The intergenerational transmission of risk and trust attitudes: Replicating and extending "Dohmen, Falk, Huffman and Sunde 2012" using genetically informed twin data.

This replication revisits an influential contribution on the intergenerational transmission of risk and trust attitudes, which, based on data from the German Socioeconomic Panel (GSOEP), reveals a positive correlation between parents' and children's attitudes. The authors of the original study argue that socialization in the family is important in the transmission process. The replication is motivated by mounting evidence indicating that within-family transmission has a considerable genetic component, which calls into question socialization as the main transmission pathway. To consider genetic transmission in addition to social transmission, the replication relies on the German twin family panel TwinLife. The findings reveal that, first, most of the variation in children's risk and social trust attitudes is attributable to differences in the non-shared environment, followed by genetic differences, whereas differences in the shared family environment - the main candidate for social transmission - do not matter. Second, correlations between parents' and children's attitudes essentially involve genetic similarity. Third, family conditions do not moderate these relationships. Thus, the findings do not support the socialization assumption.

The relationship between personality throughout adolescence and social anxiety disorder in young adulthood. A longitudinal twin study.

This study examined the longitudinal relationship between a range of personality related variables measured throughout adolescence, and social anxiety disorder (SAD) in young adulthood. In addition, we examined to what degree the phenotypic associations between personality and SAD could be attributed to shared genetic and environmental factors, respectively. A total of 3394 twins (56% females), consisting of seven national birth cohorts from Norway, participated in the study. Personality was measured with self-report questionnaires at three times throughout adolescence, and SAD was measured with a diagnostic interview in early adulthood (M = 19.1 years, SD = 1.2). Correlation and regression analyses were performed to examine phenotypic associations between personality and SAD. We then created four composite scores of personality, in which the personality variables from four different ages throughout adolescence were weighted relative to their importance for SAD. Finally, a series of Cholesky decomposition models were used to examine the underlying genetic and environmental influences on the phenotypic associations between composite scores of personality and SAD. The results showed that especially higher neuroticism, lower extraversion, higher levels of loneliness, and lower levels of resilience, self-efficacy and sense of coherence, were associated with SAD. The phenotypic correlations between composite scores of personality and SAD increased from 0.42 when personality was measured 6-7 years prior to the assessment of SAD, to 0.52 when personality was measured shortly before the assessment of SAD. These phenotypic associations were mainly due to genetic influences, indicating that personality in adolescence predicts SAD in early adulthood due to shared genetic influences rather than having direct 'causal' effects on SAD.

Genetic confounding in the association of early motor development with childhood and adolescent exercise behavior.

INTRODUCTION: Early motor development has been found to be a predictor of exercise behavior in children and adolescents, but whether this reflects a causal effect or confounding by genetic or shared environmental factors remains to be established. METHODS: For 20,911 complete twin pairs from the Netherlands Twin Register a motor development score was obtained from maternal reports on the timing of five motor milestones. During a 12-year follow-up, subsamples of the mothers reported on the twins' ability to perform seven gross motor skills ability (N = 17,189 pairs), and weekly minutes of total metabolic equivalents of task (MET) spent on sports and exercise activities at age 7 (N = 3632 pairs), age 10 (N = 3735 pairs), age 12 (N = 7043 pairs), and age 14 (N = 3990 pairs). Multivariate phenotypic and genetic regression analyses were used to establish the predictive strength of the two motor development traits for future exercise behavior, the contribution of genetic and shared environmental factors to the variance in all traits, and the contribution of familial confounding to the phenotypic prediction. RESULTS: Significant heritability (h2) and shared environmental (c2) effects were found for early motor development in boys and girls (h2 = 43-65%; c2 = 16-48%). For exercise behavior, genetic influences increased with age (boys: h2age7 = 22% to h2age14 = 51%; girls: h2age7 = 3% to h2age14 = 18%) paired to a parallel decrease in the influence of the shared environment (boys: c2age7 = 68% to c2age14 = 19%; girls: c2age7 = 80% to c2age14 = 48%). Early motor development explained 4.3% (p < 0.001) of the variance in future exercise behavior in boys but only 1.9% (p < 0.001) in girls. If the effect in boys was due to a causal effect of motor development on exercise behavior, all of the factors influencing motor development would, through the causal chain, also influence future exercise behavior. Instead, only the genetic parts of the regression of exercise behavior on motor development were significant. Shared and unique environmental parts of the regression were largely non-significant, which is at odds with the causal hypothesis. CONCLUSION: No support was found for a direct causal effect in the association between rapid early motor development on future exercise behavior. In boys, early motor development appears to be an expression of the same genetic factors that underlie the heritability of childhood and early adolescent exercise behavior.

