Cutaneous teratoma in a wild roe deer (Capreolus capreolus) in the UK.
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Animals↗
Biomedical subjects
D Couper
Publications and source records attributed to D Couper.
Leptin and incident type 2 diabetes: risk or protection?
AIMS/HYPOTHESIS: The aim of this study was to investigate the association of leptin levels with incident diabetes in middle-aged adults, taking into account factors purportedly related to leptin resistance. SUBJECTS AND METHODS: We conducted a case-cohort study (570 incident diabetes cases and 530 non-cases) representing the 9-year experience of 10,275 participants of the Atherosclerosis Risk in Communities Study. Plasma leptin was measured by direct sandwich ELISA. RESULTS: In proportional hazards models adjusting for age, study centre, ethnicity and sex, high leptin levels (defined by sex-specific cut-off points) predicted an increased risk of diabetes, with a hazard ratio (HR) comparing the upper with the lower quartile of 3.9 (95% CI 2.6-5.6). However, after further adjusting additionally for obesity indices, fasting insulin, inflammation score, hypertension, triglycerides and adiponectin, high leptin predicted a lower diabetes risk (HR=0.40, 95% CI 0.23-0.67). Additional inclusion of fasting glucose attenuated this protective association (HR=0.59, 95% CI 0.32-1.08, p<0.03 for linear trend across quartiles). In similar models, protective associations were generally seen across subgroups of sex, race, nutritional status and smoking, though not among those with lower inflammation scores or impaired fasting glucose (interaction p=0.03 for both). CONCLUSIONS/INTERPRETATION: High leptin levels, probably reflecting leptin resistance, predict an increased risk of diabetes. Adjusting for factors purportedly related to leptin resistance unveils a protective association, independent of adiponectin and consistent with some of leptin's described protective effects against diabetes.
Adiponectin↗
Association of the Lewis genotype with cardiovascular risk factors and subclinical carotid atherosclerosis: the Atherosclerosis Risk in Communities (ARIC) study.
OBJECTIVES: To evaluate the relationship of Lewis genotypes with major cardiovascular risk factors and the intima-media thickness (IMT) of carotid arteries. Lewis genotyping included four major mutations of the Lewis (FUT3) gene at nucleotide positions 59, 1067, 202 and 314. DESIGN: Two complementary population-based cross-sectional studies. SETTING: The Atherosclerosis Risk in Communities (ARIC) Study. SUBJECTS: The relationship between Lewis genotype and major cardiovascular risk factors was studied in 761 men and women aged 45-64 years without known clinical atherosclerotic disease; 577 were Caucasians and 184 were African-Americans. The association of Lewis genotype and subclinical carotid atherosclerosis was studied in 419 individuals with, and 819 controls without carotid IMT of >1.0 mm, measured by B-mode ultrasound. MAIN OUTCOME MEASURES: Mean values of cardiovascular risk factors by Lewis genotype. Lewis genotype frequencies in subclinical carotid atherosclerosis cases and controls. RESULTS: Individuals with Lewis genotypes consistent with lack of alpha(1,3/1,4)-fucosyltransferase activity (i.e. Lewis-negative genotype) had statistically significantly lower fasting glucose, factor VIIIc, von Willebrand factor and diastolic blood pressure compared with their counterparts with Lewis-positive genotypes. The distribution of Lewis genotypes and haplotypes was not significantly different between individuals with carotid IMT of >1.0 mm (cases) and their controls. The odds of carotid atherosclerosis in carriers of the Lewis-negative genotype was 1.23 (95% confidence interval 0.70-2.16) compared to individuals with Lewis-positive genotype, controlling for age, gender and race/ARIC field centre. CONCLUSION: The lack of a statistically significant association between Lewis 'genotype' and subclinical atherosclerosis in our data suggests that earlier studies reporting associations at the 'phenotypic' level may reflect aspects of the biology of the Lewis system other than an inherent genetic property.
Blood Pressure↗
Distribution of Lewis (FUT3)genotype and allele: frequencies in a biethnic United States population.
