Guest: Dr. David Furman, PhD — Immunologist & Longevity Researcher
In this episode, Dr. Regina Druz is joined by Dr. David Furman — Stanford-trained immunologist, data scientist, and creator of the iAge (Inflammatory Age) metric — to explore the biological roots of cardiovascular and brain aging. Dr. Furman explains why standard inflammation markers like hs-CRP miss the chronic inflammatory proteins that most accurately predict disease, and how proteomic testing can reveal silent arterial stiffening and organ aging years before clinical symptoms appear. The conversation covers the 1000 Immunomes Project, a landmark 17-year study at Stanford, and introduces two groundbreaking technologies: an AI-based organ aging model derived from routine blood labs, and a NASA-developed microgravity cell culture platform that functions as a personal digital twin for future aging.
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Episode Chapters
| [00:02] | Welcome & Introduction — Dr. David Furman |
| [01:31] | Dr. Furman’s Journey: From Music to Immunology at Stanford |
| [04:31] | The 1000 Immunomes Project — Mapping the Biology of Chronic Inflammation |
| [08:04] | Why Standard Biomarkers (CRP, IL-6) Often Miss Silent Inflammation |
| [11:05] | CXCL9 & Eotaxin — The Proteins That Predict Cardiovascular and Brain Aging |
| [17:30] | Clinical Evidence: Healthy Patients with Hidden Arterial Stiffening |
| [21:02] | Layer-by-Layer Interventions — From Lifestyle Foundations to Personalized Protein Targets |
| [27:39] | Organ Aging AI — Predicting System-Specific Mortality from Routine Labs |
| [34:25] | NASA Astronauts, Microgravity, and the Digital Twin for Aging |
| [38:09] | Beyond Age: Empowering Patients to Change Their Biological Future |
Podcast Transcript
[00:02] Welcome & Introduction
Dr. Regina Druz (00:02): Welcome to Own Your Heart Health. I’m Dr. Regina Druz, your holistic cardiologist. This week, we dive into common heart health concerns, uncovering root causes and unpacking scientific discoveries. Please remember that the information provided does not constitute medical advice — consult your healthcare practitioner before making any changes to your health regimen.Today I am joined by Dr. David Furman, a societal entrepreneur and prolific researcher whose goal is to redefine how we approach biomarkers of longevity. His work centers on testing that allows us to choose actionable steps for extending not just our lifespan, but our health span. Dr. David, welcome to the show.
Dr. David Furman (01:17): Thank you so much for having me, Regina.
[01:31] Dr. Furman’s Journey: From Music to Immunology at Stanford
Dr. Regina Druz (01:20): I always ask my guests: how did you grow up to become who you are today? Tell us your story.
Dr. David Furman (01:31): I was born in Argentina, moved to Israel when I was young, and by 17 or 18 I was deeply immersed in arts and music. I wanted to create impact in humanity. My father convinced me that studying biology rather than medicine would allow me to affect far more people. So I pursued biology, then immunology, then became a data scientist. Stanford recruited me while I was finishing my PhD. After analyzing data from the 1000 Immunomes Project — which we launched in 2007 — I realized that most of the signal pointed to the biology of aging. That realization shifted my entire focus around 2012.
[04:31] The 1000 Immunomes Project — Mapping the Biology of Chronic Inflammation
Dr. Regina Druz (03:47): People may not appreciate that one of the primary systems that ages as we get older is the immune system. Can you explain what is happening with the immune system, and what the 1000 Immunomes Project was designed to discover?
Dr. David Furman (04:31): The immune system is one of the most important determinants of how rapidly other organ systems age, because it senses the environment and reacts to it — producing what we call systemic chronic inflammation. Inflammation is the silent enemy that drives cardiovascular disease, Alzheimer’s disease, musculoskeletal conditions, and metabolic disorders. By 2000 we knew very little about which biomarkers were causally linked to this process. Over the past 25 years we have learned that the immune system is truly a hub for aging — hallmarks like cellular senescence and epigenetic changes are largely driven by inflammation.The 1000 Immunomes Project was designed to provide solid science around this. We recruited 1,000 relatively healthy, ambulatory individuals and secured over $70 million from federal agencies. The study ran for 15 to 17 years, allowing us to prospectively identify biomarkers of systemic chronic inflammation that predict morbidity and mortality.
