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Welcome to The Dr. Kumar Discovery, a health and wellness podcast hosted by Dr. Ravi Kumar, a board-certified neurosurgeon. This is the medical podcast for anyone who wants honest, evidence-based answers to the health questions that matter most. No corporate influence. Just a physician who reads the research, questions the dogma, and breaks it down in plain language so you can make better decisions about your own health.
Dr. Kumar is a practicing neurosurgeon who brings a surgeon's precision to topics most doctor podcasts only scratch the surface of. Each episode dives deep into the science behind metabolic health, cardiovascular disease, heart disease, hormones, nutrition, brain health, mental health, pain, inflammation, weight loss, aging, blood pressure, sleep, and longevity. Whether it's the truth about seed oils, the real data on GLP-1 drugs and weight loss, the science of cold water therapy, how light can heal the body, or why your testosterone is declining, Dr. Kumar goes straight to the peer-reviewed literature and tells you what the evidence actually shows, not what the headlines say. This is evidence-based medicine in plain English.
The show features three formats. Solo deep dives explore a single health topic from the ground up, covering everything from the biology to the practical takeaways you can use today. Expert interviews bring on leading researchers, clinicians, and forward-thinking voices in health and medicine for in-depth conversations you won't hear anywhere else. The Tribulations series tells the true stories behind medicine's greatest breakthroughs, from the discovery of penicillin to the invention of vaccines to a father's fight to save his son's life. These are the stories of the doctors, scientists, and patients who changed the course of medicine.
Topics covered on the show include testosterone and hormone optimization, sleep science, photobiomodulation and red light therapy, exercise with oxygen therapy, creatine, uric acid and gout prevention, gut health and probiotics, cardiovascular risk and Lp(a), cholesterol, PANDAS in children, PTSD and trauma, acetaminophen safety, glyphosate, foot health, and much more.
If you're tired of generic health advice and want to hear from a neurosurgeon who actually reads the studies, The Dr. Kumar Discovery is your podcast. New episodes drop regularly. Subscribe and join the discovery.
For show notes, references, and more, visit drkumardiscovery.com/podcast
Hey, everyone. Welcome back to the Dr Kumar Discovery podcast. Earlier in the week, I did a solo deep dive on lipoprotein little a, and I got a flood of really thoughtful questions in the comments and DMs. So I picked five of the best ones to do mini deep dives on. I think this will tie together most of what we talked about earlier in the week.
Ravi Kumar MD:Okay. First question. My LP little a just came back at a 180 nanomoles per liter. Should I get my kids tested? They're 14 and 17 years old.
Ravi Kumar MD:Okay. So this is a really good question, and the answer to this is yes. And this is one of the most practical things you can do with your result. LP little a is one of the most heritable cardiovascular risk factors that we know of. If yours is elevated, your kids have roughly a fifty percent or greater chance per child of also having an elevated level because it's largely driven by a single gene called LPA passed down from each parent.
Ravi Kumar MD:So that being said, the 2024 update from the National Lipid Association also formally recommends cascade screening of first degree relatives once you identify an elevated index case. So this is no longer fringe advice, it's mainstream lipidology now. So to the person who asked this question, your 14 and 17 year old can absolutely be tested. The expert consensus is that LP little a is essentially stable from around age five onward. So you basically get a single test in the teenage years, and they never need to be tested again in their whole lives.
Ravi Kumar MD:And the practical value is enormous. If their number is high, you have a thirty to forty year head start on every modifiable risk factor we talked about in the main episode. And if it's low, that's also useful information that takes worry off the table. So get them tested, get your siblings tested, get your parents tested if they're still living. In this situation, information is the whole game.
Ravi Kumar MD:Okay. So next question. You said exercise doesn't lower LP little a. So if I have a high level, is exercise even worth it for cardiovascular protection? So the answer is yes, and I want to make sure I was clear on this in the main episode because I don't want anyone thinking they shouldn't be exercising.
Ravi Kumar MD:It is true that the direct effect of exercise on the LP number itself is essentially negligible. There was a thorough review of non genetic influences on LP published in 2022 that summarized the evidence on this. They concluded that across studies, the effect of exercise on Lp ranges from no change to minimal change. And what little signal exists depends heavily on the type, intensity, and duration of exercise. So if your goal is to move the number on the lab report, exercise is not gonna do that.
