New developments in the field of epigenetics are changing our understanding of the genetic underpinnings of aging.
Sinclair, a professor of genetics at Harvard Medical School, and LaPlante, an associate professor of journalism at Utah State University, describe epigenetics using the metaphor of a piano. "If you think of your inherited genetics, your DNA, as a piano keyboard, then epigenetics determines how the keys play music," they write. "The primary players in this concert are molecular substances that affix to our genome and leave markers."
These epigenetic markers determine how genes function—essentially turning them "on" and "off"— and they are a crucial way that our bodies regulate themselves. However, as numerous markers accumulate over time, they can create "epigenetic noise," as Sinclair and LaPlante write, which can cause cells to become dysfunctional.
Researchers have discovered in recent years that the number of epigenetic markers acting on a person's cells can provide a surprisingly accurate measurement of his or her age. Now, a new "information theory" is growing in prominence, claiming that epigenetic markers may not just help us measure age—but that they may actually cause the decay associated with the aging process.
Essentially, once a cell suffers from too much epigenetic noise, the theory claims, it becomes senescent and stops reproducing. This has a cascading effect on all adjacent cells, Sinclair and LaPlante write, causing the proliferation of symptoms that we associate with aging.
Elements of this theory have been demonstrated in research on mice. When Harvard Medical School researchers altered young mice's genomes by adding epigenetic accretions, the mice experienced accelerated muscle and bone mass loss, began turning gray, experienced vision problems, and became more easily confused. In essence, they physically got older, even when they were chronologically still young.
Epigenetic mechanisms evolved in some of the earliest life forms on earth to regulate and repair cells that aren't functioning properly. However, if the information theory is true, these same mechanisms are paradoxically what cause us to suffer from aging.
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Not sure if you saw a UC San Francisco led study that identified signatures of ethnicity in the genome that appear to reflect an ethnic group’s shared culture and environment, rather than its common genetic ancestry. https://bit.ly/2LodF2q
Researchers and clinicians have known for many years that different racial and ethnic populations get diseases at different rates and ages, respond differently to medications and show very different results on standard clinical tests. So essentially, epigenetic markers are influenced by culture and environment. That said; nutrition represents one of the greatest environmental determinants of an individual’s health. While nutrient quantity and quality impart direct effects, the interaction of nutrition with genetic and epigenetic modifications is perhaps overlooked. If we accept the fact that uncontrolled inflammation plays a role in almost every major disease, including cancer, heart disease and diabetes, then perhaps a laser like focus on the role of epigenetic marks in chronic inflammation and the environment in which we live is the way forward to increased longevity?