Is zinc deficiency a risk factor for atherosclerosis?

The development of atherosclerosis is influenced by genetic, lifestyle and nutritional risk factors. Zn and metallothionein deficiency can enhance oxidative-stress-related signalling processes in endothelial cells, and since changes in available plasma Zn may affect the Zn status of the endothelium, Zn deficiency could be a risk factor for IHD. Although the association of Zn with many proteins is essential for their function, three key signalling processes are highlighted as being principal targets for the effect of Zn deficiency: the activation of NF-kappaB, the activation of caspase enzymes and the signalling of NO. The need to develop a reliable indicator of Zn status is critical to any epidemiological approach for studying the relationship between Zn status and disease incidence. Studies using appropriate animal models and investigating how the plasma Zn pool influences endothelial intracellular labile Zn would be helpful in appreciating the importance of Zn deficiency in atherogenesis.     

Is diabetes mellitus a risk factor for HCV infection?

The aim of this study was to investigate whether or not the diabetes mellitus may be considered a risk factor for the HCV infection. The HCV seroprevalence was evaluated in 254 diabetic subjects, whose anamnestic data and risk factors are known, in comparison to 223 first-time blood donors, carefully age- and gender-matched. The statistical analysis showed that the studied groups belonged to the same population (Mann-Whitney U test) and that there were no significant differences between cases and controls as regards HCV prevalence (Yates corrected chi 2 test). The obtained data underline the importance of the control group selection, especially in the studies considering age-related pathologies. The authors disprove type 2 diabetes as a risk factor for the HCV infection and consider that this is a valid hypothesis only when the hepatitis C was unknown and not adequate prevention was used.     

Is radiographic vertebral fracture a risk factor for mortality?

Clinical fractures predict increased mortality risk, but few studies report mortality based on prevalent radiographically defined vertebral fracture. This study examined whether radiographically defined vertebral fracture is a risk factor for mortality in older adults. The 1,580 participants in California (631 men, 949 women) were aged > or =50 years in 1992-1996. Lateral spine radiographs, and information about medical history and behaviors, were obtained. Overall, 55 (8.7%) men and 123 (13%) women had at least one prevalent fracture at baseline; of these, 48 women and 14 men had two or more. Over 7.6 years, 460 participants died, 27.6% without and 41.0% with prevalent fractures (p < 0.001). Prevalent vertebral fracture was not associated with all-cause mortality in both sexes combined (adjusted hazard ratio = 1.09, 95% confidence interval: 0.84, 1.42) or sex-specific analyses (women: adjusted hazard ratio = 1.15, 95% confidence interval: 0.83, 1.59; men: adjusted hazard ratio = 0.89, 95% confidence interval: 0.55, 1.46). However, women with two or more prevalent fractures had increased risk of all-cause mortality (adjusted hazard ratio = 1.56, 95% confidence interval: 1.01, 2.40; p = 0.04). Women with any prevalent vertebral fractures also had increased mortality risk from "other" causes (adjusted hazard ratio = 1.59, 95% confidence interval: 1.03, 2.45; p = 0.04) but not cardiovascular disease or cancer. A single radiographic vertebral fracture is not a risk for mortality in older women; larger, longer studies of men and those with two or more radiographic vertebral fractures are needed.     

Is vitamin A consumption a risk factor for osteoporotic fracture?

Severe vitamin A toxicity is known to have adverse effects on skeletal health. Studies involving animal models and case reports have documented that hypervitaminosis A is associated with bone resorption, hypercalcaemia and bone abnormalities. More recently, some epidemiological studies have suggested that high habitual intake of vitamin A could contribute to low bone mineral content and fracture risk. The evidence relating to the possible deleterious role of vitamin A in bone health is of variable quality and is potentially confounded by collinearity of nutrient intake and difficulties in assessing vitamin A exposure. Furthermore, because intake of vitamin A varies between studies it is not possible to define an intake threshold associated with harm.     

