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This week Longevity Technology published an article, “Mind the gap: pregnancy, recovery and the aging clock: A new review argues postpartum recovery may shape lifelong aging.” I found the article very interesting because of three reasons, firstly I’m a longevity physician, secondly, I have a daughter, and thirdly I’ve lived through exactly what this paper describes. The core argument is that biological age rises measurably during pregnancy, and it’s supposed to fall again during recovery. What the paper then says, and this is the interesting provocation, is that incomplete postpartum recovery may leave a lasting biological imprint, particularly when pregnancies arrive in quick succession. What an interesting story and question to leave us thinking, that the gap that matters the most is not between contractions, it’s between who a woman was before pregnancy and whether she ever fully recovered and returned to her baseline.

So let’s discuss the science, and dive deeper into this interesting new claim. Biological age does rise during pregnancy, and this has been confirmed by DNA methylation clocks through routine blood tests and wearable derived measures across multiple independent groups. The 2023 paper in cell metabolism showed that biological age rises under physiological stress, things like surgery or severe infection, and pregnancy was one of them. The theory is that this elevation falls once the stress resolves. But having a baby isn’t as simple as getting over a cold. You have a whole other human to look after, to feed, to nurture, to monitor constantly and keeping this little one alive can be pretty exhausting, especially in the early stages.

It’s interesting to think that pregnancy raises biological age, but if you’ve ever had a somewhat less than perfect pregnancy, this claim wouldn’t seem so abstract. It begins for most with this constant hum of nausea in the head, frequent trips to the bathroom and often struggling to eat as nutritiously as you once did. Movement can be more challenging and feel more restrictive as you have a large organ growing and your abdomen. And as you approach the final stretch, sleep can be something that is so constantly broken and never feels refreshing. When you’re carrying quite heavy it can be uncomfortable and difficult to find a position where you can truly rest, not to mention the frequent bathroom breaks as you have a heavy baby pressing against your tiny bladder that can’t seem to hold much liquid through the night. Physiological changes that are noted are an increase in resting heart rate and respiratory rate as a metabolic alkalosis is created as part of pregnancy physiology, but it can leave you feeling a pretty wiped out.

When you think about all the changes the body goes through in pregnancy, it’s no wonder to think that it is a great strain and would increase biological ageing, but what the article really pinned down on is the recovery period hypothesis. The interval between delivery and the next conception was one of the main factors that determined how completely biological age returned to baseline. If the next pregnancy began before recovery was complete, the residual burden may then compound. This is still just a hypothesis with no falsifiable predictions, not proven yet, at least at scale, but mechanistically it is quite coherent and beginning to have some empirical support.

A longitudinal study followed 130 women for nearly four years and found that those who conceived again showed disrupted postpartum deceleration in Dunedin pace of ageing. An analysis of over 300,000 pregnancies found that around half of the routine laboratory markers took between three months and one year to return to baseline.

What was quite interesting is the factors that govern recovery speed. The most important one was BMI before pregnancy, if you were in the healthy range that was protective. Secondly, breastfeeding was associated with lower biological age estimates at three months postpartum. And finally, there’s sleep, the broken late nights, the domestic variables about who takes the 3:00 AM feed and the psychological stress of it all.

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Writing this takes me back to a difficult winter, four years ago, where I was working harder than I ever had. It was cold, and dark and my daughter was three months old. It was a time my body was in constant vigilance and had no time to process any thoughts, yet it may have been the very reason why I went into longevity medicine.

It is 2:00 a.m.

The alarm is gentle now. It has to be. I have learnt that if it startles me awake, it startles her too. The room is almost completely dark, I can just make out the outline of the bottle warming beside the bed and the breast pump still sitting on the floor from the last time I used it, I must have fallen asleep before putting it away.

I lift Layla carefully from her cot.

Please.

Just this once.

Please drink.

She keeps her eyes closed as I touch the teat against her lips, for a moment I think she’s going to take it, then, with the tiniest movement of her head, she turns away.

No.

Again.

I don’t panic yet, I’ve learnt not to panic after the first attempt. I wait another fifteen minutes.

At 2:15 I try again.

Then 2:30.

Then 2:45.

Every quarter of an hour the same ritual repeats itself; warm the bottle, lift her gently enough not to wake her fully, stroke her cheek with my index finger and touch the bottle to her lips. Hope. Then watch her refuse it, by now we have become experts in tricks.

She sleeps propped up on a foam wedge that once belonged to my husband’s grandfather when he had heart failure. My husband sometimes holds her tiny hands against her chest while I try to guide the bottle into her mouth before she realises it’s there, sometimes we rock her, we always feed her asleep, sometimes we whisper and sometimes we don’t speak at all, terrified that the slightest noise will ruin the attempt.

It’s now 6:00 in the morning and she still hasn’t fed; I’m beginning to grow more and more frightened. This isn’t the first time this has happened; it happens about three times a week where she goes twenty-four hours without milk. She’s even gone twenty-six hours before. I’ve packed the overnight hospital bag enough times that I no longer have to really think about it. I throw in a change of clothes for myself, some fresh baby grows for her, a phone charger and my toothbrush. The routine is as familiar as packing for a weekend away, except this is a trip that no parent ever wants to become good at preparing for.

I changed her nappy and found red crystals; these are urates and we keep finding them because her kidneys are dehydrated and they are under pressure. Her fontanelle has sunk, and she’s now feeling feverish. Her eyes are looking very different, not just a little less bright but truly fatigued. I don’t see these things as a mother, I see them as a doctor and that’s the problem, because I know exactly what dehydration does to a three-month-old baby. I know what can happen next and for the very first time in my career, all my medical knowledge feels completely useless.

This was one of the many frightening encounters we had in the postpartum period looking after a child with a severe feeding aversion. She began rejecting milk at six weeks old and once that happened any hope of sleep, healthy whole food meals or stress regulating activity for me went out of the door. I didn’t really know much about longevity medicine before then so I don’t know what my biological age estimate was at baseline. I know what it is now and I wonder how much of an imprint the first six months of her life were on me. As a longevity medicine physician, my life’s work is in building plans protect against severe cognitive stress, maintain an adequate amount of sleep, prioritise foods that nourish microbial diversity and lift and push and pull the body and muscles to stay fit and strong. But when something like this happens, there is no plan or preparation that can keep you in line.

Medicine doesn’t currently screen for postpartum biological age recovery, there is no standard interval recommendation between pregnancies based on biological age data and the six week check is really about physical wound healing, not about systemic biological restoration. Women are told that they will feel tired after birth, but they’re not told that the sleep deprivation, stress, and breastfeeding are active variables of how fast their biological clock resets. They’re not told that conceiving before that reset is complete may compound the biological cost.

If you’re a mother and you’re reading this today, would you go back to your postpartum period and do anything differently? Would you prioritise the quick naps that you didn’t end up taking because you watched an episode on Netflix or would you take more care with meal planning and restart your personal training at an earlier date? Would you look back to having that very first child and look at it honestly, realistically, not through rose tinted longevity glasses and say but I just brought life into the world and that was my responsibility, not myself.

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References

1. Albright SM, Poganik JR. The postpartum recovery window as a determinant of maternal ageing. Trends in Endocrinology and Metabolism. 2026. doi:10.1016/j.tem.2026.09.002

2. Poganik JR, Zhang B, Baht GS, Tyshkovskiy A, Deik A, Kerepesi C, Yim SH, et al. Biological age is increased by stress and restored upon recovery. Cell Metabolism. 2023;35(5):807-820.e5. doi:10.1016/j.cmet.2023.03.015

3. [Authors TBC — iScience 2026, doi:10.1016/j.isci.2026.019218] Maternal biological aging from pregnancy through four years postpartum with disrupted recovery by subsequent pregnancy. iScience. 2026.

4. Bar A, Moran R, Mendelsohn-Cohen N, Korem Kohanim Y, Mayo A, Toledano Y, Alon U. Pregnancy and postpartum dynamics revealed by millions of lab tests. Science Advances. 2025;11(13):eadr7922. doi:10.1126/sciadv.adr7922

Recently, there has been a particular kind of surprise in medicine that is all over the news. A drug that was built for one purpose, tested, approved and prescribed for millions of people, now years into its life in the world, it is being looked at differently, and finding that the people who are taking it have an additional benefit that was never planned. This week MIT Technology published an article called “Weight-loss drugs show signs of slowing biological ageing, say drugmakers” which is a really fascinating topic in the longevity space at the moment. The GLP-1 drugs, semaglutide and tirzepatide were initially built to manage blood sugar, then they found a second life managing weight, and now, this October, their markers are quietly saying something larger: that the drugs may be slowing the body’s biological clock itself, not just its waistline.

So here is what the data is actually showing us. Novo Nordisk drew blood from just over ten thousand people, half on the drug, half on placebo, and ran it through what are called proteomic clocks, instruments that estimate biological age from the levels of specific proteins circulating in the blood rather than counting birthdays. Across tissues, the treated group’s biological age came out roughly two to three years younger than the placebo group’s. One clock, built specifically around proteins shed by the heart, showed a gap closer to four years. Eli Lilly ran a smaller study of its own, using epigenetic clocks instead, which read age off the chemical marks sitting on top of DNA, and these patterns are compared with those seen across large populations and used to estimate how old a tissue appears, or how closely its molecular profile resembles one associated with disease and death.

So what really is biological age and what are these clocks that we’re talking about? They are clocks but the actual word can somewhat mislead us as they don’t watch time passing in the way a normal clock on the wall does, they actually recognise patterns. I like to think about them as the nightly weather forecast just trained on the body, they’re able to detect pressure, movement and an approaching storm, but they’re not yet able to tell us with exact certainty what will happen to the person standing beneath the sky.

Scientists have applied proteomic clocks, which estimate biological age from proteins associated with organ function, frailty and disease and the observation we are now seeing is that semaglutide has managed to shift several of these signatures in a somewhat younger direction. It’s so interesting that the changes we are seeing are not fully explained by weight loss, or improved blood glucose, or even lower CRP which measures inflammation. Which leaves open the possibility that GLP-1 signalling is touching several connected systems all at once and communicating between systems microscopically in ways that we can’t even see.

Although very exciting, I still want a caution the ‘ring’ that we hear with every longevity headline nowadays. The first thing to remember is who ran the study, and this is not a criticism of the science itself but when a company that sells the drug, is also the company measuring the drug’s benefits, the finding deserves to be looked at with a little bit more rigour. Kevin Duffin, the Lilly scientist, was careful to call the reduction significant whilst warning against reading too much into it. The second thing to consider is the scientists behind the statements. Steve Hovarth, the biologist whose epigenetic clock was used for this work called the findings genuinely significant but then immediately qualified them he said the benefit was shown in people who were overweight or living with diabetes. So, these populations are the ones that the GLP-1 drugs were really doing clear helpful medical work. And Hovarth raised something that rarely makes headline version of the story, which is that the GLP-1 drugs carry a real risk of muscle loss alongside fat loss, and muscle loss itself is one of the better predictors of healthy ageing. So, a drug that turns back a clock while quietly eroding the tissue most associated with strength and resilience later in life is not obviously a very free win. Vadim Gladyshev, another leading voice in the ageing clock field, was asked if everybody should go on the drug then if the benefits were so universal? He responded by saying he’s not a physician so he wouldn’t be fit to give commentary on this.

So where does that leave us, honestly? I think, the biology is quite plausible and worth watching very closely as chronic inflammation and metabolic dysfunction sit at the centre of all the 12 hallmarks of ageing, so improving this would ultimately be expected to show some downstream benefit on biological age, perhaps the same way exercise or resolve diabetes would…hmm which one would be better?

And this question makes me think of several women I have treated, compressing her to one patient who I’ll call Mary. When Mary first came to see me, she didn’t ask to live to 100, she simply wanted to be able to walk up a flight of stairs, without calculating where she might need to stop. She wanted to wake up without the heavy, drugged feeling that followed her into the morning, the extreme exhaustion that sat next to her throughout her whole day. She wanted to sit in a restaurant without spending the entire meal negotiating with herself of whether she’d allow herself the bread and whether she really deserved the dessert, and quite frankly whether everyone else had noticed what she had chosen.

Her blood pressure had been rising for the past couple of years, and her glucose was beginning to drift, fat had gathered around her liver and abdomen and that’s the kind of fat that doesn’t just simply sit beneath the skin, but it behaves like an active endocrine organ releasing inflammatory signals into her blood. She had spent years being told by doctors to eat less and move more, as though the problem was a failure of her discipline rather than a physiology that had gradually become louder than her will. Eventually, a GLP -1 drug had become part of her treatment and months later the numbers had changed. Her glucose was steadier and her blood pressure was lower. She had lost the weight but that wasn’t the greatest win, what was remarkable is what she said, “I have started making plans again.”

Their moments in medicine when a laboratory result tells you less than a single ordinary sentence and this was one of the remarkable moments. Mary had not become younger, and time hadn’t simply reversed but her future had stopped narrowing. She began to age more slowly.

When discussing the GLP one’s and longevity as a whole, there is a wider story sitting behind this one. Eli Lilly has spent the last two years assembling something that looks less like a drug portfolio and more like an infrastructure for ageing itself. In September it struck a deal worth up to $2.75 billion within Insilico medicine, the same AI drug discovery company behind the pulmonary fibrosis trial. Lay on a few 100 million more in deals with companies like Fauna bio, hunting for metabolic targets beyond GLP- 1 entirely and a clearer picture forms. Lily is not simply defending its obesity franchise; it’s actually positioning itself to become as one as the first true longevity big pharma. Longevity Technology wrote about this earlier this week and the plans are astronomical.

What I’d actually tell a patient, and what I’ll tell you now, is this. If you are living with obesity or type 2 diabetes and a GLP-1 drug is already part of your care, there is genuine reason to think the metabolic benefit you’re getting runs deeper than the number on the scale, and that’s worth knowing, not as a reason to chase the drug for its own sake, but as one more piece of evidence that treating the underlying metabolic picture properly pays dividends across the whole body, including, it seems, at the level of your cells. If you are healthy and simply curious whether this is now a longevity drug for the general population, the honest answer is that nobody, including the two companies who would most like to tell you yes, actually knows yet. And if there’s a single thread worth carrying out of this essay, it’s the same one we started with all the way back at the Galapagos tortoise and its six heartbeats a minute: biology rarely hands us a single clean answer, and the companies with the clearest financial interest in a simple story are not always the ones best placed to tell it to us straight. That’s not a reason to stop paying attention, it’s the reason to keep reading carefully.

Articles for Reference:

https://longevity.technology/news/lilly-races-to-become-first-longevity-big-pharma/

https://www.technologyreview.com/2026/10/06/1145836/weight-loss-drugs-glp1-lilly-novo-aging-clocks

Did you know a Galapagos tortoise's heart beats about 6 times a minute? It’s slow, patient, and unhurried in the way that embodies everything about that animal. In contrast, a mouse’s heart flutters at close to 500 beats in that same 60 seconds; it’s a small frantic engine that never quite stops racing. Interestingly enough, the tortoise can live past 175 years, yet the mouse is lucky to see only two. Why is this?

For a while, this looked like more than a coincidence because if you collect heart rate and lifespan data across enough species, looking at mice and elephants and whales, a very interesting and strange pattern seems to emerge: if you multiply an animal’s average heart rate by its lifespan, you land somewhere close to a billion beats. So, the theory was quite interesting, and every animal seems to be issued the same allowance at birth, the difference being how quickly it spends its allowance, varying at different speeds. The tortoise rations its beats whilst the mouse burns through its budget in a very big hurry.

This concept is something that you can still apply to the patients in my clinic; those ones who have a resting heart rate of 100 have approximately double the annual risk of death compared to those sitting at a heart rate of 60. That number is real, and it does matter, but the theory of heartbeats and ageing doesn’t actually hold up as well as the data has illustrated it. This is because humans have been quite different from animals in their patterns and they’ve blown the theory apart as us homo sapiens, seem to have up to 3 billion heartbeats across an average lifespan, not the 1 billion allocated to other animals. The question arises: have humans out-engineered mortality, and effectively used technology to extend the lifespan to something that was not originally intended? Or is the theory just generally flawed at the core? Because the tighter you look at the tortoise and mouse comparison, the more tidy maths actually dissolves into something that doesn’t seem to hold up. And finally, the far more likely explanation for the human finding is that a high resting heart rate is usually a symptom of poor cardiovascular fitness, not merely a countdown clock ticking faster till the end. We all know the importance of cardiovascular fitness and all-cause mortality, so the fix isn’t just something found in a drug that slows your pulse; it’s the treadmill and the scheduled zone two training block.

It’s a shame, in a way, because the heartbeat theory is a lovely story, but biogerontology is a field littered with lovely stories that turned out to be wrong, or at best incomplete. For most of the twentieth century, theories of aging arrived one after another, each convinced it had found the single thread that, pulled hard enough, would unravel the whole process.

One of the more influential was the free radical theory. In 1954, an Argentine biochemist named Rebeca Gerschman, working at the University of Rochester, proposed that oxygen itself, or rather the unstable, reactive molecules it generates inside our cells, was slowly damaging us from within. The idea struggled to gain traction and then two years later, Denham Harman published a related theory that took the credit and the citations, though he was generous enough to acknowledge Gerschman’s work as the seed of his own. The theory eventually evolved into its modern form, focused specifically on damage generated inside our mitochondria, and it shaped decades of research and no small number of antioxidant supplements promising to mop up the damage before it accumulated. Most of those supplements, when tested properly, actually did nothing for human lifespan. But the theory was never entirely wrong, because oxidative damage is real and it does accumulate, but it simply wasn’t the whole story, and treating it as the whole story sent a great deal of research, and a great deal of money, down a path that led nowhere near a cure.

By the early 2000s, the field needed a different kind of ambition, and it found one in Aubrey de Grey, a biogerontologist who proposed a framework called Strategies for Engineered Negligible Senescence, or SENS. De Grey organized aging into seven categories of cellular damage and argued that if we could address all seven simultaneously, even imperfectly, we could buy enough time to develop better treatments before the damage caught up with us again. He has spoken of humans eventually living past a thousand years.

Then came along David Sinclair, a Harvard geneticist whose 2019 book Lifespan argued for something more unifying still: that aging is, at its root, a loss of epigenetic information, the cell’s instructions for which genes to switch on and off slowly becoming scrambled, like a CD that has been scratched one too many times. Sinclair’s own research has centered on sirtuins and NAD+, the molecules he believes help preserve that information, and his lab has shown that in animals, this information can, in principle, be restored. It’s a genuinely elegant idea, and also one that has outpaced what the evidence can currently support in humans, particularly once it reaches the version of the story sold in supplement form.

None of these theories, on their own, ever fully explained why we age. What they did, collectively, was force the field to stop hunting for one villain and start asking a better question: not what causes aging, but how many separate, overlapping processes are doing the damage, and whether there are few enough of them to name, study, and eventually treat. That is where the science has landed today, in a framework known as the hallmarks of aging, now numbering twelve.

And that is where we’re headed next.

I was recently interviewed for a Marie Claire piece on the blue zones, article found here, and it made me question something I hadn’t really thought about – something slightly uncomfortable. I often talk about the Blue Zones, with my patients in a consult or on a panel discussion and even often on my Instagram or other public facing commentary, yet the data behind some of these populations is a bit shaky. Knowing this, and being a scientist…why do I keep recommending the habits anyway?

So I want to break this down properly, let’s talk about what the Blue Zones are, what has gone wrong with the data and why I think the nine habits still survive the stories that make them famous. Why does the argument still hold, and why it really isn’t about the longevity villages at all but it is the one think, I have found, that determines whether any health advice will work.

Ready? Let’s dive in…

What are the Blue Zones

There are a handful of rural regions in the world where communities of people live extraordinarily long lives, and where we have the highest populations of centenarians. The concept is very much embedded into wellness culture and many people forget it began as a magazine story. Dan Buettner, who worked with demographers such as Michel Poulain, identified these special spots: Okinawa in Japan, Sardinia in Italy, Ikaria in Greece, Nicoya in Costa Rica, and Loma Linda in California.

From these places he distilled nine shared behaviours, the “power nine”:

1. Move naturally, through the shape of the day rather than the gym

2. Have a sense of purpose

3. Downshift, with daily rituals that lower stress

4. Eat to eighty percent fullness or “Hara Hachi Bu”

5. Eat mostly plants

6. Drink red wine, moderately and socially

7. Belong to a faith or community group

8. Put loved ones first

9. Choose the right tribe, meaning a social circle that supports healthy behaviour

It is an elegant list, and it’s origin story, is in serious trouble.

