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  • 51. 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.

  • 52.
    Lindstrom, Sara
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden.;Umea Univ, Dept Radiat Sci, Umea, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Xu, Jianfeng
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC USA..
    Zheng, S. Lilly
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC USA..
    Sun, Jielin
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC USA..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci, Umea, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Genetic variation in the upstream region of ERG and prostate cancer2009In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 20, no 7, p. 1173-1180Article in journal (Refereed)
    Abstract [en]

    A considerable fraction of prostate cancers harbor a gene fusion between the androgen-regulated TMPRSS2 and ERG, one of the most frequently over-expressed proto-oncogenes in prostate cancer. Here, we investigated if inherited genetic variation upstream of ERG alters prostate cancer risk and survival. We genotyped 21 haplotype tagging SNPs (htSNPs) covering 123 kb of 5'UTR DNA including exon 3 of ERG in 2,760 incident prostate cancer cases and 1,647 controls from a population-based Swedish case-control study (CAPS). Individual SNPs and haplotypes were tested for association with prostate cancer risk and survival. One haplotype-'CTCGTATG' located 100 kb upstream of ERG-was associated with lethal prostate cancer (HR, 1.36; 95% CI, 1.2-1.9, p = 0.006). Carriers of the variant 'T' allele of rs2836626 were diagnosed with higher TNM-stage (p = 0.009) and had an increased risk of prostate cancer-specific death (HR = 1.3; 95% CI, 1.1-1.7, p = 0.009). However, this association did not remain statistically significant after adjusting for multiple testing. We found overall no association between ERG variation and prostate cancer risk. Genetic variation upstream of ERG may alter prostate cancer stage and ultimately prostate cancer-specific death but it is unlikely that it plays a role in prostate cancer development.

  • 53. Lindstrom, Sara
    et al.
    Wiklund, Fredrik
    Adami, Hans-Olov
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Adolfsson, Jan
    Gronberg, Henrik
    Germ-line genetic variation in the key androgen-regulating genes androgen receptor, cytochrome P450, and steroid-5-alpha-reductase type 2 is important for prostate cancer development2006In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 66, no 22, p. 11077-11083Article in journal (Refereed)
    Abstract [en]

    Prostate cancer risk may be influenced by single genetic variants in the hormone-regulating genes androgen receptor (AR), cytochrome P450 (CYP17), and steroid-5-alpha-reductase type 2 (SRD5A2). In this study, we comprehensively investigated polymorphisms in these three loci and their joint effect in a large population-based study. We selected 23 haplotype-tagging single-nucleotide polymorphisms (htSNP) that could uniquely describe > 95% of the haplotypes (6 in AR, 6 in CYP17, and 11 in SRD5A2). These htSNPs were then genotyped in the Cancer Prostate in Sweden population (2,826 case subjects and 1,705 controls). We observed significant association for several SNPs in the AR gene (P = 0.004-0.02) and CYP17 (P = 0.009-0.05) and one SNP in SRD5A2 (P = 0.02). Carriers of the most common AR haplotype had a significant excess risk to develop prostate cancer [odds ratio (OR), 1.25; 95% confidence interval (95% CI), 1.1-1.5; P = 0.002], yielding an estimated population attributable risk of 16% (95% CI, 0.06-0.25). Combining risk alleles from these genes yielded a 12% risk increase for each additional high-risk allele carried (95% CI, 1.1-1.2; P for trend = 9.2 x 10(-5)), with an overall OR of 1.87 (95% CI, 1.0-3.4) for carriers of all five included risk alleles, an OR of 2.13 (P for trend = 8 x 10(-4)) for advanced disease, and an OR of 4.35 (P for trend = 7 x 10(-5)) for disease onset before age 65 years. Genetic variation in key genes in the androgen pathway is important for development of prostate cancer and may account for a considerable proportion of all prostate cancers. Carriers of rive high-risk alleles in the AR, CYP17, and SRD5A2 genes are at similar to 2-fold excess risk to develop prostate cancer.

  • 54. Lindstrom, Sara
    et al.
    Zheng, S. Lilly
    Wiklund, Fredrik
    Jonsson, Bjoern-Anders
    Adami, Hans-Olov
    Bälter, Katarina
    Brookes, Anthony J.
    Sun, Jielin
    Chang, Bao-Li
    Liu, Wennuan
    Li, Ge
    Isaacs, William B.
    Adolfsson, Jan
    Gronberg, Henrik
    Xu, Jianfeng
    Systematic replication study of reported genetic associations in prostate cancer: Strong support for genetic variation in the androgen pathway2006In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, no 16, p. 1729-1743Article, review/survey (Refereed)
    Abstract [en]

    BACKGROUND. Association studies have become a common and popular method to identify genetic variants predisposing to complex diseases. Despite considerable efforts and initial promising findings, the field of prostate cancer genetics is characterized by inconclusive reports and no prostate cancer gene has yet been established. METHODS. We performed a literature review and identified 79 different polymorphisms reported to influence prostate cancer risk. Of these, 46 were selected and tested for association in a large Swedish population-based case-control prostate cancer population. RESULTS. We observed significant (P < 0.05) confirmation for six polymorphisms located in five different genes. Three of them coded for key enzymes in the androgen biosynthesis and response pathway; the CAG repeat in the androgen receptor (AR) gene (P = 0.03), one SNP in the CYP17 gene (P = 0.04), two SNPs in the SRD5A2 gene (P = 0.02 and 0.02, respectively), a deletion of the GSTT1. gene (P = 0.006), and one SNP in the MSR1 gene, IVS5-59C > A, (P = 0.009). CONCLUSIONS. Notwithstanding the difficulties to replicate findings in genetic association studies, our results strongly support the importance of androgen pathway genes in prostate cancer etiology.

  • 55. Ludvigsson, J. F.
    et al.
    Lagerros, Y. T.
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Barna Hedenhös äter farligt2013In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, no 51-52Article in journal (Refereed)
  • 56. McKay, James D.
    et al.
    Kaaks, Rudolf
    Johansson, Mattias
    Biessy, Carine
    Wiklund, Fredik
    Bälter, Katarina
    Adami, Hans-Olov
    Boillot, Catherine
    Gioia-Patricola, Lydie
    Canzian, Federico
    Stattin, Par
    Gronberg, Henrik
    Haplotype-based analysis of common variation in the growth hormone receptor gene and prostate cancer risk2007In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 16, no 1, p. 169-173Article in journal (Refereed)
    Abstract [en]

    The growth hormone receptor (GHR) is potentially involved in prostate cancer through its role in stimulating insulin-like growth factor I production and its cellular effects on prostate epithelium. We have used a haplotype-based tagging approach within CAncer Prostate Sweden, a large retrospective case-control study of 2,863 cases and 1,737 controls to investigate if genetic variation in the GHR gene influences prostate cancer risk. One haplotype in the 3' region of the GHR gene was found associated with prostate cancer risk in elderly men (> 65 years old at the time of diagnosis), with heterozygote haplotype carriers having an odds ratio of 1.65 (95% confidence interval, 1.21-2.16; P = 0.0009, P-corrected = 0.03). GHR function has been implicated in the determination of body mass index. Interestingly, the same haplotype associated with risk in the 3' end of the GHR gene was also associated with a decrease in body mass index in controls (P = 0.003, P-corrected = 0.05), possibly indicating some functionality with this haplotype. These results suggest that whereas genetic variation in the GHR gene does not seem to play a major role in prostate cancer etiology, one haplotype in the 3' region may be potentially relevant to cases with later onset of prostate cancer.

  • 57. Michaud, D S
    et al.
    Augustsson, Katarina
    Karolinska institutet, Sweden.
    Rimm, E B
    Stampfer, M J
    Willett, W C
    Giovannucci, E
    A prospective study on intake of animal products and risk of prostate cancer2001In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 12, no 6, p. 557-567Article in journal (Refereed)
    Abstract [en]

    Objective: Association between animal products and prostate cancer have been observed in numerous observational studies, but it is not clear whether the high fat content of these foods or some other component accounts for these associations. We examine these associations among 51,529 men who contributed detailed dietary data. Methods: Participants of the Health Professionals Follow-Up Study completed a semiquantitative food-frequency questionnaire in 1986, and subsequently in 1990 and 1994. Other data on potential risk factors were collected at baseline and in subsequent questionnaires during follow-up. Between 1986 and 1996, 1897 total cases of prostate cancer (excluding stage A(1)) and 249 metastatic cancers were identified. We used pooled logistic regression for analyses of diet and prostate cancer. Results: Intakes of total meat, red meat, and dairy products were not associated with risk of total or advanced prostate cancer. An elevated risk for metastatic prostate cancer was observed with intake of red meat (relative risk (RR) = 1.6 for top vs. bottom quintile comparison, 95% confidence interval (CI) = 1.0-2.5); this association was slightly attenuated after controlling for saturated and alpha -linolenic fatty acids (RR = 1.5, 95% CI = 0.88-2.5). Processed meats, bacon and beef, pork or lamb as a main dish each contributed to an elevated risk of metastatic prostate cancer. Dairy product intake increased risk of metastatic prostate cancer (RR = 1.4, 95% CI = 0.91-2.2 for top vs. bottom quintile comparison), but no association remained after controlling for calcium and other fatty acids. A high intake in both red meat and dairy product was associated with a statistically significant two-fold elevation in risk of metastatic prostate cancer, compared to low intake of both products; however, most of the excess risk could be explained by known nutritional components of these foods. Conclusions: Intakes of red meat and dairy products appear to be related to increased risk of metastatic prostate cancer. While known nutrients, such as calcium and fatty acids, may explain most of the dairy association observed, it appears that a portion of the risk of metastatic prostate cancer associated with red meat intake remains unexplained.