The objective of the study was to examine the prevalence and distribution of four major single nucleotide polymorphisms (SNPs) (T59G, T1067G, T202C, and C314T) of the Lewis ( FUT3)gene in a biethnic United States population. This population-based cross-sectional study was based on data from the Atherosclerosis Risk in Communities (ARIC) Study, which included 761 males and females aged 45-64 years, who had no known/detected clinical atherosclerotic disease (577 Caucasians, 184 African Americans). The main outcome measures were prevalence of the Lewis genotype and allele frequencies for four SNPs of the FUT3gene. The most common genotype was the "wild type" at all four nucleotide positions ( WWWW), which was found to be present in 46.9% of ARIC participants. At least one mutant allele was detected in 51.7% of Caucasians, and 56.7% of African Americans ( P=0.59). The frequencies of mutant alleles ranged from 6.3% to 18.4% at the four FUT3gene sites examined. The distribution of the Lewis genotype and allele frequencies differed significantly by ethnicity at sites 59, 202, and 314. The prevalence of the Lewis genotype suggesting a lack of alpha(1,3/1,4) fucosyltransferase activity was 11.6% in Caucasians and 9.9% in African Americans ( P=0.67). Four specific SNPs of the Lewis genotype are common in the population at large. However, these four SNPs seem to fail to explain the majority of Lewis-negative phenotype in African Americans, given that Lewis-negative genotype prevalence was about one-third of what was expected. Use of rapid DNA sequencing and simultaneous Lewis phenotype determination could avoid the problems associated with haplotype determination and Lewis genotype grouping. Further studies testing SNPs of the Lewisgene are warranted, in particular among African Americans.
Age Factors↗
Interaction of the glutathione S-transferase genes and cigarette smoking on risk of lower extremity arterial disease: the Atherosclerosis Risk in Communities (ARIC) study.
Glutathione S-transferases M1 or T1 (GSTM1/GSTT1) affect the body's ability either to detoxify or to activate chemicals in cigarette smoke. Cigarette smoking increases the risk of lower extremity arterial disease (LEAD). We conducted a cross-sectional study to evaluate a hypothesized interaction of the genetic polymorphisms of GSTM1 and T1 with cigarette smoking in the risk of LEAD in the ARIC study. A stratified-random sample, including 212 LEAD cases (ankle-brachial index <0.9 in men or <0.85 in women) and 1277 non-cases, was selected from the ARIC cohort of 12041 middle-aged participants free of CHD, transient ischemic attack and stroke at baseline (1987-1989). Overall, the differences in the frequencies of GSTM1-0 and GSTT1-0 (the homozygous deletion genotype) were not statistically significant between cases and non-cases (44 vs. 41% and 28 vs. 18%). However, smoking was more prevalent among LEAD cases than non-cases. The results suggest that the non-deletion genotype GSTM1-1 interacts with smoking to increase the risk of LEAD, but this interaction was not statistically significant. The functional genotype GSTT1-1 was significantly associated with increased risk of LEAD given smoking after adjustment for other risk factors. In individuals with GSTT1-1, the odds ratios (ORs) (95% confidence intervals) of LEAD were 3.6 (1.4, 9.0) for current smoking and 5.0 (1.9, 13.0) for 20+ pack-years. However, in those with GSTT1-0, the ORs were 0.8 (0.2, 2.8) for current smoking and 0.6 (0.1, 2.1) for 20+ pack-years. The interaction was significant (P<0.05) on the additive scale for current smoking and on both the additive and multiplicative scales for 20+ pack-years. Among non-smokers, GSTT1-1 was not associated with LEAD. The results suggest that the GSTT1-1 polymorphism may be a susceptibility factor modifying the risk of LEAD associated with cigarette smoking.
Arteriosclerosis↗
Sources of heterogeneity in the meta-analysis of observational studies: the example of SIDS and sleeping position.
