Hallmarks Of Aging
3 min read
APRIL 5, 2023 - BY ANNIE MOBERG
LONGEVITY
Hallmarks Of Aging
3 min read
APRIL 5, 2023 - BY ANNIE MOBERG
LONGEVITY
From the moment we’re born, we all experience the effects of aging. Many of these effects are positive: improved cognitive function from birth means we learn how to read, and improved coordination helps us learn to walk.But most of us tend to think about the negative aspects of aging. From smile lines and gray hair to creaky knees and sluggish circulation, aging is something we begrudgingly accept as an inevitable part of the human condition. Bot does it have to be? That’s just one question in a series that longevity scientists have long pursued: exactly what is aging, why do we age, and what can we do to one day make age-related diseases a thing of the past?
From the moment we’re born, we all experience the effects of aging. Many of these effects are positive: improved cognitive function from birth means we learn how to read, and improved coordination helps us learn to walk.But most of us tend to think about the negative aspects of aging. From smile lines and gray hair to creaky knees and sluggish circulation, aging is something we begrudgingly accept as an inevitable part of the human condition. Bot does it have to be? That’s just one question in a series that longevity scientists have long pursued: exactly what is aging, why do we age, and what can we do to one day make age-related diseases a thing of the past?
01
What is aging?
Scientists define aging as “a progressive loss of physiological function that can increase our overall susceptibility to disease and death.” While this definition isn’t exactly cheerful for most of us, longevity scientists see it as a thrilling puzzle just waiting to be solved. Why do we lose physiological function as we get older? Why are certain diseases, like Alzheimer’s, arthritis, and osteoporosis so inextricably linked to aging? And most importantly: what can science do to slow the loss of physiological function to help people lead longer, happier, healthier lives?We may be decades away from having the answers to all of these questions. But recent scientific breakthroughs have identified the factors behind the first very important question: why do we age?
01
What is aging?
Scientists define aging as “a progressive loss of physiological function that can increase our overall susceptibility to disease and death.” While this definition isn’t exactly cheerful for most of us, longevity scientists see it as a thrilling puzzle just waiting to be solved. Why do we lose physiological function as we get older? Why are certain diseases, like Alzheimer’s, arthritis, and osteoporosis so inextricably linked to aging? And most importantly: what can science do to slow the loss of physiological function to help people lead longer, happier, healthier lives?We may be decades away from having the answers to all of these questions. But recent scientific breakthroughs have identified the factors behind the first very important question: why do we age?
02
Why do we age?
Longevity scientists have spent decades examining a range of species in search of commonalities that may hold the clue to why we age. The result: twelve common factors observed across species known as the hallmarks of aging. Although each hallmark is unique, they all interact with one another to contribute to the signs of aging. By understanding these hallmarks and how they interact, not only can we better understand aging, we can begin to understand how to reverse its impacts.
02
Why do we age?
Longevity scientists have spent decades examining a range of species in search of commonalities that may hold the clue to why we age. The result: twelve common factors observed across species known as the hallmarks of aging. Although each hallmark is unique, they all interact with one another to contribute to the signs of aging. By understanding these hallmarks and how they interact, not only can we better understand aging, we can begin to understand how to reverse its impacts.
03
The Twelve Hallmarks of Aging
Science is always learning! Researchers originally identified just nine hallmarks of aging. But more recently, three new hallmarks of aging have been classified and published in the latest version of Cell’s landmark paper, “Hallmarks of Aging”.The original 9 hallmarks:1. Genomic Instability: As we age, numerous factors can damage our DNA. The more damage our DNA accumulates over time, the higher our chances are of developing age-related disease and signs of accelerated aging.2. Telomere Attrition: Telomeres, the compound structures at the end of each of our chromosomes, shorten as we age. The shorter our telomeres get, the harder it is for our cells to multiply–making it more difficult for our tissues to regenerate and repair themselves. This compromised cell proliferation can lead to a number of age-related diseases.3. Epigenetic Alterations: Throughout the course of our lives, our DNA can be chemically modified by both internal and external factors – for example, by the foods we eat or by UV exposure. These superficial DNA modifications determine which of our genes will be expressed or not expressed. As our DNA accumulates alterations with age, we’re more likely to see the activation of genes linked to inflammation and aging.4. Loss of Proteostasis: Proteostasis maintains proper folding, degradation, trafficking, and biogenesis of proteins in our cells. As we age, proteostasis diminishes, which means our bodies start to create misfolded proteins. As these proteins accumulate in the body with time, they can lead to many issues, including chronic inflammation.5. Deregulated Nutrient-Sensing: Metabolic activity, while