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Does financial strain explain the association between children's morbidity and parental non-employment?

OBJECTIVES: To investigate whether family financial resources explain the association between parental labour market participation and children's health in families in Denmark and Sweden. DESIGN: Parent reported questionnaire data from the survey of health and welfare among children and adolescents in the Nordic countries, 1996. PARTICIPANTS: 4299 children aged 2-17 years. MEASURES: Three indicators measured children's health: recurrent psychosomatic symptoms, chronic illness, and prescribed medicine. Four variables and a composite index were used to measure family financial resources. The variable on family labour market participation consisted of five groups according to family type and parents' labour market participation. RESULTS: Children in families with one or both parents without paid work had an increased prevalence of recurrent psychosomatic symptoms (odds ratio from 1.52 to 3.20) and chronic illnesses (odds ratio from 1.43 to 2.25), whereas the use of prescribed medicine did not differ (odds ratio from 0.67 to 1.15). The five indicators on family financial resources only slightly reduced the odds ratios for recurrent psychosomatic symptoms (odds ratio from 1.12 to 2.75) and chronic illnesses (odds ratio from 1.34 to 2.22), and the odds ratios for children's use of prescribed medicine remained unchanged and non-significant (odds ratio from 0.62 to 1.18). CONCLUSIONS: Financial strain associated with non-employment does not explain the increased prevalence of health problems among children in families affected by non-employment in Denmark and Sweden. However, the associations between family labour market participation and children's health differ according to family financial status.

Adolescent↗

Does material disadvantage explain the increased risk of adverse health, educational, and behavioural outcomes among children in lone parent households in Britain? A cross sectional study.

OBJECTIVE: To test the hypothesis that material disadvantage explains the increased risk among children and young people of adverse health, educational, and behavioural problems associated with living in lone parent households in Britain STUDY DESIGN: Secondary analysis of a cross sectional survey of a representative sample of British households with children and youthMain outcomes: Parent reported fair/poor health, longstanding illness and disability, statement of special educational needs, suspension and/or expulsion from school, and in trouble with the police. PARTICIPANTS: Data were available on 15 636 (8049 boys and 7587 girls) aged 0-18 years in 8541 households in the third sweep (2001) of the British government's families and children study RESULTS: Lone parenthood was associated with increased risk of health and educational problems, and antisocial behaviour among boys and girls in a logistic regression model adjusting for child's age alone. Adding age of main carer, number of dependent children, and child's rank in the household made little difference to the associations. Addition of housing tenure, household hardship index, and an interaction term for lone parenthood and hardship eliminated the relation with lone parenthood for all outcomes except parent reported health among girls. Similar results were obtained for households headed by lone parents for at least a year. An interaction effect of lone parenthood with hardship for parent reported health and statement of special educational needs was noted. CONCLUSION: Adverse effects of lone parenthood on health, education, and antisocial behaviour were apparently explained by material disadvantage in this cross sectional sample of British households with children and youth.

Adolescent↗

Can social factors explain sex differences in insomnia? Findings from a national survey in Taiwan.

STUDY OBJECTIVE: To examine sociological explanations for the higher level of insomnia in women, including social roles and socioeconomic status (SES). DESIGN: Cross sectional survey research SETTING: Taiwanese 2001 "social trend survey" PARTICIPANTS: A nationally representative sample of 39,588 citizens aged 15 years or older living in Taiwan. MAIN RESULTS: On average, women scored 1.25 points higher than men on the insomnia inventory (p<0.001) but after controlling for social roles, the sex discrepancy in insomnia decreased slightly. SES did not, however, explain women's higher levels of insomnia. Subscale analysis showed an association between the role of homemaker and increased night time sleep disturbance and decreased daytime sequelae of poor sleep while higher educational attainment was related only to more severe daytime sequelae. CONCLUSION: The sex discrepancy in insomnia narrowed slightly after taking social role factors into consideration but was not explained by SES. The persistent sex gap in insomnia warrants further investigation.

Adolescent↗

High rates of ischaemic heart disease in Scotland are not explained by conventional risk factors.

