Anti-Inflammatory Diets

Excerpt

The average human life expectancy has more than doubled in the last 150 years worldwide; much of this increase is attributed to the rapidly advancing practice of medicine. As general medical knowledge and treatments expand and improve, many once lethal diseases are now treatable or have been eradicated, and disease prevalence has shifted away from acute, communicable processes. The chronic inflammatory state significantly contributes to the development and progression of many noncommunicable disease processes, including cancer, cardiovascular disease, and neurocognitive decline.

The inflammatory response is crucial to human survival. Inflammation is a normal and vital responsive process to internal injury and many external assaults, including foreign substances or trauma. When regulated appropriately, the inflammatory response facilitates the eradication of the invader, tissue repair, and a return to homeostasis.

Inflammation may be acute or chronic. The acute inflammatory response begins within minutes to hours, lasts for hours to days, and is typically initiated by tissue-resident macrophages and dendritic cells. In response to a stimulus perceived as harmful, these cells release a cascade of proinflammatory cytokines, chemokines, and prostaglandin E2 (PGE2). The acute inflammatory process is characterized by three main phases: enhanced blood flow to the target area via dilation of small vessels, increased vascular permeability, and phagocytic leukocyte migration into the affected tissue. An effective acute inflammatory response eradicates foreign pathogens or necrotic cells, followed by the repair of the host tissue. However, leukocytes are important causes of injury to normal cells and tissues during a normal inflammatory response. If the acute inflammatory response cannot resolve normally because of persistent tissue injury or dysregulation of normal processes, chronic inflammation will ensue.

Chronic inflammation may occur in a tissue when an inflammatory process is activated by an overabundance of triggering factors, such as free radicals, oxidative stress, or foreign pathogens. With repeated stimulus from the triggering factor, an unregulated inflammatory response can be initiated, causing chronic local or systemic organ damage. Chronic inflammation is characterized by continued proinflammatory processes being unchecked by anti-inflammatory processes. The presentation of chronic inflammation will vary with the affected tissue and the injurious agent.

Atherosclerosis is a form of chronic inflammation within the arterial vasculature that underlies the pathogenesis of peripheral, cerebral, and coronary vascular disease, predisposing to limb ischemia, stroke, and myocardial infarction. Cardiovascular disease is the most common underlying cause of death in the United States. Atherosclerosis is considered to be a chronic inflammatory response within the arterial wall to ongoing endothelial injury. As part of a complex response to injury, macrophages accumulate within the vessel wall, are chronically activated to release proinflammatory cytokines, recruit other inflammatory cells to the area, exert a catabolic effect on fibrous atheromatous plaques, and increase the overall risk of plaque rupture and thrombosis.

Cancer is another complex disease state characterized by a chronic inflammatory response. Cancer cells express antigens that may be recognized by the human immune system, thereby upregulating proinflammatory cytokines and mediators and the ongoing activation of immune cells. Cancer cells also frequently undergo necrosis, which promotes a continuous influx of leukocytes to the tumor. However, cancer cells also possess the ability to evade the normal immune system while promoting immune responses that support tumor growth. This dysregulated and dysfunctional chronic inflammatory promotes the progression of the malignancy.

An unregulated inflammatory response also significantly negatively affects neurocognitive function. The blood-brain barrier is a bidirectional communication system between the innate immune system of the brain and the peripheral immune system and was initially thought to be an insulator against peripheral inflammation. However, increased peripheral immune system activity chronically activates the specialized macrophages of the brain parenchyma known as microglia, promoting a blood-brain barrier breakdown. This breakdown may allow peripheral inflammatory mediators to enter the central nervous system, increasing neuroinflammation and the risk of neurocognitive diseases.

Chronic inflammation contributes to the risk of disease development and progression to some degree. While not completely understood, this process has encouraged healthcare practitioners to include the reduction of inflammation in preventative and treatment planning. Clinicians, particularly primary care practitioners, are uniquely poised to offer various modalities of inflammatory reduction, including adherence to an anti-inflammatory diet.