Fork U with Dr. Terry Simpson
Fork U with Dr. Terry Simpson

Fork U with Dr. Terry Simpson

Terry Simpson

Overview
Episodes

Details

Fork U(niversity) Not everything you put in your mouth is good for you. There’s a lot of medical information thrown around out there. How are you to know what information you can trust, and what’s just plain old quackery? You can’t rely on your own “google fu”. You can’t count on quality medical advice from Facebook. You need a doctor in your corner. On each episode of Your Doctor’s Orders, Dr. Terry Simpson will cut through the clutter and noise that always seems to follow the latest medical news. He has the unique perspective of a surgeon who has spent years doing molecular virology research and as a skeptic with academic credentials. He’ll help you develop the critical thinking skills so you can recognize evidence-based medicine, busting myths along the way. The most common medical myths are often disguised as seemingly harmless “food as medicine”. By offering their own brand of medicine via foods, These hucksters are trying to practice medicine without a license. And though they’ll claim “nutrition is not taught in medical schools”, it turns out that’s a myth too. In fact, there’s an entire medical subspecialty called Culinary Medicine, and Dr. Simpson is certified as a Culinary Medicine Specialist. Where today's nutritional advice is the realm of hucksters, Dr. Simpson is taking it back to the realm of science.

Recent Episodes

GLP-1 Drugs, the Mediterranean Diet, and the Science of Living Longer
DEC 18, 2025
GLP-1 Drugs, the Mediterranean Diet, and the Science of Living Longer
GLP-1 Drugs, the Mediterranean Diet, and the Science of Living LongerFor 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.Why Metabolism Matters for AgingAging 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.Retatrutide and the Next Generation of GLP-1 DrugsNewer 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.Inflammation: The Engine of AgingFor 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.Heart Disease and LongevityNothing 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.¹²The 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.⁸These 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.⁵Although 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.Dementia: Prevention, Not CureBrain 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.¹Randomized 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.Ultra-Processed Food and Brain AgingDiet 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.The Mediterranean Diet and AlcoholHere 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.What This Means for HealthspanAging 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.ReferencesUssher JR, Drucker DJ. Glucagon-Like Peptide 1 Receptor Agonists: Cardiovascular Benefits and Mechanisms of Action. Nat Rev Cardiol. 2023;20(7):463–474.Nauck MA, et al. Cardiovascular Actions and Clinical Outcomes With GLP-1 Receptor Agonists. Circulation. 2017;136:849–870.Pop-Busui R, et al. Heart Failure: An Underappreciated Complication of Diabetes. Diabetes Care. 2022;45:1670–1690.Wu Q, et al. Glucose-Independent Cardiovascular Mechanisms of GLP-1 RAs. Biomed Pharmacother. 2022;153:113517.Boshchenko AA, et al. Cardioprotective Signaling of GLP-1 Receptor Agonists. Int J Mol Sci. 2024;25:4900.Marso SP, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375:311–322.Honka H, et al. Therapeutic Manipulation of Myocardial Metabolism. J Am Coll Cardiol. 2021;77:2022–2039.FDA Orange Book.Tang H, et al. GLP-1RA Medications and Dementia Risk. JAMA Neurol. 2025;82:439–449.Seminer A, et al. Cardioprotective Glucose-Lowering Agents and Dementia Risk. JAMA Neurol. 2025;82:450–460.Au HCT, et al. GLP-1 and Neurodegenerative Pathology. Neurosci Biobehav Rev. 2025;173:106159.Inoue K, et al. GLP-1 RAs and Dementia Incidence in Older Adults. Ann Intern Med. 2025.
play-circle icon
11 MIN
Alcohol Cuts Healthspan
DEC 11, 2025
Alcohol Cuts Healthspan
The Holiday Party That Turned DeadlyIt 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.​What Is Holiday Heart?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.​Alcohol and Your HeartFor 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 and CancerAlcohol 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.​Blue Zones, Not Blue WineYou’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.Weight, Metabolism, and AgingAlcohol 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.​Why “Detox” Fixes FailPopular “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.​The Longevity HypocrisyModern 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.​When You StopOnce 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.​Bottom LineAlcohol 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.​ReferencesBerger D, De Aquino J P, Charness M E, et al. Common Alcohol-Related Concerns. NIAAA (2025).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.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.Rumgay H, Murphy N, Ferrari P, Soerjomataram I. Alcohol and Cancer: Epidemiology and Biological Mechanisms. Nutrients. 2021; 13(9): 3173. doi:10.3390/nu13093173.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.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.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.Fernández-Solà J. The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy. Nutrients. 2020; 12(2): 572. doi:10.3390/nu12020572.Domínguez F, Adler E, García-Pavía P. Alcoholic Cardiomyopathy: An Update. Eur Heart J. 2024; 45(26): 2294-2305. doi:10.1093/eurheartj/ehae362.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.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.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.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.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.
