In this episode, we discuss: 0:00:08 - Ethan’s entrepreneurial work in the cardiometabolic disease space 0:02:03 - Calcium scans (CAC scores) & CT angiography (CTA), & how it informs us about ASCVD risk 0:07:15 - Peter’s historical CAC scores, CTA results, & how one can be misled 0:12:07 - How Peter’s CTA results prompted him to lower his apoB 0:19:39 - Calcium scans vs. CT angiogram (CTA) 0:28:07 - How Ethan makes clinical decisions based on CTA results & plaque burden, & the importance of starting treatment early to prevent ASCVD 0:34:12 - Improved methods of CTA to grade plaque lesions & how it’s shaped medical decisions such as stenting 0:43:31 - Why Ethan favors optimal medical therapy over stenting outside of particular situations 0:57:23 - The need for FFR CTA, & the potential for medical therapy to eliminate ASCVD 1:01:31 - The fat attenuation index (FAI) & other ways to measure inflammation in a plaque 1:04:00 - Statins & exercise may increase the risk of calcification, but what does this mean for risk? 1:10:54 - The root cause of statin hesitation 1:17:07 - Importance of keeping blood pressure in check, defining what’s normal, & whether we should just accept higher blood pressure with age 1:28:59 - Blood pressure variability, how to best measure it, & data suggesting the enormous impact of keeping blood pressure down 1:45:05 - Drugs for treating high blood pressure recommended by the ALLHAT trial 1:48:27 - What the SPRINT trial says about the aggressive treatment of hypertension, & the risks of such treatment 1:54:04 - Confirmatory results in the STEP trial for blood pressure, & how Ethan uses the various drugs to lower blood pressure in patients 2:03:06 - The role metabolic health in ASCVD 2:08:50 - The impact of fat storage capacity & location on metabolic health & CAD
How is one and done stenting NOT better that drug therapies that can last for years and with side effects? And cost more...Come back to us peter. I know you guys are wired since med school to think pharmaceuticals - but take a hard look and listen- to what you are actually pushing for.
Peter, you won't lose your audience if you spoke in lay terms. It seems as if you feel you must speak in this medical lingo manner to impress your peers, your colleagues. They too won't be disappointed if you were to translate as you speak, your words and terms, so the average joe, those people who i hope you are trying to help, can grasp this stuff. You have said medical nomenclature starts right in med school and it's like a second language. Well for those who have english as a first language and then learn french in school - they can STILL speak all english when speaking to an english audience. This is 2 plus hours of stuff that 80 percent goes over people's head - when the title says WAYS TO PREVENT HEART DISEASE...Is your book to be done in this manner, where the critical stuff is lost on the masses? What this video is is basically two guys talking in code - and it happens to be filmed for the rest of us to try and decode - which frekin sucks!
Great discussion. I do think you should include CIMT in this discussion. CAC finds plaque late. CIMT non invasive and inexpensive. There is a lack of competent scanners but this is a great test and shows soft vulnerable plaque.
What this pathological focus on pharma interventions for high ApoB reminds me of is the historical focus on high glucose in type 2 diabetes. "We need to lower blood glucose at all cost" was the mantra of ADA for the longest time (doesn't this sound a lot like "we need to lower ApoB at all cost"). High blood glucose causes damage in small blood vessels which leads to all kinds of diabetic complication (technically true - high ApoB causes all kinds of CV complications). Disregard the fact that the underlying condition in type. diabetes is insulin resistance and let's just give type 2 diabetics more insulin (without even checking how much insulin they have). It improves their blood glucose (it does). Never mind, that it makes their insulin resistance worse over time and that if they don't change their lifestyle their condition will keep getting worse. Conclusion: type 2 diabetes is a progressive disease that cannot be reversed, it definitely has nothing to do with the way we're treating it or with the dietary recommendations (it used to be that 300g of "good" carbs per day was considered healthy for everyone). So, why does ApoB get pathologically high? Yes, we can intervene directly at the level of ApoB, but what is upstream of that? What is the underlying cause of CV? If we lower ApoB, but do not fix the actual problem, how do we know we're not making things worse over a long period of time?
The underlying cause of cardiovascular disease is apoB. The evidence points to it being a necessary cause of apoB, meaning without apoB you simply can’t get astherocletosis. Also we know what happens when you lower apoB due to the mountains upon mountains of evidence investigating just this. It seems to be the case that if you lower apoB low enough, you simply cannot get cardiovascular disease-which is why lowering apoB leads to lower cardiovascular disease mortality. ApoB is the “actual problem”. This is one of the most well established things in literally all of human biology. You seem to not be familiar with any of the mountains of studies on this topic if you’re asking if we lower apoB, how do we know we’re not making things worse over a long time”? as there are many many many studies analysing this, again more evidence than almost anything else in literally all of human biology, that clearly show that lowering apoB lowers cardiovascular disease mortality.
I had a score of 1188, 700 of which was in the LAD. I was terrified for six months that I was about to die any day. This was 11 years ago, and I haven’t had any “events” so far, but it’s still early in the day.
@@carolr.556there is a percentage of the population that needs drug intervention to lower their numbers Not everyone but some th-cam.com/video/GkWMDnTyxfo/w-d-xo.html
Peter, what was your heart rate before you fell? I've had hypotensive or rather tachycardic with some hypotension episodes after breakfast a couple of times that were really alarming. I was a bit disappointed in the blood pressure portion of this video. I feel like there's a lot more to say on the various factors (elasticity, hormonal, etc). Finally, in 2019, you did a podcast with Robert Lustig. He is now calling into question the necessity of statins and says that more adverse effects occur in those with normal LDL. While there's a good chance I'm missing the finer points of his discussion on this, it would be good to hear a conversation between the two of you on this topic.
I am exercising a lot at 77, my symptoms are when resting. Thank you, so helpful for a senior just starting cardio disease. UCSF is so back-up for cardio dept, my doctor is doing her best. I actually had my friend send my zio patch results to a cardiologist in another country to give advice for me to share with my primary
Old markers like Cholesterol LDL etc have been shown to NOT even be correlated with heart attacks… you can have sky high ldl and cholesterol. Means nothing according to the data. Insulin sensitivity is more important.
If statins are designed to lower ldl, and my ldl is 50, and if there are significant health problems such as hemophagic strokes increasing by 150% and increased diabetes over 50%, then why should I take a statin?
Good question. What I found really annoying about this interview was that both experts were either completely ignorant of increases in other risk factors, or pretended to be. As far as they were concerned, if you think statins are not 100% safe and effective (except for some annoying muscle pain for 5%), then you're an ignorant science denier. Incredible.
If you don't have plaque, don't take a statin. If you have lots of plaque, you are high risk and should take a statin. Statins do more than lower LDL, they can stabilize plaque and lower inflammation.
@@T-aka-T to reduce inflammation? Reduce/eliminate processed foods. Don’t smoke, and lower alcohol consumption. Eat whole unprocessed foods, exercise/weight lifting 3-4 times a week, 10 min walks after every meal, 150 mins of cardio a week. Get to your C-RP, APoB, Triglycerides checked.
I’m a LMHR. All biomarker are better than they ever have been. LDL a are carriers. Don’t we need more carriers when lipids are a primary energy currency?
Thanks for that. I don't know if Peter would wake up from his statin-filled dreams if a myriad LMHRs slapped him in the face ... did you see how he consistently tried to dismiss Dave Feldman's findings and speculations without even bothering to process the content of the points raised?
@@yl1487 So your comment "did you see how he consistently tried to dismiss Dave Feldman's findings and speculations without even bothering to process the content to the points raised" makes zero sense. He has an entire episode where he does just that.
@@Sobchak2 saying words and addressing things properly can be two separate, distinct things. E. G. "the sun is dangerous and leads cancer because radiation damages DNA" versus "a correlation exists between greater regular sun exposure and reduction in melanoma risk." Both could be more specific and more precise, however one is clearly less precise than the other. Cancer? Which kind of cancer? What pattern of sun exposure? Then we can talk about how the hell we have so many conflicting opinions. The data are not conflicting, opinions are. If you know anything about any electromagnetic radiation for instance, you would know that most wavelengths are essential. You would also be thinking about single versus double strand DNA breaks and repair mechanisms or lack thereof. Infrared controlling bound water of mitcochondrial ATP synthase; blue in the superior visual field activating ipRGCs (melanopsin cells); ultraviolet A producing NO and shaping the eyeballs, UVB required for vitamin (hormone) D synthesis, which controls likely over five percent of our DNA expression and heavily involved in immune system regulation. These, too, are all just words, so feel free to go fact-check. Or if you prefer popping D3 tablets crossing fingers that liver and kidneys will do their magic, feel free to do that. Good luck.
CAC tests done in Kansas City for $50 w/o insurance at St. Joseph Medical Center. I thought this was normal but doesn't appear so based on the costs discussed here.
I'm in KC...is that the location off 435/ State Line? What dept do you call foe an appointment? I'd love some details on that if you have a moment, please😊
@Lisa T yes, that is it. I will look for the contact info but if I remember correctly, I searched for CAC tests in KC and it was one of the top results!
