Aging: What to expect

From the Mayo Clinic: Aging isn’t just about growing older—it’s a journey of transformation marked by both subtle and profound shifts in body, mind, and lifestyle. As the years pass, you may notice slower reaction times, changes in skin texture, and shifts in sensory perception like hearing or vision. These are typical patterns of natural aging, not immediate cause for alarm. However, understanding what’s normal helps distinguish benign changes from early signs of disease.

Biologically, aging unfolds through intricate processes: cellular wear-and-tear, accumulation of DNA damage, reduced tissue repair, and a gradual decline in organ function. Researchers refer to these as the “hallmarks of aging”—including genomic instability, cellular senescence, and chronic low-grade inflammation. While these mechanisms underlie many age-related conditions—like cardiovascular disease, osteoporosis, and cognitive decline—the focus is shifting toward “health span”: not just how long we live, but how well.

Knowledge is empowering. By adopting targeted lifestyle changes—balanced nutrition, regular physical and mental activity, strong social ties—you can proactively support physical resilience, mental sharpness, and emotional wellness. The Mayo Clinic emphasizes prevention and adaptation, framing healthy aging as an active process rather than passive inevitability. This guide explores what to expect as we grow older—and how to navigate aging with knowledge, agency, and dignity.

Stop Blaming Willpower: The Radical Shift We Need to Fix Obesity

Picture this: a piece of advice so drilled into our collective mindset that it rarely gets questioned—“eat less and move more.” But what if that simple mantra isn’t just outdated, but actually harmful?

Over recent decades, obesity has climbed steadily, and experts say it’s time to scrap this tired narrative. Obesity isn’t a moral failing or a lack of willpower—it’s a complex, chronic, relapsing disease woven from biology, environment, economics, and culture. Blaming individuals for failing to follow basic advice not only falls short—it’s deeply misleading.

The Rising Cost of a Crisis

In England alone, obesity affects more than a quarter of adults and over 22% of ten‑ to eleven‑year‑olds. The report estimating the societal cost of overweight and obesity is staggering—£126 billion a year. That covers everything from NHS costs to lost productivity, informal care, and reduced quality of life. And without intervention, that bill could surge to £150 billion by 2035.

Blame the Environment, Not the Individual

It’s time to call out the “obesogenic environment”—a world engineered for weight gain. Cheap, ultra‑processed junk food is everywhere. Our cities are designed around cars, not pedestrians. Kids grow up glued to screens with little green space or cheap, healthy options around.

Public transport deserts. Food deserts. Tiny urban parks. None of these are bad choices—they’re design flaws in our society. And they hit the poorest communities hardest, creating gaps in access that widen health inequalities .

Why “Eat Less, Move More” Fails

Despite growing science, policy is still stuck in the past. It leans on weight‑loss programs that focus on calorie cuts and gym sessions. Those may work for some, but the moralizing tone behind them fuels weight stigma, shaming others as lazy .

Worse? That stigma actually harms physical and mental health—stress and shame sabotage health outcomes. And strangely, weight stigma is most rampant in schools and hospitals, where compassion should come first .

A New Blueprint for Obesity Care

To really turn the tide, experts urge a systemic, science-informed approach, guided by current NICE and Obesity Health Alliance frameworks. Here’s the roadmap:

  1. Recognize obesity as a chronic disease.
    It’s not about willpower—it’s a medical condition requiring long-term treatment and follow-up, not crash diets.

  2. Smash weight stigma.
    Train health professionals, educators, and employers to use respectful, bias-free language—and enforce anti-discrimination practices.

  3. Tailor care to each person.
    Treatment must reflect a person’s culture, mental health, social setting, and life realities. This means personalized plans, shared decision-making, and integrated support, including mental health resources.

  4. Change the system, not the people.
    Invest in affordable, nutritious food options. Design walkable, activity-friendly communities. Address the economic and social inequalities underpinning obesity.

A Call to Action

We’re at a crossroads. Clinging to “eat less, move more” doesn’t just fall short—it’s actively holding us back while wasting resources and harming lives. Experts now make it clear: what got us here won’t fix the problem.

Redesigning society—from zoning laws to food taxes—requires political will, public investment, and public collaboration. It’s about reframing obesity: not as a personal failure but a collective challenge.

