Fork U with Dr. Terry Simpson

For years, anti-aging has been hijacked by supplements, hacks, and promises that never hold up. Meanwhile, real science has quietly moved forward. Today, the most compelling anti-aging story does not come from a powder, a cold plunge, or a fasting app. Instead, it comes from metabolism.

A class of medications called GLP-1 receptor agonists started as diabetes drugs. Over time, clinicians discovered something bigger. These medicines now play a major role in obesity treatment, and they produce effects that reach far beyond the scale. Because obesity shortens lifespan and damages nearly every organ system, it makes sense that drugs that treat obesity could also improve healthspan—the years you live with strength, clarity, and independence.

However, weight loss alone does not explain what researchers are seeing. These drugs reduce inflammation, protect the heart, lower biological stress, and may even delay cognitive decline. Importantly, many of these effects occur independent of weight loss. That fact has forced scientists to ask a serious question: could GLP-1 drugs represent a new class of anti-aging medicine?

Even longevity-focused clinicians, such as Peter Attia, have publicly discussed using GLP-1 drugs at lower doses in select patients—not for weight loss, but for metabolic health and long-term disease prevention.

Aging is not just about time. Instead, it reflects how well your body regulates key systems over decades. Blood sugar control, inflammation, oxidative stress, and cellular repair all shape how fast—or how slowly—you age.

GLP-1 receptor agonists influence all these pathways. Originally designed to mimic a gut hormone that signals fullness, these drugs turned out to do much more. Research shows they lower systemic inflammation, improve mitochondrial function, and reduce oxidative stress. As a result, organs function better for longer.

In simple terms, when metabolism runs smoothly, cells behave younger.

Newer drugs have taken this concept even further. Retatrutide, a triple-agonist medication, targets three hormonal pathways simultaneously: GLP-1, GIP, and glucagon.

In Phase 3 trials, participants lost nearly 29% of their body weight, or more than 70 pounds on average. Yet weight loss only tells part of the story. Retatrutide also lowered inflammation, improved blood pressure, improved lipid profiles, and reduced joint pain.

Each hormone plays a role. GLP-1 reduces appetite and inflammation. GIP improves insulin sensitivity and nutrient handling. Glucagon increases energy expenditure and fat oxidation. Together, these pathways keep metabolism active, not slowing down during weight loss.

That combination does more than shrink waistlines. It restores metabolic flexibility, which declines with age.

For decades, scientists blamed aging on simple wear and tear. Modern research tells a different story. Chronic, low-grade inflammation—often called inflammaging—drives many diseases of aging.

Heart disease, stroke, arthritis, fatty liver disease, and cognitive decline all share this inflammatory background. In clinical trials, GLP-1 drugs reduced markers such as C-reactive protein, triglycerides, and blood pressure. These changes signal reduced biological aging risk, not just better lab numbers.

When inflammation falls, fewer senescent cells accumulate. Blood vessels stay healthier. Organs function longer.

Nothing ages a person faster than a heart attack. Because of that reality, cardiovascular protection matters deeply for longevity.

Multiple cardiovascular outcome trials show that GLP-1 receptor agonists reduce major adverse cardiovascular events in people with type 2 diabetes and high cardiovascular risk. Across studies, researchers observed a 13% reduction in cardiovascular death and a 9% reduction in nonfatal heart attacks compared with other treatments.¹²

The LEADER trial demonstrated that liraglutide reduced cardiovascular mortality by 22%.⁶ Similar benefits appeared with semaglutide, dulaglutide, and albiglutide.²⁷ Because of this evidence, the FDA approved several GLP-1 drugs for cardiovascular risk reduction in adults with diabetes and established heart disease.⁸

These benefits do not come from glucose control alone. GLP-1 drugs lower blood pressure, reduce inflammation, improve endothelial function, decrease oxidative stress, and reduce RAAS activity.³⁴ At the cellular level, they protect heart muscle cells from multiple forms of cell death while enhancing autophagy and mitophagy.⁵

Although GLP-1 drugs do not strongly reduce heart failure hospitalizations, meta-analyses suggest a modest benefit.³⁷ Most importantly, they safely reduce atherosclerotic risk. Preventing a heart attack remains one of the most powerful anti-aging interventions available.

Brain health deserves careful discussion. GLP-1 drugs do not reverse dementia. They do not improve cognition once dementia is established. Recent trials in patients with Alzheimer’s disease showed no meaningful cognitive improvement.

That limitation matters.

However, prevention tells a different story. Large observational studies show that GLP-1 receptor agonists are associated with 33–45% lower dementia risk compared with other glucose-lowering drugs in people with type 2 diabetes.¹² A 2025 JAMA Neurology study involving nearly 34,000 patients found a 33% lower risk of Alzheimer’s disease and related dementias among GLP-1 users.¹

Randomized trial evidence shows a more modest, but still significant effect. A 2025 JAMA Neurology meta-analysis found that GLP-1 drugs reduced dementia risk, while SGLT2 inhibitors did not.³ This finding suggests a class-specific effect, rather than a glucose-only explanation.

Mechanistically, GLP-1 drugs reduce neuroinflammation, improve insulin signaling in the brain, promote neurogenesis, and may reduce amyloid-β and tau pathology.⁵⁶ They also improve vascular health, which strongly influences cognitive aging.