  • 58.
    Moller, E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Galeone, C.
    Ist Ric Farmacol Mario Negri, Dept Epidemiol 1, Milan, Italy.;Univ Milan, Sect Med Stat Giulio A Maccacaro, Dept Occupat Hlth Luigi Devoto, Milan, Italy..
    Bellocco, R.
    Univ Milano Bicocca, Dept Stat, Milan, Italy..
    Adolfsson, J.
    Karolinska Inst, Oncol Ctr, Dept Clin Innovat & Technol CLINTEC, Stockholm, Sweden..
    Gronberg, H.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, H.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    La Vecchia, C.
    Ist Ric Farmacol Mario Negri, Dept Epidemiol 1, Milan, Italy.;Univ Milan, Sect Med Stat Giulio A Maccacaro, Dept Occupat Hlth Luigi Devoto, Milan, Italy..
    Mucci, L.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Nordic nutrition recommendations and mediterranean diet in relation to prostate cancer risk in Sweden2011In: Annals of Nutrition and Metabolism, ISSN 0250-6807, E-ISSN 1421-9697, Vol. 58, p. 273-274Article in journal (Other academic)
  • 59.
    Moller, Elisabeth
    et al.
    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..
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Univ Iceland, Ctr Publ Hlth Sci, Reykjavik, Iceland..
    Lundholm, Cecilia
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bellocco, Rino
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Johansson, Jan-Erik
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Lifetime body size and prostate cancer risk in a population-based case-control study in Sweden2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 12, p. 2143-2155Article in journal (Refereed)
    Abstract [en]

    The role of body size in prostate cancer etiology is unclear and potentially varies by age and disease subtype. We investigated whether body size in childhood and adulthood, including adult weight change, is related to total, low-intermediate-risk, high-risk, and fatal prostate cancer. We used data on 1,499 incident prostate cancer cases and 1,118 population controls in Sweden. Body figure at age 10 was assessed by silhouette drawings. Adult body mass index (BMI) and weight change were based on self-reported height and weight between ages 20 and 70. We estimated odds ratios (ORs) with 95 % confidence intervals (CIs) by unconditional logistic regression. Height was positively associated with prostate cancer. Overweight/obesity in childhood was associated with a 54 % increased risk of dying from prostate cancer compared to normal weight, whereas a 27 % lower risk was seen in men who were moderately thin (drawing 2) in childhood (P (trend) = 0.01). Using BMI < 22.5 as a reference, we observed inverse associations between BMI 22.5 to < 25 at age 20 and all prostate cancer subtypes (ORs in the range 0.72-0.82), and between mean adult BMI 25 to < 27.5 and low-intermediate-risk disease (OR 0.75, 95 % CI 0.55-1.02). Moderate adult weight gain increased the risk of disease in men with low BMI at start and in short men. Our comprehensive life-course approach revealed no convincing associations between anthropometric measures and prostate cancer risk. However, we found some leads that deserve further investigation, particularly for early-life body size. Our study highlights the importance of the time window of exposure in prostate cancer development.

  • 60.
    Moller, Elisabeth
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Galeone, Carlotta
    Ist Ric Farmacol Mario Negri, Dept Epidemiol, Milan, Italy.;Univ Milan, Luigi Devoto Dept Occupat Hlth, Milan, Italy..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Adolfsson, Jan
    Karolinska Inst, Dept Clin Innovat & Technol CLINTEC, Oncol Ctr, SE-17177 Stockholm, Sweden..
    Andersson, Therese M-L
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bellocco, Rino
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Univ Milano Bicocca, Dept Stat, Milan, Italy..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    The Nordic Nutrition Recommendations and prostate cancer risk in the Cancer of the Prostate in Sweden (CAPS) study2012In: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 15, no 10, p. 1897-1908Article in journal (Refereed)
    Abstract [en]

    Objective: The Nordic Nutrition Recommendations (NNR) aim at preventing diet-associated diseases such as cancer in the Nordic countries. We evaluated adherence to the NNR in relation to prostate cancer (PC) in Swedish men, including potential interaction with a genetic risk score and with lifestyle factors. Design: Population-based case-control study (Cancer of the Prostate in Sweden (CAPS), 2001-2002). Using data from a semi-quantitative FFQ, we created an NNR adherence score and estimated relative risks of PC by unconditional logistic regression. Individual score components were modelled separately and potential modifying effects were assessed on the multiplicative scale. Setting: Four regions in the central and northern parts of Sweden. Subjects: Incident PC patients (n 1386) and population controls (n 940), frequency-matched on age and region. Results: No overall association with PC was found, possibly due to the generally high adherence to the NNR score and its narrow distribution in the study population. Among individual NNR score components, high compared with low intakes of polyunsaturated fat were associated with an increased relative risk of localized PC. No formal interaction with genetic or lifestyle factors was observed, although in stratified analysis a positive association between the NNR and PC was suggested among men with a high genetic risk score but not among men with a medium or low genetic risk score. Conclusions: Our findings do not support an association between NNR adherence and PC. The suggestive interaction with the genetic risk score deserves further investigations in other study populations.

  • 61.
    Moller, Elisabeth
    et al.
    Karolinska Inst, Stockholm, Sweden..
    Lundholm, Cecilia
    Karolinska Inst, Stockholm, Sweden..
    Bellocco, Rino
    Karolinska Inst, Stockholm, Sweden..
    Mucci, Lorelei A.
    Karolinska Inst, Stockholm, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Stockholm, Sweden..
    LIFETIME BODY SIZE AND PROSTATE CANCER RISK IN A POPULATION-BASED CASE-CONTROL STUDY IN SWEDEN2013In: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 177, p. S5-S5Article in journal (Other academic)
  • 62.
    Moller, Elisabeth
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Wilson, Kathryn M.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Batista, Julie L.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Mucci, Lorelei A.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Univ Iceland, Ctr Publ Hlth Sci, Reykjavik, Iceland..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Giovannucci, Edward
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA..
    Body size across the life course and prostate cancer in the Health Professionals Follow-up Study2016In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 138, no 4, p. 853-865Article in journal (Refereed)
    Abstract [en]

    Current evidence of an association between body size and prostate cancer is conflicting, possibly due to differential effects of body size across the lifespan and the heterogeneity of the disease. We therefore examined childhood and adult body size in relation to total incident prostate cancer and prognostic subtypes in a prospective cohort of 47,491 US men in the Health Professionals Follow-up Study. We assessed adult height, body mass index (BMI) in early and middle-to-late adulthood, adult waist circumference, and body shape at age 10. With follow-up from 1986 to 2010, we estimated the relative risk (RR) of prostate cancer using Cox proportional hazards models. We identified 6,183 incident cases. Tallness was associated with increased risk of advanced-stage tumors, particularly fatal disease (RR=1.66, 95% CI 1.23-2.23, highest vs. lowest quintile, p(trend) < 0.001). High BMI at age 21 was inversely associated with total prostate cancer (RR=0.89, 95% CI 0.80-0.98, BMI >= 26 vs. 20-21.9, p(trend)=0.01) and with fatal and advanced disease. The association for late adult BMI differed by age (p(interaction) < 0.001); high BMI was inversely associated with total prostate cancer (RR=0.64, 95% CI 0.51-0.78, BMI >= 30 vs. 21-22.9, p(trend) < 0.001) and with non-advanced and less aggressive tumors among men <= 65 years, whereas no association was seen among men >65 years. Adult waist circumference was weakly inversely associated with less aggressive disease. Childhood obesity was unclearly related to risk. Our study confirms tall men to be at increased risk of fatal and advanced prostate cancer. The influence of adiposity varies by prognostic disease subtype and by age. The relationship between body size and prostate cancer is complex. Body size changes progressively throughout life and consequent effects on prostate cancer risk may be associated with related changes in hormonal and metabolic pathways. This large prospective study examined potential associations between the risk of various prostate cancer subtypes and multiple anthropometric measures at different ages in men. Tallness was confirmed to be associated with an elevated risk of advanced prostate cancer, particularly fatal disease. The extent to which body weight influenced risk varied according to factors such as age and disease subtype.