The Only Way Forward

Bulk‑buying produce. Zoning restrictions on fast food. Subsidies for healthy options. Those are small steps. But what’s critical is a shift in mindset—from blame to understanding, support, and system change.

As we stand looking down the road at a projected £150 billion crisis, realize this: it’s not inevitable. We can engineer our way out—literal urban engineering and policy architecture that promote health, not hinder it. But it needs more than willpower. It needs everything to change.

This isn’t about one person, one choice. It’s about architecting well-being into the fabric of our world—because when society changes, individual behaviors follow.

Eggs vs. Alzheimer’s: The Unexpected Defense in Your Fridge

Eggs. They grace our breakfasts, brunches, and bakers’ concoctions—and according to a new study, they may quietly safeguard our brains as we age.

In a large, long-running Chicago cohort known as the Rush Memory and Aging Project, researchers followed 1,024 older adults, all free of dementia at the outset. Participants filled out a detailed Harvard-style food frequency questionnaire, including how often they ate whole eggs. The scientists then tracked them for nearly seven years, assessing memory, cognition—and ultimately, digging into the brains of 578 deceased participants to look for hallmark Alzheimer’s pathology during autopsy.

Here’s where it gets impressive: those eating at least one egg a week—whether once or twice—carried approximately half the risk of developing clinical Alzheimer’s dementia compared to peers eating less than one egg monthly. Even more striking: at autopsy, their brains showed significantly fewer amyloid plaques and tau tangles, the tell‑tale signs of Alzheimer’s.

Why might eggs confer this protection? Choline—a nutrient vital for producing acetylcholine (our memory neurotransmitter) and maintaining neural cell membranes. Eggs are America’s #1 source. Mediation analysis suggested that nearly 40 % of the observed benefit stems from higher choline intake. Beyond choline, eggs offer lutein and omega‑3s—nutrients that, while less abundant, still moor brain health.

The story is far from flawless. This is observational research, which always leaves room for reverse causality and confounders—even with extensive statistical adjustments for age, education, genes, physical activity, diet, and health status. The one‑time dietary questionnaire also invites recall bias, and it missed eggs tucked into other foods. Plus, the cohort tended to be older, better educated, and female—a demographic reality that limits how far we can generalize .

Still, the dual confirmation—from clinical diagnosis and neuropathology—is rare and powerful. Capturing both real-world outcomes and the physical signatures of disease strengthens the case that something real is happening.

What should a discerning, research-savvy person like yourself take away?

First, things like eggs—simple, affordable, accessible—can still matter in late‑life brain health. We often imagine brain health interventions as expensive or high‑tech, but dietary tweaks may carry outsized public health potential, especially in underserved communities.

Second, choline is emerging as a nutrient of interest in neuroscience. If this isn’t yet on your radar, it should be—and not just in the context of pregnancy or liver health, where it’s traditionally discussed.

Third, this isn’t “eat eggs and you won’t get Alzheimer’s.” That kind of causation claim overreaches. Nonetheless, when neurology, nutrition, and pathology line up, it’s a signal worth heeding. If randomized controlled trials (RCTs) can replicate these findings, that would move the needle from suggestive to substantive.

Future steps are clear:

  • We need RCTs investigating eggs (or choline supplements) and cognitive decline or brain pathology.

  • Studies exploring dose–response: is two eggs weekly enough, or would four be better—or even worse?

  • Diverse populations—gender, ethnicity, genetic risk (like APOE4), cultural diets—must be included to ensure findings generalize.

  • Interaction effects: do eggs plus exercise or eggs plus sleep hygiene amplify protection? Are thresholds different for at‑risk individuals?

Bottom line: this study reframes eggs not just as protein and flavor, but as vehicles for brain resilience. At a bare minimum, moderate egg intake seems prudent—perhaps one to two eggs weekly doesn’t sound heroic, but these findings suggest even such modest changes may matter.

For the retired engineer, the skeptical researcher: this is real-world nutritional neuroscience—low‑hype, data‑driven, and anchored in pathology. It doesn’t promise cures, but it does deliver a plausible, biologically resonant insight that’s unequalled in simplicity.

So next time you crack an egg, consider this: you’re tapping into choline-rich, brain‑supportive nutrition—something your brain might thank you for decades down the line. Let’s keep watching the literature, and as RCTs roll in, we’ll see if eggs graduate from breakfast staple to cognitive safeguard. Until then, a modest egg habit seems a sensible, low‑risk move.

