Aging

Gut bacteria and the immune system: How aging changes the microbiome and can lead to ‘inflammaging’

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The human immune system changes with age. Immune responses start to become less robust as people get older, which makes them more vulnerable to certain infections and diseases. However, immune system aging looks different from person to person. Research has shown that changes to the composition and diversity of the microorganisms in the gut may explain these differences in immune system aging.

The gut microbiome — the population of microorganisms that lives in the gastrointestinal tract — helps the body maintain a stable internal environment when it is faced with external changes. This is known as homeostasis. The gut microbiome supports homeostasis in different ways, such as through helping to keep the immune system alert, and digesting dietary fibre into short-chain fatty acids to strengthen the intestinal wall.

The gut microbiome also helps us to regulate our inflammatory reactions. Inflammation helps the body fight microorganisms that cause disease, and helps repair damaged tissues. However, as the composition of our gut microbiome changes with age, a low level of inflammation can become constant throughout the body. This is called inflammaging.

When inflammaging develops in the gut, it leads to a decrease in immune responses, which puts people at a higher risk for infection and disease.

Let’s take a closer look at the gut microbiome and how it changes with age.

Gut microbiome imbalances in older adults

Diagram of microbial phyla
An overview of the four major gut microbial phyla. (Flore Van Leemput and Narveen Jandu), Author provided (no reuse)

Our gastrointestinal tract can be compared to a densely populated city inhabited by a variety of different bacteria, fungi, archaea and viruses collectively called the gut microbiota. In fact, compared to other parts of the body, the gut microbiome has the largest number of bacteria. In a healthy gut microbiome, there are four dominant families (or phyla) of microorganisms, including Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria.

Firmicutes and Bacteroidetes make up around 80 to 90 per cent of the gut microbiota in the digestive tract. Firmicutes help with the production of short-chain fatty acids to support intestinal health and the secretion of mucus to improve intestinal wall defence. Bacteroidetes metabolize complex carbohydrates into vitamins and nutrients, and help promote glycogen storage to improve glucose metabolism.

The gut microbiome and immune system work closely together. The microorganisms in the gut send out signals that are detected by immune sensors. This allows the immune system to regulate the beneficial bacteria in the gut, helping maintain immune homeostasis. Through this interaction, the adaptive immune system also receives stimuli from harmful substances called antigens, which trigger an immune reaction.

However, as people age, the composition and balance of microorganisms in the gut changes. This gives rise to microbial dysbiosis, which means there is a reduction in the number of beneficial bacteria in the gut, alongside a higher number and pro-inflammatory organisms and bacteria that can cause disease. In addition to this, research has also shown that the general diversity of bacteria in our gut also decreases with age.

Over time, the shortage of beneficial bacteria such as Firmicutes in older adults starts to compromise the integrity of their intestinal barrier, causing it to become leaky. This is because the Firmicutes family plays a very important role in keeping the intestinal wall healthy and strong by producing a short-chain fatty acid called butyrate. Short-chain fatty acids such as butyrate help provide nutrients to strengthen the intestinal wall, inform immune responses and lower inflammation.

When intact, the intestinal barrier works to prevent harmful bacteria from passing through the intestinal wall, entering the circulatory system and reaching important organs. However, when there are not enough gut bacteria to produce the short-chain fatty acids that are needed for the intestinal wall to function, bacteria are able to enter the bloodstream. This contributes to the formation of intestinal inflammaging, which refers to a low level of inflammation that becomes steady throughout the body with age.

How inflammaging works

Inflammaging creates an environment that is prone to inflammation, which is caused and maintained by several factors. These can include microorganism imbalances in the intestines (microbial dysbiosis), psychological stress, physical inactivity, poor nutrition and chronic infections.

When the body is exposed to these factors on a regular basis, cellular senescence occurs. Cellular senescence is a state in which cell growth is permanently arrested, which means that cells are no longer able to self-renew. Eventually, this leads to a decrease in immune responses, which are important to prevent foreign substances and pathogens from entering the body.

Diagram of interaction between human gut and microbiota
The microbiome and the human gut work together to maintain health, depicted as a handshake. The green arrows of the inner cycle represent a positive cycle, providing protection to the human gut and allowing it to provide the gut bacteria with a favourable habitat. The red arrows of the outer cycle represent a negative cycle that leads to dysbiosis and reduced immunity. (Flore Van Leemput and Narveen Jandu), Author provided (no reuse)

Maintaining a healthy balance of gut microbiota

There is a common saying that claims “you are what you eat.” Indeed, nutrition and diet play an important role in regulating the number of different microorganisms that live in the gut. This means that diet may also play a key role in the immune function of older adults.

The Mediterranean diet, known for its lower intake of refined carbohydrates, saturated fats, dairy products and red meat, has been shown to have a positive effect on the balance of microorganisms in the gut and the strength of the intestinal barrier. The Mediterranean diet has also been linked to a lower risk of Type 2 diabetes in older adults, allowing these individuals to live a longer and healthier life.

