Israel Medical Association Journal

Obesity is a growing global health concern, with its prevalence contributing to the rise of multiple chronic conditions, including autoimmune diseases. In this review I explore the intricate relationship between obesity and autoimmunity, focusing on how excess adiposity can affect immune responses and promote the development of autoimmune disorders. Obesity alters adipose tissue architecture, promoting chronic low-grade inflammation and triggering the release of pro-inflammatory cytokines, which contribute to immune system dysregulation. Adipose tissue is no longer seen as merely an energy store but as an active endocrine organ that interacts with the immune system. The review delves into mechanisms such as the role of adipokines, altered T cell function, and the recruitment of immune cells to inflamed adipose tissue, which together exacerbate autoimmune risk in obese individuals. Genetic and environmental factors also play a critical role in these processes, as polymorphisms and high-fat diets have been shown to influence both obesity and autoimmune susceptibility. Last, the review explores potential therapeutic strategies, such as lifestyle interventions and targeting obesity-driven inflammatory pathways, which could mitigate autoimmunity. Understanding the connection between obesity and autoimmunity offers insights into more effective interventions for patients suffering from these intertwined conditions.

Fasting, a practice with deep historical roots, has gained scientific attention for its potential benefits on human health, particularly in autoimmune diseases. In this review, we explored the impact of fasting on immune function and autoimmunity. Autoimmune diseases, characterized by the immune system's attack on the body’s own tissues, are influenced by genetic, environmental, and dietary factors. Various forms of fasting (intermittent, water fasting, calorie restriction, ketogenic diets, and time-restricted feeding) affect metabolism, immune modulation, and inflammation reduction. These changes can promote autophagy, stem cell renewal, and immune system rebalancing by offering potential therapeutic effects for autoimmune conditions. Although more research is needed, fasting may serve as an adjunctive therapy for immune-mediated diseases by reducing symptoms and promoting remission. However, fasting must be approached with caution, particularly for individuals with specific autoimmune disorders. We reviewed the physiological changes during fasting, types of fasting regimens, and the clinical relevance in autoimmunity. Further studies are needed to validate these observations in patient populations.

Background: Cardiovascular disease (CVD) is more frequent in patients with systemic lupus erythematosus (SLE) compared with age- and sex-matched healthy subjects. SLE is an autoimmune disease that is more prevalent in women (9:1). Women tend to develop CVD in post-menopausal years; however, women with SLE may develop endothelial dysfunction and CVD at a younger age in the pre-menopausal years.

Objectives: To study the endothelial function of adult-onset SLE patients from the north of Israel (the Galilee region) and to determine whether modern management (including biological treatments) changes the risk of developing CVD.

Methods: Thirteen females with adult-onset SLE without renal involvement were recruited to this prospective study. Clinical parameters (age, height, body mass index [BMI]), laboratory parameters (C-reactive protein [CRP] and hemoglobin level), and vascular responsiveness (flow mediated diameter percent change [FMD%]) were evaluated and compared to 11 age-matched healthy females. Student's t-test was used to find differences between the two groups.

Results: No difference was observed in adult-onset SLE female patients and their age- and sex-matched controls with regard to age (42.1 ± 11.8 years vs. 36.6 ± 10.8 years, P = NS), BMI (25 ± 1.8 kg/m² vs. 25 ± 2.5 kg/m², P = NS), and hemoglobin level (11.9 ± 0.9 gr% vs. 12.7 ± 1.2 gr%, P = NS). However, a significant difference was found in CRP (2.57 ± 2.2 mg vs. 0.60 ± 0.37 mg, P = 0.001), vascular responsiveness (0.94 ± 6.6 FMD% vs. 9.2 ± 8.1 FMD%, P = 0.012), and height (165.7 ± 4.5 cm vs. 171.6 ± 5.8 cm, P = 0.009).

Conclusions: Adult-onset SLE females had impaired endothelial function even though they were treated by modern protocols.

Inflammation is the basic mechanism leading to many pathological processes, including degenerative diseases, atherosclerosis, and cancer. We found an interesting link connecting rheumatoid arthritis and atherosclerosis that may explain the high cardiovascular event rate among patients with rheumatoid arthritis, but also may lead to a new way of thinking and a better understanding of atherosclerosis. Rheumatoid arthritis could serve as a model of accelerated atherosclerosis. Understanding the basic mechanisms of rheumatoid arthritis may solve some of the complexity of atherosclerosis.