Trillions of mutations in our cells can change each of us every day
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Beyond Inheritance
by Roxanne Kamsi
Riverhead Books (April 21st)
With approximately 30 trillion cells in the human body, around 1% are replaced daily. Unfortunately, this cellular renewal is prone to errors. As a result, there can be numerous DNA mutations occurring in our bodies each day.
“You are genetically a little different today than you were yesterday, and you will be different again tomorrow,” notes Roxanne Kamsi in her book, Beyond Inheritance: A New Understanding of Ever-Mutating Cells and Health.
These mutations can vary from minor changes in single DNA letters to the loss of entire chromosomes. While some mutations are lost when cells die, many accumulate over time. By the end of life, each of your cells could harbor thousands of mutations.
While many may associate these mutations with cancerous growths, Kamsi highlights that non-cancerous mutations can lead to various health issues as well.
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Since Darwin, many thinkers have recognized that the forces of evolution must also operate within the body.
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Some mutations can have beneficial effects. For example, the formation of purple “bruises” arises from mutations during development that impact blood vessels. Additionally, mutations in skin cells may influence melanin production, creating skin patches in lines known as Blaschko lines.
This phenomenon occurs throughout the body and across all developmental stages, demonstrating that we are all mosaics composed of various cellular types. These variations can provide certain cells with distinct advantages.
When blood stem cells divide, one cell remains a stem cell while the other becomes a blood cell. If both divide at the same rate, they maintain a balanced progeny. However, mutant cells that divide more rapidly can skew this balance over time. By age 70, it’s estimated that one in ten individuals may have a predominance of mutant blood cells, increasing risks for heart attack or stroke.
This scenario resembles an evolutionary struggle among cells, where those with even slight growth advantages gradually emerge as dominant. Remarkably, Kamsi points out that post-Darwinian thinkers understood that evolutionary principles operate within our bodies, a notion that was largely forgotten after the advent of modern genetics in the 20th century.
Numerous so-called clonal diseases, including certain cases of endometriosis, illustrate this idea, as uterine cells may grow on other organs. Moreover, many mutations can be elusive to detect, especially in hard-to-study organs like the heart or brain.
However, not all mutations spell trouble. A surprising section of the book reveals how new mutations can correct inherited conditions, with research suggesting that liver cells have evolved mechanisms to tackle issues such as fatty liver disease. Yet, advantageous mutations remain the exceptions, not the rule.
While I have some critiques about the writing style and structure of this book—there are digressions about personal attributes that seem unconnected to the main content—the core message is invaluable. This book synthesizes various studies to convey essential information that should resonate with the medical community and beyond. Our bodies are composed of cells that constantly mutate and compete, often aligning with their own interests rather than our health.
Kamsi asserts, “By abandoning the outdated idea that all cells possess identical DNA and embracing the unsettling reality that each cell’s genetic code varies slightly, we can pave the way for a new era in medicine.”
While I remain skeptical about this new era, the implications are profound. Although Kamsi does not explicitly state it, her work addresses how multicellularity weakens as cellular diversity and selfishness increase—a theme of fragmentation against a backdrop of unity.
Kamsi explains that this accumulation of mutations may be a fundamental cause of aging. Conditions associated with premature aging often correlate with DNA repair issues, which facilitate the rapid accumulation of mutations.
Regardless of whether the influx of selfish mutations is a primary cause or merely a contributing factor to aging, the notion of halting aging remains misguided. While certain drugs may slow mutation accumulation and gene editing may repair some, such interventions are ultimately transient.
Even if organ transplants become commonplace, the brain will face inevitable malfunctions. Research on individuals who died in accidents has revealed approximately 1,500 mutations in each analyzed neuron. The relentless wave of mutations cannot be fully contained.
We cannot stem this tide once we begin life in the womb. Dr. Kamsi posits, “Humans are the first beings to try to shape their own genetic destiny.” However, the logical conclusion remains that the most effective way to extend lifespan would involve redesigning the human genome to significantly decrease mutation rates.
While this may one day be feasible, it’s crucial to note that such new beings would no longer be considered human.
3 More Essential Reads on Inheritance and Change
Power, Sex, and Suicide: Mitochondria and the Meaning of Life
by Nick Lane
Mitochondria, the powerhouse of our cells, were once independent bacteria before merging symbiotically with our ancestors, facilitating complex life. As Lane discusses, their distinct nature continually shapes our lives.
Mutants: On Human Form, Diversity, and Error
by Armand Marie Leroi
Emphasizing our shared condition as mutants, Leroi discusses extraordinary cases such as babies born with single eyes. Sadly, some conditions, like albinism, can be life-threatening, yet they provide insights into our developmental processes.
Old Man’s War
by John Scalzi
Does old age signify the end? Not in Old Man’s War, a thrilling sci-fi adventure. I won’t spoil the plot, but the sequel is equally compelling and a must-read.
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Source: www.newscientist.com
