individuals with CM risk [ 17 , 18 ]. It has been suggested that these pro-inflammatory taxa con- tributes to the evolution of CM risk [ 17 , 18 ].
There are several metabolic mechanisms through which the gut microbiota may contribute to the CM risk. Lipopolysaccharide (LPS) is a known precursor for the development of obesity and insulin resistance[ 19 , 20 ] and an increase in the relative proportion of the bacteria that produce LPS in the gut has been associated with elevated systemic LPS concentration, likely resulting in high inflammation. Strong evidence for the role of LPS and TLR4 signaling in the development of atherosclerotic lesions has been shown, with the gut microbiota considered drivers of these atherosclerotic lesion formations [ 21 , 22 ]. in atherogenesis Trimethylamine N- oxide (TMAO), which derived from microbial trimethylamine metabolism, is also increased in the stool of individuals with elevated CM risk [ 23 , 24 ], although some find the inverse to be true [ 25 ] and one study found an inverse association with cardiac death in African Americans [ 26 ]. Similarly, SCFAs such as propionate, acetate and butyrate produced by bacterial fermen- tation of indigestible fibers, are known to regulate host energy intake, expenditure and storage, decreases their concentrations have been associated with elevated CM risk [ 27 , 28 ]. Finally, specific gut bacteria have also been associated with altered bile acid composition, which also seem to play an important role in diabetes, obesity, non-alcoholic fatty liver disease and other metabolic diseases via the farnesoid X receptor (FXR) and G protein-coupled bile acid receptor (GPCR) signaling pathway [ 29 – 31 ]. These metabolic pathways represent mechanisms through
Chronotype and cardiovascular diseases
Severe circadian misalignment has long been recognized to be a risk factor for the development of cardiovascular diseases ( 108 ). Most of this evidence is derived from studies on different models of shift work, which found that shift workers working during their circadian night are more likely to develop metabolic disturbances ( 109 ). This evidence has been replicated in animal models of shift work, recently reviewed ( 110 ), as well as in human interventions involving experimentally induced circadian misalignment ( 111 , 112 ). More recent research findings suggest that mild circadian misalignment, experienced as minor shifts between the sleep-awake cycle in non–shift workers, is also detrimental to health ( 50 , 113 ). For instance, data from the German MONICA/KORA Myocardial Infarction Registry indicated that specific high-risk subgroups of the population, partic- ularly men, experience a higher risk of acute myocardial infarction during transitions to and from daylight saving time ( 114 ). Although chronotype was not assessed in that study, the authors argued that men are more likely to have an evening chronotype and accumulate sleep debt during the time transition, which may lead to acute myocardial infarction. More recent data from the UK Biobank Project have demonstrated that short sleep duration in adults, particularly in those with a late chronotype, is associated with a greater tendency to engage in behaviors related to cardiovascular risk, including smoking, low intake of fruit and vegetables, and sedentary behavior ( 75 ). An adverse impact of time transitions on sleep has also been reported in adolescents with an evening chronotype ( 115 ).
hypertension) and a precursor of diabetes and cardiovas- cular disease, has also been associated with metals expo- sures in cross-sectional studies [28,29]. Thus far, however, the human evidence is limited and there is little under- standing of the underlying etiology. The underlying patho- physiology connecting the different aspects of metabolic syndrome is an area of active interest and research, but it is clear that adiposity and insulin resistance play an im- portant role . Adipose tissue, as an important endo- crine organ that modulates metabolism, inflammation and endothelial function, has been recognized in the develop- ment of metabolic syndrome, type 2 diabetes, and cardio- vascular disease  and the state of obesity, itself, is an independent risk factor for cardiovascular disease  and type 2 diabetes . However, the existence of “metabolic- ally healthy” obese and “metabolically obese” normal weight phenotypes (31.7% of obese and 23.5% of normal weight adults in NHANES 1999–2004 ) indicate that there is considerable unexplained variation in these associations [35,36] which is not explained by diet and physical activity . Although, others have shown that there is no healthy pattern of increased weight . Given the sheer magni- tude of the obesity, type 2 diabetes, and cardiovascular dis- ease epidemics, it is imperative to consider a potential role of non-traditional risk factors, such as environmental che- micals, to better understand their contribution to the glo- bal disease burden.