The use of probiotics and prebiotics can also help fight age-related inflammation. Probiotics, such as Lactobacilli and Bifidobacteria, are live microorganisms that can be consumed to support overall health. More specifically, probiotics help improve the function of the intestinal barrier and regulate immune responses by modifying the composition of the gut microbiome. However, there is still some debate around whether the acidic conditions in the stomach allow probiotics to survive long enough to be able to move into the intestine.

It is clear that the immune system has an intricate relationship with the gut microbiome. A healthy and well-balanced gut microbiome will strengthen the intestinal barrier, which helps to reduce inflammation throughout the body and support the immune system.

To achieve this, it is important to maintain a healthy and well-balanced lifestyle as we grow older. This can include lower intake of dairy products and red meats, and harnessing the benefits of probiotics and prebiotics.

Longer Genes May Drive Aging

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Summary: Four independent studies converge on the groundbreaking conclusion that the activity of long genes may be the key driver behind aging. This insight, marking a significant shift from traditional gene-specific aging theories, suggests that conditions affecting long gene activity, like smoking or caloric restriction, can accelerate or slow down aging, respectively.

The research also highlights a connection between long genes and neurodegenerative diseases, such as Alzheimer’s, offering new perspectives on disease causation and aging. The studies’ collective findings, demonstrating that longer genes are more susceptible to damage over time, pave the way for innovative aging and disease treatment strategies.

Key Facts:

  1. Long Genes at Aging’s Core: The activity of long genes, which decreases with age, is identified as a central cause of aging, connecting most existing aging knowledge into a single, measurable phenomenon.
  2. Lifestyle Impacts on Gene Activity: External factors like smoking and UV exposure reduce long gene activity, accelerating aging, whereas practices like caloric restriction enhance long gene activity, slowing aging processes.
  3. Implications for Neurodegenerative Diseases: The study suggests that the decreased activity of long genes, particularly those crucial for neural function, might underpin neurodegenerative conditions such as Alzheimer’s disease, as these cells fail to maintain essential biomaterials for neural health.

Source: Northwestern University

What causes our body to age? Four complementary studies, including one from Northwestern Medicine, have come to the same conclusion: long genes. 

In a new paper, the scientists write about their findings and how they advance existing knowledge about aging. 

“Long genes that become less active with age may be the central cause of aging in our bodies,” said co-corresponding author Thomas Stoeger, assistant professor of medicine in pulmonary and critical care at Northwestern University Feinberg School of Medicine and a member of the Potocsnak Longevity Institute.

This shows an older lady and DNA.
During aging, genes take damage as the strands of DNA that contain the genes break.

“Our finding advances the field by identifying a single phenomenon that connects most existing knowledge about aging and makes this underlying phenomenon measurable.” 

The paper, which highlighted the shared findings of four international research groups, was published in Trends in Genetics on March 21.

The groups are the first to arrive at the conclusion that most aspects of biological aging relate to gene length. 

Conditions known to accelerate aging decrease the activity of long genes. This includes smoking, alcohol, oxidative stress and UV-irradiation. Conditions known to slow aging increase the activity of long genes such as caloric restriction.

Also, genes that are very short or very long encode for cellular processes known to change in aging such as the formation of cellular energy, protein synthesis and transmission of neural signals.

“The regulation of genes is one of the most central processes of life, and our four studies explain why the activity of long genes in particular change in aging,” Stoeger said. “In addition to aging, we show that the same finding occurs in patients with Alzheimer’s disease, an age-associated disease.

“Our findings help us rethink causes of neurodegenerative diseases such as Alzheimer’s disease. Because genes with neural function are unusually long, we hypothesize that the decreased activity of long genes cells fails to produce sufficient biomaterials to properly maintain neural function.” 

The trigger of aging is a physical phenomenon related to the length of the genes and not to the specific genes involved or the function of those genes, the scientists report. The original findings were based on a mixture of molecular data from humans, mice, rats, killifish, C. elegans, D. melanogaster and experiments in mice.

Previously scientific research sought to identify specific genes responsible for aging. This new view differs from prevailing biological approaches that study the effects of single genes.

Long genes simply have more potential sites that could be damaged. The scientists compare it to a road trip — the longer the trip, the more likely that something will go wrong. And because the physiological roles of some cell types rely upon genes that are longer than those of other cell types, some cell types are more likely to be affected by DNA damage that accumulates as they age.

During aging, genes take damage as the strands of DNA that contain the genes break. This stops cells from reading the information and activating the information contained in the gene. The longer the gene, the more likely it is that at least one DNA damage site exists and stops the gene’s activation.