Age appears to matter. A 2025 target-trial emulation showed weaker effects in adults over 75, but stronger protection in younger patients.⁷ The takeaway remains clear: earlier prevention works better.

The goal is not to cure dementia. Instead, the goal is to delay its onset long enough that many people never reach it.

Diet still matters. Ultra-processed foods damage the same systems that GLP-1 drugs try to repair.

These foods hijack dopamine reward pathways, increase cravings, and weaken satiety signals. Soft textures and engineered flavors allow rapid overconsumption. High intake links to higher inflammation, worse metabolic health, reduced gray-matter density, and faster brain aging.

Additives and emulsifiers disrupt the gut microbiome and the gut-brain axis. As a result, insulin signaling in the brain worsens. GLP-1 drugs often counteract damage caused by this food environment, but prevention works better than repair.

Here is the empowering part. People can act today.

The Mediterranean diet remains the dietary pattern with the strongest evidence for protecting both the heart and the brain. Vegetables, legumes, fruit, whole grains, olive oil, fish, and minimal ultra-processed food form its foundation. This pattern reduces inflammation, improves vascular health, supports the microbiome, and slows cognitive decline.

Think of it this way: GLP-1 drugs quiet the metabolic noise. The Mediterranean diet keeps it quiet.

Alcohol also matters. Earlier beliefs about alcohol and brain protection did not hold up. Even moderate drinking increases dementia risk, worsens sleep, raises inflammation, and damages the hippocampus. If cognitive protection matters, less alcohol helps, and none works best.

Aging is not about adding years. Aging is about protecting systems.

GLP-1 drugs support metabolic health. The Mediterranean diet supports biology. Avoiding alcohol protects the brain. Movement and sleep reinforce everything else.

If heart disease, dementia, and disability are delayed long enough, many people will never experience them. That outcome does not represent immortality. Instead, it represents success at healthspan.

1. Ussher JR, Drucker DJ. Glucagon-Like Peptide 1 Receptor Agonists: Cardiovascular Benefits and Mechanisms of Action. Nat Rev Cardiol. 2023;20(7):463–474.
2. Nauck MA, et al. Cardiovascular Actions and Clinical Outcomes With GLP-1 Receptor Agonists. Circulation. 2017;136:849–870.
3. Pop-Busui R, et al. Heart Failure: An Underappreciated Complication of Diabetes. Diabetes Care. 2022;45:1670–1690.
4. Wu Q, et al. Glucose-Independent Cardiovascular Mechanisms of GLP-1 RAs. Biomed Pharmacother. 2022;153:113517.
5. Boshchenko AA, et al. Cardioprotective Signaling of GLP-1 Receptor Agonists. Int J Mol Sci. 2024;25:4900.
6. Marso SP, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375:311–322.
7. Honka H, et al. Therapeutic Manipulation of Myocardial Metabolism. J Am Coll Cardiol. 2021;77:2022–2039.
8. FDA Orange Book.
9. Tang H, et al. GLP-1RA Medications and Dementia Risk. JAMA Neurol. 2025;82:439–449.
10. Seminer A, et al. Cardioprotective Glucose-Lowering Agents and Dementia Risk. JAMA Neurol. 2025;82:450–460.
11. Au HCT, et al. GLP-1 and Neurodegenerative Pathology. Neurosci Biobehav Rev. 2025;173:106159.
12. Inoue K, et al. GLP-1 RAs and Dementia Incidence in Older Adults. Ann Intern Med. 2025.

It started at a holiday party.

Laughter, champagne, a toast — then a collapse.

A fifty-two-year-old, active and healthy, suddenly lost consciousness.

Paramedics did CPR and shocked her heart twice.

She survived — barely.

Doctors called it Holiday Heart Syndrome: an alcohol-triggered arrhythmia that can kill.​

Holiday Heart arises after binge or even moderate drinking, especially around celebrations. Alcohol irritates heart cells, disrupts electrolytes, and scrambles electrical signals, which can trigger atrial fibrillation — an erratic rhythm that raises the risk of clots, stroke, and sudden death. Even a single heavy night can set it off, and repeated use amplifies inflammation and structural damage long after the hangover fades.​

For years, the “French paradox” suggested red wine protects the heart, but newer evidence points instead to lifestyle patterns rather than wine itself. Ethanol and its metabolite acetaldehyde directly injure heart muscle, disturb calcium handling, damage mitochondria, and can lead to Alcoholic Cardiomyopathy — an enlarged, weakened heart. Harm shows up even in relatively low intake, and improvement typically requires reducing or stopping alcohol.​

Alcohol is a proven carcinogen that promotes DNA damage, inflammation, oxidative stress, and hormonal shifts that favor tumor growth. At least seven cancers — including those of the mouth, throat, larynx, esophagus, liver, colon, and breast — are directly linked to alcohol, with risk beginning above zero and rising with each additional drink. Even up to one drink a day meaningfully increases breast cancer risk, and the combined use of alcohol and tobacco multiplies risk even further.​

You’ve probably heard this one:

People in Sardinia or Ikaria drink wine every night and live to 100.

What’s missing is the math.