The data problem

In 2024, the demographer Saul Newman won an Ig Nobel Prize for a preprint arguing that the Blue Zones may be, in large part, an artefact of bad record-keeping, and his logic makes sense. Extreme old age is actually unusually hard to verify, especially in rural regions and the areas that report clusters of centenarians also happen to be the regions with poor bookkeeping: birth records, historical disruption, and financial incentives to keep a dead person on the books. For example, Okinawa’s records were substantially destroyed in the Second World War and, interestingly enough the cohorts born after the war, the ones with reliable records, seem to show markedly worse longevity outcomes than the generations before them. A little odd, right?

A similar pattern was seen in Nicoya, where the people born after 1930 seem to not have the same advantage in longevity and are worse off than their predecessors. If a place truly has a genuine culture that supports longevity and slow ageing, you really would expect the records to improve, would you not?

The next interesting point is one about Loma Linda; it’s been said that as the documentary was a National Geographic feature, there was a heavy suggestion of including a US location. Now this isn’t fraud, but it tells you something about how the map was drawn out. And finally, Newman’s paper still hasn’t passed peer review; it has actually been through nine rounds of review at the BMJ, which he attributes to resistance in the field, but his critics attribute it to the paper’s own weaknesses.

I am here, not to adjudicate the fight as the fight is the geography and the circles drawn on a map, yet the map was never the useful part. Here is why…

We are divided on data, not habits

This is the line I gave Marie Claire, and I stand by it: the scientific community is not really divided on the habits, it is divided on the data.

Almost every one of the power nine has an independent evidence base that has nothing to do with Sardinian shepherds. We knew that regular non-exercise movement lowers cardiometabolic risk before anyone counted centenarians in Ikaria and we knew that social isolation predicts mortality. We knew that chronic psychological stress is not merely unpleasant but biologically expensive. The Blue Zones did not discover these findings, they packaged them and presented them nicely in a well-fitting story.

So the honest position is this, the villages and their centenarians may or may not be real but the behaviours observed stand up perfectly well on their own evidence, with or without the story of the village.

Which raises the more interesting question. If we already had the evidence, why did the packaging matter so much?

The part nobody talks about: adherence

Here is the thing I have come to believe after years of watching patients try to change their lives.

In lifestyle medicine, the binding constraint is almost never knowledge, it truly is sustainability. We have known the broad strokes of what protects human health for decades: avoid alcohol and cigarettes, move more, sleep well, and eat your vegetables like your grandmother always used to tell you. Almost nobody fails because they were missing this information; they're missing the structure to do it consistently, day after day, and meal after meal.

They fail because the intervention required willpower to survive, and willpower is a depleting resource that competes with a job, a family, grief, travel, illness, and every ordinary Tuesday. This is precisely why each patient that comes to me asking for a “3-week detox” before going back to how they always live and eat will walk out of the consultation room rather disappointed. I work on building a longevity prescription for life, not for three weeks. And when we look at the long-term dietary intervention literature, the pattern is remarkably consistent. Initial effect, then drift, then attrition, then back to baseline. Not because the diets do not work while people follow them, but because following them is the hard part, and the trials that measure this honestly find that most people stop.

This is what makes the power nine different, and it is the reason I still teach them. They are not a regime but a set of environmental and structural defaults. In the populations they were drawn from, real or exaggerated, nobody was trying to walk ten thousand steps to hit their WHOOP goal, they lived somewhere with hills and no car, so they simply had no choice but to hit the target. Nobody was scheduling social connection; it was structurally unavoidable. Nobody was practising portion control, the plates were small and the food was slow.

These habits can be built into the architecture of life, without having to white-knuckle them through a strict regime. Given that most health advice fails because nobody can keep it up, that is not a minor feature, and it is something often overlooked by the most diligent of patients, but the structure that is repeatable is actually the whole solution.

Design beats discipline, no matter how heroic you are, you will eventually give up unless it’s built into your daily life and that is the actual lesson of the Blue Zones, and it survives even if every village turns out to be a clerical error.

Walking the nine, honestly

With that lens, here is how I would grade them.

Move naturally. Strong evidence, and structurally the easiest to install. Non-exercise activity across the day has independent cardiometabolic and mortality benefit, and it is also the one most easily destroyed by modern architecture: lifts, cars, deliveries, desk work. Rebuilding it means changing your environment, not your motivation.

Purpose. Better evidenced than most people assume. Cohort work in adults over fifty, including a well-cited 2019 analysis in JAMA Network Open, finds meaningfully lower all-cause mortality in those reporting a strong sense of life purpose, with the association holding after adjustment. The mechanism is likely a mix of behavioural, inflammatory, and stress-axis pathways. Purpose is not a soft habit; it is upstream of whether you really bother doing any of the others.

Downshift. Sound in principle, but vague in practice. The biology of chronic stress is not in dispute, and I have written elsewhere about how far it reaches into cardiovascular and metabolic function. What the Blue Zones framing does not give you is a perfect protocol, because one does not exist, it varies from person to persona and situation to situation. But the evidence supports having a reliable daily downshift ritual more than it supports any particular one.

Eat to eighty percent. Physiologically sensible, as satiety signalling lags ingestion by roughly twenty minutes, so stopping at the point of “no longer hungry” rather than “full” usually lands you at genuine sufficiency once the signal catches up. Human caloric restriction data is far weaker than the animal literature that made the idea famous, so I would not sell this as life extension. I would sell it as better post-meal energy and better glycaemic control, which is what people actually notice.

Plant slant. Correct in direction, but it is frequently misapplied. My caveat in the piece was this: we want to build a plant-forward plate, rather than just empty it of meat. Protein, B12, iron and vitamin D are all essential, and the requirement rises rather than falls with age, particularly after menopause. Remove animal foods without deliberately replacing what they carried, and you trade one longevity-related problem for another. I see the resulting iron deficiency and low protein intake in clinic constantly, usually in women who thought they were doing everything right.

Wine at five. This is the one that fails, I write this very unfortunately, as I do personally enjoy a nice glass of cabernet sauvignon. It is the single item on the list where the recommendation now runs against the evidence, and I want to be unambiguous about it. Alcohol is causally implicated in raised risk across more than two hundred conditions, including seven cancers. The old J-shaped curve suggesting a protective effect of light drinking has largely been dismantled by studies that separated lifelong abstainers from people who had stopped drinking because they were unwell. There is no dose that is protective, there are doses that are lower risk, and that is a different sentence.

If wine is doing something for you in the Blue Zones model, it is almost certainly the table it is being drunk at, not the liquid in the glass.

Belong, loved ones first, right tribe. I have grouped the last three because they are one habit wearing three coats, and collectively they are the most underrated on the list.

In the article I said that chronic loneliness carries a mortality risk roughly equivalent to smoking fifteen cigarettes a day. That figure is real and it comes from Julianne Holt-Lunstad’s meta-analytic work. That is an extraordinary finding and one worth pausing to think about for another few seconds.

What I would actually prescribe

Strip out the villages and the mythology and what remains is a design brief. Not nine things to try harder at but a small number of structural changes that make the right behaviour the path of least resistance.

Make movement the default, not the decision. Not a step target, but a commute that contains walking, and a phone call you take outdoors. The aim is that on your worst day, with zero motivation, you still move, because the alternative would require effort.

Fix the plate before you fix the diet. Protein first, plants by volume, and a deliberate answer to B12, iron and vitamin D if you are reducing animal foods. This is a shopping decision, made once a week, not a willpower decision made three times a day.

Give the downshift a fixed slot and a low bar. Ten minutes, same time daily, something you would still do while unwell or travelling. What matters to you is what is important here and the method that reduces your stress is the one that is built in here, not the one your sister-in-law does because of the latest podcast she heard. Reliability matters more than depth here.

Put connection in the calendar with the same status as work. The evidence says this belongs alongside diet and exercise as a primary health behaviour, not as a reward for finishing them. Recurring, not spontaneous, because spontaneous is the first thing a busy life deletes.

Drop the wine. Or keep the ritual and change the glass. Keep the table with the variety of vegetables and the people you love dearly.

And then the one that is not on the list, which is the honest disclaimer: none of this makes you a centenarian. The realistic promise of lifestyle medicine is compression of morbidity, more good years rather than simply more years, and better function inside the years you get. It is slowing down ageing and giving you more of the good years rather than extending the number of years on this planet indefinitely. That is a smaller promise than the Blue Zones has sold and it is also one I can defend.

Where this leaves me

I think the Blue Zones will not survive the next decade as a scientific claim but I think they will survive indefinitely as a cultural one, because they gave people something that evidence rarely provides: nine things that felt like a life rather than a protocol.

That is not nothing, because behaviour change runs on stories, and the story did more work than the data ever did.

You do not need Sardinia, you need a life shaped so that the healthy thing is the easy thing and that is the part worth keeping.

My comments appear in Marie Claire’s piece on living by the power nine, linked here.

References

• Marie Claire UK, I tried living by Blue Zone habits for a month: https://www.marieclaire.co.uk/health-fitness/wellbeing/blue-zone-habits-review

• STAT News (May 2026), Are blue zones real? New scrutiny of longevity hot spots: https://www.statnews.com/2026/05/04/are-blue-zones-real-new-scrutiny-longevity-hot-spots/

• Science, Do ‘blue zones’ rest on shaky science?: https://www.science.org/content/article/do-blue-zones-supposed-havens-longevity-rest-shaky-science

• UCL, on Saul Newman’s Ig Nobel Prize: https://www.ucl.ac.uk/ioe/news/2024/sep/ucl-demographers-work-debunking-blue-zone-regions-exceptional-lifespans-wins-ig-nobel-prize

• Blue Zones’ own response to the criticism: https://www.bluezones.com/fact-check-of-claims-blue-zones-research-validity/

• Holt-Lunstad et al., Social Relationships and Mortality Risk: A Meta-analytic Review, PLOS Medicine 2010: https://journals.plos.org/plosmedicine/article?id=10.1371%2Fjournal.pmed.1000316

• Holt-Lunstad on the accurate framing of the fifteen cigarettes comparison: https://www.julianneholtlunstad.com/15-cigarettes

• Alimujiang et al., Association Between Life Purpose and Mortality Among US Adults Older Than 50 Years, JAMA Network Open 2019: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2734064

A thirty eight year old woman sits across from me and she is tired. Not the kind of tired that resets itself after a long night of sleep, the kind that starts the day with exhaustion, she moves through the morning as though someone has quietly turned down the electricity inside her. Her voltage is low. The exhaustion seeps through the day, dimming every action and creating a feeling as though the world has lost some of its colour. Her hair is course to touch and it has lost its shine, its falling out more, she sees this as the brown clumps gather around the shower drain. Her jeans feel a lot tighter around the hips despite the fact she has reduced her calories and has been trying intermittent fasting and by three o’clock in the afternoon her thoughts have begun to move through something that feels like fog.

She has an excuse for the symptoms: Ageing. It happens right? You slow down with the responsibility of children, the pressure of work stress and perhaps her hormones are flatting out. Perhaps this simply happens to each woman they get into their later thirties.

Then her blood results come back and there it is: a raised TSH, a low thyroid hormone, and thyroid antibodies sitting quietly in the background. Suddenly the months, perhaps years, of feeling unlike herself are reduced to two words on a medical record: underactive thyroid.

But those two words do not really explain what has happened, they describe the end of the story, not always the beginning.

The metabolic house

The thyroid is tiny, it is butterfly-shaped, sits at the base of the neck and weighs less than an ounce, yet it helps set the pace at which almost every cell in the body works.

I think of it as the metabolic house of the body, it helps decide how quickly you turn food into energy, how warm you feel, how fast your heart beats, how your gut moves, how clearly you think, how regularly you menstruate and how easily you maintain muscle. When the thyroid signal slows, the whole house can begin to feel colder, darker and harder to run.

This is why thyroid health belongs within the conversation about slow ageing and by this I don’t mean thyroid medication is a new longevity hack, and perfect TSH will not somehow make you younger. But it matters because the same small gland reaches into nearly every system we are trying to preserve as we grow older: the heart, brain, bones, muscle and metabolism.

A thyroid problem is rarely experienced only in the thyroid, it is actually experienced in the life surrounding it; in the voltage of the electricity that runs the house of that particular body.

The problem may not begin in the thyroid

In many women, the most important question is not simply why the thyroid has slowed down, but what problem has happened within the immune system that has encouraged it to attack its own body.

Hashimoto’s is the most common cause of hypothyroidism in countries with adequate iodine. It is labelled as a thyroid disease, but biologically it is an autoimmune disease, the thyroid is the tissue merely just caught in the crossfire.

Your immune system has to perform a remarkable act of recognition every single day, it must decide what is you and what is not you. It must attack the virus that has invaded but spare the healthy lung tissue, it has to destroy the infected cell but leave the healthy tissue beside it alone. This ability to recognise the self and tolerate it is called immune tolerance.

In Hashimoto’s, that tolerance begins to fracture and the immune system makes antibodies against proteins within the thyroid and, over time, the gland may become less able to produce the hormone the rest of the body is waiting for.

So the thyroid becomes underactive, but the first disruption was not necessarily a lazy gland, it was actually a protective system that had become confused about what it was supposed to protect.

Women are particularly vulnerable to this confusion and around one woman in eight will develop a thyroid disorder during her lifetime, and Hashimoto’s is ten times more common in women than in men. The female immune system is generally more reactive and this can make it more effective in its response to many infections, but the same intensity comes with a greater vulnerability to autoimmune disease. Protection and misdirection can sit uncomfortably close together.

That does not mean every underactive thyroid is autoimmune, or that Hashimoto’s can be blamed on one food, one infection or one mysterious toxin, biology is rarely that obedient. Genetics, hormonal transitions, immune regulation and environmental exposures can all meet in the same person. The point is not to invent one perfect root cause but to try to understand that the thyroid result may be the final signal from a much wider system.

The prescription is essential, but it may not be the whole answer

Levothyroxine is the prescription medicine given to an underactive thyroid, and this is essential. I want to say this clearly because the wellness industry has strangely turned this into a moral argument and the rhetoric is that of you need to take the medication, you have failed to support your body naturally. And this couldn’t be further from the truth, yet it still doesn’t solve the whole story.

Levothyroxine replaces T4, the hormone an underactive thyroid can no longer make adequately. If your body cannot produce enough, replacing it is not masking the problem, it is giving your cells a signal they genuinely need. Untreated overt hypothyroidism can affect cholesterol, cardiovascular function, cognition, fertility, pregnancy and quality of life. There is no longevity benefit about leaving it untreated.

But there is another truth, and the two truths can exist together. Levothyroxine replaces the missing hormone but it does not directly treat the immune system’s loss of tolerance that caused Hashimoto’s. Which means it can correct the blood levels, whilst the pieces of inflammation still hang around, causing many of the symptoms to persist in many patients.

Many people feel completely well when their dose is right, however, some do not. Their TSH returns to the laboratory range, the result is filed as normal, yet they are still tired, still losing hair, still cold, still unable to recognise themselves inside their own body.

This does not automatically mean they need more thyroid hormone. It means the number should not be allowed to end the conversation. We have to ask about iron and B12, vitamin D, sleep, chronic under-eating, stress, insulin resistance, perimenopause, coeliac disease, medication absorption and other autoimmune conditions. Sometimes the thyroid dose needs attention, but sometimes the symptom is coming from somewhere else entirely.

The blood test matters, but the woman sitting in front of it matters more.

What does any of this have to do with how slowly you age?

Almost everything, although not in the way longevity marketing might have you believe.

Slow ageing is not the pursuit of the fastest possible metabolism or the lowest possible TSH, but it is the preservation of function for as long as we can. It means that we are arriving at seventy with the muscle to rise from the floor, the cardiovascular capacity to climb the stairs, the bone strength to survive a fall and the mental clarity to remain fully present within your own life.

Too little thyroid hormone can quietly work against each of these aims. Firstly, LDL cholesterol may rise and cardiac performance and exercise capacity can fall. Fatigue makes movement feel harder, and when movement becomes harder we do less of it. Muscle begins to disappear not only because of the hormone itself, but because the person no longer has the energy to use it. Weight may rise, mood may fall, cognition may slow and constipation may become another daily discomfort that she gradually learns to call normal.

This is how biological drift often works, it isn’t one dramatic collapse but there are small, little losses in energy, movement and metabolic health that begin to accumulate in the background.

Too much thyroid hormone is not the answer, so ensure this is seen to by a physician as an unnecessarily suppressed TSH can increase the risk of atrial fibrillation and bone loss, particularly as women grow older. The goal is not to force the metabolic house to burn hotter because a house that burns too hot is not healthier than one that has gone cold.

The goal is the right signal for your immune cells and for the cells in your thyroid gland, just the right amount to keep the systems running, but not so much that we begin to damage the very heart and bones we are trying to preserve.

What I would actually check

TSH is a useful place to begin, and its what’s found on many standard panels but is not always the whole story.

Depending on the person and the clinical context, I may also look at free T4, T3, and thyroid peroxidase antibodies, with thyroglobulin antibodies sometimes adding further information. Reverse T3 is rarely necessary in routine hypothyroidism care and should not become another expensive number collected simply because it can be measured.

Then I look beyond the thyroid because iron deficiency can produce an almost identical portrait: exhaustion, hair loss, poor exercise tolerance and brain fog. B12 deficiency, low vitamin D, inadequate food or protein, poor sleep, chronic stress and perimenopause can sit over the top of thyroid disease until it becomes impossible to know which symptom belongs to which condition. Coeliac disease is more common in people with autoimmune thyroid disease and can interfere with both nutrient and medication absorption.

Even the most ordinary details matter, such as the fact that levothyroxine generally needs to be taken consistently and separated from iron and calcium, which can reduce its absorption. A person can have the correct prescription sitting in the bathroom cabinet and still receive an inconsistent dose inside the body, and I see this happen more often than you would think.

You cannot supplement your way out of a missing hormone

The thyroid needs nutritional raw materials. Iodine is required to build thyroid hormone. Selenium, zinc and iron participate in its production and metabolism. Protein matters not only for thyroid function, but for the muscle we are trying to preserve across every decade.

Yet support is not the same as replacement: three Brazil nuts are a wonderful source of selenium that is needed for thyroid hormone production but they don’t replace the need for levothyroxine. A green powder cannot persuade damaged thyroid tissue to make a hormone it no longer has the capacity to produce and seaweed is not automatically safe because it grew in the ocean; excessive iodine can worsen thyroid dysfunction in susceptible people, particularly those with autoimmune thyroid disease.

First step is to correct what is genuinely low, do not create a new excess while trying to fix the old deficiency.

The gut matters too, although we need to be precise about what that means. The gut is one of the largest meeting places between the outside world and the immune system, and coeliac disease has a recognised relationship with autoimmune thyroid disease. Fibre, plant diversity and a nourishing diet support metabolic and immune health, but saying that every thyroid problem begins in the gut turns an interesting biological relationship into a certainty the science does not yet give us.

The most useful interventions are often quieter: eat enough, include protein, correct iron or vitamin deficiencies when they exist, build muscle, sleep properly, recover from training and finally take the medication you need in a way that allows it to be absorbed.

None of this is glamorous enough to become a thyroid ‘hack’. That is probably why it matters.

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Listen before the body has to shout

The body is rarely silent before it becomes unwell and more often than not, we become fluent in ignoring it.

We call the exhaustion adulthood, and we blame the hair loss stress. We might call the weight gain a failure of discipline and we often call the low mood a difficult season and the irregular cycle an inconvenience to deal with later. Each explanation is plausible enough that years can pass before anybody puts the symptoms beside one another and asks what they are trying to say.

Sorting out your thyroid will not stop you aging. It can, however, remove a persistent metabolic drag from the systems that determine how well you do it. It can give you back the energy required to move, help you preserve the muscle needed to remain independent, improve cardiovascular risk when hypothyroidism is contributing to it, and return a clarity that allows you to feel present inside your own days.

That is the kind of longevity I care about, not a metabolism forced to run faster or chasing a laboratory number pushed to its lowest possible edge. The answer rarely is another supplement added to an already crowded shelf.

The right signal, reaching the right tissue, in a body that still has the capacity to respond. The thyroid is small, but if we listen carefully, it can tell us a very large story about how fast the body is ageing.

