scholarly journals Alcohol Consumption, HDL-Cholesterol and Incidence of Colon and Rectal Cancer: A Prospective Cohort Study Including 250,010 Participants

Author(s):  
Aage Tverdal ◽  
Gudrun Høiseth ◽  
Per Magnus ◽  
Øyvind Næss ◽  
Randi Selmer ◽  
...  

Abstract Aims Alcohol consumption has been linked to colorectal cancer (CRC) and also to the high-density lipoprotein cholesterol level (HDL-C). HDL-C has been associated with the incidence of CRC. The aim of this study was to investigate the association between self-reported alcohol consumption, HDL-C and incidence of CRC, separately for the two sites. Methods Altogether, 250,010 participants in Norwegian surveys have been followed-up for an average of 18 years with respect to a first-time outcome of colon or rectal cancer. During follow-up, 3023 and 1439 colon and rectal cancers were registered. Results For men, the HR per 1 drink per day was 1.05 with 95% confidence interval (0.98–1.12) for colon and 1.08 (1.02–1.15) for rectal cancer. The corresponding figures for women were 1.03 (0.97–1.10) and 1.05 (1.00–1.10). There was a positive association between alcohol consumption and HDL-C. HDL-C was inversely associated with colon cancer in men (0.74 (0.62–0.89) per 1 mmol/l) and positively associated with rectal cancer, although not statistically significant (1.15 (0.92–1.44). A robust regression that assigned weights to each observation and exclusion of weights ≤ 0.1 increased the HRs per 1 drink per day and decreased the HR per 1 mmol/l for colon cancer. The associations with rectal cancer remained unchanged. Conclusion Our results support a positive association between alcohol consumption and colon and rectal cancer, most pronounced for rectal cancer. Considering the positive relation between alcohol consumption and HDL-C, the inverse association between HDL-C and colon cancer in men remains unsettled.

2018 ◽  
Vol 119 (11) ◽  
pp. 1274-1285 ◽  
Author(s):  
Toril Bakken ◽  
Tonje Braaten ◽  
Anja Olsen ◽  
Anette Hjartåker ◽  
Eiliv Lund ◽  
...  

AbstractAccording to World Cancer Research Fund International/American Institute for Cancer Research, it is ‘probable’ that dairy products decrease the risk of colorectal cancer (CRC). However, meta-analyses restricted to women have not shown associations between milk intake and risk of CRC. The aim of this study was to examine the association between milk intake and risk of CRC, colon cancer and rectal cancer among women. Data from 81 675 participants in the Norwegian Women and Cancer Cohort Study were included, and multivariable Cox proportional hazard regression models were used to investigate milk intake using two different analytical approaches: one that included repeated measurements and one that included baseline measurements only (872 and 1084 CRC cases, respectively). A weak inverse association between milk intake and risk of colon cancer may be indicated both in repeated measurements analyses and in baseline data analyses. Hazard ratios (HR) for colon cancer of 0·80 (95 % CI 0·62, 1·03, Ptrend 0·07) and 0·81 (95 % CI 0·64, 1·01, Ptrend 0·03) and HR for rectal cancer of 0·97 (95 % CI 0·67, 1·42, Ptrend 0·92) and 0·71 (95 % CI 0·50, 1·01, Ptrend 0·03) were found when comparing the high with the no/seldom milk intake group in energy-adjusted multivariable models. Our study indicates that there may be a weak inverse association between milk intake and risk of colon cancer among women. The two analytical approaches yielded different results for rectal cancer and hence CRC. Our study indicates that the use of single or repeated measurements in analyses may influence the results.


