Epigenetic Modifiers as Game Changers for Healthy Aging

Sharma, Shikha; Bhonde, Ramesh

doi:10.1089/rej.2022.0059

Cited by 3 publications

(1 citation statement)

References 157 publications

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“…The possible use in the future of drugs or interventions capable of modifying epigenetic alterations contributing to post-menopausal conditions/diseases in a controlled manner (e.g., removal, addition) may be a feasible avenue for research going forward. Such drugs have been proposed to be applied in conditions affecting bone [210], cancer [211,212], neurodegenerative disorders [213,214], cardiovascular conditions [215,216], and healthy aging [217]. The development of such "epi-drugs" is not without challenges [218], particularly since such interventions will have to be personalized for post-menopausal conditions that arise in different tissues, may not result from a single phenotypic pattern, and may occur in conjunction with multiple co-morbidities as the individual ages.…”

Section: Conclusion and The Way Forwardmentioning

confidence: 99%

The Heterogeneity of Post-Menopausal Disease Risk: Could the Basis for Why Only Subsets of Females Are Affected Be Due to a Reversible Epigenetic Modification System Associated with Puberty, Menstrual Cycles, Pregnancy and Lactation, and, Ultimately, Menopause?

Hart

2024

IJMS

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For much of human evolution, the average lifespan was <40 years, due in part to disease, infant mortality, predators, food insecurity, and, for females, complications of childbirth. Thus, for much of evolution, many females did not reach the age of menopause (45–50 years of age) and it is mainly in the past several hundred years that the lifespan has been extended to >75 years, primarily due to public health advances, medical interventions, antibiotics, and nutrition. Therefore, the underlying biological mechanisms responsible for disease risk following menopause must have evolved during the complex processes leading to Homo sapiens to serve functions in the pre-menopausal state. Furthermore, as a primary function for the survival of the species is effective reproduction, it is likely that most of the advantages of having such post-menopausal risks relate to reproduction and the ability to address environmental stresses. This opinion/perspective will be discussed in the context of how such post-menopausal risks could enhance reproduction, with improved survival of offspring, and perhaps why such risks are preserved. Not all post-menopausal females exhibit risk for this set of diseases, and those who do develop such diseases do not have all of the conditions. The diseases of the post-menopausal state do not operate as a unified complex, but as independent variables, with the potential for some overlap. The how and why there would be such heterogeneity if the risk factors serve essential functions during the reproductive years is also discussed and the concept of sets of reversible epigenetic changes associated with puberty, pregnancy, and lactation is offered to explain the observations regarding the distribution of post-menopausal conditions and their potential roles in reproduction. While the involvement of an epigenetic system with a dynamic “modification-demodification-remodification” paradigm contributing to disease risk is a hypothesis at this point, validation of it could lead to a better understanding of post-menopausal disease risk in the context of reproduction with commonalities may also lead to future improved interventions to control such risk after menopause.

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