Critique my current program. 37 Yo Man - About 6 months into doing exercise after doing little to no exercise for nearly 10 years. 180-185lbs 6'0'' Sleeping 10:30PM to 6:00AM Monday/Tuesday/Thursday/Friday 6:10 - 6:55 45 Minutes 3.5MPH 15% Incline Treadmill - Assuming Z2 Can hold conversation, but difficult Monday PM - Full Body Workout - Smith Machine - 3X12 - Light Weight 5 Minute Warmup Squat Deadlift Overhead Press Bent Over Row Bench Press 100 Captains Chairs/A couple dips/A couple pullups 20 Minute Sauna Wednesday PM - Full Body Workout - Dumbells - 4x8 - Moderate Weight 5 Minute Warmup Squat Deadlift Overhead Press Bent Over Row Bench Press 100 Captains Chairs/A Couple dips/A couple pullups Friday PM - Full Body Workout - Barbell - 5x4 - Heavier Weight 5 Minute Warmup Squat Deadlift Overhead Press Bent Over Row Bench Press 100 Captains Chairs/A Couple Dips/A couple pullups 20 Minute Sauna - Would doing three bouts of 1 Hour of Zone 2 be better or more ROI than four 45s? - If I add in 20 minutes of Zone 5 to Three of my mornings would this cardio negatively impact strength? - Or would it be better recommended to do 20 Minutes of Zone 5 after doing Strength Training? - Should I be eating more than 2000 calories if I'm attempting to just stay same weight, but become stronger? Thanks in advance!
I'm always skeptical that attacking the indicators is always going to help avoid disease. There are always deeper root causes to disease - and it is those that need to be addressed not the messenger. I wonder if Apo(b) is just going to be the new useless LDL cholesterol.
Good question. Is it just a bio-marker for something else? Probably. Although that doesn't mean it's not contributing causally to the issue in many people as well.
@@willnitschke Thanks, but that is my point the presenec of cholesterol in damaged arteries was taken as causality too, but this idea is challenged now.
@@chazwyman8951 It does seem to make causal contributions in some cases, as a statin can reduce heart attack risk by 30% in people who have already had heart attacks. Even if it's not causal, the statin is still doing something that's lowering the bio-marker AND treating the root cause. I'm not pro or anti-statins. I'm pro reality.
@@willnitschke No that is not really true. Statins reduce the "relative" risk is the claim, not the actual absolute risk. In practical terms this is the difference between 1 even in a 100 people over five years and 1.36 events in a 100 people over five years. No one thinks that LDL causes heast disease these days, and statins,(if they do work) probably act on clotting to get this tiny result.
Asymptomatic, 62yo,with high cac score >1k, and metabolically healthy. Don’t smoke, never been overweight, always active with activities, and a highly physical job for over 25yrs. This score was a complete shock and at this point I don’t have any clue of how I should proceed. My doctor just wants me to take a statin but I say no. I’m trying to improve this condition with lifestyle changes. The doctor did order a echo stress test so I’ll see how that goes. It’s a strange feeling to be at such high risk and have absolutely zero symptoms of heart disease 😢. It just leaves you not knowing what to do.
Nothing wrong with taking statins considering your high CAC score. In general, when over the score of 100, they are prescribed. You might have familial hypercholesterolemia. Apo B is lowered with statins as well. Look for Dr Brewer on youtube.
Probably WAS the problem, however I’m doing low carb now, and no processed crap. You can take statin if you want but I’ve heard too many negatives about statins and choose to get my numbers even better through diet. It all comes down to being insulin sensitive and not being insulin resistant. Insulin MUST be managed!!!
@@n2daair23 Yep. I dropped statins, PPis and CCis and most importantly carbs and processed foods. Dropped the number of meals per day to one or two, no snacking. Lost 45lbs, A1C back to normal, higher HDL lower TGL. No more wind, NAFLD, GERD,. But most importantly no more heart pain and much less being hungry.
Kaiser Permanente has opposed providing calcium scans for their heart patients. In 2020 I had Kaiser coverage and asked for a calcium scan. My cardiologist ordered a CTA instead and he instructed the radiologist to calculate a calcium score from the CTA. My score came back at 689. Two years later,.In October of 2022, I went to Harbor-UCLA Medical Center and got an EBCT calcium scan for $200 and my score was now 754. I take high-dose vitamin c, lysine, vitamin d, and vitamin k2/mk7.
Had stent placed mid LAD 3 months ago. Mild blockages in proximal LAD, proximal left circumflex, proximal RCA. CT Coronary Artery Calcium Score 261. Lipoprotein(a) 214.5 nmol/L. 54 years old. Insulin Resistant. Will target LP(a) with Repatha. Cholesterol is down as vegan since stenting. Stent pain since stenting; two mysterious runs to ER already for jaw pain and chest pain since stenting (small clots?). What do you all think I should do? Not overweight. Depressing situation. Genetics (LPa), Stress, poor diet (too much processed foods and sugar), overweight for years, and drank too much wine are my guesses for how this happened. Will try to reverse it with Esselstyn plant based diet. My recommendation is everyone should have CT Angiograms starting at 40 maybe every 3 years.
No discussion about how there are a large number of people with high LDL/apob and zero CAC?? Why? because they are insulin sensitive! Insulin sensitivity is the driver for inflammation which causes cardio diseases. Peter and his guests never touch on that. They want to fix everything with drugs. Paul Saladino has done a great job discussing this.
This is a childlike approach to science. That’s like arguing that smoking does not cause lung cancer as there are a larger number of people who smoke without having lung cancer. There is more evidence that LDL/apoB causes cardiovascular disease than almost anything in all of human biology. A paper summarises the evidence here: “Separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C.”
Hi - I was one of the "statin sceptics" for some time (side effects stuff and so on) but it took Dr Peter Attia about 1.5 podcast to convince me to use them :)
@@willnitschke mostly regarding life lastning need to stay on statins, possible side effect and the fact that most info I first got was from the antistatin side not from doctors like Peter Attia or Ethan Weiss. But I am able to change my opinions when confronted with the facts :)
@@Bjornislaw All I saw in the above video was a lot of wishful thinking, unfortunately. There has to be some sort of reasonable dose response to a statin. The argument that we don't see much in the way of improved outcomes in all cause deaths over 30 years of medication but it will work wonderfully if everyone takes a statin for 50 years of their life is the wishful thinking I'm talking about. All medications have risks and benefits, and I think these two unscientifically dismiss the risks and imagine only benefits. I would add you're not a population statistic. If you have multiple risk factors and there is evidence of plague build-up, that should logically change the risk/benefit calculation.
@@willnitschke Oh so I see you are more less in the position I once was. Well I have different view on the above video (specific when it comes to the part of everyone takes it - they never say that). And yes - my view on statins is 100% personal and based on my blood tests and family history so I am not talking about general population (as I think you might understand this and the video) but about specific health case with risk factors existing.
@@Bjornislaw It's well known from Attia's other videos that he basically wants to prescribe young people statins like candy. The fact that both of them go off into their pretend world and claim there are no risks, is also medically mischievous in my view. Let me use Yellow Fever Vax as a comparison. It's not without risks. People can die from it, although unlikely. If I live in a country that doesn't have Yellow Fever, I wouldn't take it. Everything has to be based on sensible risk/reward calculations.
Great conversation. Given the rise of the Carnivore diet and it's benefits, I have a huge dilemma I could use some feedback on. Been carnivore for 2 years. Asthma gone! No need for anti inflammatory and/or any other medications for chronic soreness, no bloating, consistent bowel movements, good energy. Have always been lean and muscular and now even leaner. Dilemma is recent blood work with higher and out of normal range markers for CVD risk (LDL,CAC, ApoB, etc) Dr's are freaking out at my numbers. Total Cholesterol 228. LDL 147, Non- HDL 156. LDL particle 2242. ApoB 106, ApoA 12, CRP .4, Lp-PLA2 136H, C-petide .46, What the heck do I do???
Had a CTA a few months ago. The cost to me was $6000 which was figured as the 20% copay. Some practices ask for this payment prior to the procedure. Wish I had followed Peter's footsteps in my 30's. I had a widow maker which triggered hfrlvef 10 years later
Does anyone know if Dr. Attia suggests intervention for someone with a positive calcium score? If it's in this podcast, I missed it. My CAC score is very low but not zero. I saw my Johns Hopkins Cardiologist yesterday actually and he said CTA or any other treatment not needed. Interesting to note that he said we need to wait for symptoms something both these docs laugh at and discuss here. Wouldn't he want to know about that atherosclerotic tissue that a CTA can see? The CAC indicated it's in the LAD but what else? We don't know w/o advance testing. Thanks for any reply!
120/80 is always the goal. But, what if the top number is good (at or below 120), but the bottom number is consistently high (say 90)? What does it mean? Is it worrisome? If so, how do you deal with it?
I'd check a1c (blood glucose) and body fat% (for metabolic syndrome). I too had an elevated bottom figure low 90's, and mid to high 120's...a few years back.
