Ep. 45: How A Vaccine Against Vascular Aging Could Prevent Heart Attacks and Stroke — with Dr. David Scieszka, Founder of Vertical Longevity Pharma

What if you could vaccinate against the world’s number-one killer? In this episode, Dr. Regina Druz walks on the wild side with Dr. David Scieszka — an Army psyop specialist turned longevity scientist and the founder and CEO of Vertical Longevity Pharma — to explore a provocative idea: a ‘vaccine’ that trains the immune system to clear out senescent ‘zombie’ cells lining our blood vessels, with the goal of preventing and even reversing atherosclerosis. They unpack the biology of cellular senescence, why the endothelium becomes ‘leaky’ with age, how the vaccine is designed to work, and where the research stands. One crucial caveat up front, and throughout: this is early, preclinical work — animal data only, not yet tested in humans, not FDA-approved, and not available. It’s a fascinating look at where the science may be heading, not a treatment you can get, and nothing here is medical advice.

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Episode Chapters

[00:00] Introduction: A Vaccine Against Atherosclerosis?
[01:37] From Army Psyop to Longevity Science
[06:03] Ultra-Processed Foods, Senolytics & Real-World Risk
[10:25] What the Vaccine Targets: Senescent Endothelial Cells
[13:37] Zombie Cells & the Leaky Endothelium
[16:44] How the Vaccine Works: A Surface-Marker Antibody
[17:38] When Senescence Begins & the Acceleration Points
[21:52] Which Cells, Safety & the Target Protein
[25:37] Mouse Results: Whole-Body Rejuvenation (Preclinical)
[29:35] Dosing, Cost & Plaque Reversal (Preclinical)
[35:28] FH, Lp(a) & the Clinical Beachhead
[47:03] What You Can Do Now & Parting Words

Transcript

[00:00] Introduction: A Vaccine Against Atherosclerosis?

Dr. Regina Druz (00:02): Welcome to Own Your Heart Health. I’m Dr. Regina Druz, your holistic cardiologist. This week we’ll dive into common heart health concerns, uncovering root causes and unpacking scientific discoveries and controversies. The information provided does not constitute medical advice. Please contact your healthcare practitioner before making any changes that may impact your health.

Dr. Regina Druz (00:40): Hi everyone, and thank you for listening to Own Your Heart Health with me, Dr. Regina Druz. I have an absolutely fascinating guest today — I feel like we’re going to walk on the wild side. I’m with Dr. David Scieszka, the CEO of a company called Vertical Longevity Pharma, and he’s bringing us news on creating a vaccine. Before you turn me off because you may be wary of vaccines, I want you to hear this in its entirety: a vaccine against the number-one disease that kills men and women in nearly every country — atherosclerosis. I’d never heard of a vaccine for atherosclerosis. We’d love to prevent it, but how would you do it with a vaccine? David, how did you grow up to be who you are today — connect the dots for us.

[01:37] From Army Psyop to Longevity Science

Dr. David Scieszka (01:37): Thanks for having me. I started my scientific career in the Army — which most people wouldn’t expect — as a psychological operations specialist. In peacetime we were essentially census takers: we’d go into friendly territories and ask how people were doing, what they needed — a hospital, a library, food, toothbrushes — and record name and age. I found that people in rural areas were aging at a much more accelerated rate than people in cities, and access to healthcare was the main driver I could identify. That was a real-world example that aging is not set — aging trajectories can be altered. So I set out to figure it out, and immediately got hit with how complicated it is. I did a biotech undergrad, moved into computational biology because this is a complex, systems-based problem, then a PhD in biomedical sciences focused on aging, and an MBA — because when this vaccine started coming together during my postdoc, I realized we’d need to understand how to run a business.

Dr. Regina Druz (03:17): It’s a fascinating story — and I’m still stuck on the psyop part. For those of us unfamiliar with that world, what is psychological operations, especially in times that aren’t so peaceful?

Dr. David Scieszka (03:40): A famous historical example: inflatable ‘balloon’ tanks staged on the shoreline of England, so Germany believed England had a massive tank battalion. That’s a psychological operation — moving attention to where you want it, away from where troops were actually landing, so nobody gets hurt. We also dropped flyers from C-130s to inform local populations, and worked to understand where threats were by talking with communities — ‘we’re providing you a hospital; could you share some intel so we can take the bad guys out of your life?’ I think of it as upgraded infantry: we can shoot and move, but we can also think deeply and try to form solutions to hard problems.