2021 ◽  
Vol 8 (1) ◽  
pp. e000644
Author(s):  
Kari Hemminki ◽  
Asta Försti ◽  
Akseli Hemminki

ObjectivesGlobal survival studies have shown favourable development in colon and rectal cancers but few studies have considered extended periods or covered populations for which medical care is essentially free of charge.DesignWe analysed colon and rectal cancer survival in Finland and Sweden over a 50-year period (1967–2016) using data from the Nordcan database. In addition to the standard 1-year and 5-year survival rates, we calculated the difference between these as a novel measure of how well survival was maintained between years 1 and 5.ResultsRelative 1-year and 5-year survival rates have developed favourably without major shifts for men and women in both countries. For Finnish men, 1-year survival in colon cancer increased from 50% to 82%, and for rectal cancer from 62% to 85%. The Swedish survival was a few per cent unit better for 1-year survival but for 5-year survival the results were equal. Survival of female patients for both cancers was somewhat better than survival in men through 50 years. Overall the survival gains were higher in the early compared with the late follow-up periods, and were the smallest in the last 10 years. The difference between 1-year and 5-year survival in colon cancer was essentially unchanged over the 50-year period while in rectal cancer there was a large improvement.ConclusionsThe gradual positive development in survival suggests a contribution by many small improvements rather than single breakthroughs. The improvement in 5-year survival in colon cancer was almost entirely driven by improvement in 1-year survival while in rectal cancer the positive development extended to survival past year 1, probably due to successful curative treatments. The current challenges are to reinvigorate the apparently stalled positive development and to extend them to old patients. For colon cancer, survival gains need to be extended past year 1 of diagnosis.


Medicina ◽  
2021 ◽  
Vol 57 (4) ◽  
pp. 361
Author(s):  
Fatma Özpamuk-Karadeniz ◽  
Yusuf Karadeniz ◽  
Adnan Kaya ◽  
Servet Altay ◽  
Günay Can ◽  
...  

Background and objectives: Mortality may increase in hypouricemia as well as inhyperuricemia. We assessed the predictive value of low serum uric acid (SUA) levels on the risk of overall mortality or a composite endpoint of death and nonfatal events. Materials and Methods: In 1013 community-based middle-aged adults, free of uncontrolled diabetes and coronary heart disease at baseline, the association of sex-specific SUA tertiles with defined outcomes was evaluated prospectively by logistic regression, stratified to gender and presence of type-2 diabetes, using recent criteria. Results: Totally, 43 deaths and additional incident nonfatal events in 157 cases were recorded at a median 3.4 years’ follow-up. Multivariable linear regression disclosed SUA to be significantly associated among non-diabetic individuals positively with creatinine, triglycerides, and body mass index in women further with fasted glucose. In multivariable-adjusted logistic regression analysis, sex-specifically dichotomized baseline uric acid (<5.1 and <4.1 mg/dL vs. higher values) significantly predicted the non-fatal events in the whole sample (relative risk (RR) 1.51 [95% confidence interval (CI) 1.02; 2.26]), as well as in men, while composite endpoint in the whole sample tended to rise (RR 1.38). Compared with the intermediate one, the top and bottom SUA tertiles combined tended to confer mortality risk (RR 2.40 [95% CI 0.89; 6.51]). Adverse outcomes in diabetic women were predicted by tertiles 2 and 3. Conclusions: Inverse association of SUA with adverse outcomes, especially in men, is consistent with the involvement of uric acid mass in autoimmune activation. The positive association of uric acid with adverse outcomes in diabetic women is likely mediated by concomitant high-density lipoprotein dysfunction.


2018 ◽  
Vol 108 (6) ◽  
pp. 1283-1290 ◽  
Author(s):  
Eke G Gruppen ◽  
Stephan J L Bakker ◽  
Richard W James ◽  
Robin P F Dullaart

