Does initial breastfeeding lead to lower blood cholesterol in adult life? A quantitative review of the evidence

BACKGROUND: Earlier studies have suggested that infant feeding may program long-term changes in cholesterol metabolism. OBJECTIVE: We aimed to examine whether breastfeeding is associated with lower blood cholesterol concentrations in adulthood. DESIGN: The study consisted of a systematic review of published observational studies relating initial infant feeding status to blood cholesterol concentrations in adulthood (ie, aged >16 y). Data were available from 17 studies (17 498 subjects; 12 890 breastfed, 4608 formula-fed). Mean differences in total cholesterol concentrations (breastfed minus formula-fed) were pooled by using fixed-effect models. Effects of adjustment (for age at outcome, socioeconomic position, body mass index, and smoking status) and exclusion (of nonexclusive breast feeders) were examined. RESULTS: Mean total blood cholesterol was lower (P = 0.037) among those ever breastfed than among those fed formula milk (mean difference: -0.04 mmol/L; 95% CI: -0.08, 0.00 mmol/L). The difference in cholesterol between infant feeding groups was larger (P = 0.005) and more consistent in 7 studies that analyzed "exclusive" feeding patterns (-0.15 mmol/L; -0.23, -0.06 mmol/L) than in 10 studies that analyzed nonexclusive feeding patterns (-0.01 mmol/L; -0.06, 0.03 mmol/L). Adjustment for potential confounders including socioeconomic position, body mass index, and smoking status in adult life had minimal effect on these estimates. CONCLUSIONS: Initial breastfeeding (particularly when exclusive) may be associated with lower blood cholesterol concentrations in later life. Moves to reduce the cholesterol content of formula feeds below those of breast milk should be treated with caution.     

Does depression increase the risk of developing type 2 diabetes?

BACKGROUND: Members of a scheme awarding injury pensions may allege that the onset of diabetes was precipitated or caused by depression induced by work in order to claim an injury award. AIMS: To quantify the association between depression and subsequent development of type 2 diabetes in order to determine whether an individual in a pension scheme that awards injury pensions, who develops type 2 diabetes, should be awarded an injury pension, if the development of the diabetes followed a work-related depressive episode. METHODS: Electronic and hand literature searches up to December 2006. Relative risk estimates from cohort studies of adults were pooled using fixed and random effects models. Attributable risk fraction was calculated using the Levin formula. RESULTS: The presence of depression or depressive symptoms was associated with increased risk of subsequently developing type 2 diabetes. The pooled fully adjusted relative risk estimate from the three highest quality studies was 1.25 (95% CI: 1.02-1.48) and was homogenous. However, depression was no more frequent among those with and without prevalent, but previously undiagnosed, type 2 diabetes. CONCLUSION: Depression is associated with subsequent development of type 2 diabetes. However, the relative risk estimate is small and only 20% of cases of diabetes can be attributed to depression in people with both conditions. Further research is needed to determine possible causal mechanisms for the association and to ascertain whether depression and diabetes may have a common aetiology.     

Does pregnancy or pregnancy loss increase later maternal risk of diabetes?

Evidence that childbearing is associated with future development of diabetes remains conflicting and the role of pregnancy loss in this association has not been investigated. We aimed to examine whether pregnancy and/or pregnancy loss (miscarriage, abortion, or stillbirth) are associated with maternal higher risk of diabetes later in life, using a population-based prospective cohort study (mean follow-up = 10.7 years), including 13,612 women (aged 35-65 at baseline). We found pregnancy per se did not change the risk of diabetes after considering the effect of education, smoking, alcohol consumption, physical activity, BMI, waist/hip ratio, hypertension, and hyperlipidemia (fully-adjusted OR: 1.04, 95 % CI: 0.82-1.31). Having more than four live births was associated with around two times higher risk of diabetes later in life (fully-adjusted OR: 1.77, 95 % CI: 1.12-2.80). Having more than two miscarriages was associated with about two-fold higher risk of diabetes (fully-adjusted Odd ratio (OR): 1.85, 95 % CI: 1.17-2.93). After further adjustment for parity, the higher risk of diabetes in those who had history of more than two miscarriages did not change substantially (OR: 1.82; 95 % CI: 1.15-2.88), but the association between more than four live births and diabetes disappeared when the role of pregnancy loss was considered (fully-adjusted HR: 1.06; 95 % CI: 0.54-2.08). No significant association was found between abortion, stillbirth and risk of maternal diabetes. Pregnancy per se did not increase risk of diabetes. Women who experience more than two miscarriages are at around two times higher risk of diabetes later in life. The association between high parity and diabetes is mediated by history of miscarriages and known risk factors of diabetes. The underlying reason for association between miscarriage and diabetes needs further investigation.     

