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- We studied cortical amyloid – episodic memory association in twin pairs - Cognitively discordant twin pairs were identified using telephone interview - 45 twin pairs participated in PET imaging and in-person neuropsychological testing - Within-twin pair differences in amyloid and memory were associated with each other - Higher amyloid is related to poorer memory even when controlling for genetic effects We studied the association between episodic memory and cortical fibrillar β-amyloid pathology within twin pairs. Using telephone-administered cognitive screening of 1415 twin pairs in a population-based older Finnish Twin Cohort study, we identified 45 (mean [SD] age 72.9 [4.0] years, 40% women) cognitively discordant same-sex twin pairs (24 dizygotic and 21 monozygotic) without neurological or psychiatric disorders other than AD or mild cognitive impairment. In-person neuropsychological testing was conducted. Cortical amyloid was measured with carbon 11-labelled Pittsburgh compound B ([11C]PiB) positron emission tomography imaging and quantified as the average standardized uptake value ratio in cortical regions affected in AD. Larger within-twin pair differences in verbal immediate (r = -0.42) and delayed free recall (r = -0.41), and visual delayed free recall (r = -0.46) were associated with larger within-twin pair differences in [11C]PiB uptake (p 's < 0.01). Correlations were not significantly different in dizygotic and monozygotic pairs suggesting that the episodic memory-cortical amyloid relationship is not confounded by genetic effects. However, larger samples are needed to draw more definitive conclusions. [ABSTRACT FROM AUTHOR]

Background Obesity susceptibility genes are highly expressed in the brain suggesting that they might exert their influence on body weight through eating-related behaviors. Objectives To examine whether the genetic susceptibility to obesity is mediated by eating behavior patterns. Methods Participants were 3977 twins (33% monozygotic, 56% females), aged 31–37 y, from wave 5 of the FinnTwin16 study. They self-reported their height and weight, eating behaviors (15 items), diet quality, and self-measured their waist circumference (WC). For 1055 twins with genome-wide data, we constructed a polygenic risk score for BMI (PRSBMI) using almost 1 million single nucleotide polymorphisms. We used principal component analyses to identify eating behavior patterns, twin modeling to decompose correlations into genetic and environmental components, and structural equation modeling to test mediation models between the PRSBMI, eating behavior patterns, and obesity measures. Results We identified 4 moderately heritable (h 2 = 36–48%) eating behavior patterns labeled "snacking," "infrequent and unhealthy eating," "avoidant eating," and "emotional and external eating." The highest phenotypic correlation with obesity measures was found for the snacking behavior pattern (r  = 0.35 for BMI and r  = 0.32 for WC; P  < 0.001 for both), largely due to genetic factors in common (bivariate h 2 > 70%). The snacking behavior pattern partially mediated the association between the PRSBMI and obesity measures (β indirect = 0.06; 95% CI: 0.02, 0.09; P  = 0.002 for BMI; and β indirect = 0.05; 95% CI: 0.02, 0.08; P  = 0.003 for WC). Conclusions Eating behavior patterns share a common genetic liability with obesity measures and are moderately heritable. Genetic susceptibility to obesity can be partly mediated by an eating pattern characterized by frequent snacking. Obesity prevention efforts might therefore benefit from focusing on eating behavior change, particularly in genetically susceptible individuals. [ABSTRACT FROM AUTHOR]

Background and Aims: Plasma apolipoprotein C3 (ApoC3) is associated with higher plasma triglyceride and type 2 diabetes incidence. We evaluated whether body mass index (BMI) or glucose metabolism were associated with ApoC3 in healthy monozygotic (MZ) twins.Methods and Results: Forty-seven MZ twin-pairs (20 man, 27 women), aged 23-42 years, were divided in subgroups according to discordance or concordance for (a) BMI (within-pair difference (Δ) in BMI≥3.0 or<3.0 kg/m2), or (b) 2-h glucose iAUC, during oral glucose tolerance test (ΔGlucose iAUC ≥97.5 or<97.5 mmol × 120 minutes). Within these discordant or concordant subgroups, we tested (Wilcoxon signed-rank test) co-twin differences in ApoC3, adiposity measures, insulin-resistance and beta-cell function indices, and plasma and lipoprotein lipids. In BMI-Discordant (p = 0.92) or BMI-Concordant (p = 0.99) subgroups, ApoC3 did not differ between leaner and heavier co-twins. In the Glucose-Discordant subgroup, ApoC3 was significantly higher in twins with higher Glucose iAUC than in their co-twins with the lower Glucose iAUC (10.03 ± 0.78 vs. 8.48 ± 0.52 mg/dl; M ± SE; p = 0.032). Co-twins with higher Glucose iAUC also had higher waist circumference, body fat percentage, liver fat content, worse insulin-sensitivity and beta-cell function and higher cholesterol and triglyceride in plasma VLDL, IDL, and LDL. In Glucose-Concordant twin-pairs, no significant differences were observed in the explored variables. In all twin-pairs, ΔApoC3 correlated with Δ in lipids and glucose metabolism variables, the closest relationship being between ΔApoC3 and ΔVLDL triglyceride (r = 0.74, p < 0.0001).Conclusions: While ApoC3 was not related to acquired differences in BMI, it associated with early dysregulation of glucose metabolism independently of obesity and genetic background. [ABSTRACT FROM AUTHOR]