The study objective was to provide an example of how risk estimates might vary across studies of observational design, even when a causal association is present and to explore the possible sources of such variation. A meta-analysis of studies on the association between prone sleeping position and sudden infant death syndrome (SIDS) is used to illustrate how risk estimates might vary across studies. Data used were reported case-control studies of the association between sleeping position and SIDS that were published between 1970 and 1994. If the pooled odds ratio had been relied on to assess the association between sleeping position and SIDS without an accompanying examination of the reasons for heterogeneity, important insights into the causal significance of the relationship may have been lost. In meta-analyses of observational studies it is important to investigate the reasons for heterogeneity across studies.
Bias↗
Sensitivity and specificity of anthropometrics for the prediction of diabetes in a biracial cohort.
OBJECTIVE: To evaluate the ability of body mass index, waist circumference, waist-to-hip ratio, and combinations of these variables to discriminate individuals who will develop diabetes in adulthood. RESEARCH METHODS AND PROCEDURES: Data were from 45- to 64-year-old men and women who were members of the Atherosclerosis Risk in Communities cohort. The analysis sample consisted of 12,814 African American and white participants who were free of diabetes at baseline. Body mass index, waist circumference, waist-to-hip ratio, and diabetes incidence (defined as one glucose measure > or =126 mg/dL after fasting for at least 8 hours, one nonfasting glucose measure > or =200 mg/dL, and self-report of diabetes or report of taking medication for diabetes). RESULTS: 1515 new cases of diabetes were identified over the 9-year follow-up. Areas under receiver operating characteristic curves ranged from 0.66 to 0.73 for single measures. The curves were smooth, with no indication of a threshold. Waist tended to have the highest receiver operating characteristic statistic in all groups, but differences were small. DISCUSSION: The three anthropometric indices tested were approximately equivalent in their ability to predict diabetes. Sensitivity and specificities differed among ethnic and gender groups.
Anthropometry↗
A prospective study of the association between home gas appliance use during infancy and subsequent dust mite sensitization and lung function in childhood.
BACKGROUND: Home gas appliance use has been associated with child respiratory illness but prospective data on the relationship between infant exposure and the development of child allergic disease has not been readily available. OBJECTIVES: (a) To determine if home gas appliance use is associated with increased risk of house dust mite (HDM) sensitization. (b) To examine whether any association between current home gas use and airway obstruction is influenced by HDM sensitization. METHODS DESIGN: an 8-year follow-up birth cohort study of children born during 1988 and 1989. PARTICIPANTS: a population-based sample (n = 498) of children who participated in the Tasmanian Infant Health Survey (TIHS) and resided in Northern Tasmania in 1997 (84% of eligible children). MAIN OUTCOME MEASURES: (a) Skin prick test reaction to nine allergens, including Dermatophagoides pteronyssinus (Der p 1) and Dermatophagoides farinae (Der f 1). (b) Spirometric lung function indices, including forced expiratory volume in one second (FEV(1)) and forced vital capacity (FVC). RESULTS: The relative risk for home gas appliance use at 1 month of age and HDM sensitization was 1.98 (1.04, 3.79) in a cohort analysis with confounder matching. Current home gas use was also associated with HDM sensitization (ARR 1.73 (1.43, 2.76)). Current home gas use was related to a stronger (P = 0.006) reduction in the FEV(1) : FVC ratio among HDM-sensitive children (adjusted difference - 6.2% (- 10.0 to - 2.4)) than non-HDM-sensitive children (adjusted difference - 0.3% (- 2.5 to 1.8)). CONCLUSION: Indoor pollutants from gas combustion may increase the likelihood of initial sensitization to HDM and play a role in the development of atopic asthma. HDM-sensitized children may be more vulnerable to indoor pollutant-induced airway obstruction. The ability of this study to detect such effects may partly reflect unflued gas appliance use among this sample.
Age Factors↗
Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities (ARIC) study.
