I know this is complicated territory.
Whatever brought you here—curiosity, concern, your own complicated relationship with what medicine recommends and what you’ve learned to question—I won’t ask you to set that aside. I’ve spent twenty years in functional medicine learning to take seriously what people carry into the room. That includes the history that makes a recommendation feel different depending on who’s making it, when, and why.
So I’ll tell you where I’m standing before I tell you what I’ve been researching.
I got the first dose of the Shingrix vaccine on a Friday just a few weeks ago. By Saturday I had a pulsing headache behind my right eye, intense enough that I stood in a parking lot and wondered whether I’d be able to drive home. I spent the rest of the day in bed. My Oura ring showed elevated autonomic stress for days. It wasn’t the kind of stress that comes from a debate or a deadline, but the behind-the-scenes kind that registers in your heart rate variability when your body is doing significant work without telling you about it.
I was hungrier than usual. Tired in a way that wasn’t explained by my schedule.
I knew what was happening. I’d done the research. I understand the work of the immune system. And I had a specific reason for finally making the decision that led me to the Safeway pharmacy for the shot that bruised my left arm.
My 87-year-old mother reminded me of the rest of it just this week.
What My Mother Told Me
I was just three years old. My sister Lori had gotten chickenpox first—mildly, the way some children do, the way the textbooks describe it, the way my son endured it twenty years ago. I caught it from Lori. But what happened next was something else entirely.
The blisters weren’t just on the surface of my skin. My parents were told there were blisters on my internal organs. My fever spiked. My eyes swelled. I lay in my orange and yellow bedroom—the one with the paper dolls and the books I couldn’t read because my eyes were too swollen—burning from the inside. My parents were beside themselves with worry. The doctor, a man named Dr. Borovsky whom I came to know like he was my uncle, went to light candles at a church with the nurses that worked in his office. They prayed for me while my parents drove me from New Jersey across state lines to Columbia Presbyterian in New York to see a specialist. There were tests. There was fear of Reye Syndrome, a rare disorder that damages many parts of the body, especially the brain and the liver. There was a baby aspirin given for the fever—later found to be contraindicated in exactly this situation.
I remember none of it.
Lori had chickenpox mildly and moved on. I had it severely and did not.
Chickenpox occupies an interesting place in the cultural memory of those of us born before about 1990. For a generation, it was a normal childhood rite of passage—chickenpox parties, deliberate exposure, the assumption that getting it once and being done was the right strategy. The varicella vaccine arrived in 1995, and the social narrative around chickenpox shifted within a generation. Children born after about 1998 mostly do not get it. Their parents (like me) did.
My mother, when I called her this week, kept returning to the same phrase. The chickenpox, she said, was the beginning of it all. Meaning my sickness. Meaning the body that would become difficult to understand, that would require a decade of investigation, repeat hospitalizations, fear, and my parents’ decision not to have more children. It would, eventually, make my career in functional medicine make sense—because, for reasons including but not limited to this childhood experience, I needed to understand what conventional medicine often fails to explain.
My mother has been holding that sentence for nearly sixty years. The beginning of it all. As if the body sends up a flare at the moments worth remembering—and then keeps the record quietly, whether we do or not.
It turns out she may have been right in ways she didn’t have language for.
What the Virus Doesn’t Do
Here is what the research is now making clear about the varicella zoster virus (VZV)—the virus that causes chickenpox.
It doesn’t leave.
After the rash clears and the fever breaks and the child recovers enough to go back to school, the virus retreats into the sensory neurons alongside the spinal cord and the cranial nerves. It establishes what we now understand as latency. It’s held there, silently, by VZV-specific T-cell immunity—the immune surveillance that runs continuously, without your awareness, for the rest of your life.
For most people, this works. The virus stays dormant. Decades pass.
But as we age, that T-cell mediated immunity naturally declines. The virus doesn’t disappear. It just faces weaker opposition. And the people contending with the steepest decline relative to their viral burden are those of us born before the 1995 vaccine—the ones carrying wild-type VZV from a childhood chickenpox infection.
Here’s something most people don’t know: before childhood vaccination became widespread, adults who’d already had chickenpox were regularly re-exposed to it. At school pickup. At family gatherings. From a neighbor’s kid with spots. That re-exposure didn’t usually give us chickenpox again—our immune systems recognized the virus and neutralized it. But in doing so, they quietly refreshed our VZV-specific T-cell immunity. We were getting passive immune top-ups throughout our adult lives without knowing it, and those top-ups kept the latent virus in our nervous systems more thoroughly suppressed.
When childhood vaccination arrived and chickenpox largely disappeared from circulation, that ambient boosting disappeared too. Adults who carry the wild-type virus stopped receiving those regular immune reminders. The latent virus faces progressively weaker opposition. This may be part of why shingles rates have risen in the decades since childhood vaccination became standard—a relationship known as the exogenous boosting hypothesis, still debated in the scientific literature. The vaccine that protected a generation of children may have quietly removed a protection the previous generation didn’t know they’d been receiving.