Because neural cells are known to rely on particularly long genes and are slow or non-dividing, they are especially susceptible to the phenomenon. Many of the genes involved in brain loss during aging and associated with Alzheimer’s disease are exceptionally long.

Pediatric cancer patients, who are cured by DNA-damaging chemotherapy, later suffer from premature aging, including neurodegeneration.

The title of the article is “Time is ticking faster for long genes in aging.”

Funding: The research from Northwestern was supported by grant R00AG068544 from the National Institute on Aging of the National Institutes of Health.

Abstract

Time is ticking faster for long genes in aging

Recent studies of aging organisms have identified a systematic phenomenon, characterized by a negative correlation between gene length and their expression in various cell types, species, and diseases.

We term this phenomenon gene-length-dependent transcription decline (GLTD) and suggest that it may represent a bottleneck in the transcription machinery and thereby significantly contribute to aging as an etiological factor.

We review potential links between GLTD and key aging processes such as DNA damage and explore their potential in identifying disease modification targets.

Notably, in Alzheimer’s disease, GLTD spotlights extremely long synaptic genes at chromosomal fragile sites (CFSs) and their vulnerability to postmitotic DNA damage. We suggest that GLTD is an integral element of biological aging.

Rethinking Aging: Could Long Genes Be the Culprits Behind Growing Older?

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Aging might be more related to gene length than the specific functions of genes, with decreased expression of long genes across species marking a key factor in aging and related diseases. This discovery opens new avenues for anti-aging research and interventions. Credit: SciTechDaily.com

Aging may be less about specific “aging genes” and more about how long a gene is. Many of the changes associated with aging could be occurring due to decreased expression of long genes, say researchers in an opinion piece publishing March 21 in the journal Trends in Genetics.

A decline in the expression of long genes with age has been observed in a wide range of animals, from worms to humans, in various human cell and tissue types, and also in individuals with neurodegenerative disease. Mouse experiments show that the phenomenon can be mitigated via known anti-aging factors, including dietary restriction.

“If you ask me, this is the main cause of systemic aging in the whole body,” says co-author and molecular biologist Jan Hoeijmakers of the Erasmus University Medical Center, Rotterdam; the University of Cologne; and Oncode Institute/Princess Maxima Institute, Utrecht.

The authors span four research groups from Spain, the Netherlands, Germany, and the United States, with each group arriving at the same conclusions using different methods.

Aging at the Molecular Level

Aging is associated with changes at the molecular, cellular, and organ level—from altered protein production to sub-optimal cell metabolism to compromised tissue architecture. These changes are thought to originate from DNA damage resulting from cumulative exposure to harmful agents such as UV radiation or reactive oxygen species generated by our own metabolism.

While a lot of research in aging has focused on specific genes that might accelerate or slow aging, investigations of exactly which genes are more susceptible to aging have revealed no clear pattern in terms of gene function. Instead, susceptibility seems to be linked to the genes’ lengths.

“For a long time, the aging field has been focused on genes associated with aging, but our explanation is that it is much more random—it’s a physical phenomenon related to the length of the genes and not to the specific genes involved or the function of those genes,” says co-author Ander Izeta of the Biogipuzkoa Health Research Institute and Donostia University Hospital, Spain.

It essentially comes down to chance; long genes simply have more potential sites that could be damaged. The researchers compare it to a road trip—the longer the trip, the more likely that something will go wrong. And because some cell types tend to express long genes more than others, these cells are more likely to accumulate DNA damage as they age. Cells that don’t (or very rarely) divide also seem to be more susceptible compared to rapidly replicating cells because long-lived cells have more time to accumulate DNA damage and must rely on DNA repair mechanisms to fix them, whereas rapidly dividing cells tend to be short-lived.

Link to Neurodegeneration

Because neural cells are known to express particularly long genes and are also slow or non-dividing, they are especially susceptible to the phenomenon, and the researchers highlight the link between aging and neurodegeneration. Many of the genes involved in preventing protein aggregation in Alzheimer’s disease are exceptionally long, and pediatric cancer patients, who are cured by DNA-damaging chemotherapy, later suffer from premature aging and neurodegeneration.

The authors speculate that damage to long genes could explain most of the features of aging because it is associated with known aging accelerants and because it can be mitigated with known anti-aging therapies, such as dietary restriction (which has been shown to limit DNA damage).

“Many different things that are known to affect aging seem to lead to this length-dependent regulation, for example, different types of irradiation, smoking, alcohol, diet, and oxidative stress,” says co-author Thomas Stoeger of Northwestern University.

However, although the association between the decline in long-gene expression and aging is strong, causative evidence remains to be demonstrated. “Of course, you never know which came first, the egg or the chicken, but we can see a strong relationship between this phenomenon and many of the well-known hallmarks of aging,” says Izeta.

In future studies, the researchers plan to further investigate the phenomenon’s mechanism and evolutionary implications and to explore its relationship with neurodegeneration.

