Prepare to have your understanding of LDL cholesterol completely revolutionized. Groundbreaking research has unveiled startling insights into the role of LDL cholesterol in cardiovascular health, challenging conventional wisdom and opening new avenues for treatment and prevention strategies.
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Research:
Show Transcript:
(00:00):
Another live session. Friends, it's Tuesday. Very grateful that you were here just waiting for the system to let me know that we are live and we are live. Just like that. Alright, we're going to dive into some pretty impressive research findings. There's a lack of strong statistical association with high LDL cholesterol levels and increased risk for cardiovascular-specific mortality as well as all cause mortality. We're also then going to transition and talk a little bit more about lipid-lowering medications and share with you some very interesting facts that I think are pretty new for a lot of folks out there, especially honing in on the absolute risk reduction with popular lipid lowering therapies. It turns out that the absolute risk reduction over the course of a treatment of a very popular lipid lowering medication is 0.35% and that is not a grammatical error and I did not misquote that 0.35%.
(00:57):
It turns out that the number needed to treat when it comes to the popular lipid lowering medications is depending upon the clinical trial about between 400 and 600 individuals. Now in pharmacologic research, A NNT closer to one or less than one is ideal. The lower the number the better and very popular lipid lowering medications have a number needed to treat greater than 600, meaning that you need to treat 600 people in order to experience one beneficial outcome, which is absolutely absurd. I apologize that I'm a little blown out here. You're just going to have to deal with that because it is very, very sunny right behind me. Thankfully Spring is here in Washington State. I would love to know where you are all from. Let me know by hitting that like button where you are viewing this, whether you're viewing it live now or later in the replay, let me know because I like to know where you are in the world, in the country.
(01:53):
We're diving into fascinating stuff, so shall we proceed? I think so. Here we go. Okay, so let's first turn our attention to, I would love to pick on, you know what? I think YouTube is censoring content. If I say the specific drug name, hint, hint, so I'm not even going to mention that. What are we're going to do is talk about this paper right here. Oh boy, you are in for a little surprise, my friends. Wait till we zoom in on this paper. Very interesting stuff out of Denmark. The title of the paper that was published in the British Medical Journal is association between low density Lepar Protein and All Cause and Cause specific mortality in Denmark, a prospective cohort study. This was published what? 2022.
(02:41):
Shoot, lemme go back to, sorry. 2020 December of 2020. Okay, so here we go. Now again, most of you have been convinced by your primary health professional that high cholesterol is the single worst thing that could ever happen to you. And if you have high cholesterol, well heaven forbid you eat butter, red meat or eggs because it will just clog your arteries. But then we have data like this that is quite interesting and let's review what this data says. Okay, I'm just going to go right to the results. Let's just skip to the results. I mean, we can talk about how many tens of thousands of people were part of this study. 108,000 people. So again, let's follow the science. 108,000 people were tracked almost 20 years I believe in this analysis. And so I'm going to zoom in for all of you that have a hard time seeing words.
(03:33):
I'm not insinuating that you have a hard time seeing, but because I'm on the screen and there's a study here, let's just make it very, very simple because I know you like to share this information with your doctor and you should because I have sold testing as well as supplemental products to doctors, medical clinics, cardiologists, you fill in the blank compounding pharmacists. And I know doctors rely upon pharmaceutical reps for their clinical information, which is a sad reality of the situation. So doctors are well-intended. They go to medical school and invest eight years of their life because they want to help people, but they're so busy managing medical records and Medicare, Medicaid insurance reimbursements. Sometimes they can't stay up on all the science, so they rely upon lunch and learns to get clinical information. And so I want to share with you this clinical information so that you can help your doctor help you.