Are you otherwise healthy, esp. metabolically? Are you insulin sensitive? If you are and the only issue is your dbp is "90“ or low 90's, I wouldn't worry too much. Otherwise, exercise tends to work for most...
Interesting the comment about statins cause calcification to worsen. It was mentioned twice but Peter let it go by without comment? Pretty concerning to say the least.
Wow “LMHR non-sense” Peter just let that go by. Why not explain that comment in detail? Discussion want’s to make his “skin fall off”? Why not politely explain without being so arrogant. If we agree ApoB is required but not sufficient why not figure out what the root cause is?
Agreed, the arrogance of certainty has already turned me off completely after 5 minutes, I thought scientists were to be curious people who always seeked the truth. Dave Feldman the engineer is more of a scientist than these guys
I think they both agree it's nonsense because of studies that examine people with familial hypercholesterolemia. People who are effectively healthy in every other way except have high blood levels of ApoB are indistinguishable from LMHR from keto or paleo or carnivore. Since those studies show independent risk from high apoB, the matter has already been settled.
@@JohnSlack89 Nothing should be settled in science as the information evolves constantly, what was dogma decades ago is obsolete today. FH is indeed very different than diet induced hypercholesterolemia, as the diet induced one can be reversed whereas the genetic one can not. If a keto or carnivore decided to go back to eating carbs, their Apo B markers would change. If we decide to use a metric that can constantly change according to eating habits, how reliable is that marker? The body is smart and adapts to the environment IMHO.
Do satin drugs really make a difference in outcomes other than just reducing a number ? Doesn't satins reduce large size LDLs and not small size LDLs which are the ones that cause problems? And lastly, where is the discussion of Dean Ornish's groundbreaking reversal of heart disease ?
Peter stated that a computerized tomography coronary angiogram (CTA) at 2mSv is equivalent to around 4% of annual natural exposure. Shouldn't that be more like 40%? And 2mSv for a CTA seems unusually low. So, perhaps radiation exposure for a CTA should be a concern.
Dr.Attia, You might want to try photobiomodulation over your cardic area QD. See if your blood pressure drops stop. Helped me to stop blood pressure drops. Great overview 😊
Where does the calcium that hardens the plaque come from? Bones, diet, calcium oxalate in the blood.? Does calcium bond with the oxalate in our bodies and attach to the injured epithelium?
It's there to repair damage. Like if you cut your knee and a scab forms. What causes the damage is the real question and I think the most convincing hypothesis is that insulin resistance is the cause. Diabetic kids show hardening of the arteries before non-diabetic kids for example. Ivor Cummins has a great podcast where he has many experts on this topic as guests. There's also a nuero surgeon called Dr Anghony Chaffee worth checking out too.
Peter, of course, you have had Kidneys as a topic of your podcast. Rick Johnson, Professor of Nephrology at the University of Colorado twice I believe and the last time February 7, 2022. It was a great podcast, as usual. :)
I think it’s funny that two doctors think you get out of your car and are getting your blood pressure taken 5 minutes later. Haha- you sit and wait for 45 minutes PAST your appointment time THEN get your pressure measured!
Peter thinks taking a statin 15 years has saved his life? Then why do we not see any reduction in mortality generally with these meds? Why did only HE get his life saved by these meds but nobody else? Wouldnt the benefit be obvious in the data??? Where is the benefit of medical intervention??? Where is the massive reduction in overall mortality?
@@connorgray2896 studies easily control for variables such as unhealthy user bias. These variables are common in epidemiology studies but in interventional case controlled trials these variables are not an issue. So again I ask where are these studies showing improvement in mortality outcomes? There isn’t any evidence that stains help
@@connorgray2896 there isn’t any data showing decreased mortality or better outcomes. Drs pushing these drugs are just parroting a narrative. They have been influenced likely? It’s like the people still out there pushing the food pyramid but we know it’s not optimal. In fact people should be eating an animal based diet but the food pyramid says eat mainly grains lol you would be surprised how common this is.
That question about blood pressure variance is very interesting when I exercise intensely including like marathons it goes way down light to 112/60 third times or I'm feeling a little not my stomach about stress it'll go to 145/88 I can test it in the mornings and it's 112/71 and then get moving have a cuppa coffee and go to 141/90. I've had it tested in my sleep wearing a cough and then just waking up tapping it and it's 108/61, it seems to me that if you can't get it down and sleep or whatever activities make a drop there is the underlying problem I just measured mine right now the first reading was 158/80 40 seconds later it was 128/72 it be very interesting to see the how the average during a day is more reflective of heart disease versus situation's.
Hi Peter . Thank you so much for a brilliant channel. I’m just wondering if you could speak to the effect RED-s has on cardiovascular health ? I have listened to your podcasts a number of times on the effect of low oestrogen on cardio health which explains that side of things really well but I am wondering about the situation where cholesterol levels are high due to Under Eating / under recovering and over training . I have seen cases where triglyceride levels are very low but HDL is high in young patients do you think this would benefit from a statin or other cholesterol lowering medication or will changes to diet , lifestyle and training address the issue. If so, how long does general lifestyle changes take to change markers like cholesterol in the blood? Thank you
That is a big mystery to me. As of today, not my cardiologist and not my GP ever mentioned that to me. If the D3 and K2 work, why don't they offer that as preventions of plaque? Let's say if you start D3/K2 at age 40, you can stop or slow down developing plague before you reach 60. Every single doctor still jumps on medication with terrible side effects. I guess we can thank to the pharmaceutical companies. They very good at convincing doctors that nothing else is good except their drugs. They just have to invite them to a fancy restaurants.
Hi Dr. Attia, I'm a high teacher that teaches a specialized advanced biotechnology course (a recent breast-cancer survivor, and recreational but committed athlete - which is why I listen to you :). I'd love to reach out to Ethan to hear more about his biotech endeavors. Would there be a way to contact him for that? I enjoy your podcast and channel very much.
If you've had a long history of blood pressure issues, please get screened for Hyperaldosteronism/Conn's Syndrome. Ask to see an endocrinologist to get screened.
@@aantix Thanks, I do not have not a history of this, but I turned 50 last year...and I am about 30 pounds overweight.... and it runs in my family... so yeah!
I don't quite understand how the pharmacological intervention to lower ApoB is equivalent to smoking cessation... Yes, both ApoB and smoking have been strongly associated with their respective diseases (cardiovascular and lung cancer). Still, the OR for smoking was incredibly larger than for ApoB. But even so, smoking is a behavior that is generally accepted to be likely harmful and can be stopped. Smoking is not necessary for life. High ApoB is a downstream effect of who knows what (too much saturated fat? high insulin? others?). ApoB is necessary for life! You cannot live with ApoB=0. These VLDLs, IDLs, LDLs are not just there for fun. Further, in comparison with smoking, where the intervention is direct, with ApoB the intervention is indirect, you take a drug (that has many side effects btw), that affects pathways we do not fully understand, and eventually lowers your ApoB. However, whatever caused your ApoB to be high is still there. On the other hand, once you stop smoking the smoking is gone. How is this equivalent? It nowhere near equivalent...
Statins lower LDL and stabilize plaque. But nobody asks how. They lower LDL by reducing only the large LDL particle. Small dense LDL particles are unchanged. It's your small dense LDL particles that causes heart disease. Statins also stabilize plaque. This is good...no? Statins stabilize plaque by calcifing your arteries. I have had 4 CAC Score scans in the last 13 years. Had 25% annual increase in my CAC Score before put on statins. 3 years on a statin and now it's a 45% annual increase in my calcium score. How does a statin stabilize plaque? Ask the question.
I have asked the same question, Kevin. I have been on statins for a number of years and while my cholesterol scores are quite low (119 total), my calcium score has continued to increase. I read that statin stabilize plaque by converting it to calcium which is more stable and less likely to break off and cause a blockage. But my question is, with very low cholesterol, where does the plaque come from to Contribute to the calcium? My Doctors cannot say. I have not found an answer. Some say that after being put on statins after an initial CAC test, they should refrain from further tests as the score will continue to rise.
@@smark404 So how do you feel about them telling you to don't do anymore CAC Score scans? True LDL is known by a Lipoprotein Fractional Ion Mobility Quest Diagnostic Test Code#91604. Know your APOB Test Code#91726 and LP-a Test Code#91729. Also the scary one is APOE Genotype Code#90649. If you have the APOE4 gene the LDL from saturated fat from a meal stays in your blood a few more days longer than other people allowing it to oxidize the LDL.
@@smark404 Steve also get a Insulin Resistance Panel with Score - Test Code#36509...and what Terra Flow said. I take K2 and D3...lots of fish oil too. Keto diet for 3 years has my insulin score down to single digits....like a 5.
Largest money maker for Big Pharma out there - statins. That's why they keep pushing it, and extending the range of who "needs" it. They want more people on it. Beware. Statins stop your body's natural production of COQ10, necessary for mitochondrial health. Statins have more risk than benefit. (Unless you are Big Pharma getting rich off it.)
