Childhood Obesity-Related Mechanisms: MicroRNome and Transcriptome Changes in a Nested Case-Control Study.
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ABSTRACT:
SUBMITTER: Kim JH
PROVIDER: S-EPMC8389653 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundThe early life course is assumed to be a critical phase for childhood obesity; however the significance of single factors and their interplay is not well studied in childhood populations.ObjectivesThe investigation of pre-, peri- and postpartum risk factors on the risk of obesity at age 2 to 9.MethodsA case-control study with 1,024 1:1-matched case-control pairs was nested in the baseline survey (09/2007-05/2008) of the IDEFICS study, a population-based intervention study on childhood obesity carried out in 8 European countries in pre- and primary school settings. Conditional logistic regression was used for identification of risk factors.ResultsFor many of the investigated risk factors, we found a raw effect in our study. In multivariate models, we could establish an effect for gestational weight gain (adjusted OR = 1.02; 95%CI 1.00-1.04), smoking during pregnancy (adjusted OR = 1.48; 95%CI 1.08-2.01), Caesarian section (adjusted OR = 1.38; 95%CI 1.10-1.74), and breastfeeding 4 to 11 months (adjusted OR = 0.77; 95%CI 0.62-0.96). Birth weight was related to lean mass rather than to fat mass, the effect of smoking was found only in boys, but not in girls. After additional adjustment for parental BMI and parental educational status, only gestational weight gain remained statistically significant. Both, maternal as well as paternal BMI were the strongest risk factors in our study, and they confounded several of the investigated associations.ConclusionsKey risk factors of childhood obesity in our study are parental BMI and gestational weight gain; consequently prevention approaches should target not only children but also adults. The monitoring of gestational weight seems to be of particular importance for early prevention of childhood obesity.
| S-EPMC3923715 | biostudies-literature
Project description:RationaleAcute lung injury (ALI) that develops 6 hours after transfusion (TRALI) is the leading cause of transfusion-related mortality. Several transfusion characteristics have been postulated as risk factors for TRALI, but the evidence is limited to retrospective studies.ObjectivesTo compare patient and transfusion risk factors between patients who do and do not develop ALI.MethodsIn this prospective cohort study, consecutive transfused critically ill patients were closely observed for development of ALI. Donor samples were collected from the transfusion bags. Risk factors were compared between patients who developed ALI after transfusion and transfused control patients, matched by age, sex, and admission diagnosis.Measurements and main resultsSeventy-four of 901 transfused patients developed ALI within 6 hours of transfusion (8%). Compared with transfused control subjects, patients with ALI were more likely to have sepsis (37 vs. 22%, P = 0.016) and a history of chronic alcohol abuse (37 vs. 18%, P = 0.006). When adjusted for patient characteristics, transfusion of plasma from female donors (odds ratio [OR], 5.09; 95% confidence interval [95% CI], 1.37-18.85) rather than male donors (OR, 1.60; 95% CI, 0.76 to 3.37), number of pregnancies among the donors (OR, 1.19; 95% CI, 1.05 to 1.34), number of donor units positive for anti-granulocyte antibodies (OR, 4.85; 95% CI, 1.32-17.86) and anti-HLA class II antibodies (OR, 3.08; 95% CI, 1.15-8.25), and concentration of lysophosphatidylcholine in the donor product (OR, 1.69; 95% CI, 1.10 to 2.59) were associated with the development of ALI.ConclusionsBoth patient and transfusion risk factors determine the probability of ALI after transfusion. Transfusion factors represent attractive targets for the prevention of ALI.
