Key Environmental Risk Factors Research Articles

Household factors associated with infant and under-five mortality in sub-Saharan Africa countries

BackgroundChild mortality has become a prominent public health issue in sub-Saharan Africa (SSA). The mortality rates can in part be translated to how communities meet the health needs of children and address key household and environmental risk factors. Though discussions on the trends and magnitude of child mortality continue as to strategize for a lasting solution, large gap exists specifically in family characteristics associated with child death. Moreover, household dynamics of child mortality in SSA is under researched despite the fact that mortality rates remain high. This study aimed to examine the influence of household structure on child mortality in SSA.MethodsSecondary data from birth histories in recent Demographic and Health Survey (DHS) in 35 SSA countries were used in this study. The total sample data of children born in the 5 years prior to the surveys were 384,747 births between 2008 and 2017. Unadjusted and adjusted Cox proportional hazard regression model was fitted to model infant and under-five mortality. The measure of association was hazard ratio (HR) with 95% confidence interval (CI). Statistical test was conducted at p < 0.05 level of significance.ResultsTotal infant mortality rates were highest in Sierra Leone (92 deaths per 1000 live births), Chad (72 deaths per 1000 live births) and Nigeria (69 deaths per 1000 live births), respectively. Furthermore, total rates of under-five mortality across 35 SSA countries were highest in Cameroon (184 deaths per 1000 live births), Sierra Leone (156 deaths per 1000 live births) and Chad (133 deaths per 1000 live births). The risk of infant mortality was higher in households of polygyny, compared with households of monogyny (HR = 1.23; CI 1.16, 1.29). Households with large number of children (3–5 and ≥ 6) had higher risk of infant mortality, compared with those with 1–2 number of children. Infants from mothers with history of multiple union had 16% increase in the risk of infant mortality, compared with those from mothers from only one union (HR = 1.16; CI 1.09, 1.24). Furthermore, under-five from female household headship had 10% significant reduction in the risk of mortality, compared with those from male household headship (HR = 0.90; CI 0.84, 0.96). The risk of under-five mortality was higher in households of polygyny, compared with monogyny (HR = 1.33; CI 1.28, 1.38). Households with large number of children (3–5 and ≥ 6) had higher risk of under-five mortality, compared with those with 1–2 number of children ever born. Under-five from mothers with history of multiple union had 30% increase in the risk of mortality, compared with those from mothers from only one union (HR = 1.30; CI 1.24, 1.36).ConclusionHousehold structure significantly influences child mortality in SSA. Knowledge of drivers of infant and child death is crucial in health policy, programmes designs and implementation. Therefore, we suggest that policies to support strong healthy families are urgently needed to improve children’s survival.

Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights.

The incidence of obesity and colorectal cancer (CRC) has risen rapidly in recent decades. More than 650 million obese and 2 billion overweight individuals are currently living in the world. CRC is the third most common cancer. Obesity is regarded as one of the key environmental risk factors for the pathogenesis of CRC. In the present review, we mainly focus on the epidemiology of obesity and CRC in the world, the United States, and China. We also summarize the molecular mechanisms linking obesity to CRC in different aspects, including nutriology, adipokines and hormones, inflammation, gut microbiota, and bile acids. The unmet medical needs for obesity-related CRC are still remarkable. Understanding the molecular basis of these associations will help develop novel therapeutic targets and approaches for the treatment of obesity-related CRC.

Posttraumatic stress disorder and breast cancer: Risk factors and the role of inflammation and endocrine function.

A breast cancer diagnosis can be a life-changing and stressful experience that can lead to chronic mental health conditions such as posttraumatic stress disorder (PTSD). Greater than one-third of patients initially diagnosed with PTSD after a diagnosis of breast cancer continue to have persistent or worsening PTSD symptoms after 4years. An emerging body of literature has indicated several key environmental and biological risk factors for PTSD among survivors of breast cancer. Well-recognized risk factors include having a history of childhood trauma, being nonwhite, obesity, younger age at the time of diagnosis, diagnosis with a higher stage of breast cancer, and short time since treatment. Of the emerging risk factors related to fear circuitry in the brain, 2 pathways of particular importance are the stress-driven activation of inflammatory pathways and the long-term effect of antiendocrine therapies. These central and peripheral responses during and after stress exposure are important because increased fear and anxiety can lead to the maintenance of PTSD and worse patient outcomes. Given the poor outcomes associated with PTSD and the high prevalence of breast cancer in women, more research to identify those women at heightened risk of PTSD after breast cancer is warranted to reduce the number of diagnoses and lessen the negative impact of this chronic mental health condition.

