# ![@healthspanmed Avatar](https://lunarcrush.com/gi/w:26/cr:twitter::1298434617549049857.png) @healthspanmed Healthspan

Healthspan posts on X about health, science, systems, has been the most. They currently have [-----] followers and [---] posts still getting attention that total [-----] engagements in the last [--] hours.

### Engagements: [-----] [#](/creator/twitter::1298434617549049857/interactions)
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- [--] Week [------] +1,057%
- [--] Month [------] +232%
- [--] Months [------] +999%
- [--] Year [------] +405%

### Mentions: [--] [#](/creator/twitter::1298434617549049857/posts_active)
![Mentions Line Chart](https://lunarcrush.com/gi/w:600/cr:twitter::1298434617549049857/c:line/m:posts_active.svg)


### Followers: [-----] [#](/creator/twitter::1298434617549049857/followers)
![Followers Line Chart](https://lunarcrush.com/gi/w:600/cr:twitter::1298434617549049857/c:line/m:followers.svg)

- [--] Week [-----] +0.42%
- [--] Month [-----] +1.10%
- [--] Months [-----] +9.90%
- [--] Year [-----] +17%

### CreatorRank: [---------] [#](/creator/twitter::1298434617549049857/influencer_rank)
![CreatorRank Line Chart](https://lunarcrush.com/gi/w:600/cr:twitter::1298434617549049857/c:line/m:influencer_rank.svg)

### Social Influence

**Social category influence**
[finance](/list/finance)  5%

**Social topic influence**
[health](/topic/health) 14%, [science](/topic/science) 7%, [systems](/topic/systems) #1751, [has been](/topic/has-been) 5%, [matter](/topic/matter) 5%, [the most](/topic/the-most) 4%, [more than](/topic/more-than) 3%, [dr](/topic/dr) 3%, [university of](/topic/university-of) 3%, [future](/topic/future) 3%

**Top accounts mentioned or mentioned by**
[@acebedoerichmd](/creator/undefined) [@mikeormsbees](/creator/undefined) [@scottz06](/creator/undefined) [@erogul1](/creator/undefined)
### Top Social Posts
Top posts by engagements in the last [--] hours

"For years rapamycin dosing has been borrowed from disease settings. But aging biology plays by different rules. New human studies are helping clarify how dose and timing shape rapamycins effects on mTOR autophagy and cellular repairsuggesting that modulation may matter more than suppression. Full Research Review https://www.gethealthspan.com/research/article/rapamycin-dosing-for-longevity https://www.gethealthspan.com/research/article/rapamycin-dosing-for-longevity"  
[X Link](https://x.com/healthspanmed/status/2021539739472683516)  2026-02-11T11:00Z [----] followers, [---] engagements


"Low-dose naltrexone has been used off-label for years in conditions marked by chronic inflammation and neuroimmune imbalance. But only recently has a deeper question come into focus: how does LDN actually work biologicallyand why might timing and delivery matter Our recent Research Review explores how LDNs effects may depend not on sustained receptor blockade but on brief time-dependent signaling that engages endogenous systems involved in immune regulation neuroinflammation and neuronal maintenance. By focusing on troche-based delivery the review examines why formulation may be part of the"  
[X Link](https://x.com/healthspanmed/status/2021675634381226130)  2026-02-11T20:00Z [----] followers, [---] engagements


"SGLT2 inhibitors are usually discussed as metabolic drugslowering glucose supporting weight loss and protecting the heart and kidneys. But emerging research suggests their influence may reach deeper. A new multi-site study examined SGLT2 inhibition through an unexpected lens: the hallmarks of aging. Instead of diabetes endpoints researchers looked at telomeres immune function metabolic reprogramming and cellular maintenance. This weeks Research Review explores what these findings begin to suggestand why common metabolic therapies may intersect with aging biology in ways were only starting to"  
[X Link](https://x.com/healthspanmed/status/2021751125767336000)  2026-02-12T01:00Z [----] followers, [---] engagements


"What if dementia doesnt begin in memory circuits at all Large population studies have revealed a quiet signal: people using GLP-1 therapies for metabolic disease develop dementia at meaningfully lower rates. Our latest Research Review explores whyby examining how metabolic health circulation and brain energy may set the conditions for cognitive decline long before symptoms appear. https://www.gethealthspan.com/research/article/glp-1-neuroprotective-benefits https://www.gethealthspan.com/research/article/glp-1-neuroprotective-benefits"  
[X Link](https://x.com/healthspanmed/status/2021947426710729165)  2026-02-12T14:00Z [----] followers, [---] engagements


"For years weve understood stress as a contributor to burnout anxiety and chronic disease. But new research is revealing something deeperstress doesnt just affect how we feel. It accelerates how we age. This month Dr. Aaron Slusher a research scientist at the Yale School of Medicine reviewed groundbreaking findings on how acute stressorslike surgery pregnancy and infectioncan rapidly increase biological age. And perhaps more importantly how those changes may be reversible. The big takeaway Stress doesnt just take a toll. It leaves a molecular signature in our DNA. Heres what the latest"  
[X Link](https://x.com/healthspanmed/status/2021388744314716636)  2026-02-11T01:00Z [----] followers, [---] engagements


"Exercise isnt just about burning calories or improving fitness. As we age two systems quietly determine how much capacity we retain: the blood vessels that deliver oxygen the mitochondria that turn it into energy In our latest Research Review we examine how different types of exercise remodel these systems over timeand why not all training shapes aging biology the same way. We step back from workouts and ask a more fundamental question: what is exercise actually rebuilding inside the body as we age Full review here"  
[X Link](https://x.com/healthspanmed/status/2022738909177024848)  2026-02-14T18:25Z [----] followers, [---] engagements


"Why do some of the fittest people on earth show pre-diabetic A1C levels even when their glucose insulin and metabolic health are excellent In this episode of Beyond Healthspan we break down the mysterious Hemoglobin A1C Paradox a surprising phenomenon where endurance athletes and highly trained individuals show higher A1C scores despite having elite metabolic markers. Watch the full episode: https://www.youtube.com/watchv=yAkqX9G33K8 https://www.youtube.com/watchv=yAkqX9G33K8"  
[X Link](https://x.com/healthspanmed/status/2017326985413095685)  2026-01-30T20:00Z [----] followers, [---] engagements


"🧠 What if Alzheimers isnt caused by plaques at allbut by an energy crisis inside your brain cells When you dig into the research of Dr. Francisco Gonzalez-Lima and Dr. Jack de la Torre on mitochondrial dysfunction in Alzheimers diseaseand the potential of methylene blue to restore neuronal energyyou begin to see a radically different framing of the disease. If you accept the premise that one of the primary drivers of AD is an energy shortfall within neurons the question becomes: where is that deficit happening The answer Gonzalez-Lima argues is almost certainly the mitochondria. His work"  
[X Link](https://x.com/healthspanmed/status/2020075093528047861)  2026-02-07T10:00Z [----] followers, [---] engagements


