Positive frequency dependent selection is a natural selection regime where the fitness of a phenotype increases with its frequency in the population. Examples can be typically found in the spread of disease tolerance strategies in a population. A characterizing feature of PFDS is that the focal allele may experience favorable selection only when it becomes more frequent in the population, while being selected against when it is rare. In this paper, by applying a solution (...) concept from evolutionary game theory, we hypothesize that the process of emergence of such alleles triggers selection for silence, where the emergence of alleles that can stay unexpressed for a period of time will be favored by selection forces. We illustrate our hypothesis using a mathematical model of a population of single locus diploid organisms with two alleles where a single mutant of an allele that experiences positive frequency dependent selection appears in a population where the other allele is a dominant. The model results show that the longer the silence interval of the new mutant before its expression, the better its chances of getting fixed in the population. However, this effect will be observable only to a certain limit after which further increase in the interval will not have an effect on the expected fixation rate. Two divergences from the simple scenario are also investigated: the nonsynchronous expression of the focal allele and its emergence in a spatial grid limited by a migration bottleneck. In all cases, it is shown that there is an evolutionary pressure inherent in the dynamics of positive frequency dependent selection on the genes to have a delayed expression. It is hypothesized that the regulation systems of such traits will be under selection for either internal silencing mechanisms or to be triggered by an external environmental condition. (shrink)

On the basis of distinctions between those properties of entities that can be defined without reference to other entities and those that (in different ways) cannot, this note argues that non-trivial forms of frequency-dependent selection of entities should be interpreted as selection occurring at a level higher than that of those entities. It points out that, except in degenerately simple cases, evolutionary game-theoretic models of selection are not models of individual selection. Similarly, models of (...) genotypic selection such as heterosis cannot be legitimately interpreted as models of genic selection. The analysis presented here supports the views that: (i) selection should be viewed as a multi-level process; (ii) upper-level selection is ubiquitous; (iii) kin selection should be viewed as a type of group selection rather than individual selection; and (iv) inclusive fitness is not an individual property. (shrink)

In what follows, I propose to evaluate Giere's analysis by applying it to a causal process considered in evolutionary theory, namely, natural selection. To say that there is selection for a given trait is to say that possessing that trait causes differential reproductive success. If there is selection for a trait and if no other evolutionary forces impinge and there is no "sampling error" due to random drift, individuals with the trait will on average have more offspring (...) than individuals without it. But sampling error can't be discounted for finite populations; so the combined effect of selection and drift will be a probability distribution of numbers of offspring. In this event, selection for a trait will imply that the mean value of the distribution associated with the individuals possessing the trait exceeds the mean value for individuals without the trait. Evolutionary theory assigns a probability distribution of possible reproductive outputs to each organism and, thereby, views organisms as stochastic systems. This implies no commitment to indeterminacy at the microlevel, of course. (shrink)

In a recent article (Sober 1982), I criticized an account of causation proposed by Giere (1979, 1980) by describing a series of examples concerning natural selection. Collier (1983) has criticized my criticisms, saying that I misapplied Giere's proposal and misconstrued the biology. More recently, Giere (1984) has defended his theory against my criticisms. Here I argue that my criticisms still stand.

This paper argues that the contextual approach to natural selection does not offer an estimation of the contributions of individual and group selection to evolutionary change in multi-level selection scenarios, and that this is so because the term “group selection”, as defined by the contextual approach, does not refer to a process taking place at the group level. In the contextual analysis framework, this term simply denotes an evolutionary change that takes place due to the fact (...) that, overall, individual types do not share similar contexts or environments, and the only way to claim that such an evolutionary change is a result of selection is by admitting that “group selection” is in fact a kind of frequency-dependent selection, i.e. a selection process taking place at the individual level. Therefore, under the names “individual selection” and “group selection”, the contextual approach actually isolates two aspects of the relation between individual types and their environment, and not two distinct levels of selection. (shrink)

