Skip to main content.

Grayhawk Healthy Aging Newsletter

Kenneth Seldeen
Dr. Kenneth Seldeen
Grayhawk Registry

Greetings Grayhawk Members to the fourth newsletter!

I appreciate the feedback from the third newsletter; hopefully a few of those green light tips were useful!  Please bear with me as we set up the response to the many comments from our previous newsletters. It is on its way, but for now I’ve entered the grant-writing season so these are busy times! 

For this newsletter, I thought I might cover one of my many journeys where a Google news health story sent me down a twisty rabbit hole – and show how I go about reading and confirming the content. With that I am pleased to present:

Newsletter 4, May 2026:

Seed oils: A Case Study in Handling Click-Bait Health News

This story starts as do many days with the swiping through the endless stream of news stories (FYI – not a good healthy aging strategy).  For others it might be social media feed, but the result likely might be the same: a catchy article discussing a better way to stay healthy. In this case, the article was “Scientists Just Debunked Every Myth About Seed Oils—Here’s What They Found”.

screenshot of google search
 A provocative title and a hot topic so I took the click bait!

First, some background. Heart disease is the #1 cause of mortality in the United States. There have been decades of research to find causes and risk factors with the finger often being pointed at dietary fat. Fat is comprised of shorter and longer molecules called fatty acids. There are three main types of fatty acids: saturated, polyunsaturated, and monounsaturated fats. The difference is the presence of 0 (saturated), 1 (monounsaturated), or 2 or more (polyunsaturated) double bonds in the chemical structure (see below image). Our body interacts with these molecules in different ways. To add more complexity, there are different types of polyunsaturated fatty acids, including omega-6 and omega-3, but we will get back to this in a bit.

diagram of the atomic bonds of different fatty acid types

The three main fatty acids — saturated fats have no double bonds, monounsaturated fats have one double bond, and polyunsaturated fats have two or more double bonds.

When it comes to heart disease the usual suspect is saturated fat. The main idea is that saturated fat increases LDL cholesterol (aka the “bad” cholesterol), which is thought to increase blockages of the heart’s arteries. As with most things, the truth of this is more nuanced and complicated, but also not the focus for this newsletter. That focus would be a second suspected cause of heart disease — omega-6 fatty acids.

This speculation picked up a lot of steam with studies suggesting the diet of our ancestors had a 1 to 1 ratio of omega-6 to omega-3 fatty acids, whereas our modern diets were a very lopsided ratio of 16 to 1 [1]. The concern is that the omega-6 fatty acid, arachidonic acid, is used to activate our immune system and therefore having too much omega-6 might cause chronic inflammation, which is linked to heart disease.

Now for the final background piece — what are seed oils? Our diets contain a wide variety of fats and oils such as butter, lard, soybean oil, canola oil, olive oil, coconut oil, avocado oil, and many more. Each of these are a blend of the various fatty acids discussed above but are mostly one type. For example, butter is mostly saturated fat, soybean oil is mostly omega-6 polyunsaturated fat, and olive oil is mostly monounsaturated fat. Now to answer the question — the term seed oil generally refers to oils derived from the seeds of plants. Some examples include corn oil, sunflower oil, soybean oil, and canola oil (rapeseed plant). The concern is that seed oils are mostly omega-6 polyunsaturated fats — which might cause inflammation and thus heart disease.

food sources for types of fatty acids

A few of the food sources and oils for saturated, polyunsaturated (Omega-6 & Omega-3), and monounsaturated fatty acids.

Now back to our healthy aging news article. The article is by Mackenzie Burgess, a registered dietary nutritionist. Her article, which covers a scientific review article, examines many of the health concerns surrounding seed oils (which includes the omega-6/omega-3 ratio issue I am focusing on here). The main points of the article are that these health concerns are overstated. Specifically with regards to the omega-6/omega-3 ratio she writes, “You might have heard people claim that our modern diets contain too much omega-6 relative to omega-3 fats (and that seed oils are largely to blame). The review pushes back on this framing, noting that this ratio isn’t a very reliable measure of diet quality.”  Not too detailed, but the take home is clear — don’t worry about it.

When I come across a health news story, my cynical nature leads me first to question the motivations of the people behind the work. Unfortunately, health news stories can make or break food industries. With so much at stake, it is not too uncommon for fabricated scientific studies, misleading news articles, and outright lies to cloud the information space.