A Genetically Informed Study of the Association Between Perceived Stress and Loneliness.

Although research shows a strong positive association between perceived stress and loneliness, the genetic and environmental etiology underlying their association remains unknown. People with a genetic predisposition to perceived stress, for example, may be more prone to feeling lonely and vice versa. Conversely, unique factors in people's lives may explain differences in perceived stress levels that, in turn, affect feelings of loneliness. We tested whether genetic factors, environmental factors, or both account for the association between perceived stress and loneliness. Participants were 3,066 individual twins (nFemale = 2,154, 70.3%) from the Washington State Twin Registry who completed a survey during April-May, 2020. Structural equation modeling was used to analyze the item-level perceived stress and loneliness measures. The correlation between latent perceived stress and latent loneliness was .68. Genetic and nonshared environmental variance components underlying perceived stress accounted for 3.71% and 23.26% of the total variance in loneliness, respectively. The genetic correlation between loneliness and perceived stress was .45 and did not differ significantly between men and women. The nonshared environmental correlation was .54 and also did not differ between men and women. Findings suggest that holding constant the strong genetic association between perceived stress and loneliness, unique life experiences underlying people's perceived stress account for individual differences in loneliness.

Are Genetic and Environmental Risk Factors for Psychopathology Amplified in Children with Below-Average Intelligence? A Population-Based Twin Study.

There is a negative association between intelligence and psychopathology. We analyzed data on intelligence and psychopathology to assess this association in seven-year-old Dutch twin pairs (ranging from 616 to 14,150 depending on the phenotype) and estimated the degree to which genetic and environmental factors common to intelligence and psychopathology explain the association. Secondly, we examined whether genetic and environmental effects on psychopathology are moderated by intelligence. We found that intelligence, as assessed by psychometric IQ tests, correlated negatively with childhood psychopathology, as assessed by the DSM-oriented scales of the Child Behavior Check List (CBCL). The correlations ranged between - .09 and - .15 and were mainly explained by common genetic factors. Intelligence moderated genetic and environmental effects on anxiety and negative affect, but not those on ADHD, ODD, and autism. The heritability of anxiety and negative affect was greatest in individuals with below-average intelligence. We discuss mechanisms through which this effect could arise, and we end with some recommendations for future research.

Continuity and change of genetic and environmental influences on reading and reading-related neurocognitive skills: A systematic review of longitudinal twin studies.

Learning to read is a dynamic and cumulative process beginning from birth and continuing through the school years. Empirical data showed a decrease of additive genetic (A) and shared environmental (C) components and an increase of non-shared environmental (E) components from preschool to middle school. However, our understanding of the aetiology of continuity and change of reading skills across this developmental period is limited. Following the PRISMA guidelines, we reviewed the results of behavioral genetic research on reading-related neurocognitive skills of 13 longitudinal twin and adoptive sibling studies spanning from preschool/kindergarten to middle/high school. Our findings suggested that continuity was mainly explained by A components throughout the study periods, and, although to a lesser extent and less consistently, by C components during the early years; change was explained by new E components throughout the years, and also by new A components in the early years. As we are interested in models relevant to traits with early onset during development, it is crucial to deepen the investigation of how developmental time can moderate the genetic and environmental variation.

Genotype-Environment Interaction in ADHD: Genetic Predisposition Determines the Extent to Which Environmental Influences Explain Variability in the Symptom Dimensions Hyperactivity and Inattention.

