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  • 1. Amundadottir, Laufey T.
    et al.
    Sulem, Patrick
    Gudmundsson, Julius
    Helgason, Agnar
    Baker, Adam
    Agnarsson, Bjarni A.
    Sigurdsson, Asgeir
    Benediktsdottir, Kristrun R.
    Cazier, Jean-Baptiste
    Sainz, Jesus
    Jakobsdottir, Margret
    Kostic, Jelena
    Magnusdottir, Droplaug N.
    Ghosh, Shyamali
    Agnarsson, Kari
    Birgisdottir, Birgitta
    Le Roux, Louise
    Olafsdottir, Adalheidur
    Blondal, Thorarinn
    Andresdottir, Margret
    Gretarsdottir, Olafia Svandis
    Bergthorsson, Jon T.
    Gudbjartsson, Daniel
    Gylfason, Arnaldur
    Thorleifsson, Gudmar
    Manolescu, Andrei
    Kristjansson, Kristleifur
    Geirsson, Gudmundur
    Isaksson, Helgi
    Douglas, Julie
    Johansson, Jan-Erik
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Wiklund, Fredrik
    Montie, James E.
    Yu, Xiaoying
    Suarez, Brian K.
    Ober, Carole
    Cooney, Kathleen A.
    Gronberg, Henrik
    Catalona, William J.
    Einarsson, Gudmundur V.
    Barkardottir, Rosa B.
    Gulcher, Jeffrey R.
    Kong, Augustine
    Thorsteinsdottir, Unnur
    Stefansson, Kari
    A common variant associated with prostate cancer in European and African populations2006In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 38, no 6, p. 652-658Article in journal (Refereed)
    Abstract [en]

    With the increasing incidence of prostate cancer, identifying common genetic variants that confer risk of the disease is important. Here we report such a variant on chromosome 8q24, a region initially identified through a study of Icelandic families. Allele -8 of the microsatellite DG8S737 was associated with prostate cancer in three case-control series of European ancestry from Iceland, Sweden and the US. The estimated odds ratio ( OR) of the allele is 1.62 (P = 2.7 x 10(-11)). About 19% of affected men and 13% of the general population carry at least one copy, yielding a population attributable risk ( PAR) of similar to 8%. The association was also replicated in an African American case-control group with a similar OR, in which 41% of affected individuals and 30% of the population are carriers. This leads to a greater estimated PAR (16%) that may contribute to higher incidence of prostate cancer in African American men than in men of European ancestry.

  • 2.
    Augustsson, Katarina
    et al.
    Karolinska institutet, Sweden.
    Lindblad, J
    Overvik, E
    Steineck, G
    A population-based dietary inventory of cooked meat and assessment of the daily intake of food mutagens1999In: Food Additives and Contaminants, ISSN 0265-203X, E-ISSN 1464-5122, Vol. 16, no 5, p. 215-225Article in journal (Refereed)
    Abstract [en]

    Frequent consumption of meat has been associated with an increased risk of colorectal cancer. Such a risk may be due to naturally occurring compounds in the meat, substances added to the meat, or agents formed during cooking. Concerning the latter alternative, mutagenic heterocyclic amines are multi-site animal carcinogens, but their relevance to human cancer has yet to be determined. In the present study, we made a population-based inventory of cooked meat dishes consumed in the county of Stockholm, ranked dishes according to cooking method and frequency of consumption and, in addition, determined levels of mutagenic activity in six commonly consumed fried meat dishes. Meat was consumed, on average, 493 times per year, giving 1.4 daily servings. Frying was the most common way to cook meat. When ranking meat dishes according to intake frequency, the top eight dishes were as follows. sausage, steak casserole, meatballs, pork chops, pork belly, bacon, ground beef patties, and, finally, mincemeat sauce. The frying sessions were pel;formed under controlled conditions at four different temperatures, and we documented the degree of surface browning and measured mutagenic activity in six frequently eaten dishes (sausage, meatballs, pork chops, pork belly, ground beef patties, and minute beef). We found extracts from all six dishes to be mutagenic, and a mean daily dose of exposure was calculated, giving 862 revertants. This investigation leaves no doubt that a major portion of the total meat consumption is fried before ingestion and that fried meat dishes frequently consumed by an elderly population in Stockholm contain mutagenic substances. Furthermore, the study provides usable information for future epidemiological research in which it is necessary to disentangle the effect of meat per se from the effect of potentially carcinogenic heterocyclic amines.

  • 3.
    Augustsson, Katarina
    et al.
    Karolinska institutet, Sweden.
    Michaud, D S
    Rimm, E B
    Leitzmann, M F
    Stampfer, M J
    Willett, W C
    Giovannucci, E
    A prospective study of intake of fish and marine fatty acids and prostate cancer2003In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 12, no 1, p. 64-67Article in journal (Refereed)
    Abstract [en]

    Experimental studies suggest that marine fatty acids have an antitumor effect on prostate tumor cells. The aim of this study was to investigate whether high consumption of fish and marine fatty acids reduces the risk of prostate cancer in humans. We followed 47,882 men participating in the Health Professionals Follow-up Study. Dietary intake was assessed in 1986, 1990, and 1994, using a validated food frequency questionnaire. During 12 years of follow-up, 2,482 cases of prostate cancer were diagnosed, of which 617 were diagnosed as advanced prostate cancer including 278 metastatic prostate cancers. Eating fish more than three times per week was associated with a reduced risk of prostate cancer, and the strongest association was for metastatic cancer (multivariate relative risk, 0.56; 95% confidence interval, 0.37-0.86, compared with infrequent consumption, i.e., less than twice per month). Intake of marine fatty acids from food showed a similar but weaker association. Each additional daily intake of 0.5 g of marine fatty acid from food was associated with a 24% decreased risk of metastatic cancer. We found that men with high consumption of fish had a lower risk of prostate cancer, especially for metastatic cancer. Marine fatty acids may account for part of the effect, but other factors in fish may also play a role.

  • 4.
    Augustsson, Katarina
    et al.
    Karolinska institutet, Sweden.
    Skog, K
    Jagerstad, M
    Dickman, P W
    Steineck, G
    Dietary heterocyclic amines and cancer of the colon, rectum, bladder, and kidney: a population-based study1999In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 353, no 9154, p. 703-707Article in journal (Refereed)
    Abstract [en]

    Background Heterocyclic amines formed in cooked meat and fish are carcinogenic in animal models and form DNA adducts in human beings. We undertook a study to assess whether these substances are related to the risks of cancer in the large bowel and urinary tract. Methods In a population-based case-control study, cases were identified from the Swedish cancer registry. Controls were randomly selected from the population register. Information on intake of various foods and was assessed by questionnaire, with photographs of foods cooked at various temperatures. We measured the content of heterocyclic amines in foods cooked under these conditions. Findings Information was retrieved from 553 controls, 352 cases of colon cancer, 249 cases of rectal cancer, 273 cases of bladder cancer, and 138 cases of kidney cancer. The response rate was 80% for controls and 70% for cases. The estimated daily median intake of heterocyclic amines was 77 ng for controls, and 66 ng, 63 ng, 96 ng, and 84 ng for cases with cancer of the colon, rectum, bladder, and kidney, respectively. The relative risk for the intake of heterocyclic amines (highest vs lowest quintile) was 0.6 (95% CI 0.4-1.0) for colon cancer, 0.7 (0.4-1.1) for rectal cancer, 1.2 (0.7-2.1) for bladder cancer, and 1.0 (0.5-1.9) for kidney cancer. Seven cases, but no controls, had an estimated daily intake of heterocyclic amines above 1900 ng. Interpretation Intake of heterocyclic amines, within the usual dietary range in this study population, is unlikely to increase the incidence of cancer in the colon, rectum, bladder, or kidney. For daily intakes above 1900 ng, our data are consistent with human carcinogenicity, but the precision was extremely low.

  • 5.
    Augustsson, Katarina
    et al.
    Karolinska institutet, Sweden.
    Skog, K
    Jagerstad, M
    Steineck, G
    Assessment of the human exposure to heterocyclic amines1997In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 18, no 10, p. 1931-1935Article in journal (Refereed)
    Abstract [en]

    Heterocyclic amines are possible human carcinogens and fried meat is an important source of exposure in the Western diet, To study the effect of heterocyclic amines in humans, accurate assessment of individual food consumption is essential, Parameters influencing the intake include the amount and type of meat ingested, frequency of consumption, cooking method, cooking temperature and the duration of cooking, The aim of the present study was to develop a practical method for assessing individual intakes of specific heterocyclic amines in a large sample of people, This has been done by combining information on food consumption and laboratory findings of heterocyclic amines in food products, Diet was assessed using a semi-quantitative food frequency questionnaire including photos of fried meat and, in all, 22 dishes were cooked and chemically analyzed. The method was employed in an elderly population in Stockholm to estimate the daily mean intake of the five heterocyclic amines 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo [4,5-f]quinoline (MeIQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-3,4,8-trimethylimidazo [4,5-f]quinoxaline (DiMeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), The total daily intake ranged from none to 1816 ng, with a mean intake of 160 ng, which is well below estimates reported previously, Highest amounts ingested were of PhIP (mean 72, range 0-865 ng/day) and MeIQx (mean 72, range 0-1388 ng/day), followed by DiMeIQx (mean 16, range 0-171 ng/day), while MeIQ and IQ were ingested only in very small amounts (mean <1 ng/day).

  • 6. Balter, O
    et al.
    Bälter, Katarina
    Demands on web survey tools for epidemiological research2005In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 20, no 2, p. 137-139Article in journal (Refereed)
    Abstract [en]

    In countries where the Internet access is high, a web-based questionnaire could save time and money compared to printed questionnaires, mainly by eliminating the two steps of transferring answers from printed to a digital data set and manually completing missing and impossible answers. However, many of the features wanted for conducting large epidemiological studies are not available in many web survey systems. Here we describe design issues the investigator needs to be aware of when using web-based questionnaires in epidemiological research.

  • 7.
    Balter, Olle
    et al.
    Royal Inst Technol, Sch Comp Sci & Commun, Stockholm, Sweden..
    Fondell, Elinor
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Karolinska Inst, Osher Ctr Integrat Med, SE-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Feedback in web-based questionnaires as incentive to increase compliance in studies on lifestyle factors2012In: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 15, no 6, p. 982-988Article in journal (Refereed)
    Abstract [en]

    Objective: We explored the use of feedback in interactive web-based questionnaires for collecting data on lifestyle factors in epidemiological studies. Design: Here we report from a cohort study on lifestyle factors and upper respiratory tract infections among 1805 men and women. We introduced interactivity in the form of personalized feedback and feedback on a group level regarding dietary intake, physical activity and incidence of infections in web-based questionnaires as incentives for the respondents to continue answering questions and stay in the study. Setting: The study was performed in Sweden. Subjects: All participants were randomly selected from the population registry. Results: Personalized feedback was offered in the baseline questionnaire and feedback on a group level in the five follow-up questionnaires. In total, 88% of the participants actively chose to get personalized feedback at least once in the baseline questionnaire. The follow-up questionnaires were sent by email and the overall compliance at each follow-up was 83-84%, despite only one reminder. In total, 74% completed all five follow-ups. However, the compliance was higher among those who chose feedback in the baseline questionnaire compared with those who did not choose feedback. Conclusions: The results show that it is possible to use feedback in web questionnaires and that it has the potential to increase compliance. The majority of the participants actively chose to take part in the personalized feedback in the baseline questionnaire and future research should focus on improving the design of the feedback, which may ultimately result in even higher compliance in research studies.