References

1. Klubo-Gwiezdzinska J, Wartofsky L. Hashimoto thyroiditis: an evidence-based guide to etiology, diagnosis and treatment. Pol Arch Intern Med. 2022;132(3):16222. doi: 10.20452/pamw.16222

2. National Institute of Diabetes and Digestive and Kidney Diseases. Hashimoto’s disease. National Institutes of Health.

3. American Thyroid Association. General information and thyroid disease statistics.

4. Klein SL, Flanagan KL. Sex differences in immune responses. Nat Rev Immunol. 2016;16(10):626–638. doi: 10.1038/nri.2016.90

5. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014;24(12):1670–1751. doi: 10.1089/thy.2014.0028

6. Jonklaas J, Bianco AC, Cappola AR, et al. Evidence-based use of levothyroxine/liothyronine combinations in treating hypothyroidism: a consensus document. Thyroid. 2021;31(2):156–182. doi: 10.1089/thy.2020.0720

7. Feldt-Rasmussen U, Effraimidis G, Bliddal S, Klose M. Risks of suboptimal and excessive thyroid hormone replacement across ages. J Endocrinol Invest. 2024;47(5):1083–1090. doi: 10.1007/s40618-023-02229-7

8. Wiesner A, Gajewska D, Paśko P. Levothyroxine interactions with food and dietary supplements: a systematic review. Pharmaceuticals. 2021;14(3):206. doi: 10.3390/ph14030206

9. Roy A, Laszkowska M, Sundström J, et al. Prevalence of coeliac disease in patients with autoimmune thyroid disease: a meta-analysis. Thyroid. 2016;26(7):880–890. doi: 10.1089/thy.2016.0108

10. Hu S, Rayman MP. Multiple nutritional factors and the risk of Hashimoto’s thyroiditis. Thyroid. 2017;27(5):597–610. doi: 10.1089/thy.2016.0635

11. Leung AM, Braverman LE. Consequences of excess iodine. Nat Rev Endocrinol. 2014;10(3):136–142. doi: 10.1038/nrendo.2013.251

An earthquake in rural Japan, sixteen women with clean arteries, and what it tells us about how much power emotion has over the body

There is a phrase people use at funerals, “she died of a broken heart.” We say it the way we say the sun rises, knowing perfectly well that it does not, using the sentence for what it carries rather than for what it claims.

I used to file it under sentiment: heart attacks were plumbing, something narrows, something ruptures, a clot forms, muscle downstream starts to die and grief was in the mind, and the mind, I assumed, stayed in its lane.

Then I read about Niigata.

Four minutes to six

On the evening of 23 October 2004, the ground under Niigata Prefecture in northern Japan lifted and dropped. The earthquake measured 6.8, and it arrived at the hour when rural Japan is indoors, the rice was in, kettles were going on. Over the weeks that followed the region absorbed roughly ninety aftershocks, several of them severe enough to feel like a fresh event, so that for the better part of a month the ground never quite finished moving, and neither did the people standing on it.

Within days, the hospitals nearest the epicentre started seeing a pattern. The patients were almost all elderly women. They came in with crushing central chest pain and breathlessness. Their ECGs carried the ST changes that mean a heart attack is unfolding in front of you. Their bloods came back positive for troponin, the protein that leaks out of heart muscle when heart muscle is dying, every single marker pointed one direction.

So the cardiologists did the obvious thing, they took them to the catheter lab, threaded a wire up from the groin, injected contrast into the coronary arteries and watched the screen for the occlusion.

There was no occlusion. The arteries were open and in several cases they were better than open, they were pristine, cleaner than you would ever expect in a woman in her seventies. Nothing narrowed, nothing ruptured, nothing to fix. And in front of them, a heart that was failing anyway.

The clay pot

The ventricle was the strange part, the base of the chamber was gripping and releasing exactly as it should. The apex, the tip, was barely moving. It had ballooned outward and gone still, so that each beat pushed out a fraction of the blood it was supposed to. The resulting silhouette on the ventriculogram did not match anything in the anatomy textbooks.

A Japanese cardiologist named Hikaru Sato had met that silhouette before, around 1990, and rather than reach for Latin he reached for something on his own coastline. Fishermen there catch octopus using a clay pot with a heavy round belly and a narrow neck. The animal climbs in for shelter and cannot climb back out. The pot is called a takotsubo. He named a cardiac syndrome after a trap.

Sixteen

Sixteen people near the epicentre were diagnosed with takotsubo cardiomyopathy in the month after the earthquake. Fifteen were women and the average age was seventy-one and a half. Most of them lived where the shaking had been most violent, and eleven of the sixteen developed symptoms on the day itself, while the aftershocks were still arriving.

Before the earthquake, that region recorded roughly one case every couple of months, in he month afterwards, near the epicentre, the incidence ran about twenty-four times higher. What makes that number worth sitting with is how specific it was. This was not a general collapse in cardiac health across a traumatised population. It was one syndrome, and it happened almost exclusively in hearts whose arteries were entirely intact.

Why the tip

A frightened body floods itself with adrenaline and noradrenaline, and it does so to save you, under an ordinary threat those quantities are useful, under an extreme one they are not ordinary at all, and the heart ends up bathed in a concentration it was never designed to receive.

The apex carries the highest density of receptors for those molecules, it takes the biggest hit, and at a certain point it simply stops answering. Cardiologists call this stunning, which is exactly the right word. The tissue is not dead. It has been struck so hard that it cannot respond.

In the largest international series of these patients, the hearts were ejecting somewhere around forty percent of their volume per beat, against the sixty or so you would want. The comparison the investigators ran is the part I have never been able to put down. They matched those patients against people who had arrived at the same hospitals with genuine infarcts, blocked arteries, muscle actively dying. The hearts with nothing wrong with their arteries were pumping worse than the hearts that were infarcting.

An emotion changed the shape of an organ, and there are images of it. Then, over days and weeks, in most people the apex wakes up. The wall starts moving, the chamber recovers its ordinary geometry. Scan the same woman three months later and you would struggle to prove anything had happened at all.

It is not about sadness

The common name is broken heart syndrome, which quietly smuggles in a theory: that grief is the cause. Grief is a cause, but it is not the main one, and the assumption falls apart the moment you look for the opposite.

In 2016 a group in Zurich did exactly that, among close to five hundred patients whose takotsubo had a clear emotional trigger, twenty had a trigger that was unambiguously joyful: a birthday party, a son’s wedding, a reunion with school friends after fifty years, a successful job interview. A favourite driver winning a race, and one patient had just become a grandmother.

They called it happy heart syndrome, and it dismantles the poetry. The muscle is not interpreting the news, it is responding to the size of the surge. A wedding and an earthquake reach the myocardium along the same road, and the tissue reads only what is dissolved in the blood arriving at it. There is no receptor for meaning. There is only magnitude, and duration.

One thing that gets left out, this is not a benign condition with an evocative name, and I think that framing has done real harm.

The chamber does recover, but the person does not always. A large Swedish registry found mortality in takotsubo broadly comparable to mortality after a true myocardial infarction. Reversible on the echo is not the same as harmless.

What I actually take from it

Almost nobody reading this is going to experience a surge on the scale of eight seconds of moving ground in your seventies. That is not the useful part, the useful part is what it establishes about the mechanism. Emotional states are not decorative, they are translated, immediately and without your permission, into instructions for blood pressure, vascular tone, glucose availability, inflammatory signalling and heart rate. Those instructions are ordinarily small and ordinarily temporary. Niigata is simply the extreme end of the same wire, the version large enough to photograph.

Which leaves an honest question; if one enormous surge can visibly deform a heart in a single night, what are the small ones doing, thousands of times, at a resolution no scanner will ever pick up, across forty years of a life?

I think about those women more than I expected to. Sitting at home on an unremarkable Saturday evening in October, kettle on, and then eight seconds that reminded them nothing is fixed.

Their arteries were flawless; it made no difference at all.

References

Sato H, Tateishi H, Uchida T, et al. Tako-tsubo-like left ventricular dysfunction due to multivessel coronary spasm.

Kodama K, Haze K, Hori M, eds. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure. Tokyo: Kagakuhyoronsha, 1990: 56 to 64. (First description and the origin of the name.)

Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol 1991; 21: 203 to 214.

Watanabe H, Kodama M, Okura Y, et al. Impact of earthquakes on takotsubo cardiomyopathy. JAMA 2005; 294(3): 305 to 307.

Sato M, Fujita S, Saito A, et al. Increased incidence of transient left ventricular apical ballooning (so-called takotsubo cardiomyopathy) after the Mid-Niigata Prefecture earthquake. Circ J 2006; 70(8): 947 to 953. (Sixteen cases within one month, one man and fifteen women, mean age 71.5; eleven developed symptoms on the day itself; incidence near the epicentre roughly twenty-four times higher than before the earthquake.)

Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of takotsubo (stress) cardiomyopathy. N Engl J Med 2015; 373(10): 929 to 938. (International

Takotsubo Registry, 1,750 patients. Mean ejection fraction 40.7 percent in takotsubo versus 51.5 percent in age- and sex-matched acute coronary syndrome.)

Ghadri JR, Sarcon A, Diekmann J, et al. Happy heart syndrome: role of positive emotional stress in takotsubo syndrome. Eur Heart J 2016; 37(37): 2823 to 2829. (Of 485 patients with a definite emotional trigger, 20 followed a pleasant event.)

Redfors B, Vedad R, Angerås O, et al. Mortality in takotsubo syndrome is similar to mortality in myocardial infarction: a report from the SWEDEHEART registry. Int J Cardiol 2015; 185: 282 to 289.

Wittstein IS, Thiemann DR, Lima JAC, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005; 352(6): 539 to 548. (The catecholamine surge mechanism.)

Lyon AR, Rees PSC, Prasad S, Poole-Wilson PA, Harding SE. Stress (takotsubo) cardiomyopathy: a novel pathophysiological hypothesis to explain catecholamine- induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008; 5(1): 22 to 29.

Bryan Johnson built his life around the belief that biological decline could be negotiated with. Measured, tracked, interrogated and adjusted, every part of the body became something to watch more closely. Food was no longer just food. Sleep was no longer just sleep. Blood work, organ function, skin, microbiome, glucose, biological age: all of it became data.

He did not merely become interested in health. He turned his body into a living experiment in control.

And then came the sentence that made the whole project feel suddenly more human.

“My stomach is eating itself.”

The diagnosis was autoimmune gastritis. His immune system had begun attacking the acid-producing cells of his stomach. For years, he had reportedly struggled with low ferritin that would not properly correct. Eventually, after further investigation, including blood work, endoscopy and gastric biopsies, the explanation became clearer. It was not a simple problem of poor intake, it was not lack of discipline. It was not that he had failed to supplement aggressively enough. It was autoimmunity.

That is the part that matters.

Johnson is not the average person ignoring his health until something breaks. He is one of the most monitored people in the world. He lives inside data, his entire public identity is built on biological vigilance and still, his immune system moved quietly against him.

This does not mean optimisation is useless. In many ways, it proves the opposite. The low ferritin was noticed. The drift was followed, the disease was caught early enough to be managed and monitored before its worst complications appeared. That is what good preventive medicine is supposed to do.

But it does mean something more uncomfortable.

You can measure everything and still not fully command the immune system. You can optimise sleep, nutrition, exercise, supplements, light exposure, glucose and body composition, and still inherit a biology that is not entirely obedient, the body is not a machine waiting for better instructions. It is an ecosystem and ecosystems do not usually fail because one input was wrong. They begin to fail when the conversation between systems changes.

The stomach was never just a stomach

Autoimmune gastritis is not ordinary gastritis, it is not the stomach feeling irritated after wine, coffee, stress or too much chilli. It is not simply reflux, or the familiar modern discomfort of digestion under pressure, it is the immune system targeting the parietal cells of the stomach.

Parietal cells are not decorative, they produce hydrochloric acid, which helps the body break down food and absorb minerals such as iron, zinc, calcium and magnesium, they also produce intrinsic factor, the protein required for vitamin B12 absorption later in the small intestine.

When parietal cells are progressively destroyed, the stomach loses acid. Iron absorption begins to falter, and ferritin can remain low for years before anything more obvious appears. As intrinsic factor falls, B12 becomes harder to absorb, however perfect the diet may look. Eventually, this can become pernicious anaemia, a B12 deficiency state that does not only affect the blood, but also the brain, nerves, mood, cognition and energy.

This is why autoimmune gastritis can be so quiet, it does not always arrive as dramatic stomach pain. It may arrive as a person who is tired in a way that does not make sense, whose ferritin does not rise, whose hair begins to shed, whose thinking feels less clear, whose recovery is slower, whose body appears to be fed but somehow not fully nourished.

The stomach is often treated as a digestive organ only. But the stomach is not just a digestive organ. It is a gatekeeper. It decides how food enters the rest of the body. It sterilises, acidifies and prepares minerals for absorption, it signals downstream to the pancreas, gallbladder, small intestine, microbiome and immune system.

When stomach acid falls, digestion does not simply become less efficient, the whole architecture of nourishment changes, food still arrives, but access is impaired. The body is not starving because there is no food, it is struggling because the door has begun to close.

The thyroid and the stomach often speak the same immune language

The other detail in Bryan Johnson’s story is not incidental. He has also spoken about having autoimmune hypothyroidism.

This overlap matters. Autoimmune thyroid disease and autoimmune gastritis have been linked for decades. The association is known as thyrogastric syndrome. In the literature, gastric autoimmunity is reported in a significant proportion of patients with Hashimoto’s thyroiditis, and Hashimoto’s is also common in patients with autoimmune gastritis.

This is not coincidence. It is shared immune architecture.

The immune system rarely reads the body in the neat categories doctors use. Endocrinology here, gastroenterology there, rheumatology somewhere else. The immune system does not care about clinic departments. It moves through tissue. A patient may arrive with Hashimoto’s and low ferritin. Another may have rheumatoid arthritis and bloating. Another may have vitiligo and B12 deficiency. Another may present with fatigue, thyroid antibodies, hair loss and poor response to levothyroxine.

Modern medicine often separates these into individual problems. The immune system may be telling one story through several organs.

This is why the combination of Hashimoto’s and autoimmune gastritis can be so punishing. Low stomach acid can impair levothyroxine absorption. Iron deficiency can worsen thyroid-related fatigue. B12 deficiency can mimic or amplify neurological and cognitive symptoms. The patient feels as though she is falling apart in fragments, but the fragments are connected.

The thyroid is not separate from the stomach. The stomach is not separate from absorption. Absorption is not separate from mitochondria. Mitochondria are not separate from fatigue. Fatigue is not separate from stress. Stress is not separate from immunity.

The body is not a collection of independent rooms. It is one house. And when the alarm keeps sounding in one room, it is rarely only one room that is on fire.

The woman who kept flying

A woman in her mid-thirties sits across from me.

She works in fashion and has her own line. From the outside, her life has the polished chaos of success: New York, shows, flights, fittings, launches, hotels, deadlines, cities entered and exited like tabs left open in the brain.

Her calendar looks impressive. Her body tells a different story.

She has Hashimoto’s, rheumatoid arthritis, fatigue that does not resolve with rest, hair that is falling out, poor absorption and a nervous system that seems to live permanently braced for the next demand.

She is not lazy. She is not careless. She is not someone who has abandoned herself. If anything, she is the opposite. She is highly functioning, highly responsible and highly adapted to pressure. That is part of the problem. Some bodies collapse early. Others become extremely good at surviving dysfunction. They keep producing, keep boarding flights, keep answering emails, keep making decisions, keep showing up, until one day the body stops asking politely.

She tells me she eats well, and I believe her.

But this is where the modern health conversation becomes too simplistic. We have become obsessed with inputs. We ask what someone eats, how much protein they get, how many steps they do, which supplements they take, what their glucose curve looks like, which fasting window they follow, which wearable they use, which protocol they are on. All of these things can matter, but the body is not only asking what came in. It is asking what state it was in when it arrived.

A meal eaten in a state of threat is not metabolised in the same way as a meal eaten in safety. Sleep after twelve hours of sympathetic overdrive is not the same as sleep after a day that resolved. Exercise layered onto an inflamed, depleted system is not always interpreted as growth. Sometimes it is interpreted as another demand.

Her immune system is not separate from her life. It is reading it. It is reading the flights, the sleep disruption, the late meals, the cortisol, the under-eating between shows, the performance pressure, the constant switching of cities, time zones and roles, and the feeling that if she stops, everything drops.

This does not mean stress “caused” her autoimmune disease. That is too crude. Autoimmunity is rarely one thing. It is genetic susceptibility meeting environmental triggers inside a body whose regulatory systems may already be strained. Genes create the possibility. The environment shapes the probability. The nervous system influences the terrain.

Autoimmunity is a loss of recognition

The immune system has two great jobs: to recognise danger and to recognise self.

Autoimmunity begins when that distinction becomes unstable. The body starts treating its own tissue as if it were threat. In autoimmune gastritis, that tissue is the acid-producing compartment of the stomach. In Hashimoto’s, it is the thyroid. In rheumatoid arthritis, the joints become a major site of immune attack.

Different tissues, but the same deeper question.

Why has the immune system lost tolerance?

Tolerance is not weakness. It is intelligence. It is the immune system knowing when not to react. It is the difference between a system that can defend you and a system that starts firing at the walls of its own house.

And tolerance is trained. It is trained by microbes, by early life exposure, by the gut, by food, by infection and recovery, by sleep, by stress resolution, by the integrity of the intestinal barrier and by the body repeatedly receiving the signal that this is safe, this is self, this does not need attack.

The gut microbiome is one of the immune system’s great teachers. It helps educate regulatory T cells, the cells that help restrain immune overreaction and maintain tolerance. When the microbiome is diverse, nourished and metabolically active, it produces compounds such as short-chain fatty acids that help maintain the gut barrier and immune regulation.

When that ecosystem is disrupted, the immune system loses part of its education. The gut lining becomes more permeable. Food antigens, bacterial fragments and inflammatory molecules cross boundaries they were not meant to cross. The immune system sees more noise, more threat and more reason to react. Over time, the system becomes less tolerant, more vigilant, more suspicious and more willing to mistake self for danger.

Modern life is training the immune system badly

The rise in autoimmune disease is not easily explained by genetics. Genes do not change meaningfully in one generation. The environment does.

Large datasets now estimate that millions of people live with at least one autoimmune disease, with women disproportionately affected and a substantial subset having more than one autoimmune diagnosis. Reviews of the field increasingly point toward modern environmental exposures, diet, stress, pollution and socioeconomic change as part of the wider autoimmune landscape.

This does not mean every case is preventable. It means the immune system is responding to a world that has changed around it.

For most of human history, the immune system was educated by contact. It met soil, animals, parasites, plants, fermented food, shared meals, outdoor life, physical work, seasonal rhythm, infection and recovery. The microbial world was not something humans encountered occasionally. It was the background condition of being alive. Through that contact, the immune system learned what required attack and what required tolerance.

Modern life has altered that conversation. We have cleaner homes, more antibiotics, more caesarean births, less soil exposure, less microbial diversity, more ultra-processed food, less fibre, more additives, more pollutants, more psychological stress, more circadian disruption, more loneliness, more sterile interiors and more life lived under artificial light, through screens, inside sealed buildings, eating food made by systems rather than soil.

We have not simply removed disease. We have also removed some of the conditions that taught the immune system restraint. And then we act surprised when it becomes reactive.

This is the paradox of modern health. We are safer in many obvious ways, but not necessarily more biologically coherent. We have reduced many acute threats, but we have created chronic ones. The immune system was designed for wounds that heal, infections that resolve, hunger that passes, stress that peaks and falls, light that changes with the sun, food that arrives with fibre and microbes, and communities that regulate the nervous system.

Instead, it now receives signals that rarely resolve. Food without fibre. Stress without completion. Light without darkness. Stimulation without recovery. Contact without connection. Cleanliness without microbial education. Abundance without nourishment.

The immune system is not malfunctioning in a vacuum. It is adapting to the world we have built. The problem is that some adaptations become disease.

Stress is not an emotion. It is an immune event.

When patients say they are stressed, the word often sounds too small for what is happening.

Stress has been made psychological, almost decorative, as if it is a feeling, a mood, a mindset problem. But stress is not just how life feels. It is how life is translated into physiology.

Stress changes cortisol, sympathetic tone, vagal tone, gut motility, stomach acid, intestinal permeability, cytokine signalling, sleep architecture, glucose handling and the way the immune system decides what kind of world it is living in.

Acute stress is not the enemy. The body is built for acute stress. It knows how to run, lift, perform, escape and then resolve. The danger is stress that never completes the loop. The email after the email. The show after the show. The flight after the flight. The decision after the decision. The phone lighting up beside the bed. The nervous system waking already braced. The body never receiving the signal that it is over now.

Chronic stress affects the gut directly. It can alter motility, secretion, visceral sensitivity, microbiota composition and gut barrier function. The gut lining is not a wall of concrete. It is a living border, one cell thick in places, negotiating constantly between the outside world and the internal immune system.

Under pressure, that border can loosen. Not enough to announce disaster, but enough to change the conversation. A little more permeability means a little more immune exposure. A little more immune exposure means a little more inflammation. A little more inflammation means a little less tolerance.

This is why telling someone with autoimmune disease to “just relax” is both biologically relevant and clinically insulting. The biology is real. The advice is useless unless it becomes specific. The question is not whether stress matters. It does. The question is whether the person has a life in which stress can actually resolve.