@@thepatternforms859 Ugh! 25 years of 'research' producing nothing more than "lower your cholesterol' while only reducing events by 1.1 percent and providing no mortality benefit (due to organ-destroying side effects) and ... that's it? At least I give Weiss credit for closing down his useless lab at UCSF.
I forgot to add. Dr. Attia please research/discuss the effectiveness of doing echo with ultrasound with Bruce protocol as a way to test for blockages without doing a full stress test with dye. I’m Marc and this is my sons acct.
If you think getting an accurate BP in a person is hard, you should try it in a cat! Yes, we in veterinary cardiology do that every day. And yes, it's just as difficult to interpret.
i had an afib episode during my yearly check up ecg. i had no symptoms of afib other than thinking that the heart rate monitor on the elliptical was broken cause in would get 180+bpm once in while. during follow ups, it was found that i had 90%+ blockage in 3 main coronary arteries. one of the arteries actually grew longer to accommodate the blockage but again no symptoms of the blockage. in japan, the internists recommended stenting and the cardiac surgeons recommended open heart triple bypass. i contemplated whether it was possible to treat by medical therapy without either but in the end i chose the open heart as a risk reduction measure because i didn't want take blood thinners for the rest of my life and there was still the potential that i would need to do the open heart later anyway. i'm curious but did i make right decision or should i have tried to medical therapy? water under the bridge but would like to hear another informed opinion...
With 3 main coronary artery stenosis,the CABG was indeed the right decision. 1.Undergoing PCA would be quite risky because during the procedure you momentarily completely seal an artery.The heart rely on adequate circulation from the 2 remaining arteries during that time ,otherwise you may sustain iatrogenic MI. 2. After extensive stenting,most likely repeatedly you would be on double ,perhaps even triple ( considering Afib too) antiplatelet therapy (blood thinners) for years .3.Long term prognosis in most cases is by far better after CABG surgery compared to PCI
Ho hum -- Weiss and Peter haven't really shed any new light other than focus on goal of 120/80 with drugs. Weiss comes off as less than fluent in his expertise.
I wonder if CAC's mean anything for a patient who has changed their life around dramatically. Meaning, an ex-smoker, ex-obese and sedentary, that used to eat crap all the time, with bad lipids, TGs, hypertension, and etc., changes his life around in every single one of those points. I wonder if an already calcified plaque Would mean anything to him. I'd guess we'd need to look for soft plaques, since it's very likely for him to have calcified plaques
@@willnitschke Good question, everyone has their opinion on that answer. Genetic / Lifestyle / Luck / etc. My answer is lifestyle, but I can’t back it up with data.
@@lpg12338 life style is the elephant in the room and more importantly under your control. But people with immaculate life styles can still die from heart attacks, suffer diabetes. So it's not as simple as one or the other.
Statins allegedly heal lesions. at least in part, through calcification. I wonder whether patients of Caldwell Esselstyn who have experienced plaque regression through a vegan diet see an increase in calcium.
Esselstyn is not a cardiologist and Pritikin had no medical background does that mean he was an expert too? There is no such thing as plant based med or doc it is not an accredited term anywhere, nice try. Just because people agree does not mean any more than smart and successful Larry King and Steven Spielberg both gave a lot of money to Bernie Madoff because they agreed he was a good investor.
Hello, in my country we are taught to treat patients not pictures. I don't understand why you would give drugs to a perfectly fine human doing 100 MET-hr/wk of endurance sports . Is this disease mongering ?
Ethan refered to the studies done on lean mass hyper-responders as nonsence, he therefore ignores the data. He gave no reason for this opinion. Without a doubt the scientists studying this fenotype and apparently Ethan has not, are varstly more qualified than Ethan, and publish all their supporting data.
It would make sense that if metabolism is basically the MOST important thing to examine than what possible sense do statins make when they straight-jacket the livers ability to process and manage cholesterol? Fix the metabolism! Function is EVERYTHING!
Ivor Cummins has a great channel for interviews with the best minds in this area and they don't speak in this manner at all. Attia is the king of confirmation bias anyway. He was on with Megyn Kelly this week and was saying seed oils are perfectly fine and suggested saturated fat wasn't great. A pusher of the experimental clot shot, what do you expect.
@peterattiamd We're really in the dark ages in terms of blood pressure control. All of the current preferred agents are giant hammers. I went 25 years with blood pressure issues without a single cardiologist or nephrologist raising the possibility of Hyperaldosteronism. I brought up the possibility to my cardiologist. I had to advocate to personally advocate to see an endocrinologist and only then, did my aldosterone/renin levels get checked. Sure enough, I had it. I had my left adrenal removed because of it. Epelernone was the needed agent. Per genetic testing (again, done on my own, not brought to attention via a doctor), I can see that I'm a slow metabolizer of caffeine (CYP1A1, C/C genotype). I had been drinking coffee my entire adult life, thinking it was a net positive per the general research, but given my slow caffeine metabolism, it actually puts me at greater risk of a cardiac event. Caffeine increases my systolic by a 20+ points and stays elevated through the evening after a single 50mg cup of coffee at 7am. Why isn't Conn's Syndrome/Hyperaldosteronism part of the screening process for blood pressure? We can sequence an entire human genome through Nebula for $150 - why isn't genetic testing part of the screening process?
In this episode, we discuss:
0:00:08 - Ethan’s entrepreneurial work in the cardiometabolic disease space
0:02:03 - Calcium scans (CAC scores) & CT angiography (CTA), & how it informs us about ASCVD risk
0:07:15 - Peter’s historical CAC scores, CTA results, & how one can be misled
0:12:07 - How Peter’s CTA results prompted him to lower his apoB
0:19:39 - Calcium scans vs. CT angiogram (CTA)
0:28:07 - How Ethan makes clinical decisions based on CTA results & plaque burden, & the importance of starting treatment early to prevent ASCVD
0:34:12 - Improved methods of CTA to grade plaque lesions & how it’s shaped medical decisions such as stenting
0:43:31 - Why Ethan favors optimal medical therapy over stenting outside of particular situations
0:57:23 - The need for FFR CTA, & the potential for medical therapy to eliminate ASCVD
1:01:31 - The fat attenuation index (FAI) & other ways to measure inflammation in a plaque
1:04:00 - Statins & exercise may increase the risk of calcification, but what does this mean for risk?
1:10:54 - The root cause of statin hesitation
1:17:07 - Importance of keeping blood pressure in check, defining what’s normal, & whether we should just accept higher blood pressure with age
1:28:59 - Blood pressure variability, how to best measure it, & data suggesting the enormous impact of keeping blood pressure down
1:45:05 - Drugs for treating high blood pressure recommended by the ALLHAT trial
1:48:27 - What the SPRINT trial says about the aggressive treatment of hypertension, & the risks of such treatment
1:54:04 - Confirmatory results in the STEP trial for blood pressure, & how Ethan uses the various drugs to lower blood pressure in patients
2:03:06 - The role metabolic health in ASCVD
2:08:50 - The impact of fat storage capacity & location on metabolic health & CAD
How is one and done stenting NOT better that drug therapies that can last for years and with side effects? And cost more...Come back to us peter. I know you guys are wired since med school to think pharmaceuticals - but take a hard look and listen- to what you are actually pushing for.
Peter, you won't lose your audience if you spoke in lay terms. It seems as if you feel you must speak in this medical lingo manner to impress your peers, your colleagues. They too won't be disappointed if you were to translate as you speak, your words and terms, so the average joe, those people who i hope you are trying to help, can grasp this stuff. You have said medical nomenclature starts right in med school and it's like a second language. Well for those who have english as a first language and then learn french in school - they can STILL speak all english when speaking to an english audience. This is 2 plus hours of stuff that 80 percent goes over people's head - when the title says WAYS TO PREVENT HEART DISEASE...Is your book to be done in this manner, where the critical stuff is lost on the masses? What this video is is basically two guys talking in code - and it happens to be filmed for the rest of us to try and decode - which frekin sucks!
I agree. The nonstop stream of acronyms few of us are familiar with is disrespectful to your audience.
@@oliverleslie7382He's an egotistical narcissist also
What about FASTING?
Great discussion. I do think you should include CIMT in this discussion. CAC finds plaque late. CIMT non invasive and inexpensive. There is a lack of competent scanners but this is a great test and shows soft vulnerable plaque.
wow tell me how to sign oN !!
Attia and Huberman have changed my life for the better; and their wonderful guests.
Me too
Same, Dr H just released another podcast w Dr A
Love listening to both of them. Knowledge is power.
How do we have the conversation without mentioning insulin sensitivity, fasting insulin, and diet?
I guess I'll skip this one, then. I don't know how you address this topic without those aspects. Waste of time.
@@getalonghome glad you agree!
And vitamin and mineral deficiencies, especially fat-soluble D3, K2, magensium.
Yeah, don't expect any of that. He's a medical doctor. Love his podcasts, but it's a weakness.
