Culture and the evolution of human cooperation

The scale of human cooperation is an evolutionary puzzle. All of the available evidence suggests that the societies of our Pliocene ancestors were like those of other social primates, and this means that human psychology has changed in ways that support larger, more cooperative societies that characterize modern humans. In this paper, we argue that cultural adaptation is a key factor in these changes. Over the last million years or so, people evolved the ability to learn from each other, creating the possibility of cumulative, cultural evolution. Rapid cultural adaptation also leads to persistent differences between local social groups, and then competition between groups leads to the spread of behaviours that enhance their competitive ability. Then, in such culturally evolved cooperative social environments, natural selection within groups favoured genes that gave rise to new, more pro-social motives. Moral systems enforced by systems of sanctions and rewards increased the reproductive success of individuals who functioned well in such environments, and this in turn led to the evolution of other regarding motives like empathy and social emotions like shame.     

Lipid reserves,fasting capability and the evolution of nestling obesity in procellariiform seabirds

Several alternative explanations have been proposed to account for the evolution of nestling obesity in a variety of avian groups. These predict quite different patterns of fat accumulation, storage and use by chicks of different ages. Yet surprisingly few studies have measured changes in body composition during chick development. We tested the applicability of these hypotheses for fulmars, Fulmarus glacialis, by direct measurement of changes in water, lipid and lean dry mass in growing chicks. Lipid and lean dry mass increased until ca. 70% of the way through chick rearing, but then levelled off. Total body water also increased until the same stage, but gradually declined thereafter, and it was this change rather than fat metabolism that resulted in mass recession. The observed pattern of a continued increase in stored lipid, and most importantly, its maintenance all the way through the mass-recession phase until chicks reach fledging, is incompatible with many of the proposed hypotheses. We suggest that the most likely ultimate explanation for large fat deposits is to fuel chicks during the initial critical period away from the nest site while they learn to forage     

Chemical evolution and the evolution of the Earth's crust

It is hypothesized that there is a close relationship between the geologic evolution of the global plates of the Earth's crust and the chemical evolution of life on the Earth. Characteristics of the axes of plate spreading are discussed in relation to postulated environments conducive to the synthesis of chemical compounds thought to be important biological precursors. Likely locations forin situ measurements to test the hypothesis are identified.     

Visceral obesity and the heart

Obesity and particularly its deleterious form, visceral adiposity, has reached a high prevalence in the industrialized world owing to the lack of exercise and the widely available energy-dense diet. As a consequence, cardiovascular diseases and metabolic disorders are afflicting an unprecedented number of individuals at a world-wide scale. Over the last decades, investigations have established firm links between visceral obesity and the development of cardiovascular diseases. Moreover, studies in the field of lipid partitioning have demonstrated that inadequacy of homeostatic mechanism ensuring adequate handling of energy surplus is associated with accumulation of visceral fat and lipid overload of internal organs, which are participating to the development of heart diseases. Visceral obesity and its metabolic consequences often referred to as the metabolic syndrome is associated with the production of an atherosclerosis prone milieu. In this review, clinical implications of visceral obesity on the development of cardiovascular disorders are reviewed along with important mechanisms participating to the development of these disorders. Implications and failure of lipid partitioning and some of the potential pathways mediating development of heart diseases are also covered in view of recent development of therapeutic options.     

Maternal obesity at conception programs obesity in the offspring

Risk of obesity in adult life is subject to programming during gestation. To examine whether in utero exposure to maternal obesity increases the risk of obesity in offspring, we developed an overfeeding-based model of maternal obesity in rats utilizing intragastric feeding of diets via total enteral nutrition. Feeding liquid diets to adult female rats at 220 kcal/kg(3/4) per day (15% excess calories/day) compared with 187 kcal/kg(3/4) per day for 3 wk caused substantial increase in body weight gain, adiposity, serum insulin, leptin, and insulin resistance. Lean or obese female rats were mated with ad libitum AIN-93G-fed male rats. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups to lean dams having ad libitum access to AIN-93G diets throughout lactation. Numbers of pups, birth weight, and size were not affected by maternal obesity. Male offspring from each group were weaned at postnatal day (PND)21 to either AIN-93G diets or high-fat diets (45% fat calories). Body weights of offspring from obese dams did not differ from offspring of lean dams when fed AIN-93G diets through PND130. However, offspring from obese dams gained remarkably greater (P < 0.005) body weight and higher % body fat when fed a high-fat diet. Body composition was assessed by NMR, X-ray computerized tomography, and weights of adipose tissues. Adipose histomorphometry, insulin sensitivity, and food intake were also assessed in the offspring. Our data suggest that maternal obesity at conception leads to fetal programming of offspring, which could result in obesity in later life.     

Maternal nutrition and the programming of obesity

The increasing incidence of obesity in the developed and developing world in the last decade has led to a need to define our understanding of the physiological mechanisms which can predispose individuals to weight gain in infancy, childhood and adulthood. There is now a considerable body of evidence which has shown that the pathway to obesity may begin very early in life, and that exposure to an inappropriate level of nutrition during prenatal and/or early postnatal development can predispose individuals to obesity in later life The brain is at the heart of the regulation of appetite and food preferences, and it is increasingly being recognised that the development of central appetitive structures is acutely sensitive to the nutritional environment both before and immediately after birth. This review will summarise the body of work which has highlighted the critical role of the brain in the early origins of obesity and presents some perspectives as to the potential application of these research findings in the clinical setting.     

Cognition and evolution: learning and the evolution of sex traits

The evolution of gender characteristics is an outcome of mate choice, which has been assumed to be genetically mediated. Recent research suggests that learning also has a role to play as an agent of sexual selection.     