  • 63. Mucci, L A
    et al.
    Dickman, P W
    Steineck, G
    Adami, H O
    Augustsson, Katarina
    Karolinska institutet, Sweden.
    Dietary acrylamide and cancer of the large bowel, kidney, and bladder: Absence of an association in a population-based study in Sweden2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 88, no 1, p. 84-89Article in journal (Refereed)
    Abstract [en]

    Recently, disturbingly high levels of acrylamide were unexpectedly detected in widely consumed food items, notably French fries, potato crisps, and bread. Much international public concern arose since acrylamide has been classified as a probable carcinogen, although based chiefly on laboratory evidence; informative human data are largely lacking. We reanalysed a population-based Swedish case-control study encompassing cases with cancer of the large bowel (N = 591), bladder (N = 263) and kidney (N = 133), and 538 healthy controls, assessing dietary acrylamide by linking extensive food frequency data with acrylamide levels in certain food items recorded by the Swedish National Food Administration. Unconditional logistic regression was used to estimate odds ratios, adjusting for potential confounders. We found consistently a lack of an excess risk, or any convincing trend, of cancer of the bowel, bladder, or kidney in high consumers of 14 different food items with a high (range 300-1200 mug kg(-1)) or moderate (range 30-299 mug kg(-1)) acrylamide content. Likewise, when we analysed quartiles of known dietary acrylamide intake, no association was found with cancer of the bladder or kidney. Unexpectedly, an inverse trend was found for large bowel cancer (P for trend 0.01) with a 40% reduced risk in the highest compared to lowest quartile. We found reassuring evidence that dietary exposure to acrylamide in amounts typically ingested by Swedish adults in certain foods has no measurable impact on risk of three major types of cancer. It should be noted, however, that relation of risk to the acrylamide content of all foods could not be studied. 

  • 64. Mucci, L A
    et al.
    Sandin, S
    Bälter, Katarina
    Adami, H O
    Magnusson, C
    Weiderpass, E
    Acrylamide intake and breast cancer risk in Swedish women2005In: Journal of the American Medical Association (JAMA), ISSN 0098-7484, E-ISSN 1538-3598, Vol. 293, no 11, p. 1326-1327Article in journal (Refereed)
  • 65. Möller, E.
    et al.
    Galeone, C.
    Andersson, T. M. -L
    Bellocco, R.
    Adami, H. -O
    Andrén, O.
    Grönberg, H.
    La Vecchia, C.
    Mucci, L. A.
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Mediterranean diet score and prostate cancer risk in a Swedish population-based case-control study2013In: Journal of Nutritional Science, ISSN 2048-6790, E-ISSN 2048-6790, Vol. 2, p. 1-13, article id e15Article in journal (Refereed)
    Abstract [en]

    Several individual components of the Mediterranean diet have been shown to offer protection against prostate cancer. The present study is the first to investigate the association between adherence to the Mediterranean diet and the relative risk of prostate cancer. We also explored the usefulness of the Mediterranean Diet Score (MDS) in a non-Mediterranean population. FFQ data were obtained from 1482 incident prostate cancer patients and 1108 population- based controls in the Cancer of the Prostate in Sweden (CAPS) study. We defined five MDS variants with different components or using either study-specific intakes or intakes in a Greek reference population as cut-off values between low and high intake of each component. Unconditional logistic regression was used to estimate the relative risk of prostate cancer for high and medium v. low MDS, as well as potential associations with the individual score components. No statistically significant association was found between adherence to the Mediterranean diet based on any of the MDS variants and prostate cancer risk (OR range: 0·96-1·19 for total prostate cancer, comparing high with low adherence). Overall, we found little support for an association between the Mediterranean diet and prostate cancer in this Northern European study population. Despite potential limitations inherent in the study or in the build-up of a dietary score, we suggest that the original MDS with study-specific median intakes as cut-off values between low and high intake is useful in assessing the adherence to the Mediterranean diet in non-Mediterranean populations. 

  • 66.
    Nystrom, Christine Delisle
    et al.
    Karolinska Inst, Dept Biosci & Nutr, Novum, S-14183 Huddinge, Sweden..
    Henriksson, Hanna
    Univ Granada, PROFITH Promoting FITness & Hlth Phys Act Res Grp, Dept Phys Educ & Sports, Fac Sports Sci, E-18071 Granada, Spain..
    Alexandrou, Christina
    Karolinska Inst, Dept Biosci & Nutr, Novum, S-14183 Huddinge, Sweden..
    Bergstrom, Anna
    Karolinska Inst, Dept Environm Med, S-17177 Stockholm, Sweden..
    Bonn, Stephanie
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Lof, Marie
    Karolinska Inst, Dept Biosci & Nutr, Novum, S-14183 Huddinge, Sweden..
    Validation of an Online Food Frequency Questionnaire against Doubly LabelledWater and 24 h Dietary Recalls in Pre-School Children2017In: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 9, no 1, article id 66Article in journal (Refereed)
    Abstract [en]

    The development of easy-to-use and accurate methods to assess the intake of energy, foods and nutrients in pre-school children is needed. KidMeal-Q is an online food frequency questionnaire developed for the LifeGene prospective cohort study in Sweden. The aims of this study were to compare: (i) energy intake (EI) obtained using KidMeal-Q to total energy expenditure (TEE) measured via doubly labelled water and (ii) the intake of certain foods measured using KidMeal-Q to intakes acquired by means of 24 h dietary recalls in 38 children aged 5.5 years. The mean EI calculated using KidMeal-Q was statistically different (p < 0.001) from TEE (4670 +/- 1430 kJ/24 h and 6070 +/- 690 kJ/24 h, respectively). Significant correlations were observed for vegetables, fruit juice and candy between KidMeal-Q and 24 h dietary recalls. Only sweetened beverage consumption was significantly different in mean intake (p < 0.001), as measured by KidMeal-Q and 24 h dietary recalls. In conclusion, KidMeal-Q had a relatively short answering time and comparative validity to other food frequency questionnaires. However, its accuracy needs to be improved before it can be used in studies in pre-school children.

  • 67.
    Olsson, Mats
    et al.
    Karolinska Univ Hosp, Dept Urol, SE-14186 Stockholm, Sweden..
    Lindstrom, Sara
    Umea Univ, Dept Radiat Sci, Umea, Sweden..
    Haggkvist, Benjamin
    Umea Univ Hosp, Ctr Oncol, S-90185 Umea, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci, Umea, Sweden..
    Ask, Birgitta
    Karolinska Univ Hosp, Dept Lab Med, Karolinska Inst, Stockholm, Sweden..
    Rane, Anders
    Karolinska Univ Hosp, Dept Lab Med, Karolinska Inst, Stockholm, Sweden..
    Ekstrom, Lena
    Karolinska Univ Hosp, Dept Lab Med, Karolinska Inst, Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    The UGT2B17 gene deletion is not associated with prostate cancer risk2008In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 68, no 5, p. 571-575Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. Deletion polymorphism of the UDP-glucuronosyltransferase 2B17 (UG'T2B17) gene has been associated with an increased prostate cancer risk in two previous independent studies. Here we determine the risk in a large-scale population-based case-control study. METHODS. Genotyping was conducted with a 5'-nuclease activity assay to distinguish those with one or two UGT2B17 gene copies (ins/del and ins/ins) from individuals homozygous for the deletion (del/del) allele. RESULTS. In contrast to previous findings, no association between the UGT2B17 deletion polymorphism and prostate cancer risk was found. Furthermore the UGT2B17 gene deletion did not affect the risk for prostate cancer specific death. CONCLUSION. The UGT2B17 deletion polymorphism does not play a major role in prostate cancer susceptibility as previously indicated.

  • 68. Pereira, M A
    et al.
    O'Reilly, E
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Fraser, G E
    Goldbourt, U
    Heitmann, B L
    Hallmans, G
    Knekt, P
    Liu, S M
    Pietinen, P
    Virtamo, J
    Spiegelman, D
    Stevens, J
    Willett, W C
    Ascherio, A
    Dietary fiber, folate, and vitamin E with coronary risk: A pooled analysis of cohort studies2006In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 113, no 8, p. E374-E375Article in journal (Other academic)
  • 69.
    Raposo, S. E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA..
    Fondell, E.
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA..
    Strom, P.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Balter, O.
    KTH Royal Inst Technol, Sch Comp Sci & Commun, Stockholm, Sweden.;Stanford Univ, Grad Sch Educ, Stanford, CA 94305 USA..
    Bonn, S. E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA..
    Nyren, O.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Plymoth, A.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bälter, Katarina
    Mälardalen University, School of Health, Care and Social Welfare, Health and Welfare. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Stanford Univ, Stanford Prevent Res Ctr, Palo Alto, CA 94304 USA..
    Intake of vitamin C, vitamin E, selenium, zinc and polyunsaturated fatty acids and upper respiratory tract infection-a prospective cohort study2017In: European Journal of Clinical Nutrition, ISSN 0954-3007, E-ISSN 1476-5640, Vol. 71, no 4, p. 450-457Article in journal (Refereed)
    Abstract [en]