play-circle icon
12 MIN
Muscle, Mitochondria, and Healthspan
DEC 4, 2025
Muscle, Mitochondria, and Healthspan
Muscle is Medicine: Why Lifting Weights is Your Best Longevity InvestmentClearly, 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.Section 1: The Enemy is Muscle Loss (Sarcopenia)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.Section 2: Big Things Help Small Things—The Cellular ConnectionAmazingly, 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.Section 3: Muscle is Your Metabolic PowerhouseLet'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.Section 4: Building an Iron SkeletonHowever, 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.Section 5: The Importance of Balance and Quality CoachingBeyond 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!Section 6: The Ultimate Goal: Getting Back UpUltimately, 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.Conclusion and Call to ActionFinally, 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.ReferencesDao 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.
play-circle icon
13 MIN
Telomeres and Time: Rewind Aging
NOV 27, 2025
Telomeres and Time: Rewind Aging
🧬 Telomeres and Time: Can We Really Rewind Aging?The Lowest Hemoglobin I’ve Ever SeenThe 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.What Are Telomeres?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.Why Everyone Talks About TelomeresTelomeres 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.What’s Being StudiedReal 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.Vitamins and Compounds That Might HelpNutrients 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.What Lifestyle Still Beats EverythingLifestyle 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.What Scientists Agree OnResearch 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.The Real TakeawayTelomeres 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.ReferencesCalado RT, Young NS. Telomere Diseases. N Engl J Med. 2009;361(24):2353-65. PMCID: PMC3401586Lai T-P, Wright WE, Shay JW. Techniques for Assessing Telomere Length. Nat Rev Genet. 2018;19(5):293-307. PMCID: PMC6380489Huang S et al. The Relationship Between Telomere Length and Aging-Related Diseases. Front Aging. 2025;6:1532. PMCID: PMC11882723Arsenis CA et al. Physical Activity and Telomere Length. Sports Med. 2017;47(3):503-512.Schellnegger T et al. Unlocking Longevity: The Role of Telomeres and Their Targeting. Front Aging Neurosci. 2024;16:1050353.
play-circle icon
9 MIN
Mitochondria Matter: The Story of Aging
NOV 20, 2025
Mitochondria Matter: The Story of Aging
The Mitochondria Problem: Why These Tiny Powerhouses Shape How We AgeMany 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.What Are Mitochondria?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 ATPFinally, mitochondria keep your organs working.You inherit all your mitochondria from your mother, which is why scientists use mitochondrial DNA to trace ancestry.How Did We Get Mitochondria? (A Very Old Story)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.What Do Mitochondria Do All Day? 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.Why Young Mitochondria Work So WellYoung 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 musclessharp thinkingfast recoveryhealthy metabolismWhen mitophagy runs smoothly, you feel energetic and resilient.What Happens When Mitochondria AgeAging 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.How Aging Mitochondria Cause TroubleAs 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 fogmuscle fatigueslower recoveryheart strainmetabolic slowdowncancer-friendly environmentsMitochondria sit at the center of how we age.Why “Mitochondrial Booster” Supplements Miss the MarkPlenty of supplements promise to “repair” mitochondria. Many sound exciting:NAD boostersUrolithin Apeptidesantioxidant stacksHowever, 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.What Does Improve Mitochondrial HealthGood news: the basics still win. And they outperform supplements every time.1. Resistance TrainingYour muscles grow new mitochondria in response to lifting weights or doing body-weight exercises.2. Zone 2 ExerciseThis “comfortably challenging” aerobic zone trains your body to use oxygen better. You can talk, but you can’t sing.3. SleepYour body repairs mitochondrial damage at night. Poor sleep means poor repair.4. Mediterranean DietWhole foods, plants, nuts, fish, and olive oil protect mitochondria from inflammation and stress.5. Treating Metabolic Disease EarlyHigh blood sugar, high LDL, and high blood pressure destroy mitochondria faster than anything else.Why Diet Tribes Get Mitochondria WrongSome 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.Alcohol Ages Mitochondria FastYour 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.Bringing It All TogetherMitochondria 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.REFERENCES1.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.
play-circle icon
12 MIN