Does the primary school attended influence self-reported health or its risk factors in later life? Aberdeen Children of the 1950s Study

BACKGROUND: Adult health and its determinants are influenced by the environment in childhood. The school attended is known to affect the health behaviours of pupils while still at school. Little is known about the long-term influence of school attended on health. METHODS: A total of 7,095 respondents (mean age 47 years) to a follow-up questionnaire who attended primary school in Aberdeen, UK, provided information on self-reported health; self-reported high blood pressure; GHQ-4; smoking status; alcohol intake; and obesity. Variance partition coefficients (VPCs) summarized the variation in adult health outcomes and behaviours across schools. Multilevel logistic regression was used to estimate the contribution of school to variation in the outcomes taking into account individual-level and school-level factors. RESULTS: There was some variation across schools in the proportion of adults reporting poor self-rated health (VPC = 0.020) and smoking (0.019). Higher VPCs were found for factors potentially confounded with school: paternal social classes (I&II) (0.45) and gender (0.44). Age at leaving secondary education (0.28) and income (0.10) varied across schools. The effects of primary school diminished after adjusting for individual-level childhood risk factors. The further addition of adult risk factors attenuated these childhood effects. After full adjustment there was no effect of the primary school attended for high blood pressure, current smoking, alcohol intake, and obesity, and negligible effects for the other outcomes. CONCLUSIONS: Contrary to our expectations, we found little evidence of any relationship between primary school and adult self-reported health or behaviour. This is surprising given the extent to which characteristics known to be associated with adult health were clustered within schools.     

Does childhood health affect chronic morbidity in later life?

Our analysis examines whether childhood health has long-term and enduring consequences for chronic morbidity. As a part of this analysis, we address two methodological issues of concern in the literature. Is adult height a surrogate for childhood health experiences in modeling chronic disease in later life? And, are the effects of adult socioeconomic status on chronic disease overestimated when childhood health is not accounted for? The analysis is based on a topical module to the third wave of the Health and Retirement Study, a representative survey of Americans aged 55-65 in 1996. Our results support the hypothesis that poor childhood health increases morbidity in later life. This association was found for cancer, lung disease, cardiovascular conditions, and arthritis/rheumatism. The associations were highly persistent in the face of statistical controls for both adult and childhood socioeconomic status. No support was found for using adult height as a proxy for the effects of childhood health experiences. Further, the effects of adult socioeconomic status were not overestimated when childhood health was excluded from the explanatory models. Our results point to the importance of an integrated health care policy based on the premise of maximizing health over the entire life cycle.     

Does maternal nutrition in pregnancy and birth weight influence levels of CHD risk factors in adult life?

The fetal-origins hypothesis suggests that maternal and fetal nutrition can have a profound and sustained impact on the health of the offspring in adult life. Although there is abundant literature reporting on the associations between birth weight and disease risk factors, only a handful of studies have been able to examine the relationship between maternal nutrition in pregnancy with the health of offspring in adult life directly. Between 1942 and 1944, nearly 400 pregnant women were recruited into a dietary study to determine whether the wartime dietary rations were sufficient to prevent nutritional deficiencies. Detailed biochemical and clinical assessments were conducted for each of the women, who were followed-up until after delivery. More than 50 years later, approximately one-quarter of the adult offspring were recruited into a study to explore the possible impact of maternal nutrition in pregnancy on CHD risk factors, including glucose tolerance, blood pressure and components of the lipid profile. Results from the present study provide no evidence to support the hypothesis that birth weight or maternal nutrition in pregnancy are associated with CHD risk factors in adult life.     