    BACKGROUND/OBJECTIVES: Antioxidants and polyunsaturated fatty acids (PUFAs) have a role in the human immune defense and may affect the susceptibility to upper respiratory tract infection (URTI). To examine dietary intake of vitamin C, vitamin E, selenium, zinc and PUFAs in relation to URTI incidence in a prospective cohort study. SUBJECTS/METHODS: A total of 1533 Swedish women and men aged 25-64 years were followed for nine months during 2011-2012. Information on dietary intake was assessed through a web-based food frequency questionnaire, and events of URTI were self-reported prospectively as they occurred. Cox proportional hazards regression was applied to obtain incidence rate ratios with 95% confidence intervals. RESULTS: The mean number of URTI events was 0.9 among all participants, 1.0 among women and 0.7 among men. In women, the incidence rate ratios ( 95% confidence interval) for high compared with low intake were 0.69 (0.55-0.88) for vitamin C, 0.77 (0.62-0.96) for vitamin E, 0.57 (0.39-0.83) for docosahexaenoic acid (DHA) and 0.80 (0.65-0.99) for arachidonic acid ( AA). No association was found for selenium or zinc among women. In men, an increased URTI incidence was seen with medium vitamin E intake (1.42 (1.09-1.85)) and high zinc intake (1.50 (1.04-2.16)). No association was found for vitamin C, selenium or PUFAs among men. CONCLUSIONS: We found an inverse association of URTI incidence among women for vitamin C, vitamin E, DHA and AA intake and a positive association among men for vitamin E and zinc intake. The observed gender differences warrant further investigation.

  • 70. Rayman, M. P.
    et al.
    Cooper, M. L.
    Vishnubhatla, I.
    Adami, H. -O
    Groenberg, H.
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Green, F. R.
    Do functional selenoprotein SNPs predict the risk of prostate cancer?2006In: Proceedings of the Nutrition Society, ISSN 0029-6651, E-ISSN 1475-2719, Vol. 65, p. 100A-100AArticle in journal (Other academic)
  • 71.
    Russnes, Kjell M.
    et al.
    Oslo Univ Hosp, Clin Canc Surg & Transplantat, N-03803 Oslo, Norway.;Univ Oslo, Dept Nutr, Inst Basic Med Sci, Sognsvannsveien 9, N-0372 Oslo, Norway..
    Moller, Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Wilson, Kathryn M.
    Harvard Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave, Boston, MA 02115 USA.;Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA..
    Carlsen, Monica
    Univ Oslo, Dept Nutr, Inst Basic Med Sci, Sognsvannsveien 9, N-0372 Oslo, Norway..
    Blomhoff, Rune
    Oslo Univ Hosp, Clin Canc Surg & Transplantat, N-03803 Oslo, Norway.;Univ Oslo, Dept Nutr, Inst Basic Med Sci, Sognsvannsveien 9, N-0372 Oslo, Norway..
    Smeland, Sigbjorn
    Univ Oslo, Dept Nutr, Inst Basic Med Sci, Sognsvannsveien 9, N-0372 Oslo, Norway..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Mucci, Lorelei A.
    Harvard Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave, Boston, MA 02115 USA.;Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Total antioxidant intake and prostate cancer in the Cancer of the Prostate in Sweden (CAPS) study. A case control study2016In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 16, article id 438Article in journal (Refereed)
    Abstract [en]

    Background: The total intake of dietary antioxidants may reduce prostate cancer risk but available data are sparse and the possible role of supplements unclear. We investigated the potential association between total and dietary antioxidant intake and prostate cancer in a Swedish population. Methods: We used FFQ data from 1499 cases and 1112 controls in the population based case-control study Cancer of the Prostate in Sweden (CAPS). The ferric reducing antioxidant potential (FRAP) assay was used to assess the total antioxidant capacity (TAC) of diet and supplements. We calculated odds ratios (ORs) for the risk of prostate cancer across quintiles of antioxidant intake from all foods, from fruit and vegetables only, and from dietary supplements using unconditional logistic regression. Results: Coffee comprised 62 % of the dietary antioxidant intake, tea 4 %, berries 4 %, chocolate 2 %, and boiled potatoes 2 %. In total 19 % and 13 % of the population took multivitamins and supplemental Vitamin C respectively, on a regular basis. Antioxidant intake from all foods and from fruits and vegetables separately measured by the FRAP assay was not associated with prostate cancer risk. For antioxidant intake from supplements we found a positive association with total, advanced, localized, high grade and low grade prostate cancer in those above median supplemental TAC intake of users compared to non-users (Adjusted ORs for total prostate cancer: 1. 37, 95 % CI 1.08-1.73, advanced: 1.51, 95 % CI 1.11-2.06, localized: 1.36. 95 % CI 1.06-1.76, high grade 1.60, 95 % CI 1.06-2.40, low grade 1.36, 95 % CI 1.03-1.81). A high intake of coffee (>= 6 cups/day) was associated with a possible risk reduction of fatal and significantly with reduced risk for high grade prostate cancer, adjusted OR: 0.45 (95 % CI: 0.22-0.90), whereas a high intake of chocolate was positively associated with risk of total, advanced, localized and low grade disease (adjusted OR for total: 1.43, 95 % CI 1.12-1.82, advanced: 1.40, 95 % CI 1.01-1.96, localized: 1.43, 95 % CI 1.08-1.88, low-grade: 1.41, 95 % CI 1.03-1.93). Conclusions: Total antioxidant intake from diet was not associated with prostate cancer risk. Supplement use may be associated with greater risk of disease.

  • 72.
    Sjors, Camilla
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat MEB, Stockholm, Sweden..
    Hedenus, Fredrik
    Chalmers Univ Technol, Gothenburg, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat MEB, SE-17177 Stockholm, Sweden..
    Tillander, Annika
    Karolinska Inst, Dept Med Epidemiol & Biostat MEB, Stockholm, Sweden..
    Bälter, Katarina
    Mälardalen University, School of Health, Care and Social Welfare, Health and Welfare. Karolinska Inst, Stockholm, Sweden.;Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, USA.
    Adherence to dietary recommendations for Swedish adults across categories of greenhouse gas emissions from food2017In: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 20, no 18, p. 3381-3393Article in journal (Refereed)
    Abstract [en]

    Objective: To explore associations between diet-related greenhouse gas emissions (GHGE), nutrient intakes and adherence to the Nordic Nutrition Recommendations among Swedish adults. Design: Diet was assessed by 4 d food records in the Swedish National Dietary Survey. GHGE was estimated by linking all foods to carbon dioxide equivalents, using data from life cycle assessment studies. Participants were categorized into quartiles of energy-adjusted GHGE and differences between GHGE groups regarding nutrient intakes and adherence to nutrient recommendations were explored. Setting: Sweden. Subjects: Women (n 840) and men (n 627) aged 18-80 years. Results: Differences in nutrient intakes and adherence to nutrient recommendations between GHGE groups were generally small. The dietary intake of participants with the lowest emissions was more in line with recommendations regarding protein, carbohydrates, dietary fibre and vitamin D, but further from recommendations regarding added sugar, compared with the highest GHGE group. The overall adherence to recommendations was found to be better among participants with lower emissions compared with higher emissions. Among women, 27% in the lowest GHGE group adhered to at least twenty-three recommendations compared with only 12% in the highest emission group. For men, the corresponding figures were 17 and 10 %, respectively. Conclusions: The study compared nutrient intakes as well as adherence to dietary recommendations for diets with different levels of GHGE from a national dietary survey. We found that participants with low-emission diets, despite higher intake of added sugar, adhered to a larger number of dietary recommendations than those with high emissions.

  • 73.
    Sjors, Camilla
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Raposo, Sara E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Harvard Univ, TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Balter, Olle
    KTH Royal Inst Technol, Sch Comp Sci & Commun, SE-10044 Stockholm, Sweden.;Stanford Univ, Grad Sch Educ, Stanford, CA 94305 USA..
    Hedenus, Fredrik
    Chalmers Univ Technol, Dept Energy & Environm, SE-41296 Gothenburg, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA 94305 USA..
    Diet-related greenhouse gas emissions assessed by a food frequency questionnaire and validated using 7-day weighed food records2016In: Environmental health, ISSN 1476-069X, E-ISSN 1476-069X, Vol. 15, article id 15Article in journal (Refereed)
    Abstract [en]

    Background: The current food system generates about 25 % of total greenhouse gas emissions (GHGE), including deforestation, and thereby substantially contributes to the warming of the earth's surface. To understand the association between food and nutrient intake and GHGE, we therefore need valid methods to assess diet-related GHGE in observational studies. Methods: Life cycle assessment (LCA) studies assess the environmental impact of different food items. We linked LCA data expressed as kg carbon dioxide equivalents (CO(2)e) per kg food product to data on food intake assessed by the food frequency questionnaire (FFQ) Meal-Q and validated it against a 7-day weighed food record (WFR). 166 male and female volunteers aged 20-63 years completed Meal-Q and the WFR, and their food intake was linked to LCA data. Results: The mean GHGE assessed with Meal-Q was 3.76 kg CO(2)e per day and person, whereas it was 5.04 kg CO(2)e using the WFR. The energy-adjusted and deattenuated Pearson and Spearman correlation coefficients were 0.68 and 0.70, respectively. Moreover, compared to the WFR, Meal-Q provided a good ranking ability, with 90 % of the participants classified into the same or adjacent quartile according to their daily average CO(2)e. The Bland-Altman plot showed an acceptable level of agreement between the two methods and the reproducibility of Meal-Q was high. Conclusions: This is the first study validating the assessment of diet-related GHGE by a questionnaire. The results suggest that Meal-Q is a useful tool for studying the link between food habits and CO(2)e in future epidemiological studies.