This dynamic was documented well enough that it delayed childhood chickenpox vaccination policy in the United Kingdom and several other countries, where public health bodies weighed the benefit to children against the cost to adults losing their natural immune reinforcement. It’s not a fringe concern, it’s a significant population-level trade-off that plays out quietly, over decades, inside individual nervous systems.
At some point—for about one in three people—the balance tips. The virus reactivates. It travels down the nerve to the skin and produces shingles: the rash, the burning, the nerve pain that can last for months or years after the blisters clear. In some cases the virus reactivates not in the skin but in the facial nerve—a condition called Ramsay Hunt syndrome, which can cause facial paralysis, vertigo, and hearing loss, and is frequently misdiagnosed as Bell’s palsy because it’s rare enough that many clinicians don’t immediately recognize it.
That much, most people know.
And when you bring up shingles, almost everyone has a story. Their own, or a partner’s, a friend’s, a parent’s—the shingles episode that wasn’t just a rash. The pain that didn’t end when the blisters did. The months of postherpetic neuralgia. The friend who hasn’t slept right in two years. For me, the story that lingers involves my maternal grandmother—my Grandma Betty. The grandma that gave me hope, confidence, and frozen chocolate chip cookies. Her shingles kept coming back. The last episode landed her in the hospital, where she had the stroke that took her life.
I was eighteen. I was just starting college. I lost the person who believed in me most. And it was the first death I can remember registering as grief and loss and longing.
What the research about shingles published in the last eighteen months has added is a bit hard to absorb. I spent the past year reading over twenty books on longevity and following the evidence as it emerged. The shingles vaccine kept showing up. It isn’t necessarily a longevity headline, but it is a finding that crosses disciplines. Cardiologists are noting it. Neurologists are noting it. The biological aging researchers are noting it. By the time I sat down to write this piece, I had read enough to know it wasn’t a single signal in a single dataset.
Here’s some of what I found:
A 2025 analysis of health records from over 100 million Americans found a consistent relationship between VZV reactivation and dementia—across nearly 400 measured variables.
Recurrent shingles episodes carried higher dementia risk than a single episode, suggesting the cumulative burden of the virus’s activity matters, not just its visible announcements.
A January 2026 study examined shingles vaccination across seven domains of biological aging—inflammation, immune function, cardiovascular health, neurodegeneration, epigenetic aging—and found that vaccinated individuals showed measurably slower aging across multiple domains, with effects persisting four or more years post-vaccination.
Four independent meta-analyses, the largest pooling data from 21 studies and over 104 million participants, have found approximately a 24% reduced risk of any dementia and a 47% reduced risk of Alzheimer’s specifically among those vaccinated against shingles.
The most methodologically rigorous study used a natural experiment in Wales, where the shingles vaccine was offered free through the NHS—but only to those born on or after September 2, 1933. Those born even days before that date were ineligible for life. The program wasn’t mandatory, but because eligibility was determined by exact date of birth rather than personal choice, the people just old enough to qualify and the people just too old to qualify were, in every meaningful way for these purposes, identical—same health histories, same socioeconomic circumstances, same proximity to care.
The only difference between them was an accident of birthdate.
Because of that, the standard objection to vaccine research largely dissolves. That objection is reasonable and has followed the field for decades: people who choose to vaccinate may have different viewpoints on health, better access to care, more regular contact with their doctors—or diverge from non-vaccinators in the many smaller ways that accumulate into any health decision. Any of those differences, not the vaccine itself, could explain better outcomes. But when eligibility is an accident of birthdate, those differences disappear. The person born one week after the cutoff and the person born one week before it are not different kinds of people. They simply live on opposite sides of a line drawn by a policy date. That’s about as close to proof as population-level vaccine research gets.
The result showed a roughly 20% reduction in new dementia diagnoses over seven years among those who were eligible.
And the results are not limited to that one study. They’ve been replicated in Wales, as well as in England, Australia, New Zealand, Canada, and multiple US health record databases, by independent research groups, using different methods. And it keeps pointing in the same direction: that vaccinating against shingles appears to reduce the risk of dementia, and possibly the broader trajectory of biological aging, in ways that the field is still working to fully explain.
What this means, practically, is that the virus my three-year-old body received from my sister in that New Jersey suburban house—the virus that drove my parents to Columbia Presbyterian, that led to candle lighting in a church, that my mother has described for nearly sixty years as the beginning of it all—has been in my nervous system ever since. It’s been held there by immune surveillance that has kept it dormant, mostly, while also, possibly, doing things we are only beginning to measure. And the evidence now suggests that what I do about that virus—at fifty-nine, with an active clinical frame of mind and decades of research capacity and an Oura ring—has potential implications for what happens to my brain and my biology over the next thirty years.
What Moves a Decision Like This
I want to recognize something candidly before I go further: Shingrix produces real side effects.
First, a note on what Shingrix actually is: It’s the second-generation shingles vaccine, approved by the FDA in 2017. It replaced an older vaccine called Zostavax that has now been discontinued in the US. Shingrix is non-live and uses an adjuvant called AS01B to drive a stronger T-cell response—the same arm of immunity that holds the virus dormant. That stronger response is why it appears to work better than its predecessor. It’s also why people feel it.