STUDY OBJECTIVES: To (1) compare prevalence of socioeconomic, behavioural, and physiological ischaemic heart disease (IHD) risk factors in Scotland with a comparable nation (England) and (2) find out if their distribution explains Scotland's comparatively higher IHD rate (1.62 (1.30, 2.02)). DESIGN, SETTING, AND PARTICIPANTS: Cross sectional, individual level observational study with data on socioeconomic, behavioural, and physiological characteristics, 6064 respondents from Scotland and England, (2362 and 3702 respectively), aged 45-74 and with data on all required items. MAIN RESULTS: There were significant and meaningful differences between the Scottish and English in the prevalence of several IHD risk factors. However, a substantially and significantly higher risk of IHD persisted among the Scottish respondents (1.50 (1.17, 1.91)) despite control for a wide range of risk factors. CONCLUSIONS: Interpretation must be cautious because these are cross sectional data, however higher levels of conventional IHD risk factors contribute to but do not explain the comparatively high rates of IHD in Scotland. Alternative explanations for, and policy interventions to tackle, Scottish rates of IHD must be considered.

Aged↗

Inequity in access to dental care services explains current socioeconomic disparities in oral health: the Swedish National Surveys of Public Health 2004-2005.

OBJECTIVE: To analyse the effects of socioeconomic disadvantage on access to dental care services and on oral health. Design, setting and outcomes: Cross-sectional data from the Swedish National Surveys of Public Health 2004 and 2005. Outcomes were poor oral health (self-rated oral health and symptoms of periodontal disease) and lack of access to dental care services. A socioeconomic disadvantage index (SDI) was developed, consisting of social welfare beneficiary, being unemployed, financial crisis and lack of cash reserves. PARTICIPANTS: Swedish population-based sample of 17 362 men and 20 037 women. RESULTS: Every instance of increasing levels of socioeconomic disadvantage was associated with worsened oral health but, simultaneously, with decreased utilisation of dental care services. After adjusting for age, men with a mild SDI compared with those with no SDI had 2.7 (95% confidence interval (CI) 2.5 to 3.0) times the odds for self-rated poor oral health, whereas odds related to severe SDI were 6.8 (95% CI 6.2 to 7.5). The corresponding values among women were 2.3 (95% CI 2.1 to 2.5) and 6.8 (95% CI 6.3 to 7.5). Nevertheless, people with severe socioeconomic disparities were 7-9 times as likely to refrain from seeking the required dental treatment. These associations persisted even after controlling for living alone, education, occupational status and lifestyle factors. Lifestyle factors explained only 29% of the socioeconomic differences in poor oral health among men and women, whereas lack of access to dental care services explained about 60%. The results of the multilevel regression analysis indicated no additional effect of the administrative boundaries of counties or of municipalities in Sweden. CONCLUSIONS: Results call for urgent public health interventions to increase equitable access to dental care services.

Adolescent↗

Failure of cigarette smoking to explain international differences in mortality from chronic obstructive pulmonary disease.

STUDY OBJECTIVE: The study aimed to explain international differences in rates and trends of chronic obstructive pulmonary disease (COPD) using two measurements of cigarette smoking, the major risk factor for this disease. DESIGN: Mortality data for COPD were obtained from the World Health Organisation for 31 countries from 1979 to 1988. Smoking data were obtained for most countries. COPD rates were compared to the percentage of current smokers and past levels of cigarette consumption. COPD trends were compared to past consumption trends. MAIN RESULTS: In men, Romania had the highest COPD mortality and Greece the lowest throughout the period. English speaking countries occupy most of the other top positions, and southern European countries and Japan the low positions. Women show a similar ranking to men (r = 0.75; p < 0.01 (1988)). Mortality rates in men are, in general, two to four times those in women. Most countries show either a decrease or no change in COPD mortality over the period. In women the opposite is true--no clear relationships are seen when comparing rates and trends of COPD with measures of smoking. CONCLUSION: This failure to explain international COPD differences suggests that national data on COPD may be unreliable or national cigarette smoking data are inadequate, or both.

