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.

You

When people talk about longevity, they usually mean how long we live.

But healthspan — the years we live well — matters far more.

That’s the time before disease steals our energy, mobility, and independence.

Modern medicine has already doubled our lifespan in the last century.

Now the goal is to extend the healthy part — without falling for pseudoscience along the way.

Longevity has become a booming business.

Some gurus, like Dr. Eric Topol, do real science.

Others, like Peter Attia, sell access: $150 000 per patient for lab tests, a VO₂ max treadmill run, and a few “optimized” workouts.

He’s also an investor in AG1 — the influencer’s green drink of choice.

Andrew Huberman promotes similar ideas under studio lights bright enough to sterilize a petri dish.

Both are clever, credentialed, and caught between data and drama.

Then there’s Dr. David Sinclair, who helped discover how cells age — and then helped turn that discovery into a supplement empire.

His company tried to patent NMN, an NAD precursor, as a drug.

The FDA briefly removed NMN from the supplement market, sending Reddit into meltdown.

It’s back now, but the episode showed how quickly science slides into sales.

And finally, we have the shirtless salesmen:

Paul Saladino, who went from carnivore crusader to “fruit influencer.”

Liver King, whose real secret wasn’t liver — it was injectable.

And Gary Brecka, who claims to predict your death date (for a fee).

These are subscription services disguised as sages.

Nicotinamide adenine dinucleotide (NAD⁺) is a molecule found in every living cell.

It helps convert food into energy and repair DNA.

As we age, NAD levels fall — metabolism slows and damage builds up.

So scientists asked: If we raise NAD again, can we slow aging?

In mice, the answer looks promising.

NAD precursors like nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) increase average lifespan by 5–15 percent and improve energy, insulin sensitivity, and activity.

That’s great for mice — but we don’t live in cages or eat lab chow.

Not directly — but your body makes NAD from dietary precursors:

tryptophan and niacin (vitamin B₃).

You’ll find them in fish, poultry, beans, milk, and whole grains — basically, a Mediterranean-style diet.

So before spending $90 on capsules, you can spend $9 at the farmers' market.

Human trials of NR or NMN (usually 500–2000 mg per day for 6–12 weeks) show they are safe and well-tolerated.

They modestly raise NAD levels and sometimes improve lipid profiles and blood pressure.

But the effects are small and inconsistent, especially in healthy adults.

NAD precursors do not reverse aging.

They don’t prevent heart attacks or extend lifespan in people — at least, not yet.

Meta-analyses show NAD precursors, especially niacin, can lower LDL (“bad”) cholesterol by about 8–12 percent.

That’s fine, but compare it to rosuvastatin (Crestor):

DoseAverage LDL Reduction5 mg≈ 45 %10 mg≈ 52 %20 mg≈ 55 %40 mg≈ 63 %

That’s the difference between...

This is it — our 100th episode of FORK U.

Over the last hundred episodes, we’ve gone from goat-gland hucksters to the microbiome, from Kellogg’s enemas to cholesterol chemistry, and from Blue Zones to bird flu.

Today, we look back — not just to celebrate the great scientists who shaped modern medicine, but to expose the modern influencers who sell that same science back to you in a bottle.

Welcome to The FORK U Hall of Fame and Shame.



Dr. Ancel Keys didn’t make guesses — he made measurements.

He and his team built one of the most detailed long-term studies in the history of medicine.

They went village by village across seven countries.

They collected what people ate, sent food samples back to labs, recorded EKGs, drew blood, and reviewed medical charts — not for a few months, but for decades.

That’s what science looks like: patient, precise, persistent.

Critics like Gary Taubes claim Keys “left out countries.”

That’s false — and it only proves they never read his work.

Keys studied cohorts of men within small villages, followed them carefully over the years to learn how diet and disease connected.

Without today’s molecular tools, he still discovered the pattern that modern science later confirmed:

ApoB — the protein attached to LDL cholesterol — is transported into the arterial wall, starting the process of atherosclerosis.

Keys didn’t chase fame. He chased truth.

His data became the foundation of preventive cardiology.

If you want to honor him, drizzle olive oil instead of conspiracy.

And a personal note — my thanks to Dr. Harry Blackburn, who worked with Keys and has kindly shared insights from those pioneering days.

In 1922, Banting and Best discovered insulin.

Before that, children with diabetes slipped into comas and died.

After the first injections, they woke up.

Their parents fed them well, but diet alone couldn’t save them.

Good science did.

It was one of medicine’s greatest moments — and still saves lives every day.

Before anyone even knew the word vitamin, Japanese surgeon Dr. Kanehiro Takaki saw sailors dying from beriberi.

Using early ideas of epidemiology, he realized the problem wasn’t infection but nutrition.

He changed their diet — adding barley and vegetables — and the disease vanished.