This was exemplified in the 1960s when the sugar industry paid off Harvard scientists to write an article pointing the finger at dietary fat as the cause of heart disease instead of sugar. Sadly, the impacts of this are still felt today — in fact only about a third of US adults are aware of the risk of sugary beverages for heart disease [2].

So first I looked into the author Mackenzie Burgess. She has covered a wide range of health nutrition topics and what generally appears to be good content. A quick AI (Copilot) investigation also revealed she has good intentions in her writing. All clear here, so next, what about the science review article itself — linked here [3]?

Screenshot of academic article

The review article with a very provocative title itself (for scientists).  A Scoping narrative review broadly summarizes the knowledge gaps on a topic without specific rules for deciding what other research studies are included or not included.

The research team is an interesting mix. Author #1 is associated with a naturalistic healthcare company. Author #2 is an academician in the Department of Public Health in Helsinki Finland and is also associated with a company that develops a nutritional focused phone app. Author #3 is in the Food Science and Technology department at The Ohio State University. Finally, author #4 works at the Soy Nutrition Institute Global, which is funded by the soybean industry. Certainly, one would expect having direct ties with the soybean industry and soybean oil (a primary oil in vegetable oil and the most used cooking oil in the United States) would have potential conflicts!

However, to be fair one must address the arguments, not the person!

Unfortunately, my focus, the omega-6/omega-3 ratio, was a section the authors hurried through. Potential deficiencies I found in the section, “Perspectives on the relevance of the dietary n-6:n-3 PUFA ratio”, include: 1) self-citing their own work, 2) stating they are not going into detail since others have discussed ‘why this ratio has fallen out of favor’, with one of those others cited being a potentially conflicted author who is associated with a company advancing a new biomarker to replace the omega-6/omega-3 ratio [4]; and 3) not addressing articles that speak to the possible importance of the ratio (I found two recent references [5, 6], in just a quick search).

They do raise an interesting point — studies where omega-6 is increased in the diet do not appear to increase inflammation [7]. I continued to investigate and confirm using AI and my own searching of the scientific literature (via pubmed.gov), and found lots of support for the notion that switching from diets higher in saturated fats to one with more omega-6 heavy polyunsaturated fats reduces the risk of heart disease (here is one of the review articles I found). Additionally, other schools of thought suggest it is not the amount of omega-6 in the diet that matters, but that it is more important that you have enough omega-3 [8]. I will have to write a future article on omega-3 supplementation (cod liver oil anyone?).

To wrap all of this up. Health news stories can be interesting, and perhaps useful. However, it is important to always be aware of motivations behind the authors and sources.

Regarding seed oils — through the trials and tribulations of the dietary fat rabbit hole I went on, and now have taken you through, I think we can all conclude it is complicated. They may not be as harmful as believed. This is good because it is difficult to avoid these oils in the average American diet. However, this article has not really changed my mind on my home habits. There, I try to avoid the whole debate about seed oils versus butter and just use monounsaturated fats, like olive oil and avocado oil, for most everything. I also feel that in the way olive and avocado oils are made, these oils might have more of the health improving bioactive compounds, which we discussed last newsletter. So, for me I suppose I’ll keep on this path, that is until I go down the next rabbit hole.

Thank you for reading the newsletter!

Sincerely,
Kenneth Seldeen, PhD
Associate Professor, Geriatrics Division, Department of Internal Medicine
Director, Grayhawk Healthy Aging Collaborative
Landon Center on Aging, University of Kansas Medical Center

References:

  1. Simopoulos, A.P., Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases. Biomed Pharmacother, 2006. 60(9): p. 502-7.
  2. Hunter, J.R., et al., Associations Between Knowledge of Health Conditions and Sugar-Sweetened Beverage Intake Among US Adults, 2021. Nutrients, 2024. 16(24).
  3. Nagra, M., et al., Concerns about the health effects of industrially produced seed oils are without scientific foundation: a scoping narrative review of the clinical and observational evidence. Crit Rev Food Sci Nutr, 2026: p. 1-61.
  4. Harris, W.S., The Omega-6:Omega-3 ratio: A critical appraisal and possible successor. Prostaglandins Leukot Essent Fatty Acids, 2018. 132: p. 34-40.
  5. DiNicolantonio, J.J. and J.H. O'Keefe, Importance of maintaining a low omega-6/omega-3 ratio for reducing inflammation. Open Heart, 2018. 5(2): p. e000946.
  6. Gutierres, D., R. Pacheco, and C.P. Reis, The Role of Omega-3 and Omega-6 Polyunsaturated Fatty Acid Supplementation in Human Health. Foods, 2025. 14(19).
  7. Rett, B.S. and J. Whelan, Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review. Nutr Metab (Lond), 2011. 8: p. 36.
  8. Calder, P.C., Omega-3 fatty acids and inflammatory processes: from molecules to man. Biochem Soc Trans, 2017. 45(5): p. 1105-1115.
Previous Newsletters

Newsletter 3, April 2026

For now, aging may be inevitable. But at any age, the human body has an amazing ability to improve, repair and adapt. There are many healthy aging strategies we can practice every day to maintain or even improve our health. To start, here are my top five.

