Ep. 29: Unlocking Longevity: How Genetic Insights Guide Lifelong Health — with Dr. Sharon Hausman-Cohen, Co-Founder of IntellxxDNA

Own Your Heart Health Podcast with Dr. Regina Druz, MD
Own Your Heart Health with Dr. Regina Druz
Ep. 29: Unlocking Longevity: How Genetic Insights Guide Lifelong Health — with Dr. Sharon Hausman-Cohen, Co-Founder of IntellxxDNA
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Your genes aren’t your destiny — but knowing them can change the trajectory of your heart, brain, and overall health. In this episode, Dr. Regina Druz sits down with genomics leader Dr. Sharon Hausman-Cohen, the co-founder and chief medical officer of IntellxxDNA, to demystify a topic that confuses patients and clinicians alike. They untangle genetics from genomics from epigenetics, explain what a SNP actually is, and make the case that for common chronic disease it’s the everyday gene variants — not the rare ‘pathogenic’ ones found on whole-genome sequencing — that matter most. Through vivid real cases — a heart attack driven by an inability to make glutathione and CoQ10, hypertension routed through salt and adrenaline genes, incretin biology that predicts GLP-1 response — they show how ‘medical genomics’ turns DNA into a personalized, actionable plan for prevention and longevity.

Watch on YouTube: A video version of this episode is available on the Own Your Heart Health YouTube channel. Subscribe to be notified of new episodes.

Episode Chapters

[00:00] Introduction & Meet Dr. Sharon Hausman-Cohen
[02:06] From a Nobel Lab to Building IntellxxDNA
[06:27] Genetics vs. Genomics vs. Epigenetics
[13:31] SNPs Explained: One Letter, Big Effects
[15:02] The Vitamin D Receptor: One Gene, Many Jobs
[18:45] Why Whole-Genome Sequencing Isn’t the Answer for Chronic Disease
[25:00] Polygenic Risk Scores & Gene Editing
[27:38] Hypertension Genomics: RAAS, Salt & Adrenaline
[28:30] A Heart-Attack Case: Glutathione, CoQ10 & Statins
[35:00] Cortisol, Incretin & Personalizing GLP-1s
[42:00] Insight & Empowerment: LPA, Aspirin & a GNC Warning
[53:30] Top Genes to Know for Heart Disease
[1:00:00] Genomics for Longevity & Closing

Transcript

[00:00] Introduction & Meet Dr. Sharon Hausman-Cohen

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): Hello everybody. Today’s topic has excited me since I was an undergraduate, and my very special guest is an undisputed leader in genetics and genomics: Dr. Sharon Hausman-Cohen. The secret is out — it’s genes. Not the genes you try on (though knowing your genes might help you fit your jeans better), but the genes that shape the trajectory of heart disease and many other chronic conditions — and that show us what we can do through lifestyle, supplements, and medications to overcome our own genetic vulnerabilities. Welcome, Dr. Sharon.

Dr. Sharon Hausman-Cohen (01:51): Thank you so much, Regina, for having me. I so appreciate it.

[02:06] From a Nobel Lab to Building IntellxxDNA

Dr. Regina Druz (01:55): I’ll ask what I ask all my guests: how did you grow up to be a leader in genetics and genomics?

Dr. Sharon Hausman-Cohen (02:06): I always wanted to understand how things work. In college I had the chance to work with a visiting Nobel laureate, Dr. Gerald Edelman, who discovered the immunoglobulin molecule, and he convinced me to pursue medicine at a molecular level. I started a PhD at Harvard, but I liked too many things to spend my life on one protein. So after a master’s I went back for my medical degree, became a family physician — birth to death — and got dual board-certified in integrative medicine. Then the 23andMe revolution hit, and patients started bringing me their genomics asking, can you help me prevent cognitive decline, or my family history of heart disease? There was no good clinical tool to use that information medically.

Dr. Sharon Hausman-Cohen (03:50): So along with my co-founder, Carol, we set out to build one. We thought we were building a research database for our own patients, and it rapidly became a huge undertaking — what’s now IntellxxDNA, a highly evidence-based, highly accurate clinical-decision-support tool that helps physicians actually practice personalized medicine.