Laboratory Comparison of Low-Cost Particulate Matter Sensors to Measure Transient Events of Pollution.

Airborne particulate matter (PM) exposure has been identified as a key environmental risk factor, associated especially with diseases of the respiratory and cardiovascular system and with almost 9 million premature deaths per year. Low-cost optical sensors for PM measurement are desirable for monitoring exposure closer to the personal level and particularly suited for developing spatiotemporally dense city sensor networks. However, questions remain over the accuracy and reliability of the data they produce, particularly regarding the influence of environmental parameters such as humidity and temperature, and with varying PM sources and concentration profiles. In this study, eight units each of five different models of commercially available low-cost optical PM sensors (40 individual sensors in total) were tested under controlled laboratory conditions, against higher-grade instruments for: lower limit of detection, response time, responses to sharp pollution spikes lasting <1 , and the impact of differing humidity and PM source. All sensors detected the spikes generated with a varied range of performances depending on the model and presenting different sensitivity mainly to sources of pollution and to size distributions with a lesser impact of humidity. The sensitivity to particle size distribution indicates that the sensors may provide additional information to PM mass concentrations. It is concluded that improved performance in field monitoring campaigns, including tracking sources of pollution, could be achieved by using a combination of some of the different models to take advantage of the additional information made available by their differential response.

Environmental Risk Factors and Geographic Distribution of Severe Fever with Thrombocytopenia Syndrome in Jiangsu Province, China

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging natural focus, tick-borne disease caused by a novel bunyavirus named SFTS virus (SFTSV). The main purpose of this study was to analyze the environmental risk factors and geographic distribution of SFTS natural foci in Jiangsu Province. A retrospective space-time analysis by SaTScan software was used to detect clusters at the town level. The maximum entropy modeling method was applied to construct the ecological niche model and analyze the environmental risk factors, and then to draw the predicted risk map. The performance of the model was assessed using the area under the curve (AUC) and known occurrence locations. During the years 2010-2016, a total of 140 laboratory-confirmed indigenous SFTS cases occurred in Jiangsu Province, with 66 occurrence locations. The reported number of SFTS cases increased year by year and SFTS cases occurred from April to October with a peak between May and August each year. Three clusters detected by space-time scan statistical analysis were connected together and shared the similar ecological environmental characteristic of hilly landscape. Fifteen environmental variables with different percent contribution can influence the ecological niche model in different degrees, whereas slope (suitable range: 0.1-4) and maximum temperature of warmest month (suitable range: 32.8-34.2°C) as the key environmental factors contributed 46.1% and 23.2%, respectively. The model had high accuracy on prediction with the averaged training AUC of 0.926. Within a predicted risk map, potential areas at high risk and 10 previously unidentified endemic regions were recognized. The distribution of SFTS natural foci was under the influence of multidimensional environmental factors. Slope and maximum temperature of warmest month were the key environmental risk factors. These results provide a valuable basis for the selection of prevention and control strategies, and the identification of potential risk areas.

Correlation Between Smoking and Passive Smoking with Multiple Sclerosis and the Underlying Molecular Mechanisms.

Multiple sclerosis (MS) is a chronic immune-mediated disease of the spinal cord and brain. Many studies have shown that smoking and passive smoking are key environmental risk factors for MS.Here, we provide an overview of the human leukocyte antigen (HLA) gene studies on smoking and MS risk, and we discuss recent studies on between epigenetics and smoking-induced MS. In addition, in this review we also summarize current research advances in biological pathways and smoking-induced MS.This review provides an overview of studies on the association between smoking, passive smoking, and MS susceptibility, and the underlying molecular mechanism.