Gut microbiota and obesity
The human gut microbiome has been linked to the obesity epidemic [ 24 , 52 – 55 ]. However, animal stud- ies comprise the majority of causative evidence linking changes in microbial composition to the obesity phe- notype (see Table 1 B). In seminal rodent-based work by Backhed et al. [ 52 ], the gut microbiota was observed to regulate the host’s ability to harvest energy from food, thus showing its role in host fat storage [ 52 ]. Sub- sequent experiments suggest that gut microbiota are affected by adiposity (with higher ratios of Firmicutes to Bacteroidetes in ob/ob mice [ 23 ]. Further work has established the potential for a particular gut microbiota ecosystem to impart an obesity phenotype, where the microbiota of ob/ob (a genetic model of obesity) or lean mice where transferred to germ-free mice [ 20 ]. It was also observed that the colonization of germ-free mice with ob/ob mouse-associated gut microbiota resulted in greater weight gain and energy extraction than the colonization with lean mouse-associated gut microbiota [ 21 ]. Providing further direct evidence for the existence of a transmissible obesity microbiota, Ridaura et al. [ 22 ] transplanted uncultured gut microbiota collected from feces from adult female twin pairs, discordant for obe- sity into germ-free mice fed the same diets. Mice receiv- ing the obesity gut microbiota experienced significantly greater increases in adiposity. It was also noted that the fecal biomass from the lean mice was significantly greater compared to the fecal biomass from the obese siblings. It should also be noted that changes in phyla are not always a result of obesity per se, but may simply be a reflection of the macronutrient composition changes [ 56 ].
As suggested by common disease and disorder pathway analyses results, a number of the identified epivariations were correlated with CVD candidate genes. DNA methylation at gene promoter regions is often associated with transcriptional repression due to interactions between DNA methylation, methyl DNA binding proteins, and histone deacetyltransferases. In contrast, promoter hypomethylation is often associated with a euchromatic state and transcriptional permissiveness . Apolipoprotein B (APOB) transcribes and translates into the main Apo lipoprotein of chylomicrons and LDL. LDL is considered as one of the main molecules leading to atherosclerosis and associated with cardiovascular risk . Higher methylation levels in APOB were reported to be associated with an increased risk of having a birth weight below the 50th percentile . The same relationship of methylation levels in APOB and birth weight was found in our study. Lower APOB methylation levels in specific CpGs located on islands were detected in the macrosomia group by 450K. We detected methylation of 399bp DNA surrounding the MVPs in enlarged samples by MASSARRAY and identified the same methylation differences. Delta-like homolog 1 (DLK1), an imprinted gene, is subject to multiple levels of epigenetic dosage control beyond conventional mechanisms of tissue- and temporal specific regulation . Upregulation of DLK1 impairs angiogenesis by inhibiting Endothelial cell (EC) proliferation  and impedes the regenerative response of ECs to the proapoptotic and antiproliferative effects of oxidized LDL . CES1, carboxylesterase 1, encodes a member of the carboxylesterase large family and participates in fatty acyl and cholesterol ester metabolism. An in vitro study showed that overexpression of CES1 in THP-1 macrophages markedly increases the rate of cholesterol efflux. Overexpression of human