Background: Developmental relationships between tobacco use and suicide-related behaviors (SRB) remain unclear. Our objective was to investigate the longitudinal associations of tobacco use in adolescence and SRB in adulthood.Methods: Using a prospective design, we examined whether tobacco use in adolescence is associated with SRB (intentional self-injury, suicide ideation) in young adulthood in a population-based sample of 1330 twins (626 males, 704 females). The baseline and follow-up data were collected by professionally administered semi-structured poly-diagnostic interviews at ages 14 and 22, respectively.Results: After adjusting for multiple potential confounders, those who reported early-onset of regular tobacco use had a significantly increased risk for intentional self-injury, such as cutting or burning, at age 22 (adjusted odds ratio [AOR] 4.57, 95% CI 1.93-10.8) in comparison to those who had not at all initiated tobacco use. Also, daily cigarette smoking at baseline was associated with future intentional self-injury (AOR 4.45, 95% CI 2.04-9.70). Early-onset tobacco use was associated with suicidal ideation in females (AOR 3.69, 95% CI 1.56-8.72) but not in males. Considering any SRB, baseline daily smokers (AOR 2.13, 95% CI 1.12-4.07) and females with early onset of regular tobacco use (AOR 3.97, 95% CI 1.73-9.13) had an increased likelihood. Within-family analyses among twin pairs discordant for exposure and outcome controlling for familial confounds showed similar, albeit statistically non-significant, associations.Conclusion: Early-onset tobacco use in adolescence is longitudinally associated with SRB (intentional self-injury and/or suicide ideation) in young adulthood, particularly among females. Further investigation may reveal whether this association has implications for prevention of SRB in adolescence and young adulthood. [ABSTRACT FROM AUTHOR]

The impact of diet on the gut microbiota has usually been assessed by subjecting people to the same controlled diet and thereafter following the shifts in the microbiota. In the present study, we used habitual dietary intake, clinical data, quantitative polymerase chain reaction, and denaturing gradient gel electrophoresis (DGGE) to characterize the stool microbiota of Finnish monozygotic twins. The effect of diet on the numbers of bacteria was described through a hierarchical linear mixed model that included the twin individuals, stratified by body mass index, and their families as random effects. The abundance and diversity of the bacterial groups studied did not differ between normal-weight, overweight, and obese individuals with the techniques used. Intakes of energy, monounsaturated fatty acids, n3 polyunsaturated fatty acids (PUFAs), n6 PUFAs, and soluble fiber had significant associations with the stool bacterial numbers (e.g., increased energy intake was associated with reduced numbers of Bacteroides spp.). In addition, co-twins with identical energy intake had more similar numbers and DGGE-profile diversities of Bacteroides spp. than did the co-twins with different intake. Moreover, the co-twins who ingested the same amounts of saturated fatty acids had very similar DGGE profiles of Bacteroides spp., whereas the co-twins with similar consumption of fiber had a very low bifidobacterial DGGE-profile similarity. In conclusion, our findings confirm that the diet plays an important role in the modulation of the stool microbiota, in particular Bacteroides spp. and bifidobacteria. [ABSTRACT FROM AUTHOR]

Background: Disparities in body mass index (BMI) between persons with different educational levels in Western countries are well documented, but the background of these education-associated disparities remains poorly understood. Objective: The objective was to examine the influence of environmental and genetic factors on education-associated disparities in self-reported BMI and weight change. Design: Longitudinal postal surveys were performed in 1975,1981, and 1990. The data were analyzed by using multivariate genetic models for twin data. The data derived from the Finnish Twin Cohort included 2482 monozygotic and 5113 dizygotic same-sex male and female twin pairs born between 1915 and 1957. Results: Education-associated differences in BMI and in weight change were clear in 1975 and 1981, respectively, whereas no differences were seen in weight change between 1981 and 1990 when age and baseline BMI were adjusted for. The trait correlation between baseline BMI and educational attainment (-0.15 in men and women) was mainly due to correlations between additive genetic factors that contributed to BMI and education in men (-0.20; 95% CI: -0.25, -0.14) and women (-0.32; 95% CI: -0.40, -0.25) when adjusted for age. Among women, a weaker positive correlation was found for the unshared environmental effects contributing to the 2traits(0.06; 95%CI: 0.02,0.12). The same factors that affected the association between education and BMI in 1975 largely explained the association between education and weight change in 1981. Conclusion: The results suggest the possibility that common genetic factors affect educational attainment and body weight, which contribute to education-associated disparities in BMI in adulthood. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this study was to determine gestational age-specific incidence and risk factors of respiratory distress syndrome (RDS) in twins compared with singletons. Study design: An analysis of 850,406 singleton and 23,278 twin infants born alive in Finland between 1987 and 2000 was performed. A number of antenatal and perinatal/intranatal factors were evaluated. Results: At less than 28 weeks of gestation, the incidence of RDS was higher in both first- and second-born twins compared with singletons. At more advanced gestation, first-born twins had a significantly lower incidence of RDS compared with the others. There was no difference in the concordance of RDS between same-sex and opposite-sex twin pairs. Vaginal delivery, female sex, being born first, and being the lighter of the twins protected from RDS. Conclusion: After taking into account gestation, twins are not at higher risk of RDS compared with singletons except at very early gestation. Environmental factors predominate over genetic ones in the predisposition to RDS in twins. [ABSTRACT FROM AUTHOR]

Presents a study which examined whether physical activity, measured at the baseline examination in 1975, was likely to play a differential role in subsequent weight changes in the following 6 y in 1571 monozygotic and 3029 dizygotic, same-sex twin pairs from the Finnish Twin Cohort Study. Study methodology used; Associations between weight change observed; What was revealed about genetic factors.

