Anders Engeland

CONOR (COhort NORway) - en oversikt over en unik forskningsdatabank

A previous study has shown that variations in threshold and intensity (lipid goal attainment) of statins for primary prevention contribute to regional differences in overall consumption of statins in Norway. Our objective was to explore how differences in prevalences of use, dosing characteristics, choice of statin and continuity of therapy in individual patients adds new information to previous results.

Objectives: The present study aimed at exploring the relations between BMI and stature and colorectal and gallbladder cancer in a huge Norwegian cohort with measured height and weight. Material and methods: Height and weight were measured in two million Norwegian men and women aged 20–74 during 1963–2001. During follow-up, 47,117 colorectal and 1715 gallbladder cancer cases were registered. Relative risks (RRs) of colorectal and gallbladder cancer were estimated using Cox proportional hazards regression. Results: The risk of colon cancer increased with increasing BMI in men; the RR of colon cancer per unit increase in BMI was 1.04 (95% CI: 1.04–1.05). For mucinous colorectal adenocarcinomas, the risk increased to a larger extent with increasing BMI in both sexes. The RR of colorectal cancer associated with 10 cm increase in height was 1.14 (95% CI: 1.11–1.16) in men and 1.17 (95% CI: 1.14–1.20) in women. The risk of gallbladder cancer increased with increasing BMI in women; the overall RR associated with one unit increase in BMI was 1.06 (95% CI: 1.04–1.07). There was no association between height and gallbladder cancer in either sex. Conclusion: The risk of colon cancer increased with increasing BMI in men, and the risk of gallbladder cancer increased with increasing BMI in women. In both sexes, the risk of colon cancer increased with increasing height.

Objective: Associations between body mass index (BMI) and stature and cancers at different sites have been explored in a number of studies. For esophageal cancer there seems to be different effects of BMI for different histological subtypes. We explored these relations in a Norwegian cohort. Material and methods: Height and weight were measured in 2 million Norwegians during 1963-2001. Duringfollow-up, 2245 histologically verified esophageal cancer cases were registered. Relative risks (RR) of esophageal cancer were estimated using proportional Cox regression. Results: Compared with normal weighted (BMI 18.5-24.9 kg/m²) an increased risk of esophageal adenocarcinoma (OA) was observed in overweight men (BMI 25-29 kg/m²): RR=1.80 (95% CI: 1.48-2.19) and in obese men (BMI ≥30kg/m²): RR=2.58 (95% CI: 1.81-3.68). The corresponding risk estimates for women were RR=1.64 (95% CI: 1.08-2.49) and RR=2.06 (95% CI: 1.25-3.39). The opposite relation was observed for esophageal squamous cell carcinoma (OSCC). For overweight men the RR of OSCC was 0.72 (95% CI: 0.63-0.82) and 0.68 (95% CI: 0.50-0.93) for obese. The corresponding RR estimates for women were 0.52 (95% CI: 0.42-0.65) and 0.43 (95% CI: 0.32-0.59). In addition, the lowest men had the highest risk of esophageal cancer in general. Adjustment for smoking did not change these relations. Conclusion: BMI had opposite relations to the two most common histological groups of esophageal cancer. While low BMI increased the risk of OSCC, high BMI increased the risk of OA. An increased risk of esophageal cancer was found in the lowest men.

BACKGROUND There are few long-term follow-up data on the relation between body mass index (BMI) in adolescence and in adulthood, and between adolescent BMI and adult mortality. The present study explores these relations. In Norwegian health surveys during 1963-1999, height and weight were measured for 128,121 persons in a standardized way both in adolescence (age 14-19 years) and 10 or more years later. Persons were followed for an average of 9.7 years after the adult measurement. Cox proportional hazard regression models were used to study the association between adolescent and adult BMI and mortality. The odds ratio of obesity (BMI >/=30) in adulthood increased steadily with BMI in adolescence, from 0.2 for low BMI up to 16 for very high BMI. Very high adolescent BMI was associated with 30-40% higher adult mortality compared with medium BMI. Adjusting for adult BMI explained most of the association of adolescent obesity and mortality, especially among men. Adjustment for smoking did not change the results. Obesity in adolescence tends to persist into adulthood. Adolescent obesity is also connected to excess mortality, but this excess seems to be explained mostly by obesity in adulthood. High BMI in adolescence seems to be predictive of both adult obesity and mortality.

