Trends in dietary intake in Switzerland, 1999 to 2009.

OBJECTIVE: To assess nutrition trends of the Geneva population for the period 1999-2009. DESIGN: Bus Santé Geneva study, which conducts annual health surveys in random samples of the Geneva population. Dietary intake was assessed using a validated FFQ and trends were assessed by linear regression. SETTING: Population-based survey. SUBJECTS: Data from 9283 participants (50% women, mean age 51·5 (sd 10·8) years) were analysed. RESULTS: In both genders total energy intake decreased from 1999 to 2009, by 2·9% in men and by 6·3% in women (both trends P < 0·005). Vegetable protein and total carbohydrate intakes, expressed as a percentage of total energy intake, increased in women. MUFA intake increased while SFA, PUFA and alcohol intakes decreased in both genders. Intakes of Ca, Fe and carotene decreased in both genders. No changes in fibre, vitamin D and vitamin A intakes were found. Similar findings were obtained after excluding participants with extreme dietary intakes, except that the decreases in SFA, vegetable protein and carbohydrate were no longer significant in women. CONCLUSIONS: Between 1999 and 2009, a small decrease in total energy intake was noted in the Geneva population. Although the decrease in alcohol and SFA intakes is of interest, the decrease in Ca and Fe intakes may have adverse health effects in the future.

Commentary : beyond vague causal effect estimation of obesity on health outcomes

In the current issue of epidemiology, Danaei and colleagues elegantly estimated both the direct effect and the indirect effect-that is, the effect mediated by blood pressure, cholesterol, glucose, fibrinogen, and high-sensitivity C-reactive protein-of body mass index (BMI) on the risk of coronary heart disease (CHD). they analyzed data from 9 cohort studies including 58,322 patients and 9459 CHD events, with baseline measurements between 1954 and 2001. Using sophisticated and cutting-edge methods for direct and indirect effect estimations, the authors estimated that half of the risk of overweight and obesity would be mediated by blood pressure, cholesterol, and glucose. Few additional percentage points of the risk would be mediated by fibrinogen and hs-CRP. How should we understand these estimates? Can we say that if obese persons reduce their body weight and reach a normal body weight, their excess risk of CHD would be reduced by half through an improvement in these mediators and by half through the reduction in BmI itself? Is that also true if these individuals are prevented from becoming obese in the first place? Can we also conclude that if these mediators are well controlled in obese individuals through other means than a body weight reduction, their excess risk of CHD would be reduced by half? Let us confront these estimates with observations from studies evaluating 2 interventions to reduce body weight, that is, bariatric surgery in patients with severe obesity and intensive lifestyle intervention in overweight patients with diabetes

PI3Kγ within a nonhematopoietic cell type negatively regulates diet-induced thermogenesis and promotes obesity and insulin resistance.

Obesity is associated with a chronic low-grade inflammation, and specific antiinflammatory interventions may be beneficial for the treatment of type 2 diabetes and other obesity-related diseases. The lipid kinase PI3Kγ is a central proinflammatory signal transducer that plays a major role in leukocyte chemotaxis, mast cell degranulation, and endothelial cell activation. It was also reported that PI3Kγ activity within hematopoietic cells plays an important role in obesity-induced inflammation and insulin resistance. Here, we show that protection from insulin resistance, metabolic inflammation, and fatty liver in mice lacking functional PI3Kγ is largely consequent to their leaner phenotype. We also show that this phenotype is largely based on decreased fat gain, despite normal caloric intake, consequent to increased energy expenditure. Furthermore, our data show that PI3Kγ action on diet-induced obesity depends on PI3Kγ activity within a nonhematopoietic compartment, where it promotes energetic efficiency for fat mass gain. We also show that metabolic modulation by PI3Kγ depends on its lipid kinase activity and might involve kinase-independent signaling. Thus, PI3Kγ is an unexpected but promising drug target for the treatment of obesity and its complications.

Trends in motor vehicle crash mortality in Europe, 1980-2007.

Recent trends (1980-2007) in mortality from road traffic crashes in European countries, and, for comparative purposes, in the USA and Japan were reviewed. Data came from the World Health Organisation database. Age-standardised rates, at all ages and at 15-24, 25-64, >=65 years, were computed. Joinpoint regression analyses to evaluate significant changes in trends were performed. In the European Union as a whole rates declined from 20.2 in 1987 to 13.5/100,000 in 2007 in men, and from 6.3 to 3.7/100,000 in women; European Union rates remained lower than USA, but higher than Japanese ones. In 2007, the highest male rates were in Lithuania (36.7/100,000), the Russian Federation (35.2), Ukraine (29.8), and Latvia (28.5), and the lowest ones in the Netherlands (6.2) and Sweden (6.9); the highest female rates were in the Russian Federation (11.3), Lithuania (9.7), Belarus, Latvia, and Ukraine (around 8), and the lowest ones in Switzerland (1.7), the UK, and Nordic countries (around 2). Mortality from motor vehicle crashes declined in northern and western European countries and - though to a lesser extent - in southern European countries, too. Mortality trends were also favourable in the Czech Republic and Poland since the mid 1990's, whereas they were still upwards in Romania and the Russian Federation. No trend was observed in Hungary and Ukraine. Trends were consistent in various age groups considered. Thus, additional urgent and integrated intervention is required to prevent avoidable deaths from motor vehicle crashes, particularly in selected central and eastern European countries.