How an Amish Gene May Add a Decade to Life

In a community of Old Order Amish near Berne, Indiana, researchers at Northwestern University uncovered a unique, “private” gene mutation in the SERPINE1 gene, which encodes the blood clotting protein PAI‑1. Individuals with one mutated copy of this gene lived almost 10 years longer than their counterparts—averaging around 85 years instead of the community’s typical 71—or early 70s.

Inspired by this mutation, scientists partnered with Tohoku University (Japan) to develop oral PAI‑1 inhibitors such as TM5614, aiming to mimic the Amish gene’s beneficial effects.

Progress so far:

  • Phase 1 trials in Japan confirmed safety and tolerability among healthy volunteers (~160 individuals).

  • Phase 2 studies are underway, including tests in individuals with type 2 diabetes, obesity, or undergoing chemotherapy, to assess metabolic improvements and stem-cell release.

Meanwhile, in animal studies, the outcomes have been extraordinary:

  • Mice genetically prone to rapid aging and high PAI‑1 levels experienced hair regrowth, improved organ health, and 4× extended lifespan when treated with the drug

The Amish are a genetically closed population, descended from just ~500 18th-century settlers. One couple likely introduced this rare SERPINE1 mutation, which then spread due to their endogamous mating patterns.

This isolation also led to amplification of other genetic disorders—both benign and harmful—but uniquely positions them as valuable subjects for genetic aging studies.

It’s crucial to remember the broader Amish lifestyle advantages seen in other studies:

  • Physical activity is intense; Amish men average ~18,000 steps/day and women ~14,000—far above average.

  • Low obesity rates (~4% vs ~36% in the general U.S.), modest diabetes, and lower cancer incidence, thanks to minimal tobacco use and strong familial support.

So, the gene is only one piece of a complex puzzle that includes environment, culture, and social structure.

So, Could This Work for Everyone?

Researchers are optimistic:

  • The Amish mutation appears safe in carriers with one mutated copy.

  • Targeted drug therapies may replicate the benefits—potentially extending both lifespan and healthspan.

  • However, caution is essential: boosting cell replication long-term might raise cancer risk.

  • Any therapeutic strategy will require rigorous, long-term trials in humans.

Why Do We Die When We Get old?

Let’s imagine for a moment that we could completely eliminate cardiovascular diseases — the world’s biggest killer, responsible for more than one in three deaths globally. You might think that eradicating such a major cause of death would dramatically boost human life expectancy. However, the reality is far less impressive: doing so would add only about two extra years to the average lifespan.

What if we also managed to completely cure cancer? That should give us a huge longevity bonus, right? In fact, curing cancer would extend life expectancy by roughly three years. Taken together, completely curing both cardiovascular diseases and cancer — which account for over half of all deaths — would only grant us about five additional years of life on average.

This is a surprising and somewhat sobering realization. Why would removing the top two killers result in such a modest gain?

The answer lies in the nature of aging and the multitude of diseases it brings. As people grow older, they become increasingly vulnerable to a wide range of chronic, degenerative conditions. By the age of 65, about half of individuals are already living with at least two chronic diseases. After 70, about half are considered multimorbid, meaning they suffer from three or more chronic conditions at the same time.

If you remove one major cause of death, another steps up to take its place. The body, already weakened and damaged by the aging process, becomes a target for other age-related diseases such as neurodegenerative disorders, kidney failure, diabetes complications, infections, and frailty-related problems.

Ultimately, what really limits human lifespan isn’t just one or two specific diseases, but the fundamental process of aging itself — a gradual, systemic decline that increases vulnerability across the board. The accumulation of cellular damage, loss of regenerative capacity, and the breakdown of biological systems all conspire to make us susceptible to a host of different fatal outcomes.

In other words, as long as we do not address the root causes of aging, simply knocking out individual diseases will only buy us small, incremental gains. If we truly want to extend healthy human life significantly, we would need to focus on slowing, stopping, or reversing the biological aging process itself — rather than playing whack-a-mole with individual diseases.

The Fountain of Youth, 1546 painting by Lucas Cranach the Elder

Obesity-Linked Cancer Cases Are Surging in the U.S.