22 - MOLECULAR GENETIC ANALYSIS SUBDIVIDED BY ADVERSITY EXPOSURE SUGGESTS ETIOLOGIC HETEROGENEITY IN MAJOR DEPRESSION

Background The extent to which Major Depression (MD) is the outcome of a single biological mechanism or represents a final common pathway of multiple disease processes remains uncertain. We suggest that genetic approaches can identify etiologic heterogeneity in MD by dividing patients on their experience of major adverse events. Methods Data are from China, Oxford, and VCU Experimental Research on Genetic Epidemiology (CONVERGE), a study of Han Chinese women with recurrent MD aimed at identifying genetic risk factors for MD in a rigorously ascertained cohort carefully assessed for key environmental risk factors (n = 9599). To detect etiologic heterogeneity, genome-wide association studies (GWAS), heritability analyses, and gene-by-environment interaction analyses were performed. Results GWAS stratified by exposure to adversity revealed three novel loci associated with MD only in subjects with no history of adversity. Significant interactions are seen between adversity and genotype at all three loci and 13.2% of MD liability can be attributed to genome-wide interaction with adversity exposure. The genetic risk in MD for samples who reported major adverse life events (26%) is partially shared with that in samples who did not (74%) (genetic correlation = +0.64). Together with results from simulation studies, these findings suggest etiologic heterogeneity within MD as a function of environmental exposures. Discussion The genetic contributions to MD in women may differ in those with and without major adverse life events. Results have implications for the molecular dissection of MD and other complex psychiatric and biomedical diseases.

Environmental public health risks in European metropolitan areas within the EURO-HEALTHY project

Urban areas in Europe are facing a range of environmental public health challenges, such as air pollution, traffic noise and road injuries. The identification and quantification of the public health risks associated with exposure to environmental conditions is important for prioritising policies and interventions that aim to diminish the risks and improve the health of the population. With this purpose in mind, the EURO-HEALTHY project used a consistent approach to assess the impact of key environmental risk factors and urban environmental determinants on public health in European metropolitan areas. A number of environmental public health indicators, which are closely tied to the physical and built environment, were identified through stakeholder consultation; data were collected from six European metropolitan areas (Athens, Barcelona, Lisbon, London, Stockholm and Turin) covering the period 2000–2014, and a health impact assessment framework enabled the quantification of health effects (attributable deaths) associated with these indicators. The key environmental public health indicators were related to air pollution and certain urban environmental conditions (urban green spaces, road safety). The air pollution was generally the highest environmental public health risk; the associated number of deaths in Athens, Barcelona and London ranged between 800 and 2300 attributable deaths per year. The number of victims of road traffic accidents and the associated deaths were lowest in the most recent year compared with previous years. We also examined the positive impacts on health associated with urban green spaces by calculating reduced mortality impacts for populations residing in areas with greater green space coverage; results in Athens showed reductions of all-cause mortality of 26 per 100,000 inhabitants for populations with benefits of local greenspace. Based on our analysis, we discuss recommendations of potential interventions that could be implemented to reduce the environmental public health risks in the European metropolitan areas covered by this study.

Carbon Metabolism Characteristics of the Karst Soil Microbial Community for Pb-Zn Mine Tailings

BIOLOG and 18S rRNA PCR-DGGE methods were used to estimate the characteristics of carbon source metabolism of the soil microbial community as well as the relationship between soil fungi and soil organic carbon in different karst land use types (corn field, citrus field, and paddy field) contaminated by Pb-Zn tailings at Sidi Village, Yangshuo, Guangxi Zhuang Autonomous Region, SW China. It was found that the concentrations of Pb, Zn, Cu, and Cd were highest in the paddy field, followed by the corn field, citrus field, and control group (dry field). In addition, the geo-accumulation index indicated that the heavy metal pollution at this area was caused by Pb and Cd and that Cd was the key environmental risk factor. With the Pb-Zn tailings, there was low microbial biomass carbon, biological entropy, and microbial carbon source metabolism in the soil samples. The highest soil organic carbon and heavy metal concentrations were found in the paddy field, followed by the corn field and citrus field. According to the DDGE results, it was found that Pycnoporus sp. ZW02.30 was found in control group soils, Fusarium solani and Fusarium oxysporum were found in the corn field and citrus field, and Penicillium decumbens was found in citrus field. These were involved in the degradation of sugars, such as starch, cellulose, hemicellulose, and lignin. However, the fungi were not found in the paddy field. Based on the low functional diversity of the soil microbial community and biological entropy as well as the high soil organic carbon concentration in the paddy field, it was concluded that soil microbial carbohydrate metabolism and the mineralization rate of the soil organic carbon was controlled by soil microorganisms, especially fungi, in different land use soils in the karst area contaminated by Pb-Zn tailings.

