Genetic and environmental effects on mortality before age 70 years

BACKGROUND: There is a familial influence on risk of many diseases and on mortality in general, which, according to studies of twins, is due to a combination of genetic and environmental effects. Adoption studies, which rest on different assumptions, may also be used to estimate separately the genetic and environmental effects on rate of dying. METHODS: The genetic influence on the rate of dying before age 70 years was investigated by estimation of the associations in total and cause-specific mortality of Danish adoptees and their biologic full and half siblings. Familial environmental influences shared at the same time in life were investigated in adoptees and their adoptive siblings. The study basis is the 14,425 nonfamilial adoptions formally granted in Denmark during the period 1924 through 1947, recorded in the Danish Adoption Register. From this register we selected the 1552 "case" adoptees (who died before 01 April 1993) and 1710 "noncase" adoptees alive at that date. The siblings of the case and noncase adoptees were traced in the archives and followed forward, and the rates of dying before age 70 years were compared. RESULTS: Compared with mortality of the biologic siblings of noncase adoptees, the mortality of biologic siblings of dead adoptees was approximately 2-fold higher for death with infections and vascular causes, and around 45% increased for natural causes and for all causes. CONCLUSION: The results suggest that there is a genetic effect on the rate of death with infections, vascular causes, natural causes and all causes, whereas there is no indication of an influence of shared sibling environment.     

Case-control study of genetic and environmental influences on premature death of adult adoptees

Genetic and environmental influence on risk of premature death in adulthood was investigated by estimating the associations in total and cause-specific mortality of adult Danish adoptees and their biological and adoptive parents. Among all 14,427 nonfamilial adoptions formally granted in Denmark during the period 1923 through 1947, we identified 976 case families in which the adoptee died before a fixed date. As control families, we selected 976 families where the adoptees were alive on that date, and matched to the case adoptees with regard to gender and year and month of birth. The data were viewed as a cohort of case parents and a cohort of control parents, and lifetime distributions in the two cohorts were compared using a Cox regression, stratified with regard to the matching variables: gender and year of birth. In the main analyses, the sample was restricted with regard to birth year of the adoptees, and age of transfer to the adoptive parents, and age at death was restricted to the same range for parents and offspring (25-64 years) in order to consider a symmetric lifetime distribution. This reduces the sample to 459 case families and 738 control families. Various truncations, restrictions, and stratifications were used in order to examine the robustness of the results. The results showed a higher mortality among biological parents who had children dying in the age range 25 through 64 years, and this was significant for death from natural causes, infectious causes, vascular causes, and from all causes combined. There were no significant effects for the adoptive parents. This study supports that there are moderate genetic influences on the risk of dying prematurely in adulthood, and only a small, if any, effect of the family environment.     

Premature death of adult adoptees: analyses of a case-cohort sample

Genetic and environmental influence on risk of premature death in adulthood was investigated by estimating the associations in total and cause-specific mortality of adult Danish adoptees and their biological and adoptive parents. Among all 14,425 non-familial adoptions formally granted in Denmark during the period 1924 through 1947, we selected the study population according to a case-cohort sampling design. As the case-control design, the case-cohort design has the advantage of economic data collection and little loss in statistical efficiency, but the case-cohort sample has the additional advantages that rate ratio estimates may be obtained, and re-use of the cohort sample in future studies of other outcomes is possible. Analyses were performed using Kalbfleisch and Lawless's estimator for hazard ratio, and robust estimation for variances. In the main analyses the sample was restricted to birth years of the adoptees 1924 and after, and age of transfer to the adoptive parents before 7 years, and age at death was restricted to 16 to 70 years. The results showed a higher mortality among adoptees, whose biological parents died in the age range of 16 to 70 years; this was significant for deaths from natural causes, vascular causes and all causes. No influence was seen from early death of adoptive parents, regardless of cause of death.     