Although earlier research has shown that individual differences on the spectrum of attention deficit hyperactivity disorder (ADHD) are highly heritable, emerging evidence suggests that symptoms are associated with complex interactions between genes and environmental influences. This study investigated whether a genetic predisposition [Note that the term 'genetic predisposition' was used in this manuscript to refer to an estimate based on twin modeling (an individual's score on the latent trait that resembles additive genetic influences) in the particular population being examined.] for the symptom dimensions hyperactivity and inattention determines the extent to which unique-environmental influences explain variability in these symptoms. To this purpose, we analysed a sample drawn from the Twins Early Development Study (TEDS) that consisted of item-level scores of 2168 16-year-old twin pairs who completed both the Strengths and Difficulties Questionnaire (SDQ; Goodman, in J Child Psychol Psychiatry 38:581-586, 1997) and the Strength and Weaknesses of ADHD Symptoms and Normal Behavior (SWAN; Swanson, in Paper presented at the meeting of the American Psychological Association, Los Angeles, 1981) questionnaire. To maximize the psychometric information to measure ADHD symptoms, psychometric analyses were performed to investigate whether the items from the two questionnaires could be combined to form two longer subscales. In the estimation of genotype-environment interaction, we corrected for error variance heterogeneity in the measurement of ADHD symptoms through the application of item response theory (IRT) measurement models. A positive interaction was found for both hyperactivity (e.g., [Formula: see text] = 2.20 with 95% highest posterior density interval equal to [1.79;2.65] and effect size equal to 3.00) and inattention (e.g., [Formula: see text] = 2.16 with 95% highest posterior density interval equal to [1.56;2.79] and effect size equal to 3.07). These results indicate that unique-environmental influences were more important in creating individual differences in both hyperactivity and inattention for twins with a genetic predisposition for these symptoms than for twins without such a predisposition.

Linking genetic foundations of sleep disturbances to personality traits: a study of mid-life twins.

Risk of sleep disturbances depends on individuals' personality, and a large body of evidence indicates that individuals prone to neuroticism, impulsivity, and (low) extraversion are more likely to experience them. Origins of these associations are unclear, but common genetic background may play an important role. Participants included 405 twin pairs (mean age of 54 years; 59% female) from the National Survey of Midlife Development in the United States (MIDUS) who reported on their personality traits (broad and specific), as well as sleep disturbances (problems with falling asleep, staying asleep, waking early, and feeling unrested). Uni- and bivariate biometric decompositions evaluated contributions of genetic and environmental factors to associations between personality and poor sleep, as well as unique contributions from individual traits. Neuroticism, extraversion, conscientiousness, and aggressiveness were the strongest phenotypic predictors of poor sleep. Genetic sources of covariance were about twice as large as non-shared environmental sources, and only shared genetic background accounted for links between aggressiveness and poor sleep. Neuroticism and extraversion accounted for most of the genetic overlap between personality and sleep disturbances. The findings shed light on developmental antecedents of ties between personality and poor sleep, suggesting a larger role of common genetic background than idiosyncratic life experiences. The results also suggest that emotion-related traits play the most important role for poor sleep, compared to other personality traits, and may partially account for genetic associations with other traits.

Shared and unique heritability of hippocampal subregion volumes in children and adults.

Behavioral genetic analyses have not demonstrated robust, unique, genetic correlates of hippocampal subregion volume. Genetic differentiation of hippocampal longitudinal axis subregion volume has not yet been investigated in population-based samples, although this has been demonstrated in rodent and post-mortem human tissue work. The following study is the first population-based investigation of genetic factors that contribute to gray matter volume along the hippocampal longitudinal axis. Twin-based biometric analyses demonstrated that longitudinal axis subregions are associated with significant, unique, genetic variance, and that longitudinal axis subregions are also associated with significant shared, hippocampus-general, genetic factors. Our study's findings suggest that genetic differences in hippocampal longitudinal axis structure can be detected in individual differences in gray matter volume in population-level research designs.

Associations between executive functions assessed in different contexts in a genetically informative sample.

