Aims The aim of the UK Biobank sample handling and storage protocol is to specify methods for the collection and storage of participant samples that give maximum scientific return within the available budget. Processing or storage methods that, as far as can be predicted, will preclude current or future assays have been avoided.
Methods The protocol was developed through a review of the literature on sample handling and processing, wide consultation within the academic community and peer review. Protocol development addressed which samples should be collected, how and when they should be processed and how the processed samples should be stored to ensure their long-term integrity. The recommended protocol was extensively tested in a series of validation studies. UK Biobank collects about 45 ml blood and 9 ml of urine with minimal local processing from each participant using the vacutainer system. A variety of preservatives, anti-coagulants and clot accelerators is used appropriate to the expected end use of the samples. Collection of other material (hair, nails, saliva and faeces) was also considered but rejected for the full cohort. Blood and urine samples from participants are transported overnight by commercial courier to a central laboratory where they are processed and aliquots of urine, plasma, serum, white cells and red cells stored in ultra-low temperature archives. Aliquots of whole blood are also stored for potential future production of immortalized cell lines. A standard panel of haematology assays is completed on whole blood from all participants, since such assays need to be conducted on fresh samples (whereas other assays can be done on stored samples). By the end of the recruitment phase, 15 million sample aliquots will be stored in two geographically separate archives: 9.5 million in a –80°C automated archive and 5.5 million in a manual liquid nitrogen archive at –180°C. Because of the size of the study and the numbers of samples obtained from participants, the protocol stipulates a highly automated approach for the processing and storage of samples. Implementation of the processes, technology, systems and facilities has followed best practices used in manufacturing industry to reduce project risk and to build in quality and robustness. The data produced from sample collection, processing and storage are highly complex and are managed by a commercially available LIMS system fully integrated with the entire process.
Conclusion The sample handling and storage protocol adopted by UK Biobank provides quality assured and validated methods that are feasible within the available funding and reflect the size and aims of the project. Experience from recruiting and processing the first 40 000 participants to the study demonstrates that the adopted methods and technologies are fit-for-purpose and robust.
]]>Small body size at birth and slow growth during the first 2 years after birth, leading to low body mass index (BMI) at 2 years, are associated with coronary heart disease and stroke in adult life. We tested the hypothesis that this path of growth is associated with an atherogenic lipid profile in later life.
We measured serum lipid concentrations at age 57–70 years in 1999 members of the Helsinki Birth Cohort. They were randomly selected from an original cohort of 8760 people and had on average 11 measurements of height and weight between birth and 2 years of age.
The 18% of subjects who used lipid-lowering medication had a lower BMI at birth and at 2 years. These subjects were excluded from the analyses of lipid profiles. A 1 kg/m2 lower BMI at birth was associated with 0.051 mmol/l (95% CI –0.001 to 0.103; P = 0.05) higher non-HDL cholesterol and 0.018 g/l higher (0.005–0.031; P = 0.006) apolipoprotein B concentrations. A slower increase in BMI during the first 6 months after birth was associated with lower HDL and higher non-HDL cholesterol concentrations. A 1 kg/m2 lower BMI at 2 years was associated with 0.020 mmol/l lower (0.004–0.036; P = 0.02) HDL cholesterol and 0.059 mmol/l (0.020–0.099; P = 0.003) higher non-HDL cholesterol and 0.018 mmol/l higher (0.008–0.028; P < 0.001) apolipoprotein B concentrations. The age at weaning off breast milk was not associated with lipid profile in later life.
Small body size at birth and slow weight gain during infancy are associated with an atherogenic lipid profile in adult life.
Methods Five variants of the CRP gene were used to investigate whether SEP differences in CRP levels are determined at conception. SEP and serum CRP were assessed in childhood (age 3–9), adolescence (age 12–18) and in adulthood (age 24–39). SEP was measured using parental education and occupational status in childhood and adolescence, and participants’ own education and occupational status in adulthood. Participants with CRP > 10 mg/l were excluded.
