scholarly journals Phosphate and Oxysterols May Mediate an Inverse Relationship Between Atherosclerosis and Cancer

EMJ Oncology ◽  
2020 ◽  
pp. 114-121
Author(s):  
Ronald B. Brown

The peer-reviewed literature has reported an inverse relationship between atherosclerosis and cancer for almost 100 years, but no causative mechanism has been established to explain this puzzling relationship. More recent research has reported an association between tumourigenesis and phosphate toxicity from dysregulated phosphate metabolism, and an association has also been reported between atherosclerosis and cholesterol oxidation products or oxysterols. The present review article synthesises these research findings and proposes that an inverse relationship between the associated risk of cancer and atherosclerosis may be mediated by tumourigenic and atherogenic dietary patterns containing inverse proportions of dietary phosphate and oxysterols. Low-fat animal-based foods generally have reduced cholesterol and oxysterol levels and relatively higher protein and phosphate levels, and dietary patterns containing these foods are associated with reduced atherosclerosis risk and increased cancer risk. By comparison, full-fat animal-based foods are higher in cholesterol and oxysterols and relatively lower in protein and phosphate, and dietary patterns containing these foods are associated with increased atherosclerosis risk and reduced cancer risk. Fruits, vegetables, and plant-based fats generally have lower phosphate levels and no cholesterol, and dietary patterns associated with increased amounts of these foods, such as the Mediterranean diet, reduce risk for both cancer and cardiovascular disease.

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2614
Author(s):  
Solbak ◽  
Al Rajabi ◽  
Akawung ◽  
Lo Siou ◽  
Kirkpatrick ◽  
...  

The objective of this study was to determine the influence of strategies of handling misestimation of energy intake (EI) on observed associations between dietary patterns and cancer risk. Data from Alberta’s Tomorrow Project participants (n = 9,847 men and 16,241 women) were linked to the Alberta Cancer Registry. The revised-Goldberg method was used to characterize EI misestimation. Four strategies assessed the influence of EI misestimation: Retaining individuals with EI misestimation in the cluster analysis (Inclusion), excluding before (ExBefore) or after cluster analysis (ExAfter), or reassigning into ExBefore clusters using the nearest neighbor method (InclusionNN). Misestimation of EI affected approximately 50% of participants. Cluster analysis identified three patterns: Healthy, Meats/Pizza and Sweets/Dairy. Cox proportional hazard regression models assessed associations between the risk of cancer and dietary patterns. Among men, no significant associations (based on an often-used threshold of p < 0.05) between dietary patterns and cancer risk were observed. In women, significant associations were observed between the Sweets/Dairy and Meats/Pizza patterns and all cancer risk in the ExBefore (HR (95% CI): 1.28 (1.04–1.58)) and InclusionNN (HR (95% CI): 1.14 (1.00–1.30)), respectively. Thus, strategies to address misestimation of EI can influence associations between dietary patterns and disease outcomes. Identifying optimal approaches for addressing EI misestimation, for example, by leveraging biomarker-based studies could improve our ability to characterize diet-disease associations.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Yasmin Bylstra ◽  
Weng Khong Lim ◽  
Sylvia Kam ◽  
Koei Wan Tham ◽  
R. Ryanne Wu ◽  
...  

Abstract Background Family history has traditionally been an essential part of clinical care to assess health risks. However, declining sequencing costs have precipitated a shift towards genomics-first approaches in population screening programs rendering the value of family history unknown. We evaluated the utility of incorporating family history information for genomic sequencing selection. Methods To ascertain the relationship between family histories on such population-level initiatives, we analysed whole genome sequences of 1750 research participants with no known pre-existing conditions, of which half received comprehensive family history assessment of up to four generations, focusing on 95 cancer genes. Results Amongst the 1750 participants, 866 (49.5%) had high-quality standardised family history available. Within this group, 73 (8.4%) participants had an increased family history risk of cancer (increased FH risk cohort) and 1 in 7 participants (n = 10/73) carried a clinically actionable variant inferring a sixfold increase compared with 1 in 47 participants (n = 17/793) assessed at average family history cancer risk (average FH risk cohort) (p = 0.00001) and a sevenfold increase compared to 1 in 52 participants (n = 17/884) where family history was not available (FH not available cohort) (p = 0.00001). The enrichment was further pronounced (up to 18-fold) when assessing only the 25 cancer genes in the American College of Medical Genetics (ACMG) Secondary Findings (SF) genes. Furthermore, 63 (7.3%) participants had an increased family history cancer risk in the absence of an apparent clinically actionable variant. Conclusions These findings demonstrate that the collection and analysis of comprehensive family history and genomic data are complementary and in combination can prioritise individuals for genomic analysis. Thus, family history remains a critical component of health risk assessment, providing important actionable data when implementing genomics screening programs. Trial registration ClinicalTrials.gov NCT02791152. Retrospectively registered on May 31, 2016.