They sip 3 to 4 ounces — not a glass, not a typical American glass, but a tasting. The flight of wine.

Their rustic wines are 10–11 percent alcohol, not the 16 percent bombs from Sonoma.

And they don’t live long because of the wine.

They live long because of everything else:

walking hills, eating beans, taking naps, sleeping well, and belonging to a community.

Their wine is cultural, not clinical.

If you want their healthspan, copy their diet, movement, and purpose — not the nightly pour.

Alcohol hijacks metabolism by forcing the liver to prioritize ethanol breakdown, pushing fat and sugar processing aside. Drinks can add substantial hidden calories, promote fatty liver, and stall fat loss, even when the rest of a diet looks reasonable.​

Popular “alcohol detox” supplements promise faster clearance or hangover prevention, but research points to ethanol itself and the inflammatory response as the main drivers of symptoms. Blocking acetaldehyde alone does not prevent mitochondrial damage, immune activation, or the residual effects that follow a night of heavy drinking.​

Modern wellness culture often warns about “toxins” while normalizing regular drinking, even framing certain spirits or wines as health tools. Yet, when viewed through a longevity lens, alcohol stands out as one of the most potent, fully optional biological stressors in the modern lifestyle.​

Once drinking stops or drops sharply, the body begins to repair: blood pressure often falls within days, heart rhythm and sleep tend to improve within weeks, and liver fat can regress over subsequent months. Over years, cancer and cardiovascular risks decline, with former light-to-moderate drinkers gradually approaching the risk profile of people who never drank or who stopped earlier in life.​

Alcohol is deeply woven into culture and celebration, but it is neither a health food nor a longevity strategy. For anyone serious about healthspan, cutting alcohol is one of the simplest, highest-impact levers available — a change your heart, DNA, and future self are strongly likely to benefit from.​

1. Berger D, De Aquino J P, Charness M E, et al. Common Alcohol-Related Concerns. NIAAA (2025).
2. Rock C L, Thomson C, Gansler T, et al. American Cancer Society Guideline for Diet and Physical Activity for Cancer Prevention. CA Cancer J Clin. 2020; 70(4): 245-271. doi:10.3322/caac.21591.
3. Jun S, Park H, Kim UJ, Choi EJ, Lee HA, Park B, Lee SY, Jee SH, Park H. Cancer risk based on alcohol consumption levels: a comprehensive systematic review and meta-analysis. Epidemiol Health. 2023;45:e2023092. doi: 10.4178/epih.e2023092. Epub 2023 Oct 16. PMID: 37905315; PMCID: PMC10867516.
4. Rumgay H, Murphy N, Ferrari P, Soerjomataram I. Alcohol and Cancer: Epidemiology and Biological Mechanisms. Nutrients. 2021; 13(9): 3173. doi:10.3390/nu13093173.
5. Gapstur S M, Mariosa D, Neamtiu L, et al. The IARC Perspective on the Effects of Policies on Reducing Alcohol Consumption. N Engl J Med. 2025; 392(17): 1752-1759. doi:10.1056/NEJMsr2413289.
6. Rumgay H, Shield K, Charvat H, et al. Global Burden of Cancer in 2020 Attributable to Alcohol Consumption. Lancet Oncol. 2021; 22(8): 1071-1080. doi:10.1016/S1470-2045(21)00279-5.
7. Yoo J E, Han K, Shin D W, et al. Association Between Changes in Alcohol Consumption and Cancer Risk. JAMA Netw Open. 2022; 5(8): e2228544. doi:10.1001/jamanetworkopen.2022.28544.
8. Fernández-Solà J. The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy. Nutrients. 2020; 12(2): 572. doi:10.3390/nu12020572.
9. Domínguez F, Adler E, García-Pavía P. Alcoholic Cardiomyopathy: An Update. Eur Heart J. 2024; 45(26): 2294-2305. doi:10.1093/eurheartj/ehae362.
10. Mackus M, van de Loo A J A E, Garssen J, et al. The Role of Alcohol Metabolism in the Pathology of Alcohol Hangover. J Clin Med. 2020; 9(11): 3421. doi:10.3390/jcm9113421.
11. van de Loo A J A E, Mackus M, Kwon O, et al. The Inflammatory Response to Alcohol Consumption and Its Role in the Pathology of Alcohol Hangover. J Clin Med. 2020; 9(7): 2081. doi:10.3390/jcm9072081.
12. Karadayian A G, Carrere L, Czerniczyniec A, Lores-Arnaiz S. Molecular Mechanism Underlying Alcohol’s Residual Effects: Acetaldehyde and Mitochondrial Dysfunction. Alcohol (Fayetteville N.Y.). 2025; doi:10.1016/j.alcohol.2025.09.004.
13. Turner B R H, Jenkinson P I, Huttman M, Mullish B H. Inflammation, Oxidative Stress, and Gut Microbiome Perturbation in Hangover. Alcohol Clin Exp Res. 2024; 48(8): 1451-1465. doi:10.1111/acer.15396.
14. Palmer E, Tyacke R, Sastre M, et al. Alcohol Hangover: Biochemical, Inflammatory, and Neurochemical Mechanisms. Alcohol Alcohol. 2019; 54(3): 196-203. doi:10.1093/alcalc/agz016.