This paper examines the links between risky health behaviors and labor market success. We provide new evidence on the joint relationships between the most prominent forms of risky health behavior − alcohol consumption, smoking and physical inactivity − and long-term labor market outcomes. We use twin data for Finnish men and women linked to register-based individual information on earnings and labor market attachment. The twin data allow us to account for shared family and environmental factors and to measure risky health behaviors in 1975 and 1981. The long-term labor market outcomes were measured in adulthood as an average over the period 1990–2009. The sample sizes are 2156 and 2498 twins, for men and women, respectively. We find that being both a smoker and a heavy drinker in early adulthood is negatively related to long-term earnings and employment later in life, especially for men. We conclude that how and why risky health behaviors cluster and how that affects individual level outcomes call for more attention. [ABSTRACT FROM AUTHOR]

• Obesity matrisome include 130 signature genes in adipose tissue and 71 in adipocytes. • Adipocyte obesity matrisome show hypertrophic inflammatory phenotype. • Adipose tissue obesity matrisome shows remodeling phenotype. • Novel metabolism-linked matrisome genes are CTSA, CSTO, FAM20B and NGLY1. Adipose tissue is a central regulator of metabolic health and its failure in obesity is a major cause of weight associated comorbidities, such as type 2 diabetes. Many extracellular matrix proteins, represented by matrisome, play a critical role in balancing adipose tissue health and dysfunction. Extracellular matrix components, produced by different cell types of adipose tissue, can modulate adipocyte function, tissue remodeling during expansion, angiogenesis, and inflammation and also form fibrotic lesions in the tissue. In this study, we investigated changes in matrisome of whole adipose tissue and adipocytes in human obesity. We investigated further the networks and biological pathways of the genes related to the changes and their association to development of metabolic dysfunction linked to type 2 diabetes. We used transcriptome data and clinical metabolic parameters from a rare weight-discordant MZ twin cohort. The Heavy-Lean differential matrisome gene expression (Δmatrisome) and differential metabolic parameters reflect changes in adipose tissue upon weight gain and changes in whole body glucose, insulin metabolism, as well as lipid status. We report that obesity Δmatrisome shows high specificity with 130 and 71 of the 1068 matrisome genes showing altered expression in the adipose tissue and adipocytes of heavier co-twin, respectively. The Δmatrisome differs considerably between adipose tissue vs adipocytes which reflects inflammation of hypertrophic adipocytes and the remodeling activity of the rest of the tissue resident cells. The obesity Δmatrisome is discussed extensively in the light of existing evidence and novel significant associations to obesity are reported to matrisome genes; cathepsin A, cathepsin O, FAM20B and N-glycanase1. [ABSTRACT FROM AUTHOR]

Abstract: Although potential environmental influences on hedonic responses to oral pungency have been identified, little is known of the possible role of genetics underlying these responses. We explored the contribution of genetic and environmental influences on the pleasantness of oral pungency and spicy foods. Respondents were young adult Finnish twins (n=331, 21–25years), including 47 complete monozygotic and 93 dizygotic twin pairs and 51 twin individuals without their co-twin. Pleasantness and intensity of strawberry jelly spiked with capsaicin (0.0001% w/v) relative to untainted strawberry jelly were rated. Furthermore, pleasantness of spicy foods and oral pungency caused by spices were rated based on food names in a questionnaire. Respondents were grouped as non-likers, medium-likers, and likers by their pleasantness responses to capsaicin spiked jelly. The contribution of genetic and environmental factors to variation and co-variation of the pleasantness traits was analyzed using quantitative genetic modeling. The non-likers perceived oral pungency as more intense (sensory) and rated pleasantness of spicy foods and pungent sensations caused by spices (questionnaire) as less pleasant than the likers. Genetic factors accounted for 18–58% of the variation in the pleasantness of oral pungency, spicy foods and pungent sensations. The rest was due to environmental factors. All pleasantness traits (sensory and questionnaire based) were shown to share a common genetic variance. This indicates that an underlying genetic aptitude to like oral pungency, and spicy foods exists and it is expressed in these measures. The findings broaden the understanding of the diverse nature of individual food preferences and motivate further search for the underlying genetic components of oral pungency. [Copyright &y& Elsevier]

Subclinical psychosis, including schizotypal indicators and psychotic experiences, predicts future suicidal ideation. This relationship may reflect unmeasured confounding from environmental factors, genetic factors, or both. We used a genetically-informative twin design to understand if the association between subclinical psychosis and suicidal ideation is independent of shared genetic and environmental factors. We analysed cross-sectional associations of age-22 self-reported subclinical psychosis (positive, negative, and disorganised features) with suicidal ideation in twins participating in the FinnTwin12 study (maximum n = 1213). Then, we analysed the reverse association of age-14 suicidal ideation with age-22 subclinical psychosis. Associations were studied first among individuals and then within monozygotic (MZ) and dizygotic (DZ) pairs. Individual-level analyses showed that all subclinical psychosis factors were associated with suicidal ideation. In within-pair analyses, estimates of associations were lower for MZ pairs than DZ pairs, except for the negative schizotypy-suicidal ideation association where estimates were consistent across individual-level and within-pair analyses. Findings provide evidence that the association between negative features and suicide ideation is not explained by familial factors and may be causal, though the possibility of confounding by individual-specific environmental factors and reverse causation cannot be ruled out. The relationships of positive and disorganised subclinical psychosis features with suicidal ideation cannot be explained by confounding due to environmental factors shared between siblings, but their associations may be due to shared genetic factors. [ABSTRACT FROM AUTHOR]