essential to life, puts stress on our cells. To prevent this, our cells have nutrient sensing pathways that make sure they’re taking in the right amount of nutrition–enough to sustain life, but not too much to stress the system. As we age, these nutrient-sensing pathways deregulate. This is thought to be a primary factor behind age-related metabolic diseases like diabetes and obesity.6. Mitochondrial Dysfunction: Known as the “powerhouse of the cell,” mitochondria keep our cells healthy and functioning. As we age, our chance of mitochondrial dysfunction increases, thereby speeding the rate of apoptosis – cell death.7. Cellular Senescence: Senescent cells are cells at the end of their life cycle that can no longer divide. When we’re young and healthy, our bodies naturally clear these cells away. But as we age, our bodies become less efficient at removing senescent cells. This leads to an accumulation of senescent cells that has been shown to increase inflammation and contribute to a number of chronic diseases.8. Stem Cell Exhaustion: Stem cells are the vital source from which all of our cells emerge. As we age, the activity of our stem cells slowly decreases. This occurs for a number of reasons; for example, pro-inflammatory signals secreted by senescent cells reduce stem cell activity. This, in turn, makes it harder for our tissues to regenerate in the same way that they do when we are young.9. Altered Intercellular Communication: Cells are constantly communicating with one another to properly function. As we age, the signaling pathways our cells use to communicate can become disrupted. Without proper communication between cells, various forms of damage can occur.The additional three hallmarks:10. Chronic Inflammation: As we age, inflammation increases throughout our bodies in a process called inflammaging. This inflammation is a result of multiple derangements caused by other hallmarks and can be observed by measuring concentrations of inflammatory cytokines and biomarkers like CRP.¹² Over time, this inflammation can have systemic manifestations, including arteriosclerosis, neuroinflammation, and osteoarthritis.11. Disabled Macroautophagy: Autophagy is the process by which our cells clean themselves. When this process is disrupted, cells can experience a build-up of waste, reduced elimination of pathogens, and enhanced inflammation. There is strong evidence that decreased autophagy is relevant to aging and age-related diseases like metabolic disorders and cancer.12. Dysbiosis: Disruption in our gut bacteria can result in dysbiosis and contributes to a variety of conditions, such as obesity, type 2 diabetes, ulcerative colitis, neurological disorders, and cancer. While bacterial diversity is established during childhood and remains relatively stable in adulthood, it undergoes gradual changes during aging, leading to an overall decrease in ecological diversity.
03
The Twelve Hallmarks of Aging
Science is always learning! Researchers originally identified just nine hallmarks of aging. But more recently, three new hallmarks of aging have been classified and published in the latest version of Cell’s landmark paper, “Hallmarks of Aging”.The original 9 hallmarks:1. Genomic Instability: As we age, numerous factors can damage our DNA. The more damage our DNA accumulates over time, the higher our chances are of developing age-related disease and signs of accelerated aging.2. Telomere Attrition: Telomeres, the compound structures at the end of each of our chromosomes, shorten as we age. The shorter our telomeres get, the harder it is for our cells to multiply–making it more difficult for our tissues to regenerate and repair themselves. This compromised cell proliferation can lead to a number of age-related diseases.3. Epigenetic Alterations: Throughout the course of our lives, our DNA can be chemically modified by both internal and external factors – for example, by the foods we eat or by UV exposure. These superficial DNA modifications determine which of our genes will be expressed or not expressed. As our DNA accumulates alterations with age, we’re more likely to see the activation of genes linked to inflammation and aging.4. Loss of Proteostasis: Proteostasis maintains proper folding, degradation, trafficking, and biogenesis of proteins in our cells. As we age, proteostasis diminishes, which means our bodies start to create misfolded proteins. As these proteins accumulate in the body with time, they can lead to many issues, including chronic inflammation.5. Deregulated Nutrient-Sensing: Metabolic activity, while essential to life, puts stress on our cells. To prevent this, our cells have nutrient sensing pathways that make sure they’re taking in the right amount of nutrition–enough to sustain life, but not too much to stress the system. As we age, these nutrient-sensing pathways deregulate. This is thought to be a primary factor behind age-related metabolic diseases like diabetes and obesity.6. Mitochondrial Dysfunction: Known as the “powerhouse of the cell,” mitochondria keep our cells healthy and functioning. As we age, our chance of mitochondrial dysfunction increases, thereby speeding the rate of apoptosis – cell death.7. Cellular Senescence: Senescent cells are cells at the end of their life cycle that can no longer divide. When we’re young and healthy, our bodies naturally clear these cells away. But as we age, our bodies become less efficient at removing senescent cells. This leads to an accumulation of senescent cells that has been shown to increase inflammation and contribute to a number of chronic diseases.8. Stem Cell Exhaustion: Stem cells are the vital source from which all of our cells emerge. As we age, the activity of our stem cells slowly decreases. This occurs for a number of reasons; for example, pro-inflammatory signals secreted by senescent cells reduce stem cell activity. This, in turn, makes it harder for our tissues to regenerate in the same way that they do when we are young.9. Altered Intercellular Communication: Cells are constantly communicating with one another to properly function. As we age, the signaling pathways our cells use to communicate can become disrupted. Without proper communication between cells, various forms of damage can occur.The additional three hallmarks:10. Chronic Inflammation: As we age, inflammation increases throughout our bodies in a process called inflammaging. This inflammation is a result of multiple derangements caused by other hallmarks and can be observed by measuring concentrations of inflammatory cytokines and biomarkers like CRP.