Reversing the aging clock: A tiny plant protein holds the secret

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Scientists might have hacked the secret of anti-aging. A particular organelle in plant cells is now the subject of scrutiny that might be the key

A new plant cell discovery promises human anti-aging potential

Researchers Heeseung Choi and Katie Dehesh holding young, green and old, yellow arabidopsis plants in the laboratory

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Scientists might just be getting closer to achieving their goal of hacking the aging process as they recently discovered a new challenger in this race. There’s a particular organelle in plant cells that has been known for over a century now. However, this is a gem that has been underlooked over the years as not a lot of research has been conducted to understand it. 

Recently, a UCR research team decided to study these plant cells to determine which parts of the plant cells are responsible for controlling their responses to stress from factors like stress, too little light, or too much salt. To their surprise, they learned about this organelle and an understudied protein that is responsible for maintaining the organelle by controlling whether plants survive being left too often in the dark. 

Katie Dehesh, distinguished professor of molecular biochemistry at UCR, and co-author of the study published in Nature Plants Journal, said, “For us, this finding is a big deal. For the first time, we have defined the profound importance of an organelle in the cell that was not previously implicated in the process of aging.”

This organelle, the Golgi body, is composed of a series of cup-shaped membrane-covered sacs, and it is responsible for sorting the molecules in the cell to ensure they get to the right places. The protein called COG functions by controlling and coordinating the movement of small sac “envelopes” that transport other molecules around the cell. 

The COG protein and the Golgi bodies work hand in hand, as this protein is what will help the Golgi bodies to attach sugars to other proteins or lipids before they are sent to the needed places in the plant. 

Heeseung Choi, a researcher in UCR’s Botany and Plant Sciences Department and first author of the new study, described how the protein and the organelle work together. Choi wrote, “Golgi are like the post office of the cell. They package and send out proteins and lipids to where they’re needed. A damaged Golgi can create confusion and trouble in the cell’s activities, affecting how the cell works and stays healthy.”

COG protein effect on plant cells

After discovering how important the COG protein is to plant health, the research team decided to dig deeper to learn more about how this protein impacted the growth of these plants. Working with two groups of plants, they modified some so they could not produce these proteins. As expected, the modified plants had no issues growing under normal conditions and could not be told apart from the unmodified plants. 

Choi noted, “In the dark, the COG mutants showed signs of aging that typically appear in wild, unmodified plants around day nine. But in the mutants, these signs manifested in just three days.” This is because depriving plants of light restricts their access to sunlight to make sugar to aid their growth. 

After reversing the mutation and reversing this protein into the plant, the research team noted that it immediately brought the plants back to life as though they weren’t almost dying. 

The real excitement now lies in the fact that the Golgi bodies do not only exist in plants as they are also present in humans and all eukaryotic organisms. Dehesh noted that this research has effectively advanced knowledge about how plants age, which will be really helpful in discovering clues about the human aging process. 

Hence, the team is planning to continue studying the molecular mechanisms behind the results from this study to see just how close they will get to reaching a breakthrough relating to age-related diseases in humans. 

The Hidden Trigger of Aging: New Discovery Could Change Longevity Research.

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A groundbreaking study has discovered that cell membrane damage can lead to cellular senescence, a state associated with aging and disease. This adds a third possible outcome to the previously understood consequences of cell damage—recovery or death. The research highlights the impact of moderate membrane damage on cell fate and opens new paths for promoting healthy aging by understanding and manipulating the underlying mechanisms of cellular senescence.

Recent research has discovered that physical harm to the cell’s outer layer can trigger aging at the cellular level in human cells.

The delicate membrane encasing our cells measures just 5 nanometers in thickness—merely 1/20th the width of a soap bubble. This membrane is susceptible to damage from everyday physiological activities, such as muscle movements and injuries to tissues. In response to this vulnerability, cells possess repair systems capable of mending membrane damage to some extent.

Mechanical damage to the cell membrane was previously believed to trigger two simple cellular outcomes: recovery or death. In this study, however, the researchers uncovered a third outcome – cellular senescence.

“When I started this project, I simply aimed to understand the repair mechanisms of the damaged cell membrane,” recalls Professor Keiko Kono, head of the Membranology unit and senior author of this study, which involved multiple members from the unit, including Kojiro Suda, Yohsuke Moriyama, Nurhanani Razali, and colleagues. “Unexpectedly, we ended up discovering that cell membrane damage, in a sense, switches cell fate.”