Two questions are raised for Grafen’s formal darwinism project of aligning evolutionary dynamics under natural selection with the optimization of phenotypes for individuals of a population. The first question concerns mean fitness maximization during frequency-dependent selection; in such selection regimes, not only is mean fitness typically not maximized but it is implausible that any parameter closely related to fitness is being maximized. The second question concerns whether natural selection on inclusive fitness differences can be (...) regarded as individual selection or whether it leads to a departure from the central motivation that led to the formal darwinism project, viz., to show that “Darwinian” evolution through individual selection leads to “good design” or phenotypic adaptation through trait optimization. (shrink)

In this paper I critically evaluate Reisman and Forber’s :1113–1123, 2005) arguments that drift and natural selection are population-level causes of evolution based on what they call the manipulation condition. Although I agree that this condition is an important step for identifying causes for evolutionary change, it is insufficient. Following Woodward, I argue that the invariance of a relationship is another crucial parameter to take into consideration for causal explanations. Starting from Reisman and Forber’s example on drift and after (...) having briefly presented the criterion of invariance, I show that once both the manipulation condition and the criterion of invariance are taken into account, drift, in this example, should better be understood as an individual-level rather than a population-level cause. Later, I concede that it is legitimate to interpret natural selection and drift as population-level causes when they rely on genuinely indeterministic events and some cases of frequency-dependent selection. (shrink)

There is surprisingly little philosophical work on conceptually spelling out the difference between the traits on which natural selection may be said to act (e.g. “having a high running speed”) and mere circumstantial traits (e.g. “happening to be in the path of a forest fire”). I label this issue the “selectable traits problem” and, in this paper, I propose a solution for it. I first show that, contrary to our first intuition, simply equating selectable traits with heritable ones is (...) not an adequate solution. I then go on to argue that two recent philosophical solutions to this problem—due to Peter Godfrey-Smith and Pierrick Bourrat—are unconvincing because they cannot accommodate frequency-dependent selection. The way out of this difficulty is, I argue, to accept that extrinsic properties dependent on relations between intrinsic properties of the population members should also count as selectable traits. I then show that my proposal is legitimized by more than the simple accommodation of frequency-dependent selection. (shrink)

Complexity and life as we know it depend crucially on the laws and constants of nature as well as the boundary conditions, which seem at least partly “fine-tuned.” That deserves an explanation: Why are they the way they are? This essay discusses and systematizes the main options for answering these foundational questions. Fine-tuning might just be an illusion, or a result of irreducible chance, or nonexistent because nature could not have been otherwise (which might be shown within a fundamental theory (...) if some constants or laws could be reduced to boundary conditions or boundary conditions to laws), or it might be a product of selection: either observational selection (weak anthropic principle) within a vast multiverse of many different realizations of physical parameters, or a kind of cosmological natural selection making the measured parameter values quite likely within a multiverse of many different values, or even a teleological or intentional selection or a coevolutionary development, depending on a more or less goal-directed participatory contribution of life and intelligence. In contrast to observational selection, which is not predictive, an observer-independent selection mechanism must generate unequal reproduction rates of universes, a peaked probability distribution, or another kind of differential frequency, resulting in a stronger explanatory power. The hypothesis of Cosmological Artificial Selection (CAS) even suggests that our universe may be a vast computer simulation or could have been created and transcended by one. If so, this would be a far-reaching answer – within a naturalistic framework! – of fundamental questions such as: Why did the big bang and fine-tunings occur, what is the role of intelligence in the universe, and how can it escape cosmic doomsday? This essay critically discusses some of the premises and implications of CAS and related problems, both with the proposal itself and its possible physical realization: Does CAS deserve to be considered as a convincing explanation of cosmic fine-tuning? Is life incidental, or does CAS revalue it? And are life and intelligence ultimately doomed, or might CAS rescue them? (shrink)

The process of partner selection reflects ethnographic realities where cooperative rewards obtain that would otherwise be lost to loners. Baumard et al. neglect frequency-dependent processes exemplified by games of coordination. Such games can produce multiple equilibria that may or may not include fair outcomes. Additional, group-selection processes are required to produce the outcomes predicted by the models.