Ravi Kumar MD:But that's not the goal. Remember the framework. LP little a only becomes harmful in the presence of two things, chronic endothelial injury and oxidizable fuel loaded onto those particles. Exercise hits the first one of those two conditions hard. Regular aerobic exercise lowers blood pressure, which directly reduces mechanical shear injury to your vessel walls.
Ravi Kumar MD:It improves insulin sensitivity, which reduces the chronic glycation and inflammation of your endothelium, and it boosts nitric oxide production from your endothelial cells, which is the master signaling molecule that keeps your vessels healthy and pliable. I did a whole episode on nitric oxide last week with Doctor. Nathan Bryan. Please listen to it if you haven't already. You'll definitely be glad you did.
Ravi Kumar MD:Okay, so back to this question. I really like this analogy when thinking about exercise and LPLA. Exercise doesn't change the cards you're dealt, but it dramatically changes the table you're playing on. A vascular system that's getting daily exercise is fundamentally less receptive for LP little a to deposit cholesterol and start a plaque. That's how you should be thinking about it if you live with high LP little a.
Ravi Kumar MD:So here's my advice to you. You should be doing both aerobic exercise and resistance training. Do three to four resistance training sessions per week in a hundred and fifty to three hundred minutes of moderate aerobic activity every week as well. If you do that, you'll be doing your vascular system a big solid. Okay.
Ravi Kumar MD:Next question. The tokoloins and Maasai thing blew my mind. Is this for real or is it cherry picked? Because every cardiologist I've seen says saturated fat is the problem. Okay, so this is a topic of debate for sure, because pretty much all doctors are trained in traditional and conventional ways of thinking that is largely dictated by pharmaceutical company influence on medical education.
Ravi Kumar MD:That's just the truth of it, guys. I'm one of them. I went through the same educational system. So I know that it takes bucking of the conventional system, it takes being identified as an outlier, and it takes thinking creatively to actually look at what the data really says. And not many doctors do that.
Ravi Kumar MD:This is one of those examples where conventional dogma still has the minds of most doctors and patients trapped in flawed thinking because they haven't opened their minds and actually looked at the data with an unbiased lens. I have a whole cardiovascular disease series. It's episodes one through five where I talk about the history and science behind cardiovascular disease and the misconceptions and the misunderstanding that determine conventional dogma. So if you want to learn more about it, those are some fantastic episodes to listen to. Okay, so the Tokelauan data that you're asking about comes from a long running series of studies called the Tokelau Island Migrant Study.
Ravi Kumar MD:The foundational paper was published in the American Journal of Clinical Nutrition in 1981, and the Tokelauans on their Homotols were getting more than 50% of their daily energy from coconut, which is overwhelmingly saturated fat. They also smoked like chimneys because they traded coconut for cigarettes as their primary currency. By any conventional logic, they should have had catastrophic rates of heart disease, but they didn't. Atherosclerotic disease was rare. What's even more telling is that when those same Tokelauans migrated to New Zealand and shifted toward a more Western diet with more refined carbohydrates, sugar, and seed oil exposure, their lipid profiles deteriorated and cardiovascular risk climbed.
Ravi Kumar MD:The Maasai data, which is a group of nomadic herders in Africa, is even more striking. The original field survey was published in 1964. They examined 400 Maasai men who were eating an essentially exclusive diet of meat, milk, and blood from their cattle. Despite that, the men had low cholesterol levels and almost no clinical or autopsy evidence of atherosclerotic heart disease. A follow-up paper in 1972 confirmed those findings.
Ravi Kumar MD:Saturated fat was a huge fraction of their diet, and the cardiovascular disease just wasn't there. So what's going on? Well, I laid out the framework in the main episode, you should definitely go back and listen to it. But let me recap it here. Saturated fats are chemically stable.