The present study explored body mass index (BMI), height, and risk of prostate cancer in a large Norwegian cohort of 950 000 men aged 20–74 years, whose height and weight were measured in a standardised way in the period 1963–1999. These were followed for an average of 21 years. The Cox proportional hazard models were used in the analyses. During follow-up, 33 300 histologically verified cases of prostate cancer were registered. The risk of prostate cancer increased by both BMI and height. The magnitude of the increase by BMI was modest, the relative risk (RR) of obese men (BMI30) compared with normal weighted was 1.09 (95% CI: 1.04–1.15). However, the RR at age 50–59 years was 1.58 (95% CI: 1.29–1.94) in men being obese at about age 45 years compared with normal weighted men. The tallest men had an RR of 1.72 (95% CI: 1.46–2.04) compared with the shortest men. The overall effect of BMI on the incidence of prostate cancer was modest. The larger effect found in men aged 50–59 years might partly explain the previous inconsistent findings.

Body mass index (BMI) has shown both positive and negative associations with ovarian cancer. Whether a possible association between height and ovarian cancer exists is unknown. We explored whether BMI and height were associated with ovarian cancer risk in a Norwegian cohort of approximately 1.1 million women, aged 14–74 years who were measured between 1963 and 1999. The cohort was followed for an average of 25 years through linkage to population-based cancer and death registries. Among the cohort, 7882 histologically verified cases of ovarian cancer were registered. Relative to women with a medium BMI (18.5–24.9 kg/m²), women who were overweight or obese in adolescence or young adulthood had an increased risk of ovarian cancer; women with a very high BMI in adolescence had a relative risk of 1.56 (95% confidence interval = 1.04 to 2.32) compared with women with medium BMI. No such association was seen in older women. A positive association between height and risk of ovarian cancer, particularly endometrioid ovarian cancer, was observed in women younger than 60 years of age.

The relation between body mass index (BMI) and mortality is not clear in the literature. An inverse relation between height and mortality has been suggested. We explore these relations in a very large cohort in Norway. We studied two million men and women, age 20–74 years, who were measured during 1963–2000. These persons were followed for an average of 22.1 years. We used Cox proportional hazard models in the analyses. Also, the optimal BMI (the BMI at the time of measurement that was subsequently related to the lowest mortality) was estimated. Over the study period, 723,000 deaths were registered. The relative risk of death by BMI showed a J- or U-shaped curve, with the lowest rates of death at BMI between 22.5 and 25.0. In men, the optimal BMI increased from 21.6 when measured at age 20–29 to 24.0 when measured at age 70–74. In women, the optimal BMI was consistently higher, increasing from 22.2 to 25.7. Mortality decreased with increased height in men; in women, mortality decreased with height only up to heights of about 160–164 cm and then increased among the tallest women. The relation between BMI and mortality was J- or U-shaped, with the “optimal” BMI varying by age and sex. Height was inversely related to mortality in men and in women up to a height of 165 cm.

A large number of studies have explored the relation between body mass index (BMI) and mortality in adults. The relation between BMI in adolescence and mortality has been investigated to a lesser extent. It has been suggested that all-cause mortality is elevated among those who were overweight during adolescence, but the limitation of previous studies has been study size. The present study explored this relation in a Norwegian cohort of 227,003 boys and girls, aged 14–19 years, whose height and weight were measured during tuberculosis screening in 1963–1975. These persons were followed for an average of 31.5 years (about 7.2 million person-years). A total of 7,516 deaths were registered. Multivariate Cox proportional hazards regression models were used in the analyses. An increasing risk of death by increasing BMI in adolescence was observed. Mortality among males whose baseline BMI was between the 85th and 95th percentiles and above the 95th percentile in the US reference population was 30% and 80% higher, respectively, than that among those whose baseline BMI was between the 25th and 75th percentiles. The corresponding rates among females were 30% and 100%. The excess mortality among adolescents whose BMI was high was not clearly manifested before they reached their thirties. Hence, BMI in adolescence is predictive of adult mortality.