So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

Human biochemical genetics

Attachment--and loss.

Evolutionary-biological reasoning suggests that individuals should be differentially susceptible to environmental influences, with some people being not just more vulnerable than others to the negative effects of adversity, as the prevailing diathesis-stress view of psychopathology (and of many environmental influences) maintains, but also disproportionately susceptible to the beneficial effects of supportive and enriching experiences (or just the absence of adversity). Evidence consistent with the proposition that individuals differ in plasticity is reviewed. The authors document multiple instances in which (a) phenotypic temperamental characteristics, (b) endophenotypic attributes, and (c) specific genes function less like “vulnerability factors” and more like “plasticity factors,” thereby rendering some individuals more malleable or susceptible than others to both negative and positive environmental influences. Discussion focuses upon limits of the evidence, statistical criteria for distinguishing differential susceptibility from diathesis stress, potential mechanisms of influence, and unknowns in the differentialsusceptibility equation.

/pdf/beyond-diathesis-stress-differential-susceptibility-to-5357tarjg7.pdf

Beyond Diathesis Stress: Differential Susceptibility to Environmental Influences.

Biological reactivity to psychological stressors comprises a complex, integrated, and highly conserved repertoire of central neural and peripheral neuroendocrine responses designed to prepare the organism for challenge or threat. Developmental experience plays a role, along with heritable, polygenic variation, in calibrating the response dynamics of these systems, with early adversity biasing their combined effects toward a profile of heightened or prolonged reactivity. Conventional views of such high reactivity suggest that it is an atavistic and pathogenic legacy of an evolutionary past in which threats to survival were more prevalent and severe. Recent evidence, however, indicates that (a) stress reactivity is not a unitary process, but rather incorporates counterregulatory circuits serving to modify or temper physiological arousal, and (b) the effects of high reactivity phenotypes on psychiatric and biomedical outcomes are bivalent, rather than univalent, in character, exerting both risk-augmenting and risk-protective effects in a context-dependent manner. These observations suggest that heightened stress reactivity may reflect, not simply exaggerated arousal under challenge, but rather an increased biological sensitivity to context, with potential for negative health effects under conditions of adversity and positive effects under conditions of support and protection. From an evolutionary perspective, the developmental plasticity of the stress response systems, along with their structured, context-dependent effects, suggests that these systems may constitute conditional adaptations: evolved psychobiological mechanisms that monitor specific features of childhood environments as a basis for calibrating the development of stress response systems to adaptively match those environments. Taken together, these theoretical perspectives generate a novel hypothesis: that there is a curvilinear, U-shaped relation between early exposures to adversity and the development of stress-reactive profiles, with high reactivity phenotypes disproportionately emerging within both highly stressful and highly protected early social environments.

https://cals.arizona.edu/fcs/sites/cals.arizona.edu.fcs/files/D&P%20Boyce%20&%20Ellis%202005.pdf

Biological sensitivity to context: I. An evolutionary–developmental theory of the origins and functions of stress reactivity

argument is often, if not acrimonious, at least heated. It gives an impression of the fluidity of opinion on many fundamental ideas under discussion and of the urgency with which cardiac cyanosis in the newborn is regarded. When Dr. William Muscott says that the earliest he has operated for pulmonary stenosis is on an infant 3 days old, and Sir Russell Brock agrees that the earlier in the first month that operation is undertaken the better, and when Dr. Varco asks Dr. Senning 'so far as I know they have never yet catheterized any child intrauterine in Sweden, but they have done it through the delivery canal sometimes-would you tell us the indications of the Scandinavian group for catheterization in the immediate newborn period?', one is indeed being kept up with the times. But that was two years ago and already some of the questions then debated have since been answered. This beautifully printed and well-illustrated stiff paperbacked volume is, and will for a few years yet remain, an invaluable companion to a full-scale textbook on congenital heart disease.

Growth at Adolescence.

Prior studies have reported an association between the presence of the 7 repeat allele of the 48 bp repeat polymorphism of the third cytoplasmic loop of the dopamine D4 receptor gene (DRD4) and novelty seeking behaviors, attention deficit hyperactivity disorder (ADHD), Tourette syndrome (TS), pathological gambling, and substance abuse. However, other studies have failed to replicate some of these observations. To determine whether we could replicate these associations we genotyped 737 individuals from four different groups of control subjects, and 707 index subjects from four different groups of impulsive, compulsive addictive behaviors including substance abuse, pathological gambling, TS, and ADHD. Chi-square analysis of those carrying the 7 allele versus non-7 allele carriers was not significant for any of the groups using a Bonferroni corrected alpha of.0125. However, chi-square analysis of those carrying any 5 to 8 allele versus noncarriers was significant for pathological gambling (p <.0001), ADHD (p </=.01) and the total index group (p </=.0004). When the comparison included all 7 alleles the results were significant for gamblers (p <.0001), TS (p </=.003), ADHD (p </=.003), and the total group (p </=.0002). There was a significant increase in the frequency of heterozygosity versus homozygosity for all alleles for pathological gamblers (p </=.0031) and the total index group (p </=.0015), suggesting that heterosis played a role. In the substance abuse subjects a quantitative summary variable for the severity of drug dependence, based on the Addiction Severity Index, showed that the scores varied by increasing severity across the following genotypes: 44 </= heterozygotes </= 77 </= 22. Studies of other quantitative traits indicated an important role for the 2 allele and the 22, 24, and 27 genotypes. All studies indicated that the role of the DRD4 gene in impulsive, compulsive, addictive behaviors is more complex than a sole focus on the 7 versus non-7 alleles.