Dr. Regina Druz (04:53): Two takeaways: one, there’s a roundabout route to Harvard Medical School via the PhD track — I’m kidding. Two, more seriously, there’s a tremendous need for robust, verified clinical-decision-support tools in genetics, because there’s a lot of misunderstanding. Many patients think all genetic analysis is the same, and don’t distinguish genetics from genomics from epigenetics. Let’s start there — what are those terms?

[06:27] Genetics vs. Genomics vs. Epigenetics

Dr. Sharon Hausman-Cohen (06:27): Great place to start — even geneticists aren’t necessarily specialists in genomics. Genetics is the study of inheritance: Mendelian traits and inheritable diseases like Tay-Sachs, cystic fibrosis, sickle cell, or the BRCA breast-cancer gene — specific genes tied to specific outcomes. Genomics is different: it’s the study of small, one-letter changes in your DNA that, most of the time, don’t cause any disease by themselves, but combined with diet, lifestyle, and each other can be very significant. The best-known example is APOE4 and Alzheimer’s — but APOE4 is in almost 25% of the population, so it’s not pathogenic on its own. I have APOE4/4 patients in their 80s above the 90th percentile for cognition. What it does depends on the eight or nine other variants it interacts with — some double the risk, some cut it in half.

Dr. Sharon Hausman-Cohen (09:30): Epigenetics — ‘on top of genetics’ — is the idea that we can modify how our genes are expressed by what we do. The classic example is methylation, but everything counts: eating more fruits and vegetables, or chili peppers and lion’s mane mushrooms, lowers expression of an inflammatory gene called TNF-alpha — and there’s a TNF-alpha variant that, combined with APOE4, can raise Alzheimer’s risk about six-fold. So in our IntellxxDNA reports, the diet, lifestyle, supplement, and medication recommendations targeted to someone’s specific variants are really the science of epigenetics: you inherit your genes, but what you do changes how they manifest.

Dr. Regina Druz (10:46): I tell patients genetics is like an alphabet — a language — while genomics is the book that tells the story, with its interactions of protagonists and antagonists, and epigenetics is how the story plays out. It’s complex, but the great part is we now have tools that are relatively inexpensive (things that didn’t exist or cost hundreds of thousands of dollars a decade ago), decision-support systems, and a way to integrate it with labs, imaging, and biometrics into a whole phenotype.

[13:31] SNPs Explained: One Letter, Big Effects

Dr. Sharon Hausman-Cohen (13:31): Let’s define a variant — the other name is a SNP, a single-nucleotide polymorphism. DNA is built from just four base pairs, symbolized A, T, C, and G — like the ones and zeros of computer language, but four letters. There are about 3 billion of them in the human genome, and most stay the same in everyone, or we’d be wildly different. But a little over a million can differ between individuals. A SNP is one little place that changes — it might do nothing, or it might significantly affect how a gene works.

Dr. Regina Druz (22:22): Hi everyone, it’s Dr. Regina here. I know there are contradictory opinions about nutrition for heart health and longevity — the discussion gets heated and confusing. Some push low-fat, low-cholesterol; others are fans of a ketogenic diet; and there are many voices urging vegan or vegetarian eating. To cut through the clutter, my team and I created Holistic Heart University: on-demand courses, nutrition and lifestyle resources, and supplement guidance to make healthy choices for your heart easier to understand. I’m especially proud of our open office hours and the Q&A feature where you can put us in the hot seat. Head to the show notes for the link and use promo code OWNER20 for 20% off our annual subscription. I’ll see you in office hours.

[15:02] The Vitamin D Receptor: One Gene, Many Jobs

Dr. Sharon Hausman-Cohen (15:02): Our body makes a human with only about 28,000 genes because each gene does different things. Take the vitamin D receptor — vitamin D can’t work alone; it binds its docking station, and its job there is to turn things off. If your vitamin D receptor isn’t working, you can’t turn things off: you can’t turn off bone remodeling and get osteoporosis; you can’t turn off immunity and get autoimmunity; you can’t turn off cell growth and risk cancer.

Dr. Regina Druz (16:39): If you don’t turn off plaque progression, you get what follows downstream.