  • 8. Barrett, J H
    et al.
    Smith, G
    Waxman, R
    Gooderham, N
    Lightfoot, T
    Garner, R C
    Augustsson, Katarina
    Karolinska institutet, Sweden.
    Wolf, C R
    Bishop, D T
    Forman, D
    Investigation of interaction between N-acetyltransferase 2 and heterocyclic amines as potential risk factors for colorectal cancer2003In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 24, no 2, p. 275-282Article in journal (Refereed)
    Abstract [en]

    Fast N-acetyltransferase 2 (NAT2) acetylators may be at increased risk of colorectal cancer through the activation of carcinogenic heterocyclic amines (HA), which are produced by meat cooked at high temperatures and are found in cigarette smoke. A study of 500 incident colorectal cancer cases and population controls, matched for age, sex and general practitioner, was conducted in the UK to investigate this hypothesis. Usual meat intake and lifetime smoking habits were estimated using a detailed questionnaire administered by interview. Subjects also indicated how well cooked they ate their meat. Subjects were classified as fast or slow NAT2 acetylators on the basis of NAT2 genotype. Complete genotype data were available on 433 matched pairs. The risk of colorectal cancer showed a steady increase with meat intake, rising to an odds ratio of 1.51 [95% confidence interval (1.03, 2.23)] for the highest versus the lowest quartile, after adjustment for total energy intake, and this was even more pronounced for red meat [odds ratio 1.97 (1.30, 2.98)]. However, this effect was not influenced by the preference for well-done meat. Smoking was also associated with an increased risk [odds ratio 1.47 (1.10, 1.98) for ever- versus never-smokers]. In both cases and controls similar to40% of subjects were classified as fast acetylators, and the risks associated with (red) meat intake and smoking did not vary with NAT2 status. This study provides no support for the hypothesis that fast NAT2 acetylators are at increased risk of colorectal cancer, even if exposed to high levels of HA from well-cooked meat or smoking.

  • 9. Bonn, S. E
    et al.
    Surkan, P. J.
    Trolle Lagerros, Y.
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Feasibility of a novel web-based physical activity questionnaire for young children2012In: Pediatric Reports, ISSN 2036-749X, E-ISSN 2036-7503, Vol. 4, no 4, article id e37Article in journal (Refereed)
    Abstract [en]

    Accurate assessment of children's physical activity is critical in determining associations between childhood physical activity and health later in life. We have developed a web-based questionnaire, KidActive-Q, to assess physical activity in early childhood. The feasibility and reproducibility of KidActive-Q were assessed in a sample of 20 children aged 2 to 6 years. The questionnaire was distributed to parents via e-mail on two occasions. The median time required to complete KidActive-Q was 2.5 minutes. All the parents reported that the questionnaire was easy or very easy to fill. The intraclass correlations for test-retest reliability were 0.60 (95% confidence interval: 0.31-0.88) for daily time spent outdoors, and 0.85 (95% confidence interval: 0.72-0.97) for daily time watching television. Our results suggest that KidActive-Q is a user-friendly tool for assessing physical activity in early childhood. To our knowledge, this is the first web-based questionnaire specifically developed for young children. 

  • 10.
    Bonn, S. E.
    et al.
    Karolinska Inst, Stockholm, Sweden..
    Wiklund, F.
    Karolinska Inst, Stockholm, Sweden..
    Sjolander, A.
    Karolinska Inst, Stockholm, Sweden..
    Szulkin, R.
    Karolinska Inst, Stockholm, Sweden..
    Stattin, P.
    Umea Univ, Umea, Sweden..
    Holmberg, E.
    Univ Gothenburg, Sahlgrenska Acad, Gothenburg, Sweden..
    Gronberg, H.
    Karolinska Inst, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Stockholm, Sweden..
    Body Mass Index and Weight Change in Men with Prostate Cancer: Progression and Mortality.2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, p. 141-142Article in journal (Other academic)
  • 11.
    Bonn, Stephanie E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Lagerros, Ylva Trolle
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, S-17177 Stockholm, Sweden..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Holmberg, Erik
    Univ Gothenburg, Inst Clin Sci, Dept Oncol, Sahlgrenska Acad, Gothenburg, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Physical Activity and Survival among Men Diagnosed with Prostate Cancer2015In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 24, no 1, p. 57-64Article in journal (Refereed)
    Abstract [en]

    Background: Few studies have investigated the association between post-diagnosis physical activity and mortality among men diagnosed with prostate cancer. The aim of this study was to investigate the effect of physical activity after a prostate cancer diagnosis on both overall and prostate cancer-specific mortality in a large cohort. Methods: Data from 4,623 men diagnosed with localized prostate cancer 1997-2002 and followed-up until 2012 were analyzed. HRs with 95% confidence intervals (CI) were estimated using Cox proportional hazards models to examine the association between post-diagnosis recreational MET-h/d, time spent walking/bicycling, performing household work or exercising, and time to overall and prostate cancer-specific death. All models were adjusted for potential confounders. Results: During the follow-up, 561 deaths of any cause and 194 deaths from prostate cancer occurred. Statistically significantly lower overall mortality rates were found among men engaged in 5 recreationalMET-h/d (HR, 0.63; 95% CI, 0.52-0.77), walking/ bicycling 20 min/d (HR, 0.70; 95% CI, 0.57-0.86), performing householdwork > 1 h/d (HR, 0.71; 95% CI, 0.59-0.86), or exercising > 1 h/wk (HR, 0.74; 95% CI, 0.61-0.90), compared with less active men within each activity type. For prostate cancer-specific mortality, statistically significantly lower mortality rates were seen among men walking/bicycling >= 20 min/d (HR, 0.61; 95% CI, 0.43-0.87) or exercising 1 h/wk (HR, 0.68; 95% CI, 0.48-0.94). Conclusions: Higher levels of physical activity were associated with reduced rates of overall and prostate cancer-specific mortality. Impact: Our study further strengthens previous results indicating beneficial effects of physical activity on survival among men with prostate cancer. Cancer Epidemiol Biomarkers Prev; 24(1); 57-64. (C) 2014 AACR.

  • 12.
    Bonn, Stephanie E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17177 Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17177 Stockholm, Sweden..
    Tillander, Annika
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17177 Stockholm, Sweden..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17177 Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17177 Stockholm, Sweden.;Stanford Univ, Stanford Prevent Res Ctr, Stanford, CA 94305 USA..
    Body mass index in relation to serum prostate-specific antigen levels and prostate cancer risk2016In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 139, no 1, p. 50-57Article in journal (Refereed)
    Abstract [en]

    High Body mass index (BMI) has been directly associated with risk of aggressive or fatal prostate cancer. One possible explanation may be an effect of BMI on serum levels of prostate-specific antigen (PSA). To study the association between BMI and serum PSA as well as prostate cancer risk, a large cohort of men without prostate cancer at baseline was followed prospectively for prostate cancer diagnoses until 2015. Serum PSA and BMI were assessed among 15,827 men at baseline in 2010-2012. During follow-up, 735 men were diagnosed with prostate cancer with 282 (38.4%) classified as high-grade cancers. Multivariable linear regression models and natural cubic linear regression splines were fitted for analyses of BMI and log-PSA. For risk analysis, Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) and natural cubic Cox regression splines producing standardized cancer-free probabilities were fitted. Results showed that baseline Serum PSA decreased by 1.6% (95% CI: -2.1 to -1.1) with every one unit increase in BMI. Statistically significant decreases of 3.7, 11.7 and 32.3% were seen for increasing BMI-categories of 25<30, 30<35 and 35 kg/m(2), respectively, compared to the reference (18.5<25 kg/m(2)). No statistically significant associations were seen between BMI and prostate cancer risk although results were indicative of a positive association to incidence rates of high-grade disease and an inverse association to incidence of low-grade disease. However, findings regarding risk are limited by the short follow-up time. In conclusion, BMI was inversely associated to PSA-levels. BMI should be taken into consideration when referring men to a prostate biopsy based on serum PSA-levels. What's new? High body mass index (BMI) has been associated with risk of aggressive or fatal prostate cancer. One possible explanation may be an effect on serum prostate-specific antigen (PSA) levels. Here, the authors assessed the association between BMI and serum PSA level and prostate cancer risk in a large prospective cohort study. While no statistically significant associations were found between BMI and overall risk of prostate cancer, increasing BMI was associated with decreased serum PSA levels among men with no previous prostate cancer diagnosis. BMI should be taken into consideration when referring men to a prostate biopsy based on PSA-test results.

  • 13.
    Bonn, Stephanie E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Szulkin, Robert
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Holmberg, Erik
    Univ Gothenburg, Dept Oncol, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Body mass index and weight change in men with prostate cancer: progression and mortality2014In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, no 8, p. 933-943Article in journal (Refereed)
    Abstract [en]

    Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study. Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models. Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03-2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss > 5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41-2.66), while a weight gain > 5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18-3.16). Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.

  • 14.
    Bonn, Stephanie Erika
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12a, SE-17177 Stockholm, Sweden..
    Bergman, Patrick
    Linnaeus Univ, Dept Sport Sci, Kalmar, Sweden..
    Lagerros, Ylva Trolle
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, SE-17177 Stockholm, Sweden.;Karolinska Univ, Huddinge Hosp, Dept Endocrinol Metab & Diabet, Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12a, SE-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12a, SE-17177 Stockholm, Sweden..
    A Validation Study of the Web-Based Physical Activity Questionnaire Active-Q Against the GENEA Accelerometer2015In: JMIR Research Protocols, ISSN 1929-0748, E-ISSN 1929-0748, Vol. 4, no 3, article id UNSP e86Article in journal (Refereed)
    Abstract [en]

    Background: Valid physical activity assessment in epidemiological studies is essential to study associations with various health outcomes. Objective: To validate the Web-based physical activity questionnaire Active-Q by comparing results of time spent at different physical activity levels with results from the GENEA accelerometer and to assess the reproducibility of Active-Q by comparing two admissions of the questionnaire Methods: A total of 148 men (aged 33 to 86 years) responded to Active-Q twice and wore the accelerometer during seven consecutive days on two occasions. Time spent on six different physical activity levels including sedentary, light (LPA), moderate (MPA), and vigorous (WA) as well as additional combined categories of sedentary-to-light and moderate-to-vigorous (MVPA) physical activity was assessed. Validity of Active-Q was determined using Spearman correlation coefficients with 95% confidence intervals (CI) and the Bland-Altman method. Reproducibility was assessed using intraclass correlation coefficients (ICCs) comparing two admissions of the questionnaire Results: The validity correlation coefficients were statistically significant for time spent at all activity levels; sedentary (r=0.19, 95% CI: 0.04-0.34), LPA (r=0.15, 95% CI: 0.00-0.31), sedentary-to-light (r=0.35, 95% CI: 0.19-0.51), MPA (r=0.27, 95% CI: 0.12-0.42), WA (r=0.54, 95% CI: 0.42-0.67), and MVPA (r=0.35, 95% CI: 0.21-0.48). The Bland-Altman plots showed a negative mean difference for time in LPA and positive mean differences for time spent in MPA, WA and MVPA. The ICCs of test-retest reliability ranged between r=0.51-0.80 for the different activity levels in Active-Q. Conclusions: More moderate and vigorous activities and less light activities were reported in Active-Q compared to accelerometer measurements. Active-Q shows comparable validity and reproducibility to other physical activity questionnaires used today.

