How persistent pathogens could accelerate the aging process | Amy Proal

Core Argument - The prevailing aging models inadequately address the role of persistent pathogens (viruses, bacteria, parasites) as a significant driver of human aging and healthspan reduction [1] - Persistent pathogens can embed themselves in tissues and nerves, potentially driving various health problems later in life [2][3][4] - These pathogens can actively distort the signaling of human genes, impacting multiple hallmarks of aging [8] Pathogen Prevalence and Impact - Approximately 95% of individuals harbor one or more strains of herpes virus [5] - Around 11% of people in the US and up to 87% in some global regions carry the chronic parasite toxoplasma [6] - Persistent SARS-CoV-2 virus has been found in tissue samples months or years after initial infection [7] - Pathogens can drive mitochondrial dysfunction by hijacking host cell metabolism [10][11][12] - Viruses can integrate into telomeres, leading to shorter and more unstable telomeres [13][14] - Viral proteins can interact with and distort the signaling of human aging pathways [15] Proposed Solutions and Recommendations - The industry needs to seriously consider the impact of persistent pathogens when developing healthspan extending interventions [17] - Curbing the activity of pathogens should precede interventions like gene editing [18] - Integrating existing antiviral and anti-parasite medications into healthspan protocols is recommended [18] - Individuals with herpes simplex virus who regularly took anti-herpes virus medications had a 10 times lower risk of developing dementia [19] - Investment in new diagnostic test platforms to identify persistent pathogens is crucial [20][21] - Incorporating the activity of persistent pathogens into aging models is essential for successfully extending healthspan [22]