Obesity and major depressive disorder (MDD) are associated, but evidence about how they relate over time is conflicting. The goal of this study was to examine prospective associations between ...depression and obesity from early adolescence through early adulthood.
Participants were drawn from a statewide, community-based, Minnesota sample. MDD and obesity with onsets by early adolescence (by age 14), late adolescence (between 14 and 20) and early adulthood (ages 20-24) were assessed via structured interview (depression) and study-measured height and weight.
Cross-sectional results indicated that depression and obesity with onsets by early adolescence were concurrently associated, but the same was not true later in development. Prospective results indicated that depression by early adolescence predicted the onset of obesity (odds ratio (OR)=3.76, confidence interval =1.33-10.59) during late adolescence among female individuals. Obesity that developed during late adolescence predicted the onset of depression (OR=5.89, confidence interval=2.31-15.01) during early adulthood among female individuals.
For girls, adolescence is a high-risk period for the development of this comorbidity, with the nature of the risk varying over the course of adolescence. Early adolescent-onset depression is associated with elevated risk of later onset obesity, and obesity, particularly in late adolescence, is associated with increased odds of later depression. Further investigation into the mechanisms of these effects and the reasons for the observed gender and developmental differences is needed. Prevention programs focused on early-onset cases of depression and adolescent-onset cases of obesity, particularly among female individuals, may help in reducing risk for this form of comorbidity.
Epidemiological research is believed to underestimate the lifetime prevalence of mental illness due to recall failure and a lack of rapport between researchers and participants.
In this prospective ...study, we examined lifetime prevalence and co-morbidity rates of substance use disorders, antisocial personality disorder (ASPD) and major depressive disorder (MDD) in a representative, statewide Minnesota sample (n = 1252) assessed four times between the ages of 17 and 29 years with very low attrition.
Lifetime prevalence rates of all disorders more than doubled between the ages of 17 and 29 years in both men and women, and our prospective rates at the age of 29 years were consistently higher than rates from leading epidemiological surveys. Although there was some variation, the general trend was for lifetime co-morbidity to increase between the ages of 17 and 29 years, and this trend was significant for MDD-alcohol dependence, MDD-nicotine dependence, and ASPD-nicotine dependence.
Overall, our results show that emerging adulthood is a high-risk period for the development of mental illness, with increases in the lifetime prevalence and co-morbidity of mental disorders during this time. More than a quarter of individuals had met criteria for MDD and over a fifth had experienced alcohol dependence by the age of 29 years, indicating that mental illness is more common than is estimated in cross-sectional mental health surveys. These findings have important implications for the measurement of economic burden, resource allocation toward mental health services and research, advocacy organizations for the mentally ill, and etiological theories of mental disorders.
A number of studies reports reduced hippocampal volume in individuals who engage in problematic alcohol use. However, the magnitude of the difference in hippocampal volume between individuals with v. ...without problematic alcohol use has varied widely, and there have been null findings. Moreover, the studies comprise diverse alcohol use constructs and samples, including clinically significant alcohol use disorders and subclinical but problematic alcohol use (e.g. binge drinking), adults and adolescents, and males and females.
We conducted the first quantitative synthesis of the published empirical research on associations between problematic alcohol use and hippocampal volume. In total, 23 studies were identified and selected for inclusion in the meta-analysis; effects sizes were aggregated using a random-effects model.
Problematic alcohol use was associated with significantly smaller hippocampal volume (d = -0.53). Moderator analyses indicated that effects were stronger for clinically significant v. subclinical alcohol use and among adults relative to adolescents; effects did not differ among males and females.
Problematic alcohol use is associated with reduced hippocampal volume. The moderate overall effect size suggests the need for larger samples than are typically included in studies of alcohol use and hippocampal volume. Because the existing literature is almost entirely cross-sectional, future research using causally informative study designs is needed to determine whether this association reflects premorbid risk for the development of problematic alcohol use and/or whether alcohol has a neurotoxic effect on the hippocampus.