  • 74. Skog, K
    et al.
    Augustsson, Katarina
    Steineck, G
    Stenberg, M
    Jagerstad, M
    Polar and non-polar heterocyclic amines in cooked fish and meat products and their corresponding pan residues1997In: Food and Chemical Toxicology, ISSN 0278-6915, E-ISSN 1873-6351, Vol. 35, no 6, p. 555-565Article in journal (Refereed)
    Abstract [en]

    Fourteen cooked dishes with their corresponding pan residues were analysed for polar and non-polar heterocyclic amines using HPLC. The choice of foods, including beef, pork, poultry, game, fish, egg and sausages, was based on an investigation of an elderly population in Stockholm participating in an analytical epidemiological case-control study on cancer risks after intake of heterocyclic amines. The food items were prepared using normal household cooking practices, and to reflect the wide range of surface browning of the cooked dishes that would be encountered in this population, four cooking temperatures were used in the range 150-225 degrees C. For all food samples, the total amount of heterocyclic amines formed at 150 degrees C was less than 1 ng/g cooked product, and at 175 degrees C less than 2 ng/g. The highest concentrations of heterocyclic amines were detected in fillet of pork, reindeer meat and chicken breast fried at 200 and 225 degrees C and their corresponding pan residues. The total sum of 2-amino-3,8-dimethylimidazo-[4,5-f]quinoxaline 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine was about 1 mu g per 100 g portion (including pan residues) for reindeer meat and chicken breast, and between 1.9 and 6.3 mu g per 100-g portion for fillet of pork. PhIP was the most abundant heterocyclic amine, identified in 73 of 84 samples, and the highest concentration of PhIP, 32.0 ng/g, was found in the pan residue from fillet of pork cooked at 225 degrees C. The non-polar heterocyclic amines 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole and 3-amino-1-methyl-5H-pyrido[4,3-b]indole were detected in the range of 0.5-7.4 ng/g in most foods cooked at 225 degrees C, and also in meat sauce prepared at 200 and 175 degrees C. The other heterocyclic amines tested for: 2-amino-3-methylimidazo- [4,5-f]quinoline, 2-amino-3,4-dimethylimidazo[4,5-f]quinoline, 2-amino-6-methyl-pyrido-[1,2-a:3',2'-d]-imidazole and 2-aminodipyrido-[1,2-a:3',2'-d]imidazole were present only at very low or non-detectable levels. The low recoveries of the amino-alpha-carbolines 2-amino-9H-pyrido[2,3-b]indole and 2-amino-3-methyl-9H-pyrido[2,3-b]indole made it impossible to quantify them. However, the co-mutagenic substances 1-methyl-9H-pyrido-[3,4-b]indole and 9H-pyrido[3,4-b]indole were detected at levels of about 1-30 ng/g in most of the dishes cooked at 200 and 225 degrees C. 

  • 75. SKOG, K
    et al.
    STEINECK, G
    Augustsson, Katarina
    Karolinska institutet, Sweden.
    JAGERSTAD, M
    EFFECT OF COOKING TEMPERATURE ON THE FORMATION OF HETEROCYCLIC AMINES IN FRIED MEAT-PRODUCTS AND PAN RESIDUES1995In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 16, no 4, p. 861-867Article in journal (Refereed)
    Abstract [en]

    Frequent consumers of meat have an increased risk of colorectal cancer and possibly also of breast, stomach, pancreas and urinary bladder cancer. Bacon, 'Falusausage', ground beef, meatballs, pork belly, pork chops and sliced beef account for more than one-third of the intake of fried meat of the population of Stockholm of age 50-75. These dishes were fried at four temperatures (150, 175, 200 and 225 degrees C) representing normal household cooking practices in Stockholm. Heterocyclic amines in these dishes were analysed using solid-phase extraction and HPLC. The heterocyclic amines 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 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) were recovered. The formation of IQ was favoured by moderate cooking temperatures; IQ was detected in one meat sample cooked at 150 degrees C and in some pan residues. The yield of MeIQx, DiMeIQx and PhIP increased with the temperature. For several of the meat dishes, the content of heterocyclic amines in the pan residue was as large or larger than for corresponding piece of meat. The highest levels of MeIQx were 23.7 ng/g in the meat and 23.3 ng/g in the pan residue, Corresponding data for DiMeIQx were 2.7 and 4.1 ng/g and for PhIP 12.7 and 82.4 ng/g. The study leaves little doubt that mutagenic heterocyclic amines are ingested by the population of Stockholm, and added to previous epidemiological studies from the same area, the combined data are consistent with human carcinogenicity of heterocyclic amines, However, analytical epidemiological studies are needed before any statement on causality can be made.

  • 76. Sun, J L
    et al.
    Wiklund, F
    Hsu, F C
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Zheng, S L
    Johansson, J E
    Chang, B L
    Liu, W N
    Li, T
    Turner, A R
    Li, L W
    Li, G
    Adami, H O
    Isaacs, W B
    Xu, J F
    Gronberg, H
    Interactions of sequence variants in interieukin-1 receptor-associated kinase4 and the Toll-like receptor 6-1-10 gene cluster increase prostate cancer risk2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 3, p. 480-485Article in journal (Refereed)
    Abstract [en]

    Chronic or recurrent inflammation has been suggested as a causal factor in several human malignancies, including prostate cancer. Genetic predisposition is also a strong risk factor in the development of prostate cancer. In particular, Toll-like receptors (TLR), especially the TLR6-1-10 gene cluster, are involved in prostate cancer development. Interleukin-1 receptor-associated kinases (IRAK) 1 and 4 are critical components in the TLR signaling pathway. In this large case-control study, we tested two hypotheses: (a) sequence variants in IRAK1 and IRAK4 are associated with prostate cancer risk and (b) sequence variants in IRAK1/4 and TLR1-6-10 interacts and confers a stronger risk to prostate cancer. We analyzed 11 single nucleotide polymorphisms (four in IRAK1 and seven in IRAK4) among 1,383 newly diagnosed prostate cancer patients and 780 population controls in Sweden. Although the single-nucleotide polymorphisms in IRAK1 and IRAK4 alone were not significantly associated with prostate cancer risk, one single-nucleotide polymorphism in IRAK4, when combined with the high-risk genotype at TLR6-1-10, conferred a significant excess risk of prostate cancer. In particular, men with the risk genotype at TLR6-1-10 and IRAK4-7987 CG/CC had an odds ratio of 9.68 (P = 0.03) when compared with men who had wildtype genotypes. Our findings suggest synergistic effects between sequence variants in IRAK4 and the TLR 6-1-10 gene cluster. Although this study was based on a priori hypothesis and was designed to address many common issues facing this type of study, our results need confirmation in even larger studies.

  • 77. Sun, J L
    et al.
    Wiklund, F
    Zheng, S L
    Chang, B L
    Bälter, Katarina
    Li, L W
    Johansson, J E
    Li, G
    Adami, H O
    Liu, W N
    Tolin, A
    Turner, A R
    Meyers, D A
    Isaacs, W B
    Xu, J F
    Gronberg, H
    Sequence variants in toll-like receptor gene cluster (TLR6-TLR1-TLR10) and prostate cancer risk2005In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 97, no 7, p. 525-532Article in journal (Refereed)
    Abstract [en]

    Background: Chronic inflammation plays an important role in several human cancers and may be involved in the etiology of prostate cancer. Toll-like receptors (TLRs) are important in the innate immune response to pathogens and in cross-talk between innate immunity and adaptive immunity. Our previous finding of an association of TLR4 gene sequence variants and prostate cancer risk provides evidence for a role of TLRs in prostate cancer. In this study, we investigated whether sequence variants in the TLR6-TLR1-TLR10 gene cluster, residing within a 54-kb region on 4p14, were associated with prostate cancer risk. Methods: We selected 32 single-nucleotide polymorphisms (SNPs) covering these three genes and genotyped these SNPs in 96 control subjects from the Cancer Prostate in Sweden (CAPS) population-based prostate cancer case-control study. Five distinct haplotype blocks were inferred at this region, and we identified 17 haplotype-tagging SNPs (htSNPs) that could uniquely describe < 95% of the haplotypes. These 17 htSNPs were then genotyped in the entire CAPS study population (1383 case subjects and 780 control subjects). Odds ratios of prostate cancer for the carriers of a variant allele versus those with the wild-type allele were estimated using unconditional logistic regression. Results: The allele frequencies of 11 of the 17 SNPs were statistically significantly different between case and control subjects (P = .04-.001), with odds ratios for variant allele carriers (homozygous or heterozygous) compared with wild-type allele carriers ranging from 1.20 (95% confidence interval [CI] = 1.00 to 1.43) to 1.38 (95% CI = 1.12 to 1.70). Phylogenetic tree analyses of common haplotypes identified a clade of two evolutionarily related haplotypes that are statistically significantly associated with prostate cancer risk. These two haplotypes contain all the risk alleles of these 11 associated SNPs. Conclusion: The observed multiple associated SNPs at the TLR6-TLR1-TLR10 gene cluster were dependent and suggest the presence of a founder prostate cancer risk variant on this haplotype background. The TLR6-TLR1-TLR10 gene cluster may play a role in prostate cancer risk, although further functional studies are needed to pinpoint the disease-associated variants in this gene cluster.

