Abstract
The aging process is driven by multiple mechanisms that lead to changes in energy production, oxidative stress, homeostatic dysregulation and eventually to loss of functionality and increased disease susceptibility. Most aged individuals develop chronic low-grade inflammation, which is an important risk factor for morbidity, physical and cognitive impairment, frailty, and death. At any age, chronic inflammatory diseases are major causes of morbimortality, affecting up to 5–8% of the population of industrialized countries. Several environmental factors can play an important role for modifying the inflammatory state. Genetics accounts for only a small fraction of chronic-inflammatory diseases, whereas environmental factors appear to participate, either with a causative or a promotional role in 50% to 75% of patients. Several of those changes depend on epigenetic changes that will further modify the individual response to additional stimuli. The interaction between inflammation and the environment offers important insights on aging and health. These conditions, often depending on the individual’s sex, appear to lead to decreased longevity and physical and cognitive decline. In addition to biological factors, the environment is also involved in the generation of psychological and social context leading to stress. Poor psychological environments and other sources of stress also result in increased inflammation. However, the mechanisms underlying the role of environmental and psychosocial factors and nutrition on the regulation of inflammation, and how the response elicited for those factors interact among them, are poorly understood. Whereas certain deleterious environmental factors result in the generation of oxidative stress driven by an increased production of reactive oxygen and nitrogen species, endoplasmic reticulum stress, and inflammation, other factors, including nutrition (polyunsaturated fatty acids) and behavioral factors (exercise) confer protection against inflammation, oxidative and endoplasmic reticulum stress, and thus ameliorate their deleterious effect. Here, we discuss processes and mechanisms of inflammation associated with environmental factors and behavior, their links to sex and gender, and their overall impact on aging.
Highlights
Reviewed by: Christine Noel Metz, Feinstein Institute for Medical Research, United States Luciele Guerra Minuzzi, State University of Campinas, Brazil
The aging process is driven by multiple mechanisms that lead to changes in energy production, oxidative stress, homeostatic dysregulation and eventually to loss of functionality and increased disease susceptibility
Some diet types can result in metabolic and epigenetic changes that affect immune function [81], as reported in populations that consume a high-fat and low-fiber western diet, who show a prevalence of noncommunicable diseases (NCDs) higher than populations that consume a Mediterranean diet or a diet based on bioactive compounds, like the hydroxytyrosol in olive oil [82,83,84]
Summary
The systemic chronic low-grade inflammation observed in aged individuals has been coined as “inflammaging” [1], and leads to metabolic dysfunction, physical limitations, and frailty in older adults [reviewed in [2]]. Inflammaging leads to an increased secretion of interleukin 1beta (IL1b), interferons (IFNs), and tumor necrosis factor a (TNFa) [3] This inflammatory response appears to depend on biological factors like sex, being higher in older women, and is influenced by many environmental factors. Estrogen is the sex hormone with the greatest impact on the immune response, being described as one of the non-modifiable regulators of the immune system, due to its immunoregulatory and protective effects in many inflammatory models [46] This is contradictory with the fact that women have a higher prevalence of autoimmune diseases than men, estrogens should be a protective condition [47]. For a better general view of estrogens mechanisms and effect on the innate immune system cells we recommend reviews that have extensively covered those topics [53,54,55,56]
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