Dr. Regina Druz (04:56): That explains a lot about how you carried that mindset into longevity — from observing patients in under-resourced rural areas. We know there are real healthcare disparities; we’re a big country and we still haven’t solved access even to basic care, and we’re behind a lot of other countries on that. So how did that translate into wanting to pursue longevity, rather than, say, going into policy?

[06:03] Ultra-Processed Foods, Senolytics & Real-World Risk

Dr. David Scieszka (06:03): Funny you mention it — I wanted to be a politician, because I thought access to care was immediately solvable. It turns out that’s a problem we’ll be addressing for decades; we still have food deserts in the U.S. with nothing but fast food, which feeds the health disparities, diabetes, and cardiovascular issues. I later worked in a College of Pharmacy in environmental toxicology, looking at population-wide studies, and it’s striking how far behind we still are. I couldn’t quite do the political route, so I took the science detour.

Dr. Regina Druz (06:56): You took the ‘easier’ path — a biotech PhD. It’s fascinating, because I just read a study in the Journal of the American College of Cardiology on ultra-processed foods and cardiovascular events, with a direct dose relationship: each extra serving raised risk by about 5%. Two things stood out. First, the classification — the NOVA system — isn’t straightforward, because it’s based on the degree of processing, not the nutrients, so fried fish or soy milk can count as ultra-processed. Second, and troubling, there was an interaction with race: in Black patients the risk per serving was higher — around 6% or more. So even within an imperfect system, factors were interacting. So tell me — you went into biotech to help people age more slowly. What did you find in the lab that propelled you toward Vertical Longevity?

Dr. David Scieszka (08:41): A lot of testing — I’ve been in this field for fourteen years. To your point on ultra-processed foods, we know a lack of fiber plus increased sugar does real damage, and fiber can offset some of the fat. We studied longevity therapies in real-world context, because mice in a sterile environment don’t reflect how we actually live — we’re constantly affronted by bacteria, secondhand smoke, diesel exhaust. When we stress-tested some longevity therapeutics, we saw heart failure in mice after wildfire-smoke events with a class of compounds called senolytics — and those are being sold over the counter right now. The epidemiology is hard, because it’s statistically difficult to lift that harm signal high enough to prove it, so they’ll keep being sold. But it turns out they can be a lot more dangerous than people expect — and that was part of the impetus for our vaccine and our current work at Vertical Longevity.

[10:25] What the Vaccine Targets: Senescent Endothelial Cells

Dr. Regina Druz (10:25): So what is the concept of a vaccine against atherosclerosis actually based on — what are we vaccinating against? As a clinical cardiologist, I think of vaccines for infectious agents, like chickenpox. But atherosclerosis is a complex disease. We’d love primordial prevention — getting people to where they don’t even have risk factors — but in my mind, atherosclerosis is aging, because aging is vascular: the vascular system shows all the damage and even participates in other diseases like cancer. So how do you conceptualize a vaccine here — what exactly are you doing?

Dr. David Scieszka (11:35): The cells that line the inside of arteries and veins are called endothelium. Those cells can transform into a senescent state — a state of cell-cycle arrest that, crucially, is pro-inflammatory and no longer functions properly: vascular tone drops, signaling goes awry. The inside of your artery needs to be a very tight barrier, but when cells become senescent they permeabilize that barrier — they can’t hold onto their neighbors as well, so gaps open up. There’s a growing body of evidence for this that isn’t yet well known in cardiology. We’ve known for decades that arterial branch points are hotbeds for atherosclerosis — this is a mechanistic explanation of why: the barrier permeabilizes, turbulent flow drives LDL into the gaps and initiates plaque, and the senescent cells, being pro-inflammatory, hinder the immune system’s clearance of that plaque. So the vaccine targets the senescent endothelial cells. In preclinical studies, clearing them gave the entire mouse body a therapeutic benefit, including the ability to prevent plaque — and we’re now testing in primates whether it can fully clear plaque, which we believe is mechanistically plausible.

