The standard annual exam is failing women through menopause. We still treat this transition as mainly a conversation about hot flashes or dryness. It’s so much more than that.

I’m starting to see the menopause transition as a cardiovascular inflection point. Markers shift. Risk factors change. What you do in that transition affects the decades ahead.

The changes can seem small individually. They’re easy to dismiss one by one. As a provider, I know that it’s often easiest to say “let’s monitor that.”

But if you compare a woman’s body the year before menopause to ten years after, here’s what’s different: Blood pressure rises. Cholesterol rises. Lp(a) rises. Visceral fat increases. Lean muscle decreases. Blood vessels stiffen. Plaque progression accelerates too.

Heart disease is still the leading cause of death in women, by far, and a disproportionate share of that risk accumulates during this time. Menopause should be seen as a huge opportunity to protect and improve your heart health.

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What Happens During the Menopause Era

Clinically, menopause is defined as one year after your last period. But that definition fails women. Menopause isn’t a single event. It’s a menopause “era.” It’s the years before, during, and after this major hormonal transition. It’s a slow progression over years, and those years are very important.

The key hormonal driver is estrogen. In menopause, levels eventually drop. But during the transition, they fluctuate — which is its own kind of stress on the system.

Estrogen isn’t usually thought of as a heart-health hormone, but it clearly is one:

• It supports vasodilation, keeping blood vessels flexible and responsive.

• It improves your cholesterol profile — keeping HDL (protective cholesterol) higher, and reducing triglycerides and LDL.

• It supports endothelial function — the lining of your blood vessels, which helps limit plaque buildup.

• It regulates fat distribution and insulin sensitivity.

• It suppresses Lp(a), a genetic cardiovascular risk factor.

When estrogen drops, all of these protective effects shift together. That’s why this era functions like a cardiovascular turning point, not a collection of unrelated symptoms.

What Markers Actually Change

This is where the “annual physical” falls short — because these shifts are often missed or dismissed in routine care.

• Lipids shift. This can be subtle, but total cholesterol rises, LDL rises, HDL falls — even with no change in diet or exercise. It’s tied to the estrogen drop.

• Lp(a) rises. Estrogen suppresses Lp(a) and as estrogen falls, Lp(a) can climb. Roughly 20 to 25% of the population carries a genetically elevated Lp(a) — this transition can push it even higher.

• Blood pressure rises, often slowly and subtly. This is tied to the loss of estrogen’s vasodilating effect and increasing arterial stiffness.

• Visceral fat accumulates. Fat storage shifts from under the skin to around the organs. Weight and BMI may barely change while fat distribution changes substantially — and visceral fat is inflammatory.

• Insulin resistance worsens. Estrogen supports insulin sensitivity. As it declines, glucose dysregulation can begin well before it shows up on routine labs.

• Inflammation increases. Hormone therapy generally lowers markers of vascular inflammation (though important nuance: oral estrogen actually raises CRP through a first-pass effect in the liver, while transdermal estrogen doesn’t. It’s one more reason route of hormone administration matters).

• Endothelial function worsens. The inner lining of blood vessels becomes less responsive, less flexible, more prone to plaque.

All of this can happen while a woman looks completely fine on a standard physical. Normal weight and BMI. Normal-ish cholesterol and blood pressure.

What We’re Missing for Women

This is what we’re missing for women in this time of life:

1. Most cardiovascular risk calculators were built from male-dominated data and don’t factor in menopausal status as a risk variable. A 55-year-old woman with rising LDL and rising blood pressure will often still calculate as “low risk” even as her actual risk factors are moving in the wrong direction.

2. Cardiovascular disease looks different in women. Women more often think their own cardiac symptoms are something else — symptoms like fatigue, nausea, shortness of breath, and jaw pain get attributed to stress, anxiety, or perimenopause instead of the heart.

3. Perimenopause care is most often discussed around quality of life: treating hot flashes, sleep, mood. That matters, but we’re not talking nearly enough about the cardiovascular piece happening underneath all of it.

What Menopause Markers to Watch for

Here are the markers we should be tracking:

• A lipid panel with ApoB — total cholesterol, HDL, LDL, triglycerides, and ideally ApoB, which directly counts atherogenic particles rather than estimating them.

• Lp(a), checked at least once in every adult, and this transition is a particularly important moment to know your number if you haven’t already.

• Blood pressure trend, not a single clinic reading. A few weeks of home monitoring gives a far more accurate picture than one number taken in an office.

• Fasting insulin and glucose, alongside A1c. A1c misses early insulin resistance; fasting insulin can reveal metabolic dysfunction before A1c ever moves.

• hs-CRP, reflecting systemic inflammatory load and functioning as an independent cardiovascular risk predictor in its own right.

• Waist circumference. BMI is a poor proxy here — a woman can have a completely normal BMI with significant visceral fat accumulation underneath it.

• A DEXA scan. For bone density, but also visceral fat and lean muscle mass, which can shift through this transition without changing the scale.

• A coronary calcium score, if risk factors are present. A CAC score can show subclinical atherosclerosis — plaque that’s already there, before symptoms appear. It’s one of the most powerful tools we have for reclassifying risk in women who present as “low risk” on standard calculators despite real risk factors.

• A conversation about hormone therapy, with timing in mind. It isn't right for everyone. But for many women without contraindications, starting therapy close to the onset of menopause provides real cardiovascular benefit (in addition to all the other benefits): improved lipids, reduced visceral fat, better insulin sensitivity — while starting more than 10 years past menopause can flip that picture toward increased risk instead. This is the timing hypothesis, and it's why this time matters. Your primary care provider can start this conversation — you don't need a specialist.

What Can Move the Needle

With the right markers, we can identify interventions that can actually move the needle on a women’s heart health. Here are some examples:

• Statins. These should be in the conversation. A lot of people are hesitant, but statins reduce heart attack and stroke risk significantly. They’re safe and effective, and the menopause is a time we can see the most benefit.

• Strength training. This addresses visceral fat and lean muscle loss. Muscle is metabolically protective, and this is the time you’re losing it fastest.

• Diet matters. A Mediterranean diet is associated with improved inflammation markers, glucose regulation, and body composition.

• Sleep is critical. Poor sleep during the menopause transition is linked to worse cardiovascular health markers. Treating the sleep disruption (through hormone therapy or otherwise) protects more than your rest.

• Hormone therapy, discussed above, with timing in mind.

• Blood pressure, once you have a good trend from home monitoring, may need treatment beyond lifestyle changes. Careful that “let’s watch it” doesn’t become the default for years if the trend is climbing.

All of this should be a conversation with your doctor.

The Bottom Line

Perimenopause and the menopause transition should be treated as a cardiovascular inflection point. It should shape how we evaluate cardiovascular risk and where we intervene.

This is so much more than a conversation about hot flashes or vaginal dryness. It’s a defined time period where real, meaningful intervention for cardiovascular health is possible.

Your primary care provider is in a unique position — the one person positioned to see all of you, your symptoms, your risk factors, your habits, and to have the real conversation about what’s right for you.

That’s longevity medicine. It’s the practice of catching this time window.

I joke with my husband that he’s a sucker for supplements. Every week, more boxes and trial memberships show up on our doorstep — creatine, uric acid support, apple cider vinegar, “focus” gummies, salt supplements, protein powders. His algorithm knows him too well.

The supplement industry is huge, and most of what gets sold has little real evidence behind it — including a lot of what’s currently on our countertop.

But a small handful of supplements do have strong, consistent evidence behind them, because they address real issues that diet and modern life leave open. Here are the ones I actually think are worth it, why, and what I’d watch out for.

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1. Vitamin D3

This is one of the most common deficiencies I see. Most of us spend our days indoors, wear sunscreen when we do go out, and live somewhere far enough from the equator that winter sun barely produces vitamin D in skin at all. Low vitamin D is linked to increased mortality risk, and correcting a deficiency supports immune function, bone health, and mood.

The best evidence here is in people who are actually deficient — so it’s a good idea to get your level checked before assuming you need it. Typical dosing is 1,000 to 4,000 IU daily depending on where you’re starting from; some people need a prescription-strength dose short-term to correct a significant deficiency.

We can’t really get much Vitamin D from food, but here’s a fun fact: mushrooms exposed to UV light produce vitamin D2. After just 15 minutes of sun exposure, sliced mushrooms reach vitamin D2 levels comparable to fatty fish like salmon. Even a sunny windowsill for a day works. It’s one of the only real food-based sources of vitamin D that isn’t fortified or animal-derived.

There’s a real risk worth knowing too. You can get too much, and I’ve seen this in practice. Vitamin D toxicity happens from over supplementation. This can raise blood calcium levels, causing symptoms like nausea, fatigue, excessive thirst, and over time, kidney damage.

It happens most often when people take high-dose drops or gummies without realizing how concentrated they are, or stack multiple vitamin D-containing products without realizing it. More is not better. If you’re supplementing above 4,000 IU daily long-term, your levels need to be monitored.

2. Omega-3 (EPA and DHA)

The strongest evidence for omega-3 supplementation is cardiovascular. Omega-3s at higher doses lower triglycerides, and can reduce major cardiovascular events in high-risk patients.

If you’re already eating salmon, sardines, or mackerel a couple of times a week, you likely get enough. If not, 1 to 2 grams of combined EPA and DHA daily is a good target. Algae-based omega-3 supplements are a good vegetarian and vegan option — they’re actually the original source fish get their omega-3s from in the first place.

Beyond cardiovascular health, there’s some evidence connecting omega-3 status to mood regulation, and some early research on hormonal and inflammatory benefits during perimenopause and menopause specifically.

3. Magnesium

Magnesium is a cofactor in hundreds of enzymatic reactions — muscle function, nerve signaling, energy production, bone health, heart rhythm. Our diets fall short in providing the magnesium we need. A deficiency is linked to poor sleep, muscle cramps, and elevated blood pressure.

Not all forms are equal:

• Magnesium glycinate — best-tolerated, least GI disruption, a good general choice including for sleep.

• Magnesium citrate — well-absorbed, but more likely to have a laxative effect at higher doses. Useful if constipation is part of what you’re addressing, but less ideal if it isn’t.

• Magnesium oxide — cheapest, most common in generic multivitamins, but also the most poorly absorbed of the common forms.

• Magnesium threonate — early, interesting research specifically around cognitive effects, though the evidence for this is thinner.

Typical range across forms is 200 to 400 mg daily.

4. Creatine

Creatine has a lot of research behind it. And a lot of people still think it’s only for bodybuilders. The evidence is strong for strength, power, and lean muscle mass, and increasingly there’s real evidence for cognitive benefit too.

The benefit for women in the perimenopause and menopause transition is fascinating. A small 2025 study found creatine supplementation improved reaction time and mood stability in perimenopausal and menopausal women. Most creatine studies have focused on young male athletes, and I love seeing studies on women in this life stage who were previously left out.

Muscle mass is a key longevity variable. And creatine is one of the cheapest, safest, most well-studied ways to support it. Standard dose is 3 to 5 grams of creatine monohydrate daily — no loading phase necessary, no cycling required. It dissolves easily in coffee, water, or a smoothie without changing the taste much.

5. B12

This one is conditional, but important when it applies. A few groups are at real risk of deficiency, since stomach acid is required to absorb B12 properly from food:

• Vegetarians and vegans

• Older adults (absorption naturally declines with age)

• Anyone on long-term acid-suppressing medication, like a PPI

• Anyone on long-term metformin, which interferes with B12 absorption

• Worth watching: GLP-1s reduce overall food intake, and some researchers are now asking whether that could affect B12 and other nutrient levels too

A blood test can confirm whether you’re actually low. If you are, oral supplementation can restore levels and supports both red blood cell production and nerve function. If absorption itself is the problem rather than intake, B12 injections bypass the gut entirely and are a good option.

A quick note on iron

Ferritin deficiency is extremely common, especially in women — and it’s also one of the most dismissed, since standard reference ranges are wide enough that a low number often gets waved off as normal. I’ve written about this before: My Ferritin Was 5.

But unlike the others on this list, iron isn’t something I recommend broadly. Getting too much can be a real problem — iron accumulates in the body and, over time, can affect the liver and heart. This is one to test, not guess on. If you are iron-deficient, supplementation is important and works well. If you are not, don’t supplement.

The risks of supplements

Supplements are regulated far more loosely than medications. The FDA doesn’t have authority to approve dietary supplements before they’re marketed. This means nobody verifies that what’s on the label is actually what’s in the supplement before it reaches shelves. Contamination, mislabeled doses, and products that simply don’t contain what they claim are all problems.

A couple of examples worth knowing, because they’re more common than people expect and rarely traced back to the actual cause:

• Vitamin B6 can cause peripheral neuropathy — numbness and nerve damage, sometimes irreversible — with long-term use, and not just at extreme doses. This often shows up when people are taking ordinary multivitamins and magnesium supplements, often without realizing B6 was even in them.

• Niacin (B3), in high supplemental doses, raises uric acid levels and can trigger gout. Worth checking labels since niacin hides in supplements and energy drinks: B-complex vitamins, most energy drinks (Red Bull, Monster, Celsius, 5-Hour Energy all contain it), and many pre-workout formulas.

My husband actually developed gout not long after starting several new supplements at once (no other risk factors whatsoever). We never found a good answer, because when you’re taking six new things at once, it’s hard to figure out cause and effect.

This is why third-party testing matters: look for a USP, NSF Certified for Sport, or ConsumerLab seal on the label. That means an independent lab has verified the contents match the label and screened for contaminants.

Supplements can also interact with medications in ways people don't expect. For example: omega-3s have mild blood-thinning properties, and at higher doses (above 3g/day) can add to the effect of anticoagulants like warfarin. Magnesium can also bind to certain antibiotics, including some of the most commonly prescribed ones, and reduce their absorption if taken too close together. This is why your doctor needs the full list of everything you take, not just your prescriptions.

Overdosing on a fat-soluble vitamin like D is a real risk too. More isn’t better with any of these. Each one on this list has a recommended dose range, and going above it doesn’t add benefit — it can add real risk.

When to actually take these

• Vitamin D3 — with food that has some fat in it, like morning coffee with cream or breakfast with avocado.

• Magnesium — evening, ideally with dinner or before bed. It won’t sedate you but can support winding down.

• Omega-3 — with a meal, any meal, to reduce the GI upset that can come from taking it on an empty stomach.

• Creatine — timing doesn’t matter much; consistency does. Whenever you’ll actually remember it daily.

• B12 — morning, on an empty stomach if oral, for best absorption.

The bottom line

The things that actually work tend to be boring and cheap. And the things marketed hardest on our algorithms often have the least evidence behind them.

Five supplements cover most of our common needs. Everything else should have a specific reason behind it — a real deficiency, a real goal, a conversation with your doctor. And if you're not deficient in any of these and already eating a nutritious and varied diet, you may not need most of this list either.

It’s the same practice as reviewing your medications: know what you’re taking, and why, and keep asking if it still earns its spot.

Getting outside first thing in the morning can be one of the first things to go on a busy morning.

In my ideal state, I get outside, before coffee, before the phone, before anything else. No sunglasses. Just outside, with my face to the sky.

It’s a real intervention… and it’s very simple.

I won’t lie and say I do this daily. I don’t, but it’s something I want to work on, practice, and make a daily habit. This post is about why.

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How it works

Your eyes aren’t just for seeing. Behind the retina is a separate population of cells called photosensitive retinal ganglion cells, which detect light and then report to the suprachiasmatic nucleus, the master clock sitting in your hypothalamus.

That clock controls your circadian rhythm as well as sets the timing for cortisol, melatonin, body temperature, and metabolic processes in your body. Morning light is one of the strongest signals that clock receives to know what time it actually is.

The cortisol spike

Cortisol is often thought of as a problem in the wellness space. But in reality, that morning cortisol spike — the cortisol awakening response — is very healthy and important. It’s what makes us alert and functional.

And bright light exposure, especially in the early morning, increases this response.

The morning cortisol spike is a small and necessary stress signal. Some stress signals are important, like a hard workout. This trains our system to be more resilient. And a blunted or delayed morning cortisol rise is associated with fatigue and disrupted circadian rhythms.

Why morning light shifts your clock the right direction

Sleep

Timing matters for this. Light exposure in the early morning advances your circadian phase, pulling your internal clock earlier. This makes it easier to fall asleep at a reasonable hour later that night.

Light exposure in the evening does the opposite: it delays your clock, pushing your natural sleep time later. This is why scrolling on a bright phone in the evening is harmful. It pulls your internal clock in the opposite direction.

Morning light also suppresses melatonin, which you want in the morning. Melatonin is the signal for sleep, and clearing it efficiently in the morning helps you feel alert.

Mood

Morning light exposure is linked to increased serotonin turnover and better mood regulation. This is a consistent finding in seasonal affective disorder research, and timed morning bright-light therapy is an established, evidence-backed treatment.

Metabolism

People who get the majority of their daily bright light exposure earlier in the day tend to have lower body weight than people whose light exposure is later. But interestingly, short-term lab studies show that bright light exposure can acutely increase insulin resistance right after exposure, with evening light producing the larger effect.