Mechanisms of Cellular Fate Determination

The key to determining cell fate is the extent of damage and subsequent calcium ion influx. The thin cell membrane damage can be easily repaired, allowing the cells to continue cell division without any trouble. The highest level of cell membrane damage induces cell death. However, a middle level of cell membrane damage turns the cells into senescent cells several days later, even though membrane resealing seems successful

Kintsugi, the traditional Japanese art of repairing broken pottery by mending cracks with lacquer and gold. Kintsugi visibly incorporates the history of an object into its new form. In this analogy, cell membrane damaged is repaired, however, rather than restoring the cell to its original form, the new cellular nature is irreversibly changed and the cells behave differently in our body. Credit: Amy Cao, Salk Institute

Cancer cells divide unlimitedly. In contrast, non-cancerous normal cells have a limited capacity for cell division – around 50 times before division is irreversibly stopped, and the cells enter a state known as cellular senescence. Senescent cells are still metabolically active, but unlike young and healthy cells, they produce various secretory proteins that upregulate immune responses in both nearby tissues and distant organs. This mechanism can induce both beneficial and detrimental changes in our body, including acceleration of wound healing, cancer promotion, and aging. During the last decade, numerous studies have reported that senescent cells exist in animal bodies, including humans, and that the removal of senescent cells can rejuvenate body functions in experimental animals.

New Insights into Cellular Senescence

However, the cause of cell senescence in the human body remains a controversial topic. “The gene expression profile and bioinformatics suggested that cell membrane damage explains the origin of senescent cells in our bodies, specifically the ones near damaged tissues,” explains Professor Kono.

The best-established inducer of cellular senescence is repeated cell division. Many other stresses also induce cellular senescence in a laboratory setting, such as DNA damage, oncogene activation, and epigenetic changes. The long-standing dogma in the research field was that various stresses induce cellular senescence ultimately via the activation of DNA damage response. However, the authors uncovered that cell membrane damage induces cellular senescence via a different mechanism that involves calcium ions and the tumor suppressor gene p53. These findings may contribute to develop a strategy to achieve healthy longevity in the future.

Embrace the Beauty of Aging With Our Guide to Aging Joyfully

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Our celebratory guide’s skincare, haircare, health, and nutrition tips will have you feeling your best at any age.

embrace the beauty of aging with our guide to aging joyfully woman gray hair smiling looking down

Growing older doesn’t mean letting younger generations have all the fun. Our guide to aging joyfully is packed with expert advice on all things aging and will inspire you to look and feel your best!

You’ll find beauty, nutrition, fitness, and mental health tips inside to help you feel more vibrant every day. Life doesn’t stop because of aging, and you shouldn’t either—so download the Prevention Premium member-exclusive guide, Age Joyfully, to make sure you’re getting all of our experts’ brilliant tips. There’s something in here for everyone, and you’ll definitely want to share all of these helpful tidbits with friends and family!

What you’ll find in your member-exclusive guide

Age Joyfully is full of information to help you embrace your age. Here, you’ll discover ways to maintain beautiful hair and skin, keep your body at its healthiest, and sharpen your mind. The Age Joyfully guide contains 70 pages of helpful advice, practical wisdom, and inspiring ideas to help you on your path to embracing the joy and beauty of aging.

✔️ Your healthiest body at any age

Keep your eyes, heart, and bones at their healthiest throughout life. Our science-backed advice for maintaining a healthy body takes you through every decade, from your 40s to your 70s, with practical advice and fascinating insight into how your body works and what it needs from you.

✔️ Easy shortcuts to ageless skin

woman smiling

You’ll likely need to shift your approach to skincare with age. It’s normal for skin needs to change, but the chapter on “Easy Shortcuts to Ageless Skin” will help you maintain vibrant, healthy skin. Find out how to apply your vitamins, soften wrinkles, and personalize your SPF for a youthful and radiant complexion.

“What Doctors Tell Their Friends About Aging” is full of secrets from M.D.s who see hundreds of patients a year—they know what foods will help you feel young, what gets better as you get older, and what the happiest older people have in common (hint: it isn’t working more!).

You’ll also find tasty and nutritious recipes to help you enjoy the process of keeping your body strong (thanks to antioxidants necessary for aging healthfully). In “The Colors of Health,” you’ll discover how eating five hues every day will supply you with the nutrients your body needs. Some quick and easy recipes inside:

  • Herb-roasted potato medley
  • Corn, mango, and edamame salad
  • Cauliflower soup with grilled shrimp

fruits and vegetables

Here’s a sneak peek at advice you can start using today

  • Use an at-home gloss treatment once a week to keep your silver mane as shiny as possible. (From “Keep Your Hair Forever Young” on page 16).
  • Eat every three to four hours to maintain a healthy metabolism and energy levels. (From “Speed Up Your Metabolism” on page 47).
  • Add eye friendly nutrients like lutein, zeaxanthin, vitamins C and E, essential fatty acids, and zinc to your diet to reduce your risk of developing eye disease and degeneration.