Dr. Regina Druz (06:29): Were these participants volunteers from the general public, or patients from the Stanford healthcare system?
Dr. David Furman (06:41): Completely healthy volunteers who came in for a flu vaccine. People with serious uncontrolled disease were excluded, although those with well-managed conditions — hypertension being very common in individuals over 65, for example — were included. This design allowed us to prospectively predict who developed various conditions as the study progressed.
[08:04] Why Standard Biomarkers (CRP, IL-6) Often Miss Silent Inflammation
Dr. Regina Druz (07:25): Most of my patients have had high-sensitivity C-reactive protein (hs-CRP) and interleukin-6 (IL-6) measured. These are the classic inflammation markers. But the immune system aging and chronic inflammation you describe — is that the same thing we see on a standard blood panel?
Dr. David Furman (08:04): The key distinction is acute versus chronic inflammation. For roughly two decades, research has shown that hs-CRP and IL-6 are very poor predictors of non-communicable diseases. Cardiovascular disease can be predicted only marginally better than chance using hs-CRP, and most cardiologists no longer rely on it. These markers do rise dramatically with acute infection — a cut finger, a flu — but systemic chronic inflammation shows up as entirely different proteins in the blood. Because there was a gap in knowledge, we took an unbiased approach: we measured hundreds of thousands of parameters from those thousand individuals to find the most predictive ones.
[11:05] CXCL9 & Eotaxin — The Proteins That Predict Cardiovascular and Brain Aging
Dr. Regina Druz (09:43): What did you find? Which biomarkers emerged as the most important predictors of aging?
Dr. David Furman (11:05): Out of all the data we analyzed — gene expression, proteins, cell frequencies, metabolites — proteins were the most predictive of chronological aging and disease risk. The single most predictive protein was not IL-6. It was CXCL9, also called MIG. CXCL9 circulates in the blood, increases with age, and causes damage to the endothelium — the inner lining of blood vessels. Elevated CXCL9 is associated with cellular senescence of the endothelium, left ventricular hypertrophy, and arterial stiffening.The second key protein is eotaxin, also known as CCL11. Eotaxin-1 is produced largely in response to airborne exposures — air pollution, cooking vapors, allergens. Macrophages in the lungs produce it, and it enters the bloodstream where it crosses the blood-brain barrier easily. There it causes cognitive dysfunction and is associated with dementia and memory loss.The other three important proteins are gamma interferon (involved in immune system activation), GRO-alpha, and TRAIL. TRAIL is particularly interesting: it sensitizes senescent cells to undergo apoptosis. Low TRAIL means senescent cells are not being cleared, and they accumulate throughout the body — a core driver of tissue aging.
Dr. Regina Druz (14:23): Fascinating. CXCL9 — is it produced by immune cells, or by the endothelium itself as it ages?
Dr. David Furman (14:39): In the textbook, CXCL9 is produced by immune cells to call lymphocytes to a site of infection. But in aging, what we see is that damaged endothelium itself produces CXCL9 — and then that CXCL9 damages neighboring endothelial cells. You get a propagating senescence signal: more senescence leads to stiffer tissue, higher vascular resistance, elevated pressure on the heart, and eventually hypertrophy — which is very difficult to reverse.
[17:30] Clinical Evidence: Healthy Patients with Hidden Arterial Stiffening
Dr. Regina Druz (15:38): We can measure endothelial dysfunction and plaque progression in clinical practice. Recently, AI tools have been able to detect inflammation in epicardial adipose tissue — the fat surrounding the heart, sometimes abbreviated EAT. When this tissue infiltrates the cardiac muscle it leads to stiffening and a syndrome called heart failure with preserved ejection fraction (HFpEF), strongly linked to obesity. At what age should people begin testing these proteomic markers? Because someone could have a beautiful lipid profile, normal hs-CRP, and no cardiac hypertrophy on ultrasound, and yet already carry these protein signatures of endothelial dysfunction.