Genetic and environmental influences on the relation between parental social class and mortality

BACKGROUND: Genetic and maternal prenatal environmental factors as well as the post-natal rearing environment may contribute to the association between childhood socioeconomic circumstances and later mortality. In order to disentangle these influences, we studied all-cause and cause-specific mortality in a cohort of adoptees, in whom we estimated the effects of their biological and adoptive fathers' social classes as indicators of the genetic and/or prenatal environmental factors and the post-natal environment, respectively. METHODS: In all 12 608 children born 1924-47 in Denmark who were placed early in life with adoptive parents were followed up for causes of death until 2000. Hazard ratios for paternal social class retrieved from adoption records were estimated using Cox regression models. RESULTS: Adoptees with biological fathers from higher social classes had a lower rate of mortality after their fifth decade of life, mainly due to a lower risk of cardiovascular, infectious, and respiratory diseases. Adoptive father's social class showed no clear relation with adoptee's mortality risk. The risk estimates for paternal social class were slightly attenuated after adjustment for adoptee's adult social class, which as expected was inversely related to mortality from both natural and external causes. CONCLUSION: Genetic and/or prenatal environmental factors contribute to the development of the relation of paternal social class to mortality from natural causes later in adult life independently of the effect of own social class, whereas there is no evidence for such long-term effect of the rearing environment.     

Influence of genes and family environment on adult smoking behavior assessed in an adoption study.

Twin studies suggest that genetic factors influence smoking behavior. However, in these studies, genetic and environmental influences may be confounded. We examined whether smoking behavior of adoptees is associated with smoking behavior in adoptive and biological relatives in a design in which this confounding is minimized. Data on smoking status were collected using a mailed questionnaire in a sample of 840 adoptive families from the Danish Adoption Register including all non-familial adoptions from 1924 through 1947. Smoking data were available for 706 adoptees, 451 biological fathers, 580 biological mothers, 641 adoptive fathers, 693 adoptive mothers, 199 biological full-siblings, 684 maternal half-siblings, and 576 paternal half-siblings. Adoptees' status as ever, current, heavy, or former (ex-)smokers was related to their relatives' smoking status. Adoptees ever smoking was associated with their full-siblings' status as ever smokers (OR = 3.6 [1.5-8.7]). Adoptees' current smoking was also associated with their full-siblings' ever (OR = 3.2 [1.5-7.7]) and current (OR = 2.6 [1.3-5.0]) smoking, whereas adoptees' heavy smoking was associated with their full-siblings ever (OR = 5.5 [2.1-14.3]), current (OR = 4.0[1.9-8.6]) and heavy (OR = 2.0[1.0-4.2]) smoking. Compared with current smokers, adoptee ex-smokers had full-siblings who were ex-smokers more often (OR = 3.5 [1.0-11.6]), current (OR = 0.4 [0.2-0.8]), and heavy (OR = 0.3 [0.1-0.9]) smokers less often. Adoptees' smoking behavior was not associated with adoptive or biological parents' status as current smokers. This study of smoking behavior in adult adoptees and their biological and adoptee family supports the finding in twin studies of a genetic influence on smoking within the same generation.     

Cardiovascular risk factors in a French Canadian population: resolution of genetic and familial environmental effects on blood pressure using twins, adoptees, and extensive information on environmental correlates

Genetic and environmental influences on systolic (SBP), diastolic (DBP), and mean arterial (MBP) blood pressure were examined using an expanded version of a path model in which parents and their singleton, twin, and adopted offspring were incorporated, and which also included an environmental index as an estimate of the underlying familial environmental component. Estimates of genetic heritability are lower in parents (10-15%) than in offspring (40-50%). Cultural heritability was significant for SBP (0.31) and MBP (0.40), and an intergenerational effect was found for DBP, with higher estimates in parents (0.42) than in offspring (0.21). Marital resemblance was significant, and no support was found for differential maternal and paternal cultural transmission. Two novel results arising from this study are 1) gender-specific sibling effects, with greater female than male resemblance for SBP and MBP and the opposite pattern for DBP, and 2) the suggestion of extra twin resemblance arising on account of additional shared environments and resulting in greater like-sex than opposite-sex twin resemblance. The major conclusions drawn from this study are that 1) parameter estimates are stable with or without the use of extensive environmental indices, and 2) the addition of twins and adoptees did not significantly impact the results, with the exception of a possible influence of the adoptees in estimates of cultural heritability for DBP. Combining both these features (i.e., extended relatives and environmental indices) enables testing for additional sources of familial aggregation, which is not possible using the traditional nuclear family approach and results in a more accurate assessment of the relative roles of heredity and environment on blood pressure than has been previously possible.     