Periodontitis has been linked to clinical cardiovascular disease but not to subclinical atherosclerosis. The purpose of this study was to determine whether periodontitis is associated with carotid artery intima-media wall thickness (IMT). Cross-sectional data on 6017 persons aged 52 to 75 years were obtained from the Atherosclerosis Risk in Communities Study 1996 to 1998 examination. The dependent variable was carotid IMT >/=1 mm. Periodontitis was defined by extent of attachment loss >/=3 mm: none/mild (<10%), moderate (10% to <30%), or severe (>/=30%). Covariates included age, sex, diabetes, LDL cholesterol, HDL cholesterol, triglycerides, hypertension, smoking, waist-hip ratio, education, and race/study center. Odds of IMT >/=1 mm were higher for severe periodontitis (OR 2.09, 95% CI 1.73 to 2.53) and moderate periodontitis (OR 1.40, CI 1.17 to 1.67) compared with no periodontitis. In a multivariable logistic regression model, severe periodontitis (OR 1.31, CI 1.03 to 1.66) was associated with IMT >/=1 mm, while adjusting for the other factors in the model. These results provide the first indication that periodontitis may play a role in the pathogenesis of atheroma formation, as well as in cardiovascular events.
Arteriosclerosis↗
The relation between infant indoor environment and subsequent asthma.
Our aim was to examine the contribution of an infant's indoor environment to childhood asthma using prospective data. We conducted a cross-sectional asthma survey in 1995 on 92% (6,378/6,911) of 7-year-olds in Tasmania, Australia. We linked these data with data collected in 1988 as part of the Tasmanian Infant Health Survey, which was designed to investigate sudden infant death. We were able to match 863 records out of the 1,111 in the 1988 survey and the 6,378 in the 1995 survey. The former group was interviewed at home at 1 month of age. In homes where at least one adult smoked in 1988, reported infant exposure to smoking in the same room in 1988 was associated with increased asthma by 1995 (relative risk = 1.52; 95% confidence interval = 1.01-2.29) after adjustment for confounders. The associations between infant exposure to environmental tobacco smoke and asthma were not consistent, however. Gas heater use in 1988 was associated with asthma (relative risk = 1.92; 95% confidence interval = 1.33-2.76). Markers of aeroallergen exposure at 1 month of age were not materially associated with asthma or wheeze. In some settings, air circulation practice with regard to bedroom door closure appeared important. Poor indoor air quality may play an important role in the development of childhood asthma.
Adult↗
Tobacco smoke exposure at one month of age and subsequent risk of SIDS--a prospective study.
The aim of this investigation was to identify the sources of postnatal exposure to tobacco smoke at 1 month of age and to examine their relation to sudden infant death syndrome (SIDS). The Tasmanian Infant Health Survey was a prospective cohort study undertaken from 1988 to 1995. It involved 9,826 infants (89% of eligible infants) at higher risk of SIDS. Subsequently 53 eligible infants died of SIDS. Hospital interviews were available on 51 and home interviews on 35 SIDS infants. Urinary cotinine assays were conducted using gas-liquid chromatography (n = 100). Within a predictive model that explained 63% of urinary cotinine variance, the strongest predictor of cotinine and also of SIDS was maternal smoking, though the effects of prenatal and postnatal smoking could not be separated. However, for particular smoking-related behaviors, there was a discordance between prediction of cotinine concentration and prediction of risk of SIDS. If smoking mothers did not smoke in the room with the baby, the cotinine level in the infant's urine was reduced by a little more than a half (p = 0.009), but this was not associated with a reduction in SIDS risk (odds ratio = 1.09, 95% confidence interval 0.47-2.55). Similarly, the presence of other adult resident smokers was associated with a 63% increase in urinary cotinine (p = 0.047) but not with increased SIDS risk (odds ratio = 0.69, 95% confidence interval 0.34-1.40). However, the study lacked the power to detect modest effects, that is, those altering risk less than twofold.
Adult↗
Short-term morbidity and infant mortality among infants who slept supine at 1 month of age--a follow-up report.