To me, this suggests that metabolism also has its own cyclical rhythm, and getting the right light cues at the right time of day may be what’s important for metabolic health.

Hormones

You may have heard claims that morning sunlight raises testosterone but the evidence is thin here. It probably doesn’t hurt.

What actually counts

Saying “get sunlight” in the morning is pretty vague, so here are some specifics:

• Outdoor light, even on an overcast day, is much brighter than indoor lighting.

• Glass filters out a significant portion of the wavelengths your retina responds to. This is why standing outside works, but standing near a bright window may not work as well.

• You don’t need direct sun on your skin, and staring at the sun is a bad idea. Your eyes should be exposed to outdoor light, unobstructed by sunglasses.

• How much? Ten minutes on a bright, clear morning is likely enough. On cloudier days twenty to thirty minutes may be needed to get an equivalent signal.

• Earlier is better than later, but the consistent practice matters more. The same time window most days is more important than the occasional perfect sunrise walk.

The bottom line

Morning sun doesn't cost anything. No one is selling it to you. It has good evidence behind it. And most of us skip it anyway, while easily reaching for practices that cost money or come in a bottle.

Our eyes are doing work every morning, whether we know it or not.

I had a clinic day recently where four different patients, back to back, came in on the same medication: a proton pump inhibitor. Omeprazole, mostly. One started it after reflux symptoms. One after a hospital stay. One couldn’t remember why. They had just kept refilling it, for years.

None of these prescriptions were wrong when they were started. The problem is when a drug designed for short-term use is still being taken years later, and nobody's asked if it's still needed.

Below are the five I probably see most often, and how I think about them.

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1. Proton pump inhibitors

PPIs work. They’re often essential for persistent reflux, esophagitis, ulcers, Barrett’s esophagus, and more. The problem is that they often continue indefinitely, and in practice, patients stay on them for years, sometimes decades.

Stopping isn’t easy, which is why people don’t often try for too long. Long-term use suppresses acid production, and when stopped, the body compensates by ramping it back up. If you quit cold turkey, many people get a rebound surge of symptoms, which most read that as proof they still need it.

There are some scary headlines about these meds longterm causing kidney disease, c diff, dementia, fractures, but there isn’t great data behind most of those. I see the bigger and real issue being nutrient absorption: magnesium, B12, and iron all depend on stomach acid, and years of suppression can slowly drop levels.

It deserves a conversation with your doctor. Often you can taper the dose slowly, step down to as-needed, use a milder acid reducer, expect a rough few weeks, and follow up. Some people with a real reason to stay on it — Barrett’s, severe esophagitis, high bleeding risk — should stay on it.

2. Sedative sleep medications — benzodiazepines and Z-drugs

Ambien, Xanax, Valium, Restoril — different drug classes, same problem. The American Geriatrics Society’s Beers Criteria, the standard reference for medications to avoid in aging patients, recommends against all of them. The risk is cognitive impairment, delirium, falls, fractures, and car crashes.

These drugs are associated with an increased risk of hip fracture in older adults — a fracture that, for a lot of people, is the injury that starts the decline into lost independence.

Most of these prescriptions started during a specific bad stretch — grief, a divorce, a diagnosis — and then never revisited once the stretch ended. Tapering off is very hard. But “hard to stop” is not the same as “still necessary,” and it’s critical to address especially for the people most at risk from staying on it.

3. NSAIDs — ibuprofen, naproxen, diclofenac

Taken occasionally, NSAIDs are fine for most people. Taken daily for chronic pain, they’re one of the more dangerous habits. All NSAIDs carry some cardiovascular risk — increased odds of heart attack and stroke, doubled risk of hospitalization for heart failure. In adults over 65, regular use increases risk of acute kidney injury. And the GI bleeding risk climbs with age.

NSAIDs treat the symptom of inflammation without asking why it’s there. Chronic joint pain, chronic back pain — often there’s an underlying driver (weight, muscle imbalance, an unaddressed injury, inflammatory disease). Years of that lead to real cardiovascular and renal risk that compounds.

4. Calcium supplements

For years the advice was simple: aging woman, worry about bone health, recommend a calcium pill. Not anymore. Large trials now show calcium supplements carry real downsides: GI side effects, a higher risk of kidney stones, and a significant increase in heart attack risk.

The mechanism makes sense — a supplement delivers a concentrated dose all at once, spiking blood calcium in a way food doesn’t. Calcium from food arrives slowly and alongside the other nutrients. We don’t see the increased cardiovascular risk with dairy or leafy greens. Bone health matters, we just shouldn’t default to a pill. Food first.

5. First-generation antihistamines

Diphenhydramine — Benadryl, and the sleep aids built on it (like Tylenol PM, Unisom) is often not thought of as a long-term medication to most people. It’s sold over the counter, taken almost automatically, for allergies or for sleep. It’s also strongly anticholinergic with real concerns long-term.

People using the daily diphenhydramine for over three years significantly increased risk of developing dementia.

The fix depends on which reason you’re actually taking it for. If it’s for allergies, switching to a second-generation antihistamine — cetirizine, loratadine, fexofenadine — works just as well without the anticholinergic risk, because these drugs are specifically designed not to cross into the brain.

If it’s for sleep, that switch won’t help. Second-generation antihistamines don’t cause drowsiness — that’s the entire reason they’re safer. Reaching for Benadryl at night usually means an underlying sleep problem. That’s worth a discussion with your doctor — about sleep hygiene, stress, or an evaluation for what’s causing the insomnia.

The prescribing pattern

None of these are bad drugs in the moment. But they are often prescribed on repeat without anyone circling back. And in a fragmented system with short visits, we are failing at revisiting these. Like asking if the sleep aid started during a divorce still makes sense five years later, or whether the PPI from a stressful period still has a place.

The risk also rarely comes from one drug in isolation. It’s usually a combination, like a sedative plus an antihypertensive increasing fall risk. Or a PPI plus reduced dietary absorption creating a nutrient deficiency. It’s usually a build up of factors over time.

What to do

Consider making a visit simply to review medications. Go one by one and ask: what was this for, when did it start, and do I still benefit from this.

For long-term PPI use, consider periodic magnesium, B12, and iron checks. For a sedative sleep aid or benzodiazepine, ask about options and a taper. For daily NSAID use, ask what’s actually driving the pain, and whether the drug is treating the cause or just hiding it. For calcium, ask if you actually need the pill, or if your diet already covers it. For an antihistamine you reach for nightly, ask why you’re taking it and if a second-generation version would be an option.

For anything you’ve been on for more than a year ask: is this still the right medication for who I am now?

The bottom line

Part of aging is what accumulates in your medication and supplement list. The goal is not to avoid medication, but to stay in an active relationship with what you’re taking. Know what you’re on, why you’re on it, and keep asking if there’s a good reason to continue.

Medication and supplement review is its own kind of practice. Not a one-time cleanup, but something you keep doing.

Can you squeeze in this patient, they really need to be seen? Yes.
Can you join this meeting? Yes.
Can you volunteer at the school event? Yes.
Can you make it to the thing, even though you're exhausted? Yes.
Can you reach out and smooth this over? Yes. Yes. Yes.

I'm working through something right now and you may know the feeling — a request I don't want to say yes to, from people I don't want to disappoint.

The hard part was not actually deciding what I wanted to do. I knew that right away. The hard part was after. When the younger, more obedient version of myself doesn’t feel like they can say no.

Saying yes was never really a decision

For a lot of us — especially for a lot of women — “yes” is often something we are trained into. Say yes to the extra project, the invitation, the favor, the thing you don’t really have room for.

Saying no requires a kind of confrontation, and the path of least resistance becomes: just go along with it.

But, this gets more expensive with time. A “yes” you didn’t really mean in your 20s might cost you an afternoon. But in your 40s and 50s and beyond, the yeses compound, and can turn into years spent living in other people’s expectations rather than your own.

The longevity connection

A sense of autonomy is actually tied to health and longevity. This isn’t just a self-help topic. Chronic resentment affects sleep, inflammation, our nervous system staying activated.

There’s real evidence that a sense of autonomy — believing your choices are your own — is tied to markers of stress, resilience, and longevity itself.

In one study that I love, researchers analyzed essays written in the 1930s by young women who later became nuns, looking for markers of autonomous decision-making, meaning a sense of choice, autonomy, and resistance to outside pressure. Decades later, the women who showed more of these traits in their twenties had lived significantly longer than those who didn’t.

And a more recent 2025 study following nearly 23,000 adults over 12 years found that a stronger sense of control over one’s own life was associated with significantly lower risk of death. And interestingly, people whose sense of control increased over the study period — not people who started out high, people who gained it — had the lowest mortality risk of all.

I especially like that last part because it shows that this is something you can build. You can increase your sense of control. This can grow over time. You don’t have to be born with it, but you can develop it.

What “sense of control” means

Researchers who study this break it into two pieces: how much you believe you can shape your own life (mastery), and how much you feel blocked by outside forces — other people, circumstances, obligations (constraints). One of the standard measures asks people to rate: “Other people determine most of what I can and cannot do.”

Saying no is one lever on this — maybe the most obvious one. But it’s not the only one. A sense of control also comes from things like: making a decision deliberately instead of defaulting to whatever’s easiest, structuring even small parts of your day around what you actually want rather than what’s expected, and noticing where you’ve handed your choices to someone else’s expectations.

This is about making the life that’s happening to you the life you’re actually choosing.

Every “yes” is a “no” to something else

Underneath every hard no is an identity question: who am I allowed to be, if I’m not the person who always says yes? For a lot of us, that can be unfamiliar territory. We’ve never tested it.

Here’s what helps me: every yes is a no to something else. Rest. A relationship you want to invest in. A project that matters to you. An unstructured evening that restores you instead of depletes you. You have a finite amount of time and energy, and a yes you didn’t mean spends both on something you didn’t choose.

Try asking one question: if I say yes to this, what am I saying no to instead? Sometimes the answer makes the yes worth it. Often it doesn’t — and knowing the trade-off makes the no easier to say.

A practice, not a milestone

I’m still working on this — probably always will be, honestly. It’s a practice, not a milestone, and something you get better at by doing it badly a few times first.

What helps is identifying the struggle: this is hard because I was trained to avoid this exact feeling. It’s not because the no is actually wrong.

The goal was never to feel confident before you say it. Confidence is mostly what happens after — you say it enough times, notice your life didn’t fall apart, and neither did the relationship, and neither did you.

The practice gets easier. You get stronger.

Vaginal estrogen might be the most underused intervention in women's health.

It is not new. It is not expensive. It does not require a specialist. There's good evidence behind it — including data showing it can cut a woman's risk of hospitalization and sepsis from recurrent UTIs by more than half. The safety profile is excellent. But only a fraction of women who could benefit are using it.

There are many reasons it’s so underutilized, including fear, confusion, and inadequate provider training.

This is a great example of how the most powerful longevity interventions are often the simplest, most accessible, and most ignored.

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What Genitourinary Syndrome of Menopause Actually Is

Genitourinary syndrome of menopause (GSM) affects most women at some point after 40. This is the term used to describe the many changes that happen in the vagina, vulva, bladder, and urethra when estrogen declines during perimenopause and menopause.

Unlike hot flashes, which often improve over time, GSM is progressive and without treatment, it gets worse.

Symptoms include:

Vaginal dryness and irritation. The vaginal walls thin, lose elasticity, and produce less natural lubrication. This can cause daily discomfort — walking, sitting, wearing certain clothing, intimacy.

Painful sex. Pain with intercourse is not inevitable and it is not something women simply have to accept. It is a treatable medical condition.

Urinary urgency and frequency. The urethra and bladder are estrogen-sensitive, and as estrogen declines, the ability to hold urine comfortably decreases.

Recurrent urinary tract infections. This is potentially the most medically serious and more below on this.

The urinary consequences of untreated GSM lead to functional decline, loss of independence, and institutionalization in older women. The sexual health consequences affect relationships, connection, and purpose — all of which are longevity variables.

UTI Problems

Recurrent UTIs in postmenopausal women are a significant public health problem. They are often treated with repeated courses of antibiotics, which works short-term but contributes to antibiotic resistance, disrupts the gut and vaginal microbiome, and doesn’t address the underlying cause.

In older women these can progress to urosepsis — a life-threatening infection and a leading cause of hospitalization and death in elderly women.

The underlying cause, in most postmenopausal women with recurrent UTIs, is estrogen deficiency. Because estrogen maintains the health of the vaginal epithelium, which supports a Lactobacillus-dominant microbiome, and an acidic pH that inhibits pathogen colonization. When estrogen declines, the vaginal pH rises, Lactobacillus populations fall, and uropathogens, like E. coli, colonize more easily and then move to the urethra and bladder.

A large retrospective study last year found that among postmenopausal women with recurrent UTIs, those using vaginal estrogen had less than half the sepsis rate and a quarter the death rate compared to those who weren't. A 2023 study of over 5,600 women found vaginal estrogen reduced UTI frequency by over 50 percent. And the 2025 AUA/SUFU/AUGS guideline gives local low-dose vaginal estrogen a strong recommendation for vulvovaginal symptoms of GSM.

Vaginal estrogen is one of the most effective tools we have for women’s health, and we are not using it nearly enough.

This is Not Systemic Hormone Therapy

Importantly, vaginal estrogen is very different from systemic hormone therapy.

After the Women’s Health Initiative study in 2002 raised concerns about systemic hormone therapy, a generation of women and physicians became afraid of anything estrogen-related. That fear has persisted despite reanalyzed and reinterpreted data.

When applied locally at low doses, vaginal estrogen acts on local tissue: the vagina, vulva, urethra, and bladder. Systemic absorption is minimal. Blood estrogen levels do not significantly change. The concerns about systemic estrogen do not apply to vaginal estrogen at the doses used for GSM.

The FDA actually removed the black box warning from low-dose vaginal estrogen, specifically because it was causing confusion and discouraging appropriate use.

Even women with a history of breast cancer (who are often told to avoid all estrogen) may be candidates for vaginal estrogen. A 2025 meta-analysis of breast cancer survivors found vaginal estrogen use was not associated with increased recurrence risk, and was actually linked to significantly lower all-cause mortality.

What to Know About Formulations

Vaginal estrogen comes in several forms — cream, tablet, suppository, ring, and gel. There is no single best type, all have similar efficacy.

Vaginal estrogen cream. The oldest formulation, widely available, can be used for both internal vaginal application and external vulvar symptoms. Some women find it messier than other options.

Vaginal tablets or suppositories. Easy to use, less mess, deliver estrogen directly to vaginal tissue. Vagifem and its generic equivalents fall in this category.

Vaginal ring. Inserted every three months, delivers continuous low-dose estrogen. Good option for women who don’t want to remember a daily or weekly application.

Vaginal gel. Newer formulations, including ultra-low-dose options.

Intravaginal DHEA (prasterone). Converts locally to both estrogen and testosterone, can be an option for women concerned about estrogen specifically.

Why This Is Underused and Under-discussed

There are many reasons. Fear from WHI misinterpretation. Physician discomfort discussing sexual and urinary symptoms. Inadequate training. Patient embarrassment. The ongoing myth that these symptoms are just part of aging and nothing can be done.

But none of these are acceptable reasons for leaving women with treatable symptoms untreated.

You do not have to live with vaginal dryness, painful sex, urinary urgency, or recurrent UTIs. Vaginal estrogen is the most effective treatment we have.

The Bottom Line

The practice of longevity in women isn’t just about what we add, like exercise, sleep, purpose, connection. But it’s also about what medicine too often fails to offer, and what we should know to ask for.

You don’t need to see a specialist. You can see your primary care provider or of the many accessible telehealth options now.

Vaginal estrogen is one of the most evidence-based, accessible, and underutilized tools we have for helping women not just live longer, but live better in the years they have.

Ask about it. Ask for it. It belongs in the conversations, and in our practice.

My ferritin was 5.

Not my hemoglobin. Not my hematocrit. Those were fine. No anemia. No flags.

But my ferritin — the protein that stores iron in your body, the number that tells you how much iron your body actually has in reserve — was 5. It should be closer to 70. I was running on empty.

In retrospect, I knew exactly why my ferritin got low. I’ve had 4 pregnancies and births. I lose blood every month. I have a vegetarian diet. I wasn’t eating enough iron to replace what I was losing. And the fix was straightforward once I knew there was a problem.

Despite regular and routine medical care, nobody checked it until I asked them to.

My hemoglobin was always normal and that is what standard care looks at.

It is costing people their energy, hair, cognitive function, fertility, and sometimes much more.

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What Ferritin Actually Is

Ferritin is not the same as hemoglobin.

Hemoglobin is the protein in red blood cells that carries oxygen. It’s what a standard CBC measures. When hemoglobin falls below a certain level, you have anemia.

Ferritin is different. It’s your iron reserve. It’s found in every cell, but concentrated primarily in the liver, spleen, and bone marrow. A small amount circulates in your blood, and that's what the ferritin test measures, providing a window into how much iron your body actually has in storage. Think of hemoglobin as the fuel in your engine and ferritin as the fuel in your tank.

