Hi there,
Last week, I joined a panel on “The Rise of the Provider-Influencer.” My view: sharing a result is only part of the job. We also have to help people make sense of it.
Then this week delivered a perfect example of why that matters.
A January 2026 Science paper estimated that genetic differences explain more than half the variation in modeled intrinsic lifespan. That is different from saying half of your own lifespan is fixed.
If that’s true, it brings up feelings of futility. If so much of longevity is predetermined, how much do our protocols, habits, and interventions really matter?
What does that percentage actually describe?
It doesn’t tell us how many years one person can gain from a habit or medicine.
The TL;DR if you only have 30 seconds:
- Genes and lifespan: Heritability describes variation in a population, not a personal deadline.
- Exercise: A small study found a change in a protein-based age estimate, not proof of ten months of rejuvenation.
- My routine: How I fit lifting, cardio, and recovery into the week.
🏋️ Exercise and a younger protein-clock result. A small study found a lower proteomic age estimate after 12 weeks of combined strength and endurance training. It did not test whether walking works less well or whether people live longer.
⚡ Quick Hits: An early human trial of partial epigenetic reprogramming, weight regain after GLP-1 withdrawal, and the limits of consumer tests.
What the lifespan heritability estimate means
Earlier estimates often put lifespan heritability around twenty to twenty-five percent. Estimates differ with the population, methods, and causes of death included.
The new analysis asked how deaths from external causes affect that estimate.
The authors used mathematical models and twin data to account for deaths from causes such as accidents and infections. Their estimate for intrinsic lifespan was above fifty percent.
That may sound discouraging. But a population-level percentage is not a division of your own life into years you can and cannot change.
Heritability describes how much variation relates to genetic differences under the conditions studied. Changing those conditions can still change outcomes.
Why the methods matter
External causes can mask differences in intrinsic lifespan. A person who dies in an accident cannot reveal how long they might otherwise have lived.
The analysis changes an estimate under its model assumptions. It doesn’t make every earlier lifespan study wrong.
What it means for treatment research
Genetic differences may help researchers find pathways that affect disease and aging.
A high estimate does not show that aging is a single programmed process. It also does not establish that modifying mTOR, APOE, or another pathway will extend human life.
A genetic contribution can guide a hypothesis. A treatment still needs its own evidence for benefits and harms.
For example, cholesterol-lowering treatments have clinical outcome evidence for selected patients. That evidence comes from their trials, not from a lifespan heritability estimate.
Risk changes with age
Genetic contributions can differ by age and cause of death. That doesn’t give us a universal age range in which to overcome our DNA.
Family history and inherited factors such as Lp(a) can matter to preventive care. Their value depends on the disease and the decision they change.
Living to a certain age does not mean you have outlived all genetic risk. Prevention remains useful, but it is not a way to pass through a fixed genetic boundary.
What This Means For You
For prevention, I would start here:
Start with risk factors that change care
Review family history, blood pressure, lipids, diabetes risk, and smoking. ApoB and Lp(a) can add useful cardiovascular information in the right context. This paper does not show that everyone needs deep genetic sequencing.
Judge each intervention on its own evidence
The study does not validate rapamycin, metformin, or another drug for healthy people’s longevity. Any off-label use needs a separate assessment of evidence, harms, and the person’s goals.
Medication and habits can both matter
Needing medicine for an inherited risk is not a failure of lifestyle. The right choice depends on the clinical evidence and your own risk.
Genes influence health, and prevention can still help. A population estimate cannot settle the choices for one person.
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Exercise changed a protein-based age estimate
The exercise study looked at a different question: what happens to a protein-based age score after training?
The MyoGlu analysis in npj Aging measured a protein-based age score before and after a twelve-week exercise program.
A lower score is interesting. It doesn’t prove that the whole person became younger.
The Study:
Researchers took 26 sedentary men (aged 40–65) and didn't just tell them to "exercise more." They put them through a 12-week boot camp: 4 sessions a week, mixing heavy whole-body strength training with high-intensity endurance cycling.
They used Olink proteomics to measure 204 specific age-related proteins (ProtAge) and performed deep tissue biopsies to see what was happening at the cellular level.
The Result:
After twelve weeks, the average protein-based age gap was lower.
