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This argues that the human immune system evolved optimal function in a dirtier world, including the presence of various microbes and helminth parasites, whose removal leads to pathogenic immunological hyperactivity ( Rook et al., 2004). One interpretation of the cause of such dysbiotic effects utilizes the ‘old friends’ hypothesis (derived from the hygiene hypothesis ). Such imbalance can manifest as loss of immunomodulatory microbial species and is exacerbated by pro-dysbiotic aspects of the modern lifestyle, including antibiotic usage and the so-called Western diet ( Buford, 2017). One cause of inflammaging is gut dysbiosis, an imbalance in the composition of the intestinal microbiome.
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Such inflammation is a contributory factor in diverse age-related pathologies, including cardiovascular disease, dementia, cancer, chronic obstructive pulmonary disease (COPD), osteoporosis, age-related macular degeneration ( Xia et al., 2016), and perhaps even symptom severity during SARS-CoV-2 (COVID-19) infections ( Akbar and Gilroy, 2020). How does aging cause senescent multimorbidity? While there are clearly multiple contributory factors, one determinant whose importance is becoming increasingly clear is inflammaging, the state of systemic, low-grade inflammation that increases with age, independent of attack by infectious pathogens ( Franceschi et al., 2000). The geroscience approach views preventative intervention in the aging process as a means to simultaneously pre-empt the development of multiple age-related diseases ( Austad, 2016). The aging process is the main cause of senescent multimorbidity, the co-occurrence of multiple chronic pathologies that includes the major diseases of late life. Could worm infections provide broad-spectrum protection against age-related disease? Introduction Here, we explore the hypothesis that restorative helminth therapy would have anti-inflammaging effects. Interestingly, Crowe et al., 2020 recently reported that treatment with a secreted glycoprotein from a parasitic nematode can protect against murine aging by induction of anti-inflammatory mechanisms. A further possibility is that loss of old friend commensals also increases the sterile, aging-associated inflammation known as inflammaging, which contributes to a range of age-related diseases, including cardiovascular disease, dementia, and cancer.
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Accordingly, probiotic therapies that restore ‘old friend’ microbes and helminths have been explored as Darwinian treatments for these disorders. For example, a decline in exposure to commensal microbes and gastrointestinal helminths in developed countries has been linked to increased prevalence of allergic and autoimmune inflammatory disorders (the hygiene hypothesis). Evolutionary medicine argues that disease can arise because modern conditions do not match those in which we evolved.
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