Dietary trans-fatty acid intake in relation to cancer risk: a systematic review and meta-analysis

Abstract

Context Apart from ruminant fat, trans-fatty acids are produced during the partial hydrogenation of vegetable oils, (eg, in the production of ultraprocessed foods). Harmful cardiovascular effects of trans-fatty acids are already proven, but the link with cancer risk has not yet been summarized. Objective A systematic review (following PRISMA guidelines) – including observational studies on the association of trans-fatty acid intake with any cancer risk – was conducted, with no limitations on population types. Data Sources The electronic databases PubMed and Embase were searched to identify relevant studies. Data Extraction This systematic review included 46 articles. Quality was assessed via the Newcastle-Ottawa scale. Meta-analyses were conducted if at least 4 articles exploring the same transfat-cancer pairings were found. Data analysis Nineteen cancer types have been researched in cohort and case-control studies on trans-fatty acids, with breast cancer (n = 17), prostate cancer (n = 11), and colorectal cancer (n = 9) as the most researched. The meta-analyses on total trans-fat showed a significant positive association for prostate cancer (odds ratio [OR] 1.49; 95%CI, 1.13–1.95) and colorectal cancer (OR 1.26; 95%CI, 1.08–1.46) but not for breast cancer (OR 1.12; 95%CI, 0.99–1.26), ovarian cancer (OR 1.10; 95%CI, 0.94–1.28), or non-Hodgkin lymphoma (OR 1.32; 95%CI, 0.99–1.76). Results were dependent on the fatty acid subtype, with even cancer-protective associations for some partially hydrogenated vegetable oils. Enhancing moderators in the positive transfat-cancer relation were gender (direction was cancer-site specific), European ancestry, menopause, older age, and overweight. Conclusion Despite heterogeneity, higher risk of prostate and colorectal cancer by high consumption of trans-fatty acids was found. Future studies need methodological improvements (eg, using long-term follow-up cancer data and intake biomarkers). Owing to the lack of studies testing trans-fatty acid subtypes in standardized ways, it is not clear which subtypes (eg, ruminant sources) are more carcinogenic. Systematic Review Registration PROSPERO registration no. CRD42018105899

Ultra‐processed food consumption and the risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial

“…48 Second, ultra-processed foods possibly include some neoformed processing contaminants that are produced during physical, chemical and/or biological industrial processes, such as acrylamide, which has been classified as a Group 2A carcinogen (probably carcinogenic to humans) by International Agency for Research on Cancer due to its mutagenic effect 49 and trans fatty acids, which have been indicated to play a harmful role in carcinogenesis by epidemiological and animal studies. 50,51 Also, ultra-processed foods may contain some detrimental compounds derived from packaging materials. For example, it is suggested that ultra-processed food consumption may increase the exposure to di(2-ethylhexyl) phthalate, an endocrine-disruptor compound frequently used as a plasticizer 11,52 ; notably, human and laboratory studies both indicate that exposure to di(2-ethylhexyl) phthalate may promote carcinogenesis via various molecular signals, such as DNA damage.…”

Macronutrients Intake and Risk of Stomach Cancer: Findings from Case-Control Study

“…As for trans-fats, higher intake was also associated with increased GC risk. Limited and inconsistent results exist in the literature on the role of trans-fats in cancer risk [50] although associations with increased risk of gastrointestinal (GI) cancer have been reported [51]. Consistently, Elaidic acid, a trans-fatty acid, was found to enhance the metastasis of GI cancer cells [52].…”

Do Pathophysiologic Mechanisms Linking Unhealthy Lifestyle to Cardiovascular Disease and Cancer Imply Shared Preventive Measures? ― A Critical Narrative Review ―

“…56 Of note, smoking and alcohol abuse together lead to an even more than additive and dose-related increase in foods promote atherosclerosis, 43 and may play a pathophysiological role in cancer development due to their proinflammatory effects and induction of oxidative stress. 44 High sodium intake as salt is associated with CVD risk, 33 and seems to promote certain types of cancer, such as gastric cancer. 45 In clinical practice, improving a harmful dietary pattern is obviously one of the shared measures for prevention of both cancer 32 and CVD.…”