The average change was about ten months on the ProtAge scale. Changes in proteins such as CLEC14A may help explain exercise biology, but a blood-protein change does not show that participants built a “younger blood supply.”
What this does not tell us about walking
The intervention combined resistance and endurance training. It did not randomly compare that program with casual walking, so it cannot show that walking failed.
In the larger observational dataset, some activity associations may reflect fitness, illness, or why people chose an activity. They should not be read as proof that walking makes people biologically older.
The Big Takeaway
Both endurance and strength work can help health. This paper does not establish a threshold of intensity needed to activate autophagy or make someone younger.
The useful goal is a routine you can sustain and recover from, with enough challenge to improve fitness.
My weekly exercise routine
This research, along with other studies, has helped me refine my routine. I’m sharing it to show how I fit the pieces together. Your goals and constraints may be different.
Here is how I arrange lifting, cardio, and recovery.
I lift on weekdays and take rapamycin on Saturday. I separate them because of a possible effect on muscle signaling. That scheduling hypothesis has not been shown to prevent interference or improve longevity in humans. My Friday intervals serve my fitness goals; they are not a proven ProtAge-reversal protocol.
The Daily Non-Negotiable: 7,000+ Steps
I use a treadmill desk for two to four miles of walking, plus twenty to thirty minutes of deliberate Zone 2 cardio. That keeps me moving during the workday, though walking alone can’t guarantee good insulin sensitivity.
The Weekly Split
Monday: Lower Body (Posterior Chain)
I focus on hip-hinge movements and the muscles at the back of my lower body. Strength here helps the activities I want to keep doing.
Tuesday: Upper Body Strength (Push Focus)
I work on pushing strength and loading my upper body. I’d also like to do more push-ups.
Wednesday: Zone 2 Cardio & Core
I do moderate cardio and core work. I keep a thick yoga mat by my desk for dead bugs and bird dogs between meetings, and practice pelvic-floor, transverse-abdominal, and breathing exercises.
Thursday: Unilateral Lower Body
I prioritize single-leg work such as Bulgarian split squats. I can challenge my legs with less external weight, although that doesn’t mean the load on my spine drops by half.
Friday: back, biceps, and intervals
I use four-by-four intervals: four minutes of hard effort, three minutes of active recovery, repeated four times. I aim for roughly ninety percent of maximum heart rate during the hard periods. This is my training choice, not a threshold this aging study proved everyone needs.
Saturday and Sunday: cardio and recovery
I do thirty to seventy-five minutes of Zone 2 cardio each day and skip weights. I take rapamycin on Saturday morning. Whether this schedule changes autophagy or training gains remains unproved.
⚡ Longevity Quick Hits
👁️ ER-100 enters clinical testing: Life Biosciences received authorization for a first-in-human study in January 2026. The initial aims include safety and tolerability in optic neuropathy. Permission to conduct a trial is not approval of a treatment or proof of age reversal.
📉 Regain after medication stops: The 2026 BMJ review found substantial weight regain after weight-management medication ended. Several marker estimates relied on projections. It supports a maintenance plan with a clinician, not a universal requirement to take a GLP-1 drug forever.
🚫 Consumer tests: A Wired review of Viome raised questions about useful clinical advice and product sales. A consumer review is not a validation study. Before buying, ask what decision the result can reliably change.
🫀 Until Next Week
If you want to change your routine, choose one slot this week for activity you can repeat.
Walking remains useful. You can add strength or harder cardio as your health, fitness, and recovery allow.
Build gradually. If hard intervals are new to you, start with a manageable effort and seek advice when your health or symptoms call for it.
Aim to improve fitness while staying healthy enough to keep training. You don’t need to chase “metabolic panic” or a ninety-percent heart rate to make progress.
To your healthspan,
Hillary Lin, MD
Co-Founder & CEO
Curator
Learn about Curator’s platform.
Events listed when this issue was published
I'll be at the Integrative Healthcare Symposium in NYC – Feb 19-21. Let me know if you're there and we can sync up!
👱🏻♀️👩🏻🦰👩🏻👧🏽👧🏾 Livelong Women’s Health Summit – April 17-18, 2026, SF, CA. Delighted to join 50 other thought leaders in speaking on women's longevity! (Code HILLARY50 for $50 off)
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GlycanAge reports an age estimate from IgG glycosylation. It doesn’t diagnose the cause of inflammation or establish a treatment.
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