Dr. David Furman (17:30): That happens all the time. We conducted a study in 150 people who were matched for CRP, BMI, and every conventional cardiovascular risk factor. Those with elevated Inflammatory Age — our metric — had measurable arterial stiffening on pulse wave velocity testing and increased left ventricular changes, despite having no clinical symptoms and never presenting to a clinic for cardiovascular concerns.The molecular and cellular changes that precede disease begin 15 to 20 years before any clinical presentation. I would say the early 30s is a reasonable starting point for measuring these biomarkers — that is when we can intercept the molecular trajectory of disease before it becomes irreversible.
[21:02] Layer-by-Layer Interventions — From Lifestyle Foundations to Personalized Protein Targets
Dr. Regina Druz (20:00): What are the most powerful interventions? What can actually be changed, and on what timeline?
Dr. David Furman (21:02): There are several layers. Layer one is the foundation — the one-size-fits-all baseline that everyone must establish first. Without it, advanced interventions provide no benefit and may even cause harm. Layer one includes: quality sleep and sleep hygiene; regular movement (sedentary behavior measurably raises inflammation); time in nature (even viewing greenery reduces inflammatory markers in peer-reviewed studies); and a whole-food diet rich in nutrients.From a dietary standpoint, refined wheat products — bread, pasta — are among the strongest drivers of organ aging in our data. Dairy products are also inflammatory. Conversely, berries and small fish are highly beneficial. Microplastics from plastic food storage accumulate in blood and tissues and are now recognized as contributors to inflammation.Layer two is fine-tuning based on your specific protein deviations. For example, if your eotaxin is elevated, we investigate your air quality at home and at work and recommend air purification. Each deviated protein has a corresponding environmental or behavioral trigger.Layer three involves newer technologies — including AI-based organ aging analysis from standard labs, and the microgravity-based digital twin technology.
Dr. Regina Druz (25:47): Resilience is the word I always come back to. The foundation has to come first. Patients often tell me: I exercise, I eat well, I don’t smoke, I sleep, I manage stress — why is my blood pressure still elevated? The honest answer is that effort intensity does not always match the cellular processes already in motion. The proteome gives us a window into those processes so we can address them specifically.
[27:39] Organ Aging AI — Predicting System-Specific Mortality from Routine Labs
Dr. Regina Druz (27:00): Tell me more about the organ aging AI. Is this an algorithm that takes standard blood work and correlates it to the proteomic signatures from the Immunomes Project?
Dr. David Furman (27:39): Close, but distinct. We use a comprehensive panel of 33 standard biomarkers — cardiovascular, metabolic, and others — from standard labs. The algorithm is agnostic to textbook organ assignments; we simply took all available biomarkers from half a million people and trained it to predict system-specific mortality across ICD-10 disease chapters: cardiovascular, Alzheimer’s and dementia, musculoskeletal, and metabolic.The assumption is that the older a system biologically, the higher its mortality risk. We validated the model in 10,000 individuals from the Health and Retirement cohort. For example, creatinine — typically used for kidney function — turns out to be predictive of metabolic syndrome in our model. Cystatin C similarly crosses traditional organ boundaries. The AI captures these cross-system interactions naturally, telling the clinician not just what’s aging, but what to do about it.
Dr. Regina Druz (30:47): What is your view on epigenetic age clocks? I have patients with stellar epigenetic biological ages who nevertheless have significant coronary artery disease, pristine blood work, and extensive plaque burden.
Dr. David Furman (31:47): Epigenetic clocks were the first technology developed for biological age estimation and they remain the best at predicting chronological age — but who needs to predict something they already know? The problems are: (1) they are very difficult to change because we do not know how to intervene on the epigenome; (2) test-retest precision is poor — the same person tested at different labs may see a 10-to-20 year spread in results. In contrast, if inflammatory protein markers are elevated, we know exactly which interventions move those proteins. With standard lab-based organ aging, we have 120 years of clinical research behind the levers to optimize those values.
[34:25] NASA Astronauts, Microgravity, and the Digital Twin for Aging
Dr. Regina Druz (33:38): You’ve mentioned Holistic Heart Centers is now offering immune system age testing. Can you also tell our listeners about your NASA collaboration and what you discovered with astronauts?