Following evidence that prone sleeping is causally related to sudden infant death syndrome (SIDS), intervention campaigns to avoid prone sleeping in many countries have led to a large reduction in SIDS and total infant mortality. The supine position has been recommended for healthy infants in several countries. The objective of this report was to determine how usual sleep position at 1 month relates to morbidity indicators at 1 month and 12 weeks and to SIDS and postneonatal mortality using a prospective population-based live birth cohort in Tasmania, Australia. Eligible infants were the one-fifth of Tasmanian live births at higher risk of SIDS using a perinatal score. From 1 January 1988 to 31 December 1995, 9826 (89% of eligible) infants participated in the home interview. Fifty-three eligible infants died of SIDS, 51 (96%) with hospital interview data and 35 (81% of those eligible for home visit) with home visit data. The main outcome measures were SIDS, postneonatal mortality and parentally reported infant morbidity. The postneonatal mortality rates (cases per 1000 live births) by usual sleep position at 1 month of age were supine 1.60 [95% CI 0.04, 8.87], side 2.87 [1.79, 4.35], prone 10.27 [5.62, 17.18] and other (including no usual position) 6.37 [0.16, 34.98]. None of the study infants who slept supine died of SIDS at a later time. Of 25 morbidity indicators studied, only noisy breathing was increased for supine compared with side-sleeping babies. In this study, there was no evidence to suggest that supine sleeping at 1 month of age was associated with an increase in important short-term morbidity or postneonatal mortality. These findings provide further support for the recent recommendations of the American Academy of Pediatrics that healthy infants should preferably sleep in the supine position.
Analysis of Variance↗
Water fluoridation, bone mass and fracture: a quantitative overview of the literature.
OBJECTIVE: To use the technique of meta-analysis to address the following research questions: Is water fluoridation associated with altered fracture risk at a population level and are the differences between studies consistent with confounding or chance variation between studies? METHOD: The data sources utilised were Medline 1966-97, reviews and bibliographies. The search terms were fluoridation, bone mass and/or fracture. We included all observational studies published in English relating water fluoridation to bone mass and/or fracture in the initial assessment. RESULTS: Water fluoridation had no evident effect on fracture risk (RR 1.02, 95% CI 0.96-1.09, n = 18 studies). There was marked heterogeneity between studies which could be explained, in part, by the combination of gender, urbanicity and study quality (R2 0.25, p = 0.05, weighted analysis). CONCLUSIONS: Water fluoridation both at levels aimed at preventing dental caries and, possibly, at higher naturally occurring levels appears to have little effect on fracture risk, either protective or deleterious, at a population level. The small effect on bone mass seen in studies performed at the individual level is consistent with this finding. Variation between studies is also likely to be due to differences in the distribution of other recognised fracture risk factors between different populations. Confirmation of these findings is required in large studies performed at the individual level.
Analysis of Variance↗
Relationship between early life respiratory illness, family size over time, and the development of asthma and hay fever: a seven year follow up study.
BACKGROUND: The timing and mechanism of the inverse association between increasing sibling number and atopic disease are not yet understood. A study was undertaken to examine how family size at birth predicts early respiratory illness, to report the association between infant respiratory illness and childhood atopic disease, and to determine whether the protective effect of large family size operates during infancy or later childhood. METHODS: A prospective follow up study was carried out on 863 children (78%) of 1111 participants in the Tasmanian Infant Health Survey performed in 1988. In 1988 household size and history of respiratory illness were obtained by parental interview at home (median age 35 days) and later by telephone (median age 85 days). In 1995 asthma, hay fever, and household size were assessed by parental questionnaire in a large cross sectional survey. RESULTS: In 1988 increasing resident number (per resident) (adjusted odds ratio (AOR) 1.17 (95% CI 1.05 to 1.31)) and resident density (AOR 1.77 (95% CI 1.07 to 2.94)) were related to parental report of an upper respiratory tract infection (URTI) by one month of age. Children with a reported URTI by home interview were more likely to have subsequent asthma (adjusted relative risk (ARR) 1.27 (95% CI 1.05 to 1.53)). The association between lower respiratory tract infection (LRTI) at telephone interview (relative risk (RR) 1.34 (95% CI 1.02 to 1.75) and asthma was reduced after adjustment for family history of asthma (ARR 1.27 (95% CI 0.98 to 1.66)). Antibiotic use by home interview was not associated with subsequent asthma or hay fever. Indicators of family size in 1988 were associated with hay fever but not asthma but, in contrast, resident number in 1995 was inversely associated with asthma (AOR 0.82 (95% CI 0.72 to 0.92) per resident) and hay fever (AOR 0.82 (95% CI 0.71 to 0.96) per resident). Children with no siblings were at risk for current asthma, particularly if symptoms began after the age of four (RR 2.81 (95% CI 1.36 to 5.84)). CONCLUSIONS: The apparent protective effect of large household size and asthma could not be explained by an increase in reported early respiratory illness. The first year of life may not be the most critical time for the protective effect of large household size to be mediated in relation to asthma, but this effect occurred by the seventh year of life.
