Dietetic lectins cause disease

Rheumatism and nutrition

In addition, there are other mechanisms by which omega-3 fatty acids can influence the inflammatory process. Since omega-3 fatty acids have a high affinity for the enzymes cyclooxygenase and lipoxygenase, but can only be metabolized to a lesser extent due to the additional double bond, they reduce overall eicosanoid formation [2]. In addition, eicosapentaenoic acid is able to displace arachidonic acid from the membrane phospholipids, so that less substrate is available for the formation of the arachidonic acid derivatives [10]. In addition, omega-3 fatty acids reduce the concentration of inflammatory cytokines: for example, high-dose administration of omega-3 fatty acids lowers the interleukin-1β level in patients with chronic polyarthritis [55]. An influence on the expression of adhesion molecules and other inflammatory genes (e.g. genes of cyclooxygenase-2) by omega-3 fatty acids is also discussed [16; 26].

The supply of eicosapentaenoic acid depends primarily on the dietary intake of this fatty acid, which occurs almost exclusively in fatty fish such as salmon, mackerel and herring. Docosahexaenoic acid (C22: 6ω3) is also found in fatty fish, which can easily be converted into eicosapentaenoic acid [23]. In principle, the human organism is also capable of de novo synthesis of eicosapentaenoic acid from alpha-linolenic acid (C18: 3ω3) which occurs in plants (especially linseed oil) and which is considered to be the parent substance of omega-3 fatty acids. However, this multi-stage conversion - similar to the conversion of linoleic acid into arachidonic acid - is very inefficient and also shows a clear dependence on genetic factors and diet. The conversion rate is approx. 5%, so that the supply of 20 g alpha-linolenic acid would be necessary to synthesize 1 g eicosapentaenoic acid.

Oxidative stress

The excessive inflammatory reaction that occurs in rheumatoid arthritis leads to an increased formation of free radicals and ROS in the affected joints. Phagocytic cells such as activated macrophages and granulocytes cause a respiratory burst, which is mediated by a NADPH oxidase complex and results in a considerable increase in oxygen consumption and the production of highly toxic ROS. The resulting oxidative stress potentiates the inflammatory process through various mechanisms [44; 53]. Free radicals activate phospholipase A2 and thus increase the release of arachidonic acid from the phospholipids. As a result, the formation of pro-inflammatory eicosanoids is also increased [69]. In addition, free radicals act on various connective tissue structures in the joint, such as B. proteoglycans, hyaluronic acid, lipids and proteins (e.g. collagen) destructive [39; 53]. An increased formation of pro-inflammatory substances such as cytokines and chemokines [75] is also triggered by free radicals and the induction of the transcription factor NFκB (nuclear factor kappa B).

In the affected tissues, the concentration of antioxidants decreases due to their increased consumption, which in turn leads to an increase in oxidative stress. In the event of an insufficient supply of antioxidants and a resulting increase in oxidative stress in the joint, the inflammation process is further intensified [57]. This results in "excessive phagocytosis", which further increases the formation of ROS and the inflammatory process gets out of control.

It has long been known that increased oxidative stress leads to the development of various diseases such as atherosclerosis [49; 85; 101], cancer [34; 48], Parkinson's disease [29; 35] and Alzheimer's disease [5; 20; 89] favored. The clinical manifestation of atherosclerosis poses a risk of relevant concomitant and secondary diseases for rheumatoid patients. Patients with rheumatoid arthritis have been shown to have a two to four-fold higher risk than non-RA patients of suffering a cardiovascular event [108]. According to research using the Norfolk Arthritis Register, cardiovascular disease was the leading cause of death in a cohort of 1,362 rheumatoid arthritis patients who were newly registered between 1990 and 1994 and were re-recorded in late 1999 [42]. It is crucial that the cardiovascular manifestations are not solely due to classic risk factors (hypertension, nicotine, diabetes mellitus).

Possible starting points for a connection between cardiovascular complications and rheumatoid arthritis are the inflammatory genesis of both diseases. Supported by the constantly increased concentration of cytokines and oxidative stress, endothelial dysfunctions are increased and the formation of atherosclerotic plaques is promoted.

Optimizing nutrient delivery in rheumatoid arthritis patients, including with antioxidant nutrients, is therefore not only important in connection with the actual disease process, but also relevant with regard to other cardiovascular or metabolic secondary diseases.

Starting points for dietary measures

The relationships between nutrition and inflammatory rheumatic diseases resulting from the mechanisms presented above are confirmed by a large number of experimental and clinical data [45; 60; 79; 99]. The focus of a dietary influence on inflammatory joint diseases is the targeted supply of anti-inflammatory food factors and antioxidant nutrients as well as the reduction of the intake of arachidonic acid-containing foods (Fig. 3).