  • 78.
    Tolstrup, Janne S.
    et al.
    Univ Southern Denmark, Natl Inst Publ Hlth, DK-1353 Copenhagen K, Denmark..
    Hvidtfeldt, Ulla A.
    Univ Copenhagen, Dept Publ Hlth, Social Med Sect, DK-1168 Copenhagen, Denmark..
    Flachs, Esben Meulengracht
    Univ Southern Denmark, Natl Inst Publ Hlth, DK-1353 Copenhagen K, Denmark..
    Spiegelman, Donna
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Heitmann, Berit L.
    Copenhagen Univ Hosp, Inst Prevent Med, Res Unit Dietary Studies, Ctr Hlth & Soc, Copenhagen, Denmark..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Goldbourt, Uri
    Tel Aviv Univ, Sect Epidemiol & Biostat, Henry N Neufeld Cardiac Res Inst, Dept Epidemiol & Prevent Med, IL-69978 Tel Aviv, Israel..
    Hallmans, Goeran
    Umeaa Univ, Dept Publ Hlth & Clin Med, Umea, Sweden..
    Knekt, Paul
    Natl Inst Hlth & Welf, 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..
    Stevens, June
    Univ N Carolina, Sch Publ Hlth, Dept Nutr, Chapel Hill, NC 27599 USA..
    Virtamo, Jarmo
    Natl Inst Hlth & Welf, Helsinki, Finland..
    Feskanich, Diane
    Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Smoking and Risk of Coronary Heart Disease in Younger, Middle-Aged, and Older Adults2014In: American Journal of Public Health, ISSN 0090-0036, E-ISSN 1541-0048, Vol. 104, no 1, p. 96-102Article in journal (Refereed)
    Abstract [en]

    Objectives. We investigated associations of smoking and coronary heart disease (CHD) by age. Methods. Data came from the Pooling Project on Diet and Coronary Heart Disease (8 prospective studies, 1974-1996; n = 192 067 women and 74 720 men, aged 40-89 years). Results. During follow-up, 4326 cases of CHD were reported. Relative to never smokers, CHD risk among current smokers was highest in the youngest and lowest in the oldest participants. For example, among women aged 40 to 49 years the hazard ratio was 8.5 (95% confidence interval [CI] = 5.0, 14) and 3.1 (95% CI = 2.0, 4.9) among those aged 70 years or older. The largest absolute risk differences between current smokers and never smokers were observed among the oldest participants. Finally, the majority of CHD cases among smokers were attributable to smoking. For example, attributable proportions of CHD by age group were 88% (40-49 years), 81% (50-59 years), 71% for (60-69 years), and 68% (70 years) among women who smoked. Conclusions. Among smokers, the majority of CHD cases are attributable to smoking in all age groups. Smoking prevention is important, irrespective of age.

  • 79. Torniainen, Suvi
    et al.
    Hedelin, Maria
    Autio, Ville
    Rasinpera, Heli
    Bälter Augustsson, Katarina
    Klint, Asa
    Bellocco, Rino
    Wiklund, Fredrik
    Stattin, Par
    Ikonen, Tarja
    Tammela, Teuvo L. J.
    Schleutker, Johanna
    Gronberg, Henrik
    Jarvela, Irma
    Lactase persistence, dietary intake of milk, and the risk for prostate cancer in Sweden and Finland2007In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 16, no 5, p. 956-961Article in journal (Refereed)
    Abstract [en]

    Prostate carcinoma is the most common cancer in men. Its primary pathogenesis is mostly unknown. Dairy products containing lactose have been suggested to be risk factors for prostate cancer. Digestion of lactose is dependent on lactase activity in the intestinal wall. A single nucleotide polymorphism C to T residing 13,910 bp upstream of the lactase gene has been shown to associate with the developmental down-regulation of lactase activity underlying persistence/nonpersistence trait. To find out whether lactase persistence is related to the risk for prostate cancer, we genotyped 1,229 Finnish and 2,924 Swedish patients and their 473 Finnish and 1,842 Swedish controls using solid-phase minisequencing. To explore if dairy products have an association with prostate cancer, we analyzed the milk consumption in the Swedish study consisting of 1,499 prostate cancer patients and 1,130 controls (Cancer Prostate in Sweden I study) using a questionnaire. Only the consumption of low-fat milk was found to be associated with increased risk of prostate cancer [odds ratio (OR), 1.73; 95% confidence interval (95% CI), 1.162.391. A statistically significantly higher (P < 0.01) lactose intake was observed among subjects with high lactase activity (C/T and T/T genotypes) compared with those with low lactase activity (C/C genotype). Lactase persistence did not associate with increased risk for prostate carcinoma in the Finnish (OR, 1.11; 95% CI, 0.83-1.47, P = 0.488) or in the Swedish populations (OR, 1.16; 95% CI, 0.91-1.46; P = 0.23). In conclusion, lactase persistence/nonpersistence contains no risk for prostate cancer. Analysis of different milk products showed some evidence for low-fat milk as a potential risk factor for prostate cancer.

  • 80.
    Trinh, T.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Christensen, S. E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Brand, J. S.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Cuzick, J.
    Queen Mary Univ London, Wolfson Inst Prevent Med, Ctr Canc Prevent, London EC1M 6BQ, England..
    Czene, K.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Sjolander, A.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Hall, P.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Background risk of breast cancer influences the association between alcohol consumption and mammographic density2015In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 113, no 1, p. 159-165Article in journal (Refereed)
    Abstract [en]

    Background: Alcohol consumption has been suggested to increase risk of breast cancer through a mechanism that also increases mammographic density. Whether the association between alcohol consumption and mammographic density is modified by background breast cancer risk has, however, not been studied. Methods: We conducted a population-based cross-sectional study of 53 060 Swedish women aged 40-74 years. Alcohol consumption was assessed using a web-based self-administered questionnaire. Mammographic density was measured using the fully-automated volumetric Volpara method. The Tyrer-Cuzick prediction model was used to estimate risk of developing breast cancer in the next 10 years. Linear regression models were used to evaluate the association between alcohol consumption and volumetric mammographic density and the potential influence of Tyrer-Cuzick breast cancer risk. Results: Overall, increasing alcohol consumption was associated with higher absolute dense volume (cm(3)) and per cent dense volume (%). The association between alcohol consumption and absolute dense volume was most pronounced among women with the highest (>= 5%) Tyrer-Cuzick 10-year risk. Among high-risk women, women consuming 5.0-9.9, 10.0-19.9, 20.0-29.9, and 30.0-40.0 g of alcohol per day had 2.6 cm(3) (95% confidence interval (CI), 0.2-4.9), 2.9 cm(3) (95% CI, -0.6 to 6.3), 4.6 cm(3) (95% CI, 1.5-7.7), and 10.8 cm(3) (95% CI, 4.8-17.0) higher absolute dense volume, respectively, as compared with women abstaining from alcohol. A trend of increasing alcohol consumption and higher absolute dense volume was seen in women at low (<= 3%) risk, but not in women at moderate (3.0-4.9%) risk. Conclusion: Alcohol consumption may increase breast cancer risk through increasing mammographic density, particularly in women at high background risk of breast cancer.