Background: Longitudinal studies enhance understanding of the complex reciprocal relationship between smoking and depression from adolescence to young adulthood. Examining bi-directional associations between cigarette smoking and depressive symptoms in a genetically informative twin design can help to understand whether the associations are independent of shared genetic and environmental factors.Methods: We analyzed longitudinal data on smoking and depressive symptoms in twins participating in the adolescent (mean age 17.5) and young adult (mean age 21.9) surveys of the FinnTwin12 study (maximum N = 2,954 individuals; 1,154 twin pairs). At both waves, self-reported depressive symptoms, assessed with the 10-item version of the General Behavior Inventory (GBI), and smoking status were analyzed. The bi-directional associations were first studied among individuals and then within monozygotic and dizygotic twin pairs.Results: When adjusted for multiple covariates and baseline depressive symptoms, daily smokers at age 17 had higher depressive symptom scores at age 22 than never smokers (Incidence Rate Ratio = 1.17, 95% CI: 1.03-1.33). Similarly, when adjusted for covariates and baseline smoking, higher score in GBI at age 17 was associated with an increased likelihood of being a non-daily (Relative Risk Ratio (RRR) = 1.06, 95% CI: 1.01-1.11) or daily (RRR = 1.05, 95% CI: 1.00-1.10) smoker at age 22. No associations were found in within-pair analyses, suggesting that the individual-level association is explained by shared familial liabilities.Conclusion: During the developmental period from adolescence to adulthood, cigarette smoking and depressive symptoms are reciprocally associated. However, these associations are confounded by shared genetic and other familial liabilities. [ABSTRACT FROM AUTHOR]

Background: Cigarette smoking and depression are major public health concerns, but longitudinal research on the association between smoking and antidepressant use is scarce. The purpose of this study was to investigate, whether smoking predicts antidepressant medication during a 10-year follow-up.Methods: A questionnaire was administered to Finnish adult twins in 1990. Antidepressant prescription data during 1995-2004 were obtained from the register of the Finnish Social Insurance Institution and linked to the survey data. Cox Proportional Hazard Models among 10,652 individuals (1075 cases, 9577 controls) assessed the risk for depression in the cohort, whereas within-pair comparisons of smoking twins with their non-smoking co-twins controlled for shared familial influences.Results: Daily smokers had a significantly elevated likelihood for having antidepressant prescriptions in the follow-up. Based on the analysis among those without baseline depression, heavy daily smokers had a significantly elevated likelihood (HR 1.56, 95% CI 1.17-2.08) for antidepressant prescription when adjusted for all confounders. Similar analysis using pairs discordant for antidepressant medication confirmed that daily smoking twins had a higher likelihood for prescriptions (HR 1.98, 95% CI 1.11-3.54) compared with their non-smoking co-twins. The estimates were for MZ pairs (HR 1.78, 95% CI 0.48-6.55) and DZ pairs (HR 1.92, 95% CI 0.99-3.72), respectively.Limitations: Changes in smoking status after baseline cannot be accounted for. Reversed association between depression and smoking cannot be ruled out.Conclusion: Daily smoking predicts antidepressant medication, even when controlling for essential confounders and familial factors. This study highlights the need of systematically assessing depressive symptoms among smokers. [ABSTRACT FROM AUTHOR]

The consequences of heavy alcohol use remain a serious public health problem. Consistent evidence has demonstrated that both genetic and social influences contribute to alcohol use. Research on gene-environment interaction (GxE) has also demonstrated that these social and genetic influences do not act independently. Instead, certain environmental contexts may limit or exacerbate an underlying genetic predisposition. However, much of the work on GxE and alcohol use has focused on adolescence and less is known about the important environmental contexts in young adulthood. Using data from the young adult wave of the Finnish Twin Study, FinnTwin12 ( N = 3402), we used biometric twin modeling to test whether education moderated genetic risk for alcohol use as assessed by drinking frequency and intoxication frequency. Education is important because it offers greater access to personal resources and helps determine one’s position in the broader stratification system. Results from the twin models show that education did not moderate genetic variance components and that genetic risk was constant across levels of education. Instead, education moderated environmental variance so that under conditions of low education, environmental influences explained more of the variation in alcohol use outcomes. The implications and limitations of these results are discussed. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Little is known about the associations of serum fatty acids with lipoprotein profile and the underlying genetic and environmental etiology of these relationships. We aimed to analyze the phenotypic association of serum n-6 and n-3 polyunsaturated (PUFAs), monounsaturated (MUFAs) and saturated (SFAs) fatty acids (relative proportion to total fatty acids) with lipids and lipoproteins, and to quantify common genetic and environmental factors determining their covariation. Methods: Two cohorts of healthy Finnish twins were assessed in young adulthood. Data were available for 1269 individual twins including 561 complete pairs. Serum metabolites were measured by nuclear magnetic resonance spectroscopy. Bivariate quantitative genetic models were used to decompose the phenotypic covariance between the pairs of traits into genetic and environmental components. Results: Among the strongest correlations observed, serum total n-6 PUFAs and linoleic acid were inversely (max. r = −0.65) and MUFAs positively (max. r = 0.63) correlated with triglycerides and very low-density lipoprotein (VLDL) particle concentration, particularly with large VLDL (for n-6 PUFAs) and medium VLDL (for MUFAs). Genetic factors significantly contributed to their covariance with bivariate heritability estimates ranging from 44% to 56% for n-6 PUFAs and 58% to 66% for MUFAs. Genetic correlations with lipid traits were moderate to high (max. r A = −0.59 and 0.70 for n-6 PUFAs and MUFAs, respectively). Statistically significant, but substantially weaker phenotypic correlations of total n-3 PUFAs, docosahexaenoic acid (DHA) and SFAs with lipoprotein profile were not decomposed into their genetic and environmental components. Conclusion: Shared genetic factors are important in explaining why higher concentrations of serum n-6 PUFAs and lower concentrations of serum MUFAs strongly associate with lower triglyceride and VLDL particle concentrations. [Copyright &y& Elsevier]