Adult↗

Can regional variation in "avoidable" mortality be explained by deaths outside hospital? A study from Sweden, 1987-90.

STUDY OBJECTIVE: This study aimed to calculate the proportion of deaths outside hospital in Sweden for some conditions for which the acute medical management may be important to the outcome and to analyse whether the proportion of deaths outside hospital can explain regional variations in mortality from these causes of death. DESIGN: The place of death was registered on all death certificates in Sweden during the period 1987-90. The proportion of deaths outside hospital was calculated at the national level for selected causes of death. Variation in cause-specific mortality among the 26 administrative health areas in Sweden was analysed. Death rate ratios were calculated with standardisation for age and sex using the national rate as standard. The correlation between the proportion of deaths outside hospital in each health area and the cause specific mortality irrespective of place of death was calculated. For areas with a significantly high death rate the ratios for mortality outside hospital as well as in hospital were analysed in order to decide which component of mortality represented a high mortality risk. SETTING AND PARTICIPANTS: All death registration in Swedish citizens and other residents in Sweden aged under 70 years between 1987 and 1990 which gave diabetes, asthma, ischaemic heart disease, cerebrovascular diseases, or ulcer of the stomach or duodenum as the underlying cause of death. MAIN RESULTS: For asthma (58%) and ischaemic heart disease (54%), most deaths occurred outside hospital. For most causes of death, however, no correlation was found among the health areas between the proportion of deaths outside hospital and the SMR for mortality irrespective of the place of death. A high death rate was associated with a high proportion of deaths outside hospital, for diabetes in one area in the north of Sweden (Norrbotten) and for ulcer of the stomach and duodenum in one large municipality (Göteborg). CONCLUSIONS: The high proportion of deaths outside hospital at the national level for some of the conditions studied suggests that in-depth studies of the process preceding death and the functioning of medical care are needed. In most cases, however, no evidence was found that regional variation in mortality could be explained by death outside hospital. The results for diabetes in Norbotten and ulcer of stomach and duodenum in Göteborg indicate that in-depth studies on the quality of care are required.

Adolescent↗

Can confounding by sociodemographic and behavioural factors explain the association between size at birth and blood pressure at age 50 in Sweden?

STUDY OBJECTIVE: To evaluate whether socioeconomic confounding explains the relationship between size at birth and blood pressure at age 50. DESIGN: Cross sectional study with retrospectively collected data on size at birth. SETTING: Uppsala, Sweden. PARTICIPANTS: 1333 men born in 1920-24, and a subset of 615 men for analyses including early social circumstances. MAIN OUTCOME MEASURES: Blood pressure measured after 10 minutes rest in supine position. Crude and adjusted effect measures were compared. MAIN RESULTS: Controlling for sociodemographic characteristics at age 50, such as socioeconomic position, highest education achieved and marital status did not reduce the strength of the association between birth weight and systolic blood pressure at 50 years. In the total population, the slope of the body mass index adjusted relationship changed from -3.4 mmHg/kg to -3.5 mmHg/kg on additional adjustment for sociodemographic characteristics at age 50 (both p values < 0.01). Controlling for behavioural characteristics at age 50, such as smoking and recent alcohol drinking, did not affect the relationship between birth weight and blood pressure at 50. In the 615 men for whom information on sociodemographic circumstances in early life was available, adjustment for factors such as social class of the family, mother's marital status or area of residence, led to a slight reduction of the effect of birth weight on systolic blood pressure at age 50. The slope of the body mass index adjusted relationship changed from -2.8 mmHg/kg to -2.6 mmHg/kg after additional adjustment for early life circumstances in the sample as a whole (p values 0.09 and 0.12). Simultaneous adjustment for sociodemographic characteristics at birth together with sociodemographic and behavioural characteristics at age 50 led to only a slight reduction of the effect of birth weight on systolic blood pressure at 50 years. CONCLUSION: The strong inverse associations between birth weight and blood pressure among 50 year old Swedish men are highly unlikely to be explained by confounding with socioeconomic circumstances at birth or in adult life.