¹² Over time, this inflammation can have systemic manifestations, including arteriosclerosis, neuroinflammation, and osteoarthritis.11. Disabled Macroautophagy: Autophagy is the process by which our cells clean themselves. When this process is disrupted, cells can experience a build-up of waste, reduced elimination of pathogens, and enhanced inflammation. There is strong evidence that decreased autophagy is relevant to aging and age-related diseases like metabolic disorders and cancer.12. Dysbiosis: Disruption in our gut bacteria can result in dysbiosis and contributes to a variety of conditions, such as obesity, type 2 diabetes, ulcerative colitis, neurological disorders, and cancer. While bacterial diversity is established during childhood and remains relatively stable in adulthood, it undergoes gradual changes during aging, leading to an overall decrease in ecological diversity.
Key Takeaways:
- Longevity scientists study why we age and how to reverse the impacts of age-related disease.
- These researchers have uncovered 12 hallmarks of aging common to many different species.
- From DNA damage to the accumulation of senescent cells, these 12 hallmarks interact to cause age-related diseases like Alzheimer’s and arthritis.
- Some lifestyle practices like cold exposure, plant-based eating, and daily exercise can help slow some of these 12 hallmarks, improving our overall longevity.
Key Takeaways:
- Longevity scientists study why we age and how to reverse the impacts of age-related disease.
- These researchers have uncovered 12 hallmarks of aging common to many different species.
- From DNA damage to the accumulation of senescent cells, these 12 hallmarks interact to cause age-related diseases like Alzheimer’s and arthritis.
- Some lifestyle practices like cold exposure, plant-based eating, and daily exercise can help slow some of these 12 hallmarks, improving our overall longevity.
Reviewed by Alessandra Zonari, PhD, Chief Scientific Officer (CSO) and Co-Founder of OneSkin
Alessandra earned her Master’s degree in stem cell biology, and her PhD in skin regeneration and tissue engineering at the Federal University of Minas Gerais in Brazil in collaboration with the 3B’s Research Group in Portugal. Alessandra did a second post-doctoral at the University of Coimbra in Portugal. She is a co-inventor of three patents and has published 20 peer-reviewed papers in scientific journals.
Reviewed by Alessandra Zonari, PhD, Chief Scientific Officer (CSO) and Co-Founder of OneSkin
Alessandra earned her Master’s degree in stem cell biology, and her PhD in skin regeneration and tissue engineering at the Federal University of Minas Gerais in Brazil in collaboration with the 3B’s Research Group in Portugal. Alessandra did a second post-doctoral at the University of Coimbra in Portugal. She is a co-inventor of three patents and has published 20 peer-reviewed papers in scientific journals.
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Yes, You Need Sunscreen During Winter
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Exploring the skin’s purpose in whole-body health
Stressed Skin: 4 Stress Effects on the Skin
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What Causes Dark Circles Under and Around Your Eye...
How to Brighten Eyes and Under-Eyes
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6 Benefits of Jojoba Oil
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7 Benefits of Andiroba Oil For Skin
Why is my Skin Peeling on My Face?
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PREP enhances the effects of OS-01 FACE, and the p...
Why cellular senescence is more than just one of t...
Allantoin For Skin: A Comprehensive Guide
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A Simplified Guide To The Different Skin Texture T...
How OS-01 Works With Different Skin Types
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Does Niacinamide Help With Acne & Scarring?
Skin Microbiome: What It Is, Why it’s Important, A...
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The 101 Guide To Understanding Acne-Prone Skin
The Top 4 Prickly Pear Benefits for Skin
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OneSkin Notable Mention: Dave Asprey's The Human U...
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Clean Beauty: What “clean” really means and why “s...
Retinol 101: Debunking Retinol as the Gold Standar...
Menopause & Skin: What you need to know
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101 Guide on The Benefits of Cleansing Your Face
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Celebrating Black History Month: A Discussion With...
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Peptides: the first piece of th...
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Health Is The New Wealth
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