Showing papers by "Carol E. Franz published in 2010"

Genetic and Environmental Influences on Cortisol Regulation Across Days and Contexts in Middle-Aged Men

Abstract: Cortisol is an indicator of hypothalamic–pituitary–adrenal axis responsivity to stress, but few twin studies have examined the heritability of cortisol concentrations in adults across the diurnal cycle and in different contexts. Saliva samples were provided by 783 middle-aged male twins on one laboratory and two home days as part of the Vietnam Era Twin Study of Aging. Significant cortisol heritability estimates were found for laboratory measures only: awakening (.56); 30 min after awakening (.48); 1000 h (.42); mean output across the day (.43); and mean cortisol awakening response (.64). Twin correlations at home were low. In the laboratory, they were unchanged for fraternal twins, but increased for identical twins. Greater measurement error at home did not appear to account for home-laboratory differences. The results suggest that genetic factors influence cortisol responses to specific environmental stressors. Thus, cortisol levels are correlated in identical twins only when they undergo similar experiences.

Does Parental Education have a Moderating Effect on the Genetic and Environmental Influences of General Cognitive Ability in Early Adulthood

Abstract: Hereditary influences account for a substantial proportion of the variance in many cognitive abilities. However, there is increasing recognition that the relative importance of genetic and environmental influences may vary across different socioeconomic levels. The overall goal of the present study was to examine whether parental education has a moderating effect on genetic and environmental influences of general cognitive ability in early adulthood (age 19.6 ± 1.5). Participants were 5,955 male twins from the Vietnam Era Twin (VET) Registry. Significant effects of parental education on mean level of general cognitive ability scores were found, but a model without moderating effects of parental education on genetic or environmental influences on cognitive scores proved to be the best fitting model. Some, but not all, previous studies have found significant moderating effects; however, no consistent pattern emerged that could account for between-study differences regarding moderating effects on genetic and environmental influences.

Testosterone modifies the effect of APOE genotype on hippocampal volume in middle-aged men

Abstract: Background: The APOE e4 allele is an established risk factor for Alzheimer disease (AD), yet findings are mixed for how early its effects are manifest. One reason for the mixed results could be the presence of interaction effects with other AD risk factors. Increasing evidence indicates that testosterone may play a significant role in the development of AD. The aim of the present study was to examine the potential interaction of testosterone and APOE genotype with respect to hippocampal volume in middle age. Methods: Participants were men from the Vietnam Era Twin Study of Aging (n = 375). The mean age was 55.9 years (range 51–59). Between-group comparisons were performed utilizing a hierarchical linear mixed model that adjusted for the nonindependence of twin data. Results: A significant interaction was observed between testosterone and APOE genotype (e4-negative vs e4-positive). Those with both low testosterone (≥1 SD below the mean) and an e4-positive status had the smallest hippocampal volumes, although comparisons with normal testosterone groups were not significant. However, individuals with low testosterone and e4-negative status had significantly larger hippocampal volumes relative to all other groups. A main effect of APOE genotype on hippocampal volume was observed, but only when the APOE -by-testosterone interaction was present. Conclusions: These findings demonstrate an interaction effect between testosterone and the APOE e 4 allele on hippocampal volume in middle-aged men, and they may suggest 2 low testosterone subgroups. Furthermore, these results allude to potential gene–gene interactions between APOE and either androgen receptor polymorphisms or genes associated with testosterone production.

When help becomes a hindrance: mental health referral systems as barriers to care for primary care physicians treating patients with Alzheimer's disease.

Abstract: Objectives: To describe structural barriers to mental health specialists and consequences of these barriers to care for patients with dementia and neuropsychological symptoms and their primary care physicians (PCPs). Design: Cross-sectional qualitative interview study of PCPs. Setting: Physicians' offices, primarily managed care. Participants: Forty PCPs in Northern California. Measurements: Open-ended interviews lasted 30–60 minutes. The interview guide covered clinician background, practice setting, clinical care of a particular patient, and general approach to managing patients with Alzheimer disease or related dementias. Interviews were transcribed and themes reflecting referrals identified. Results: Ninety-three percentage of the PCPs described problematic access to and communication with mental health specialists (in particular psychiatrists and neuropsychologists) as impediments to effective care for dementia patients. Thematic analysis identified structural barriers to mental health referrals ranging from problems with managed care and reimbursement policies to lack of trained providers and poor geographic distribution of specialists. Structural barriers compromised care for patients with dementia because the barriers limited PCP treatment options, and resources, impacted office staff and time with other patients, impeded and delayed care, and fostered poor communication and lack of coordinated care. Negative consequences for PCPs included increased frustration, conflict, and burnout. Conclusion: PCPs viewed problems created by onerous referral systems, such as mental health carve outs, as particularly burdensome for elderly patients with comorbid dementia and neuropsychiatric problems. These problems were cited by PCPs across different types of practice settings. PCPs managed treatment of neurobehavioral symptoms as best they could despite lack of specialist support.

Psychopathic personality traits in middle-aged male twins: a behavior genetic investigation.

Abstract: Psychopathic personality is characterized by interpersonal dominance, impulsivity, sensation seeking, poor planning, and aggressiveness. Studies have shown that the Multidimensional Personality Questionnaire (MPQ) can be used to estimate scores on the fearless-dominant (FD) and the impulsive-antisocial (IA) dimensions of the Psychopathic Personality Inventory (PPI), the best validated self-report measure of psychopathic personality traits. Prior behavior genetic studies reported roughly equal genetic and nonshared environmental influences for both FD and IA, which remained stable from adolescence to young adulthood. However, no prior studies address genetic and environmental influences on these dimensions beyond early adulthood. We utilized the classic twin method to examine genetic and environmental influences on variance in FD and IA in a sample of middle-aged male twins. Biometric modeling indicated that the variance in both factors is best explained by additive genetic and nonshared environmental influences. FD showed roughly equal contributions from genetic and environmental factors, whereas IA showed greater contributions from environmental than genetic factors. Additionally, the small phenotypic correlation between FD and IA was explained entirely by nonshared environmental factors.