Dr. David Furman (34:25): NASA reached out about five years ago because they observed accelerated aging in astronauts during and after space missions. Using a NASA-developed cell culture system that simulates zero-gravity, we can expose a person’s own cells to microgravity conditions and observe how they age — creating what is essentially a digital twin of your future biological state. A recently pre-printed paper shows that this microgravity model can predict, for each hallmark of aging, how an individual will age — compared not against a population, but against themselves. The product is called Beyond Age and is available through concierge medicine and longevity clinics.
Dr. Regina Druz (36:35): At Holistic Heart Centers we are building a longevity suite, including HeartWell.ai — our simulation platform for cardiovascular risk modeling. The trials of the future will likely be pragmatic, n-of-1 investigations at scale. The idea that we could take a simple swab, simulate your cellular future in microgravity, and return a personalized risk profile — that is genuinely transformative preventive medicine.
[38:09] Beyond Age: Empowering Patients to Change Their Biological Future
Dr. David Furman (38:58): The most important message is this: biological aging is malleable. You can change the future of your health. This is not fatalism — it is empowerment. With the right measurements and the right interventions, patients can take meaningful control of how they age.
Dr. Regina Druz (39:17): One hundred percent. Be there for your family and friends. Dr. David, this has been immense. I have learned a tremendous amount, and I am ordering my Beyond Age testing kit as soon as we finish recording. We will revisit this topic once my results come in. Thank you for tuning in to Own Your Heart Health with Dr. Regina Druz. This podcast is powered by Holistic Heart Centers. Please rate and review us on your favorite platform, 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 Inflammatory Age (iAge), and how is it different from my regular inflammation blood test?
Inflammatory Age — or iAge — is a biological aging metric developed by Dr. Furman’s team at Stanford based on a panel of inflammatory proteins identified in the 1000 Immunomes Project. Unlike standard inflammation markers such as hs-CRP (high-sensitivity C-reactive protein) or IL-6, which primarily reflect acute infection or injury, iAge captures chronic, low-grade systemic inflammation — the kind that silently drives cardiovascular disease, brain aging, and cellular senescence over decades. The key proteins measured include CXCL9 (linked to endothelial damage and arterial stiffening), eotaxin/CCL11 (linked to brain and memory decline), gamma interferon, GRO-alpha, and TRAIL. Standard panels can appear completely normal even when iAge reveals significant underlying inflammation. If you are interested in getting your immune system age measured, ask your physician about iAge testing or visit holisticheartcenters.com.
At what age should I start testing for immune aging and inflammatory biomarkers?
Dr. Furman recommends starting in the early 30s, because the molecular and cellular changes that precede disease typically begin 15 to 20 years before clinical symptoms appear. By the time a patient develops hypertension, arterial stiffening, or cardiac hypertrophy, the underlying inflammatory processes have often been active for well over a decade. In the research study, 150 individuals who were matched for every conventional cardiovascular risk factor — normal CRP, normal BMI, no known disease — were found to have measurable arterial stiffening detected only through iAge and pulse wave velocity testing. Testing earlier gives patients and clinicians the opportunity to intercept these processes before they become irreversible. Individuals with a family history of heart disease, high polygenic risk scores, or early lipid abnormalities may benefit from starting even sooner.
What lifestyle changes can lower inflammatory proteins like CXCL9 and eotaxin?
Dr. Furman describes a layered intervention approach. The essential foundation — what he calls Layer One — applies to everyone and must be in place before anything else: consistent quality sleep, regular physical movement (sedentary behavior is a measurable driver of inflammation), time in natural environments, and a whole-food diet free of refined grains and processed dairy. Berries and small fish are particularly beneficial. Reducing microplastic exposure by switching from plastic to glass food storage also matters. Layer Two is personalized: if eotaxin is elevated, for instance, improving indoor air quality through air purifiers and monitoring outdoor pollution becomes a priority target. The key insight is that chronicity of exposure is the risk factor — an occasional pizza does not undo a strong baseline. Sustainable daily habits are what move the needle on these proteins.