@@getalonghomez p in
What this pathological focus on pharma interventions for high ApoB reminds me of is the historical focus on high glucose in type 2 diabetes. "We need to lower blood glucose at all cost" was the mantra of ADA for the longest time (doesn't this sound a lot like "we need to lower ApoB at all cost"). High blood glucose causes damage in small blood vessels which leads to all kinds of diabetic complication (technically true - high ApoB causes all kinds of CV complications). Disregard the fact that the underlying condition in type. diabetes is insulin resistance and let's just give type 2 diabetics more insulin (without even checking how much insulin they have). It improves their blood glucose (it does). Never mind, that it makes their insulin resistance worse over time and that if they don't change their lifestyle their condition will keep getting worse. Conclusion: type 2 diabetes is a progressive disease that cannot be reversed, it definitely has nothing to do with the way we're treating it or with the dietary recommendations (it used to be that 300g of "good" carbs per day was considered healthy for everyone). So, why does ApoB get pathologically high? Yes, we can intervene directly at the level of ApoB, but what is upstream of that? What is the underlying cause of CV? If we lower ApoB, but do not fix the actual problem, how do we know we're not making things worse over a long period of time?
The underlying cause of cardiovascular disease is apoB. The evidence points to it being a necessary cause of apoB, meaning without apoB you simply can’t get astherocletosis. Also we know what happens when you lower apoB due to the mountains upon mountains of evidence investigating just this. It seems to be the case that if you lower apoB low enough, you simply cannot get cardiovascular disease-which is why lowering apoB leads to lower cardiovascular disease mortality. ApoB is the “actual problem”. This is one of the most well established things in literally all of human biology. You seem to not be familiar with any of the mountains of studies on this topic if you’re asking if we lower apoB, how do we know we’re not making things worse over a long time”? as there are many many many studies analysing this, again more evidence than almost anything else in literally all of human biology, that clearly show that lowering apoB lowers cardiovascular disease mortality.
I had a score of 1188, 700 of which was in the LAD. I was terrified for six months that I was about to die any day. This was 11 years ago, and I haven’t had any “events” so far, but it’s still early in the day.
Most of this is about drug interventions..What about other therapies?
@@carolr.556 I do lots of things (exercise, supplements, diet) but I have no idea what’s actually helpful.
th-cam.com/play/PLxyjOraXh0-ndvUEstSZJ2hPgXR2DqKwR.html
Statins do work
@@carolr.556there is a percentage of the population that needs drug intervention to lower their numbers
Not everyone but some
th-cam.com/video/GkWMDnTyxfo/w-d-xo.html
What was your diet up until you got those results?
thank you both. Exactly, never apologize for repeating. Human beings forget! thank you for repeating.
Peter, what was your heart rate before you fell? I've had hypotensive or rather tachycardic with some hypotension episodes after breakfast a couple of times that were really alarming. I was a bit disappointed in the blood pressure portion of this video. I feel like there's a lot more to say on the various factors (elasticity, hormonal, etc). Finally, in 2019, you did a podcast with Robert Lustig. He is now calling into question the necessity of statins and says that more adverse effects occur in those with normal LDL. While there's a good chance I'm missing the finer points of his discussion on this, it would be good to hear a conversation between the two of you on this topic.
The cost of health care in US is astonishing imo. In my country, in eastern Europe, a Calcium Score is $90
I am exercising a lot at 77, my symptoms are when resting. Thank you, so helpful for a senior just starting cardio disease. UCSF is so back-up for cardio dept, my doctor is doing her best. I actually had my friend send my zio patch results to a cardiologist in another country to give advice for me to share with my primary
Old markers like Cholesterol LDL etc have been shown to NOT even be correlated with heart attacks… you can have sky high ldl and cholesterol. Means nothing according to the data. Insulin sensitivity is more important.
That's why they are backing off the LDL claim and now focusing on the ApoB claim.
Deadly wrong
That’s right. Current research developments are key to our understanding.
@@JoeS97756 the major risk calculators for heart attack don't even ask for your LDL level presumably because it lacks predictive value.
@@willnitschkeand probably Lp (a) too.
If statins are designed to lower ldl, and my ldl is 50, and if there are significant health problems such as hemophagic strokes increasing by 150% and increased diabetes over 50%, then why should I take a statin?
Good question. What I found really annoying about this interview was that both experts were either completely ignorant of increases in other risk factors, or pretended to be. As far as they were concerned, if you think statins are not 100% safe and effective (except for some annoying muscle pain for 5%), then you're an ignorant science denier. Incredible.
If you don't have plaque, don't take a statin. If you have lots of plaque, you are high risk and should take a statin. Statins do more than lower LDL, they can stabilize plaque and lower inflammation.
@@T-aka-T to reduce inflammation? Reduce/eliminate processed foods. Don’t smoke, and lower alcohol consumption. Eat whole unprocessed foods, exercise/weight lifting 3-4 times a week, 10 min walks after every meal, 150 mins of cardio a week. Get to your C-RP, APoB, Triglycerides checked.
@@T-aka-T ok
@@longshanks5531 great list. Looking for sunlight in the list though ... and circadian rhythm is just one facet of it.
Peter is still a gift. I paid $99 for my CAC in May 2018.
Ouch here in NM I paid 150 around that date..
I’m a LMHR. All biomarker are better than they ever have been. LDL a are carriers. Don’t we need more carriers when lipids are a primary energy currency?
Thanks for that. I don't know if Peter would wake up from his statin-filled dreams if a myriad LMHRs slapped him in the face ... did you see how he consistently tried to dismiss Dave Feldman's findings and speculations without even bothering to process the content of the points raised?
@@yl1487 there is an entire episode, with Dave Feldman, where he addresses this very point.
@@Sobchak2 Exactly. To say he addresses it is one way of putting it.
@@yl1487 So your comment "did you see how he consistently tried to dismiss Dave Feldman's findings and speculations without even bothering to process the content to the points raised" makes zero sense.
He has an entire episode where he does just that.
@@Sobchak2 saying words and addressing things properly can be two separate, distinct things.
E. G. "the sun is dangerous and leads cancer because radiation damages DNA" versus "a correlation exists between greater regular sun exposure and reduction in melanoma risk."
Both could be more specific and more precise, however one is clearly less precise than the other. Cancer? Which kind of cancer? What pattern of sun exposure?
Then we can talk about how the hell we have so many conflicting opinions. The data are not conflicting, opinions are.
If you know anything about any electromagnetic radiation for instance, you would know that most wavelengths are essential. You would also be thinking about single versus double strand DNA breaks and repair mechanisms or lack thereof. Infrared controlling bound water of mitcochondrial ATP synthase; blue in the superior visual field activating ipRGCs (melanopsin cells); ultraviolet A producing NO and shaping the eyeballs, UVB required for vitamin (hormone) D synthesis, which controls likely over five percent of our DNA expression and heavily involved in immune system regulation. These, too, are all just words, so feel free to go fact-check. Or if you prefer popping D3 tablets crossing fingers that liver and kidneys will do their magic, feel free to do that. Good luck.
CAC tests done in Kansas City for $50 w/o insurance at St. Joseph Medical Center. I thought this was normal but doesn't appear so based on the costs discussed here.
I'm in KC...is that the location off 435/ State Line? What dept do you call foe an appointment? I'd love some details on that if you have a moment, please😊
@Lisa T yes, that is it. I will look for the contact info but if I remember correctly, I searched for CAC tests in KC and it was one of the top results!
@@TheD_R_G thank you so much for the info & taking the time to answer 😀
Critique my current program.
37 Yo Man - About 6 months into doing exercise after doing little to no exercise for nearly 10 years.
180-185lbs 6'0''
Sleeping 10:30PM to 6:00AM
Monday/Tuesday/Thursday/Friday 6:10 - 6:55
45 Minutes 3.5MPH 15% Incline Treadmill - Assuming Z2 Can hold conversation, but difficult
Monday PM - Full Body Workout - Smith Machine - 3X12 - Light Weight
5 Minute Warmup
Squat
Deadlift
Overhead Press
Bent Over Row
Bench Press
100 Captains Chairs/A couple dips/A couple pullups
20 Minute Sauna
Wednesday PM - Full Body Workout - Dumbells - 4x8 - Moderate Weight
5 Minute Warmup
Squat
Deadlift
Overhead Press
Bent Over Row
Bench Press
100 Captains Chairs/A Couple dips/A couple pullups
Friday PM - Full Body Workout - Barbell - 5x4 - Heavier Weight
5 Minute Warmup
Squat
Deadlift
Overhead Press
Bent Over Row
Bench Press
100 Captains Chairs/A Couple Dips/A couple pullups
20 Minute Sauna
- Would doing three bouts of 1 Hour of Zone 2 be better or more ROI than four 45s?
- If I add in 20 minutes of Zone 5 to Three of my mornings would this cardio negatively impact strength?
- Or would it be better recommended to do 20 Minutes of Zone 5 after doing Strength Training?
- Should I be eating more than 2000 calories if I'm attempting to just stay same weight, but become stronger?
Thanks in advance!
I'm always skeptical that attacking the indicators is always going to help avoid disease. There are always deeper root causes to disease - and it is those that need to be addressed not the messenger. I wonder if Apo(b) is just going to be the new useless LDL cholesterol.