Ravi Kumar MD:They don't oxidize easily. So even when these populations had some baseline vascular insult, their lipoproteins, including Lp little a, weren't loaded with oxidized inflammatory cargo. The atherogenic cascade simply wasn't being triggered the way it gets triggered in someone eating a modern industrial diet rich in polyunsaturated seed oils, which oxidize like crazy. I did a full episode on seed oils, which goes much deeper on this topic, and if you want to keep pulling this thread, that's a good one to listen to. The science on dietary fat has moved a lot in the last twenty years, and the public health messaging just hasn't caught up yet.
Ravi Kumar MD:Okay, next question. I have high LP low A and a family history of heart attacks. Should I just start taking a baby aspirin? Okay, well this is a question you should bring up to your doctor. This is not a decision you make on your own because aspirin has real bleeding risks, and the answer depends on your full clinical picture.
Ravi Kumar MD:But, I can tell you, the science is interesting here, and there's a specific genetic angle that makes LP little a different from other cardiovascular risk factors when it comes to aspirin. The key paper here is a post hoc analysis of the Woman's Health Study that was published in the Journal of Atherosclerosis. They looked at about twenty five thousand women who had been randomized to either low dose aspirin or placebo, and they genotyped them for a specific variant in the LPA gene. About three point seven percent of the women carried this variant, and those carriers had dramatically higher LP levels and roughly double the cardiovascular risk of non carriers. So here's the part that matters.
Ravi Kumar MD:Among carriers who got randomized to aspirin, that excess cardiovascular risk was effectively wiped out. The relative risk reduction in cardiovascular events with aspirin on board in the setting of this Lp little a gene was fifty six percent, and it was statistically significant. Among non carriers, aspirin allocation gave essentially no significant benefit. A more recent analysis from the ASPREE trial found a similar pattern in older adults. Carriers of the high Lp little a variant got disproportionate benefit from aspirin, and non carriers didn't.
Ravi Kumar MD:What this means in plain English is that for the subset of people with genetically high Lp aspirin's antiplatelet effect appears to specifically counteract LP little a's tendency to promote stickier, more durable clots. It's a beautiful example of mechanistic alignment. So the same structural features that made LP little a good at sealing wounds in our ancestors, mimicking plasminogen, and slowing clot break down, is also what makes a clot in the coronary artery more dangerous today if you have high LP levels. Aspirin tilts that back the other way. So the clinical takeaway is, if your LP level is high, your bleeding risk is low, and you and your physician are weighing primary prevention strategies, this is a worthwhile conversation to have.
Ravi Kumar MD:The evidence is not yet at the level of guideline mandate, but it's far better than guesswork. Okay, question number five. I keep hearing about new drugs that can lower Lp by 90%. When are those going to be available, and should I just wait for them? Okay, so that's a great question, and the pipeline here is genuinely exciting.
Ravi Kumar MD:In about a decade, we've gone from having essentially nothing that meaningfully lowers Lp little a to having multiple drugs in late stage development that can drop it by more than 90%. The two leading candidates are pelicarcin and opacirin. Pelicarcin is an antisense oligonucleotide. Think of it as a tiny molecule that goes into your liver and tells the LPA gene's messenger RNA to get destroyed before it can make any apo protein, which is the main protein that defines LPA's characteristics. The phase two trials published in the New England Journal of Medicine showed reduction in Lp at around eighty percent with monthly injections.
Ravi Kumar MD:Pelicarcin is now in large phase three trials with final results expected in 2026. Now, opacirin, the other drug, is a small interfering RNA, which is a similar concept but slightly different molecular mechanism. And the phase two trials here were published in the New England Journal of Medicine in 2022, and they showed reductions of greater than 95% of your LP levels at higher doses, and they dosed it every twelve weeks instead of monthly. Both of these trials I just talked about are designed to answer the most important question we don't yet have an answer to, and that is, Does specifically lowering LP reduce heart attacks, strokes, and cardiovascular death? We have very strong genetic and mechanistic evidence to think the answer is yes, but until we have a randomized outcomes trial showing it, we don't truly know.
Ravi Kumar MD:We know these drugs lower LP, don't know if that reduces death or injury from cardiovascular outcomes. Okay, so now back to this question you asked. Let me give you a practical answer here. Should you wait for these drugs? My honest answer is no, and here's why.