[13:37] Zombie Cells & the Leaky Endothelium

Dr. Regina Druz (13:37): Let’s unpack that step by step. Our bodies have living cells and dead cells, but there’s an in-between stage — in my upcoming book, Longevity Decoded, readers will see them called ‘zombie cells.’ Like movie zombies, they’re sort of dead but behave as if alive, and they can do a lot of damage. That’s what senescent cells are. You might think they just sit there taking up space, but they send signals to surrounding tissues that promote inflammation — and our declining ability to clear them is one of the hallmarks of aging. Eventually we can’t clear them, the damage accumulates and compounds. Am I tracking with you?

Dr. David Scieszka (15:02): That’s a fantastic explanation — and they also transform their neighbors into senescence, which is exactly the zombie effect.

Dr. Regina Druz (15:10): So they’re major influencers — and dangerous. Let’s step back: the endothelium is the inner lining of our blood vessels, only one cell thick, present in every vessel down to the capillaries. It’s effectively the largest organ in the body — spread out, it would cover a football field or more. So the endothelium can become leaky — like leaky gut, but here we have leaky vessels. Does that sound right?

Dr. David Scieszka (16:14): Yes, exactly.

[16:44] How the Vaccine Works: A Surface-Marker Antibody

Dr. Regina Druz (16:16): So how does the vaccine actually work — what’s in it, and what’s happening mechanistically to help clear those senescent cells from the blood vessels?

Dr. David Scieszka (16:44): Senescence is incredibly complicated biology — the expression profile isn’t always the same. But thankfully, in the endothelium, once cells turn senescent they pop out a surface marker, almost like a flag. We target that marker with a vaccine-based antibody approach: we have the immune system generate antibodies against the surface marker, and then your own immune system clears out those cells — just as it did when you were younger. That ability to clear senescent cells used to be robust and declines with age, so we’re re-engaging the immune system to work like it did when we were younger.

[17:38] When Senescence Begins & the Acceleration Points

Dr. Regina Druz (17:38): At what age does our own immune clearance of senescent cells start to decline, without any extra stimulation?

Dr. David Scieszka (17:54): Roughly once growth has stopped — around twenty-five, as a rough number, though it varies. And the process accelerates: it starts very slowly but is essentially exponential, because senescence begets senescence — one cell becomes two, two become four — while the body’s declining ability to clear them makes it worse.

Dr. Regina Druz (18:33): It’s a little disheartening to learn this starts in the late twenties; I was hoping for forty or fifty.

Dr. David Scieszka (18:56): The underlying process starts earlier, but there’s a fascinating wrinkle in ‘what is aging.’ Population-wide statistics show two acceleration points — around forty and around sixty. As a systems biologist, I picture the body as an equilibrium where everything is interconnected; around forty, some support pillars crumble and the equilibrium has to shift, accelerating aging, then again around sixty. We can see this physiologically, but we can’t point to one single cause — it’s senescence, environment, genes, everything around us.

Dr. Regina Druz (20:02): It’s fascinating — I was reading about a woman, Maria, who lived to 116 and was studied by Spanish investigators, abbreviated M116. Counter to some of our assumptions, she was the opposite in several ways — her telomeres were extra short, which researchers theorized may have protected her from cancer, because her cells weren’t dividing as fast. So what we think we know keeps getting complicated. Now, senescent cells — do they occur in every organ, and is vascular senescence the earliest, given how much work our vessels do?

[21:52] Which Cells, Safety & the Target Protein

Dr. David Scieszka (21:52): Every cell type can transform senescent — that was debated for a long time. A researcher out of UC Irvine showed neurons can become senescent, and despite pushback, she was vindicated; that was one of the last cell types in question. Cardiac cells, liver cells — everything can, to different degrees. I’d love human data across age ranges, but that often requires donated tissue, which isn’t available for every age outside disease scenarios, so I don’t know if those studies exist yet. Based on the constant stress the endothelium endures, I’d bet it and the liver transform a lot of senescent cells — though the liver has internal mechanisms to recognize and clear its own defunct cells, more so than the endothelium, and certainly more than the heart, where there are no stem cells to replace cleared cells.

Dr. Regina Druz (23:24): So is the surface marker on senescent cells the same one healthy cells carry, or is it specific — so the antibody won’t damage healthy tissue?