Molecular Genetic Analysis Subdivided by Adversity Exposure Suggests Etiologic Heterogeneity in Major Depression.

The extent to which major depression is the outcome of a single biological mechanism or represents a final common pathway of multiple disease processes remains uncertain. Genetic approaches can potentially identify etiologic heterogeneity in major depression by classifying patients on the basis of their experience of major adverse events. Data are from the China, Oxford, and VCU Experimental Research on Genetic Epidemiology (CONVERGE) project, a study of Han Chinese women with recurrent major depression aimed at identifying genetic risk factors for major depression in a rigorously ascertained cohort carefully assessed for key environmental risk factors (N=9,599). To detect etiologic heterogeneity, genome-wide association studies, heritability analyses, and gene-by-environment interaction analyses were performed. Genome-wide association studies stratified by exposure to adversity revealed three novel loci associated with major depression only in study participants with no history of adversity. Significant gene-by-environment interactions were seen between adversity and genotype at all three loci, and 13.2% of major depression liability can be attributed to genome-wide interaction with adversity exposure. The genetic risk in major depression for participants who reported major adverse life events (27%) was partially shared with that in participants who did not (73%; genetic correlation=+0.64). Together with results from simulation studies, these findings suggest etiologic heterogeneity within major depression as a function of environmental exposures. The genetic contributions to major depression may differ between women with and those without major adverse life events. These results have implications for the molecular dissection of major depression and other complex psychiatric and biomedical diseases.

LPG fuel subsidies in Latin America and the use of solid fuels to cook

The use of solid fuels (USF) for cooking is a key environmental health risk factor, affecting more than 2.8 billion people globally. The Sustainable /Development Goal seven (SDG7) aspires to ensure access to affordable, reliable, sustainable and modern energy for all by 2030. This will require transition toward modern cooking fuels such as Liquefied Petroleum Gas (LPG) and electricity. In Latin American and the Caribbean (LAC), 90 million people still rely on solid fuels for cooking. Access and price have been identified as the main factors that limit substitution of solid fuels by clean fuels.In this paper, we present an exploratory analysis of the effects of subsidy policies for LPG in reducing USF in LAC countries when controlling for indicators of socioeconomic development and urbanization. In LAC, subsidies to LPG have substantially contributed to accelerate the transition from USF to clean fuels for cooking. Targeted subsidies should be considered as a policy option to implement the SDG7 on clean energy. Making clean energy accessible to all has the co-benefits of preventing diseases and premature deaths. Understanding the transition processes from USF to cleaner fuels made by LAC countries can better inform policy making in other regions.

EVALUATING KEY ENVIRONMENTAL RISK FACTORS FOR POLLUTION AT INTERNATIONAL PORTS IN TAIWAN

UDC 629.5:614.7:627.74 Professional paper Summary The main purpose of this paper is to use the fuzzy analytic hierarchy process (FAHP) approach to evaluate the key environmental risk factors for pollution at international ports in Taiwan. Relying on the literature and experts’ opinions, a hierarchical structure with three risk aspects and thirteen risk factors is first constructed, and a FAHP model then proposed. Based on data from the AHP experts’ questionnaires, we use the FAHP approach to determine key environmental risk factors. Finally, the results show that: (1) Air pollution is the most important aspect of environmental pollution at international ports in Taiwan. (2) In order of relative importance, the top five key environmental risk factors for pollution at international ports in Taiwan are the oil leaks from ships, volatile organic compounds (VOCs), exhaust emissions from ships at berth, harmful coatings on ships' hulls, and ships' failure to use lowpollution fuel. Furthermore, some discussions are provided for port authority in Taiwan.

Unified theory of Alzheimer's disease (UTAD): implications for prevention and curative therapy.