The central point of this essay is to demonstrate the incommensurability of ‘Darwinian fitness’ with the numeric values associated with reproductive rates used in population genetics. While sometimes both are called ‘fitness’, they are distinct concepts coming from distinct explanatory schemes. Further, we try to outline a possible answer to the following question: from the natural properties of organisms and a knowledge of their environment, can we construct an algorithm for a particular kind of organismic life-history pattern that itself will (...) allow us to predict whether a type in the population will increase or decrease relative to other types? Introduction Darwinian fitness Reproductive fitness and genetical models of evolution The models of reproductive fitness 4.1 The Standard Viability Model 4.2 Frequency-dependent selection 4.3 Fertility models 4.4 Overlapping generations Fitness as outcome 5.1 Fitness as actual increase in type 5.2 Fitness as expected increase in type 5.2.1 Expected increase within a generation 5.2.2 Expected increase between generations 5.2.3 Postponed reproductive fitness effects The book-keeping problem Conclusion. (shrink)

Maynard Smith’s defenses of adaptationism and of the value of optimization theory in evolutionary biology are both criticized. His defense does not adequately respond to the criticism of adaptationism by Gould and Lewontin. It is also argued here that natural selection cannot be interpreted as an optimization process if the objective function to be optimized is either (i) interpretable as a fitness, or (ii) correlated with the mean population fitness. This result holds even if fitnesses are frequency-independent; the (...) problem is further exacerbated in the frequency-dependent context modeled by evolutionary game theory. However, Eshel and Feldman’s new results on “long-term” evolution may provide some hope for the continuing relevance of the game-theoretic framework. These arguments also demonstrate the irrelevance of attempts by Intelligent Design creationists to use computational limits on optimization algorithms as evidence against evolutionary theory. It is pointed out that adaptation, natural selection, and optimization are not equivalent processes in the context of biological evolution. (shrink)

A hypothesis on the evolutionary origin of the genetic pathway of sex determination in the nematode Caenorhabditis elegans is presented here. It is suggested that the pathway arose in steps, driven by frequency‐dependent selection for the minority sex at each step, and involving the sequential acquisition of dominant negative, neomorphic genetic switches, each one reversing the action of the previous one. A central implication is that the genetic pathway evolved in reverse order from the final step in (...) the hierarchy up to the first. The possible applicability of the model to the other well‐characterized sex determination pathway, that of Drosophila melanogaster, and to sex determination in mammals, is discussed, along with some potential implications for pathway evolution in general. Finally, the specific molecular and population genetic questions that the model raises are described and some tests are proposed. (shrink)

Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable mutational load (...) on the thousands of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior. (Published Online November 9 2006) Key Words: adaptation; behavior genetics; Darwinian psychiatry; evolution; evolutionary genetics; evolutionary psychology; mental disorders; mutation-selection balance; psychiatric genetics; quantitative trait loci (QTL). (shrink)

This paper is a commentary on the focal article by Grafen and on earlier papers of his on which many of the results of this focal paper depend. Thus it is in effect a commentary on the “formal Darwinian project”, the focus of this sequence of papers. Several problems with this sequence are raised and discussed. The first of these concerns fitness maximization. It is often claimed in these papers that natural selection leads to a maximization of fitness and (...) that this view is claimed in Fisher’s “fundamental theorem of natural selection”. These claims are refuted, and various incorrect statements about the meaning and interpretation of the fundamental theorem of natural selection, in this sequence and in other papers by other authors, are discussed. Next, much of the work in this sequence rests on the first Price equation. In the deterministic (infinite population) case this equation is no more than the standard classical equation relating to changes in gene frequencies. In the stochastic case the equation gives the change in gene frequencies as the sum of two terms (the second of which vanishes in the deterministic case). These two terms are of essentially equal importance in the situation considered in the focal article, yet one of Grafen’s results ignores the second term in the stochastic analysis. This is associated with a wavering between deterministic and stochastic analyses and the use of the Price fitness concept and the classical fitness concept. These comments cast doubts on Grafen’s optimization theory. (shrink)