When iron stores start to fall, your body protects hemoglobin first. It drains the reserve (ferritin) to keep hemoglobin normal for as long as possible. This means you can have extremely low ferritin with a completely normal hemoglobin and hematocrit. The standard lab panel misses it completely unless someone is specifically checking ferritin.

And by the time anemia appears on labs, ferritin has often been low for months or years.

Why Ferritin Goes Low

Low ferritin has different causes and it’s critical to identify this for the right treatment. Here is how I think about it:

Blood loss — the most common cause in women. Menstruation is the leading cause of iron deficiency in premenopausal women. Heavy periods, fibroids, and other sources of regular blood loss deplete iron stores over time. This is what happened to me. The fix requires both addressing the loss and replacing the iron, and understanding that oral supplementation takes time.

Poor absorption. Even with adequate dietary iron, some people can’t absorb it properly. Autoimmune gastritis — the condition Bryan Johnson was recently diagnosed with — destroys the stomach’s acid-producing cells, which are essential for iron absorption. Celiac disease, H. pylori infection, and chronically low stomach acid (often from long-term PPI use) all decrease iron absorption. This is why some people with low ferritin don’t respond to oral iron supplementation.

Inadequate dietary intake. Plant-based diets are a common dietary contributor. Non-heme iron — the form found in plants — is less bioavailable than heme iron from animal sources. Vegetarians and vegans need nearly double the dietary iron than meat eaters to absorb the same amount.

Increased demand. Pregnancy increases iron requirements. Endurance athletes have higher requirements. Rapid growth in adolescence creates similar demands.

Chronic inflammation. This one is tricky because in chronic inflammation, ferritin can actually be falsely elevated. Ferritin actually rises with inflammation and so can mask true iron deficiency. A full iron panel is needed to sort this out.

What Low Ferritin Does to You

Iron is not just about red blood cells. It is essential for mitochondrial function, neurotransmitter synthesis, thyroid hormone conversion, immune function, and cellular energy production. When ferritin is low, every system that depends on iron starts to underperform.

Fatigue. This is the most common and most dismissed symptom. Iron is required for mitochondrial energy production. Low ferritin means your cells are running inefficiently at the most basic level.

Hair loss. This can be one of the most distressing consequences of low ferritin. Hair follicles are metabolically active cells and among the first to be affected by iron deficiency. Ferritin below 30 — even 50 by some research — is associated with significant hair shedding. Many women are treated for “hormonal hair loss” when the real driver is ferritin.

Brain fog and cognitive changes. Iron is essential for dopamine and serotonin synthesis. Low ferritin affects concentration, working memory, and mood. Many women attribute these symptoms to perimenopause when ferritin can be the missing variable.

Thyroid disruption. Iron is required to produce thyroid hormone. Iron deficiency impairs both thyroid hormone synthesis and the conversion of T4 to the active T3 form. Low ferritin can cause or worsen hypothyroid symptoms — fatigue, brain fog, weight changes, hair loss, feeling cold.

Fertility and reproductive health. The connection between ferritin and fertility is strong. Low ferritin impairs follicular development, egg quality, and ovulation. Ferritin below 30 is much more common in women with unexplained infertility compared to fertile controls. A 2025 study found that treating iron deficiency with IV iron nearly doubled live birth rates in women with infertility.

For women in perimenopause: heavier and more irregular periods during the transition can accelerate ferritin depletion at the same time as hormonal changes are already compounding fatigue, brain fog, and mood changes. Low ferritin and perimenopausal symptoms overlap so significantly that one is frequently mistaken for the other. Checking ferritin is one of the first things I do when a perimenopausal woman comes in feeling depleted.

Exercise intolerance. Iron is essential for oxygen delivery to working muscles. Even without anemia, low ferritin impairs aerobic capacity, endurance, and recovery. Athletes with low ferritin often plateau in performance without understanding why.

Restless legs syndrome. One of the most consistent associations in the restless legs literature is iron deficiency — specifically low ferritin, not necessarily anemia. Ferritin below 50 is associated with higher rates of restless legs symptoms.

If you have been told your labs are normal while experiencing any combination of these symptoms — fatigue, hair loss, brain fog, poor exercise tolerance, mood changes — ask specifically about your ferritin number.

Bryan Johnson’s Ferritin — And Why His Story Is Different

By now you may have seen Bryan Johnson’s announcement. He spends millions annually tracking his health, and announced last month that he has autoimmune gastritis — a chronic condition in which the immune system attacks the stomach’s acid-producing cells, impairing iron and B12 absorption. His earliest signal was eleven years of persistently low ferritin without anemia.

His story and mine share the same number — low ferritin, normal hemoglobin — but the clinical picture is completely different.

In a premenopausal woman with low ferritin, blood loss and low dietary intake are the first and most likely explanation.

Iron deficiency in a man without an obvious dietary explanation is a GI bleed until proven otherwise. This means endoscopy. In his particular case, he had low ferritin and known autoimmune thyroid disease — which should immediately prompt investigation for autoimmune gastritis. The connection between autoimmune thyroid disease and autoimmune gastritis is well established. Anti-parietal cell antibodies and an upper endoscopy should have been ordered years earlier.

Johnson credits his eventual diagnosis to overhauling his medical team and launching a systematic investigation. What he describes — a clinician finally looking at the full picture and connecting the dots — is exactly what good primary care does. It doesn’t require millions annually. It requires a physician who knows your history, tracks your trends, and has good clinical training.

How to Raise Your Ferritin

The approach depends on why your ferritin is low. Know your cause first.

For women with blood loss as the primary driver: You cannot supplement your way out of ongoing loss without addressing the source. If you have heavy periods or fibroids, it’s important to have a plan to minimize the bleeding alongside iron replacement.

Dietary iron. Heme iron is from meat, poultry, and fish. Non-heme iron comes from plant sources like lentils, beans, tofu, spinach, pumpkin seeds, fortified grains, and dark chocolate. Non-heme iron is absorbed at lower rates — but plant-based diets can definitely support healthy ferritin with deliberate food choices.

Worth knowing: premenopausal women need 18mg of iron per day — more than double the 8mg recommended for men and postmenopausal women. This helps exlplain why low ferritin is so common in women of reproductive age.

Vitamin C is important. Eating vitamin C-rich foods alongside iron-rich plant foods — citrus, bell peppers, strawberries, broccoli — increases non-heme iron absorption significantly. This should be a habit at every meal.

What to avoid around iron intake. Calcium, coffee, and tea all impair iron absorption. Wait at least an hour after coffee before taking supplements or eating your most iron-rich meal.

Oral supplementation. Ferrous bisglycinate is better tolerated than ferrous sulfate and better absorbed — look for "bisglycinate" or "chelated iron" on the label. Take it with vitamin C, away from coffee and calcium. Every other day dosing may actually improve net absorption for some people. Expect 3-6 months to meaningfully raise ferritin. It takes time and that’s normal.

What level to aim for. The normal reference range includes levels associated with significant symptoms. Most longevity and functional medicine physicians aim for at least 50-70 ng/mL. For hair loss specifically, some research suggests levels above 70 are needed for follicle recovery.

When oral iron doesn’t work: If ferritin doesn’t respond to supplementation, the problem is likely absorption — not intake. This is when autoimmune gastritis, celiac disease, H. pylori, or chronic PPI use need to be ruled out. IV iron infusions bypass the GI tract entirely and worth asking about if oral supplementation has failed.

What to Ask Your Doctor

If you haven’t had your ferritin checked recently — ask for it specifically. It is not automatically included in a standard CBC or metabolic panel. You have to ask.

If your ferritin is below 50 and you have symptoms — fatigue, hair loss, brain fog, poor exercise tolerance — push for treatment even if you’re told your labs are “normal.” Normal and optimal are not the same thing.

If you’re a man with low ferritin without an obvious dietary explanation — ask for a GI workup. Don’t accept “take iron supplements” as the complete answer.

If your ferritin doesn’t respond to oral supplementation — ask about IV iron and ask why absorption might be impaired.

One important caveat: more iron is not always better. Iron overload is real and can damage the liver, heart, and pancreas over time. Hemochromatosis — a genetic condition causing excess iron absorption — is more common than most people realize. And elevated ferritin doesn’t always mean iron stores are high; it can also signal inflammation or liver disease.

The goal is not to supplement blindly. The goal is to know your number, understand what’s driving it, and treat accordingly. Get the level first, then act on what you find.

The Longevity Connection

I view ferritin as a longevity marker.

Iron is built into the machinery of your mitochondria. The electron transport chain — the series of protein complexes that produce ATP — depends on iron to function. Without adequate iron, mitochondrial energy production drops. This is why low ferritin fatigue is not ordinary tiredness. Your cells are producing less energy. Iron deficiency and mitochondrial dysfunction reinforce each other. You cannot fully support your mitochondria while your ferritin is critically low.

For women — who are at higher risk of iron deficiency due to menstruation and pregnancy — this is one of the most common and most correctable longevity variables being missed in routine care.

The Bottom Line

My ferritin was 5. I wasn’t anemic. My standard labs looked fine.

Ferritin is one of the most important numbers you can know. It is not routinely checked. It is not routinely treated until anemia appears. And by that point, you’ve often been symptomatic for months or years.

Ask for it. Know your number. Don’t accept “normal” when optimal is what you actually need.

That is the practice of longevity medicine. It doesn’t require millions. It requires the right questions, asked by someone who knows you well enough to connect the dots.

My father is 78 years old.

He plays tennis almost every day and still stands on his hands for minutes at a time. He has a plant-based diet, he’s lean, and he has more energy than most people half his age. He had a coronary artery bypass graft years ago — related to high Lp(a), one of the most common inherited cardiovascular risk factors. His heart wasn’t damaged. It functions beautifully. He is, by almost any measure, thriving.

Then he came home from a recent appointment and told me what his doctor said.

That he thought my father would probably live until 85. And that he would likely die from heart disease.

He sounded defeated when he told me. He sounded like someone who had just been handed a verdict.

That's not a prognosis. That's a nocebo effect.

I have to say this upfront: my father asked for it. He looked his doctor in the eye and directly asked “How long do you think I’ll live?” Most patients don’t do that. And most physicians aren’t prepared for it. I’m sure it caught his doctor off guard.

But how a physician answers that question matters more than we might think.

His bypass was successful. His heart function is excellent. His LDL is optimally managed. Blood pressure normal. He exercises daily, eats well, and his most significant cardiovascular risk — Lp(a) — is being managed as well as current tools allow.

The diagnosis is real. The risk is real. The prognosis as delivered — without accounting for who he actually is — is incomplete.

And as I’ll explain, it may actually be harmful.

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The Nocebo Effect: What Your Doctor Says About Your Future Actually Changes It

There is a good body of research on what happens when physicians communicate prognosis, and it’s more consequential than what most of us were taught in medical school.

Most people have heard of the placebo effect — the measurable biological benefit that comes from positive expectation. Fewer people know its twin: the nocebo effect. Where placebo describes what happens when we expect to get better, nocebo describes what happens when we expect to get worse. Negative expectations activate stress pathways, alter immune function, and affect health behaviors in ways that can make a pessimistic prognosis self-fulfilling.

In other words: what you believe about your future changes your future. And what your physician tells you shapes what you believe.

A study of patients with heart disease found that those who held more negative beliefs about their condition faced worse health outcomes than those with similar disease burden who held more optimistic beliefs. The belief itself was predictive.

Research on subjective age and longevity is equally fascinating. People who feel younger than their chronological age live longer — in one study, up to 7.5 years longer — than those who feel their age or older.

And your physician prognosis influences all of it. What a doctor says about your future shapes how you think about your future. How you think about your future shapes how you live. How you live shapes how long and how well you live.

Your doctor’s prognosis is actually a clinical intervention. And most physicians are making it without knowing they are.

What We Were Taught, and What We Weren’t

Medicine trains physicians to be accurate. To be honest. To avoid false hope. These are foundational values, and I hold them too.

But there is a difference between telling a patient the truth about their condition, and telling them a future that closes doors rather than opening them.

My father’s doctor was probably trying to be honest. He was probably trying to set realistic expectations. Or he may have been trying to encourage my father to take his health seriously.

What he may not have considered is that he was also, in that moment, practicing medicine that has real consequences. That telling a 78-year-old man — who plays tennis every day and does handstands and does everything he can to improve his heart health — that he will probably die from heart disease at 85 is not a neutral act.

It is a prediction that can shape their trajectory.

I am sure I’ve been that doctor. I’m sure I’ve given prognostic information without fully thinking about with what it does to the person receiving it. Medical training doesn’t teach us to think about this carefully enough.

What Good Prognostic Communication Looks Like

Patients deserve honesty and physicians have an ethical obligation to it. This is not about giving false optimism.

But we can acknowledge what is true while also acknowledging what is possible. We can say: here is your condition, here is what the data shows, and here is what I have seen people like you — people who live well, who move their bodies, who take their health seriously — actually do.

For my father, that could have sounded something like this:

“You have a history of coronary artery disease, but your heart function is excellent and your risk factors are extremely well controlled. People with your lifestyle and your numbers do better than the statistics suggest. I can’t tell you exactly how long you’ll live — nobody can — but I can tell you that everything you’re doing is working, and that your body is responding. Keep doing what you’re doing.”

That is honest. It is also accurate. And it does something the other version does not: it gives a person confidence in their own body. It makes them a partner in their health rather than a passive recipient of a predetermined outcome.

Giving patients confidence in their bodies is one of the most important interventions we have.

What Patients Can Do

If a physician gives you a prognosis that feels like it closes doors rather than opening them — you can push back. You can ask:

“Is that based on my specific numbers and lifestyle, or on general statistics for people with my diagnosis?”

“What would I need to do to change that trajectory?”

“What does the best-case picture look like for someone like me?”

You are also allowed to seek a second opinion, and not because your physician is wrong about your diagnosis, but because prognosis is also an interpretation, and interpretations vary.

A Note to Physicians

We have more power than we sometimes realize, and also more responsibility.

When we tell a patient what their future looks like, we are shaping expectations that will influence outcomes. That is a clinical intervention.

The research on nocebo effects and the biology of expectation belongs in medical education. And not to make us falsely optimistic, but to make us thoughtful about the full clinical consequences of what we say.

My father left that appointment with a ceiling on his future that his body contradicts every time he walks onto a tennis court or stands on his hands.

He is 78 and he is thriving. And his doctor should have said so.

The Bottom Line

I’m still working on convincing my father that his doctor’s prognosis is not his destiny.

What we say about your future matters. How you think about your future matters. The belief that your body is capable, that the trajectory is modifiable, that 85 is not a ceiling — that belief is medicine.

That is the practice of longevity. And it starts with what we say.

It was 3am. My son had croup — that distinctive seal-bark cough that every parent recognizes with a specific kind of dread. I was holding him in a steaming shower, his small body against mine, feeling his breathing slowly ease. Terrified and steady at the same time. Knowing I would do anything for him. Knowing that I would never let anyone else do this.

I wasn’t thinking about my sleep. I wasn’t thinking about my cortisol levels or my cardiovascular risk or the research on chronic sleep deprivation. I was thinking about him.

That moment — exhausted, scared, present, and exactly where I needed to be — is the paradox at the heart of women’s longevity.

Women Live Longer. But They Don’t Live Better.

Here is what the data shows: Women outlive men by an average of five to six years. But they spend nearly three more years of their lives in poor health. They carry a higher burden of chronic disease, disability, and pain in the years they do live. They defer their own healthcare more consistently than men. They are more likely to be undiagnosed, undertreated, and dismissed.

We have studied why women live longer for decades, but we have not figured out why they live worse.

I think the caregiving burden is a significant part of the answer.

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The Invisible Burden Has Biological Consequences

Women carry a disproportionate share of the invisible labor that sustains families. The night wakings. The sick days. The mental load of knowing everyone’s schedule, everyone’s needs, everyone’s fears. The healthcare appointments made and attended. The emotional labor of holding a family together through stress, loss, sickness, transition.

Chronic stress activates the body’s stress response systems and accumulates over time. Cortisol dysregulation contributes to cardiovascular disease, metabolic dysfunction, immune suppression, and accelerated cellular aging. And chronic sleep disruption impairs mitochondrial function, increases inflammatory burden, and accelerates the oxidative damage that drives aging at the cellular level.

Studies of mothers caring for chronically ill children show that the longer the duration of caregiving, the shorter their telomeres and the lower their telomerase activity — a signature of accumulated stress. The biology of caregiving is measurable. It ages women at the cellular level.

For many women, this burden doesn't end when the kids grow older. Nearly half of adults in their 40s and 50s are now caring for an aging parent — the so-called sandwich generation. The 3am moments don't always end. Sometimes they just change from a crying infant to an aging parent's late-night phone call.

And this labor isn’t just personal — it’s structural. The unpaid caregiving women provide is what keeps families functioning and people out of hospitals. The system depends on it. It just never says so.

This has real consequences.

The Caregiving Paradox

Here is where it gets a little complicated.

Purpose is one of the strongest longevity predictors we have. The research is as robust as almost any biomarker we measure. And the effect is more pronounced in women than in men — a strong sense of purpose lowers mortality risk significantly.

Motherhood and caregiving provide that purpose. Deeply and in ways that are difficult to articulate and impossible to quantify. The love I felt holding my son in that shower at 3am — terrified and steady, and knowing I was exactly where I needed to be — is also protective.