Clearly, your body changes as you age. I learned this lesson years ago when my son was three years old. We started him skiing, and he loved every minute of it. When he fell, he tumbled onto his behind, jumped right back up, and skied down the hill like nothing had happened. He was pure rubber and resilience.

However, I was 53 years his senior that year. I did an inadvertent 360-degree twirl on the slopes myself. His mother saw me and immediately asked if I had broken my wrist, wondering when I could return to surgery. The difference between a flexible young body and an older body is critical. Consequently, I retired from skiing that season and now enjoy the lodge, where I write and make them great dinners.

Indeed, your older body desperately needs work to stay flexible, strong, and balanced as time goes on. I have seen too many independent seniors lose everything after a simple fall in their own home. They go from living on their own to spending their last days in a care center, sometimes never leaving bed. This outcome is not healthspan. Instead, you want a fall to be like my son’s—just on your butt and back up. Sadly, too many fall and cannot get up. This isn't a commercial for a safety pendant, but a sincere plea for you to start working your muscles.

Specifically, we talk frequently about heart health and clear arteries in longevity. Those things are unquestionably crucial. Nevertheless, the biggest threat to functional independence as we age is a condition called sarcopenia. This is the medical term for age-related muscle loss.

Unfortunately, we start losing about 3 to 8 percent of our muscle mass every decade after age 30. That loss accelerates quickly once you hit 70. This problem is not just about looking less toned; fundamentally, it is about losing the ability to stand up from a chair, carry groceries, or, most importantly, catch yourself when you trip. The falls that result are often catastrophic.

Amazingly, resistance training is effective at the microscopic level, too. We have talked extensively about the tiny, complex mechanisms of the cell, but here is the key takeaway: small things benefit from big things.

In fact, increasing muscle mass through training has direct, positive effects on two major microscopic drivers of aging: mitochondrial function and telomere health.

To elaborate, when you challenge your muscles, you signal your cells to create more energy. This signal forces your mitochondria—the cellular powerhouses—to become both more numerous and more efficient. Better mitochondrial function equals more energy and less cellular stress.

Moreover, studies show that resistance training actually increases the activity of the enzyme telomerase in some cells. Telomerase helps maintain the protective caps on your DNA called telomeres.

Therefore, you don’t need to buy fancy, expensive supplements like NAD or telomere boosters. Picking up a dumbbell costs less money but yields more results. You gain muscular strength, better metabolism, stronger bones, and the cellular benefits all at once.

Let's consider how muscle mass influences your diet. Your muscle is actually your body’s largest organ for glucose disposal. Think of it like this: when you eat, your body releases glucose (sugar) into your bloodstream. Insulin then works to escort that glucose out of your blood and into your cells for energy. The vast majority of that glucose gets parked in your muscle cells.

Clearly, if you have more muscle mass, you automatically have a bigger parking lot for that glucose.

Consequently, more muscle means your body gains better insulin sensitivity. It becomes more efficient at regulating blood sugar. This effect is the absolute bedrock of preventing and managing Type 2 diabetes. Ultimately, resistance training is a powerful pharmaceutical intervention for your metabolic health.

However, the benefits don't stop at the muscles. Let's talk about bone density, which is crucial for everyone, especially women. We know calcium and Vitamin D are important, yet they are only one part of the solution.

Remember that bone is living tissue; it responds to stress. When you lift a weight—even if it is just your own body weight in a squat—the mechanical force signals to your bones that they must get stronger. This process is known as the Mechanostat principle. Conversely, without that heavy, high-intensity mechanical load, bone density naturally declines, leading to osteoporosis.

In conclusion, if you only do low-impact cardio, you are helping your heart, but you are not sending the signal needed to maintain or increase bone mineral density. Specifically, you must load your bones to strengthen them.

Beyond pure strength, true independence depends on mobility and balance. This is where functional training, including Yoga, plays a huge role. My favorite Yoga classes are a combination of bodyweight resistance and cardiovascular movement. I look for the physics—the movement, the resistance, and the balance—and keep the "woo" out of it. Furthermore, a Yoga mat costs far less than some supplements, but it will make a fall much easier to recover from.

Therefore, if you are getting started, please get professional help! Having a great gym coach to help with proper form is paramount—shout out to my friends Jeremy the Hulk and the Zeigler Monster! Additionally, it is equally important to enlist a private Yoga instructor to ensure you are not malaligned and that you know what to look for. A special shout-out to my yogi Xuan—and yes, I will be doing more classes this year!

Ultimately, the reason we train is not just to be strong; rather, it is so that if you fall when you are 65, 75, or 80, you possess the strength, stability, and awareness to get up by yourself. This ability is the true mark of functional longevity.

Let me give you two examples of why this ability matters so much. A fellow was admitted to a facility after he broke his hip. Before he fell, he lived alone, was a champion bowler, and enjoyed his life. He simply slipped on a rug, fell, and was found a day later. After his hip was fixed, he spent the next year of his life mostly in bed, eventually dying of COVID-19 in a long-term care facility. One single fall that he couldn't get up from changed his life and his outlook completely.