OR 'prostaglandin derivative'/de OR 'C reactive protein '/de OR (autacoid* OR chemokine* OR prostaglandin* OR ((inflammat*) NEAR/3 (marker* OR mediator*)) OR 'C reactive protein' OR 'creactive protein' OR crp OR 'c reaction protein'):ab,ti) OR ('anthropometric parameters'/de OR 'body height'/de OR 'body size'/de OR 'head circumference'/de (((body) NEAR/3 (height OR size)) OR 'head circumference' OR (height NEAR/3 age)):ab,ti) OR ('respiratory tract disease'/exp OR 'respiratory function'/exp OR 'lung function test'/exp OR 'cystic fibrosis'/de OR (((respirat* OR breath* OR pulmonar* OR lung* OR airway* OR bronchopulmon*) NEAR/3 (disease* OR function* OR disorder* OR obstruct*)) OR COPD OR bronchitis):ab,ti) OR ('mental disease'/exp OR Epilepsy/exp OR cognition/exp OR 'mental function'/de OR 'brain function'/de OR memory/de OR (((cognit* OR learn* OR brain* OR neurolog* OR mental*) NEAR/3 (disorder* OR disease* OR function* OR develop* OR impair*)) OR memor* OR dyslex* OR (Attention NEAR/3 Defic*) OR adhd OR epilep* OR cognit* OR dement*):ab,ti) OR ('nonalcoholic fatty liver'/de OR ((nonalcoholic OR 'non alcoholic' ) NEAR/3 ('fatty liver' OR steatohepatitis)):ab,ti)) AND (Epidemiology/exp OR 'cohort analysis'/de OR 'prospective study'/de OR 'follow up'/de OR 'longitudinal study'/de OR 'retrospective study'/de OR 'case control study'/de OR 'intervention study'/de OR 'clinical study'/de OR 'clinical trial'/exp OR (((Hazard OR odds OR risk*) NEXT/1 Ratio*) OR ((Prospectiv* OR Populat* OR Observat* OR Retrospect* OR intervent* OR clinical) NEXT/1 (stud* OR trial*)) OR (case* NEAR/3 control*) OR (Cross NEXT/1 section*)):ab,ti) NOT ([animals]/lim NOT [humans]/lim)
by members of the Bcc are diverse. Some of these include pyrrolnitrin, a broad spectrum compound with activity against phytopathogenic fungi and some Gram- positive bacteria, cepacidines A and B which are peptides with high antifungal acitivity, and glidobactins that exhibit broad activity against yeast and fungi, as well as having anti-tumour properties (Vial et al. 2007). Bcc members are also known for their ability to degrade synthetic compounds. This is due to their broad metabolism which can utilise different, and often complex carbon sources. The beneficial properties of the Bcc led the Environmental Protection Agency in America to register certain Bcc strains for commercial use as biopesticides, allowing the reduction of toxic chemical pesticides; however a 1999 risk assessment, investigating the potential pathogenicity of Bcc members, led to a moratorium being placed on any new products containing Bcc strains (Mahenthiralingam et al. 2008). Until more research is undertaken on the risk posed by environmental isolates, the routes of infection, and whether the removal of virulence genes by genetic modification results in a stable non-pathogenic organism, caution should still be taken when considering Bcc strains for use in the agricultural industry.
Investigations of the impact that patent infections by soil-transmitted gastrointestinal nema- tode parasites exert on the composition of the host gut commensal flora are attracting grow- ing interest by the scientific community. However, information collected to date varies across experiments, and further studies are needed to identify consistent relationships between parasites and commensal microbial species. Here, we explore the qualitative and quantitative differences between the microbial community profiles of cohorts of human vol- unteers from Sri Lanka with patent infection by one or more parasitic nematode species (H +), as well as that of uninfected subjects (H-) and of volunteers who had been subjected to regular prophylactic anthelmintic treatment (Ht). High-throughput sequencing of the bacte- rial 16S rRNA gene, followed by bioinformatics and biostatistical analyses of sequence data revealed no significant differences in alpha diversity (Shannon) and richness between groups (P = 0.65, P = 0.13 respectively); however, beta diversity was significantly increased in H+ and Ht when individually compared to H-volunteers (P = 0.04). Among others, bacteria of the families Verrucomicrobiaceae and Enterobacteriaceae showed a trend towards increased abundance in H+, whereas the Leuconostocaceae and Bacteroidaceae showed a relative increase in H- and Ht respectively. Our findings add valuable knowledge to the vast, and yet little explored, research field of parasite—microbiota interactions and will pro- vide a basis for the elucidation of the role such interactions play in pathogenic and immune- modulatory properties of parasitic nematodes in both human and animal hosts.