| S-EPMC2048675 | biostudies-literature
Project description:BACKGROUND:Smoking and alcohol consumption are the most common social habits in patients with sialolithiasis. Moreover, obesity has been reported to have a significant association with poor oral hygiene, one of the causes of sialolithiasis. The purpose of this study was to evaluate the relationships among tobacco smoking, drinking alcohol, obesity and sialolithiasis in a Korean population. METHODS:The Korean National Health Insurance Service-Health Screening Cohort, which includes patients ≥40 years old, was assessed from 2002 to 2013. A total of 947 sialolithiasis participants were matched with 3788 control subjects at a ratio of 1:4 with respect to age group, sex, income group, region of residence, hypertension, diabetes, and dyslipidemia. We analyzed the participants' previous histories of smoking (current or past smokers compared to nonsmokers) and alcohol consumption (≥ 1 time per week compared to < 1 time per week) in the sialolithiasis and control groups. Obesity was measured using body mass index (BMI, kg/m2), which was categorized as < 18.5 (underweight), ≥ 18.5 and < 23 (normal), ≥ 23 and < 25 (overweight), ≥ 25 and < 30 (obese I), and ≥ 30 (obese II). Crude and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression analyses. RESULTS:The rate of smoking was higher in the sialolithiasis group (32.4% [307/947]) than in the control group (29.1% [1103/3788], P = 0.047). The adjusted OR of smoking for the sialolithiasis group was 1.31 (95% CI = 1.08-1.59, P = 0.006). Alcohol consumption and obesity were not statistically significantly related to sialolithiasis. CONCLUSION:The odds of smoking were increased in sialolithiasis patients compared with control subjects in the population ≥ 40 years of age.
| S-EPMC7164270 | biostudies-literature
Project description:BackgroundAlthough obesity is an established risk factor for renal cell carcinoma (RCC), it is unclear whether this relationship varies across histologic subtypes.MethodsWe conducted a nested case-control study within the Kaiser Permanente Northern California (KPNC) health care network, and meta-analysis combining our results with those of previously published studies. Our KPNC study included 685 RCC cases [421 clear cell; 65 papillary; 24 chromophobe; 35 other; 141 not otherwise specified (NOS)] and 4266 controls. Subtype-specific odds ratios (ORs) and 95% confidence intervals (CIs) for categories of body mass index (BMI) and were computed from the case-control data using polytomous logistic regression. Findings from this and other relevant studies were combined by meta-analysis using a random effects model.ResultsIn the KPNC study, obesity (BMI ≥ 30 kg/m2) was associated with clear cell RCC (OR 1.5, 95% CI 1.1-2.1) and chromophobe RCC (OR 2.5, 95%CI 0.8-8.1), but not with papillary RCC (OR 1.0, 95% CI 0.5-1.9). In meta-analysis including three additional studies, a similar pattern of summary relative risks (SRR) for obesity was observed across subtypes (clear cell: SRR 1.8, 95% CI 1.5-2.2; chromophobe: SRR 2.2, 95% CI 1.3-3.7; papillary, SRR 1.2, 95% CI 0.8-1.6).ConclusionsThese findings support the hypothesis that histologic subtypes of RCC possess distinct etiologic pathways, with obesity important for the development of clear cell and, possibly, chromophobe RCC, but not papillary RCC.
| S-EPMC6151870 | biostudies-literature
Project description:The purpose of this study was to improve prediction of patients at high-risk for metastatic disease utilizing a nested case-control design that uniquely enables enrichment for relevant phenotypes. We identified all women diagnosed with primary breast cancer from January 1, 1997, to December 31, 2005, in the Stockholm health care region. Patients developing distant metastatic disease (cases) were selected and controls (free from distant disease) were randomly matched by adjuvant therapy, age and calendar period at diagnosis. The nested case-control study included 768 study subjects with clinical information and gene expression arrays (Human Cancer G110). Study subjects were randomly and equally divided into training set (discovery) or testing (validation) set. Metastatic onset prediction was then compared including either clinical variables only or combining clinical and genetic information. Differentially expressed genes and pathways between cases and controls included a wide-spectrum of well known as well as candidate regulators of the metastatic cascade.