But the same role that gives women their deepest sense of meaning is also the role most likely to deplete their sleep, elevate their cortisol, accelerate their cellular aging, and defer their own healthcare for years at a time. Both are true. The love is real and the cost is real.

Caregiving stress is not the same as work stress or financial stress or acute crisis stress. It is relentless and chosen and soaked in love. It may not feel like burden even when it is one. And that’s what can make it invisible.

The 3am Moment

I would not trade that shower at 3am for anything. Not for a full night of sleep, not for optimal cortisol levels, not for a better score on any longevity metric we have. The love is the point. The connection is the point. The being the one who knows exactly how to take care of someone — that is the point.

This is not an argument that motherhood or caregiving is bad for your health. It is an argument that medicine needs to see the full picture. When a woman comes in exhausted, with elevated inflammatory markers and disrupted sleep and deferred healthcare, the clinical response needs to be better. We can’t just say “reduce your stress.” We need to understand what her life actually looks like. Find out what she’s carrying. And find out who is helping carry her.

We should ask about caregiving responsibilities the same way we ask about smoking history. It’s a clinical variable and belongs in the history.

The love is real. The cost is real. A medicine that only sees one of those is not adequately serving the women in its care.

What We Can Do Better

Putting yourself on your own list is not selfishness. It is how you sustain the capacity to care for everyone else. Your longevity is also your children’s longevity.

Name the burden. Not just to yourself, but out loud — to your partner, your physician, your people. The invisible load becomes more manageable when it is made visible. Research consistently shows that social support is one of the strongest buffers against the kind of chronic stress that accumulates in caregiving.

Ask for help specifically. Specific asks: can you take the kids Tuesday? Can you handle the appointment? Specificity makes help easier to give and easier to receive.

Defer your own healthcare less. I know this is easier said than done. But the pattern of women postponing their own care is one of the main ways the caregiving burden shows up. Your appointment matters. Your labs matter. Your sleep study matters. Schedule it the way you’d schedule it for those you love.

And tell your doctor what your life actually looks like. Not just your symptoms, but your context. A physician who understands what you’re carrying can practice differently. That conversation starts with you being willing to say: here is what my life actually looks like right now.

The Bottom Line

Women live longer. They don’t live better. And the gap between those two facts has a biology that medicine has barely begun to address.

The caregiving burden is real. The love that makes it worth it is real. Both things are true and both things have consequences. A longevity medicine that only sees one of them is leaving women behind.

I held my son in that shower until his breathing eased and he was calmer. Then I lay awake listening to him breathe for another hour before I could sleep.

I would do it again tonight.

I want medicine to see what that cost is. But also what it gives. Medicine should hold both things at once, the way mothers do, every single day.

A patient came to me two years ago with rheumatoid arthritis so severe she’d stopped gardening — the thing she loved most. Her hands were stiff by morning, swollen by afternoon. She was on multiple medications, managing symptoms but never quite ahead of them.

She had also been gradually gaining weight over years, with rising blood sugar. We started a GLP-1 for weight loss and metabolic health. Within four months, her inflammation markers had dropped dramatically. Within six, she was back in her garden. Her rheumatologist began tapering her medications. We were able to reduce her blood pressure medications too.

I’ve been practicing medicine for many years, and can’t say I’ve seen another drug class do what I’m seeing GLP-1s do.

I believe the most powerful longevity interventions are free — sleep, movement, connection, purpose. GLP-1s are not free, not simple, and not without real risk. But the evidence is strong enough, and what I’m seeing in practice is significant enough, that I think it deserves real attention.

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What I’m Seeing in Practice

The stories aren’t about the number on the scale. They’re about the person who got their life back.

I’ve had patients come off blood pressure medications they’d been on for decades. I’ve watched people who hadn’t exercised in years start walking, then jogging, then signing up for 5Ks — because for the first time in a long time, their body doesn’t hurt enough to stop them. I’ve seen drinking lessen. Sleep improve. Brain fog lift.

I’ve seen inflammatory conditions — like arthritis and chronic pain syndromes — improve in ways that have surprised both me and my patients. They weren’t taking GLP-1s for inflammation. They were taking them for weight and metabolic health, and the inflammation relief came as a surprise.

Patients are proud, grateful, motivated, hopeful. Some describe a quieting of what researchers call “food noise” — the constant, intrusive mental chatter about eating, craving, and self-judgment. And when that noise goes down, something else comes up: presence, energy, a renewed relationship with their own body.

These are some of the best most motivating follow-up visits I have.

The Perimenopause and Menopause Relationship

This is the part of the GLP-1 conversation I think we need to talk about and explain better.

Something specific happens to a woman’s body during perimenopause and menopause that has nothing to do with willpower or habits. As estrogen declines, fat storage shifts — moving from the hips and thighs to the abdomen. Visceral fat accumulates around the organs, and visceral fat is metabolically active and inflammatory in a way subcutaneous fat is not. It raises cardiovascular risk, worsens insulin resistance, and low-grade systemic inflammation that accelerates aging.

This shift can happen even when a woman’s weight on the scale doesn’t change at all and her habits are identical to five years earlier.

This is where it gets clinically interesting. A 2024 study published in the journal Menopause found that postmenopausal women on semaglutide plus hormone therapy lost significantly more weight, at every checkpoint, than those on semaglutide alone. Estrogen therapy alone can reduce visceral fat gain, improve insulin sensitivity, and help preserve lean muscle mass. Combined with a GLP-1, the effect appears to compound.

The metabolic shift of perimenopause deserves a distinct treatment approach, rather than a generic weight loss conversation that ignores what’s actually happening hormonally.

Why This Makes Scientific Sense

The explanation for how GLP-1 drugs work is usually kept simple: they mimic a gut hormone that signals fullness, so people eat less.

But it’s much bigger than this. GLP-1 receptors are found throughout the body: in the brain, the heart, the kidneys, the immune cells, the gut. At therapeutic doses, these drugs do more than simply suppress appetite. The brain’s reward circuitry shifts. Inflammatory signaling reduces. Metabolism changes.

The clearest proof of this came from the SELECT trial, one of the most rigorous studies in this space. In patients with obesity and established cardiovascular disease but no diabetes, semaglutide reduced major adverse cardiovascular events — heart attack, stroke, cardiovascular death — by 20% compared to placebo. When researchers examined how much of that benefit came from weight loss itself, they found only about a third of the cardioprotective effect was explained by reduced waist circumference, and the rest came from somewhere else. The trial's own authors concluded that semaglutide should be “reconceptualized as a disease-modifying treatment” rather than simply a weight loss drug.

We treat chronic diseases as separate, distinct problems. But one idea coming out of GLP-1 research is that many of them share common root causes, such as chronic inflammation and metabolic dysfunction. A drug that addresses those roots doesn’t just treat one condition, but it improves the whole terrain.

From a longevity standpoint, that matters. We don’t age in a single organ. We age systemically.

What We Actually Know About Cancer

I find this really fascinating and worth tracking.

Observational studies — including a large 2025 analysis published in JAMA Oncology — found GLP-1 users had lower rates of obesity-related cancers, and earlier data showed similar patterns in people with diabetes. This makes biological sense: obesity itself is a known driver of multiple cancer types, so a drug that treats obesity might reasonably reduce cancer risk as a downstream effect.

Then, in December 2025, an analysis of 48 randomized controlled trials found GLP-1 drugs ‘probably have little or no effect’ on obesity-related cancer risk. The likely explanation: people who stay on these medications tend to have better healthcare access and lower baseline cancer risk to begin with. That’s confounding. I’d treat this the same way I treat the Alzheimer’s story: promising, unresolved, not yet something to count on.

The one specific safety signal worth knowing: GLP-1s carry a caution for people with a personal or family history of medullary thyroid cancer, based on early animal studies. The actual incidence in human trials has been under 1%, and some researchers think the signal may reflect increased screening and detection rather than the drug causing new cancers. If you have a family history of this specific cancer, it’s worth a direct conversation with your physician before starting.

The Addiction Research

If you’d told me years ago that a diabetes drug would become one of the most promising treatments for alcohol use disorder, I don’t think I would have believed you. The evidence here is pretty interesting.

A randomized controlled trial published in JAMA Psychiatry in 2025 found that low-dose semaglutide significantly reduced alcohol cravings, drinks per drinking day, and heavy drinking episodes.

The mechanism seems to involve the same brain reward circuitry implicated in food noise. GLP-1 receptors sit in regions of the brain governing craving and reward, and animal studies show these drugs reduce alcohol intake by modulating dopamine release.

This is still early. We need head-to-head trials against existing addiction treatments. But for a condition that doesn’t have many effective pharmacological treatments, this deserves attention.

Where the Hype Outpaces the Evidence

Not everything in this space is solid ground.

Microdosing — taking smaller-than-prescribed doses — has become a popular trend, largely driven by people trying to reduce side effects or save money. The evidence for it is thin. Standard dosing is what’s actually been studied in clinical trials. Interesting to watch, not something to recommend yet.

The newer multi-receptor drugs deserve caution. Retatrutide and similar emerging compounds are showing strong early results, and the online enthusiasm has outpaced the data. But our long-term safety data comes largely from earlier, simpler formulations like semaglutide, and we don’t yet know what years of triple-receptor agonism does in a broad population.

Compounded versions are a separate and more serious problem. Some telehealth platforms and peptide vendors sell compounded versions of GLP-1 drugs. These products have unverified purity, sterility, and dosing and I cannot recommend them.

The Real Risks and Downsides

Muscle and bone loss is the one I think about most. Lean mass is one of the most powerful predictors of longevity we have. Some patients lose significant muscle and bone density alongside fat — particularly concerning in perimenopausal and postmenopausal women, who are already losing both at an accelerated rate from declining estrogen. Resistance training and adequate protein intake are essential.

We don’t yet have good studies for most off-label uses. We need controlled trials, especially publicly funded research into areas pharmaceutical companies have less financial incentive to prioritize.

Discontinuation is its own problem. Many patients regain weight when they stop, and we don’t yet know the right long-term strategy for someone who wants to eventually come off the medication.

And there’s an equity problem I don’t want to gloss over. These drugs are expensive, often poorly covered by insurance, and largely accessible to people who can pay out of pocket or navigate a complicated prior authorization system.

Good medicine shouldn’t be a luxury product. Right now, for many people, this one still is.

A Tool, Not a Destination

In my practice, I think of GLP-1s the way I think of any powerful longevity intervention: as a tool that creates a window of opportunity. The drug can lower inflammation, quiet the metabolic noise, reduce the physiologic burden that was preventing a patient from exercising, sleeping, and engaging fully with their life.

The patients I’ve seen thrive most are the ones who used that window. They built the muscle. They addressed the sleep. They worked on the stress and the relationships and the purpose. The drug gave them back enough capacity to do that work — and they did it.

We are at the beginning of understanding how a single molecule, acting across many biological systems simultaneously, might reshape what aging looks like.

I still believe the most powerful longevity interventions are free. But that doesn’t mean every powerful intervention has to be.

A drug is not a practice. But it can clear the path back to one. The sleep, the movement, the connection, the purpose — none of that disappeared for my patient in her garden. It was simply waiting for her, on the other side of a molecule that gave her hands back.

GLP-1s are not the practice of longevity. But for some patients, they are what makes the practice possible again.

I came to the Nicoya Peninsula in Costa Rica thinking I’d get to experience an idyllic blue zone life. That I’d exercise, eat well, sleep well, and feel healthy. Confirm what I thought I already knew about Blue Zones.

Instead, it taught me what I needed to learn.

It rained. A lot. Our first week, two of our tires blew on flooded roads. A tropical storm knocked out the power and water for 2 days. We were covered in mosquito bites, waking up through the night to itch. An earthquake woke me from sleep one night. A kitchen circuit blew and we had no way to refrigerate food for a few days.

What I learned was how to respond to this. What I learned was the art and practice of what the locals call 'tranquila.'

What Tranquila Means

Tranquila is a Spanish word that roughly translates to “calm” or “relax” or “don’t worry.” But the translation doesn’t quite capture it. It’s less an instruction than an offering. A small gift passed between people multiple times a day.

Our son dropped a glass at a restaurant and it shattered across the floor. The waiter crouched down, started cleaning, looked up with a smile. ‘Tranquila,’ he said.

I dropped the kids at school on a stormy morning, visibly worried. The teacher put her hand on my arm. 'Tranquila,' she said — we will keep them safe and dry.

At the grocery checkout I realized I’d forgotten bananas and started to rush back. The clerk waved her hand. 'Tranquila,' she said. I will wait.

Every time someone said it to me I noticed the same thing: they meant it. It wasn’t performative reassurance. It was a transmission of calm from one person to another. As if they had enough to spare.

This is what I kept trying to understand. Where does that come from? What do they have that makes it so available, so reflexive, so real?

What I Expected to Find

The Nicoya Peninsula is one of the Blue Zones identified by researcher Dan Buettner — one of a handful of places on earth where people routinely live into their 90s and beyond, with unusually low rates of heart disease, cancer, and diabetes.

The contributing factors are well documented: a plant-based diet centered on beans, corn, and tropical fruit. Daily movement embedded in ordinary life. Strong family and community ties. Purpose and a reason to wake up every morning.

And low stress. Researchers identify low psychological stress as one of the central features of Blue Zone life.

I understood this intellectually before I arrived. I thought I understood what it meant.

I did not.

The Storm

It started with rain. Then more rain and strong wind. The kind of rain that makes you understand why people build their homes on higher ground. I had nightmarish visions of my children being swept away in floodwater.

The power went out. The water turned off. The roads flooded. Trees came down across the paths. We had no internet to get weather updates or check for evacuation orders.

The next morning the fallen trees blocking the main roads were gone. Nobody organized it. Nobody was asked. The locals got up early and just did it.

And the people around me — neighbors, locals, the teachers, the cafe owners — were tranquila. Just another storm. This happens. Matter of fact. Calm in a way that wasn’t practiced. We help each other. We wait for the sun. We clear the roads.

Tranquila.

The Gap

We know what chronic stress does to the body — the cortisol dysregulation, the inflammatory burden, the telomere shortening, the cardiovascular risk. I know this, yet I was probably one of the most stressed people on the peninsula.

That gap — between knowing something and embodying it — is probably the most important thing the Blue Zone has taught me.

People there weren’t practicing tranquility. They weren’t meditating, doing breathwork, tracking metrics, taking adaptogens, or following a stress management protocol. Tranquility is a disposition — something so embedded in the culture that it didn’t need a name or a method.

You cannot buy that. You cannot download it. You cannot arrive at it through a certification program or a morning routine or a supplement stack.

It is the accumulation of a culture organized around different values than ours. Around mutual aid. Around accepting what cannot be controlled. Around trusting that the sun will come out and the roads will be cleared, because it’s always been that way.

What the Research Actually Shows

The Nicoya Blue Zone data is compelling — average life expectancy in this low-income region reaches 85, among the highest in the world. But here is what the research also shows, and what most Blue Zone coverage misses:

Nicoyans who are born here but move away don’t take the longevity with them. People who move here at retirement age don’t gain it. The Blue Zone effect isn’t in the water or the beans or the sunshine — though all of those contribute. It’s in a lifetime of accumulated cultural practice. I think a big part of it is the disposition that forms when you grow up watching strangers stop to help with tires, watching roads cleared at sunrise, watching your grandmother sit with a storm.

You cannot move into a Blue Zone and absorb its longevity. And the Blue Zone itself is changing — modernization and migration have already weakened longevity patterns in Nicoya as the region has developed.

A Note on the Controversy

The Blue Zone data has come under serious scrutiny. A 2024 study found that in some Blue Zone regions, the majority of reported supercentenarians were missing, imaginary, clerical errors, or had died — and in at least one case, families were misreporting deaths to continue collecting pension benefits.

Research specific to Nicoya found that people born here after 1930 didn’t show exceptional longevity compared to the rest of Costa Rica. Poor birth registration, weak historical record keeping, and confirmation bias appear to have inflated the longevity numbers significantly.

The specific statistical claims deserve skepticism. But it doesn’t change what I observed about how people live here. The food, the movement, the community, the pace, the tranquila — these are real. Whether they produce centenarians or not, they represent a way of organizing human life that is profoundly different from ours. And the gap between that culture and ours — the chronic anxiety, the optimization, the performing — is worth examining regardless of whether the longevity data holds up.

Maybe the lesson of the Blue Zones was never really about how long people live. Maybe it was always about how they live.

What Makes This Place Different

Even if the longevity data is overstated, what I observed about how people live here is real. Before the storm, I had been cataloguing the factors.

The food — rice and beans at every meal, plantains, fresh fruit, light early dinners that amount to time-restricted eating practiced culturally for generations.

The movement — everyone moves, soccer in the evenings, walking everywhere, surfing, gardening, sweating in the heat just by existing.

The community — neighbors who gather without scheduling it, families that are multi-generational and present, social connection as the texture of daily life rather than something you carve out time for.

The light — people wake with the sun and sleep when it’s dark, circadian alignment happening by default rather than by design.