Takaki brought Japan into modern medicine.

Even Dr. Charles Mayo admired him.

Had he lived longer, he would likely have shared a Nobel Prize.

In 1961, Dr. Leonard Hayflick discovered something remarkable:

Human cells divide about fifty times, then stop — the Hayflick Limit.

He proved aging isn’t mystical. It’s biological.

Every division shortens a cell’s life clock until it retires.

His research wasn’t about nutrition, but it changed everything about how we understand aging and regeneration.

He was the first true longevity doctor — without supplements, slogans, or selfies.

The DASH Diet — Dietary Approaches to Stop Hypertension — came from a dream team of researchers.

• Dr. Lawrence Appel at Johns Hopkins led the NIH...

Thanksgiving is more than a meal — it’s a worldwide celebration of gratitude built around foods that started here in the Americas. Corn, beans, potatoes, and turkey didn’t just feed a nation; they changed global cuisine. Today, we blend culinary history with medical sense to show how to enjoy the feast without the nap.

Our Canadian friends already finished their celebration. For their Thanksgiving, I roasted a chicken with Swiss Chalet sauce — if you know, you know. Thank you, Canada, for giving us Tim Hortons, Swiss Chalet, and the perfect excuse for early gravy season.

In the United States, we wait for the fourth Thursday in November to celebrate. And while Thanksgiving began as a survival story between settlers and Native Americans, it’s become a global holiday. Whether you’re in Edinburgh, London, or Los Angeles, if there’s a turkey on your table, you’re part of it.

Turkey is a ridiculously large bird. Cooking one whole is like putting a cow in the oven and hoping all the parts turn out right — it just doesn’t work.

That’s why I separate mine. The breast goes into a sous vide bath until juicy and tender, and the legs roast separately until golden brown. This approach keeps everyone happy and the meat perfectly cooked.

Another reason to love turkey: it’s naturally low in saturated fat, especially compared to red meat. So, when prepared well, it’s one of the healthiest centerpieces for your table.

Stuffing the bird might seem traditional, but it can also be dangerous. Baking bread inside raw poultry turns your dinner into a bacteria incubator. Instead, bake it separately.

My favorite? Cornbread stuffing — a true dish of the Americas. Combine cornbread cubes, sautéed onions, celery, herbs, mushrooms, and broth. For extra flavor, crisp up some turkey skin like “poultry bacon” and crumble it on top.

(You’ll find the full recipe at terrysimpson.com)

Long before Europeans knew what a potato was, Indigenous farmers in the Andes were cultivating hundreds of varieties. Those humble tubers crossed the ocean and reshaped diets from Dublin to Delhi. Yes, the Italians perfected Gnochi - and the Irish love of the potato brought many of our finest folks to the United States.

At my table, I keep mashed potatoes simple — Yukon Golds, butter, olive oil, milk, salt, and pepper. No truffle oil. No mountain of bacon. Just creamy, honest comfort food.

Green beans are another gift from the Americas. Native farmers grew them with corn and squash — the Three Sisters that nourished generations. The beans climbed the corn stalks while enriching the soil — the original regenerative farming.

In Culinary Medicine, we love beans for their fiber, plant protein, and heart-healthy nutrients.

If you’re remaking the classic green bean casserole, skip the canned soup. Use fresh mushrooms, milk, and a touch of cornstarch. Or, sauté the beans in olive oil and garlic for a lighter, Mediterranean twist.

(Full recipe posted at terrysimpson.com)

Before the main event, try Cowboy Caviar — a colorful bean salad from the American Southwest. It’s bright, high in fiber, and helps you eat more slowly (and more sanely).

Mix black beans, black-eyed peas, corn,...

Vitamin D is sold as bottled sunshine. Social media says it boosts immunity, prevents cancer, and makes you live longer. But science says something very different — and megadoses pushed by influencers like Dr. Eric Berg can do more harm than good. Here’s what you need to know.

Vitamin D has been called the sunshine vitamin for over a century.

We discovered it when children in industrial cities developed rickets — bones so soft they bent like rubber.

The cure wasn’t pills. It was sunlight and milk fortified with Vitamin D.

Today, that history is lost under a pile of influencer ads.

Scroll through TikTok or YouTube, and you’ll see people claim Vitamin D cures everything — from fatigue to depression to cancer.

One of the loudest voices is Dr. Eric Berg, who calls himself a “doctor.”

Here’s the problem: he’s not a physician. He’s a chiropractor.

And in California, chiropractors aren’t allowed to call themselves physicians. For good reason.

Dr. Berg recommends doses of Vitamin D that are ten to twenty times higher than medical guidelines. That’s dangerous advice.

Let’s look at what real science — not social media — tells us.

Vitamin D isn’t really a vitamin. It’s a hormone that helps your body absorb calcium, strengthen bones, and regulate parts of your immune system.