New trends in the kitchen: propellants assessment of edible food aerosol sprays used on food.

New products available for food creations include a wide variety of "supposed" food grade aerosol sprays. However, the gas propellants used cannot be considered as safe. The different legislations available did not rule any maximum residue limits, even though these compounds have some limits when used for other food purposes. This study shows a preliminary monitoring of propane, butane and dimethyl ether residues, in cakes and chocolate after spraying, when these gases are used as propellants in food aerosol sprays. Release kinetics of propane, butane and dimethyl ether were measured over one day with sprayed food, left at room temperature or in the fridge after spraying. The alkanes and dimethyl ether analyses were performed by headspace-gas chromatography-mass spectrometry/thermal conductivity detection, using monodeuterated propane and butane generated in situ as internal standards. According to the obtained results and regardingthe extrapolations of the maximum residue limits existing for these substances, different delays should be respected according to the storage conditions and the gas propellant to consume safely the sprayed food.

Obesity markers and estimated 10 year fatal cardiovascular risk in Switzerland

Objective: To assess the effectiveness of obesity markers to detect high (>5%) 10- year risk of fatal cardiovascular disease (CVD) as estimated using the SCORE function. Methods: Cross-sectional study including 3,047 women and 2,689 men aged 35-75 years (CoLaus study). Body fat percentage was assessed by tetrapolar bioimpedance. CVD risk was assessed using the SCORE risk function and gender and age-specific cut points for body fat were derived. The diagnostic accuracy of each obesity marker was evaluated through receiver operating characteristics (ROC) analysis. Results: Body fat presented a higher correlation with 10-year CVD risk than waist/hip ratio (WHR), waist or BMI: in men, r=0.31, 0.22, 0.19 and 0.12 and for body fat, WHR, waist and BMI, respectively; the corresponding values in women were 0.18, 0.15, 0.11 and 0.05, respectively (all p<0.05). In both genders, body fat showed the highest area under the ROC curve (AUC): in men, the AUC (and 95% confidence interval) were 76.0 (73.8 - 78.2), 67.3 (64.6 - 69.9), 65.8 (63.1 - 68.5) and 60.6 (57.9 - 63.5) for body fat, WHR, waist and BMI, respectively. In women, the corresponding values were 72.3 (69.2 - 75.3), 66.6 (63.1 - 70.2), 64.1 (60.6 - 67.6) and 58.8 (55.2 - 62.4). The use of body fat percentage criterion enabled to capture three times more subjects with high CVD risk than BMI criterion, and almost twice as much as WHR criterion.. Conclusions: Obesity defined by body fat percentage is more accurate to detect high 10-year risk of fatal CVD than obesity markers based on WHR, waist or BMI.

Genetic studies of body mass index yield new insights for obesity biology

Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

Obesity-related phenotypes are associated to parental longevity in a Swiss population-based study

METHODS. We analyzed data from a population-based sample of 2561 participants (1163 men and 1398 women) aged 55-75 years from the city of Lausanne, Switzerland (CoLaus study). Participants were stratified by the number of parents (0, 1, 2) who survived to 85 years or more. Trend across these strata was assessed using a non-parametric kmean test. The associations of parental age (independent covariate used as a proxy for longevity) with fasting blood glucose, blood pressures, blood lipids, body mass index (BMI), weight, height or liver enzymes (continuous dependent variables) were analyzed using multiple linear regressions. Models were adjusted for age, sex, alcohol consumption, smoking and educational level, and BMI for liver enzymes. RESULTS. For subjects with 0 (N = 1298), 1 (N = 991) and 2 (N = 272) long-lived parents, median BMI (interquartile range) was 25.4 (6.5), 24.9 (6.1) and 23.7 (4.8) kg/m2 in women (P <0.001), and 27.3 (4.8), 27.0 (4.5) and 25.9 (4.9) kg/m2 in men (P = 0.04), respectively; median weight was 66.5 (16.1), 65.0 (16.4) and 63.4 (13.7) kg in women (P = 0.003), and 81.5 (17.0), 81.4 (16.4) and 80.3 (17.1) kg in men (P = 0.36). Median height was 161 (8), 162 (9) and 163 (8) cm in women (P = 0.005) and 173 (9), 174 (9) and 174 (11) cm in men (P = 0.09). The corresponding medians for AST (Aspartate Aminotransferase) were 31 (13), 29 (11) and 28 (10) U/L (P = 0.002), and 28 (17), 27 (14) and 26 (19) U/L for ALT (Alanin Aminotransferase, P = 0.053) in men. In multivariable analyses, greater parental longevity was associated with lower BMI, lower weight and taller stature in women (P < 0.01) and lower AST in men (P = 0.011). No significant associations were observed for the other variables analyzed. Sensitivity analyses restricted to subjects whose parents were dead (N = 1844) led to similar results, with even stronger associations of parental longevity with liver enzymes in men. CONCLUSIONS. In women, increased parental longevity was associated with smaller BMI, attributable to lower weight and taller stature. In men, the association of increased parental longevity with lower liver enzymes, independently of BMI, suggests that parental longevity may be associated with decreased nonalcoholic fatty liver disease.