The aim of this review is to propose a Unified Theory of Alzheimer’s disease (UTAD) that integrates all key behavioural, genetic and environmental risk factors in a causal chain of etiological and pathogenetic events. It is based on three concepts that emanate from human’s evolutionary history: (1) The grandmother-hypothesis (GMH), which explains human longevity due to an evolutionary advantage in reproduction by trans-generational transfer of acquired knowledge. Consequently it is argued that mental health at old-age must be the default pathway of humans’ genetic program and not development of AD. (2) Therefore, mechanism like neuronal rejuvenation (NRJ) and adult hippocampal neurogenesis (AHN) that still function efficiently even at old age provide the required lifelong ability to memorize personal experiences important for survival. Cumulative evidence from a multitude of experimental and epidemiological studies indicate that behavioural and environmental risk factors, which impair productive AHN, result in reduced episodic memory performance and in reduced psychological resilience. This leads to avoidance of novelty, dysregulation of the hypothalamic–pituitary–adrenal (HPA)-axis and cortisol hypersecretion, which drives key pathogenic mechanisms of AD like the accumulation and oligomerization of synaptotoxic amyloid beta, chronic neuroinflammation and neuronal insulin resistance. (3) By applying to AHN the law of the minimum (LOM), which defines the basic requirements of biological growth processes, the UTAD explains why and how different lifestyle deficiencies initiate the AD process by impairing AHN and causing dysregulation of the HPA-axis, and how environmental and genetic risk factors such as toxins or ApoE4, respectively, turn into disease accelerators under these unnatural conditions. Consequently, the UTAD provides a rational strategy for the prevention of mental decline and a system-biological approach for the causal treatment of AD, which might even be curative if the systemic intervention is initiated early enough in the disease process. Hence an individualized system-biological treatment of patients with early AD is proposed as a test for the validity of UTAD and outlined in this review.

Decline of cell viability and mitochondrial activity in mouse skeletal muscle cell in a hypomagnetic field.

Hypomagnetic field (HMF), one of the key environmental risk factors for astronauts traveling in outer space, has previously been shown to repress locomotion of mammalians. However, underlying mechanisms of how HMF affects the motor system remains poorly understood. In this study, we created an HMF (<3 μT) by eliminating geomagnetic field (GMF, ∼50 μT) and exposed primary mouse skeletal muscle cells to this low magnetic field condition for a period of three days. HMF-exposed cells showed a decline in cell viability relative to GMF control, even though cells appeared normal in terms of morphology and survival rate. After a 3-day HMF-exposure, glucose consumption of skeletal muscle cells was significantly lower than GMF control, accompanied by less adenosine triphosphate (ATP) and adenosine diphosphate (ADP) content and higher ADP/ATP ratio. In agreement with these findings, mitochondrial membrane potential of HMF-exposed cells was also lower, whereas levels of cellular Reactive Oxygen Species were higher. Moreover, viability and membrane potential of isolated mitochondria were reduced after 1 h HMF-exposure in vitro. Our results indicate that mitochondria can directly respond to HMF at functional level, and suggest that HMF-induced decline in cell functionality results from a reduction in energy production and mitochondrial activity.

Abstract MP82: The Effect of Nicotinic Acetylcholine Receptor Genes CHRNA3/5 on Thoracic Aortic Calcium is Mediated by Smoking

Introduction: Coronary artery calcium (CAC) and thoracic aortic calcium (TAC), markers of subclinical atherosclerosis, have been shown to strongly correlate with the amount of atheromatous plaque and subsequently predict future coronary disease events and mortality. CAC and TAC are complex heritable traits with both genetic and environmental risk factors such as cigarette smoking. We investigated the role of smoking, a key environmental risk factor, as a mediator of the genetic risk of subclinical atherosclerosis in the COPDGene study. Hypothesis: We hypothesized that smoking will mediate a portion of the genome-wide significant SNPs with subclinical atherosclerosis as measured by TAC and CAC. Methods: We performed genome wide genotyping of common and rare variants in COPDGene, a study of 10,192 current and former smokers with at least 10 pack-years of smoking history. CAC and TAC were measured using high dose, inspiration chest CT scans, following an established protocol in 8,739 individuals (6,150 non-Hispanic Whites and 2,589 African Americans). Mediation analysis, using the significant SNPs from the GWA of common and rare variants, was performed using R software adjusting for genetic ancestry using principal components as well as recognized risk factors (age, gender, BMI, diabetes, high blood pressure, steroid use, high cholesterol, and presence of a coronary stent). We used the log transformation of CAC plus 1 and the log transformation of TAC plus 1 as the quantitative phenotypes. Results: There were 3 SNPs on chromosome 15q25 [CHRNA5/3] achieving genome-wide significance with TAC in non-Hispanic Whites, with the most significant result being rs951266 (p= 3.074e-8). We previously replicated 9 SNPs on chromosome 9 [CDKN2B-AS1] reaching genome-wide significance with CAC in non-Hispanic Whites. In African Americans, no genome-wide significant associations were identified. Given these findings, we tested for mediation of these genetic signals by pack-years of smoking among non-Hispanic Whites in the COPDGene study. Pack-years of smoking history was a significant mediator of CHRNA5/3 [rs951266] on TAC (p &lt;0.001, 13% indirect effect), while smoking was not a significant mediator of CDKN2B-AS13 on CAC (p =0.58). Conclusions: The nicotinic acetylcholine receptor genes on chromosome 15 (CHRNA5/3) were significantly associated with thoracic aortic calcium in this cohort of heavy smokers. Cigarette smoking mediates this genetic risk for subclinical atherosclerosis and may offer an avenue for intervening on the genetic susceptibility to coronary artery disease.

