Paola Bressan Why babies look like their daddies: paternity uncertainty and the evolution of self-deception in evaluating family resemblance

http://www.psy.unipd.it/~pbressan/papers/why_babies.pdf

Abstract

It has been suggested that in a socially monogamous system where fathers invest in their mate’s offspring but paternity is far from certain, it will be adaptive on the part of infants to conceal their father’s identity; but the opposite claim has also been made that this is against the genetic interests of the fathers, and a high frequency of adulterine births will select instead for paternal resemblance. In this article, I present a simple theoretical model that suggests that neonatal anonymity benefits fathers, mothers, and children. Once anonymity becomes established, however, all babies start paying the cost of paternity uncertainty, that is, the reduction in paternal care due to fathers not knowing whether they have truly sired their mate’s offspring. By diminishing the fitness of babies, such a cost bounces back as lowered fitness for parents as well. We should then expect the evolution of maternal strategies directed to decrease paternity uncertainty, in the form of instinctive and unsolicited comments on babies’ resemblance to their putative fathers. In contradiction to the widespread belief that it would be in fathers’ interest to be skeptical of these allegations, the model suggests that, under conditions of infant anonymity, fathers will actually promote their own fitness by believing their spouses.

Keywords Resemblance · Confidence of paternity · Parental investment · Kin recognition · Evolutionary psychology

Review

Neurobiology of overeating and obesity: The role of melanocortins and beyond

Rahul Pandita,

Johannes W. de Jong a,

Louk J.M.J. Vanderschuren a, b,

Roger A.H. Adan a

a Rudolf Magnus Institute of Neuroscience, Department of Neuroscience and Pharmacology, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands

b Department of Animals in Science and Society, Division of Behavioural Neuroscience, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 2, 3584 CM Utrecht, The Netherlands

http://dx.doi.org/10.1016/j.ejphar.2011.01.034, How to Cite or Link Using DOI

Abstract

The alarming increase in the incidence of obesity and obesity-associated disorders makes the etiology of obesity a widely studied topic today. As opposed to ‘homeostatic feeding’, where food intake is restricted to satisfy one's biological needs, the term ‘non-homeostatic’ feeding refers to eating for pleasure or the trend to over-consume (palatable) food. Overconsumption is considered a crucial factor in the development of obesity. Exaggerated consumption of (palatable) food, coupled to a loss of control over food intake despite awareness of its negative consequences, suggests that overeating may be a form of addiction. At a molecular level, insulin and leptin resistance are hallmarks of obesity. In this review, we specifically address the question how leptin resistance contributes to enhanced craving for (palatable) food. Since dopamine is a key player in the motivation for food, the interconnection between dopamine, leptin and neuropeptides related to feeding will be discussed. Understanding the mechanisms by which these neuropeptidergic systems hijack the homeostatic feeding mechanisms, thus leading to overeating and obesity is the primary aim of this review. The melanocortin system, one of the crucial neuropeptidergic systems modulating feeding behavior will be extensively discussed. The inter-relationship between neuronal populations in the arcuate nucleus and other areas regulating energy homeostasis (lateral hypothalamus, paraventricular nucleus, ventromedial hypothalamus etc.) and reward circuitry (the ventral tegmental area and nucleus accumbens) will be evaluated and scrutinized.

Keywords: Obesity; Leptin resistance; Addiction; Craving; Melanocortin

Article of the month

Rational drug design

European Journal of Pharmacology

Volume 625, Issues 1–3, 25 December 2009, Pages 90–100

Soma Mandala, Mee'nal Moudgila, Sanat K. Mandalb, c, , ,

Abstract

In this article, current knowledge of drug design is reviewed and an approach of rational drug design is presented. The process of drug development is challenging, expensive, and time consuming, although this process has been accelerated due to the development of computational tools and methodologies. The current target based drug design approach is incomplete because most of the drugs developed by structure guided approaches have been shown to have serious toxic side effects. Otherwise these drugs would have been an ideal choice for the treatment of diseases. Hence, rational drug design would require a multidisciplinary approach. In this regard, incorporation of gene expression technology and bioinformatics tools would be indispensable in the structure based drug design. Global gene expression data and analysis of such data using bioinformatics tools will have numerous benefits such as efficiency, cost effectiveness, time saving, and will provide strategies for combination therapy in addition to overcoming toxic side effects. As a result of incorporation of gene expression data, partial benefit of the structure based drug design is slowly emerging and rapidly changing the approach of the drug development process. To achieve the full benefit of developing a successful drug, multidisciplinary approaches (approaches such as computational chemistry and gene expression analysis, as discussed in this article) would be necessary. In the future, there is adequate room for the development of more sophisticated methodologies.