The lowest hemoglobin I’ve ever seen belonged to a young woman who was still standing. Her blood count was one-fourth of normal. She was pale, short of breath, and strong enough to walk into the clinic.

Doctors soon learned her bone marrow had stopped making new blood cells. The diagnosis was aplastic anemia — a true telomere disease.

She survived thanks to her fitness, modern science, and a bone marrow transplant from a generous donor in Germany. Two years later, she’s in law school, healthy, and full of life.

Each cell in your body carries chromosomes — long strands of DNA. At the ends of those chromosomes sit telomeres, tiny caps that keep the DNA from unraveling, like plastic tips on shoelaces.

Every time a cell divides, its telomeres shorten a little. When they get too short, the cell can no longer divide. Scientists call that stage cellular senescence — cellular retirement.

In 2009, researchers Elizabeth Blackburn and Carol Greider won the Nobel Prize for discovering telomerase, an enzyme that can rebuild telomeres. Their discovery sparked dreams of reversing aging. But there’s a catch: cancer cells also use telomerase to live forever. Turning that enzyme on everywhere might turn back time — or turn on tumors.

Telomeres became the poster child for longevity marketing.

Social media ads promise to “measure your biological age.” Supplement companies claim to “lengthen your telomeres” for hundreds of dollars a bottle.

The problem? Telomere tests vary between labs. Results can change by 20 percent depending on the method. They show trends, not destiny.

Real scientists are studying how telomeres behave under different conditions.

• Danazol — a synthetic sex hormone that slows telomere loss in people with inherited marrow failure. It works but brings side effects, so it’s not an anti-aging trick.
• Henagliflozin — a diabetes drug that increased telomere length in one small study. Whether that helps humans live longer is still unknown.
• Aripiprazole — an antipsychotic that repaired telomeres in cells after oxidative stress. That’s a Petri dish result, not a prescription for youth.

These drugs show that we can nudge biology, but they’re for disease, not for vanity.

Nutrients influence telomere health, too.

• Vitamin D supports telomerase. Long-term studies show it slows telomere shortening.
• Vitamins C and E help reduce chemical stress that wears telomeres down.
• Gamma-tocotrienol, a form of vitamin E, may reverse telomere loss — so far only in lab work.
• TA-65, from the Astragalus plant, may activate telomerase but carries risk. Turning on telomerase could also fuel cancer.
• Telomir 1 is experimental and not available outside research.

None of these is proven to extend life. They’re promising ingredients, not miracles in a capsule.

Lifestyle matters more than any supplement.

A large study at UCSF showed that people who ate a Mediterranean diet, exercised, and managed stress boosted telomerase activity within months.

No powder required.

Telomeres respond to care. They’re markers of how you live, not the cause of how long you live.

Longer telomeres don’t guarantee longer life — they reflect how your body has handled time, inflammation, and stress.

Many people suddenly talk about mitochondria. You hear them in political speeches, on podcasts, and across social media. RFK Jr said he can “see” kids with weak mitochondria just by watching them walk through an airport. Others claim special diets or powders can “fix” aging by supercharging these organelles.

However, most of that chatter misses the actual science.

This post breaks down what mitochondria do, why they matter for aging, and how you can keep them healthy. No hype. No detox teas. Just biology you can use.

Every cell in your body contains tiny structures called mitochondria. They act like miniature cells living inside your larger cells. Each mitochondrion even has its own DNA.

Mitochondria divide independently from your regular cells.

They manage your energy, converting glucose to ATP

Finally, mitochondria keep your organs working.

You inherit all your mitochondria from your mother, which is why scientists use mitochondrial DNA to trace ancestry.

About 1.5 billion years ago, a simple cell swallowed a bacterium and refused to digest it. Instead, they formed a partnership.

The bacterium supplied energy.

The host cell provided safety.

That partnership became the mitochondrion. Every person alive today runs on that ancient deal.

Mitochondria take glucose from your food and convert it into ATP — the energy your body uses to move, think, heal, and grow. This process runs every second of your life.