2021 ◽  
Vol 10 (1) ◽  
pp. 153
Author(s):  
Hong Jin Yoon ◽  
Jie-Hyun Kim ◽  
Gi Hyeon Seo ◽  
Hyojin Park

N-nitrosodimethylamine (NDMA), a known carcinogenic agent, was recently detected in some products of ranitidine. Several studies have investigated the detectability of NDMA, in drugs and their risks. However, only a few epidemiological studies have evaluated cancer risk from the use of such individual drugs. This study investigates the risk of cancer in ranitidine users. We conducted an observational population-based cohort study using the Health Insurance Review and Assessment databases, which contain information about the use of medicines in South Korea. The primary study cohort consisted of ranitidine users (n = 88,416). For controls, we enrolled users of famotidine, another H2-receptor antagonist in which no NDMA has been detected. A 4:1 matched cohort was constructed to compare cancer outcomes of the two groups. Our matched cohort comprised of 40,488 ranitidine users and 10,122 famotidine users. There was no statistical difference in the overall cancer risk between the ranitidine and famotidine groups (7.45% vs. 7.56%, HR 0.99, 95% CI 0.91–1.07, p = 0.716). Additionally, no significant differences were observed in the analysis of 11 single cancer outcomes. We found no evidence that exposure to NDMA through ranitidine increases the risk of cancer.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.C Van 't Klooster ◽  
P.M Ridker ◽  
N.R Cook ◽  
J.G.J.V Aerts ◽  
J Westerink ◽  
...  

Abstract Background As treatment for cardiovascular disease (CVD) has improved substantially over the last decades, more patients survive acute CVD manifestations and are at risk for developing cancer as well as recurrent CVD. Due to similar risk factors, including smoking and obesity, patients with established CVD are at higher risk for cancer. Objectives The aim of this study was to develop and externally validate prediction models for the estimation of 10-year and lifetime risk for total, colorectal, and lung cancer in patients with established CVD. Methods Data from patients with established CVD from the UCC-SMART prospective cohort study (N=7,280) were used for model development, and data from the CANTOS trial (N=9,322) were used for model validation. Predictors were selected based on previously published cancer risk prediction models or cancer risk factors, easy clinical availability, and availability in the derivation dataset (UCC-SMART cohort). A Fine and Gray competing risk-adjusted lifetime model was developed for total, colorectal, and lung cancer. Results Selected predictors were age, sex, smoking status, weight, height, alcohol use, antiplatelet use, diabetes mellitus, and C-reactive protein. External calibration for 4-year risks of the total cancer, colorectal cancer, and lung cancer models was good (Figure 1), and C-statistics were 0.63–0.74 in the CANTOS trial population. Median predicted lifetime risks in CANTOS were 26% (range 1%-52%) for total cancer, 4% (range 0%-13%) for colorectal cancer, and 5% (range 0%-37%) for lung cancer. Conclusions Lifetime and 10-year risk of cancer can be estimated with easy to measure variables in patients with established CVD, showing a wide distribution of predicted lifetime risks for total cancer and lung cancer. Using these lifetime models in clinical practice could increase understanding of cancer risk and aid in emphasizing healthy lifestyle changes. Figure 1. Calibration plots of cancer models Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): University Medical Center; Additional funding: CANTOS trial was funded by Novartis Pharmaceuticals.


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2662
Author(s):  
Anna Palomar-Cros ◽  
Ana Espinosa ◽  
Kurt Straif ◽  
Beatriz Pérez-Gómez ◽  
Kyriaki Papantoniou ◽  
...  

Nighttime fasting has been inconclusively associated with a reduced risk of cancer. The purpose of this study was to investigate this association in relation to prostate cancer risk. We examined data from 607 prostate cancer cases and 848 population controls who had never worked in night shift work from the Spanish multicase-control (MCC) study, 2008–2013. Through an interview, we collected circadian information on meal timing at mid-age. We estimated odds ratios (OR) and 95% confidence intervals (CI) with unconditional logistic regression. After controlling for time of breakfast, fasting for more than 11 h overnight (the median duration among controls) was associated with a reduced risk of prostate cancer compared to those fasting for 11 h or less (OR = 0.77, 95% 0.54–1.07). Combining a long nighttime fasting and an early breakfast was associated with a lower risk of prostate cancer compared to a short nighttime fasting and a late breakfast (OR = 0.54, 95% CI 0.27–1.04). This study suggests that a prolonged nighttime fasting duration and an early breakfast may be associated with a lower risk of prostate cancer. Findings should be interpreted cautiously and add to growing evidence on the importance of chrononutrition in relation to cancer risk.


