The Impact of Familial Predisposition to Obesity and Cardiovascular Disease on Childhood Obesity

The prevalence of childhood obesity has reached alarming rates world-wide. The aetiology seems to be an interplay between genetic and environmental factors, and a surrogate measure of this complex interaction is suggested as familial predisposition. Familial predisposition to obesity and related cardiovascular disease (CVD) complications constitute the presence of obesity and/or obesity-related complications in primarily blood-related family members. The approaches of its measurement and applicability vary, and the evidence especially of its influence on obesity and obesity treatment in childhood is limited. Studies have linked a familial predisposition of obesity, CVD (hypertension, dyslipidaemia and thromboembolic events), and type 2 diabetes mellitus to BMI as well as other adiposity measures in children, suggesting degrees of familial aggregation of metabolic derangements. A pattern of predispositions arising from mothers, parents or grandparents as being most influential have been found, but further comprehensive studies are needed in order to specify the exact implications of familial predisposition. In the scope of childhood obesity this article reviews the current literature regarding familial predisposition to obesity and obesity-related complications, and how these familial predispositions may impact obesity in the offspring.Key Words: Pediatric obesity, Familial predisposition, Cardiovascular diseases, Diabetes mellitus type 2     

Functional trait space and the latitudinal diversity gradient

The processes causing the latitudinal gradient in species richness remain elusive. Ecological theories for the origin of biodiversity gradients, such as competitive exclusion, neutral dynamics, and environmental filtering, make predictions for how functional diversity should vary at the alpha (within local assemblages), beta (among assemblages), and gamma (regional pool) scales. We test these predictions by quantifying hypervolumes constructed from functional traits representing major axes of plant strategy variation (specific leaf area, plant height, and seed mass) in tree assemblages spanning the temperate and tropical New World. Alpha-scale trait volume decreases with absolute latitude and is often lower than sampling expectation, consistent with environmental filtering theory. Beta-scale overlap decays with geographic distance fastest in the temperate zone, again consistent with environmental filtering theory. In contrast, gamma-scale trait space shows a hump-shaped relationship with absolute latitude, consistent with no theory. Furthermore, the overall temperate trait hypervolume was larger than the overall tropical hypervolume, indicating that the temperate zone permits a wider range of trait combinations or that niche packing is stronger in the tropical zone. Although there are limitations in the data, our analyses suggest that multiple processes have shaped trait diversity in trees, reflecting no consistent support for any one theory.Species richness increases toward the equator (1, 2) in major clades of both extant and extinct species of plants and animals (3, 4). The generality of the pattern hints at a correspondingly general explanation, yet the latitudinal gradient in species richness remains one of ecology’s greatest unsolved puzzles. Long-running debates over the causes of the latitudinal gradient of species richness have focused on ecological, evolutionary, and geographic explanations (5–10). Although there has been some progress (11), it is also increasingly clear that there are numerous obstacles to understanding the primary drivers of the latitudinal gradient, including an ever-increasing number of hypotheses (12, 13), challenges in clearly separating their interdependencies (14, 15), and difficulties in rigorously falsifying their assumptions and predictions (16).More powerful tests of biodiversity theories need to move beyond species richness and instead explicitly focus on the mechanisms generating the gradient, by recasting the theories in terms of other measures of diversity, such as functional diversity (17–19). For example, explanations that assume species richness is limited by resource availability have often focused on the strength of species interactions, life history differences, and environmental constraints on how species pack into niche space (20). Evolutionary hypotheses have focused on differences in diversification rates, as well as the influence of species interactions on diversification rates (9). These interaction-based explanations implicitly refer to the degree of ecological differentiation among species, and therefore to trait dispersion within clades and assemblages, suggesting that patterns of functional diversity may provide a more powerful test of theory than taxonomic richness (21).A particularly important concept that unifies many ecological and evolutionary theories is the concept of the Hutchinsonian multidimensional niche (22). Hutchinsonian niches can be quantified by assessing the functional trait hypervolumes that characterize phenotypic space occupied by a set of species. Quantifying the volume, overlap, and packing of functional trait space at different spatial scales enables inferences about how differing ecological and evolutionary processes structure functional diversity and ecological strategies (23, 24).Here, we recast several contrasting hypotheses for the latitudinal gradient in terms of functional trait space. We focus on the proximate ecological mechanisms that ultimately can influence evolutionary processes. We quantify tree functional trait space across latitude at three spatial scales: (i) within assemblages (alpha), (ii) among assemblages (beta), and (iii) among biomes (gamma). For alpha and beta analyses, we use tree species assemblage data from 620 standardized 0.1-ha forest plots (Fig. 1A); for gamma analyses, we calculated the latitudinal range distributions for 520 New World tree species where we had sufficient data on geographic distribution and functional traits. In total, across all analyses, we used paired geographic occurrence data with trait data for 6,839 tree species.Open in a separate windowFig. 1.(A) Spatial distribution of the 620 0.1-ha forest plots used in this study. Plots are colored by richness. Plots cover most of the New World forested climate space (Fig. S1). (B) Relationship between absolute latitude and alpha hypervolume for tropical (red triangles) and temperate (blue pluses) plots. (C) Alpha hypervolume as a function of effective species richness (number of species with full trait coverage). We compare this hypervolume with a null expectation based on sampling the same number of species from the regional pool (median, dark gray line; 90% quantile range, light gray envelope).We primarily measured hypervolumes for three central traits hypothesized to characterize major axes of ecological strategy variation (25): specific leaf area (SLA), maximum height, and seed mass. SLA represents the tradeoff between leaf longevity and maximum photosynthetic rate (26); height is important for light competition and dispersal (27); and seed mass represents tradeoffs between fecundity, dispersal, and seedling survival (27). Although whole-plant resource strategies can be more fully assessed in higher dimensions (28, 29), we focus on these traits because of data availability (Materials and Methods). We use a hypervolume algorithm for calculating the volume and overlap of trait space (30) (Materials and Methods). All hypervolumes are reported in units of SDs of centered and scaled log-transformed trait values, raised to the power of the number of trait dimensions used.At all scales, our overall results and conclusions are similar (i) with and without gap-filling missing data, (ii) if we use convex hulls instead of hypervolumes to calculate trait spaces, and (iii) if we include additional trait axes. Additional details are given in Figs. S2–S7.     