Does menopause increase diabetes risk? Strategies for diabetes prevention in midlife women

Menopause is a significant milestone for midlife women. The characteristic changes in sex hormones and associated symptoms mark a time of increased risk for chronic disease, most notably cardiovascular disease. The diabetes epidemic, combined with recent epidemiologic studies linking sex hormone profiles with incident diabetes risk, have recently raised the possibility that the menopause may increase diabetes risk as well. This report reviews studies of menopause and diabetes risk, as well as the potential mechanisms through which menopause might affect traditional and more novel diabetes risk factors. Diabetes risk appears to be more strongly linked with factors associated with chronological aging and sex hormones rather than changes in menopausal status per se. Strategies to reduce diabetes risk, namely lifestyle changes, hormone therapy and other pharmacologic interventions are also discussed vis à vis midlife women and menopause.     

Whose quality of life is it anyway? Discrepancies between youth and parent health-related quality of life ratings in type 1 and type 2 diabetes

Purpose

Health-related quality of life (HRQOL) is a critical diabetes outcome, yet differences between youth and parent-proxy ratings can make interpretation difficult. This study aims to explore potential differences between self- and parent-reports of Pediatric Quality of Life Inventory (PedsQL) scores from youth with type 1 (T1D) or type 2 diabetes (T2D) and to evaluate associations between discrepancies, PedsQL scores, and glycemic control (HbA1c).

Methods

Youth and parents in the SEARCH for Diabetes in Youth Study (T1D: age 5–18, n = 3402; T2D: age 8–18, n = 353) completed the PedsQL Generic and Diabetes Modules, and youth provided a blood sample to assess HbA1c. Discrepancies (youth minus parent PedsQL ratings) were calculated and examined by age and diabetes type, and associations with youth PedsQL scores and HbA1c were evaluated.

Results

Discrepancies existed between youth and parent-proxy reports of generic and diabetes PedsQL scores in T1D and T2D (all p values < 0.01). Higher (more favorable) ratings were reported by youth except for those 5–7-years old, where parents’ scores were higher. When parent-proxy scores were higher, discrepancies were largest when the child reported low PedsQL scores. Higher HbA1c was associated with larger discrepancies (youth scores higher) for adolescents with T1D.

Conclusions

Discrepant PedsQL ratings suggest that parents may often underestimate youths’ HRQOL except in the youngest children. Although examining both reports is optimal, the youth report should be prioritized, particularly for young children with T1D and for adolescents with either T1D or T2D.

     

Does the Belgian diabetes type 2 care trajectory improve quality of care for diabetes patients?

Background

The Belgian care trajectory (CT) for diabetes mellitus type 2 (T2DM), implemented in September 2009, aims at providing integrated, evidence-based, multidisciplinary patient- centred care, based on the chronic care model.The research project ACHIL (Ambulatory Care Health Information Laboratory) studied the adherence of CT patients, in the early phases of CT programme implementation, with CT obligations, their uptake of incentives for self-management, whether the CT programme was targeting the appropriate group of patients, how care processes for these patients evolved over time and whether CT start led to better quality in the processes and outcomes of care.

Methods

This observational study took place in the period 2006–2011 and covered T2DM patients who started a CT between 01/09/2009 and 31/12/2011.Four data sources were used: outcome data, from electronic patient records (EPRs) on all CT patients, provided by general practitioners (GPs); reimbursement process data on all CT patients and clinically comparable patients; and data from a sample of CT patients and clinically comparable patients from an EPR-based regional GP network and a paper-based national GP network, respectively.Through multilevel analysis of cross-sectional and longitudinal data, the effect of CT inclusion on processes and outcome was estimated, controlling for potential confounders.

