AMA #3: When Can You Actually Stop a Statin? Plus Plaque, Lp(a), Sleep Apnea & Heart Scans

Two hours, your questions, and no script. You brought the good stuff: when it's actually safe to come off a statin, whether the enzyme supplements are worth it, what sleep apnea does to your arteries, how I build and read a full lab panel, and which heart-imaging test to get if you can only get one.

I answer fast, and I answer honestly — including the parts where the real answer is "we don't know yet." If you want the short version of how I think about metabolic and vascular risk, this is a good place to start. Grab a coffee, skip around with the chapters, and take what's useful for you.

⏱️ CHAPTERS
0:00 Welcome, and how these AMAs work
0:33 Shockwave therapy for ED, and how it grows new blood vessels
3:05 Can an ultrasound tech get CIMT-qualified? Why CardioRisk controls quality
6:52 Aspirin after a stent: how long, and who actually needs it
11:04 Small vessel disease and brain bleeds: the stroke signs to watch
13:01 Nattokinase, lumbrokinase, serrapeptase: do the enzymes work?
16:20 The genetic lottery: 45 years of partying and still standing
18:15 How long does a statin take to work? (and the clotting angle)
21:02 How often should you really see your preventive cardiologist?
25:23 Soft plaque, leg cramps, and the statin-intolerance playbook
29:52 Age 73: when can I stop my statin, aspirin, and lisinopril?
33:47 Supplements worth the money: magnesium, creatine, D3/K2, fish oil
40:05 Why all the statin hate? Relative vs. absolute risk, and trust
45:15 Lp(a): who should test, and why it matters for your family
49:48 Will Lp(a)-lowering drugs be covered for prevention?
53:36 Thyroid and heart health: why I check free T3 and free T4
55:26 Sleep, sleep apnea, and metabolic health
57:32 Walking after meals: GLUT4, meal timing, and insulin resistance
1:06:50 Testosterone and heart disease, for men and for women
1:10:51 What sleep apnea physically does to your arteries
1:13:31 The real problem with long-term PPIs
1:16:52 Is a carotid ultrasound worth it? It depends who reads it
1:19:35 Is plaque stabilization real science, or a gamble?
1:23:12 Nitric oxide lozenges, ADMA, and the oral microbiome
1:30:44 Building a lab panel: the tests I want, and how I read them
1:35:31 Microalbumin (UACR): the underused early-warning test
1:41:50 Why there's no one perfect diet (and why nutrition science is so hard)
1:53:25 Retatrutide, peptides, and the "just buy it online" problem
1:59:35 CAC vs. CIMT vs. CCTA: which imaging should you get?
2:14:18 CAC of 8 at 47, LDL 110: do you need a statin?
2:15:32 Wrap-up, and where to find me

📚 STUDIES & TERMS REFERENCED
JUPITER (rosuvastatin lowers events via hsCRP): Ridker PM, Danielson E, Fonseca FAH, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. PMID: 18997196. https://pubmed.ncbi.nlm.nih.gov/18997196/

Multivitamin and cognition (COSMOS-Mind): Baker LD, Manson JE, Rapp SR, et al. Effects of cocoa extract and a multivitamin on cognitive function: a randomized clinical trial. Alzheimers Dement. 2023;19(4):1308-1319. PMID: 36102337. https://pubmed.ncbi.nlm.nih.gov/36102337/

▶️ WATCH NEXT
AMA #2 — Why a "Perfect" LDL Won't Save You: https://youtu.be/v2Pa7UUTLO8
AMA #1 — Lp(a), Microplastics, Testosterone & CAC: https://youtu.be/r1p-LpCruHc
Try THIS Instead of Nattokinase (the enzyme deep dive): https://youtu.be/yA26H0_7-_U
My video on statins and the brain: https://youtu.be/pgfNT7o08_g

⚕️ DISCLAIMER
This channel is for education, not medical advice. I'm a board-certified vascular surgeon, but I'm not your surgeon, and nothing here replaces a conversation with your own physician. Supplements and medications carry real risks, including bleeding. Talk to your doctor before starting, stopping, or changing anything — especially statins, aspirin, or any supplement if you take blood thinners or antiplatelet medication.

💬 If you got something out of this, subscribe and share it with a friend.  Every new viewer helps our small channel grow one curious mind at a time.

___________________________
🧬 About Dr. Lily Johnston
  
Dr. Johnston is a double board-certified vascular and general surgeon in San Diego, specializing in metabolic and cardiovascular prevention. She’s the founder of CorSight Health and a passionate advocate for reimagining how medicine approaches chronic disease.

Transcript

SPEAKER_00 0:05

Hey everybody, welcome back to a live Ask Me Anything. I'm Dr. Lily Johnston, board certified vascular surgeon, and I hope a cardiometabolic specialist. So I hope you'll never need me as a surgeon. There are a bunch of you already in the chat. We have some anonymous questions.

SPEAKER_01 0:23

Hey everybody.