Good question. Is it just a bio-marker for something else? Probably. Although that doesn't mean it's not contributing causally to the issue in many people as well.
@@willnitschke Thanks, but that is my point the presenec of cholesterol in damaged arteries was taken as causality too, but this idea is challenged now.
@@chazwyman8951 It does seem to make causal contributions in some cases, as a statin can reduce heart attack risk by 30% in people who have already had heart attacks. Even if it's not causal, the statin is still doing something that's lowering the bio-marker AND treating the root cause. I'm not pro or anti-statins. I'm pro reality.
@@willnitschke No that is not really true. Statins reduce the "relative" risk is the claim, not the actual absolute risk. In practical terms this is the difference between 1 even in a 100 people over five years and 1.36 events in a 100 people over five years. No one thinks that LDL causes heast disease these days, and statins,(if they do work) probably act on clotting to get this tiny result.
@@chazwyman8951 Exactly how is your "correction" to what I wrote not exactly the same as what I wrote? Please read my comment again.
Two heart attacks two angioplasties with four stents. We know we have problems. Should I get a calcium scan?or CT
Once you have a tent, CAC is useless
Asymptomatic, 62yo,with high cac score >1k, and metabolically healthy. Don’t smoke, never been overweight, always active with activities, and a highly physical job for over 25yrs. This score was a complete shock and at this point I don’t have any clue of how I should proceed. My doctor just wants me to take a statin but I say no. I’m trying to improve this condition with lifestyle changes. The doctor did order a echo stress test so I’ll see how that goes. It’s a strange feeling to be at such high risk and have absolutely zero symptoms of heart disease 😢. It just leaves you not knowing what to do.
Nothing wrong with taking statins considering your high CAC score. In general, when over the score of 100, they are prescribed. You might have familial hypercholesterolemia. Apo B is lowered with statins as well. Look for Dr Brewer on youtube.
Try bergamot pro might help
Is your problem diet?
Probably WAS the problem, however I’m doing low carb now, and no processed crap. You can take statin if you want but I’ve heard too many negatives about statins and choose to get my numbers even better through diet. It all comes down to being insulin sensitive and not being insulin resistant. Insulin MUST be managed!!!
@@n2daair23 Yep. I dropped statins, PPis and CCis and most importantly carbs and processed foods. Dropped the number of meals per day to one or two, no snacking. Lost 45lbs, A1C back to normal, higher HDL lower TGL. No more wind, NAFLD, GERD,. But most importantly no more heart pain and much less being hungry.
Pre-ordered your book and cant wait for it.
i'm peter will never see that but thanks for sharing little buddy
Kaiser Permanente has opposed providing calcium scans for their heart patients. In 2020 I had Kaiser coverage and asked for a calcium scan. My cardiologist ordered a CTA instead and he instructed the radiologist to calculate a calcium score from the CTA. My score came back at 689. Two years later,.In October of 2022, I went to Harbor-UCLA Medical Center and got an EBCT calcium scan for $200 and my score was now 754. I take high-dose vitamin c, lysine, vitamin d, and vitamin k2/mk7.
do you mean that you take the high dose supplements in response to your calcium scores or you have always taken those?
@WorkComp Sorry, I didn't see your comment until now. I started taking g the supplements after learning that I have heart disease.
1:52:28 Cholesterol does show a U-shaped mortality curve: Yi, Yi, Ohrr, Sci Rep
. 2019 Feb 7
epidemiology study. Check the mendelian randomization studies for causation.
Had stent placed mid LAD 3 months ago. Mild blockages in proximal LAD, proximal left circumflex, proximal RCA.
CT Coronary Artery Calcium Score 261. Lipoprotein(a) 214.5 nmol/L. 54 years old. Insulin Resistant. Will target LP(a) with Repatha. Cholesterol is down as vegan since stenting. Stent pain since stenting; two mysterious runs to ER already for jaw pain and chest pain since stenting (small clots?). What do you all think I should do? Not overweight. Depressing situation.
Genetics (LPa), Stress, poor diet (too much processed foods and sugar), overweight for years, and drank too much wine are my guesses for how this happened. Will try to reverse it with Esselstyn plant based diet. My recommendation is everyone should have CT Angiograms starting at 40 maybe every 3 years.
Plus relaxation therapy three times a day ,moderate exercise five days a week .
No discussion about how there are a large number of people with high LDL/apob and zero CAC?? Why? because they are insulin sensitive! Insulin sensitivity is the driver for inflammation which causes cardio diseases. Peter and his guests never touch on that. They want to fix everything with drugs. Paul Saladino has done a great job discussing this.
It's tragic how they want to fix everything with drugs - and what they really do is compound and or create metabolic issues. Bad job by them.
High LDL , 590 calcium score , perfect blood sugar level !!!!
This is a childlike approach to science. That’s like arguing that smoking does not cause lung cancer as there are a larger number of people who smoke without having lung cancer. There is more evidence that LDL/apoB causes cardiovascular disease than almost anything in all of human biology. A paper summarises the evidence here: “Separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C.”
Hi - I was one of the "statin sceptics" for some time (side effects stuff and so on) but it took Dr Peter Attia about 1.5 podcast to convince me to use them :)
Remarkable, given he provided no sound rational arguments as to why.
@@willnitschke mostly regarding life lastning need to stay on statins, possible side effect and the fact that most info I first got was from the antistatin side not from doctors like Peter Attia or Ethan Weiss. But I am able to change my opinions when confronted with the facts :)
@@Bjornislaw All I saw in the above video was a lot of wishful thinking, unfortunately. There has to be some sort of reasonable dose response to a statin. The argument that we don't see much in the way of improved outcomes in all cause deaths over 30 years of medication but it will work wonderfully if everyone takes a statin for 50 years of their life is the wishful thinking I'm talking about. All medications have risks and benefits, and I think these two unscientifically dismiss the risks and imagine only benefits. I would add you're not a population statistic. If you have multiple risk factors and there is evidence of plague build-up, that should logically change the risk/benefit calculation.
@@willnitschke Oh so I see you are more less in the position I once was. Well I have different view on the above video (specific when it comes to the part of everyone takes it - they never say that). And yes - my view on statins is 100% personal and based on my blood tests and family history so I am not talking about general population (as I think you might understand this and the video) but about specific health case with risk factors existing.
@@Bjornislaw It's well known from Attia's other videos that he basically wants to prescribe young people statins like candy. The fact that both of them go off into their pretend world and claim there are no risks, is also medically mischievous in my view.
Let me use Yellow Fever Vax as a comparison. It's not without risks. People can die from it, although unlikely. If I live in a country that doesn't have Yellow Fever, I wouldn't take it. Everything has to be based on sensible risk/reward calculations.
Great conversation. Given the rise of the Carnivore diet and it's benefits, I have a huge dilemma I could use some feedback on. Been carnivore for 2 years. Asthma gone! No need for anti inflammatory and/or any other medications for chronic soreness, no bloating, consistent bowel movements, good energy. Have always been lean and muscular and now even leaner. Dilemma is recent blood work with higher and out of normal range markers for CVD risk (LDL,CAC, ApoB, etc) Dr's are freaking out at my numbers. Total Cholesterol 228. LDL 147, Non- HDL 156. LDL particle 2242. ApoB 106, ApoA 12, CRP .4, Lp-PLA2 136H, C-petide .46, What the heck do I do???
Had a CTA a few months ago. The cost to me was $6000 which was figured as the 20% copay. Some practices ask for this payment prior to the procedure. Wish I had followed Peter's footsteps in my 30's. I had a widow maker which triggered hfrlvef 10 years later
Does anyone know if Dr. Attia suggests intervention for someone with a positive calcium score? If it's in this podcast, I missed it. My CAC score is very low but not zero. I saw my Johns Hopkins Cardiologist yesterday actually and he said CTA or any other treatment not needed. Interesting to note that he said we need to wait for symptoms something both these docs laugh at and discuss here. Wouldn't he want to know about that atherosclerotic tissue that a CTA can see? The CAC indicated it's in the LAD but what else? We don't know w/o advance testing. Thanks for any reply!
120/80 is always the goal. But, what if the top number is good (at or below 120), but the bottom number is consistently high (say 90)? What does it mean? Is it worrisome? If so, how do you deal with it?
I'd check a1c (blood glucose) and body fat% (for metabolic syndrome). I too had an elevated bottom figure low 90's, and mid to high 120's...a few years back.
Yes to have chronically high diastolic is a problem because this is the pressure your heart needs to push against
Are you otherwise healthy, esp. metabolically? Are you insulin sensitive? If you are and the only issue is your dbp is "90“ or low 90's, I wouldn't worry too much. Otherwise, exercise tends to work for most...
Interesting the comment about statins cause calcification to worsen. It was mentioned twice but Peter let it go by without comment? Pretty concerning to say the least.
They're both very weak
Wow “LMHR non-sense” Peter just let that go by. Why not explain that comment in detail? Discussion want’s to make his “skin fall off”? Why not politely explain without being so arrogant. If we agree ApoB is required but not sufficient why not figure out what the root cause is?