Results

By the end of 2011, data on 18,250 CT patients had been collected. Approximately 50 % of these CT patients had received reimbursement for a glucometer and nearly 60 % had had at least one encounter with a diabetes educator. The CT programme recruited T2DM patients who had been difficult to control in the past. In the years prior to CT start, there had been a gradual improvement in the follow up of these patients. Moreover, compared to non-CT patients, the proportion of CT patients adhering to the recommended frequency for monitoring of parameters, such as HbA1c, increased significantly around CT start. Some data sources, albeit not all, suggested there had been an improvement in certain outcomes, such as HbA1c, after CT inclusion.

Conclusions

According to this study, CT enrolment is associated with better quality of care processes compared to non-CT patients. This improvement was found in several of the data sources used in this study. However, results on outcome parameters remain inconclusive.

     

Does the type of treatment supporter influence tuberculosis treatment outcomes in Zimbabwe?

Zimbabwe National Tuberculosis Guidelines advise that direct observation of anti-tuberculosis treatment (DOT) can be provided by a family member/relative as a last resort. In 2011, in Nkayi District, of 763 registered tuberculosis (TB) patients, 59 (8%) received health facility-based DOT, 392 (51%) received DOT from a trained community worker and 306 (40%) from a family member/relative. There were no differences in TB treatment outcomes between the three DOT groups, apart from a higher frequency rate of ‘no reported outcomes’ for those receiving family-based DOT. Family members should be trained to use a suitable DOT support package.     

Does vehicle color influence the risk of being passively involved in a collision?

BACKGROUND: Bright- or light-colored vehicles are sometimes regarded as safer because they are presumably more visible. We examined the effect of vehicle color on the risk of being passively involved in a collision. METHODS: This paired case-control study used data from the Spanish database of traffic crashes. We selected those collisions from 1993 to 1999 in which only one of the drivers committed an infraction. The violators constituted the control group; the other drivers formed the case group. Information about the color of the vehicle and other confounding variables was also collected. RESULTS: When white was compared with the remaining colors, a protective estimate was obtained (adjusted odds ratio [aOR] = 0.97; 95% confidence interval = 0.94-1.00). The results were similar for light colors (white plus yellow) compared with all remaining colors (aOR = 0.96; 0.94-0.99). The protective effect of light colors was specifically observed for open roads and under daylight conditions. It was stronger in conditions other than good weather (aOR = 0.91; 0.86-0.99) than in good weather conditions. CONCLUSIONS: Light colors (white and yellow) were associated with a slightly lower risk of being passively involved in a collision, although only under certain environmental conditions.     

Dietary fiber intake and risk of type 2 diabetes: a dose–response analysis of prospective studies

Observational studies suggest an association between dietary fiber intake and risk of type 2 diabetes, but the results are inconclusive. We conducted a meta-analysis of prospective studies evaluating the associations of dietary fiber intake and risk of type 2 diabetes. Relevant studies were identified by searching EMBASE (from 1974 to April 2013) and PubMed (from 1966 to April 2013). The fixed or random-effect model was selected based on the homogeneity test among studies. In addition, a 2-stage random-effects dose–response meta-analysis was performed. We identified 17 prospective cohort studies of dietary fiber intake and risk of type 2 diabetes involving 19,033 cases and 488,293 participants. The combined RR (95 % CI) of type 2 diabetes for intake of total dietary fiber, cereal fiber, fruit fiber and insoluble fiber was 0.81 (0.73–0.90), 0.77 (0.69–0.85), 0.94 (0.88–0.99) and 0.75 (0.63–0.89), respectively. A nonlinear relationship was found of total dietary fiber intake with risk of type 2 diabetes (P _{for nonlinearity} < 0.01), and the RRs (95 % CI) of type 2 diabetes were 0.98 (0.90–1.06), 0.97 (0.87–1.07), 0.89 (0.80–0.99), 0.76 (0.65–0.88), and 0.66 (0.53–0.82) for 15, 20, 25, 30, and 35 g/day. The departure from nonlinear relationship was not significant (P _{for nonlinearity} = 0.72), and the risk of type 2 diabetes decreased by 6 % (RR 0.94, 95 % CI 0.93–0.96) for 2 g/day increment in cereal fiber intake. Findings from this meta-analysis indicate that the intakes of dietary fiber may be inversely associated with risk of type 2 diabetes.     