SPEAKER_00 0:23

I'm gonna go ahead and get started with those and we will kick it off. All right. So the first question I have here is thanks for doing these AMAs. During number two, I mentioned a colleague that does shockwave or ultrasound-based treatments for erectile dysfunction. Can I share his name and specialty to look him up? Absolutely. His name is Zachary Lott. He is a nurse practitioner extraordinaire. He is with Nexus HealthSpan. That is his practice in Mission Viejo, California. So please go look up Zach and uh tell him I said hi. The next question related is: can I explain how shockwave and ultrasound-based treatments create more small blood vessels and why this is helpful? Shockwave therapy is used for many things. Erectile dysfunction is one. It's also used for wound healing, chronic injuries. And the way that this works is the ultrasound waves encounter receptors in the tissue called mechanoreceptors. And they actually take the sound and they interpret it as mechanical stress. And those receptors take that information and convert it into a signal in the body. And that signal generates something called vascular endothelial growth factor or VEGF. You may know VEGF if you are in the cancer sphere because we have anti-VEGF drugs that will suppress angiogenesis or the formation of new blood vessels. And that helps suppress the tumor from growing new blood vessels and a blood supply to you know take over. But if you are struggling with erectile dysfunction or poor wound healing or chronic inflammation, you will want new blood vessels to help bring extra blood flow to that area and either support erection quality or wound healing, whatever the case may be. So the sound waves trigger this, these particular types of receptors. Those receptors generate the signal to grow new blood vessels. So that's how it works. I am not a super expert in that. Zach could tell you more, but that is in general how that works. All right, let's pop over to the chat. Donut time is here with so many questions. Thank you for that. We are going to get into a sum of these. Let's see. What are the three best donuts to eat to improve cardiovascular health and why? Well, I think this is a really important question. Um eat one every so often because you love it and because it brings you joy in life. And get rid of the other two. That's my advice on that. Can anyone that's already an ultrasound tech easily become a CIMT qualified tech? What's the period of training and potential cost? Good question. Uh, there are levels of ultrasound techs as well. So there are people who can do any kind of ultrasound. There's a special type of tech called a vascular tech, and they specialize, of course, in doing ultrasound exams on blood vessels and making sure that they know exactly how to arrange the uh probes so that they get good velocities, which is usually how ultrasound is going to measure the narrowing in a blood vessel. They measure the speed of the blood going past the narrowing. It's like when you put your thumb over a hose, the water sprays and goes faster. Um CIMT is a separate exam, as we've talked about. The companies will have their own thoughts about who gets to scan for them. So Cardio Risk, which is the lab I use, the company that I work with. Um, no financial affiliation, by the way. I just like their product and use them and um have a good relationship with their executive team. But they, because they are their whole company is focused on the reliability and repeatability of their examination, they have a very specific protocol. And as a company, they made a decision. And the decision was we know this test is highly dependent on the quality of the people and the images that we get. Therefore, we are going to control that quality by controlling who can scan for us. So it's not enough to be a registered vascular tech for ultrasound to scan for cardio risk. You actually have to prove to cardio risk that your tests are up to their standards. So the truth is anybody can scan for cardio risk as long as you can give them good pictures. I am not a vascular tech, but I have some ultrasound-based credentials. I'm qualified to read ultrasound. I have something called RPVI, Registered Physician for Vascular Interpretation. That was a separate test I had to take as part of my vascular surgery board certification. And that says I can interpret vascular ultrasound. It does not say anything about my ability to actually do the tests myself, like with the ultrasound probe in my hand and look at the pictures. However, because as a surgeon, I use ultrasound a lot in my practice personally, just to go find the vessel that I want and assess whether it's open or shut down. It was not hard for me to practice enough to go take the test for cardia risk. It was the only double-blinded randomized test I have ever had to do in my entire medical training, which means most doctors, most surgeons are never put up against that level of scrutiny. Now, it's a little bit of an artificial metric because you don't blind people for surgery testing, right? That's just not how we evaluate the level of skill that a surgeon or a doctor of any kind has. However, I will say it was an interesting experience. I was not sure that I had passed when I took their test. And I really respect the integrity of a company that says you have to give us the level of quality that is necessary to have a reliable test, which is why I feel so strongly in using their services. Um, because I know what it takes to provide images for them, how seriously they take the reproducibility and reliability of their test. Anyway, I will stop going on about CIMT. It's a good um question, but not every company will have that level of testing and um sophistication about who gets to submit for them. All right. Let's see. Lisa had a question about aspirin. So this was actually in the comments from the other video. Uh I should I be taking anyone forever or not at all, or for just a year or two after stent placement. So the stent placement is the key to this question, Lisa, because if you have had a stent put in, we know a couple things. One, you have cardiovascular disease, you have plaque. In fact, you had enough of it that needed a stent to make sure that that blood vessel stayed open. And two, you have an artificial piece of metal and and well, for coronary stent would be metal in the body. And the body doesn't like stuff that's not its own. It wants to wall that off and protect itself from any foreign intruders or invaders. And stents are like that. So stents, especially when they're just put in, have this propensity to create clot. We don't want that. Uh, so that means that dual antiplatelet therapy for drug eluding stents. So sorry, back up. Um, some stents are just like a little metal cage, little plastic or sorry, metal tube, and it goes on the inside of the artery and just mechanically holds it open. Then we have a new generation of stents that are drug-eluding stents or DES, and those actually have a coating on the metal, and the coating is designed to prevent the immune system from like attacking that stent and growing new plaque and new fibrosis in and around it and re-narrowing the artery. For all kinds of reasons, drug eluding stents are even more thrombotic in the initial period than regular bare metal stents. So patients who have drug eluding stents, especially in the coronary arteries, are going to be on dual antiplatelet therapy. So aspirin and usually um plavex or clopidogril, sometimes brylinta, checkagrillor, other agents, two of them for sometimes a year, sometimes six months, depends on the cardiologist, but commonly a year after the stent procedure. At that time, many can be de-escalated to single antiplatelet therapy. But again, you had disease severe enough to require a stent. I would leave you on one antiplatelet agent, whether that's pelavix only or aspirin only, depends a little on the severity of the disease, what disease you might have elsewhere, whether that's been treated or not. That's um that's a more nuanced question, which antiplatelet agent you would pick, but I would probably leave you on one indefinitely or until we ran into bleeding complications that necessitated us uh to come up with a new plan. So that's different than if you just have some plaque but no stent, and that's different than if you have no plaque. So if you have no plaque and you're over 70, you should not be on aspirin. If you have some plaque and you're under 70, that's a nuanced conversation. It depends a little bit on why you have plaque and how much, how high risk it is. Um, and then you know, with stents with known disease or severe disease, we're gonna say yes, probably should be on at least aspirin or maybe even something stronger for a longer period of time, maybe indefinitely, or at least until it causes issues. Okay. What else we got? 30-day challenge, welcome. 69-year-old female, total cholesterol is 325. Your C I M T. Okay, I don't see a question in there. Um, great. Well, thanks for sharing. Plaque burden is three. Okay, so I don't know what the question is, but uh arterial age is normal. I don't know, that's not quite right. You have positive LP little A, you have a plaque burden of three. If you're 69 and your average is 0.78, I'm actually gonna guess that your IMT was a little bit above average uh for your age. I can't say for sure, but I would guess. So yeah, you have you have disease. Um Sandran, welcome. My father has just been diagnosed with small vessel disease and small brain bleeds because of it. What should we watch for in case it happens again? So, great question. Not a neurologist, don't even play one on television. Um, small vessel disease is usually the result of hypertension, high blood pressure, and may also be the result of poor cardiovascular risk factors in other ways, like diabetes type 2, especially, and uh dyslipidemia or problems with atherogenic particles in our blood. So make sure those are under good control. And then if there is small vessel disease in the brain, really any problem with the brain is going to be a stroke-like symptom. Now, the classic stroke-like symptoms are weakness or numbness in an arm or a leg, facial droop, slurred or garbled speech. Those are really the classic, but those are only for the territory of the middle cerebral artery. We actually have an anterior circulation in the brain, which is the front half, middle, which is obviously little, and then posterior circulation, which is the back half. And strokes present differently depending on what parts of the brain are impacted. So the classic symptoms are usually for that MCA territory, middle cerebral artery, things in the front that shows up very variable. Could be vision changes, could be, you know, executive function issues like attention. Hard to know whether that's an acute issue with a stroke or if that's somebody, quote unquote, just getting older. Posterior circulation, back half of the brain circulation strokes tends to be vision issues or balance issues. And sometimes that's all of a sudden people just are like wobbly and tipping over one direction. Hard to know, but my best advice would be to make sure that all of those risk factors are under good control as best you can. And listen to your neurologist, they're actually the experts in that one. All right. Hello, Rina. Hi. Regarding aminos, enzymes, effects on vascular health. Do they help vascular health? And what do you know have a preventive effect? Short chain, mid-chain, long-chain aminos enzymes. Um, that is a question I don't exactly know how to answer. Aminos are amino acids. Those are just building blocks for proteins. So, yes, there are essential amino acids. Those are typically referenced as it relates to um muscle performance and gym performance, typically. Things like um citrulline and arginine can impact the nitric oxide pathway. They are precursor molecules, and so they may have some indirect effect on that. That is a little bit of a more specific answer to your question. Enzymes. Um, we just did a bunch of videos on the common enzymes to be able to talk about like natokinase, lembrokinase, and serapeptase. Uh, my personal opinion is that the jury is still very much out on those. There is some interesting initial research. Um, it's all really coming out of China, and that is neither good or bad, but I have not seen a lot of it replicated in the US. And so I'm still waiting for that to happen before I go whole hog on the enzymes. That said, we should not be totally US-centric or Western-centric in our thinking or approach. And I think there may be some utility in some of these. Um, natokinase was very pop is very popular. It's probably the most commonly used one. I have some concerns about the bleeding risk at higher doses. And everybody uh wants to tell me in the comments that only the higher doses work because of the one paper. And so, um, yes, we can think about that for many people. Maybe it's useful, but again, bleeding risks are an issue. Lumbrokinase, I think, is a little safer based on one or two papers that think that that whole and lumbrokinase is not one compound, it's six or so, all derived from an earthworm. So that one fact we don't get from functional foods. We actually just, well, I won't speak for all of you. I will not be getting lymbrokinase from any functional foods because I will not be eating earthworms. Um, the idea that we know exactly how all things, all those six things that we call one lumbokinase work is beyond me. I'm not sure that we know that. I think, based on a couple of the papers I saw, that it might be a bit safer just because it's not so broad in its activation of the fibrinolytic systems, meaning the clot breakdown systems that are in the body. However, does it work to reduce plaque? There's one paper that says yes. There are one or two papers that say that for natokinase, too. We've not seen it replicated outside of um that SETI group for notokinase. So I don't know. Jury is out. They are interesting compounds. I know many of you are using them and trying them, some with good and good effect, right? I won't dispute that. Um, so I don't know. I think it's an interesting concept. There are a lot of other things we have in our arsenal to help manage and reduce plaque. Okay. Sunshine 316, first time watching live. Thank you for being here. I'm excited to have you. I'm excited you made it. Thanks. All right. Adam Summerhill, why am I alive and stronger than kids half my age? I partied, shod dope, drank for 45 years, and they can't find anything but hypertension. You know, you won the genetic lottery, my friend. You won the genetic lottery. Uh this is the same, you know, same thing as people who smoked two packs a day for their whole lives and outlived their kids. I don't know what to say, other than sometimes we get away with stuff we shouldn't. Other people who are very diligent still end up with a lot of disease. And I think, you know, people give me a hard time when I say that a lot of this is genetics. Like, you know, we didn't get obese from genetic. Well, actually, we did. Um, obesity in many ways is a genetically driven disease for some people. And there is a huge component of lifestyle that's relevant for all of our patients, no matter what set of cards you were handed from mom and dad. But I truly believe that a lot of, especially the really aggressive disease that I see is not from people who just didn't give a damn about themselves for the first 50 years of life. Um, most people are operating kind of in the same bell curve of modern American disaster diet and not quite as active as we should be, and a little overstressed chronically, and a little underslept chronically. And like most people are kind of operating in that same bell curve, and yet some people have really terrible disease. Other people who have terrible labs have no disease, like none. I've looked. So I have to conclude that a fair amount of this is driven genetically, and some of those genes we understand and know about, and many we don't. So, congratulations, you won the genetic lottery. Um, now that you're here, I'm gonna guess that perhaps you are partying less and sleeping more and maybe exercising more. I hope that's true. And uh, thanks for being