Contrast that with my own dad. He took a fall at age 96 trying to trim a tree. It took a bit of effort, and he received a stern warning from his son and the EMTs, but he got up. He lived independently until age 98.

Consequently, this kind of preparation matters because the statistics are sobering: falls are the leading cause of injury death for people over 65. Tragically, studies show that up to 30% of seniors who fracture a hip lose their independence entirely.

Finally, resistance training, combined with functional movement, is the macroscopic lever that pulls all those microscopic switches. It is the closest thing to a fountain of youth that doesn’t require a prescription. It just requires effort.

Remember that you must continually increase the demand on your body—this is called progressive overload. Most importantly, remember that resistance training is the stimulus, but protein is the building material. Aim for a high protein intake daily, and definitely enjoy that protein smoothie right after your workout!

On that note, we’re even taking this training on the road this year with our Mediterranean Cruise, where we’ll have an instructor to help you with simple movements—things so that if you fall, you can get up by yourself.

• Dao T, Green AE, Kim YA, Bae SJ, Ha KT, Gariani K, Lee MR, Menzies KJ, Ryu D. Sarcopenia and Muscle Aging: A Brief Overview. Endocrinol Metab (Seoul). 2020 Dec;35(4):716-732. doi: 10.3803/EnM.2020.405. Epub 2020 Dec 23. PMID: 33397034; PMCID: PMC7803599.
• Sun L, Zhang T, Luo L, Yang Y, Wang C, Luo J. Exercise delays aging: evidence from telomeres and telomerase -a systematic review and meta-analysis of randomized controlled trials. Front Physiol. 2025 Jun 26;16:1627292. doi: 10.3389/fphys.2025.1627292. PMID: 40642293; PMCID: PMC12241061.
• Massini DA, Nedog FH, de Oliveira TP, Almeida TAF, Santana CAA, Neiva CM, Macedo AG, Castro EA, Espada MC, Santos FJ, Pessôa Filho DM. The Effect of Resistance Training on Bone Mineral Density in Older Adults: A Systematic Review and Meta-Analysis. Healthcare (Basel). 2022 Jun 17;10(6):1129. doi: 10.3390/healthcare10061129. PMID: 35742181; PMCID: PMC9222380.
• Jeon YK, Jeong J, Shin SD, Song KJ, Kim YJ, Hong KJ, Ro YS, Park JH. The effect of age on in-hospital mortality among elderly people who sustained fall-related traumatic brain injuries at home: A retrospective study of a multicenter emergency department-based injury surveillance database. Injury. 2022 Oct;53(10):3276-3281. doi: 10.1016/j.injury.2022.07.036. Epub 2022 Jul 23. PMID: 35907679.
• McKendry J, Lowisz CV, Nanthakumar A, MacDonald M, Lim C, Currier BS, Phillips SM. The effects of whey, pea, and collagen protein supplementation beyond the recommended dietary allowance on integrated myofibrillar protein synthetic rates in older males: a randomized controlled trial. Am J Clin Nutr. 2024 Jul;120(1):34-46. doi: 10.1016/j.ajcnut.2024.05.009. Epub 2024 May 16. PMID: 38762187; PMCID: PMC11291473.

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.

Research tells a simple story:

• Telomeres shorten as cells divide.
• Stress, smoking, and inflammation speed that process.
• Healthy diets and regular movement slow it.
• Some medications affect telomere biology but aren’t for general use.
• We still don’t know if lengthening telomeres increases lifespan.

So far, no pill or powder beats sleep, exercise, and plants on a plate.

Telomeres aren’t countdown clocks. They’re mileage markers.

Protect them by doing the basics well: eat plants and fish, move daily, sleep enough, manage stress, and don’t smoke.

Simple. Sustainable. Supported by science.

1. Calado RT, Young NS. Telomere Diseases. N Engl J Med. 2009;361(24):2353-65. PMCID: PMC3401586
2. Lai T-P, Wright WE, Shay JW. Techniques for Assessing Telomere Length. Nat Rev Genet. 2018;19(5):293-307. PMCID: PMC6380489
3. Huang S et al. The Relationship Between Telomere Length and Aging-Related Diseases. Front Aging. 2025;6:1532. PMCID: PMC11882723
4. Arsenis CA et al. Physical Activity and Telomere Length. Sports Med. 2017;47(3):503-512.
5. Schellnegger T et al. Unlocking Longevity: The Role of Telomeres and Their Targeting. Front Aging Neurosci. 2024;16:1050353.

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.

Plenty of supplements promise to “repair” mitochondria. Many sound exciting:

• NAD boosters
• Urolithin A
• peptides
• antioxidant stacks

However, evidence in actual humans remains limited.

NAD boosters don’t show meaningful anti-aging benefits.

Urolithin A can help with muscle endurance, but doesn’t reverse aging.

Antioxidant megadoses may even interfere with exercise benefits.

People want a miracle switch. We don’t have one.

Good news: the basics still win. And they outperform supplements every time.

Your muscles grow new mitochondria in response to lifting weights or doing body-weight exercises.

This “comfortably challenging” aerobic zone trains your body to use oxygen better. You can talk, but you can’t sing.

Your body repairs mitochondrial damage at night. Poor sleep means poor repair.

Whole foods, plants, nuts, fish, and olive oil protect mitochondria from inflammation and stress.

