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Purpose: Lifestyle-related conditions such as obesity are associated with prostate cancer progression, but the associations with hyperglycemia and dyslipidemia are unclear. This study, therefore, aims to examine the association of glucose, triglycerides, and total cholesterol with prostate cancer death., Methods: From the Swedish AMORIS cohort, we selected 14,150 men diagnosed with prostate cancer between 1996 and 2011 who had prediagnostic measurements of serum glucose, triglycerides, and total cholesterol. Multivariable Cox proportional hazards regression models were used to determine the hazard ratios for death in relation to the aforementioned metabolic markers., Results: Using clinical cut-off points, a non-significant positive association was observed between glucose and prostate cancer death. When compared to those with glucose in the lowest quartile, those in the highest quartile had greater risk of prostate cancer death (HR 1.19; 95% CI 1.02-1.39). However, neither total cholesterol nor triglycerides were associated with prostate cancer death. Glucose and triglycerides were positively associated with overall, cardiovascular, and other deaths. Hypercholesterolemia was only associated with risk of CVD death., Conclusion: Our results suggest that glucose levels may influence prostate cancer survival, but further studies using repeated measurements are needed to further elucidate how glucose levels may influence prostate cancer progression.

Lifestyle-related risk factors such as hyperglycemia and dyslipidemia have been associated with several cancers. However, studies exploring their link with prostate cancer (PCa) clinicopathological characteristics are sparse and inconclusive. Here, we investigated the associations between serum metabolic markers and PCa clinicopathological characteristics. The study comprised 14,294 men from the Swedish Apolipoprotein MOrtality RISk (AMORIS) cohort who were diagnosed with PCa between 1996 and 2011. Univariate and multivariable logistic regression were used to investigate the relation between glucose, triglycerides and total cholesterol and PCa risk categories, PSA, Gleason score, and T-stage. Mean age at time of PCa diagnosis was 69 years. Men with glucose levels >6.9 mmol/L tend to have PSA<4 μg/L, while those with glucose levels of 5.6-6.9 mmol/L had a greater odds of PSA>20 μg/L compared to PSA 4.0-9.9 μg/L. Hypertriglyceridemia was also positively associated with PSA>20 μg/L. Hyperglycemic men had a greater odds of intermediate- and high-grade PCa and advanced stage or metastatic PCa. Similarly, hypertriglyceridemia was positively associated with high-grade PCa. There was also a trend toward an increased odds of intermediate risk localized PCa and advanced stage PCa among men with hypertriglyceridemia. Total cholesterol did not have any statistically significant association with any of the outcomes studied. Our findings suggest that high serum levels of glucose and triglycerides may influence PCa aggressiveness and severity. Further investigation on the role of markers of glucose and lipid metabolism in influencing PCa aggressiveness and severity is needed as this may help define important targets for intervention., (© 2016 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

With exception of cholesterol and total fat intake, associations between lipid biomarkers and kidney cancer have not often been researched. We aimed to assess possible links between lipid profiles and kidney cancer risk in a large prospective cohort study, while also taking into account glucose levels and BMI. A cohort based on 542,924 persons with baseline information on glucose, triglycerides (TGs), total cholesterol (TC) and creatinine was selected from the Swedish Apolipoprotein Mortality Risk study. A subgroup of 85,621 also had baseline measurements of HDL, LDL, apolipoprotein A-I and apoB. Multivariate Cox proportional hazard models were used to analyze associations between quartiles and dichotomized values of these lipid components and kidney cancer risk. During a mean follow-up of 13 years, 958 persons developed kidney cancer. TGs were the only lipid component for which a statistically significant association was found with kidney cancer risk when using both quartiles and a clinical cutoff (hazard ratio: 1.25 (95% CI: 0.99-1.60), 1.29 (1.01-1.66) and 1.66 (1.30-2.13) for the 2nd, 3rd and 4th quartile, compared to the 1st, with p-value for trend: <0.001). The association remained after exclusion of the 95% percentile of TG. Quartiles of glucose were also positively associated with kidney cancer risk, whereas quartiles of TC were negatively associated with kidney cancer risk. This detailed analysis of lipid components only showed a consistent relation between TG levels and kidney cancer risk. Further mechanistic studies are required to assess links between lipid abnormalities and kidney cancer., (Copyright © 2011 UICC.)