Notably, besides the similarities shared by Pers ⬍ 12m and Pers ⬎ 12m, the disparity in psAF of short or long duration was also revealed, which may be linked to the maintenance of AF progression. For example, Clostridium bolteae (a species enriched in Pers ⬎ 12m) is a bacterium that has been shown to be overabundant in the intestinal tract of autistic children suffering from gastric intestinal ailments, which produces a conserved speciﬁc capsular polysaccharide (39). Faecalibacterium prausnitzii (a species decreased in Pers ⬎ 12m), is an abundant obligate anaerobe that colonizes during weaning and is thought to maintain colonic health throughout life. This species may be a useful potential biomarker to assist in ulcerative colitis and Crohn’s disease discrim- ination (40). It has been previously revealed that Faecalibacterium prausnitzii induced Toll-like receptor 2 (TLR2) activation, which is linked to enhanced tight junction formation, while its role in enhancing epithelial barrier integrity requires further inves- tigation (41). Meanwhile, Faecalibacterium prausnitzii treatment improved hepatic health and reduced adipose tissue inﬂammation in mice fed a high-fat diet (42). The alterations of the GM were coupled with metabolic phenotype, which was inﬂuenced by interaction with the intestinal bacteria. A 20-year cohort study following ⬎ 74,000 participants revealed that oleic acid (decreased in Pers ⬍ 12m and Pers ⬎ 12m compared with the control) consumption signiﬁcantly reduced the risk for developing cardiovas- cular diseases. Oleic acid prevents coronary heart disease by suppressing oxidative stress, mitigating cardiomyocyte cell damage. In addition, octadecanedioic acid- induced lipotoxicity, as mentioned above, could be antagonized by the unsaturated fatty acid oleic acid (32). Niacin (decreased in Pers ⬎ 12m) is a potent high-density lipoprotein cholesterol-raising drug and has been proposed as an attractive approach to reduce cardiac events in patients with or at risk of atherosclerotic cardiovascular disease (43). Niacin has been used for primary and secondary coronary heart disease prevention for over 40 years. Until recently, clinical trials incorporating niacin as part of an intervention strategy consistently demonstrated reduction in clinical events and lesion improvement (44). Furthermore, recent studies have demonstrated that choline (decreased in Pers ⬎ 12m), an essential dietary nutrient for humans, is required for the synthesis of the neurotransmitter acetylcholine, the methyl group donor betaine, and phospholipids. Therefore, choline is involved in a broad range of critical physiological functions across all stages of the life cycle (45). Notably, a previous study concluded that choline prevents angiotensin II (Ang II)-induced cardiac hypertrophy through inhibition of reactive oxygen species (ROS)-mediated p38 mitogen-activated protein kinase (MAPK) activation as well as regulation of the Ca 2 ⫹ -mediated calcineurin signal
samples, and curative treatment of these infections had no effect on faecal microbiota composition in the short-term (i.e. at 3 weeks after treatment). We chose T. trichiura as the model infection to measure the effects of STH infections on intestinal microbiota because this parasite has been shown to affect immune regulation in humans in previous studies and it resides in the large intestine. Trichuris spp. are natural parasites of a wide variety of different mammalian hosts . Evidence from previous studies indicates that Trichuris infections of animals may modify the intestinal microbiota. Experimental infections with Trichuris suis in 7 pigs showed a disturbed microbiota in the proximal colon at 21  and 53  weeks following infection that was associated with changes in the abundance of approximately 13% of bacterial genera and particularly with declines in the relative abundance of Fibrobacter and Ruminococcus, although these were not reflected in changes in diversity indices at the genus level . Rhesus macaques with idiopathic chronic diarrhoea, an inflammatory bowel disease of monkeys, were infected with T. trichiura ova and although patent infections were not established, there was some evidence of clinical improvement in four out of the five monkeys investigated : T. trichiura infection was associated with a reduction in bacterial attachment to the colonic mucosa 14 weeks after infection but an increase in bacterial diversity with an increase in the abundance of Tenericutes and Bacteroidetes . Such apparent beneficial effects of T. trichiura on diarrhoea could have been mediated through immune mechanisms rather than through changes in microbiota, with the latter being a conse- quence of the resolution of diarrhoea rather than a direct effect of the parasites.