And the pace. The heat and humidity makes urgency structurally impossible. Nobody rushes because the climate won’t allow it. The low-grade chronic stress of modern life — the performing, the optimizing, the never quite finishing simply cannot sustain itself here.

These practices emerged from a culture organized around different priorities — community over productivity, presence over optimization, acceptance over control.

Tranquila isn’t a wellness practice. It’s what happens when a culture has never separated from the conditions human biology was designed to thrive in.

What I’m Taking Home

I won’t pretend the storm made me tranquila. I was anxious and I stayed anxious until the rain stopped and the roads cleared and the kids came home safely from school.

But something shifted.

I watched strangers help us without being asked. I watched my children sit with boredom and discover it wasn’t dangerous. I watched a community absorb a significant storm with the calm of people who have absorbed many storms before and know that the sun comes back.

And I thought about what medicine can and cannot do.

Medicine can lower your LDL. It can manage your blood pressure. It can screen for the diseases most likely to kill you and intervene before they do. These things matter a lot.

But medicine cannot give you the disposition that helps strangers reflexively, sits with storms without catastrophizing, clears roads at sunrise not because someone asked but because that is simply what you do.

The longevity research points to this untranslatable and unpurchasable accumulation of a life lived in community, in acceptance, in mutual aid, in the absence of the particular kind of chronic anxiety that characterizes modern life.

We can learn from it even if we cannot replicate it. We can build toward it even if we cannot buy it.

We can practice, in whatever small ways are available to us.

The Bottom Line

I came to a Blue Zone expecting to confirm what I already believed — that the most powerful interventions are simple, free, and boring. That the practice of longevity is built in the daily accumulation of ordinary things.

I still believe that. But I also understand it differently now.

Because the most powerful thing I observed here wasn’t the food or the movement or the community. It was the absence of something. The absence of the particular strain of anxious striving that I carried here with me from home — the kind that was hard to fully put down even in a beautiful place, even on sabbatical, even knowing everything I know about what chronic stress does to the body.

Tranquila.

The locals said it to me like a gift. Like something obvious. Like of course.

And I’ll keep practicing it.

I’m writing this from the Nicoya Peninsula in Costa Rica, where I’m spending the month on sabbatical after five years with my employer. It is a rare gift, and I don’t take it for granted.

A sabbatical is, at its core, a practice of rest. And rest isn’t defined by how long it lasts, but how you hold it.

This doesn’t feel much like a vacation. We’re in a different environment with new routines for what feels like a long time. The kids are in a school here. Some moments have been quite tough. A tropical storm knocked out our power and water for two days. Roads flooded. We were far from home with uncertain information and kids to keep calm. It made us really appreciate home and normal life that we’ll be excited to get back to.

But I’ve been trying to identify what makes this time feel different from a vacation, and I don’t think it’s the amount of time as much as the intention behind it.

Which I love because it means almost anyone can have one and we don’t have to depend on our employers.

What a Sabbatical — and Rest — Actually Is

The word comes from the Hebrew shabbat, which means rest. This was a practice built into the structure of time itself. Every seventh year, farmers let their fields rest. Not because they were tired, but because the land needed discontinuity to remain productive. The fallow period was a preparation for what would follow.

We lost that rhythm somewhere. We replaced it with vacation, one or maybe two weeks of compressed activity, and often more exhausting than the work it was meant to interrupt.

A sabbatical is something different. It is intentional discontinuity. A deliberate pause. A pause not just from the tasks of your work, but from the identity of being a worker. Time to rest at a deeper level. Time to remember who you are when you aren’t performing a role.

It doesn’t have to be a month in another country. It can be two weeks held differently. It could be a slow August reframed with intention. Or even a long weekend structured around something else.

The duration doesn’t matter as much as the decisions around it.

Why It Matters and the Science of Rest

We have treated rest as the absence of work. But it’s actually something more active than that.

Chronic work stress accumulates in ways that don’t resolve with a normal weekend. Cortisol dysregulation, elevated inflammatory markers, impaired immune function, accelerated cellular aging are measurable consequences of sustained high-demand work without recovery. It builds over months and years, and a two-day weekend does not clear it.

Cognitive restoration research shows that rest in natural environments, with reduced demands on directed attention, restores the capacity for creativity, complex problem-solving, and emotional regulation. The brain needs discontinuity to consolidate learning, process experience, and generate insights.

There is also growing research on what happens to identity and purpose during sustained rest. People who take sabbaticals — not just vacations — report returning with greater clarity about what matters, what they want to change, and who they want to become. That has downstream effects on performance, relationships, and health.

Rest is a necessity.

The Rest Spectrum

Rest doesn’t require months or a formal employer benefit. Here is what’s possible across different amounts of time:

Two weeks. This can be enough time to decompress if the first week is protected from work and the second week is structured with intention. The research on stress recovery suggests it takes most people five to seven days to actually downregulate their nervous system after sustained high-demand work. Which means a two-week sabbatical gives you one week of rest and one week of something new.

A slow summer or intentional season. I think this may be the most accessible version for most people. Not a formal sabbatical but a reframing of a period of time. Protecting certain hours. Saying no to certain commitments. Giving yourself permission to move more slowly and notice more carefully.

A long weekend or a single week. This is not enough time to fully decompress, but enough to practice the intention. A weekend with no plans and no screens. A week where you protect mornings for something that isn't work. You can practice sabbatical as a habit even when you can't access it as a block of time.

A month. Enough time to establish a different rhythm and notice what you actually enjoy when nobody is asking anything of you. To read something long, learn something new, observe something carefully. I think a month is when the sabbatical can start to change you rather than just rest you.

Three to six months. This is the traditional academic sabbatical. Enough time for a project, a significant learning, a creative or intellectual creation. Let’s be honest, this is rare outside academia. Maternity leave was the closest I came to this kind of sabbatical. And of course that sabbatical creation was a newborn — which, as any new mother knows, not restful but certainly changes you.

How to Create One — Regardless of Your Situation

If you have a formal sabbatical benefit: Use it fully. Resist the urge to stay partially connected. The value of a sabbatical is proportional to your willingness to actually leave. Trust the people you work with to handle things. The organization will survive. And you will return restored.

If you have two weeks of PTO: Reframe it before it begins. A sabbatical starts with a decision. Ask yourself: what do I want to be different about how I think, feel, or live when these two weeks are over? That question changes how you spend the time. Protect the first four to five days from any work contact. Use the second week for something that requires your attention in a different way — maybe a project, maybe a place, maybe a practice, maybe a person.

If you have a slow summer or season: Identify two or three things you want to protect in that period. Time with people you love. Something you want to learn. A slower morning. A regular walk. The sabbatical can be an intentional thread running through a summer.

If you have neither time nor benefit: Micro-sabbaticals are real. A weekend with no plans and no screens. A morning a week protected for something that isn’t work. A deliberate slow day once a month. None of these are the same as a month somewhere, but the intention matters regardless of the duration. You can practice sabbatical as a habit even when you can’t access it as a block of time.

What to Actually Do on One

A lot of people plan a sabbatical and then fill it with productivity — a book to write, a course to complete, a project to finish. That is work with a different title.

A sabbatical includes some or all of the following:

Rest that goes deeper than sleep. Unstructured time. Slow mornings. Naps without guilt. Time that isn’t accounted for.

Movement that feels like play. Not a training protocol, but something you actually enjoy, with other people.

Nature. Natural environments restore cognitive capacity in ways that urban environments do not. You need to go outside, regularly, without an agenda.

Something new to learn. Not for your career development but for curiosity. A language, a craft, a subject that has nothing to do with your work. Learning activates the brain differently.

Reflection. Some regular practice of asking: what am I noticing? What do I want to be different? What am I grateful for? What have I been avoiding? Reflection is what makes it generative.

Social connection. Time with people you love, without an agenda. Not networking. Presence.

Deliberate non-optimization. This is the hardest one. A sabbatical is not the time to fix your sleep, overhaul your diet, start a new supplement protocol, or become a different person. It is time to be, not to improve. The improvement comes from the being, not from adding more.

A Note to Physicians

Physician burnout is not a personal failure. It is a systems problem — a predictable outcome of sustained high-demand work without adequate recovery, in a culture that has historically treated rest as weakness and self-sacrifice as virtue.

Burned-out physicians make more errors. They leave medicine. They get sick. They die younger. And they cannot practice the kind of attentive, curious, longitudinal care that their patients deserve.

A sabbatical is a clinical intervention — for you, and for every patient you will see when you return.

If your employer offers this benefit, use it without guilt. If they don’t, advocate for it. If that’s not possible yet, find the version of it you can access — a protected week, a slow month, a regular practice of rest.

How to Come Back

A sabbatical isn’t just about the time away. It’s about who you are when you return.

The return is where most sabbaticals are wasted. People come back and within a week are indistinguishable from who they were before — same pace, same habits, same patterns, same overwhelm. The insights of the sabbatical dissolve on contact with the ordinary.

Before returning, it’s helpful to think about what to protect from this time, what to do differently, what to say no to.

Then actually do those things. The sabbatical’s value isn’t in the time. It’s in what you carry back and refuse to give up.

I'm still figuring out what to carry home from this month. But I know I'll be back to this sabbatical practice, if not this place.

The Bottom Line

A sabbatical isn’t a reward for working hard enough. And it shouldn’t be a luxury available only to academics and people with generous employers.

It is a practice. One that can be scaled to the time you have, held with intention, and returned to again and again across a working life.

I came here burned out in ways I hadn't fully admitted. I'm leaving with something I don't have a word for yet. But it feels like the beginning of something.

My parents are in their late 70s. They still play tennis. They show up, they compete, they have a community built around a shared language that has nothing to do with their age. They are part of something. They belong somewhere.

Whenever I see 80 year olds on the tennis court, I think the same thing: This is it. This is actually what healthy aging looks like.

As a physician, I have become increasingly convinced that one of the most underrated prescriptions I could write has nothing to do with medication, supplements, or biomarker optimization.

It is play.

Not exercise. Not a workout. No structured training protocol.

Play. The kind of physical activity that involves other people, challenges your brain, and that you look forward to. The kind that feels less like medicine and more like Saturday morning.

I’m writing this from Nosara, Costa Rica, where I’m on sabbatical for the month. And I keep noticing the same thing here that I notice watching my parents on the court.

People play. Kids and adults on the same soccer field in the evenings. Swimmers of every age in the water. Neighbors gathering. Nobody is tracking their Zone 2 heart rate. Nobody is optimizing. They are just moving their bodies with other people. I think communities where people live longest are also the communities where play never stops being part of life.

More on that soon.

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What Play Actually Does

For most of human history, movement and social connection were not separate activities. You moved with other people. You competed, cooperated, navigated, adapted together.

Modern life separated exercise from play. We turned exercise into a solo activity and something you did in a gym, on a treadmill, with headphones in. We optimized for efficiency and lost the social dimension.

The Copenhagen City Heart Study followed over 8,500 adults for up to 25 years, tracking leisure-time physical activity and all-cause mortality. Researchers compared eight sports and activities, and the pattern that emerged was not about intensity or duration.

It was about social connection.

Tennis players gained nearly 9.7 additional years of life expectancy compared to sedentary individuals. Badminton players gained 6.2 years. Soccer players 4.7 years. Joggers gained 3.2 years. Health club activities added 1.5. This is observational data so we don’t know causality, but the pattern is consistent.

Why Social Play Is Different

The loneliness epidemic is happening alongside every other health crisis. Social isolation is linked to lower brain volume, a 26% higher risk of developing dementia, and higher mortality risk (similar to smoking). It is particularly problematic in midlife and older adulthood, when the built-in social structures of school, early career, and young family life have dissolved.

Most exercise doesn’t solve this. A gym membership doesn’t give you a community. A solo run doesn’t give you someone who knows your name. What play does is put you in relationship with other people around a shared activity. It gives you somewhere to belong that isn’t defined by your age, your job title, or your health status.

My parents aren’t just playing tennis. They are maintaining a social world. They are showing up somewhere where people know their name.

That is medicine. We just don’t write it on a prescription pad.

What Play Does to the Brain

Cognitive decline is what patients fear most, and it’s one of the areas where we have more leverage than people realize.

The activities with the strongest cognitive benefits tend to be what researchers call “open-skill” sports. These are activities that require constant adaptation rather than repetitive predictable movement. Tennis, racket sports, dancing, martial arts, team sports — all of these ask you to read another person, adjust your movement, make decisions under pressure, and respond to the unexpected.

This is cognitive training.

Playing these activities regularly is linked to improvements in executive function and working memory, reduced risk of age-related cognitive decline including Alzheimer’s and dementia, and increased neuroplasticity.

One data point I love: a landmark 21-year study published in the New England Journal of Medicine found that of all the physical activities studied, dancing was the only one that significantly reduced the risk of dementia — by 76%. Not jogging. Not swimming. Dancing. Because dancing requires you to move, adapt to music, navigate space, and respond to a partner simultaneously. It is cognitively demanding in a way that solo exercise is not.

It Scales With Your Entire Life

This is what I find most compelling about play as a longevity practice — it doesn’t have an expiration date.

My boys play tennis. My husband plays at a 5.0 level. My parents play. I play. Three generations, one court, one language. And the research backs what I observe in my own family: unlike many high-impact activities, socially embedded play can be sustained across the entire lifespan, from youth well into older adulthood.

It’s not the same with football. Or basketball. The best play finds you at every stage of life, asks you to keep adapting, and keeps rewarding you for showing up.

There is no age limit on a good rally. Or a good dance.

What This Looks Like in Practice

The prescription is not any specific sport. It is the combination of physical challenge, cognitive demand, and social connection. Here is what the evidence supports across different activities:

Tennis and racket sports — the longevity data is the strongest here. Tennis added nearly a decade of life expectancy in the Copenhagen study. Badminton added 6.2 years. If you want the benefits of a racket sport with a lower barrier to entry, badminton and pickleball are both great options.

Pickleball — the long-term longevity data is still young on pickleball, but a national survey of over 800 adults found that older adults who play pickleball had significantly lower odds of being lonely and experienced less social isolation. It’s also lower-impact, which makes it more accessible across the lifespan.

Dancing — dancing is at the top of the cognitive protection list. If you have always wanted to dance, this is a good reason to start.

Team sports — recreational soccer, adult volleyball, basketball leagues. What matters is showing up for other people. The Copenhagen data suggests the social dimension is doing significant work independent of the physical benefit.

Martial arts and yoga — both offer something the others don’t always guarantee: a built-in community with a progression structure that keeps people engaged long-term. The community of a dojo or a regular yoga studio is its own form of social medicine.

The common thread is showing up somewhere, with other people, doing something that asks something of your body and your brain.

A Note on Joy

The tennis court makes my parents alive: competitive, engaged, laughing, frustrated, connected. The tennis court is somewhere to be with someone waiting for them.

Joy changes cortisol levels, immune function, cardiovascular response, neural engagement. The research on purpose and meaning and social connection is research on what it feels like to be a human being who has something to look forward to.

The best longevity practices don’t feel like medicine. They feel like something you’d do anyway. They feel like play.

Find it. Protect it. Practice it.

I keep getting ads in my inbox. Invitations to longevity medicine training programs — certifications, masterclasses, conferences. Five figure price tags to learn how to practice the medicine I already believe in. Medicine that should already be taught in medical school.

Something about these invitations bothers me. The price tag. The exclusivity. The implicit message that this kind of medicine requires a special credential — one that costs five figures to obtain — and that positions the physician who holds it as something apart from primary care.

I understand the impulse. There is real knowledge in some of these. The science of longevity medicine is evolving and physicians should be learning it. Primary care training doesn’t currently teach this framework well enough. Programs like these exist partly because medical education failed to fill it. But the answer to that failure shouldn’t be a five figure credential that most physicians can’t afford and that most patients never benefit from.

It shouldn’t work that way. For physicians or for patients.

There is a growing belief that longevity medicine requires wealth — to access as a patient, and to learn as a physician. I want to challenge both.

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What Longevity Medicine Looks Like In Practice

The best longevity medicine I practice is billed as primary care. Let me show you what I mean.

I’ve been seeing a patient in his 60s by video every month for three years. In that time: bypass surgery, a diabetes diagnosis, COPD, major family stress. Also in that time: 50 pounds lost, smoking stopped, diabetes reversed. I want to note: he did this through lifestyle changes alone. While I had encouraged him to consider a GLP-1, he was motivated to try without medication.

No concierge membership. No five-figure annual fee. His visits are covered by insurance.

The medicine that actually changes trajectories — comprehensive testing, longitudinal thinking, a clinical framework built around prevention — is not proprietary to elite clinics. It is what good primary care has always been. We just stopped funding it that way.

And in the space that a broken primary care system left behind, a world of elite longevity medicine has emerged — one that promises what primary care used to deliver, at a price most people can't afford. The medicine at its core can be good. Some not. But the exclusivity, the price tags, the bundling of some evidence based care with non-evidence based expensive add-ons — has a values problem.

I never went into medicine for the elite clinic. I went into it for the opposite reason. I wanted this for everyone, especially for the ones who couldn’t pay.

Here’s what I believe: longevity medicine is not a luxury product. It is what good primary care should be. And what we need to build back toward.