"Most Alzheimers conversations start with plaques and tangles. This one starts somewhere else: fuel failure. In this clip from Beyond Healthspan Dr. Francisco Gonzalez-Lima breaks down a finding that flips the usual narrative: The brain has almost no energy backup. When metabolism slips function starts to slip with it. And that metabolic decline can appear long before obvious neurodegeneration. Using rare fresh-frozen postmortem brain tissue and quantitative cytochrome oxidase mapping his team found a clear pattern: High demand brain networks showed early metabolic compromise FDG-PET"  
[X Link](https://x.com/healthspanmed/status/2020213363754889594)  2026-02-07T19:09Z [----] followers, [---] engagements


"New human data are beginning to clarify how rapamycin should be dosed for agingnot by constant suppression but through dose and timing that engage cellular maintenance pathways. We synthesized findings across animal models dog trials and emerging human studies to ask a simple question: how do you harness rapamycins healthspan biology without disrupting normal cellular function Our latest Research Review explores what the biologyand new human evidenceare starting to reveal. https://www.gethealthspan.com/research/article/rapamycin-dosing-for-longevity"  
[X Link](https://x.com/healthspanmed/status/2020549323461890224)  2026-02-08T17:24Z [----] followers, [----] engagements


"Why do some of the fittest people on earth show pre-diabetic A1C levels even when their glucose insulin and metabolic health are excellent In this episode of Beyond Healthspan we break down the mysterious Hemoglobin A1C Paradox a surprising phenomenon where endurance athletes and highly trained individuals show higher A1C scores despite having elite metabolic markers. Watch the full episode: https://www.youtube.com/watchv=yAkqX9G33K8 https://www.youtube.com/watchv=yAkqX9G33K8"  
[X Link](https://x.com/healthspanmed/status/2020588461695414740)  2026-02-08T20:00Z [----] followers, [---] engagements


"What if cognitive aging isnt primarily a problem of memory neurotransmitters or plaquesbut a problem of energy In this episode of Beyond Healthspan we sit down with Dr. Francisco Gonzalez-Lima Professor of Neuroscience Pharmacology and Toxicology at the University of Texas at Austin to unpack decades of research on brain energy metabolism mitochondria and aging. In this episode we cover: Why energy metabolism has been overlooked in neuroscience How mitochondrial dysfunction appears before Alzheimers pathology The central role of cytochrome c oxidase (Complex IV) in brain energy How red and"  
[X Link](https://x.com/healthspanmed/status/2020663962212421709)  2026-02-09T01:00Z [----] followers, [---] engagements


"Exercise is biological remodeling. The question is: what systems are being remodeledand for how long Our latest Research Review explores mitochondrial and vascular adaptation through an aging lens. Read https://www.gethealthspan.com/research/article/exercise-modalities-and-mitochondrial-and-vascular-remodeling https://www.gethealthspan.com/research/article/exercise-modalities-and-mitochondrial-and-vascular-remodeling"  
[X Link](https://x.com/healthspanmed/status/2020784759967011112)  2026-02-09T09:00Z [----] followers, [---] engagements


"For decades dementia research has focused on memory loss plaques and neurotransmitters. But what if those are late-stage signalsnot the beginning A growing body of population data points to something unexpected: people on GLP-1 therapies develop dementia at lower rates. Not because these drugs target cognition directly but because they appear to influence the systems that fail before memory does. Our latest Research Review follows that signal upstreaminto brain energy supply circulation and metabolic resilienceand asks a different question: what if dementia risk is shaped years earlier than"  
[X Link](https://x.com/healthspanmed/status/2020950862605308235)  2026-02-09T20:00Z [----] followers, [---] engagements


"For decades calorie restriction has been one of the most reliable ways to improve metabolic health and extend lifespan in animals. But sustained restriction is hard to maintainand not without tradeoffs. This weeks Research Review explores a deeper question: if fasting works because of the biological signals it triggers can those same signals be engaged without long-term deprivation By examining a randomized human trial of a fasting-mimicking diet we explore whether short-term dietary stress reaches deep enough into human biology to engage autophagythe cells internal maintenance system thought"  
[X Link](https://x.com/healthspanmed/status/2021313265889079639)  2026-02-10T20:00Z [----] followers, [---] engagements


"For years perimenopause has been framed as a simple hormonal decline. But new research suggests something more complex is happeninginside the brain. As estrogen signaling becomes erratic the hypothalamus begins to rewire. This disrupts how hunger energy use and body weight are coordinated setting the stage for many of the metabolic changes women experience in midlife. Our latest Research Review explores what this rewiring meansand why perimenopausal weight gain may be less about behavior and more about biology."  
[X Link](https://x.com/healthspanmed/status/2021237771034316830)  2026-02-10T15:00Z [----] followers, [---] engagements


"ME/CFS is often described as fatigue. Clinically its something else entirely: a failure to recover after stress. Even modest exertion can push patients into prolonged collapsenot because of weakness but because the system fails to reset. A recent human study approached this problem through aging biology focusing on autophagythe cells maintenance systemand what happens when it slows. Our latest Research Review explores why ME/CFS may be less of an anomaly and more of a stress test for aging biology itself."  
[X Link](https://x.com/healthspanmed/status/2022234321340469648)  2026-02-13T09:00Z [----] followers, [---] engagements


"For decades protein nutrition has been evaluated almost entirely through one lens: muscle. Fast digestion leucine content and muscle protein synthesis made whey protein the gold standard for recovery and aging muscle. But protein interacts with far more than skeletal muscle. Sleep regulation circadian timing metabolic efficiency immune signaling and brain chemistry are all influenced by amino acid compositionyet these systems are often studied in isolation. This weeks Research Review examines evidence that not all whey proteins function identically and why protein compositionnot just total"  
[X Link](https://x.com/healthspanmed/status/2022400414952624578)  2026-02-13T20:00Z [----] followers, [---] engagements


"What if the key to rapamycin and aging isnt how much but how often New human data are reshaping how scientists think about dosing timing and the biology of cellular maintenance. Our latest Research Review dives into the evidence. https://www.gethealthspan.com/research/article/rapamycin-dosing-for-longevity https://www.gethealthspan.com/research/article/rapamycin-dosing-for-longevity"  
[X Link](https://x.com/healthspanmed/status/2022611796767764810)  2026-02-14T10:00Z [----] followers, [---] engagements