Adolescent↗

Trends in cigarette consumption cannot fully explain trends in British lung cancer rates.

STUDY OBJECTIVES: To determine whether British lung cancer (LC) trends are adequately explained by cigarette smoking trends, and whether modelling using aggregated smoking prevalence estimates can validly replace modelling using individual smoking histories. METHODS: Observed LC trends for 1955-1985 for both sexes and three age groups were compared with multistage model predictions using smoking history data from two surveys (HALS, AHIP). The modelling used the individual smoking data directly or aggregated prevalence estimates. It allowed for variation in age of starting and stopping smoking, amount smoked, tar levels, and environmental tobacco smoke (ETS) exposure. RESULTS: Observed male LC rates fell faster than predicted by a model (with the first and penultimate stages assumed affected by smoking) that allowed for variation in amount smoked and in tar level (with some provision for "compensation"), and was based on aggregated smoking data from HALS. The discrepancy equated to an annual change unexplained by smoking of -2.4%, -2.8%, and -1.9% for ages 35-44, 45-54, and 55-64. The annual unexplained changes were less in women, and reversed at age 55-64; -1.7%, -0.8%, and +0.8% for the three ages. They were similar using individual smoking histories (-2.6%, -1.8%, and -1.6%; women, -0.9%, -0.5%, and +0.2%). The discrepancies were unexplained by plausible alternative multistage parameters, full allowance for tar reduction, alternative estimates of amount smoked, or ETS. CONCLUSIONS: British LC trends cannot be fully explained by cigarette consumption trends, implying factors other than cigarette smoking contribute importantly to overall risk. Predictions using aggregated prevalence estimates provide useful information.

Adult↗

Xenon kinetics in muscle are not explained by a model of parallel perfusion-limited compartments.

Experimental tissue gas kinetics do not follow the prediction for a single stirred perfusion-limited compartment. One hypothesis proposes that the kinetics might be explained by considering the tissue as a collection of parallel compartments, each with its own flow, reflecting the tissue microcirculatory flow heterogeneity. In this study, observed tissue gas kinetics were compared with the kinetics predicted by a model of multiple parallel compartments. Gas exchange curves were generated by recording the time course of tissue radioactivity in the intact calf muscles of anesthetized ventilated dogs exposed to step function changes of 133Xe in the inspired air for 5-h periods. Microcirculatory flow heterogeneity in the same tissue was determined by the radioactive microsphere method. Observed mean tissue transit times were on average longer than predicted by a factor of 6.7. Observed means averaged 52.1 min compared with 8.3 min predicted by the perfusion-limited model. Relative dispersions of tissue transit times were also uniformly larger than predicted. We conclude that Xe gas kinetics in intact canine skeletal muscle are not explained by a model of multiple parallel perfusion-limited compartments. Countercurrent exchange of gas between vessels is a possible explanation.

Animals↗

Maternal weight differences do not explain ethnic differences in biochemical screening.

In previous work, we and others have shown that serum levels of alpha-fetoprotein, human chorionic gonadotropin, and estriol vary among the four commonly defined racial/ethnic groups seen in the United States: white, African-American, Asian, and Hispanic. We have suggested that better sensitivity and specificity could improve screening sensitivity and specificity. However, it has been argued that systematic weight differences among the groups could explain the variation. We evaluated the results from 208,257 patients having screening and found systematic weight differences. However, these differences were not as large as the racial/ethnic differences, showing that weight does not fully explain the discrepancy, and, therefore, four separate data bases give more accurate results.

Asian↗

Didymosis aplasticosebacea: coexistence of aplasia cutis congenita and nevus sebaceus may be explained as a twin spot phenomenon.