What Longevity Medicine Is

There are some really interesting emerging interventions — rapamycin, senolytic therapies, NAD+ precursors — that may prove important. I follow this research closely. But the evidence is early, and most aren't ready for routine clinical use. But a good physician will watch this space with you, and integrate what becomes validated as the science matures.

And if we strip away the marketing and the biological age clocks, the millions spent on annual protocols, the aggressive supplement stacks, what you find at the core of longevity medicine is pretty ordinary.

It is a physician who knows your full picture. Who has a longitudinal view of your health — where you’ve been, where you’re headed, and what we can do now while the trajectory is still highly modifiable.

Who identifies metabolic dysfunction early. Who considers your hormonal health in your 30s and 40s as a cardiovascular and cognitive issue, not just a quality-of-life issue. Who asks about your sleep, and follows up when the answer is bad. Who thinks about nutrition as a clinical variable, not a lifestyle suggestion. Who looks at your ApoB and Lp(a) alongside your LDL, and knows what to do when they’re elevated. Who thinks about your muscle mass as a metabolic organ and prescribes resistance training accordingly. Who knows your VO2 max because cardiorespiratory fitness predicts longevity better than almost any biomarker we have.

And who asks about your purpose, your stress, what’s actually going on in your life.

That physician exists. They are called a primary care doctor. They just need the time to practice this way.

The failure is that this kind of care — which every patient deserves — has become financially accessible only to a small fraction of the population. And the system that should be delivering it has been compressed into fifteen-minute appointments, leaving almost no room for the kind of thinking longevity medicine requires.

And in that gap, something has grown: direct-to-consumer testing, longevity influencers, n=1 self-experimentation documented publicly. The information is available, but biomarkers need context. An Lp(a) of 150 means something very different in a 35-year-old with no family history than in a 52-year-old woman entering perimenopause with a father who had a bypass at 58. The practice of medicine is a judgment applied to a specific person in a specific context.

Your PCP is Already a Longevity Doctor

Your primary care physician is not unaware of longevity medicine. Most of us went into primary care specifically because we wanted to do this kind of work: to know patients over time, to be proactive about prevention, to catch things early and change trajectories, to help people live their longest and best lives.

To be fair — practicing this way requires training and curiosity that the current medical education system doesn't currently produce. Not every PCP is a longevity doctor yet. But the knowledge is learnable, and the framework is available.

In a fifteen-minute appointment, in the current system, your PCP is expected to address your presenting complaint, review your medications, update your preventive care, manage your chronic conditions, think about your family history, your hormonal picture, your supplements, your fatigue, your sleep quality, and how to improve your cardiovascular risk. And document everything in an electronic medical record.

The math does not work.

What patients are paying for at a five-figure longevity clinic is not secret knowledge. It is not access to treatments unavailable elsewhere. It is time. And, it is continuity. The same physician, who knows your history, watching your trajectory over years. That longitudinal relationship is itself a clinical intervention.

Primary Care Should be the Future of Longevity Medicine

I want to believe that the future of longevity medicine is not more exclusive clinics. It is primary care, practiced the way it was always meant to be practiced — with smaller panels, more time, continuity, and a clinical framework oriented toward prevention.

The physicians leaving traditional practice to build DPC and concierge models are trying to reclaim primary care. And the patients seeking out longevity clinics are recognizing, correctly, that their long-term health deserves more than fifteen minutes, and they are paying for it because the system has given them no other option.

The goal should be to make that option available to everyone.

We're not there yet. But while the system catches up, here's what you can ask for today.

What You Can Ask For Right Now

The tests matter, but what matters more is the clinical thinking around them. You want a physician who uses these tools as part of a longitudinal relationship — who knows what to do when results come back, and who thinks about your health as a trajectory rather than a snapshot.

That said, knowing what to ask for gives you a starting point. Here is some of what is available in primary care today, without a concierge membership.

On cardiovascular risk: A standard lipid panel is not enough. ApoB is more informative than LDL. Lp(a) — one of the most common inherited cardiovascular risk factors, affecting one in five people — should be measured at least once in every adult. A coronary calcium score, if you have family history or elevated risk markers, gives you a direct look at subclinical atherosclerosis years before a cardiac event.

On metabolic health and fitness: Fasting insulin alongside glucose reveals dysfunction years before A1c becomes abnormal. hs-CRP reflects inflammatory burden. VO2 max should be treated as a vital sign. Cardiorespiratory fitness is one of the strongest mortality predictors we have — stronger than most biomarkers we routinely measure. Your wearable gives a reasonable estimate, and your physician should be asking about it.

On sleep: Not just hours, but quality, continuity, restoration. Unrefreshing sleep, frequent waking, and daytime fatigue that sleep doesn’t fix deserve formal evaluation, including screening for sleep apnea.

On hormonal health in your 40s and 50s: Especially through perimenopause and menopause. This conversation should include cardiovascular risk, bone density, and hormone therapy.

On exercise: Not as a lifestyle suggestion but as a prescription. Resistance training and cardiorespiratory fitness targets for your specific age and health status. The data on muscle mass and VO2 max as longevity predictors is stronger than most pharmaceuticals we prescribe.

On purpose and meaning: A physician practicing longitudinal primary care should know whether you are thriving or just functioning. Whether you have something to look forward to. Whether the stress you're under is acute or chronic. The research on purpose, social connection, and meaning as longevity variables is as good as most of the biomarker data. It belongs in the clinical conversation.

None of this requires a concierge membership. It requires a physician with the time and framework to think about your health as a trajectory — and a patient who knows enough to ask.

The Bottom Line

Longevity medicine is not a luxury product that only the wealthy deserve.

At its best it is attentive, longitudinal, prevention-oriented primary care — practiced with enough time and curiosity to actually think. The knowledge exists. The tests exist. The evidence exists. What is missing is the system that makes it accessible to everyone, not just those who can afford to pay outside of it.

I think about the patient I mentioned at the beginning. Three years of monthly video visits. Bypass surgery, diabetes, COPD. Also: 50 pounds lost, smoking stopped, diabetes reversed. No concierge membership. No five-figure fee. Just a physician with enough time and enough continuity to actually practice this way.

That is longevity medicine and it was billed as primary care.

Primary care physicians are already longevity doctors. We just need the conditions to practice that way. And patients deserve to know that the medicine they’re being sold at a premium is the same medicine their primary care physician would gladly provide, if the system gave them the time to do it.

This is a practice, not a product. It’s something you build over years, with a physician who knows you, returning to it again and again as your body and your life change.

I always felt like I had something of my mother and maternal grandmother that was hard to put into words. An energy. A drive. Something deeper.

I think I figured out what it is.

Mitochondria.

Every cell in your body contains mitochondria. These are the small structures responsible for producing the energy that powers everything you do. Your heartbeat. Your brain and thoughts. Your movement. And unlike almost everything else in your biology, your mitochondria didn’t come from both of your parents.

They come from your mother. Who got hers from her mother. Who got hers from hers.

An unbroken maternal line, stretching back further than any of us can trace. When I think about the energy I feel in my body — the drive, the capacity, the something I could never name — I now think of it as a living inheritance. Passed generation to generation from women. And carried forward in every cell.

I find that beautiful.

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The Biology — an Unbroken Line

Mitochondria have their own separate DNA, and it’s completely different from the nuclear DNA you inherit from both parents.

Your nuclear DNA contains roughly 20,000 genes inherited from both your mother and father, shuffling and recombining with every generation.

Your mitochondrial DNA contains just 37 genes. It lives outside the nucleus, replicates independently, and passes essentially unchanged from mother to child. It accumulates rare, small mutations over thousands of years. Your mitochondria connect you to your mother. To her mother. To hers. And on.

Those slow mutations create haplogroups that are associated with different VO2 max capacity, different oxidative stress responses, different disease risks. Your maternal inheritance influences how your mitochondria actually function.

The biohacking world treats mitochondria as a problem to optimize. But I think it’s important we remember we are carrying something that has been selected, refined, and passed forward across generations of human survival.

What Mitochondria Actually Are

Mitochondria are often called the powerhouses of the cell, and that is accurate but I also think it undersells them. They also regulate how cells age, how they respond to stress, and when they die. Mitochondrial dysfunction is implicated in cardiovascular disease, metabolic disease, neurodegeneration, and emerging evidence links mitochondrial function to fertility.

Two places in the human body stand out for their massive mitochondrial load: the heart muscle, which has the highest mitochondrial density of any organ, and the egg cell, which contains many more mitochondria than any other cell in the human body.

It’s interesting when you think about it. The heart is the organ that constantly beats to keep you alive, and the ovaries that carry the eggs that carry your children. Evolution decided these two things needed more mitochondria than anything else.

The Ovarian Connection Nobody Talks About

A mature human egg contains between 100,000 and 600,000 mitochondria. A heart cell (with huge energy demands) contains around 5,000 to 8,000. Most other cells contain just a few hundred to a few thousand. The egg is the most mitochondria-rich cell in the human body, by a lot.

This matters because mitochondrial function in eggs is linked to egg quality, fertilization success, embryo development, and reproductive aging. As women age, mitochondrial function in oocytes declines, thought to be one of the main mechanisms behind age-related fertility decline.

This also helps explain something many women notice but struggle to get answers about in perimenopause: the changes in energy, metabolism, cognition, and sleep. Mitochondrial function in the ovaries declines during the transition, and that decline is felt everywhere. The fatigue has a cellular explanation. We are not imagining it.

This is almost never discussed in primary care or really anywhere outside of reproductive medicine. But it connects directly to something every woman in her 30s and 40s should understand: mitochondrial health is reproductive health, and reproductive health is long-term metabolic health.

Mitochondrial Stewardship (Not Optimization)

There is a growing world of mitochondrial optimization — red light therapy panels, NAD+ IV infusions, expensive supplement stacks, elaborate morning protocols. NAD+ IV infusions run hundreds of dollars per session. Red light panels cost thousands. Elaborate longevity protocols can run tens of thousands annually.

The people promoting these interventions have actually done something helpful: they’ve brought mitochondrial health into the conversation and made people care about cellular biology in a way medicine has largely failed to do.

But I think they’ve missed something important about what mitochondria actually are.

These are not broken systems waiting to be upgraded. They are an ancient inheritance, passed forward through every mother who ever lived. They have been supporting us, generation after generation, through ice ages and famine and migration and childbirth. They don’t need to be hacked. They need to be respected. And the most powerful interventions are free.

Respecting them looks like giving them what they have always needed to do their work: sustained movement, deep sleep, stable blood sugar, clean air, real food, connection.

The supplements and interventions are interesting and some may prove important. But they are at the margins of a foundation that exercise, sleep, and metabolic health have already built — or not. You cannot supplement your way past a sedentary lifestyle and disrupted sleep.

Your Mitochondria Respond to How You Live

You can’t change the mitochondrial DNA your mother gave you — that’s your inheritance, and it’s yours permanently. But you can help them do their best work — by influencing the number of mitochondria in your cells, their efficiency, and how well your body maintains them. That is all responsive to your daily choices.

The evidence on mitochondrial health is pretty clear, and here is what drives it:

Exercise: especially sustained aerobic exercise. Low to moderate intensity aerobic exercise, sustained over time, is among the most powerful stimuli for mitochondrial biogenesis, which is the creation of new mitochondria. Resistance training matters too, particularly for preserving mitochondrial function in muscle as we age. This applies to the ovaries too.

Sleep. Mitochondrial repair happens during sleep. Chronic sleep deprivation impairs mitochondrial function and accelerates the kind of oxidative stress that damages mitochondrial DNA. Sleep deprivation has been shown to cause mitochondrial dysfunction and oxidative stress directly in oocytes.

Blood sugar stability. Chronic glucose dysregulation generates oxidative stress that damages mitochondria. Keeping fasting insulin low and avoiding the blood sugar spikes that drive inflammation is mitochondrial medicine practiced every day, at every meal.

Not smoking. Cigarette smoke directly damages mitochondrial DNA. This is one of the most well-established mechanisms of smoking-related disease.

Limiting alcohol. Alcohol impairs mitochondrial function in a dose-dependent way. In the ovaries, alcohol use is associated with reduced egg quality and quantity.

That’s most of it. It doesn’t require a membership or a panel or a morning routine filmed for social media.

What the Biohackers Are Actually Talking About

Some of what’s out there in the mitochondrial optimization world is actually pretty interesting science and something to keep an eye on.

CoQ10. Coenzyme Q10 plays a direct role in mitochondrial energy production. We know statins deplete CoQ10 and people on statins may benefit from supplementation. Outside of that, the evidence for routine supplementation in healthy people is modest. But the fertility story is more interesting. CoQ10 levels in oocytes decline with age, and a 2024 systematic review of six randomized controlled trials found that CoQ10 supplementation in women with diminished ovarian reserve improved oocyte quality, fertilization rates, and embryo quality before IVF. For women navigating reproductive aging or fertility treatment, this is one of the more evidence-based mitochondrial supplements we have.

NAD+ precursors (NMN and NR). NAD+ is important for mitochondrial function. The precursor supplements: nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR), have plausible mechanisms and some real research behind them. Human trial data is still early and effect sizes modest. A recent study shows blood levels may not fall with age like we thought, though some studies do show tissue-level decline in muscle and brain. I think this is a space worth watching, though not ready for routine clinical recommendation.

Urolithin A. Urolithin A supports mitophagy, the process by which cells clear out damaged mitochondria and replace them with healthier ones. Urolithin A is produced naturally when gut bacteria, particularly Akkermansia muciniphila and Lactobacillus species, metabolize pomegranates, walnuts, and berries. Research suggests up to 60% of Americans may not have the gut microbiome composition to produce it effectively, which supports the argument for the supplement form. Worth watching.

Red light therapy. There is a plausible mechanism — it can influence mitochondrial function at the cellular level. The clinical evidence is thin and inconsistent. Not yet sure the evidence justifies the investment for most people.

Methylene blue, hyperbaric oxygen, elaborate IV protocols. Very early, very limited. Not ready. Not recommended.

Some of these may prove important as the science matures. But they are working at the margins of a foundation that exercise, sleep, and metabolic health have already built, or not.

I think the biohacking world has inverted the hierarchy, optimizing the 5% while underselling the 95%.

Your Maternal Inheritance

I think about the maternal line. How mothers pass something forward. Not just in memory or personality or the shape of a face. But in the mitochondria that power every heartbeat I have, that powered every egg I carried my children in, that my children now carry forward themselves.

The biohacking world wants to sell you back something that was given to you by the women who came before you. Something you can protect with the same boring but powerful things your grandmother probably already knew.

My grandmother had five kids, a full social life, tons of friends, played tennis, and laughed a lot. She moved her body not because anyone told her to, but because that's just how she lived. She wasn't optimizing anything. She didn't have a protocol. She probably got some things wrong. But she moved her body, she laughed, she loved her people. Turns out that's most of it.

Sleep. Move. Eat well. Don’t smoke.

Honor what was passed to you. And pass something good forward.

The Bottom Line

Your mitochondria came from your mother. Who got hers from her mother. Who got hers from hers. The most powerful thing you can do with that inheritance is also the simplest: protect it.

The science is real. The interventions are real. But they are not new, and they are not expensive, and they did not require anyone to discover them. The women who came before you already knew. They just called it living well.

My father told me a story recently that I keep thinking about.

He was at his "Medicare Wellness Visit” with his primary care physician. Blood pressure, labs, the usual. At some point in the visit, his doctor looked at him and asked: do you have a purpose in life?

My father paused. Not because he didn’t have an answer (he did), but because he’d never been asked that question in a medical setting before. In decades of annual exams, nobody had thought to ask it. And yet when his doctor asked him, it felt, he said, like the most important question of the whole appointment.

It wasn't on the standard questionnaire. His doctor just asked.

I’ve been thinking about why that is. I think that question represents something that most of medicine has slowly abandoned: the idea that a person’s sense of meaning is a clinical one. That it belongs in the exam room alongside blood pressure and cholesterol. That it is, in fact, a longevity metric.

Because the evidence says it is.

We spend a lot of time in medicine asking about what you eat, how much you exercise, and whether you sleep enough. We rarely ask why you want to be here for the long haul. But that question may matter just as much.

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What the research actually shows

The relationship between purpose and longevity is not soft science or wishful thinking.

A 2019 study published in JAMA Network Open followed nearly 7,000 adults over age 50 and found that those with the lowest sense of life purpose were more likely to die during the follow-up period than those with the highest, even after controlling for health status, demographics, and health behaviors.

The Japanese have a word for this: ikigai — roughly translated as the reason you wake up in the morning. Nowhere has it been more associated with longevity than Okinawa. Research on Blue Zones populations consistently identifies a strong sense of purpose as one of the common denominators among centenarians. Interestingly, Okinawa has no word for retirement. The concept of an abrupt end to purposeful contribution doesn’t exist there.

Purpose is also associated with lower rates of Alzheimer’s disease, reduced stroke risk, better metabolic health, healthier sleep, and greater physical function in older adults. It seems to work through multiple biological pathways simultaneously: reducing chronic inflammation, supporting cortisol regulation, promoting health behaviors, and buffering the physiological impact of stress.