There is a tension between, on the one hand, the view that natural selection refers to individual-level causes, and on the other hand, the view that it refers to a population-level cause. In this article, I make the case for the individual-level cause view. I respond to recent claims made by McLoone that the individual-level cause view is inconsistent. I show that if one were to follow his arguments, any causal claim in any context would have to be regarded (...) as vindicating a form of population-level cause view. I show why this is implausible and how a consistent individual-level cause position can be held within the interventionist account of causation. Finally, I argue that there is one sense in which natural selection might be said to refer to population-level causes of evolutionary change. The upshot is that, as noted by others, natural selection can be regarded as referring to a population-level cause in the context of frequency-dependent selection and other situations of fitness-altering interactions between the individuals of a population. But whether this statement is true will depend on the empirical case investigated, not some a priori conceptual distinction. Thus, even though situations of frequency dependence might be ubiquitous, it is orthogonal to the conceptual question of whether frequency-independent natural selection—McLoone’s target—refers to individual- or population-level causes. (shrink)

Sound is an inherent component of the environment that provides conditions and information necessary for many animal activities. Soniferous species require specific acoustic and physical conditions suitable for their signals to be transmitted, received, and effectively interpreted to successfully identify and utilize resources in their environment and interact with conspecifics and other heterospecific organisms. We propose the Acoustic Habitat Hypothesis to explain how the acoustic environment influences habitat selection of sound-dependent species. We postulate that sound-dependent species select (...) and occupy habitats with unique acoustic characteristics that are essential to their functional needs and conducive to the threshold of sound frequency they produce and detect. These acoustic habitats are based on the composition of biophony, geophony, and technophony in the soundscape and on the biosemiotics mechanisms described in the eco-field hypothesis. The Acoustic Habitat Hypothesis initiates questions of habitat selection that go beyond the physical attributes of the environment by applying ecoacoustics theory. We outline the theoretical basis of the Acoustic Habitat Hypothesis and provide examples from the literature to support its assumptions. The concept of acoustic habitats has been documented in the literature for many years but here, we accurately and extensively define acoustic habitat and we put this concept into a unified theory. We also include perspectives on how the Acoustic Habitat Hypothesis can stimulate a paradigm shift in conservation strategies for threatened and endangered species. (shrink)

Recent research into the evolution of higher cognition has piqued an interest in the effect of natural selection on the ability of creatures to respond to their environment. It is believed that environmental variation is required for plasticity to evolve in cases where the ability to be plastic is costly. We investigate one form of environmental variation: frequency dependent selection. Using tools in game theory, we investigate a few models of plasticity and outline the cases where (...) selection would be expected to maintain it. Ultimately we conclude that frequency dependent selection is likely insuffcient to maintain plasticity given reasonable assumptions about its costs. This result is very similar to one aspect of the well-discussed Baldwin effect, where plasticity is first selected for and then later selected against. We show how in these models one would expect plasticity to grow in the population and then be later reduced. Ultimately we conclude that if one is to account for the evolution of behavioral plasticity in this way, one must appeal to a very particular sort of external environmental variation. (shrink)

If humans have an evolved moral psychology, then we should not expect it to function in an identical way between individuals. Instead, we should expect a diversity in the function of our moral psychology between individuals that varies along genetic lines, and a corresponding diversity of moral attitudes and moral judgements that emerge from it. This is because there was no one psychological type that would reliably produce adaptive social behaviour in the highly heterogeneous environments in which our minds evolved. (...) As such, there was no single psychological type towards which evolution could gravitate. Instead we evolved a stable polymorphism of psychological types, maintained by frequency-dependent selection, each predisposed towards particular social and moral attitudes and behaviours. This can help explain the existence of moral diversity, particularly intra-cultural moral diversity, and seemingly intractable moral disagreement. (shrink)