  • 15.
    Bonn, Stephanie Erika
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Lagerros, Ylva Trolle
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, SE-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    How Valid are Web-Based Self-Reports of Weight?2013In: Journal of Medical Internet Research, ISSN 1438-8871, E-ISSN 1438-8871, Vol. 15, no 4, article id UNSP e52Article in journal (Refereed)
    Abstract [en]

    Background: Many studies rely on self-reported anthropometric data. While paper-based self-reports have been the standard collection mode, the number of studies collecting self-reported data via the Web is increasing rapidly. Although numerous studies have shown good agreement between self-reported and measured weight using paper-based questionnaires, the validity of using the Web to inquire about weight is unknown. Objective: The objective of this study was to validate Web-based self-reports of bodyweight compared to weight measured at the study center. Methods: The validity of weight self-reported via the Web was assessed by comparing self-reports against measurements of weight in a convenience sample of 149 individuals (77.2% women, 115/149), aged 20-65 years. Study participants self-reported their weight via a Web-based questionnaire and thereafter had their weight measured in the research center. Results: The Spearman correlation coefficient between self-reported and measured weight was 0.98 (P<.001). The mean difference between self-reported and measured weight was -1.2 (SD 2.6) kg. There was a statistically significant difference between self-reported and measured weight with the self-reported being lower (P<.001). Subjects with a body mass index (BMI) >= 25 kg/m(2), and subjects >= 30 years of age, under-reported their weight statistically significantly more than subjects with a BMI <25 kg/m(2), and subjects <30 years of age, respectively. Conclusions: Our results show that self-reported weight via the Web can be a valid method of data collection.

  • 16.
    Bonn, Stephanie Erika
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Lagerros, Ylva Trolle
    Karolinska Inst, Clin Epidemiol Unit, Dept Med, SE-17177 Stockholm, Sweden..
    Christensen, Sara Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Moller, Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Wright, Antony
    MRC, Cambridge, England..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Active-Q: Validation of the Web-Based Physical Activity Questionnaire Using Doubly Labeled Water2012In: Journal of Medical Internet Research, ISSN 1438-8871, E-ISSN 1438-8871, Vol. 14, no 1, article id e29Article in journal (Refereed)
    Abstract [en]

    Background: Increased use of the Internet provides new opportunities for collecting data in large studies. The aim of our new Web-based questionnaire, Active-Q, is to assess total physical activity and inactivity in adults. Active-Q assesses habitual activity during the past year via questions in four different domains: (1) daily occupation, (2) transportation to and from daily occupation, (3) leisure time activities, and (4) sporting activities. Objective: The objective of our study is to validate Active-Q's energy expenditure estimates using the doubly labeled water (DLW) method, and to assess the reproducibility of Active-Q by comparing the results of the questionnaire completed by the same group on two occasions. Methods: The validity and reproducibility of Active-Q were assessed in a group of 37 individuals, aged 20 to 65 years. Active-Q was distributed via email to the participants. The total energy expenditure of the participants was assessed using DLW for 11 consecutive days. Results: The median time to complete Active-Q was 6.1 minutes. The majority of participants (27/37, 73%) reported that the questionnaire was "easy" or "very easy" to answer. On average, Active-Q overestimated the total daily energy expenditure by 440 kJ compared with the DLW. The Spearman correlation between the two methods was r = 0.52 (P < .001). The intraclass correlation coefficient for total energy expenditure between the results of Active-Q completed on two occasions was 0.83 (95% CI 0.73-0.93). Conclusions: Active-Q is a valid and reproducible method of assessing total energy expenditure. It is also a user-friendly method and suitable for Web-based data collection in large epidemiological studies.

  • 17.
    Brown, David A.
    et al.
    St Vincents Hosp, Ctr Appl Med Res, Sydney, NSW 2010, Australia.;Univ New S Wales, Sydney, NSW, Australia..
    Lindmark, Fredrik
    Umea Univ, Dept Radiat Sci, Umea, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Preoperat Sci, Umea, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Zheng, Sigun L.
    Wake Forest Univ, Ctr Human Genom, Winston Salem, NC 27109 USA..
    Xu, Jianfeng
    Wake Forest Univ, Ctr Human Genom, Winston Salem, NC 27109 USA..
    Isaacs, William B.
    Johns Hopkins Univ, Dept Urol, Baltimore, MD USA..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Breit, Samuel N.
    St Vincents Hosp, Ctr Appl Med Res, Sydney, NSW 2010, Australia.;Univ New S Wales, Sydney, NSW, Australia..
    Wiklund, Fredrik E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Macrophage Inhibitory Cytokine 1: A New Prognostic Marker in Prostate Cancer2009In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 15, no 21, p. 6658-6664Article in journal (Refereed)
    Abstract [en]

    Purpose: High serum levels of macrophage inhibitory cytokine 1 (MIC-1) are strongly associated with metastatic prostate cancer, suggesting MIC-1 is a biomarker for prostate cancer prognosis. Experimental Design: We conducted a prospective cohort study of 1,442 Swedish men with a pathologically verified diagnosis of prostate cancer between 2001 and 2003. Blood was drawn either pretreatment (n = 431) or posttreatment (n = 1,011) and cases were followed for a mean time of 4.9 years (range, 0.1-6.8 years). Results: MIC-1 serum levels independently predicted poor cancer-specific survival with an almost 3-fold higher cancer death rate in patients with serum levels in the highest quartile compared with men with serum levels in the lowest quartile (adjusted hazard ratio, 2.98; 95% confidence interval, 1.82-4.68). Pretreatment MIC-1 levels revealed an even stronger association with disease outcome with an 8-fold higher death rate in the highest compared with the lowest category (adjusted hazard ratio, 7.98; 95% confidence interval, 1.73-36.86). Among patients considered to have localized disease, MIC-1 significantly increased the discriminative capacity between indolent and lethal prostate cancer compared with the established prognostic markers clinical stage, pathologic grade, and prostate-specific antigen level (P = 0.016). A sequence variant in the MIC-1 gene was associated with decreased MIC-1 serum levels (P = 0.002) and decreased prostate cancer mortality (P = 0.003), suggesting a causative role of MIC-1 in prostate cancer prognosis. Conclusions: Serum MIC-1 concentration is a novel biomarker capable of predicting prostate cancer prognosis. (Clin Cancer Res 2009;15(21):6658-64)

  • 18. Bälter, Katarina
    et al.
    Balter, O
    Fondell, E
    Lagerros, Y T
    Web-based and mailed questionnaires: A comparison of response rates and compliance2005In: Epidemiology, ISSN 1044-3983, E-ISSN 1531-5487, Vol. 16, no 4, p. 577-579Article in journal (Refereed)
    Abstract [en]

    Background: We assessed response rates and compliance for a printed questionnaire and a Web questionnaire in a Swedish population-based study and explored the influence of adding personalized feedback to the Web questionnaire. Methods: We assigned 875 subjects to I of 3 groups: printed questionnaire, plain Web questionnaire, or Web questionnaire with personalized feedback. The questionnaire had 2 parts, first a general section and then a dietary section. Results: The response rate for the general section was 64% for the printed questionnaire, compared with 50% for the Web questionnaire with feedback. For the dietary questionnaire, the rates were reversed, resulting in a total response rate for the dietary questionnaire that did not differ between printed and web questionnaire with feedback. Conclusions: Interactivity in the Web questionnaire increased compliance in completion of the second section of the questionnaire. Web questionnaires can be useful for research purposes in settings in which Internet access is high.

  • 19.
    Bälter, Katarina
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Moller, Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Fondell, Elinor
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    The effect of dietary guidelines on cancer risk and mortality2012In: Current Opinion in Oncology, ISSN 1040-8746, E-ISSN 1531-703X, Vol. 24, no 1, p. 90-102Article, review/survey (Refereed)
    Abstract [en]

    Purpose of review Dietary guidelines are important tools for educating the general public and helping health professionals promote good health and prevent chronic diet-related diseases. However, it is of major public health relevance that the effect of the guidelines per se is evaluated to make sure that they serve their purpose. The aim of this article is to review the current research on dietary guidelines and their effect on cancer risk and mortality. Recent findings Since the last 30-40 years, most industrialized countries have had dietary guidelines. The guidelines are based on thorough reviews of the current scientific evidence regarding dietary intake and health. Potential health benefits associated with good adherence to the guidelines have been evaluated in observational studies during the last 15 years, with an increase in the number of studies during the most recent years. Summary Available data on the potential association between dietary guidelines and cancer are limited and inconclusive. A meta-analysis of studies on overall cancer risk shows no protective effect for good adherence to the dietary guidelines as compared with poor adherence. However, good adherence was associated with a 21% reduced risk of colorectal cancer, and 22% reduced cancer-specific mortality.

  • 20.
    Bälter, Katarina
    et al.
    Karolinska institutet, Sweden.
    Möller, E.
    Fondell, E.
    The effect of dietary guidelines on cancer risk and mortality.2012In: Current Opinion in Oncology, ISSN 1040-8746, E-ISSN 1531-703X, Vol. 24, no 1, p. 90-102Article in journal (Refereed)
    Abstract [en]

    Dietary guidelines are important tools for educating the general public and helping health professionals promote good health and prevent chronic diet-related diseases. However, it is of major public health relevance that the effect of the guidelines per se is evaluated to make sure that they serve their purpose. The aim of this article is to review the current research on dietary guidelines and their effect on cancer risk and mortality. Since the last 30-40 years, most industrialized countries have had dietary guidelines. The guidelines are based on thorough reviews of the current scientific evidence regarding dietary intake and health. Potential health benefits associated with good adherence to the guidelines have been evaluated in observational studies during the last 15 years, with an increase in the number of studies during the most recent years. Available data on the potential association between dietary guidelines and cancer are limited and inconclusive. A meta-analysis of studies on overall cancer risk shows no protective effect for good adherence to the dietary guidelines as compared with poor adherence. However, good adherence was associated with a 21% reduced risk of colorectal cancer, and 22% reduced cancer-specific mortality.

  • 21.
    Bälter, Katarina
    et al.
    Mälardalen University, School of Health, Care and Social Welfare, Health and Welfare. Karolinska Institutet, Stockholm, Sweden.
    Sjörs, C.
    Karolinska Institutet, Stockholm, Sweden.
    Sjölander, A.
    Karolinska Institutet, Stockholm, Sweden.
    Gardner, C.
    Stanford School of Medicine, USA.
    Hedenus, Fredrik
    Chalmers University of Technology, Sweden.
    Tillander, A.
    Karolinska Institutet, Stockholm, Sweden.
    Is a diet low in greenhouse gas emissions a nutritious diet?: - Analyses of self-selected diets in the LifeGene study2017In: Archives of Public Health, ISSN 0778-7367, E-ISSN 2049-3258, Vol. 75, no 1, article id 17Article in journal (Refereed)
    Abstract [en]

    Background: Climate change is an urgent global issue and the food sector is a major contributor to greenhouse gas emissions (GHGE). Here we study if a diet low in GHGE could be a nutritious diet compared to the Nordic Nutrition Recommendations (NNR). Methods: The environmental impact of foods from Life Cycle Assessment (LCA) data was linked to a food frequency questionnaire (FFQ) filled out by 5,364 participants in the Swedish LifeGene study. Thereafter, we calculated the daily emission of CO2 equivalents (CO2e) as well as the intake of selected nutrients associated with vegetables, fruits, meat and dairy products. The CO2e was divided into quartiles were quartile 1 corresponds to a diet generating the lowest CO2e, and quartile 4 corresponds to a diet with the highest CO2e. Results: The overall diet-related emission was 4.7kg CO2e/day and person, corresponding to 1.7 ton CO2e/year. In general, there were only small differences in nutrient intake between groups of varying levels of CO2e, regardless if the intake was analyzed as absolute intake, energy percent or as nutrient density. Moreover, adherence to NNR was high for the group with the lowest CO2e, except for saturated fat where the intake was higher than recommended for all CO2e groups. On the other hand, only the group with the lowest CO2e fulfilled recommended intake of fiber. However, none of the CO2e groups reached the recommended intake of folate and vitamin D. Conclusions: Here we show that a self-selected diet low in CO2e provides comparable intake of nutrients as a diet high in in CO2e. 

