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The expansion of general medical knowledge has led to an increase in the average lifespan of humans. This increased longevity has caused a shift in disease prevalence toward noncommunicable diseases. The chronic inflammatory state has been identified as a significant contributor to many chronic diseases, including cardiovascular disease, type 2 diabetes, and certain malignancies. Consistent evidence demonstrates that healthy dietary habits, including anti-inflammatory diets, decrease overall risk, morbidity, and mortality from these and other chronic diseases. Anti-inflammatory diets are based on a holistic life approach with a dietary focus on whole foods that are biodiverse and not overly processed. The bioactive components in high quantities within an anti-inflammatory diet work synergistically to reduce the inflammatory state. Adherence to these diets can reduce the symptom burden of chronic, noncommunicable diseases, but the highest level of efficacy comes from long-term adherence. This activity highlights the mechanisms by which adherence to an anti-inflammatory diet reduces the overall risk of developing chronic disease processes and highlights the role of the interprofessional, multidisciplinary healthcare team in promoting acceptance of and adherence to an anti-inflammatory diet. Objectives: Apply evidence-based tools to evaluate the inflammatory potential of a patient's current dietary habits. Differentiate the anti-inflammatory properties of select foodstuffs. Select patients with disease processes characterized by a chronic inflammatory state who may benefit from adopting an anti-inflammatory dietary plan. Collaborate with the interprofessional team to educate patients on the benefits of adopting and adhering to an anti-inflammatory diet. Access free multiple choice questions on this topic.

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.[1] 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.[2] 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.[2] In response to a stimulus perceived as harmful, these cells release a cascade of proinflammatory cytokines, chemokines, and prostaglandin E2 (PGE2).[2] 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.[2] If the acute inflammatory response cannot resolve normally because of persistent tissue injury or dysregulation of normal processes, chronic inflammation will ensue.

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.[2] In response to a stimulus perceived as harmful, these cells release a cascade of proinflammatory cytokines, chemokines, and prostaglandin E2 (PGE2).[2] 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.[2] 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.[3] 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.[4]

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.[4] 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.[5] 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.[6] 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.[6]

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.[6] 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.[6] 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.

Evidence has consistently demonstrated that adherence to a healthy diet reduces overall morbidity and mortality and the risk of cardiovascular disease and certain malignancies.[1][18][23] Long-term adherence to an anti-inflammatory diet requires a paradigm shift for patients, from expecting readily observable changes in a short timeframe to making lifestyle modifications for the sustainment or improvement of their current health status over their lifetime. Several factors are associated with better patient adherence to lifestyle modifications.[35] Behavioral habits, including current dietary habits, high levels of physical activity, and self-monitoring of health statistics, play a role in successful adherence. Cognitive components such as reduced disinhibition and confidence in achieving personal goals, personality traits like resiliency, and buy-in and support from family members all promote adherence to lifestyle modifications.[35] Comprehensive programs facilitated by multidisciplinary, interprofessional teams that combine dietary recommendations with specific cognitive and behavioral strategies result in greater long-term patient adherence to lifestyle modifications.[35] A lifestyle modification team may include, but is not limited to, physicians, advanced practice providers, dietitians, nutritionists, psychologists, clinical nursing staff, and trained lifestyle counselors.[35]. This interprofessional team can create individualized plans tailored to disease prevention, symptom management, current lifestyle, and access to necessary resources, providing the patient with personalized, comprehensive, supportive care to improve long-term outcomes.

Comprehensive programs facilitated by multidisciplinary, interprofessional teams that combine dietary recommendations with specific cognitive and behavioral strategies result in greater long-term patient adherence to lifestyle modifications.[35] A lifestyle modification team may include, but is not limited to, physicians, advanced practice providers, dietitians, nutritionists, psychologists, clinical nursing staff, and trained lifestyle counselors.[35]. This interprofessional team can create individualized plans tailored to disease prevention, symptom management, current lifestyle, and access to necessary resources, providing the patient with personalized, comprehensive, supportive care to improve long-term outcomes. The increasing average life expectancy of the general population also requires a paradigm shift for providers, expanding our focus on increasing the quality of these extended years by reducing the burden of chronic disease. Working with patients to implement an anti-inflammatory diet can help accomplish this goal. Each recommended anti-inflammatory diet, implemented individually or in combination, exhibited long-term, positive effects on chronic diseases such as cardiovascular disease, cancer, and neurocognitive decline. The overall risk reduction afforded by adherence to these diets comes from a synergistic combination of protective bioactive components in high quantities within these anti-inflammatory diets. To achieve the overall risk reduction and positive health effects of these anti-inflammatory diets, they should be incorporated as a lifestyle modification with a mindset of long-term sustainability. By integrating these anti-inflammatory diets, the goal of a life with both quality and quantity is achievable.