Familial aggregation of blood pressure and weight in adoptive families. I. Comparisons of blood pressure and weight statistics among families with adopted, natural, or both natural and adopted children

Tests of homogeneity of means, variances and correlations for systolic blood pressure (BP), diastolic BP and weight among subdivisions of a smple of adoptive families are presented. The means and variances of either type of BP, but not weight, were not significantly heterogeneous among families grouped according to the number of parents and children, natural and/or adopted, in the family unit. Estimates of correlation between family members wree not heterogeneous among subdivisions for each of the three variables. Our results indicate that these data are suitable for a genetic analysis of familial aggregation. Pooled correlations suggest that the degree of resemblance of BP and of weight between family members varies within and across generations. Correlations involving the adoptees were significantly different from zero only for diastolic BP.     

Familial aggregation of blood pressure and weight in adoptive families. III. Analysis of the role of shared genes and shared household environment in explaining family resemblance for height, weight and selected weight/height indices

This study presents an analysis of the role of genetic and household environment in explaining the familial aggregation of height (HT), weight (WT), and body mass indices (WT/HT1.2 and WT/HT2.0). The biologic model used for the analysis partitions the covariances between family members into the contributions of genetic and environmental variability shared within and across generations, including a variance component shared only by a mother and her natural children. Tests of hypotheses suggest that shared genes and shared household environmental factors make significant contributions to the familial aggregation of WT (adjusted for age and sex) and of HT (adjusted for age and sex), whereas family resemblance of WT adjusted for age and HT can be attributed mostly to the effects of shared genes. The familial aggregation of selected WT/HT indices is attributed to the effects of shared household environment only, suggesting that these variables measure a characteristic of stature that is independent of height and weight.     

Familial patterns of covariation for cardiovascular risk factors in adults: The Victorian Family Heart Study

The Victorian Family Heart Study was established to address the causes of familial patterns in cardiovascular risk factors. From 1990 to 1996, a representative population sample of 783 adult families (2,959 individuals), each comprising both parents (40-70 years) and at least one natural adult offspring (18-30 years), was recruited in Melbourne, Australia. Included in both generations were 461 monozygotic and dizygotic twins as pairs or singletons. A multivariate normal model was used for pedigree analysis of height, weight, body mass index, diastolic and systolic blood pressure, pulse rate, and total and high density lipoprotein cholesterol. All traits showed evidence for additive genetic variation, explaining from 55% (height) to 26% (pulse) of age- and sex-adjusted variance. An effect persisting into adulthood of shared family environment during cohabitation explained from 39% (body mass index) to 13% (systolic blood pressure) of variance (not nominally significant for diastolic blood pressure). These shared environmental effects were strongest within twin pairs, less so for sibling pairs, and least for parent-offspring pairs (in which an effect was not observed for weight, diastolic and systolic blood pressure, and total cholesterol). On a background of genetic influences, there are periods in early life during which the family environment cements long-term correlations between adult relatives in cardiovascular risk factors.     

Substantial intergenerational increases in body mass index are not explained by the fetal overnutrition hypothesis: the Cardiovascular Risk in Young Finns Study

BACKGROUND: According to the fetal overnutrition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the offspring. If the hypothesis is true, then the association between maternal body mass index (BMI; in kg/m(2)) and offspring BMI should be stronger than the association between paternal BMI and offspring BMI, because only the mother directly influences the fetal environment. OBJECTIVES: We prospectively examined intergenerational change in BMI and tested the fetal overnutrition hypothesis. DESIGN: Data on offspring weight were obtained from mothers. BMI was assessed from 2980 complete parent-offspring trios when the offspring were 3 to 18 y of age. The assessment of offspring BMI was repeated 21 y later at age 24-39 y. RESULTS: Adult BMI of the offspring was 1.21 units higher than the BMI of their parents at the same age, which indicates an increase in obesity levels across generations (P < 0.0001). Maternal BMI was more strongly associated with offspring birth weight than was paternal BMI (P = 0.0009). However, there were no such differences in parent-offspring associations for BMI at later developmental stages when offspring were aged 3-39 y (P > 0.35). The results did not materially change in a sensitivity analysis for 1% to 15% nonpaternity. CONCLUSIONS: Because offspring share all genes with their parents, the observed substantially higher adult BMI for offspring than for parents is likely explained by environmental influences. No support was found for any specific influence from fetal environment on this intergenerational increase in adult obesity. The findings were consistent with the fetal overnutrition hypothesis only in relation to birth weight.     