2021 ◽  
Vol 22 (4) ◽  
pp. 1680
Author(s):  
Mariusz Dąbrowski

In the last decade, cancer became the leading cause of death in the population under 65 in the European Union. Diabetes is also considered as a factor increasing risk of cancer incidence and mortality. Type 2 diabetes is frequently associated with being overweight and obese, which also plays a role in malignancy. Among biological mechanisms linking diabetes and obesity with cancer hyperglycemia, hyperinsulinemia, insulin resistance, increased levels of growth factors, steroid and peptide hormones, oxidative stress and increased activity of pro-inflammatory cytokines are listed. Antidiabetic medications can modulate cancer risk through directly impacting metabolism of cancer cells as well as indirectly through impact on risk factors of malignancy. Some of them are considered beneficial (metformin and thiazolidinedions—with the exception of bladder cancer); on the other hand, excess of exogenous insulin may be potentially harmful, while other medications seem to have neutral impact on cancer risk. Inhibitors of the sodium-glucose cotransporter-2 (SGLT-2) are increasingly used in the treatment of type 2 diabetes. However, their association with cancer risk is unclear. The aim of this review was to analyze the anticancer potential of this class of drugs, as well as risks of site-specific malignancies associated with their use.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Weiqing Liu ◽  
Shumin Ma ◽  
Lei Liang ◽  
Zhiyong Kou ◽  
Hongbin Zhang ◽  
...  

Abstract Background Studies on the XRCC3 rs1799794 polymorphism show that this polymorphism is involved in a variety of cancers, but its specific relationships or effects are not consistent. The purpose of this meta-analysis was to investigate the association between rs1799794 polymorphism and susceptibility to cancer. Methods PubMed, Embase, the Cochrane Library, Web of Science, and Scopus were searched for eligible studies through June 11, 2019. All analyses were performed with Stata 14.0. Subgroup analyses were performed by cancer type, ethnicity, source of control, and detection method. A total of 37 studies with 23,537 cases and 30,649 controls were included in this meta-analysis. Results XRCC3 rs1799794 increased cancer risk in the dominant model and heterozygous model (GG + AG vs. AA: odds ratio [OR] = 1.04, 95% confidence interval [CI] = 1.00–1.08, P = 0.051; AG vs. AA: OR = 1.05, 95% CI = 1.00–1.01, P = 0.015). The existence of rs1799794 increased the risk of breast cancer and thyroid cancer, but reduced the risk of ovarian cancer. In addition, rs1799794 increased the risk of cancer in the Caucasian population. Conclusion This meta-analysis confirms that XRCC3 rs1799794 is related to cancer risk, especially increased risk for breast cancer and thyroid cancer and reduced risk for ovarian cancer. However, well-designed large-scale studies are required to further evaluate the results.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ying-Yi Lu ◽  
Hung-Pin Tu ◽  
Chieh-Hsin Wu ◽  
Chien-Hui Hong ◽  
Kuo-Chia Yang ◽  
...  

AbstractKeloid is a skin disease characterized by exaggerated scar formation, excessive fibroblast proliferation, and excessive collagen deposition. Cancers commonly arise from a fibrotic microenvironment; e.g., hepatoma arises from liver cirrhosis, and oral cancers arise from submucosal fibrosis. As keloids are a prototypic fibroproliferative disease, this study investigated whether patients with keloids have an increased cancer risk. In a matched, population-based study, first 17,401 patients treated for keloids during 1998–2010 with 69,604 controls without keloids at a ratio of 1:4 were evaluated. The association between keloids and risk of cancer was estimated by logistic regression or Cox proportional hazard regression models after adjustment of covariates. In total, 893 first-time cases of cancer were identified in the 17,401 patients with keloids. The overall cancer risk was 1.49-fold higher in the keloids group compared to controls. Regarding specific cancers, the keloids group, had a significantly higher risk of skin cancer compared to controls (Relative risk = 1.73). The relative risk for skin cancer was even higher for males with keloids (Relative risk = 2.16). Further stratified analyses also revealed a significantly higher risk of developing pancreatic cancer in female patients with keloids compared to controls (Relative risk = 2.19) after adjustment for known pancreatic cancer risk factors. This study indicates that patients with keloids have a higher than normal risk for several cancer types, especially skin cancers (both genders) and pancreatic cancer (females). Therefore, patients with keloids should undergo regular skin examinations, and females with keloids should regularly undergo abdominal ultrasonography.


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