"GLP-1 medications are often framed as weight-loss drugs. But the biology tells a much bigger story. In Episode [--] of our GLP-1 & Longevity Series the Healthspan clinical team explores why this class of medications may represent one of the most important medical developments of our generationaffecting metabolism cardiovascular health liver function brain resilience and potentially the trajectory of aging itself. We move beyond headlines to examine what GLP-1s are actually doing inside the bodyand why many of their benefits appear independent of weight loss."  
[X Link](https://x.com/healthspanmed/status/2022785626790334901)  2026-02-14T21:30Z [----] followers, [----] engagements


"20/ In the trial BHB increased from [----] [----] mmol/L with henagliflozin. Thats not keto diet territory. Its tinybarely above baseline. But in aging biology small persistent changes in BHB can have meaningful effects: Cleaner mitochondrial energy production Less reactive oxygen species Lower activation of the NLRP3 inflammasome More antioxidant gene expression Support for FOXO and SIRT pathways involved in cellular repair Improved neuronal resilience in animal models This is why BHB is increasingly viewed as an endogenous anti-aging metabolitea molecule that gently tilts the cell toward"  
[X Link](https://x.com/healthspanmed/status/2004190656575746444)  2025-12-25T14:01Z [----] followers, [--] engagements


"21/ Why would an SGLT2 inhibitor raise BHB at all Because losing glucose in urine creates a mild steady energy deficit. The body compensates by tapping into fat stores and increasing ketone production. Its not fastingbut it mimics some of fastings metabolic choreography: Less reliance on glucose More reliance on fatty acids Mild activation of nutrient-sensing pathways A quiet shift toward maintenance In essence henagliflozin induces a tiny metabolic pivot toward the physiology of caloric restrictionwithout the individual needing to change diet"  
[X Link](https://x.com/healthspanmed/status/2004190668588306808)  2025-12-25T14:01Z [----] followers, [--] engagements


"27/ When you combine:  Thiamine  PC / PE / sphingosine  BHB  IGFBP-3  CTL granzyme B Slightly longer telomeres a clear motif emerges: A gentle shift away from growth and overload toward efficiency cleanup and metabolic balance. This is the same multi-system pattern seen during caloric restriction one of the most robust longevity interventions in animal models. The trial doesnt prove were inducing CR in humans. But the metabolomics fingerprint looks like a cousin of that physiology. Its a coordinated low-amplitude recalibration not dramatic but directionally meaningful"  
[X Link](https://x.com/healthspanmed/status/2004190740755406862)  2025-12-25T14:01Z [----] followers, [--] engagements


"28/ [--] Short-term metabolic outcomes still matter As expected the drug also improved traditional metabolic markers vs placebo: Larger reductions in HbA1c and fasting glucose Greater weight and BMI loss Bigger drop in serum uric acid These alone dont make a longevity drugbut they reduce chronic stressors that accelerate cellular damage"  
[X Link](https://x.com/healthspanmed/status/2004190752726008236)  2025-12-25T14:01Z [----] followers, [--] engagements


"Why do some of the fittest people on earth show pre-diabetic A1C levels even when their glucose insulin and metabolic health are excellent In this episode of Beyond Healthspan we break down the mysterious Hemoglobin A1C Paradox a surprising phenomenon where endurance athletes and highly trained individuals show higher A1C scores despite having elite metabolic markers. Watch the full episode: https://www.youtube.com/watchv=yAkqX9G33K8 https://twitter.com/i/web/status/2004356504061669870 https://www.youtube.com/watchv=yAkqX9G33K8 https://twitter.com/i/web/status/2004356504061669870"  
[X Link](https://x.com/healthspanmed/status/2004356504061669870)  2025-12-26T01:00Z [----] followers, [---] engagements


"🧬 Hair Loss as a Window into Aging: How Autophagy & Senescence Drive Follicle Decline Hair loss is often dismissed as a mere cosmetic issuebut mounting evidence suggests its a powerful biomarker of systemic aging. Recent research highlights two cellular processes at the heart of follicle health: senescence (where cells cease to divide but remain active) and autophagy (a cellular cleanup program). When these processes go awry hair follicle stem cells (HFSCs) falter hair thins and the scalp gradually loses its regenerative spark. Below is a deep dive into the science behind hair loss detailing"  
[X Link](https://x.com/healthspanmed/status/2004854789709127861)  2025-12-27T10:00Z [----] followers, [----] engagements


"🧬 If youve been waiting to start a longevity protocol this is your moment. For a limited time Healthspan is taking 20% off every protocol program and lab panelfrom metabolic optimization to mitochondrial support and advanced biomarker testing. Your future self will thank you. Use code NEW20 at checkout https://gethealthspan.com https://gethealthspan.com"  
[X Link](https://x.com/healthspanmed/status/2005016198795460666)  2025-12-27T20:41Z [----] followers, [----] engagements


"🧬 What if aging isnt caused by cellular declinebut by cellular overactivity What if the same molecular programs that build and repair our bodies in youth never truly shut offand slowly begin to harm us Thats the premise of hyperfunction theory and a [----] Nature Aging study has just revealed its most compelling evidence yet. 👇"  
[X Link](https://x.com/healthspanmed/status/2005081281613496517)  2025-12-28T01:00Z [----] followers, [---] engagements


"1 The Core Question For years longevity research revolved around a single molecule: rapamycin an inhibitor of mTORC1the master growth controller. But the question remained: Could targeting one pathway ever be enough in a system as complex as aging In [----] a team led by Gkioni et al. tested that idea by adding a second molecule: trametinib a MEK inhibitor that blocks a parallel growth signal the RasERK pathway. What they found changed the field"  
[X Link](https://x.com/healthspanmed/status/2005081293638566125)  2025-12-28T01:00Z [----] followers, [--] engagements


"2 The Breakthrough When combined rapamycin + trametinib extended mouse lifespan by: +34.9% in females +27.4% in males Thats not additive noiseits a systems-level synergy. For comparison: rapamycin alone extends lifespan by 1520%. The implication Aging may not be governed by one pathway but by an interconnected network of pro-growth signals that need to be quieted together"  
[X Link](https://x.com/healthspanmed/status/2005081305516777538)  2025-12-28T01:00Z [----] followers, [--] engagements


"3 The Big Idea Aging as Overactivity Traditionally aging was seen as decline: systems breaking down cells failing DNA wearing out. But hyperfunction theorypioneered by Dr. Mikhail Blagosklonnyflips this narrative. It suggests aging arises from too much function. Cells keep doing their jobs past their useful window: secreting growing signaling. Over time that chronic overdrive causes hypertrophy inflammation and senescence. Not failureoverfunction"  
[X Link](https://x.com/healthspanmed/status/2005081317483184513)  2025-12-28T01:00Z [----] followers, [--] engagements