here. At Sunshine316, how long does it take for a statin to start working? So depends on what you mean by work. The impact on your lipids, the cholesterol molecules and the proteins that carry them, more importantly, is within days to weeks. So I could retest you in a month and I would expect to see about the effect on your cholesterol numbers that we would see. But that's not all they do. They also mitigate inflammation in the blood vessel wall. That was shown with the Jupiter trial. Don't come for me. I know people have issues with Jupiter. Nevertheless, the data are the data, and it reduced high-sensitivity C-reactive protein, uh, and seems to do so reliably in larger studies and cohorts as well. It also has an impact on clotting. Statins have an impact on clotting. This is not talked about, and it's not universally true. It seems to be particularly true for Resuvastatin. We are also seeing a signal for it in bempadoic acid and to some degree with the PCS canine inhibitors. Whether this is a direct result of the molecule on the clotting pathways, or more likely a result of inflammation reduction. I'm not entirely sure. It's not totally spelled out as I have started looking into this. I was actually going to do a video on this a couple of weeks ago, and then I got all spun up about the vitamin K study instead. But a paper just came out looking at a reduction in deep vein thrombosis or DVT. Those are the scary blood clots in your legs that can go to your lungs. And they showed a substantial reduction in DBT in patients taking bempidoic acid. So bempadoic acid is one of the newer medications that's available to help reduce APOB or apolipoprotein B or our atherogenic plaque-forming particles in the blood, LDLC as well. Um, it's not super commonly used yet because it's still expensive on patent and much many insurances aren't really covering it easily yet. I have my first couple of patients just getting started on it. But interestingly, the clotting signal for bempadoic acid is there. So, how long does that take to start working? I don't really know. And I don't know exactly how long HSCRP will take to come down with statins either. Usually I see HSCRP move more slowly, probably in the order of months. Um, inflammation, especially when it's chronic, is a little bit slow to spin down, but I don't exactly know how many months. I would say I usually reassess total lab values at about three months after starting lipid lowering therapy in my patients, or really any intervention, but lipid lowering therapy particularly, and reassess at that time. And if we need to change therapy for whatever reason, that is a good time to reassess and go on from there. I'm gonna pop back over to our anonymous questions for just one second, because somebody had a question about how often they should see their preventive cardiologist. There was a long, you know, diatribe about the lab values and coronary calcium score and medications and all of these things. Long story short, this person had some heart failure and is now on a path to success, doing really, really well. And they are doing so well, in fact, that their cardiologist only wants to see them once a year. This person asks, that's great news, but I want to better myself even more. Wouldn't I benefit by seeing a preventive cardiologist every three months instead? I'm gaining a lot of knowledge, and how can I improve even more going forward? I really wanted to get to this question because I think we end up making a hobby out of our health and our health care. And for a period of time, I Really encourage people to like lean into this drive. But the ultimate goal is not to be dependent on your preventive cardiologist or your favorite YouTube doctor. It is to create a system that allows you to go do the things in life that are worth doing. Coming to see your doctor is not what most people would consider a deeply fulfilling, like joy-producing activity in their life. Now, I have a couple patients that bring me deep joy when I see them because usually they're doing well and I love them and it's awesome. And perhaps for them it is a fraction of that. I don't know. What I will say though is the whole goal is to not be dependent on me. The goal is to get you to a place where you are thriving and able to like forget about the meds and the stuff and like go do things, right? Go cook, go travel, go see the world, go take a crochet class. I don't know, whatever it is that drives you, as long as it's not the donut shop, don't um make a world tour of donut shops. But the um goal should be for your own accountability. So if what you need is somebody to remind you every three months that you need to still be paying attention to your nutrition and what goes in your mouth, and you need to still be paying attention to your exercise, great. You may not need your doctor, you may need a coach, or you may need a community of people who can help keep you accountable. You might want to get your labs done every so often, again, as an accountability measure, but it's not because you're changing something and expecting the number to be different in three months. Okay. My hope is by the time I get my patients dialed in, we should be able to follow at least every six months, maybe every year. That said, I know that there is accountability that comes from coming to see me. And there is accountability that uh, you know, it becomes top of mind, right? People are like, oh, I'm gonna come see Dr. J in a few months. Like, better, better keep with the diet, better keep keep up the exercise. We're gonna be checking that ultrasound again next year, like better keep up with it. But I don't think you need to do that in the office. What is the best way to do that? I don't really know. Um, I think you should be checking your blood pressure regularly. And I think until you get your supplements and meds and lifestyle stuff all dialed in, yeah, every three months is probably reasonable. But once you're optimized, get out of here, man. Get out, go, go do something else, go touch grass, go exercise, go for a long bike ride, whatever it might be. Uh, the goal is for you to not be dependent on me. All right. WD25A. Careful taking supplementary potassiums if on ACE inhibitors like ramapril. Um, yeah, the the ACE inhibitors don't cause as much potassium retention as um things like spironalctone. That is one of the diuretics that's potassium-sparing. So, spironal lactone, I worry a lot more about people taking supplementary potassium. Uh, I don't worry as much about it on the ACE inhibitors. And okay, I'm scrolling back up. You guys are so busy in the chat. I'm excited. All right. Jeck Grin, I had CCTA showing soft plaque. Pretty sure doctor will want me on a statin, but my existing horrific leg cramp problem has me scared to try that. Should I see a cardiologist or a vascular surgeon? You should absolutely make sure that you do not have peripheral artery disease. So you should get at least an ankle brachial index, preferably a complete duplex. So ankle brachial index, stop, let me back up. That is a pressure measurement. We're gonna take the blood pressure in your ankles, both from your uh dorsalis pedus artery, which runs on the top of the foot, and the posterior tibial artery, which runs right behind your meat um middle ankle bone. And we're gonna compare that to the blood pressure in your arm. The normal ankle brachial index is anything above 0.9, or like your pressure in your feet is about 90% of the pressure in your arm, that it would be normal. Anything less than that is abnormal. If you're only getting cramps with walking, then you may need an exercise ABI because your pressures might be normal at rest. But then when you exercise and increase the demand for blood flow and oxygen to the muscles, then you may expose an area of narrowing that causes you to have ischemia, which could be causing the cramps. So I think getting that checked is an absolute necessity for a first step. Uh, if the cramps are irregular or they're nocturnal, then that's a kind of a separate issue. I would make sure that you get your ferritin level checked. Uh, low ferritin, which is an iron storage form, is associated with restless leg syndrome and can absolutely be part of a cramping issue. And then, as somebody mentioned, the electrolytes are the next thing that I typically recommend for people, um, particularly if cramping is associated with sweating, exercise, dehydration. That can absolutely be a thing. The other thing I have accidentally diagnosed in patients who have intermittent cramping pain is gout. So make sure you've got a uric acid that is normal or not elevated. Um, I had a patient who thought that it was like nocturnal leg cramps, and it turns out it was basically gouty arthritis causing pain in his legs at night. So all of those things are possibilities and could be worked up. And if you are still having issues and you are having to kind of go through the lipid lowering therapy conversation, you can start at a low dose and then decide. And what I do with my patients is say, we're gonna try it. If you get symptoms, then you stop for a week and tell me if your symptoms get better. If they get better, then we rechallenge at the low dose. And if they come back, then I am quite sure that you're intolerant at least at that dose. Then the question becomes can we do a lower dose? Can we do alternate day dosing? Do we try a different statin? If by the time we have gone through a lot of these hoops and and it sounds like a lot, it really takes a few weeks to like get rid of one of these medicines because you don't tolerate them. So maybe six weeks to like get past all of the statins, then fine. We say that you are statin intolerant and we work on the next thing. Right now is how we get that's how we get access to things like bepadoic acid through your insurance or the injectables, the PCSK9 inhibitors like Repatha or Praluent. Those are really great drugs. Um Rapatha is now available cash for I think 250 or 300 a month, which is not cheap, but it's way better than it used to be. It used to be a grand a month, um, even for people with insurance. So it's coming down. Oral PCSK9 inhibitors are on the horizon and will be coming out any day, and that should further lower the price of the injectables. Um, small interfering RNA and glycerin is actually available for a twice-a-year infusion. So you can't do it at home, but twice a year, not bad. Lots of options out there for lipid lowering if you don't tolerate statins. And I would say you don't need to be on them and suffering for weeks and weeks and weeks before you make that call. You can take them for a week, decide if it's a problem for you, report back to your physician, and hopefully move on. So I hope that helps. All right. Rick Guthrie, age 73, 40% plaque, 40% narrowing, maybe. Uh aspirin, lysinapril, 20 milligrams of one of the statins, working diligently to remove plaque. How do I know when I can stop aspirin, statin, lysinapril? Okay, so we don't know for sure, but when your markers are normal, so let's start with blood pressure because that's the easy one. Um, figuring out why you have high blood pressure, for many people it is hyperinsulinemia, too much insulin circulating in the blood, which tends to be an excess energy problem. And sometimes reducing carbohydrates or reducing total energy from our food supply can help with that. If we can get your blood pressure into the normal range without medication, then we can stop your blood pressure medication. So for many people, weight loss or fat loss will help accomplish that. Low carbohydrate will help accomplish that. For some people, a plant-based approach can do that. Okay, I don't want to pick on any one strategy here, the DASH diet, right? People, people seem to really like that one for hypertension. Um I have other concerns about it. That's another topic for another question. We, if we can get your blood pressure down to a place where you don't need the medicine, great, we can stop it. Aspirin. Uh, this goes back to Lisa's question. It kind of depends on how much risk you want to take and how severe we think that plaque is and what your other risk factors are. Do you have LP little A? Do you have a CAC over 300? And are you at risk for bleeding complications? Are you taking other blood thinners? Are you above a certain age? All those things would contribute to a discussion about aspirin. People will tell you that we need to be on statins forever. I am not convinced that's true, and I have zero data that support a de-escalation or a stopping. That said, I would absolutely be willing to work with patients who wanted to do that. And if it were me making that call, I would do it based on the soft plaque imaging. So whether that's another CCTA or a CIMT that shows stabilization and I, again, stable or reduced IMT year over year, CCTA showing that total plaque burden is the same and the non-calcified plaque burden is decreasing. Perhaps the calcified plaque burden is increasing, but that is transforming our vulnerable lipid-rich plaque into the more stable calcified paved over dormant plaque, that's fine. Does that effect go away as you reduce your statins? Depends. Do you still have the underlying risk factors that will drive new plaque to form? Maybe. But again, if we're monitoring carefully over time and we can catch it in short order, I'm okay with that. If your inflammation goes up though, I may, you know, recommend that we readdress and figure out where that's coming from. Destatin doesn't have to be the answer for inflammation, but it's one approach to reducing it in a hurry and stabilizing arterial plaques. So long answer to a short question, we don't know. There are probably some physicians who are willing to work with you on that. The classic textbook answer is that if nothing else changes, then nothing changes and you'll be on these meds indefinitely. Um, for aspirin, I don't feel terribly about that. The lysinipril, you need it as long as you need it. If your blood pressure can get better without it, great, fine, happy to take that away. And then the statin is probably something that could be de-escalated over time once we've stabilized all of your soft plaque. How long that's gonna take, don't know. Um, and does anybody actually recommend that in the literature? Absolutely not. That is not a thing, uh, to be really clear. But, you know, it's your body, it's your life. You get to decide um how much risk you're willing to tolerate and what you want to do. And I don't think it's a crazy idea, inherently. All right, Alicia Cunningham, thank you for being here. Supplements can be expensive. Which do you believe are worth the money for vascular health? Awesome question. Uh overall, there are a couple of supplements that I recommend for almost everybody, not lab-based. So magnesium glycinate at night to help support sleep and muscle relaxation. I think most people generally benefit from it at least a little bit, and the risks are super low. I take a fair amount of it and recommend it to a lot of patients. It is hard to check magnesium. So it's easy to check magnesium levels. It's hard to get a meaningful number. Um, you'll get a magnesium level on your regular chemistry panel from your lab, but it doesn't mean you're not depleted if it's normal. Even red blood cell magnesium, which is probably the more advanced test that some people get, I'm not convinced that that number is particularly well calibrated or reliable or super helpful. So I've quit checking it. And I just give people magnesium if they are not, you know, perfect, amazing sleepers or they have any cramping issues or anything like that. I think magnesium is a good one. Creatine is another one that I think is super safe and supports almost everybody who is doing a strength-based training program, which you probably should be. Um, and for that reason, it's good. There is also a very interesting signal, possibly for creatine and brain health and brain energy. Uh, the data for that are a little less solid, but I'm curious. And again, it's so safe that I feel reasonably good recommending that. Uh, I personally take five grams a day of creatine. I am close to upping it to 10 regularly. I have been spot dosing extra creatine on nights where