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 Chronic inflammation: a central mechanism in human systemic deterioration, aging, heart attacks, dementia, and cancer.

Abstract

Inflammation is a crucial physiological response that enables the body to defend against external and internal aggressions. However, when it becomes chronic and dysregulated, it becomes a pathological agent of multiple systemic diseases. This article reviews the role of chronic inflammation in the genesis and progression of cardiovascular, neurodegenerative, autoimmune, metabolic, and oncological diseases. Its molecular mechanisms, the oxidative factors that trigger it, and therapeutic strategies focused on its control are addressed.

1. Introduction

Inflammation is a complex immunological process that aims to eliminate pathogens and repair damaged tissues. In the short term, it is beneficial; however, its persistence—even in the absence of an obvious stimulus—gives rise to a condition known as chronic low-grade inflammation, which is implicated in a wide range of non-communicable diseases (1,2).

2. Molecular Mechanisms of Chronic Inflammation

Chronic inflammation is mediated by the continuous activation of macrophages, T lymphocytes, and endothelial cells, along with the production of proinflammatory cytokines such as IL-1β, IL-6, and TNF-α, and reactive oxygen species (ROS) (3, 4).
The most common contributing factors include a proinflammatory diet, smoking, sedentary lifestyle, environmental pollution, and intestinal dysbiosis (5).

3. Systemic Implications of Chronic Inflammation

3.1 Cardiovascular Diseases

Inflammation is key to atherogenesis. Endothelial damage perpetuates an inflammatory cascade that promotes the formation of unstable plaques, with a high risk of rupture and thrombosis (6). Studies such as CANTOS have shown that blocking IL-1β reduces cardiovascular events independently of lipid levels (7).

3.2 Neurodegenerative Diseases

Prolonged microglial activation generates a proinflammatory environment that promotes neurodegeneration. This mechanism has been identified in Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis.

3.3 Aging and Impotence

The term “inflammation” describes the phenomenon of persistent basal inflammation with age, linked to mitochondrial dysfunction, cellular aging, sarcopenia, and sexual dysfunction.

3.4 Cancer

Inflammation promotes carcinogenesis through mechanisms such as NF-κB activation, inhibition of apoptosis, and angiogenesis.  Examples include gastric cancer caused by H. pylori and hepatocellular carcinoma caused by chronic hepatitis.

3.5 Autoimmune and Intestinal Diseases

Diseases such as lupus, rheumatoid arthritis, celiac disease, and psoriasis present systemic inflammation mediated by dysfunction of the adaptive and innate immune systems.

4. Strategies for Controlling Inflammation

4.1 Natural Antioxidants

Several studies support the use of antioxidants such as vitamins C, E, coenzyme Q10, and polyphenols (resveratrol, curcumin) as modulators of the inflammatory response.

4.2 Anti-Inflammatory Diet

A Mediterranean diet, rich in unsaturated fats, fruits, vegetables, and anti-inflammatory spices, has been shown to reduce inflammatory markers such as CRP and IL-6.

4.3 Regular Physical Activity

Regular exercise modulates immunity and reduces systemic inflammation, improving insulin sensitivity and vascular function.

4.4 Sleep, Blood Glucose Control, and Blood Glucose Control  Stress and Microbiota

Sleep deprivation and chronic stress increase cortisol and cytokine production. Furthermore, intestinal dysbiosis is associated with increased intestinal permeability and chronic endotoxemia.

5. Conclusion

Chronic inflammation represents a common denominator in the leading causes of global morbidity and mortality. Its early identification and control through nutritional, pharmacological, and behavioral interventions is a priority in preventive medicine. A comprehensive approach must consider individual, genetic, and environmental factors.

References

1. Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454(7203):428–35.

2. Furman D, et al. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019;25(12):1822–32.

3. Libby P. Inflammation in atherosclerosis. Nature.  2002;420(6917):868–74.

4. Nathan C, Ding A. Nonresolving inflammation.  Cell.  2010;140(6):871–82.

5. Calder PC, et al.  Dietary factors and low-grade inflammation in relation to overweight and obesity.  Br J Nutr.  2011;106 Suppl 3:S5–78.

6. Hansson GK, Hermansson A. The immune system in atherosclerosis.  Nat Immunol.  2011;12(3):204–12.

7. Ridker PM, et al.  Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease.  N Engl J Med 2017;377(12):1119–31.

Raul Ayala MD @MyDoctorOnCall.com