High blood sugar, high LDL, and high blood pressure destroy mitochondria faster than anything else.

Some diet influencers insist that insulin resistance is the One True Cause of aging and that keto or carnivore diets fix it all. That was tested in high-quality metabolic ward studies.

It failed.

Low-carb diets did not outperform other diets when calories and protein were controlled. Fat loss was the same. Metabolism behaved the same. Insulin wasn’t the magic dial.

Mediterranean-style eating continues to show the strongest data for longevity.

Your liver breaks down alcohol by generating large amounts of oxidative stress. That stress directly damages mitochondrial DNA, mitochondrial enzymes, and mitochondrial membranes.

It also disrupts their normal fuse-and-divide rhythm, which accelerates aging inside your cells. The hangover fades, but the mitochondrial damage does not.

Mitochondria are real, essential organelles — not a buzzword. Yet some people use the term “mitochondria” the same way Deepak Chopra uses the word “quantum": to describe everything and explain nothing.

Here’s the truth:

When mitochondria age, you age.

Driving inflammation.

Increasing cancer risk.

Slowing your metabolism.

They weaken your heart and muscles.

Finally, they cloud your thinking.

If we’re going to blame mitochondria for aging, let’s at least understand them — and learn how to keep them healthy.

Strength training, aerobic exercise, sleep, nutrition, and treating metabolic disease remain the most powerful tools we have.

Your mitochondria are trying their best.

Help them do their job.

1.Somatic Mutations of Mitochondrial DNA in Aging and Cancer Progression.

Lee HC, Chang CM, Chi CW. Ageing Research Reviews. 2010;9 Suppl 1:S47-58. doi:10.1016/j.arr.2010.08.009.

2. Mitochondrial DNA Mutations in Ageing and Cancer.

Smith ALM, Whitehall JC, Greaves LC.Molecular Oncology. 2022;16(18):3276-3294. doi:10.1002/1878-0261.13291.

3. Age-Associated Mitochondrial DNA Mutations Cause Metabolic Remodelling That Contributes to Accelerated Intestinal Tumorigenesis.

Smith AL, Whitehall JC, Bradshaw C, et al. Nature Cancer. 2020;1(10):976-989. doi:10.1038/s43018-020-00112-5.

4.Understanding the Impact of Mitochondrial DNA Mutations on Aging and Carcinogenesis (Review).

Kobayashi H, Imanaka S International Journal of Molecular Medicine. 2025;56(2):118. doi:10.3892/ijmm.2025.5559.

5.Mitochondrial Dysfunction and Oxidative Stress in Aging and Cancer.

Kudryavtseva AV, Krasnov GS, Dmitriev AA, et al. Oncotarget. 2016;7(29):44879-44905. doi:10.18632/oncotarget.9821.

6.Role of Mitochondrial Dysfunction in Cancer Progression.

Hsu CC, Tseng LM, Lee HC. Experimental Biology and Medicine (Maywood, N.J.). 2016;241(12):1281-95. doi:10.1177/1535370216641787.

7. Mitochondrial Dysfunction and Mitochondrial Dynamics-the Cancer Connection.

Srinivasan S, Guha M, Kashina A, Avadhani NG. Biochimica Et Biophysica Acta. Bioenergetics. 2017;1858(8):602-614. doi:10.1016/j.bbabio.2017.01.004.

8.Dysregulation of Mitochondrial Function in Cancer Cells.

Awad AMAM, Abdul Karim N. International Journal of Molecular Sciences. 2025;26(14):6750. doi:10.3390/ijms26146750.

 9. Premalignant Progression in the Lung: Knowledge Gaps and Novel Opportunities for Interception of Non-Small Cell Lung Cancer. An Official American Thoracic Society Research Statement.

Moghaddam SJ, Savai R, Salehi-Rad R, et al. American Journal of Respiratory and Critical Care Medicine. 2024;210(5):548-571. doi:10.1164/rccm.202406-1168ST.

10. Mitochondria in Oxidative Stress, Inflammation and Aging: From Mechanisms to Therapeutic Advances.

Xu X, Pang Y, Fan X. Signal Transduction and Targeted Therapy. 2025;10(1):190. doi:10.1038/s41392-025-02253-4.

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 cannot get Urolithin A directly from food. You only get the precursors, and only people with the right gut bacteria turn those precursors into Urolithin A.

Supplements bypass the microbiome entirely and give everyone measurable Urolithin A, even non-producers.

Foods that contain ellagitannins include:

• pomegranates
• walnuts
• raspberries
• blackberries
• some teas, especially green tea

But none of these will raise Urolithin A levels if your gut bacteria cannot perform the conversion.

Short-term human studies show that Urolithin A is safe and well-tolerated. Most people experience no side effects. When side effects do show up, they are usually mild digestive symptoms like bloating or softer stools.

What we don’t know:

• long-term safety
• pregnancy or breastfeeding safety
• multi-year use
• effects in chronic disease

In other words, the short-term data look good, but the long-term story hasn’t been written yet.

Here is the simple answer:

Urolithin A is biologically promising but clinically modest.

It improves certain cellular markers and may boost muscle endurance in older adults.

It does not reverse aging or change major health outcomes—not yet.