I get poor sleep, and I have found that helpful. I know Rhoda Patrick does 10 a day routinely, and I'm I'm toying with the idea of going there myself. So those two are pretty easy. Uh, vitamin D3, I base on lab testing. So I will measure vitamin D levels in my patients. I try to get people at least 40 to 60. Um, 60 to 100 is really what I think is optimal. Again, the data are not like overall, the endocrine societies, yada yada. Most people are not recommending that. They are just recommending getting people above that 30 threshold, which is probably too low, in my opinion, but not well supported by big clinical trials. K2, I supplement with D3. If you watch the K2 videos, you know that this is a little bit of a loaded issue. I don't think the risks for K2 are very high at all. It's very, very safe. I think it probably supports bone health, may support some metabolic uh issues, right? Like blood glucose actually may help with a little bit K2. So, for all those reasons, I think it's a good idea. What it's doing for arterial plaque and calcification, probably if we take enough of it in the long run, it may slow down arterial calcification. Whether that's a good thing or not, we absolutely do not know. Um, but I still recommend it and personally take it. Fish oil is another one I commonly recommend, but not universally. Why not universally? Um, I also check omega-3 levels in patients. And if you are replete all by yourself, you're getting two to three servings of fatty fish a week, and your omega levels are great, you probably don't need it. Uh, for the rest of us who don't manage to quite get that much fish in our in our diet, I think low-level omega-3 supplementation is probably a good idea. It's generally anti-inflammatory, it helps with the membranes of our cells, the packaging of our cells that should be like just a little bit fluid and that's good. And it seems to support cardiovascular health and brain health separately. The EPA is more cardiovascular and inflammation, the DHA is good brain health support for all those reasons. Most people probably could be on good, high-quality fish oil supplements. Be careful about your heavy metals, be careful that that's third-party tested, be careful about oxidation, store it in a dark, cold environment if you can. Uh, and probably a multivitamin. Again, hard to pin down exactly why that's absolutely necessary for everybody. I don't recommend it always. But if you're doing supplements, there is one study that showed people who take Centrum daily get less dementia than people who don't. And I will say, even if you are really conscientious about getting whole, minimally processed foods, whatever that means to you, our food environment is not what it used to be 100 years ago. The quality of our soil, the quality of our animal feed, the quality of our oceans, none of it is what it used to be. So just making sure that you're getting an adequate supply of, you know, vitamins, minerals, micronutrients, all of those things, probably worthwhile. I don't feel really strongly about it, but I don't think it's harmful. So those are the ones that I commonly recommend. Other things that I do are typically based on lab testing. So homocysteine is a good example, or B vitamin supplementation. I don't think everybody needs to be on a B vitamin, but if your homocysteine is greater than eight, certainly greater than 10, I'm gonna recommend that you take a methylated B vitamin to get your homocysteine down. Um, and it works quite well. What dose of vitamin D am I gonna recommend? That's gonna be based on your lab tests. Uh, what what is your level? How deficient are you? Yes, you should get some more sunshine too if you're deficient, but even in Southern California, I have a surprising number of people who are out in the sun who are still not quite getting enough vitamin D. Uh I think those are the big ones for supplements. If I think of any more, I'll come back to that. But that's what I got for now. Alright. Adam Summer Hill, thanks. I don't even have a cavity and was adapted. Good. So you know dental health is critically important to your cardiovascular health. Awesome. Alright. Hell Arena here. Statins are huge money. There are natural remedies that can address many issues, billions of dollars a year. Statins can be issued to younger people more dementia early. Um the issues with statins and money. So the doctors don't get any money to prescribe these drugs, to be very clear. Almost all the statins are now generic. Uh, in fact, I think they're all generic. So of the drugs we prescribe, they are the least expensive. There is no doubt a big pharmaceutical industrial complex that is invested in people being on drugs. Um, and this was a question from uh Donut Time earlier. Why all the hate with statins? I think that there has been a lot of demonization of these drugs because people were not told about possible side effects, and so they feel lied to. The side effects are real. They are also not universal, not everybody gets them. They are not necessarily related to the entire class uniformly, which means older drugs, older statins tended to have issues that some of the newer ones do not. There are some that are more soluble in water that may travel more places in the body, versus the ones that are more soluble in fat, which might be more able to penetrate into the brain, which is mostly a fatty organ. So as a class, I mean, they all have the same general mechanism of action, but all of the drugs are not the same. So if you are intolerant to one, you may tolerate another. Um and the lack of transparency with some of the clinical trial data has been a huge concern. So there is something called the Cholesterol Treatment Trialists Collaborative, and they are really controlling all of the raw data for most of the randomized controlled trials that have been done in the US around statins. Uh, that's an issue, right? Those data should be available for everybody to reanalyze and you know deal with as we see fit. When it gets controlled, everybody's concerned that there's lack of transparency and what that people are hiding something. The presentation of reduction in risk related to statin therapy, which is all of lipid lowering therapy, right? But we talk about relative risk versus absolute risk. 40% reduction in cardiovascular events, like that's a relative risk reduction. If you look at the absolute risk reduction, it's like 1% or half a percent. It really depends on the population you're talking about and the outcome that you're talking about, but it doesn't help as many people as the marketing would suggest, right? Is anybody surprised by that? Probably not. But I think there has been this bigger issue of like cholesterol is the whole problem. It cannot be the whole problem. If cholesterol were the entire problem with heart disease, we would have cured heart disease 30 years ago. That does not mean it's irrelevant. It does not mean it's not part of a solution. It means that coming into your doctor's office being told that you should take a statin and come back in a year and forget about your insulin resistance and forget about your high blood pressure and forget about your nutrition and your exercise and your sleep apnea and all these other things that we talk about here, like that's bad medicine, right? It doesn't mean that statins are the devil, but it does mean that we have to be more holistic in our approach. So statins are a tool. Lipid lowering is a tool. It is one of many that I have in my arsenal and may or may not deploy for any particular patient at a given time. Uh, again, a propos of the earlier question, we might do it for a period of time with some intensity to get through an acute event like a heart attack or a bypass, but are we gonna do it at that intensity? Forever. Gosh, I hope not. Maybe we could de-escalate. I don't know. Nobody studied it. So, in my opinion, yes, statins have some risk for new onset diabetes if you're not doing anything to control your metabolic health. Statins have a risk for muscle symptoms. They may have some issue with, you know, myo mitochondrial toxicity and like strength impairment. And these are other signals that are out there, but not as well delineated. The risks for dementia are actually, in my opinion, fairly low as long as you're not getting a huge amount of statin through your blood-brain barrier and reducing your desmosterol. Another question for another day. I did a video about this and can link that for you guys. Some people will have brain fog, and if that's you, you should stop. Okay. Other people don't. And for those people who do not actually have an immediate cognitive symptom, I don't believe that it's going to cause dementia for them early, or else I wouldn't prescribe it. As somebody living with a parent with dementia, I would not wish that on anybody. So I absolutely wouldn't give it if that's what I thought would happen. But patients have been told that this is the only problem with their heart health. That's obviously incorrect. And where we've gotten in trouble is a trust issue, right? And so uh this is the this is a problem for everybody. And once we have lost trust with our patients, then it's really hard to like stand there and go, like, you have to do this, right? And we had this issue in COVID too. Everybody from public health stood up and said, We know this to be true as a fact, and like you must do this. And it turns out much of that was wrong. And rather than have some curiosity and humility and say, gosh, this is really scary, we don't know. Here's what we think might help, but we're gonna study it and get back to you. That's not what happened, right? We came out and said a lot of stuff with a lot of certainty and then got a bunch of egg on our face, and we lost a lot of trust. And I'm not sure that that was wrong. Like people um we we didn't do right. So, anyway, long story short, uh, that's what I that's my takeaway on the statin issue. Uh, we can we can always get back into that if there are other issues. Uh one up 008. Hey, patavastatin versus rosuvastatin, switching to pattavastatin due to an A1C of 5.8. Any drawbacks? So um rosuvastatin at is either a moderate or a high intensity statin. Patavostatin is a low, maybe a moderate intensity statin. So you will get less APOB lowering with the patavastatin than you were getting with the rosuvastatin. Um I appreciate the desire to go down or to go to a less intense statin based on the A1Z. I would also offer, you know, making sure that you're getting your nutrition dialed in for that, making sure that you've tried lower dosing of the Rosuvastatin, two and a half milligrams every day, two and a half every other day. Um, play with it and see. But I would just encourage you to get a fair amount of uh close follow-up testing to understand what's going on for you there. All right, Alicia Cunningham, I'm 62 with no symptoms. Is it still useful for me to get a LP little A test? Yes, the recommendations are that everybody should be tested at least once in a lifetime. That is both for your benefit and potentially for the benefit of some family members. If you have siblings or children who could also be impacted if they knew that you were LP little A positive or had elevated levels, because it is a genetically determined risk factor. And also, if your levels were sky high, you may find that you just have not presented with disease yet. But if we knew that, we might screen you more aggressively and potentially find those issues either with a heart valve or with plaque in your blood vessels before they ever turned into a real problem. All right. The real McCoy. Thanks for all the valuable information. You're very welcome. Thank you for being here. All right. Jane Tindley, why have I developed the worst heartburn since commencing aspirin, a torvostatin into cagrilor? Feels as bad as the heart attack. Oh no, I'm sorry. Um I would think about making sure your aspirin is enteric coated or EC, making sure that that's not what's doing it, and then trying to think about when you're taking them. Um, I would try to switch them to the morning. If you're taking them at night, sometimes taking them and lying down can worsen uh acid reflux. But those are a couple of issues off the top of my head. I'm not getting that a lot in my own patients. Um both lipophilic and hydrophilic statins get into the brain. Yes. Um they they do at least, as best we know. I know that Tom Dayspring says that. And as a very smart lepidologist, I tended to believe him on that. Um, but it's hard for us to test, right? It's like, how do you know what's getting into the brain? We don't do spinal taps on everybody. And so I do think that's right. Um the number of people who have problems in their brain and their heart who end up on statins is really high, which means I'm I'm not saying this didn't happen, Rena. Like, don't get me wrong, I'm not picking a fight. Um, but I will say that vascular dementia is a real thing. So if you have enough blood vessel disease that somebody put you on a statin, you may also have disease in the brain. And all of these things are possibilities. I'm really sorry that people in your life got sick when they were on statins. Will LPA lowering drugs be widely available and insurance coverage for primary prevention? They will probably be available for primary prevention eventually. The first trials that are gonna come out, I believe, are for secondary prevention. Uh, one of them is actively still enrolling for primary prevention, but those data will probably come out later and will be harder to interpret. That's not true. They won't be harder to interpret. Um, it's gonna be a bigger lift to get your insurance approval for primary prevention until they are widely used for secondary prevention and we have good data for outcomes reduction. Hopefully they'll come out for both. Uh, it depends a little bit on how the companies decide to apply for approval. And what that means is once the studies are done, a drug company goes to the FDA and says, here's what we want the drug label to say. We want it to say that people who have not yet had a heart attack should take this because they have elevated LP little A and this is primary prevention. Or they could go to the FDA and say, you know what, we're just going to write it right now for secondary prevention because we want it on the market as fast as possible. And those are the data we have. If that's true, and the FDA approval is only for secondary prevention, then they will be accessible for cash, but insurance won't cover it if it's not on the label for a while. So I don't know how that's gonna go. I am sure that the companies will want as wide an approval as possible, but uh stay tuned. We are still waiting for phase three outcomes for pelicarcin, I think will be the first to come out, and we are hoping for that in the last half of 2026. Stay tuned. All right. Yes, um, Paul Elkins says if you go to patavostatin and APOB is still too high, talk to your doc about adding a zetomybe and uh much more effective to add a zetomide rather than max the statin dose. A little bit of this depends on whether you're a hypersum secreter or hyperabsorber. If you're a hyperabsorber, for sure azetamib is probably disproportionately useful. I try to put almost all my patients on both, uh, if they're gonna be on lipid lowering therapy, I will be on very low dose statins and azetomib. Um and I have several patients on azetomide monotherapy, totally in the absence of evidence, but um for so far, so good. So far, so good. All right. Anything is better than resorting to proton pump inhibitors. I generally agree with that. Um PPIs are uh tough on the gut in the long-term term in terms of long-term gut health. Um one thing that helps statin cramps with statin with dinner instead of the morning. So the other thing potentially is making sure if you're concerned about having side effects, especially muscle side effects with your statins, make sure your vitamin D level is replete, meaning uh for at least 40 to 60, but probably 60 to 100 before you start statin therapy. And CoQ10 has mild to moderate evidence in support of it, but 100 milligrams twice a day. So morning and evening would be the other thing to max out your chances of