The primary objective of this study was to determine whether disc degeneration, as assessed through magnetic resonance imaging, is greater in smokers than in nonsmokers. To control for the maximum number of potentially confounding variables, pairs of identical twins highly discordant for cigarette smoking were selected as study subjects. Data analyses revealed 18% greater mean disc degeneration scores in the lumbar spines of smokers as compared with nonsmokers. The effect was present across the entire lumbar spine, implicating a mechanism acting systemically. This investigation demonstrates the efficiency of using carefully selected controls in studying conditions of multifactorial etiology, such as disc degeneration.
To determine the independent associations of dietary preference for fat with obesity without the confounding by genetic effects.
Descriptive comparison of the responses of monozygotic twins discordant for obesity to questions concerning current and past preference for dietary fat, current overconsumption of fatty items and recalled food consumption compared to the co-twin.
The Research and Development Centre of the Social Insurance Institution, Finland.
Twenty-three healthy monozygotic twin pairs who were discordant for obesity (BMI difference at least 3 kg/m(2)).
Obesity status of the twin, as a function of the current and recalled dietary preferences and selected psychosocial variables.
The obese twins reported current preference for fatty foods three times more frequently than the lean co-twin. Moreover, when comparing recalled taste for fat at the time the twins left their parental homes, both the obese and lean co-twins consistently recalled that the obese twin had greater preference for fatty foods in young adulthood, and that the lean twin had less. Psychological characteristics of lean and obese co-twins did not differ.
Acquired preference for fatty foods is associated with obesity, independent of genetic background. Modification of fat preferences may be an important step in the prevention of obesity in the general population.
Alcohol intake may be associated with cancer risk, but epidemiologic evidence for prostate cancer is inconsistent. We aimed to prospectively investigate the association between midlife alcohol intake and drinking patterns with future prostate cancer risk and mortality in a population-based cohort of Finnish twins.
Data were drawn from the Older Finnish Twin Cohort and included 11,372 twins followed from 1981 to 2012. Alcohol consumption was assessed by questionnaires administered at two time points over follow-up. Over the study period, 601 incident cases of prostate cancer and 110 deaths from prostate cancer occurred. Cox regression was used to evaluate associations between weekly alcohol intake and binge drinking patterns with prostate cancer risk and prostate cancer-specific mortality. Within-pair co-twin analyses were performed to control for potential confounding by shared genetic and early environmental factors.
Compared to light drinkers (=3 drinks/week; non-abstainers), heavy drinkers (>14 drinks/week) were at a 1.46-fold higher risk (HR 1.46; 95 % CI 1.12, 1.91) of prostate cancer, adjusting for important confounders. Among current drinkers, binge drinkers were at a significantly increased risk of prostate cancer (HR 1.28; 95 % CI 1.06, 1.55) compared to non-binge drinkers. Abstainers were at a 1.90-fold higher risk (HR 1.90; 95 % CI 1.04, 3.47) of prostate cancer-specific mortality compared to light drinkers, but no other significant associations for mortality were found. Co-twin analyses suggested that alcohol consumption may be associated with prostate cancer risk independent of early environmental and genetic factors.
Heavy regular alcohol consumption and binge drinking patterns may be associated with increased prostate cancer risk, while abstinence may be associated with increased risk of prostate cancer-specific mortality compared to light alcohol consumption.
Notes
Cites: Adv Exp Med Biol. 2015;815:59-7025427901
Cites: Am J Epidemiol. 2002 Dec 1;156(11):985-9312446254
Cites: Br J Cancer. 2015 Feb 3;112(3):580-9325422909
Cites: Eur J Cancer Prev. 2012 Jul;21(4):350-922095143
Cites: Nutr Cancer. 2006;56(1):50-617176217
Cites: Int J Cancer. 2006 Sep 15;119(6):1501-416615108
Cites: Hum Hered. 1978;28(4):241-54566252
Cites: Epidemiol Rev. 2001;23(1):110-411588834
Cites: Urology. 2004 Oct;64(4):717-2215491708
Cites: Am J Epidemiol. 2010 Oct 1;172(7):773-8020813803
Mortality and morbidity from ischaemic heart disease (IHD) was studied in 5404 Finnish males aged 35-64 years who had been hospitalised for alcohol-related disease in 1972 without any admissions for IHD during that same period. By record-linkage, morbidity and mortality were followed up to the end of 1975. The mortality of patients with alcohol-related diseases was compared to 1120 patients with acute appendicitis by calculating indirectly age-standardised mortality ratios (SMR). The mortality and morbidity of 5963 patients with acute myocardial infarction or angina pectoris was also studied. The following SMRs for IHD mortality, non-fatal-IHD-hospitalisation and for mortality from all causes respectively, were found: acute myocardial infarction 11.6, 7.2 and 7.2; alcohol intoxication 6.0, 4.5 and 4.5; angina pectoris 5.2, 10.5 and 3.4; liver cirrhosis 2.2, 2.5 and 11.8; alcoholism 1.9, 1.9 and 3.6; pancreatitis 1.8, 1.2 and 4.4; alcohol psychosis 1.7, 2.5 and 4.2. IHD mortality and morbidity appeared to be more prevalent in patients hospitalised with alcohol intoxication than in patients with other alcohol-related diseases. This suggests that rapid drinking predisposes both to serious intoxication and to fatal disturbances of cardiac rhythm.