Dr. David Scieszka (23:50): It’s specific. As a functional peptide it otherwise appears only in the context of extreme bone fractures — it’s associated with a bit of bone remodeling — and it’s also on some foam cells, so we may clear foam cells inside plaques, which could be a good thing. We brought the data to bone experts, who told us they don’t expect any problems given how little of it is around normally, and they’ll run the study for us in Australia. I’m still going to test it — I’m obsessed with safety, even where the FDA wouldn’t require it.

Dr. Regina Druz (24:49): What’s the name of that protein?

Dr. David Scieszka (24:59): I’ll share that with you afterward.

Dr. Regina Druz (25:02): Fair enough — the point is making sure healthy tissues aren’t impaired. So what have you seen in mice so far? Give us some hope, since so much jeroscience runs through mouse models.

[25:37] Mouse Results: Whole-Body Rejuvenation (Preclinical)

Dr. David Scieszka (25:37): In our preclinical work we saw a therapeutic benefit in every organ and system we could monitor — and I want to be clear this is in mice. We stress-tested the vaccine using the same metrics that showed heart failure from the senolytics dasatinib and quercetin: we ran echocardiograms and, where those senolytics drove toward heart failure, after vaccination we saw movement in the opposite direction — cardiac rejuvenation. We saw improved pulmonary function on several measures, organ-prolapse prevention, even hair-loss prevention, and we’d expect effects on chronic kidney disease and possibly vascular dementia mechanistically, though we haven’t shown those. The idea is whole-body rejuvenation, because this assists every organ that touches blood.

Dr. David Scieszka (27:41): On the human side, there have actually been a few prior clinical trials using antibody-drug conjugates — a chemotherapy linked to an antibody — against this exact protein, in breast cancer. They passed phase-one safety in humans but didn’t cure the cancer, so those trials stopped. That tells us roughly what antibody levels we should generate, which informs our dosing to keep the risk of a serious adverse event statistically very low. It’s a cancer-associated protein in humans, so there could even be anti-cancer effects. I know it sounds like a magic pill.

Dr. Regina Druz (27:45): It does sound very sci-fi and futuristic.

Dr. Regina Druz (28:14): It’s striking to picture tiny echo probes on mice — I do echo on every patient in person with a handheld transducer. Reversal of a weakened heart muscle to the point that heart failure reverses is remarkable; in humans there’s a known discordance between ejection fraction and the clinical syndrome, and heart failure with preserved ejection fraction is harder still. But restoring diminished function is real progress.

[29:35] Dosing, Cost & Plaque Reversal (Preclinical)

Dr. Regina Druz (29:35): In the mouse studies, was it one-and-done, or does it require repeated injections — how much immune stimulation is needed for a durable effect, say over a year?

Dr. David Scieszka (29:35b): It was a three-dose series to ramp up the immune response. And to the worry some people have about vaccines: a lot of those concerns center on adjuvants, and ours has no adjuvant at all — it’s a virus-like particle, recognized by the body like a virus, so we sidestep that issue, though some people may still be put off by the word ‘vaccine.’

Dr. Regina Druz (30:10): But it is a vaccine — it stimulates the immune system, so mechanistically that’s what it is.

Dr. David Scieszka (30:15): Exactly — no alum, no adjuvant, just recognized like a virus. We deliberately chose the virus-like-particle approach because it can be produced very cheaply, on par with statins, which are inexpensive. We don’t want this to be only for the wealthy — this isn’t stem-cell therapy. The vision is: go to your doctor once a year, get your flu shot and your senolytic vaccine, ideally covered by insurance through a billing code. The roughly one-year timeframe, which would likely need a booster, also adds a safety feature: if anyone ever had an issue, you simply stop boosting and the antibodies gradually fade.

Dr. Regina Druz (31:42): How much plaque regression or reversal have you seen — recognizing these are animal models?

Dr. David Scieszka (31:42b): For plaque specifically we lean on external, independent validation — there are now three labs testing this approach in different vaccine modalities. Our own work focused largely on safety. A separate group showed that clearing senescent endothelial cells, targeting the same marker, can prevent plaque by up to 50%, and another showed it can clear existing plaque by up to 40% — whole plaques that were once there, gone.

Dr. Regina Druz (32:25): So the endothelium is regenerated — the foam cells, the calcium deposits, all of it cleared?