not having any muscle side effects. Many of my patients like being on CoQ10. I have been checking CoQ10 levels, and almost all of my patients, whether they're taking it or not, whether they're on statins or not, seem to have adequate levels of CoQ10, which I'm not sure if that's just a problem with the lab test. Like maybe our test just isn't measuring that well because really what we measure is in the serum. What the issue is is in the mitochondria. I don't know. Um, stay tuned on whether I think CoQ10 testing is actually all that helpful. Uh at most alpha, hyperthyroidism and heart health. So the thyroid gland obviously makes thyroid hormone, and we can be too high, which is hyperthyroidism, or too low, hypothyroidism. The hyperthyroidism with Graves disease, which is an autoimmune condition where we have an immune reaction to our own thyroid gland and we actually activate it, we overactivate it, and we get a lot of thyroid hormone. That is very serious and can actually be something requiring hospitalization. We don't tend to see issues with people who are just a little bit extra therapeutic on their thyroid replacement hormone. Um, but yes, there is some issue with especially Graves' disease-associated hyperthyroidism. The other common thing is hypothyroidism also has some ramifications for cardiovascular disease. So it is always a good thing to just double check your thyroid levels. I personally think everybody should have a, in addition to the TSH, which is what is standardly checked, a free T4 and a free T3. Free T4 is pretty well accepted. The free T3, both of those are versions of the circulating form of your thyroid hormone. T4 is the inactivated form, T3 is the activated form. Uh the endocrine societies are not super excited about people measuring T4 and T3 levels, but I do think that they are helpful for people who particularly have some kind of fatigue or possible hypothyroid-related symptoms. Um, if you're just screening for classic hyper hypothyroidism, a TSH is probably adequate. And let's go to some anonymous questions. Does REM sleep disorder impact fasting glucose or ketones? Very low REM and often deep sleep according to wearables. Um I think I don't know about all sleep disorders. Um, I am, again, not a sleep specialist, but anything that impacts sleep is gonna impact your metabolic function. And a poor night of sleep will absolutely raise my fasting glucose and most of the people that I know. A stressful situation will raise fasting glucose. And frankly, lack of sleep or lack of restorative sleep is a stressor on the body. It's a chronic stressor if it's happening on an ongoing basis, right? So I don't know about the REM sleep disorder specifically, but I would say wear a glucose monitor or check your glucose and ketones and see what you notice about the quality of your sleep versus your metabolic status. I would not at all be surprised to know that it was having an adverse impact. Uh, that if it's a chronic condition, it may be hard to know because if you're not getting good sleep most nights, what are you comparing it to? Don't know. Uh, but I do think sleep in general is a really wildly underappreciated problem in metabolic health. And, you know, sleep apnea is a great thing. Like I screen a lot of people for sleep apnea. Some people have it, some people don't. Um, helping people manage sleep is a great, very, very satisfying thing because when people start sleeping well, they feel amazing. Uh, and the two things that I do that I think help people the most are getting them referred for sleep testing and diagnosing sleep apnea if they have it. And for women, uh menopausal hormone therapy can be life-changing in terms of recovering sleep issues that started in the menopausal transition? It won't fix anything for you if it's been a chronic issue your whole life. But certainly if you had sleep issues that started postmenopause, uh, menopausal hormone therapy is potentially life-changing for you. Okay. Does smoothing CGM glucose elevations, for example, by exercise right after eating, help reduce insulin resistance? Absolutely, it does. Uh so the, you know, total glucose spike, lowering that is very helpful. So walking after a meal or even air squats after a meal can be really helpful for opening up those Glute 4 channels in the muscle. Those are the um pathways that allow blood glucose to become muscle glucose. And once you activate the muscles, you're like, hey, we're gonna do some work. Your muscle's like, great, we want energy. So they will open up those GLUT4 channels and bring the sugar from your blood into the muscle. That is an insulin-independent action, which is great because it means that even if you're insulin-resistant, you can bring your glucose from the circulation into the muscles. That is a great way to help mitigate that impact. Obviously, adjusting your nutrition so that you eat things that don't spike you as much can help. Many uh people will try to eat carbs at the end of the meal. So get your protein and your fiber in first if you eat that, and put the carbs at the end again, so it just has to sift through all of the other foodstuffs in your belly before getting processed and metabolized, so that um again, it doesn't spike as high as quickly, and your body has time to process and mobilize that. Most people optimally will do better if your eating window is earlier rather than later. Those of us who fast in the morning and have our eating window from like noon to 8 p.m. tend to still have more insulin circulating total than people who have their window from 8 a.m. until 4 p.m. or whatever that is. Um, but from a social standpoint, it's just very difficult for a lot of us to eat early and not late. Um, like I have a hard time eating my big meal of the day while I'm still at work. That's just hard to do. So for me, the easiest thing is to eat it after I get home, but that tends to be in the evening. And so that's how I change my fasting or like restricted eating window. Um, it's better than nothing. But yeah, if you talk to like Dr. Boz or other people who are um using a lot of therapeutic fasting, they will tell you that the earlier you can shift your eating window overall, the better that is, and the better your body will deal with uh overnight. Your sleep quality is also better if you can stop eating at least three hours before you go to bed. I also have a problem with that. I have a struggle to make that happen. So I appreciate that that is not easy. And if you could, it's a good idea. What is my opinion of Ivy plaque X treatment if you have a high CAC score to reduce and or stabilize plaque? I have no idea what that is. Uh more information, please, or I will go look it up and think about it. I am concerned. Uh if I have not heard of it, I am concerned. I will look into it. Um if one is statin intolerant and has a high normal LDL and an LPA of 135 nanomoles, what is the best course of treatment? Thanks. So again, um, first question is do you have plaque? How how aggressively are we gonna be with your lipids? And if you have plaque and you want your lipids to be lowered, then that's fairly straightforward. You go to a different agent, like the PCS canine inhibitors or a zetamib or bempadoic acid or enclycerin, yada yada. Um, if you don't have plaque, then the question is, do you need to lower it? There are a lot of people, especially in the prevention space, who will tell you that the lower the better and there's no consequence to it and the side effects are all overblown. Uh, you've seen in the chat here that is not exactly the case. And I do think there's always a cost to making an intervention. But if you have a strong family history, you're very concerned. I think you can lower lipids safely. I think the PCSK9 inhibitors are quite safe. Um the side effect profile is much better than for statins. So that would probably be you could try Zedia first. Probably my next step would be to just try Zetamib and see how that goes. And you can on average expect 15 to 20% reduction in LDLC with that. Um, the other thing you could do would be to check your APOB and check your particle counts because it may be that your LDLC, the cholesterol, is high, but the particles are normal or low, and your APOB is fine. That's the other consideration here. We didn't talk a lot about advanced lipid testing, but we probably will soon because I just had my labs done and uh we will go through all of that because I have a very similar story. I have elevated LDLC, but my APOB is normal and my particle counts are great. Um, so that is a conversation and a teaching point that we will have probably in an upcoming dedicated video. But because you guys are the best and you're here with me on a Saturday afternoon, you get a sneak peek. All right, overnight hours of hypoglycemia, 50s and 60s, plaque causing. So um is that symptomatic hypoglycemia in somebody who is diabetic, or is that just your CGM that you're wearing because you're very conscientious, alarming that it's 50 to 60 overnight? Those are very, very different things. So um the average metabolically well human can be totally fine at a blood glucose of 50 or 60, and I don't consider that hypoglycemic unless you're waking up in a sweat feeling terrible. Then your body is unhappy. But if it is that you have a CGM that is waking you up at night because you're sleeping on your arm, um it's either a sensor malfunction or a physiologic number that is not actually impacting your body in a bad way. So we'll need a little more information before we can uh hone in on that one specifically. Plaque won't cause that, but if you're diabetic, then your diabetes medicines that lower blood sugar can cause it. Um, if you had a high glucose spike, then your body's own insulin response can cause your blood sugar to crash later. That is a fairly common thing, like with the roller coaster of kids, right? Like they eat a really super sugary meal, they have a blood sugar spike, they then they have an insulin spike, then they have a blood sugar crash. Uh, and that tends to be the common way that that happens in people who are metabolically not on diabetes medications. Um, all right, long-term high-volume endurance athlete training can force the cardiovascular system to adapt in ways that become pathological. While the health benefits of exercise seem to outweigh these negative impacts during an athlete's career, what is the long-term health impact after retiring from competition and training? I think you need to image and test, don't guess. So you need your heart checked out. Um, it depends, right? So there are athletes that have, I mean, professional athletics takes a toll. A lot of things take a toll, right? Football players have traumatic brain injury and soccer players and hockey players, any contact sport people have these this issue. Um the like endurance athletes, ultra-marathoners, marathoners, triathletes seem to get more arterial calcification. They may also get more arrhythmias. Um, these, you know, but but what's done is done, right? Your career is happened, it's behind you now. All you can do is evaluate where you are today and make the best of it, right? And and be grateful that uh that you are, you know, probably still very fit and have a lot of metabolic engine behind you to help manage um whatever comes next for you. But yeah, you may have a struggle with arrhythmia. You may have some more calcification than the average bear. Um, the good news is that will impact you less than had you not been an athlete. But I think you should, you know, there's um there's a guy on there's a physician. He's not a guy, he's uh a physician in Utah who's a cardiologist, his uh practices called Cardiostrong, I believe. And he Is somebody who's worked a lot with athletes. I do not know him personally. I can't vouch for his care, but uh I certainly see him quite a bit in social media circles and online. And uh that would be one option, would be to sort of connect with somebody who's got a lot of experience working with endurance athletes and seeing what they have to offer. Again, I'm not a cardiologist, so that's not uh a forte of mine per se, but there are people out there who are sensitive to those issues and might be able to help you get a better sense for where you are today and what you should be concerned about and what you get to take to the bank because you spent a lifetime being really, really fit. What is the highest CAC score I have ever seen? Um, several thousand I've seen, and I've seen people walking around fine with that. Um how important is your testosterone level if you have heart disease? Hmm, this is an interesting question. Uh the answer to that is it depends on why your testosterone level is abnormal. So testosterone is relevant from a metabolic standpoint, and it can be artificially, not artificially, it can be driven low by metabolic disease, in particular sleep apnea, sedentary lifestyle, uh, overweight obesity, all of those things can drive testosterone levels low. From that standpoint, fixing those root causes will not only improve your testosterone level, but it will improve your cardiometabolic health and help you do better and be less likely to have cardiac events. Um, replacing testosterone that is low is not proven to have any beneficial cardiac effect. It could maybe sometimes in some people have a positive metabolic effect in terms of reducing blood sugar a little, reducing progression to diabetes a little. Um, but there is a black box warning on it for cardiac events, because in older studies that were not particularly well done, there was an increase in a couple of those studies for heart attack and stroke, um, probably related to excess levels. That's another topic for another day. But the bottom line is I think it's safe to do testosterone replacement for um, I'm gonna assume this is a man. That's not a fair assumption. We'll talk about women in a second. Um, for men who are symptomatic from low testosterone, it is reasonable to replace the testosterone to a physiologic level, even in the presence of some plaque or heart disease with appropriate cautions, particularly if the symptoms are severe. Um, figuring out why people have low testosterone, particularly if they have those lifestyle risk factors we talked about, will be much more helpful in the long run, but that can take some time. And I have no evidence that it's going to directly impact your plaque. Uh, it's probably not going to hurt you, but again, there have been some studies that did show harm, and we have to be a little bit aware of that. In the bigger, broader picture, I don't really think that that's helpful, but or I don't really think it's harmful, but just be aware that that is out there. And depending on who you talk to, you may hear that. Uh, for women, I think it's even less likely to be important. Um, not because testosterone is not important for women, but just because the zeitgeist that has come up around testosterone for women has, I think, really distorted what it can and cannot do. We don't know that there's any abnormal, low level of testosterone in women. There is what is below average. Um, and there is some utility in testosterone replacement for women for low libido in the postmenopausal state. But women's sexual function is really complicated. And testosterone can make people feel really, really good no matter what the problem is. And at that point, it's basically just a legal drug. Uh, and so just because it makes you feel better does not actually mean it's correcting a problem. It just means you're getting a boost from a substance and you're now at a super physiologic state. So um the uh moral of the story is testosterone in women is a little bit loaded. It's very popular right now on social media. It may have a role in a specific number of women, but it's not necessarily something that I am super aggressive about replacing. And uh I don't necessarily think it's particularly helpful for cardiac health in particular. Okay, going back to our chat. Okay. When someone has sleep apnea, what exactly does it do physically to the arterial system? Okay, this is an interesting thing. It does many things. So you are, if you have sleep apnea, what that means is that you stop breathing somewhere between five and a