Ravi Kumar MD:Even if the trials succeed and the drugs hit the market in the late twenty twenty's, they will likely be expensive, and they'll likely first be approved for people with established cardiovascular disease as secondary prevention. And primary prevention coverage will probably take years longer to sort out. More importantly, the lifestyle levers we talked about in the main episode are available right now. They cost nothing, they have no side effects, and they directly address the root cause of how Lp little a causes harm. Get the seed oils out of your body, control your blood pressure, lock in your metabolic health, move your body, don't smoke.
Ravi Kumar MD:If you do those things, your high LP becomes a much less interesting number on your lab report. So, the drugs are coming, and if you have high cardiovascular risk with elevated LP, you may end up on one of those drugs. But your real protection can start today with the lifestyle changes I just mentioned. Okay. So now on to some bonus topics.
Ravi Kumar MD:These weren't questions I received, but they were things I thought were worth talking about. The first one is a saturated fat finding I didn't get into in the main episode. If you listened to my seed oils episode, you know I'm pretty firmly in the camp that the war on saturated fat has been one of the most consequential nutritional mistakes of the last fifty years. So here's an extra piece of the puzzle. When you reduce dietary saturated fat and replace it with carbohydrates or with monounsaturated fat or polyunsaturated fats, your LP little a number goes up, not down.
Ravi Kumar MD:A 2024 review and meta analysis pulled together the randomized control trials on this question. They found that lower saturated fat diets modestly but consistently increased LP little a compared to high saturated fat diets. The effect was more pronounced when saturated fats were replaced with carbohydrates or trans fats, but the direction was the same across different replacement strategies. The most detailed data on this comes from a series of metabolic feeding trials called the Delta trials, where LP little a increased by 11 to 20% when saturated fat was cut and replaced with carbohydrates or monounsaturated fats. And remember, African American populations and South Asian populations on average have higher baseline LP levels when compared to European populations.
Ravi Kumar MD:So this matters a lot for that community in particular. So what does this mean? It means that the standard cardiology playbook of cut your saturated fat, replace it with whole grains and vegetable oils, may be actually raising one of the most important cardiovascular risk factors. You might be lowering your LDL number while simultaneously cranking up your LP level. And someone who already has elevated LP, that could be a net negative trade.
Ravi Kumar MD:So this doesn't mean go pour butter on everything. It means the simplistic narrative around saturated fats needs to go away. Real, whole food saturated fats from quality sources are not the enemy they've been painted as. And if you've got high LP, people telling you to swap out your eggs and butter for industrial seed oils or margarines may be making your underlying risk much worse. Okay, so here's the next bonus topic.
Ravi Kumar MD:I thought it would be nice to briefly review why this LPA gene even exists in the first place. And I want to bring this up because I think it's fascinating. We know that Lp little a is essentially confined just to humans, old world primates, and weirdly, the European hedgehog. And that's it. No other mammals have it.
Ravi Kumar MD:And the hedgehog version actually evolved completely independently from the primate version by something called convergent molecular evolution. So here we have two different mammalian lineages independently duplicating and modifying the same gene, plasminogen, to produce the apol a molecule. So why does that matter? Well, when evolution independently invents the same thing twice in two unrelated species over tens of millions of years, that's not a random accident. That's a design feature being selected for repeatedly because it confers a survival advantage.
Ravi Kumar MD:It's one of the strongest pieces of evidence we have that Lp was protective in the ancestral world. So the modern story, where we treat it purely as a disease gene, just doesn't fit the evolutionary record. So if you've got high Lp, you're not broken. You inherited a survival adaptation from your ancestors who needed it to live long enough to reproduce. Your job is just to give that adaptation the right environment where it doesn't end up causing you harm.
Ravi Kumar MD:So stop chronically injuring your endothelium, stop loading your lipoproteins with oxidizable fuel, and LP little a remains a wound healing superhero rather than a cardiovascular villain. Okay, so that's it for this week, folks. If you found this helpful, do me a favor and share it with someone in your life who's been told they have high LP and doesn't know what to do about it. This information changes how people think about their cardiovascular future, and there's still way too little about it out there. Okay, so that wraps it up.
Ravi Kumar MD:I'll see you next week. Cheers.