Dr. David Scieszka (32:58): Over a relatively short duration — in humans it would probably take about a year, which is reassuring because it’s a slow mechanism, so you’re not worried about destabilizing or rupturing plaque. If a 40% reduction is possible in that window, imagine two years — potentially complete rejuvenation of the endothelium. We still have to show that, of course.

[35:28] FH, Lp(a) & the Clinical Beachhead

Dr. Regina Druz (33:00): My mind is racing. Last year at the European Society of Cardiology, a company presented CRISPR gene-editing work targeting familial hypercholesterolemia and lipoprotein(a). Lipids matter enormously, but in the best-case lipid scenario you address only about 30% of a person’s risk. Cardiology calls the other 70% ‘residual risk’ — a misnomer, since the majority can’t be a residual. We know that residual risk — endothelial dysfunction and more — shapes outcomes. Even powerful drugs like PCSK9 inhibitors show plaque regression in some trials, yet we’re not certain regression always translates to fewer events. So imagine a young person with bad genetics — early coronary disease in the family, or Lp(a), or familial hypercholesterolemia — with just fatty streaks. If your vaccine were approved and safe, would they get a prevention shot at, say, eighteen, so they never form plaque?

Dr. David Scieszka (35:28): That’s exactly the beachhead we’re approaching first — we’re mirroring a ‘go after FH first’ playbook to try to prevent major cardiac events. I believe in the FH story: by repairing those barriers, you can have circulating cholesterol through the roof, but if it can’t permeabilize the gaps, it can’t get in. With Lp(a), I picture its sharp tails dragging along and cutting the endothelium; if those cells turn senescent, we clear them and let stem cells replace them. We have to show the outcomes — I get ahead of myself because I can visualize it — but I hope we can help both populations and make this a thing of the past.

Dr. Regina Druz (36:46): It’s amazing that rare diseases, which rarely get funding, inspired CRISPR approaches to one of the most common killers — and now potentially a vaccine that melts a meaningful amount of plaque. Forty percent is nothing to sneeze at. How far are you from human trials?

Dr. David Scieszka (37:32): Going in through an orphan-drug designation for familial hypercholesterolemia would allow a seamless phase one-two, in close contact with the FDA. If everything goes right, we’re hoping to be out of phase two by 2029 — which assumes a lot, including investors who like our primate data. We’re testing three diseases: atherosclerosis, metabolic disease, and pulmonary hypertension, and we expect positive outcomes in all three. We still need the investment to complete the preclinical pathway and secure that orphan designation, which is up to the FDA.

Dr. Regina Druz (38:33): You mentioned metabolic disease — how would this work there? Could it potentially put type 2 diabetes into remission?

Dr. David Scieszka (38:52): In mice, glucose-tolerance and insulin-sensitivity tests came back to a much more normal level — and I have to be careful: type 2 diabetes can go into remission but doesn’t truly disappear, so I won’t say ‘cure.’ The mechanism is senescent adipose tissue, which is pro-inflammatory and heavily vascularized; fat is now recognized as its own signaling organ. Clearing those senescent fat cells reduced the aberrant signaling and reversed glucose intolerance and insulin insensitivity toward normal — again, in mice. We’ll measure that next in diabetic primates.

Dr. Regina Druz (40:12): In cardiology we’re in the era of weight-loss medications as paradigm-shifters, going beyond weight loss because we’ve recognized epicardial adipose tissue — a ‘zombified’ fat that can invade the heart muscle itself. One of the fastest-rising forms of heart failure is what I call ‘fat-heart syndrome’ — heart failure with preserved ejection fraction — a huge, hard-to-treat epidemic, until SGLT2 inhibitors and then semaglutide and tirzepatide showed benefits beyond weight loss. Do you foresee trials aimed specifically at that preserved-EF, obesity-related heart failure?

Dr. David Scieszka (41:52): That’s the strategy: get initial approval in FH, which grants seven years of market exclusivity, then expand the indications — potentially into heart failure with preserved ejection fraction, and we’re hoping to prevent ventricular fibrillation too; a potential Northwestern collaborator may study this in mouse models. We want this approved as broadly as possible, because forcing patients off-label raises the price. We can also eventually produce it in a room-temperature-stable format, no refrigeration — so it could reach deserts, jungles, and lower-resource countries where refrigeration is the rate-limiting step.