Are schizophrenia or antipsychotic drugs a risk factor for cataracts?

Lens changes and ocular disturbances have been reported in conjunction with the use of antipsychotic drugs. We estimated the incidence rate of a clinical diagnosis of cataract in patients with a psychotic disorder, schizophrenia, and compared it with the rate in the general population. Among the schizophrenic patients, we also examined the role of dose and duration of antipsychotic drugs on the risk of cataract development. We followed up two cohorts of patients 30-85 years of age who were included in the United Kingdom General Practice Research Database. Patients in one group had a diagnosis of schizophrenia (N = 4,209). The other group was an age- and sex-matched cohort of 10,000 patients sampled from the source population. The incidence of cataracts was 4.5 per 1,000 person-years among the general population and 3.5 in the schizophrenia population. Overall, antipsychotic drug use was not associated with the occurrence of cataracts. Nevertheless, among long-term users of chlorpromazine at daily doses of 300 mg or greater, and among users of prochlorperazine, the relative risks were 8.8 (95% confidence interval = 3.1-25.1) and 4.0 (95% confidence interval = 0.8-20.7), respectively. There is no indication that schizophrenia per se is associated with an increased risk of developing cataracts.     

Is teenage pregnancy a neonatal risk factor?

Maternal characteristics and neonatal outcome of 421 primiparas aged 15–19 years who delivered at Bikur Cholim Hospital in Jerusalem were examined. The study group included 190 teenage mothers from the Mea Shearim community who marry young and who receive extensive social and economic support. The control group included 231 teenage mothers from other areas of Jerusalem, characterized by a predominantly low social class, Oriental ethnic origin, and a high rate of out-of-wedlock births (28.6%). The Mea Shearim mothers had a significantly lower incidence of low birth weight (<2500 g) infants compared to the control group (6.3% vs. 14.7%, p < 0.01). The differences could not be explained by maternal age distribution, ethnicity, smoking, or marital status. These results suggest that in a community that provides extensive social and economic support and good access to free prenatal care of high standard, teenage pregnancy is not a neonatal risk factor.     

Is maternal age a risk factor for mental retardation among children?

The purpose of this study was to determine whether older or very young maternal age at delivery is associated with mental retardation in children. Ten-year-old children with mental retardation (an intelligence quotient of 70 or less) were identified in 1985-1987 from multiple sources in the metropolitan Atlanta, Georgia, area. These children were subdivided into two case groups according to whether they had concomitant developmental disabilities or birth defects affecting the central nervous system (codevelopmental retardation) or did not have such disabilities (isolated retardation). Control children were randomly chosen from the regular education files of the public school systems in the study area. Data on sociodemographic variables were gathered from birth certificates. Children of teenaged mothers were not at increased risk for either form of retardation and children of mothers aged > or =30 years were not at increased risk for isolated retardation, in comparison with children of mothers aged 20-29 years. A markedly elevated risk of codevelopmental retardation was seen among black children of mothers aged > or =30 years that was not attributable to Down syndrome. A modest increase in risk for codevelopmental retardation was observed among white children born to older mothers, but it was entirely due to Down syndrome.     

Is household antibiotic use a risk factor for antibiotic-resistant pneumococcal infection?