(04:22):
Okay? So 108,000 people were tracked for, I can't remember the exact number of years, I think 15 years in this particular analysis. What the investigators found here is compared with individuals with concentration of LDL cholesterol between 132 and 154 milligrams per deciliter. The multivariate adjusted hazard ratio for all cause mortality was 1.25 for individuals with LDL concentrations less than 70 milligrams per deciliter. I'll explain in a moment reverse causality here and 1.15 for individuals that had LDL concentrations greater than 189 milligrams per deciliter. So essentially what that means is the individuals with the lowest risk of death in this particular analysis from all causes cardiovascular specific causes as well as cancer had LDL cholesterol levels between 132 and 154 milligrams per deciliter, which less I remind you, is much higher than what are the current recommendations per the American Association for the American Heart Association and other family practice and internal medicine guidelines.
(05:36):
When an LDL cholesterol level is over 130 milligrams per deciliter, it's recommended that clinicians prescribe a statin, a lipid loid medication. But let's zoom down. I know these words don't convey the story, so we're going to focus on pretty little pictures. These pictures are showing all cause mortality and you're seeing here are cholesterol levels on this Y axis and hazard ratios for all cause mortality. The individuals with the lowest risk for all cause mortality had an LDL cholesterol that is higher than the current recommendations 140 milligrams per deciliter and the same holds true for people not on lipid lowering medication. This I think is quite interesting. The people that are on lipid lowering medication tend to have pretty low LDL cholesterol levels and we'll talk about that in just a moment. Talk about why that might be, probably because they have preexisting cardiovascular disease. But if you look at these numbers here, you have 95,000 subjects in this arm versus just 13,000.
(06:41):
So as a proportion of individuals that have died, turns out that the people on lipid lowering medication represent a much higher proportion of the deaths, most likely because they have underlying cardiovascular disease, high blood pressure, obesity in the sort. But let's go on down. There's another beautiful image here. This is figure three. And just so you know what we're looking at, we're looking at the multi-variable adjusted hazard ratios for cause specific mortality according to levels of low density lipoprotein cholesterol, the so-called bad cholesterol. Alright, so let's look at just cardiovascular specific mortality. The lowest risk group here, the group that is sort of what everything is based upon because they had the lowest risk of dying, have pretty high LDL cholesterol levels, 132 milligrams per deciliter. So when you go to your doctor and they're freaking out because your LDL is one 15 or one 40, you might want to take a screenshot of this and say, look, I've been diving into some research doc based upon everything that I see, it doesn't appear that my LDL is really probably contributing to a significant atherosclerotic risk, especially if and only if your triglycerides are low and your HCL is high and you have low body fat percentage.
(07:54):
Now what's interesting is the relationship with low LDL cholesterol and higher odds of dying from cancer. And this highlights potentially this, so-called reverse causality, meaning some people that have really low LDL cholesterol levels probably have already preexisting disease occurring. And so that's what the individuals that are in the low cholesterol camp will say. When we share these studies, they'll say, oh, well you're just cherry picking data and highlighting reverse causality in the sort. But it is quite interesting, this idea that low LDL cholesterol lower the better doesn't seem to really hold true for all cause mortality as well as cancer specific and even cardiovascular related mortality. So anyway, I think this is quite interesting. Here's fatal myocardial infarctions, non myocardial infarctions only heart failure. Again, the sweet spot in terms of cholesterol, it's significantly higher. The people that had the lowest risk had pretty high LDL cholesterol levels. Again, we're talking here, 140 milligrams per deciliter with heart failure with, oh, oops, sorry. Oh man, we somehow got out of there quick. Let's go back to the PDF. My apologies here.
(09:15):
And we look here at non-fatal myocardial infarctions. Again, the lowest risk group was the people that had pretty high LDL cholesterol. So we're going to get back into this data. I just want to check in. I want to say thank you for being here live. I really, really enjoy you all being here. Any comments, any questions? I did receive an Instagram comment that I do want to address. I think it's really interesting. I see some live comments here from Mike. What about NMR particle size count tests, things like that. Okay, so we're going to get into that in a moment. We really will. But gosh, this, if you go to my Instagram page and maybe I can look it up on this screen here. Let me just see. Just give me half a second metabolic mic. Perfect. So hopefully we can see this video. Oh dang, it's not.