The best part: purpose in life is not a personality trait you either have or don’t. It is a modifiable risk factor. And it belongs in the same conversation as blood pressure and cholesterol.

Why doctors rarely ask the question

There are obvious reasons. The fifteen-minute appointment doesn’t leave a lot of room for existential questions. The electronic health record doesn’t have a field for ikigai. Purpose is hard to quantify, and medicine is increasingly organized around what can be measured, billed, and documented.

There is also, I think, a subtler reason. Medicine has become very good at treating disease, and less comfortable with the fuller question of what makes a life worth living. We are trained to identify pathology, not to explore meaning. And so we ask about symptoms and skip the question that might tell us the most about a patient’s actual trajectory.

My father’s doctor asked it anyway. And it didn’t feel like an intrusion, rather, it was one of the most humanizing moments he’d had in a clinical setting.

A physician with fifteen minutes cannot ask this question. A physician with time can, and that gap is worth closing.

What ‘purpose’ actually means, and what it doesn’t

The word “purpose” can sound grand in a way that makes people feel they are failing if they don’t have an answer that involves changing the world.

It doesn’t have to be that. Purpose, in the research, is defined broadly: a self-organizing life aim that provides a sense of direction. It can be creative work, faith, family, community, craft, mentorship, advocacy, or service. It can be tending a garden that your grandchildren will grow up in. It can be the research you’ve dedicated your career to, or the neighborhood you’re trying to improve, or the friendships you maintain with intention.

The specific form it takes is deeply personal. It’s different for everyone. Having something that organizes your attention, that pulls you forward, that makes getting up in the morning feel like more than maintenance — that is what predicts the outcomes.

What it is not: a to-do list or a career goal. Those things can serve purpose but they are not the same as it. A lot of high-achieving people in their 40s and 50s mistake busyness for meaning, and then discover the difference when the busyness stops.

How having a purpose works in the body

Purpose is actually biologically active. Here is what the research suggests is happening:

• Inflammation. Higher purpose in life is associated with lower levels of inflammatory markers, including IL-6 and CRP. Chronic low-grade inflammation is one of the central drivers of accelerated aging. Purpose appears to dampen it, possibly through its effects on cortisol regulation.

• Health behaviors. People with a strong sense of purpose sleep better, exercise more consistently, use preventive health services at higher rates, and are more likely to follow through on medical recommendations. Purpose is, in part, what makes other healthy behaviors sustainable over time — it provides the why that makes the habits stick.

• Stress response. Purpose acts as a buffer against the physiological impact of acute and chronic stress. It doesn’t eliminate stress, but it changes how the body responds to it. People with high purpose show faster cortisol recovery after stressors.

• Cognitive resilience. A sense of purpose is associated with reduced risk of Alzheimer’s disease and slower cognitive decline in aging adults, independent of baseline cognitive status. One proposed mechanism is that purpose promotes neural reserve — the richness of cognitive engagement that protects against neurodegeneration.

• Cardiovascular protection. Purpose is independently associated with reduced cardiovascular events, lower rates of stroke, and lower all-cause cardiovascular mortality. The mechanism is likely related to reduced inflammation, better blood pressure regulation, and the downstream effects of more consistent health behaviors.

Why this question matters, especially in midlife

This conversation tends to surface in people’s 40s and 50s. Midlife is often when the structures that provided meaning by default — building a career, raising young children, establishing a home — begin to shift.

People who have organized their sense of purpose around those external structures sometimes find themselves, for the first time, uncertain about what they are here for.

This is a moment worth taking seriously. The research suggests that purpose levels in midlife are particularly predictive of health outcomes in later decades. This is a time when the question has a lot of leverage.

Do you have a purpose?

The answer may not come easily. If it does, that’s worth appreciating. Many people have more purpose than they give themselves credit for. It just doesn’t feel dramatic enough to call a purpose.

Showing up consistently for the people you love is a purpose. Building something that will outlast you is a purpose. Practicing a craft with intention across decades is a purpose.

If the answer doesn’t come easily, here are the questions that tend to open things up:

• What do you want to have contributed by the time you are 80?

• Who needs you in a way that only you can fill?

• What are you doing when time disappears?

• What would you do if the outcome didn’t depend on recognition or reward?

• What problems in the world make you feel called rather than just concerned?

Purpose is often developed gradually. What matters is that you are asking. And that someone in your life, ideally including your physician, thinks it’s worth asking too.

It’s okay for your answer to change. It probably will.

My father’s answer was immediate. To help others, care for his family, write books that matter, give talks that inspire. He didn't hesitate for a second.

When I ask myself the same question, my answer has two parts. The first is close to home: a happy family and kids who feel loved. The second is to practice medicine in a way that actually sees people.

Neither of those answers would win a TED talk. Both of them are real. And I think that’s exactly the point.

Purpose is a practice. Not something you arrive at once and carry forever, but something you return to, tend to, and let evolve.

One of my healthiest patients in her 80s would say she has never “exercised.”

She walks every morning. She gardens. She takes the stairs. She plays with her grandchildren.

She is one of the healthiest people I know. And she laughs at the idea that she “exercises.”

What she does instead is move. Constantly, naturally, as part of how she lives.

It turns out that might be more important than anything she could do in a gym.

Because the fact is: an hour at the gym will not undo eight hours of sitting. The body responds to how it is used throughout the entire day — not just the hour we set aside for it. We’ve confused exercise with movement.

We Confused Exercise With Movement

We’ve separated movement from life, and called the separated piece exercise. We built gyms. We designed classes. We scheduled workouts. We created a domain of physical activity that was intentional, structured, and contained. It became something you did for an hour, then stopped.

We forgot that for most of human history, movement was not a separate activity. It was woven into everything. Walking between places. Carrying things. Squatting, climbing, lifting, working with the body. The body was in motion because life required it.

Modern life has removed almost all of that. We sit in cars, at desks, on sofas. We have engineered movement out of daily life… delivery services, remote work, drive-throughs, elevators.

And then we think an hour at the gym might compensate.

It doesn’t. The body evolved for regular movement. It was not designed for prolonged stillness interrupted by occasional intensity.

The research on sedentary behavior has made this increasingly clear: prolonged inactivity has its own metabolic consequences, independent of whether you exercised that morning. The body responds to how it is used throughout the day, not just to the hour you set aside for it.

But Exercise Still Matters

Exercise is also important, but is a different practice. Structured workouts, like lifting weights, running, a workout class, do things that regular movement cannot fully replicate.

They build cardiovascular fitness, strengthen muscle, and do something for mental health that a walk to the mailbox doesn’t. The intensity, the completion, the feeling of having pushed through something difficult. This is its own practice with its own returns, and it matters a lot.

What this post is about is simpler: exercise shouldn’t be the only movement in your day. It should add to a life already full of physical activity. For most of us, that foundation has been removed, and an hour at the gym cannot fully replace what we lost.

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Your Body Needs Frequent Signals

I think about it this way: the body is not a battery you charge with exercise and then spend down through the day. The body is a system that responds to repeated inputs, all day long.

Movement throughout the day does things that a single workout cannot. It keeps metabolism active between meals. It supports circulation and lymphatic flow. It lubricates joints and maintains range of motion. It regulates blood sugar. It supports mood and cognition. A ten-minute walk after a meal measurably blunts the glucose spike, and is one of the simplest metabolic interventions available.

The body needs regular reminders that it’s alive.

This is why the small regular movements that modern life has removed matter so much. The walk to the store instead of the drive. The stairs instead of the elevator. The standing during the phone call. The trip to a colleague’s office instead of the slack message. These are regular signals for your body.

The cumulative effect of those signals — across a day, a year, a decade — is what the body is built on.

One of the Biggest Longevity Mistakes We Make

This is a common pattern I see in practice: a patient in their fifties comes to see me with stiffness, fatigue, and some low-grade mild chronic pain. They brush it off as “aging” and often, by the time they mention it to me, they’ve started thinking of it as inevitable.

Sometimes it is aging. But often, it is adapting to inactivity. The body is very good at becoming what it is asked to be. Ask it to sit most of the day and it will adapt. That means muscles will shorten, joints will stiffen, metabolism will slow, circulation will become less efficient, and energy will become harder to generate and sustain.

Sometimes what we think is “aging” is actually the body adapting to being underused.

Modern life makes regular activity almost structurally impossible. The stiffness that comes from sitting too much can be improved by moving more. The fatigue that comes from a sedentary life often responds to the very thing that seems counterintuitive: more movement, not more rest.

Thinking about adaptation, rather than inevitable aging, is one of the most hopeful things I can offer a patient. Because it changes what is possible.

Movement Protects Muscle, and Muscle Protects Everything

Muscle is actually one of the body’s great survival systems.

Muscle is your metabolic reserve. It regulates blood sugar, supports hormone function, generates heat, and provides the fuel your body draws on when you’re sick, injured, or under stress. It supports your bones and your joints. It is what keeps you upright, stable, and capable of getting up off the floor.

We lose muscle with age, called sarcopenia, and the rate of loss increases significantly after fifty. But it doesn’t have to — this is strongly influenced by how much the muscles are asked to do.

The body tends to keep what it is asked to use.

Resistance training — lifting weights, bodyweight work, anything that loads your muscles against resistance, is one of the most important things most people over forty can do for their long-term health.

This doesn’t require a gym membership or a structured strength training program (though don’t get me wrong, those are valuable). It requires asking your muscles to work regularly: carrying groceries rather than using a cart, climbing hills rather than flat routes, getting up from the floor without using your hands, lifting your grandchildren or your kids, choosing the harder physical option when the easier one is available.

Cardiovascular Fitness Predicts Longevity

There is a number I think we should start treating as a vital sign, and it’s now more accessible than ever thanks to wearables: VO2 max.

VO2 max is the measure of cardiorespiratory fitness. It is your body’s capacity to use oxygen during sustained effort. It reflects the health of your heart, lungs, blood vessels, muscles, and mitochondria all at once. And it is one of the strongest predictors of longevity we have.

A large study found that low cardiorespiratory fitness (low VO2 max) was associated with a higher risk of death than hypertension, smoking, diabetes, or end-stage renal disease. The least fit patients had mortality rates 5 times higher than the most fit. This is one of the most striking results in the longevity literature.

What makes this hopeful: VO2 max is highly trainable. Even small improvements can make a big difference. You don’t need to become a competitive athlete, just become less sedentary.

VO2 max is now easily measurable. Garmin, Apple Watch, Whoop, Oura — these all estimate VO2 max from heart rate data during exercise. They aren’t perfect, but they’re good enough to track trends over time. I think we should be recording VO2 max estimates the way we record blood pressure — a routine vital sign that tells us something important about trajectory.

A high VO2 max is built over time through sustained cardiovascular effort. Walking briskly. Hiking. Cycling. Swimming. Tennis. We need to ask something of our cardiovascular system, regularly, across years.

The People Who Age Well Usually Keep Moving

In my primary care practice I’ve seen a pattern that no study fully captures.

The patients who age well, in the sense of remaining vital, engaged, and physically confident, are almost universally people who never stopped moving. It’s not necessarily the people who exercised intensely or trained seriously. But people who walked, who gardened, who played with their grandchildren, who took the stairs, who remained physically curious about what their bodies could do.

The eighty-year-olds I see playing tennis doubles on Tuesday mornings are not remarkable athletes, but they are remarkable in their consistency. They show up, week after week, year after year. They never told themselves they were too old to move.

They have a relationship with their body that is still active, instead of resigned. A sense that the body is still a participant in life, and not just a container for it. People who continue moving tend to stay connected to life itself.

The Goal Isn’t Optimization

You do not need to optimize your movement any more than you need to optimize your breathing.

You do not need a structured strength training program five days a week (though this is good). You do not need a standing desk, a walking pad, a continuous glucose monitor tracking your post-meal glucose response (though this can sometimes be useful).

What most people need is simpler and more available than any of that.

More movement woven into the ordinary day. Fewer hours of unbroken sitting. More willingness to choose the physical option when the convenient one is also available. A sport or activity that brings enough enjoyment to keep showing up. The best movement practice is always the one you actually do and actually enjoy.

Movement doesn’t need to be extreme to change your health trajectory. It needs to be consistent. It needs to be a daily practice.

What the Body Is Teaching Itself Right Now

Longevity is not built through isolated moments of discipline. It is built through patterns the body recognizes over years. Through regular signals of a life that keeps moving.

Through the ten thousand walks and the flights of stairs and the afternoons in the garden and the times you got up off the floor without thinking about it, because getting up off the floor was still something your body knew how to do.

The body is always adapting. Always becoming what it is asked to be.

The question is what we are teaching it to expect.

Let’s start with something most sleep content leaves out: There will be periods when you don’t sleep well. That is okay.

Grief. New parenthood. Sick kids. A difficult season at work. Perimenopause. Relationship stressors. A move. A diagnosis.

Life contains periods of disrupted sleep that are a normal response to being human.

What I want you to know is this: a few bad weeks do not undo years of good habits. The research on acute sleep deprivation is meaningfully different from the research on chronic deprivation. The body is more resilient than the optimization content often suggests.

What matters is not that you sleep perfectly, but that you return to the practice when the acute period passes.

My Sleep Story

There have been many periods in my life when I stopped sleeping well, and I know there will be more to come.

My sleep deprivation accumulated gradually. It started in my twenties with the stress of medical school. Then residency, working through the night, biking through San Francisco streets in the middle of the night to get to or from the hospital. Then new motherhood, and the interrupted nights that stretch into years.

Sleep became something that happened after everything else was done.

I noticed that my normal had become irritability, fogginess, and a feeling of being behind myself all day. When my sleep improved (gradually, intentionally, as a practice) almost everything else improved with it.

That is what this post is about.

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Before we get into the science, one thing I want to say upfront: if you are not sleeping well and you are not exercising consistently, the most impactful thing isn't a supplement or a sleep hygiene tip. It's to lift weights. I'll explain the science behind this later. I wanted to say it upfront because it surprises almost everyone and it's the most underused sleep intervention I know of.

Sleep Is Active Repair

We talk about sleep as if it is passive. Like the body simply powers down.

But sleep is actually an incredibly metabolically active state.

While you sleep, the brain clears metabolic waste through the glymphatic system. This is essential for long-term cognitive health. The body repairs tissue, consolidates memory, regulates hormones, resets the immune system, and processes emotional experience. Growth hormone, which is critical for muscle maintenance and metabolic health, is released primarily during deep sleep.

When we cut it short, chronically, we are interrupting a biological process that has no substitute and no way to fully catch up.

What Sleep Deprivation Does

The research on chronic sleep deprivation should make all of us take this more seriously.

Metabolically, even one week of five to six hours per night impairs insulin sensitivity, elevates cortisol, and disrupts the hormones that regulate hunger (ghrelin rises, leptin falls) making overeating a biological response to insufficient sleep.

Cardiovascularly, consistently sleeping less than six hours is associated with significantly higher rates of hypertension, heart attack, and stroke. A large study across multiple countries found short sleep duration linked to an increased risk of dying from coronary heart disease.

Cognitively, the amyloid plaques associated with Alzheimer’s accumulate faster in people who sleep poorly. Chronically disrupted sleep in midlife is one of the strongest modifiable risk factors for dementia we know of.

And mentally, poor sleep worsens anxiety and depression (and anxiety and depression worsen sleep). Improving sleep is one of the most reliable interventions for mood and emotional resilience available.

The Perimenopause Connection

For women in their 40s and 50s, sleep deserves a specific conversation.

Estrogen and progesterone both play significant roles in sleep architecture. Progesterone has a sedative effect and promotes deeper sleep. Estrogen helps regulate body temperature and REM sleep.

As these hormones fluctuate and decline through the perimenopause transition, sleep is often one of the first to go, through night sweats, early waking, difficulty falling back asleep, and a general lightening of sleep quality.

If you are a woman in your 40s or 50s and your sleep has changed, even subtly, this is worth discussing with a provider who understands the hormonal dimension.

What Your Sleep Tracker Is Actually Telling You

Most people with a sleep tracker look at their score and move on. Here’s what to pay attention to:

• Total sleep time. The target most adults need is 7 to 9 hours. Not time in bed, but time actually asleep.

• Deep sleep (slow wave sleep). This is where physical restoration happens. Growth hormone is released almost exclusively during deep sleep. Tissue repairs. The immune system resets. Most adults should be getting roughly 15 to 20 percent of their total sleep as deep sleep, so about one to one and a half hours for a seven to eight hour night. Alcohol or eating late are reliable destroyers of deep sleep.

• REM sleep. This is where emotional processing, memory consolidation, and creative thinking happen. REM is also where your brain processes the experiences of the day. Most adults need 20 to 25 percent of total sleep as REM, so roughly one and a half to two hours. REM is suppressed by alcohol, cannabis, and many sleep medications. It is also the first thing to recover when sleep improves, which is why people often report vivid dreaming when they start sleeping better.

• Sleep efficiency. Time asleep divided by time in bed. Above 85 percent is considered good. If yours is consistently lower, it suggests either trouble falling asleep, frequent waking, or spending too much time in bed awake.