Major depressive disorder (MDD) that onsets by adolescence is associated with various deficits in psychosocial functioning. However, adolescent-onset MDD often follows a recurrent course that may ...drive its associated impairment.
To tease apart these two clinical features, we examined the relative associations of age of onset (adolescent versus adult) and course (recurrent versus single episodes) of MDD with a broad range of psychosocial functioning outcomes assessed in early adulthood. Participants comprised a large, population-based sample of male and female twins from the Minnesota Twin Family Study (MTFS; n = 1252) assessed prospectively from ages 17 to 29 years.
A recurrent course of MDD predicted impairment in several psychosocial domains in adulthood, regardless of whether the onset was in adolescence or adulthood. By contrast, adolescent-onset MDD showed less evidence of impairment in adulthood after accounting for recurrence. Individuals with both an adolescent onset and recurrent episodes of MDD represented a particularly severe group with pervasive psychosocial impairment in adulthood.
The negative implications of adolescent-onset MDD for psychosocial functioning in adulthood seem to be due primarily to its frequently recurrent course, rather than its early onset, per se. The results highlight the importance of considering both age of onset and course for understanding MDD and its implications for functioning, and also in guiding targeted intervention efforts.
Gender differences in the prevalence of alcohol use disorder (AUD) have motivated the separate study of its risk factors and consequences in men and women. However, leveraging gender as a third ...variable to help account for the association between risk factors and consequences for AUD could elucidate etiological mechanisms and clinical outcomes.
Using data from a large, community sample followed longitudinally from 17 to 29 years of age, we tested for gender differences in psychosocial risk factors and consequences in adolescence and adulthood after controlling for gender differences in the base rates of AUD and psychosocial factors. Psychosocial factors included alcohol use, other drug use, externalizing and internalizing symptoms, deviant peer affiliation, family adversity, academic problems, attitudes and use of substances by a romantic partner, and adult socio-economic status.
At both ages of 17 and 29 years, mean levels of psychosocial risks and consequences were higher in men and those with AUD. However, the amount of risk exposure in adolescence was more predictive of AUD in women than men. By adulthood, AUD consequences were larger in women than men and internalizing risk had a stronger relationship with AUD in women at both ages.
Despite higher mean levels of risk exposure in men overall, AUD appears to be a more severe disorder in women characterized by higher levels of adolescent risk factors and a greater magnitude of the AUD consequences among women than men. Furthermore, internalizing symptoms appear to be a gender-specific risk factor for AUD in women.
Although common sense suggests that environmental influences increasingly account for individual differences in behavior as experiences accumulate during the course of life, this hypothesis has not ...previously been tested, in part because of the large sample sizes needed for an adequately powered analysis. Here we show for general cognitive ability that, to the contrary, genetic influence increases with age. The heritability of general cognitive ability increases significantly and linearly from 41% in childhood (9 years) to 55% in adolescence (12 years) and to 66% in young adulthood (17 years) in a sample of 11 000 pairs of twins from four countries, a larger sample than all previous studies combined. In addition to its far-reaching implications for neuroscience and molecular genetics, this finding suggests new ways of thinking about the interface between nature and nurture during the school years. Why, despite life's 'slings and arrows of outrageous fortune', do genetically driven differences increasingly account for differences in general cognitive ability? We suggest that the answer lies with genotype-environment correlation: as children grow up, they increasingly select, modify and even create their own experiences in part based on their genetic propensities.
The personality traits of neuroticism and extraversion are predictive of a number of social and behavioural outcomes and psychiatric disorders. Twin and family studies have reported moderate ...heritability estimates for both traits. Few associations have been reported between genetic variants and neuroticism/extraversion, but hardly any have been replicated. Moreover, the ones that have been replicated explain only a small proportion of the heritability (<~2%). Using genome-wide single-nucleotide polymorphism (SNP) data from ~12,000 unrelated individuals we estimated the proportion of phenotypic variance explained by variants in linkage disequilibrium with common SNPs as 0.06 (s.e. = 0.03) for neuroticism and 0.12 (s.e. = 0.03) for extraversion. In an additional series of analyses in a family-based sample, we show that while for both traits ~45% of the phenotypic variance can be explained by pedigree data (that is, expected genetic similarity) one third of this can be explained by SNP data (that is, realized genetic similarity). A part of the so-called 'missing heritability' has now been accounted for, but some of the reported heritability is still unexplained. Possible explanations for the remaining missing heritability are that: (i) rare variants that are not captured by common SNPs on current genotype platforms make a major contribution; and/ or (ii) the estimates of narrow sense heritability from twin and family studies are biased upwards, for example, by not properly accounting for nonadditive genetic factors and/or (common) environmental factors.