Background: In a cohort including 5112 prostate cancer (pCa) patients, the authors investigated associations among triglycerides (TG), total cholesterol (TC), and pCa while taking into account glucose., Methods: A cohort (n = 200,660) based on 4 groups of men, according to age at cohort entry, with TG, TC, and glucose measurements was selected from the Apolipoprotein MOrtality RISk (AMORIS) database. Of these, 5112 men developed pCa. Multivariate Cox proportional hazard models were used to analyze associations among TG, TC, and pCa. Competing risks were assessed graphically., Results: Age-stratified analyses for quartiles of TG, TC, and glucose showed a negative association between glucose and pCa risk (HR, 0.93; 95% CI, 0.86-1.01), 0.93 (0.86-1.01), 0.87 (0.81-0.94) for the second, third, and fourth quartiles compared with the first (P(trend) = .001). Stratified analysis by glucose levels (<6.11 or ≥ 6.11 mmol/L) showed a positive association between hypertriglyceridemia (TG ≥ 1.71 mmol/L) and pCa risk, when there were high glucose levels (HR, 1.23; 95% CI, 1.01-1.48). No association was found for hypercholesterolemia (TC ≥ 6.50 mmol/L). Competing risk analysis showed that protective effects of glucose were overestimated in conventional Cox proportional hazard models and strengthened positive findings between TG and pCa risk., Conclusions: The authors'; findings supported the hypothesis that factors of the glucose and lipid metabolism influence pCa risk. Competing risk assessment showed that it is important to take into account the long natural history and age distribution of pCa when interpreting results. The authors'; findings indicate another reason to fight the increasing prevalence of obesity and dyslipidemia., (2010 American Cancer Society.)

Aims: To describe trajectories for metabolic risk factors for type 2 diabetes (T2D) up to 25 years prior to diagnosis and to estimate the absolute 20‐year risk for T2D based on a simple set of commonly measured key risk factors. Methods: From the Swedish AMORIS cohort we included 296 428 individuals with data on fasting glucose obtained in health examinations during 1985–1996 (baseline period). All participants were followed until 2012 for development of incident T2D. The 20‐year T2D risk based on age, sex, body mass index (BMI), fasting glucose and triglycerides was estimated. Trajectories for biomedical risk factors of T2D starting from >20 years before diagnosis and including fasting glucose, triglycerides and BMI were evaluated according to yearly means for cases and controls. Results: We identified 28 244 new T2D cases during the study period, with an average 20‐year risk of 8.1%. This risk was substantially increased in overweight and obese participants and those with elevated fasting glucose and triglyceride levels, in both men and women. T2D cases had higher mean BMI and fasting glucose and triglyceride levels compared with controls >20 years before diagnosis and the difference in fasting glucose levels increased over time. Conclusions: Development of T2D is associated with subtle elevations in glucose and lipid levels >20 years before diagnosis. This suggests that diabetogenic processes tied to chronic insulin resistance operate for decades prior to the development of T2D. A simple risk classification can help in early identification of individuals who are at increased risk. [ABSTRACT FROM AUTHOR]

Background: The lipid and glucose metabolisms are postulated as possible intermediary mechanisms in linking obesity and breast cancer (BC). Links between serum lipid and glucose biomarkers and BC risk has been observed in the Swedish Apolipoprotein MORtality RISk (AMORIS) cohort. We conducted a follow-up analysis including information on tumour characteristics.Methods: One thousand eight hundred twenty-four women diagnosed with BC, with serum biomarker levels of glucose, triglycerides, cholesterol (total, HDL, and LDL), and apolipoproteins A-1 and B recorded in a routine health check at baseline were included. BC severity was split into categories (good, moderate, and poor prognosis) based on ER status, TNM stage, and age at diagnosis. Proportional odds models were used to obtain odds ratios (ORs) and 95% confidence intervals (CI), with the interval time between baseline measurement and BC diagnosis accounted for.Results: Serum glucose and the ApoB/ApoA-1 ratio showed a non-statistically significant positive association with BC severity (proportional OR: 1.25 (95%CI: 0.92-1.70) for glucose (Conclusions: Despite the size and detail of data in AMORIS, we only found a modest positive association between serum levels of glucose, apoB/ApoA-1 and BC severity, suggesting that these factors are not the main players in linking obesity and BC aggressiveness. [ABSTRACT FROM AUTHOR]

Background: The role of cholesterol levels in the development of atrial fibrillation (AF) is still controversial. In addition, whether and to what extent apolipoproteins are associated with the risk of AF is rarely studied. In this study, we aimed to investigate the association between blood lipid levels in midlife and subsequent risk of new-onset AF.Methods and Findings: This population-based study included 65,136 individuals aged 45 to 60 years without overt cardiovascular diseases (CVDs) from the Swedish Apolipoprotein-Related Mortality Risk (AMORIS) cohort. Lipids were measured in 1985 to 1996, and individuals were followed until December 31, 2019 for incident AF (i.e., study outcome). Hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated using Cox regression, adjusting for age, sex, and socioeconomic status. Over a mean follow-up of 24.2 years (standard deviation 7.5, range 0.2 to 35.9), 13,871 (21.3%) incident AF cases occurred. Higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) were statistically significantly associated with a lower risk of AF during the first 5 years of follow-up (HR = 0.61, 95% CI: 0.41 to 0.99, p = 0.013; HR = 0.64, 95% CI: 0.45 to 0.92, p = 0.016), but not thereafter (HR ranging from 0.94 [95% CI: 0.89 to 1.00, p = 0.038] to 0.96 [95% CI: 0.77 to 1.19, p > 0.05]). Lower levels of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (ApoA-I) and higher triglycerides (TG)/HDL-C ratio were statistically significantly associated with a higher risk of AF during the entire follow-up (HR ranging from 1.13 [95% CI: 1.07 to 1.19, p < 0.001] to 1.53 [95% CI: 1.12 to 2.00, p = 0.007]). Apolipoprotein B (ApoB)/ApoA-I ratio was not associated with AF risk. The observed associations were similar among those who developed incident heart failure (HF)/coronary heart disease (CHD) and those who did not. The main limitations of this study include lack of adjustments for lifestyle factors and high blood pressure leading to potential residual confounding.Conclusions: High TC and LDL-C in midlife was associated with a lower risk of AF, but this association was present only within 5 years from lipid measurement and not thereafter. On the contrary, low HDL-C and ApoA-I and high TG/HDL-C ratio were associated with an increased risk of AF over almost 35 years of follow-up. ApoB/ApoA-I ratio was not associated with AF risk. [ABSTRACT FROM AUTHOR]