Results All CRP gene variants were associated with circulating CRP concentrations in childhood, but there were no differences in the distribution of these variants by SEP. No strong evidence was found of associations between parental SEP and CRP. A graded association between higher SEP and lower CRP was observed in adulthood for education (P = 0.0005) but not for occupational status. Trajectories that led to high educational achievement both in the participants and their parents were associated with lower (P ≤ 0.047) CRP levels in adulthood. Excluding participants with infectious diseases, pregnant or lactating women and women using oral contraceptives did not change the findings.
Conclusion In this cohort, SEP differences in CRP concentrations seen in adulthood appear not to be determined at conception or evident in childhood or adolescence.
]]>Methods We studied 1167 participants in Project Viva, a longitudinal cohort study of pregnant women and their children. We estimated first and second trimester maternal iron intake from food frequency questionnaires. We used an electronic laboratory database to identify haemoglobin and MCV levels in pregnancy. We measured child BP up to five times with a Dinamap and used mixed-effects regression models in our analysis.
Results Mean (SD) child SBP at 3 years was 92.0 (9.9) mmHg. Adjusting for confounders, for each 10 mg increase in first trimester iron intake, child SBP was not lower, but was in fact 0.4 mmHg higher (95% CI 0.1, 0.7). For second trimester iron intake, and for first or second trimester haemoglobin and MCV levels, we did not find any appreciable association with 3 year SBP.
Conclusions In contrast to animal studies, we did not find that lower maternal iron status during pregnancy was associated with higher offspring BP.
]]>Methods A Poisson regression model relating the daily fluctuations in summer temperature and mortality in France from 1975 to 2003 was used to estimate the daily expected number of deaths over the period 2004–2006 as a function of the observed temperatures.
Results During the 2006 heat wave (from 11 to 28 July), about 2065 excess deaths occurred in France. Considering the observed temperatures and with the hypothesis that heat-related mortality had not changed since 2003, 6452 excess deaths were predicted for the period. The observed mortality during the 2006 heat wave was thus markedly less than the expected mortality (~4400 less deaths).
Conclusions The excess mortality during the 2006 heat wave, which was markedly lower than that predicted by the model, may be interpreted as a decrease in the population's vulnerability to heat, together with, since 2003, increased awareness of the risk related to extreme temperatures, preventive measures and the set-up of the warning system.
]]>A recent monograph by the International Agency for Research on Cancer (IARC) has identified indoor air pollution from coal usage as a known human carcinogen, while that from biomass as a probable human carcinogen. Although as much as 74% of the Indian population relies on solid fuels for cooking, very little information is available on cancer risk associated with these fuels in India.
Using data from a multicentric case–control study of 799 lung and 1062 hypopharyngeal/laryngeal cancer cases, and 718 controls, we investigated indoor air pollution from various solid fuels as risk factors for these cancers in India.
Compared with never users, individuals who always used coal had an increased risk of lung cancer [odds ratio (OR) 3.76, 95% confidence interval (CI) 1.64–8.63]. Long duration of coal usage (>50 years) was a risk factor for hypopharyngeal (OR 3.47, CI 0.95–12.69) and laryngeal (OR 3.65, CI 1.11–11.93) cancers. An increased risk of hypopharyngeal cancer was observed among lifelong users of wood (OR 1.62, CI 1.14–2.32), however this was less apparent among never-smokers. Increasing level of smokiness inside the home was associated with an increasing risk of hypopharyngeal and lung cancer (Ptrend < 0.05).
This study showed differential risks associated with indoor air pollution from wood and coal burning, and provides novel evidence on cancer risks associated with solid fuel usage in India. Our findings suggest that reducing indoor air pollution from solid fuels may contribute to prevention of these cancers in India, in addition to tobacco and alcohol control programs.
Methods The search was concluded in April 2006. Bibliographic databases consulted included PubMed, EMBASE, Cochrane Library and NIOSHTIC2. Pooled estimates were obtained using random-effects meta-analysis. Sources of heterogeneity between studies were explored, as was publication bias.