tissue. Obesity on the other hand is characterised by hypertrophy of white adipocytes together with increased release of FA into the circulation due to both elevated basal lipolytic rate as well as a reduced regulated lipolysis response to insulin [3,4]. The decreased response of expanded WAT to insulin can be a result of increased WAT inflammation. For example, extensive WAT hypertrophy stresses adipocytes and induces the secretion of inflammatory proteins (adipokines) which subsequently attract pro-inflammatory leukocytes that also release pro-inflammatory cytokines and chemokines into the circulation [5,6]. In the presence of WAT inflammation, the inflammatory cytokines tumour necrosis factor α (Tnf-α) and interleukin-6 (IL-6) have been shown to directly inhibit the insulin signalling pathway and thereby induce insulin resistance predominately in WAT itself, liver, and muscle [7–10]. The numbers of pro-inflammatory M1 macrophages and cytotoxic T cells in expanded WAT are increased, whereas the numbers of anti-inflammatory M2 macrophages and regulatory T cells are reduced [11,12]. In addition to macrophages and T cells, increased abundance of B cells and neutrophils and reduced abundance of eosinophils are also hallmarks of WAT inflammation [13–15]. This increased pro-inflammatory state in expanded WAT is also associated with the development of glucose intolerance and type 2 diabetes. After a meal, plasma glucose levels rise and in response insulin is released by the pancreas. Insulin acts on its target tissues including muscle, liver and adipose tissues and induces the uptake of glucose by these tissues which subsequently lowers plasma glucose again . However, inhibition of insulin signalling by e.g. dysfunctional expanded WAT leads to hyperglycemia, signalling the pancreas to produce more insulin. Progressive insulin resistance and compensatory increases in insulin production will ultimately result in failure of the pancreas and the development of type 2 diabetes [9,17,18].
Another way to address the sample selection problem is to use a within-subjects design and examine the effects of being married or unmarried on individual offending over time. Stud- ies using these designs have, on the whole, found that being married is associated with lower offending in young adulthood. The weakness of these designs is that they must eliminate rival hypotheses linking “being married” in a given year and offend- ing. While it is easy to control for factors such as income or age, such studies have not adequately controlled for factors such as “maturity” which might cause both successful marriage and desistance from antisocial behavior. In a very complex analysis of the Glueck and Glueck follow-up sample, employing “in- verse probability of treatment weighting” (IPTW) to control for confounds related to selection bias in married subjects as well as within-subjects sources of bias, Sampson, Laub and Wimer (2006) estimated an average reduction of approximately 35% in the odds of committing a crime when a given subject was mar- ried compared to not married. More research employing pro- pensity score matching and within-subjects designs is needed to test the tightly confined research question (is it really being married that changes the behavior?). Nonetheless, marriage as observed in the population, encompassing all the reasons a person gets married and stays married, appears to be associated with lower rates of offending.
Recognized traditional risk factors for CVD include age, sex, family history, hypertension, dysglycemia, dyslipi- demia, and smoking. Newer cardiovascular risk factors include abdominal obesity (measured by waist circum- ference), insulin resistance, infl ammation as measured by high-sensitivity C-reactive protein (hsCRP) levels, lack of consumption of fruits and vegetables, sed- entary lifestyle, and psychosocial stress. While trad- itional parameters are routinely assessed in the clinic, waist circumference should be added to the routine evaluation of cardiovascular risk. In patients whose triglyceride levels are elevated, an apolipoprotein B measurement can replace that of low-density lipopro- tein cholesterol (LDL-C) for the purpose of risk assess- ment and management of CMR.