Previous work reports an association between familial risk factors stemming from parental characteristics and offspring disruptive behavior disorders (DBDs). This association may reflect (a) the ...direct effects of familial environment and (b) a passive gene-environment correlation (r(GE)), wherein the parents provide both the genes and the environment. The current study examined the contributions of direct environmental influences and passive r(GE) by comparing the effects of familial risk factors on child DBDs in genetically related (biological) and non-related (adoptive) families.
Participants were 402 adoptive and 204 biological families. Familial environment was defined as maternal and paternal maladaptive parenting and antisociality, marital conflict and divorce; offspring DBDs included attention deficit hyperactivity disorder (ADHD), conduct disorder (CD) and oppositional defiant disorder (ODD). Mixed-level regressions estimated the main effects of familial environment, adoption status and the familial environment by adoption status interaction term, which tested for the presence of passive r(GE).
There was a main effect of maternal and paternal maladaptive parenting and marital discord on child DBDs, indicating a direct environmental effect. There was no direct environmental effect of maternal or paternal antisociality, but maternal and paternal antisociality had stronger associations with child DBDs in biological families than adoptive families, indicating the presence of a passive r(GE).
Many familial risk factors affected children equally across genetically related and non-related families, providing evidence for direct environmental effects. The relationship of parental antisociality and offspring DBDs was best explained by a passive r(GE), where a general vulnerability toward externalizing psychopathology is passed down by the parents to the children.
Previous research indicates that alcohol and drug dependence constitute aspects of a general vulnerability to externalizing disorders that accounts for much of the parent-offspring resemblance for ...these and related disorders. This study examined how adolescent offspring risk for externalizing psychopathology varies with respect to parental alcoholism and illicit drug dependence.
Data from the Minnesota Twin Family Study, a community-based investigation of adolescents (age 17 years, n=1252) and their parents, were used. Lifetime diagnoses of alcohol and drug dependence (among both parents and offspring) and offspring attention deficit hyperactivity disorder, oppositional defiant disorder, conduct disorder, adult antisocial behavior, and nicotine dependence were assessed via structured interviews.
Parental alcohol dependence and parental drug dependence were similarly associated with increased risk for nearly all offspring disorders, with offspring of alcohol and drug-dependent parents having approximately 2-3 times the odds for developing a disorder by late adolescence compared to low-risk offspring. Compared to parental dependence on other illicit drugs, parental cannabis dependence was associated with weaker increased risk for offspring externalizing disorders.
Both parental alcohol and drug dependence are independently associated with an increased risk for a broad range of externalizing psychopathology among late-adolescent offspring.
One variant of substance-use disorder is characterized by behavioral disinhibition. In this report, we martial evidence for a model for the development of this variant. We hypothesize that genetic ...liability for this variant is reflected in a spectrum of risk indicators linked to the inability or unwillingness to inhibit behavioral impulses. Included in this spectrum are personality traits suggesting low constraint, and externalizing psychopathology, including conduct, oppositional defiant, and attention-deficit disorder in children and antisocial personality disorder and behavior in adults. We further hypothesize that these individual differences in behavioral disinhibition are manifestations of underlying central nervous system processes associated with various psychophysiological anomalies, some of which may index genetic risk for substance abuse. Support for the model is derived from the analysis of findings from the Minnesota Twin Family Study, an epidemiological investigation of approximately 2,700 adolescent twins and their parents.
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