Inflammation, not Cholesterol, Is a Cause of Chronic Disease

Abstract

Since the Seven Countries Study, dietary cholesterol and the levels of serum cholesterol in relation to the development of chronic diseases have been somewhat demonised. However, the principles of the Mediterranean diet and relevant data linked to the examples of people living in the five blue zones demonstrate that the key to longevity and the prevention of chronic disease development is not the reduction of dietary or serum cholesterol but the control of systemic inflammation. In this review, we present all the relevant data that supports the view that it is inflammation induced by several factors, such as platelet-activating factor (PAF), that leads to the onset of cardiovascular diseases (CVD) rather than serum cholesterol. The key to reducing the incidence of CVD is to control the activities of PAF and other inflammatory mediators via diet, exercise, and healthy lifestyle choices. The relevant studies and data supporting these views are discussed in this review.

Impact of combined healthy lifestyle factors on survival in an adult general population and in high‐risk groups: prospective results from the Moli‐sani Study

“…Our findings are in agreement with previous evidence showing a role of inflammation in CVD onset , and also support the common soil hypothesis according to which both CVD and cancer diseases share a common soil of pathogenetic mechanisms and consequently risk/protective factors .…”

The effect of green tea on inflammatory mediators: A systematic review and meta‐analysis of randomized clinical trials

“…KEYWORDS catechin, C-reactive protein, green tea, interleukin-6, tumor necrosis factor-alpha 1 | INTRODUCTION Inflammation is a physiological reaction of the innate immune system that aims to decrease the harmful effect of agents that causes tissue injury. A growing body of evidence proposed that chronic systemic inflammation is the main cause of chronic diseases such as endothelial dysfunction, cardiovascular disease, lung diseases (Firoozabadi et al, 2017;Shahriary, Ghanei, & Rahmani, 2017;Shahriary, Panahi, Shirali, & Rahmani, 2017), metabolic syndrome, and type 2 diabetes (Tsoupras & Lordan, 2018). The main inflammatory mediators that have been extensively investigated in relation to health status are high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).…”

“…Lymphocyte and macrophages produce IL-6 and TNF-α (Gabay, 2006). In response to increased levels of IL-6 and TNF-α, liver cells secrete CRP into blood circulation (Pepys & Hirschfield, 2003), and the enhancement of CRP, IL-6, and TNF-α concentrations will lead to chronic diseases (Tsoupras & Lordan, 2018). Several studies have indicated that dietary intakes, particularly those with plant based, can change the concentrations of inflammatory mediators (Haghighatdoost & Hariri, 2019a, 2019bHariri & Ghiasvand, 2016;Vallianou, Tsang, Taghizadeh, Davoodvandi, & Jafarnejad, 2019).…”

In vitro Anti‐atherogenic Properties of N‐Heterocyclic Carbene Aurate(I) Compounds

“…These chronic multifactorial inflammatory diseases are characterized by the development of lesions on the intima wall of medium and large‐sized arteries, called atheromata or atherosclerotic plaques. After decades of lethargic progression, these lesions progress suddenly and cause stenosis, thus limiting blood‐flow or even arterial rupture causing characteristic clinical manifestations such as distal ischemia, progressive clot formation, and stroke …”

“…After decades of lethargic progression,t hese lesions progress suddenly and causes tenosis, thusl imiting blood-flow or even arterial rupture causing characteristic clinical manifestations such as distal ischemia, progressive clot formation, and stroke. [4] One of the most potent mediators of inflammationt hat plays ac rucial role in atherosclerosis is platelet-activating factor (PAF) (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine); [5] which is aw ell-established biologically active glyceryl-ether phospholipid with 16-18 carbonsa tsn-1p osition of the glycerol backbone ( Figure 1). [5] PAFm odulates angiogenesis, thrombosis, oncogenic transformation,t umor growth, metastasis and the mechanism of atherogenesis (atheromatosis).…”