How does the AI-based organ aging test work, and is it different from epigenetic age clocks?
The AI-based organ aging model developed by Dr. Furman’s team analyzes 33 standard blood biomarkers — the kind already available from labs like Superpower or Function — and predicts system-specific mortality risk across major organ categories including cardiovascular, neurological, musculoskeletal, and metabolic. Validated in over 500,000 individuals and a separate 10,000-person cohort, the model assigns a biological age to each organ system and identifies which may be aging fastest. This differs significantly from epigenetic age clocks, which estimate chronological age from DNA methylation patterns but have limited actionability and poor test-retest precision (results can vary by 10-20 years across labs). The organ aging model is grounded in biomarkers that clinicians already know how to move — giving both doctor and patient a clear target for intervention.
What is the ‘Beyond Age’ microgravity test, and is it available to the general public?
Beyond Age is a personalized aging prediction tool developed in collaboration with NASA. A sample of a patient’s own cells is exposed to a simulated zero-gravity environment using a cell culture system originally designed for space medicine research. Because microgravity accelerates cellular aging processes, this allows scientists to observe how that individual’s cells will age across the hallmarks of aging — not compared to a population average, but relative to the patient’s own baseline. The result is a form of biological digital twin: a window into your cellular future. The technology is currently available through concierge medicine practices and longevity clinics. Holistic Heart Centers is exploring its incorporation into the longevity suite alongside iAge and HeartWell.ai cardiovascular risk modeling. Please note that this is an emerging technology and has not yet completed full clinical validation as of the recording of this episode.
Show Notes & Resources
Guest: Dr. David Furman, PhD
Immunologist | Data Scientist | Longevity & Aging ResearcherStanford-trained; former researcher, 1000 Immunomes ProjectCreator of iAge (Inflammatory Age) and co-developer of Beyond AgeLocation: San Francisco Bay Area, CA
Resources Mentioned:
• iAge Immune System Age Test — available through longevity/concierge medicine clinics including Holistic Heart Centers
• Beyond Age (microgravity digital twin) — beyondage.com (confirm current URL with Dr. Furman’s team)
• 1000 Immunomes Project — Stanford University longitudinal study on immune aging biomarkers
Key Terms Referenced in This Episode
• Inflammatory Age (iAge): A biological aging score based on five inflammatory proteins predictive of morbidity and mortality.
• CXCL9 (MIG): A protein that increases with age and drives endothelial senescence, arterial stiffening, and left ventricular hypertrophy.
• Eotaxin (CCL11): A chemokine produced in the lungs in response to air quality exposures; crosses the blood-brain barrier and is associated with cognitive decline.
• TRAIL: A protein that promotes apoptosis (programmed cell death) of senescent cells. Low TRAIL = accumulation of senescent cells throughout the body.
• Cellular Senescence: A state in which damaged cells stop dividing but do not die, instead releasing inflammatory signals that damage surrounding tissue.
• hs-CRP: High-sensitivity C-reactive protein — a common acute-phase inflammation marker with limited utility for predicting chronic cardiovascular aging.
• Proteomics: The large-scale study of proteins in a biological system, including their structure, function, and interactions.
• Epicardial Adipose Tissue (EAT): Fat surrounding the heart that, when excessive, can infiltrate cardiac muscle and contribute to heart failure with preserved ejection fraction (HFpEF).
• Pulse Wave Velocity: A clinical measure of arterial stiffness — higher values indicate stiffer arteries and greater cardiovascular risk.
• ICD-10: International Classification of Diseases, 10th revision — the global standard for disease classification used in clinical and research settings.
• HFpEF: Heart failure with preserved ejection fraction — a form of heart failure where the heart muscle contracts normally but the ventricles are stiff.
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Medical Disclaimer
The information in this transcript is for educational purposes only and does not constitute medical advice. The discussions about stem cells, exosomes, peptides, and regenerative therapies reflect the clinical experiences and opinions of the physicians involved. These treatments are not FDA-approved for all applications discussed. Individual results vary. Please consult your licensed healthcare practitioner before making any changes to your health regimen.