is likely that perceived lack of parental support and poor general hygiene are proxy measures of the same aspect of parental neglect. These assessments were made independently by two different professionals. Although there was no significant association with childhood obesity, the association of the two variables with later obesity was very strong. These results are consistent with our previous finding of a more than 4-fold risk of overweight in young adults whose mothers claimed not to know about the offspring’s sweet-eating habits as a child; reported actual sweet-eating habits had less influence.1o The relation between a mother’s attitude to her child and obesity in the child was considered by Bruch.7 She suggested that a mother who does not like her child may react to this dislike by overprotecting and overfeeding the child, and thereby induce obesity. We had no information about whether overprotection and rejection were present at the same time. Children suffering from parental neglect seem to be at high risk of obesity in accordance with Bruch’s findings, but overprotective support, and particularly being well-groomed or being an only child, did not increase the risk significantly in our study. The association between parental neglect and later obesity is far stronger than those for other psychosocial risk factors, such as parental education or occupation,9 quality of dwelling,9 or child’s school performance.15 Future studies should address the inter-relation between the psychosocial risk factors in terms of their association with later obesity. The mechanisms by which psychosocial factors act are not known. Dietary habits and physical activity may have roles, but in studies in the general population, neither have shown effects on obesity as large as those observed in this 326
study. We suggest that parental neglect may cause a psychological state that affects energy balance by altering behaviour (overeating and physical inactivity) or hormone balances, influencing fat storage (corticosteroids, catecholamines, or insulin). A previous adoption study has shown that genetic relationship can account for the familial resemblance in obesity in adulthood.16.17 This finding suggests that the rearing environment, as assessed by degree of obesity of the family members, has no sustained effect into adulthood. Other features of family life, unrelated to degree of obesity in the family, may have roles, however. Whether parental neglect acts independently of the genetic effect or is a mediator of it must be addressed in future studies, including information on degree of obesity of the parents, which was not available in this study. However, by controlling for the effect of body-mass index in childhood we partly addressed this drawback. The parent-offspring association in body-mass index seems to be fully expressed by the age of 7.18 Furthermore, the genetic effect observed in the adoption study produces much smaller odds ratios (about 2) than those in our study.16 For the prevention of cardiovascular diseases in adulthood, it is important to begin with preventive programmes at early school age.19 Garrow20.21 argues that there is an opportunity to prevent obesity in primary school children, which may be better than at any other stage in life. By taking advantage of linear growth, the child can become thinner simply by keeping the weight constant. Furthermore, primary school children may be easier to deal with than teenagers. Thus, modification of pertinent psychosocial risk factors in early childhood may be worth while to test in intervention studies. For preventive purposes, it may also be important to identify children suffering from parental neglect. This study
was supported by Sygekassernes Helsefond (30-90, 262-90, 247-91, 244-92), the Danish Heart Foundation (Hjerteforeningen), Novo Nordisk Foundation, and the Danish Medical Research Council (5.22.99.98).
References 1
Dietz WH. Prevention of childhood
obesity. Pediatr Clin North Am
1986; 33: 823-33. 2 Dietz WH, Gortmaker SL. Factors within the physical environment associated with childhood obesity. Am J Clin Nutr 1984; 39: 619-24. 3 Johnston FE. Health implications of childhood obesity. Ann Intern Med 1985; 103: 1068-73. 4 Loader P. Childhood obesity: the family perspective. Int J Eating Disord 1985; 4: 211-25. 5 Kinston W, Loader P, Miller L, Rein L. Interaction in families with obese children. J Psykosom Res 1988; 32: 513-32. 6 Silverman WK, Israel AC. The development and treatment of childhood obesity: parental and family factors. Behav Therapist 1987; 10: 197-201. Bruch H. The importance of overweight. New York: WW Norton, 1957. 8 Quaade F. Obese children: anthropology and development. Copenhagen: Dansk Videnskabs Forlag, 1955. 9 Lissau-Lund-Sørensen I, Sørensen TIA. Prospective study of the influence of social factors in childhood on risk of overweight in young adulthood. Int J Obes 1992; 16: 169-75. 10 Lissau I, Breum L, Sørensen TIA. Maternal attitude to sweet eating habits and risk of overweight in offspring: a ten-year prospective population study. Int J Obes 1993; 17: 125-29. 11 Lissau I. Tandplejeadfaerd og parodontal sygdom. En 10 års histotisk prospektiv kohorteundersøgelse. Dissertation. Copenhagen: University of Copenhagen, 1993. 12 Friis-Hasché E. Skolebørns sundhedstilstand (Thesis). Copenhagen; 7
Odontologisk boghandels forlag, 1981. 13 Power C, Moynihan C. Social class and changes in weight-for-height between childhood and early adulthood. Int J Obes 1988; 12: 445-53.