It is generally accepted that RF signals from cellular telephones do not possess enough energy to break chemical bonds or damage DNA (FCC 1999; NRPB 2000), and some have argued on physical grounds alone that the extremely low intensities and associated low energy from these non-ionizing radiations are not capable of causing cancer, either by initiation or promotion or progression (Moulder et al. 1999; Park 2001). Scientific interest was raised when Lai and Singh (1995) reported increased numbers of DNA breaks in rat brain cells after two hour expo- sures to RF radiation of 2.45 GHz (SAR 0.5-2.0 W/kg). Subsequent studies, however, failed to replicate these findings (Malyapa et al. 1998). Similarly, it was reported that micronuclei were inducible in human lymphocytes in vitro by relatively high power density microwave radiation of 2.45 GHz and 7.7 GHz (Zotti-Martelli et al. 2000). Subsequent studies at cellular telephone frequencies did not replicate these findings and found no evidence for induction of chromosome aberrations or micronuclei in human blood lymphocytes exposed in vitro for 24 h to 835.62 MHz or 847.74 MHz RF radiation at SARs of 4.9 or 5.5 W/kg (Vijayalaxmi et al. 2001a, 2001b). A recent study reported that micronuclei were induced in human lymphocytes in vitro at an average SAR of at least 5.0 W/kg at 837 MHz and1909.8 MHz (Tice et al. 2002). How- ever, these findings were not consistent with several previous ones (Vijayalaxmi et al. 2001a, 2001b) nor were they replicated in a more recent study of C3H 10T (½) cells exposed to RF waves (835.62 MHz or 847.74 MHz) at SARs of 3.2 to 5.1 W/kg (Bisht et al. 2002). It was pos- tulated that the positive findings might be related to thermal effects resulting from hot spots due to significant inhomogeneities in the SAR distributions (Bisht et al. 2002). RF signals in the frequency range of relevance to mobile phones have been judged not to be directly mutagenic and adverse effects from such exposures are predominantly the result of thermal effects caused by high power intensities (Brusick et al. 1998).
All statistical analyses were performed by using SAS software version 9.1 (SAS Institute, Cary, NC). Normal distribution of each cardiometabolic component mea- surement was checked by using a Shapiro- Wilks test in combination with graphical methods. Bivariate analyses between all the variables under study were tested by using a Pearson ’ s correlation. Descriptive characteristics were examined across strength tertiles and between genders and are provided as means, standard errors, and percentages. Differences in these characteristics across strength categories were tested by using linear regression and logistic regression for continuous and categorical variables respectively, after creating appropriate categories and dummy coding for each. Gender-strati ﬁ ed multiple regression analyses were conducted to test the
OBJECTIVES: The purpose of this study was to determine the gender- speci ﬁ c independent association between muscular strength and cardiometabolicrisk clustering in a large cohort (n = 1421) of children. METHODS: Principal component analysis was used to determine the pattern of risk clustering and to derive a continuous aggregate score (MetScore) from various cardiometabolicrisk components: percent body fat (%BF), fasting glucose, blood pressure, plasma triglycerides levels, and HDL-cholesterol. Gender-strati ﬁ ed risk and MetScore were assessed by using general linear models and logistic regression for differences between strength tertiles, as well as independent associations with age, BMI, estimated cardiorespiratory ﬁ tness (CRF), physical activity, and muscular strength (normalized for body mass). RESULTS: In both boys (n = 670) and girls (n = 751), there were signi ﬁ cant differences in cardiometabolic pro ﬁ les across strength tertiles, such that stronger adolescents had lower overall risk. Age, BMI, cardiorespiratory ﬁ tness, physical activity participation, and strength were all individually correlated with multiple risk compo- nents, as well as the overall MetScore. However, in the adjusted model, only BMI ( b = 0.30), physical inactivity ( b = 0.30), and normal- ized strength capacity ( b = – 1.5) emerged as signi ﬁ cant (P , .05) predictors of MetScore. %BF was the strongest loading coef ﬁ cient within the principal component analysis – derived MetScore outcome. CONCLUSIONS: Normalized strength is independently associated with lower cardiometabolicrisk in boys and girls. Moreover, %BF was as- sociated with all cardiometabolicrisk factors and carried the stron- gest loading coef ﬁ cient. These ﬁ ndings bolster the importance of early strength acquisition and healthy body composition in childhood. Pediatrics 2014;133:e896 – e903