In clinical trials, 17% of recipients had at least one Grade 3 reaction—severe enough to prevent normal everyday activity. For people with autoimmune conditions—rheumatoid arthritis, MS, Crohn’s, or Hashimoto’s, like myself—there are legitimate questions the clinical trials have not fully answered, because those populations were largely excluded from the studies. There is a small but documented increased risk of Guillain-Barré Syndrome (another autoimmune condition affecting the peripheral nerves and muscles) in adults sixty-five and older within 42 days post-vaccination, acknowledged on the vaccine manufacturer’s label. Women tend to report stronger reactions than men. (Though who knows if that’s due to biological reaction or to women being more likely to report what they feel.)
For me, these aren’t reasons to dismiss the vaccine. They are reasons to make an informed decision with someone who knows your full picture, and not to hand that decision to an algorithm or a blanket prescription of what should or should not be done.
Shingles is also not communicable in the way most diseases we vaccinate against are. You cannot give shingles to anyone. A person with active shingles can, through direct contact with the rash, transmit the virus to someone who has never had chickenpox or been vaccinated against it—in which case that person develops chickenpox, not shingles—but the reactivation that becomes shingles in your nervous system stays your reactivation. The virus that has been latent in your dorsal root ganglia since childhood, waking up now, is your virus.
Unlike the childhood varicella vaccine, whose use shifts patterns of exposure across the population, the biological risk Shingrix reduces lands on the person who takes it. The potential benefit lands on the same person. The side effects, the same. That makes the Shingrix decision different from decisions about vaccines where my choice has implications for the people around me—where what one person does affects what another person catches.
The immediate biological calculus is mostly interior. The risk it reduces is mine. The benefit, mine. The side effects, mine. Which is exactly the kind of decision that belongs to the person inside the body, made by or with the help of someone who knows it well.
But interior doesn’t mean uninfluenced.
The selective vaccinator among us is not making a decision like this on biomedical evidence alone. We’re making it inside a cultural moment that has its own complicated history, where institutional trust has been fractured in ways that are sometimes justified and sometimes not, where the line between skepticism and misinformation has become genuinely difficult to locate. I would never suggest that your hesitation is uninformed. But I do want to share what I found when I went looking, and what it meant against the backdrop of my own body’s long relationship with this particular virus, so that the thinking, when and if you do it, is your own—and richer for the company.
The research on Shingrix is, by the standards of preventive medicine, unusually strong. The Wales natural experiment is the kind of evidence we rarely get. The replication in Canada makes it harder to dismiss. Four meta-analyses across more than 100 million people pointing in the same direction is not a signal to ignore because it comes from a cultural moment we’ve learned to distrust.
But evidence alone is not what moves people. What moves people is understanding what’s at stake in their specific body. Mine has been carrying this virus since I was three years old, since the blisters went internal, since my parents drove me to New York in fear and my sister was already fine.
My mother called it the beginning of it all.
My grandmother’s shingles was closer to the end.
I am trying, at fifty-nine, to keep it from claiming the middle.
It is making me wonder, though.
My mother held that one sentence about my childhood for nearly sixty years, and the body that received it has been holding the virus for just as long. The term for what was happening inside me—viral latency—did not exist in the room when I was three. Not quite. A British general practitioner named Robert Hope-Simpson was formulating it in 1965, working from sixteen years of careful observation of 3,500 patients in a rural practice in England. He proposed that following chickenpox, the virus becomes latent in the sensory ganglia, where it can be reactivated from time to time.
I was born in 1966—a year after Hope-Simpson published his hypothesis. I got sick in 1969.
The concept of viral latency as it applies to VZV was being written into the medical record in essentially the same moment my body was writing the virus into its memory. Neither my mother nor Dr. Borovsky, lighting candles at a church while my parents drove me to Columbia Presbyterian, had access to it yet. The confirmation that Hope-Simpson’s hypothesis of viral latency was correct didn’t arrive until 1983. We now know that T-cell immunity is what holds the virus dormant—the immune system’s long memory, the quiet surveillance that keeps the latent virus from stirring. That particular understanding developed through the 1980s and 1990s, the decade in which we lost my grandmother. The dementia connection is only from the last eighteen months.
The keep thinking about what else I have filed away as resolved.
Not as a wound, or as trauma. Just as: that happened, and then it ended, and then we moved on. The cystic acne that appeared in moments of extreme change and pressure. The car accidents I walked away from. The pregnancy that didn’t continue. The grief that I metabolized, I told myself, in the appropriate amount of time.
My mother said it was the beginning of it all and meant my sickness. And she was right about that.
But I’m starting to think that she was expressing more than she realized. That what we name as beginnings are sometimes just the moments where the body started keeping a record nobody asked it to keep and that didn’t make it into the chart. But the body has been keeping every record of every one of those moments ever since, faithfully, without request or permission, waiting for someone to finally pay attention.
What in your body is still holding what you decided was over?
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