14 SAS Institute. SAS user’s guide: statistics, version 5 edition. Cary, NC: SAS Institute, 1985. 15 Lissau I, Sørensen TIA. School difficulties in childhood and risk of overweight and obesity in young adulthood: a ten-year prospective population study. Int J Obes 1993; 17: 169-75. 16 Stunkard AJ, Sørensen TIA, Hanis C, et al. An adoption study of human obesity. N Engl J Med 1986; 314: 193-98. 17 Sørensen TIA, Holst C, Stunkard AJ, Skovgaard LT. Correlations of body mass index of adult adoptees and their biological and adoptive relatives. Int J Obes 1992; 16: 227-36.
C, Stunkard AJ. Childhood body mass indexgenetic and familial environmental influences assessed in a longitudinal adoption study. Int J Obes 1992; 16: 705-14. 19 Hertzel BS, Berenson GS, eds. Cardiovascular risk factors in childhood: epidemiology and prevention. Amsterdam: Elsevier, 1987. 20 Garrow JS. The management of obesity: another view. Int J Obes 1992; 16 (suppl 2): 59-63. 21 Garrow JS. Management and prevention of obesity in children. In: obesity and related diseases. Edinburgh: Churchill Livingstone, 18 Sørensen TIA, Holst
1988.
QT dispersion and sudden unexpected death in chronic heart failure
Summary Death in chronic heart failure (CHF) can be from progression of disease or sudden and unexpected. We have attempted to identify factors that predict sudden death in CHF. We followed up 44 patients with CHF for 12-50 (mean 36) months. 4 patients died of non-cardiovascular causes and were excluded from analysis. There were 7 sudden deaths (symptoms for less than 1 h in a previously stable patient) and 12 from progressive CHF. Patients who died of progressive CHF had lower left-ventricular ejection fractions and higher concentrations of atrial natriuretic factor than the 21 survivors, but there were no differences in these variables between survivors and those who died suddenly. However, the sudden death group had significantly (p<0·05) greater inter-lead variability in the QT interval on the electrocardiogram (QT dispersion; 98·6 [95% Cl 79·1-118] ms½) than survivors (53·1 [41·9-64·3] ms½) or the group who died from progressive CHF (66·7 [51·8-81·6] ms½). QT dispersion is a marker of myocardial electrical instability. The association of increased QT dispersion with sudden death suggests that patients at high risk of such death could be identified by means of this simple, reproducible test. This group might benefit from more intensive treatment. Lancet 1994; 343: 327-29
Introduction Chronic heart failure (CHF) is the most important public health problem in cardiovascular medicine. In the Framingham Heart Study, 2.5 % of people over 45 years old were affected; median survival time was 3-2 years in men and 5-4 years in women.’ 50% of deaths in mild CHF and 25% of those in severe CHF are sudden and unexpected.2,3 The distinction between sudden and non-sudden death is unclear, as are the causes and mechanisms of sudden death. Many studies have identified risk factors for all deaths in CHF; low values of left-ventricular ejection fraction, maximum exercise tolerance, serum sodium, potassium, and magnesium, and mean arterial pressure all increase the risk.4-6 Activation of the renin-angiotensin system and the
Department of Clinical Pharmacology, Nlnewells Hospital and Medical School, Dundee DD1 9SY, UK (C S Barr MRCP, A Naas MB, M Freeman, C C Lang MRCP, Prof A D Struthers FRCP) Correspondence to: Dr Craig S Barr