Over the past two decades, the U.S. has witnessed a troubling trend: cancer types linked to obesity have nearly tripled, signaling a serious public health crisis.

What the Data Reveal

  • A review of over 33,000 obesity-related cancer deaths showed a threefold increase nationwide.

  • Breast, colorectal, endometrial, kidney, liver, thyroid, gallbladder, pancreatic, and multiple myeloma are among the cancers most strongly linked to obesity.

  • The National Cancer Institute estimates that in 2019 alone, approximately 43,700 new cancer cases in men (4.8%) and 92,200 in women (10.6%) were caused by excess weight.

Who’s Being Affected?

Originally, obesity-related cancers mostly affected older adults. Now, rising obesity rates in younger Americans are shifting incidence toward early-onset cancers.

  • Worldwide data link excess weight to increases in colon, rectal, pancreatic, and kidney cancers among people under 50.

  • In the U.S., early-onset colorectal, breast, kidney, and uterine cancers have spiked by as much as 80% between 2010–2019, with obesity cited as a key driver.

How Obesity Drives Cancer

Obesity influences cancer risk via several biological mechanisms:

  1. Hormonal imbalances: Fat tissue produces extra estrogen, elevating risks for breast, endometrial, and ovarian cancers.

  2. Insulin and growth factors: Elevated insulin and IGF-1 promote cell proliferation and tumor development—linked to colorectal, prostate, endometrial, ovarian, and breast cancers.

  3. Chronic inflammation: Ongoing inflammation from excess fat damages DNA—fuelling cancer initiation.

  4. Increased organ size: Studies show obese individuals may have larger livers, kidneys, and pancreases—creating more cells susceptible to cancerous change .

Early Weight Gain Matters

It’s not just adult obesity—early-life excess weight dramatically raises future cancer risk. A Spanish cohort study of 2.6 million people linked higher BMI in ages 18–40 with up to 18 different cancers over a lifetime. The longer excess weight persists, especially from youth, the greater the cumulative damage.

Consequences & Cost

The surge in obesity-associated cancers threatens to undo decades of cancer mortality decline. Roughly 1 in 20 cancers in the U.S. are now estimated to result from excess weight . These diseases carry both human suffering and significant healthcare costs, straining medical systems and public health initiatives.

What Can Be Done

Several strategies could curb this trend:

  • Weight-loss interventions: Evidence suggests that reducing body weight lowers cancer risk and improves outcomes—especially in breast and colorectal cancers .

  • Medication support: Drugs like Ozempic, used alongside diet and exercise, show promise for weight control and may help reduce cancer risk.

  • Early prevention: Promoting healthy weight from childhood through adulthood is key, as early exposure has the most significant impact .

  • Public health policy: Improving access to nutritious foods, promoting physical activity, and addressing socioeconomic factors affecting early obesity are essential long-term strategies.

A Global Issue

The U.S. isn’t alone—obesity has more than doubled globally over recent decades, mirroring increases in obesity-linked cancers globally. But U.S. trends, especially early-onset cases, reflect the urgent need for domestic action.

(c)Cal Breskovic

The Downsides of Diet Drugs

Diet drugs like Ozempic (semaglutide) have become increasingly popular for weight loss, especially among people with obesity or type 2 diabetes. While they can be highly effective, there are important downsides and risks that users should understand before starting them. Here’s a balanced look at the potential drawbacks:

Gastrointestinal Side Effects

The most common downsides of Ozempic and similar GLP-1 receptor agonists are digestive issues, including:

* Nausea
* Vomiting
* Diarrhea
* Constipation
* Abdominal pain or bloating
These symptoms can be especially strong when starting the drug or increasing the dose.

Risk of Pancreatitis

Although rare, Ozempic may increase the risk of acute pancreatitis (inflammation of the pancreas). Symptoms include severe abdominal pain, nausea, and vomiting. If suspected, immediate medical attention is needed.

Gallbladder Problems

Weight loss itself can raise the risk of gallstones, and GLP-1 drugs may further increase this risk. Gallbladder inflammation or gallstones may require surgery.

Possible Thyroid Cancer Risk

In animal studies, semaglutide has been linked to thyroid C-cell tumors. While this hasn’t been definitively shown in humans, people with a personal or family history of medullary thyroid carcinoma (MTC) or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2) are advised not to take Ozempic.