2015-07-08 | GSE48091 | GEO
Project description:OBJECTIVES:To investigate the relationship between dyslipidemia and obesity status among Viet-namese adolescents. METHODS:In this case-control study, 282 adolescents (6-11 years), including 88 obese cases and 194 normal-weight controls, were recruited from a population-based cross-sectional study from two provinces in Vietnam. The anthropometric, blood lipid, and other laboratory test results of the study subjects were analyzed. RESULTS:Obese children tended to have more visceral fat (Pearson's r = 0.795, p < 0.0001) than subcutaneous fat (Pearson's r = 0.754, p < 0.0001), and this difference was associated with an increase in blood triglyceride level (Pearson's r = 0.232, p < 0.05) and a strikingly high rate of hypertriglyceridemia (38.6%). We also found that birth weight and parental body mass index were related to the status of obesity among the study subjects. However, only birth weight was significantly higher in the obese group than in the normal weight group. These findings indicate the effect of prenatal nutrition on childhood obesity. Furthermore, high-birth weight children had a surprisingly high rate of obesity. CONCLUSION:Together, our data suggest that obesity increased the risk for hypertriglyceridemia, which was, at least partially, due to prenatal nutrition.
| S-EPMC5441441 | biostudies-literature
Project description:Inflammation in utero is linked to childhood respiratory and infectious complications. Obesity is an increasingly common chronic inflammatory state, yet little is known about its role in childhood respiratory illness. We sought to examine the association between maternal pre-gravid BMI and early childhood respiratory hospitalization. We conducted a population-based case-control study using the Washington State Comprehensive Hospital Abstract Reporting System and linked birth certificate data. Cases were children age 0-5 years, born in Washington state, with a respiratory hospitalization between 2003 and 2008. We identified 15,318 cases, frequency matching each case to two controls by birth year (total 31,060 controls). We used logistic regression to estimate the risk (approximated by odds ratios) of early childhood respiratory hospitalization according to maternal pre-gravid body mass index (BMI) category (underweight, normal, overweight, obese), after adjustment for maternal and infant characteristics. An elevated maternal pre-gravid BMI was associated with increased risk of childhood respiratory hospitalization, with an adjusted odds ratio OR [95 % CI] = 1.08 [1.03-1.14] for overweight mothers (BMI 25-29.9 kg/m(2)), and OR = 1.29 [1.22-1.36] for obese mothers (BMI ? 30 kg/m(2)). An elevated maternal pre-gravid BMI was associated with higher risk of early childhood respiratory hospitalization. Childhood respiratory illness may be an important complication of excess maternal weight that should be shared with expectant mothers.
| S-EPMC3538085 | biostudies-literature
Project description:BackgroundTo assess the association of hospital-treated infections with the subsequent risk of two Epstein-Barr virus (EBV)-related malignancies, namely Hodgkin's lymphoma (HL) and nasopharyngeal carcinoma (NPC).MethodsWe performed a nested case-control study based on several national registers in Sweden. Cases were individuals newly diagnosed with HL or NPC during 1994-2016 in Sweden, according to the Swedish Cancer Register. For each case, we randomly selected five controls individually matched to the case on sex and year of birth from the general Swedish population. Hospital-treated infections (i.e., infections requiring either inpatient or outpatient hospital care) were identified from the Swedish Patient Register. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) of HL and NPC, in relation to hospital-treated infections, after adjustment for age, sex, calendar period, educational achievement, and region of residence.ResultsThe study included a total of 890 cases of HL and 306 cases of NPC. A hospital-treated infection three years ago or earlier was associated with a higher risk of HL (OR = 1.49, 95%CI: 1.26-1.75) as well as NPC (OR = 1.36; 95%CI: 1.01-1.83). The positive association was noted for both bacterial and viral infections and primarily for respiratory and skin infections. A monotonous dose-response relationship was found between a number of hospital-treated infections and the risk of HL (p = 0.02) but less compelling for NPC (p = 0.06). Using a 5-year lag time rendered similar results (OR = 1.43, 95%CI: 1.21-1.70 for HL; OR = 1.43, 95%CI: 1.05-1.95 for NPC).ConclusionsThese findings suggest that infections requiring hospital treatment might contribute to the carcinogenesis of malignancies potentially related to EBV.