Executive functions (EFs) are cognitive functions that help direct goal-related behavior. EFs are usually measured via behavioral tasks assessed in highly controlled laboratory settings under the supervision of a research assistant. Online versions of EF tasks are an increasingly popular alternative to in-lab testing. However, researchers do not have the same control over the testing environment during online EF assessments. To assess the extent to which EFs assessed in-lab and online are related, we used data from the Colorado Online Twin Study (CoTwins; 887 individual twins aged 13.98-19.05) and constructed an Lab Common EF factor and an Online Common EF factor from four EF tasks assessed in-lab and online. The Lab Common and Online Common EF factors were genetically identical (rA = 1.00) but phenotypically separable (r = .77, 95% confidence interval [0.59, 0.94]) indicating that these EF factors have the same genetic underpinnings but may be differentially influenced by environmental factors. We examined phenotypic, genetic, and environmental correlations between the EF factors and a general cognitive ability factor (g) assessed in the lab and found similar relationships between Lab Common EF and g and Online Common EF and g. Overall, these results suggest that Common EF factors assessed in different contexts are highly related to each other and similarly related to other cognitive outcomes. These findings indicate that online task-based EF assessments could be a viable strategy for increasing sample sizes in large-scale studies, particularly genetically informed studies. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Reconsidering the failure model: Using a genetically controlled design to assess the spread of problems from reactive aggression to internalizing symptoms through peer rejection across the primary school years.

According to the failure model (Patterson & Capaldi, 1990), peer rejection is the intermediary link between problem behaviors and internalizing symptoms. The present study tested the model with 464 monozygotic and same-sex dizygotic twin pairs (234 female, 230 male dyads). Teacher-reported reactive aggression and internalizing symptoms, and peer-reported peer rejection were collected at ages 6, 7, and 10 (from 2001 to 2008). Support for the failure model emerged in conventional non-genetically controlled analyses, but not twin-difference score analyses (which remove shared environmental and genetic contributions). Univariate biometric models attributed minimal variance in failure model variables to shared environmental factors, suggesting that genetic factors play an important unacknowledged role in developmental pathways historically ascribed to nonshared experiences in the failure model.

Connecting loneliness with pathological personality traits: Evidence for genetic and environmental mediation from a study of older twins.

Loneliness has broad public health importance, especially in older adulthood, and there is some evidence suggesting it is associated with several personality disorders (PDs). The etiology of these PD-loneliness associations, however, has rarely been studied, especially in the context of the maladaptive traits of the DSM-5 alternative model of personality disorder (AMPD). To address these limitations, we estimated phenotypic, genetic, and unique environmental associations between loneliness and maladaptive personality traits in a sample of older adults from the Minnesota Twin Registry (n = 1,356, Mage = 70.4). Loneliness was moderately to strongly associated with each of the AMPD domains of negative affect, detachment, antagonism, disinhibition, and psychoticism (r = .22-.58), with evidence of both genetic (rg = .45-.75) and unique environmental (re = .10-.48) influences explaining the associations to varying degrees. We argue that loneliness may be an underappreciated concomitant of personality pathology, with PD traits perhaps underlying its development. Indeed, these findings suggest that loneliness may be a manifestation of the genetic and environmental forces that also lead to pathological personality variation. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Genetic and shared environmental factors explain the association between adolescent polysubstance use and high school noncompletion.

OBJECTIVE: Examine the nature of the relationship between adolescent polysubstance use and high school noncompletion. METHOD: Among a sample of 9,579 adult Australian twins (58.63% female, Mage = 30.59), we examined the association between the number of substances used in adolescence and high school noncompletion within a discordant twin design and bivariate twin analysis. RESULTS: In individual-level models controlling for parental education, conduct disorder symptoms, childhood major depression, sex, zygosity, and cohort, each additional substance used in adolescence was associated with a 30% increase in the odds of high school noncompletion (OR = 1.30 [1.18, 1.42]). Discordant twin models found that the potentially causal effect of adolescent use on high school noncompletion was nonsignificant (OR = 1.19 [0.96, 1.47]). Follow-up bivariate twin models suggested genetic (35.4%, 95% CI [24.5%, 48.7%]) and shared environmental influences (27.8%, 95% CI [12.7%, 35.1%]) each contributed to the covariation in adolescent polysubstance use and early school dropout. CONCLUSIONS: The association between polysubstance use and early school dropout was largely accounted for by genetic and shared environmental factors, with nonsignificant evidence for a potentially causal association. Future research should examine whether underlying shared risk factors reflect a general propensity for addiction, a broader externalizing liability, or a combination of the two. More evidence using finer measurement of substance use is needed to rule out a causal association between adolescent polysubstance use and high school noncompletion. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

The Heritability of Psychopathology Symptoms in Early Adolescence: Moderation by Family Cultural Values in the ABCD Study.