  • 22.
    Cantarutti, Anna
    et al.
    Univ Milano Bicocca, Dept Stat & Quantitat Methods, I-20126 Milan, Italy.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bellocco, Rino
    Univ Milano Bicocca, Dept Stat & Quantitat Methods, I-20126 Milan, Italy.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Body mass index and mortality in men with prostate cancer2015In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 75, no 11, p. 1129-1136Article in journal (Refereed)
    Abstract [en]

    BACKGROUNDBody Mass index (BMI) has been shown to affect risk and mortality of several cancers. Prostate cancer and obesity are major public health concerns for middle-aged and older men. Previous studies of pre-diagnostic BMI have found an increased risk of prostate cancer mortality in obese patients. OBJECTIVETo study the associations between BMI at time of prostate cancer diagnosis and prostate cancer specific and overall mortality. METHODSBMI was analyzed both as a continuous variable and categorized into four groups based on the observed distribution in the cohort (BMI<22.5, 22.5<25, 25<27.5 and 27.5kg/m(2)). The association between BMI and mortality was assessed using stratified Cox proportional hazards models and by fitting regression splines for dose response analysis in 3,161 men diagnosed with prostate cancer. After 11 years of follow up via linkage to the population-based cause of death registry, we identified 1,161 (37%) deaths off which 690 (59%) were due to prostate cancer. RESULTSHigh BMI (BMI27.5kg/m(2)) was associated with a statistically significant increased risk of prostate cancer specific mortality (HR:1.44, 95%CI: 1.09-1.90) and overall mortality (HR:1.33, 95%CI: 1.09-1.63) compared to the reference group (BMI 22.5<25kg/m(2)). Additionally, men with a low BMI (<22.5kg/m(2)), had a statistically significant increased risk of prostate cancer specific mortality (HR:1.33, 95%CI: 1.02-1.74) and overall mortality (HR:1.36, 95%CI: 1.11-1.67) compared to the reference. However, this effect disappeared when men who died within the first two years of follow-up were excluded from the analyses while the increased risk of prostate cancer specific mortality and overall mortality remained statistically significant for men with a BMI27.5kg/m(2) (HR:1.44, 95%CI: 1.09-1.90 and HR: 1.33, 95%CI: 1.09-1.63, respectively). CONCLUSIONThis study showed that a high BMI at time of prostate cancer diagnosis was associated with increased overall mortality. Prostate 75: 1129-1136, 2015. (c) 2015 Wiley Periodicals, Inc.

  • 23. Chang, E T
    et al.
    Hedelin, M
    Adami, H O
    Gronberg, H
    Bälter Augustsson, Katarina
    Alcohol drinking and risk of localized versus advanced and sporadic versus familial prostate cancer in Sweden2005In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 16, no 3, p. 275-284Article in journal (Refereed)
    Abstract [en]

    Background: It is unknown whether the association of alcohol consumption with prostate cancer risk varies between localized and advanced cases, or between sporadic and familial cases. Methods: We assessed recent alcohol drinking in a population-based case-control study of Swedish men, including 1499 cases and 1130 controls. Drinking status and average volume, frequency, and type of alcohol consumed were evaluated. Unconditional logistic regression was performed to estimate the odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for associations between alcohol consumption and prostate cancer risk. Results: Prostate cancer cases were more likely than controls to be current or former, rather than never, drinkers. However, there was no association between recent total alcohol, beer, wine, and liquor consumption and risk of overall prostate cancer, nor advanced, sporadic, or familial prostate cancer. The OR for risk of overall disease among men who drank more than 135 g of total alcohol per week versus non-drinkers was 1.2 (95% CI: 0.9, 1.5), p(trend)=0.12. There was a marginal positive association between alcohol intake and risk of localized disease. Conclusions: We detected no association between recent alcohol consumption and risk of advanced, sporadic, or familial prostate cancer, and a borderline positive association with localized disease.

  • 24. Chang, E T
    et al.
    Hedelin, M
    Adami, H O
    Gronberg, H
    Bälter, Katarina
    Re: Zinc supplement use and risk of prostate cancer2004In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 96, no 14, p. 1108-1108Article in journal (Refereed)
  • 25. Chang, E. T.
    et al.
    Hedelin, M.
    Adami, H. -O
    Grönberg, H.
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Leitzmann, M. F.
    Giovannucci, E.
    Re: Zinc supplement use and risk of prostate cancer (multiple letters) [1]2004In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 96, no 14, p. 1108-1109Article in journal (Refereed)
  • 26.
    Christensen, S.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Moller, E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bonn, S.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Lissner, L.
    Univ Gothenburg, Sahlgrenska Dept Publ Hlth & Community Med, Gothenburg, Sweden..
    Ploner, A.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Sjolander, A.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Meal-Q - a new meal-based FFQ on the web2011In: Annals of Nutrition and Metabolism, ISSN 0250-6807, E-ISSN 1421-9697, Vol. 58, p. 414-414Article in journal (Other academic)
  • 27.
    Christensen, Sara E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Moller, Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Ploner, Alexander
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Balter, Olle
    KTH Royal Inst Technol, Sch Comp Sci & Commun, Stockholm, Sweden..
    Lissner, Lauren
    Univ Gothenburg, Dept Publ Hlth & Community Med, Gothenburg, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Relative Validity of Micronutrient and Fiber Intake Assessed With Two New Interactive Meal- and Web-Based Food Frequency Questionnaires2014In: Journal of Medical Internet Research, ISSN 1438-8871, E-ISSN 1438-8871, Vol. 16, no 2, article id e59Article in journal (Refereed)
    Abstract [en]

    Background: The meal-and Web-based food frequency questionnaires, Meal-Q and MiniMeal-Q, were developed for cost-efficient assessment of dietary intake in epidemiological studies. Objective: The objective of this study was to evaluate the relative validity of micronutrient and fiber intake assessed with Meal-Q and MiniMeal-Q. The reproducibility of Meal-Q was also evaluated. Methods: A total of 163 volunteer men and women aged between 20 and 63 years were recruited from Stockholm County, Sweden. Assessment of micronutrient and fiber intake with the 174-item Meal-Q was compared to a Web-based 7-day weighed food record (WFR). Two administered Meal-Q questionnaires were compared for reproducibility. The 126-item MiniMeal-Q, developed after the validation study, was evaluated in a simulated validation by using truncated Meal-Q data. Results: The study population consisted of approximately 80% women (129/163) with a mean age of 33 years (SD 12) who were highly educated (130/163, 80% with >12 years of education) on average. Cross-classification of quartiles with the WFR placed 69% to 90% in the same/adjacent quartile for Meal-Q and 67% to 89% for MiniMeal-Q. Bland-Altman plots with the WFR and the questionnaires showed large variances and a trend of increasing underestimation with increasing intakes. Deattenuated and energy-adjusted Spearman rank correlations between the questionnaires and the WFR were in the range rho=.25-.69, excluding sodium that was not statistically significant. Cross-classifications of quartiles of the 2 Meal-Q administrations placed 86% to 97% in the same/adjacent quartile. Intraclass correlation coefficients for energy-adjusted intakes were in the range of .50-.76. Conclusions: With the exception of sodium, this validation study demonstrates Meal-Q and MiniMeal-Q to be useful methods for ranking micronutrient and fiber intake in epidemiological studies with Web-based data collection.

  • 28.
    Christensen, Sara E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Moller, Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Ploner, Alexander
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Wright, Antony
    UK Med Res Council, MRC Collaborat Ctr Human Nutr Res, Cambridge, England..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Balter, Olle
    KTH Royal Inst Technol, Sch Comp Sci & Commun, Stockholm, Sweden..
    Lissner, Lauren
    Univ Gothenburg, Dept Publ Hlth & Community Med, Gothenburg, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Two New Meal- and Web-Based Interactive Food Frequency Questionnaires: Validation of Energy and Macronutrient Intake2013In: Journal of Medical Internet Research, ISSN 1438-8871, E-ISSN 1438-8871, Vol. 15, no 6, article id UNSP e109Article in journal (Refereed)
    Abstract [en]

    Background: Meal-Q and its shorter version, MiniMeal-Q, are 2 new Web-based food frequency questionnaires. Their meal-based and interactive format was designed to promote ease of use and to minimize answering time, desirable improvements in large epidemiological studies. Objective: We evaluated the validity of energy and macronutrient intake assessed with Meal-Q and MiniMeal-Q as well as the reproducibility of Meal-Q. Methods: Healthy volunteers aged 20-63 years recruited from Stockholm County filled out the 174-item Meal-Q. The questionnaire was compared to 7-day weighed food records (WFR; n=163), for energy and macronutrient intake, and to doubly labeled water (DLW; n=39), for total energy expenditure. In addition, the 126-item MiniMeal-Q was evaluated in a simulated validation using truncated Meal-Q data. We also assessed the answering time and ease of use of both questionnaires. Results: Bland-Altman plots showed a varying bias within the intake range for all validity comparisons. Cross-classification of quartiles placed 70%-86% in the same/adjacent quartile with WFR and 77% with DLW. Deattenuated and energy-adjusted Pearson correlation coefficients with the WFR ranged from r=0.33-0.74 for macronutrients and was r=0.18 for energy. Correlations with DLW were r=0.42 for Meal-Q and r=0.38 for MiniMeal-Q. Intraclass correlations for Meal-Q ranged from r=0.57-0.90. Median answering time was 17 minutes for Meal-Q and 7 minutes for MiniMeal-Q, and participants rated both questionnaires as easy to use. Conclusions: Meal-Q and MiniMeal-Q are easy to use and have short answering times. The ranking agreement is good for most of the nutrients for both questionnaires and Meal-Q shows fair reproducibility.

  • 29. Duggan, D.
    et al.
    Zheng, S. L.
    Knowlton, M.
    Benitez, D.
    Dimitrov, L.
    Wiklund, F.
    Robbins, C.
    Isaacs, S. D.
    Cheng, Y.
    Li, G.
    Sun, J.
    Chang, B. -L
    Marovich, L.
    Wiley, K. E.
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Stattin, P.
    Adami, H. -O
    Gielzak, M.
    Yan, G.
    Sauvageot, J.
    Liu, W.
    Kim, J. W.
    Bleecker, E. R.
    Meyers, D. A.
    Trock, B. J.
    Partin, A. W.
    Walsh, P. C.
    Isaacs, W. B.
    Grönberg, H.
    Xu, J.
    Carpten, J. D.
    Two genome-wide association studies of aggressive prostate cancer implicate putative prostate tumor suppressor gene DAB2IP2007In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 99, no 24, p. 1836-1844Article in journal (Refereed)
    Abstract [en]

    Background: The consistent finding of a genetic susceptibility to prostate cancer suggests that there are germline sequence variants predisposing individuals to this disease. These variants could be useful in screening and treatment. Methods: We performed an exploratory genome-wide association scan in 498 men with aggressive prostate cancer and 494 control subjects selected from a population-based case-control study in Sweden. We combined the results of this scan with those for aggressive prostate cancer from the publicly available Cancer Genetic Markers of Susceptibility (CGEMS) Study. Single-nucleotide polymorphisms (SNPs) that showed statistically significant associations with the risk of aggressive prostate cancer based on two-sided allele tests were tested for their association with aggressive prostate cancer in two independent study populations composed of individuals of European or African American descent using one-sided tests and the genetic model (dominant or additive) associated with the lowest value in the exploratory study. Results: Among the approximately 60000 SNPs that were common to our study and CGEMS, we identified seven that had a similar (positive or negative) and statistically significant (P<.01) association with the risk of aggressive prostate cancer in both studies. Analysis of the distribution of these SNPs among 1032 prostate cancer patients and 571 control subjects of European descent indicated that one, rs1571801, located in the DAB2IP gene, which encodes a novel Ras GTPase-activating protein and putative prostate tumor suppressor, was associated with aggressive prostate cancer (one-sided P value =. 004). The association was also statistically significant in an African American study population that included 210 prostate cancer patients and 346 control subjects (one-sided P value =. 02). Conclusion: A genetic variant in DAB2IP may be associated with the risk of aggressive prostate cancer and should be evaluated further.