Induction of Bim and Bid gene expression during accelerated apoptosis in severe sepsis

Introduction  

In transgenic animal models of sepsis, members of the Bcl-2 family of proteins regulate lymphocyte apoptosis and survival of sepsis. This study investigates the gene regulation of pro-apoptotic and anti-apoptotic members of the Bcl-2 family of proteins in patients with early stage severe sepsis.     

A single nucleotide polymorphism of macrophage migration inhibitory factor is related to inflammatory response in coronary bypass surgery using cardiopulmonary bypass.

OBJECTIVE: Cardiac surgery causes induction and release of inflammatory mediators that may be regulated by genetic background. Macrophage migration inhibitory factor (MIF) is a proinflammatory mediator that is known to be up-regulated in patients undergoing cardiac operations. Here we analyzed genotype distribution and allele frequency of the MIF-173*G/C single nucleotide polymorphism (SNP) and MIF plasma levels in patients undergoing surgical revascularization with (on-pump, n=45) and without (off-pump, n=34) cardiopulmonary bypass (CPB). METHODS: Genotyping was performed using a real-time PCR-based system with a hybridization probe system specific for the MIF-173*G/C SNP. In on-pump patients, blood samples were drawn before start of CPB, after termination of CPB and 12h postoperatively. In off-pump patients, blood samples were collected before stabilizer placement, after removal of the stabilizer and 12h postoperatively. MIF levels were measured using ELISA technique. RESULTS: Genotype distribution and allele frequencies were comparable between on-pump and off-pump patients. When comparing patients according to MIF genotype, a significant increase of MIF plasma levels after completed coronary bypass grafting using CPB was found in patients heterozygous for the MIF-173*G/C SNP (p<0.05). Moreover, on-pump patients showed significantly decreased MIF plasma levels after 12h postoperatively (p<0.05). In off-pump patients, MIF plasma levels were not significantly different over the time-course and were independent of the genotype. CONCLUSIONS: Patients carrying the C-allele showed significantly increased levels of the proinflammatory cytokine MIF compared to G/G homozygous when revascularization was carried out using CPB. The G/C genotype may be associated with a severe inflammatory reaction and therefore preoperative screening could be beneficial for patients undergoing cardiac surgery using CPB.     

Parenteral vaccination against influenza does not induce a local antigen-specific immune response in the nasal mucosa

The immune response in the nasal mucosa to influenza vaccination in 23 patients scheduled for tonsillectomy was studied. A statistically significant increase in influenza virus-specific serum and oral fluid antibodies was observed 7 days after vaccination. The numbers of influenza virus-specific antibody-secreting cells (ASCs) in peripheral blood also increased significantly 1 week after vaccination. The numbers of ASCs in tonsils and nasal mucosa were compared with data from a recent study of nonvaccinated volunteers. The numbers of influenza virus-specific ASCs in tonsils were significantly higher in the vaccinated group, but, surprisingly, there was no significant difference between the groups in the numbers of ASCs in nasal mucosa. This suggests that the influenza virus-specific antibodies detected in oral fluid are not produced locally in the nasal mucosa and may originate from a systemic source, indicating that the vaccination may favor a systemic immune response.     