The genetics of Alzheimer's disease (AD) are obscure. Although most cases are sporadic half the patients with sporadic AD have a positive family history. The mode of genetic transmission and the role of environmental factors are unknown. The purpose of this study was to examine the contribution of genetic factors to the pathogenesis of AD in a twin cohort.
The Finnish Twin Cohort consists of all Finnish same-sexed twin pairs born before 1958 with both co-twins alive in 1975. The total number of twin pairs is 13 888, of whom 4307 are monozygotic (MZ) and 9581 ar dizygotic (DZ). These data were linked with the Hospital Discharge Register from 1972 to 1991 to identify twins who had dementia or related disease as a discharge diagnosis. The linkage of the registries yielded a total of 285 twin individuals. The medical records of these twins and their co-twins were reviewed to confirm and classify dementia (AD, vascular dementia, mixed dementia, and other dementia). The incidence, concordance, and age at onset of AD were examined.
The incidence of AD was significantly higher in MZ than in DZ twin individuals, with and adjusted MZ/DZ incidence ratio of 1.8 (95% confidence intervals 1.2 to 2.7). In contrast, the incidence of vascular or mixed dementia did not differ between MZ and DZ individuals (MZ/DZ ratio 0.6 [0.3 to 1.2]) for vascular and 1.0 [0.5 to 2.1] for mixed dementia). The pairwise concordance for AD was 18.6% in MZ pairs and 4.7% in DZ pairs and the corresponding probandwise concordance rates were 31.3% and 9.3%. The pairwise concordance for vascular dementia was 18.2% in MZ pairs and 6.7% in DZ pairs with corresponding probandwise rates of 30.8% and 12.5%. The onset age of AD concordant MZ pairs was identical in two pairs and diverged by up to 15 years.
The higher incidence of AD in MZ individuals than in DZ individuals may provide a clue to the aetiology of AD. The higher concordance rate of MZ pairs confirms the contribution of the major genetic component while indicating the need to identify environmental triggers.
Besides familial Alzheimer's disease (AD), the genetic susceptibility has also been found in sporadic cases of AD, mostly related to the apolipoprotein E polymorphism. The penetrance of AD is determined by age and probably by environmental exposure. Gene-environment interaction of a disease can be examined through studies of twins. The relative roles of genetic and environmental influences can be estimated by comparing the concordance rates between monozygotic (MZ) and dizygotic (DZ) twins. Genetic models can be used to specify contributions both from genetic as well as shared and unique environmental effects. The role of environmental factors can be investigated in the co-twin control study, either by comparing environmental exposure in MZ twins discordant for a disease or by comparing MZ twins discordant for an exposure suspected of causing a particular disease. The sampling of twin pairs AD can be carried out using voluntary recruitment, linkage of twin and hospital discharge registries or screening of twin registry population. Potential sources of biases in sampling are discussed. The majority of the published twin studies on AD are case reports or based on selected materials. In MZ pairs, the concordance rates for AD have varied between 31% and 83%. Only one co-twin control study in twins discordant for AD has been published. Published twin studies on AD are briefly reviewed.