We used microbiology and pharmacy data from health-maintenance organizations to determine whether antibiotic use by a household member increases the risk of penicillin-non-susceptible pneumococcal disease. Though it has been well established that an individual's antibiotic use increases one's risk of antibiotic-resistant infection, it is unclear whether the risk is increased if a member of one's household is exposed to antibiotics. We therefore conducted a case-control study of patients enrolled in health maintenance organizations in Western Washington and Northern California. Cases were defined as individuals with penicillin-non-susceptible pneumococcal infection; controls were individuals with penicillin-susceptible pneumococcal infection. Socioeconomic variables were obtained by linking addresses with 1997 census block group data. One-hundred and thirty-four cases were compared with 798 controls. Individual antibiotic use prior to diagnosis increased the odds of penicillin non-susceptibility, with the strongest effect seen for beta-lactam use within 2 months (OR 1.8, 95% CI 1.2, 2.8). When household antibiotic use by persons other than the patient were considered, at 4 months prior to diagnosis there was a trend towards an association between penicillin non-susceptibility and beta-lactam antibiotic use, and a possible association in a small subgroup of patients with eye and ear isolates. However, no significant overall pattern of association was seen. We conclude that though antibiotic use of any kind within 2 months prior to diagnosis is associated with an increased risk of penicillin-non-susceptible pneumococcal disease, there is no significant overall pattern of association between household antibiotic use and penicillin-non-susceptible pneumococcal infection.     

Is restrained eating a risk factor for weight gain in a general population?

BACKGROUND: In modern societies characterized by abundant and accessible foods, restrained eating may become an adaptive behavior to limit weight gain. OBJECTIVE: We assessed the relations between eating behavior (EB) and adiposity in a general population over a 2-y period. DESIGN: We recruited 466 adults and 271 adolescents in 1999 on a geographical basis to participate in a longitudinal study. At the initial examination and 2 y later, they answered an EB questionnaire, the Three-Factor Eating Questionnaire-R18, which measured cognitive restraint (CR), uncontrolled eating, and emotional eating. On the same occasions, several measures of adiposity were also obtained: body mass index (BMI; in kg/m2), waist circumference, the sum of 4 skinfold thicknesses, and percentage body fat. Relations between EB and adiposity were tested separately in adults and adolescents by using mixed linear regressions after adjustment for age, sex, and (in adolescents) Tanner pubertal stage. RESULTS: At baseline, CR was positively associated with BMI in normal-weight subjects (mean BMI: 21.4 in the lowest to 23.3 in the highest CR quintile; P < 0.001) but not in overweight adults (P = 0.25). Initial CR did not predict change in adiposity variables (BMI change: P = 0.79 in adults, P = 0.57 in adolescents and young adults). Conversely, a high initial BMI was associated with a larger increase in CR (beta = 20.1, P < 0.0001 in adults; beta = 21.7, P = 0.003 in adolescents and young adults). CONCLUSIONS: Restrained eating is strongly associated with adiposity in normal-weight subjects but not in overweight subjects. However, restrained eating does not promote weight gain.     

Is calcium supplementation a risk factor for cardiovascular diseases in older women?

Low intake of dietary calcium is related to bone loss and fragility fracture in older adults, especially postmenopausal women. Contradictory findings have been reported from studies that investigated the association between calcium supplementation and hypertension and the risk of stroke and cardiovascular disease. Misinterpretation of findings from studies that are not primarily designed to address these issues might overshadow the benefits of dietary calcium. Until well-designed studies address the current uncertainties, the possible detrimental effect (e.g., hypercalcemia and its complications) of higher-than-recommended calcium intake should be balanced against the likely benefits of calcium on bone, particularly in elderly women.     

Is early enteral nutrition a risk factor for gastric intolerance and pneumonia?

BACKGROUND: Early enteral nutrition (EN) after injury reduces septic complications, but upper digestive intolerance (UDI) occurring immediately post-trauma is a risk factor for pneumonia. Our study aimed to determine whether early intragastric feeding may lead to gastric intolerance and subsequent pneumonia in ventilated multiply injured patients. METHODS: This prospective study involved two groups of patients randomized either to immediate intragastric EN, or to delayed intragastric EN started later than 24 h after admission. UDI was diagnosed when gastric residual volume, measured with a 50-ml syringe after stopping the feeding for 2 h, exceeded 200 ml at least at two consecutive measurements, and/or when vomiting occurred. RESULTS: Out of 52 patients, 27 were included in the early EN group, and 25 in the delayed-EN group. On day 4, the early EN group received a greater amount of feeding because of intolerance problems occurring in the delayed-EN group (1175 +/- 485 ml vs. 803 +/- 545 ml). Twenty-five subjects--33% of the early EN patients and 64% of the delayed-EN patients--met the criteria for pneumonia (P = 0.050). On average, patients with pneumonia were older, more severely injured, and therefore required more ventilator days and a longer stay in the intensive care unit than patients without pneumonia. CONCLUSIONS: If properly administered, early enteral nutrition can decrease the incidence of upper intestinal intolerance and nosocomial pneumonia in patients with multiple injuries.     