  • 30.
    Fondell, Elinor
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden.;Karolinska Inst, Osher Ctr Integrat Med, S-17177 Stockholm, Sweden..
    Axelsson, John
    Karolinska Inst, Osher Ctr Integrat Med, S-17177 Stockholm, Sweden.;Karolinska Inst, Dept Clin Neurosci, S-17177 Stockholm, Sweden..
    Franck, Kristina
    Swedish Inst Infect Dis Control, Stockholm, Sweden..
    Ploner, Alexander
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Lekander, Mats
    Karolinska Inst, Osher Ctr Integrat Med, S-17177 Stockholm, Sweden.;Stockholm Univ, Stress Res Inst, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Gaines, Hans
    Swedish Inst Infect Dis Control, Stockholm, Sweden..
    Short natural sleep is associated with higher T cell and lower NK cell activities2011In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 25, no 7, p. 1367-1375Article in journal (Refereed)
    Abstract [en]

    Short sleep duration increases the risk of several diseases, possibly involving compromised immune function. However, most previous studies are based on experimentally induced sleep deprivation, and only a few have studied natural variations in sleep duration. Thus our aim was to study how natural variations in sleep duration affect immune function. In total, 36 healthy men and women, aged 20-54, donated blood; 29 on three consecutive mornings, and seven on one morning. Each morning, participants selfreported sleep duration the night prior to blood draw. General sleep patterns, physical activity and stress were also assessed. A flow-cytometric assay was used to measure natural killer cell activity (NKCA). T cell function (in response to PHA, influenza, and SEA + B), and B cell function (in response to PWM) per volume whole blood. Short sleep duration prior to blood draw (<7 h) was associated with 49% higher PHA-induced T cell function (95% CI 7/109%) and 30% lower NKCA compared with normal prior sleep (7-9 h) (95% CI -46/-8%). In addition, high perceived stress was associated with 39% higher PHA-induced T cell function (95% CI 0/94%). High general physical activity was associated with 47% increased numbers of B cells and 28% increased numbers of T cells, but not with immune function. Our results suggest strong relationships between short sleep duration and T- and NK-cell functions. The stability of the findings as well as the clinical consequences of the link between short sleep and immune function should be explored in future studies. 

  • 31.
    Fondell, Elinor
    et al.
    Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Osher Ctr Integrat Med, Stockholm, Sweden..
    Balter, Olle
    Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Karolinska Inst, Sch Comp Sci & Commun, Royal Inst Technol, Stockholm, Sweden..
    Rothman, Kenneth J.
    RTI Hlth Solut, Res Triangle Pk, NC USA.;Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.;Boston Univ, Sch Publ Hlth, Dept Med, Boston, MA USA..
    Bälter, Katarina
    Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Dietary Intake and Supplement Use of Vitamins C and E and Upper Respiratory Tract Infection2011In: Journal of the American College of Nutrition (Print), ISSN 0731-5724, E-ISSN 1541-1087, Vol. 30, no 4, p. 248-258Article in journal (Refereed)
    Abstract [en]

    Objective: Antioxidants are regulators of immune function and may play a role in upper respiratory tract infections (URTI). We investigated the potential effects of dietary intake from food and supplement use of vitamins C and E on the risk of self-reported URTI. Methods: We conducted a population-based cohort study of 1509 Swedish men and women ages 20 to 60 with a follow-up period of 4 months. Participants reported a total of 1181 occurrences of URTI. Poisson regression model was used to control for age, sex, and other confounding factors. Results: Among women, we found that the incidence rate ratio (IRR) for high intake of vitamin C (>200 mg/d) from food was 0.69 (95% CI 0.49-0.98) compared with low intake (<100 mg/d). This association was not seen among men, for whom the IRR was 1.16 (95% CI 0.79-1.70) for high intake of vitamin C (>150 mg/d) compared with low intake (<50 mg/d). We saw no protective effect of vitamin E from food among either men or women, but a possible protective effect of vitamin C and E supplement use among men (vitamin C, 0.69 [95% CI 0.47-1.02]; vitamin E, 0.56 [95% CI 0.33-0.95]), although not among women. Conclusion: The present study is the first observational study to suggest that intake of vitamin C from food is sufficient to lower the risk of URTI among women. In addition, it appears that supplement use of vitamin E and vitamin C may reduce the risk of URTI among men, who overall had a lower intake of vitamin C from food than women.

  • 32.
    Fondell, Elinor
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Karolinska Inst, Osher Ctr Integrat Med, SE-17177 Stockholm, Sweden..
    Christensen, Sara E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Royal Inst Technol, Sch Comp Sci & Commun, Stockholm, Sweden..
    Adherence to the Nordic Nutrition Recommendations as a measure of a healthy diet and upper respiratory tract infection2011In: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 14, no 5, p. 860-869Article in journal (Refereed)
    Abstract [en]

    Objective: The Nordic countries have published joint dietary recommendations, the Nordic Nutrition Recommendations (NNR), since 1980. We evaluated adherence to the NNR as a measure of a healthy diet and its potential association with self-reported upper respiratory tract infection (URTI). Design: A prospective, population-based study with a follow-up period of 4 months. Dietary intake was assessed using a semi-quantitative FFQ with ninety-six items, along with other lifestyle factors, at baseline. URTI was assessed every three weeks. A Poisson regression model was used to control for age, sex and other confounding factors. Setting: A middle-sized county in northern Sweden. Subjects: Swedish men and women (n 1509) aged 20-60 years. Results: The NNR include recommendations on macronutrient proportions, physical activity and intake of micronutrients, sodium, fibre and alcohol. We found that overall adherence to the NNR was moderately good. In addition, we found that high adherence to the NNR (>5.5 adherence points) was not associated with a lower risk of URTI (incidence rate ratio (IRR) 0.89, 95% CI 0.73, 1.08) compared with low adherence (<4.5 adherence points). When investigating individual components of the NNR, only high physical activity was associated with lower URTI risk (IRR=0.82, 95% CI 0.69, 0.97) whereas none of the dietary components were associated with risk of URTI. Conclusions: Overall adherence to the NNR was moderately good. Overall adherence to the NNR was not associated with URTI risk in our study. However, when investigating individual components of the NNR, we found that high physical activity was associated with lower URTI risk.

  • 33.
    Fondell, Elinor
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostatist, S-17177 Stockholm, Sweden.;Osher Ctr Integrat Med, Karolinska Inst, Stockholm, Sweden..
    Lagerros, Ylva Trolle
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, S-17177 Stockholm, Sweden..
    Sundberg, Carl Johan
    Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden..
    Lekander, Mats
    Osher Ctr Integrat Med, Karolinska Inst, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Clin Neurosci, Stockholm, Sweden.;Stockholm Univ, Stress Res Inst, S-10691 Stockholm, Sweden..
    Balter, Olle
    Karolinska Inst, Dept Med Epidemiol & Biostatist, S-17177 Stockholm, Sweden.;Sch Comp Sci & Commun, Royal Inst Technol, Stockholm, Sweden..
    Rothman, Kenneth J.
    RTI Hlth Solut, Res Triangle Pk, NC USA.;Boston Univ, Dept Epidemiol, Sch Publ Hlth, Boston, MA 02215 USA.;Boston Univ, Dept Med, Sch Publ Hlth, Boston, MA 02215 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostatist, S-17177 Stockholm, Sweden..
    Physical Activity, Stress, and Self-Reported Upper Respiratory Tract Infection2011In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 43, no 2, p. 272-279Article in journal (Refereed)
    Abstract [en]

    FONDELL, E., Y. T. LAGERROS, C. J. SUNDBERG, M. LEKANDER, O. BALTER, K. J. ROTHMAN, and K. BALTER. Physical Activity, Stress, and Self-Reported Upper Respiratory Tract Infection. Med. Sci. Sports Exerc., Vol. 43, No. 2, pp. 272-279, 2011. Purpose: Upper respiratory tract infection (URTI) is the most common reason for seeking primary care in many countries. Still, little is known about potential strategies to reduce susceptibility. We investigated the relationships between physical activity level, perceived stress, and incidence of self-reported URTI. Methods: We conducted a population-based prospective cohort study of 1509 Swedish men and women aged 20-60 yr with a follow-up period of 4 months. We used a Web-based questionnaire to assess disease status and lifestyle factors at the start of the study. We assessed physical activity and inactivity as total MET-hours (MET task) per day and perceived stress by the 14-item Perceived Stress Scale. Participants were contacted every 3 wk via e-mail to assess incidence of URTI. They reported a total of 1181 occurrences of URTI. We used Poisson regression models to control for age, sex, and other potential confounding factors. Results: We found that high levels of physical activity (>= 55 MET.h.d(-1)) were associated with an 18% reduced risk (incidence rate ratio (IRR) = 0.82, 95% confidence interval (CI) = 0.69-0.98) of self-reporting URTI compared with low levels of physical activity (< 45 MET.h.d(-1)). This association was stronger among those reporting high levels of stress (IRR = 0.58, 95% CI = 0.43-0.78), especially among men (IRR = 0.37, 95% CI = 0.24-0.59), but absent in the group with low levels of stress. Conclusions: We found that high physical activity was associated with a lower risk of contracting URTI for both men and women. In addition, we found that highly stressed people, particularly men, appear to benefit more from physical activity than those with lower stress levels.

  • 34. Hedelin, M
    et al.
    Klint, A
    Chang, E T
    Bellocco, R
    Johansson, J E
    Andersson, S O
    Heinonen, S M
    Adlercreutz, H
    Adami, H O
    Gronberg, H
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Dietary phytoestrogen, serum enterolactone and risk of prostate cancer: the Cancer Prostate Sweden Study (Sweden)2006In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 17, no 2, p. 169-180Article in journal (Refereed)
    Abstract [en]

    Based on evidence that phytoestrogens may protect against prostate cancer, we evaluated the associations between serum enterolactone concentration or dietary phytoestrogen intake and risk of prostate cancer. In our Swedish population-based case-control study, questionnaire-data were available for 1,499 prostate cancer cases and 1,130 controls, with serum enterolactone levels in a sub-group of 209 cases and 214 controls. Unconditional logistic regression was performed to estimate multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with risk of prostate cancer. High intake of food items rich in phytoestrogens was associated with a decreased risk of prostate cancer. The OR comparing the highest to the lowest quartile of intake was 0.74 (95% CI: 0.57-0.95; p-value for trend: 0.01). In contrast, we found no association between dietary intake of total or individual lignans or isoflavonoids and risk of prostate cancer. Intermediate serum levels of enterolactone were associated with a decreased risk of prostate cancer. The ORs comparing increasing quartiles of serum enterolactone concentration to the lowest quartile were, respectively, 0.28 (95% CI: 0.15-0.55), 0.63 (95% CI: 0.35-1.14) and 0.74 (95% CI: 0.41-1.32). Our results support the hypothesis that certain foods high in phytoestrogens are associated with a lower risk of prostate cancer.

