Parties and voters in Iceland: A study of the 1983 and 1987 Althingi elections.

This thesis analyses the 1983 and 1987 Althingi elections in Iceland, a micro state with rich literary and historical traditions, including the Althingi which Icelanders claim to be the oldest parliament in the world. Three theoretical approaches - a party identification approach, a rational approcah, and a social-structural approach - are used. A special effort is made to compare the Icelandic findings to voting behaviour in Norway and Sweden. Direct party switching (23% in 1983 and 36% in 1987) is shown to be the main reason for the major changes in election results, while the impact of new voters and mobilization and demobilization of voters was small. As in many European countries, voters often change party identification when they switch parties, thus limiting the usefulness of the party identification model. Nevertheless party identification, while weaker than in Scandinavia, serves to tie parties to voters, along with party membership, participation in primaries, and exposure to the press. In accord with a rational approach, Icelandic voters have a cognitive map of the party system along left-right lines, as is the case in Scandinavia. Most voters can rank the parties on a left-right continuum, which is related to party choice, like and dislike for the parties and party leaders, and voters' stance on issues. A left- right issue factor is by far most strongly related to party choice, as in Scandinavia, while an urban-rural factor on which the ranking of parties is different, reduces the correspondence between the left-right spectrum and vote switching. While issue voting in Iceland is high, it is lower than in Norway and Sweden. The thesis argues, that the main reason is that Icelandic parties offer less clear and stable alternatives in elections. Social-structural variables are generally weakly related to party choice. Class voting has decreased dramatically, and is much weaker than in Norway and Sweden. The thesis is based on the first election surveys in Iceland, conducted by the author. Three data sets are used, based on random samples from the National Register: from 1983 (N=1003), from 1987 (N=1745), and a 1983-1987 panel (N=67 8)

The association between glucose abnormalities and heart failure in the population-based Reykjavik study

To access publisher full text version of this article. Please click on the hyperlink in Additional Link fieldOBJECTIVE: Diabetes is an independent risk factor for heart failure, whereas the relation between heart failure and abnormal glucose regulation (AGR) needs further evaluation. We studied this combination in the Reykjavik Study. RESEARCH DESIGN AND METHODS: The Reykjavik Study, a population-based cohort study during 1967-1997, recruited 19,381 participants aged 33-84 years who were followed until 2002. Oral glucose tolerance tests and chest X-rays were obtained from all participants. Cases were defined in accordance with World Health Organization criteria for type 2 diabetes or AGR (impaired glucose tolerance or impaired fasting glucose) and European Society of Cardiology guidelines for heart failure. RESULTS: The overall prevalence of type 2 diabetes and heart failure was 0.5% in men and 0.4% in women, while AGR and heart failure were found in 0.7% of men and 0.6% of women. Among participants with normal glucose regulation, heart failure was diagnosed in 3.2% compared with 6.0 and 11.8% among those with AGR and type 2 diabetes, respectively. The prevalence of type 2 diabetes in the age-group 45-65 years increased in both sexes during the period (P for trend = 0.007). The odds ratio was 2.8 (95% CI 2.2-3.6) for the association between type 2 diabetes and heart failure and 1.7 (1.4-2.1) between AGR and heart failure. CONCLUSIONS: There is a strong association between any form of glucometabolic perturbation and heart failure. Future studies in this field should focus on all types of glucose abnormalities rather than previously diagnosed diabetes only

Glucose abnormalities and heart failure predict poor prognosis in the population-based Reykjavík Study

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldBACKGROUND: The risk of cardiovascular disease increases progressively with increasing blood glucose from levels well below the diabetic threshold. In the Reykjavík Study the relationship between heart failure and abnormal glucose regulation was already apparent at the level of impaired glucose tolerance. The aim of this study was to determine the prognosis of participants with any glucose abnormality and heart failure and to test whether the combination of these conditions may adversely affect the subsequent prognosis. DESIGN: A prospective population-based study. METHODS: Data from the first visit of 19 381 participants were used. Participants were divided into groups according to their glycaemic and heart failure level, and comparisons were made between the groups and disease-free participants serving as a reference group. The risk of mortality and morbidity was calculated with adjustments for main cardiovascular risk factors and ischaemic heart disease. RESULTS: Participants in the reference group were younger, had lower body mass indices and more seldom a history of myocardial infarction compared with diseased groups. Mortality was lowest in the reference group (P<0.0001) increasing to a maximum in participants with the combination of glucose abnormality and heart failure. Prognostically, the mortality risk associated with abnormal glucose regulation was increased but was lower than the risk of diabetes. The risk of a new myocardial infarction was highest in participants with diabetes [hazard ratio (HR) 1.6; 95% confidence interval (CI) 1.3-2.0] or diabetes in combination with heart failure (HR 1.8; CI 1.1-2.7). CONCLUSIONS: Heart failure or glucose abnormalities are related to increased morbidity and mortality. The combination of glucose abnormality and heart failure did, however, not add further to the unfavourable prognosis in the presence of ischaemic heart disease

Linkage of essential hypertension to chromosome 18q

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldWe performed a genomewide scan with 904 microsatellite markers using 120 extended Icelandic families with 490 hypertensive patients. The families were identified by cross-matching a list of hypertensive patients from the Hypertension Clinic of the University Hospital (Landspitalinn) in Iceland with a genealogy database of the entire Icelandic nation. After adding 5 markers, we found linkage to chromosome 18q with an allele-sharing LOD score of 4.60 (P=2.1x 10(-6)). These results provide evidence for a novel susceptibility gene for essential hypertension on chromosome 18q and show that it is possible to study the genetics of essential hypertension without stratifying by subphenotypes

A genetic risk factor for periodic limb movements in sleep

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldBACKGROUND: The restless legs syndrome (RLS) is a common neurologic disorder characterized by an irresistible urge to move the legs. It is a major cause of sleep disruption. Periodic limb movements in sleep are detectable in most patients with RLS and represent an objective physiological metric. METHODS: To search for sequence variants contributing to RLS, we performed a genomewide association study and two replication studies. To minimize phenotypic heterogeneity, we focused on patients with RLS who had objectively documented periodic limb movements in sleep. We measured serum ferritin levels, since iron depletion has been associated with the pathogenesis of RLS. RESULTS: In an Icelandic discovery sample of patients with RLS and periodic limb movements in sleep, we observed a genomewide significant association with a common variant in an intron of BTBD9 on chromosome 6p21.2 (odds ratio, 1.8; P=2x10(-9)). This association was replicated in a second Icelandic sample (odds ratio, 1.8; P=4x10(-4)) and a U.S. sample (odds ratio, 1.5; P=4x10(-3)). With this variant, the population attributable risk of RLS with periodic limb movements was approximately 50%. An association between the variant and periodic limb movements in sleep without RLS (and the absence of such an association for RLS without periodic limb movements) suggests that we have identified a genetic determinant of periodic limb movements in sleep (odds ratio, 1.9; P=1x10(-17)). Serum ferritin levels were decreased by 13% per allele of the at-risk variant (95% confidence interval, 5 to 20; P=0.002). CONCLUSIONS: We have discovered a variant associated with susceptibility to periodic limb movements in sleep. The inverse correlation of the variant with iron stores is consistent with the suspected involvement of iron depletion in the pathogenesis of the disease