You cannot swallow ATP and get more energy. ATP supplements don’t work. Only your mitochondria make the usable fuel your body needs.

Young mitochondria act like teenagers. They run fast, bounce back quickly, and handle stress with ease. Cells constantly recycle old mitochondria through a process called mitophagy. This system works beautifully in childhood.

Fresh mitochondria power:

• strong muscles
• sharp thinking
• fast recovery
• healthy metabolism

When mitophagy runs smoothly, you feel energetic and resilient.

Aging slows everything down. Mitochondria begin to leak more “exhaust,” build up mutations, and lose efficiency. Damaged ones don’t get removed as well, because mitophagy weakens with age.

Unfortunately, mitochondria do something worse than slow down:

They fuse with healthy mitochondria.

Imagine pouring spoiled milk into a fresh gallon. The whole jug goes bad. Aging mitochondria do the same thing inside your cells. They spread dysfunction to the healthy ones.

As mitochondria fail, they change how cells function. They send distress signals back to the nucleus that alter gene expression. These messages push cells toward inflammation, stress, and survival pathways that your body normally keeps quiet.

Even more concerning, changes in mitochondrial shape — too much splitting (fission) and not enough merging (fusion) — appear in both aging and cancer. These shifts support tumor growth, help cancer cells spread, and make some treatments less effective.

Aging mitochondria increase the risk of:

• brain fog
• muscle fatigue
• slower recovery
• heart strain
• metabolic slowdown
• cancer-friendly environments

Mitochondria sit at the center of how we age.

By Dr. Terry Simpson

Most people hear the name Urolithin A and think it belongs in a commercial about prostate health. It sounds like something a man named “Gary, 62,” would talk about while fishing. But Urolithin A has nothing to do with plumbing. Instead, it sits at the center of a new wave of longevity science focused on how our cells clean up old, broken parts.

As we age, our mitochondria—the tiny power centers inside our cells—start to slow down. They build up damage and stop working well. Eventually, this pile-up makes us lose strength and energy. That’s where Urolithin A comes in. It helps switch back on a process called mitophagy, which is basically the cell’s recycling program for old mitochondria.

You cannot eat Urolithin A directly. Instead, your body makes it when your gut bacteria break down special plant compounds called ellagitannins. These are found in foods like:

• pomegranates
• walnuts
• berries
• green tea (yes, really)

Green tea is usually known for its catechins, but it also contains ellagitannins like strictinin. After you drink it, your gut bacteria break these tannins apart and create ellagic acid, which can later turn into Urolithin A.

However, this only works if you have the right microbes. And here’s the surprising part:

Most people do not.

Studies show that only 12% to 40% of adults naturally produce Urolithin A from food. Everyone else makes little to none because their gut bacteria simply aren’t built for the job.

Your microbiome—the community of bacteria living in your digestive system—decides whether you make Urolithin A or not.

People who produce Urolithin A usually have:

• more diverse gut microbes
• special bacteria like Enterocloster and Gordonibacter
• the right genes inside those microbes to do the chemical conversion

People who don’t produce it (called “metabotype zero”) lack those bacteria or the gene pathways needed. Eating more pomegranates or drinking more green tea does not fix this. No diet, including keto or Mediterranean, has been shown to turn a non-producer into a producer.

This is why two people can eat the same food, and only one makes Urolithin A.

In older adults, researchers have tested Urolithin A supplements for up to 4 months. These studies show several encouraging results:

• muscle endurance improves
• inflammation markers decrease
• mitochondrial health markers look better

Even so, there are limits. Trials show no meaningful improvement in:

• walking distance
• ATP (cellular energy) production
• overall physical function

So the biology looks better, but major clinical outcomes have not changed.

Scientists also study Urolithin A in senescent cells—cells that have stopped dividing but still cause inflammation. In the lab, Urolithin A can:

• reduce senescence markers
• calm inflammatory signals
• restore mitophagy
• improve oxidative stress
• even strengthen circadian rhythms inside aging cells

All of this sounds exciting. However, these findings are from cell culture, not humans. They give us clues, not guarantees.

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