"4 The mTOR Pathway: The Growth Command Center mTORC1 senses nutrients amino acids insulin and energy. When active it drives growth and protein synthesisvital in youth destructive when chronic. In adulthood persistent activation (especially from excess calories and leucine-rich diets) locks cells into an anabolic state. Autophagythe cleanup processshuts down. Damaged mitochondria accumulate. Rapamycin acts like a brake pedal restoring equilibrium and extending lifespan by up to 20% in mice"  
[X Link](https://x.com/healthspanmed/status/2005081329374036213)  2025-12-28T01:00Z [----] followers, [--] engagements


"5 The RasERK Pathway: The Inflammatory Amplifier If mTORC1 is the builder RasERK is the communicator. It relays external growth signalslike insulin and EGFstraight to the nucleus. In aging this pathway gets stuck on. The result: chronic inflammation excessive proliferation and metabolic noise. RasERK overactivation fuels inflammagingthe slow burn that drives everything from arterial stiffening to neurodegeneration"  
[X Link](https://x.com/healthspanmed/status/2005081341344579973)  2025-12-28T01:00Z [----] followers, [--] engagements


"6 Why Combine Them Both pathways evolved to handle short bursts of stress or growth. But in modern conditionsconstant food stress and insulintheyre chronically stimulated. Inhibiting mTORC1 slows growth and re-activates cellular repair. Inhibiting MEK/ERK dampens inflammatory feedback and cellular stress signaling. Together they address two sides of the same coin: metabolic overdrive and inflammatory amplification"  
[X Link](https://x.com/healthspanmed/status/2005081353256402975)  2025-12-28T01:00Z [----] followers, [--] engagements


"🔬 [--] Tissue-Level Changes Liver: Fewer tumors and reduced inflammatory gene expression Muscle: Preserved mitochondrial function and mass Kidney: Improved morphology and filtration capacity Heart (from RAPACAT trial in cats): left ventricular wall thickness by 1722% The pattern is consistent: dual inhibition preserves tissue integrity across systems"  
[X Link](https://x.com/healthspanmed/status/2005081401042108925)  2025-12-28T01:00Z [----] followers, [--] engagements


"⚖ [--] Dose Matters At high doses (11.5 mg/kg) trametinib caused liver steatosis spleen enlargement and testicular degeneration. But at low doses (1.44 mg/kg) benefits appeared with minimal toxicity. This highlights the need for precision dosinga hallmark of future longevity medicine. More isnt better; balance is"  
[X Link](https://x.com/healthspanmed/status/2005081412920336744)  2025-12-28T01:00Z [----] followers, [--] engagements


"🧭 [--] The Road Ahead The next frontier: - Clinical trials testing low-dose combinations of safe pathway modulators - Mapping sex-specific responses - Identifying molecular biomarkers for hyperfunction control - Designing adaptive dosing algorithms for precision gerotherapy Longevity medicine is moving from single hits to orchestration"  
[X Link](https://x.com/healthspanmed/status/2005081484366053792)  2025-12-28T01:00Z [----] followers, [---] engagements


"💡 [--] The Takeaway Aging isnt a clock running downits an orchestra playing too loudly for too long. Rapamycin and trametinib taught us that longevity doesnt come from silencing one instrument but from retuning the whole symphony. For the full breakdown of mechanisms data and translational insights: https://www.gethealthspan.com/research/article/rapamycin-and-trametinib https://www.gethealthspan.com/research/article/rapamycin-and-trametinib"  
[X Link](https://x.com/healthspanmed/status/2005081496592547916)  2025-12-28T01:00Z [----] followers, [---] engagements


"Why the timeline matters These cardiovascular improvements emerged far sooner than would be expected if they were driven primarily by: Weight loss Changes in lipid profiles Improved insulin sensitivity Instead the rapid onset points toward mTORs role in vascular tone endothelial signaling and cardiac relaxation dynamics. In animal models mTOR inhibition has long been linked to improved vascular elasticity and reduced age-associated cardiac hypertrophy. This study provided early human evidence consistent with that biology"  
[X Link](https://x.com/healthspanmed/status/2006452541836636416)  2025-12-31T19:48Z [----] followers, [--] engagements


"Safety signals were reassuringbut not definitive Importantly no adverse events directly attributable to rapamycin were observed over the 8-week period. There were: No infections No clinically meaningful immunosuppression No study discontinuations That said the authors were careful not to overstate safety. Six participants. Eight weeks. Proof-of-concept only. This study doesnt establish long-term safetybut it does reinforce existing data suggesting that low-dose short-term mTOR inhibition behaves very differently from transplant-level exposure."  
[X Link](https://x.com/healthspanmed/status/2006452553731682562)  2025-12-31T19:49Z [----] followers, [--] engagements


"A reframing of metabolic drugs By [----] the picture had shifted. SGLT2 inhibitors were no longer viewed solely as glucose-lowering agents but as system-level modulators of aging biologyinfluencing inflammation mitochondrial health telomere dynamics and cellular senescence through a shared metabolic lens. Not a silver bullet. Not a classic senolytic. But a biologically coherent way to reduce the pressure that drives tissues toward senescence in the first place"  
[X Link](https://x.com/healthspanmed/status/2006452755834245280)  2025-12-31T19:49Z [----] followers, [--] engagements


"8 Hormone replacement therapy: a regulatory course correction One of the most consequential changes of [----] wasnt molecularit was regulatory. The FDA initiated removal of the black-box warning on menopausal hormone replacement therapy. Re-analyses showed that for women initiating HRT near menopause: Quality of life improves Bone density is preserved Cardiometabolic outcomes improve All-cause mortality may decrease The takeaway wasnt HRT for everyone. It was that timing and personalization matter. https://twitter.com/i/web/status/2006452767662186644"  
[X Link](https://x.com/healthspanmed/status/2006452767662186644)  2025-12-31T19:49Z [----] followers, [--] engagements


"For decades rapamycin has been recognized for its ability to extend lifespan in animals by targeting one of the central drivers of agingthe mTOR pathway. But what does that actually look like in humans A new pilot study from the University of Texas Health Science Center explored this question by administering low-dose rapamycin (1 mg/day) to six healthy men in their seventies for eight weekscloser to the longevity-style dosing now being studied not the high immunosuppressive doses used in transplant medicine. The results were small but meaningful: Improved diastolic function (the hearts"  
[X Link](https://x.com/healthspanmed/status/2009263988975259893)  2026-01-08T14:00Z [----] followers, [---] engagements


"8/ In the brain this same overactivity drives neurodegeneration as misfolded proteins pile up faster than neurons can clear them. In muscle it contributes to sarcopenia weakening contractile fibers and exhausting mitochondrial capacity"  
[X Link](https://x.com/healthspanmed/status/2009354545005244898)  2026-01-08T20:00Z [----] followers, [--] engagements


"9/ In metabolic organs like the liver and pancreas the same imbalance leads to nutrient overload and insulin resistance. Across systems cells forget how to pausebuilding when they should be repairing producing when they should be cleaning up"  
[X Link](https://x.com/healthspanmed/status/2009354556753498311)  2026-01-08T20:00Z [----] followers, [--] engagements