Dr. Regina Druz (43:19): It sounds phenomenal — I almost feel for Brian Johnson, doing so much to not age, when in five or six years a vaccine like this might arrive. Of course lifestyle still matters — stress, environmental exposures, poor diet, and bad habits keep the endothelium leaky, and you can override the benefit — but it would give people a real chance to start early and go preventive. When do you expect the primate study to read out across those three buckets?

Dr. David Scieszka (44:35): We’re funded for six months, expecting a downward plaque trend within the first three and overt clearance within six, with metabolic biomarkers improving within about three months; pulmonary hypertension is more of an unknown to me. We also have a rare opportunity to extend into a primate lifespan study. The FDA doesn’t yet recognize aging as a disease, and we need it to be a target to run a trial against it. A human-relevant primate lifespan study showing meaningful extension after a senolytic intervention could help change that — and because these are already geriatric, diabetic primates, we could potentially do it in about five years rather than twenty or thirty.

Dr. Regina Druz (46:12): What’s the life expectancy of these geriatric diabetic primates, and how much additional lifespan might the vaccine drive if it works?

Dr. David Scieszka (46:29): In the control group we wouldn’t expect many to last more than about five more years. In the vaccinated group, even in the diabetic case — which itself shortens lifespan — we’d hope to see years of life extension; in a healthy case we honestly don’t know how far it could go. We’ll have to find out.

[47:03] What You Can Do Now & Parting Words

Dr. Regina Druz (47:03): To be inclusive of people who can’t wait for a vaccine — there are other ways to lower senescent-cell burden, even if they’re less targeted than vaccinating against a specific marker. As a biologist of nearly fifteen years, what are your top approaches?

Dr. David Scieszka (47:39): I’ll sound cautious — I don’t even like taking ibuprofen. Senolytics can do real good, and there are natural products, like capers, that have gentler senolytic activity — just watch the salt, because too much salt does its own damage. Many natural foods carry this benefit at a low, safer level. My worry with potent senolytic supplements is subtle damage we can’t initially detect — a bit like how smoking harms you over decades rather than immediately. So if I were going to take anything, I’d first get a complete baseline blood panel, then test and re-check — if I saw liver function trending down, I’d stop immediately. Start with natural foods before reaching for supplements.

Dr. Regina Druz (49:05): For sure. We tell patients about foundational diets — an anti-inflammatory, high-phytonutrient Mediterranean style that improves nutrient sensing and helps clear senescent cells — and interventional diets like a fasting-mimicking diet, which has patented protocols shown to drive autophagy and degrade senescent cells in animals and humans. There’s renewed interest in fasting and caloric restriction as a powerful, multi-hallmark switch — and then a vaccine like yours could augment all of it and potentially reverse some of these dreaded chronic diseases. David, you’re a person to watch — I’ll keep my eyes peeled for the preprints. Any parting words for our listeners?

Dr. David Scieszka (50:56): Keep going. Sometimes the world seems its darkest, but keep pushing through — we’ve got this, and we’ll get there together. Thank you again, Dr. Druz, for having me. This has been a lot of fun.

Dr. Regina Druz (51:13): Same here — I learned a ton, and I can’t wait. Make the vaccine happen sooner. Take care. Thank you for tuning in to Own Your Heart Health with Dr. Regina Druz. This podcast is powered by Holistic Heart Centers. If you enjoyed the show, please rate and review us on your favorite platform. To learn more about our services, visit holisticheartcenters.com and subscribe to our YouTube channel — the link is in the show notes. See you next week.

Frequently Asked Questions

What is a “vaccine against atherosclerosis,” and how would it work?

Dr. Scieszka’s idea is to train the immune system to clear out senescent (‘zombie’) cells lining the blood vessels. As the endothelium (the single-cell-thick inner lining of arteries and veins) accumulates senescent cells with age, it becomes ‘leaky,’ which lets LDL slip in to seed plaque while the pro-inflammatory senescent cells hinder the immune system’s cleanup. The vaccine — built on a virus-like particle that displays a surface marker found on senescent endothelial cells — prompts the body to make antibodies against that marker, so a person’s own immune system removes those cells, as it did more efficiently when younger. Importantly, this mechanism has been studied in animals; it is not an approved or available treatment, and this is an explanation of the science, not medical advice.