A Secret Factor Accelerates Aging, Scientists Say—the Clue Could Help Us Conquer Death

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New research unveils a hidden element that speeds up the biological clock—and its implications for longevity.

young man holding picture of old eyes over his

  • Our bodies can’t keep up as we age, and a new study puts forth damage to our DNA as the potential culprit.
  • When new proteins aren’t created fast enough to keep our bodily functions moving efficiently, it leads to symptoms of aging.
  • Looking at the reason for the start of aging symptoms led researchers to discover our DNA struggling to repair itself.

If only we could figure out a way to keep our DNA healthy. Forever healthy.

We’ve long known about the symptoms of aging, but a new study published in Nature Genetics mined the root of those symptoms and found that damaged DNA may be a key reason our bodies break down.

“DNA damage,” the authors wrote, “functionally underlies major aspects of normal aging.”

Understanding just how the aging symptoms occur requires looking at each step in the process. In the study, the team from Erasmus University Medical Center in the Netherlands looked at mice and studied how protein production slows down as we age. Walking it all the way back shows that we can likely blame damaged DNA.

As explained by former Harvard Medical School professor William Haseltine in a Forbes essay, that protein production slow-down stems from damaged DNA.

Proteins are produced from RNA, which need to copy DNA. The process of DNA converting to RNA is known as transcription—the act of taking the genetic information from DNA and moving it outside a stored cell. You could think of it as DNA acting as long-term safe storage for our genetic makeup. The RNA comes into play when the DNA gets copied and moved to a different facility within the body for manufacturing proteins.

Cumulative damage to DNA gets in the way of that transcription process.

In the study, the team found that the RNA-making phase tended to stall in older mice, leading to a build-up in the DNA behind it and muddying the DNA strand until the process played itself out. The larger the gene, the more prevalent this behavior was.

With one transcription process interrupted, entire gene expressions got delayed. With interruptions and delays, proteins don’t get created fast enough to stave off those pesky aging symptoms we see, introducing hiccups in our once problem-free bodily functions. When transcription gets stuck or slowed, it causes cellular pathways to malfunction.

“We demonstrate that this transcriptional stress is caused by endogenous DNA damage and explains the majority of gene expression changes in aging,” study authors wrote. They say that this specifically impacts aging hallmarks, such as nutrient sensing, autophagy, proteostasis, energy metabolism, immune function, and cellular stress resilience.

Premature aging disorders tend to play out as a result of DNA repair mechanisms malfunctioning, and normal aging may just function that way as well. When the DNA can’t repair itself, it obviously remains damaged. That, then, backs up the protein-producing pipeline and leads to the outward-facing symptoms of aging.

“In other words, the genetic fingerprint produced by interrupted transcription is the same as that produced by aging, suggesting that the two are intimately connected,” Haseltine wrote.

When our bodies can’t produce the proper protein responses and our bodily systems start to decay, it may all stem from damaged DNA. Now, if only we could figure out how to keep the damage from happening.Tim Newcomb is a journalist based in the Pacific Northwest. He covers stadiums, sneakers, gear, infrastructure, and more for a variety of publications, including Popular Mechanics. His favorite interviews have included sit-downs with Roger Federer in Switzerland, Kobe Bryant in Los Angeles, and Tinker Hatfield in Portland. 

A Secret Factor Accelerates Aging, Scientists Say. The Clue Could Help Us Conquer Death.

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New research unveils a hidden element that speeds up the biological clock—and its implications for longevity.

young man holding picture of old eyes over his

Gear-obsessed editors choose every product we review. We may earn commission if you buy from a link. Why Trust Us?

  • Our bodies can’t keep up as we age, and a new study puts forth damage to our DNA as the potential culprit.
  • When new proteins aren’t created fast enough to keep our bodily functions moving efficiently, it leads to symptoms of aging.
  • Looking at the reason for the start of aging symptoms led researchers to discover our DNA struggling to repair itself.

If only we could figure out a way to keep our DNA healthy. Forever healthy.

We’ve long known about the symptoms of aging, but a new study published in Nature Genetics mined the root of those symptoms and found that damaged DNA may be a key reason our bodies break down.

“DNA damage,” the authors wrote, “functionally underlies major aspects of normal aging.”

Understanding just how the aging symptoms occur requires looking at each step in the process. In the study, the team from Erasmus University Medical Center in the Netherlands looked at mice and studied how protein production slows down as we age. Walking it all the way back shows that we can likely blame damaged DNA.

As explained by former Harvard Medical School professor William Haseltine in a Forbes essay, that protein production slow-down stems from damaged DN

Proteins are produced from RNA, which need to copy DNA. The process of DNA converting to RNA is known as transcription—the act of taking the genetic information from DNA and moving it outside a stored cell. You could think of it as DNA acting as long-term safe storage for our genetic makeup. The RNA comes into play when the DNA gets copied and moved to a different facility within the body for manufacturing proteins.

Cumulative damage to DNA gets in the way of that transcription process.