Is birthweight a good marker for gestational exposures that increase the risk of adult disease?

There is much evidence of a link between low birthweight and elevated risk of adult cardiovascular disease, from humans and experimental animals. However, if one relies on data linking birthweight to coronary heart disease to estimate the public health implications of this association, the effects are likely to be modest. The focus on birthweight may be misplaced, because reduced size at birth may not be in the causal pathway linking gestational factors to disease in adult offspring. We need to know more about this before we can estimate the public health implications of gestational factors and assess the potential for intervention. The most studied gestational factor is maternal nutrition. We review here evidence for and against birthweight being in the causal pathways between suboptimal maternal nutrition and increased risk of adult disease in the offspring and provide evidence suggesting that birthweight is not in all of them. From a public health point of view, we suggest that future research in this field should focus on modifiable gestational exposures that may be linked to adult disease, whether or not they influence size at birth.     

Is birth weight a risk factor for ischemic heart disease in later life?

BACKGROUND: An inverse association between birth weight and ischemic heart disease (IHD) has been seen in observational studies. OBJECTIVE: We wanted to determine the strength and consistency of the association between birth weight and subsequent IHD. DESIGN: We conducted a systematic review of observational studies. RESULTS: Seventeen published studies of birth weight and subsequent IHD were identified that included a total of 144,794 singletons. Relative risk estimates for the association between birth weight and IHD were available from 16 of these studies. Additional data from 2 unpublished studies of 3801 persons were also included. In total, the analyses included data from 18 studies on 4210 nonfatal and 3308 fatal IHD events in 147,009 persons. The mean weighted estimate for the association between birth weight and the combined outcome of nonfatal and fatal IHD was 0.84 (95% CI: 0.81, 0.88) per kilogram of birth weight (P<0.0001). No significant heterogeneity was observed between estimates in different studies (P=0.09), nor was there evidence of publication bias (P=0.3, Begg test). Neither restricting the analysis to fatal IHD events nor adjusting for socioeconomic status had any appreciable effect on the findings. CONCLUSIONS: These findings are consistent with a 1 kg higher birth weight being associated with a 10-20% lower risk of subsequent IHD. However, even if causal, interventions to increase birth weight are unlikely to reduce the incidence of IHD materially. Further studies are needed to determine whether the observed association reflects a stronger underlying association with a related exposure or is due (at least in part) to residual confounding.     

Is the duration of poverty and unemployment a risk factor for heavy drinking?

Research on the influence of socioeconomic status (SES) on heavy drinking of alcohol has provided contradictory findings. A limitation of the literature is that studies have primarily measured SES at one point in time. Inspired by the life course perspective and sociological research on chronic stress, this study uses data from the US National Longitudinal Survey of Youth (1979-1992 wave) to examine whether the duration of poverty and unemployment is a risk factor for heavy drinking. Results from logistic and ordinary least squares regression analyses demonstrate that longer durations of poverty and involuntary unemployment across a span of 13 years significantly predict being a heavy drinker and more frequent heavy drinking at ages 27-35 years. These effects are independent of gender, age, race/ethnicity, marital status, prior heavy drinking, and present SES. Overall, this study contributes to the literature that histories of poverty and involuntary unemployment have lasting effects on heavy drinking. More studies should use longitudinal data to explore the temporal dimension of SES.