From the Cover: Strong upslope shifts in Chimborazo's vegetation over two centuries since Humboldt

Global climate change is driving species poleward and upward in high-latitude regions, but the extent to which the biodiverse tropics are similarly affected is poorly known due to a scarcity of historical records. In 1802, Alexander von Humboldt ascended the Chimborazo volcano in Ecuador. He recorded the distribution of plant species and vegetation zones along its slopes and in surrounding parts of the Andes. We revisited Chimborazo in 2012, precisely 210 y after Humboldt’s expedition. We documented upward shifts in the distribution of vegetation zones as well as increases in maximum elevation limits of individual plant taxa of >500 m on average. These range shifts are consistent with increased temperatures and glacier retreat on Chimborazo since Humboldt’s study. Our findings provide evidence that global warming is strongly reshaping tropical plant distributions, consistent with Humboldt’s proposal that climate is the primary control on the altitudinal distribution of vegetation.The biological impacts of ongoing climate change (1) are already apparent in species’ poleward and upslope range shifts and earlier spring events (2–9). However, most studies stem from high-latitude areas and are generally restricted to dynamics across the past few decades (10). To our knowledge, only three previous resurveys have studied range shifts of tropical plant taxa, all at <4,000 m in elevation (7, 8, 11). Modeling (12) and paleoecological studies (13) suggest that tropical montane vegetation should be highly sensitive to climate change. However, researchers strongly debate whether tropical plants are tracking warming temperatures along elevation gradients, with most (although scarce) studies indicating they are lagging behind (cf. 14, 15). Such lags could have negative effects on the distributions of species dependent on certain plant taxa, e.g., as a food source (16). The question is particularly urgent given the growing evidence of systematically stronger warming rates in high-mountain environments (17).The legacy and works of Alexander von Humboldt (1769–1859) not only constitute the foundation of biogeography, but also what is likely the oldest dataset on altitudinal ranges of plant species. The observations recorded by Humboldt and Aimé Bonpland (1773–1858) during their travels in Central and South America, and synthesized in a Tableau of Mt. Chimborazo (summit 6,268 m above sea level) and accompanying essay (18), provide a unique opportunity to study tropical vegetation changes over a period of 210 y. To our knowledge, this period is more than twice as long as any previous resurvey study based on historical biodiversity records (11, 19). We revisited the upper slopes of the Chimborazo volcano in June 2012. Our aim was to record the current elevational distribution of plants and test for upward shifts since Humboldt’s expedition, as a response to anthropogenic global warming. We sampled plant species presence and abundance along transects every 100 m of elevation between 3,800 and 5,200 m. Three main findings, comparing our surveys to Humboldt’s data, support strong upward shifts of plant distributions: a higher upper limit for plant growth, increased elevation of vegetation zones, and upward shifts in the upper range limits of most individual taxa.     

Birthweight,Childhood Body Mass Index,Height and Growth,and Risk of Polycystic Ovary Syndrome

IntroductionAdult obesity is linked with polycystic ovary syndrome (PCOS), but the importance of body size at ages before PCOS is diagnosed is unknown.ObjectiveTo investigate associations between a woman''s own birthweight, childhood body mass index (BMI), height and growth patterns in relation to her risk of PCOS.MethodsWe included 65,665 girls from the Copenhagen School Health Records Register, born in the period 1960–1996, with information on birthweight and measured weight and height at the ages of 7–13 years. Overweight was defined using International Obesity Task Force (IOTF) criteria. From the Danish National Patient Register, 606 women aged 15–50 years were identified. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated by Cox regression analysis.ResultsBirthweight was not associated with PCOS. At the age of 7–13 years, girls with overweight had a higher risk of developing PCOS than girls without overweight; HR 2.83 (95% CI 2.34–3.42) at age 7 years and 2.99 (95% CI 2.38–3.76) at age 13 years. Furthermore, girls with overweight at both 7 and 13 years had a higher risk of developing PCOS than girls without overweight or overweight at only one age. Height was positively associated with PCOS risk at all ages. Girls who were persistently tall or changed from tall to average height had a higher risk of developing PCOS than girls with average height growth.ConclusionOverweight and tall stature in childhood are positively associated with PCOS risk, but birthweight is not.