Agreed, the arrogance of certainty has already turned me off completely after 5 minutes, I thought scientists were to be curious people who always seeked the truth. Dave Feldman the engineer is more of a scientist than these guys
@@lk-ky3rw Agreed
I think they both agree it's nonsense because of studies that examine people with familial hypercholesterolemia. People who are effectively healthy in every other way except have high blood levels of ApoB are indistinguishable from LMHR from keto or paleo or carnivore. Since those studies show independent risk from high apoB, the matter has already been settled.
@@JohnSlack89 Nothing should be settled in science as the information evolves constantly, what was dogma decades ago is obsolete today. FH is indeed very different than diet induced hypercholesterolemia, as the diet induced one can be reversed whereas the genetic one can not. If a keto or carnivore decided to go back to eating carbs, their Apo B markers would change. If we decide to use a metric that can constantly change according to eating habits, how reliable is that marker? The body is smart and adapts to the environment IMHO.
LMHR is what? I have not watched this yet and may not given the comments. Sorry for asking the obvious.
Do satin drugs really make a difference in outcomes other than just reducing a number ? Doesn't satins reduce large size LDLs and not small size LDLs which are the ones that cause problems? And lastly, where is the discussion of Dean Ornish's groundbreaking reversal of heart disease ?
The whole large vs. small particles is old science. Disproven. All particles are atherogenic.
Your discussion is much appreciated!
Peter stated that a computerized tomography coronary angiogram (CTA) at 2mSv is equivalent to around 4% of annual natural exposure. Shouldn't that be more like 40%? And 2mSv for a CTA seems unusually low. So, perhaps radiation exposure for a CTA should be a concern.
It considering the number one cause of death is CVD. In the face of this even a scan that is 100% of your Annual radiation is probably worth it.
Thank's both of you, for the content.
Dr.Attia,
You might want to try photobiomodulation over your cardic area QD.
See if your blood pressure drops stop. Helped me to stop blood pressure drops.
Great overview 😊
Where does the calcium that hardens the plaque come from? Bones, diet, calcium oxalate in the blood.? Does calcium bond with the oxalate in our bodies and attach to the injured epithelium?
It's there to repair damage. Like if you cut your knee and a scab forms. What causes the damage is the real question and I think the most convincing hypothesis is that insulin resistance is the cause. Diabetic kids show hardening of the arteries before non-diabetic kids for example. Ivor Cummins has a great podcast where he has many experts on this topic as guests. There's also a nuero surgeon called Dr Anghony Chaffee worth checking out too.
Is it due to low vit k through life
Peter, of course, you have had Kidneys as a topic of your podcast. Rick Johnson, Professor of Nephrology at the University of Colorado twice I believe and the last time February 7, 2022. It was a great podcast, as usual. :)
I think it’s funny that two doctors think you get out of your car and are getting your blood pressure taken 5 minutes later. Haha- you sit and wait for 45 minutes PAST your appointment time THEN get your pressure measured!
Peter thinks taking a statin 15 years has saved his life? Then why do we not see any reduction in mortality generally with these meds? Why did only HE get his life saved by these meds but nobody else? Wouldnt the benefit be obvious in the data??? Where is the benefit of medical intervention??? Where is the massive reduction in overall mortality?
Maybe because most people that use statins still participate in terrible lifestyle behaviours?
@@connorgray2896 studies easily control for variables such as unhealthy user bias. These variables are common in epidemiology studies but in interventional case controlled trials these variables are not an issue. So again I ask where are these studies showing improvement in mortality outcomes? There isn’t any evidence that stains help
@@thepatternforms859 interesting. I wonder why Peter is so convinced of their utility then? Surely he is examining the data?
@@connorgray2896 there isn’t any data showing decreased mortality or better outcomes. Drs pushing these drugs are just parroting a narrative. They have been influenced likely? It’s like the people still out there pushing the food pyramid but we know it’s not optimal. In fact people should be eating an animal based diet but the food pyramid says eat mainly grains lol you would be surprised how common this is.
Perhaps statins don't work that well for people that are on an animal high fat western diet.
A real acronym festival occurred here.
How can I get a cta scan for prevention? I have a calcium score of zero. I will gladly pay
Find a provider in your area. Get a doctor’s order.
You dont
That question about blood pressure variance is very interesting when I exercise intensely including like marathons it goes way down light to 112/60 third times or I'm feeling a little not my stomach about stress it'll go to 145/88 I can test it in the mornings and it's 112/71 and then get moving have a cuppa coffee and go to 141/90. I've had it tested in my sleep wearing a cough and then just waking up tapping it and it's 108/61, it seems to me that if you can't get it down and sleep or whatever activities make a drop there is the underlying problem I just measured mine right now the first reading was 158/80 40 seconds later it was 128/72 it be very interesting to see the how the average during a day is more reflective of heart disease versus situation's.
Any talk about telimisartan
Hi Peter . Thank you so much for a brilliant channel. I’m just wondering if you could speak to the effect RED-s has on cardiovascular health ? I have listened to your podcasts a number of times on the effect of low oestrogen on cardio health which explains that side of things really well but I am wondering about the situation where cholesterol levels are high due to Under Eating / under recovering and over training . I have seen cases where triglyceride levels are very low but HDL is high in young patients do you think this would benefit from a statin or other cholesterol lowering medication or will changes to diet , lifestyle and training address the issue. If so, how long does general lifestyle changes take to change markers like cholesterol in the blood? Thank you
Interesting. Nothing on vitamin K and slowing coronary calcium?
That is a big mystery to me. As of today, not my cardiologist and not my GP ever mentioned that to me. If the D3 and K2 work, why don't they offer that as preventions of plaque? Let's say if you start D3/K2 at age 40, you can stop or slow down developing plague before you reach 60. Every single doctor still jumps on medication with terrible side effects. I guess we can thank to the pharmaceutical companies. They very good at convincing doctors that nothing else is good except their drugs. They just have to invite them to a fancy restaurants.
Hi Dr. Attia, I'm a high teacher that teaches a specialized advanced biotechnology course (a recent breast-cancer survivor, and recreational but committed athlete - which is why I listen to you :). I'd love to reach out to Ethan to hear more about his biotech endeavors. Would there be a way to contact him for that? I enjoy your podcast and channel very much.
Ethan is great. Glad that you got him on again
This guy never really answered your question about blood pressure variations and fluctuations throughout the day during different activities. SMH
Can someone define what' pulling all the levers' would be?
So, surgically removing belly fat will, theoretically, worsen the metabolic profile due to higher risk of "bathtub overflow"? Is that the assumption?
My blood pressure increased over time, but immediately after serious
12 hour back surgery, the lack of constant pain decreased my blood pressure immediately.
I read years ago that the highest percentage of heart attacks occur in men at age 49 years; is this still accurate?
FFR is based on inducing hyperemia to see if a lesion is truly flow limiting under stress
Blood Pressure…. mine is through the roof!! Was recently 180/112…so yeah, I’m a goner. 💀💀
If you've had a long history of blood pressure issues, please get screened for Hyperaldosteronism/Conn's Syndrome. Ask to see an endocrinologist to get screened.
@@aantix Thanks, I do not have not a history of this, but I turned 50 last year...and I am about 30 pounds overweight.... and it runs in my family... so yeah!
@@aantix Thank you for that. May help me.
Greetings
Interested in a discussion on elevated blood pressure in the 20-30 year old
The latency of some of Weiss’ responses lols like cognitive decline due to statin ingesting.
I don't quite understand how the pharmacological intervention to lower ApoB is equivalent to smoking cessation... Yes, both ApoB and smoking have been strongly associated with their respective diseases (cardiovascular and lung cancer). Still, the OR for smoking was incredibly larger than for ApoB. But even so, smoking is a behavior that is generally accepted to be likely harmful and can be stopped. Smoking is not necessary for life. High ApoB is a downstream effect of who knows what (too much saturated fat? high insulin? others?). ApoB is necessary for life! You cannot live with ApoB=0. These VLDLs, IDLs, LDLs are not just there for fun. Further, in comparison with smoking, where the intervention is direct, with ApoB the intervention is indirect, you take a drug (that has many side effects btw), that affects pathways we do not fully understand, and eventually lowers your ApoB. However, whatever caused your ApoB to be high is still there. On the other hand, once you stop smoking the smoking is gone. How is this equivalent? It nowhere near equivalent...
Statins lower LDL and stabilize plaque. But nobody asks how. They lower LDL by reducing only the large LDL particle. Small dense LDL particles are unchanged. It's your small dense LDL particles that causes heart disease. Statins also stabilize plaque. This is good...no? Statins stabilize plaque by calcifing your arteries. I have had 4 CAC Score scans in the last 13 years. Had 25% annual increase in my CAC Score before put on statins. 3 years on a statin and now it's a 45% annual increase in my calcium score. How does a statin stabilize plaque? Ask the question.