ABSTRACT Background Paraoxonase-1 (PON-1) is a high-density lipoprotein (HDL)-associated enzyme with antioxidative properties, which may protect against the development of cardiovascular disease. Alcohol consumption increases HDL cholesterol, but the extent to which alcohol consumption gives rise to higher serum PON-1 activity is uncertain. Objective In a population-based study, we determined the relation of serum PON-1 activity with alcohol consumption when taking account of HDL cholesterol and apolipoprotein A-I (apoA-I), its major apolipoprotein. Design A cross-sectional study was performed in 8224 participants of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort. Alcohol consumption was categorized as 1) no/rarely (25.3%); 2) 0.1–10 g/d (49.3%); 3) 10–30 g/d (20.1%); and 4) >30 g/d (5.2%) with 1 drink equivalent to 10 g alcohol. Serum PON-1 activity was measured as its arylesterase activity (phenyl acetate as substrate). Results Median serum PON-1 activity was 50.8, 53.1, 54.4, and 55.7 U/L in the 4 categories of alcohol consumption, respectively (P < 0.001). Its increase paralleled the increments in HDL cholesterol and apoA-I. Notably, there was no further increase in PON-1 activity, HDL cholesterol, and apoA-I when alcohol consumption was increased from 10–30 g/d to >30 g/d. Multivariable linear regression analysis demonstrated that PON-1 activity was related to alcohol consumption independently from clinical covariates, high sensitivity C-reactive protein, and lipid concentrations, including HDL cholesterol (P < 0.001 for each category of alcohol consumption with no alcohol consumption as the reference category). Notably, as inferred from standardized β-coefficients, there was no difference in PON-1 activity between 10–30 g alcohol/d and >30 g alcohol/d. Conclusions Alcohol consumption is associated with an increase in serum PON-1 activity, but its effect seems to reach a plateau with alcohol consumption of 10–30 g/d.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lei Kuang ◽  
Nathan.D Wong

Introduction: The protective relation of high density lipoprotein-cholesterol (HDL-C) with coronary heart disease may be weakened in the presence of inflammation; however, whether inflammation may attenuate any association of HDL-C with peripheral arterial disease (PAD) is unknown. Hypothesis: We hypothesized that inflammation measured by high-sensitivity C-reactive protein (hs-CRP) will attenuate any inverse association of HDL-C with PAD. Methods: We studied 6512 men and women aged ≥ 40 years who participated in the National Health and Nutrition Examination Survey (NHANES ) from 1999-2004 who had measures of ankle brachial index (positive for PAD defined as <0.9 or ≥1.5), lipids, high-sensitivity CRP (hs-CRP) and other risk factors. Groups were categorized by low (<40 mg/dL for men or <50 mg/dl or women), intermediate (40 or 50-59 mg/dL), and high (≥60 mg/dL) HDL-C, and low (<1 mg/L), normal (1-3), and high (3 mg/L) hs-CRP levels. We evaluated the odds ratio (ORs) for PAD by logistic regression adjusted for age, race, gender, low density lipoprotein-cholesterol, smoking, diabetes, body mass index, systolic blood pressure waist circumference and triglycerides. Results: Those with the highest hs-CRP levels had the highest prevalence of PAD (8.5-10.8%), regardless of level of HDL-C (figure 1). Using high HDL-C/low hs-CRP as the reference, the likelihood of PAD was significantly increased among those with normal and high hs-CRP within the intermediate HDL-C group: OR 4.7 (95%CI 1.6, 14.1) and OR 4.5 (95% CI 1.4,14.2) , respectively. Among those with normal and high hs-CRP within the low HDL-C group, the likelihood of PAD was also increased:OR 5.0 (95% CI 2.1,12,1) and OR 6.4 (95% CI 2.2,18.1), respectively. Conclusion: High hs-CRP is associated with higher likelihood of PAD across all ranges of HDL-C, but especially when HDL-C is normal or low. These results support the value of combined hs-CRP and HDL-C in risk stratification for PAD which should be validated by prospective studies.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Catherine Rahilly-Tierney ◽  
Howard D Sesso ◽  
J. Michael Gaziano ◽  
Luc Djousse