Most adults need 600 to 800 IU per day — not 10,000.

If your level is low, your doctor may recommend a short course of higher doses, but chronic mega-dosing can lead to toxicity.

So how much Vitamin D do you actually need?

That depends on your sun exposure, skin color, diet, and where you live. People who live in northern climates or rarely go outside might need a supplement — but the rest of us get plenty from sunlight and food.

The VITAL Trial, published in The New England Journal of Medicine (2019), followed over 25,000 people taking Vitamin D or a placebo.

The result? No meaningful reduction in cancer, heart disease, or death.

Other major studies say the same thing.

If your Vitamin D levels are normal, taking more doesn’t improve health — it just makes your urine more expensive.

There are benefits for people who are deficient, but that’s not most of us.

A simple blood test can tell you if you truly need supplementation.

Vitamin D toxicity is not rare.

Excess doses can cause calcium levels in your blood to spike, leading to nausea, confusion, kidney stones, and even heart rhythm problems.

There is no benefit to megadoses of vitamin D (link)

Here’s the truth: you can get enough Vitamin D the way nature intended.

Good sources include:

• Salmon, sardines, and tuna
• Eggs and fortified milk
• Mushrooms
• And, of course, sunlight

Ten to fifteen minutes of midday sun on your arms and legs a few times a week is usually enough.

If you live in Alaska in January, sure — take a supplement.

But for most of us, a walk outside beats a handful of pills.

It’s easy to see why Vitamin D is so popular.

It promises health without effort.

Pop a pill instead of taking a walk, eat poorly, but believe you’re fixing it — it’s the illusion of health without the habit of health.

But biology isn’t fooled.

Our bodies need balance, not...

Recently, Mark Hyman posted on X (formerly Twitter) that a new study suggests eating more animal protein might actually lower your risk of cancer. The study he pointed to came from the NHANES dataset—a U.S. survey of diet and health. It sounded reassuring, but it doesn’t line up with the bulk of the evidence. Here is the story about Animal protein and cancer risk:

Let’s dig into what the science really shows.

If you want the strongest evidence, look at red and processed meats. Large prospective cohort studies and systematic reviews consistently show that higher intake of these foods increases cancer risk. The effect is clearest for colorectal cancer, but we also see it in breast, endometrial, and even lung cancer.[1–6]

How big is the risk? Recent meta-analyses and systematic reviews find relative risks (RRs) and hazard ratios (HRs) in the 1.10–1.30 range for the highest vs. lowest intakes. For example, a comprehensive meta-analysis reported that every 50–70 grams per day of red or processed meat increased colorectal cancer risk by 15–32% (HR 1.15–1.32).[3,5] Processed meat generally carries more risk than unprocessed red meat.[2–3,6]

That’s why the American Cancer Society recommends limiting red and processed meats. Their advice is clear: swap them out for fish, poultry, or legumes when possible.[15]

The data on fish tells a different story. Multiple studies and meta-analyses find a modest reduction in colorectal cancer risk with higher fish intake (SRR 0.94, 95% CI 0.89–0.99).[7–8] In fact, adding 50 grams of fish per day reduces risk by about 4%.

Pescatarian diets (no red meat, but including fish) show even more protection. Compared to meat-eaters, pescatarians had a 9% lower overall and colorectal cancer risk (RR 0.91, 95% CI 0.86–0.96).[9]

Chicken and turkey usually get lumped in with “animal protein.” But when you pull the data apart, poultry tells a different story. Most meta-analyses show a neutral or even slightly protective association with colorectal cancer (RR 0.79, 95% CI 0.63–0.99 for white meat).[10–12]

That said, a few studies hint at possible links with certain blood cancers, but those findings aren’t strong or consistent.[5,10] For most people, poultry is a much safer choice than red or processed meats.

Dairy is tricky. On one hand, milk and calcium-rich foods are consistently linked to a lower risk of colorectal cancer (RR 0.93, 95% CI 0.91–0.94).[4,13] On the other hand, high intake of milk or calcium may slightly increase the risk of prostate and endometrial cancers (RR 1.09–1.10).[13–14]

No consistent associations are found for breast or ovarian cancer. Cheese intake in particular may even have protective effects, but results vary.

So why did that NHANES study Mark Hyman highlighted find a small reduction in cancer mortality with higher animal protein? A few reasons:

• NHANES relies on a single dietary recall—one snapshot in time that may not reflect long-term habits.
• It doesn’t separate red and processed meat from healthier animal proteins like fish or poultry.
• Residual confounding (differences in lifestyle factors that aren’t fully accounted for) may skew the results.

When you put NHANES side by side with larger, longer-term studies and meta-analyses, it looks like the outlier. The overwhelming weight of evidence shows that