Dr. Sharon Hausman-Cohen (16:46): Exactly — and that’s why you can’t just talk about a gene; you have to talk about a gene variant, because the same gene interacts differently with the heart, bone, and immune system. Some variants reduce how many vitamin D receptors you make — and resveratrol from red grapes, sulforaphane from broccoli sprouts, and estrogen can all increase them. That’s epigenetics in action: understanding what’s going on in someone’s genome and how to respond. Those vitamin-D-receptor SNPs wouldn’t show up on whole-genome sequencing, even though two copies are found in 5 to 14% of people.

[18:45] Why Whole-Genome Sequencing Isn’t the Answer for Chronic Disease

Dr. Sharon Hausman-Cohen (18:45): Whole-genome sequencing sounds like the best — ‘I want it all’ — and we both have that personality. But you can only use a test if you know what to do with it. The research world of whole-genome sequencing is built to identify rare, pathogenic, disease-causing variants — missing or extra pieces of DNA tied to serious diseases like muscular dystrophy. For the average person already in their 30s, 40s, or beyond, they won’t learn much, because if they had a pathogenic variant of importance, they’d likely already know. What they need is to understand common chronic disease — and that’s medical genomics, which my IntellxxDNA team is pioneering.

Dr. Sharon Hausman-Cohen (20:30): In 2015 the Precision Medicine Initiative funded precision approaches in cancer and pharmacogenomics, but making genomics useful for chronic disease got largely ignored by public research. That’s what my co-founder and I took on: take someone’s genome, find the variants most associated with cognitive decline, heart disease, diabetes, depression, and more, figure out what each does, and how to respond with diet, lifestyle, supplements, and medications. By 2016 it was clearly working — we saw improved cognition in mild impairment and early dementia, and we could tell people with strong family histories of heart disease, ‘even though your cholesterol is normal, you may want advanced testing,’ because of specific variants.

[25:00] Polygenic Risk Scores & Gene Editing

Dr. Regina Druz (22:30): At the European Society of Cardiology meeting there was a lot on genetics. Years ago we were excited about polygenic risk scores — adding up many SNPs using computational biology that accounts for prevalence and effect size. They have a role, but when we added a top-of-the-heap coronary score to what we already knew from biomarkers and imaging, the improvement in risk stratification was real but modest — not off the charts. I came to understand why: the actionable points are the individual SNPs, the points of influence. Whole-genome sequencing mostly matters when there’s gene editing or substitution — like Verve Therapeutics, recently acquired by Eli Lilly, editing the gene in familial hypercholesterolemia to radically drop cholesterol, now being tested for Lp(a). For most people with common chronic disease, whole-genome sequencing won’t add much. Do you agree?

Dr. Sharon Hausman-Cohen (26:49): One hundred percent. Whole-genome sequencing looks at things generally found in fewer than one in 5,000 — often one in 100,000 — people. It’s not designed to help a physician understand how to address this person’s heart disease, and most heart-disease-related variants aren’t rare, because heart disease isn’t rare. Speaking of which — hypertension might be a fun place to start.

[27:38] Hypertension Genomics: RAAS, Salt & Adrenaline

Dr. Sharon Hausman-Cohen (27:43): We have a system meant to raise blood pressure if we’re injured — the renin-angiotensin-aldosterone system, the RAAS, with lots of checks and balances. If variants make it overactive, you over-raise blood pressure; some pathways are salt-sensitive and respond well to ACE inhibitors or angiotensin receptor blockers. But other genes contribute to hypertension through inflammation (TNF-alpha with oxidative stress) or mitochondrial regulation — and those need completely different approaches. There’s even a variant that makes people less salt-sensitive, so a low-salt diet won’t help them. One of the top variants relates to your adrenaline receptors: for a bit over half of people the receptors are more active, which raises blood pressure — and that’s why exercise, meditation, yoga, and ashwagandha, which lower adrenaline, help keep it down.

[28:30] A Heart-Attack Case: Glutathione, CoQ10 & Statins

Dr. Sharon Hausman-Cohen (28:30): A case: a 61-year-old man came to me a year after a heart attack. He didn’t have high cholesterol, his blood pressure was fairly controlled, and his blood sugar was fine — he just wanted to understand what happened. What had his doctors done? The classic: drive his LDL down toward 46 and put him on a low-salt diet — neither of which addressed his actual drivers.