Adult↗
Association between use of a quilt and sudden infant death syndrome: case-control study.
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Bedding and Linens↗
Determinants of dust mite allergen concentrations in infant bedrooms in Tasmania.
BACKGROUND: High exposure to house dust mite allergen during the first year of life has been found to increase the risk of subsequent asthma and mite sensitization. Environmental factors, home construction and cleaning methods used are associated with levels of dust mites in the home. OBJECTIVE: To investigate determinants of levels of Der p 1 and Der f 1 mite allergens in homes of infants in southern Tasmania. METHODS: Dust samples were collected from 72 homes of infants participating in the Tasmanian Infant Health Survey (TIHS). The Der p 1 and Der f 1 allergen concentrations in these samples were measured. The TIHS interviewers obtained information from the mothers of the infants via a questionnaire, observed specified aspects of the home environment, and took readings of bedroom temperature and humidity. The effect of each item on allergen concentration in dust from bedroom floors was examined in a variety of ways. Those items which in this study appeared to be significantly related to allergen concentrations plus items which in other studies have been found to be related to allergen concentrations were then investigated further in multivariate models. RESULTS: Der p 1 allergen concentration (microg/g) and density (microg/m2) in dust from bedroom floors were found to be related to several home environment factors. In the univariate analyses, indoor humidity, 24 h maximum temperature, number of residents and a combination of floor covering and cleaning methods appeared to have a significant effect on allergen levels. These factors remained important in the multivariate model except that indicators for mould in the bathroom and drying washing on an outside line replaced indoor humidity. CONCLUSION: Features related to home dampness, the number of residents and floor covering and cleaning were major determinants of Der p 1 levels in the bedrooms studied.
Allergens↗
Cross sectional study of the relation between sibling number and asthma, hay fever, and eczema.
OBJECTIVES: To document the relation between sibling number and atopic disease, and to assess the contribution of possible confounding factors to the protective effect of siblings in relation to asthma and hay fever. DESIGN AND SUBJECTS: Cross sectional survey by parental questionnaire in Tasmania, Australia, on 6378 children (92% of those eligible) who reached 7 years of age during 1995. METHODS: Exercise challenge lung function testing was conducted on 428 children. Analyses reported were conducted on singleton births only (n = 6158). RESULTS: The prevalences of a history of asthma ever, hay fever, and eczema were 27%, 19%, and 22%, respectively. Asthma and hay fever, but not eczema, were inversely related to sibling number, with evidence of a dose-response trend. The mean age at onset for asthma or wheezy breathing decreased as the number of siblings increased. The inverse association between sibling number and asthma or hay fever persisted after adjustment for several confounders, such as parental smoking or breast feeding, but did not persist after adjustment for household size in 1995. CONCLUSIONS: The protective effect of high sibling number could not be separated from household size at age 7, and it appears to be operating after birth and influences the age at onset of asthma symptoms. Further work to increase knowledge of how the protective effect of the presence of siblings works might have important implications for the understanding of the pathogenesis of asthma.
Age of Onset↗
Waterproof mattress linings and SIDS.
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Bedding and Linens↗