Abstract: Background: Few twin studies have examined nutrition-related phenotypes among children, and none has investigated energy and macronutrient intakes. Objective: The objective was to quantify genetic and environmental influences on variations in energy and macronutrient intakes among children aged 9years. Design: We conducted a nutrition study among children participating in the Quebec Newborn Twin Study, a population-based birth cohort of twins. We derived dietary data from two multiple-pass 24-hour dietary recalls with a parent and his or her child. The analysis employed a classic twin study design and used data from 379 twin pairs. Results: Univariate analyses indicate that heritability for mean daily energy (kcal) and macronutrient (g) intakes was moderate, ranging from 0.34 (95% CI: 0.22, 0.46) to 0.42 (0.31, 0.53). Genetic effects also accounted for 0.28 (0.16, 0.40) of the variance in percent of energy from lipids, while only environmental (shared and unique) effects accounted for the variance in percent of energy from proteins and carbohydrates. The shared environment did not contribute to variations in daily intakes for most of the nutritional variables under study. Multivariate analyses suggest the presence of macronutrient-specific genetic influences for lipids and carbohydrates, estimated at 0.12 (0.04, 0.19) and 0.20 (0.11, 0.29) respectively. Conclusions: The unique environment (i.e., not shared by family members) has the largest influence on variances in daily energy and macronutrient intakes in 9-year-old children. This finding underscores the need to take obesogenic environments into account when planning dietary interventions for younger populations. [Copyright &y& Elsevier]

Abstract: Background: Studies on diet and high-density lipoprotein (HDL) subspecies distribution are limited. Objective: We examined the relationship between macronutrient composition and lipoprotein particle size and HDL subspecies independent of genetic effects by studying monozygotic (MZ) twins. Methods: 24 healthy MZ twin pairs aged 23–33 years were identified from two longitudinal population-based studies, FinnTwin16 and FinnTwin12. Total energy and nutrient intake were assessed with 3-day food records and physical activity was measured by the Baecke index. HDL subspecies distribution was determined by non-denaturing gradient gel electrophoresis. Associations between diet composition and HDL mean particle size were determined by multivariate nutrient density models adjusted for confounding variables. Results: Substituting one energy percentage from omega-3 polyunsaturated fatty acids (n-3 PUFAs) for a corresponding amount of energy from other type of fats was related to changes in the relative proportions of the HDL subspecies 2b, 3a and 3b toward a larger mean particle size in men (β ±SE: 1.00±0.26nm, p =0.004) and women (β ±SE: 0.90±0.21nm, p =0.001). This association remained significant in analyses controlling for genetic and shared environmental influences using within-pair differences of the measures in MZ twin pairs (β ±SE: 0.37±0.14nm, p =0.019). Twins with the higher n-3 PUFA intake had significantly higher proportions of large HDL2b particles and lower proportions of smaller-sized HDL3a and HDL3b particles as compared to their co-twins with lower intakes (p <0.05). Conclusions: Our data suggest that n-3 PUFA intake is associated with a favorable change in the distribution of HDL subspecies towards larger particles independent of genetic and shared environmental factors. [Copyright &y& Elsevier]

Background & Aims: Ectopic fat in muscle and liver is linked to obesity and type 2 diabetes. Recently, pancreatic lipid accumulation has also been associated with β-cell dysfunction and reduced insulin production, leading to the development of type 2 diabetes. Physical exercise training has been shown to attenuate β-cell dysfunction in patients, but little is known about its effects on pancreatic and hepatic fat accumulation. In this study, we validated in-vivo proton magnetic resonance spectroscopy (1H MRS) in pancreatic fat measurement with biochemical measurements in a pig model. Thereafter, the effects of increased physical activity on the amounts of pancreatic and liver fat were studied in eight monozygotic twin pairs who have discordant physical activity and fitness. Methods: Pancreatic fat content was studied in 15 pigs using 1H MRS and/or biochemical analyses. In addition, liver and pancreatic fat were assessed using 1H MRS in eight monozygotic male twin pairs with 18% mean difference in VO2max between the twin brothers. Results: Twins with higher physical fitness had 23% less liver fat (1.3±1.3% vs. 2.1±2.6%, p =0.022) but no such difference was observed in the pancreatic fat (8.2±9.3% vs. 9.8±8.5%, respectively, p =0.3). Hepatic fat content was inversely associated with VO2max. A positive association was found between pancreatic and liver fat contents (β =5.18, p =0.012). Pancreatic fat content was also associated with insulin sensitivity indexes and plasma adiponectin and glutamyltransferase concentrations. Conclusions: Pancreatic fat content is associated with insulin resistance and hepatic fat content. An active lifestyle seems to beneficially influence hepatic fat metabolism. [Copyright &y& Elsevier]