Dr. Sharon Hausman-Cohen (29:46): His genomics showed the number-one contributor to his cardiac risk was an inability to make glutathione, our master antioxidant. Think of an apple: cut it and it browns quickly, because fruits keep their antioxidants in the skin; we keep ours in our blood and muscle. If you can’t make glutathione, that’s associated with about 3.2 times the risk of heart disease, because you can’t protect the heart from oxidative stress. He also couldn’t make CoQ10 well. These aren’t common variants — each in under 10% of people — but he had both. Putting him on a statin (which depletes CoQ10 and creates oxidative stress) without replacing CoQ10, plus a low-salt diet, was the wrong regimen. When we lowered his oxidative stress — and addressed his chemical and metal hobby exposures with masks, gloves, and ventilation — his blood pressure stayed great. That’s a very different cause of heart disease you can’t reach with standard testing.

[35:00] Cortisol, Incretin & Personalizing GLP-1s

Dr. Regina Druz (33:25): This points to where genomics may find wide application — the pleiotropic effects of common drugs. Statins have plaque-stabilizing, anti-inflammatory effects beyond cholesterol. And in the era of GLP-1 and dual/triple incretins, cardiac studies show a direct vascular, anti-inflammatory effect independent of weight loss — and there’s now a specific genetic combination that may predict who responds with appropriate weight loss. There’s also growing attention to high cortisol as a driver of hypertension, beyond rare Cushing syndrome — and a lot of it is genetically driven.

Dr. Sharon Hausman-Cohen (36:21): Absolutely. The number-one gene related to diabetes is TCF7L2 — the only diabetes gene 23andMe reported — and more than 45% of people carry one copy. It codes for the incretin GIP, one of the targets of tirzepatide; each copy means about 35% less. So that’s hugely helpful: those people aren’t making much incretin to start with, so they can choose to eat far fewer carbohydrates, support their gut (for example, Akkermansia), or replace incretin with a GLP-1 based on their other risk factors. As for cortisol, the adrenaline-receptor variant we mentioned is a major contributor for over half of people — and exercise, meditation, yoga, and ashwagandha help.

Dr. Sharon Hausman-Cohen (38:30): I get back a genomics report and can almost tell the person’s story beforehand. A 70-year-old physician asked me to review his — he had variants affecting vitamin C and glutathione (big effects on cataracts) and a cluster affecting heart disease, Lp(a), and plaque, including an inflammation combination that can give five times the risk of heart disease and heart failure. Before he told me his history I asked, have you had cataracts or heart disease? He went blank and said he’d had bad cataracts since his late 40s and a quadruple bypass at 60. Showing people it isn’t their fault, and how to be proactive, is very empowering.

Dr. Regina Druz (41:04): Hi everyone, it’s Dr. Regina here. Many of my colleagues and I are seeing patients arrive with self-ordered blood tests. When this trend started, I thought it would help — who doesn’t want more access to their health data? But too often self-ordered labs lead to more confusion and frustration: patients come in with a pile of results and are no better off. That’s why we created HeartWell Toolkits — a curated collection of at-home blood and genetic markers focused on heart and brain health that gives you the data you need to make informed, actionable decisions. You can order them at the shop on holisticheartcenters.com — the link is in the show notes. Use code TESTING10 for 10% off and free shipping.

[42:00] Insight & Empowerment: LPA, Aspirin & a GNC Warning

Dr. Regina Druz (42:00): For most people with common chronic diseases, the genetics isn’t a single gene — the large-effect pathogenic variants are rare. But they still have variants that are very impactful, because when you align your interventions to overcome the gaps your genes create, you get results. It’s actionable.

Dr. Sharon Hausman-Cohen (43:59): And you get insight. About 5% of people have an Lp(a)-associated SNP that more than doubles — almost triples — heart-disease risk (higher still in Hispanic populations). Lp(a) normally helps stop micro-clotting; if you can’t, that matters. In a large women’s health study, women with that specific Lp(a) variant who took low-dose aspirin a few times a week cut their heart-disease risk by more than half, while women without it saw only a small benefit. So don’t do the ‘GNC approach’ — walking into a store where a clerk says ‘this is good for the heart, this is good for the heart.’ One person needs glutathione support, another needs aspirin, another benefits most from a statin (there’s even a gene that predicts strong statin benefit). Patients turned to biohacking because they couldn’t find physicians to help them in a precision way. Our mission is to stop labeling people with broad disease categories — and stop blaming them — and instead find the root cause.