"27/ The treatment also reduced reactive oxygen species (ROS) inside ovarian cells lowering the oxidative stress that damages mitochondria and DNA. In aging tissues oxidative overload is one of the most persistent barriers to proper repairand here it visibly eased"  
[X Link](https://x.com/healthspanmed/status/2009354771044712721)  2026-01-08T20:01Z [----] followers, [--] engagements


"28/ Taken together these results painted a consistent picture from cell to organism: Rapamycin restored order not by stimulating growth but by rebalancing metabolismallowing the ovarys energy systems to prioritize quality over quantity"  
[X Link](https://x.com/healthspanmed/status/2009354783271080436)  2026-01-08T20:01Z [----] followers, [--] engagements


"31/ This was not traditional hormone stimulation. The goal wasnt to increase egg countit was to improve the quality and developmental potential of the eggs already present by restoring balance in the ovarian microenvironment"  
[X Link](https://x.com/healthspanmed/status/2009354819186905376)  2026-01-08T20:01Z [----] followers, [--] engagements


"32/ Even this short course produced clear benefits. Women who received Rapamycin generated more fertilized eggs more developing embryos and more top-grade blastocysts compared with standard IVF protocols. Success rates effectively doubled"  
[X Link](https://x.com/healthspanmed/status/2009354831023268205)  2026-01-08T20:01Z [----] followers, [--] engagements


"34/ Importantly this improvement came without additional hormone exposure or longer treatment cycles. It reflected a change in cellular health not ovarian stimulationsuggesting that a brief metabolic reset can meaningfully enhance fertility potential"  
[X Link](https://x.com/healthspanmed/status/2009354855006261618)  2026-01-08T20:01Z [----] followers, [--] engagements


"35/ Underneath the statistics lies a deeper biological narrative: Rapamycin didnt make new eggsit helped existing ones function better. By restoring order to how ovarian cells manage growth repair and energy use the ovary regained part of its youthful rhythm"  
[X Link](https://x.com/healthspanmed/status/2009354866859376910)  2026-01-08T20:01Z [----] followers, [--] engagements


"39/ Taken together this research forms one of the clearest bridges yet between reproductive biology and longevity science. It shows that the ovary long considered one of the first organs to age follows the same molecular rules as every other tissue in the body"  
[X Link](https://x.com/healthspanmed/status/2009354914049520103)  2026-01-08T20:01Z [----] followers, [--] engagements


"40/ In a healthy ovary the cells internal clock oscillates between growth and repair. Protein synthesis rises autophagy clears the debris and the cycle repeats a rhythm that keeps the oocyte and its surrounding cells in sync"  
[X Link](https://x.com/healthspanmed/status/2009354925910995259)  2026-01-08T20:02Z [----] followers, [--] engagements


"41/ With age that rhythm falters. Growth signals remain switched on ribosome activity accelerates and cleanup processes slow. The ovary becomes metabolically congested unable to clear oxidative debris and communication between the egg and its support cells begins to break down. https://twitter.com/i/web/status/2009354937957011679 https://twitter.com/i/web/status/2009354937957011679"  
[X Link](https://x.com/healthspanmed/status/2009354937957011679)  2026-01-08T20:02Z [----] followers, [--] engagements


"42/ Rapamycin restores the pause. By temporarily slowing protein production it gives the cell time to repair and recycle. In doing so it doesnt reverse aging it rebalances it allowing old systems to operate with younger efficiency"  
[X Link](https://x.com/healthspanmed/status/2009354949856252311)  2026-01-08T20:02Z [----] followers, [--] engagements


"43/ This patterntoo much growth not enough repairhas been seen in almost every aging system studied: the brain heart muscle and immune cells. Now for the first time we see it clearly in the ovary. The same biology that governs lifespan also governs fertility"  
[X Link](https://x.com/healthspanmed/status/2009354961554165859)  2026-01-08T20:02Z [----] followers, [--] engagements


"45/ For reproductive medicine that means fertility decline after [--] may not be an irreversible countdown. It may be a reflection of lost cellular coordination; something that at least in part can be restored"  
[X Link](https://x.com/healthspanmed/status/2009354985474265536)  2026-01-08T20:02Z [----] followers, [--] engagements


"46/ For longevity science it offers validation that interventions like Rapamycin act on fundamental cellular economics; reallocating energy from endless growth toward maintenance and repair. That shift improves not just lifespan but healthspan"  
[X Link](https://x.com/healthspanmed/status/2009354997159616648)  2026-01-08T20:02Z [----] followers, [--] engagements


"47/ The ovary is showing us what happens when that balance is restored: fewer errors higher efficiency and renewed functioneven after age [--]. Its a microcosm of what every tissue in the body seeks with age: equilibrium between building and cleaning ambition and restraint"  
[X Link](https://x.com/healthspanmed/status/2009355008991707261)  2026-01-08T20:02Z [----] followers, [--] engagements


"The latest research reveals mitochondrial breakdown as a root driver of aging. We created a framework to track their health diagnose decline and apply interventions that protect lifespan. https://www.youtube.com/watchv=QpWZheUD1_Y https://www.youtube.com/watchv=QpWZheUD1_Y"  
[X Link](https://x.com/healthspanmed/status/2009716835340693621)  2026-01-09T20:00Z [----] followers, [---] engagements


"3 Low-dose daily rapamycin and cardiovascular aging For decades rapamycins clinical identity was shaped almost entirely by its use in transplantation. High doses. Continuous exposure. Intentional immunosuppression. That history made many clinicians wary of rapamycin as a preventive or longevity-focused interventionparticularly for cardiovascular aging. A small [----] pilot study began testing a very different question"  
[X Link](https://x.com/healthspanmed/status/2010863453087699102)  2026-01-12T23:56Z [----] followers, [--] engagements


"A proof-of-concept study with a narrow but precise aim Rather than asking whether rapamycin improves metabolic markers researchers asked something more specific: If you briefly inhibit mTOR signaling in older adultsusing low daily dosingdo you see measurable changes in vascular and cardiac function independent of weight loss or long-term metabolic remodeling To test this six healthy men aged [----] received [--] mg of rapamycin daily for [--] weeks. This was intentionally conservative: Low dose Short duration Carefully monitored Designed to probe physiology not outcomes"  
[X Link](https://x.com/healthspanmed/status/2010863465175663091)  2026-01-12T23:56Z [----] followers, [--] engagements


"A biologically coherent explanation From a mechanistic perspective the result aligns with what SGLT2 inhibitors consistently do: Lower glucose excursions Reduce oxidative and inflammatory load Improve mitochondrial efficiency Shift cells toward fat oxidation and mild ketone use All of these factors are known contributors to telomere erosion. Reducing them doesnt require activating telomerase or altering DNA replication directlyit simply reduces the cellular stress environment that accelerates telomere loss"  
[X Link](https://x.com/healthspanmed/status/2010863646218564014)  2026-01-12T23:57Z [----] followers, [--] engagements