My patient in fashion does not need a wellness quote about boundaries. She needs her biology to stop living as though every season is a threat. She needs meals that are not inhaled between obligations, sleep that is not treated as leftover time, strength that is not just thinness under pressure, a gut that is fed consistently enough to repair, a nervous system that has daily evidence of safety, and an immune system that is not being asked to regulate inside a life that never lets anything settle.

The biohacker and the fashion founder are not opposites

At first, Bryan Johnson and my patient seem like opposite figures.

He represents maximal measurement. She represents maximal motion. He lives through control. She lives through demand. He tries to reduce every variable. She is surrounded by variables.

But biologically, they meet in the same place: the immune system.

One body tracked everything and still developed autoimmunity. Another body kept performing and found itself inflamed, exhausted and increasingly unable to absorb.

Both reveal the same problem with the modern fantasy of health. We keep pretending the body can be managed from the outside, as if enough data will solve it, enough discipline will solve it, enough productivity can coexist indefinitely with biological strain. We behave as though the body will keep accepting instructions without eventually answering back.

But the body is not passive. It listens, and then it adapts.

The skeleton listens to load. The gut listens to microbes. The nervous system listens to safety. The immune system listens to threat. The stomach listens to stress, inflammation and autoimmunity. The thyroid listens to energy availability, inflammation and absorption.

The body is always listening. The question is what modern life keeps saying.

What optimisation gets right

It would be easy to use Bryan Johnson’s diagnosis as proof that biohacking is absurd. That would be lazy.

His diagnosis does not prove that tracking is pointless. It proves that tracking has limits. There is a difference.

A low ferritin that does not correct should be investigated. A B12 level that keeps falling should be taken seriously. A thyroid condition that becomes hard to stabilise should raise questions about absorption. Symptoms that appear across systems should not be dismissed just because each individual result looks only mildly abnormal.

This is where longevity medicine can be useful. Not as fantasy, but as early interpretation. The goal is not to become immortal. The goal is to catch biological drift before it becomes structural damage.

That is what seems to have happened in Johnson’s case. The ferritin was the whisper. The workup followed. The diagnosis emerged.

The problem is not measurement. The problem is believing measurement equals mastery. It does not. Measurement tells you where to look. It does not guarantee you can control what you find.

What optimisation gets wrong

Modern optimisation often treats the body as something to perfect.

But the body is not asking for perfection. It is asking for coherence.

You can take the supplements and still be inflamed. You can eat the clean diet and still fail to absorb. You can lift weights and still be under-recovered. You can have a perfect morning routine and still live in a life that keeps your nervous system braced. You can track your sleep and still not feel safe enough to restore.

The body does not care how impressive the protocol looks. It reads the whole environment.

This is why autoimmune disease cannot be reduced to “do this and you will not get it.” That is not medicine. That is marketing. There is no clean promise here. No perfect anti-autoimmune diet. No supplement stack that guarantees immune tolerance. No meditation app that reverses parietal cell destruction. No wearable that can make the immune system recognise self again.

But there are signals that matter. Fibre, sleep, vitamin D, protein, muscle, microbial diversity, reducing ultra-processed food, treating infections, addressing H. pylori where present, correcting iron and B12 deficiency, reducing chronic inflammatory load, stress physiology and connection all matter. Not because these are soft lifestyle extras, but because they are biological inputs. They are part of the terrain in which the immune system decides how aggressively to behave.

What I would look for clinically

In a patient with Hashimoto’s, unexplained low ferritin, fatigue, hair loss, poor absorption, bloating, reflux, low B12, poor response to levothyroxine or another autoimmune condition, I would think about the stomach. Not as an afterthought, but as part of the immune story.

I would want to understand whether ferritin is low because intake is poor, blood is being lost, inflammation is trapping iron, or absorption is impaired. I would consider anti-parietal cell antibodies, intrinsic factor antibodies, B12, folate, ferritin and full iron studies, zinc, thyroid antibodies, coeliac screening where appropriate and H. pylori testing. In the right clinical context, gastroenterology referral for upper endoscopy with biopsies matters.

Because if autoimmune gastritis is present, oral supplements may not behave the way people expect. Oral iron may not correct ferritin. Oral B12 may not be enough. Levothyroxine dosing may become harder to stabilise. The patient may be blamed for inconsistency when the problem is absorption.

Once autoimmune gastritis is established, management is not glamorous. B12 often needs to bypass the stomach through injections if intrinsic factor is impaired. Iron may need to be given intravenously if oral absorption fails. H. pylori should be treated if present. The stomach may need surveillance over time because autoimmune gastritis is associated with increased risk of gastric neuroendocrine tumours and gastric cancer.

This is not wellness theatre. This is basic clinical consequence.

But the deeper management cannot stop there. Replacing nutrients is not the same as restoring regulation. You can inject B12 and still leave the immune system inflamed. You can infuse iron and still leave the gut barrier compromised. You can adjust thyroid medication and still leave the patient living in a state of threat. You can manage the disease and still ignore the terrain.

Medicine needs both: the replacement and the repair, the diagnosis and the context, the antibody and the life.

The stomach as a metaphor

There is something almost too poetic about autoimmune gastritis.

The stomach, the organ of receiving, begins to lose its ability to receive.

Food arrives, but nourishment becomes harder. The body is fed, but not fully supplied. The patient eats, but the system cannot access what it needs.

This is not only true of the stomach. It is true of modern life.

We are surrounded by abundance and still depleted. Connected and still lonely. Stimulated and still tired. Informed and still confused. Optimised and still inflamed. Fed and still undernourished.

We keep adding more data, more supplements, more productivity, more tracking, more interventions, more plans. But the body may not need more noise. It may need fewer contradictions.

It may need food it recognises, sleep it can trust, microbes that teach tolerance, movement that builds capacity rather than punishment, stress that resolves, relationships that regulate and a life that does not constantly ask the immune system to stand guard.

The long view

The man who optimised everything still developed autoimmunity.

That sentence will be used by some people to mock him. I do not think that is the useful response.

The useful response is more sober.

His story shows us both the promise and the limit of modern longevity. The promise is early detection. The limit is control.

We should measure. We should investigate. We should not ignore quiet signals like low ferritin, unexplained fatigue, B12 deficiency, poor absorption or multiple autoimmune conditions clustering together.

But we should also stop pretending that the body can be hacked into silence.

The immune system is not a spreadsheet. It is memory. It remembers genes, microbes, infections, stress, chemicals, sleep loss, the gut barrier and the life around it. And sometimes, when the signals become too distorted, it begins to mistake the body for the enemy.

That is autoimmunity.

Not a failure of willpower. Not a failure of discipline. Not a failure of clean eating. A failure of recognition. The body no longer fully recognises itself.

And perhaps that is the deeper warning inside this diagnosis.

Modern life has become so biologically confusing that even the immune system, the system designed to know what belongs to us, is starting to lose the distinction.

The question is no longer only how we live longer.

It is how we build a life the body can still recognise as safe.

Because the future of medicine will not belong only to the people who measure the most. It will belong to the people who can interpret the signal beneath the measurement: the low ferritin, the thyroid antibody, the tired woman on her tenth flight, the stomach losing acid, the immune system losing tolerance, the body whispering long before diagnosis that something in this life is no longer being received.

References

1. Bryan Johnson publicly described his diagnosis as autoimmune gastritis and used the phrase “my stomach is eating itself”; subsequent reporting described years of low ferritin, elevated anti-parietal cell antibodies and biopsy-supported diagnosis.

2. Cellini M, Santaguida MG, Virili C, et al. Hashimoto’s Thyroiditis and Autoimmune Gastritis. Frontiers in Endocrinology. 2017;8:92.

3. Belkaid Y, Hand TW. Role of the Microbiota in Immunity and Inflammation. Cell. 2014;157(1):121–141.

4. Abend AH, et al. Estimation of Prevalence of Autoimmune Diseases in the United States Using Electronic Health Record Data. Journal of Clinical Investigation. 2024/2025.

5. Zheng JF, Lee YH, Leong PY. The Modern Epidemic of Autoimmunity. International Journal of Rheumatic Diseases. 2024.

6. Konturek PC, Brzozowski T, Konturek SJ. Stress and the Gut: Pathophysiology, Clinical Consequences, Diagnostic Approach and Treatment Options. Journal of Physiology and Pharmacology. 2011;62(6):591–599.

7. Toh BH. Diagnosis and Classification of Autoimmune Gastritis. Autoimmunity Reviews. 2014;13:459–462.

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He almost didn’t come.

His wife is a patient of mine. She had spent the better part of a year working on her health, quietly, methodically, in the way that people do when they finally decide to take it seriously. She had improved considerably. And somewhere in that process, she had decided her husband needed to do the same.

He was in Dubai for one day. A business trip. He had meetings, calls, a flight to catch. He sat down across from me with the particular politeness of a man who has been sent somewhere he does not believe he needs to be.

“I’m perfectly fine,” he said. “I don’t really know why I’m sitting in a GP’s office.”

He was thirty-seven. No symptoms. No diagnosis. No reason, by any conventional measure, to be concerned.

We talked about his life. His work, his habits, his family. And then he mentioned, almost in passing, that his father had died at sixty-two. A round of golf on a Sunday morning. A heart attack on the seventh hole. No prior history. No warning. Just a man who had been well, and then was not, and then was gone.

I asked if we could run some markers.

His Lp(a) came back at 260. The upper limit of normal is 75. His LDL was approaching 200. His ApoB was elevated. None of these numbers had ever been checked. None of them had ever needed to be, because nothing had gone wrong yet.

It is not a frightening story. It is not meant to be. It is simply a biological reality, one that, found at thirty-seven, changes everything about what comes next. The cascade of management that follows is not punitive. It is protective. A statin to begin. A PCSK9 inhibitor to bring Lp(a) into a range where decades of arterial exposure carry less consequence. Cardiac imaging to understand what the vasculature has already quietly recorded. Behavioural changes, compounding slowly, across years he still has ahead of him.

None of this is fair. A genetic hand he did not choose, a history he cannot rewrite. But fairness is not the point of medicine before the drift.

Protection is.

He has two young daughters and a wife who sent him to me because she had seen, in her own body, what it means to catch something early. He does not want to leave at sixty. He said it plainly, without drama, the way a man says something he has probably thought about more than he lets on. He wants more decades. More years with the three people he loves most, his wife, and his two daughters.

He came in perfectly fine.

He left with the best possible chance of staying that way.

When death was immediate

There was a time when the body did not have the luxury of decline. It did not accumulate disease nor did it not drift slowly into dysfunction.

It was interrupted.

A cut became infected and sepsis ensued. A birth became fatal, for mother and child, and a cough followed by fever that rose and did not ever come down. For most of human history, death was acute, visible, and fast. This is not metaphor, it is demographic reality.

In England in 1800, nearly 30–40% of children died before the age of five¹. Across Europe, life expectancy hovered between 30 and 40 years, not because adults could not live longer, but because so many never survived childhood².

If you plotted mortality as a curve, it did not rise gradually with age as it does today. It spiked early, fell for those who survived, and then rose again in later life. The beginning and the end of life carried comparable risk. The body was not failing slowly, it was being overwhelmed early.

And medicine, in that world, was not a system of prevention. It was a system of response. It was built around the only question that mattered:

What is wrong with you?

Semmelweis and the first fracture in ignorance

In 1847, at the Vienna General Hospital, two maternity wards sat side by side. One was staffed by physicians and the other by midwives. The difference between them was not subtle. Women in the physician-led ward were dying of puerperal fever at rates approaching 10–18% and in the midwife ward, mortality was closer to 2–3%³.

Ignaz Semmelweis did something deceptively simple. He observed. Doctors moved directly from autopsies to the labour ward without washing their hands. These hands carried the residue of death into the act of birth.

Midwives did not. He then introduced a policy; handwashing with chlorinated lime and mortality fell immediately. From nearly one in five women dying, to fewer than one in fifty within months³.

He could not explain the mechanism, the germ theory had not been classified, but he recognised there was a pattern. This was the first fracture in a long-held assumption: that death in these settings was inevitable.

For the first time, medicine did not simply respond to death, it interrupted its cause.

The great transition

What followed was not one discovery, but many. Clean water systems removed pathogens from the bloodstream of cities⁴, sewerage separated waste from life and hygiene became infrastructure, not habit.

Then vaccination changed something deeper. Smallpox, once responsible for hundreds of millions of deaths, was eradicated entirely⁵. Measles mortality fell by more than 70% globally with immunisation⁶.

Then there was Fleming and the discovery of penicillin. Antibiotics transformed infection from inevitability to option and the result was not subtle. It actually reshaped the human lifespan.

Childhood stopped being the most dangerous phase of life and early mortality collapsed. Life expectancy rose. This is the defining success of modern medicine, not that it made us immortal, but that it allowed us to live long enough for something else to emerge.

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The emergence of slow death

When death is delayed, biology does not remain still, it reveals itself. The diseases that now define modern life were not created in this era, they were uncovered by it.

Atherosclerosis develops over decades, beginning silently long before any event⁷, type 2 diabetes is preceded by years of insulin resistance, with glucose remaining deceptively normal⁸ and neurodegeneration begins long before cognition changes⁹.

The body does not collapse, it compensates: quietly, continuously, intelligently. Which is precisely why these conditions are so difficult to detect early because nothing appears wrong. Until it is.

The unseen phase: biology before diagnosis

The problem is not that medicine lacks tools, it is that it is not structured to act in the phase where biology is most dynamic which are the years before diagnosis. In the period where systems are compensating. Where fasting glucose remains normal because insulin is elevated, where liver fat accumulates before transaminases rise and where vascular inflammation precedes structural change.

This is not absence of disease, it is disease in motion and it is where trajectory is most modifiable.

The three questions

I did not arrive at this framework through theory, I arrived at it through practice. I used to work at the end.

In acute medicine, and then during COVID, I stood in the part of the system where the body has already declared itself. Where physiology is no longer negotiating quietly, but failing in a way that demands intervention.

A patient arrives with a heart attack, another cannot breathe, another is septic, their systems beginning to collapse in real time.

There is no ambiguity in that space, something is definitely wrong and medicine, at its most powerful, responds with clarity and force. We intervene, we stabilise and we save lives that, not long ago, would have been lost without question. This is where medicine asks its first question:

What is wrong with you?

It is a necessary question, it built modern medicine, but over time, I moved away from that edge and into general practice and there, the landscape changed.

Patients were no longer arriving in crisis but they were arriving with diagnoses. Chronic conditions and age-related disease: diabetes, coronary artery disease, heart failure and cancer.

The body had already crossed a line and here, medicine takes on a different shape. It measures, it classifies and it manages. It asks:

How far have you crossed the threshold?

And again, this matters because this is where disease is slowed and where complications are prevented. Here is where lives are extended, but not necessarily good years added, just years, added.

So even here, something felt late because the biology did not begin at diagnosis, it had been moving for years before that moment and that is where the third question emerged, not from theory, but from observation. From the recognition that the most important phase of disease was happening in a space we were not truly engaging with.

So I began to organise medicine differently in my mind, not by specialty, not by organ system but by time. There are three forms of medicine.

Medicine at the end, you arrive in crisis, something has broken and it asks: What is wrong with you?

Medicine at the threshold, a line has been crossed, a diagnosis has been made and it asks: How far have you crossed the line?

And then there is a third. One which is earlier, quieter and more difficult to see.

Medicine before the drift.

This is where I now work. Here, the body is still compensating, the biology has not failed but it is moving, directionally and the question changes again:

What is the body remembering?

Because physiology is not a snapshot, it is a record, of sleep and its absence, of movement and its loss, of stress that resolved, and stress that did not, of food that nourished, and food that signalled excess.

Every system carries memory. The liver remembers repeated metabolic load, the vasculature remembers pressure and inflammation and the brain remembers safety or threat.

Long before disease is named, the direction is already set and this is not prevention as it is traditionally framed, it is the reading of biology while it is still adaptive, while it still has options.

Why this matters now

I am not suggesting that the other forms of medicine are flawed, they are unbelievably essential. The doctor in the emergency department will stabilize and save a life, the cardiologist managing heart failure will reduce symptom burden and find a way to improve the quality of his patient’s days and the oncologist administering chemotherapy is trying to kill the runaway cells that are trying to colonize the rest of the healthy tissue.

Without them, we lose everything we have built but the dominant diseases of our time are not acute, they are cumulative and they unfold over years. And by the time they reach the end, or even the threshold, much of the trajectory has already been written. The kind of doctor I am today sits earlier in that story, not replacing what exists but extending care to earlier, where it matters just as much.

The future is not new treatment. It is earlier understanding

Medicine does not need to become more aggressive, it needs to become earlier, it needs to extend its field of view into the years where biology is still negotiating. Where nothing is obviously wrong and everything is already changing, because the future of medicine will not be defined by how well we treat disease.

It will be defined by how precisely we learn to see it before it is forced to declare itself.

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References

1 Wrigley, E.A. & Schofield, R.S. (1981). The Population History of England 1541–1871. Cambridge University Press.

2 Riley, J.C. (2005). Estimates of regional and global life expectancy, 1800–2001. Population and Development Review. 31(3):537–543.

3 Semmelweis, I. (1861). The Etiology, Concept, and Prophylaxis of Childbed Fever. (Carter KC, trans.) University of Wisconsin Press; 1983.

4 Cutler D, Miller G. (2005). The role of public health improvements in health advances: the twentieth-century United States. Demography. 42(1):1–22.

5 Fenner F, Henderson DA, Arita I, Ježek Z, Ladnyi ID. (1988). Smallpox and Its Eradication. World Health Organization.

6 World Health Organization. (2019). Measles. WHO Global Health Observatory data.

7 McGill HC Jr, McMahan CA, Zieske AW, et al. (1993). Association of coronary heart disease risk factors with microscopic qualities of coronary atherosclerosis in youth. Circulation. 102(4):374–379. (PDAY Study)

8 Tabák AG, Jokela M, Akbaraly TN, et al. (2009). Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes. Lancet. 373(9682):2215–2221.

9 Jack CR Jr, Knopman DS, Jagust WJ, et al. (2010). Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurology. 9(1):119–128.

https://drrheakotecha.substack.com/p/microplastics-pcospmos-and-the-quiet

She doesn’t sit down. She holds the chair for a moment, like she might change her mind, and then she breaksinto tears. Not gradually, not hesitantly, fully.

“I don’t understand,” she says. “We’ve been trying for a year.” She was thirty years old with no diagnosis. Noobvious reason.

The kind of patient medicine still calls unexplained.

She has done everything right, she’s tracked ovulation, cleaned up her diet, reduced alcohol and seen two obstetricians. And still, nothing.

Around her, life seems careless. Her sister conceived without trying a few months ago. Soon after, her best friend announced her “accident”. Fertility, for everyone else, appears effortless. But for her, it has become work.

She is holding a coffee. Hot oat milk latte in a takeaway cup. Paper, technically, but not really. Because that cup is lined with polyethylene. A thin plastic film. Invisible but necessary because without it, the cup dissolves.With it, the cup holds, and with heat, it leaches¹.

The exposure we do not see

We are trained to fear toxins that arrive dramatically. Contaminated water, heavy metals and industrial disasters. But most exposure does not arrive like that anymore. It arrives as design. Engineered into convenience, embedded into packaging and scaled into invisibility. Microplastics are not an event. They are an environment.

Fragments smaller than 5 mm. Down to nanoplastics measured in billionths of a metre². Small enough to pass through barriers that evolution never prepared us for. Small enough to enter blood³.

The average human now ingests or inhales tens of thousands of these particles every year through water, food, and air⁵. Not once. Continuously.

Scale

This is not a failure of awareness but it is a consequence of scale. Plastic production has increased more than 200-fold since the mid-20th century⁶. It was designed to last, to resist decay and to survive environments that break everything else.

That is its advantage and its problem. Because what does not degrade in the environment does not degrade easily in biology⁷.

So the same properties that made plastic economically irresistible have made it biologically persistent.

Capitalism optimises for durability, scalability, and cost. The body requires adaptability, turnover, and signal precision. These are not aligned systems.

The metaphor we are living inside

If fibre was the architecture we removed from food then plastic is the architecture we have added to life. An external scaffolding. Lightweight. Durable. Everywhere. But unlike fibre, it does not nourish the system it enters. It occupies it.

Microplastics are not nutrients. They are debris. Biologically inert in purpose. But not in consequence. Because the body still has to respond to them. And that response is rarely neutral.

The body does not ignore anything

The body is not passive, it reads everything. Particles. Chemicals. Signals. And then it decides: inflame, adapt, compensate or, over time, fail. Microplastics do not need to be toxic in the traditional sense, they need only to exist in the wrong place.