Recent research into the evolution of higher cognition has piqued an interest in the effect of natural selection on the ability of creatures to respond to their environment (behavioral plasticity). It is believed that environmental variation is required for plasticity to evolve in cases where the ability to be plastic is costly. We investigate one form of environmental variation: frequency dependent selection. Using tools in game theory, we investigate a few models of plasticity and outline the (...) cases where selection would be expected to maintain it. Ultimately we conclude that frequency dependent selection is likely insufficient to maintain plasticity given reasonable assumptions about its costs. This result is very similar to one aspect of the well-discussed Baldwin effect, where plasticity is first selected for and then later selected against. We show how in these models one would expect plasticity to grow in the population and then be later reduced. Ultimately we conclude that if one is to account for the evolution of behavioral plasticity in this way, one must appeal to a very particular sort of external environmental variation. (shrink)

Mealey argued that sociopathy is an evolutionary stable strategy subject to frequency-dependent selection – high levels of sociopathy being advantageous to the individual if population-wide frequencies of it are low, and vice versa. I argue that at least one alternative hypothesis exists that explains her data equally well. Alternative hypotheses must be formulated and tested before any theory can be validated.

This article utilizes three premises. There are commonly ecologically oriented, naturally selected specialized differences in frequency and/or quality as well as sexually selected differences between the sexes. Sex in the sense of coming together and going apart or going apart and coming together is trade in these naturally selected differences, i.e., there is a mating market in sexual species. While such trade is beneficial to the population as a whole, sexual competition and selection is conflict over the profits (...) of that trade and can be detrimental to the population as a whole. These premises yield a naturally selected sex allocation theory of the possible directions and forms of sexual selection, i.e., one that includes costs as well as frequencies. This can explain conventional sex roles, the sex-role reversed, inter- as well as intrasexual selection, and passive as well as active choice. Any of these alternatives may be over mates, over gametes, or both. A hypothetical example based on density dependence relative to resources is provided, one that suggests that centrioles may be a cytoplasmic resource in males in multicellular animals, and which are the target of active choice and the mechanism of manipulation in passive female choice. As a whole, the approach yields a truly general theory of sexual selection, provides an alternative to the mechanism for Fisher’s principle, and gives a theoretical explanation for Mayr’s biological species definition. (shrink)

The strategic pluralism model depends upon pathogen prevalence and environmental hardship being independent. Evidence is presented that they are positively correlated. The rise in short-term mating strategy in the United States is better explained by changes in the operational sex ratio than by increases in pathogen prevalence. Nonetheless, in highlighting the advantages of a high-investment strategy to less attractive males, Gangestad & Simpson's model helps to clarify the dynamics of frequency-dependent selection.

The widespread potential for somatic fusion among different conspecific multicellular individuals suggests that such fusion is adaptive. However, because recognition of non‐kin (allorecognition) usually leads to a rejection response, successful somatic fusion is limited to close kin. This is consistent with kin‐selection theory, which predicts that the potential cost of fusion and the potential for somatic parasitism decrease with increasing relatedness. Paradoxically, however, Crozier1 found that, in the short term, positive‐frequency‐dependent selection eliminates the required genetic polymorphism (...) at allorecognition loci. The ‘Crozier paradox’ may be solved if allorecognition is based on extrinsically balanced polymorphisms, for example at immune loci. Alternatively, the assumption of most models that self fusion is mutually beneficial is wrong. If fusion is on average harmful, selection will promote unconditional rejection. However, we propose that fusion within individuals is beneficial, selecting for the ability to fuse, but fusion between individuals on average costly, selecting for non‐self recognition (rather than non‐kin recognition). We discuss experimental data on fungi that are consistent with this hypothesis. BioEssays 30:1193–1203, 2008. © 2008 Wiley Periodicals, Inc. (shrink)