What are senescent (‘zombie’) cells, and what do they have to do with heart disease?

Senescent cells are an in-between state — not dividing, not dead — that Dr. Druz nicknames ‘zombie cells’ in her forthcoming book. They secrete pro-inflammatory signals that damage surrounding tissue and can even push neighboring cells into senescence (the ‘zombie effect’). The declining ability to clear them is considered one of the hallmarks of aging. In blood vessels, senescent endothelial cells are thought to weaken the barrier and promote inflammation, linking cellular aging directly to atherosclerosis — and, because nearly every tissue touches blood, potentially to many age-related conditions. This is a general explanation of an active area of research, not a diagnosis or treatment recommendation.

Is this vaccine available — has it been tested in people?

No. This is early, preclinical work. The results discussed — plaque prevention and clearance, cardiac and metabolic rejuvenation, and lifespan extension — come from mouse studies (some from independent labs) or are aspirational, and primate studies are underway. Dr. Scieszka describes hoping to reach human trials via an orphan-drug pathway for familial hypercholesterolemia, with a target of completing phase two around 2029 — contingent on funding and FDA decisions. The vaccine is not FDA-approved, not available, and not proven in humans. Anyone interested should follow the published research and consult their own clinician; nothing here is medical advice or an investment recommendation.

What can I do now to reduce senescent-cell burden?

Both physicians urge caution with over-the-counter ‘senolytic’ supplements — Dr. Scieszka notes potential hidden harms (he cites a mouse heart-failure signal with the senolytics dasatinib and quercetin after wildfire-smoke exposure) and recommends baseline and follow-up blood work before and during any such experiment, stopping immediately if markers worsen. He suggests starting with natural foods rather than potent supplements. Dr. Druz points to foundational, anti-inflammatory, high-phytonutrient (Mediterranean-style) eating and, as an interventional option, a fasting-mimicking diet with published protocols that support autophagy. These are general wellness ideas, not personalized medical advice — talk with your own clinician before starting any supplement or dietary program.

Show Notes & Resources

Guest: Dr. David Scieszka, PhD, MBA

Dr. David Scieszka is the founder and CEO of Vertical Longevity Pharma, a startup developing a senolytic ‘vaccine’ intended to prevent and reverse atherosclerosis and extend healthy lifespan. A former U.S. Army psychological-operations specialist, he holds a biotechnology undergraduate degree and earned a PhD in biomedical sciences (focused on aging) alongside an MBA, with a background in computational biology, bioinformatics, and environmental toxicology. His company reports preclinical mouse data on plaque prevention and organ rejuvenation, with primate studies underway and collaborations including Wake Forest University and a research group in Australia. (Disclosure: Dr. Scieszka is the founder and CEO of the company developing the product discussed and has been raising investment for it; he has a direct financial and commercial interest in this work.)

Vertical Longevity Pharma — Dr. Scieszka’s company developing the senolytic vaccine (investigational / preclinical)

Resources Mentioned in This Episode

Vertical Longevity Pharma — Dr. Scieszka’s company developing the senolytic vaccine. DISCLOSURE: the guest is founder/CEO and has been raising investment; this is descriptive, NOT an endorsement or an investment recommendation, and the product is investigational and preclinical
Clinical-trial status — the vaccine is PRECLINICAL: mouse data (some from independent labs), primate studies underway, with human trials only targeted (the guest cites ~2029 for completing phase two via an orphan-drug pathway). It is not FDA-approved and not available
Cellular senescence & the hallmarks of aging — background on senescent (‘zombie’) cells, the endothelium, and vascular aging
A caution on over-the-counter senolytics — the guest describes a mouse heart-failure signal with dasatinib + quercetin after wildfire-smoke exposure; do not self-treat with senolytic supplements without clinician guidance
Nutrition foundations — anti-inflammatory, high-phytonutrient Mediterranean-style eating; a fasting-mimicking diet (autophagy) as an interventional option
‘Longevity Decoded’ — Dr. Druz’s forthcoming book (where she discusses ‘zombie cells’)
NOVA food classification — the JACC ultra-processed-food study referenced (verify before citing)
Heartwell AI (heartwell.ai) — Holistic Heart Centers’ personalized cardiovascular-risk tool
Schedule a consult with Holistic Heart Centers — go.holisticheartcenters.com/apply

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