In the lung, they activate macrophages and increase pro-inflammatory cytokines such as IL-6 and TNF-α⁸.

In the liver, they induce oxidative stress and mitochondrial dysfunction⁹. In blood, they circulate as particulate cargo, interacting with endothelium and immune cells³. In reproductive tissue, they alter cellular signalling.

This is not poisoning. It is distortion.

The chemistry they carry

Microplastics are rarely just particles, they are vehicles.

BPA.

BPS.

Phthalates.

PFAS.

Endocrine disruptors. They do not destroy hormones, they imitate them. BPA behaves like a weak estrogen. It binds to estrogen receptors (ERα and ERβ), altering transcriptional signalling and downstream gene expression¹⁰.

Not strong enough to replace physiology. But strong enough to confuse it. It also disrupts the hypothalamic–pituitary–gonadal (HPG) axis, altering GnRH pulsatility and downstream LH/FSH signalling¹¹.

And fertility is built on precision.

A note on ‘BPA-free’: The widespread shift to BPA-free products has not resolved the problem. BPS and BPF(the most common replacements) bind to the same estrogen receptors and disrupt the same hormonal pathways. The label changed. The chemistry did not.

In women with PCOS, this disruption lands on already disrupted ground. The HPG axis is already dysregulated, LH/FSH ratios already skewed, androgen signalling already elevated, insulin resistance already compounding the picture. BPA does not create PCOS. But the evidence suggests it amplifies the conditions that make it worse. Studies consistently show higher urinary and serum BPA concentrations in women with PCOS compared to controls, with positive correlations between BPA levels and free androgen index, testosterone, and LH/FSH ratio²²²³. For a condition already defined by hormonal noise, endocrine disruption is not a new problem. It is more of the same problem, arriving from a different direction.

Fertility is not a switch

It is a sequence. Signal → response → timing → coordination. Ovulation must occur, the endometrium must respond and implantation must align with a narrow window. Even small disruptions in signalling reduce success, they do not eliminate it but they do reduce it.

At the ovarian level, BPA has been shown to impair granulosa cell function and reduce estradiol synthesis¹². At the uterine level, it alters endometrial receptivity markers such as integrins and HOXA10 expression¹³.

At the embryonic level, oxidative stress and endocrine disruption impair implantation signalling. Not failure, but friction.

What we are seeing clinically

In IVF cohorts, higher BPA levels; fewer viable oocytes¹⁴ and lower implantation rates¹⁵. And in men, microplastics detected in semen samples¹⁶ are associated with reduced motility and abnormal morphology via oxidative stress and mitochondrial impairment¹⁷. Not sterility. Reduction.

And when both sides are slightly impaired, the probability curve shifts.

Quietly.

But meaningfully.

Back to her

She is not asking about microplastics. She is asking: “Why me?” And the honest answer is, there is no single cause, there is only cumulative load.

The cup.

The bottle.

The air.

The packaging.

The receipts.

The water.

Each one small but together, constant.

Medicine’s blind spot

Medicine is built to detect failure such as blocked tubes, hormonal disorders and structural abnormalities.Microplastics do not present like that. They do not create disease you can name, they create environments you do not measure.

They belong to a different type of medicine. I call it medicine before the drift, where nothing is wrong and everything is changing.

The deeper question

The question is not are microplastics the cause? They are not. The question is, what kind of biology are they quietly shaping?

Because fertility is not guaranteed, it is permitted. And the body permits reproduction when conditions suggest safety such as energy sufficiency, hormonal integrity and low inflammatory burden.

Chronic low-grade inflammation, oxidative stress, and endocrine disruption shift this internal signal away from reproduction toward preservation¹⁸. Microplastics do not remove that permission. They erode it.

Capitalism and the invisible trade

This is not accidental, plastic solved a problem. It allowed cheap packaging, global transport, and food preservation. Essentially, convenience at scale. It allowed systems to move faster than biology ever could. But the trade was silent. We removed friction from life and introduced particles into it. You do not see them. You do not feel them. But your body records them.

The way it records everything.

The poetry of it

We built a world that does not decay and then placed it inside a body that depends on decay to renew itself. So, we created permanence and introduced it into systems that survive through turnover.

We engineered stability and inserted it into biology that requires rhythm and now we are asking the body to make life in an environment it no longer recognises.

What do we do about it

Not fear but direction. Not elimination but reduction. Because this is not a problem you can solve completely.However, it is one you can meaningfully shift.

Reducing exposure: a clinical framework

1. Heat and plastic never meet

• No hot drinks in takeaway cups

• No microwaving in plastic

• Avoid hot food in plastic containers

Heat increases polymer breakdown and accelerates chemical leaching¹.

2. Water is a daily dose

• Use filtered water (reverse osmosis where feasible)

• Avoid bottled water when possible

• Never leave bottles in heat or sunlight.

Bottled water contains significantly higher microplastic loads compared to tap water⁵.

3. Food storage is cumulative exposure

• Prefer glass or stainless steel

• Reduce long-term plastic storage

• Avoid reheating in plastic

Lipophilic chemicals like BPA leach more readily into fatty foods¹⁹.

4. Reduce ultra-processed packaging load

• Whole foods over packaged foods

• Fewer cans, fewer wrappers

Canned linings are a major source of BPA exposure²⁰.

5. Air is underestimated

• Ventilation matters

• Reduce synthetic textiles where possible

Microplastic fibres are inhaled and deposited in lung tissue⁸.

6. Receipts and dermal exposure

• Limit handling of thermal receipts

BPA is absorbed transdermally and contributes to systemic load²¹.

7. Do not aim for perfection

You are shifting probability.

Not eliminating exposure.

Support your body’s response from within

You cannot fully avoid exposure, that is no longer realistic. So the second question becomes, what does the body do with what it cannot avoid? Because the body is not passive, it does not simply accumulate and surrender. It responds.

Detoxification is not a trend, it is physiology. The liver, gut, kidneys and cellular antioxidant systems work together. The issue is not that these systems do not exist. It is that they are now handling a load they were never designed for.

So the goal is not elimination, the goal is support.

Sulforaphane: activating the signal for detoxification

Sulforaphane, found in broccoli sprouts at concentrations up to 100 times higher than mature broccoli, activates the NRF2 pathway²⁴. NRF2 is not a supplement trend. It is a master regulator of cellular defence.

When activated, it upregulates phase II detoxification enzymes, including glutathione S-transferases. These enzymes conjugate compounds like BPA and phthalates, converting them into water-soluble forms that can be excreted in urine²⁵.

Human trials have shown that sulforaphane-rich broccoli sprout beverages increase the excretion of airborne pollutants such as benzene and acrolein by up to 60%²⁶.

Direct human evidence for microplastic clearance is still limited but the pathway is established, and the intervention is food.

Dietary fibre: reducing contact, increasing elimination

Fibre does not just regulate digestion, it regulates exposure. Insoluble fibre acts mechanically. It binds particles within the gut lumen and increases stool bulk, reducing the contact time between microplastics and the intestinal wall. Less time, less interaction and less opportunity for translocation.

Soluble fibre acts chemically. It binds bile acids and disrupts enterohepatic circulation. This matters because PFAS and similar compounds are reabsorbed through bile recycling²⁷. Interrupt that cycle, and you increase excretion.

Large population studies consistently show that higher fibre intake is associated with lower circulating PFAS levels²⁸.

Again, not elimination, but reduction.

N-acetylcysteine (NAC): protecting the cell

NAC is not removing particles, it is protecting biology. It acts as a precursor to glutathione, the body’s primary intracellular antioxidant. Glutathione sits at the centre of oxidative balance.

When microplastics and endocrine disruptors enter tissue, one of the first responses is oxidative stress.Reactive oxygen species increase, mitochondrial function becomes impaired, inflammatory signalling rises.Experimental data consistently show that NAC attenuates this response²⁹. Reduced oxidative damage, improved mitochondrial stability and lower inflammatory signalling.

It does not change exposure. It changes response.

What this section is not

This is not a detox protocol, this is not a promise of removal. Microplastics are persistent. Some will remain, but biology is not binary, between exposure and disease, there is a spectrum.

And along that spectrum, there is room to support the system.

The principle

None of these eliminate exposure, they support the biology that responds to it, and that distinction matters.Because the body is not failing. It is adapting.

The question is whether we are giving it enough capacity to adapt well.

The closing

She finishes her coffee slowly. We move on to tests, to cycles, to what we can measure.

But the cup stays, because it represents something larger than itself. A world where exposure is not exceptional. It is ambient, constant, uninvited.

The question is no longer whether microplastics are in the body. They are.

The question is:

What signals are we giving our biology, every single day, and what kind of life that biology now believes it is safe enough to create, not just for yourself, but the next generation.

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References

1 Cao X, Bhatta M, Bhatt DL, et al. Release of microplastics and chemicals from takeaway containers under heat. Environmental Science & Technology. 2022;56(21):15507–15516. doi:10.1021/acs.est.2c04993

2 Gigault J, ter Halle A, Baudrimont M, et al. Current opinion: What is a nanoplastic? Environmental Pollution. 2018;235:1030–1034. doi:10.1016/j.envpol.2018.01.024

3 Leslie HA, van Velzen MJM, Brandsma SH, Vethaak AD, Garcia-Vallejo JJ, Lamoree MH. Discovery and quantification of plastic particle pollution in human blood. Environment International. 2022;163:107199. doi:10.1016/j.envint.2022.107199

4 Ragusa A, Svelato A, Santacroce C, et al. Plasticenta: First evidence of microplastics in human placenta. Environment International. 2021;146:106274. doi:10.1016/j.envint.2020.106274

5 Cox KD, Covernton GA, Davies HL, et al. Human consumption of microplastics. Environmental Science & Technology. 2019;53(12):7068–7074. doi:10.1021/acs.est.9b01517

6 Geyer R, Jambeck JR, Law KL. Production, use, and fate of all plastics ever made. Science Advances. 2017;3(7):e1700782. doi:10.1126/sciadv.1700782

7 Andrady AL. Microplastics in the marine environment. Marine Pollution Bulletin. 2011;62(8):1596–1605. doi:10.1016/j.marpolbul.2011.05.030

8 Jenner LC, Rotchell JM, Bennett RT, et al. Detection of microplastics in human lung tissue using μFTIR spectroscopy. Science of the Total Environment. 2022;831:154907. doi:10.1016/j.scitotenv.2022.154907

9 Deng Y, Zhang Y, Lemos B, Ren H. Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure. Scientific Reports. 2017;7:46687. doi:10.1038/srep46687

10 Rubin BS. Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects. Journal of Steroid Biochemistry and Molecular Biology. 2011;127(1–2):27–34. doi:10.1016/j.jsbmb.2011.05.002

11 Peretz J, Vrooman L, Ricke WA, et al. Bisphenol A and reproductive health: update of experimental and human evidence, 2007–2013. Environmental Health Perspectives. 2014;122(8):775–786. doi:10.1289/ehp.1307728

12 Ehrlich S, Williams PL, Missmer SA, et al. Urinary bisphenol A concentrations and early reproductive health outcomes among women undergoing IVF. Human Reproduction. 2012;27(12):3583–3592. doi:10.1093/humrep/des328

13 Varayoud J, Ramos JG, Bosquiazzo VL, et al. Neonatal exposure to bisphenol A alters rat uterine implantation-associated gene expression. Endocrinology. 2011;152(8):3101–3111. doi:10.1210/en.2010-1044

14 Bloom MS, Kim D, vom Saal FS, et al. Bisphenol A exposure reduces the estradiol response to gonadotropin stimulation during in vitro fertilization. Fertility and Sterility. 2011;96(3):672–677. doi:10.1016/j.fertnstert.2011.06.063

15 Fujimoto VY, Kim D, vom Saal FS, Lamb JD, Taylor JA, Bloom MS. Serum unconjugated bisphenol A concentrations in women may adversely influence oocyte quality during in vitro fertilization. Fertility and Sterility. 2011;95(5):1816–1819. doi:10.1016/j.fertnstert.2010.11.008

16 Zhao Y, Feng Y, Shi R, et al. Microplastics detected in human follicular fluid and in vitro fertilization outcomes. Science of the Total Environment. 2023;899:165356. doi:10.1016/j.scitotenv.2023.165356

17 Hou L, Wang X, Zhao Z, et al. Adverse effects of polystyrene microplastics on male reproductive functions. Environment International. 2021;146:106254. doi:10.1016/j.envint.2020.106254

18 Berntsen S, Strømkjaer K, Kristensen SL, et al. Chronic inflammation and reproductive suppression: mechanistic pathways. Endocrinology. 2019;160(4):753–764. doi:10.1210/en.2018-00653

19 Geens T, Aerts D, Berthot C, et al. A review of dietary and non-dietary exposure to bisphenol-A. Food and Chemical Toxicology. 2012;50(10):3725–3740. doi:10.1016/j.fct.2012.07.059

20 Carwile JL, Luu HT, Bassett LS, et al. Polycarbonate bottle use and urinary bisphenol A concentrations. Environmental Health Perspectives. 2009;117(9):1368–1372. doi:10.1289/ehp.0900604

21 Biedermann S, Tschudin P, Grob K. Transfer of bisphenol A from thermal printer paper to the skin. Analytical and Bioanalytical Chemistry. 2010;398(1):571–576. doi:10.1007/s00216-010-3936-9

22 Michałek B, Skrzypulec-Plinta V, Drosdzol-Cop A. Urinary bisphenol A in women with polycystic ovary syndrome: a possible suppressive effect on steroidogenesis. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2021;264:28–33. doi:10.1016/j.ejogrb.2021.06.014

23 Bae J, Thévenot P, Amoah SK, et al. Polycystic ovary syndrome and endocrine disruptors (bisphenols, parabens, and triclosan) — a systematic review. Life. 2023;13(1):201. doi:10.3390/life13010201

24 Fahey JW, Talalay P. Antioxidant functions of sulforaphane: a potent inducer of Phase II detoxication enzymes. Food and Chemical Toxicology. 1999;37(9–10):973–979. doi:10.1016/S0278-6915(99)00082-4

25 Dinkova-Kostova AT, Kostov RV. Glucosinolates and isothiocyanates in health and disease. Trends in Molecular Medicine. 2012;18(6):337–347. doi:10.1016/j.molmed.2012.04.003

26 Egner PA, Chen JG, Zarth AT, et al. Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. Cancer Prevention Research. 2014;7(8):813–823. doi:10.1158/1940-6207.CAPR-14-0103

27 Genuis SJ, Birkholz D, Ralitsch M, Thibault N. Human detoxification of perfluorinated compounds. Public Health. 2010;124(7):367–375. doi:10.1016/j.puhe.2010.03.002

28 Dhingra R, Winquist A, Darrow LA, Klein M, Steenland K. A study of reverse causation: examining the associations of perfluorooctanoic acid serum levels with two outcomes. Environmental Health Perspectives. 2017;125(3):416–421. doi:10.1289/EHP125

29 Wang Y, Qian H. Phthalates and their impacts on human health. Healthcare. 2021;9(5):603. doi:10.3390/healthcare9050603

From PCOS (recently renamed PMOS) and hormonal signalling to inflammation, oxidative stress and IVF outcomes, we examine how modern environmental exposures may be influencing reproductive health in ways medicine is only beginning to understand.

It’s a conversation about fertility, modern life and the invisible exposures the body is now adapting to every single day.

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He didn’t come in because he felt ill. He came in because something had stopped making sense. Not pain. Not fatigue in any language he could clearly name. Just a quiet misalignment.

At night, his heart rate sat too high. Ninety-five. Sometimes a hundred. Lying still. No anxiety trigger, no late caffeine and no alcohol binge. By morning, it disappeared.

His Oura ring had been flagging it and his WHOOP had been watching it. His HRV was drifting downward for weeks and his resting heart rate was edging up. His sleep was more fragmented than he realised.

“I feel fine,” he said. “But something’s off.” That was the only language he had. So we ran an ECG.

Paroxysmal atrial fibrillation¹

Not constant or dramatic, but just intermittent enough to remain invisible, unless you were watching continuously, and for the first time in his life, he was.

The body has never lived in snapshots

Medicine still works in moments. A blood test, a reading, a single number taken once, and then interpreted as if it were stable. But physiology is not stable. It is rhythmic.

The autonomic nervous system oscillates between sympathetic activation and parasympathetic recovery, second by second,² cortisol follows a diurnal curve, it is not a constant value³ and glucose rises and falls in response to eating behaviour, not intention⁴

The body moves in trajectories, not states and a single number is just a photograph but health is a film. Wearables did not give us more data, they changed the unit of measurement, from moment to pattern.

The signal is still there. The interpretation is what we’ve lost

There is a term for sensing the internal state of the body: Interoception.⁵

It is the brain’s ability to interpret signals from the heart, lungs, gut, and immune system, to feel fatigue before collapse, hunger before dysregulation and strain before injury. This system is not abstract. It is neuroanatomical.

The insular cortex integrates visceral signals with emotional awareness⁶ and the vagus nerve carries afferent information from organs to brainstem nuclei⁷. Heart rate variability reflects this entire feedback loop, the flexibility of the system to respond and recover,² and for most of human history, this was enough.

Because life created contrast. Light and dark were distinct, movement was continuous and stress resolved.

Now, the inputs have flattened.

Artificial light suppresses melatonin and disrupts circadian rhythm⁸. Ultra-processed food overrides satiety signaling through dopaminergic reward pathways⁹. Chronic stress maintains elevated cortisol and sympathetic tone¹⁰. Sedentary behaviour reduces mitochondrial signaling and metabolic flexibility¹¹.

The signal hasn’t disappeared but the noise has increased to the point that the signal feels like baseline. Fatigue becomes normal, poor sleep becomes identity and low resilience becomes personality. The body is still speaking. We’ve just lost fluency.

Wearables are not technology. They are compensation

When a system loses function, medicine sometimes replaces it. Not perfectly, but enough to compensate. Wearables are doing something similar, they are not improving physiology. They are translating it.

HRV becomes visible autonomic strain²
Resting heart rate becomes visible inflammatory and metabolic load¹²
Sleep becomes visible neurophysiological repair¹³

They are not giving you new information but they are restoring access to information you no longer reliably perceive. A prosthesis for perception.

What your wearable is actually measuring

It looks like a fitness tracker but it is actually a map of biological ageing across systems.

Autonomic system: HRV reflects vagal tone and autonomic flexibility. Chronically low HRV is associated with increased all-cause mortality and reduced adaptability²

Cardiorespiratory system: VO₂ max remains one of the strongest predictors of mortality. Each 1 MET increase reduces risk by ~13%¹⁴

Neurological system: Slow-wave sleep facilitates glymphatic clearance of neurotoxic waste including amyloid-β¹⁵

This is not performance data, it is system integrity. The wearable does not show how fit you are, it shows how well your systems are holding together.

Why behaviour changes when biology becomes visible

This is where wearables become incredibly powerful. Not because they inform but because they make physiology impossible to ignore.

Alcohol

Alcohol suppresses parasympathetic activity and reduces HRV via autonomic imbalance¹⁶, it fragments sleep architecture by reducing slow-wave sleep and REM¹⁷. But most people don’t feel that clearly, until they see it on their WHOOP dashboard the next morning. Red recovery with lowered HRV, sky high resting heart rate and very fragmented sleep.

This is not theory but personal physiology and this really leads to positive behavioral changes. That third glass of red wine will be contemplated and then skipped. You don’t want a red recovery when you have a big meeting the following day, it will just throw you off your game. When the proof is flashing on your dashboard first thing in the morning, the body becomes harder to lie to.

Sleep

Sleep is not rest, it is active repair. Growth hormone pulses during slow-wave sleep¹⁸
and synaptic pruning and memory consolidation occur during REM¹³. A late night is not just fatigue, it is missed biology.Wearables don’t create discipline. They expose cost.

Glucose

HbA1c is an average, it hides variability. It tells you how you ate over the last 3 months. CGMs tell you how you are eating right now. They reveal postprandial spikes, which are independently associated with oxidative stress and endothelial dysfunction¹⁹. For the first time, eating behaviour has immediate metabolic feedback. Not retrospective but real-time.

Movement

Exercise is scheduled as an event, but it is a signal the body desperately needs daily. Skeletal muscle acts as an endocrine organ, releasing myokines that regulate inflammation and insulin sensitivity²⁰ and regular movement improves mitochondrial biogenesis and metabolic flexibility¹¹

Did your WHOOP age lower because of the three strength training sessions you put in over the course of the week? Did that drop in biological age feel good and did it encourage you to repeat the pattern the following week, rather than skipping the weights whilst getting caught up in your busy life? Busy, is what is like to call, modern life’s euphemism for sedentary.