"How to interpret it responsibly This single study doesnt prove that SGLT2 inhibitors lengthen telomeres in the general population. But it does challenge a long-held assumption: that adult telomere dynamics are strictly unidirectional. As a proof-of-concept it suggests that metabolic interventions can influence genomic stability markers in humans at least under certain conditions. If replicated this would position SGLT2 inhibitors as one of the first widely used drug classes with direct effects on a canonical hallmark of aging alongside their established cardiometabolic benefits."  
[X Link](https://x.com/healthspanmed/status/2010863658784711058)  2026-01-12T23:57Z [----] followers, [--] engagements


"A reframing of metabolic drugs By [----] the picture had shifted. SGLT2 inhibitors were no longer viewed solely as glucose-lowering agents but as system-level modulators of aging biologyinfluencing inflammation mitochondrial health telomere dynamics and cellular senescence through a shared metabolic lens. Not a silver bullet. Not a classic senolytic. But a biologically coherent way to reduce the pressure that drives tissues toward senescence in the first place"  
[X Link](https://x.com/healthspanmed/status/2010863718515818555)  2026-01-12T23:57Z [----] followers, [--] engagements


"8 Hormone replacement therapy: a regulatory course correction One of the most consequential changes of [----] wasnt molecularit was regulatory. The FDA initiated removal of the black-box warning on menopausal hormone replacement therapy. Re-analyses showed that for women initiating HRT near menopause: Quality of life improves Bone density is preserved Cardiometabolic outcomes improve All-cause mortality may decrease The takeaway wasnt HRT for everyone. It was that timing and personalization matter. https://twitter.com/i/web/status/2010863731249713531"  
[X Link](https://x.com/healthspanmed/status/2010863731249713531)  2026-01-12T23:57Z [----] followers, [--] engagements


"What if cognitive aging isnt primarily a problem of memory neurotransmitters or plaquesbut a problem of energy In this episode of Beyond Healthspan we sit down with Dr. Francisco Gonzalez-Lima Professor of Neuroscience Pharmacology and Toxicology at the University of Texas at Austin to unpack decades of research on brain energy metabolism mitochondria and aging. In this episode we cover: Why energy metabolism has been overlooked in neuroscience How mitochondrial dysfunction appears before Alzheimers pathology The central role of cytochrome c oxidase (Complex IV) in brain energy How red and"  
[X Link](https://x.com/healthspanmed/status/2012631390295408846)  2026-01-17T21:01Z [----] followers, [---] engagements


"For decades scientists have attributed the decline in fertility after age [--] mainly to chromosomal errors in aging eggs. Yet new evidence suggests the process begins earlierand within the cellular machinery that maintains egg quality and longevity. A new study examined the use of rapamycin a compound long studied in longevity research in women undergoing IVF. The results were notable: short-term low-dose rapamycin doubled the success rate of IVF compared with standard protocols. The study also traced the biology behind this improvement showing that as women reach their mid-30s ovarian cells"  
[X Link](https://x.com/healthspanmed/status/2016315318667563089)  2026-01-28T01:00Z [----] followers, [---] engagements


"🧠 Is Alzheimers really a disease of misfolded proteinsor a crisis of cellular energy For decades the dominant theory of Alzheimers disease (AD) has focused on the accumulation of amyloid plaques and tau tangles. But a growing body of research points to a different culprit that may come earlier: mitochondrial dysfunction. Neurons are energy-intensive cells. They require enormous amounts of ATP to support everything from electrical signaling and synapse formation to protein recycling and structural maintenance. When mitochondrial function falterswhether due to aging inflammation or poor oxygen"  
[X Link](https://x.com/healthspanmed/status/2016466309207507225)  2026-01-28T11:00Z [----] followers, [---] engagements


"Researchers gave obese micewho had been on a high-fat diet for [--] weeksdaily doses of rapamycin. These mice had all the hallmarks of leptin resistance: High leptin levels Excess body fat Unchecked food intake Sluggish POMC neuron activity Within days of rapamycin treatment changes began to appear. 🧠 POMC neurons reawakened. Firing rates increased. Genes linked to appetite suppression turned back on. And the brain started responding to leptin again"  
[X Link](https://x.com/healthspanmed/status/2016964705647243276)  2026-01-29T20:00Z [----] followers, [--] engagements


"When leptin was administered after rapamycin pretreatment its effectspreviously mutedbecame potent once more: Food intake dropped Fat mass decreased Leptin signaling cascades lit up again Even more telling: in mice without rapamycin pretreatment leptin had no effectconfirming that the drug had re-sensitized the brain to this crucial hormone. And this wasnt just about eating less. ⚙ Mice that responded to rapamycin showed: Increased energy expenditure https://twitter.com/i/web/status/2016964717668159677 https://twitter.com/i/web/status/2016964717668159677"  
[X Link](https://x.com/healthspanmed/status/2016964717668159677)  2026-01-29T20:00Z [----] followers, [--] engagements


"Most obesity medications focus on suppressing appetite or altering digestion Many lifestyle interventions eventually stall because the brain adapts Weight regain is common because the underlying signaling dysfunction isnt corrected But what if we could fix the signal What if we could re-sensitize the brain to leptinso that satiety returns cravings decrease and metabolism becomes more responsive Thats what rapamycin appears to do in these studies"  
[X Link](https://x.com/healthspanmed/status/2016964839747571788)  2026-01-29T20:01Z [----] followers, [--] engagements


"By turning down mTOR it allows leptin to be heard again. By restoring that signal it breaks the cycle of persistent hunger and fat accumulation. It reframes obesity not as a failure of discipline but as a neuronal feedback errorone thats potentially reversible. And that opens up a much bigger question: Could this same approach be applied in humansnot just for obesity but for age-related metabolic dysfunction as well We dont know yet. But the path forward is clear: https://twitter.com/i/web/status/2016964852267569305 https://twitter.com/i/web/status/2016964852267569305"  
[X Link](https://x.com/healthspanmed/status/2016964852267569305)  2026-01-29T20:01Z [----] followers, [--] engagements


"By restoring leptin sensitivity through mTOR inhibition in POMC neurons rapamycin offers a completely new way to think about treating obesitynot by forcing the body to eat less but by helping the brain feel full again. This is still early-stage science. The doses used in mice arent yet applicable to humans. And more research is needed before clinical translation. But the implications are enormous. What if fixing metabolism starts with fixing the brain"  
[X Link](https://x.com/healthspanmed/status/2016964876208656899)  2026-01-29T20:01Z [----] followers, [--] engagements


