A Brief Note on Evolutionary History of Human Health and Diseases

Received: 01-Jun-2022, Manuscript No. jem-22-69282 ;;Accepted Date: Jun 22, 2022; Editor assigned: 03-Jun-2022, Pre QC No. jem-22-69282 (PQ); Reviewed: 17-Jun-2022, QC No. jem-22-69282 ; Revised: 22-Jun-2022, Manuscript No. jem-22-69282 (R); Published: 29-Jun-2022, DOI: 10.4303/jem/236068

Introduction

Almost all genetic variants that influence disease risk have human-specific origins; however, the systems they influence have ancient roots that often trace back to evolutionary events that occurred long before humans existed. We discuss how advances in our understanding of disease genetic architectures, recent human evolution, and deep evolutionary history can help explain how and why humans become ill in modern environments. The prevalence of many common and rare genetic diseases varies across human populations. These differences are largely the result of modern human populations’ diverse environmental, cultural, demographic, and genetic histories. Combining our growing understanding of evolutionary history with genetic medicine, while taking environmental and social factors into account, will help to realise the promise of personalised genomics and realise the potential hidden in an individual’s DNA sequence to guide clinical decisions. In short, precision medicine is fundamentally evolutionary medicine, and incorporating evolutionary perspectives into clinical practise will help it reach its full potential. Within the last 200,000 years, modern humans evolved from their most likely common ancestor, Homo erectus, which means “upright man” in Latin.

Description

Within the last 200,000 years, modern humans evolved from their most likely common ancestor, Homo erectus, which means “upright man” in Latin. Homo erectus was a human species that existed between 1.9 million and 135,000 years ago.

Chemical toxins have been a constant source of evolutionary challenges throughout the history of life, and ancient adaptations to various chemical poisons can be found deep within the genomic storehouse of evolutionary history. However, the rate of change in modern environments mediated by human-introduced pollutants, is rapidly screening this storehouse and putting many species’ adaptive potential to the test. In this chapter, we review the long history of evolutionary adaptation to environmental toxins before going on to describe the characteristics of stressors and populations that may aid in modern adaptation to pollutants introduced by humans. We emphasise that phenotypes derived to enable survival in polluted environments may be multidimensional, necessitating global genome-scale tools and approaches to uncover their mechanistic basis, and we provide examples of recent progress in this area.

Marine pollution is widespread and is one of the major factors influencing contemporary marine biodiversity around the world. How do we monitor, document, and predict the short- and long-term effects of pollutants on at-risk species in order to protect marine biodiversity? Modern genomics tools provide high-throughput, information-rich, and increasingly cost-effective approaches to characterising biological responses to environmental stress, and are important tools in an ever-expanding toolkit for monitoring and assessing the effects of pollutants on marine species. We show how genomics tools can be used to screen chemicals and pollutants for biological activity and reveal specific mechanisms of action using recent research in marine killifish. The above-mentioned macro evolutionary events laid the groundwork for genetic disease, but considering more recent changes that occurred during the evolutionary history of the human lineage is required to illuminate the full context of human disease.

Comparing humans to their closest living primate relatives, such as chimps, has revealed diseases that do not exist in other species or take very different paths. We’re getting a better understanding of the genetic differences that underpin some of these human-specific conditions, with a focus on infectious diseases. However, this link later in life causes a clinical trade-off. Hormone replacement therapy reduces the risk of osteoporosis and ovarian cancer in postmenopausal women, but increases the risk of breast cancer due to its effects on breast tissue. Given the similarity of the maintenance versus proliferation trade-off, this is just one of many examples of cancer risk emerging as a result of trade-offs in immune, reproductive, and metabolic systems56,84. Given the interaction of multiple individuals and genomes with different goals, pregnancy is also fraught with clinically relevant trade-offs. Cellular trade-offs have medical implications as well. Cellular senescence, for example, is a necessary and beneficial part of many basic bodily responses, but the accumulation of senescent cells is at the root of many age-related disorders.

Conclusion

As a result, people with different answers to this trade-off may have very different ‘molecular’ versus ‘chronological’ ages. Although evolutionary assumptions are implicit in medical practise, self-reported family history remained the best representation of our evolutionary ancestors’ imprint on disease risk until recently. A family history, on the other hand, cannot fully capture each individual’s complex evolutionary and demographic history. New technologies now allow for the collection and interpretation of a person’s family history in a much longer and more comprehensive form their genome. New data and methods are significantly improving the resolution and depth with which these histories can be quantified, allowing evolution to inform medical practise.

Acknowledgment

None.

Conflict of Interest

None.

Copyright: © 2022 Gomez-Jacinto L. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.