sympathetic nervous system’ are associated with a poor prognosis. Attempts have been made lately to separate predictors of death from progressive CHF and predictors of sudden unexpected death. In one study, an increasing plasma noradrenaline distinguished patients who died of progressive CHF from those who died suddenly.8 Prolongation of the QT interval has been found to predict sudden death in patients with coronary artery disease9 (although not in patients with cardiac dysfunction1O) and alcoholic cirrhosis,lO,l1 and cardiovascular death in normal, apparently healthy, individuals in large population studies.12 Another measure that might be useful in this context is inter-lead variability in the QT interval (dispersion). This index reflects regional variation in ventricular repolarisation,13 which represents an electrophysiological substrate for arrhythmias.14 Among patients with acute myocardial infarction, there is increased dispersion in those who develop ventricular tachyarrhythmias but not in those without such complications. is Similarly, QT dispersion is increased in patients with long QT syndromes who are at high risk of ventricular arrhythmias.16 Patients with acute myocardial infarction1S or hypertrophic cardiomyopathy 17 who die suddenly also have increased QT dispersion. In CHF, variable of the electrophysiological properties myocardium, coupled with an already failing heart, might be associated with alterations in ventricular repolarisation that could identify patients at risk of sudden death. If this hypothesis is correct, measurement of QT dispersion might be a simple non-invasive screening procedure to identify CHF patients at greater risk of sudden death. We have prospectively examined haemodynamic, neurohormonal, and biochemical variables and retrospectively assessed QT interval measurements in a cohort of patients with CHF to see which factors predict sudden unexpected death. Patients and methods 44 patients of mean age 76 (range 53-85) years, with symptomatic left-ventricular systolic dysfunction secondary to ischaemic heart disease (New York Heart Association class III-IV) were followed up for a mean of 36 (range 12-50) months, and endpoints of survival, sudden unexpected death, or death from progressive CHF were assessed. The patients were receiving aspirin, diuretics, and angiotensin-converting-enzyme (ACE) inhibitors but no other cardioactive drugs; in particular, none was taking anti-arrhythmic therapy or drugs that can affect the QT interval. The study was approved by the Tayside Committee on Medical Research Ethics.
327
2
3
4 5
Milliner DS, Shinaberger JH, Shuman P, Coburn JW. Inadvertent aluminium administration during plasma exchange due to aluminium contamination of albumin-replacement solutions. N Engl J Med 1985; 312: 165-67. Gupta RK, Relyveld EH, Lindbald EB, Bizzini B, Ben-Efraim S, Gupta CK. Adjuvants-a balance between toxicity and adjuvancy. Vaccine 1993; 11: 293-06. Gluck R, Mischler R, Brantschen S, Just M, Althaus B, Cryz SJ Jr. Immunopotentiating reconstituted influenza virus virosome (IRIV) vaccine delivery system for immunization against hepatitis A. J Clin Invest 1992; 90: 2491-95. Herzenberg LA, Tokuhisa T. Epitope specific regulation. J Exp Med 1982; 155: 1730-40. Etlinger HM, Gillessen D, Lahm HW, Matile H, Schonfeld HJ,
Parental neglect young adulthood
Trzeciak A. Use of prior vaccinations for the development of new vaccines. Science 1990; 249: 423-25. 6 Schutze MP, Deriaud E, Przewlocki G, Le Clerc C. Carrier-induced epitopic suppression is initiated through clonal dominance.J Immunol 1989; 142: 2635-40. 7 André FE, Hepburn A, D’Hondt E. Inactivated candidate vaccines for hepatitis A. Prog Med Virol 1990; 37: 72-95. 8 Ambrosch F, Wiedermann G, André FE, et al. Comparison of HAV antibodies induced by vaccination, passive immunization and natural infection. In: Hollinger FB, Lemon SM, Margolis HS, eds. Viral hepatitis and liver disease. Baltimore: Williams and Wilkins, 1991: 98-100. 9 Anon. Hepatitis A: a vaccine at last. Lancet 1992; 339: 1198-99. 10 André FE, D’Hondt E, Delem A, Safary A. Clinical assessment of safety and efficacy of an inactivated hepatitis A vaccine: rationale and summary of findings. Vaccine 1992; 10 (suppl 1): S160-68. 11 Poovorawan Y, Tieamboonlers A, Chumdermpadetsuk S, Glück R, Cryz SJ. Control of a hepatitis A outbreak by active immunization of high-risk susceptibles. J Infect Dis (in press). 12 Gluck R. Towards a universal IRIV traveller vaccine. Third Conference on International Travel Medicine, April 26-29, 1993. Paris (abstr). International Society of Travel Medicine, Paris, 1993.