Strategy 1: Maintaining and Expanding Social Interactions

Social isolation is one of the hallmarks of aging. Unfortunately, loneliness is on the rise, and the risks are great — as described in this news story about social isolation. Yes, we are social creatures, and the benefits of being social are many: stress reduction, better cognition, higher physical activity and more (figure below). So how best to maintain social interactions? Although family and close friends help, it has been shown that “larger social networks have a protective influence on cognitive function” (Reference 1) — in other words, meeting fresh faces and different kinds of people can help our health.

Illustration showing social interaction supporting healthy aging, including reduced stress, better sleep, cognitive function, physical activity, and lower blood pressure

Staying social may be one of the best anti-aging
strategies available. The figure above touches on
just a few of the many benefits. See references
1-6 at the end of the article.

How do we do that? I would start by asking: What activities do you like to do? Your hobbies and interests are often shared by others. Clubs and meetups can be found online. For me, my pickleball addiction has already led to dozens of new friends.

Strategy 2: Using Sleep Hygiene

We need to sleep. The benefits are wide ranging — so why is sleep so difficult?

Illustration showing sleep hygiene leading to healthy sleep, including reduced stress, sharper focus, better immunity, improved mood, and a consistent sleep schedule

Sleep hygiene refers to the habits to support
consistent sleep, and the health benefits are
abundant. See references 7-11 at the end of the
article.

Here are the goals for sleep:

Duration: Generally, about 6-8 hours per night. Some researchers lean more towards 8 hours.

Quality: Sleeping through the night, with fewer middle-of-the-night wakeups. It also refers to the overnight cycling between light, REM and deep sleep.

Although no magic pills exist to accomplish this, sleep hygiene can certainly help. Covered nicely by this Cleveland clinic article, sleep hygiene refers to habits that improve sleep duration and quality. This includes:

  • Having regular sleep and wake-up times.
  • Keeping the bedroom cool and dark (sleep mask helps too).
  • Having a comfortable bed and pillow.
  • Taking a warm bath or shower right before can help.
  • Having a standard quiet routine leading up to sleep (like reading or meditation).
  • Avoiding late night snacks, cell phone usage (no news sites), alcohol, caffeine, stress inducing activities (do not watch the news before bed).

I would also add that if you regularly wake up to use the bathroom, make sure the path is clear, safe and well lit to avoid falls. Using red lighting may be preferable so you can quickly return to sleep.

Strategy 3: Nutrition - Eat your fruits and vegetables

There may be no area of greater confusion than identifying the perfect longevity diet. With so many options and strategies — ranging from scientifically grounded to straight fad — how does one navigate? You may have heard of a few of these — vegetarian, Mediterranean, DASH, longevity, Nordic, Atkins, Paleo, Carnivore, Whole30, Alkaline — perhaps hundreds or even a thousand more!

My view is that a common thread in about 90-95% of healthy diets is the inclusion of fruits and even more so, vegetables. Why is this the case? Well, beyond the vitamins and mineral benefits, fruits and vegetables have bioactive compounds. These are molecules that have the potential to affect our health and enhance the action of vitamins naturally found in the food. There are tens of thousands, maybe hundreds of thousands of different types of these molecules found in fruits and vegetables. Here are a few major classes:

  • Polyphenols like anthocyanin found in blueberries - give antioxidant benefits.
  • Carotenoids like lycopene found in red tomatoes - reduce risk of cardiovascular disease.
  • Terpenoids like ursolic acid found in apple skin - increase muscle mass.
  • Saponins like ginsenosides found in ginseng - relieve stress.
  • Still so many more classes to go — I’ll stop here.
Broccoli, citrus, tomatoes, berries, carrots, and avocado labeled with nutrients such as sulforaphane, flavonoids, lycopene, anthocyanins, lutein, oleic acid, and phytosterols, respectively

Fruits and vegetables are each packed with unique bioactive
compounds. Diversity in diet may be a key to aging well.

