Abstract

Chronic inflammation has been identified as a necessary step to mediate atherosclerosis and cardiovascular disease and as a relevant stage in the onset and progression of several types of cancer. Considerable attention has recently been focused on the identification of dietary bioactive compounds with anti-inflammatory activities as an alternative natural source for prevention of inflammation-associated diseases. The remarkable capacity of cocoa flavanols as antioxidants, as well as to modulate signaling pathways involved in cellular processes, such as inflammation, metabolism and proliferation, has encouraged research on this type of polyphenols as useful bioactive compounds for nutritional prevention of cardiovascular disease and cancer. Data from numerous studies suggest that cocoa and cocoa-derived flavanols can effectively modify the inflammatory process, and thus potentially provide a benefit to individuals with elevated risk factors for atherosclerosis/cardiovascular pathology and cancer. The present overview will focus on the most recent findings about the effects of cocoa, its main constituents and cocoa derivatives on selected biomarkers of the inflammatory process in cell culture, animal models and human cohorts.

Highlights

  • Inflammation is a protective physiological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, that involves immune cells, blood vessels, and molecular mediators [1]

  • The increase found in high density lipoproteins (HDL)-cholesterol in the previously mentioned study is in line with other results in similar populations after an intake of flavanol-rich cocoa [76], of cocoa powder with milk [97] and in agreement with the results described by Jenkins and colleagues [98] who reported a significant increase in HDL-cholesterol after consumption of a cocoa bran (25 g dietary fiber/day) for two weeks by healthy subjects

  • A number of studies of cell cultures and animals have unequivocally demonstrated that cocoa flavanols reduce pro-inflammatory cytokines and inhibit inflammatory mediators NF-κB, COX-2 and inducible nitric oxide (NO) synthase (iNOS)

Read more

Summary

Introduction

Inflammation is a protective physiological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, that involves immune cells, blood vessels, and molecular mediators [1]. The purpose of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. Inflammation is normally closely regulated by the body, chronic inflammation may lead to a host of diseases, including the two most lethal pathologies of our time, cardiovascular disease and cancer [1]

Inflammation and Cardiovascular Dysfunction
Inflammation and Cancer
Cocoa Flavonoids as Anti-Inflammatory Compounds
Bioavailability and Distribution of Cocoa Flavanols
Cocoa Flavanols in the Prevention of Cardiovascular Disease and Cancer
Studies of Cell Culture
Studies of Experimental Animals
Cocoa and Cardiovascular Disease in Animal Models
Cocoa and Colon Inflammation and Cancer in Animal Models
Cocoa and Colon Inflammation
Cocoa and Colon Cancer
Studies in Humans
Cocoa and Human Cardiovascular Disease
Cocoa and Inflammatory Interleukins and CRP
Cocoa and Soluble Adhesion Molecules
Cocoa Fiber and Theobromine
Cocoa in the Context of a Healthy Diet
Findings
Conclusions
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.