Trends in risk factors, patterns and causes in hospitalized strokes over 25 years: The Lausanne Stroke Registry.

BACKGROUND AND OBJECTIVE: The Lausanne Stroke Registry includes, from 1979, all patients admitted to the department of Neurology of the Lausanne University Hospital with the diagnosis of first clinical stroke. Using the Lausanne Stroke Registry, we aimed to determine trends in risk factors, causes, localization and inhospital mortality over 25 years in hospitalized stroke patients. METHODS: We assessed temporal trends in stroke patients characteristics through the following consecutive periods: 1979-1987, 1988-1995 and 1996-2003. Age-adjusted cardiovascular risk factors, etiologies, stroke localizations and mortality were compared between the three periods. RESULTS: Overall, 5,759 patients were included. Age was significantly different among the analyzed periods (p < 0.001), showing an increment in older patients throughout time. After adjustment for age, hypercholesterolemia increased (p < 0.001), as opposed to cigarette smoking (p < 0.001), hypertension (p < 0.001) and diabetes and hyperglycemia (p < 0.001). In patients with ischemic strokes, there were significant changes in the distribution of causes with an increase in cardioembolic strokes (p < 0.001), and in the localization of strokes with an increase in entire middle cerebral artery (MCA) and posterior circulation strokes together with a decrease in superficial middle cerebral artery stroke (p < 0.001). In patients with hemorrhagic strokes, the thalamic localizations increased, whereas the proportion of striatocapsular hemorrhage decreased (p = 0.022). Except in the older patient group, the mortality rate decreased. CONCLUSIONS: This study shows major trends in the characteristics of stroke patients admitted to a department of neurology over a 25-year time span, which may result from referral biases, development of acute stroke management and possibly from the evolution of cerebrovascular risk factors.

A genetic risk score combining 32 SNPs is associated with body mass index and improves obesity prediction in people with major depressive disorder.

BACKGROUND: Obesity is strongly associated with major depressive disorder (MDD) and various other diseases. Genome-wide association studies have identified multiple risk loci robustly associated with body mass index (BMI). In this study, we aimed to investigate whether a genetic risk score (GRS) combining multiple BMI risk loci might have utility in prediction of obesity in patients with MDD. METHODS: Linear and logistic regression models were conducted to predict BMI and obesity, respectively, in three independent large case-control studies of major depression (Radiant, GSK-Munich, PsyCoLaus). The analyses were first performed in the whole sample and then separately in depressed cases and controls. An unweighted GRS was calculated by summation of the number of risk alleles. A weighted GRS was calculated as the sum of risk alleles at each locus multiplied by their effect sizes. Receiver operating characteristic (ROC) analysis was used to compare the discriminatory ability of predictors of obesity. RESULTS: In the discovery phase, a total of 2,521 participants (1,895 depressed patients and 626 controls) were included from the Radiant study. Both unweighted and weighted GRS were highly associated with BMI (P <0.001) but explained only a modest amount of variance. Adding 'traditional' risk factors to GRS significantly improved the predictive ability with the area under the curve (AUC) in the ROC analysis, increasing from 0.58 to 0.66 (95% CI, 0.62-0.68; χ(2) = 27.68; P <0.0001). Although there was no formal evidence of interaction between depression status and GRS, there was further improvement in AUC in the ROC analysis when depression status was added to the model (AUC = 0.71; 95% CI, 0.68-0.73; χ(2) = 28.64; P <0.0001). We further found that the GRS accounted for more variance of BMI in depressed patients than in healthy controls. Again, GRS discriminated obesity better in depressed patients compared to healthy controls. We later replicated these analyses in two independent samples (GSK-Munich and PsyCoLaus) and found similar results. CONCLUSIONS: A GRS proved to be a highly significant predictor of obesity in people with MDD but accounted for only modest amount of variance. Nevertheless, as more risk loci are identified, combining a GRS approach with information on non-genetic risk factors could become a useful strategy in identifying MDD patients at higher risk of developing obesity.