during childhood and increased risk of obesity in
Summary
Introduction
The association of various features of family life with obesity in childhood is well established, but less is known about the effect of these influences on the risk of later obesity. In this prospective, population-based study, we examined the influence of parental care in childhood on the risk of obesity in the offspring in young adulthood. In 1974, 1258 pupils aged 9-10 years were randomly selected from the third grade of Copenhagen schools. Information on 987 pupils was obtained from the form teachers on family structure and the perceived support from the parents; school medical services reported on the child’s general hygiene. 756 (86%) of the 881 eligible participants were followed up 10 years later. The influence of family factors in childhood on the risk of obesity (body-mass index >95th centile) in young adulthood was estimated by odds ratios with control for age and body-mass index in 1974, sex, and social background. Family structure (biological or other parents and number of siblings) did not significantly affect the risk of adult obesity. Parental neglect greatly increased the risk in comparison with harmonious support (odds ratio 7·1 [95% Cl 2·6-19·3]). Dirty and neglected children had a much greater risk of adult obesity than averagely groomed children (9·8
Although it is generally accepted that characteristics of family life are closely linked to the development and maintenance of obesity in children,l the extent to which they determine the child’s later propensity to obesity has not been much investigated.2-4 The possible influence of family factors5,6 has been debated for several decades. Bruchmade interesting observations while treating obese
[3·5-28·2]). However, being an only child, receiving overprotective parental support, or being well-groomed had no effect. Parental neglect during childhood predicts a great risk of obesity in young adulthood, independent of age and bodymass index in childhood, sex, and social background. Lancet 1994; 343: 324-27
Institute of Preventive Medicine, Copenhagen Health Services, Kommunehospltalet, DK-1399 Copenhagen (I Lissau PhD, Prof T I A Sørensen Dr Med Sci); and Department of Paediatrics, Rigshospitalet, University of Copenhagen (I Lissau), Denmark
Correspondence to: Dr Inge Lissau 324
children. She described a prototype of a mother of an obese child as ambivalent, exerting overprotection and rejection at the same time. Many obese children were unwanted, only children, or an afterthought. In a cross-sectional study of Copenhagen schoolchildren, Quaade8 could not replicate her findings. In this 10-year follow-up study of a randomly selected cohort of 9-10-year-old children,9-11 we examined the effects of family structure and parents’ care for their offspring’s well-being during childhood on risk of obesity in young adulthood.
Subjects and methods In 1974, a random sample of children, mostly aged 9-10 years, was drawn from the population of pupils attending the third school grade in the Copenhagen municipality.12 The sample comprised 1258 children, 25% of the population. The key professionals at school (the form teacher and the school nurse or doctor) and the parent or guardian answered questionnaires about the child. Complete information from school sources was obtained at the first examination for 987(78%).881 children who were still living on the island of Sjaelland were followed up 10 years later by a mailed questionnaire and a subsequent home visit in 1984-85." The participation rate in follow-up was 86% (756). The 231 children who were not followed up (106 not available for 10-year follow-up and 125 non-respondents) showed, as expected, more school difficulties and health problems, and were of lower social class than
participants." The form teachers’ questionnaire was completed for 1120 children (89%); it included questions on family structure and an assessment of the teacher’s perceived support by the parents of their child (table 1). In Denmark, the form teacher normally has
*With control for body-mass index, age at examination in childhood, sex, and confounder score.