Summary: Studies of singletons suggest that right-handed individuals may have higher levels of testosterone than do left-handed individuals. Prenatal testosterone levels are hypothesised to be especially related to handedness formation. In humans, female members from opposite-sex twin pairs may experience elevated level of prenatal exposure to testosterone in their intrauterine environment shared with a male. We tested for differences in rates of left-handedness/right-handedness in female twins from same-sex and opposite-sex twin pairs. Our sample consisted of 4736 subjects, about 70% of all Finnish twins born in 1983–1987, with information on measured pregnancy and birth related factors. Circulating testosterone and estradiol levels at age 14 were available on 771 and 744 of these twins, respectively. We found significantly (p =.006) lower prevalence of left-handedness in females from opposite-sex pairs (5.3%) compared to females from same-sex pairs (8.6%). The circulating levels of neither testosterone nor estradiol related to handedness in either females or males. Nor were there differences in circulating testosterone or estradiol levels between females from opposite-sex and same-sex twin pairs. Birth and pregnancy related factors for which we had information were unrelated to handedness. Our results are difficult to fully explain by postnatal factors, but they offer support to theory that relates testosterone to formation of handedness, and in a population-based sample, are suggestive of effects of prenatal testosterone transfer. [ABSTRACT FROM AUTHOR]

Purpose: To examine the heritability of spherical equivalent (SE) in older women. Design: Population-based twin study. Participants: Ninety monozygotic (MZ) and 86 dizygotic (DZ) female twin pairs aged 63 to 76 years who were born from 1924 through 1937. Methods: Ocular refraction was measured using an autorefractor and controlled by the subjective method. The contributions of genetic and environmental factors to individual differences in SE were estimated by applying an independent pathway model to twin data. Main Outcome Measures: Contribution of genetic and environmental effects to the variation in SE. Results: Mean SE of the study population was 1.68 (standard deviation, ±1.82) with no differences observed either between the MZ and the DZ individuals or between the left and the right eyes. The pairwise correlations were higher in the MZ sisters (intraclass correlation coefficient [ICC], 0.803 right eye and 0.807 left eye) than DZ sisters (ICC, 0.406 right eye and 0.435 left eye). Quantitative genetic modelling showed that 83% (95% confidence interval, 77%–87%) of the variance in SE could be explained by heritable factors. Conclusions: Additive genetic influences explained most of the individual differences in SE among older Finnish women. Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article. [ABSTRACT FROM AUTHOR]

Abstract: The purpose of this study was to examine how resting electrocardiographic (ECG) and other clinical variables, which can be included in a routine clinical examination, predict walking ability in older women. Three hundred and twenty women (63–75 years) without overt cardiac diseases and apparent mobility limitations were studied. Measurements performed were clinical examination (standard 12-lead resting ECG, assessment of physical activity level, presence of chronic diseases, use of beta-blockers, body mass index (BMI), ability to squat, resting blood pressure) and six-minute walking test. Participants walked 533±75m in the six-minute walking test. The best electrocardiographic predictors of long walking distance were high TV5 and TII, but their explanation rates were small (4.5% and 3.8%, respectively). In hypertensive participants (systolic blood pressure=SBP≥160mmHg), the respective values were 9.3% and 5.8%. The best predictors of long walking distance were ability to squat without limitations and low BMI (15.5% and 13.6%, respectively). Altogether the studied variables explained 36% of the variation in walking distance. The data gathered in clinical examination give useful information for the assessment of walking ability in relatively healthy older women. Resting ECG does not give clinically significant additional information for the assessment in subjects without overt cardiac disease. [ABSTRACT FROM AUTHOR]

It has been suggested that certain health behaviours, such as smoking, may operate as mediators of the well-established inverse association between IQ and mortality risk. Previous research may be afflicted by unadjusted confounding by socioeconomic or psychosocial factors. Twin designs offer a unique possibility to take genetic and shared environmental factors into account. The aim of the present national twin study was to determine the interrelations between IQ at age 18, childhood and attained social factors and smoking status in young adulthood and mid-life. We studied the association between IQ at age 18 and smoking in later life in a population of 11 589 male Swedish twins. IQ was measured at military conscription, and data on smoking and zygosity was obtained from the Swedish Twin Register. Information on social factors was extracted from censuses. Data on smoking was self-reported by the twins at the age of 22–47 years. Logistic regression models estimated with generalised estimating equations were used to explore possible associations between IQ and smoking among the twins as individuals as well as between-and within twin-pairs. A strong inverse association between IQ and smoking status emerged in unmatched analyses over the entire range of IQ distribution. In within-pair and between-pair analyses it transpired that shared environmental factors explained most of the inverse IQ–smoking relationship. In addition, these analyses indicated that non-shared and genetic factors contributed only slightly (and non-significantly) to the IQ–smoking association. Analysis of twin pairs discordant for IQ and smoking status displayed no evidence that non-shared factors contribute substantially to the association. The question of which shared environmental factors might explain the IQ–smoking association is an intriguing one for future research. [Copyright &y& Elsevier]

Abstract: It has been proposed that patients with schizophrenia and some of their relatives suffer from reduced neurocognitive efficiency, increasing their sensitivity to experimental task demands. The present study evaluated such a possibility during performance of a working memory task by schizophrenia patients and their co-twins along with a healthy control sample. Electrophysiological data were obtained from sets of nine twin pairs (monozygotic and dizygotic pairs collapsed) discordant for a diagnosis of schizophrenia and from nine matched healthy control twin pairs, during administration of a variable-load spatial working memory task. Event-related potentials (ERPs) were measured immediately after memory set onset and during a delay period. For correctly performed trials, slow-wave ERP activity measured during the late stimulus encoding and delay periods exhibited a significant Diagnostic Group-by-Memory Load interaction, with schizophrenia patients showing a differentially strong load effect. Patients'' co-twins displayed an intermediate level of load sensitivity while healthy controls showed no significant load effect. These results support an inefficiency model of neurocognitive dysfunction in schizophrenia, a pattern that appears to be related to the pathogenesis and inheritance of the disorder. Furthermore, this inefficiency appeared during the late stimulus encoding stage of working memory functioning, possibly reflecting disruptions in stimulus representation consolidation. [Copyright &y& Elsevier]