Breastfeeding and the risk of childhood obesity

Breastfeeding is suggested to be a potential obesity prevention strategy, but the evidence that breast-fed infants have a lower risk of later obesity is equivocal. Fourteen studies published between 2003 and 2006 that considered the relationship between breastfeeding and risk of childhood overweight and obesity were reviewed. Three studies reported a protective effect in children (i.e., increased duration of breastfeeding was associated with a lower risk of childhood overweight/obesity), 4 reported a partial protective effect (i.e., only evident in a subgroup), 6 reported no protective effect, and 1 reported a protective effect in children but not in adults. While there is some evidence that breastfeeding may help to prevent childhood obesity, it should not be viewed as the only preventative nutrition measure. In the U.S., rates of breastfeeding have risen while rates for childhood obesity have increased dramatically. This finding reinforces the view that many factors are involved in maintaining a healthy body weight.     

Protein evolution drives the evolution of the genetic code and vice versa

A model for the developmental pathway of the genetic code, grounded on group theory and the thermodynamics of codon-anticodon interaction is presented. At variance with previous models, it takes into account not only the optimization with respect to amino acid attributes but, also physicochemical constraints and initial conditions. A 'simple-first' rule is introduced after ranking the amino acids with respect to two current measures of chemical complexity. It is shown that a primeval code of only seven amino acids is enough to build functional proteins. It is assumed that these proteins drive the further expansion of the code. The proposed primeval code is compared with surrogate codes randomly generated and with another proposal for primeval code found in the literature. The departures from the 'universal' code, observed in many organisms and cellular compartments, fit naturally in the proposed evolutionary scheme. A strong correlation is found between, on one side, the two classes of aminoacyl-tRNA synthetases, and on the other, the amino acids grouped by end-atom-type and by codon type. An inverse of Davydov's rules, to associate the amino acid end atoms (O/N and non-O/non-N) of 18 amino acids with codons containing a weak base (A/U), extended to the 20 amino acids, is derived.     

The structure of protein evolution and the evolution of protein structure

The observed distribution of protein structures can give us important clues about the underlying evolutionary process, imposing important constraints on possible models. The availability of results from an increasing number of genome projects has made the development of these models an active area of research. Models explaining the observed distribution of structures have focused on the inherent functional capabilities and structural properties of different folds and on the evolutionary dynamics. Increasingly, these elements are being combined.     

The evolution of the environment and its influence on the evolution of life

Thermodynamic data and known paleogeological data were used to deduce when and what elements (compounds) were readily available during the whole history of the earth. On the basic assumption that available compounds would dictate the type of organisms to emerge, we attempted to derive a kind of evolutionary tree. This was then compared with the existing evolutionary trees derived from the sequences of proteins and polynucleotides.     

microRNAs in the regulation of adipogenesis and obesity

Worldwide obesity is a growing health problem, associated with increased risk of chronic disease. Understanding the molecular basis of adipogenesis and fat cell development in obesity is essential to identify new biomarkers and therapeutic targets for the development of anti-obesity drugs. microRNAs (miRNAs) appear to play regulatory roles in many biological processes associated with obesity, including adipocyte differentiation, insulin action and fat metabolism. Recent studies show miRNAs are dysregulated in obese adipose tissue. During adipogenesis miRNAs can accelerate or inhibit adipocyte differentiation and hence regulate fat cell development. In addition miRNAs may regulate adipogenic lineage commitment in multipotent stem cells and hence govern fat cell numbers. Recent findings suggest miR-519d may be associated with human obesity, but larger case-control studies are needed. Few miRNA targets have been experimentally validated in adipocytes but interestingly both miR-27 and miR-519d target PPAR family members, which are well established regulators of fat cell development. In this review recent advances in our understanding of the role of miRNAs in fat cell development and obesity are discussed. The potential of miRNA based therapeutics targeting obesity is highlighted as well as recommendations for future research which could lead to a breakthrough in the treatment of obesity.     

Frameworks of population obesity and the use of cultural consensus modeling in the study of environments contributing to obesity

Obesity in Eastern Europe has been linked to privilege and status prior to the collapse of communism, and to exposure to free-market economics after it. Neither formulation is a complete explanation, and it is useful to examine the potential value of other models of population obesity for the understanding of this phenomenon. These include those of: thrifty genotypes; obesogenic behaviour; obesogenic environments; nutrition transition; obesogenic culture; and biocultural interactions of genetics, environment, behaviour and culture. At the broadest level, obesity emerges from the interaction of thrifty genotype with obesogenic environment. However, defining obesogenic environments remains problematic, especially in relation to sociocultural factors. Furthermore, since different identity groups may share different values concerning the obesogenicity of the environment, a priori assumptions about group homogeneity may lead to flawed interpretations of the importance of sociocultural factors in obesogenic environments. A new way to identify cultural coherence of groups and populations in relation to environments contributing to obesity is put forward here, that of cultural consensus modeling.     

PPARs and the complex journey to obesity

Obesity and the related disorders of dyslipidemia and diabetes (components of syndrome X) have become global health epidemics. Over the past decade, the elucidation of key regulators of energy balance and insulin signaling have revolutionized our understanding of fat and sugar metabolism and their intimate link. The three 'lipid-sensing' peroxisome proliferator-activated receptors (PPAR-alpha, PPAR-gamma and PPAR-delta) exemplify this connection, regulating diverse aspects of lipid and glucose homeostasis, and serving as bona fide therapeutic targets. With molecular underpinnings now in place, new pharmacologic approaches to metabolic disease and new questions are emerging.     

FTO and obesity: the missing link

The field of vascular molecular imaging is searching for the "holy grail" of an imaging technique that will quantitatively and reliably assess vulnerable coronary plaques. Fluorescence imaging with indocyanine green specifically identifies lipid-rich plaques in rabbits and in humans and represents a promising, though invasive, approach.