Table 2: Likelihood of obesity In young adulthood In relation to family factors estimation 14 with
Table 1: Prevalence of obesity In childhood and young adulthood In relation to family factors In childhood
daily contact with the pupils and teaches them at least one major subject, usually for several years. He or she is the person mainly responsible for contact with parents and coordination of class work. 97% (247) of the form teachers had known the participating pupil for
least 6 months.12 The school medical service (59 school nurses, 16 school medical officers) at the same time, but independently, answered a questionnaire (for 1100 children [87%]) about the general hygiene of the child (table 1) and reported the height and weight. The reported height (without shoes, to the nearest cm) and weight (naked or in light underwear, to the nearest kg) were those recorded at the latest examination.12 The age of the child (in months) at the time of measurement was recorded for all but 11 qf the participants. In 1984-85, the participants (aged 20-21 years) were re-examined. Height and weight were obtained by the questionnaire.9 Body-mass index (weight/height2) was used to define degree of overweight (90th centile) and obesity (95th centile). Limits of overweight for male participants were 18.7 kg/m2 at age 9-10 and 25.9 kgfm2 at age 20-21; the limits for females were 18.9 kg/m2 and 24-2 kg/m2, respectively. The corresponding cut-offs for obesity were 20-2 kg/m2 and 26-9 kgfm2 for male participants and 20-1 1 kgfm2 and 26-3 kg/m2 for females. It has been shown previously that obesity in young adults is related to parental social factors.9,13 The mother or guardian reported by mailed questionnaire (for 887 children [71 %]) on her own and the father’s school education and on householder’s occupation. We defined low education as 7 years of primary school, middle as 9 years of school (leaving with a general certificate, ordinary level), and high as 10-12 years (leaving with secondary school certificate of education or general certificate of education, advanced level). Occupational status was classified low for unskilled manual workers and pensioners; middle for lower-level salaried employed, non-academic self-employed, and skilled manual workers; and high for those with academic university degrees, managing directors, factory owners, and upper-level salaried employed. Quality of housing was classified according to the Commission of Dwellings in areas with poor and good houses (known by postal code for all 1258 children).12 We controlled for the possible confounding effect of these four social variables by a confounder score, as well as by the four variables separately.99 Overweight and obesity were used as dependent variables. The main analysis comprised two steps. In the first step, prevalence of overweight and obesity in young adulthood was calculated in relation to family factors in childhood. In the second step, we carried out logistic regression analysis by maximum likelihood
body-mass index and age at examination in the social confounder score as covariates. and childhood,15 sex, CI for odds ratios were calculated from the standard errors of 95% the coefficients. The social confounder score for each individual was made by a separate logistic regression analysis with overweight as the dependent variable, and the four social factors as independent nominal scale variables; a value of zero was assigned to missing information. Thus, the confounder score is a single continuous variable that brings together information on the four social variables.
at
Results The prevalence of obesity in childhood and young adulthood in relation to the family factors in childhood is shown in table 1. Other results are based on the prospective analysis of obesity in young adulthood while controlling for body-mass index in childhood. Family structure in childhood had no significant effect on the likelihood of obesity in young adulthood when bodymass index and age at examination in childhood, sex, and the social confounder score were included as covariates
(table 2). By contrast, parental support as perceived by the form teacher had a highly significant effect on the child’s risk of obesity in young adulthood (table 2). Children receiving no support had a significantly higher risk than those raised with harmonious parental support. Overprotective support tended to increase the risk of obesity, but the effect was not significant. General hygiene in childhood also had a highly significant effect on the risk of obesity in young adulthood. In comparison with averagely groomed children, those considered dirty and neglected were 9 8 times more likely to be obese in young adulthood. The analysis was repeated in several other ways, with essentially the same results. We analysed the risk of being overweight rather than obese (body-mass index above the 90th centile), the risk of becoming obese or overweight excluding the children already obese (36) or overweight (76) in childhood, and the risk of being or of becoming obese or overweight with control for the four social variables separately and together (instead of using the confounder score) in the multivariate analysis.