A large number of studies have shown that obesity is both under genetic control and influenced by several environmental factors, including energy expenditure and intake. Several studies in animals and humans have furthermore suggested that certain environmental factors, such as a high fat intake, may modify the expression of the genes responsible for weight gain. The present study 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. A hierarchical multiple-regression analysis was used to test for gene-environment interactions by identifying significant three-way interactions between genetic factors, physical activity, and weight change. The results showed that associations between weight change in twin A and twin B were significantly stronger for monozygotic than for same-sex dizygotic twins at all levels of physical activity. Additionally, in the monozygotic men the strength of the association varied with physical activity level, and the association between the change in body mass index between the twin pairs with the highest physical activity level was about three times stronger (beta = 0.40) than the association in twin pairs with the lowest physical activity level (beta = 0.15, P for trend = 0.002). In pairs of dizygotic men, and in both monozygotic and dizygotic women, similarity in body mass index change was independent of physical activity level (all P > 0.14). The present study showed that genetic factors may modify the effects of physical activity on weight change, and suggests that a sedentary lifestyle may have an obesity-promoting effect in men with a genetic predisposition.
BACKGROUND: The prevalence of asthma is rising and there are recent reports of increasing asthma rates among top level skiers and runners in the Nordic countries. METHODS: The lifetime occurrence of pulmonary diseases (asthma, chronic bronchitis, emphysema) and current bronchitis symptoms was compared in former elite male athletes (n = 1282) who represented Finland between 1920 and 1965 at least once in international competitions and controls (n = 777) who, at the age of 20, were classified as healthy and who responded to a questionnaire in 1985. The presence of disease and symptoms was identified from the questionnaire and, in the case of asthma, also from a nationwide reimbursable medication register. The death certificates of the subjects of our original cohort who died between 1936 and 1985 were also investigated to determine the cause of death. RESULTS: The occurrence of the pulmonary diseases was associated with age, smoking habits, occupational group, and a history of exposure to chemicals. After adjusting for these variables, athletes who participated in mixed sports (odds ratio (OR) 0.46, 95% confidence interval (CI) 0.23 to 0.92) and power sports (OR 0.43, 95% CI 0.21 to 0.87) had lower odds ratios for emphysema, and endurance sports athletes had a lower odds ratio for the presence of at least one pulmonary disease (OR 0.53, 95% CI 0.28 to 0.98) when compared with controls. Athletes also tended to have fewer reimbursable medications for asthma and fewer current symptoms for chronic bronchitis. Between 1936 and 1985 two controls but none of the athletes died of asthma. CONCLUSIONS: The lifetime occurrence of asthma or other pulmonary diseases is not increased in former elite athletes, and exercise alone, even in a cold environment, did not appear to increase the prevalence of asthma, at least up to the mid 1980s.
To investigate the predictive value of atopy, smoking, and living in a farm environment in the development of chronic bronchitis.
This was a cross sectional and longitudinal study.
Postal surveys carried out in Finland in 1975 and 1981.
The study was part of the Finnish twin cohort study, which included adult twin pairs born in Finland before 1958. The cross sectional sample consisted of 18,351 subjects, including 1025 prevalent cases, and the follow up sample comprised 17,134 subjects, 553 of whom were incident cases of chronic bronchitis.
According to the cross sectional data, chronic bronchitis was associated with atopy (relative risk 1.41) and smoking (2.43). In the follow up data, chronic bronchitis was related to atopy (1.28), smoking (2.31), and farming (1.45).
The results confirm the earlier finding in the Finnish farming population that, in addition to smoking, atopy predisposes the development of chronic bronchitis. A farm environment was also found to be a predisposing factor. The results give further support to the "Dutch hypothesis" on the etiology of chronic bronchitis, according to which atopy is a predisposing factor.
Notes
Cites: J Epidemiol Community Health. 1987 Dec;41(4):300-53502671
Cites: Am Rev Respir Dis. 1984 Nov;130(5):759-656497158
Cites: Med Lav. 1984 Mar-Apr;75(2):101-96749046
Cites: J Occup Med. 1983 Feb;25(2):131-416834161
Cites: Am Rev Respir Dis. 1980 Feb;121(2):329-387362139
We estimated genetic and environmental variance of BMI among 7245 non-pregnant MZ and DZ pairs of the same sex from the population-based Finnish Twin Cohort. The contributions of additive genetic effects, shared and non-shared environmental effects on age-adjusted BMI-variance were estimated by LISREL structural equation models. Genetic effects contribute 72% in men and 66.4% in non-pregnant women of total variance, while 27.8% of variance among men and 33.6% among women is due to non-shared environmental effects. Shared environmental effects were nonsignificant (0% for women and 0.2% for men). Similar values were obtained for hereditary and non-shared environmental effects, when shared environmental effects were not included in the model. The inclusion of pregnant women did not substantially change heritability estimates.