BACKGROUND: Few studies have examined prospectively the relationship between baseline high-density lipoprotein (HDL) cholesterol and longevity. OBJECTIVES: We sought to examine whether higher HDL levels were associated with lower risk of all-cause, cardiovascular (CVD), and non-CVD mortality prior to age 90 in the Physicians’ Health Study (PHS). METHODS: We considered a baseline cohort of 1351 PHS participants who provided bloods between 1997 and 2001 and were old enough to reach age 90 by March 4, 2009. Included subjects had complete baseline data on HDL and total cholesterol; lifestyle factors including smoking, exercise, alcohol consumption, and BMI; and comorbidities including hypertension, diabetes mellitus, congestive heart failure, cancer, and stroke. We used Cox proportional hazards to determine the HRs and 95% CIs for all-cause, CVD, and non-CVD mortality prior to age 90, adjusting for baseline age, co-morbidities, and non-HDL cholesterol. RESULTS: At baseline, the cohort had a mean (SD) age of 81.9 (2.9) years and a mean (SD) HDL cholesterol of 44.8(16.5) mg/dL. After a mean follow-up of 6.8 years (maximum 12.3 years), 501 (37.1%) of men died prior to age 90. In multi-variable adjusted analyses, men in the highest HDL-C quartile (≥54.1 mg/dL) had a 28% lower risk (HR 0.72, 95% CI 0.55-0.95) of all-cause mortality prior to age 90 compared to men in the lowest HDL-C quartile (<32.8 mg/dL). From the lowest to highest HDL quartile, age-adjusted HR(95%CI) for CVD mortality prior to age 90 were 0.66 (0.44-0.99), 0.58 (0.38-0.90), and 0.53 (0.34-0.82) (p for trend 0.004). There was no significant association between baseline HDL cholesterol and non-CVD death. CONCLUSION: In a cohort of older male physicians with long-term follow-up, baseline HDL cholesterol was inversely associated with the risk of dying prior to age 90, largely explained by an inverse association between HDL and CVD mortality.


Mutagenesis ◽  
2019 ◽  
Vol 35 (3) ◽  
pp. 207-219
Author(s):  
Hongyao Yu ◽  
Kari Hemminki

Abstract We review here data on familial risk in colorectal cancer (CRC) generated from the Swedish Family-Cancer Database, the largest resource of its kind in the world. Although the concordant familial risk for CRC (i.e. CRC risk in families of CRC patients) has been reasonably well established, the studies on discordant familial risks (i.e. CRC risk in families with any other cancers) are rare. Because different cancers could be caused by shared genetic susceptibility or shared environment, data of associations of discordant cancers may provide useful information for identifying common risk factors. In analyses between any of 33 discordant cancers relative risks (RRs) for discordant cancers were estimated in families with increasing numbers of probands with CRC; in the reverse analyses, RRs for CRC were estimated in families with increasing numbers of probands with discordant cancers. In separate analyses, hereditary non-polyposis colorectal cancer (HNPCC) families were excluded from the study, based on HNPCC related double primary cancers, to assess the residual familial RRs. We further reviewed familial risks of colon and rectal cancers separately in search for distinct discordant associations. The reviewed data suggested that colon cancer was associated with a higher familial risk for CRC compared to rectal cancer. The previous data had reported associations of CRC with melanoma, thyroid and eye cancers. Nervous system cancer was only associated with colon cancer, and lung cancer only associated with rectal cancer. The reviewed data on discordant association may provide guidance to gene identification and may help genetic counseling.


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Wahyu Wulaningsih ◽  
Hans Garmo ◽  
Lars Holmberg ◽  
Niklas Hammar ◽  
Ingmar Jungner ◽  
...  

Background. Metabolic syndrome has been linked to an increased cancer risk, but the role of dyslipidaemia in gastrointestinal malignancies is unclear. We aimed to assess the risk of oesophageal, stomach, colon, and rectal cancers using serum levels of lipid components.Methods. From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected 540,309 participants (> 20 years old) with baseline measurements of total cholesterol (TC), triglycerides (TG), and glucose of whom 84,774 had baseline LDL cholesterol (LDL), HDL cholesterol (HDL), apolipoprotein B (apoB), and apolipoprotein A-I (apoA-I). Multivariate Cox proportional hazards regression was used to assess glucose and lipid components in relation to oesophageal, stomach, colon, and rectal cancer risk.Results. An increased risk of oesophageal cancer was observed in persons with high TG (e.g. HR: 2.29 (95% CI: 1.42–3.68) for the 4th quartile compared to the 1st) and low LDL, LDL/HDL ratio, TC/HDL ratio, log (TG/HDL), and apoB/apoA-I ratio. High glucose and TG were linked with an increased colon cancer risk, while high TC levels were associated with an increased rectal cancer risk.Conclusion. The persistent link between TC and rectal cancer risk as well as between TG and oesophageal and colon cancer risk in normoglycaemic individuals may imply their substantiality in gastrointestinal carcinogenesis.