Evolutionary gradualism, the randomness of mutations, and the hypothesis that natural selection exerts a pervasive and substantial influence on evolutionary outcomes are pair-wise logically independent. Can the claims about selection and mutation be used to formulate an argument for gradualism? In his Genetical Theory of Natural Selection, R.A. Fisher made an important start at this project in his famous “geometric argument” by showing that a random mutation that has a smaller effect on two or more phenotypes will (...) have a higher average fitness than a random mutation that has a larger phenotypic effect. Motoo Kimura’s demonstration that a gene’s probability of fixation depends on both the selection coefficient and the effective population size shows that Fisher’s argument for gradualism was mistaken. Here we analyze Fisher’s argument and explain how Kimura’s theory leads to a conclusion that Fisher did not anticipate. We identify a fallacy that reasoning about fitness differences and their evolutionary consequences should avoid. We then distinguish forward-directed from backward-directed versions of gradualism. The backward-directed thesis about a single mutation may be correct, but the forward-directed thesis is not. After that we consider a sequence of random mutations that all affect the same cluster of phenotypes and Allen Orr’s idea that there is an optimal sequence of mutation sizes, moving from larger to smaller as the population approaches a fixed optimum. This provides a likelihood justification for a forward-directed version of gradualism when there is a fixed optimum, but it also provides an argument against forward-directed gradualism if the optimum shifts substantially as the population evolves. Finally, we consider whether genome-wide association studies (GWASs) can furnish empirical evidence that bears on the truth of gradualism. The version of gradualism that GWASs directly bear on concerns the phenotypic effect size of a gene after it arises by mutation and has reached an appreciable frequency, not the phenotypic size of the mutation event itself. (shrink)

To the evolutionarily oriented clinical psychiatrist, the discipline of behavioural ecology is a fertile basic science. Human psychology discusses variation in terms of means, standard deviations, heritabilities, and so on, but behavioural ecology deals with mutually incompatible alternative behavioural strategies, the heritable variation being maintained by negative frequency-dependent selection. I suggest that behavioural ecology should be included in the interdisciplinary dialogue recommended by Keller & Miller (K&M). (Published Online November 9 2006).

In their paper “Is psychopathy a mental disease?”, Thomas Nadelhoffer and Walter Sinnott-Armstrong argue that according to any plausible account of mental disorder, neural and psychological abnormalities correlated with psychopathy should be regarded as signs of a mental disorder. I oppose this conclusion by arguing that at least on a naturalistically grounded account, such as Wakefield’s ‘Harmful Dysfunction’ view, currently available empirical data and evolutionary considerations indicate that psychopathy is not a mental disorder.

Since the solution to many public health problems depends on research, it is critical for the progress and well-being for the patients that we can trust the scientific literature. Misconduct and poor laboratory practice in science threatens the scientific progress, leads to loss of productivity and increased healthcare costs, and endangers lives of patients. Data duplication may represent one of challenges related to these problems. In order to estimate the frequency of data duplication in life science literature, a systematic (...) screen through 120 original scientific articles published in three different cancer related journals [journal impact factor 20] was completed. The study revealed a surprisingly high proportion of articles containing data duplication. For the IF 20 journals, 25 % of the articles were found to contain data duplications. The IF 5–10 journal showed a comparable proportion. The proportion of articles containing duplicated data was comparable between the three journals and no significant correlation to journal IF was found. The editorial offices representing the journals included in this study and the individual authors of the detected articles were contacted to clarify the individual cases. The editorial offices did not reply and only 1 out of 29 cases were apparently clarified by the authors, although no supporting data was supplied. This study questions the reliability of life science literature, it illustrates that data duplications are widespread and independent of journal impact factor and call for a reform of the current peer review and retraction process of scientific publishing. (shrink)

How much bacterial evolution occurs in our intestines and which factors control it are currently burning questions. The formation of new ecotypes, some of which capable of coexisting for long periods of time, is highly likely in our guts. Horizontal gene transfer driven by temperate phages that can perform lysogeny is also widespread in mammalian intestines. Yet, the roles of mutation and especially lysogeny as key drivers of gut bacterial adaptation remain poorly understood. The mammalian gut contains hundreds of bacterial (...) species, each with many strains and ecotypes, whose abundance varies along the lifetime of a host. A continuous high input of mutations and horizontal gene transfer events mediated by temperate phages drives that diversity. Future experiments to study the interaction between mutations that cause adaptation in microbiomes and lysogenic events with different costs and benefits will be key to understand the dynamic microbiomes of mammals. Also see the video abstract here: https://youtu.be/Zjqsiyb5Pk0. (shrink)