Results Fourteen different studies (nine case-control and five cohort studies) accomplished inclusion criteria. All these studies followed standardized criteria for AD diagnosis and most of them obtained quantitative estimates of exposure. Pooled estimates suggest an increased risk of AD from case-control studies (ORpooled 2.03; 95% CI 1.38–3.00) and from cohort studies (RRpooled 1.62; 95% CI 1.16–2.27), with moderate to high statistical heterogeneity in both cases (respectively, I2 = 58% and I2 = 54%). Cohort studies showed consistently increased risks for exposed men (RRpooled 2.05; 95% CI 1.51–2.80, I2 = 0%). Evidence of dose–response relationship was not present. Test for publication bias suggests small study effects, mostly for case-control studies.
Conclusions Available epidemiological evidence suggests an association between occupational exposure to ELF-EMF and AD. However, some limitations affecting the results from this meta-analysis should be considered. More information on relevant duration and time windows of exposure, on biological mechanisms for this potential association and on interactions between electromagnetic fields exposure and established risk factors for AD is needed.
]]>Methods A case-control study was carried out from June to December 2006. Cases were recruited at Amudat hospital, Nakapiripirit district, Uganda, after clinical and parasitological confirmation of symptomatic VL infection. Controls were individuals that tested negative using a rK39 antigen-based dipstick, which were recruited at random from the same communities as the cases. Data were analysed using conditional logistic regression.
Results Ninty-three cases and 226 controls were recruited into the study. Multivariate analysis identified low socio-economic status and treating livestock with insecticide as risk factors for VL. Sleeping near animals, owning a mosquito net and knowing about VL symptoms were associated with a reduced risk of VL.
Conclusions VL affects the poorest of the poor of the Pokot tribe. Distribution of insecticide-treated mosquito nets combined with dissemination of culturally appropriate behaviour-change education is likely to be an effective prevention strategy.
]]>Although measles incidence has been reduced to low levels in many countries, the potential exists for HIV-1 infection to enhance measles virus (MV) transmission and hinder measles control and elimination efforts.
HIV-1 infection was incorporated into an age-structured, deterministic compartmental model of MV transmission. Parameter estimates were obtained from published studies. The model was then adapted to simulate the introduction of antiretroviral therapy (ART).
The model suggests that prior to the introduction of ART, HIV-1 infection has little impact on the transmission dynamics of MV. High mortality rates in HIV-1-infected children without access to ART counteract the higher rates of vaccine failure, shorter duration of maternal antibody protection and longer duration of infectiousness in HIV-1-infected children, as many of these children die before they are able to contribute to MV transmission. The introduction of ART into the model resulted in an increase in measles prevalence.
High overall mortality among HIV-1-infected children without access to ART limits the impact of the HIV-1 epidemic on MV transmission and may help to explain the initial success of measles control strategies in Africa. The scaling-up of ART should improve children's survival but could lead to an increase in measles prevalence in the absence of sustained measles control efforts. Further study of the duration of immunity in HIV-1-infected children receiving ART and their response to revaccination is needed to determine whether a second dose of measles vaccine will protect these children and further reduce MV transmission.
Methods Within the European Prospective Investigation into Cancer and Nutrition (EPIC), a calibration study was set up to express individual dietary intakes according to the same reference scale. A linear regression calibration model was used to correct the association between diet and disease for measurement errors in dietary exposures. In the present work, we describe an approach for analysing the EPIC data, using as an example the evaluation of the association between fish intake and colorectal cancer incidence.
Results Sex- and country-specific attenuation factors ranged from 0.083 to 0.784, with values overall higher for men compared with women. Hazard ratio estimates of colorectal cancer for a 10 g/day increase in fish intake were 0.97 [95% confidence interval (CI): 0.95–0.99] and 0.93 (0.88–0.98), before and after calibration, respectively.
Conclusions In a multicentre study, the diet/disease association can be evaluated by exploiting the whole variability of intake over the entire study. Calibration may reduce between-centre heterogeneity in the diet–disease relationship caused by differential impact of measurement errors across cohorts.