• HRV during sleep. Heart rate variability during sleep is your nervous system’s recovery score. It reflects how well your body is restoring itself overnight. Consistently low HRV during sleep, especially if it’s trending downward over weeks, is often a signal of accumulated stress, poor recovery, or illness before symptoms appear.

Here's what I've learned from my own data, because personal observations are sometimes more convincing than statistics. Alcohol tanks my deep sleep every time. Even one glass drops my deep sleep percentage, raises my resting heart rate overnight, and lowers my HRV. Eating late has a similar but milder effect. Altitude is worth mentioning too. If you travel to altitude and your tracker scores tank, this is normal.

HRV during sleep tends to be higher in the follicular phase and lower in the luteal phase for women. In the week or two before your period, progesterone rises and then falls, and this reliably affects sleep quality for many women — lighter sleep, more waking, lower HRV. I see it in my own data every time. This isn’t really a sleep problem, but it’s a hormonal pattern worth knowing.

One important caveat: trackers are imperfect. Consumer devices are pretty good at distinguishing sleep stages, and it’s best to use them to look at trends over weeks and months rather than a single bad score.

The Exercise Connection We Don’t Talk About Enough

Exercise is one of the most powerful sleep interventions available.

• Resistance training and deep sleep. Lifting weights, bodyweight training, anything that challenges your muscles increases the proportion of deep sleep. If your deep sleep percentage is consistently low, adding or increasing resistance training is one of the first things I would suggest.

• Aerobic exercise and REM. Regular aerobic exercise is associated with reduced time to fall asleep and increased REM sleep. This builds over weeks of consistent training.

Exercise improves sleep, and better sleep improves exercise performance, recovery, and the motivation to keep training. This is one of the best cycles in all of longevity medicine… and also one of the worst when it breaks down. The person who stops exercising sleeps worse. The person who sleeps worse has less energy to exercise.

If you are not sleeping well and you are not exercising consistently, this is where I would start before anything else. Before the sleep supplements, before the blackout curtains, before the magnesium. Move your body consistently, and watch what happens to your nights.

On Sleep Meds and Supplements

On supplements: magnesium glycinate is the most evidence-based option worth trying. Melatonin works best for timing issues like jet lag, not as a nightly sedative. Alcohol feels like it helps but will damage sleep quality even at one to two drinks.

On prescriptions: traditional sleep medications (benzodiazepines like Ativan and Valium, and Z-drugs like Ambien and Lunesta) suppress deep sleep and REM, meaning you're unconscious but not fully restored. Long-term use is associated with dependence and cognitive decline. Trazodone is commonly prescribed off-label and is generally safer, though the evidence for sleep quality improvement is just okay. The newer orexin antagonists like Belsomra (suvorexant) and Dayvigo (lemborexant) are more targeted by blocking the wake-promoting signal rather than sedating the brain, and so may preserve sleep architecture better. These are worth discussing with your physician if you need pharmacological support.

CBT-I outperforms all of them for chronic insomnia — we should really be using this more.

Sleep as a Practice

Sleep content usually presents sleep as a problem to solve…. blue light blocking glasses, blackout curtains, the perfect sleep stack, the optimal bedroom temperature. These things can help, but I think the framing is wrong.

Sleep is a practice you build a relationship with. It’s a practice, not just on the nights when conditions are perfect, but on the ordinary nights, the difficult nights, the nights when your mind won’t settle.

I slept badly for years because I hadn’t yet decided that sleep was worth protecting. I now know that it’s a priority, and protecting it even before I feel finished for the day is good medicine. A good practice.

That shift, to sleep being foundational, is what changed things for me. It wasn’t a gadget or a supplement. It was a decision.

What the Practice Actually Looks Like

Sleep as a practice means building the conditions for sleep into the structure of your day, not just the hour before bed.

• Light and timing. Your circadian rhythm is set by light. Morning light exposure, even ten minutes outside within an hour of waking, sets your biological clock in ways that make falling asleep easier that evening. And evening light, including screens and overhead lighting, signals wakefulness at exactly the wrong time. This is one of the lowest-cost interventions available.

• Consistency. A consistent wake time, even on weekends, is a powerful sleep intervention most people are not doing. Your circadian rhythm depends on regularity. Sleeping in on weekends feels restorative but it’s actually not.

• Temperature. Core body temperature needs to drop to initiate sleep. A cool bedroom, around 65 to 68 degrees, helps this. A warm bath or shower an hour before bed also can help by pulling heat to the surface and then releasing it.

• The wind-down. Sleep begins in the hours before closing your eyes. The nervous system needs transition, from the activated state of the day to the settled state that sleep requires. Screens deserve special mention here. Because of blue light, but also because of the cognitive and emotional activation they produce right before bed. The content itself is often the problem, not just the light.

• Alcohol. Worth naming again: alcohol disrupts sleep architecture even when it feels like it helps you fall asleep.

• When sleep doesn’t come. The relationship with sleep matters here too. Lying in bed anxious can make sleep less likely. Getting up and doing something quiet until you feel sleepy again can be more effective than staying in bed willing sleep to come.

Sleep Makes Today Better

Most sleep content focuses on the long-term stakes, which are real and worth knowing, but what I think is more important: Sleep makes today better.

The meeting where you actually follow the thread of the conversation. The patience you have with your kids at the end of the day. The run that feels good instead of like survival. The emotional steadiness that lets you respond rather than react. The appetite that doesn’t require willpower to manage because the hormones are calibrated.

Sleep is the longevity practice that pays the fastest returns, and a lot of people still treat it as optional.

It is foundational. Everything else you do for your health works better with adequate sleep and worse without it. Exercise, nutrition, stress management, relationships — all of this is downstream of whether you are sleeping.

You don’t have to be perfect at it. You just have to return to the practice.

I still have bad weeks, and will have more in the future. But I return to it. That is the practice.

Something shifted in my clinic a few months ago.

I started using an AI scribe. This is a tool on my phone that listens to my patient visits and generates the clinical note in real time. I knew it would save me time. What I didn’t expect was what it would do to the quality of that time.

I can look at my patients now. Actually look at their face, their hands, the way they pause before answering a question. Instead of splitting my attention between the person in front of me and the screen beside me, I am just there.

But the change I didn’t anticipate was what happens between patients.

Before, I would immediately open the next chart, still mentally in the previous visit. My mind was never quite where my body was. There was no transition.

Now I close the chart with the note complete and often have a minute, sometimes a few. I can sit with what just happened before moving to what’s next. I can arrive at the next patient as my best self: curious, settled, actually ready.

I am someone who has been very bad at this. I have always moved from patient to patient, meeting to meeting, task to task. Multitasking, always mid-something, with no space between any of it. Feeling busy became my norm. It became my practice.

But the AI scribe helped me realize what I’d been missing. And once I noticed it in clinic, I started noticing its absence everywhere.

Always Mid-Something

I’ve been thinking about this in the context of the burnout conversation in medicine. We talk a lot about volume and having too many patients, too little time. We talk about administrative burden. Both are real.

I also wonder if part of what makes the current model so depleting is something subtler: the absence of space between.

When you move from patient to patient to documentation to inbox to patient again without a single moment of transition, something accumulates. It’s not tiredness. It’s a kind of fragmentation and the sense that you are never quite whole in any one moment because the last moment hasn’t finished and the next one has already started. You are always mid-thought, mid-feeling, mid-something.

Over time, I think it erodes the very things that drew most of us to medicine: the curiosity, the connection, the sense that this work means something. Those things need space to breathe.

What the Space Between Actually Is

The space between is not downtime. It is not inefficiency. It is not the absence of something useful and productive.

It is when things become possible.

It’s where a thought that was forming in the background finally has room to surface. It’s where curiosity gets to ask its question.

In medicine, the space between is where you notice the thing the patient didn’t say. Where empathy has a moment to catch up. Where a physician can remember that they are a human being caring for another human being, not just moving through a queue.

This is not only true in medicine. It is true in every life. And I think protecting it is one of the most underrated longevity practices we have.

Stillness and presence are what help make life feel rich rather than just full. And this richness of life is what the longevity practices are actually for.

We Have Engineered the Space Between Out of Existence

Our days now have minimal gaps. Phone to meeting to email to podcast to scroll to phone again. We fill every available moment. Silence feels like a problem to solve instead of a resource to protect.

For most of human history, transition was built into the structure of daily life… the walk between places, the wait without a screen, the meal without a notification. These were the moments in which the mind processed, integrated, and reset. We have replaced them with stimulation and called it productivity.

Research on the brain's default mode network (the system that activates during rest and mental quiet) shows that these unstructured moments are when the brain consolidates memory, processes emotion, and generates creative thought. Stillness is a different kind of work.

The Space Between as a Longevity Practice

Protecting the space between is a practice. It’s a practice that compounds over time in ways that matter for how we age.

Research confirms that regular periods of present-moment awareness consistently improve outcomes across chronic pain, stress, depression, sleep, and immune function. This is a daily longevity practice.

Periods of mental stillness are good for you. They are good for you today, and they are good for your future decades.

What This Looks Like in Practice

The space between doesn’t require an intensive meditation retreat or a digital detox. It is about the small, repeated decisions to not fill every moment.

It is the walk taken without headphones, just once this week. The few minutes between finishing one task and starting the next, spent looking out a window rather than at a screen. The meal eaten without a phone on the table. The transition between work and home life that is actually a transition.

It is also something worth asking of the systems we work within. The AI scribe in my clinic gave me back the space between patients… for now. But health systems, administrators, and employers are not always inclined to protect this for us. We need to actively resist the default toward filling the space between. We have to protect it and treat it like the resource it is.

I’ve been in recent meetings where the conversation has turned to productivity, and the idea that now that providers have AI scribes, we should have capacity for more. More patients, tighter schedules, greater outputs. I completely understand the business reality behind these conversations.

But I also find myself sitting in these meetings thinking: this is exactly how the space between gets taken away again. The efficiency gain gets absorbed back into volume, and the provider is still busy but with better software.

I want the space between to be treated as a clinical asset. Because a provider who arrives at each patient curious, settled, and actually present is not wasting time.

The Space Between Is Where You Live

Most of our life is made up of ordinary moments in ordinary days. It’s made up of the transitions between events. It’s made up of our quiet minutes.

How these moments feel, whether they are rushed or spacious, reactive or present, shapes everything including your relationships, your health, your capacity for joy and curiosity and connection.

I‘ll be honest… I’m still bad at this. The AI scribe gave me back some space between patients, but I still fill the space between everything else. I still pick up my phone in the transition between work and home. I still multitask when I could pause. I am practicing this imperfectly.

But that’s what a practice is. You don’t arrive. You just keep returning.

My AI scribe gave me back some of that space in clinic. It changed what my time feels like. And it reminded me of something I think I knew but had forgotten how to practice: The space between is not just time to fill between the things that matter.

The space between IS what matters.

I had a tough day in clinic last week, finding myself almost crying in the parking lot. Nothing bad happened. There was no bad outcome. There was no particularly hard diagnosis.

I simply ran out of time when my patients needed more of me. I felt the recognizable feeling… a massive and familiar overwhelm.

One patient needed to walk through years of lab trends, understand what they meant for her cardiovascular health, and feel heard in her anxiety about it. Another was frustrated (rightfully so) that she couldn’t get the appointment soon enough to adjust her medications and get her feeling like herself again.

Both deserved more, and both got a version of me watching the clock while trying to be fully present.

That tension is exhausting in a way that’s hard to describe.

This raised a question: If longevity is about the long game, building health over decades, then what happens when the physicians responsible for that long game can’t sustain it themselves?

The Model is Built on Volume, Not Value

The quiet crisis in primary care is structural. There is nothing personal about it. The current model runs on volume. It runs on fully booked panels, compressed visits, 15 minutes to address whatever walks through the door.

That works great for a straightforward ear infection. It doesn’t work for the complex, layered, emotionally nuanced conversations that actually move the needle on someone’s long-term health.

The result is a system where patients feel rushed and dismissed, and physicians feel like they’re practicing a diminished version of the medicine they trained for.

Primary care physicians are among the most affected by burnout. The drivers are consistently: excessive administrative burden, loss of autonomy, and the persistent feeling that there simply isn’t enough time to care for patients well.

Burnout Is a Predictable System Output

Burnout is the word we use, but it's not quite right. Burnout can imply that the physician ran out of fuel. What it actually feels like is being forced, repeatedly, to practice below your own standard of care. To know what your patient needs and be structurally prevented from providing it. Framing physician burnout as an individual resilience problem is inaccurate and harmful. This is not a personal failing.

Occupational burnout identifies six mismatches between worker and workplace that predict burnout: workload, control, reward, community, fairness, and values. Primary care, as currently structured, fails on nearly all six. Primary care providers see 20 to 25 patients a day, spend more time on documentation than direct care, and feel distressed when the system can’t provide what their patients actually need.

Most physicians I know don’t lose their passion. But they don’t have the conditions to make practicing with passion possible.

The Visits That Matter Most Get the Least Time

Here is the central paradox of primary care in the context of longevity medicine: the visits that matter most receive the least time.

Prevention, risk stratification, metabolic health, cardiovascular trends, mental wellness, and the slow work of helping a patient understand where their body is headed… these are not problems you solve in 15 minutes. They require continuity, time, trust, and real partnership built over years.

We know that comprehensive care is associated with lower costs and fewer hospitalizations. Comprehensiveness is good medicine, and it's also good economics. This comprehensiveness is what the volume-based model erodes, because rushed visits become single-issue visits, and single-issue visits reduce the ability to see the whole person. And seeing the whole person, over time, is exactly what primary care is for.

The Longevity of the Physician-Patient Relationship

We also know that seeing the same physician over time leads to better outcomes. Studies show that having this long-term relationship can actually help reduce hospital admissions and ER visits. So that relationship between PCP and patient itself is a clinical intervention.

But continuity requires something often not talked about in policy discussions: a physician who stays. The sustainability of primary care depends not only on training enough physicians, but maybe more importantly, on keeping them fulfilled and supported enough to stay in practice for a long time.

This is a longevity question.

What Fulfillment in Medicine Actually Requires

What does it take for a primary care physician to feel that their work is fulfilling, and sustainable over the long arc of a career? Luckily, it isn’t complicated.

Physicians thrive when they have real autonomy. Autonomy in clinical decision-making, but also in something more basic: control over their own time.

They thrive when they have enough time to actually be present with a patient.

When the work aligns with why they entered medicine in the first place.

When they feel competent in the deeper sense of being able to do the job as it deserves to be done.

When they feel connected, both to the patients they’re caring for and to the team around them.

And when there is still room to learn, to grow, to be curious.

These should be minimum requirements for practicing medicine well. Good medicine can’t happen without them. The therapeutic relationship that comes from knowing a patient over time depends on a physician who is present, motivated, and not simply surviving the day.

This is what makes the current model so quietly destructive. It harms physicians, but it also harms the quality of care provided.

The Models Getting It Right

Something is shifting. There are now many more models built around smaller patient panels, longer visits, and continuity. This is driven by physicians seeking a better way to practice, and also patients seeking something better. Direct primary care, concierge medicine, and hybrid models are growing because they are solving a problem for both physicians and patients.

In direct primary care, physicians typically carry panels of 400 to 600 patients rather than the conventional 2,000+. They have time to answer messages, review trends, coordinate care proactively, and know their patients as whole people.

These models are not a complete solution. The out-of-pocket costs create real access barriers, and the equity implications matter. But they are proof that the math can change. And when the math changes, so does the medicine.

AI and the Revival of Primary Care

For all the anxiety about AI replacing physicians, I think the more exciting story is this: AI may be one of the most powerful tools we have for giving primary care physicians their practice back.

The administrative burden on PCPs alone is staggering. We spend about twice as much time on documentation (inbox management, prior authorizations, administrative tasks, etc) than on patient care. AI is already beginning to change this. My AI scribe saves me significant time, and maybe most importantly, gives me presence with patients, and some mental breathing room as I move between patients.

AI can also summarize and integrate data. It can flag lab trends. It can draft a prior authorization. It can draft administrative messages to patients. This frees the physician to do what only a physician can do: think with the patient about their life, their values, and their health.

Of course, there is caution worth naming. AI that is deployed primarily to increase volume, to see more patients in the same amount of time, will not save primary care. This will accelerate the same broken model, just with better software.

The measure of success should be whether physicians feel more capable, more present, and more able to practice the kind of medicine that actually changes outcomes over the long run.

Used well, AI will not replace the relationship at the center of primary care, but will protect it. It will allow a physician and patient to sit together, without the clock as the third person in the room, and actually talk about where things are headed.

That is the version of AI in medicine worth building toward.

What This Moment In Primary Care Is Really About

The physicians leaving traditional practice aren’t giving up on medicine. Many of them are trying to save it by building something that restores the relationship at the center of it. Patients seeking out new models do it because they recognize that their long-term health deserves more than 15 minutes.

The future of primary care is smaller, slower, and more personal. It is a system where the physician can remain present, fulfilled, and effective for the full arc of a patient’s life.

If we are serious about longevity medicine and about changing the trajectory of chronic disease, cardiovascular risk, and healthspan, we have to be equally serious about the longevity of the physicians practicing it.