(10:03):
Okay, so lemme go back to this screen here. So this is my Instagram page. I recently shared this video right here. It's not letting me, but gosh, it's not letting me log in. So we won't look at that at this exact moment, but there's a comment and the comment was actually really, really good. The comment was from a gentleman that said, Hey look, my LDL cholesterol is high and my triglycerides are high and my hhl is low. So I just want to make a disclaimer here. When we're talking about problematic issues with high LDL cholesterol, we need to create a more nuanced conversation. And many people have been talking about this. Dave Feldman has, bless his heart, has been sharing this information for the better part of six years now, I think since 2016 he's been talking about this. We need to look at this lean mass hypers responder phenotype.
(10:50):
So if your LDL is high and your triglycerides are low and HDL is high and you have the lean mass hypers responder phenotype and the cut points, we've done many videos on that, then we probably don't need to be really concerned about your LDL. But if your LDL is high and your triglycerides are over 100 milligrams per deciliter and your HDL is low, less than 50 milligrams per deciliter, that's a problem. Okay? So if you have that triad where you have high LDL, low HDL and high triglycerides, that's problematic. And so again, we've interviewed Dr. Philia, he talked about this at length, and I can share that in the, I'll put a little link here after the fact. So I just want to clarify because a lot of people are saying, well, my LDL is high, so that's okay. It can be problematic. But if you have insulin resistance and you have high triglycerides in low HGL, so that's just, I want to offer that disclaimer, but many of you have low body fat, low fasting insulin, low triglycerides, and high HDL and high LDL. So it seems that in that phenotype
(11:52):
Your is pretty low from developing atherosclerotic plaque. And again, we've talked about why that may be the lipid energy model and the so-called lean mass, hypers respond or phenotype. So we're going to dive into that in just a moment. But because exercise is so important for all aspects of health, including cardiovascular health, I just want to remind you of the creatine contending electrolyte six by myo signs. Look, if you're not taking creatine during your workouts, you are missing out. This is one of the most studied ergogenic aids on the market. Hands down, it turns out that electrolytes enhance the absorption of creatine. Creatine helps with cellular hydration, with bringing water into your cells, which is how it helps with exercise. So there's over 820 reviews over at myoxcience.com. This is the only therapeutically dosed creatine electrolyte combo on the market. You have albion chelated minerals, you have touring, you have creatine, obviously magnesium, potassium, it's a phenomenal product.
(12:53):
Click the link in the description below to save on that and use the code podcast at checkout. Okay, so let's get into some messy business here. I'm honestly a little bit reluctant to share this information about statins because I feel sort of like statins are sort of like the covid thing. And if you want to get your research published, you have to say favorable things about the statins. All the cardiologists are recommending this is first line therapy for hyperlipidemia. But when you look at the research, it's really, really unimpressive in terms of what statins do in terms of outcomes, and that's what we're going to focus on. Now, again, if you're on a lipid medication, I'm not saying get off, I'm not not playing doctor here. First of all, I'm not a physician. I have not been to medical school. I'm just offering this disclaimer.
(13:51):
I think you should work with your healthcare practitioner, but there's something that you should know about because we are told over and over and over again that this medication save so many lives and we need to be taking lipid lowering medication. It turns out that the process of atherosclerosis and developing a heart attack is much more multifaceted and multifactorial. There's chronic inflammatory pathways, there's insulin resistance, hypercoagulable pathways, blood viscosity. I mean there's a lot of stuff going on, blood pressure. So just to think that this one medication is going to offer all these benefits, I was blown away here at the A RD, this is the absolute risk difference between individuals taking statins or placebo. This is not a mistake here. This is not a typo 0.39%. So when your doctor's like Sally, oh my gosh, you eat butter and have eggs and red meat, you have to take this medication. You're like, well, I've actually looked at an analysis of 26 different studies, including 22 clinical trials and the absolute risk reduction, the difference between the placebo and the treatment group is 0.39%. That's less than 1% difference. I mean, think about that. This stuff has been the number one selling drug for the past 20 years, and we have clinical trials suggesting the absolute risk reduction is less than 1%.