This is the uncomfortable truth

Longevity is not built in interventions. It is built in repetition of the pillars of longevity: sleep, movement, light, food and stress

Daily. Quietly. For years.

Wearables don’t change physiology but they change awareness and awareness changes behaviour. This is where the gold dust lies. The four age related diseases that are the causal effect of shortened healthspan today are diseases of lifestyle. Of the way the body moves through the world. Governed by the behaviors and habits of its host.

When you change that behavior, when you reinforce the positive feedback from the wearable device you then automatically reduce the risk of chronic disease and extend healthspan.

What could be more important to longevity?

Where wearables fail

They are not precise.

Sleep staging is inferred, not measured (no EEG)¹³. VO₂ max is estimated, not directly tested and HRV varies with measurement conditions. They are directionally useful but not diagnostically definitive and more importantly, they can disconnect you from your body if misused.

I had a patient, a woman in her early fifties, a couple of years into menopause, meticulous by nature, the kind of person who reads the footnotes. She came to me three months after getting her first wearable. She wasn’t sleeping better. She was sleeping worse.

Not because her sleep had changed. But because she was now watching it. Every morning before she had even sat up, she was reading her scores. A readiness of 67 sent her into a quiet spiral. She would cancel her morning walk, the one thing that was actually helping her, because the device had told her to rest. She had stopped trusting the feeling of waking up refreshed and started trusting the number instead.

Her HRV hadn’t dropped. Her anxiety had risen. And anxiety, as it turns out, is one of the most reliable ways to suppress the very metrics she was trying to improve. The wearable hadn’t made her more connected to her body. It had made her more afraid of it.

When a number overrides sensation, the prosthesis replaces the system it was meant to support. And that is regression. If you wake up on a red day, but you feel okay and you use it as your excuse to cancel on your personal trainer, then the whole point is lost in this disconnection. Use it as a tool to motivate and assist, not as a diagnosis or a clutch to fuel anxiety.

They measure the body. They don’t actually question the environment it’s in.

A raised heartrate may mean you are fighting the beginning of a virus, and you should take it easy, it may mean you had too much caffeine too late in the day or it could be a signal that the body hasn’t fully recovered from training. All are very different inputs, so they shouldn’t warrant the very same output.

Anthropology got here first

In Sardinia and Ikaria, no one tracks HRV because nothing in their environment chronically disrupts it. Movement is continuous and meals are structured. Stress resolves through social regulation and social connection alone improves survival by ~50%²¹. The body reads safety and it invests in repair.

We replaced regulation with measurement

We removed light, movement, community and rhythm and replaced them with data, metrics and tracking. We now measure what the environment once regulated. The wearable is not innovation. It is evidence of loss.

The man who paid attention

He went on to have the pathway ablated, a small, precise intervention. Electrical silence where there had been noise, thenrhythm settled. The risk that had been quietly accumulating; stroke, instability, the slow erosion of cardiac function now fell away before it ever had the chance to declare itself.

Nothing dramatic happened and that is the point because from the outside, it looks like the wearable did something but it simply revealed a pattern. He chose not to ignore it and that decision changed the trajectory of his physiology. That is what matters, not the device but the relationship to what it shows.

So the question is not: Which wearable should I buy?

The question is: What has changed in my life that I need one to see what my body is already trying to tell me?

And more importantly: What will I do with what it shows?

Because used well, a wearable does not replace the body. It restores a line of communication that has been made harder to access. A way of seeing pattern again, of responding earlier, of intervening while biology is still reversible.

Not optimisation or control but something quieter: a return to paying attention, while there is still something left to change.

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References

1. Perez MV et al. Large-scale assessment of a smartwatch to identify atrial fibrillation. NEJM. 2019. https://doi.org/10.1056/NEJMoa1901183

2. Thayer JF, Lane RD. Neurovisceral integration model. Neurosci Biobehav Rev. 2009. https://doi.org/10.1016/j.neubiorev.2008.08.004

3. Czeisler CA. Circadian rhythms and sleep. Nature. 2013. https://doi.org/10.1038/497S13a

4. Monnier L et al. Glucose variability and complications. Diabetes Care. 2006. https://doi.org/10.2337/dc06-0197

5. Craig AD. Interoception and the sense of the physiological condition. Nat Rev Neurosci. 2002. https://doi.org/10.1038/nrn894

6. Critchley HD et al. Neural systems supporting interoception. Nat Neurosci. 2004. https://doi.org/10.1038/nn1176

7. Berthoud HR, Neuhuber WL. Vagal afferent pathways. Auton Neurosci. 2000. https://doi.org/10.1016/S1566-0702(00)00215-0

8. Walker MP. Sleep and circadian biology. Ann NY Acad Sci. 2009. https://doi.org/10.1111/j.1749-6632.2009.04416.x

9. Hall KD et al. Ultra-processed diets and energy intake. Cell Metab. 2019. https://doi.org/10.1016/j.cmet.2019.05.008

10. McEwen BS. Stress physiology. NEJM. 1998. https://doi.org/10.1056/NEJM199801153380307

11. Booth FW et al. Inactivity and chronic disease. Compr Physiol. 2012. https://doi.org/10.1002/cphy.c110025

12. Fox K et al. Resting heart rate and mortality. JACC. 2007. https://doi.org/10.1016/j.jacc.2007.04.079

13. de Zambotti M et al. Wearables vs PSG sleep accuracy. Sleep. 2019. https://doi.org/10.1093/sleep/zsy198

14. Myers J et al. Exercise capacity and mortality. NEJM. 2002. https://doi.org/10.1056/NEJMoa011858

15. Xie L et al. Sleep drives glymphatic clearance. Science. 2013. https://doi.org/10.1126/science.1241224

16. Saghir Z et al. Alcohol and HRV. J Clin Med. 2018. https://doi.org/10.3390/jcm7030058

17. He S, Hasler BP, Chakravorty S. Alcohol and sleep-related problems. Current Opinion in Psychology.2019;30:117–122. doi:10.1016/j.copsyc.2019.03.007

18. Van Cauter E et al. Sleep and growth hormone. Endocr Rev. 2000. https://doi.org/10.1210/edrv.21.3.0390

19. Ceriello A et al. Postprandial hyperglycemia. Diabetes Care. 2008. https://doi.org/10.2337/dc08-0369

20. Pedersen BK. Muscle as endocrine organ. Physiol Rev. 2019. https://doi.org/10.1152/physrev.00024.2018

21. Holt-Lunstad J et al. Social relationships and mortality. PLoS Med. 2010. https://doi.org/10.1371/journal.pmed.1000316

The Patient Who Could Not Answer the Question

A ninety-year-old woman sits across from me. She has come in for gastric discomfort. Pain after eating. A slow withdrawal from food. On paper, this is straightforward. Ageing, reduced gastric acid, mucosal atrophy.

I ask her what a typical day of eating looks like. She pauses.

“We used to get sandwiches from Marks and Spencer,” she says.
“My husband and I, we’d eat on the go. Always busy. Always out…”

Her husband died a few years ago.

I ask again, gently.
“And now?”

She returns to the same place. The same memories. The same life. Her daughter, sitting beside her, leans forward.

“Mum,” she says, more firmly,
“Dr Rhea is asking what you eat now. Not before when you and Papa used to live in London.”

But the question is already answered. This is not just about food. This is a nervous system still organised around a life that no longer exists. A body that once regulated in the presence of another now left to stabilise itself.

And slowly, quietly, everything begins to change.

We Built a World Where Survival No Longer Requires Each Other

There was a time when being alone was not an inconvenience. It was a risk.

Not emotional discomfort. Not a passing feeling. A biological disadvantage.

To be alone once meant you did not eat. No shared hunt. No collective effort. No guarantee of food the next day.Protection was not optional. It was communal. Sleep required someone watching. Movement required coordination. You did not survive alone.

Now we live in a world where you can order food on Deliveroo without speaking to another person. You can find a home through Property Finder without ever meeting the people who built it, sold it, or lived in it before you. You can work, eat, move, and exist entirely independently.

We have engineered out the necessity of each other. But we have not changed the biology that still expects it. And so something subtle has happened.

The conditions that once signalled safety are no longer guaranteed.

Stress Was Designed to Resolve. Loneliness Does Not.

Stress, in the body, follows a rhythm.

It rises.
It peaks.
It resolves.

A clean physiological loop. But loneliness disrupts that loop. Loneliness is the store that never closes.

The lights are still on. The door is slightly open. No one is quite sure who might walk in. Nothing dramatic is happening.And yet nothing is settled.

The body does not fully downshift. It does not fully switch off. It does not complete the cycle. It remains slightly activated.

Not in crisis. But not safe enough to close.

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Loneliness Is Processed as Threat, Not Emotion

We often speak about loneliness as though it belongs to psychology. But the brain does not process it that way.

The anterior cingulate cortex (the same region activated in physical pain) is activated during social exclusion¹. From a neural perspective, the distinction between emotional pain and physical pain is not clean.

It is shared.

The amygdala increases threat signalling. The hypothalamus activates the HPA axis. Cortisol rises.

The body prepares. Not for sadness. But for danger. Because evolution never updated the code.

To be alone once meant vulnerability. No tribe meant no protection. No shared resources. No survival advantage. So the system responds accordingly.

We speak about loneliness as though it belongs to emotion. Something subjective. Something optional. Something soft.But the body does not experience it that way.

A meta-analysis of over 300,000 individuals found that social isolation increases mortality risk by 29% — a magnitude comparable to smoking 15 cigarettes a day¹.

More recent data shows that loneliness accelerates biological ageing by approximately four years, measured through epigenetic clocks².

This is not language. This is measurement.

What Chronic Isolation Does to the Body

Loneliness behaves less like a feeling and more like a sustained biological exposure. Cortisol remains elevated.Sympathetic tone increases. Vagal tone declines.

Gene expression shifts. Studies show increased pro-inflammatory signalling and reduced antiviral responses in chronically lonely individuals².

Cytokines rise — IL-6, TNF-alpha. Inflammation becomes baseline, not response. Sleep becomes fragmented. Not always shorter — but less restorative. Metabolism shifts subtly. Glucose regulation becomes less efficient.

Over time, this leads to:

• Increased cardiovascular risk³

• Accelerated epigenetic ageing (≈ +4 years)⁴

• Higher rates of dementia⁵

• Immune dysregulation

This is not an abstract concept. The body encodes isolation.

The gut is not separate from this story.

The enteric nervous system, the vast neural network lining the gastrointestinal tract, communicates with the brain primarily through the vagus nerve. This bidirectional channel regulates digestion, motility, and the composition of the gut microbiome.

When the body registers social isolation as threat, vagal tone declines. The parasympathetic state, the one in which digestion functions well, in which the gut lining maintains its integrity, in which the microbiome is nourished and diverse, is suppressed.

This is why the ninety-year-old woman’s gastric symptoms are not simply mechanical. They are partly functional — a gut responding to a nervous system that has lost its co-regulator. Lost its companion to life.

The body digests differently when it is unaccompanied. We rarely account for that. But the physiology does.

The Mismatch Between Modern Life and Ancient Biology

Modern life has removed friction. You no longer need a tribe to eat. To move. To find shelter. But the body still expects the signals that came with that life.

Eye contact.
Shared meals.
Physical proximity.
Co-regulation.

Instead, we have replaced them with efficiency. Faster systems. Cleaner independence. Less reliance.

And in doing so, we have removed something the body quietly depended on: The repeated confirmation that it is safe.

What We Learn from the Longest-Lived Populations

Across Okinawa, Sardinia, Icaria, Nicoya, and Loma Linda, a consistent pattern emerges. Not perfection. Connection.

In Okinawa, moai, lifelong social groups, ensure no one moves through life alone⁶.

In Sardinia, daily life is structured around shared rhythm. Meals are communal. Evenings are collective. Sleep aligns with natural light. These populations still experience stress. But it resolves. They do not live in prolonged isolation.

Their biology reflects that.

The Body Does Not Regulate Alone

The body is not a collection of independent systems. It is coordinated. Like an orchestra. Each system, immune, endocrine, nervous, playing in time.

Connection maintains that timing. It acts as a conductor. Remove it, and nothing stops immediately. But something shifts.

It becomes like a violinist left on stage after the orchestra has gone. She continues to play. The instrument still works. The notes still sound. But without the quartet, without the conductor — the timing falters. The pitch drifts. The coherence dissolves. Not because the instrument is damaged.

But because it was never meant to play alone.

Returning to the Woman

What she needed was not just acid support. Not just dietary adjustment. Not just treatment for gastritis. She needed rhythm.

Shared meals.
Conversation.
Presence.

Because eating is not only digestive. It is relational. The body prepares differently when it is alone. It digests differently when it is unaccompanied. We rarely account for that.

But the physiology does.

What This Means in Practice

The intervention is not to socialise more broadly.

It is to reconnect intentionally.

• Call someone you have been meaning to speak to

• Share a meal instead of eating alone when you can

• Prioritise one or two relationships of depth over many of surface

• Reintroduce small rituals — walking, coffee, conversation — done in presence

These are not lifestyle extras. They are biological inputs.

The Closing

We have built a world where you can meet your needs without people.

Food arrives.
Homes are found.
Work is done.

But the body still waits for something else. A signal it was designed to receive. That it is safe enough to soften. Safe enough to repair. Safe enough to close the loop.

Longevity is not only about how you live. It is about whether your biology is being conducted or left to play alone.

Because the most powerful signals for repair were never just nutrients or movement.

They were other humans.

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References

1. Eisenberger NI et al. Science. 2003

2. Cole SW et al. Genome Biology. 2007

3. Valtorta NK et al. Heart. 2016

4. Sutin AR et al. Nature Aging. 2022

5. Livingston G et al. Lancet. 2020

6. Buettner D. Blue Zones research

7. Holt-Lunstad J et al. Perspectives on Psychological Science. 2015

Happy listening!

A forty-eight-year-old woman sits across from me and says something that has become strangely common in modern medicine.

“I’m not ill,” she says. “I just don’t recover the way I used to.”

She is not describing disease in any conventional sense. Her blood work is unremarkable. Her scans are normal. She still exercises, still works, still functions in the way modern life requires.

But something in the deeper rhythm of her biology has changed.

The body used to move like a quiet orchestra. Signals rising and falling in rhythm. Inflammation arriving, then dissolving.Collagen laid down, then remodelled. Sleep descending like a tide, restoring what the day had quietly worn away.

Repair was never something we noticed. Because it never asked for attention. It happened in the background, like silk being rewoven, thread by invisible thread, across the architecture of tissue.

Now, that silk doesn’t tear dramatically. It loosens. Frays at the edges. Holds, but not quite as it used to.

A strained tendon takes months instead of weeks. A poor night’s sleep seems to echo into the week. Bruises linger. Inflammation settles into tissues and remains there longer than it should.

Nothing dramatic has happened. And yet something unmistakable has been lost.

This is one of the defining biological experiences of contemporary aging: not sudden pathology, but the slow erosion of repair.

It is this quiet biological deceleration that helps explain one of the fastest-growing fascinations in longevity medicine: Peptides.

The body heals through signals, not intentions

Healing is not passive. The body does not repair simply because tissue is damaged. It repairs because cells receive instructions.¹

Every phase of regeneration depends on signaling molecules telling tissues: repair here, reduce inflammation here, build collagen here, restore blood supply here.²

Peptides are fragments of this signaling language. They are short chains of amino acids that act like biochemical messengers, carrying instructions between cells.³

What makes them medically intriguing is that many of the peptides now in demand are tied directly to processes modern humans feel are failing: slower tendon healing, poorer muscle recovery, weaker sleep restoration, declining tissue resilience.

The peptide story is not really about innovation. It is about replacement.

Repair used to be built into life

For most of human history, the body did not need pharmacological reminders to regenerate. Humans lived inside conditions that constantly reinforced repair. Movement was not scheduled exercise. It was survival.

Muscle was loaded daily through carrying, climbing, walking, lifting.⁶ Growth hormone pulses were stimulated naturally through deep sleep, fasting, physical exertion, and circadian rhythm.⁷

Collagen remodeling occurred in bodies repeatedly exposed to real mechanical challenge.⁸ Inflammation rose in response to injury and then resolved.⁹

The body received constant environmental signals telling it: use this tissue, preserve this muscle, repair this damage.

Now compare that to modern life. Many people sit for ten hours a day, then attempt to compress movement into one or two gym sessions a week. We no longer load our tissues often enough to justify the body investing heavily in maintaining them.

And yet we expect those tissues to remain youthful. So instead, increasingly, we turn to molecules.

BPC-157 and the modern wound that never quite heals

BPC-157 is perhaps the clearest example of what the peptide age is really revealing. Its full name, Body Protection Compound 157, sounds almost mythological, as though it belongs in a laboratory designed by science fiction writers.

Derived from a protective protein sequence first isolated from gastric juice, BPC-157 has become one of the most fashionable peptides in sports medicine, longevity clinics, and wellness circles because it promises something people increasingly feel they have lost: the ability to heal normally.

If peptides were people at a dinner party, BPC-157 would be impossible to miss. He’s the stocky one. Broad-shouldered. Grounded. The kind of person who doesn’t say much, but when something breaks, he’s already fixing it before anyone else has stood up.

Someone spills a glass. A chair leg snaps. A guest twists their ankle on the way in.

BPC doesn’t panic. He just moves quietly through the room, binding, reinforcing, stabilising. He is not glamorous. He is not the centre of attention. But he is the reason things hold together.

And perhaps that is why he has become so popular, because increasingly, people feel like something in their bodies is no longer holding the way it should.

It is used for stubborn tendon injuries. Slow ligament recovery. Persistent inflammation. Gut irritation. Soft tissue repair.People turn to it when their bodies seem reluctant to mend themselves. And that is the deeper cultural clue. Why are so many bodies now reluctant to mend?

When I use oral BPC-157 clinically, it is often in a very specific subset of patients: those with severe gut barrier disruption, high ultra-processed food exposure, chronic stress physiology, and signs of intestinal permeability dysfunction.

In some carefully selected patients, I have trialed oral BPC-157 where conventional gut restoration strategies alone were insufficient, particularly in those with suspected barrier compromise and elevated zonulin-associated permeability patterns.

Because what we call “leaky gut” is often not mysterious at all.

It is frequently the predictable consequence of modern living: ultra-processed diets, microbiome depletion, alcohol burden, sleep loss, persistent cortisol excess, and inflammatory food exposure damaging a barrier system that was never designed for this level of assault.¹⁸ ¹⁹

The gut lining was never meant to be a battlefield.

It is a single-cell border, soft, selective, alive. A membrane that decides, moment by moment, what belongs inside your body and what does not. It was designed for plants, for fibre, for rhythm, for microbes that knew your name.

Not for emulsifiers. Not for alcohol most nights of the week. Not for cortisol that never quite settles. And so the barrier does what all biological systems do under pressure.

It loosens. Not enough to fail, but enough to leak.

BPC becomes attractive because it offers the fantasy of shortcut healing: repair the gut lining without rebuilding the life that damaged it. That is why it is culturally irresistible.

CJC-1295, Ipamorelin, and the muscle shortcut fantasy

CJC-1295 and Ipamorelin reveal another version of the same modern longing. These peptides stimulate growth hormone signaling pathways, attempting to amplify anabolic pulses that naturally decline with age.⁵

They are sought after for: better recovery, improved sleep repair, lean muscle gain, faster training adaptation.

Across the room, you’ll find a very different pair. CJC-1295 and Ipamorelin don’t sit still.

They are the ones circulating, energised, persuasive, quietly influential. They lean in when they speak. They make you feel like something is about to happen.

They don’t build muscle themselves. They don’t repair tissue directly. They convince the room to do it. They tap the shoulder of the endocrine system and say: “Now would be a good time to grow.”

They are not the labour. They are the signal. And like all signals, they only make sense if the rest of the environment is ready to respond.

But here too, the question is not simply pharmacological. It is anthropological. Growth hormone evolved to respond dynamically to: deep sleep, intense exertion, fasting, repeated muscular demand.⁷

Historically, muscle was preserved because it was constantly required. Now many people spend five days sitting still, lift weights once or twice a week, and then ask why their bodies are not maintaining youthful muscle mass.

Muscle is metabolically expensive. The body will not preserve it unless life repeatedly proves it is needed. So peptides become seductive because they seem to offer a biochemical workaround: the signaling of hard-earned physiological demand without the volume of actual demand.

They promise the gains without the ancestral conditions that once justified them.

TB-500 and the biology of unfinished repair

TB-500 belongs to the same family of modern compensation. Derived from thymosin beta-4, it is used for tissue regeneration, wound healing, injury recovery, and accelerated repair after strain.²¹

TB-500 is different again. If BPC is the one who fixes what’s broken,
TB-500 is the one who moves through the room before you even realise something is wrong.