Familial aggregation of blood pressure and weight in adoptive families. II. Estimation of the relative contributions of genetic and common environmental factors to blood pressure correlations between family members

An analysis of the familial aggregation of blood pressure (BP) was conducted to provide estimates of the role of genes and household environment in determining the phenotypic resemblance between biologically related family members. The biological model used for this analysis parameterizes the correlations between family members into the contributions of genetic and environmental variability shared within and across generations. Hypothesis testing about different parameters in the model suggests that shared environment explains larger fractions of the parent-natural child and the full sib correlations for diastolic BP than for systolic BP. For diastolic BP, children in a household share the effects of common environment in addition to the effects which they share with their parents. Dependence of the degree of resemblance between household members on the effects of environmental factors shared within and a-ross generations is not explained by the variability of length of cohabitation among individuals.     

Symptom patterns and causes of somatization in men: II. Genetic and environmental independence from somatization in women

The genetic and environmental antecedents of clinically distinct disorders leading to somatization were compared in 807 Swedish men and 859 Swedish women adopted at an early age by non-relatives. Asthenic somatization, the predominant form in men, was a neurotic disorder associated with a lower incidence of criminality in the somatizers' biological parents than in the biological parents of non-somatizers of either sex. In contrast, most female somatizers and a minority of men with diversiform somatization had disorders that were associated with a higher incidence of criminality in their biological parents than in other biological parents. Likewise, female somatizers, but not male somatizers, had an excess of alcoholic biological fathers when compared to other adoptees. In addition, different postnatal environmental background factors contributed to the risk for somatization in each sex. These findings support the distinctions among the different types of somatizers and show that the usual causes of somatization are fundamentally different in men and women. This illustrates the utility of the adoption paradigm in resolving genetic and environmental contributions to the familial aggregation of developmentally complex phenotypes.     

Familial resemblance of adiposity-related parameters: results from a health check-up population in Taiwan

The mechanisms of obesity is still unclear, however, genetic and environmental factors are two major possible causes of obesity. The purpose of this study was to assess the degree of familial resemblance of different obesity-related parameters in a health check-up population in Taiwan. We measured body mass index (BMI), waist-to-hip ratio (WHR) and percentage of body fat (BFAT) anthropometrics in 1724 members of 431 families participating in the MJ Health Screening program. Each family contributed four members, i.e. father, mother, son, and daughter. All the participants were free from coronary heart disease, hypertension, diabetes, dyslipidemia, and generally in good health. The degree of familial aggregation was measured by heritability that was calculated based on age-adjusted familial (parent-offspring, sibling, spouse) correlations. The maximal heritability estimates were 39, 30 and 35% for BMI, WHR and BFAT, respectively. For WHR, the correlation between spouses was not significant and the heritability appears to be predominantly due to genetic causes. Furthermore, for BMI and BFAT, the spouse correlations were 0.08 and 0.11, respectively. The heritabilities for BMI and BFAT were mostly explained by genetic factors and familial environmental factors such as dietary habits or physical activity. The familial resemblance of various obesity-related parameters was moderate in a health check-up population in Taiwan. While the heritability for WHR appears to be mainly due to genetic factors, the familial resemblance for BMI and percentage of BFAT may involve both genetic and familial environmental factors.     

Genetic Epidemiology of Obesity

Obesity has become a global epidemic and contributes to theincreasing burden of type 2 diabetes, cardiovascular disease,stroke, some types of cancer, and premature death worldwide.Obesity is highly heritable and arises from the interactionsof multiple genes, environmental factors, and behavior. In thispaper, the authors reviewed recent developments in genetic epidemiologicresearch, focusing particularly on several promising genomicregions and obesity-related genes. Gene-gene and gene-environmentinteractions of obesity were also discussed. Published studieswere accessed through the MEDLINE database. The authors alsosearched the Obesity Gene Map Database (http://obesitygene.pbrc.edu/)and conducted a manual search using references cited in relevantpapers. Heritabilities for obesity-related phenotypes variedfrom 6% to 85% among various populations. As of October 2005,253 quantitative trait loci for obesity-related phenotypes havebeen localized in 61 genome-wide linkage scans, and geneticvariants in 127 biologic candidate genes have been reportedto be associated with obesity-related phenotypes from 426 positivefindings. Gene-gene interactions were also observed in severalgenes, and some genes were found to influence the effect ofdietary intake and physical activity on obesity-related phenotypes.Integration of genetic epidemiology with functional genomicsand proteomics studies will be required to fully understandthe role of genetic variants in the etiology and preventionof obesity. body mass index • genes • obesity • overweight     