(15:34):
That's insane to me. When you actually look at this, this is really unimpressive. If this was creatine, I mean let's just be honest, if creatine gave you less than 1% sports performance benefit, would you take it? Why would you waste your money on something that was offering less than 1% of a benefit? I mean, if it was like, oh, increase your strength by 0.35%, you'd be like, who cares? Point three five. I mean, that's nothing. That's the difference between having a little coffee or not. I mean, that's nothing. Why are we recommending this to so many people? How did this become a blockbuster? I literally don't get it. Okay, so I get a little passionate about this stuff because I really want to help people and so many people have been duped, I feel like. And so what we're going to look at here is what's known as the number needed to treat.
(16:36):
And this is interesting when it comes to satin this stuff is. So this is a supplementary material here. This is going to blow your mind. I'm not even kidding you right now. This is going to blow your fricking mind. Okay, so as I mentioned, these are randomized controlled trials comparing statins to placebo O, and all sorts of these different trials have different names. A-C-A-P-S trial, the all heart trial, the Jupiter trial, the Aspen trial. Yeah, you've heard of these things. And in these trials what they list is what's known as NNT. This is known as the number needed to treat. And NNT essentially is trying to ask the question in pharmacologic jargon, if we were to give this medication to 50 people, or how many people would we need to give this medication to in order to achieve one beneficial outcome? So when it comes to an NNT, the lower the number the better.
(17:41):
Let's just think about something like this. Lemme just break it down to you. If we think about antibiotics, let's say you step on a rusty screw and you get staph thermophilus or staph aureus in your foot and you start to get an infection and it's coming up your leg, your leg is red. This has happened to me before. Thank God for western medicine. I stepped on a screw. I got this infection. I did everything natural I could, but I was getting this staph aureus running up my leg. So what did I do? I went to the doctor. I got Keflex. This stuff worked like magic. I mean, I'm telling the infection gone within 12 hours, the redness went away, the swelling went away. It was remarkable. I probably would've lost my leg or died had I not had the antibiotics. So antibiotics have an NNT of like 0.5 or even better.
(18:29):
They almost work 100% of the time unless the bacterial infection is antibiotic resistant and you might need to pair different antibiotics together. So now that you have a general idea of what an NNT is, so when we have a higher number needed to treat, that's not very good. So this trial, five years long known as the A-F-C-P-A-S trial, the number needed to treat to prevent one life loss from cardiovascular disease is 417, which is not very, very good. Let's go on down. I think the Jupiter, oh, this one's interesting. The A-S-C-O-T trial, this was a three-year trial, NNT 625, not very good.
(19:19):
The Aspen trial, NNT to prevent a heart attack 149. This is the C-A-I-U-S trial, the NNT 3000 3025. I mean these are, you need to treat 3000 people in order to get one prevention of a heart attack. I don't know, this is crazy to me. We look at the card study 116, the hope study 263 to prevent one heart attack, NNT, the Jupiter trial, 223 people needed to treat to prevent a fatal heart attack. 2,500 people. You need to give this medication that has been shown to have side effects, exercise intolerance, possibly memory loss, possibly diabetes increase. You need to treat 25, I'm sorry, 223 people before you prevent one heart attack. How many of those 233 people are going to get diabetes or have other side effects? I mean, I dunno. Like I said, I feel like talking about statins puts you at risk for censorship.
(20:33):
So I am trying to tread lightly here, but this is science that's just on the internet and you can download it for free. Here's the article, again, I'm not trying to be reckless. If you're on a lipid lower medication, you need to work with your doctor. But if your doctor's foisting this on you and you sort of look at this research and you scratch your head a little bit, that's just called, in my opinion, critical thinking. And I am trying to promote critical thinking here. I think we should all think a little bit more critically. And again, we need to have a little bit more of a nuanced conversation and look at the LDL cholesterol numbers. Not in a vacuum, but in constellation of other biomarkers. What's your blood pressure? What's your body fat percentage? Where's that fat distributed? Is it in the abdomen or the buttocks or non high risk areas?