hundred times a minute every night, all night long. So you are intermittently choking to death, briefly, all night long. So that does a couple of things. First, your oxygen levels may drop. If your oxygen levels drop, your tissues become hypoxic. They don't have oxygen. That creates a huge set of alarm bells, and many bad things happen when oxygen levels get low. That is why your heart hurts when you have chest pain related to a heart attack because your muscles are screaming for oxygen. That's why the leg cramps for PAD are an issue. It's because the muscles are screaming for oxygen. They do not like, not part of your body wants to be without oxygen. It is a huge stressor, creates all kinds of chemical issues. Uh, it's bad news bears. Point number two is that that also sets off a stress response, a cortisol response, because you're choking to death. Your body doesn't know whether that's somebody else who's coming to choke you to death or your tongue just getting in the way of normal breathing. It thinks you're briefly dying. So there is a huge stress response that happens every single time you stop breathing. That hormone creates a lot of sympathetic tone. So sympathetic nervous system is your fight and flight uh nervous system, and it wants to be ready to fend off a tiger. Well, that's great for an acute response, but this is happening, again, five to a hundred times an hour, every hour, all night long. That's a lot. Every night for years, that's a lot of stress hormone that was meant for a one-time situation. That causes problems with blood sugar, that causes uh problems with your heart rate variability and dropping that, and increasing your heart rate uh and tone, all of those things. Finally, there is an actual pressure problem in the chest wall, on the chest cavity, um, because your try your diaphragm is trying to pull against the tongue that has flopped in the back of your throat and is physically obstructing the airway. And so you're generating a huge amount of negative intrathoracic pressure, right? You're it's like sucking on a closed straw, basically. Um, and that ultimately causes the heart to be under more stress. So lots of different ways than in which sleep apnea is a problem for your whole body, but in particular your cardiovascular system. Great question. All right. Good morning from Melbourne. Thank you. Welcome, Pamica. What is wrong with proton pump inhibitors if they stop the heartburn? Uh, they really change the pH of your stomach, right? So they inhibit the secretion of acid. Your stomach is acidic for a reason. It's acidic to protect you from the bacteria that we eat normally in our foods. It's acidic to help digest your food. And when we lose the acidity in the stomach, all of those things go away. So I think we are more prone to getting pathogens in our DI system and our digestion is impaired. It does tend to create some issues in terms of like gut dysbiosis. We change the different kinds of bacteria that are living in our intestines and where they're living in the intestines. And so chronically, that is a problem. Using it as a you know, issue, like a one-time thing or for a week while you're eating really spicy food somewhere because you're traveling, I don't have a problem with that. Um, but chronic use, I do think, is is an issue. It causes problems with absorption of micronutrients so people can become iron deficient on PPIs long term, because again, uh the normal way that we absorb things from our diet is totally changed when we change the chemistry in the gut. All right, I have been using natokinase for three years. Is there any way I can use it with aspirin? Um you can. It's a question of what is it doing for you and is it safe and at what dose? Those are questions we don't have good answers to. Um, I'm gonna guess you watch the video. Uh, lower doses seem to be safer, but I don't know how safe, and I don't know what it's helping at lower doses, right? So all of these are good unanswered questions, and I wish I had a better, more compelling answer for you. A lot of people are doing it and not bleeding to death, but I gotta say, um, I'm just not sure it's worth the risk, especially because I'm not convinced that the outcomes are that much better. Uh, Nate the Menace, hey, how are you? Welcome. Does reactive hypoglycemia affect vascular health in any way? Uh probably. I mean, reactive hypoglycemia, do you mean reactive from being hyperglycemic? I think the hyperglycemia and the hyperinsulinemia are probably worse. I think dropping into the you know 50s for a brief minute is probably not the end of the world. But I'd be more concerned about why it's why it's getting that way in the first place and what the set of circumstances that led us to that reactive hyper hypoglycemia would be. And probably that is more relevant for the vascular health piece, but I don't have an easy pithy answer to that question. You need cholesterol, it protects the myelin sheaths. Um, that's true. The uh cholesterol synthesis in the brain tends to be independent of the cholesterol synthesis elsewhere in the body. All right. Oh, thank you, donut, for answering that question as well. Yes, it puts your heart at greater oxygen struggle, doesn't allow a system to rest. Perfect. Oh, you guys are answering all the questions for me. I don't even need to be here. You guys got this. You guys got this. Do I think a sonogram of the carotid arteries is at all helpful in seeing any problems? Depends entirely on who does it and who's looking at the pictures. Uh, yes, a CIMT is basically a sonogram of the carotid arteries, but it's a very specific question and done in a very specific way. I personally will take an ultrasound to anybody's neck and take a quick look and see what I see. And I can give you sort of a, you know, low, medium, high risk assessment based on what I see, but that's because I do a lot of carotid ultrasound and I do CIMT testing, so I have a good eyeball for what I'm seeing. If you ask your doctor to order a carotid ultrasound, there's some chance they may find something really unexpected, but you could also get what looks like a normal report and still have disease there, plaque, that went undetected because it didn't rise to the threshold of narrowing the blood vessel so much that it caused a change in speed. Some sonographers will report the presence of plaque that doesn't change the blood velocity. Others don't. Not everybody who orders the ultrasound will actually ever look at the pictures. Most people will look at the report. So it really depends on who's doing it and what they're looking for. Um, it's a great test in the right hands. Uh used poorly, it's not very helpful. Was that city called the Men's Health Initiative? No, it was not. I'll look it up for you though, um, Paul, and uh grab it. And you know what? I meant to bring in my um, I don't I don't see Gerard here, but I did mean to bring in my official life. If Gerard was here, I was gonna I was gonna do that on camera for you guys. Um if I had ended up not being a doctor, what other skills do I have and what would I have enjoyed doing in life? I have no idea because I have spent my entire adult life doing this. Um that's not entirely true. I spent three years working as a science and tech analyst for the government and found that really interesting. And it's a lot like what I do here, which is to say reading the literature, the science, the studies, the research, and trying to translate that and bring it to people who had a lot of interest in the topic, but not the same depth of knowledge and understanding. Uh some of the other people on our channel will probably argue the degree to which I'm effective at doing that, because I still use words that are too big and concepts that I don't explain very well. But nevertheless, I enjoy trying to help bring information to people who are interested, but not quite as nerdy as I am. And that I think is probably what I would end up doing if I weren't uh doing the whole surgery thing. All right. Um D25A stabilizing plaque is only a theory which may or may not be correct. It's not proven science, it's a gamble basically. So, yes and no. I think what we can say is that there is absolutely an evolution of plaque. So if we do repeated imaging studies over time, what we can see is that the fibrous cap overlying lipid-rich plaques can thicken or become thin and rupture. And that seems to be relevant. We also can see, like Dr. Agatston has presented data. So Agatsten of the Agathan Calcium Score, he's now doing a lot of work with CCTA. I sat on a panel with him in January and he showed a lot of his own data, uh, his patients' data, which again, anecdotes, not published studies, but over time we see that the areas of plaque that were soft and lipid-rich have become calcified and what we would call like higher density on the CT scan, meaning more firm, calcified, stable-ish. Uh, and we know that if we consider the amount of calcified plaque versus the amount of lipid-rich plaque, it's really the lipid-rich plaque that is driving risk. All of that together creates a very compelling story for plaque stabilization. And while I think I agree that there's not been a study of that per se, what do we think is happening that is reducing event rates in trials where we're doing secondary prevention with successful interventions, right? So whether that's PCS canon inhibitors, whether that's semaglutide, ozempic, wagovi, um, we have trials that show reduction in events. What do we think is happening? The plaques are not rupturing. So that ergo probably means that we are stabilizing them. Perhaps it means that we are just not triggering rupture events in a different way, but the imaging data would support, in my mind, a change in the plaque characteristics. And we have that both with um intravascular ultrasound, we have it on MRI and the carotids. We have a lot of different imaging modalities that do show a change in plaque characteristics over time and acceleration of those changes with intensive medical therapy. So I do think we have a pretty compelling story. Uh, plaque regression is perhaps the more controversial piece of this, right? So that's not just taking the lipid-rich plaque and turning it into something much more stable, but actually causing the body to reabsorb um the material that's in there. Plaque regression, I think, is more controversial. It has been shown in a couple of studies with uh very high quality imaging, right? We can show it with intravascular ultrasound. Um, maybe we can see it on CCTA, although, again, the level of detection of that technology is not quite where we want it to be yet to demonstrate compelling plaque regression. Uh so that one, I agree, is probably better in the hypothesis category, although I'm again, I'm reasonably comfortable saying I think we're gonna see it. It just depends on how aggressive people are being managed. Whether it matters or not, again, there's at least one paper that showed that if you saw more plaque regression, you had fewer events. Um, not prime time yet, but there are some studies that speak to this. Okay. Do I have experience opinion on using nitric oxide lozenges for improving vessel health? Uh, jet grand. So I have used them. I don't know whether they really improve health or not. Um, measuring nitric oxide is tricky. The best that we have is a proxy marker, ADMA, SDMA. Um, and this actually also came up in one of the questions about nitric oxide. So nitric oxide has a very, very fast half-life in the blood, um, milliseconds maybe. So we can't measure it directly. We have these metabolites or byproducts that are associated with nitric oxide levels. Uh, ADMA is the one that is commonly measured. And then we have physical measurements like flow-mediated dilation. This is a test where they restrict the blood flow to the arm and then release it and see how much dilation you get of the blood vessel in the brachial artery. Um, these are not super well correlated with clinical events, and so they are not widely used in clinical practice. I used to check ADMA more often than I do now. It's an expensive test and it doesn't move the needle for many of my patients. Um there are a bunch of things that purport to improve nitric oxide. The uh lozenges are one, the um like arginine citrulline are another, and exercise is probably the best one, uh, leafy greens for some. And then part of that is do you have the oral microbiome? Do you have the bacteria in your mouth that will actually convert nitrite to nitrates or nitrates to nitrites? I forget. Sorry, I did not actually do that well in chemistry. Um, so in any case, there is that conversion goes one way or the other, and it's facilitated by the oral microbiome. Uh, people who use alcohol-based mouthwash every day, for example, will get rid of a lot of those good bacteria and may have issues converting. And um, so that's part of the issue. If your oral microbiome isn't in the right place and you're using the lozenges, you may not actually get as much impact because you're not getting that conversion. So that's the best of my answer on that one. I don't think it's harmful. Um, some people may notice an impact for exercise and using vasodilators that way to support exercise. I don't have a lot of evidence for that either. Uh, there is intro, I'm seeing another question in the anonymous group. Um, does the use of doxazosin or other vasodilators affect mortality outcomes? Doxazoscin is not one I know as well. The more common one that I get asked about is cialis or the phospho diastase 5 inhibitors, the erectile dysfunction drugs. Um, they work by stopping the enzyme that breaks down nitric oxide. So they don't create more nitric oxide, but they at least allow it to circulate longer. So that causes vasodilation. The reason they work for erectile dysfunction is because that vasodilation increases blood flow to the penis and creates more blood flow there for the erections, but also it works everywhere. It is not organ-specific. So you get more blood flow everywhere. There are people who are using it in the longevity space for that purpose, right? Perhaps it even improves cerebral oxygenation and perfusion. I don't know yet. There are some like little inklings. I have not done my own deep dive into this yet. Um, again, I don't think the risk is that high if you're not on a bunch of other meds that might impact your blood pressure, but I don't know that there's a strong signal for mortality yet. Uh, I don't even know that there's a strong signal for any improvement in cardiovascular markers other than maybe blood pressure. If I had one patient who actually had took it chronically and had an improvement in blood pressure, but nobody does it for that specifically on purpose. All right. Can I comment on the utility of vigorous intensity cardio versus moderate on arteries? I think um this is from Kushik, Czech Rebote. Thank you for coming. Thanks for your comments. Um, mostly I think this is an efficiency question. The um moderate versus high intensity, I think you can probably get good impact of moderate. I like high intensity just because it's more efficient. I don't have to do it for as long. Um, what is the magic equation that allows you to convert moderate to high intensity? Don't know off the top of my head. Uh, but in general, it's this idea of how long versus how high is your heart rate elevation, right? Duration versus versus intensity. And I think that you can make up for in intensity what you lack in duration, or you can extend in duration what you lack in intensity. Intensity, that eventually creeps down to a place where we're just doing low intensity steady state, which is different. So low intensity steady state is me on a walking pad doing this, but still able to have a conversation. Anything moderate or high is going to be me sweating and not able to speak in full sentences. And that is really the bucket of cardiorespiratory fitness that we're talking about. And my take on some of the literature, I'm not a deep dive expert in that, but I have heard it presented. And what I have taken away is it is about efficiency. If you like long or moderate efforts, by all means. If you don't love cardio as much and you just want to get it over with, try your high intensities.