Associations Between Jet Lag and Cortisol Diurnal Rhythms After Domestic Travel

Abstract: Millions of people travel across time zones each year for business and pleasure. In 2001, U.S. residents reported an average of nine long distance trips per person per year with a median length of 210 (SE = 3) miles (Department of Transportation [USDOT], 2001). Fatigue, disturbance in sleep, and anxiety have all been associated with traveling long distances (Boulos et al., 1995; Cho, Ennaceur, Cole, & Suh, 2000; Gander, Nguyen, Rosekind, & Connell, 1993; Waterhouse, Reilly, & Atkinson, 1997). These symptoms, commonly referred to as “jet lag,” are attributed to the desynchronization of the circadian rhythm in the body due to changes in the light and dark cycle. Jet lag is associated with lack of alertness, poor sleep, irritability, stress, impaired performance in athletes, and depressed mood (Waterhouse et al., 1997). The degree of jet lag varies by the number of time zones crossed and direction of travel; eastward travel is associated with slower acclimation to the new time zone than westward travel (Boulos et al., 1995; Minors & Waterhouse, 1981). Jet lag has been of interest to those concerned with the productivity and health of frequent business travelers (Striker, Dimberg, & Liese, 2000); frequent travelers have higher rates of insurance claims for psychological problems, infectious diseases, back disorders, and injuries than nontravelers, and the number of claims increases with the number of trips (Liese, Mundt, Dell, Nagy, & Demure, 1997). Several studies have determined that travel across times zones alters hormonal patterns linked to circadian rhythm, such as diurnal rhythms of melatonin and cortisol (Cho, 2001; Cho et al., 2000; Klein & Wegmann, 1974; Lemmer, Kern, Nold, & Lohrer, 2002; Winget, DeRoshia, & Holley, 1985). Of particular interest may be jet-lag effects on the diurnal rhythm of cortisol, a stress hormone and a primary product of the hypothalamic-pituitary-adrenal axis (HPA axis; Kirschbaum & Hellhammer, 1989), as cortisol levels have been associated with individual differences in physical and mental health (for review, see Sapolsky, Romero, & Munck, 2000), and aging (Van Cauter, Leproult, & Kupfer, 1996). Previous studies of jet lag and cortisol have found that cortisol diurnal rhythms have been altered by flights over six or more times zones either westward or eastward (Bullock, Martin, Ross, Rosemond, & Marino, 2007; Klein & Wegmann, 1974; Lemmer et al., 2002; Winget et al., 1985). Other research on jet lag and cortisol has drawn links between repeated long-term flights, elevated cortisol levels after such flights, and later cognitive deficits (Cho, 2001; Cho et al., 2000). In general, results from previous studies provide estimates of 1 day of recovery needed for every one to two time zones crossed for circadian rhythms to adjust (Bullock et al., 2007; Eastman, Gazda, Burgess, Crowley, & Fogg, 2005; Loat & Rhodes, 1989). Although prior studies have demonstrated associations between jet lag and cortisol, most have been conducted on small, selective samples of less than 25 participants. None have examined the associations between cortisol and jet lag within a large national sample of community participants and with control days in their own naturalistic settings. Furthermore, the majority of these studies have examined chronic jet lag (i.e., many trips within a short amount of time) or extreme jet lag (i.e., travel over six or more time zones). Given that only a small minority of long-distance trips cross more than three time zones (Department of Transportation, 2001), prior research may not generalize to the average traveler. The current research focuses on a large sample of middle-aged men, comparing variations in diurnal cortisol regulation based on number of time zones traveled eastward or westward. This study addresses the following questions: (a) Are cortisol diurnal rhythms altered by domestic travel across three or fewer time zones?; (b) does this vary by eastward or westward travel?; and (c) are there potential confounds such as mood, sleep quality and disturbances, and wake time that can account for the dysregulation of the cortisol rhythms?

Genetic vulnerability and phenotypic expression of depression and risk for ischemic heart disease in the Vietnam era twin study of aging.

Abstract: Objective To determine if depression contributes to incident heart disease after accounting for genetic, behavioral, and medical factors associated with both conditions. Methods We used a prospective twin study with a 12-year follow-up. In 1992, lifetime diagnosis of depression was assessed in 1159 male-male twins and merged with longitudinal health data from the Vietnam Era Twin Registry Study of Aging. Incident heart disease was defined as having myocardial infarction, heart surgery, or angina at 12-year follow-up when twins were 55.4 years (standard deviation, 2.5 years) of age. Risks for heart disease were computed in a logistic regression model that included comparing twins at different levels of phenotypic expression of depression and varying levels of genetic vulnerability at the same time adjusting for pertinent covariates. Results After adjusting for sociodemographics, co-occurring psychopathology, smoking, obesity, diabetes, hypertension, and social isolation, twins at high genetic risk and exposed to depression remained at greater risk of developing ischemic heart disease (IHD) (odds ratio, 2.55; 95% confidence interval, 1.44-4.49) compared with those at low genetic risk and without phenotypic expression of depression. Odds ratios suggest that twins at genetic liability but without phenotypic expression were at risk of IHD, but the effect was not statistically significant. Conclusions A history of depression is a risk factor for incident heart disease after adjusting for numerous covariates. Twins with both high genetic vulnerability and phenotypic expression of depression were at greatest risk of IHD. Trends suggest the genetic contribution to IHD that overlaps with depression may partly explain this association, but studies in larger samples are warranted.