In the study, the team found that the RNA-making phase tended to stall in older mice, leading to a build-up in the DNA behind it and muddying the DNA strand until the process played itself out. The larger the gene, the more prevalent this behavior was.

With one transcription process interrupted, entire gene expressions got delayed. With interruptions and delays, proteins don’t get created fast enough to stave off those pesky aging symptoms we see, introducing hiccups in our once problem-free bodily functions. When transcription gets stuck or slowed, it causes cellular pathways to malfunction.

“We demonstrate that this transcriptional stress is caused by endogenous DNA damage and explains the majority of gene expression changes in aging,” study authors wrote. They say that this specifically impacts aging hallmarks, such as nutrient sensing, autophagy, proteostasis, energy metabolism, immune function, and cellular stress resilience.

Premature aging disorders tend to play out as a result of DNA repair mechanisms malfunctioning, and normal aging may just function that way as well. When the DNA can’t repair itself, it obviously remains damaged. That, then, backs up the protein-producing pipeline and leads to the outward-facing symptoms of aging.

“In other words, the genetic fingerprint produced by interrupted transcription is the same as that produced by aging, suggesting that the two are intimately connected,” Haseltine wrote.

When our bodies can’t produce the proper protein responses and our bodily systems start to decay, it may all stem from damaged DNA. Now, if only we could figure out how to keep the damage from happening.

Doctor Reveals His Daily Tips to Live a Longer Life

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Biological Clocks Have Been ‘Rewired’ To Increase Lifespan By 80 Percent

For most of human history, aging has been seen as an inevitable consequence of life. But thanks to an explosion of medical and technological breakthroughs in recent decades, some scientists are beginning to consider aging as a disease that we can actually treat, or at least delay.

One such scientist is Peter Diamandis, a medical doctor and serial entrepreneur with a portfolio of more than 20 companies.

“As an entrepreneur, my early passions were in space,” Diamandis, who was nominated as one of the World’s 50 Greatest Leaders by Fortune in 2014, told Newsweek. “But in the last decade, my passion has been about what I consider the most important revolution of our time, which is what I refer to as the healthspan revolution.”

But what is healthspan, and how does it compare to the traditional concept of lifespan?

“Your lifespan is how long you live, how long your heart is ticking,” Diamandis said. “But healthspan is how long you feel healthy, vibrant and have the ability to enjoy life. And while we’ve extended lifespan, we haven’t fully extended healthspan yet.”

Among Diamandis’ many founded companies is the non-profit XPRIZE, which designs and hosts public competitions intended to encourage technological development in specific areas. In 2023, the company announced its largest XPRIZE to date: a $101 million prize offered to a team that can develop and test therapeutics capable of extending our healthspan by restoring and maintaining function in our cognition, immune systems and muscles as we age.

Diamandis is hopefully that these technologies will begin to be available within the next seven years. But the question is, what can we do now to live a longer, healthier life?

“I talk about something called longevity mindset,” Diamandis said. “And longevity mindset is having enough confidence that these breakthroughs are coming our way. And it’s your job to remain healthy to intercept these breakthroughs coming our way.”

To support this longevity mindset, we need to adopt a longevity lifestyle.

“Genetics only account for something between 7 [percent] and 20 percent of our longevity,” Diamandis said. “The majority is your lifestyle.”

So what does a longevity expert like Diamandis do every day to optimize his health and support this longevity mindset?

  1. Exercise: “The number one thing for me is exercise. I’m in the gym lifting weights at least four days a week, I’m on my Technogym bike getting 45 minutes of zone 2 cardio three to four times a week. I’ve added 10 pounds of muscle mass in the last year. You know, I’m at the best health that I’ve been and I’m 62.
  2. Sleep: “Number two is sleep. I am monomaniacal about getting eight hours of sleep. And now, I’m in bed by 9:30 because I wake up at 5:30 a.m.
  3. Diet: “The next thing is diet. There are very few absolutes [in diet] but there are some: sugar is a poison. The body never evolved to eat that much sugar. So I minimize my sugar, I’m wearing a continuous glucose monitor and I’m measuring it constantly. And if I’m going to eat something sweet I will eat it with intention. I will savor it, rather than just shoveling it down. I also focus on taking in 150 grams of protein; I weigh 150 pounds so it’s a gram per pound to maintain and grow muscle.”
  4. Positive mindset: “A large study published in the Proceedings of the National Academy of Science [in 2019] said that optimists live 15 percent longer than pessimists. [So] I don’t watch the news. You couldn’t pay me to watch the crisis news network TV.”

A Natural Fountain of Youth for Aging Men

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Looking for a simple antiaging tool to boost your physical, psychological and sexual health? This natural blend of antioxidant-rich compounds may be just what the doctor ordered

We can’t slow down the hands of time, but it is possible to put the brakes on biological aging, at least to some extent. In men, a natural combination of pomegranate fruit rind and cocoa seed extract does just that, effectively mitigating the effects of aging.[i]

Men between the ages of 36 and 55 who took the supplement blend had improvements in several areas that typically decline with age, including boosts to physical, psychological and sexual functions.