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Now that I tease the omega-3 test, yeah. I will take one for the team. Yep, you're right. All right. 23-year-old male currently experiencing idiopathic post-meal palpitations. Ooh, that sounds unpleasant. Um, I'm glad you're working with a cardiologist. Yeah. Um, UCI also has a good integrative medicine program if you're uh interested in checking that out. All right. Sunshine 316, arugula is good. Yes, that's apropos of the nitric oxide conversation. It is one of the uh leafy greens that is high in those compounds. Holter echo, all normal, but doing a tilt table for possible pots. Yeah. Um you can try working on higher electrolytes and seeing if that helps. That seems to be um what helps a lot of the pots folks, but I am not an expert there. Yeah, compelling story is not settled science. You're right. Science should never be settled, um, to be fair. I think we are always learning more and getting more, and the answers are never straightforward. And if, you know, if you're here, then you know that that's how I feel about all of these things. And it's a challenge to be in the social media space with that message. Um, it's not a popular one, but I believe in it. So here we are, and you guys are here with me, which I'm really excited about. So many confounding factors. Absolutely. These are hard things to study. The longer the time course of the disease, the harder this is to deal with uh and to study well because more and more of those things come into play over time and we just can't control for them very well. B plus in chemistry. I am human. Yeah, um, that was my first semester of organic chemistry. I got a B plus. I got an A in the second half, but I don't remember any of it. I just studied my ass off. All right. Okay, guys, I'm gonna go back through these questions one more time and see if I missed anything. Um, let me know what else you want to hear about today. Somebody left a question about uh lab testing. So I'm gonna go through a list of lab tests that they mentioned and talk about that while you guys get your last questions in here. If I missed one up top, um just put it back down below. I'll try to get to it, but I am at the bottom of the chat. So if I missed something that you really wanted to get answered, please just put it down again because I am trying to read and talk at the same time, and uh that is a challenge. So this person said lipid panel, comprehensive metabolic panel, C reactive protein, good. I would ask for high sensitivity C reactive protein, that is more helpful. Apollipoprotein each. Uh, I hope you mean B, but you may have also meant A or little A. No, lipoprotein little A is down below. Okay, so apolipoprotein, probably B is what you mean. Apo B, good. Um, insulin total should be a fasting insulin test. I would love for you to have that fasted. I would love for you to do your lipid panel tested. That is not actually the common recommendation, but I think it's more helpful so that I can interpret your triglycerides and not make you go back and get them checked again. All right. Hemoglobin A1C with estimated average glucose. Yep, uric acid, good. Vitamin B12, cynocobalamin. I prefer to check homocysteine because that tells me much more about your ability to convert the inactivated forms of your B vitamins, like cynocobalamin, into methylcobalamin and the methylated forms that your body actually uses. So overall B12 levels are fine, but I have seen people with replete or normal or high B12 levels who still have elevated homocysteine because they're getting inactivated B vitamins in their multi or in their B complex that they're taking, and they're still not able to convert them. And if your homocysteine is still high, then that's still a problem. Vitamin D25 hydroxy, great. Zinc, iron T I B C ferritin, great. Magnesium, so again, serum magnesium will already be in your metabolic panel. If this is RBC magnesium, maybe that's more helpful. But I saw a paper recently that showed that that was actually even not that well correlated with magnesium uptake, which is probably the true marker for magnesium depletion in the body, which is only a research-based tool where they bring people in, give them an enormous load of magnesium, either orally or IV, and then measure how much they excrete, which if you subtract how much you gave from how much is excreted, then that's how much the body absorbed, which is a sense of how much the body wanted or needed to absorb. And that is how it has been measured previously. But I don't know how well the red blood cell magnesium levels really correlate to that. So I have quit measuring RBC magnesium too, and I just give people more magnesium and don't measure, don't care too much about it. And then uh we already talked about the CoQ10 levels. I have checked them in my patients and sometimes still do, but honestly, the reference ranges for that are not as helpful as I would want them to be, and I am not really changing my management based on that. All right, okay, a few more coming in here at the last minute. Great. 66-year-old male peaked P waves on EKG, pulmonary hypertension with no clinical symptoms except for sleep apnea. Is there a connection between pulmonary hypertension and sleep apnea? Yes, there can be. Again, um, when you are trying to breathe against a closed airway, you create a lot of pressure in the thoracic cavity and it can cause pulmonary hypertension over time. Absolutely. Thank you for addressing our questions. You're very welcome. Thank you for being here and having such a good and friendly discussion. Science should never be settled. Yes, I agree. Hi from Luxembourg. Hi, Antonio. Awesome, welcome, great to have you. What about L-citrulline for people with atherosclerosis or high blood pressure? Um, L-citrulline is part of that nitric oxide pathway. And uh by itself, if I didn't know anything else about nitric oxide, maybe it's helpful, but I'd love to that's again, uh, try to figure out what is the root cause. And if we do think it's nitric oxide, maybe based on one of those ADMA measurements, maybe L-citrulline is the good choice for that. Again, we talked a little bit about all the supplements and interventions for nitric oxide. Uh, they all make good sense on paper, whether they are really impactful in practice is kind of variable. Some people seem to respond really well, others not so much, and I don't yet have a great sense for who that's gonna be, but I think they're pretty low risk. Meaning worth a try. 24-hour medical seminar? No, not quite. Uh, but I don't know, we're we're at two and a half or one and a half, that's pretty good. Um, why is an UACR part of testing panel for hypertensives? So this is um microalbumin to creatinine ratio. It is commonly used in diabetic patients, but not in hypertensives. And it's a great question because again, we do see people so let me start, let me back up. The kidneys have two jobs. The kidneys filter out bad stuff, but their other job is to keep good stuff. And that sounds like it's one and the same thing, but it's not exactly. So um when you think about how like the kidney is a really remarkable organ, uh, it cannot possibly know all of the toxins that could possibly be required to filter out in the world, right? The chemical memory that you would have to have to figure out exactly which things to keep and throw away is too high. So the way that it really works is that the kidney kind of gets rid of everything and then reabsorbs the good stuff. So what it should keep is actually a much more bounded and finite list, right? It should keep all of a certain amount of sodium, it should keep a certain amount of potassium, it should keep all of our protein. So microalbumin is a microscopic amount of protein that is inappropriately spilled into the urine, meaning the kidney did not reabsorb it. Most people's kidney function tests are about whether the kidney is clearing out the toxins, and that's helpful and good information to have. Microalbumin also says, is the kidney able to keep the good stuff, especially the protein? And when people start spilling protein in the urine, it means that this reabsorption mechanism is under stress. And the two most common reasons for that are high blood pressure and diabetes or hyperglycemia poorly controlled. Typically, it takes diet, a true diagnosis of diabetes and being profoundly insulin resistant for years before people get that diagnosis. Um, we have a mechanism to help manage it in diabetic patients, which is to say once there is an once there's evidence that there's impaired kidney function, people will escalate therapy. Why it takes that particular marker and not just their A1C being over 6.5, which, you know, 6.5 to 7 is considered good control in the modern endocrinology space. Uh, I think those of us in the metabolic health space would say we would love to be able to get people under 6.5 again and put their diabetes into remission by uh predominantly lifestyle, but with or without targeted therapeutics as well, is always possible. So from that standpoint, the microalbumin to creatinine is you know a target for more aggressive intervention in the diabetic population. In the hypertensives, all we know is that you know we should better control their hypertension. And usually if their hypertension is well controlled and they still have microalbumin, then we're looking at an insulin resistance problem. But I actually had somebody recently who is well controlled from a hyperglycemia standpoint. She was pre-diabetic, but has gotten that under really good control and is not, as far as we know, hypertensive, never has been, and her microalbumin is creeping up. And it's unclear exactly what we are supposed to do about that. She is not at a threshold where she has a diagnosis or a pathologic amount of protein in the urine. So I don't really want to put her on medicine for anything because I'm not sure what I'm treating. So I it's an underused test, 100%. It's an underused test, mostly because it helps us identify insulin resistance and hypertension before people have real catastrophic consequences and their kidney damage is irreversible or other organ damage is irreversible. So I like it as an early warning sign. Um, but you know, is it gonna help us know that we're still supposed to get people's blood pressure normal? No, we already know their blood pressure should be normal. Um, does it help us understand if insulin resistance might be at the root cause of their hypertension? That's a possibility. So it's a cheap test and it's a good idea. I think we should probably be using it more, but there's no current guidance for the use of it in people with high blood pressure alone. Do I do second opinion appointments? Uh yes and no. You I'm only licensed in a few states, and mostly I see people through my practice at Scripps Clinic in California. Um, but you can reach out to me by email info at core site, C-O-R-S-I-G-H-Thealth.com, and I can let you know whether that is something I can help with or not. Or maybe I know somebody who I can send you to it's licensed where you are. That's pretty unlikely. I don't know very many people, but um I will help if I can. Jorge, do I believe high-fat diet impairs glucose metabolism? I personally reduced my fat intake and triglycerides dropped. Aguincy improved too. Yes, I actually do believe this, which is really unpopular in keto carnivore circles, but excess energy from either carbohydrates or fat will cause insulin resistance. And there are very good data from this, especially in muscle cells, where excess free fatty acids will cause insulin resistance on the myocytes. Um again, for a lot of people, it depends on where you're starting. Um, not everybody needs to control fat right away if you're on a low-carb diet. But for a lot of people, if we are still struggling with metabolic health, even on a low-carb diet, then the next question is how much energy overall is coming in. And if it's in excess, then your body's system to manage energy, which is your metabolism, will be under stress. It is possible to eat too much fat. I personally believe that. All right. Do I take MMA tests with homocysteine? Um, typically I don't, although I know many people recommend it. I just haven't done it, and I don't know that it adds a lot to my own personal thing, but it may just be that I'm not smart enough. Uh, MMA is often with just methylmalanic acid, sorry, for the abbreviation. Um, often MMA is tested along with homocysteine. I personally don't do it very often. All right. I upped fat protein eggs and cut the carb significantly, dramatic improvement in lipid numbers. Why didn't any of my doctors know about this? Are they being trained better? Um, nutrition is becoming very politicized, and it's a challenge, and I don't have a good answer for you. The right diet for any given individual is not universally the same. So I get a lot of comments being like, well, what do you recommend for everybody? I don't recommend the same thing for everybody. The diet that works best for me may not be what works best for you. The diet that works best for me today is not the diet that worked best for me five years ago. So things change over time within ourselves, and we are all different unicorns between each other. And so 90% of the time I recommend a low carbohydrate approach for my patients. I have some people who come in who are already doing a very low-fat plant forward approach, and I won't argue about that if they're doing well. Uh, if they're not doing well and are open to talking about it, I do offer some thoughts. But again, I try to be really data-driven. Like, what is the actual problem? And what am I, what do I think I'm fixing by changing their nutrients? Um, we don't know enough about this. The science is really, really hard because we eat one to three times a day under the best case scenario, right? Some people eat more than that. And there's so much else that happens. It's really hard to study. If you study it very deliberately, like you lock people in a lab and you control every morsel that they eat, well, you can only do that for a couple of weeks because it's too expensive to do it for any longer, and nobody will sign up for that unless they're going to Mars or the moon. Um, if you're just gonna ask people what they eat in the last year, you can imagine how unreliable that is. And unfortunately, the vast majority of our nutrition studies, and I use that word loosely, but the information that has been published about nutrition is by and large coming from Food Frequency Questionnaires, which is a piece of paper or an online forum that you get that says, How many times do you think you've eaten broccoli in the last two months or six months or 12 months, or how many times per week on average in the last year do you eat broccoli? And do you eat chicken? And do you eat red meat? And do you eat corn and do you eat chips and do you eat french fries and do you eat donuts and do you eat whatever eggs? And so you can imagine how much bias would be involved in your own recall of what you eat, right? If you identify as a person who eats a healthful diet, then you're gonna answer those questions the right way. If you identify as somebody who doesn't give a shit what they eat, then you're gonna answer those questions in the standard American disaster way. So, you know, the standard American disaster diet is a problem for everybody, whether that is your springboard to a ketogenic diet, to a low carbohydrate diet, to a Mediterranean diet, to the DASH diet, to a mind diet, to the Esselstein diet, whatever it is, if you're departing from standard American disaster, you're probably gonna do better. And this is where all the fights come from, right? Because people are like, vegans do great. And people are like, well, carnivores do great. And like, we're gonna fight it out and talk about, you know, which defects there are in each of these approaches. Well, there's not enough fiber, well, there's not enough iron, well, there's not enough protein, there's not enough fat-soluble vitamins, there's not um a lot of people do well on a low carb diet. Some people do well on a low-fat diet, some people do well on a vegetarian diet, and some people do well on a carnivore diet. We eat in the way that we eat for all kinds of different reasons. Some people are doing it for their mental illness or their autoimmune disease, or because their child has epilepsy, or whatever the case may be. There are a hundred reasons to eat in a particular style or way that have nothing to do with your cardiovascular system. And I am totally on board with helping you continue your way of eating if it is serving you in some good way. And whatever unintended consequences it has, and they all have some, let's talk about it and see what we can do. Um, I wish more doctors had a sense for how to help people do that and how important food as medicine is. That is not something that is changing quickly enough, in my opinion. Okay. Take iodine as supplements. Um, I this is really with respect to thyroid function. And I know that there are some people who do this or talk about this a lot. I don't feel strongly about it. I don't have a I don't have a strong deep dive for you on this. Um, short answer, generally not something I'm recommending routinely for my patients. Okay. L-citrulline is effective to increase nitric oxide and enough. Yeah, uh, it's supposed to be for sure. I increase my carbs just prior to exercise, like Dr. Cy was suggested, feels good. Ketogenic six years, maybe too long. So, um, Jorge, I think some people do better with exercise with a little bit of targeted carbohydrate replacement. Other people don't, and you do you. Um it's possible to continue to exercise fat adapted, but if you want better performance and you notice better performance, I don't think replacing some small volume of carbohydrates is going to be the end of the world unless it triggers food addiction issues for you. I think you have to measure and figure out what is working for you. Um, and again, it may have changed. I also have introduced a few more carbohydrates than I used to, but I'm exercising a lot more than I used to. And um certainly my resistance training is much more demanding than it used to be. So I don't know. I don't have the right answer. I don't think any of us are totally figured it out, but keep playing with it, keep being willing to experiment and test and get more information. And if it's working, do it. Do it. All right. Imagine if all doctors were required to do 20 hours of asking anything live. Uh hey Steven, welcome. Chris Cardell, long-term detriment from taking uh THC gummies or CBN for sleep. And the solution, only solution I've ever had. We don't know for sure. Um, there are a lot of sleep people that will say that THC is a problem for the quality of sleep. I have certainly parroted that myself from time to time. But I will say if your alternative is doing nothing and getting crappy sleep forever, that seems like a bad deal. So I don't know. I would recommend trying to actually get in with a sleep person and talking about it. I don't know if you've ever tried trazidone. I don't know if I like trazidone better than I like THC gummies. I just don't have a great sense for that. My knee-jerk reaction is that any chemical substance is changing the quality of sleep. However, getting sleep, big deal. So if you have come up with something that's working for you, um, I hate to take that away without trying to offer some kind of something in its place. So um stay tuned on that, see if you can uh work with somebody to help with help with that issue. Sam, hi, Moroccan, Canadian now from Morocco. Uh causes behind extra systole, probably extra systolic beats like PVCs. I don't know. I'm not sure about that. And also not as much of a not not as much of an expert in heart rhythms as I wish I were. So I'm not gonna give you an answer because I don't know. Sunshine, is that an okay to take with GLP1? Yes, yes, no concerns there. All right. Lisa, ah, you're so sweet. George, thanks for common sense. Uh you guys are great. Uh you guys are the best. All right. Paul, what biomarkers will show vascular inflammation even before MPO or LPPLA2 are elevated? Are F2 isoprostains, OxalDL adhesion molecules, or other that are early indicators of early atherosclerosis? You know, I don't know. And I feel like less than 1% of the population is even getting MPO or LPPLA2. Um, my buddy used to call F2 isoprostains the lie detector test for lifestyle. And basically, if you were pretending that you were eating okay and exercising and sleeping and you weren't, that's how you would see F2 isoprostains. In general, I don't test F2 isoprostains because I don't know how it really changes management. People are going to do what they're going to do or not. Um, LPPLA2 is the one that I still use most often. I only check myeloperoxidase or MPO if I'm really worried about somebody's periodontal disease or um periodontal pathogens. Uh I don't routinely check MPO anymore, only in cases where there's elevation in CRP and maybe there's a dental issue that's uh unclear to me. I'm not sure that that's correct, but that's what I have learned from from Brad Bale and Amy Denin. So that's what I have been doing. Ox LDL, overall a better predictor. I don't know how early it goes up in the pathogenesis of plaque. Um, not something I'm routinely testing. It's a pain in the ass for my patients to get it done, and uh, it comes from very different labs, and I get different reference ranges every time. So, unless people come in specifically asking for Ox LDL, I'm not checking it. Um MMP9 might be interesting. Again, matrix metalloprotenase 9 is one of the enzymes that will degrade that thin fibrous cap overlying our plaque. There is some evidence that MMP9 levels are interesting, at least on a research side. Clinically, not sure. Uh interleukin 6 is another one that comes up as a marker for systemic inflammation, not being used commonly in clinical practice. I still think imaging is the best thing we have, but I don't know. It's a good question. Luxembourg, yes, what kind of magnesium is good for insomnia? Um, I