Dr. Sharon Hausman-Cohen (47:30): Another: a woman with two copies of ENPP1 had over six times the risk of diabetes and higher atherosclerosis risk, yet ate well and wasn’t overweight, and couldn’t understand her high hemoglobin A1c. Her genomics gave the insight; a continuous glucose monitor confirmed her sugars ran high all the time. Because metformin downregulates that overactive gene, within 48 hours her sugars dropped more than 20 points and eventually under 100. She came to me for an integrative approach — but for her, a conversation about medication made complete sense.

[53:30] Top Genes to Know for Heart Disease

Dr. Regina Druz (48:34): We see the same with statins — patients want to reduce or stop them, and over 10 to 15 years we detect early signals of statin-associated insulin resistance, more often in women. Genetic testing tells us their predispositions for insulin sensing, glucose regulation, beta-cell function, and lipid pathways, so we can lean in with a less-medicated or differently-medicated plan.

Dr. Sharon Hausman-Cohen (50:01): For beta-cell-related variants, alcohol is especially detrimental; for mitochondrial-related diabetes risk, alpha-lipoic acid, CoQ10, and PQQ help. With your map, you can choose the most important diet, lifestyle, and supplements — and it’s been hugely helpful for brain health too, since heart and brain health are cousins and twins.

Dr. Sharon Hausman-Cohen (53:30): Give listeners your top genes for someone with heart disease to know — all testable through physician-ordered medical genomics. Start with the one you can get almost anywhere, even from 23andMe: 9p21, now often called CDKN2A. Around 45 to 47% have a copy. It can make you deposit calcium in your arteries instead of your bones — and vitamin K2 helps overcome it very directly. Next, Lp(a), which we can confirm by gene and by blood. Then soluble ST2 (the IL1RL1 gene), which you won’t find on consumer tests — combined with another inflammatory pathway it contributes to about 4.5 times the risk of heart disease and heart failure, and completely changes management (watch NT-proBNP; it responds to spironolactone and early anti-inflammatories). Also your haptoglobin type — haptoglobin 2-2 raises heart risk when blood sugar rises or vitamin C drops — and the clotting genes (Factor II and Factor V), which drive stroke risk and contribute to soft plaque.

[1:00:00] Genomics for Longevity & Closing

Dr. Regina Druz (56:39): On testing, in Europe there’s a fat attenuation index — a CT-angiography technique that measures inflammation in the fat around the heart and coronaries — which will be a breakthrough for tailoring heart-failure treatment to inflammation, and advanced plaque imaging like Cleerly can catch soft, inflammatory plaque that isn’t calcified.

Dr. Sharon Hausman-Cohen (1:00:46): For longevity, these tests really help. Several genes overrepresented in the Blue Zones are in our reports. The number-one longevity protein is Klotho — and people with low Klotho benefit much more from aerobic exercise (resistance training is less helpful for them) and from resveratrol. There’s a nutrient-sensor gene tied to heart health and longevity, and APOE2, the opposite of APOE4, is a longevity variant. Longevity is the science of knowing yourself — your macular, diabetes, osteoporosis, stroke, and cardiac risks — and even cancer, which mostly isn’t from cancer genes but from an impaired ability to clear carcinogens. The more you know, the more precise and thoughtful your plan, instead of taking 20 or 30 random things. Note that nothing is for everyone: Valter Longo’s fasting-mimicking diet has good evidence, but people with certain mitochondrial variants (who can’t transport carnitine well) can get sick on it.

Dr. Regina Druz (1:05:51): I agree completely. At Holistic Heart Centers we offer a full longevity panel built on IntellxxDNA, paired with vascular imaging — because aging is vascular on almost every level. To forge a great longevity path you have to ask how to de-risk your vascular situation, and everything follows from inflammation, detoxification, and oxidative stress. Dr. Sharon, this was a pleasure — we’ll have to have you back, because this is just the tip of the iceberg.

Dr. Sharon Hausman-Cohen (1:07:01): My pleasure — happy to come back. Thank you.