Studies of the 48 bp repeat polymorphism of the DRD4 gene in impulsive, compulsive, addictive behaviors: Tourette syndrome, ADHD, pathological gambling, and substance abuse.

The published literature on the relationship between behavioral intentions and fertility behavior exhibits four major problems: inconsistent and confusing use of theoretical constructs, limited use of different types of intentions, use of nonbehavioral outcomes, and failure to explore adequately the couple aspects of the intentions/behavior relationship. The study reported here addresses these problems by using a theoretical framework that characterizes the psychological/behavioral sequence leading to a planned conception, three different types of fertility intentions, a behavioral outcome variable, and data from 196 married couples with no children and 185 married couples with one child. Data analysis results in a simultaneous equation, constrained regression model which indicates that child-timing intentions are the most important predictors of proceptive behavior over a 3-1/2 year period and that childbearing intentions are next in importance; that behavioral intentions are the final common pathway through which fertility motivations, attitudes, beliefs, and desires affect behavior; that the use of proceptive behavior as an outcome variable improves the explanatory power of our models; and that the interaction of couple intentions do not demonstrate greater husband or wife influence over couple proceptive behavior but do demonstrate that disagreement has a delaying effect on the onset of that behavior.

Behavioral Intentions: Which Ones Predict Fertility Behavior in Married Couples?1

After briefly reviewing different approaches in the social and behavioral sciences to conceptualize the reasons that humans become motivated to bear children, I present a theoretical framework that incorporates many elements of these approaches. The framework is based on a four-step psychological sequence: the formation of traits, the activation of traits into desires, the translation of desires into intentions, and the implementation of intentions in the form of behavior. I use data from 401 married couples to develop regression models of the two middle steps of this sequence that indicate how childbearing motivational traits lead to childbearing desires and how the latter lead to childbearing intentions. I also develop a regression model that indicates how childbearing motivation affects an individual's perception of his or her spouse's childbearing desires.

Childbearing motivations, desires, and intentions: A theoretical framework.

We present a theoretical framework that organizes individual-level fertility motivations into a couple-level model. One feature of this framework is the Traits-Desires-Intentions-Behaviour (TDIB) sequence through which the fertility motivations of individuals produce instrumental behaviours that are designed to promote or prevent childbearing. A second feature of this framework is the cognitive capacity of individuals to perceive a partner's motivational structure. We combine these two features into a dyad-level model that addresses interactions between partners at each step of the motivational sequence. We elaborate this model first with respect to the perception of partner's motivational structure and second with respect to the combination of partner's and own motivational structure. In the process we consider how couple-level processes of communication, influence, and disagreement can be measured and studied through these interactions. We conclude with a summary discussion of the framework and a consideration of the implications it has for a theory of reproductive psychology, population surveys, and family planning services.

https://www.jstor.org/stable/pdfplus/4148229.pdf

A framework for modelling fertility motivation in couples

Childbearing motivation may be conceptualized as based upon psychological traits and shaped by experiences during childhood, adolescence, and early adult life. This paper explores what those traits and developmental experiences are. Two measures of childbearing motivation, one positive and the other negative, are described. Using a sample of 362 married men and 354 married women, the paper systematically examines the factors associated with these measures. In addition to a set of basic personality traits, these factors include parental characteristics, teenage experiences, and a number of variables from young adult behavior domains such as marriage, education, work, religion, and parental relationships. Stepwise multiple regression analyses lead to two final constrained, simultaneous-equation regression models. These models indicate the importance of both personality traits and diverse life-cycle experiences in the development of childbearing motivation, the differential gender distribution of predictors, and the different experiential antecedents of positive and negative motivation

Warren B. Miller

Papers

Studies of the 48 bp repeat polymorphism of the DRD4 gene in impulsive, compulsive, addictive behaviors: Tourette syndrome, ADHD, pathological gambling, and substance abuse.

Behavioral Intentions: Which Ones Predict Fertility Behavior in Married Couples?1

Childbearing motivations, desires, and intentions: A theoretical framework.

A framework for modelling fertility motivation in couples

Personality traits and developmental experiences as antecedents of childbearing motivation.