  • 81.
    Trinh, Thang
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Eriksson, Mikael
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Darabi, Hatef
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Brand, Judith S.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Cuzick, Jack
    Queen Mary Univ London, Wolfson Inst Prevent Med, Ctr Canc Prevent, London EC1M 6BQ, England..
    Czene, Kamila
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Hall, Per
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Background risk of breast cancer and the association between physical activity and mammographic density2015In: Breast Cancer Research, ISSN 1465-5411, E-ISSN 1465-542X, Vol. 17, article id 50Article in journal (Refereed)
    Abstract [en]

    Introduction High physical activity has been shown to decrease the risk of breast cancer, potentially by a mechanism that also reduces mammographic density. We tested the hypothesis that the risk of developing breast cancer in the next 10 years according to the Tyrer-Cuzick prediction model influences the association between physical activity and mammographic density. Methods We conducted a population-based cross-sectional study of 38,913 Swedish women aged 4074 years. Physical activity was assessed using the validated web-questionnaire Active-Q and mammographic density was measured by the fully automated volumetric Volpara method. The 10-year risk of breast cancer was estimated using the Tyrer-Cuzick (TC) prediction model. Linear regression analyses were performed to assess the association between physical activity and volumetric mammographic density and the potential interaction with the TC breast cancer risk. Results Overall, high physical activity was associated with lower absolute dense volume. As compared to women with the lowest total activity level (<40 metabolic equivalent hours [MET-h] per day), women with the highest total activity level (>= 50 MET-h/day) had an estimated 3.4 cm(3) (95% confidence interval, 2.3-4.7) lower absolute dense volume. The inverse association was seen for any type of physical activity among women with <3.0% TC 10-year risk, but only for total and vigorous activities among women with 3.0-4.9% TC risk, and only for vigorous activity among women with >= 5.0% TC risk. The association between total activity and absolute dense volume was modified by the TC breast cancer risk (P-interaction = 0.05). As anticipated, high physical activity was also associated with lower non-dense volume. No consistent association was found between physical activity and percent dense volume. Conclusions Our results suggest that physical activity may decrease breast cancer risk through reducing mammographic density, and that the physical activity needed to reduce mammographic density may depend on background risk of breast cancer.

  • 82. Ullen, H
    et al.
    Augustsson, Katarina
    Karolinska institutet, Sweden.
    Gustavsson, C
    Steineck, G
    Supplementary iron intake and risk of cancer: Reversed causality?1997In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 114, no 1-2, p. 215-216Article in journal (Refereed)
    Abstract [en]

    Dietary iron intake and body iron stores have been suggested to increase cancer risk, especially colorectal cancer. Within a population-based case-control study in Stockholm county 1993-94, information on dietary and supplementary iron intake were collected through a food frequency questionnaire. An initially noted positive association between intake of supplementary iron and colorectal cancer risk was reversed when intake 5 years prior to cancer diagnosis was subtracted. Reversed causality due to early disease giving symptoms of iron shortage, resulting in iron supplementation, is an issue to consider when a possible association between intake of iron and cancer risk is investigated. 

  • 83. Voskuil, D W
    et al.
    Augustsson, Katarina
    Karolinska institutet, Sweden.
    Dickman, P W
    van't Veer, P
    Steineck, G
    Assessing the human intake of heterocyclic amines: Limited loss of information using reduced sets of questions1999In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 8, no 9, p. 809-814Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to evaluate loss of information from a reduced food frequency questionnaire as compared with an extensive reference method developed to assess the intake of heterocyclic amines (HCAs), Food frequency data were linked to concentrations of HCAs in cooked foods to estimate the individual daily exposure to a combination of five HCAs. The number of food items in the questionnaire was reduced and selected in three ways: (a) according to the contribution to the estimated total intake; (b) the between-person variance; or (c) dishes included in other studies. The effect on sensitivity, specificity, concordance, the correlation coefficient, kappa, and simulated relative risks was determined using information from a population-based study conducted in Stockholm. Only a limited amount of misclassification was introduced when the number of dishes was reduced from 39 to 15 or 20, and no major difference was seen when dishes were selected according to the total intake or the between-person variance. Our data indicate that for a specific exposure, such as HCAs, the loss of accuracy in an analytical epidemiological study is small and may not be relevant when the number of dishes in a food frequency questionnaire is decreased, if the initially chosen dishes are carefully selected and cover a reasonable part of the total intake or between-person variance.

  • 84.
    Westerlund, A.
    et al.
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Div Clin Canc Epidemiol,Dept Oncol, Gothenburg, Sweden..
    Steineck, G.
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Div Clin Canc Epidemiol,Dept Oncol, Gothenburg, Sweden.;Karolinska Inst, Dept Pathol & Oncol, Div Clin Canc Epidemiol, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Stattin, P.
    Umea Univ Hosp, Dept Surg & Perioperat Sci, S-90185 Umea, Sweden..
    Gronberg, H.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Hedelin, M.
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Div Clin Canc Epidemiol,Dept Oncol, Gothenburg, Sweden.;Karolinska Inst, Dept Pathol & Oncol, Div Clin Canc Epidemiol, Stockholm, Sweden..
    Dietary supplement use patterns in men with prostate cancer: the Cancer Prostate Sweden Study2011In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 22, no 4, p. 967-972Article in journal (Refereed)
    Abstract [en]

    Background: In a European setting, we know little about the use of dietary supplements among men with prostate cancer (PCa) and to what extent lifestyle, disease or other factors influence such use. Patients and methods: We evaluated supplement use in 1127 men with incident PCa and in 900 population controls in Sweden. Age-adjusted binary regression with an identity link was carried out to estimate prevalence differences and corresponding 95% confidence intervals (CIs). Modifying effects of lifestyle-and diet-related factors were explored by statistical assessment of additive interaction. Results: Among men with PCa, 542 individuals (48%) had used supplements, which was a 10% (95% CI: 5.9%-15%) higher prevalence than among population controls. Among individuals with high intake of fatty fish, vegetables, and phytoestrogens, but low intake of saturated fat, supplement use was 29% (95% CI: 18%-41%) more common in men with PCa than in population controls. We found no evidence of heterogeneity by categories of education, smoking history, body mass index, fiber, fruit, or phytoestrogen intake, treatment, or disease stage. Conclusion: Supplement use is common in Swedish men with PCa, especially among those with a healthy dietary pattern.

  • 85.
    Wiklund, C. A.
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, R.
    Karolinska Institutet, Stockholm, Sweden.
    Thornton, L. M.
    Karolinska Institutet, Stockholm, Sweden.
    Bälter, Katarina
    Mälardalen University, School of Health, Care and Social Welfare, Health and Welfare. Karolinska Institutet, Stockholm, Sweden.
    Welch, E.
    Karolinska Institutet, Stockholm, Sweden.
    Bulik, C. M.
    Karolinska Institutet, Stockholm, Sweden.
    Childhood body mass index and development of eating disorder traits across adolescence2018In: European eating disorders review, ISSN 1072-4133, E-ISSN 1099-0968, Vol. 26, no 5, p. 462-471Article in journal (Refereed)
    Abstract [en]

    Objective: Understanding the role of premorbid body mass index (BMI) in the emergence of eating disorders may be key to identifying effective prevention strategies. We explore relations between BMI and eating disorders traits in young twins. Method: The effect of BMI at age 9/12 and 15 on eating disorder traits measured using the Eating Disorders Inventory-2 (EDI) at ages 15 and 18 was examined using bivariate modelling in a longitudinal population sample of Swedish twins. Results: The correlation between BMI and EDI within individuals was stable across all ages and remained significant after adjusting for later BMI. Bivariate analysis indicated significant positive genetic correlations between BMI ages 9/12 and 15 and subsequent EDI scores. The relationship remained significant for BMI age 9/12 and EDI age 15 in the adjusted model, indicating a longitudinal association. Conclusion: Our results have implications for conceptualizing the interrelation of BMI and eating disorders across childhood and adolescence. 

  • 86.
    Wiklund, Fredrik
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Lageros, Ylva Trolle
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, S-17176 Stockholm, Sweden..
    Chang, Ellen
    No Calif Canc Ctr, Fremont, CA 94538 USA.;Stanford Univ, Sch Med, Dept Hlth Res & Policy, Div Epidemiol, Stanford, CA 94305 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Johansson, Jan-Erik
    Orebro Univ Hosp, Dept Urol, S-70116 Orebro, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden.;Harvard Univ, Dept Epidemiol, Boston, MA 02115 USA..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Lifetime total physical activity and prostate cancer risk: a population-based case-control study in Sweden2008In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 23, no 11, p. 739-746Article in journal (Refereed)
    Abstract [en]

    The etiologic role of physical activity in prostate cancer development is unclear. We assessed the association between lifetime total physical activity and prostate cancer risk in a Swedish population-based case-control study comprising 1,449 incident prostate cancer cases and 1,118 unaffected population controls. Information regarding physical activity was obtained via a self-administered questionnaire assessing occupational, household, and recreational activity separately at various ages throughout an individual's lifetime. Clinical data (TNM-classification, Gleason sum and PSA) was obtained from linkage to the National Prostate Cancer Registry. Overall, we observed no association between lifetime total physical activity and prostate cancer risk (odds ratio [OR] = 1.04, 95% confidence interval [CI] = 0.77-1.41 for a parts per thousand yen49.7 vs. < 41.9 metabolic equivalent-hours per day). There was a significantly increased risk of prostate cancer in the most active men compared with the least active men in household (OR = 1.44, 95% CI = 1.08-1.92) and recreational physical activity (OR = 1.56, 95% CI = 1.16-2.10). Comparing the most active with the least active men, total physical activity was not associated with either localized disease (OR = 0.95, 95% CI = 0.67-1.34) or advanced disease (OR = 1.19, 95% CI = 0.83-1.71). These findings do not support the hypothesis that physical activity uniformly protects against prostate cancer development.