Supplements make the most sense for:

• adults over 60
• people with early muscle loss
• individuals who are non-producers
• those wanting to support mitochondrial health

But nothing replaces the basics:

• resistance training
• movement
• eating well
• sleep
• stress control

That is still the foundation of a longer, healthier life.

(For the blog — as provided)

1. Kuerec AH, Lim XK, Khoo AL, et al. Targeting Aging With Urolithin A in Humans: A Systematic Review. Ageing Research Reviews. 2024;100:102406.
2. Heilman J, Andreux P, Tran N, et al. Safety Assessment of Urolithin A… Food and Chemical Toxicology. 2017;108:289-297.
3. Hasheminezhad SH, Boozari M, Iranshahi M, et al. Biological Activities of Urolithins… Phytotherapy Research. 2022;36(1):112-146.
4. Singh A, D'Amico D, Andreux PA, et al. Direct Supplementation With Urolithin A… European Journal of Clinical Nutrition. 2022;76(2):297-308.
5. Aichinger G, Stevanoska M, Beekmann K, et al. PBPK Modeling of Urolithin A… Molecular Nutrition & Food Research. 2023;67(15).
6. D'Amico D, Andreux PA, Valdés P, et al. Impact of Urolithin A on Health, Disease, and Aging. Trends in Molecular Medicine. 2021;27(7):687-699.
7. Gandhi GR, Antony PJ, Ceasar SA, et al. Health Functions of Ellagitannin-Derived Urolithins. Critical Reviews in Food Science and Nutrition. 2024;64(2):280-310.
8. Zhang M, Cui S, Mao B, et al. Ellagic Acid and Urolithin A: Sources and Metabolism. Critical Reviews in Food Science and Nutrition. 2023;63:6900-6922.
9. García-Villalba R, Giménez-Bastida JA, Cortés-Martín A, et al. Urolithins: Metabolism and Microbiota. Molecular Nutrition & Food Research. 2022;66:2101019.

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 “interesting biochemistry” and “fewer funerals.”

So NAD may nudge your cholesterol; statins save lives.

Older adults with metabolic syndrome, prediabetes, or early neurodegenerative disease could see modest improvements in inflammation or blood lipids.

Younger, healthier people mostly see lighter wallets.

No serious drug interactions have been documented, though theoretical ones exist with some chemotherapy or DNA-repair drugs.

As always, talk to your doctor before combining anything with prescription therapy.

The best way to support NAD and longevity is still food, sleep, and movement.

A Mediterranean diet rich in legumes, vegetables, olive oil, and fish fuels NAD pathways naturally — and has proven benefits for heart and brain health.

No influencer code required.

We’ll explore all of this — diet, longevity, and a little wine science — on next summer’s Mediterranean Longevity Cruise.

World-class physicians, scientists, and chefs will join me for ten days of evidence-based indulgence.

It’ll cost less than a Peter Attia consult — and no one will force you to drink AG1.

(For the record, I still do. It’s gentle on my stomach, but I’m hunting for less bougie vitamins.)

Boosting NAD may someday help extend healthspan, but for now, the best evidence still supports:

• Eat Mediterranean-style food.
• Move daily.
• Sleep enough.
• Manage stress.
• See your doctor before your supplement dealer.

That’s how you live longer and better — no silver bullet, just science and common sense.

Effects of NAD+ Precursor Supplementation on Glucose and Lipid Metabolism in Humans: A Meta-Analysis. Zhong O, Wang J, Tan Y, Lei X, Tang Z. Nutrition & Metabolism. 2022;19(1):20. doi:10.1186/s12986-022-00653-9.

2 Niacin: An Old Lipid Drug in a New NAD+ Dress. Romani M, Hofer DC, Katsyuba E, Auwerx J. Journal of Lipid Research. 2019;60(4):741-746. doi:10.1194/jlr.S092007.

3.Nicotinamide Adenine Dinucleotide in Aging Biology: Potential Applications and Many Unknowns. Bhasin S, Seals D, Migaud M, Musi N, Baur JA. Endocrine Reviews. 2023;44(6):1047-1073. doi:10.1210/endrev/bnad019.

4. Crestor. FDA Drug Label. Food and Drug Administration Updated date: 2024-07-31

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 trial.
• Drs. George Bray, Donna Ryan, and Catherine Champagne built the menu at Pennington Biomedical.
• Dr. Frank Sacks at Harvard analyzed the data.

They showed that a diet rich in fruits, vegetables, and low-fat dairy could lower blood pressure without weight loss.

Then came the Portfolio Diet, developed by Dr. David Jenkins and his team at the University of Toronto.

They combined soy, nuts, soluble fiber, and plant sterols — lowering LDL cholesterol by up to 17 percent.

That’s culinary medicine — research that feeds both the lab and the kitchen.

And yet some influencers still say we need “more salt.”

The DASH team proved the opposite — unless, of course, you’re selling $39 mango-flavored electrolytes on TikTok.

If you ever visit Edinburgh, skip the castle and go straight to the Surgeons’ Hall Museum.

Inside are the breakthroughs that transformed surgery:

Lister’s antisepsis, Syme’s anatomy, and James Young Simpson’s chloroform.