He’s fluid.
Restless.
Always in motion.

He notices the tension before it becomes injury. He crosses spaces others don’t. Connective, adaptive, hard to pin down. Where BPC reinforces, TB-500 reorganises. He doesn’t just repair the structure, he changes how the structure responds to strain.

And that is why people are drawn to him when recovery feels incomplete, when the body heals, but never quite returns to what it was.

Athletes use it. Longevity clinics prescribe it. Patients seek it when inflammation lingers and tissues fail to rebound.

Its popularity tells the same story: modern bodies are increasingly unable to recover at the pace people expect. Not because biology is broken. Because life has become anti-regenerative.

The peptide pharmacy comedy nobody explains

And then there is the strange comedy of how people actually obtain these molecules. Because peptide culture has split into two parallel universes.

In one universe: regulated compounding pharmacies prepare peptides under controlled sterile conditions, with purity standards, dosing oversight, endotoxin testing, and pharmaceutical-grade manufacturing safeguards.

In the other: the internet.

A curious wilderness of “research-grade peptides” sold in tiny mysterious vials that often sound as though they were produced by a moonlighting chemist in a warehouse next to a vape distributor.

“Not for human consumption,” the label solemnly declares — while entire online forums are dedicated to humans consuming exactly that.

This distinction matters enormously.

Research-grade peptides are often not subject to the same sterility controls, endotoxin screening, contaminant testing, or batch consistency standards as regulated pharmacy compounds.

And endotoxins are not trivial.

Even tiny bacterial residue contamination can provoke inflammatory reactions that have nothing to do with the peptide itself.

Which means that sometimes when people say: “This peptide made me feel awful,”
what they may actually be experiencing is not the biology of regeneration —
but the biological consequences of injecting something that was never adequately purified in the first place.

The peptide world, in this sense, is part medicine, part frontier economy. And not all frontiers are safe.

Every party has a back room.

This is where things become less certain.
Less regulated.
Less… explained.

And not everything served there is what it claims to be.

The evidence problem

And yet here the story becomes more uncertain. Despite enormous enthusiasm, many peptides now circulating in wellness medicine still lack the level of evidence required for confident long-term endorsement.

BPC-157, for example, has compelling animal data and mechanistic promise, but robust large-scale human randomized trials remain sparse.¹⁶

The same is true for many growth hormone secretagogues used in anti-ageing clinics.¹⁷ Some may ultimately prove transformative.

Some may become indispensable tools in regenerative medicine. But right now, for many of the compounds most widely discussed, the market has moved faster than the science. Potential is not proof. Mechanism is not outcome. Promise is not certainty.

What the peptide boom is really telling us

The rise of peptides tells us something profound about modern civilisation. It tells us that increasing numbers of people feel their bodies are no longer recovering under ordinary conditions.

They sleep, but do not restore. They exercise, but do not rebuild. They rest, but do not repair. And often, they are right.

But the deeper question is not whether peptides work. The deeper question is: What kind of world have we built, that so many people now need synthetic biochemical messengers
to recreate instructions that ordinary life once provided freely?

That question is larger than medicine. It is anthropological.

Because underneath all of this, the molecules, the protocols, the fascination; is something quieter.

A body that remembers how to repair, but is no longer living in conditions that allow it to. A system waiting for signals it used to receive effortlessly.

Light.
Movement.
Rest.
Challenge.
Resolution.

Things that once told the body, without question: You are safe enough to rebuild.

The patients at the edge of the evidence

Some report remarkable benefit. Some feel no difference. Some return convinced they have found something transformative.

And yet the uncomfortable truth remains unchanged: We still do not have enough data.

Not enough long-term safety data.
Not enough large human trials.
Not enough certainty to speak with the confidence the market often pretends to have.

And that is where modern medicine now finds itself. Not in the certainty of endorsement,
nor in the simplicity of rejection, but in a more difficult ethical space:

If the science is still incomplete, would you still take the message; simply because modern life has made the body so desperate to hear one?

References

¹ Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 6th ed. Garland Science; 2015.

² Gurtner GC, Werner S, Barrandon Y, Longaker MT. Wound repair and regeneration. Nature. 2008;453(7193):314–321. doi:10.1038/nature07039

³ Fosgerau K, Hoffmann T. Peptide therapeutics: current status and future directions. Drug Discov Today.2015;20(1):122–128. doi:10.1016/j.drudis.2014.10.003

⁴ Sikiric P, Seiwerth S, Rucman R, et al. Stable gastric pentadecapeptide BPC 157: novel therapy in gastrointestinal tract and wound healing. Curr Pharm Des. 2011;17(16):1612–1632. doi:10.2174/138161211796197084

⁵ Teichman SL, Neale A, Lawrence B, et al. Prolonged stimulation of growth hormone secretion by CJC-1295. J Clin Endocrinol Metab. 2006;91(3):799–805. doi:10.1210/jc.2005-1537

⁶ Lieberman DE. The Story of the Human Body: Evolution, Health and Disease. Pantheon Books; 2013.

⁷ Van Cauter E, Plat L, Copinschi G. Interrelations between sleep and the somatotropic axis. Sleep. 1998;21(6):553–566. doi:10.1093/sleep/21.6.553

⁸ Kjaer M. Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. Physiol Rev.2004;84(2):649–698. doi:10.1152/physrev.00031.2003

⁹ Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454(7203):428–435. doi:10.1038/nature07201

¹⁰ McEwen BS. Protective and damaging effects of stress mediators. N Engl J Med. 1998;338(3):171–179. doi:10.1056/NEJM199801153380307

¹¹ Frost HM. Bone’s mechanostat: a 2003 update. Anat Rec A Discov Mol Cell Evol Biol. 2003;275A(2):1081–1101. doi:10.1002/ar.a.10119

¹² Wolfe RR. The underappreciated role of muscle in health and disease. Am J Clin Nutr. 2006;84(3):475–482. doi:10.1093/ajcn/84.3.475

¹³ Magnusson SP, Kjaer M. The impact of loading, unloading, ageing and injury on the human tendon. J Physiol.2019;597(5):1283–1298. doi:10.1113/JP275450

¹⁴ Hood DA. Mechanisms of exercise-induced mitochondrial biogenesis in skeletal muscle. Appl Physiol Nutr Metab.2009;34(3):465–472. doi:10.1139/H09-045

¹⁵ Veldhuis JD, Roemmich JN, Richmond EJ, Rogol AD. Endocrine control of body composition in infancy, childhood, and puberty. Endocr Rev. 2005;26(1):114–146. doi:10.1210/er.2003-0038

¹⁶ Sikiric P, Hahm KB, Blagaic AB, et al. BPC 157 and gastrointestinal tract healing: experimental evidence and future perspectives. Curr Pharm Des. 2020;26(26):3071–3089. doi:10.2174/1381612826666200113100905

¹⁷ Smith RG, Sun Y, Jiang H. Growth hormone secretagogues: biology and clinical relevance. Endocr Rev.2005;26(3):346–360. doi:10.1210/er.2003-0017

¹⁸ Zinöcker MK, Lindseth IA. The Western diet–microbiome-host interaction and its role in metabolic disease. Nutrients.2018;10(3):365. doi:10.3390/nu10030365

¹⁹ Vanuytsel T, Tack J, Farre R. The role of intestinal permeability in gastrointestinal disorders and current methods of evaluation. Gastroenterology. 2021;160(5):1617–1629. doi:10.1053/j.gastro.2020.12.062

²⁰ Dattilo M, Antunes HKM, Medeiros A, et al. Sleep and muscle recovery: endocrinological and molecular basis. Med Hypotheses. 2011;77(2):220–222. doi:10.1016/j.mehy.2011.04.017

²¹ Goldstein AL, Hannappel E, Kleinman HK. Thymosin β4: actin-sequestering protein wound repair and regeneration molecule. Expert Opin Biol Ther. 2005;5(5):593–601. doi:10.1517/14712598.5.5.593

This piece is also available as a podcast episode. If you prefer to listen, you can find it on Apple Podcasts and Spotify under “RE:Age Reflections on Body, Time and Longevity”.

When I first arrived in Japan, I found it more difficult than I expected.

There were no bins anywhere. I kept holding onto rubbish, unsure where it was meant to go. There were rules for everything. Where to stand, how to queue, how to behave in shared spaces. It felt rigid, almost excessive at first.

And I think part of that reaction was also me.

I had just left Dubai during a period of uncertainty. We didn’t even know until the very last moment whether this trip would happen, constantly looking at updated flight schedules and repeated alerts on our phones about intercepted missiles. I arrived carrying more than I realised; not obvious stress, but a low, constant tension that had been sitting quietly underneath everything.

So stepping into a place that felt so controlled, so ordered, almost amplified that feeling. At first, it was overwhelming.And then, gradually, something shifted.

The detail I didn’t understand at first

It took me a few days to realise what I was actually reacting to. The rules are not there for control. They are there for respect.

You don’t speak loudly in lifts, not because you’ve been told not to, but because someone else might want quiet. You don’t litter, not because there’s a consequence, but because it would change the space for someone else. You don’t pick a cherry blossom, not because it’s forbidden, but because it’s beauty belongs to everyone.

There is a quiet understanding that your actions are never isolated.

They land somewhere.
They affect someone.

And when enough people live like that, the environment itself changes.

It becomes calmer.
More predictable.
Easier to exist within.

You feel it before you can explain it. Environments like this don’t just change behaviour. They change biology.

The thing we have slowly lost

In the Western world, we’ve become very good at building life around the individual.

Your health.
Your goals.
Your progress.
Your outcomes.

And none of that is wrong. But it is incomplete. Because a life optimised only for the self is often a life the body never fully learns to relax into.

Because we’ve quietly deprioritised something fundamental: the idea that we exist within a shared system. That our behaviours shape not just our own experience, but the baseline environment that everyone else lives in.

And biologically, that matters far more than we give it credit for.

Ikigai: and why I thought I understood it

I had always known the word ikigai. Your reason for being. And I always thought I understood it.

But being here reframed it for me. Because in the Western world, we often interpret purpose as something quite individual: your career, your achievements, your identity.

But here, it feels different. It feels embedded. Relational.

Less about what you extract from life, and more about how you exist within it.

Why I love this medicine

And it made me think about my own work. Because I feel incredibly lucky to have a strong sense of ikigai. Practising longevity medicine — and actually living it — is something I care deeply about.

Not just because of the science. But because of the people. What I enjoy most is not diagnosing a condition. It’s understanding a life.

Sitting with someone and learning: who they are, what they care about, what drives them, what they’re afraid of, what they want their life to look like.

And then building something together. A plan that comes from a place of strength, not just fixing what’s wrong. That’s what makes it meaningful.

The fifth pillar we don’t measure properly

In longevity medicine, we tend to focus on what we can quantify.

Nutrition.
Exercise.
Sleep.
Metabolic health.

But there is a fifth pillar that is consistently present in the longest-living populations in the world:

Community.

If you look at places like Loma Linda, longevity is not built purely through individual optimisation. It’s built through structure — shared meals, collective routines, social integration, a sense of belonging.

People are embedded in something.

They are known.
They are expected.
They are part of a system that extends beyond themselves.

And that has measurable effects on biology.

A large meta-analysis of over 300,000 individuals showed that stronger social relationships are associated with a 50% increased likelihood of survival¹.

Loneliness and social isolation are consistently associated with increased mortality risk, with effect sizes comparable to major risk factors like smoking².

Cardiovascular risk increases significantly in socially isolated individuals, including higher rates of heart disease and stroke³.

And perhaps most importantly, a sense of purpose, having a reason to wake up, to contribute, to be part of something, is associated with improved cognitive function and longer lifespan across multiple longitudinal studies⁴.

This is not abstract. It is biological.

It is mediated through the nervous system, through inflammatory pathways, and through the way the brain continuously interprets the world around us⁷ ⁸.

Why this works

Because the body is not just responding to what you eat or how you move. It is responding to the environment you exist within.

And social connection changes that environment. It reduces baseline stress signalling⁵.
It regulates the nervous system, increasing vagal tone and heart rate variability, both of which are strongly associated with emotional regulation, cardiovascular health, and longevity⁷.
It dampens chronic inflammatory activation⁶.

It gives the body something it is constantly searching for: A sense of safety.

From a neurophysiological perspective, this matters more than we realise. The nervous system is constantly scanning the environment for cues of safety or threat, and it is only in states of perceived safety that the body shifts into parasympathetic dominance, the state required for repair, restoration, and long-term health⁸.

And when the body feels safe, it behaves differently.

It repairs.
It restores.
It lets go.

The second lesson: Makoto

There was another word that stayed with me: Makoto.

Sincerity. Authenticity. Truth. The idea that trust — both in yourself and from others — comes from alignment. Not from performance. Not from presentation. But from being genuinely consistent with who you are.

And I realised something slightly unexpected. My word for this year had been trust. And I hadn’t consciously connected the two.

But when I looked back on my diary where I write my manifestations and words of daily gratitude - I realised how deeply this idea had already shaped the way I think.

What this place does to you

There is something about Japan that is difficult to explain until you feel it. There is space here. Not just physical space.But mental space.

You’re not constantly pushed to react, to optimise, to move faster than you need to. You have room to notice how you feel.

And that, in itself, changes something.

The thing I will take back

Japan didn’t give me a new protocol. It didn’t change my biomarkers. It didn’t offer a shortcut.

What it did was far more confronting.

It made me realise that we have become very good at extending life, while quietly neglecting the conditions that make that life meaningful.

Because longevity, as we practise it in the West, is still largely centred around the self.

Your health.
Your optimisation.
Your outcomes.

And all of that matters. But it is incomplete.

Because a body that lives longer, without connection, without contribution, without meaning, is not necessarily a body that has lived well.

And perhaps that is the shift Japan forced me to confront. Longevity isn’t just a biological pursuit. It’s a reflection of the environments we create for each other.

It’s shaped by how you move through the world, how you affect the people around you, and how you contribute to something beyond yourself.

So maybe the question is not only:

How do I live longer?

But:

What does my life give back, not someday, but in the way I live it, every day?

Because in the end, it is not just the length of life that stays behind. It is what that life leaves within others.

References:

¹ Holt-Lunstad J, Smith TB, Layton JB. Social relationships and mortality risk: a meta-analytic review. PLoS Medicine. 2010;7(7):e1000316. https://doi.org/10.1371/journal.pmed.1000316

² Holt-Lunstad J, Smith TB, Baker M, Harris T, Stephenson D. Loneliness and social isolation as risk factors for mortality: a meta-analytic review. Perspectives on Psychological Science. 2015;10(2):227–237. https://doi.org/10.1177/1745691614568352

³ Valtorta NK, Kanaan M, Gilbody S, Ronzi S, Hanratty B. Loneliness and social isolation as risk factors for coronary heart disease and stroke. Heart. 2016;102(13):1009–1016. https://doi.org/10.1136/heartjnl-2015-308790

⁴ Boyle PA, Barnes LL, Buchman AS, Bennett DA. Purpose in life is associated with mortality among community-dwelling older persons. Psychosomatic Medicine. 2009;71(5):574–579. https://doi.org/10.1097/PSY.0b013e3181a5a7c0

⁵ McEwen BS. Protective and damaging effects of stress mediators. New England Journal of Medicine. 1998;338(3):171–179. https://doi.org/10.1056/NEJM199801153380307

⁶ Slavich GM, Irwin MR. From stress to inflammation and major depressive disorder. Psychological Bulletin. 2014;140(3):774–815. https://doi.org/10.1037/a0035302

⁷ Thayer JF, Lane RD. Claude Bernard and the heart–brain connection: further elaboration of a model of neurovisceral integration. Neuroscience & Biobehavioral Reviews. 2009;33(2):81–88. https://doi.org/10.1016/j.neubiorev.2008.08.004

⁸ Porges SW. The polyvagal theory: phylogenetic substrates of a social nervous system. International Journal of Psychophysiology. 2001;42(2):123–146. https://doi.org/10.1016/S0167-8760(01)00162-3

He came in for antibiotics.

Thirty-eight years old, a banker, immaculate in presentation. Crisp shirt, polished shoes, efficient speech. He was apologetic about taking up time. “Sinus infection again,” he said. Second one this month.

He wanted what most patients want in these moments: a quick prescription, a quick fix, a quick return to function.

But recurrent illness is rarely just about the infection itself.

When the body begins failing in patterns, medicine must ask a deeper question:
What terrain is this infection growing in?

So we checked his bloodwork. His vitamin D was low. Not catastrophically low. Not dramatic enough to make headlines. Just quietly, chronically insufficient — exactly the kind of deficiency modern medicine has normalised because it has become so common.

And that is the real story.

The striking thing about vitamin D deficiency today is not that it exists. It is that it has become ordinary.

We were not designed to live like this

For most of human history, humans lived in regular contact with sunlight.

We rose with dawn.
We worked outdoors.
Skin met ultraviolet light as part of ordinary life, not as an occasional event. Vitamin D is not simply something we eat. It is a hormone-like signal the body manufactures when sunlight touches skin.

But modern life has steadily broken that relationship.

We wake indoors.
Commute indoors.
Work under artificial light.
Exercise in enclosed spaces.
Spend long days behind glass, where UVB rays cannot penetrate.

And even when sunlight is available, not every body produces vitamin D equally.

Melanin, the pigment that gives skin its colour, acts as a natural sunscreen. This is biologically protective, but it also means darker skin requires longer sun exposure to produce the same amount of vitamin D as lighter skin.¹

Age changes the equation too.

As skin ages, its ability to synthesize vitamin D declines significantly. A person in their seventies may generate only a fraction of the vitamin D that a younger adult can produce from the same sunlight exposure.²

So deficiency is not only about spending too little time outside.

It is also shaped by pigmentation, latitude, season, clothing, sunscreen use, and the simple biological reality that ageing skin becomes less efficient at making what it once produced easily.

This is why vitamin D becomes more important, not less, as we grow older. The older body needs the signal just as much — sometimes more — but receives it less efficiently.

We have built a civilisation that protects us from the elements, but in doing so has distanced us from one of the oldest biological inputs human physiology depends upon.

Vitamin D deficiency is, in many ways, a disease of indoor civilisation: but also of modern longevity itself.

The immune system: where deficiency first whispers

Most people still associate vitamin D with bones. That is only the beginning.

Vitamin D receptors are expressed throughout the immune system — macrophages, dendritic cells, T lymphocytes, B cells, respiratory epithelium.¹ When activated, vitamin D helps regulate innate immune defense, antimicrobial peptide production such as cathelicidin, and inflammatory balance.²

In the respiratory tract, this matters profoundly.

Low vitamin D status has been associated with increased susceptibility to upper respiratory infections, impaired mucosal immune defense, and recurrent airway inflammation.³ A major meta-analysis in the BMJ found that vitamin D supplementation reduced risk of acute respiratory tract infections, particularly in those who were deficient at baseline.⁴

Several studies have also found lower serum 25(OH)D levels in patients with chronic rhinosinusitis compared with healthy controls, suggesting deficiency alters the inflammatory terrain in which sinus disease persists.⁵

Vitamin D does not “cause” sinusitis. But deficiency creates a biological environment in which immune resilience weakens. That banker’s second sinus infection this month was not caused by one low vitamin D reading. But his low vitamin D was part of the story.

A terrain marker.
A clue that the immune system was operating below optimal capacity.

The brain: sunlight is also neurochemistry

Vitamin D is deeply involved in the central nervous system.

Receptors for vitamin D are found in the hippocampus, hypothalamus, substantia nigra, and cortex — regions intimately involved in mood regulation, cognition, and emotional processing.⁶

This matters because vitamin D helps regulate synthesis of serotonin, dopamine, and neurotrophic factors involved in neuronal resilience.⁷

Low vitamin D has repeatedly been associated with higher rates of depression, seasonal mood decline, fatigue syndromes, and impaired cognitive performance.⁸

What many people describe as winter brain fog, flattened mood, or unexplained emotional fatigue is often interpreted psychologically first.

But sometimes it is biochemical. A body deprived of light becomes, quite literally, neurochemically dimmer.

Gene expression: vitamin D is not passive, it edits biology

What makes vitamin D extraordinary is that it behaves less like a conventional vitamin and more like a genomic regulator.

Its active form, calcitriol, binds to the vitamin D receptor (VDR), which enters the nucleus of the cell and interacts directly with DNA.⁹

This receptor complex influences hundreds of genes involved in:

• immune signaling

• inflammatory control

• insulin regulation

• oxidative stress defense

• cellular repair

• mitochondrial function

Vitamin D is not simply supporting systems.
It is helping orchestrate them.

This is why deficiency has such diffuse effects: when vitamin D is low, regulation becomes less precise across multiple biological pathways at once.