Genetic “Mysteries” and International Adoption: The Cultural Impact of Biomedical Technologies on the Adoptive Family Experience*

This paper argues that the increasing medicalization and geneticization of North American society may be influencing how and why adoptive families think—and worry—about their children's birthparents, their children's ‘health risks’, and about their own role as parents in genetic terms. It further discusses why these processes may be causing adoptive parents unnecessary anxieties. It suggests that family professionals and social workers should be aware of the effects of these socio‐cultural processes and of the real limitations of genetic techniques to predict, diagnose, and cure disease in order to better respond to prospective adoptive parents' need for support and information.     

Why are children in the same family so different from one another?

One of the most important findings that has emerged from human behavioral genetics involves the environment rather than heredity, providing the best available evidence for the importance of environmental influences on personality, psychopathology, and cognition. The research also converges on the remarkable conclusion that these environmental influences make two children in the same family as different from one another as are pairs of children selected randomly from the population. The theme of the target article is that environmental differences between children in the same family (called "nonshared environment") represent the major source of environmental variance for personality, psychopathology, and cognitive abilities. One example of the evidence that supports this conclusion involves correlations for pairs of adopted children reared in the same family from early in life. Because these children share family environment but not heredity, their correlation directly estimates the importance of shared family environment. For most psychological characteristics, correlations for adoptive "siblings" hover near zero, which implies that the relevant environmental influences are not shared by children in the same family. Although it has been thought that cognitive abilities represent an exception to this rule, recent data suggest that environmental variance that affects IQ is also of the nonshared variety after adolescence. The article has three goals: (1) To describe quantitative genetic methods and research that lead to the conclusion that nonshared environment is responsible for most environmental variation relevant to psychological development, (2) to discuss specific nonshared environmental influences that have been studied to date, and (3) to consider relationships between nonshared environmental influences and behavioral differences between children in the same family. The reason for presenting this article in BBS is to draw attention to the far-reaching implications of finding that psychologically relevant environmental influences make children in a family different from, not similar to, one another.     

Contributors to childhood obesity in Iran: the views of parents and school staff

Objective

To explore the contextual influences on childhood obesity in Tehran, Iran to inform future development of an obesity prevention intervention for Iranian primary school children.

Study design

Qualitative study.

Methods

Focus groups and interviews with parents and school staff were convened to explore their perceptions of the causes of childhood obesity. Eleven focus groups and three interviews were held with parents and school staff (88 participants in total) from three different socio-economic areas in Iran's capital city, Tehran. All the discussions were transcribed verbatim in Persian. An iterative thematic approach was used for data analysis.

Results

Overall, the causes of childhood obesity were perceived to relate to macro-level policy influences, the school environment, sociocultural factors, and family and individual behavioural factors, acting in combination. A key emergent theme was the pervasive influence of Government policies on children's food intake and physical activity. Another key theme was the political and sociocultural context that does not support girls and women in Iran in having active lifestyles.

Conclusion

The findings suggest that parents and school staff have sophisticated views on the possible causes of childhood overweight and obesity which encompassed behavioural, structural and social causes. A prominent emerging theme was the need for state level intervention and support for a healthy environment. Any local initiatives in Iran are unlikely to be successful without such support.

What is known on this subject

Childhood obesity is growing in Iran and it is seen as one of the features of the nutrition transition in developing countries. Findings from cross-sectional studies suggest a range of lifestyle factors contribute to obesity in the Iranian population.

What this study adds

This qualitative study explores the socioenvironmental changes contributing to childhood obesity in primary school-aged children in Iran. Findings have provided important contextual data on the perceived contributors to childhood obesity in Iran, such as macro-level policy influences on accessibility to healthy food and physical activity, competing priorities at school level, sociocultural influences on diet and physical activity and limited knowledge and skills of parents. This has laid the foundation for the development of appropriate childhood obesity prevention interventions.     