"What if the future of obesity treatment lies not in suppressing appetitebut in restoring the brains ability to respond to it naturally This research marks a powerful step in that direction. 📖 Want to explore the full science behind this breakthrough Dr. Aaron Slusher research scientist at the Yale School of Medicine breaks it all down in our latest Research Review: 👉 Read the full article here: If you care about metabolism aging or the neuroscience of hunger this is a must-read. https://gethealthspan.com/science/article/rapamycin-and-leptin-resistance"  
[X Link](https://x.com/healthspanmed/status/2016964888284058091)  2026-01-29T20:01Z [----] followers, [--] engagements


"1. 🧬 A protein found in human milk is now showing up in adult nutrition researchfor reasons that go well beyond muscle. Most people think protein quality = muscle protein synthesis. But a growing body of evidence suggests protein composition may influence sleep circadian timing metabolism and cognitionnot just recovery. Heres the science on alpha-lactalbumin 👇 https://twitter.com/i/web/status/2017402473632440509 https://twitter.com/i/web/status/2017402473632440509"  
[X Link](https://x.com/healthspanmed/status/2017402473632440509)  2026-01-31T01:00Z [----] followers, [---] engagements


"2. 🔍 Background: Why protein quality has been oversimplified For decades whey has been the gold standard because its: fast-digesting high in essential amino acids strong at stimulating muscle protein synthesis (MPS) So we judged protein mostly by anabolic output. But protein is also a signalnot just building material"  
[X Link](https://x.com/healthspanmed/status/2017402485674254403)  2026-01-31T01:00Z [----] followers, [--] engagements


"3. 🍼 Why human milk matters here Alpha-lactalbumin is a major protein in human milk accounting for 22% of total protein. Human milk supports more than growth: neurodevelopment immune maturation metabolic programming circadian rhythm formation That raises a legitimate question: Is its amino acid design doing more than building tissue https://twitter.com/i/web/status/2017402497514770446 https://twitter.com/i/web/status/2017402497514770446"  
[X Link](https://x.com/healthspanmed/status/2017402497514770446)  2026-01-31T01:00Z [----] followers, [--] engagements


"4. 🧬 The key idea: composition not just grams Whey isnt one compoundits a mixture of fractions with different amino acid profiles. Alpha-lactalbumin has an interesting amino acid profile: ✅ fairly high BCAAs (for MPS signaling) ✅ unusually high tryptophan (for serotonin/melatonin pathways) Because of this mix it sits at the intersection of muscle + neurochemistry. https://twitter.com/i/web/status/2017402509745393825 https://twitter.com/i/web/status/2017402509745393825"  
[X Link](https://x.com/healthspanmed/status/2017402509745393825)  2026-01-31T01:00Z [----] followers, [--] engagements


"5. 💪 1) Muscle recovery: the leucine trigger still holds Leucine isnt just a building block in the way that we traditionally think about amino acids. Its a metabolic signal. It stimulates mTOR to initiate muscle protein synthesis. Both whey and alpha-lactalbumin are 10% leucine by weight. So a 20g serving 2g leucine aligning with the leucine threshold often cited for maximizing muscle protein synthesisespecially in older adults with anabolic resistance. https://twitter.com/i/web/status/2017402521623617762 https://twitter.com/i/web/status/2017402521623617762"  
[X Link](https://x.com/healthspanmed/status/2017402521623617762)  2026-01-31T01:00Z [----] followers, [--] engagements


"6. 📈 Fast leucine kinetics matter Data comparing protein fractions show alpha-lactalbumin can produce a rapid rise in circulating leucine similar to whey. Thats the point of fast proteins: hit the leucine threshold within the post-meal window when muscle protein synthesis machinery is most responsive https://twitter.com/i/web/status/2017402537104838962 https://twitter.com/i/web/status/2017402537104838962"  
[X Link](https://x.com/healthspanmed/status/2017402537104838962)  2026-01-31T01:00Z [----] followers, [--] engagements


"7. 🧬 2) What makes alpha-lactalbumin different: tryptophan density Alpha-lactalbumins tryptophan content is nearly double standard whey: [--] mg/g (alpha-lactalbumin) vs [--] mg/g (standard whey) Thats a non-trivial signaling difference"  
[X Link](https://x.com/healthspanmed/status/2017402549247287461)  2026-01-31T01:00Z [----] followers, [--] engagements


"8. 😴 3) Sleep biology starts with tryptophan but the bottleneck isnt intake. Here's why Tryptophan is the precursor for: serotonin melatonin But the rate-limiting step is often transport into the brain because tryptophan competes with other LNAAs (leucine isoleucine valine tyrosine phenylalanine) for the same transporters. Translation: more protein more brain tryptophan Sometimes its the opposite. There's a bottleneck of amino acids that get to the brain"  
[X Link](https://x.com/healthspanmed/status/2017402561272418498)  2026-01-31T01:00Z [----] followers, [--] engagements


"9. 🥛 Why warm milk makes you sleepy is usually overstated Bovine milk has: relatively low absolute tryptophan a competing LNAA profile that can limit brain uptake So the sleep effect often isnt about milk tryptophan. Its about tryptophan-to-LNAA ratio"  
[X Link](https://x.com/healthspanmed/status/2017402573255545025)  2026-01-31T01:00Z [----] followers, [--] engagements


"10. 🧠 Alpha-lactalbumin changes the ratio Because its tryptophan-rich relative to other LNAAs alpha-lactalbumin can improve the odds that tryptophan crosses into the brain despite competition. Some studies estimate: 130% increase in brain tryptophan availability pre-bed (model-based) https://twitter.com/i/web/status/2017402585620390256 https://twitter.com/i/web/status/2017402585620390256"  
[X Link](https://x.com/healthspanmed/status/2017402585620390256)  2026-01-31T01:00Z [----] followers, [--] engagements


"11. 📊 And the plasma data is striking Controlled human work shows alpha-lactalbumin can raise plasma tryptophan up to 3x. Example: A 40g dose produced 3-fold higher plasma tryptophan vs carbohydrate and other proteins. Thats a meaningful biochemical shift"  
[X Link](https://x.com/healthspanmed/status/2017402601327956081)  2026-01-31T01:00Z [----] followers, [--] engagements


"12. ⚖ Clinical sleep outcomes: mixed (and that matters) Some randomized trials report improvements in: sleep latency sleep efficiency next-day alertness Others show neutral effects. This doesnt kill the mechanismbut it flags that sleep is context-dependent: dose timing energy intake participant characteristics https://twitter.com/i/web/status/2017402613428588764 https://twitter.com/i/web/status/2017402613428588764"  
[X Link](https://x.com/healthspanmed/status/2017402613428588764)  2026-01-31T01:00Z [----] followers, [--] engagements