Generally, the research is still too thin (yellow / red light level) to recommend supplementation with any specific bioactive molecule. But overall, the potential of these compounds are why I support a wide variety of fruits and vegetables in your diet.

Strategy 4: Nutritional Supplements — Vitamin D for me

There are many yellow light supplements, and many could/should be green light — but, as this newsletter is getting on the longer side, I will recommend only vitamin D for now. Vitamin D is very interesting scientifically. As of writing, there are 99,926 scientific publications on pubmed.gov regarding vitamin D — yet so much controversy still exists regarding the benefits of supplementation.

Generally, those with higher serum vitamin D levels fare better in many areas (figure below) — but studies using vitamin D supplements to improve health often show mixed results. My view is with the low risk profile and relatively low cost, along with potential for many benefits, I put vitamin D on my green light list. Supplementing with 1,000 to 2,000 IU daily of vitamin D3 is in the safe range (upper limit 4,000 IU daily). For most adults, this dose will successfully increase serum 25-OH vitamin D levels above the sufficiency threshold — technically above 30 ng/ml or 75 nmol/L depending on the units used in a serum test. A cautionary note: those with a history of calcium kidney stones or hyperparathyroidism should talk with their physician before undertaking significant vitamin D supplementation.

Illustration showing vitamin D supplementation supporting bone health, muscle function, immune health, fall prevention, mood, and well‑being.
Vitamin D has a very low risk profile and great
potential to enhance our health in many ways.
See references 12-16 at the end of the article.

Strategy 5: Exercise — keep it fun and do not get injured

We have all heard the recommendations — 30 minutes a day, 5 days a week, plus strength training. Yet less than 15% of those 65 and older meet these goals! These recommendations are a big step from the 1970s recommendations — that being aerobic exercise only. But there is so much more exercise can do for us (figure below).

My primary expertise is aging research, but muscle has been an interest area for the past 10 years. Two main observations that guide my exercise recommendations are: 1) we need exercise to challenge our muscle, cardiovascular, and cognitive systems in a variety of ways (figure below); and 2) it does not take much time per exercise to see benefits.

Illustration showing exercise as key to physical fitness, supporting endurance, muscle mass, balance, strength, mobility, and flexibility.

Unfortunately, there is no pill or single exercise
that accomplishes all the wide-ranging benefits
the body needs. Therefore, keep your exercises
different, keep them safe, and most importantly
keep them fun!

Lots to talk about in a newsletter, so to keep this short: we need all types of exercise — gentle walks for stress relief, heavy-breathing challenges for cardiovascular fitness, a variety of resistance exercises for muscle mass, strength and power, balance training, flexibility and more. How does one fit all this into a busy schedule?

Admittedly, that question has always been a curiosity for me. I frame it this way: what is the least amount of exercise that we can do and still receive benefits? A long walk will take a long time, but can this be done once a week to achieve long term benefits? Can a 30-minute stationary bike session be replaced with a shorter one if high intensity intervals are included? In the gym, are three sets of 10 needed? Can one set work if the weight is a little greater? Early indications to all these questions are yes.

Plus, some activities accomplish multiple exercise goals at the same time. Activities such as sports, gardening and even activities that do not seem like exercise but are fun and include social interaction can be beneficial. Aside from the physical benefits, exercise should be enjoyable and engaging. The strategy should not be to focus solely on what exercise can improve for you, but rather on having a more active lifestyle.

Finally, whatever exercise you choose, keeping injury-free is important. Injuries can halt exercise programs for lengthy periods of time and cause dramatic declines. A few recommendations to avoid injuries:

  • Consult a physician to clear you for exercise before starting.
  • Seek out expertise, such as a gym trainer, to learn proper techniques for exercises.
  • Plan ahead for the activity; think about the possible risks and what you will do if you encounter problems.
  • Do not speed from 0 to 100. If new to exercise, start with easy-to-accomplish goals to identify your starting levels and build slowly from there (especially with weightlifting).
  • Likewise, until you get a sense of your exercise capacity, do not do too much in one day (no 10 mile runs on day 1).
  • Rest days are needed - all your exercise goals do not need to be accomplished in a day.
  • If you are feeling concerned or unsure about certain exercises, do not take the risk — there is no need to rush anything when it comes to exercise.

More about exercise is sure to come in future newsletters. Thank you for reading.