The cardiovascular and metabolic system: silent long-term consequences

Vitamin D deficiency is increasingly linked with hypertension, insulin resistance, endothelial dysfunction, and adverse cardiometabolic risk profiles.¹⁰

Part of this relationship is inflammatory.
Part is vascular.
Part is endocrine.

Vitamin D helps regulate the renin-angiotensin system, influences vascular tone, and plays a role in glucose metabolism.¹¹

Low levels are associated with higher rates of metabolic syndrome and type 2 diabetes progression.¹²

This does not mean vitamin D is a miracle cure. But it does mean chronic deficiency quietly destabilizes systems that age us faster when unsupported.

Mortality: what long-term data reveals

Perhaps the most striking evidence comes from mortality studies.

Large epidemiological cohorts consistently show that low serum 25(OH)D is associated with increased all-cause mortality risk.¹³

Individuals with chronically deficient levels have higher rates of:

• respiratory mortality

• cancer mortality

• frailty-related decline

• immune-mediated illness

This is not because vitamin D alone determines lifespan. It is because vitamin D status reflects whether the body has access to one of its most fundamental regulatory inputs: light.

Low vitamin D is often not the disease itself. It is the biomarker of a body living too far from its design.

Why are so many people deficient now?

Because almost every force in modern life pushes us toward deficiency.

1. We no longer receive consistent UVB exposure

Vitamin D synthesis requires UVB radiation directly on skin. Glass blocks UVB.

2. Skin pigmentation changes synthesis efficiency

Melanin reduces UV penetration; darker skin requires longer exposure.

3. Age reduces production dramatically

A 70-year-old produces roughly 25% of the vitamin D a 20-year-old makes from identical sun exposure.

4. Sunscreen blocks the pathway

Essential for skin cancer prevention — but it also reduces UVB penetration.

5. Geography matters

In many regions, winter sunlight angle makes adequate production impossible for months.

6. Obesity alters bioavailability

Vitamin D becomes sequestered in adipose tissue, lowering circulating levels.

In short: Modern humans are biologically underlit.

The blood level that matters

Clinically we measure serum 25-hydroxyvitamin D [25(OH)D].

General functional ranges:

• Deficiency: <20 ng/mL (50 nmol/L)

• Insufficiency: 20–30 ng/mL

• Optimal for most adults: 30–50 ng/mL

• In recurrent infection or immune dysregulation: often aim closer to 40 ng/mL

You cannot reliably guess vitamin D status by symptoms alone. You test.

What do we do to fix it?

Not with vague advice. Not with “get more sun.” With deliberate correction.

Sunlight

10–30 minutes of midday exposure to arms and legs several times weekly, depending on latitude, season, skin tone, and age. The goal is not burning. The goal is biologically meaningful UVB contact — enough to trigger endogenous synthesis without damaging the skin barrier.

Supplementation

For many deficient adults, vitamin D3 is the preferred form because it is the same type your skin naturally makes from sunlight, and it raises blood levels more effectively than vitamin D2.

Typical correction ranges for deficiency often fall between: 2,000–4,000 IU vitamin D3 daily, depending on your blood level, body size, absorption, and medical guidance.

But vitamin D does not work alone.

It is often paired with vitamin K2, because once vitamin D increases calcium absorption from the gut, K2 helps activate proteins that move that calcium into bones and teeth, where it is needed most, and away from places it does not belong, such as arteries and soft tissues.¹⁴
This is particularly important for long-term cardiovascular health, because calcium balance is not just about how much you absorb — it is about where that calcium is deposited over time.

In other words:
Vitamin D helps absorb calcium.
Vitamin K2 helps tell calcium where to go.

Why vitamin A matters too

Vitamin A is part of this same fat-soluble network.

It helps maintain the health of blood vessel linings, supports immune barriers such as the respiratory and gut mucosa, and works alongside vitamin D at the level of gene signaling, where both nutrients help regulate how cells grow, repair, and respond to inflammation.¹⁵

This matters because cardiovascular health is not only about cholesterol or blood pressure. It is also about keeping arteries flexible, preventing inappropriate calcification, and maintaining healthy tissue repair.

Together, vitamins A, D, and K form a coordinated system:

• Vitamin D improves calcium absorption

• Vitamin K2 directs calcium into the skeleton

• Vitamin A supports healthy vessels and balanced signaling

The goal is not megadosing. The point is balance.

These vitamins were never designed to act as isolated pills. In the body, they function as a connected system: each one helping the others work properly.

Re-test

Always repeat bloodwork after 8–12 weeks to ensure levels are moving into optimal range safely.

Cofactors matter

Magnesium remains essential for vitamin D metabolism. Without magnesium, both hepatic and renal activation of vitamin D becomes less efficient.¹⁶

A person can supplement vitamin D faithfully and still fail to correct deficiency if magnesium status is poor.

Think terrain, not pills

If recurrent infections persist, ask deeper questions: Sleep? Stress? Gut absorption? Chronic inflammation? Nasal structural issues? Metabolic dysfunction?

Vitamin D is foundational, but never isolated.

What vitamin D deficiency is really telling us

The epidemic of low vitamin D is not a failure of individual discipline. It is a reflection of how profoundly human life has changed.

We have built lives increasingly disconnected from the environmental signals that once regulated us: sunlight, darkness, movement, season, exposure.

And then we are surprised when biology begins to fail quietly. Low vitamin D is not just about a vitamin. It is about a species living outside its design.

The deeper lesson

That banker left with antibiotics. But he also left with something more important than a prescription: a clue.

Not just about why he had been ill twice in one month, but about the quieter ways modern life erodes us long before disease becomes dramatic enough to name.

Because vitamin D deficiency rarely announces itself loudly.

It does not arrive like a heart attack or a fracture or a diagnosis that changes everything overnight. It arrives silently. As the tiredness people explain away. The lowered mood mistaken for stress. The winter immunity that never quite recovers.The infections that recur just often enough to become normal.

And that is what makes it so dangerous. It hides inside ordinary life.

Inside office towers where daylight is seen but never touched. Inside commutes that begin before sunrise and end after dusk. Inside children growing up indoors beneath artificial light, and adults whose skin no longer meets the sun except through glass.

We have built lives of extraordinary convenience, and in doing so, removed ourselves from one of biology’s oldest relationships: the relationship between human skin and natural light.

The body keeps count of that absence.

It remembers every season lived under ceilings.
Every year spent disconnected from morning light.
Every signal it expected and never received.

Low vitamin D is not simply a vitamin deficiency.

It is evidence of a species living increasingly detached from the conditions that once made it well.

And perhaps that is the real warning hidden in these blood tests: That many of the illnesses we call modern are not mysterious at all. They are, in part, the physiological consequences of living too far from the world we were designed to inhabit.

Sometimes medicine is not about discovering something rare. Sometimes it is about noticing what has become so common we have stopped seeing it.

And vitamin D may be the quietest epidemic of all.

References

¹ Aranow C. Vitamin D and the immune system. J Investig Med. 2011;59(6):881–886. doi:10.2310/JIM.0b013e31821b8755

² Hewison M. An update on vitamin D and human immunity. Clin Endocrinol (Oxf). 2012;76(3):315–325. doi:10.1111/j.1365-2265.2011.04261.x

³ Ginde AA, Mansbach JM, Camargo CA Jr. Association between serum 25-hydroxyvitamin D level and upper respiratory tract infection in the United States population. Arch Intern Med. 2009;169(4):384–390. doi:10.1001/archinternmed.2008.560

⁴ Martineau AR, Jolliffe DA, Hooper RL, et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. 2017;356:i6583. doi:10.1136/bmj.i6583

⁵ Mulligan JK, White DR, Wang EW, et al. Vitamin D3 deficiency increases sinus mucosa dendritic cells in pediatric chronic rhinosinusitis with nasal polyps. Otolaryngol Head Neck Surg. 2012;147(4):773–781. doi:10.1177/0194599812450832

⁶ Eyles DW, Smith S, Kinobe R, Hewison M, McGrath JJ. Distribution of the vitamin D receptor and 1α-hydroxylase in human brain. J Chem Neuroanat. 2005;29(1):21–30. doi:10.1016/j.jchemneu.2004.08.006

⁷ Patrick RP, Ames BN. Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism. FASEB J.2014;28(6):2398–2413. doi:10.1096/fj.13-246546

⁸ Anglin RE, Samaan Z, Walter SD, McDonald SD. Vitamin D deficiency and depression in adults: systematic review and meta-analysis. Br J Psychiatry. 2013;202(2):100–107. doi:10.1192/bjp.bp.111.106666

⁹ Carlberg C, Campbell MJ. Vitamin D receptor signaling mechanisms: integrated actions of a well-defined transcription factor. Steroids. 2013;78(2):127–136. doi:10.1016/j.steroids.2012.10.019

¹⁰ Pilz S, Verheyen N, Grübler MR, Tomaschitz A, März W. Vitamin D and cardiovascular disease prevention. Nat Rev Cardiol. 2016;13(7):404–417. doi:10.1038/nrcardio.2016.73

¹¹ Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D₃ is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest. 2002;110(2):229–238. doi:10.1172/JCI15219

¹² Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes: systematic review and meta-analysis. J Clin Endocrinol Metab. 2007;92(6):2017–2029. doi:10.1210/jc.2007-0298

¹³ Schöttker B, Jorde R, Peasey A, et al. Vitamin D and mortality: meta-analysis of individual participant data from a large consortium of cohort studies. BMJ. 2014;348:g3656. doi:10.1136/bmj.g3656¹⁴ Knapen MHJ, Braam LAJLM, Drummen NEA, Bekers O, Hoeks APG, Vermeer C. Menaquinone-7 supplementation improves arterial stiffness in healthy postmenopausal women. Thromb Haemost. 2015;113(5):1135–1144. doi:10.1160/TH14-08-0675

¹⁵ Ross AC. Vitamin A and retinoic acid in T cell-related immunity. Am J Clin Nutr. 2012;96(5):1166S–1172S. doi:10.3945/ajcn.112.034637

¹⁶ Uwitonze AM, Razzaque MS. Role of magnesium in vitamin D activation and function. J Steroid Biochem Mol Biol.2018;180:35–43. doi:10.1016/j.jsbmb.2017.01.014

There is a specific moment in the modern food story that looks trivial until you realise it was a template.

It wasn’t a war. It wasn’t a famine. It wasn’t a scientific discovery. It was a milkshake.

McDonald’s, in its earliest form, was fast but recognisable: beef patties, potatoes, milkshakes made with ice cream. Then scale arrived.

And when scale arrives, it does not ask, is this nourishing? It asks, is this reproducible? It asks, will it survive transport?It asks, will it hold texture, mouthfeel, colour, and profit margin?

Real ice cream is fragile. It requires a cold chain. It melts. It refreezes. It costs money. So the solution wasn’t better food. The solution was chemistry. Powdered mixes. Emulsifiers. Thickeners. Stabilisers. Add water. Same texture. Longer shelf life. Higher profit.

That is not a niche story about one menu item. That is the origin story of ultra-processing.¹ ³

And once you see it, you begin to recognise it everywhere: the conversion of food from a living, perishable, seasonal object into an industrial product engineered for stability and scale.

Not because anyone set out to harm human biology. But because capitalism does not optimise for biology. It optimises for repeatability.

Food did not become worse. It became scalable.

Most people talk about ultra-processed foods as if they are simply “junk.” As if the problem is moral weakness or bad choices.

But the most honest way to understand ultra-processing is not to start with the consumer. It is to start with the supply chain.⁴ A food system designed to deliver cheap, uniform, always-available calories at industrial scale has a predictable consequence: it removes what is expensive, variable, slow, and fragile.

It removes structure. It removes fibre. It removes the food matrix — the thing that makes a carbohydrate arrive slowly, a fat arrive with signals, a protein arrive buffered.⁵⁻⁸

And then it replaces that structure with what industry can control: extracted starches, refined oils, isolated proteins, flavour systems, and additives that simulate what whole foods once carried naturally.

The front of the packaging is marketing. The back is biology. Because the biology isn’t in the claim. It’s in what had to be removed to make the product viable.

The biology of removing structure

Humans did not evolve eating nutrients. We evolved eating food in form. In texture. In time. Chewing is a signal. Stretch is a signal. Fermentation is a signal. Arrival rate in the small intestine is a signal.⁹–¹¹

Whole foods deliver redundancy - multiple checkpoints that allow the brain, gut, pancreas, and immune system to agree on what is happening. Ultra-processed foods compress those signals into one dominant message: fast reward, fast absorption, minimal work.¹² Once structure is removed, the physics of eating changes. And something else changes that is harder to measure. Hunger becomes unreliable.

Ultra-processed foods do not simply deliver calories differently. They distort the feedback loop between brain and body. Rapid absorption, compressed texture, engineered hyper-palatability - these alter dopaminergic signalling and reward anticipation¹². The body receives energy before it receives fullness.

Satiety becomes delayed. Craving becomes anticipatory. Eating becomes less about need and more about cue. Over time, people lose something subtle but profound: hunger literacy.

They can no longer reliably tell the difference between appetite and stimulation. Between nourishment and reward. Between physical hunger and environmental trigger. This is not gluttony. It is neural recalibration. And when hunger becomes unreliable, restraint becomes heroic rather than automatic.

People eat faster. Satiety arrives later. Calories arrive earlier. Glucose excursions widen. Insulin demand rises. The microbiome receives different substrates.¹³–¹⁴

This is not ideology.

In the NIH inpatient randomised controlled trial by Hall et al., participants eating an ultra-processed diet consumed around 500 kcal per day more and gained weight, despite diets matched for calories, macronutrients, sugar, sodium, and fibre.¹⁵ Not because they were careless. Because the food was engineered to make restraint metabolically late.

Additives: not toxic, but not neutral

It is tempting to make this simple. Ingredients are chemicals. Chemicals are bad. That is not scientifically serious.

But neither is pretending that emulsifiers, stabilisers, and texturisers are biologically inert simply because they are approved for use. Many exist to solve industrial problems: separation, spoilage, texture collapse.

The gut is not a passive pipe. It is a boundary ecosystem protected by a mucus layer, immune signalling, microbial metabolites, and tight junctions.¹⁶–¹⁷

In animal and ex vivo human microbiome studies, common dietary emulsifiers such as carboxymethylcellulose and polysorbate-80 alter microbial composition and inflammatory signalling.¹⁸

More importantly, human feeding trials now show that exposure to carboxymethylcellulose changes gut microbiota and metabolomic profiles in a subset of individuals, consistent with adverse gut effects.¹⁹

This does not mean all emulsifiers are poison. It means industrial solutions to food stability become biological variables at population scale. Biology is rarely indifferent to inputs repeated daily for decades.

Ultra-processed food is not just an obesity story

Obesity is the visible outcome, so it dominates the conversation. But ultra-processed food exposure is associated with cardiometabolic disease, some cancers, depression, anxiety, and increased all-cause mortality across large observational cohorts and meta-analyses.²⁰–²²

Definitions vary. Not all processing is equivalent. Nuance matters. But the pattern remains: diets dominated by industrial formulations are consistently associated with worse health outcomes than diets dominated by minimally processed foods.

The system does not make ultra-processed foods because it hates humans. It makes them because they are efficient commodities.

They last.
They transport.
They standardise.
They scale.

And in scaling, they become less like food and more like a platform.

If your grandparents wouldn’t recognise it, it isn’t food

There is an anthropological shortcut that is often more accurate than any nutrition label: if your grandparents would not recognise it as food, it probably isn’t food.

For most of human history, eating was not abstract. Food had lineage. It came from a plant or an animal. It had seasonality, weight, smell, texture. It spoiled. It required preparation. It demanded time. Ultra-processed foods break that continuum.

A protein bar engineered for shelf life, a flavoured yoghurt stabilised with gums, a meal assembled from powders, oils, and flavour systems, these are edible products, but they are not culturally continuous with human eating.

No grandparent would recognise them as nourishment. They would recognise them as objects. Anthropology matters because biology follows culture. And culture is learned early.

A child born today does not meet food the way previous generations did. Their first exposures are often sweetened yoghurts, pouches, cereals extruded into shapes, engineered snacks designed for compliance and shelf stability.

Their microbiome is seeded in an environment without seasonal scarcity. Without fermentation variability. Without textural friction. By adolescence, the neural reward circuits that respond to food have already adapted to intensity.

This is not nostalgia. It is developmental programming. Ultra-processing did not just scale adult food. It scaled early exposure. And early exposure writes deeply.

The human digestive system evolved in dialogue with foods that had limits; limits of availability, perishability, texture, and effort. When food loses those limits, appetite loses its brakes.

Limits were once biological. Food spoiled. It required effort. It required chewing. It required time. It required stopping.Ultra-processed food removes those boundaries. It is soft. It is portable. It is available at midnight. It requires no preparation, no interruption, no friction.

When friction disappears, regulation weakens. Appetite evolved inside constraint. When constraint vanishes, appetite becomes unbounded, not because humans changed, but because the environment did.

The loss of limits is not indulgence. It is physics. Calling something “food” because it fits through a mouth is a modern convenience, not a biological truth.

What it looks like in clinic

This becomes painfully clear in practice. A large proportion of the people I see — intelligent, motivated, health-conscious individuals who have actively sought out an advanced longevity programme, are consuming more than half of their daily calories from ultra-processed foods without realising it.

They present with hormonal dysregulation, gut symptoms, mood instability, fatigue, poor sleep, inflammatory markers that never quite settle.

They believe they are eating well.

So I ask them to send photographs of everything they eat and drink over three days.

Not a food diary.
Not a summary.
Photographs.

When the images arrive, there is often a moment of quiet shock. Protein powders. “Healthy” snack bars. Flavoured yoghurts. Seed-oil dressings. Fortified milks. Sugar-free drinks. Convenience foods marketed as wellness.

None of it registers as non-food until it is seen laid out in sequence. These are not disengaged or careless people.

These are people trying to do everything right, navigating a food environment where industrial products masquerade as nourishment.

If this is the case among those actively seeking longevity, it raises an uncomfortable question: how much of the population - less informed, less resourced, less reflective - is eating a diet that no human body was ever designed to interpret as food at all?

The closing

There is a reason the milkshake is the perfect metaphor. Because the moment you turn ice cream into powder and ask water to pretend, you have crossed a boundary.

You have taken something living, fragile, perishable, real, and rebuilt it as a product that can survive capitalism.

And the body notices. Not morally. Not emotionally. Physiologically.

The gut notices. The pancreas notices. The brain notices. The question is not whether you can “handle” ultra-processed food. The question is how much of your life you want to spend eating things that required your biology to be removed in order to be profitable.

References

¹ Monteiro CA, Cannon G, Levy RB, et al. Increasing consumption of ultra-processed foods and likely impact on human health. Public Health Nutr. 2011.
² Monteiro CA, Cannon G. The UN Decade of Nutrition, NOVA classification and ultra-processing. Public Health Nutr.2018.
³ FAO. Ultra-processed foods, diet quality and health. 2019.
⁴ Pineda E, et al. Food environments and obesity. BMJ Nutr Prev Health. 2024.
⁵ Fardet A. Food matrix effects. Nutr Rev. 2016.
⁶ Jenkins DJA, et al. Glycaemic index and food structure. Am J Clin Nutr.
⁷ Reynolds A, et al. Carbohydrate quality and health. Lancet. 2019.
⁸ Monteiro CA. Ultra-processed foods: what they are and why they matter. World Nutr.
⁹ Teff KL. Cephalic-phase responses. Am J Physiol.
¹⁰ de Graaf C. Texture and satiety. Physiol Behav.
¹¹ Lentle RG, et al. Mastication and digestion. Comp Biochem Physiol.
¹² DiFeliceantonio AG, et al. Ultra-processed foods and reward pathways. Cell Metab.
¹³ Sonnenburg JL, Sonnenburg ED. Microbiota-accessible carbohydrates. Cell Metab.
¹⁴ Zinöcker MK, Lindseth IA. UPFs and metabolic health. BMJ Open.
¹⁵ Hall KD, et al. Ultra-processed diets cause excess intake. Cell Metab. 2019.
¹⁶ Johansson MEV, et al. Intestinal mucus barrier. Nat Rev Gastroenterol Hepatol.
¹⁷ McGuckin MA, et al. Mucus and gut defence. Nat Rev Microbiol.
¹⁸ Chassaing B, et al. Dietary emulsifiers alter microbiota. Nature.
¹⁹ Chassaing B, et al. CMC feeding trial. Gastroenterology. 2022.
²⁰ Lane MM, et al. Ultra-processed foods and mortality. BMJ. 2024.
²¹ Pagliai G, et al. UPFs and mental health. Nutrients.
²² Srour B, et al. UPFs and cancer risk. BMJ.