  • 35. Hedelin, Maria
    et al.
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Chang, Ellen T.
    Bellocco, Rino
    Klint, Asa
    Johansson, Jan-Erik
    Wiklund, Fredrik
    Thellenberg-Karlsson, Camilla
    Adami, Hans-Olov
    Gronberg, Henrik
    Dietary intake of phytoestrogens, estrogen receptor-beta polymorphisms and the risk of prostate cancer2006In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, no 14, p. 1512-1520Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. The causes of prostate cancer are poorly understood, but genetic factors may be more important than for many other malignancies, and dietary phytoestrogens may be protective. Because phytoestrogens bind tightly to the estrogen receptor-beta, we conducted an epiderniologic investigation of synergistic effects between phytoestrogen intake and estrogen receptor-beta gene polymorphisms. METHODS. We performed a population-based case-control study in Sweden. All participants reported their phytoestrogen intake and donated a blood sample. We identified four haplotype-tagging single nucleotide polymorphisms (htSNPs) and genotyped these htSNPs in 1314 prostate cancer patients and 782 controls. Odds ratios were estimated by multivariate logistic regression. Interactions between phytoestrogen intake and estrogen receptor-beta SNPs on prostate cancer risk were evaluated considering both multiplicative and additive effect scales. RESULTS. We found a significant multiplicative interaction (P = 0.04) between dietary intake of phytoestrogens and a promoter SNP in the estrogen receptor-beta gene (rs 2987983-13950), but not with any of the three other htSNPs (P = 0.11, 0.69, 0.85). Among carriers of the variant promoter alleles, we found strong inverse associations with increasing intake of total phytoestrogens (odds ratio for highest vs. lowest quartile = 0.43; P for trend < 0.001), isoflavonoids (odds ratio = 0.63; P for trend = 0.05), and coumestrol (odds ratio = 0.57; P for trend = 0.003). We found no association between phytoestrogens and prostate cancer among carriers homozygous for the wild-type allele (TT). CONCLUSIONS. Our study provides strong evidence that high intake of phytoestrogens substantially reduce prostate cancer risk among men with specific polymorphic variation in the promoter region of the estrogen receptor-beta gene.

  • 36. Hedelin, Maria
    et al.
    Chang, Ellen T.
    Wiklund, Fredrik
    Bellocco, Rino
    Klint, Asa
    Adolfsson, Jan
    Shahedi, Katarina
    Xu, Jianfeng
    Adami, Hans-Olov
    Gronberg, Henrik
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism2007In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, no 2, p. 398-405Article in journal (Refereed)
    Abstract [en]

    Dietary intake of marine fatty acids from fish may protect against prostate cancer development. We studied this association and whether it is modified by genetic variation in cyclooxygenase (COX)-2, a key enzyme in fatty acid metabolism and inflammation. We assessed dietary intake of fish among 1,499 incident prostate cancer cases and 1,130 population controls in Sweden. Five single nucleotide polymorphisms (SNPs) were identified and genotyped in available blood samples for 1,378 cases and 782 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by multivariate logistic regression. Multiplicative and additive interactions between fish intake and COX-2 SNPs on prostate cancer risk were evaluated. Eating fatty fish (e.g. salmon-type fish) once or more per week, compared to never, was associated with reduced risk of prostate cancer (OR: 0.57, 95% CI: 0.43-0.76). The OR comparing the highest to the lowest quartile of marine fatty acids intake was 0.70 (95% CI: 0.51-0.97). We found a significant interaction (p < 0.001) between salmon-type fish intake and a SNP in the COX-2 gene (rs5275: +6365 T/C), but not with the 4 other SNPs examined. We found strong inverse associations with increasing intake of salmon-type fish among carriers of the variant allele (OR for once per week or more vs. never = 0.28, 95% CI: 0.18-0.45; p(trend) < 0.01), but no association among carriers of the more common allele. Frequent consumption of fatty fish and marine fatty acids appears to reduce the risk of prostate cancer, and this association is modified by genetic variation in the COX-2 gene. 

  • 37.
    Henriksson, Hanna
    et al.
    Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.;Karolinska Inst, Dept Biosci & Nutr, S-14183 Huddinge, Sweden..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bergstrom, Anna
    Karolinska Inst, Inst Enviromental Med, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Balter, Olle
    Royal Inst Technol, Sch Comp Sci & Commun, Stockholm, Sweden..
    Delisle, Christine
    Karolinska Inst, Dept Biosci & Nutr, S-14183 Huddinge, Sweden..
    Forsum, Elisabet
    Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden..
    Lof, Marie
    Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.;Karolinska Inst, Dept Biosci & Nutr, S-14183 Huddinge, Sweden..
    A New Mobile Phone-Based Tool for Assessing Energy and Certain Food Intakes in Young Children: A Validation Study2015In: JMIR mhealth and uhealth, E-ISSN 2291-5222, Vol. 3, no 2, article id e38Article in journal (Refereed)
    Abstract [en]

    Background: Childhood obesity is an increasing health problem globally. Obesity may be established already at pre-school age. Further research in this area requires accurate and easy-to-use methods for assessing the intake of energy and foods. Traditional methods have limited accuracy, and place large demands on the study participants and researchers. Mobile phones offer possibilities for methodological advancements in this area since they are readily available, enable instant digitalization of collected data, and also contain a camera to photograph pre- and post-meal food items. We have recently developed a new tool for assessing energy and food intake in children using mobile phones called the Tool for Energy Balance in Children (TECH). Objective: The main aims of our study are to (1) compare energy intake by means of TECH with total energy expenditure (TEE) measured using a criterion method, the doubly labeled water (DLW) method, and (2) to compare intakes of fruits and berries, vegetables, juice, and sweetened beverages assessed by means of TECH with intakes obtained using a Web-based food frequency questionnaire (KidMeal-Q) in 3 year olds. Methods: In this study, 30 Swedish 3 year olds were included. Energy intake using TECH was compared to TEE measured using the DLW method. Intakes of vegetables, fruits and berries, juice, as well as sweetened beverages were assessed using TECH and compared to the corresponding intakes assessed using KidMeal-Q. Wilcoxon matched pairs test, Spearman rank order correlations, and the Bland-Altman procedure were applied. Results: The mean energy intake, assessed by TECH, was 5400 kJ/24h (SD 1500). This value was not significantly different (P=.23) from TEE (5070 kJ/24h, SD 600). However, the limits of agreement (2 standard deviations) in the Bland-Altman plot for energy intake estimated using TECH compared to TEE were wide (2990 kJ/24h), and TECH overestimated high and underestimated low energy intakes. The Bland-Altman plots for foods showed similar patterns. The mean intakes of vegetables, fruits and berries, juice, and sweetened beverages estimated using TECH were not significantly different from the corresponding intakes estimated using KidMeal-Q. Moderate but statistically significant correlations (rho=.42-.46, P=.01-.02) between TECH and KidMeal-Q were observed for intakes of vegetables, fruits and berries, and juice, but not for sweetened beverages. Conclusion: We found that one day of recordings using TECH was not able to accurately estimate intakes of energy or certain foods in 3 year old children.

  • 38.
    Hsu, Fang-Chi
    et al.
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA.;Wake Forest Univ, Sch Med, Div Publ Hlth Sci, Winston Salem, NC 27157 USA..
    Lindstrom, Sara
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Sun, Jielin
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Chen, Shyh-Huei
    Natl Yunlin Univ Sci & Technol, Dept Ind Management, Yunlin, Taiwan..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Turner, Aubrey R.
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA..
    Liu, Wennuan
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Kim, Jin Woo
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA..
    Stattin, Par
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Chang, Bao-li
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA..
    Isaacs, William B.
    Johns Hopkins Med Inst, Dept Urol, Baltimore, MD 21205 USA. Translat Genom Res Inst, Phoenix, AZ USA..
    Xu, Jianfeng
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA.;Wake Forest Univ, Sch Med, Div Publ Hlth Sci, Winston Salem, NC 27157 USA..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Zheng, S. Lilly
    Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA..
    A multigenic approach to evaluating prostate cancer risk in a systematic replication study2008In: Cancer Genetics and Cytogenetics, ISSN 0165-4608, Vol. 183, no 2, p. 94-98Article in journal (Refereed)
    Abstract [en]

    Although it is well known that multiple genes may influence prostate cancer risk, most current efforts at identifying prostate cancer risk variants rely on single-gene approaches. In previous work using mostly single-gene approaches, we observed significant associations (P < 0.05) for 6 of 46 polymorphisms in five genes in a Swedish prostate cancer case-control study population. We now report on the higher-order gene-gene interactions among those 46 genetic variants and the combined effect of the six polymorphisms with significant main effects for association with prostate cancer risk in 795 controls and 1,461 cases. Classification and regression tree analysis was used to evaluate higher-order gene-gene interactions. No interactions were confirmed by the result from logistic regressions. For the combined analysis, we tested the hypothesis that individuals carrying multiple copies of risk variants are at increased risk for prostate cancer. Individuals carrying more than eight copies of any risk variant were almost twofold more likely to get prostate cancer (OR = 1.99, P = 0.0014). A significant trend relationship was observed (P < 0.0001). In the present study, additive effects but not multiplicative effects among these six polymorphisms with significant main effects were observed. 

  • 39.
    Hvidtfeldt, Ulla A.
    et al.
    Univ So Denmark, Alcohol Res Ctr, Natl Inst Publ Hlth, DK-1399 Copenhagen K, Denmark.;Univ Copenhagen, Dept Publ Hlth, Social Med Sect, Copenhagen, Denmark..
    Tolstrup, Janne S.
    Univ So Denmark, Alcohol Res Ctr, Natl Inst Publ Hlth, DK-1399 Copenhagen K, Denmark..
    Jakobsen, Marianne U.
    Aarhus Univ Hosp, Dept Clin Epidemiol, Aalborg, Denmark..
    Heitmann, Berit L.
    Copenhagen Univ Hosp, Ctr Hlth & Soc, Inst Prevent Med, Res Unit Dietary Studies, Copenhagen, Denmark..
    Gronbaek, Morten
    Univ So Denmark, Alcohol Res Ctr, Natl Inst Publ Hlth, DK-1399 Copenhagen K, Denmark..
    O'Reilly, Eilis
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Goldbourt, Uri
    Tel Aviv Univ, Dept Epidemiol & Prevent Med, Henry N Neufeld Cardiac Res Inst, Epidemiol & Biostat Sect, IL-69978 Tel Aviv, Israel..
    Hallmans, Goran
    Umeaa Univ, Dept Publ Hlth & Clin Med, Umeaa, Sweden..
    Knekt, Paul
    Natl Publ Hlth Inst, Helsinki, Finland..
    Liu, Simin
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Pereira, Mark
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA..
    Pietinen, Pirjo
    Natl Publ Hlth Inst, Helsinki, Finland..
    Spiegelman, Donna
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA..
    Stevens, June
    Univ N Carolina, Sch Publ Hlth, Dept Nutr, Chapel Hill, NC 27599 USA.;Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA..
    Virtamo, Jarmo
    Natl Publ Hlth Inst, Helsinki, Finland..
    Willett, Walter C.
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA..
    Rimm, Eric B.
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA..
    Ascherio, Alberto
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA..
    Alcohol Intake and Risk of Coronary Heart Disease in Younger, Middle-Aged, and Older Adults2010In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 121, no 14, p. 1589-1597Article in journal (Refereed)
    Abstract [en]

    Background-Light to moderate alcohol consumption is associated with a reduced risk of coronary heart disease. This protective effect of alcohol, however, may be confined to middle-aged or older individuals. Coronary heart disease incidence is low in men <40 years of age and in women <50 years of age; for this reason, study cohorts rarely have the power to investigate the effects of alcohol on coronary heart disease risk in younger adults. This study examined whether the beneficial effect of alcohol on coronary heart disease depends on age. Methods and Results-In this pooled analysis of 8 prospective studies from North America and Europe including 192 067 women and 74 919 men free of cardiovascular diseases, diabetes, and cancers at baseline, average daily alcohol intake was assessed at baseline with a food frequency or diet history questionnaire. An inverse association between alcohol and risk of coronary heart disease was observed in all age groups; hazard ratios among moderately drinking men (5.0 to 29.9 g/d) 39 to 50, 50 to 59, and >= 60 years of age were 0.58 (95% confidence interval [CI], 0.36 to 0.93), 0.72 (95% CI, 0.60 to 0.86), and 0.85 (95% CI, 0.75 to 0.97) compared with abstainers. However, the analyses indicated a smaller incidence rate difference between abstainers and moderate consumers in younger adults (incidence rate difference, 45 per 100 000; 90% CI, 8 to 84) than in middle-aged (incidence rate difference, 64 per 100 000; 90% CI, 24 to 102) and older (incidence rate difference, 89 per 100 000; 90% CI, 44 to 140) adults. Similar results were observed in women. Conclusion-Alcohol is also associated with a decreased risk of coronary heart disease in younger adults; however, the absolute risk was small compared with middle-aged and older adults. (Circulation. 2010; 121: 1589-1597.)