personally like magnesium bisglycinate or magnesium glycinate. I think ultimately what I have begun to learn from other people that are smart in this space is that all of the chelated magnesiums, so that's glycinate, taurate, threonate, malate, um, all end up getting cleaved from the thing. The magnesium becomes separate from the other thing. But glycine by itself is also helpful for sleep. So there are people who will take five grams of glycine before bed. So even if you take mag3-8, you know, whether it's it's probably magnesium in general that's helpful, but probably you get some extra benefit from the glycine or the glycinate that's coming with your magnesium, you could also just take five grams of glycine at night uh and whatever kind of magnesium you want. All of the chelated magnesiums, which is to say not magnesium oxide and not magnesium citrate, are gentler on the intestinal system and should not cause uh loose stools. So, for all of those reasons, I always prefer those chelated magnesiums, and glycinate is the one that I most commonly use. Some people say 3-8 has better brain penetration. Maybe that's all bullshit. We don't really know. Um yeah, okay. Do I have an opinion on retitrutide? Yes. Um, I am generally very excited about the GLP1 receptor agonists and their cousin molecules, GIP, glucagon. Um, I think retitrutide is going to be an amazing adjunct for patients with severe fatty liver overweight and obesity. Uh, I think it's being used now, prior to any FDA approval, in a way that is creating a lot of angst in the general population for kind of this, what what people are calling like looks maxing and um titrating Jimbro, like they're running anabolic steroids and REDA because it's really effective at fat loss and doesn't tank people's appetites. And I had a friend's 18-year-old son get on a phone call with me and start asking me about whether he should start taking retitrutide with his BMI of 22 because he wants to do a cut and he wants to do this and he wants to do that, and he knows that people can just buy it on the internet. I think that's not safe. Um it is possible to get these peptides from wherever, and it could be baking soda or it could be meth. If you're not sending it out for third-party testing, you don't know. I know a lot of people using peptides, and many of them are using it safely, and I am happy to engage in a harm reduction conversation about that. As a physician with a license, they are not things I can prescribe, right? Redatrutide is not FDA approved, it's not available for prescription yet. I can't tell you to go take that. That seems like a bad idea. Um, BPC 157, TB500, like these are things that exist that might even be helpful, but I can't prescribe them. And I don't think it's within my scope to tell you to go reconstitute a powder sterily and try to pull up the dosing yourself and inject it and like be fine with that. I have a hard time with that. That is a line that other people in this space have happily crossed and don't feel as strongly about. Maybe I'm just a big stick in the mud and overly concerned about the safety and truthfully the legal implications of doing that as a physician with a license. Um, but the bigger picture is retotrutite is going to be a great molecule. I'm not sure that it's that much magically above and beyond trisepatite. I think trisepatite is a great drug. Uh, and I prescribe it for appropriate patients when the opportunity arises and they're and they're interested in that. But um, RETA will have more weight loss, more fat loss, and it may have some additional indications, potentially for fatty liver disease. And um, you know, it's it's just a different molecule with the glucagon. We'll see about the heart rate, we'll see about the impact on uh other side effects. People get a lot of skin sensitivity or allydynia that is potentially um problematic. So stay tuned. I think we, you know, the data are still coming in. Let's get the trials and let's figure out where it fits in our armamentarium of molecules to manage metabolic disease, overweight, and obesity. All right. Mark Suave Suave, great. LPAA high, 80 milligrams per deciliter. APOB is 55, and Doc wants it lower. Should I be worried? Um, I worried is an interesting term. I don't know. Are you worried? Your LDL is 55. That's at oh sorry, Apo B is 55. Depends on what your LDLC is. Um, I think an Apo B of 55 is pretty darn good. The question is, how else do they want it lowered and how do you feel about that? And do you have imaging that suggests that your LP little A is problematic? Do you have a lot of plaque? If you do, then maybe getting your APOB even lower is helpful. If you don't, then maybe uh Apo B of 55 is adequate. I don't know. Um, I would ask your doctor why they want it lower than that and see what they say. All right, apple fritter live next time. Okay, so what I think I'll do is I'll do the fish oil capsule and then I'll chase it with a little bit of apple fritter just to get rid of the fish taste. And I think that's the plan. I like this is coming together, guys. It's gonna be great. It's gonna be great. Uh what is the true risk of having my LPA at 80 milligrams per deciliter? 45-year-old black male lost 90 pounds. Awesome, good job. BP is controlled, HDL is 60, other lipids are perfect. So, you know, 50 milligrams per deciliter is that cutoff. Um, 80 is elevated. I don't know what the percentile is for you at that. Um, but again, if it were me, I would aggressively manage your APOB, which you're doing, and get imaging and see what's going on and make sure that other sources of residual risk, like homocysteine, you could consider polygenic risk scoring if you've got significant premature history in the family of cardiac events, heart attack, stroke, limb loss. Um, but I think looking at your family history is also a good indicator. If you have a lot of people in your family who have premature cardiac disease, then I would get right on that and figure out what else you need to do to tackle. Um, if people have LP Letol A that's high and yet everybody is like hanging out and eating barbecue in their 80s and doing great and not in the hospital and hasn't had stents and heart attacks and whatever, maybe it's not so bad for you. Um sorry, I don't mean to laugh at you. I'm not, I'm not trying to, I'm laughing because we don't know as much as we think we do, right? A number is just a number and the context is really important. And so I struggle with these how much does it matter questions because I want to have a more concrete answer for you, and we don't, right? There are people who have elevated LP little A who go their whole lives and do fine, especially those who are in metabolically good shape. I think your weight loss control and your blood pressure, these are like among the best things you could have done for every disease you might develop later in life. So I think you're on the right track. You're absolutely on the right track. Keep going, good job. All right, Chris Cardell, handful of marathons, then keto for years, genetic markers. Do I get CIMT or other tests? Um yeah, so which imaging test should you get? CIMT, coronary calcium score, or CCTA. Depends a lot on what is available to you, how old you are, and uh how much money you want to spend doing all of this. Um, for people that are younger, coronary calcium is less helpful, and CIMT or CCTA would be better choices because they'll image the soft plaque that shows up earlier in life before it becomes calcified. But those two tests are harder to get to. So a good high-quality CIMT can be very tough to come by if there isn't somebody who scans for cardio risk near you. And a CCTA is gotta get a doctor's order, gotta go in, get an IV, get the contrast, then you might want to get your CD and send it off to heart flow or cardio risk. I'm sorry, clearly, uh for an AI analysis or total plaque volume analysis. So that ends up costing around $2,000 out of pocket, which is a hefty toll plus the radiation. Not everybody is is that invested. I think if you are looking for a quick and dirty answer and you're over 50, a CAC is the easiest, most straightforward first stop. It's only calcified plaque, it's not a perfect test, but it's the easiest to get to for many people and it starts a good conversation. Um CIMT is my next favorite because it's no radiation, because I can do them every year for people, but I totally appreciate that they are hard to get if you do not live near somebody who scans for cardio risk or um brings them in to scan patients. So um this is this is the conundrum of what kind of imaging you should get, but pick one and start somewhere is is what I would say. Some imaging is better than no imaging. Get what you can get and we'll go from there. That's where that's where I am with all of my patients. All right. Thank you, Lisa. I appreciate you. All right, all right, all right. Question C D, hi. APOB 195, LPA less than 10, CAC was zero, HDL79, triglyceride 77, carnivore lost 90 pounds. What's my opinion on your labs? So the interpretation of your CAC zero is a little bit again, just a as I said, dependent on your age. Um, that is much more reassuring if you're in your 60s and 70s than it is if you're in your 40s. If you're in your 40s and then you want to know whether you're okay to hang out at those labs, then I would get soft plaque imaging of some kind, C I M T with an ultrasound or a CT angiogram of your coronary arteries with an AI overlay tool, so you have some sense. Um, in the absence of other information about your family history, uh, other things like that, I don't really know. Like I would say you could be a lean mass hyperresponder. I don't know if you have familial hypercholesterolemia or if you are a lean mass hyperresponder. Either of those are possible with those labs. And my answer would be a lot dependent on what happened. Um, and how attached are you to carnivore and a super low carb approach. You could probably, if you're a lean mass hyperresponder, you could drop your Apo B down with reintroducing some carbs that will come at a price for you, whatever that price might be, and why you decided to go to carnivore. Maybe that's worth it to you, maybe it's not. You can certainly do it pharmacologically or maybe with supplements. Um, whether that's important to you may or may not matter, right? Again, no calcified plaque is a little reassuring in the short term. Whether it's reassuring in the long term is very much less clear to me. And we don't know, I don't know based on what you've told me what the etiology of your lipoprotein problem is, whether you're a lean mass hyperresponder or whether you have FH. Um that's not right. What if you can't get access to any of those tests, any of the imaging tests? Um tough place, tough place to be. And you may have to travel to go get them done. Uh, you you know, everybody is gonna do their best with biomarkers, meaning lab tests and your blood pressure. I mean, that's what we've been working on for a long time, and that is still what's in the guidelines. Like, let me be clear, imaging is used as an adjudicator for sort of borderline cases, but nobody in the guidelines is yet recommending routine imaging for patients. That is something I personally believe in. I'm out on a ledge there. Uh and most people in the regular prevention space would say you can get it done mostly with the biomarkers. I don't think that's adequate because I know people with perfect biomarkers who have more plaque than they should, which is to say any. And I know people with horrible biomarkers who, even looking for soft plaque, have none. Cool. Guess what? Those are different scenarios and we should manage them differently. So I do think that the imaging is helpful. But if you can't get access to it, then you do the best with what you have. You make sure your blood pressure is as good as you can make it, you make sure your metabolic health is as good as you can get it, you manage your energy, you manage your visceral adiposity, the fat around our organs, the belly fat, you exercise like it's your job, you eat a healthful nutritional strategy for you, whatever that means, whatever goal you have about that, um, pick your poison, pick your, pick your medicine, right? Pick your strategy that makes the most sense for you, that you think you can do sustainably in a long-term way, and then measure your labs and all of whatever to make sure that that is actually working for you, that your blood sugar isn't going up, that your lipids aren't going out of control with a pro, you know. Again, we just talked about that. Maybe that's a problem, maybe it's not. We don't know for sure. But uh, all that to say test, don't guess, do the best you can with what you have now. And if you get to a place where you need more information, think about traveling to go get it. But that's a big lift. And, you know, that's not what's available to you right now. Do the best you have with what you got. All right. CAC is zero. Yeah. I CIMT I think would be helpful. Um, I again I love that test. I don't mean to to beat a dead horse about that, but uh certainly I have found some plaque in people and and others not, right? I've had people with positive calcium scores who come to me and had um pretty good CIMT. So it's not perfect. The overlap's about 90%, but I do think it would be informative. All right. Donut time. Remember to hit that like button and share. Yes, thank you. Thank you, donut time. Uh type 2 diabetic, no carbs for me. Okay, yep, totally get it. Totally get it. I appreciate the the conundrum there. Mm-hmm. Pick the brain of a vascular surgeon on a random Saturday. Life is freaking awesome. Yes, it is. Yes, it is. I'm excited to be here with you guys. You guys have been awesome. All right. Um, I think, no, oh, nope. More, more, more. Value of one hour fasting glucose versus a two-hour test. Um, I think that an oral glucose tolerance test is usually more helpful than a fasting glucose if you're highly suspicious for metabolic dysfunction and your fasting test doesn't show it, or you think your fasting test is inaccurate for whatever reason. A two-hour glucose tolerance test is better, especially if you get it with insulin. So make sure they draw your glucose and your insulin at baseline one hour, two hours. And if you are low carb, you will want to be on a pretest carb reintroduction protocol. Otherwise, uh you will absolutely get wildly hyperglycemic and hyperinsulinemic because your low carb way of eating most of the time causes physiologic glucose sparing. So before you, if you were a low carb, before you go do a two-hour glucose tolerance test, um, take three or four days and up your carbs, 150 a day at least, probably, uh, to try to get a better answer on that test. Okay. Is this too much for a lab panel? Followed by a long list of things. Um, TMAO, estradiol, reverse T3, sex hormone binding globulin, DHA, magnesium, testosterone, PSA, uric acid, salivary cortisol, salivary cortisol, I don't know what to do with. Um, I don't routinely do that anymore. Homocysteine, UA, ADMA, TPO antibodies, lipoprotein without a specification. I don't know what that is. Uh IgF1, I have also generally quit measuring because it's hard to act be make that actionable if people's growth hormone is low. It's so expensive to replace that uh most people choose not to do that. And again, outcomes data are lacking for that. Pregnetolone, uh GGT, good. Hybrinogen, good. C-reactive protein. Again, high sensitivity, C-reactive protein would be my preference. Uh free T3, aldosterone. Metanephrines, you don't need metanephrines unless you think you have a phyochromocytoma or an adrenal tumor causing wildly high blood pressure. Interleukin 8, I have never ordered once in my life. Uh, tell me why you're getting that, and I'll be excited to learn about that. Alpha fetal protein tumor marker. Um, I also don't order that. Okay. How important is the fractionation test? So this is the um NMR, sometimes I am mobility. I prefer NMR with the lipoproteins. So not just your LDL cholesterol, but your LDL particles and how big are the particles and how many HDL particles do you have? And what about your VLDL particles and your IDL particles, all that stuff. I find the fractionation personally helpful for my patients who may be discordant, meaning their LDL cholesterol does not totally match their APOB or doesn't match something else. Getting more information from the fractionation and understanding their particle number and counts or sizes, excuse me, is potentially helpful. It's like the last 5%. Um, I think you can get 90% of the way there with a regular fasting lipid panel and an APOB and an LPA. The NMR is nice to have. Uh, the lipidologists, by the way, have totally gone away from using it. They don't get it anymore. They think it's a total waste of time and money. And they say that the particle sizes are not that relevant. I mean, they're interesting from a research standpoint, but they would be totally happy just going off of fasting or non-fasted lipid panels. So from the lipidology side of things, they're not that interested in it anymore and they're not doing it. I still find it interesting. When we uh go over my labs soon, I will show you why it matters for some of us who are potentially uh lower carb or have interesting discordance. So um you'll you'll see that when we go over mine. And the plaquex person comes back and says, I had 52 plaquex treatment, my CAC went down 700 points. Interesting, I have never seen that. Um, I will investigate. I will investigate that. I have not ever seen a calcium score go down that much. And I am curious, is the word I'll use. Um Paul, is HOMA IR sensitive and accurate to detect insulin resistance? I think so. What we don't know about HOMA IR is exactly what the threshold should be. So a lot of research, it's mostly a research tool. It's not been deployed clinically with a lot of evidence or data behind it. Most of us in the space would use two, uh like below two, and you feel reasonably confident that somebody is insulin sensitive. Over two is a good cutoff for insulin resistance. Maybe. I've also seen somebody say one is like the better cutoff for optimal insulin sensitivity. But yeah, I use it. Um, usually I can tell just from a Fasting glucose and insulin, like just eyeball it and tell whether somebody's insulin resistant. If your fasting insulin is less than five, the chances of your HOMA IR being over two are pretty low. Um, but yeah, it's a reasonable adjunct. And for people whose eyeball picture smells like metabolic dysfunction, but their labs are not as bad as I was expecting. I will calculate the HOMA IR and see what that is. Um, but just be aware that from a sort of endocrinology metabolic health standpoint, it's mostly been used in research and there's not a lot of clinical um, there's not a lot of clinical support built around HOMA IR. At the end of the day, do I think that 90% of our issues come from eating too much food and having high body fat? Maybe. I I think a lot of atherosclerotic disease is also inflammatory, which can come from high body fat, but and also genetics. I really do believe, I think I said this at the beginning of the episode. There's a huge number of people who just have a bad card hand from mom and dad with respect to plaque formation. Um, they do worse if they have excess body fat. And I think that there's a lot about our modern food environment and environment environment that is causing us to eat energy in excess. Um, I don't think that this is a moral failing of society that we're all just lazy and overeat. So I don't think that's it. Um, but I do think that in general, yes, that has happened as a society. We have gotten bigger and it's a problem. Uh, and certainly from the insulin resistance standpoint, that is a huge contributor in that space. Do I suggest calcium supplements for bone? Generally not, unless you eat no animal products and no dairy uh and you have osteoporosis. Other than that, I don't like calcium supplements very much. Find out lab codes tried to order LP little A and they don't know what it is. Um dropped a comment in the anonymous things knows the lab codes. The lab codes are different by provider. So Lab Core and Quest will have different lab codes, and then you may not even be in the US, at which point I don't know what the lab code is for you. Um, but I would call it lipoprotein little A and see if that helps. Doop doop doo. 47 male, LDL down with lifestyle changes in diet, calcium score is eight. Do you need to start statins? 47-year-old with a calcium score of eight, and your LDL is down to 110. Um, do you need to? Need is a strong word. Um with the presence of plaque, I would target an LDLC less than 70 for you, but uh less than 90 for sure would be guideline driven. And it depends on what your APOB is, because it may be that your LDL cholesterol is overrepresented in terms of your particle number. So that's one of these times where fractionation might be helpful because if your particle numbers are totally perfect, then you could argue for again sticking with that lifestyle that you've you've gone through. You could try uh lipid lowering light, you could try Zetia only. Depends what's your high sensitivity C reactive protein. Um, that won't get better with Zetia, but it might get better with statins or additional fat loss. I don't know. Loaded question, hard to answer without more information. Paul, thank you for that lab code. Amazing. You guys are the best. All right. Okay, we have been at this for a couple of hours. I am out of questions. And am I licensed in Utah? No, I am sorry that I am not. Um, but you can find me by email info at courseitehealth.com C-O-R-S-I-G-H-Thealth.com. Um I am really only seeing people in California at this point, but happy to help if I can. Cardio risk is in Utah, so I know you can get a C I M T done there. All right, guys, I'm gonna wrap it here. You have been amazing. This was so much fun. I hope you guys got something out of this and learned. Please share this episode with friends and family. I will get a uh set of timestamps in the description for folks. You guys are the best. Until next time, take really good care.