Testosterone Declines With Age, but Nature May Help

In men, testosterone regulates sexual function, bone and muscle mass, muscular strength, production of red blood cells, psychological wellness and metabolic homeostasis, among other important functions.

But testosterone levels decrease with age, beginning with a 1% drop per year in the 30s and increasing to declines of 2% to 3% per year after age 50. This drop in testosterone can have a significant impact on daily functions.[ii] As noted in the International Journal of Medical Sciences:[iii]

“Low testosterone level decreases aging adults’ physical performance, mood status, energy level, and quality of life (QOL). A low level of FT [free testosterone] causes erectile dysfunction, loss of muscle mass, reduced sexual desire, abnormal abdominal fat gain, low bone mineral density, joint pain, sleep disturbances, fatigue, depression, and a decline in cognitive functions.”

Natural compounds, such as velvet bean (Mucuna prurines), ashwagandha and the plant Tribulus terrestris, have a long history of use to boost hormone levels and harnessing plant compounds for this purpose continues to this day.

Pomegranate-Cocoa Blend Increases Testosterone, Grip Strength and More

The study involved 120 men who took a blend of pomegranate fruit rind and cocoa seed extracts, at a dose of either 200 milligrams (mg) or 400 mg, or a placebo for 56 days. The researchers compared aging males’ symptoms (AMS) scores, along with muscular strength and serum testosterone levels before and after the supplement usage.

Both doses of the supplement significantly reduced mean AMS scores, while improving general, psychological and physical well-being. Testosterone levels also increased significantly compared with levels before the supplement usage as well as to placebo.

Hand-grip strength, a widely used biomarker of overall muscle strength and aging, also significantly improved, while perceived stress scale scores went down. Separate research also found the pomegranate-cocoa blend effectively increased testosterone level and muscle strength in young men between the ages of 21 and 35 as well.[iv]

Pomegranate Is a Symbol of Fertility

Traditionally, pomegranate is regarded as a boon to fertility, so its role in boosting testosterone isn’t entirely surprising. The rind is also heralded for a range of beneficial pharmacological activities, including:[v]

AntioxidantImmune-modulatoryAnti-diabetic
Anti-plasmodialAntimicrobialWound healing
Anti-hyperglycemicHepatoprotectiveAnti-diarrheal

Pomegranate is an antiaging superstar in part due to urolithin A (UA), a compound your gut bacteria produce when you eat ellagitannins and ellagic acid found in pomegranates, berries and nuts. UA offers benefits to mitochondrial and cellular health, age-related conditions, metabolic function, gastrointestinal homeostasis and acute diseases.[vi]

“UA enhances cellular health by increasing mitophagy and mitochondrial function and reducing detrimental inflammation. Several preclinical studies show how UA protects against aging and age-related conditions affecting muscle, brain, joints, and other organs,” researchers noted in Trends in Molecular Medicine.[vii]

Unfortunately, it’s estimated that only 40% of people can naturally produce meaningful levels of UA from dietary compounds, so supplementation or attention to improving gut health may be useful. Nonetheless, pomegranate and pomegranate extracts are rich in polyphenols known to reduce inflammation and oxidative stress, which may be useful for erectile dysfunction, benign prostatic hyperplasia[viii] and other ailments.

When you browse through our pomegranate research database, you can learn much more about the powerful health benefits of pomegranate.

Cocoa Reverses Cardiovascular Aging

In addition to boosting testosterone, cocoa contains flavanols that may help reverse age-related changes in the cardiovascular system. “Increased vascular stiffness, endothelial dysfunction, and isolated systolic hypertension are hallmarks of vascular aging,” a research team wrote in the journal Age. But, “Regular cocoa flavanol (CF) intake can improve vascular function in healthy young and elderly at-risk individuals.”[ix]

In a study of 22 young and 20 older men, consuming a cocoa flavanol drink for just 14 days reversed the age-related burden of cardiovascular risk.[x] Further, in terms of aging, consuming cocoa is linked to a number of beneficial effects, including:[xi]

  • Lower risk of heart failure hospitalization and death
  • Decreased risk of cognitive decline
  • Increased cerebral blood flow
  • Reduced body weight
  • One-third reduction in the risk of developing cardiovascular disease.

Use our cocoa research database to discover even more reasons why eating cocoa is good for you.

Looking for More Ways to Boost Testosterone Naturally?

There are many ways to fight back against the natural declines in testosterone that occur with age. First, learn more about the importance of this hormone via our testosterone research database. Then, discover these five evidence-based ways to boost your testosterone naturally — when you do, you’ll also learn five common things to avoid to keep your production optimal.