BACKGROUND: Co-occurrence of aplasia cutis congenita and nevus sebaceus has sometimes been observed. OBJECTIVE: We propose a genetic mechanism that may explain this coexistence of two different congenital skin disorders. METHODS AND RESULTS: We review 15 cases as reported in the literature and present an additional case. To explain the temporal and spatial proximity of the two skin lesions we advance the concept of twin spotting for which we propose the term didymosis (Greek didymos = twin). In an embryo heterozygous for two different recessive mutations localized on either of a pair of homologous chromosomes, an event of somatic recombination would occur at an early developmental stage, giving rise to two different cell clones homozygous for either mutation. CONCLUSION: The concept of didymosis aplasticosebacea is so far hypothetical. Future molecular research may show whether this concept holds true.

Child↗

Paradominant inheritance may explain familial occurrence of Cutis marmorata telangiectatica congenita.

Cutis marmorata telangiectatica congenita (CMTC) is a rare congenital vascular anomaly that virtually always occurs sporadically and in a patchy, quadrant, unilateral or otherwise segmental manifestation. This would suggest mosaicism of a postzygotic mutation. Some authors, however, described CMTC occurring in several members of a family. This paradox may be explained by the concept of paradominant inheritance. Heterozygous individuals carrying a 'paradominant' mutation are, as a rule, phenotypically normal. The mutation can therefore be transmitted unperceived through many generations. The trait only becomes manifest when a postzygotic mutation occurring during early embryogenesis gives rise to loss of heterozygosity and forms a mosaic population of cells being either homozygous or hemizygous for the mutation. This concept may explain the occasional familial occurrence of CMTC.

Child, Preschool↗

Extraventricular intracisternal obstructive hydrocephalus--a hypothesis to explain successful 3rd ventriculostomy in communicating hydrocephalus.

The basis of successful 3rd ventriculostomy in cases of communicating hydrocephalus is not yet understood. We performed 3rd ventriculostomies in 5 patients with free cerebrospinal fluid (CSF) communication from the ventricles to the cisterna magna. Preoperative magnetic resonance images (MRIs) showed dilated ventricles, a downward bulging floor of the 3rd ventricle (interpreted as a sign of pressure gradient between the ventricles and basal cisterns) and a free communication to an enlarged cisterna magna. The other basal cisterns were of normal or smaller size. All patients recovered from their clinical symptoms and none of them needed a shunt. The hypothesis of an intracisternal CSF pathway obstruction (e.g. between the cisterna magna and the prepontine cistern) could explain the MRI findings, although such an obstruction cannot be directly visualized. It would also explain the successful 3rd ventriculostomies in these cases.

Child, Preschool↗

Four additional CLCN5 exons encode a widely expressed novel long CLC-5 isoform but fail to explain Dent's phenotype in patients without mutations in the short variant.

BACKGROUND: Dent's disease is caused by mutations in the CLCN5 gene coding for the chloride channel CLC-5. However, sequencing of CLCN5 exonic regions in some patients presenting with low-molecular-weight proteinuria and hypercalciuria - the hallmarks of Dent's disease - failed to identify causative mutations. AIM: Given the observation that some species harbour a CLCN5 mRNA encoding an extended CLC-5 aminoterminus compared with the so far known human form, we worked on the presumption that an orthologous (longer) CLCN5 transcript is also present in humans and that our patients may have mutations herein. METHODS: Extensive databank mining, reverse transcription polymerase chain reaction (RT-PCR) and automated sequencing were used in the search for novel CLCN5 transcripts. The human CLCN5 gene was investigated in 7 patients out of five families by direct automated sequencing of PCR-amplified DNA products. RESULTS: Two new human CLCN5 transcripts expressed in kidney and various other tissues could be identified. These arise from a novel site of transcription initiation, alternative splicing and the use of four additional CLCN5 exons. If being translated, both these mRNAs would lead to an enlarged CLC-5 protein consisting of 816 amino acids by adding 70 aminoterminal residues to the so far known 746-amino-acid-long isoform. Sequence analysis of the henceforward 17 CLCN5 exons revealed no mutation in the patients with a phenotype resembling Dent's disease. CONCLUSIONS: Despite the identification of further targets to explain Dent's disease, the molecular defect in our patients remains to be elucidated. Hence, their phenotype may be explained by mutations that affect so far unknown regulating elements of the CLCN5 gene or another gene(s), probably encoding CLC-5 accessory protein(s).