I have asked the same question, Kevin. I have been on statins for a number of years and while my cholesterol scores are quite low (119 total), my calcium score has continued to increase. I read that statin stabilize plaque by converting it to calcium which is more stable and less likely to break off and cause a blockage. But my question is, with very low cholesterol, where does the plaque come from to Contribute to the calcium? My Doctors cannot say. I have not found an answer. Some say that after being put on statins after an initial CAC test, they should refrain from further tests as the score will continue to rise.
@@smark404 What is your HDL/trig ratio and markers of inflammation (CRP, A1c etc.) Diet? D3 and K2 supplementation?
@@smark404 So how do you feel about them telling you to don't do anymore CAC Score scans? True LDL is known by a Lipoprotein Fractional Ion Mobility Quest Diagnostic Test Code#91604. Know your APOB Test Code#91726 and LP-a Test Code#91729. Also the scary one is APOE Genotype Code#90649. If you have the APOE4 gene the LDL from saturated fat from a meal stays in your blood a few more days longer than other people allowing it to oxidize the LDL.
@@terraflow__bryanburdo4547 Hey good questions for Steve! You know your stuff.
@@smark404 Steve also get a Insulin Resistance Panel with Score - Test Code#36509...and what Terra Flow said. I take K2 and D3...lots of fish oil too. Keto diet for 3 years has my insulin score down to single digits....like a 5.
Is Ethan still pushing toxic statins which carry no mortaity benefi?
Yep!
Largest money maker for Big Pharma out there - statins. That's why they keep pushing it, and extending the range of who "needs" it. They want more people on it. Beware. Statins stop your body's natural production of COQ10, necessary for mitochondrial health. Statins have more risk than benefit. (Unless you are Big Pharma getting rich off it.)
@@thepatternforms859 Ugh! 25 years of 'research' producing nothing more than "lower your cholesterol' while only reducing events by 1.1 percent and providing no mortality benefit (due to organ-destroying side effects) and ... that's it? At least I give Weiss credit for closing down his useless lab at UCSF.
He ignores data that shows that all-cause mortality is HIGHER at total cholesterol 260 for older age cohorts. He can take his poison elsewhere.
Oh God, find something worthwhile to put your scepticism into.
I forgot to add. Dr. Attia please research/discuss the effectiveness of doing echo with ultrasound with Bruce protocol as a way to test for blockages without doing a full stress test with dye. I’m Marc and this is my sons acct.
I received your new book yesterday 🥳
If you think getting an accurate BP in a person is hard, you should try it in a cat! Yes, we in veterinary cardiology do that every day. And yes, it's just as difficult to interpret.
i had an afib episode during my yearly check up ecg. i had no symptoms of afib other than thinking that the heart rate monitor on the elliptical was broken cause in would get 180+bpm once in while. during follow ups, it was found that i had 90%+ blockage in 3 main coronary arteries. one of the arteries actually grew longer to accommodate the blockage but again no symptoms of the blockage. in japan, the internists recommended stenting and the cardiac surgeons recommended open heart triple bypass. i contemplated whether it was possible to treat by medical therapy without either but in the end i chose the open heart as a risk reduction measure because i didn't want take blood thinners for the rest of my life and there was still the potential that i would need to do the open heart later anyway. i'm curious but did i make right decision or should i have tried to medical therapy? water under the bridge but would like to hear another informed opinion...
What was your diet when this happened?! Specifically, how much oil and red meat did you consume?
With 3 main coronary artery stenosis,the CABG was indeed the right decision. 1.Undergoing PCA would be quite risky because during the procedure you momentarily completely seal an artery.The heart rely on adequate circulation from the 2 remaining arteries during that time ,otherwise you may sustain iatrogenic MI. 2. After extensive stenting,most likely repeatedly you would be on double ,perhaps even triple ( considering Afib too) antiplatelet therapy (blood thinners) for years .3.Long term prognosis in most cases is by far better after CABG surgery compared to PCI
@@OverdrivePacingthanks!
Happy birthday 🎉
What can prevent sudden cardiac death particular due to total vessel obstruction ,remember adherence to total medical therapy needs adherence .
Ho hum -- Weiss and Peter haven't really shed any new light other than focus on goal of 120/80 with drugs. Weiss comes off as less than fluent in his expertise.
My thoughts exactly too much waffling!
Geeze, did I miss the segment on abbreviations and acronyms?? But cytokines? Go on.
I wonder if CAC's mean anything for a patient who has changed their life around dramatically. Meaning, an ex-smoker, ex-obese and sedentary, that used to eat crap all the time, with bad lipids, TGs, hypertension, and etc., changes his life around in every single one of those points. I wonder if an already calcified plaque Would mean anything to him. I'd guess we'd need to look for soft plaques, since it's very likely for him to have calcified plaques
No one knows...time and degrees matter, the body heals itself and age also factors in as well.
What I would wonder about is how much of the problem was life style related and how much of it remains genetic.
@@willnitschke Good question, everyone has their opinion on that answer. Genetic / Lifestyle /
Luck / etc. My answer is lifestyle, but I can’t back it up with data.
@@lpg12338 life style is the elephant in the room and more importantly under your control. But people with immaculate life styles can still die from heart attacks, suffer diabetes. So it's not as simple as one or the other.
@@willnitschke Very true, like most things in life, it is multifaceted.
Statins allegedly heal lesions. at least in part, through calcification. I wonder whether patients of Caldwell Esselstyn who have experienced plaque regression through a vegan diet see an increase in calcium.
Esselstyn is not a RD or Cardiologist. Would you get dental advice from a plumber?
@@StanDupp6371 poor analogy. he's an MD. With many yrs. treating heart patients. Many plant-based mds fully agree with him. Nice try.
Esselstyn is not a cardiologist and Pritikin had no medical background does that mean he was an expert too? There is no such thing as plant based med or doc it is not an accredited term anywhere, nice try. Just because people agree does not mean any more than smart and successful Larry King and Steven Spielberg both gave a lot of money to Bernie Madoff because they agreed he was a good investor.
Too many undefined acronyms in this podcast. FH? ApoB, CAC, CT? What are those?
Google
$99 for my Coronary Calcium Score test
Just had mine last month $55.00 cash.
Hello, in my country we are taught to treat patients not pictures. I don't understand why you would give drugs to a perfectly fine human doing 100 MET-hr/wk of endurance sports . Is this disease mongering ?
Wow...just shows how much we dont know
Guyyyyys! What about a HOT TUB and SAUNA? APPLE CIDER VINEGAR? SLEEP?!
Round and round we go, where the truth is, nobody knows. Men will be on Mars before they know what the root cause of heart disease is.
Did he just say that a Starbucks is $20?
As time goes on the statin pushers are becoming a smaller circle of prescribers.
Too technical and nerdy for me, need to come back later after I learn some basics 😂
Ethan refered to the studies done on lean mass hyper-responders as nonsence, he therefore ignores the data. He gave no reason for this opinion. Without a doubt the scientists studying this fenotype and apparently Ethan has not, are varstly more qualified than Ethan, and publish all their supporting data.
Dr Attica,you promote dangerous gene therapy shots and call yourself a health expert?
Sorry, but this episode is way too heavy on medical jargon and undefined acronyms. I had to stop after about an hour - very frustrating.
I said the same thing - it's as if they need to impress us, or their colleagues etc. and it's frekin annoying on these life and death matters.
@@oliverleslie7382It is never a good idea to stoke fear in people! Every person has a completely different cardiovascular profile!
It would make sense that if metabolism is basically the MOST important thing to examine than what possible sense do statins make when they straight-jacket the livers ability to process and manage cholesterol? Fix the metabolism!
Function is EVERYTHING!
Ivor Cummins has a great channel for interviews with the best minds in this area and they don't speak in this manner at all. Attia is the king of confirmation bias anyway. He was on with Megyn Kelly this week and was saying seed oils are perfectly fine and suggested saturated fat wasn't great. A pusher of the experimental clot shot, what do you expect.
Doctor ford brewer is more knowledgeable than either of these guys
@peterattiamd We're really in the dark ages in terms of blood pressure control. All of the current preferred agents are giant hammers.
I went 25 years with blood pressure issues without a single cardiologist or nephrologist raising the possibility of Hyperaldosteronism. I brought up the possibility to my cardiologist. I had to advocate to personally advocate to see an endocrinologist and only then, did my aldosterone/renin levels get checked. Sure enough, I had it. I had my left adrenal removed because of it. Epelernone was the needed agent.
Per genetic testing (again, done on my own, not brought to attention via a doctor), I can see that I'm a slow metabolizer of caffeine (CYP1A1, C/C genotype). I had been drinking coffee my entire adult life, thinking it was a net positive per the general research, but given my slow caffeine metabolism, it actually puts me at greater risk of a cardiac event. Caffeine increases my systolic by a 20+ points and stays elevated through the evening after a single 50mg cup of coffee at 7am.
Why isn't Conn's Syndrome/Hyperaldosteronism part of the screening process for blood pressure?
We can sequence an entire human genome through Nebula for $150 - why isn't genetic testing part of the screening process?
Thanks for this information. I am going to check into it.