Bayesian Geostatistical Analysis and Ecoclimatic Determinants of Corynebacterium pseudotuberculosis Infection among Horses.

Kansas witnessed an unprecedented outbreak in Corynebacterium pseudotuberculosis infection among horses, a disease commonly referred to as pigeon fever during fall 2012. Bayesian geostatistical models were developed to identify key environmental and climatic risk factors associated with C. pseudotuberculosis infection in horses. Positive infection status among horses (cases) was determined by positive test results for characteristic abscess formation, positive bacterial culture on purulent material obtained from a lanced abscess (n = 82), or positive serologic evidence of exposure to organism (≥1:512)(n = 11). Horses negative for these tests (n = 172)(controls) were considered free of infection. Information pertaining to horse demographics and stabled location were obtained through review of medical records and/or contact with horse owners via telephone. Covariate information for environmental and climatic determinants were obtained from USDA (soil attributes), USGS (land use/land cover), and NASA MODIS and NASA Prediction of Worldwide Renewable Resources (climate). Candidate covariates were screened using univariate regression models followed by Bayesian geostatistical models with and without covariates. The best performing model indicated a protective effect for higher soil moisture content (OR = 0.53, 95% CrI = 0.25, 0.71), and detrimental effects for higher land surface temperature (≥35°C) (OR = 2.81, 95% CrI = 2.21, 3.85) and habitat fragmentation (OR = 1.31, 95% CrI = 1.27, 2.22) for C. pseudotuberculosis infection status in horses, while age, gender and breed had no effect. Preventative and ecoclimatic significance of these findings are discussed.

Paleolithic hunter-gatherers’ dietary patterns: Implications and consequences

The human diet has passed through several revolutionary changes since the introduction of agriculture, which has led to substantial modifications in individuals’ nutrition behavior. Overwhelming evidence supporting that diet is a key environmental risk factor affecting the now rampant incidence of the diseases of affluence such as obesity, type 2 diabetes mellitus, cardiovascular diseases, and certain types of cancer. Findings on the health implications of low carbohydrate-high protein diet are inconsistent and controversial. Unlike modern humans, it was argued that the eating patterns of the Paleolithic hunter-gatherers could have beneficial effects on human health by reducing diet-induced chronic lifestyle diseases. Hence, the objective of this review was to outline the main aspects of Paleolithic hunter-gatherers’ dietary patterns and its main long-term health consequences. Paleolithic diet is based on the assumption that our hunter-gatherer ancestors were nourished on low carbohydrate-high protein diet. Yet, the majority of literature on Paleolithic diet is anecdotal and reflects two opposite viewpoints. First, advocates and proponents argued that human’s genome could have been modified a little since the early stages of agriculture. Thus, genetically, humans remain Stone Agers adapted for a Paleolithic dietary regimen. As such, consuming a diet similar to that consumed during the Paleolithic era would be more compatible with our genetic makeup and might reduce the occurrence of diet-related lifestyle diseases. Second, critics asserted that the Paleolithic dietary recommendations and restrictions are not evidence-based. Adherents of Paleolithic nutrition claimed that modern populations who maintained Paleolithic lifestyle are totally free of the diseases of affluence. Nonetheless, information about the Paleolithic diet have been drawn from studies of surviving hunter-gatherer populations, archeological records, and analysis of wild plants and animals plus other methods. Recommendations of the Paleolithic nutrition are not based on interventional studies, thus the adoption of which could have negative health consequences. Hence, before adopting low carbohydrate-high protein diet, it seems logical to undertake a well designed population-based longitudinal studies to evaluate the long-term health consequences of the Paleolithic nutrition.