Sincerely,
Kenneth Seldeen, Ph.D.
Associate Professor, Geriatrics Division, Department of Internal Medicine
Director, Grayhawk Healthy Aging Collaborative
Landon Center on Aging, University of Kansas Medical Center

References:

  1. Social network, cognitive function, and dementia incidence among elderly women. American Journal of Public Health. https://www.pubmed.gov/18511731
  2. The relationship between social support and sleep quality in older adults: A review of the evidence. Archives of Gerontology and Geriatrics. https://www.pubmed.gov/37717378
  3. The Effects of Social Interaction Intervention on Cognitive Functions Among Older Adults Without Dementia: A Systematic Review and Meta-Analysis. Innovation in Aging. https://www.pubmed.gov/39450376
  4. Anomaly Detection Based on Time Series Data of Hydraulic Accumulator. Sensors (Basel). https://www.pubmed.gov/36502152
  5. Longitudinal Analysis of the Relationship Between Social Isolation and Hypertension in Early Middle Adulthood. Journal of the American Heart Association. https://www.pubmed.gov/38619293
  6. Could social relationships be key to reaching healthy longevity? Aging (Albany NY). https://www.pubmed.gov/37387546
  7. Sleep loss and emotion: A systematic review and meta-analysis of over 50 years of experimental research. Psychological Bulletin. https://www.pubmed.gov/38127505
  8. Sleep deprivation effects on basic cognitive processes: which components of attention, working memory, and executive functions are more susceptible to the lack of sleep? Sleep Science. https://www.pubmed.gov/34381574
  9. A Narrative Review on How Timing Matters: Circadian and Sleep Influences on Influenza Vaccine Induced Immunity. Vaccines (Basel). https://www.pubmed.gov/40872930
  10. Assessment of an App-Based Sleep Program to Improve Sleep Outcomes in a Clinical Insomnia Population: Randomized Controlled Trial. JMIR mHealth and uHealth. https://www.pubmed.gov/40267472
  11. The importance of sleep regularity: a consensus statement of the National Sleep Foundation sleep timing and variability panel. Sleep Health. https://www.pubmed.gov/37684151
  12. Effect of supplemental vitamin D3 on bone mineral density: a systematic review and meta-analysis. Nutrition Reviews. https://www.pubmed.gov/36308775
  13. Effect of vitamin D supplementation on muscle strength, gait and balance in older adults: a systematic review and meta-analysis. Journal of the American Geriatrics Society. https://www.pubmed.gov/22188076
  14. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. https://www.pubmed.gov/28202713
  15. Effect of Vitamin D Supplementation on Depression in Adults: A Systematic Review of Randomized Controlled Trials (RCTs). Nutrients. https://www.pubmed.gov/36839310
  16. Effect of Vitamin D Supplementation on Risk of Fractures and Falls According to Dosage and Interval: A Meta-Analysis. Endocrinology and Metabolism (Seoul). https://www.pubmed.gov/35504603

Understanding why we age has been a long unanswered question over the history of mankind. The first scientific model of aging arose from the often-called father of medicine, Hippocrates, who proposed aging is due to a gradual loss of heat and moisture. More specifically, Hippocrates described humans as possessing four humors: blood, phlegm, yellow bile and black bile. During aging the warmth and moisture of blood and phlegm humors give way to the coldness and dryness of the "bile" humors during aging. These concepts for aging dominated western thought for nearly 2,000 years until the dawn of the scientific revolution in the 1600s, when René Descartes proposed the body is like that of a machine and aging is simply the wear and tear of time.

A black-and-white cartoon illustration depicts a worn-out car with smoke coming from its engine, labeled as a "Wear and-Tear Model of Aging." Various parts of the car are annotated with boxes representing organs, senses, cellular damage, and functions, symbolizing how aging affects different body systems through gradual deterioration.
Wear-and-tear models compare aging
to the way machines break down.

Over the next several hundred years wear and tear models of aging (also known as stochastic aging, figure right) continued to develop. Ideas thought to drive aging included DNA damage and mutation accumulation, runaway inflammation, reactive oxygen species (ROS) accumulation - also known as the free radical theory of aging, mitochondrial failure, and more - 40 to 50 more and similar ideas. Although wear and tear models are enticing, one might expect that through optimal care we should hope to see people living 200 years or more - yet the oldest anyone has reached is 122 years of age (Jean Clement) and she smoked until 117 years of age and ate a pound of chocolate every day (allegedly).