"13. 🍽 A practical issue: energy load can confound sleep Many trials used 40g alpha-lactalbumin [--] hours before bed. Thats [---] kcaland energy intake itself affects sleep initiation. A scoping review in athletes found: each additional [--] MJ (240 kcal) in the evening +5 minutes sleep onset latency (p = 0.011) So big pre-bed boluses can create competing effects. https://twitter.com/i/web/status/2017402625390727342 https://twitter.com/i/web/status/2017402625390727342"  
[X Link](https://x.com/healthspanmed/status/2017402625390727342)  2026-01-31T01:00Z [----] followers, [--] engagements


"14. Notably a randomized crossover trial from Dr. @mikeormsbee's lab administered alpha-lactalbumin [--] minutes before sleep rather than [--] hours prior. While group-level sleep outcomes were neutral the design highlights an emerging point: supplement timing relative to circadian physiology may be critical. https://twitter.com/i/web/status/2017402637185073512 https://twitter.com/i/web/status/2017402637185073512"  
[X Link](https://x.com/healthspanmed/status/2017402637185073512)  2026-01-31T01:00Z [----] followers, [--] engagements


"15. 🥩 Protein timing has its own signal That same review found: each additional [--] g/kg evening protein [--] minutes faster sleep onset (p = 0.013) And: each extra hour between last intake and bedtime [--] minutes less total sleep time (p = 0.014) Translation: Too much energy can delay sleep but modest protein may support sleep transitiontiming matters"  
[X Link](https://x.com/healthspanmed/status/2017402649214390550)  2026-01-31T01:00Z [----] followers, [--] engagements


"16. 🔥 4) Metabolic and body composition signals Pre-sleep protein (in general) has been associated with: increased overnight MPS higher overnight energy expenditure improved satiety (even when total calories are controlled) Alpha-lactalbumin also has preclinical support: In animals it reduced weight gain and improved markers like glucose/insulin/HOMA-IR despite high-fat diets. Human metabolic data is still narrower but intriguing. https://twitter.com/i/web/status/2017402661306515765 https://twitter.com/i/web/status/2017402661306515765"  
[X Link](https://x.com/healthspanmed/status/2017402661306515765)  2026-01-31T01:00Z [----] followers, [--] engagements


"17. 🧬 PCOS: a notable human signal (adjunctive) In women with PCOS alpha-lactalbumin + myo-inositol (2g) has been reported to improve: body weight ovulation rates menstrual cycle regularity Some studies used alpha-lactalbumin doses as low as [--] mgsuggesting a potential synergistic/transport role rather than macro nutrition. This needs careful interpretation and replication but its not nothing. https://twitter.com/i/web/status/2017402673096757473 https://twitter.com/i/web/status/2017402673096757473"  
[X Link](https://x.com/healthspanmed/status/2017402673096757473)  2026-01-31T01:00Z [----] followers, [--] engagements


"18. 🧠 5) Cognition stress resilience and central fatigue Because alpha-lactalbumin influences serotonin pathways via tryptophan availability studies have examined: next-day attention (especially under sleep restriction/circadian disruption) stress resilience central fatigue during prolonged effort Signals appear context-dependentstronger in states of stress sleep loss or high demand. https://twitter.com/i/web/status/2017402684933034037 https://twitter.com/i/web/status/2017402684933034037"  
[X Link](https://x.com/healthspanmed/status/2017402684933034037)  2026-01-31T01:00Z [----] followers, [--] engagements


"19. ✅ What this review argues (carefully) Alpha-lactalbumin isnt better protein in a universal sense. But its a good case study for why protein quality may be expanding beyond: ❌ How anabolic is it to include: ✅ amino acid signaling ✅ circadian timing ✅ neurochemical pathways ✅ metabolic context Protein is a biological input not just a macronutrient. https://twitter.com/i/web/status/2017402696727466418 https://twitter.com/i/web/status/2017402696727466418"  
[X Link](https://x.com/healthspanmed/status/2017402696727466418)  2026-01-31T01:00Z [----] followers, [--] engagements


"20. 🧾 Bottom line The mechanism (tryptophan availability + LNAA competition) is biologically plausible and supported by strong biochemical data (e.g. 3x plasma tryptophan). Clinical outcomes are mixedsuggesting timing dose and energy context are critical. More RCTs are needed to define: optimal dosing best timing window which populations benefit most https://twitter.com/i/web/status/2017402708567986669 https://twitter.com/i/web/status/2017402708567986669"  
[X Link](https://x.com/healthspanmed/status/2017402708567986669)  2026-01-31T01:01Z [----] followers, [--] engagements


"21. 🧬 If protein quality has been defined too narrowly alpha-lactalbumin offers a useful case study. Not as a silver bulletbut as evidence that amino acid composition timing and biological context may matter as much as grams or macros. Dr. Richard LaFountains full research review explores the datastrengths limits and open questions. 🔗 https://www.gethealthspan.com/research/article/alpha-lactalbumin-research https://www.gethealthspan.com/research/article/alpha-lactalbumin-research"  
[X Link](https://x.com/healthspanmed/status/2017402720622453017)  2026-01-31T01:01Z [----] followers, [--] engagements


"The latest research reveals mitochondrial breakdown as a root driver of aging. We created a framework to track their health diagnose decline and apply interventions that protect lifespan. https://www.youtube.com/watchv=QpWZheUD1_Y https://www.youtube.com/watchv=QpWZheUD1_Y"  
[X Link](https://x.com/healthspanmed/status/2017538361922388127)  2026-01-31T10:00Z [----] followers, [---] engagements


"Zone [--] training has become one of the most talked-about ideas in fitness and longevity often portrayed as the sweet spot for building mitochondrial health improving fat metabolism and extending endurance. But is the science really that simple In our latest Beyond Healthspan episode muscle physiology researcher Kristi Storoschuk PhDc joins Rich LaFountain PhD and Brandon Fell MS NBC-HWC to break down what her new Sports Medicine review actually found and why much of the Zone [--] hype leaves out critical context. They explore: Why intensity not just duration drives mitochondrial adaptation How"  
[X Link](https://x.com/healthspanmed/status/2019697598249210164)  2026-02-06T09:00Z [----] followers, [---] engagements


"Intermittent mTOR inhibition is one of the most important ways to prolong healthspan. Were here to provide patients with options to do just that. Join our beta program: https://gethealthspan.com/ https://gethealthspan.com/"  
[X Link](https://x.com/healthspanmed/status/1489629318678401027)  2022-02-04T15:58Z [----] followers, [---] engagements


"RT @AcebedoErichMD: This is why I take Rapamycin once a week. https://x.com/i/status/2020200076921172276 https://x.com/i/status/2020200076921172276"  
[X Link](https://x.com/anyuser/status/2020311527723765933)  2026-02-08T01:39Z [----] followers, [--] engagements

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