]]>Methods A total of 14 445 participants, aged 39–54 in 1993, completed the personality questionnaires composed of the Bortner Type-A scale, the Buss–Durkee Hostility Inventory (for total, neurotic and reactive hostility) and the Grossarth-Maticek–Eysenck Personality Stress Inventory that assesses six personality types [cancer-prone, coronary heart disease (CHD)-prone, ambivalent, healthy, rational, anti-social]. The association between personality traits and mortality, during a mean follow-up of 12.7 years, was assessed using the Relative Index of Inequality (RII) in Cox regression.
Results In models adjusted for age, sex, marital status and education, all-cause and cause-specific mortality were predicted by ‘total hostility’, its ‘neurotic hostility’ component as well as by ‘CHD-prone’, ‘ambivalent’ ‘antisocial’, and ‘healthy’ personality types. After mutually adjusting personality traits for each other, only high ‘neurotic hostility’ remained a robust predictor of excess mortality from all causes [RII = 2.62; 95% confidence interval (CI) = 1.68–4.09] and external causes (RII = 3.24; 95% CI = 1.03–10.18). ‘CHD-prone’ (RII = 2.23; 95% CI = 0.72–6.95) and ‘anti-social’ (RII = 2.13; 95% CI 0.61–6.58) personality types were associated with cardiovascular mortality and with mortality from external causes, respectively, but CIs were wider. Adjustment for potential behavioural mediators had only a modest effect on these associations.
Conclusions Neurotic hostility, CHD-prone personality and anti-social personality were all predictive of mortality outcomes. Further research is required to determine the precise mechanisms that contribute to these associations.
]]>Methods We included all person-time in women aged 15–50 between 1983 and 2001 and compared mortality rates by time since pregnancy outcome (live birth, stillbirth, induced and spontaneous abortion) using Poisson regression, adjusting for socio-demographic factors.
Results Mortality was highest on the first day after pregnancy (adjusted RR compared with third to fourth year post-partum 105.74, 95% CI: 76.08, 146.95) and remained elevated until 180 days (adjusted RR 1.55, 95% CI: 1.13, 2.11). Pregnancies ending in abortions and stillbirths accounted for 50% of deaths in women within 6 weeks of the end of pregnancy, and mortality after these outcomes was between two and four times as high as mortality after a livebirth.
Conclusion The high mortality rates immediately after birth provide strong support for a skilled attendance strategy. After abortions or stillbirths, women should be under surveillance for up to 1 week. Further work on the cause of deaths in the late post-partum period is required to understand the mechanisms behind increased mortality risks at these times.
]]>Methods The study population included patients aged 40+ years who received a prescription for Cox-2 inhibitors and were included in the General Practice Research Database. The incidence of upper GI events, myocardial infarction (MI) and stroke was estimated in this cohort. It was assumed that patients had experienced the upper GI and cardiovascular effects, as observed in clinical trials [relative rate (RR) of 0.49 for upper GI and 1.86 for MI]. Simulation methodology was used to estimate attributable risks, i.e. the difference between exposed and unexposed event probabilities.
Results The study population included 155 439 Cox-2 users. The number of upper GI events prevented by Cox-2 inhibitors was 179, while the number of excess MI cases was 83 per 10 000 patients treated for 4 years. A strong association was found between extent of GI benefit and cardiovascular harm. There was a large difference in the frequency of benefit over harm in only 6% of the patients (difference of 1% or more); 23% of the patients had more harm than benefit, including those with a history of ischaemic heart disease.
Conclusions The benefit of Cox-2 inhibitors in reducing the frequency of upper GI events may be offset by their cardiovascular harm, particularly in patients with risk factors for cardiovascular disease.
]]>Back pain (BP) is a frequent disorder affecting currently up to 40% of adults inWestern Europe. Most of it is said to be ‘non-specific’, i.e. lacking an obvious patho-anatomical explanation. It is seldom the consequence of a contagious disease caused by microorganisms. This does not exclude it from being communicable if ‘communicable’ is to refer to something being transmitted by sharing or exchanging information.