Impact of childhood life events and childhood trauma on the onset and recurrence of depressive and anxiety disorders.

To investigate the effect of childhood life events and childhood trauma on the onset and recurrence of depressive and/or anxiety disorders over a 2-year period in participants without current psychopathology at baseline. Longitudinal data in a large sample of participants without baseline DSM-IV depressive or anxiety disorders (n = 1,167, aged 18 to 65 years; assessed between 2004-2007) were collected in the Netherlands Study of Depression and Anxiety (NESDA). Childhood life events and childhood trauma were assessed at baseline with a semistructured interview. The Composite International Diagnostic Interview, based on DSM-IV criteria, was used to diagnose first onset or recurrent depressive and/or anxiety disorders over a 2-year period. At baseline, 172 participants (14.7%) reported at least 1 childhood life event, and 412 (35.3%) reported any childhood trauma. During 2 years of follow-up, 226 participants (19.4%) developed a new (n = 58) or recurrent (n = 168) episode of a depressive and/or anxiety disorder. Childhood life events did not predict the onset and recurrence of depressive or anxiety disorders. Emotional neglect and psychological, physical, and sexual abuse were all associated with an increased risk of first onset and recurrence of either depressive or comorbid disorders (P < .001), but not of anxiety disorders. In multivariate models, emotional neglect was the only significant independent predictor of first onset and recurrence of any depressive or comorbid disorder (P = .002). These effects were primarily mediated by the severity of (subclinical) depressive symptoms at baseline and, to a lesser extent, by a prior lifetime diagnosis of a depressive and/or anxiety disorder. Childhood maltreatment is a key environmental risk factor, inducing vulnerability to develop new and recurrent depressive and comorbid anxiety and depressive episodes.

Participatory risk mapping of malaria vector exposure in northern South America using environmental and population data

Malaria elimination remains a major public health challenge in many tropical regions, including large areas of northern South America. In this study, we present a new high spatial resolution (90 × 90 m) risk map for Colombia and surrounding areas based on environmental and human population data. The map was created through a participatory multi-criteria decision analysis in which expert opinion was solicited to determine key environmental and population risk factors, different fuzzy functions to standardize risk factor inputs, and variable factor weights to combine risk factors in a geographic information system. The new risk map was compared to a map of malaria cases in which cases were aggregated to the municipio (municipality) level. The relationship between mean municipio risk scores and total cases by muncipio showed a weak correlation. However, the relationship between pixel-level risk scores and vector occurrence points for two dominant vector species, Anopheles albimanus and Anopheles darlingi, was significantly different (p < 0.05) from a random point distribution, as was a pooled point distribution for these two vector species and Anopheles nuneztovari. Thus, we conclude that the new risk map based on expert opinion provides an accurate spatial representation of risk of potential vector exposure rather than malaria transmission as shown by the pattern of malaria cases, and therefore it may be used to inform public health authorities as to where vector control measures should be prioritized to limit human-vector contact in future malaria outbreaks.

Prenatal immune activation and subsequent peripubertal stress as a new model of schizophrenia

Evaluation of: Giovanoli S, Engler H, Engler A et al. Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice. Science 339(6123), 1095–1099 (2013).Epidemiological studies show that maternal viral infection during pregnancy plays a key role in the etiology of neurodevelopmental disorders, such as schizophrenia and autism. Prenatal maternal immune activation and peripubertal psychological stress are key environmental risk factors for neurodevelopmental disorders. Viral mimic polyriboinosinic-polyribocytidylic acid is known to act as a Toll-like receptor-3 agonist. Polyriboinosinic-polyribocytidylic acid has been typically used to establish this rodent model of prenatal immune activation. Recently, Giovanoli et al. reported on a new neurodevelopmental model of schizophrenia based on combined prenatal immune activation and peripubertal stress. In this report, we place these findings into context and discuss their significance.