This present study presents novel fındings in regard to the relationship between TV and fat mass and depot-specifıc adiposity, utilizing DXA and MRI: the gold standards for these measurements. Having a TV in the bedroom and viewing TV ⬎2 hours/day were each associated with 2 to 2.5 times the odds of being in the top quartile of fat mass, even when adjustments were made for age, gender, eth- nicity, MVPA level, and diet. Similarly, both having a TV in the bedroom and viewing TV ⬎2 hours/day were associated with 2.1 to 2.9 times the odds of being in the top quartile of subcutaneous adipose tissue mass, and viewing TV ⱖ5 hours/day was associated with two times the odds of being in the top quartile of VAT mass. Prior studies supporting the link between TV viewing and higher likelihood of being overweight/obese relied on anthropometric measurements of obesity. 4
Higher perceptions of disorder were not significantly associated with greater
cardiometabolicrisk. It is possible that cohesion is a more enduring social feature of a neighborhood, having more lasting associations with health than disorder, which may fluctuate more over time (our measure of disorder was captured with items such as trash in the streets). Meanwhile, the lack of an association between disorder and health in the present study is inconsistent with some others’ findings (Bowling et al., 2006; Rios et al., 2012; Wen et al., 2005). We believe these disparate findings may be explained both by features of the different samples and specific indices used to operationalize neighborhood hazards. Some previous investigations of health in the context of neighborhood disorder have used fairly racially/ethnically homogeneous samples of adults (e.g. Bowling, et al., 2006). Both the level of neighborhood disorder and residents’ interpretation of signs of disorder may vary across racial and ethnic groups which may be better represented in the present sample. After taking racial/ethnic background into account, the relation between neighborhood disorder and health was not significant, a phenomenon observed by others (Mendes de Leon et al., 2009). Furthermore, other researchers have defined neighborhood hazards with questions asking participants about fights, violence, gang activity, and assaults (e.g., Wen et al., 2005). These items may elicit stronger affective and physiological responses from residents than perceiving trash and vandalism, as was measured in the present study.
Academic Editor: Paul B. Tchounwou
Received: 13 April 2017; Accepted: 5 June 2017; Published: 16 June 2017
Abstract: Cardiovascular disease (CVD) and associated behavioural and metabolic risk factors
constitute a major public health concern at a global level. Many reports worldwide have documented different risk profiles for populations with demographic variations. The objective of this study was to examine geographic variations in the top leading cardio metabolic and behavioural risk factors in Luxembourg, in order to provide an overall picture of CVD burden across the country. The analysis conducted was based on data from the nationwide ORISCAV-LUX survey, including 1432 subjects, aged 18–69 years. A self-reported questionnaire, physical examination and blood sampling were performed. Age and sex-adjusted risk profile maps were generated using multivariate Bayesian geo-additive regression models, based on Markov Chain Monte Carlo techniques and were used to evaluate the significance of the spatial effects on the distribution of a range of cardio metabolic risk factors, namely smoking, high body mass index (BMI), high blood pressure, high fasting plasma glucose, alcohol use, high total cholesterol, low glomerular filtration rate, and physical inactivity. Higher prevalence of smoking was observed in the northern regions, higher overweight/obesity and abdominal obesity clustered in the central belt, whereas hypertension was spotted particularly in the southern part of the country. Maps revealed that subjects residing in Luxembourg canton were significantly less likely to be hypertensive or overweight/obese, whereas they were less likely to practice physical activity of ≥8000 Metabolic Equivalent of Task (MET)-min/week. These patterns were also observed at the municipality level in Luxembourg. Statistically, there were non-significant spatial patterns regarding smoking, diabetes, total serum cholesterol and low glomerular filtration rate risk distribution. This comprehensive risk profile mapping showed remarkable geographic variations in cardio metabolic and behavioural risk factors. Considering the prominent burden of CVD this research provides opportunities for tailored interventions and may help to better fight against this escalating public health problem.