Random Variations’ and their Role in our Longevity; Can we Avoid them?

USC investigates a new model of aging that takes into account not only genetics and environmental exposures, but also the tiny changes that randomly arise at the cellular level.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436990/
https://academic.oup.com/biomedgerontology/article-abstract/76/10/1740/6134451?redirectedFrom=fulltext
https://www.researchgate.net/publication/349289535_Gene-Environment_Interactions_and_Stochastic_Variations_in_the_Gero-Exposome

University Professor Caleb Finch introduced the "Tripartite Phenotype of Aging" as a new conceptual model that addresses why lifespan varies so much, even among human identical twins who share the same genes. According to Finch only about 10 to 35 percent of longevity can be traced to genes inherited from our parents, Finch mentioned.
Finch authored the paper with a former graduate student of his, Amin Haghani. In the article, they propose that the limited heritability of aging patterns and longevity in humans is an outcome of gene-environment interactions, as well as random variations in the body's cells. These random changes can include cellular changes that happen during development, molecular damage that occurs later in life, and more. Caleb Finch said "We wanted to introduce a conceptual map and some new terminology that will motivate a more comprehensive understanding of what the limitations of genetic determinants in aging are, how important it is to consider the genetic variance in relationship to the environment, and include this new domain of stochastic variations, which is very well recognized by different fields. It hasn't really been put in a formal context in which the complete package can be discussed, and that's what I hope our article achieves."

The new model is a natural extension of the idea of the exposome, which was first proposed by cancer epidemiologist Christopher Paul Wild in 2005 to draw attention to the need for more data on lifetime exposure to environmental carcinogens. The exposome concept illustrates how external factors, ranging from air pollution and socioeconomic status to individual diet and exercise patterns, interact with endogenous, or internal, factors such as the body's microbiome and fat deposits.

Professor Finch went on to say “The new model illustrates that cell-by-cell variations in gene expression, variations arising during development, random mutations, and epigenetic changes - turning genes "off" or "on" - should be explicitly considered apart from traditional genetic or environmental research regarding aging. More detailed study into these chance processes has been enabled by cutting-edge research techniques, including the study of gene transcription within single cells as well as ChIP-sequencing, which can illustrate how individual proteins interact with DNA.”
In the paper, Finch and Haghani discussed several examples of how risks of age-related disease are poorly predicted by DNA alone, but are heavily influenced by environmental exposures as well as the time and duration of the exposure. One well-known example of a gene that is associated with increased Alzheimer's risk is ApoE-4; however, having the ApoE-4 gene doesn't definitively mean someone will get Alzheimer's. Studies in both mice and humans revealed that ApoE-4, and clusters of related genes, interact with exposure to things such as air pollution or cigarette smoke to influence risk. Alzheimer's patients also show differences in their epigenetics as compared to individuals without the disease.

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