To propose the hypothesis of BP being a communicable disease.
We base our hypothesis on a reanalysis of five German health surveys. They show a wide gap in BP prevalence between West and East Germany early after reunification. The gap consistently decreased to nearly zero in 2003. Work disability data followed a comparable course.
Various processes may have contributed to the observed changes. Our hypothesis is corroborated by experimental research showing that BP-related beliefs, attitudes and behaviour could positively be influenced by media campaigns and by insights from another recent epidemic.
Complicated HIV transmission dynamics make it unclear how to design and interpret results from community-randomized controlled trials (CRCT) of interventions to prevent infection.
Mathematical modelling was used to investigate the effectiveness of interventions to prevent HIV transmission aimed at high-risk groups and factors related to the chance of recording a statistically significant result.
Behaviour change by high-risk groups can substantially reduce HIV incidence in the whole population, although its effect is sensitive to the structure of the sexual network and the phase of the epidemic. There is a delay between the behaviour change happening and its full effect being realized in the low-risk group and this can pull the measured incidence rate ratio towards one and reduce the chance of recording a statistically significant result in a CRCT. Our simulations suggest that only with unrealistically favourable study conditions would a statistically significant result be likely with 5 years follow-up or less. Small differences in the epidemiological parameters between communities can lead to misleading incidence rate ratios. Behaviour change independent of the intervention can increase the epidemiological impact of the intervention and the chance of recording a statistically significant result.
HIV prevention interventions, especially those targeted at high-risk groups may take longer to work at the population level and need more follow-up time in a CRCT to generate statistically significant results. Mathematical modelling can be used in the design and analysis of CRCTs to understand how the impact of the intervention could develop and the implications this has for statistical power.
In recent years, HIV prevalence has begun to decline in Zimbabwe, which has been associated with reductions in sexual risk behaviour. Here, we analyse the determinants of HIV incidence in this period of decline and estimate the population-level impact of identified risk factors.
A population-based cohort of 1672 HIV-negative adult males and 2465 HIV-negative adult females was recruited between 1998 and 2000. Each individual was then followed-up 3 years later. The influence and inter-relationship of social, behavioural and demographic variables were examined using a proximate determinants framework. To explore the population-level influence of a variable, methods were developed for estimating a risk factor's contribution to the reproductive number (CRN).
HIV incidence was 19.9 [95% confidence interval (CI) 16.3–24.2] per 1000 person years in men and 15.7 (95% CI 13.0–18.9) in women. Multiple sexual partners, having an unwell partner, and reporting another sexually transmitted disease were risk factors that captured the main aspects of the proximate determinants framework: individual behaviour, partnership characteristics and the probability of transmission, respectively. If the proximate determinants fully captured risk of HIV infection, underlying factors would not influence a fully parameterized model. However, a number of underlying social and demographic determinants remained important in regression models after including the proximate determinants. For both sexes, having multiple sexual partners made a substantial CRN, but, for women, no behaviour explained more than 10% of new infections.
The proximate determinants did not explain the majority of new infections at the population level. This may be because we have been unable to measure some risks, but identifying risk factors assumes that those acquiring infections are somehow different from others who do not acquire infections. That they are not suggests that in this generalized epidemic there is little difference in readily identifiable characteristics of the individual between those who acquire infection and those who do not.
Historical data are necessary to establish long-term trends in disease incidence but pose analytical problems since their accuracy and reliability may be poorly specified.
A robust measure of the spatial velocity, R0A, of epidemic waves from space-time series is proposed using binary data. The method was applied to the historical records of influenza morbidity for the island of Iceland over a 61-year period of influenza seasons from 1915–16 to 1975–76.
The onset of influenza waves tended to speed up over the period studied and the three pandemic waves associated with viral shifts in influenza A [Spanish influenza H1N1 (1918–19), Asian influenza H2N2 (1957–58) and Hong Kong influenza H3N2 (1968–69)] spread more rapidly around the island and struck earlier in the influenza season than did inter-pandemic waves, even when the latter were equally intensive as measured by total number of cases and case incidence.