Background/Aims: This study aimed to determine the heritability of serum alanine aminotransferase (S-ALT) and fasting serum insulin (fS-insulin) concentration as well as determine the association of these measures with liver fat content in young adult monozygotic (MZ) and dizygotic (DZ) twins. Methods: Three hundred and thirteen individual twins were recruited from a population-based cohort (n =4929). The study subjects represented a wide range of body mass indexes (BMI), were free of any diseases or regular medications and had an intake of less than two drinks of alcohol/day. To verify that S-ALT is a marker of liver fat, it was measured by proton magnetic resonance spectroscopy (1H MRS) in 66 subjects. Heritability estimations were performed using BMI- and gender-adjusted values. Results: Intra-pair correlations were significantly higher in the MZ twins than the DZ twins for both S-ALT (0.65 for MZ and 0.04 for DZ) and fS-insulin (0.58 and 0.34, respectively). Heritability of S-ALT was 55% and that of fS-insulin 61%. In the 66 subjects S-ALT (r =0.70 for women and r =0.50 for men, p ⩽0.01 for both) and fS-insulin (r =0.58 and r =0.59, respectively, p ⩽0.01 for both) concentrations correlated significantly with liver fat content. Conclusions: These twin data suggest that approximately 60% of the variation in S-ALT, a marker of liver fat content, is genetically determined. [Copyright &y& Elsevier]

Abstract: The origins of human handedness remain unknown. Genetic theories of handedness have received much attention, but some twin studies suggest modest, perhaps negligible genetic effects on handedness. A related question concerning handedness is whether twins have higher rates of left-handedness than do singletons. We studied handedness, with information on forced right-handedness, in a sample of 30161 subjects aged 18–69 from a questionnaire survey of the older Finnish Twin Cohort. Left-handedness was found to be more common in twins (8.1%) and triplets (7.1%) than in singletons (5.8%), whereas ambidextrousness was more common in triplets (6.4%) than in twins (3.4%) and singletons (3.5%). As in many other studies, males were more likely to be left-handed. Ambidextrous subjects were more likely to become right-handed writers even if not forced to use their right hand. We fit maximum likelihood models to our twin data to estimate the contribution of additive genetic, common environment and unique environmental effects to hand preference. Results, depending on the model, indicate that unique environmental effects account for most observed variance in handedness, both in childhood (92–100%) and adulthood (74–86%). When forced right-handedness was taken into account, estimates of familial effects increased. Concordance for left-handedness in twins is rare, and accordingly, very large samples are needed to detect the familial effects. Our results show that forced-handedness can have an effect on estimates of genetic effects. [Copyright &y& Elsevier]

Abstract: The nature, neural underpinnings, and etiology of deficits in verbal declarative memory in patients with schizophrenia remain unclear. To examine the contributions of genes and environment to verbal recall and recognition performance in this disorder, the California Verbal Learning Test was administered to a large population-based Finnish twin sample, which included schizophrenic and schizoaffective patients, their non-ill monozygotic (MZ) and dizygotic (DZ) co-twins, and healthy control twins. Compared with controls, patients and their co-twins showed relatively greater performance deficits on free recall compared with recognition. Intra-pair differences between patients and their non-ill co-twins in hippocampal volume and memory performance were highly positively correlated. These findings are consistent with the view that genetic influences are associated with reduced verbal recall in schizophrenia, but that non-genetic influences further compromise these abnormalities in patients who manifest the full-blown schizophrenia phenotype, with this additional degree of disease-related declarative memory deficit mediated in part by hippocampal pathology. [Copyright &y& Elsevier]

Abstract: The contribution of genetic factors to individual differences in food use was estimated in a large population-based twin cohort of young adults (22- to 27-year-old). Male and female twins (n =2009 complete twin pairs) evaluated use-frequencies of 24 food items using 5 categories (1=never–5=several times a day) in a postal questionnaire. Foods were categorized by factor analysis. Estimates of the relative proportions of additive genetic, shared environmental, and unshared environmental effects on the use-frequency of food items and factor scores were obtained by quantitative genetic modeling of twin data based on linear structural equations. Four factors of food use were identified: “healthy” foods, high-fat foods, sweet foods, and meats. The variance of the use-frequency of food items and food categories was explained by additive genetic and unshared environmental influences, whereas shared environmental factors did not contribute to food use. The average proportions of genetic effects on the total variance of the use-frequency of food items and food categories were 40% and 45%, respectively. Sex differences were observed in the magnitude of genetic influences for use-frequency of four food items (chocolate, other sweets, fried foods, and meat), and in genetic factors underlying the use of three (fresh vegetables, fruits, and cheeses) items. In conclusion, family environment does not appear to influence the food use of young adults and thus nutritional education should be targeted at this age group to support development of healthy eating patterns. In addition, the results illuminate the importance of the sex-specific genetic effects on food use. [Copyright &y& Elsevier]

Abstract: The purpose of the present study was to examine the effect of a second task on postural balance and to determine the role of genetic influences on postural balance when dual tasking among 206 monozygotic and 227 dizygotic female twins, aged 63–76 years. Balance was measured as medio-lateral and antero-posterior velocity of the centre of pressure (COP) (mm/s) and velocity moment (mm2/s) while standing on a force platform. Doing an arithmetic task increased movement of the COP while the hand motor task had no effect on movement of the COP. The genetic contribution to balance in the single task situation was minor (14%, 95% confidence interval, CI: 11–35%) whereas in the dual task situation it was moderate (28%, 95% CI: 0.02–42%). The finding can be explained in the light of the underlying phenotypes of dual tasking, such as cognitive processing that is found to be under considerable genetically controlled even in old age. Moreover, the present study supports previous studies suggesting that, especially among older people, when simultaneously maintaining balance and performing another cognitively demanding task, additional central processing is recruited. [Copyright &y& Elsevier]