It was here that Arthur Conan Doyle, as a medical student, learned from Dr. Joseph Bell, the sharp observer who inspired Sherlock Holmes.

From those halls, medicine shifted from superstition to study — from anecdote to anatomy.

It’s where modern diagnosis began.

And this month on TikTok, we’ll walk those halls together.

Every generation gets its snake-oil salesman; ours just live-streams.

Gary Brecka calls himself a biologist who can predict your date of death — and change it for a price.

He has no medical degree, just a bachelor’s in biology and a borrowed pair of scrubs.

He never finished chiropractic school.

He sells hydrogen-water bottles, claiming there are 1,400 studies — there aren’t.

He says cold plunges melt fat — they don’t.

If they did, every Alaskan fisherman would look like Thor.

Brecka’s not a scientist. He’s a salesman with a ring light.

Barbara O’Neill preaches more than she practices science.

She claims cayenne pepper stops heart attacks and cholesterol is a Big Pharma hoax.

She charges thousands for seminars, dismisses evidence, and wraps it all in Seventh-Day Adventist fervor.

Meanwhile, my Crestor costs $2.36 for three months.

You do the math.

Now for the shirtless side of pseudoscience.

Compare the scientists who built the Mediterranean, DASH, and Portfolio diets to today’s supplement influencers.

The difference? The scientists do science. The influencers do sales.

There’s Paul Saladino — the carnivore who rediscovered fruit when steak stopped trending.

The salt bros selling electrolyte powder at $39 a bag.

Dr. Gundry, the ex-surgeon who says beans are dangerous — unless you buy his Bean Guard for $60 a month.

And the Liver King — whose biggest muscle came from a syringe, not a steak.

They don’t test ideas — they test lighting.

They make millions selling powders, not progress.

Science doesn’t need an affiliate link.

While the supplement crowd surfed and sold, real heroes — doctors, nurses, respiratory therapists, and dietitians — showed up every day during the pandemic.

Before there was a vaccine.

Before there was safety.

They went anyway.

Those are the people who save lives — not the ones selling shortcuts.

After 100 episodes, one truth stands out:

Science doesn’t need to be sexy to save lives.

My job — our job — is to build the bridge between real scientists and the public.

My background is in medicine, but my mission is communication.

To bring you work done in labs and clinics — not under ring lights.

The people I feature here aren’t influencers.

They’re the scientists whose glory comes from a colleague’s handshake, not a sales link.

Because behind every breakthrough is someone who’ll never trend on TikTok — but they’re the ones who truly change the world.

That’s what FORK U stands for — separating noise from nutrition, hype from health, and always choosing evidence over ego.

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, peppers, red onion, avocado, olive oil, lime juice, and cilantro. Chill it and watch it vanish.

Everyone blames tryptophan, but the real reason for that post-Thanksgiving crash is carbs, alcohol, and portion size.

When you load up on potatoes, rolls, and pie, your insulin spikes, helping tryptophan turn into melatonin — your sleep hormone. Add a glass (or three) of wine and you’re down for the count.

To avoid it, eat slowly, take a short walk after dinner, and save dessert for later. Your pancreas will thank you.

I’m a surgeon, not a baker. So, I buy my pumpkin pie from Costco and serve it with vanilla ice cream. Sometimes, simplicity really is the secret ingredient.

We’re launching a new live cooking show called FORK U with Flavor!

Join me on TikTok (@drterrysimpson) and maybe Instagram (@drterrysimpsonmd) as we cook together, talk food science, and share a few laughs.

Paid Substack subscribers at drsimpson.com get ingredient lists and recipes ahead of time so you can cook along live. Everyone else gets the replay links and recipes afterward.

If you can’t watch me set off the occasional smoke alarm, you haven’t lived.

Wherever you live — America, Canada, or across the pond — Thanksgiving reminds us that food connects us all.

Eat well. Be grateful. And remember, food isn’t just medicine — it’s connection, culture, and joy.

Happy Thanksgiving from me, Dr. Terry Simpson, and the FORK U team.

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 shortcuts.

Supplements can help fill a true gap — not when they replace good food and lifestyle.

Vitamin D is essential — just not magical.

If you’re deficient, fix it.

If you’re not, skip the megadoses and save your kidneys.

And please — don’t take medical advice from a chiropractor on YouTube.

The best way to get your Vitamin D?

Eat well. Move more. Go outside.

That’s the real sunshine therapy.

1. Manson JE et al. Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease (VITAL Trial). NEJM 2019; 380:33–44.
2. Bolland MJ et al. Effect of Vitamin D Supplementation on Mortality and Disease Outcomes. Lancet Diabetes Endocrinol. 2022; 10(2):120–130.
3. Marcinowska-Suchowierska E et al. Toxic Effects of Vitamin D Overdose. Front Endocrinol. 2018; 9:550.
4. Ataide FL, Carvalho Bastos LM, Vicente Matias MF, Skare TL, Freire de Carvalho J. Safety and effectiveness of vitamin D mega-dose: A systematic review. Clin Nutr ESPEN. 2021 Dec;46:115-120. doi: 10.1016/j.clnesp.2021.09.010. Epub 2021 Sep 25. PMID: 34857184.
5. Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. National Academies Press, 2011.