Adult↗

An effect of the PAI-1 4G/5G polymorphism on cholesterol levels may explain conflicting associations with myocardial infarction and stroke.

BACKGROUND AND PURPOSE: The gene-encoding plasminogen activator inhibitor type 1 (PAI-1) has a common 4G/5G 'functional' polymorphism, and people homozygous for the 4G allele have higher PAI-1 plasma concentrations. The 4G/4G genotype is associated with increased risk of myocardial infarction but paradoxically protects against stroke. We hypothesized that this paradox may be explained via an effect of the PAI-1 polymorphism on plasma lipids. METHODS: We studied 71 consecutive Italian patients referred to our Institute for first stroke or vascular cognitive impairment. PAI-1 gene 4G/5G polymorphism, total plasma cholesterol, plasma triglycerides, sex, age, smoking, oral contraceptive use, statin therapy, hypertension, diabetes, and history of myocardial infarction were examined. RESULTS: The 4G/4G genotype was significantly associated with high cholesterol (p = 0.003) but not with triglycerides (p = 0.39). Adjusted odds ratios were: 5.8 for 4G/4G vs. 4G/5G (95% CI, 3.1-23.0), and 15.9 for 4G/4G vs. 5G/5G (95% CI, 2.4-105.0). CONCLUSIONS: This finding may explain the involvement of the PAI-1 polymorphism in the clustering of atherothrombotic risk factors, and why people with the 4G/4G genotype are at increased risk for myocardial infarction. Stroke is not so clearly related to hypercholesterolemia and other effects of the 4G/4G genotype (perhaps increased PAI-1 expression) may protect against stroke.

Adult↗

Differential initiation of translation of a single estrogen receptor mRNA could explain some estradiol resistance cases.

Cell response to steroid stimulation is generally acknowledged to be mediated by an intracellular protein known as a receptor. Response intensity is related to the affinity of the receptor and to the number of sites occupied by its specific ligand. Although verified in the majority of experimental and clinical studies, certain phenomena of steroid hormone resistance would seem to challenge this assertion. Application of gene molecular biology to determine the action mechanisms of steroid hormones has partially explained cell resistance in terms of genetic modifications. The work presented here shows that in certain cases, estrogen resistance could be explained by regulation of translation of the single messenger RNA coding for the receptor.

Animals↗

Endothelial dysfunction and low-grade inflammation explain much of the excess cardiovascular mortality in individuals with type 2 diabetes: the Hoorn Study.

OBJECTIVE: The mechanisms responsible for the increased cardiovascular disease risk that accompanies type 2 diabetes (T2D) remain poorly understood. It is commonly held that endothelial dysfunction and low-grade inflammation can explain, at least in part, why deteriorating glucose tolerance is associated with cardiovascular disease. However, there is no direct evidence for this contention. METHODS AND RESULTS: In this population-based study (n=631), T2D was cross-sectionally associated with both endothelial dysfunction and low-grade inflammation, whereas impaired glucose metabolism (IGM) was associated only with low-grade inflammation. These findings were independent of other risk factors that accompany T2D or IGM. During a follow-up of 11.7 years (median; range 0.5 to 13.2 years), low-grade inflammation was associated with a greater risk of cardiovascular mortality (hazard ratio, 1.43 [95% CI, 1.17 to 1.77] per 1 SD difference). For endothelial dysfunction, the association with cardiovascular mortality was stronger in diabetic (hazard ratio, 1.87 [95% CI, 1.43 to 2.45]) than in nondiabetic individuals (hazard ratio, 1.23 [95% CI, 0.86 to 1.75]; P interaction=0.06). Finally, T2D-associated endothelial dysfunction and low-grade inflammation explained approximately 43% of the increase in cardiovascular mortality risk conferred by T2D. CONCLUSIONS: These data emphasize the necessity of randomized controlled trials of strategies that aim to decrease cardiovascular disease risk by improving endothelial function and decreasing low-grade inflammation, especially for T2D patients.

Aged↗