Dr. Regina Druz (1:07:10): To the professionals listening: if you’re thinking of launching a cardiometabolic or integrative cardiology program in your practice, we can help. Holistic Heart Centers helps physicians expand into hybrid or concierge services — head to the show notes and click the application link; your intro call is entirely free. Ready to schedule a practice review? Use code DOC10 for 10% off our Practice Power Hour, a 60-minute coaching session. 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, and visit holisticheartcenters.com and subscribe to our YouTube channel. See you next week.

Frequently Asked Questions

What’s the difference between genetics, genomics, and epigenetics?

Dr. Hausman-Cohen draws a clear line. Genetics is the study of inheritance — specific genes tied to specific outcomes, like the single-gene diseases Tay-Sachs, cystic fibrosis, sickle cell, or the BRCA breast-cancer gene. Genomics is the study of small, one-letter DNA changes (SNPs) that mostly don’t cause disease on their own but, combined with diet, lifestyle, and each other, can be very significant — APOE4 and Alzheimer’s is the famous example (APOE4 is in nearly 25% of people, so it’s not pathogenic by itself). Epigenetics — literally ‘on top of genetics’ — is how your choices change the way your genes are expressed; for instance, certain foods lower expression of the inflammatory gene TNF-alpha. Dr. Druz’s analogy: genetics is the alphabet, genomics is the book that tells the story, and epigenetics is how the story plays out. This is educational information, not medical advice.

Is whole-genome sequencing or a 23andMe kit enough for heart health?

Not really, and for different reasons. Whole-genome sequencing is designed to find rare, pathogenic, disease-causing variants (often found in fewer than one in 5,000 to one in 100,000 people) — so a healthy adult usually won’t learn much about their everyday heart risk from it. Direct-to-consumer kits like 23andMe were pioneering and report some useful SNPs, but they’re limited. What matters most for common chronic disease, Dr. Hausman-Cohen argues, is ‘medical genomics’ — interpreting the common gene variants that actually shape heart disease, diabetes, and cognition, and translating them into actions. That kind of physician-ordered analysis (the focus of IntellxxDNA) is generally not available through consumer kits. This is general education; testing decisions should be made with a qualified clinician.

How can knowing my genes change how my heart disease is treated?

It can change the plan entirely, because it points to the root cause. Dr. Hausman-Cohen shared cases: a man whose heart attack was driven not by cholesterol but by an inability to make glutathione and CoQ10 — for whom a standard statin plus low-salt diet was the wrong regimen, and lowering oxidative stress was the right one; a patient whose hypertension ran through salt-sensitivity and adrenaline-receptor genes; and a woman whose diabetes-risk gene (ENPP1) responded dramatically to metformin, confirmed on a continuous glucose monitor. Genomics can also flag who benefits most from aspirin (certain Lp(a) variants), statins, or anti-inflammatories (the soluble ST2 / IL1RL1 pathway). The goal is precision — the right intervention for your biology, rather than a one-size-fits-all or ‘GNC’ approach. Always work with a qualified clinician on your own situation.

Can genetic testing really help with longevity?

Dr. Hausman-Cohen makes the case that it’s foundational to a serious longevity plan. Several genes overrepresented in the Blue Zones appear in IntellxxDNA’s longevity reports — notably Klotho, the top longevity protein (people with low Klotho benefit more from aerobic exercise and resveratrol, and less from resistance training), and APOE2, the protective counterpart to APOE4. She frames longevity as ‘the science of knowing yourself’ — your cardiac, diabetes, osteoporosis, stroke, macular, and even cancer risks (most cancer risk relating to impaired clearance of carcinogens rather than cancer genes). Knowing your variants lets you build a tighter, more thoughtful plan instead of taking dozens of random supplements — and avoid pitfalls, since nothing works for everyone (some people do poorly on a fasting-mimicking diet, for example). Dr. Druz adds that aging is fundamentally vascular, so genomics pairs naturally with vascular imaging. This is educational information, not personalized medical advice.