(21:17):
What are your triglycerides? What's your hgl L? What are your liver enzymes? What's your fasting insulin? What's your fibrinogen? What's your CRP? I mean, all these things need to be considered. And that's why over at our website, high intensity health.com, we have the free blood work cheat sheet. Definitely download it. Print out page one and share that either with your doctor or your friends and family. Again, friends, what do you think of this content? Hit that like button if you are enjoying it. Should we do more breakdowns like this? I would love to know what your thoughts are. Hopefully you've been hearing me okay in the comment section. I did a mic check and I couldn't hear how my microphone was, so lemme know if the audio has been okay this whole time. So a lot of folks here live right now. I want to get you live questions.
(22:03):
I know when you watch replay, you get annoyed by this, but let's just get to live questions. People are here live and we want to address this. Okay? Statins lower testosterone. I wasn't aware of that, but that makes sense from a mechanism of action standpoint. Statins are in the category of medications known as MG coa reductase inhibitors, and so they suppress a critically important upstream pathway in the isoprenoid and cholesterol biosynthetic pathway. And of course we know that testosterone ultimately is derived from cholesterol. And so if we completely crushed cholesterol, we're probably going to affect DHEA, which is an important precursor to testosterone. We're going to affect testosterone and more. So yeah, okay, audio is good. Thank you for letting me know that. Great. We have folks from Vietnam, south Florida, Miami, Wisconsin, love that. You guys are so good. Fall City, Washington. Sherry, thank you for being here from Fall City, Washington, amazing eastern Washington in the house here in Western Washington.
(23:08):
We're having great sunny weather. Hope you are as well. Jerry Cash, great question here from Jerry Crash, and I'm just going to throw this on the screen right here because I'm addressing this question. Jerry says, how soon before a workout do I take creatine? Well, I'm biased of course, because we sell creatine paired with electrolytes. You want to take it during your workout, so a little bit before and while you're exercising. It turns out, guys, that creatine is best absorbed when you're exercising. People are like, well, you need to take 20 grams of creatine per day to load. No, you don't need to load creatine. If you're an omnivore, if you've been a vegan for 20 years, you might need to front load creatine. But if you eat an omnivore diet, you're getting plenty of creatine in your diet. It turns out that when you're exercising, when you take creatine in real time, it increases the absorption and it might help with cellular energy production during exercise.
(24:01):
And so that's why we have the creatine containing electrolytes sticks. Because electrolytes increase the absorption of creatine. You have to have electrolytes when to get creatine into your cells. You need sodium and ease and potassium. It's that simple. There's a creatine transport protein on your cells. They depend upon electrolytes. So if you're just taking creatine by itself, you're not getting the best bang for your buck. And again, that's why we created the creatine electrolyte sticks by bioscience because you get everything together. You don't have to mix this stuff together and it's really affordable. Okay, all Bruce Lee says, the fact that atherosclerosis only occurs in the artery in predictable locations clearly shows is not a cholesterol or lipoprotein issue. Alright, this is a good point that this individual has, but I want to add a little bit of a disclaimer here.