Genetic covariation between neuroticism and the symptoms of anxiety and depression

A genetic analysis of the trait of neuroticism and symptoms of anxiety and depression in 3,810 pairs of adult MZ and DZ twins is reported. Differences between people in these measures can be explained simply by differences in their genes and in their individual environmental experiences. There is no evidence that environmental experiences that are shared by cotwins, such as common family environment or social influences, are important. There are differences between the sexes in gene action affecting neuroticism, and genetic effects become more pronounced with age in females. The lack of evidence for dominance variance affecting neuroticism contrasts well with the detection of considerable genetical nonadditivity for extraversion in the same sample and reinforces the view that these two traits are not only statistically, but also genetically, quite independent. An analysis of the causes of covariation between anxiety, depression, and neuroticism shows that additive gene effects are more important causes of covariation than environmental factors. Genetic variation in symptoms of anxiety and depression is largely dependent on the same factors as effect the neuroticism trait. However, there is also evidence for genetic variation specific to depression.     

Familial aggregation of morbid obesity

Recent studies have shown major gene effects for obesity in randomly ascertained families. To investigate the familial aggregation of a specific subset of obesity, which is particularly prone to medical complications, families with morbid obesity were studied. This condition occurs in 1%-2% of the population and is defined as 45.5 kg (100 pounds) or more over ideal weight. First-degree relatives of 221 morbidly obese probands (1560 adults) were identified, and height and weight (current and greatest) were obtained from each family member. Morbid obesity occurred in the family members of the probands 8 times more often than in the general population. Of the morbidly obese probands, 48% had one or more first-degree relatives who were also morbidly obese compared to a 6% population estimate. By the ages of 20-24, 12% of the morbidly obese probands were already 45.5 kg or more overweight, and 45% were 22.7 kg (50 pounds) or more overweight. There was little difference in the prevalence of familial morbid obesity by the gender of the probands: 47% of the male probands and 48% of the female probands had another morbidly obese relative, while 67% and 53% of the early onset (before age 25) male and female probands, respectively, had one or more first-degree relatives who were also morbidly obese. In addition to the extreme degree of familial aggregation, the prevalence of morbid obesity in parent-offspring sets was calculated within the morbidly obese families. Morbidly obese families who have one or two morbidly obese parents have a 2.6 times increased risk (p<0.002) of having one or more morbidly obese adult offspring, compared to families who have neither parent morbidly obese. Evidence for trimodality of the body mass index distribution was found for each gender (p = 0.0006 for male relatives and p = 0.075 for female relatives). The strong familial aggregation of morbid obesity indicates the need for further understanding of the genetic determinants of this extreme clinical disorder and how environmental factors affect the genetic expression of the trait.     

Influence of heredity on dietary restraint, disinhibition, and perceived hunger in humans

OBJECTIVE: Dietary restraint, disinhibition, and perceived hunger have been shown to affect food intake and body weight and are thought to be risk factors for eating disorders, but little is known about their origins. We investigated the influence of heredity, shared (familial) environment, and individual environment on dietary restraint disinhibition, perceived hunger and their relation to body size and food intake. METHODS: Scores on the Three Factor Eating Questionnaire and the Restraint Scale in addition to height, weight, body mass index, and 7-d diary reported nutrient intakes were obtained from 39 identical, 60 fraternal same-sex, and 50 fraternal opposite-sex adult twin pairs who were living independently. Linear structural modeling was applied to investigate the nature and degree of genetic and environmental influences. RESULTS: Analysis showed significant genetic and individual environmental, but not shared (familial) environmental, influences on cognitive restraint, perceived hunger, and Restraint Scale scores, with genes accounting for 44%, 24%, and 58% of the variance, respectively. In contrast, disinhibition was found to be significantly influenced by the shared (familial) environment, accounting for 40% of the variance. Further analysis showed that cognitive restraint and perceived hunger heritabilities could not be accounted for by significant heritabilities of body weight, height, or body mass index. In contrast, the heritability of Restraint Scale scores was found to be related to body size. Cognitive restraint was negatively correlated with nutrient intake, and differences in cognitive restraint were found to be related to differences in the body sizes of identical twin pairs. CONCLUSIONS: Dietary restraint appears to be another component in a package of genetically determined physiologic, sociocultural, and psychological processes that regulate energy balance, whereas dietary disinhibition may be the intermediary between upbringing and the development of overweight and/or eating disorders.