| S-EPMC9367337 | biostudies-literature
Project description:BackgroundPrescription opioid use is highly associated with risk of opioid-related death, with 1 of every 550 chronic opioid users dying within approximately 2.5 years of their first opioid prescription. Although gabapentin is widely perceived as safe, drug-induced respiratory depression has been described when gabapentin is used alone or in combination with other medications. Because gabapentin and opioids are both commonly prescribed for pain, the likelihood of co-prescription is high. However, no published studies have examined whether concomitant gabapentin therapy is associated with an increased risk of accidental opioid-related death in patients receiving opioids. The objective of this study was to investigate whether co-prescription of opioids and gabapentin is associated with an increased risk of accidental opioid-related mortality.Methods and findingsWe conducted a population-based nested case-control study among opioid users who were residents of Ontario, Canada, between August 1, 1997, and December 31, 2013, using administrative databases. Cases, defined as opioid users who died of an opioid-related cause, were matched with up to 4 controls who also used opioids on age, sex, year of index date, history of chronic kidney disease, and a disease risk index. After matching, we included 1,256 cases and 4,619 controls. The primary exposure was concomitant gabapentin use in the 120 days preceding the index date. A secondary analysis characterized gabapentin dose as low (<900 mg daily), moderate (900 to 1,799 mg daily), or high (≥1,800 mg daily). A sensitivity analysis examined the effect of concomitant nonsteroidal anti-inflammatory drug (NSAID) use in the preceding 120 days. Overall, 12.3% of cases (155 of 1,256) and 6.8% of controls (313 of 4,619) were prescribed gabapentin in the prior 120 days. After multivariable adjustment, co-prescription of opioids and gabapentin was associated with a significantly increased odds of opioid-related death (odds ratio [OR] 1.99, 95% CI 1.61 to 2.47, p < 0.001; adjusted OR [aOR] 1.49, 95% CI 1.18 to 1.88, p < 0.001) compared to opioid prescription alone. In the dose-response analysis, moderate-dose (OR 2.05, 95% CI 1.46 to 2.87, p < 0.001; aOR 1.56, 95% CI 1.06 to 2.28, p = 0.024) and high-dose (OR 2.20, 95% CI 1.58 to 3.08, p < 0.001; aOR 1.58, 95% CI 1.09 to 2.27, p = 0.015) gabapentin use was associated with a nearly 60% increase in the odds of opioid-related death relative to no concomitant gabapentin use. As expected, we found no significant association between co-prescription of opioids and NSAIDs and opioid-related death (OR 1.11, 95% CI 0.98 to 1.27, p = 0.113; aOR 1.14, 95% CI 0.98 to 1.32, p = 0.083). In an exploratory analysis of patients at risk of combined opioid and gabapentin use, we found that 46.0% (45,173 of 98,288) of gabapentin users in calendar year 2013 received at least 1 concomitant prescription for an opioid. This study was limited to individuals eligible for public drug coverage in Ontario, we were only able to identify prescriptions reimbursed by the government and dispensed from retail pharmacies, and information on indication for gabapentin use was not available. Furthermore, as with all observational studies, confounding due to unmeasured variables is a potential source of bias.ConclusionsIn this study we found that among patients receiving prescription opioids, concomitant treatment with gabapentin was associated with a substantial increase in the risk of opioid-related death. Clinicians should consider carefully whether to continue prescribing this combination of products and, when the combination is deemed necessary, should closely monitor their patients and adjust opioid dose accordingly. Future research should investigate whether a similar interaction exists between pregabalin and opioids.
| S-EPMC5626029 | biostudies-literature
Project description:The identification of early biological changes associated with the psychotic disorder (PD) is important as it may provide clues to the underlying pathophysiological mechanisms. We undertook the first proteomic profiling of blood plasma samples of children who later develop a PD. Participants were recruited from the UK Avon Longitudinal Study of Parents and Children (ALSPAC) cohort who also participated in psychiatric assessment interviews at age 18. Protein expression levels at age 11 were compared between individuals who developed PD at age 18 (n = 37) with population-based age-matched controls (n = 38). Sixty out of 181 plasma proteins profiled were found to be differentially expressed (P < .05) in children with an outcome of the PD. Thirty-four of these proteins were found to be differentially expressed following correction for multiple comparisons. Pathway analysis implicated the complement and coagulation cascade. A second, targeted proteomic approach was used to verify these findings in age 11 plasma from subjects who reported psychotic experiences at age 18 (n = 40) in comparison to age-matched controls (n = 66). Our findings indicate that the complement and coagulation system is dysregulated in the blood during childhood before the development of the PD.
| S-EPMC5814944 | biostudies-literature