The potential for using R0A in a real-time context is explored using French influenza data.
The new measure of wave velocity appears to be applicable to those historical time series where breakdown into regional or local areas is available. The study is being extended to (i) other countries where similar influenza time series are available and (ii) to other diseases within Iceland.
To explore the association between low serum vitamin D and risk of active tuberculosis in humans.
Systematic review and meta-analysis.
Observational studies published between 1980 and July 2006 (identified through Medline) that examined the association between low serum vitamin D and risk of active tuberculosis.
For the review, seven papers were eligible from 151 identified in the search. The pooled effect size in random effects meta-analysis was 0.68 with 95% CI 0.43–0.93. This ‘medium to large’ effect represents a probability of 70% that a healthy individual would have higher serum vitamin D level than an individual with tuberculosis if both were chosen at random from a population. There was little heterogeneity between the studies.
Low serum vitamin D levels are associated with higher risk of active tuberculosis. Although more prospectively designed studies are needed to firmly establish the direction of this association, it is more likely that low body vitamin D levels increase the risk of active tuberculosis. In view of this, the potential role of vitamin D supplementation in people with tuberculosis and hypovitaminosis D-associated conditions like chronic kidney disease should be evaluated.
It is often recommended that control groups in meta-analyses of genetic association studies are checked for Hardy-Weinberg equilibrium (HWE) as a surrogate for assessing study quality. However, tests for HWE have low power and there is currently no consensus about how to handle studies that deviate significantly from HWE.
We identified 72 papers describing 114 meta-analyses of 1603 primary gene–disease comparisons. Based on these studies and on related simulations, we evaluated four different strategies for handling studies that appear not to be in HWE: (i) include them in the meta-analysis; (ii) exclude them if the test for HWE results in P < 0.05; (iii) exclude them if a measure of the size of departure from HWE is large and (iv) exclude them if (ii) and (iii).
Of the 72 papers, 26 did not report information on HWE, with a trend toward increased reporting with time. HWE was evaluated through testing, with only three papers assessing the size of departure. On re-analysis, 9% of the 1603 primary comparisons showed significant deviation from HWE. The chance of an extreme departure from HWE was inversely related to the sample size of the study. Simulations suggest that there is no advantage in excluding studies that appear not to be in HWE.
Meta-analyses should report both the magnitude and the statistical significance of departures from HWE. Studies that appear to deviate from HWE should be investigated further for weaknesses in their design, but these studies should not be excluded unless there are other grounds for doubting the quality of the study.
Data are limited regarding cancer incidence among Indians residing in different geographic regions around the world. Examining such rates may provide us with insights into future aetiological research possibilities as well as screening and prevention.
Incidence rates for all cancers combined and 19 specific cancers were obtained for India from Globocan 2002, for Indians in Singapore from Cancer Incidence in Five Continents (VIII), and from national data sources for South Asians (SA) in the United Kingdom (UK) and for Asian Indians/Pakistanis (AIP) and whites in the United States (US).
We observed the lowest total cancer incidence rates in India (111 and 116 per 100 000 among males and females, respectively, age-standardized to the 1960 world population) and the highest among US whites (362 and 296). Cancer incidence rates among Indians residing outside of India were: intermediate Singapore (102 and 132), UK (173 and 179) and US ranges 152–176 and 142–164. A similar pattern was observed for cancers of the colorectum, prostate, thyroid, pancreas, lung, breast and non-Hodgkin lymphoma. In contrast, rates for cancers of the oral cavity, oesophagus, larynx and cervix uteri were highest in India. Although little geographic variability was apparent for stomach cancer incidence, Indians in Singapore had the highest rates compared with any other region. The UK SA and the US AIP appear with adopt the cancer patterns of their host country.
Variations in environmental exposures such as tobacco use, diet and infection, as well as better health care access and knowledge may explain some of the observed incidence differences.
Ethnicity is a consistent correlate of excess weight in youth. We examine the influence of lifestyles on ethnic differences in excess weight in early adolescence in the UK.