Muscle Loss with Weight Loss

Rapid weight loss from Ozempic may include not just fat but also lean muscle mass, especially in older adults. This can lead to frailty, reduced mobility, and increased fall risk if not addressed with strength training and adequate protein intake.

Dependency and Weight Regain

Many users regain weight after stopping Ozempic. This raises concerns about “long-term dependency”—patients may need to stay on the drug indefinitely to maintain weight loss.

Cost and Insurance Issues

Ozempic can be expensive, especially if not covered by insurance. Some plans may not cover it if prescribed for weight loss rather than diabetes. Out-of-pocket costs can reach hundreds or even over \$1,000 per month.

Limited Long-Term Safety Data

Although semaglutide is approved and generally considered safe, long-term data (10+ years) is still lacking for people using it specifically for obesity. Unknown risks may emerge over time.

Psychological Effects

Some people report changes in food preferences, taste, or a diminished desire to eat, which may sound like a benefit—but can also interfere with the enjoyment of food and social eating, and in some cases may lead to disordered eating behaviors.

Summary:

Ozempic and similar drugs can be powerful tools for weight loss, particularly for people struggling with obesity or metabolic issues. But they’re not a magic fix, and the side effects, risks, and long-term consequences need to be weighed carefully. Ideally, they should be used as part of a broader health plan that includes nutrition, exercise, and regular medical monitoring.

If you’re considering Ozempic for weight loss, it’s best to have a detailed discussion with your healthcare provider about the benefits and realistic expectations—and what alternatives might work better for your body and lifestyle.

20 Ailments Commonly Associated with Obesity

Obesity isn’t just about weight — it’s a complex health condition that can affect nearly every system in the body. While no two people experience it the same way, carrying excess body fat over time can increase the risk of developing a number of chronic health issues.

Some of these conditions are well-known, like type 2 diabetes and high blood pressure. Others are less obvious, such as sleep apnea, joint pain, and certain types of cancer. Together, they can create a web of health challenges that impact energy, mobility, mood, and overall quality of life.

This list outlines 20 common ailments that are more likely to occur in people living with obesity, not to shame or alarm — but to inform, empower, and support anyone seeking to understand their body better. With awareness comes the ability to take steps toward better health.

  1. Type 2 Diabetes
    Higher body fat can lead to insulin resistance and blood sugar dysregulation.
  2. Heart Disease
    Obesity increases risk of high blood pressure, high cholesterol, and atherosclerosis.

  3. Hypertension (High Blood Pressure)
    Extra weight puts more strain on the heart and blood vessels.

  4. Stroke
    Due to increased risk of blood clots and narrowed arteries.

  5. Sleep Apnea
    Fat deposits around the neck can obstruct the airway during sleep.

  6. Osteoarthritis
    Added weight puts extra pressure on joints, especially knees and hips.

  7. Fatty Liver Disease (NAFLD)
    Fat buildup in the liver not related to alcohol use, which can lead to inflammation.

  8. Gallstones
    Obesity increases cholesterol levels in bile, which can form stones.

  9. Certain Cancers
    Higher risk of cancers such as breast, colon, endometrial, kidney, and esophageal.

  10. Gastroesophageal Reflux Disease (GERD)
    Abdominal fat can increase pressure on the stomach, pushing acid upward.

  11. Depression & Anxiety
    Linked both biologically (inflammation, hormones) and socially (stigma, isolation).

  12. Infertility or Hormonal Imbalances
    Particularly in women, obesity can disrupt estrogen and insulin levels.

  13. Polycystic Ovary Syndrome (PCOS)
    Obesity worsens hormonal imbalances and insulin resistance in PCOS.

  14. Chronic Back Pain
    Extra weight strains the spine and lower back muscles.

  15. Incontinence
    Increased pressure on the bladder can lead to stress urinary incontinence.

  16. Gout
    Obesity raises uric acid levels, increasing risk of painful joint flare-ups.

  17. Asthma or Breathing Difficulties
    Fat around the chest and abdomen can reduce lung capacity.

  18. Skin Conditions
    Including fungal infections, rashes, and intertrigo in skin folds.

  19. Venous Insufficiency & Varicose Veins
    Extra weight can impair blood return from the legs to the heart.

  20. Reduced Immune Function
    Chronic inflammation from excess fat may weaken immune responses.