Discussion
parental care for the offspring’s well-being has a highly significant association with obesity in young adulthood: parental neglect during childhood predicts a Lack of
325
greatly increased risk of obesity in young adulthood. Neither overprotective parental support nor family structure was significantly associated with the risk. Johnston3concluded after reviewing work published up to 1985, "Despite 45 years of concentrated research, our ignorance about childhood obesity is amazing. There are plenty of correlations and risk ratios, but few in depth prospective data allow us to disaggregate a condition that has been a complex and heterogeneous collection of causes".3This statement still seems to be valid. Our results are difficult to compare with those of other studies addressing this problem because of differences in design (cross-sectional or prospective), setting (general or clinic population), sample selection (random or non-random), age group, definition of obesity, control of confounding, and assessment of family factors. The advantages and limitations of our study have been discussed,9,lO but the main point is that the temporal sequence between assessment of family factors and obesity is established. The assessment of the family factors was based on limited information from a mailed questionnaire. The reliability was checked,12 but the questionnaire was not directly validated. However, the information was collected many years before the assessment of obesity in young adulthood. We believe that no other key professionals know as much about the parents and the family homes as the form teachers. In view of the reservations, it is surprising that parental neglect was such a strong predictor of prospective obesity. The strength of the association suggests that the questions used elicit information on a very important component of the psychosocial influence on obesity. For screening of individuals at risk it is an obvious advantage that the risk factors can be easily investigated. It is likely that perceived lack of parental support and poor general hygiene are proxy measures of the same aspect of parental neglect. These assessments were made independently by two different professionals. Although there was no significant association with childhood obesity, the association of the two variables with later obesity was very strong. These results are consistent with our previous finding of a more than 4-fold risk of overweight in young adults whose mothers claimed not to know about the offspring’s sweet-eating habits as a child; reported actual sweet-eating habits had less influence.1o The relation between a mother’s attitude to her child and obesity in the child was considered by Bruch.7 She suggested that a mother who does not like her child may react to this dislike by overprotecting and overfeeding the child, and thereby induce obesity. We had no information about whether overprotection and rejection were present at the same time. Children suffering from parental neglect seem to be at high risk of obesity in accordance with Bruch’s findings, but overprotective support, and particularly being well-groomed or being an only child, did not increase the risk significantly in our study. The association between parental neglect and later obesity is far stronger than those for other psychosocial risk factors, such as parental education or occupation,9 quality of dwelling,9 or child’s school performance.15 Future studies should address the inter-relation between the psychosocial risk factors in terms of their association with later obesity. The mechanisms by which psychosocial factors act are not known. Dietary habits and physical activity may have roles, but in studies in the general population, neither have shown effects on obesity as large as those observed in this 326
study. We suggest that parental neglect may cause a psychological state that affects energy balance by altering behaviour (overeating and physical inactivity) or hormone balances, influencing fat storage (corticosteroids, catecholamines, or insulin). A previous adoption study has shown that genetic relationship can account for the familial resemblance in obesity in adulthood.16.17 This finding suggests that the rearing environment, as assessed by degree of obesity of the family members, has no sustained effect into adulthood. Other features of family life, unrelated to degree of obesity in the family, may have roles, however. Whether parental neglect acts independently of the genetic effect or is a mediator of it must be addressed in future studies, including information on degree of obesity of the parents, which was not available in this study. However, by controlling for the effect of body-mass index in childhood we partly addressed this drawback. The parent-offspring association in body-mass index seems to be fully expressed by the age of 7.18 Furthermore, the genetic effect observed in the adoption study produces much smaller odds ratios (about 2) than those in our study.16 For the prevention of cardiovascular diseases in adulthood, it is important to begin with preventive programmes at early school age.19 Garrow20.21 argues that there is an opportunity to prevent obesity in primary school children, which may be better than at any other stage in life. By taking advantage of linear growth, the child can become thinner simply by keeping the weight constant. Furthermore, primary school children may be easier to deal with than teenagers. Thus, modification of pertinent psychosocial risk factors in early childhood may be worth while to test in intervention studies. For preventive purposes, it may also be important to identify children suffering from parental neglect. This study
was supported by Sygekassernes Helsefond (30-90, 262-90, 247-91, 244-92), the Danish Heart Foundation (Hjerteforeningen), Novo Nordisk Foundation, and the Danish Medical Research Council (5.22.99.98).