The ABO histo‐blood group, first discovered over a century ago, is found not only in humans but also in many other primate species, with the same genetic variants maintained for at least 20 million years. Polymorphisms in ABO have been associated with susceptibility to a large number of human diseases, from gastric cancers to immune or artery diseases, but the adaptive phenotypes to which the polymorphism contributes remain unclear. We suggest that variation in ABO has been maintained by frequency‐ (...) class='Hi'>dependent or fluctuating selection pressures, potentially arising from co‐evolution with gut pathogens. We further hypothesize that the histo‐blood group labels A, B, AB, and O do not offer a full description of variants maintained by natural selection, implying that there are unrecognized, functionally important, antigens beyond the ABO group in humans and other primates. (shrink)

Objective: To estimate the level of complementary feeding pattern among children aged between 6 to 23 months and to identify the determinants in individual, household and community level in Bangladesh. Methods: From secondary data of Bangladesh Demographic Health Survey 2011 was used in this study. A total of 2,373 children aged between 6 to 23 months were selected. To estimate the level of CFP “dimension index” was used and the score of the index was used as dependent variables. Statistical (...) analyses and tests were guided by the nature of the variables. Multivariable logistic regression analyses were performed to identify the significant determinants of CFP. Results: The overall level of CFP among children aged between 6 to 23 months was low. More than 95% of the children experienced either no or inadequate CFP. The mean levels of CFP as well as percentages of no or inadequate CFP were significantly lower among children of the youngest age group, uneducated parents, unemployed/laborer fathers, socio-economically poor families, food insecure families and rural areas. No weekly exposure to mass media also revealed significant associations with CFP. However, only few variables remained significant for adequate CFP in the multivariable logistic regression analysis. Adequate CFP was significantly lower among the children aged between 6 to 23 months, children of illiterate fathers and socio-economically middle-class families as compared to their reference categories. Conclusion: Inappropriate and inadequate CFP may cause serious health hazards among children of 6 to 23 months in Bangladesh. It is ethical to take effective interventions and strategies by the government and other concerned stakeholders to improve the overall situation of CFP in Bangladesh. (shrink)

Objective: To estimate the level of complementary feeding pattern (CFP) among children aged between 6 to 23 months and to identify the determinants in individual, household and community level in Bangladesh. Methods: From secondary data of Bangladesh Demographic Health Survey (BDHS) 2011 was used in this study. A total of 2,373 children aged between 6 to 23 months were selected. To estimate the level of CFP dimension index and the “score of the index” was used as dependent variables. Statistical (...) analyses and tests were guided by the nature of the variables. Multivariable logistic regression analyses were performed to identify the significant determinants of CFP. Results: The overall level of CFP among children aged between 6 to 23 months was low. More than 95% of the children experienced inadequate (92.7%) CFP level. The mean levels of CFP as well as percentages of no or inadequate (94.1%) CFP were significantly lower among children of the youngest age group (06 months), uneducated parents, unemployed/laborer fathers, socio-economically poor families, food insecure families and rural areas. However, only few variables remained significant for adequate CFP in the multivariable logistic regression analysis. Adequate CFP was significantly lower among the children aged between 6 to 23 months (OR: 0.22, 95% CI: 0.10-0.47), children of illiterate fathers (OR: 0.32, 95% CI: 0.11-0.95) and socio-economically middle-class families (OR: 0.28, 95% CI: 0.09-0.86) as compared to their reference categories. Conclusion: Inappropriate and inadequate CFP may cause serious health hazards among children of 6 to 23 months in Bangladesh. It is ethical to take effective interventions and strategies by the government and other concerned stakeholders to improve the overall situation of CFP in Bangladesh. (shrink)

This paper identifies the major failings of mainstream economics and the rational choice theory it relies upon. These failures were identified by the four figures mentioned in the title: economics treats agents as rational fools; by the time the long … More ›.

