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- Landgren, Sara, 1980, et al.
(författare)
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Genetic variation of the ghrelin signaling system in females with severe alcohol dependence
- 2010
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Ingår i: Alcoholism: Clinical and Experimental Research. - : Wiley. - 0145-6008 .- 1530-0277. ; 34:9, s. 1519-1524
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Tidskriftsartikel (refereegranskat)abstract
- INTRODUCTION: Central ghrelin signaling is required for the rewarding effects of alcohol in mice. Because ghrelin is implied in other addictive behaviors such as eating disorders and smoking, and because there is co-morbidity between these disorders and alcohol dependence, the ghrelin signaling system could be involved in mediating reward in general. Furthermore, in humans, single nucleotide polymorphisms (SNPs) and haplotypes of the pro-ghrelin gene (GHRL) and the ghrelin receptor gene (GHSR) have previously been associated with increased alcohol consumption and increased body weight. Known gender differences in plasma ghrelin levels prompted us to investigate genetic variation of the ghrelin signaling system in females with severe alcohol dependence (n = 113) and in a selected control sample of female low-consumers of alcohol from a large cohort study in southwest Sweden (n = 212). METHODS: Six tag SNPs in the GHRL (rs696217, rs3491141, rs4684677, rs35680, rs42451, and rs26802) and four tag SNPs in the GHSR (rs495225, rs2232165, rs572169, and rs2948694) were genotyped in all individuals. RESULTS: We found that one GHRL haplotype was associated with reports of paternal alcohol dependence as well as with reports of withdrawal symptoms in the female alcohol-dependent group. Associations with 2 GHSR haplotypes and smoking were also shown. One of these haplotypes was also negatively associated with BMI in controls, while another haplotype was associated with having the early-onset, more heredity-driven, type 2 form of alcohol dependence in the patient group. CONCLUSION: Taken together, the genes encoding the ghrelin signaling system cannot be regarded as major susceptibility genes for female alcohol dependence, but is, however, involved in paternal heritability and may affect other reward- and energy-related factors such as smoking and BMI.
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| 2. |
- Mehlig, Kirsten, 1964, et al.
(författare)
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Cohort Profile: The INTERGENE Study.
- 2017
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Ingår i: International journal of epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 1464-3685 .- 0300-5771. ; 46:6
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Tidskriftsartikel (refereegranskat)abstract
- In 2001, the INTERGENE research programme established a population-based cohort of 3614 adults living in south-western Sweden. The aim was to assess environmental, lifestyle and hereditary risk factors for cardio-metabolic and respiratory diseases, and to document secular changes in many of these characteristics. Because the focus is on coronary heart disease (CHD), the population cohort was complemented with 618 patients with acute or chronic CHD who were sampled during the examination period for the cohort (2001–04), following the same protocol. More than 800 variables describe lifestyle and socio-demographic characteristics from questionnaires, anthropometric characteristics from physical examinations, and biomarkers from blood sampled during the examination. Additional blood samples and extracted DNA are stored in biobanks. Data from the case-control study of CHD were used to investigate associations between common risk factors (overweight, smoking, alcohol consumption, sedentary behaviour) and different candidate genes with respect to CHD, and explore interactions. In addition, a biomarker for airway inflammation (Fraction of Exhaled Nitric Oxide, FENO) was investigated as a risk factor for respiratory disease, and collaboration was established with international consortia to identify genes related to respiratory and cardiovascular diseases. An update of registry information on cohort members from hospitals, general practitioners and pharmacies provides a wide spectrum of incident diagnoses and treatments between 2001 and 2014. A recently completed longitudinal follow-up of the baseline cohort will provide a further measurement point to describe changing cardiovascular risk factors in south-west Sweden. Participation at baseline was 42%, and 61% of these participated at the follow-up.
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| 3. |
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| 4. |
- Berg, Christina, 1963, et al.
(författare)
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Eating patterns and portion size associated with obesity in a Swedish population.
- 2009
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Ingår i: Appetite. - : Elsevier BV. - 1095-8304 .- 0195-6663. ; 52:1, s. 21-6
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Tidskriftsartikel (refereegranskat)abstract
- The objective of this study was to describe the association between meal pattern and obesity. The study is based on data from the INTERGENE research programme, and the study population consists of randomly selected women and men, aged 25-74, living in the V?stra G?taland Region in Sweden. A total of 3610 were examined. Participants with measured BMI>/=30 were compared with others (BMI<30) with respect to questionnaire data on habitual meal patterns and intake of energy estimated from food frequencies and standard portions. Odds ratios (OR) with 95% confidence intervals were adjusted for age, sex, smoking and physical activity in logistic regression models. Being obese was significantly associated with omitting breakfast, OR 1.41 (1.05-1.90), omitting lunch OR 1.31 (1.04-1.66) and eating at night OR 1.62 (1.10-2.39). Obesity was also related to significantly larger self-reported portion sizes of main meals. No statistically significant relationship with intake of total energy was revealed. Thus, the results indicate that examination of meal patterns and portion sizes might tell us more about obesogenic food patterns than traditional nutrient analyses of food frequencies. Being obese was associated with a meal pattern shifted to later in the day and significantly larger self-reported portions of main meals.