Data were collected from 6599 pupils, aged 11–13 years in 51 schools, on dietary practices and physical activity, parental smoking and overweight, and on overweight and obesity (using International Obesity Task Force criteria).
Skipping breakfast [girls odds ratio (OR) 1.74, 95% confidence interval (CI) 1.30–2.34; boys OR 2.06; CI 1.57–2.70], maternal smoking (girls OR 2.04, CI 1.49–2.79; boys OR 1.63, CI 1.21–2.21) and maternal overweight (girls OR 2.01, CI 1.29–3.13; boys OR 2.47, CI 1.63–3.73) were associated with obesity. Skipping breakfast, more common among girls, was associated with other poor dietary practices. Compared with White UK peers, Black Caribbeans (girls OR 1.62, CI 1.24–2.12; boys OR 1.49, CI 1.15–1.95) and Black Africans (girls OR 1.96, CI 1.52–2.53; boys OR 2.50, CI 1.92–3.27) were more likely to skip breakfast and engage in other poor dietary practices, and Indians were least likely. White Other boys reported more maternal smoking (OR 1.37, CI 1.03–1.82). All these reports were more common among those born in the UK than those born elsewhere. Black Caribbean girls were more likely to be overweight (OR 1.38, CI 1.02–1.87) and obese (OR 1.65, CI 1.05–2.58), Black African girls to be overweight (OR 1.35, CI 1.02–1.79) and White Other boys to be overweight (OR 1.37, CI 1.00–1.88) and obese (OR 1.86, CI 1.15–3.00). Adverse dietary habits and being born in the UK contributed to these patterns.
These findings signal a potential exacerbating effect on ethnic differences in obesity if adverse dietary habits persist. Combined adolescent and parent-focused interventions should be considered.
Studies have shown a positive association between trans fatty acids (TFA) intake and risk of coronary heart disease (CHD), primarily accounted for by industrially produced TFA. Some of these studies indicate an inverse association between ruminant TFA (R-TFA) intake and CHD implying that R-TFA intake is innocuous or even protective against CHD. The aim of this study was to describe the association between R-TFA intake and risk of CHD evaluating both the absolute and the energy-adjusted intake.
The study was an 18-year follow-up study of 3686 Danes, aged 30–71 years, at baseline without previous CHD.
There were no overall associations between absolute or energy-adjusted R-TFA intakes and risk of CHD. However, among women, indications of inverse associations between R-TFA intake and risk of CHD were found: hazard ratio (HR) per 0.5 g increase in absolute R-TFA intake = 0.84 [95% confidence interval (CI): 0.70, 1.01] and HR per 0.5 g increase in energy-adjusted R-TFA intake = 0.77 (95% CI: 0.55, 1.09). No associations between absolute or energy-adjusted R-TFA intakes and CHD were found among men.
This study suggests that R-TFA intake is not associated with a higher risk of CHD. Whether R-TFA intake is even protective against CHD among women cannot be concluded from this study.
It is hypothesized that associations found between birth weight and subsequent risk of type-2 diabetes are due to inherited genes affecting both fetal growth and metabolism of insulin.
To study whether there is a familial (shared environmental and genetic) link between birth weight and type-2 diabetes, the authors used a sample of 11 411 Swedish like-sexed twins born from 1926 to 1958 with at least one offspring, to study the association between offspring birth weight for gestational age and parental risk of type-2 diabetes.
Decreasing offspring birth weight for gestational age (with 1 SD) was associated with an increased risk of type-2 diabetes among father's [odds ratio (OR) = 1.72, 95% confidence interval (CI): 1.33–2.23] and decreased risk among mothers (OR=0.43, 95% CI: 0.30–0.62), independent of grand parental and parental socio-economic status and parental smoking. In paired twin analysis, the association between offspring birth weight and mothers with risk of type-2 diabetes was similar within- and between-twin pairs, whereas father's risk was slightly smaller within than between pairs (ORBetween=1.90, 95% CI: 1.10–3.28, and ORWithin=1.71, 95% CI: 1.10–2.67, respectively).