Show Notes & Resources

Guest: Dr. Sharon Hausman-Cohen, MD

Dr. Sharon Hausman-Cohen is a Harvard-trained family physician, dual board-certified in integrative medicine, and a leader in clinical (‘medical’) genomics. She is the co-founder and chief medical officer of IntellxxDNA, an evidence-based genomic clinical-decision-support platform that helps clinicians translate a person’s gene variants into personalized strategies for heart, brain, metabolic, and longevity health. Her work focuses on the genomics of common chronic disease — and on what diet, lifestyle, supplements, and medications can do in response.

IntellxxDNA — medical-genomics clinical decision support (physician-ordered): intellxxdna.com

Resources Mentioned in This Episode

IntellxxDNA — Dr. Hausman-Cohen’s evidence-based medical-genomics clinical decision support for clinicians (physician-ordered; intellxxdna.com)
Medical genomics vs. whole-genome sequencing — medical genomics focuses on common SNPs that shape chronic disease, rather than the rare pathogenic variants WGS targets
Heart-relevant gene variants discussed — 9p21/CDKN2A (+ vitamin K2/MK-7), an Lp(a) SNP, soluble ST2 (IL1RL1), haptoglobin 2-2, glutathione & CoQ10, clotting (Factor II/V), TCF7L2 (incretin), ENPP1 (diabetes)
Advanced cardiac testing referenced — Cleerly and the fat attenuation index (FAI) for coronary plaque and inflammation; NT-proBNP for heart failure
Gene editing — Verve Therapeutics (acquired by Eli Lilly) editing genes for familial hypercholesterolemia, now being explored for Lp(a)
Longevity genes — Klotho, APOE2, and Blue Zones-associated variants; referenced reading: Eric Topol’s Super Agers and Valter Longo’s longevity / fasting-mimicking work
HHC full longevity panel — built on IntellxxDNA and paired with vascular imaging
‘Chat with the podcast’ on NotebookLM — Google’s public notebook loaded with OYHH episodes (holisticheartcenters.info/notebook)
Holistic Heart University — on-demand courses and resources (use code OWNER20 for 20% off annual)
HeartWell Toolkits — at-home heart and brain health lab + genetic panels (use code TESTING10 for 10% off and free shipping)
For clinicians: Practice Power Hour coaching with Holistic Heart Centers (use code DOC10 for 10% off)

Key Terms Referenced in This Episode

Genetics vs. Genomics: Genetics = inheritance of specific genes/traits; genomics = small one-letter DNA changes that combine with lifestyle to shape risk.

Epigenetics: How diet, lifestyle, and environment change the expression of your genes — the basis of responding to your genomics.

SNP: Single-nucleotide polymorphism — a one-letter DNA change that may do nothing or significantly alter how a gene works.

Medical Genomics: Interpreting common variants that drive chronic disease (vs. the rare pathogenic variants whole-genome sequencing targets).

APOE4 / APOE2: APOE4 (in ~25%) interacts with other variants to raise risk; APOE2 is a protective, longevity-associated variant.

Vitamin D Receptor: A receptor that ‘turns things off’; variants are linked to bone, immune, cancer, and cardiac effects.

Polygenic Risk Score: A computed sum of many SNPs — useful but often only modestly additive over biomarkers and imaging.

9p21 / CDKN2A: A very common variant that can deposit calcium in arteries instead of bone — helped directly by vitamin K2.

Soluble ST2 (IL1RL1): An inflammatory variant that, combined with another pathway, sharply raises heart-disease and heart-failure risk.

Glutathione & CoQ10: Antioxidant pathways; inability to make them raises cardiac risk — and statins can deplete CoQ10.

TCF7L2: The top diabetes-related gene; it codes for the incretin GIP and helps predict GLP-1 response.

Haptoglobin 2-2: An oxidative-stress type that raises heart risk when blood sugar rises or vitamin C drops.

Klotho: The number-one longevity protein; low levels favor aerobic exercise and resveratrol.

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Medical Disclaimer

The information in this podcast is for educational purposes only and does not constitute medical advice. The discussions reflect the clinical experiences and opinions of the physicians involved, and references to specific genes, tests, supplements, medications, or companies are not endorsements. Genomic results require professional interpretation, and any changes to supplements or medications should be made with a qualified clinician. Patient cases are shared for illustration and are not predictive of any individual’s results. Do not start, stop, or change any treatment based on this episode. Please consult your licensed healthcare practitioner before making any changes to your health regimen.