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| 5. |
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| 6. |
- Berg, Christina, 1963, et al.
(författare)
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Food patterns and cardiovascular disease risk factors: the Swedish INTERGENE research program.
- 2008
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 88:2, s. 289-97
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Analyzing the impact of the intake of many foods simultaneously provides additional knowledge about analyses of nutrients and might make it easier to implement recommendations for the public. OBJECTIVE: The objective was to examine food patterns in a Swedish population and determine how they are related to metabolic risk factors for cardiovascular disease. DESIGN: The study is based on data from the INTERGENE population study of women and men aged 25-74 y in western Sweden. Dietary patterns were identified with cluster analysis of 93 food frequencies reported by 3452 participants. Associations with features of the metabolic syndrome, including blood lipids, blood pressure, and anthropometric measures, were analyzed. RESULTS: Five distinct food patterns were identified, of which one was interpreted as a "healthy" reference pattern. This healthy cluster was distinguished by more frequent consumption of high-fiber and low-fat foods and lower consumption of products rich in fat and sugar. The 4 other clusters differed significantly from the reference cluster with respect to prevalence of cardiovascular disease risk factors and the metabolic syndrome. For example, body mass index and waist-to-hip ratio were significantly higher in a cluster characterized by high consumption of energy-dense drinks and white bread and low consumption of fruit and vegetables (P < 0.0001 and P = 0.004, respectively). CONCLUSIONS: It is possible to distinguish food patterns that are related to obesity and obesity-related cardiovascular disease risk factors in contrast with a more healthy pattern conforming with current dietary guidelines. Thus, the results indicate no reason for questioning the current recommendations.
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| 7. |
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| 8. |
- Berg, Christina, 1963, et al.
(författare)
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Normal weight adiposity in a Swedish population: how well is cardiovascular risk associated with excess body fat captured by BMI?
- 2015
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Ingår i: Obesity Science & Practice. - : Wiley. - 2055-2238. ; 1:1, s. 50-58
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Tidskriftsartikel (refereegranskat)abstract
- Objective The aim of this study was to examine how well body mass index (BMI) reflects cardiovascular risk associated with excess adiposity in a Swedish population by examining the association between body fat, BMI and cardiovascular risk factors. Methods A total of 3,010 adults participated. Normal weight adiposity was defined as the combination of BMI<25 kg/m2 and percentage body fat ≥35% for women and ≥25% for men. Associations with blood pressure, blood lipids, apolipoproteins and C-reactive protein were analysed in age-adjusted regression models. Results The majority of the individuals with overweight and obesity were correctly classified to adiposity, while a wide range of body fat was observed among the normal weight subjects. In total, 9% of the participants were categorised as normal weight with adiposity. Compared with the normal weight leanness group, participants with normal weight adiposity had higher levels of serum triglycerides, low-density lipoprotein cholesterol, C-reactive protein, apolipoptotein B and the apolipoprotein B/A-I ratio. In normal weight men, adiposity was also associated with higher blood pressure and lower high-density lipoprotein cholesterol. Conclusions Higher percentage of body fat was associated with less favourable risk factor profile even in subjects who were normal weight. Thus, it might be relevant to screen for metabolic risk factors in the upper end of the normal weight category.
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| 10. |
- Gustavsson, Jaana, 1974, et al.
(författare)
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Interaction of apolipoprotein E genotype with smoking and physical inactivity on coronary heart disease risk in men and women.
- 2012
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Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 220:2, s. 486-492
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Apolipoprotein E genotype (APOE) polymorphism affects lipid levels and coronary heart disease (CHD) risk. However, these associations may be modified by lifestyle factors. Therefore, we studied whether smoking, physical inactivity or overweight interact with APOE on cholesterol levels and CHD risk. METHODS: Combining two Swedish case-control studies yielded 1735 CHD cases and 4654 population controls (3747 men, 2642 women). Self-reported questionnaire lifestyle data included smoking (ever [current or former regular] or never) and physical inactivity (mainly sitting leisure time). We obtained LDL cholesterol levels and APOE genotypes. CHD risk was modelled using logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for relevant covariates. RESULTS: Smoking interacted with APOE on CHD risk; adjusted ORs for ever versus never smoking were 1.45 (95% CI 1.00-2.10) in ɛ2 carriers, 2.25 (95% CI 1.90-2.68) in ɛ3 homozygotes and 2.37 (95% CI 1.85-3.04) in ɛ4 carriers. Female ɛ4 carriers had OR 3.62 (95% CI 2.32-5.63). The adjusted ORs for physical inactivity were 1.09 (95% CI 0.73-1.61), 1.34 (95% CI 1.12-1.61), and 1.79 (95% CI 1.38-2.30) in ɛ2, ɛ3ɛ3 and ɛ4 groups, respectively. No interaction was seen between overweight and APOE for CHD risk, or between any lifestyle factor and APOE for LDL cholesterol levels. CONCLUSION: The APOE ɛ2 allele counteracted CHD risk from smoking in both genders, while the ɛ4 allele was seen to potentiate this risk mainly in women. Similar ɛ2 protection and ɛ4 potentiation was suggested for CHD risk from physical inactivity.
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