Illustration of a computer screen titled "Programmed Aging" displaying a list of sensory and cognitive functions with corresponding ages when decline or changes typically begin. Key details include wrinkles appearing around age 35, vision declining after 40, muscles and bones after 30, touch and pain after 50, hearing and taste & smell after 60, and cognition declining after 70, each accompanied by relevant icons.
Programmed models compare aging to
a timely scheduled list. 

Emerging during the 20th century, an alternative model for aging arose that suggested we age because we are biologically programmed to age. On the surface the concept of programmed aging makes sense. As a population humans generally learn to walk, talk, grow permanent teeth, enter puberty all on schedule. Then, unsurprisingly, there also appears to be a schedule for the appearance of wrinkles, loss of senses and the decline in strength and cognition that comes with aging (figure right).  Although many aspects of this model are sensible, the concept has two major challenges. The first is from an evolutionary perspective. Why would such a mechanism that makes one less fit to survival evolve in the first place? Although this has been debated previously, it could be argued aging allows newer generations to outcompete older generations, improving overall survival of the species.

Second, however, if such a system does exist, then is there a specific aging gene that we could knock-out to live forever? Is the new search for the fountain of youth finding this gene? Unfortunately, the aging gene has not yet been found and therefore the debate continues: Is aging because of wear and tear OR is it programmed? The answer appears to be what is always a good response to a this-or-that question — YES. Enter geroscience.

The scientific field of geroscience emerged about 15 years ago, guided by the core concept that it is the underlying biology of aging that drives age-related diseases (like osteoporosis, heart disease, cancer, dementia, etc.). A key tenet of geroscience are the "hallmarks of aging", initially published in 2013 that identified nine hallmarks, with three more being added in 2023, and two more added just this last year, for a total of 14 (figure below).

Circular diagram illustrating hallmarks of psychosocial isolation and mental illness, divided into three categories: primary hallmarks (blue-green) including genomic instability, telomere attrition, epigenetic alterations, and proteostasis loss; antagonistic hallmarks (yellow-orange) featuring disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, and cellular senescence; and integrative hallmarks (red-purple) showing extracellular matrix changes, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. Each segment contains icons representing specific biological processes, emphasizing complex interactions contributing to mental health conditions.
The 14 hallmarks of aging by Lopez-Otin et al Geromedicine (2025).  

The hallmarks describe aging at the level of cellular breakdown, including DNA damage, the telomere attrition (i.e., loss of the protective DNA endcaps, loss of autophagy - i.e., protein recycling systems, and breakdown of the cellular energy-producing organelles, mitochondria); at the level of tissues breakdown, including chronic inflammation, decline of the tissue replenishing stem cells, cellular senescence (i.e., cells that enter a zombie-like state, driving inflammation and tissue dysfunction and changes in the microbiome, the intestinal bacteria); and even at the level of organismal breakdown, including the newly added hallmark, social isolation.

With all this being said, why then do we age? The short answer is that the hallmarks of aging contribute to accruing cellular damage, reducing tissue and organ function until the point function, well, unfortunately, "ceases." But why is aging so different from one person to the next? Why does one person at 60 have trouble walking a block while another at age 80 can run a marathon? Not unexpectedly, the key players are environment, lifestyle choices and genetics. But why?

The answer lies in how the body and cells defend against the hallmarks of aging. As depicted in the figure below, aging is an ongoing battle between the hallmarks of aging and the cellular defenses against the hallmarks. The key to why aging differs from one person to the next is that environment, lifestyle, and genetics both positively or negatively impact the interplay between the hallmarks and cellular defenses. For example, let us examine one hallmark of aging, mitochondrial failure. Over time these energy producing organelles decline in both number and efficiency. On an environmental level, exposure to heavy metals or air pollution have been known to harm mitochondria, while access to clean water and green natural settings can benefit mitochondria. Lifestyle choices like alcohol consumption or stress can diminish mitochondria, while access to exercise or consumption of fruits and vegetables, increasing exposure to bioactive molecules can improve mitochondria. And on a genetic/biologic level, specific DNA differences (called mitotypes) in the DNA or damaged mitochondrial protein components may reduce function, while cells have the capability to generate fresh fully functional mitochondria as needed to improve function. These are but a snippet of the hundreds, maybe thousands of factors affecting just this single hallmark. Add to this the complexity that each hallmark affects other hallmarks: for example, as we age our epigenetic profile changes, reducing the ability of cells to create the protein to defend against other hallmarks!