Background. Few studies have analysed the importance of haptoglobin (Hp) as a risk factor for acute myocardial infarction (AMI), stroke, and heart failure (HF) in large healthy populations. Aims. We examined Hp as risk factor for AMI, stroke, and HF in the Apolipoprotein MOrtality RISk (AMORIS) Study and compared its predictive strength with that of total serum cholesterol (TC). Methods. Prospective study (11.8 years) of AMI, stroke, and HF through linkage with Swedish hospital discharge and mortality registers with measurements of Hp in 342,125 subjects. Results. Hp is a significant risk factor of AMI, stroke, and HF. Relationships were stronger for men than women with regard to stroke and HF, but not AMI. Hp was almost as predictive as TC for AMI and about equally predictive of stroke with a stronger relationship to ischaemic than haemorrhagic stroke. A 4.2-fold increase in risk of AMI was observed comparing subjects in the joint lower quartiles of TC and Hp to those in the upper. For stroke, the risk increase was 2-fold, and 1.5-fold for HF. Interpretation. The inflammation marker Hp carried as much additional predictive information value on AMI and stroke as TC. Hp was also a risk factor of HF. [ABSTRACT FROM AUTHOR]

Hypercholesterolemia and hypertriglyceridemia are risk factors for cardiovascular disease. The potentially atherogenic very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), large buoyant, and small dense low-density lipoprotein (LDL) particles are all transported by apolipoprotein (apo) B, one protein per particle. The anti-atherogenic HDL contains apoA-I. In the apolipoprotein-related mortality risk (AMORIS) study, 98,722 males and 76,831 females aged 20–80 years were investigated at health check-ups. They were followed for 98 months, and 1267 males and 586 females died from myocardial infarction. The aim of the study is to investigate if apoB and apoA-I are more closely related to cardiac risk than lipids. The most common lipid phenotype in those who died was combined hypercholesterol- and hypertriglyceridemia (type IIB, 48%), followed by isolated hypercholesterolemia (type IIA, 40%). However, irrespective of lipid phenotype, and also in subjects with normal lipids, the highest CV risk was seen in those with a high apoB/apoA-I (>0.9 in males, >0.8 in females) compared with those with values below these cut-points. It is concluded that the balance of apoB/apoA-I is a simple and precise indicator strongly reflecting CV risk irrespective of lipid levels or combinations of lipids. [Copyright &y& Elsevier]

Background: Lipoproteins are associated with acquired aortic valve stenosis (AS). This study investigated whether an elevated apolipoprotein (apo)B/apoA-1 ratio was associated with an increased risk of AS and if this association was influenced by a history of a major adverse cardiovascular event (MACE) defined as stroke, myocardial infarction or revascularisation.Methods: A study was undertaken of 131,816 individuals, aged ≥30 years, from the Swedish Apolipoprotein MOrtality RISk (AMORIS) cohort, with measurements of apolipoproteins B and A-1 at health examinations during 1985-1996.Results: There were fewer women and the average age was 4 years older in the highest apoB/apoA-1 quintile compared with the lowest. Being overweight, having reduced renal function and diabetes mellitus were more frequent. Low-density lipoprotein cholesterol, triglyceride and apolipoprotein B levels were higher in the top apoB/apoA-1 quintile. During follow-up through 2011, non-rheumatic aortic valve disease was diagnosed in 2,999 individuals (2.3%). Using ICD-10 codes from 1997, AS was identified in 1,887 patients. An elevated apoB/apoA-1 ratio was associated with an increased incidence of aortic valve disease after multivariable adjustment [hazard ratio (HR) (95% CI) for the fifth vs first quintile of 1.28 (1.09-1.50)]. Restricting the analyses to incident AS during 1997-2011 yielded an HR of 1.41 (1.15-1.72). This increased incidence was primarily seen in women and individuals aged ≥65 years. History of MACE did not influence these associations.Conclusions: An elevated apoB/apoA-1 ratio was associated with an increased incidence of AS, particularly in women and individuals aged ≥65 years, regardless of previous MACE. [ABSTRACT FROM AUTHOR]