  • 40.
    Jakobsen, Marianne U.
    et al.
    Aarhus Univ Hosp, Dept Clin Epidemiol, DK-9000 Aalborg, Denmark.;Copenhagen Univ Hosp, Ctr Hlth & Soc, Res Unit Dietary Studies, Inst Prevent Med, Copenhagen, Denmark.;Glostrup Univ Hosp, Res Ctr Prevent & Hlth, Glostrup, Denmark.;Aarhus Univ Hosp, Cardiovasc Res Ctr, Aalborg Hosp, DK-9000 Aalborg, Denmark..
    O'Reilly, Eilis J.
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Heitmann, Berit L.
    Copenhagen Univ Hosp, Ctr Hlth & Soc, Res Unit Dietary Studies, Inst Prevent Med, Copenhagen, Denmark..
    Pereira, Mark A.
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Fraser, Gary E.
    Loma Linda Univ, Dept Epidemiol & Biostat, Loma Linda, CA 92350 USA..
    Goldbourt, Uri
    Tel Aviv Univ, Epidemiol & Biostat Sect, Henry N Neufeld Cardiac Res Inst, Dept Epidemiol & Prevent Med, IL-69978 Tel Aviv, Israel..
    Hallmans, Goran
    Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden..
    Knekt, Paul
    Natl Publ Hlth Inst, Helsinki, Finland..
    Liu, Simin
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA..
    Pietinen, Pirjo
    Natl Publ Hlth Inst, Helsinki, Finland..
    Spiegelman, Donna
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA..
    Stevens, June
    Univ N Carolina, Sch Publ Hlth, Dept Nutr, Chapel Hill, NC 27599 USA.;Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA..
    Virtamo, Jarmo
    Natl Publ Hlth Inst, Helsinki, Finland..
    Willett, Walter C.
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Harvard Ctr Canc Prevent, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA..
    Ascherio, Alberto
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies2009In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 89, no 5, p. 1425-1432Article in journal (Refereed)
    Abstract [en]

    Background: Saturated fatty acid (SFA) intake increases plasma LDL-cholesterol concentrations; therefore, intake should be reduced to prevent coronary heart disease (CHD). Lower habitual intakes of SFAs, however, require substitution of other macronutrients to maintain energy balance. Objective: We investigated associations between energy intake from monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs), and carbohydrates and risk of CHD while assessing the potential effect-modifying role of sex and age. Using substitution models, our aim was to clarify whether energy from unsaturated fatty acids or carbohydrates should replace energy from SFAs to prevent CHD. Design: This was a follow-up study in which data from 11 American and European cohort studies were pooled. The outcome measure was incident CHD. Results: During 4-10 y of follow-up, 5249 coronary events and 2155 coronary deaths occurred among 344,696 persons. For a 5% lower energy intake from SFAs and a concomitant higher energy intake from PUFAs, there was a significant inverse association between PUFAs and risk of coronary events (hazard ratio: 0.87; 95% CI: 0.77, 0.97); the hazard ratio for coronary deaths was 0.74 (95% CI: 0.61, 0.89). For a 5% lower energy intake from SFAs and a concomitant higher energy intake from carbohydrates, there was a modest significant direct association between carbohydrates and coronary events (hazard ratio: 1.07; 95% CI: 1.01, 1.14); the hazard ratio for coronary deaths was 0.96 (95% CI: 0.82, 1.13). MUFA intake was not associated with CHD. No effect modification by sex or age was found. Conclusion: The associations suggest that replacing SFAs with PUFAs rather than MUFAs or carbohydrates prevents CHD over a wide range of intakes. Am J Clin Nutr 2009;89:1425-32.

  • 41.
    Jan, Michael
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Temple Univ Hosp & Med Sch, Dept Internal Med, Philadelphia, PA 19140 USA..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Preoperat Sci, Urol, Umea, Sweden..
    Holmberg, Erik
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Oncol, Gothenburg, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    The roles of stress and social support in prostate cancer mortality2016In: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 50, no 1, p. 47-55Article in journal (Refereed)
    Abstract [en]

    Objective: This study aimed to evaluate the association between perceived stress, social support, disease progression and mortality in a nationwide population-based cohort of men with prostate cancer. Materials and methods: The study surveyed 4105 Swedish men treated for clinically localized prostate cancer regarding stress, grief, sleep habits and social support. Associations between these factors and mortality were assessed using multivariate Cox regression analysis. Results: Men with the highest levels of perceived stress had a statistically significantly increased rate of prostate cancer-specific mortality compared with men with low stress levels (hazard ratio 1.66, 95% confidence interval 1.05-2.63). Men with high stress levels also had a high frequency of grieving and sleep loss. They also had fewer people with whom to share their emotional problems and felt an inability to share most of their problems with partners, friends and family. Conclusions: This study contributes to the growing field of psychosocial quality of life research in men with prostate cancer. The findings show a significant association between prostate cancer-specific mortality and perceived stress in patients initially diagnosed with localized, non-metastatic prostate cancer. Significant associations between perceived stress and various psychosocial factors were also seen. The findings of this study could prove useful to target interventions to improve quality of life in men with prostate cancer.

  • 42. Johansson, Mattias
    et al.
    Mckay, James D.
    Stattin, Par
    Canzian, Federico
    Boillot, Catherine
    Wiklund, Fredrik
    Adami, Hans-Olov
    Bälter, Katarina
    Gronberg, Henrik
    Kaaks, Rudolf
    Comprehensive evaluation of genetic variation in the IGF1 gene and risk of prostate cancer2007In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, no 3, p. 539-542Article in journal (Refereed)
    Abstract [en]

    Insulin-like growth factor-I (IGF1) stimulates cell proliferation, decreases apoptosis, and has been implicated in cancer development. Epidemiological studies have shown elevated levels of circulating IGF1 to be associated with increased risk of prostate cancer. To what extent genetic variation in the IGF1 gene is related to prostate cancer risk is largely unknown. We performed a comprehensive haplotype tagging (HT) assessment of single nucleotide polymorphisms (SNPs) representing the common haplotype variation in the IGF1 gene. We genotyped 10 SNPs (9 haplotype tagging SNPs (htSNPs)) within Cancer Prostate in Sweden (CAPS), a case-control study of 2,863 cases and 1,737 controls, in order to investigate if genetic variation in the IGF1 gene is associated with prostate cancer risk. Three haplotype blocks were identified across the IGF1 gene and 9 SNPs were selected as haplotype tagging SNPs. Common haplotypes in the block covering the 3' region of the IGF1 gene showed significant global association with prostate cancer risk (p = 0.004), with one particular haplotype giving an odds ratio of 1.46 (95% CI = 1.15-1.84, p = 0.002). This haplotype had a prevalence of 5% in the study population. Our results indicate that common variation in the IGF1 gene, particularly in the 3' region, mail affect prostate cancer risk. Further studies on genetic variations in the IGF1 gene in relation to prostate cancer risk as well as to circulating levels of IGF1 are needed to confirm this novel finding. (c) 2006 Wiley-Liss. Inc.

  • 43.
    Johansson, Mattias
    et al.
    Int Agcy Res Canc, F-69372 Lyon 08, France.;Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Stockholm, Sweden..
    Mckay, James D.
    Int Agcy Res Canc, F-69372 Lyon 08, France..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Rinaldi, Sabina
    Int Agcy Res Canc, F-69372 Lyon 08, France..
    Hallmans, Goran
    Umea Univ Hosp, Dept Publ Hlth & Clin Med, S-90185 Umea, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard Univ, Dept Epidemiol, Boston, MA 02115 USA..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Stockholm, Sweden..
    Kaaks, Rudolf
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany..
    Genetic Variation in the SST Gene and its Receptors in Relation to Circulating Levels of Insulin-Like Growth Factor-I, IGFBP3, and Prostate Cancer Risk2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 5, p. 1644-1650Article in journal (Refereed)
    Abstract [en]

    Background: Somatostatin (SST) and its receptors (SSTR1-5) may have a role in prostate cancer by influencing the IGFI hormone axis or through direct effects on prostate epithelia. We have investigated if genetic variation in the SST and SSTR1-5 genes influences prostate cancer risk and/or circulating IGFI and IGFBP3 hormone levels. Materials and Methods: We analyzed 28 haplotype tagging single nucleotide polymorphisms in the SST and SSTR1-5 genes in a case-control/genetic association study to investigate the association between genetic variation and prostate cancer risk. The study included 2863 cases and 1737 controls from the Cancer Prostate in Sweden (CAPS) study. To investigate the genetic influence on circulating hormone levels, plasma concentrations of IGFI and IGFBP3 were analyzed in 874 controls of the CAPS study and 550 male subjects from the Northern Sweden Health and Disease Cohort (NSHDC). Results: No clear association between prostate cancer risk and genetic variation of the SST and SSTR1-5 genes was identified. The SSTR5 missense single nucleotide polymorphism rs4988483 was associated with circulating IGFI (P = 0.002) and IGFBP3 (P = 0.0003) hormone levels in CAPS controls, with a per allele decrease of similar to 11%. This decrease was replicated in NSHDC for circulating IGFBP3 (P = 0.01) but not for IGFI (P = 0.09). Combining CAPS and NSHDC subjects indicated evidence of association between rs4988483 and both IGFBP3 (P = 2 x 10(-5)) and IGFI (P = 0.0004) hormone levels. Conclusions: Our results suggest that genetic variation in the SSTR5 gene and, particularly, the rs4988483 single nucleotide polymorphism influence circulating IGFI and IGFBP3 hormone levels with no measurable effect on prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):164.4-50)

  • 44. Johansson, Mattias
    et al.
    Mckay, James D.
    Wiklund, Fredrik
    Rinaldi, Sabina
    Verheus, Martijn
    van Gils, Carla H.
    Hallmans, Goran
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Adami, Hans-Olov
    Gronberg, Henrik
    Stattin, Paer
    Kaaks, Rudolf
    Implications for prostate cancer of insulin-like growth factor-I (IGF-I) genetic variation and circulating IGF-I levels2007In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 92, no 12, p. 4820-4826Article in journal (Refereed)
    Abstract [en]

    Background: Elevated levels of circulating IGF-I have consistently been associated with increased prostate cancer risk. We recently found a haplotype in the 3 ' region of the IGF-I gene associated with increased risk of prostate cancer, and we hypothesized that the observed association is mediated by circulating IGF-I. Materials and Methods: We analyzed haplotypes and three haplotype-tagging single nucleotide polymorphisms (htSNPs) in the 3 ' region of the IGF-I gene in relation to circulating levels IGF-I in 698 control subjects from the CAncer Prostate in Sweden ( CAPS) study and 575 cases and controls from the prospective Northern Sweden Health and Disease Cohort ( NSHDC) study. We also performed a meta-analysis of these two and four other association studies on genetic variation in the 3 ' region of the IGF-I gene in relation to circulating IGF-I levels. Results: The IGF-I haplotype previously associated with prostate cancer risk, labeled "TCC," was associated with elevated levels of IGF-I in the CAPS study (P = 0.02), but not in the NSHDC study. In contrast, two of the three IGF-I htSNPs tagging this haplotype, rs6220 and rs7136446, were associated with elevated levels of IGF-I in the NSHDC ( P = 0.03 and P = 0.04, respectively), but not in the CAPS study. In the meta-analysis, the TCC haplotype and the rs6220 SNP were associated with elevated levels of circulating IGF-I ( P = 0.001 and P < 0.0001, respectively). Conclusions: Genetic variation in the 3 ' region of the IGF-I gene seems to influence circulating levels of IGF-I. This observation is consistent with the hypothesis that variation in the IGF-I gene plays a role in prostate cancer susceptibility by influencing circulating levels of IGF-I.