  • 87.
    Wilson, Kathryn M.
    et al.
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, Hans-Olov
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Vikstrom, Anna C.
    Stockholm Univ, Dept Environm Chem, S-10691 Stockholm, Sweden..
    Paulsson, Birgit
    Stockholm Univ, Dept Environm Chem, S-10691 Stockholm, Sweden..
    Tornqvist, Margareta
    Stockholm Univ, Dept Environm Chem, S-10691 Stockholm, Sweden..
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Acrylamide exposure measured by food frequency questionnaire and hemoglobin adduct levels and prostate cancer risk in the Cancer of the Prostate in Sweden Study2009In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 124, no 10, p. 2384-2390Article in journal (Refereed)
    Abstract [en]

    Acrylamide, a probable human carcinogen, is formed during the cooking of many commonly consumed foods. Data are scant on whether dietary acrylamide represents an important cancer risk in humans. We studied the association between acrylamide and prostate cancer risk using 2 measures of acrylamide exposure: intake from a food frequency questionnaire (FFQ) and acrylamide adducts to hemoglobin. We also studied the correlation between these 2 exposure measures. We used data from the population-based case-control study Cancer of the Prostate in Sweden (CAPS). Dietary data was available for 1,499 cases and 1, 118 controls. Hemoglobin adducts of acrylamide were measured in blood samples from a subset of 170 cases and 161 controls. We calculated odds ratios (ORs) for the risk of prostate cancer in high versus low quantiles of acrylamide exposure using logistic regression. The correlation between FFQ acrylamide intake and acrylamide adducts in non-smokers was 0.25 (95% confidence interval: 0.14-0.35), adjusted for age, region, energy intake, and laboratory batch. Among controls the correlation was 0.35 (95% CI: 0.21-0.48); among cases it was 0.15 (95% CI: 0.00-0.30). The OR of prostate cancer for the highest versus lowest quartile of acrylamide adducts was 0.93 (95% CI: 0.47-1.85, p-value for trend = 0.98). For FFQ acrylamide, the OR of prostate cancer for the highest versus lowest quintile was 0.97 (95% CI: 0.75-1.27,p trend = 0.67). No significant associations were found between acrylamide exposure and risk of prostate cancer by stage, grade, or PSA level. Acrylamide adducts to hemoglobin and FFQ-measured acrylamide intake were moderately correlated. Neither measure of acrylamide exposure-hemoglobin adducts or FFQ-was associated with risk of prostate cancer. (C) 2008 Wiley-Liss. Inc.

  • 88.
    Wilson, Kathryn M.
    et al.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Moller, Elisabeth
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, Hans-Olov
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Andren, Ove
    Orebro Univ Hosp, Orebro, Sweden..
    Andersson, Swen-Olof
    Orebro Univ Hosp, Orebro, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA..
    Coffee and risk of prostate cancer incidence and mortality in the Cancer of the Prostate in Sweden Study2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 8, p. 1575-1581Article in journal (Refereed)
    Abstract [en]

    Coffee intake has recently been associated with significantly lower risk of lethal and advanced prostate cancer in a US population. We studied the association between coffee and prostate cancer risk in the population-based case-control study Cancer of the Prostate in Sweden. Dietary data were available for 1,499 cases and 1,112 controls. We calculated odds ratios (ORs) for the risk of prostate cancer in high versus low categories of coffee intake using logistic regression. We studied overall prostate cancer risk as well as risk of fatal, advanced, localized, high-grade, grade 7, and low-grade disease. Mean coffee intake was 3.1 cups per day among both cases and controls. Coffee intake was not associated with overall prostate cancer risk. Risk of fatal prostate cancer was inversely, but not statistically significantly, associated with coffee intake, with an odds ratio of 0.64 [95 % confidence interval (CI) 0.34-1.19, p value for linear trend = 0.81] for men consuming greater than 5 cups per day compared to men drinking less than 1 cup per day. The highest intake of coffee was associated non-significantly with lower risk of advanced disease (OR = 0.73, 95 % CI 0.41-1.30, p trend = 0.98) and associated significantly with lower risk of high-grade cancer (Gleason 8-10; OR = 0.50, 95 % CI 0.26-0.98, p trend = 0.13). Risk of localized, grade 7, and low-grade cancers was not associated with coffee intake. This study provides some support of an inverse association between coffee and lethal and high-grade prostate cancer.

  • 89. Ye, W
    et al.
    Romelsjo, A
    Augustsson, Katarina
    Karolinska institutet, Sweden .
    Adami, H O
    Nyren, O
    No excess risk of colorectal cancer among alcoholics followed for up to 25 years2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 88, no 7, p. 1044-1046Article in journal (Refereed)
    Abstract [en]

    We conducted a population-based retrospective cohort study among 179 398 Swedish patients hospitalised for alcoholism from 1970 to 1994, and found no excess risk for colorectal cancers, overall or at any anatomical subsite. Our findings challenge the hypothesis that alcohol intake is a risk factor for cancer of the large bowel.

  • 90. Zheng, S. Lilly
    et al.
    Liu, Wennuan
    Wiklund, Fredrik
    Dimitrov, Latchezar
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Sun, Jielin
    Adami, Hans-Olov
    Johansson, Jan-Erik
    Sun, Jishan
    Chang, Baoli
    Loza, Matthew
    Turner, Aubrey R.
    Bleecker, Eugene R.
    Meyers, Deborah A.
    Carpten, John D.
    Duggan, David
    Isaacs, William B.
    Xu, Jianfeng
    Gronberg, Henrik
    A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study2006In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, no 14, p. 1556-1564Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. Recently identified associations of prostate cancer risk with several genes involved in innate immunity support a role of inflammation in the etiology of prostate cancer. Considering inflammation is regulated by a complex system of gene products, we hypothesize sequence variants in many other genes of this pathway are associated with prostate cancer. METHODS. We evaluated 9,275 SNPs; in 1,086 genes of the inflammation pathway using a MegAlleleTM genotyping system among 200 familial cases and 200 unaffected controls selected from a large Swedish case-control population (CAPS). RESULTS. We found that significantly more than the expected numbers of SNPs were significant at a nominal P-value of 0.01, 0.05, and 0.1, providing overall support for our hypothesis. The excess was largest when using a more liberal nominal P-value (0.1); we observed 992 significant SNPs compared with the 854 significant SNPs expected by chance, and this difference was significant based on a permutation test (P = 0.0025). We also began the effort of differentiating true associated SNPs by selecting a small subset of significant SNPs (N = 26) and genotyped these in an independent sample of similar to 1,900 CAPS1 subjects. We were able to confirm 3 of these 26 SNPs. It is expected that many more true associated SNPs will be confirmed among the 992 significant SNPs identified in our pathway screen. CONCLUSIONS. Our study provides the first objective support for an association between prostate cancer and multiple modest-effect genes in inflammatory pathways.

  • 91.
    Zheng, S. Lilly
    et al.
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Sun, Jielin
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Smith, Shelly
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Stattin, Par
    Univ Umea Hosp, Dept Urol, S-90185 Umea, Sweden..
    Li, Ge
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Hsu, Fang-Chi
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA.;Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA..
    Zhu, Yi
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Kader, A. Karim
    Wake Forest Univ, Bowman Gray Sch Med, Dept Urol, Winston Salem, NC 27157 USA..
    Turner, Aubrey R.
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Liu, Wennuan
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Bleecker, Eugene R.
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Meyers, Deborah A.
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Duggan, David
    Translat Genom Res Inst, Phoenix, AZ USA..
    Carpten, John D.
    Translat Genom Res Inst, Phoenix, AZ USA..
    Chang, Bao-Li
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Isaacs, William B.
    Johns Hopkins Med Inst, Baltimore, MD 21205 USA..
    Xu, Jianfeng
    Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Cumulative association of five genetic variants with prostate cancer2008In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 358, no 9, p. 910-919Article in journal (Refereed)
    Abstract [en]

    Background Single-nucleotide polymorphisms (SNPs) in five chromosomal regions -- three at 8q24 and one each at 17q12 and 17q24.3 -- have been associated with prostate cancer. Each SNP has only a moderate association, but when SNPs are combined, the association may be stronger. Methods We evaluated 16 SNPs from five chromosomal regions in a Swedish population (2893 subjects with prostate cancer and 1781 control subjects) and assessed the individual and combined association of the SNPs with prostate cancer. Results Multiple SNPs in each of the five regions were associated with prostate cancer in single SNP analysis. When the most significant SNP from each of the five regions was selected and included in a multivariate analysis, each SNP remained significant after adjustment for other SNPs and family history. Together, the five SNPs and family history were estimated to account for 46% of the cases of prostate cancer in the Swedish men we studied. The five SNPs plus family history had a cumulative association with prostate cancer (P for trend, 3.93x10(-28)). In men who had any five or more of these factors associated with prostate cancer, the odds ratio for prostate cancer was 9.46 (P=1.29x10(-8)), as compared with men without any of the factors. The cumulative effect of these variants and family history was independent of serum levels of prostate-specific antigen at diagnosis. Conclusions SNPs in five chromosomal regions plus a family history of prostate cancer have a cumulative and significant association with prostate cancer.

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