Sociopaths are “outstanding” members of society in two senses: politically, they draw our attention because of the inordinate amount of crime they commit, and psychologically, they hold our fascination because most ofus cannot fathom the cold, detached way they repeatedly harm and manipulate others. Proximate explanations from behavior genetics, child development, personality theory, learning theory, and social psychology describe a complex interaction of genetic and physiological risk factors with demographic and micro environmental variables that predispose a portion of the population (...) to chronic antisocial behavior. More recent, evolutionary and game theoretic models have tried to present an ultimate explanation of sociopathy as the expression of a frequency-dependent life strategy which is selected, in dynamic equilibrium, in response to certain varying environmental circumstances. This paper tries to integrate the proximate, developmental models with the ultimate, evolutionary ones, suggesting that two developmentally different etiologies of sociopathy emerge from two different evolutionary mechanisms. Social strategies for minimizing the incidence of sociopathic behavior in modern society should consider the two different etiologies and the factors that contribute to them. (shrink)

Most research on transmission biases in cultural evolution has treated different biases as distinct strategies. Here I present a model that combines both frequency dependent bias (including conformist bias) and payoff bias in a single decision-making calculus and show that such an integrated learning strategy may be superior to relying on either bias alone. Natural selection may operate on humans’ relative dependence on frequency and payoff information, but both are likely to contribute to the spread of (...) variants with high payoffs. Importantly, the magnitude of conformist bias affects the evolutionary dynamics, and I show that an intermediate level of conformity may be most adaptive and may spontaneously evolve as it resists the invasion of low-payoff variants yet enables the fixation of high-payoff variants in the population. (shrink)

Ronald Giere's analysis of causal effectiveness in populations involves the comparison of two hypothetical populations, one in which every individual has the suspected causal factor, and the other in which none do. Elliott Sober has argued that in cases where causal effectiveness depends on relative population sizes, Giere's analysis breaks down. I take issue with this claim, and argue to the contrary that Giere's analysis can help provide insight into these cases.

BackgroundSubjective cognitive decline, non-amnestic mild cognitive impairment, and amnestic mild cognitive impairment are regarded to be at high risk of converting to Alzheimer’s disease. Amplitude of low-frequency fluctuations can reflect functional deterioration while diffusion tensor imaging is capable of detecting white matter integrity. Our study aimed to investigate the structural and functional alterations to further reveal convergence and divergence among SCD, naMCI, and aMCI and how these contribute to cognitive deterioration.MethodsWe analyzed ALFF under slow-4 and slow-5 bands and white (...) matter fiber integrity among normal controls, SCD, naMCI, and aMCI groups. Correlation analyses were further utilized among paired DTI alteration, ALFF deterioration, and cognitive decline.ResultsFor ALFF calculation, ascended ALFF values were detected in the lingual gyrus and superior frontal gyrus within SCD and naMCI patients, respectively. Descended ALFF values were presented mainly in the LING, SFG, middle frontal gyrus, and precuneus in aMCI patients compared to CN, SCD, and naMCI groups. For DTI analyses, white matter alterations were detected within the uncinate fasciculus in aMCI patients and within the superior longitudinal fasciculus in naMCI patients. SCD patients presented alterations in both fasciculi. Correlation analyses revealed that the majority of these structural and functional alterations were associated with complicated cognitive decline. Besides, UF alterations were correlated with ALFF deterioration in the SFG within aMCI patients.ConclusionsSCD shares structurally and functionally deteriorative characteristics with aMCI and naMCI, and tends to convert to either of them. Furthermore, abnormalities in white matter fibers may be the structural basis of abnormal brain activation in preclinical AD stages. Combined together, it suggests that structural and functional integration may characterize the preclinical AD progression. (shrink)

Incorporating theoretic insights from ageing biology could advance the “staying alive” hypothesis. Higher male extrinsic mortality can weaken selection against ageing-related diseases and self-preservation, leading to high male intrinsic mortality. This may incidentally result in female-biased longevity-promoting traits, a possibility that will require rigorous testing in order to disentangle from the adaptive self-preservation hypothesis presented in the target article.