Family cultural values that emphasize support, loyalty, and obligation to the family are associated with lower psychopathology in Hispanic/Latino/a youth, but there is a need to understand the implications of family cultural values for youth development in racially/ethnically heterogeneous samples. This study examined phenotypic associations between parent- and youth-reported family cultural values in late childhood on youth internalizing and externalizing symptoms in early adolescence, and whether family cultural values moderated genetic and environmental influences on psychopathology symptoms. The sample comprised 10,335 children (Mage=12.89 years; 47.9% female; 20.3% Hispanic/Latino/a, 15.0% Black, 2.1% Asian, 10.5% other) and their parents from the Adolescent Brain Cognitive Development (ABCD) Study, and biometric models were conducted in the twin subsample (n = 1,042 twin pairs; 43.3% monozygotic). Parents and youth reported on their family cultural values using the Mexican American Cultural Values Scale at youth age 11-12, and parents reported on youth internalizing and externalizing symptoms using the Child Behavior Checklist at youth ages 11-12 and 12-13. Greater parent- and youth-reported family cultural values predicted fewer youth internalizing and externalizing symptoms. Biometric models indicated that higher parent-reported family cultural values increased the nonshared environmental influences on externalizing symptoms whereas youth-reported family cultural values decreased the nonshared environmental influences on internalizing symptoms. This study highlights the need for behavior genetic research to consider a diverse range of cultural contexts to better understand the etiology of youth psychopathology.

The Challenges and Opportunities for Mental Health Twin Research in Nigeria.

The recent interest in increasing diversity in genetic research can be useful in uncovering novel insights into the genetic architecture of mental health disorders - globally and in previously unexplored settings such as low- and middle-income settings like Nigeria. Genetic research into mental health is potentially promising in Nigeria and we reflect on the challenges and opportunities for twin research which may be particularly suited to Nigeria. The higher rates of twinning in Africa and Nigeria specifically, make the twin design an affordable and readily maintainable approach for genetic research in the country. Despite potential challenges with recruitment, data collection, data analysis and dissemination; the success of current efforts suggest that the twin design can tapped even further for greater impact in the country. We highlight some ways in which the scope of twin research can be increased and suggest some ways in which existing challenges can be overcome including recent Patient Participant Involve and Engagement activities.

The interaction between polygenic risk and environmental influences: A direct test of the 3P model of insomnia in adolescents.

BACKGROUND: Stress is a universal phenomenon and one of the most common precipitants of insomnia. However, not everyone develops insomnia after experiencing a stressful life event. This study aims to test aspects of Spielman's '3P model of insomnia' (during adolescence) by exploring the extent to which: (a) insomnia symptoms are predicted by polygenic scores (PGS); (b) life events predict insomnia symptoms; (c) the interaction between PGS and life events contribute to the prediction of insomnia symptoms; (d) gene-environment interaction effects remain after controlling for sex. METHODS: The sample comprised 4,629 twins aged 16 from the Twin Early Development Study who reported on their insomnia symptoms and life events. PGS for insomnia were calculated. In order to test the main hypothesis of this study (a significant interaction between PGS and negative life events), we fitted a series of mixed effect regressions. RESULTS: The best fit was provided by the model including sex, PGS for insomnia, negative life events, and their interactions (AIC = 26,158.7). Our results show that the association between insomnia symptoms and negative life events is stronger for those with a higher genetic risk for insomnia. CONCLUSIONS: This work sheds light on the complex relationship between genetic and environmental factors implicated for insomnia. This study has tested for the first time the interaction between genetic predisposition (PGS) for insomnia and environmental stressors (negative life events) in adolescents. This work represents a direct test of components of Spielman's 3P model for insomnia which is supported by our results.

Evaluating alternative models of youth externalizing using quantitative genetic analyses.