Diagram illustrating the "Battlefield of Aging," showing interactions between environment and genetics influencing cellular damage and defenses, which impact cellular health. Key elements include a circular infographic on aging factors, arrows indicating cellular damage and defenses, and a depiction of cellular health leading to tissue health, healthspan, and lifespan.
Aging is a constant war between the aggressive hallmarks of aging and stalwart cellular defenses - with genetic and environment playing both sides.

As you can see, the process of aging is complicated. As might be expected, at present there is no single pill that can cure all of it, but there are many things we can do that help reduce the burden. Some strategies are more generalized like exercise, where our preliminary data in mice that we are looking to publish soon show that with exercise we can reduce burden from multiple hallmarks and in multiple tissues! Other strategies can be very focused, including the emerging use (in early/safety clinical trials) of senolytics (i.e., compounds that target the "zombie-like" pro-inflammatory senescent cells for removal — a topic for a future newsletter!). 

We are in an exciting time for aging research. Now armed with the strongest yet understanding of why we age, we are hopeful for what the future will bring for keeping all of us healthier physically and cognitively as long as possible.  With this being said, thank you again to our Grayhawk Registry members. Your efforts in joining with us in our efforts to perform healthy aging research will lay the foundation for new understandings that lead to better aging for all.


Thank you also for your time reading! If you would like to participate in aging research, learn more by clicking on this link: https://www.kumc.edu/research/landon-center-on-aging/research/information-for-research-volunteers.html

Understanding why we age has been a long unanswered question over the history of mankind. The first scientific model of aging arose from the often-called father of medicine, Hippocrates, who proposed aging is due to a gradual loss of heat and moisture. More specifically, Hippocrates described humans as possessing four humors: blood, phlegm, yellow bile and black bile. During aging the warmth and moisture of blood and phlegm humors give way to the coldness and dryness of the "bile" humors during aging. These concepts for aging dominated western thought for nearly 2,000 years until the dawn of the scientific revolution in the 1600s, when René Descartes proposed the body is like that of a machine and aging is simply the wear and tear of time.

A black-and-white cartoon illustration depicts a worn-out car with smoke coming from its engine, labeled as a "Wear and-Tear Model of Aging." Various parts of the car are annotated with boxes representing organs, senses, cellular damage, and functions, symbolizing how aging affects different body systems through gradual deterioration.
Wear-and-tear models compare aging
to the way machines break down.

Over the next several hundred years wear and tear models of aging (also known as stochastic aging, figure right) continued to develop. Ideas thought to drive aging included DNA damage and mutation accumulation, runaway inflammation, reactive oxygen species (ROS) accumulation - also known as the free radical theory of aging, mitochondrial failure, and more - 40 to 50 more and similar ideas. Although wear and tear models are enticing, one might expect that through optimal care we should hope to see people living 200 years or more - yet the oldest anyone has reached is 122 years of age (Jean Clement) and she smoked until 117 years of age and ate a pound of chocolate every day (allegedly).

Illustration of a computer screen titled "Programmed Aging" displaying a list of sensory and cognitive functions with corresponding ages when decline or changes typically begin. Key details include wrinkles appearing around age 35, vision declining after 40, muscles and bones after 30, touch and pain after 50, hearing and taste & smell after 60, and cognition declining after 70, each accompanied by relevant icons.
Programmed models compare aging to
a timely scheduled list. 

Emerging during the 20th century, an alternative model for aging arose that suggested we age because we are biologically programmed to age. On the surface the concept of programmed aging makes sense. As a population humans generally learn to walk, talk, grow permanent teeth, enter puberty all on schedule. Then, unsurprisingly, there also appears to be a schedule for the appearance of wrinkles, loss of senses and the decline in strength and cognition that comes with aging (figure right).  Although many aspects of this model are sensible, the concept has two major challenges. The first is from an evolutionary perspective. Why would such a mechanism that makes one less fit to survival evolve in the first place? Although this has been debated previously, it could be argued aging allows newer generations to outcompete older generations, improving overall survival of the species.

Second, however, if such a system does exist, then is there a specific aging gene that we could knock-out to live forever? Is the new search for the fountain of youth finding this gene? Unfortunately, the aging gene has not yet been found and therefore the debate continues: Is aging because of wear and tear OR is it programmed? The answer appears to be what is always a good response to a this-or-that question — YES. Enter geroscience.

The scientific field of geroscience emerged about 15 years ago, guided by the core concept that it is the underlying biology of aging that drives age-related diseases (like osteoporosis, heart disease, cancer, dementia, etc.). A key tenet of geroscience are the "hallmarks of aging", initially published in 2013 that identified nine hallmarks, with three more being added in 2023, and two more added just this last year, for a total of 14 (figure below).