Background: Information on the inheritance of neurophysiological abnormalities might help elucidate the molecular genetic basis of schizophrenia. We used magnetoencephalography (MEG) and electroencephalography (EEG) to investigate the inheritance of auditory-cortical deficiencies in twin pairs discordant for schizophrenia. Methods: Auditory EEG/MEG responses to frequent standard and occasional deviant tones were measured in mono- and dizygotic (MZ and DZ) twin pairs discordant for schizophrenia and demographically matched healthy twin pairs, recruited from a total population cohort. The MEG/EEG results were regressed against the genetic resemblance to patients with schizophrenia across the patients’ unaffected MZ/DZ co-twins and control subjects (with genetic correlations of 1, .5, and 0 to schizophrenia patients, respectively). Results: The EEG responses P50, N100, and mismatch negativity (MMN), as well as the MEG response P50m, were reduced in the schizophrenic patients. P50 and N100 were significantly decreased also in their unaffected co-twins, as compared with the control subjects. Importantly, the P50 and N100 decrease correlated with the unaffected subjects’ genetic resemblance to schizophrenia patients. Conclusions: Our results suggest inherited abnormalities in cortical auditory processing in schizophrenia, reflected by the decreased P50/P50m and N100 amplitudes, whereas the MMN abnormalities might reflect predominantly state-dependent neurodegeneration. [Copyright &y& Elsevier]

Abstract: The dopamine hypothesis of schizophrenia postulates that a dysfunctional dopaminergic system is a major pathophysiological mechanism in the disease. Most studies have focused on striatal dopamine D2 receptors, but a disturbed link between dopamine D1 and D2 receptors has also been proposed. Schizophrenia is highly heritable, and recent evidence suggests that alterations in the dopaminergic system confer susceptibility for schizophrenia instead of being solely related to the to overt expression of the disease. To explore the impact of genetic vulnerability for schizophrenia on the balance of striatal dopamine D1 and D2 receptors, we studied monozygotic (MZ) and dizygotic (DZ) unaffected co-twins from twin pairs discordant for schizophrenia as well as healthy control twins using positron emission tomography (PET). Both [11C]SCH 23390 and [11C]raclopride were used to quantitate D1 and D2 receptor binding, respectively, in the same individuals during the same day. The association between D1 and D2 receptor binding was analyzed using conventional region of interests as well as voxel-wise D1/D2 ratio maps. All levels of analyses failed to show any differences in D1/D2 ratio between the unaffected MZ or DZ co-twins and control twins. We noted rostrocaudally declining and dorsoventrally increasing gradients in D1/D2 ratio in the striatum, with no differences between groups in these gradients. In this sample, we did not find evidence for an association between increased genetic risk for schizophrenia and altered D1/D2 receptor balance in the striatum. [Copyright &y& Elsevier]

Background: Family studies are in conflict as to whether schizophrenia and bipolar disorder have independent genetic etiologies. Given the relatively low prevalence (approximately 1%) of these disorders, the use of quantitative endophenotypic markers of genetic liability might provide a more sensitive strategy for evaluating their genetic overlap. We have previously demonstrated that spatial working memory deficits increase in a dose-dependent fashion with increasing genetic proximity to a proband among the unaffected co-twins of schizophrenic patients. Here, we evaluated whether such deficits might also mark genetic susceptibility to bipolar disorder. Methods: The Wechsler Memory Scale-Revised Visual Memory Span and Digit Span subtests were administered to 46 schizophrenic patients, 32 of their unaffected co-twins, 22 bipolar patients, 16 of their unaffected co-twins, and 100 control twins, representing unselectively nationwide twin samples. Results: Schizophrenic patients and their unaffected co-twins performed significantly worse than control subjects on the spatial working memory task, whereas only the schizophrenic patients performed significantly below the control subjects on the verbal working memory task. Neither bipolar patients nor their unaffected co-twins differed from control subjects on these measures. Conclusions: Our findings support the hypothesis that impairment in spatial working memory might effectively reflect an expression of genetic liability to schizophrenia but less clearly to bipolar disorder. [Copyright &y& Elsevier]

: BackgroundAlthough the heritability of bipolar I disorder (BPI) is high, few magnetic resonance imaging (MRI) studies of siblings of bipolar patients exist. We performed MRI brain scans on a nationwide sample of twins with BPI, as well as on their co-twins and a demographically balanced sample of control twin subjects, to detect any structural alterations related to the disorder and to the increased genetic risk.: MethodsThe National Hospital Discharge Register, National Population Register, and Finnish Twin Cohorts were used to identify bipolar twins. Structured diagnostic interviews and MRI scans were obtained for 24 twins with BPI, 15 healthy co-twins, and 27 control twin subjects.: ResultsPatients and co-twins showed a significant decrease in left hemispheric white matter volume. The disparity in patients was −16.1 cm3 (95% confidence interval [CI] −26.6, −5.6) and in co-twins −11.3 cm3 (95% CI −22.1, −0.4) compared with control twin subjects. No gray matter decrease was seen in patients or co-twins.: ConclusionsThe results of this first large-scale MRI study of twins with BPI, their co-twins, and appropriate control twin subjects, suggest that alterations of the left hemisphere white matter in BPI may reflect genetic factors predisposing to the disorder. [Copyright &y& Elsevier]