Interest has increased in the recent literature on characterizing psychopathology dimensionally in hierarchical models. One dimension of psychopathology that has received considerable attention is externalizing. Although extensively studied and well-characterized in late adolescents and adults, delineation of the externalizing spectrum in youth has lagged behind. As a complement to structural analyses of externalizing, in this study, we use quantitative genetic analyses of twin data to adjudicate among alternative models of youth externalizing that differ in granularity. Specifically, we compared model fit, estimates of genetic and environmental influences on the externalizing dimension, and the average, variability, and precision of genetic and environmental influences on individual symptoms due to the externalizing dimension, specific symptom dimensions, and unique etiological influences. Given that none of these criteria are definitive on their own, we looked to the confluence of these criteria to exclude particular models while highlighting others as leading contenders. We analyzed parent-report data on 38 externalizing symptoms from a population-representative, ethnically diverse sample of 883 youth twin pairs (51% female), who were on average 8.5 years old. Although models including an externalizing composite and attention deficit hyperactivity disorder, oppositional defiant disorder, and conduct disorder diagnoses and symptom dimensions showed similar heritability to latent variable models of externalizing, models that included latent dimensions of externalizing and more fine-grained symptom dimensions fit better and were more balanced in the magnitude of genetic and environmental influences on individual symptoms due to the externalizing dimension and specific symptom dimensions. Pending replication, these more granular and elaborated model(s) can be useful for advancing research on causes and outcomes of youth externalizing and its fine-grained specific components. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Structural and functional network analysis of twins using fMRI data.

Similarities between twins have been widely demonstrated, underscoring the remarkable influence of genetics across numerous traits. In this study, we explore the genetic underpinnings of the human brain by examining MRI data from the Queensland Twin Imaging study. Specifically, this study seeks to compare brain structure and function between twins and unrelated subjects, with an emphasis on describing the effects of genetic factors. To achieve these goals, we employed the source-based morphometry method to extract intrinsic components and elucidate recognizable patterns. Our results show that twins exhibit a higher degree of similarity in gray and white matter density compared with unrelated individuals. In addition, four distinct states of brain activity were identified using coactivation patterns analysis. Furthermore, twins demonstrated a greater degree of similarity in the temporal and spatial features of each state compared with unrelated subjects. Taken together, these results support the hypothesis that twins show greater similarity in both brain structure and dynamic functional brain activity. Further exploration of these methods may advance our understanding of the complex interplay between genes, environment, and brain networks.

Nonlinear Catch-Up Growth in Height, Weight, and Head Circumference from Birth to Adolescence: A Longitudinal Twin Study.

Owing to high rates of prenatal complications, twins are, on average, substantially smaller than population norms on physical measurements including height, weight, and head circumference at birth. By early childhood, twins are physically average. This study is the first to explore the process of catch-up growth by fitting asymptotic growth models to age-standardized height, weight, and head circumference measurements in a community sample of twins (n = 1281, 52.3% female) followed at up to 17 time points from birth to 15 years. Catch-up growth was rapid over the first year and plateaued around the population mean by early childhood. Shared environmental factors accounted for the majority of individual differences in initial physical size (57.7-65.5%), whereas additive genetic factors accounted for the majority of individual differences in the upper asymptotes of height, weight, and head circumference (73.4-92.6%). Both additive genetic and shared environmental factors were associated with variance in how quickly twins caught up. Gestational age and family SES emerged as important environmental correlates of physical catch-up growth.

Genetic Influence on Gyral Peaks.

Genetic mechanisms have been hypothesized to be a major determinant in the formation of cortical folding. Although there is an increasing number of studies examining the heritability of cortical folding, most of them focus on sulcal pits rather than gyral peaks. Gyral peaks, which reflect the highest local foci on gyri and are consistent across individuals, remain unstudied in terms of heritability. To address this knowledge gap, we used high-resolution data from the Human Connectome Project (HCP) to perform classical twin analysis and estimate the heritability of gyral peaks across various brain regions. Our results showed that the heritability of gyral peaks was heterogeneous across different cortical regions, but relatively symmetric between hemispheres. We also found that pits and peaks are different in a variety of anatomic and functional measures. Further, we explored the relationship between the levels of heritability and the formation of cortical folding by utilizing the evolutionary timeline of gyrification. Our findings indicate that the heritability estimates of both gyral peaks and sulcal pits decrease linearly with the evolution timeline of gyrification. This suggests that the cortical folds which formed earlier during gyrification are subject to stronger genetic influences than the later ones. Moreover, the pits and peaks coupled by their time of appearance are also positively correlated in respect of their heritability estimates. These results fill the knowledge gap regarding genetic influences on gyral peaks and significantly advance our understanding of how genetic factors shape the formation of cortical folding. The comparison between peaks and pits suggests that peaks are not a simple morphological mirror of pits but could help complete the understanding of folding patterns.