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.     

Does high vitamin K1 intake protect against bone loss in later life?

The findings of a number of cross-sectional studies suggest benefits of high phylloquinone (vitamin K₁) intake on bone health in later life. Until recently these observational data were supported by the findings of an intervention study that showed a protective role for vitamin K₁ (together with calcium, magnesium, zinc, and vitamin D₃) on bone loss over 3 years in early postmenopausal women. Over the last 18 months, two further important intervention studies have been published, which investigated the effect of vitamin K₁ on bone loss in older subjects. These two studies add to the evidence-base but cast some doubt on the benefits of high vitamin K₁ intake on bone health in later life.     

Role of pancreatic-derived factor in type 2 diabetes: evidence from pancreatic β cells and liver

Pancreatic-derived factor (PANDER) is a cytokine-like protein that is highly expressed in pancreatic islets. In vitro, PANDER pretreatment or viral-mediated overexpression promotes apoptosis of islet β cells. Under conditions of insulin resistance, chronic hyperglycemia potently activates PANDER expression and stimulates the cosecretion of insulin and PANDER in β cells. PANDER binds to the liver cell membrane and induces insulin resistance, resulting in increased gluconeogenesis. Recently, PANDER was found to be expressed in rodent and human liver, and its expression is increased in the liver of diabetic mice and rats. Hepatic overexpression of PANDER promotes lipogenesis in the liver and induces insulin resistance in C57BL/6 mice, whereas the inactivation of hepatic PANDER markedly reduces steatosis, insulin resistance, and hyperglycemia in db/db mice. PANDER deficiency protects mice from high-fat-diet-induced hyperglycemia by decreasing gluconeogenesis in the liver. In summary, PANDER plays an important role in the progression of type 2 diabetes by negatively regulating islet β-cell function and insulin sensitivity in the liver.     

Who is responsible for food risks? The influence of risk type and risk characteristics

The influence of food risk type and risk characteristics on food risk responsibility judgments was studied. A total of 1270 Finnish consumers judged their personal responsibility and the responsibility of three non-personal targets, industry, retail, and society, in relation to six food-related risks. They also evaluated the risks on several psychometric dimensions. The ratings were gathered via internet questionnaire. Industry and society were considered to be most responsible for all risks but the risk of cardiovascular disease, for which personal responsibility was considered to be highest. Judgments of personal controllability predicted personal responsibility judgments, and unnaturalness judgments predicted non-personal targets’ judged responsibility. Personal responsibility judgments were related to different risk dimensions than judgments of non-personal targets’ responsibility.     

The role of early life environmental risk factors in Parkinson disease: what is the evidence?

Parkinson disease (PD) is of unknown but presumably multifactorial etiology. Neuropathologic studies and animal models show that exposure to environmental neurotoxicants can determine progressive damage in the substantia nigra many years before the onset of clinical parkinsonism. Therefore, PD, like other neurologic diseases related to aging, may be determined by exposures present in the environment early during the life span or even during pregnancy. Recent epidemiologic studies have focused on the possible role of environmental risk factors present during adult life or aging. Smoking and coffee drinking have consistently been identified to have protective associations, whereas roles of other risk factors such as pesticide and infections have been reported in some studies but not replicated in others. Both genetic inheritance and sharing of common environment in the same family explain the increased risk of PD of relatives of PD cases compared with relatives of controls in familial aggregation studies. Much evidence indicates that risk factors that have a long latency or a slow effect could be important for late-onset PD. Further epidemiologic studies are warranted in this area.