References 1
Dietz WH. Prevention of childhood
obesity. Pediatr Clin North Am
1986; 33: 823-33. 2 Dietz WH, Gortmaker SL. Factors within the physical environment associated with childhood obesity. Am J Clin Nutr 1984; 39: 619-24. 3 Johnston FE. Health implications of childhood obesity. Ann Intern Med 1985; 103: 1068-73. 4 Loader P. Childhood obesity: the family perspective. Int J Eating Disord 1985; 4: 211-25. 5 Kinston W, Loader P, Miller L, Rein L. Interaction in families with obese children. J Psykosom Res 1988; 32: 513-32. 6 Silverman WK, Israel AC. The development and treatment of childhood obesity: parental and family factors. Behav Therapist 1987; 10: 197-201. Bruch H. The importance of overweight. New York: WW Norton, 1957. 8 Quaade F. Obese children: anthropology and development. Copenhagen: Dansk Videnskabs Forlag, 1955. 9 Lissau-Lund-Sørensen I, Sørensen TIA. Prospective study of the influence of social factors in childhood on risk of overweight in young adulthood. Int J Obes 1992; 16: 169-75. 10 Lissau I, Breum L, Sørensen TIA. Maternal attitude to sweet eating habits and risk of overweight in offspring: a ten-year prospective population study. Int J Obes 1993; 17: 125-29. 11 Lissau I. Tandplejeadfaerd og parodontal sygdom. En 10 års histotisk prospektiv kohorteundersøgelse. Dissertation. Copenhagen: University of Copenhagen, 1993. 12 Friis-Hasché E. Skolebørns sundhedstilstand (Thesis). Copenhagen; 7
Odontologisk boghandels forlag, 1981. 13 Power C, Moynihan C. Social class and changes in weight-for-height between childhood and early adulthood. Int J Obes 1988; 12: 445-53.
14 SAS Institute. SAS user’s guide: statistics, version 5 edition. Cary, NC: SAS Institute, 1985. 15 Lissau I, Sørensen TIA. School difficulties in childhood and risk of overweight and obesity in young adulthood: a ten-year prospective population study. Int J Obes 1993; 17: 169-75. 16 Stunkard AJ, Sørensen TIA, Hanis C, et al. An adoption study of human obesity. N Engl J Med 1986; 314: 193-98. 17 Sørensen TIA, Holst C, Stunkard AJ, Skovgaard LT. Correlations of body mass index of adult adoptees and their biological and adoptive relatives. Int J Obes 1992; 16: 227-36.
C, Stunkard AJ. Childhood body mass indexgenetic and familial environmental influences assessed in a longitudinal adoption study. Int J Obes 1992; 16: 705-14. 19 Hertzel BS, Berenson GS, eds. Cardiovascular risk factors in childhood: epidemiology and prevention. Amsterdam: Elsevier, 1987. 20 Garrow JS. The management of obesity: another view. Int J Obes 1992; 16 (suppl 2): 59-63. 21 Garrow JS. Management and prevention of obesity in children. In: obesity and related diseases. Edinburgh: Churchill Livingstone, 18 Sørensen TIA, Holst
1988.