BMJ Open ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. e035556
Author(s):  
Heigo Reima ◽  
Jaan Soplepmann ◽  
Anneli Elme ◽  
Mari Lõhmus ◽  
Rena Tiigi ◽  
...  

ObjectivesLarge disparities in colorectal cancer (CRC) management and survival have been observed across Europe. Despite recent increases, the survival deficit of Estonian patients with CRC persists, particularly for rectal cancer. The aim of this study was to examine diagnostic, staging and treatment patterns of CRC in Estonia, comparing clinical data from 1997 and 2011.DesignNationwide population-based retrospective study.SettingEstonia.ParticipantsAll incident cases of colon and rectal cancer diagnosed in 1997 and 2011 identified from the Estonian Cancer Registry. Clinical data gathered from medical records.Outcome measuresDifferences in diagnostic, staging and treatment patterns; 5-year relative survival ratios.ResultsThe number of colon cancer cases was 337 in 1997 and 498 in 2011; for rectal cancer, the respective numbers were 209 and 349. From 1997 to 2011, large increases were seen in the use of colonoscopy and lung and liver imaging. Radical resection rate increased from 48% to 59%, but emergency surgeries showed a rise from 18% to 26% in colon and from 7% to 14% in rectal cancer. The proportion of radically operated patients with ≥12 lymph nodes examined pathologically increased from 2% to 58% in colon cancer and from 2% to 50% in rectal cancer. The use of neoadjuvant radiotherapy increased from 6% to 39% among stage II and from 20% to 50% among patients with stage III rectal cancer. The use of adjuvant chemotherapy in stage III colon cancer increased from 42% to 63%. The 5-year RSR increased from 50% to 58% in colon cancer and from 37% to 64% in patients with rectal cancer.ConclusionsMajor improvements were seen in the diagnostics, staging and treatment of CRC in Estonia contributing to better outcomes. Increase in emergency surgeries highlights possible shortcomings in timely diagnosis and treatment.


2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 468-468
Author(s):  
John Hogan ◽  
Kathryn Dejulius ◽  
Xiaoxia Li ◽  
John Calvin Coffey ◽  
Matthew Kalady

468 Background: Dissimilarity exists between colon and rectal cancer at a genetic, clinical, and molecular level. This is likely to reflect variation at a transcriptomic level. Transcriptional studies of colorectal cancer have previously combined colonic and rectal adenocarcinoma in a single group. Consequently few studies accurately describe the transcriptional profile of colon and/or rectal cancer. This study aims to develop classifiers based on transcriptomic differences between colon and rectal cancer and utilize these classifiers to predict tumor origin (colon vs. rectum). Methods: Comparisons were made between cDNA microarrays derived from colon (87) and rectal (125) adenocarcinomas. Gene expression data was filtered according to standard deviation to retain only highly dysregulated genes. Genes differentially expressed between colon and rectal adenocarcinoma were identified on two groups t test (p<0.05, Bonferroni p value adjustment) and further analysed. Genes were rank ordered in terms of descending fold change. Comparisons included a) colon adenocarcinoma vs. rectal adenocarcinoma (stages I - III), b) stage II colon adenocarcinoma vs. stage II rectal adenocarcinoma and c) stage III colon adenocarcinoma vs. stage III rectal adenocarcinoma. For each comparison, those five genes with the greatest positive fold change were grouped in a classifier. Five separate tests were applied to evaluate the discriminatory capacity of each classifier and summary receiver operating characteristic curves generated for each classifier. Results: Genetic classifiers dervied from a comparison of stage II colon and stage II rectal adenocarcinoma were the most accurate in distinguishing tumor type (mean sensitivity 82.5%, mean specificity 81.7%). Classifiers derived from a pooled analysis comparing colon and rectal cancers (stages I - III) (mean sensitivity 79.8%, mean specificity 71.1%) and those derived from a comparison of stage III colon and stage III rectal cancers (mean sensitivity 57.1%, mean specificity 98.6%) were also accurate in determining tumor type (colon vs. rectum). Conclusions: Colon and rectal adenocarcinoma differs at a transcriptomic level. These findings provide insight into underlying biologic differences.


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