  • 45. Johansson, Mattias
    et al.
    Van Guelpen, Bethany
    Hultdin, Johan
    Wiklund, Fredrik
    Adami, Hans-Olov
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Gronberg, Henrik
    Stattin, Par
    The MTHFR 677C -> T polymorphism and risk of prostate cancer: results from the CAPS study2007In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 18, no 10, p. 1169-1174Article in journal (Refereed)
    Abstract [en]

    The methylenetetrahydrafolate reductase (MTHFR) enzyme may influence cancer development by affecting DNA methylation, synthesis and repair. The MTHFR 677C -> T single nucleotide polymorphism (SNP) has been associated with decreased enzyme activity and has therefore been implicated in cancer development. We analyzed the MTHFR 677C -> T SNP in 2,777 incident prostate cancer cases and 1,639 population controls from the CAncer Prostate in Sweden study (CAPS). No significant association was found overall between prostate cancer risk and the 677C -> T SNP (p = 0.27) with heterozygote (CT) and homozygote (TT) allele carriers showing ORs of 1.12 (95% CI: 0.98-1.27) and 1.02 (95% CI: 0.80-1.30), respectively. In the subgroup of low risk prostate cancer, heterozygote-but not homozygote-allele carriers displayed a slight over-risk with an OR of 1.21 (95% CI: 1.03-1.41). Among men under 65 years of age, the 677C -> T SNP was associated with prostate cancer risk (p = 0.007), with odds ratios of 1.33 (95% CI: 1.09-1.63) for heterozygote allele carriers and 0.86 (95% CI: 0.6-1.24) for homozygote allele carriers. However, this association was attributed to a shift in the genotype distribution in the young controls. In conclusion, our results do not provide strong support for the hypothesis that the MTHFR 677C -> T polymorphism is related to prostate cancer risk.

  • 46. Lagerros, Y T
    et al.
    Mucci, L A
    Bellocco, R
    Nyren, O
    Balter, O
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Validity and reliability of self-reported total energy expenditure using a novel instrument2006In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 21, no 3, p. 227-236Article in journal (Refereed)
    Abstract [en]

    Improved methods for quantitative self-reports of total physical activity in epidemiological studies are needed. We evaluated randomly selected individuals' ability to integrate their perception of physical activity over time to produce an estimate of the "usual" level, using a novel instrument for self-quantification of energy expenditure. A population-based sample of 418 Swedish men and women, age 20-59, completed a questionnaire containing the new instrument. For validation, three 24 hour recalls by phone served as gold standard. Reproducibility was assessed through administering the instrument another three times. The validation involved 133 subjects and another 160 completed the reproducibility evaluation. Pearson correlation between usual daily energy expenditure measured by the instrument and the mean of the 24 hour recalls was 0.73. After subdividing the self-reported daily energy expenditure and the mean of the 24 hour recalls into quintiles, 83.5% of the participants remained in the same quintile, or one quintile apart. There was a tendency towards overestimation of usual daily physical activity. This was significantly associated with low education. Reproducibility showed an intraclass correlation of 0.55. Although integrated reports of usual daily energy expenditure over longer periods seem to be afflicted with a tendency of overestimation, total energy expenditure can be estimated with reasonable validity and reproducibility using our instrument.

  • 47. Lindmark, F
    et al.
    Zheng, S L
    Wiklund, F
    Bensen, J
    Bälter Augustsson, Katarina
    Karolinska Inst, Stockholm, Sweden.;Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, USA.
    Chang, B L
    Hedelin, M
    Clark, J
    Stattin, P
    Meyers, D A
    Adami, H O
    Isaacs, W
    Gronberg, H
    Xu, J F
    H6D polymorphism in macrophage-inhibitory cytokine-1 gene associated with prostate cancer2004In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 96, no 16, p. 1248-1254Article in journal (Refereed)
    Abstract [en]

    Background: Accumulating epidemiologic and molecular evidence suggest that inflammation is an important component in the etiology of prostate cancer. Macrophage-inhibitory cytokine-1 (MIC-1), a member of the transforming growth factor beta superfamily, is thought to play an important role in inflammation by regulating macrophage activity. We examined whether sequence variants in the MIC-1 gene are associated with the risk of prostate cancer. Methods: The study population, a population-based case-control study in Sweden, consisted of 1383 prostate cancer case patients and 780 control subjects. From 94 of the control subjects, we constructed gene-specific haplotypes of MIC-1 and identified four haplotype-tagging single-nucleotide polymorphisms (SNPs): Exon1+25 (V9L), Exon1+142 (S48T), IVS1+1809, and Exon2+2423 (H6D). All study subjects were genotyped for the four SNPs, and conditional logistic regression analysis was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). Results: A statistically significant difference (P = .006) in genotype frequency was observed for the nonsynonymous change H6D) (histidine to aspartic acid at position 6) between prostate cancer patients and control subjects. Carriers of the GC genotype, which results in the H6D change, experienced a lower risk of sporadic prostate cancer (OR = 0.80, 95% CI = 0.66 to 0.97) and of familial prostate cancer (OR = 0.61, 95% CI = 0.42 to 0.89) than the CC genotype carriers. In the study population, the proportion of prostate cancer cases attributable to the CC genotype was 7.2% for sporadic cancer and 19.2% for familial cancer. None of the other SNPs or haplotypes was associated with prostate cancer. Conclusion: This study shows an association between a nonsynonymous change (H6D) in the MIC-1 gene and prostate cancer. This finding supports the hypothesis that genetic variation in the inflammatory process contributes to prostate cancer susceptibility.

  • 48. Lindmark, F
    et al.
    Zheng, S L
    Wiklund, F
    Bälter Augustsson, Katarina
    Sun, J
    Chang, B
    Hedelin, M
    Clark, J
    Johansson, J E
    Meyers, D A
    Adami, H O
    Isaacs, W
    Gronberg, H
    Xu, J
    Interleukin-1 receptor antagonist haplotype associated with prostate cancer risk2005In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 93, no 4, p. 493-497Article in journal (Refereed)
    Abstract [en]

    IL1-RN is an important anti-inflammatory cytokine that modulate the inflammation response by binding to IL1 receptors, and as a consequence inhibits the action of proinflammatory cytokines IL1 alpha and IL1 beta. In this study, we hypothesise that sequence variants in the IL1-RN gene are associated with prostate cancer risk. The study population, a population-based case - control study in Sweden, consisted of 1383 prostate cancer case patients and 779 control subjects. We first selected 18 sequence variants covering the IL1-RN gene and genotyped these single-nucleotide polymorphisms ( SNPs) in 96 control subjects. Gene-specific haplotypes of IL1-RN were constructed and four haplotype-tagging single-nucleotide polymorphisms (htSNPs) were identified (rs878972, rs315934, rs3087263 and rs315951) that could uniquely describe 495% of the haplotypes. All study subjects were genotyped for the four htSNPs. No significant difference in genotype frequencies between cases and controls were observed for any of the four SNPs based on a multiplicative genetic model. Overall there was no significant difference in haplotype frequencies between cases and controls; however, the prevalence of the most common haplotype (ATGC) was significantly higher among cases (38.7%) compared to controls (33.5%) ( haplotype-specific P = 0.009). Evaluation of the prostate cancer risk associated with carrying the 'ATGC' haplotype revealed that homozygous carriers were at significantly increased risk ( odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.2 - 2.2), compared to noncarriers, while no significant association was found among subjects heterozygous for the haplotype ( OR = 1.0, 95% CI = 0.8 - 1.2). Restricting analyses to advanced prostate cancer strengthened the association between the 'ATGC' haplotype and disease risk (OR for homozygous carriers vs noncarriers 1.8, 95% CI = 1.3 - 2.5). In conclusion, the results from this study support the hypothesis that inflammation has a role of in the development of prostate cancer, but further studies are needed to identify the causal variants in this region and to elucidate the biological mechanism for this association.

  • 49. Lindstrom, S
    et al.
    Wiklund, F
    Jonsson, B A
    Adami, H O
    Bälter, Katarina
    Brookes, A J
    Xu, J F
    Zheng, S L
    Isaacs, W B
    Adolfsson, J
    Gronberg, H
    Comprehensive genetic evaluation of common E-cadherin sequence variants and prostate cancer risk: strong confirmation of functional promoter SNP2005In: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 118, no 3-4, p. 339-347Article in journal (Refereed)
    Abstract [en]

    The E-cadherin gene (CDH1) has been proposed as a prostate cancer (PC) susceptibility gene in several studies. Aberrant protein expression has been related to prognosis and progression in PC. In addition, a functional promoter SNP (rsl6260) has been found to associate with PC risk. We performed a comprehensive genetic analysis of CDH1 by using the method of haplotype tagged SNPs in a large Swedish population-based case-control study consisting of 801 controls and 1,636 cases. In addition, Swedish PC families comprising a total of 157 cases sampled for DNA were analyzed for selected SNPs. Seven SNPs, including the promoter SNP rsl6260, that captured over 96% of CDH1 haplotype variation were selected as haplotype tagging SNPs and analyzed for associated PC risk. We observed significant confirmation of rsl6260 (P=0.003) for cases with a positive family history of PC (FH+) both in an independent case-control population and in PC families. In addition, a common haplotype (HapB, 25%) including the variant allele of rsl6260 was associated (P=0.004) with PC risk among FH+ cases. The promoter SNP rsl6260 as well as HapB were significantly transmitted to affected offspring in PC families. We report strong confirmation of the association between PC risk in FH+ cases and a functional CDH1 promoter SNP in an independent population. In conjunction with the biological importance of CDH1 our findings encourage further evaluation of genetic variation in CDH1 in relation to PC etiology. Due to the difficulties in replication of genetic association studies. this finding is unusual and novel.

  • 50. Lindstrom, Sara
    et al.
    Adami, Hans-Olov
    Bälter, Katarina Augustsson
    Xu, Jianfeng
    Zheng, S. Lilly
    Stattin, Paer
    Gronberg, Henrik
    Wiklund, Fredrik
    Inherited variation in hormone-regulating genes and prostate cancer survival2007In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 13, no 17, p. 5156-5161Article in journal (Refereed)
    Abstract [en]

    Purpose: Hormonal manipulation is the mainstay treatment of prostate cancer, notably in advanced stages. Despite initial favorably response, the cancer eventually develops hormone resistance resulting in disease progression and death. However, little is known about genetic determinants of disease progression and prostate cancer-specific death. Experimental Design: We analyzed a population-based cohort comprising 2,761 men diagnosed with prostate cancer from March 2001 to October 2003 and with complete follow-up through July 2006. During a median follow-up time of 3.8 years, a total of 300 men had died from prostate cancer. We genotyped 23 haplotype tagging single nucleoticle polymorphisms in the genes AR, CYP17, and SRD5A2 and used Cox proportional hazards analyses to quantify associations between genotype and risk of dying from prostate cancer. Results: The variant 'A': allele of an AR promoter single nucleoticle polymorphism, rs17302090, was borderline associated with a 50% increased risk of dying from prostate cancer (95% confidence interval, 1.0-2.3; P = 0.07). This finding was more pronounced in patients who received hormonal therapy as primary treatment at diagnosis (hazard ratio, 19; 95% confidence interval, 1.3-2.9; P = 0.007). We did not identify any associations between CYP17 or SRD5A2 variation and prostate cancer-specific death. Conclusions: Our results suggest that inherited genetic variation in the androgen receptor gene affects hormonal treatment response and ultimately prostate cancer death.

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