QT dispersion and sudden unexpected death in chronic heart failure
Summary Death in chronic heart failure (CHF) can be from progression of disease or sudden and unexpected. We have attempted to identify factors that predict sudden death in CHF. We followed up 44 patients with CHF for 12-50 (mean 36) months. 4 patients died of non-cardiovascular causes and were excluded from analysis. There were 7 sudden deaths (symptoms for less than 1 h in a previously stable patient) and 12 from progressive CHF. Patients who died of progressive CHF had lower left-ventricular ejection fractions and higher concentrations of atrial natriuretic factor than the 21 survivors, but there were no differences in these variables between survivors and those who died suddenly. However, the sudden death group had significantly (p<0·05) greater inter-lead variability in the QT interval on the electrocardiogram (QT dispersion; 98·6 [95% Cl 79·1-118] ms½) than survivors (53·1 [41·9-64·3] ms½) or the group who died from progressive CHF (66·7 [51·8-81·6] ms½). QT dispersion is a marker of myocardial electrical instability. The association of increased QT dispersion with sudden death suggests that patients at high risk of such death could be identified by means of this simple, reproducible test. This group might benefit from more intensive treatment. Lancet 1994; 343: 327-29
Introduction Chronic heart failure (CHF) is the most important public health problem in cardiovascular medicine. In the Framingham Heart Study, 2.5 % of people over 45 years old were affected; median survival time was 3-2 years in men and 5-4 years in women.’ 50% of deaths in mild CHF and 25% of those in severe CHF are sudden and unexpected.2,3 The distinction between sudden and non-sudden death is unclear, as are the causes and mechanisms of sudden death. Many studies have identified risk factors for all deaths in CHF; low values of left-ventricular ejection fraction, maximum exercise tolerance, serum sodium, potassium, and magnesium, and mean arterial pressure all increase the risk.4-6 Activation of the renin-angiotensin system and the
Department of Clinical Pharmacology, Nlnewells Hospital and Medical School, Dundee DD1 9SY, UK (C S Barr MRCP, A Naas MB, M Freeman, C C Lang MRCP, Prof A D Struthers FRCP) Correspondence to: Dr Craig S Barr
sympathetic nervous system’ are associated with a poor prognosis. Attempts have been made lately to separate predictors of death from progressive CHF and predictors of sudden unexpected death. In one study, an increasing plasma noradrenaline distinguished patients who died of progressive CHF from those who died suddenly.8 Prolongation of the QT interval has been found to predict sudden death in patients with coronary artery disease9 (although not in patients with cardiac dysfunction1O) and alcoholic cirrhosis,lO,l1 and cardiovascular death in normal, apparently healthy, individuals in large population studies.12 Another measure that might be useful in this context is inter-lead variability in the QT interval (dispersion). This index reflects regional variation in ventricular repolarisation,13 which represents an electrophysiological substrate for arrhythmias.14 Among patients with acute myocardial infarction, there is increased dispersion in those who develop ventricular tachyarrhythmias but not in those without such complications. is Similarly, QT dispersion is increased in patients with long QT syndromes who are at high risk of ventricular arrhythmias.16 Patients with acute myocardial infarction1S or hypertrophic cardiomyopathy 17 who die suddenly also have increased QT dispersion. In CHF, variable of the electrophysiological properties myocardium, coupled with an already failing heart, might be associated with alterations in ventricular repolarisation that could identify patients at risk of sudden death. If this hypothesis is correct, measurement of QT dispersion might be a simple non-invasive screening procedure to identify CHF patients at greater risk of sudden death. We have prospectively examined haemodynamic, neurohormonal, and biochemical variables and retrospectively assessed QT interval measurements in a cohort of patients with CHF to see which factors predict sudden unexpected death. Patients and methods 44 patients of mean age 76 (range 53-85) years, with symptomatic left-ventricular systolic dysfunction secondary to ischaemic heart disease (New York Heart Association class III-IV) were followed up for a mean of 36 (range 12-50) months, and endpoints of survival, sudden unexpected death, or death from progressive CHF were assessed. The patients were receiving aspirin, diuretics, and angiotensin-converting-enzyme (ACE) inhibitors but no other cardioactive drugs; in particular, none was taking anti-arrhythmic therapy or drugs that can affect the QT interval. The study was approved by the Tayside Committee on Medical Research Ethics.
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