Circular diagram illustrating hallmarks of psychosocial isolation and mental illness, divided into three categories: primary hallmarks (blue-green) including genomic instability, telomere attrition, epigenetic alterations, and proteostasis loss; antagonistic hallmarks (yellow-orange) featuring disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, and cellular senescence; and integrative hallmarks (red-purple) showing extracellular matrix changes, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. Each segment contains icons representing specific biological processes, emphasizing complex interactions contributing to mental health conditions.
The 14 hallmarks of aging by Lopez-Otin et al Geromedicine (2025).  

The hallmarks describe aging at the level of cellular breakdown, including DNA damage, the telomere attrition (i.e., loss of the protective DNA endcaps, loss of autophagy - i.e., protein recycling systems, and breakdown of the cellular energy-producing organelles, mitochondria); at the level of tissues breakdown, including chronic inflammation, decline of the tissue replenishing stem cells, cellular senescence (i.e., cells that enter a zombie-like state, driving inflammation and tissue dysfunction and changes in the microbiome, the intestinal bacteria); and even at the level of organismal breakdown, including the newly added hallmark, social isolation.

With all this being said, why then do we age? The short answer is that the hallmarks of aging contribute to accruing cellular damage, reducing tissue and organ function until the point function, well, unfortunately, "ceases." But why is aging so different from one person to the next? Why does one person at 60 have trouble walking a block while another at age 80 can run a marathon? Not unexpectedly, the key players are environment, lifestyle choices and genetics. But why?

The answer lies in how the body and cells defend against the hallmarks of aging. As depicted in the figure below, aging is an ongoing battle between the hallmarks of aging and the cellular defenses against the hallmarks. The key to why aging differs from one person to the next is that environment, lifestyle, and genetics both positively or negatively impact the interplay between the hallmarks and cellular defenses. For example, let us examine one hallmark of aging, mitochondrial failure. Over time these energy producing organelles decline in both number and efficiency. On an environmental level, exposure to heavy metals or air pollution have been known to harm mitochondria, while access to clean water and green natural settings can benefit mitochondria. Lifestyle choices like alcohol consumption or stress can diminish mitochondria, while access to exercise or consumption of fruits and vegetables, increasing exposure to bioactive molecules can improve mitochondria. And on a genetic/biologic level, specific DNA differences (called mitotypes) in the DNA or damaged mitochondrial protein components may reduce function, while cells have the capability to generate fresh fully functional mitochondria as needed to improve function. These are but a snippet of the hundreds, maybe thousands of factors affecting just this single hallmark. Add to this the complexity that each hallmark affects other hallmarks: for example, as we age our epigenetic profile changes, reducing the ability of cells to create the protein to defend against other hallmarks!

Diagram illustrating the "Battlefield of Aging," showing interactions between environment and genetics influencing cellular damage and defenses, which impact cellular health. Key elements include a circular infographic on aging factors, arrows indicating cellular damage and defenses, and a depiction of cellular health leading to tissue health, healthspan, and lifespan.
Aging is a constant war between the aggressive hallmarks of aging and stalwart cellular defenses - with genetic and environment playing both sides.

As you can see, the process of aging is complicated. As might be expected, at present there is no single pill that can cure all of it, but there are many things we can do that help reduce the burden. Some strategies are more generalized like exercise, where our preliminary data in mice that we are looking to publish soon show that with exercise we can reduce burden from multiple hallmarks and in multiple tissues! Other strategies can be very focused, including the emerging use (in early/safety clinical trials) of senolytics (i.e., compounds that target the "zombie-like" pro-inflammatory senescent cells for removal — a topic for a future newsletter!). 

We are in an exciting time for aging research. Now armed with the strongest yet understanding of why we age, we are hopeful for what the future will bring for keeping all of us healthier physically and cognitively as long as possible.  With this being said, thank you again to our Grayhawk Registry members. Your efforts in joining with us in our efforts to perform healthy aging research will lay the foundation for new understandings that lead to better aging for all.


Thank you also for your time reading! If you would like to participate in aging research, learn more by clicking on this link: https://www.kumc.edu/research/landon-center-on-aging/research/information-for-research-volunteers.html

Landon Center on Aging

University of Kansas Medical Center 
Landon Center on Aging
Mail Stop 1005
3901 Rainbow Boulevard 
Kansas City, KS 66160 
Fax: 913-945-7544