The well-established association between paternal type-2 diabetes and offspring birth weight seems to primarily be due to as yet unidentified non-shared environmental factors. However, familial factors shared within twin pairs may contribute to the association.
The Demographic and Health Surveys (DHSs) have been used throughout the developing world for the last 20 years to provide data on the distribution of disease in order to inform planning. Data on child illness and death are reported by mothers and are susceptible to error.
We conducted an in-depth study of the Iranian DHS carried out in 2000–2001 and reviewed 110 DHS carried out around the world to check for bias by assessing the social gradient in reported child morbidity and mortality.
We found that the reported under-5 child morbidity and mortality rates for the 28 Iranian provinces were inversely correlated (r = –0.592, P < 0.001) and that the adjusted social gradient of child morbidity implied increased illness in those who had literate vs illiterate mothers (OR = 1.26, 95% CI 1.20–1.32) compared with a decrease in mortality with increased literacy (OR = 0.52, 95% CI 0.46–0.59). Many of the other DHSs also show increased rates of reported child diarrhoea in households with higher levels of maternal education, access to piped water and urban (vs rural) dwellings, the reverse of what is found with mortality rates.
This suggests that there may be significant recall and reporting bias in under-5 childhood morbidity in DHSs. Caution should be used in the interpretation and use of data from DHSs and the survey methods should be reviewed.
We analyse the NHANES III sample to assess the suitability of measured stature and sitting height to estimate leg length (tibia + femur) and predict fatness. High rates of overweight in the United States population may lead to greater gluteo-femoral fat mass which will increase sitting height and artificially decrease estimates of both absolute and relative leg length.
The analyses include 3076 women and 3233 men, 20.0–49.9 years of age of White, Black or Mexican-American ethnicity. The poverty index ratio, measured stature, sitting height, upper leg length, weight, four skinfolds, buttocks circumference and elbow, biacromial and biiliac breadths were extracted from the database. The sitting height ratio, % body fatness, % upper leg length (ULL/stature), and other indices were estimated. Correlation and principle component analysis were used to assess the relationship between measures of body fatness, relative leg length and the other variables.
For adults in the NHANES III % body fat is more strongly correlated with buttocks circumference (r = 0.87 and 0.78 for women and men), than with any measure of estimated leg length (r's range from –0.28 to –0.10 for both sexes). Principle components analysis separates fatness, stature and estimated leg length into uncorrelated factors for this sample.
Reports of a negative association between leg length and fatness for adults of the NHANES III are likely spurious, due to greater gluteo-femoral fat thickness increasing sitting height. Future rounds of the NHANES, and similar surveys in other nations with high body fat populations, should measure lower extremity length directly to better assess its relationship to health and disease risk.
The concept of priming of childhood obesity by prenatal exposure to maternal smoking is based on a number of consistent studies. A recent paper found similar associations between paternal smoking and childhood obesity, questioning the presumed causal effect attributed to the prenatal exposure. Is the relation to paternal smoking consistent? Does it explain the effect of maternal smoking before or in pregnancy?
Data from a cross sectional study on 5899 children in the setting of the 2005 school entrance health examinations in Bavaria were analysed. Associations between paternal smoking or maternal smoking before or in pregnancy and childhood obesity were assessed with adjustment for potential confounders.
The children's mean age was 5.8 years. The unadjusted odds ratio for obesity and paternal smoking was 2.0 (95% CI: 1.5, 2.6) and similar to that for maternal smoking before or in pregnancy with 2.3 (95% CI: 1.8, 3.1). After adjustment for a number of potential confounders and paternal smoking at interview the odds ratio for maternal smoking before or in pregnancy and childhood obesity was 1.9 (95% CI: 1.3, 2.7). There was no evidence for interaction between paternal smoking and maternal smoking before or in pregnancy (P = 0.38).
Although of similar magnitude, the association of paternal smoking could only partially explain the effect of maternal smoking before or in pregnancy on childhood obesity. Whether this persistent association reflects residual confounding or causality is unclear.