(25:03):
Where are we at? Where are we at? Where are we at? Okay, fuck this one. I just say the F word all. What I want to share with you guys is this picture right here. I thought this was really interesting. So this shows subclinical. This shows the regions of the body where you see subclinical atherosclerosis and it turns out that the femoral artery gets clogged as well. And so we talk a lot about atherosclerosis in the heart, but it seems like in young high risk individuals, you actually see more carotid artery atherosclerosis as well as femoral artery atherosclerosis. The paper that we're talking about here, again, we're going to do a journal club and we're going to have all these things accessible to you guys, but this is a great article titled Progression of Early Subclinical Atherosclerosis Study. And this was really interesting trying to help clinicians better understand the biomarkers that are linked with atherosclerosis. And I thought it was pretty cool that they had this image to show regions of the body where individuals actually had atherosclerosis. This is really, of course, exercise has been shown to be helpful, as you already know. Yeah, it happens. Atherosclerosis happens in the Corona where arteries, but the carotid arteries, the femoral artery and throughout the body, but we just notice it more in the heart. It turns out that the arteries of the heart, the coronary arteries are very
(26:42):
Small. So when they get occluded or narrowed for atherosclerosis, then you have issues and emia and heart attacks and so on. Okay, great comment though. Sherry says, husband had three strokes getting out of rehab tomorrow, trashing his statin, never took drugs before. Sherry, how did your husband have three strokes? What happened? I would love to know the lifestyle medications, toxin exposure, blood viscosity, blood pressure, Phyllis in at some point. Okay, so Stan is getting off Crestor four days ago after 15 years. So Stan, you're probably just fine. You know what you might want to benefit from? Look, and some people that have already had a heart attack, they do benefit from the anti-inflammatory effects of statins. Take zyme Q 10. That's what I would suggest. A bioavailable K MQ 10, not just from Costco or Walmart. Get a good brand. Take some cozy Q 10.
(27:44):
Okay, CTB says a lot of the studies on creatine are done on vegans to exaggerate the positive effects. Most of the studies are actually just on athletes. I mean, I see what you mean. CCTB. But look, creatine works. I mean, this is the thing. If you try it, you try to have a good workout, take a little creatine, taking electrolyte sticks, you will notice a benefit from that. So good. I hear your comment though, but I get it. Pure absolute says, for me it's simple. You need LDL. If your LDL is lowered artificially, you're causing harm. But we also know that statins lower normal LDL and don't touch oxidized LDL. Yeah, I don't know if there's a specific, yeah, I mean LDL oxidation, I don't know if there's any treatment to lower specifically oxidized LDL. And again, I'm not saying in all causes, LDL is benign as Nick Noritz and Peter T have talked about. LDL is necessary, but it's insufficient to cause atherosclerosis. There are other factors going on. Okay, thoughts on glycocalyx and atherosclerosis? You know what? This is such a good comment. What I'm going to do here is just share with you guys a video on my channel of glycocalyx, and so we glycocalyx high intensity health. I'm going to drop it in the comment section below.
(29:15):
We have been talking a lot about glycocalyx over the past several years. I don't even know where this video is to be honest with you. But yeah, I'll share this in today's section. We're going to unpack. Sorry that was hot. So glycocalyx, it's an interesting phenomenon and I will see, so this is the video right here. I'm going to dump this in the chat section right here. Okay. I don't know why my pace is not working. If you want to hear more about the glycocalyx, it has to do with cell membranes and cell fluidity and the structure of cells and some of the cell to cell communication. So I think it's quite interesting more on that later. So Bill Cook says, do statins cause liver damage? Yeah, I think that's rare. Honestly, I think that the challenge with statins is more related to exercise intolerance and potentially increasing risk for diabetes.
(30:21):
And I think honestly, low dose statins a couple of times a week may not be that big of a deal, but you see so many people that are on 20 milligrams of Crestor every day for years, and I think that might be problematic. Okay. Amy says, I have elevated lipoprotein little lay and statins are recommended to lower LEL and produce overall risk of atherosclerotic cardiovascular disease. I eat low carb, high fat exercise, sleep, sun, ground, et cetera. Torn about what to do with lp. Little lay. Yeah, Amy, I'm with you. Yeah, I don't know. I mean, if I was in your shoes, would I take 10 milligrams of Crestor? Lipitor twice a week maybe. I'm not sure.
(31:03):
People talk about, well, what is LP ate? Is it just an oxidized low density lipoprotein circulating? We do know that it's associated with increased risk of clotting. So you would want to stay well hydrated. Look at your blood viscosity, your hemoglobin hematocrit, RDWR, bbc, et cetera. So those are things to consider blood donation. But Amy, I can't tell you, you should never take a statin. I don't know. This is all something that you should consider an experiment with yourself, but I do know people from a longevity perspective because statins have unique anti-inflammatory properties. Again, here I was just kind of trashing the number needed to treat and so forth. But microdosing these just like you wouldn't want to take super high dose of rapamycin or super high dose metformin, tinkering around with these things microdosing a couple times a week. I don't know, see what that might do. But I think I would look at David Diamond's work. He's talked a lot about lipoprotein little a and fibrinogen and clotting cascades. I think that's something to consider.
(32:08):
So DC says, my LDL is 1 74. I would love to know what are your triglycerides in HGL? That would be super interesting. Susan says, I'm not an athlete obese, but losing weight and regarding health on a caramel diet, I clean houses for a living on my feet all day and I'm active, but not an athlete. Well, CRE benefit me, Susan. That's a good question. I honestly think the only way to know is just to try and just see what it does. Again, you can save with the code podcast over at my science, the electrolyte sticks. You get two and a half grams of the cleanest ine on the market known as creapure. Save the code podcast. You have a 30 day money back guarantee. So that's what I would just give it a try. You're on your feet all day. I think Susan, the biggest thing that I would worry about in your case is exposure to the chemicals and cleaning products.
(32:59):
So I'd make sure that you're using the best cleaning products that you can go as sauna if you have access to that and so forth. Alright, Amy says, I've one copy of the a PE four genotype, as do I Amy. We are alike in that way. We have two arms, 10 fingers. Just kidding. Okay, so you're an APOE four, maybe a three four, maybe a two four. I'm not sure. So don't want to affect my brain with statins. Yeah, I'm with you. That's why I'm not going to take that as well. Okay. Stan says, MK seven is a better form of vitamin K two lots of literature on it compared to MK four. Yeah, so chasing illa. The research is on vitamin MK seven, sorry, vitamin K two, MK seven. These monoclone chains, the length, it's not really that important. People market NK four, they market mk whatever it, a lot of good research is on MK seven.
(34:01):
Darlene had a heart attack six years ago. She's on Lipitor, 40 milligrams since then. Now my leg hurt all the time. Lipitor. Hopefully I can increase my exercise tolerance. My pharmacist says statins will crip you. So Darlene, I would suggest getting coenzyme Q 10 and start to eat as other people have commented to hear beef, heart, lamb, heart. That should help over time. Frank says, I think creatine will help Susan. I take a daily dose and it has helped my energy levels significantly. Thank you for that, Frank. Janet says all good three months in, but LDL is over 400 up from 1 63 in November. Total cholesterol is over 500 triglycerides since November are from 83 to 1 41. HCL has gone down. Janet, what changes did you make three months ago? I'm sorry, the changes in your lipids are going in the wrong direction.
(34:59):
I don't know why your triglycerides have gone up so much. Did you test them fasted initially and then test them in a post meal state? That would be very interesting. Very interesting to note. Well, friends, what'd you think of this episode, this live show? I would love to know what you think by simply hitting that like button. And you could do us all a huge favor by sharing this video with a friend. Just say, Hey, check this out. You might get some benefit from this and that would help me so that I know that you guys are digging these live shows. But that would probably help your friend if you in fact did enjoy this live session.
(35:37):
We will catch you next Tuesday. Again, hopefully you got some value from this conversation. I myself, I'm going to go work out. I don't know about you. Who's going to go work out? Lemme know in the comment section below. We will catch you next Tuesday. I very much appreciate your likes, your comments, share shares. Be sure to check this channel tomorrow, 7:30 AM Pacific Standard Time. We have a really good episode all about exercise intolerance and exercise resistance, but I think you'll think is pretty fascinating. So until then, we will catch you later, my friends. Take care. Bye.
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