Robb Wolf – Death by Lab Work, ApoB Confusion, Cholesterol and Diet
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News Topic:
Show Notes:
Web3 Working Group – DarkHorse Podcast
Dr. Aseem Malhotra – Joe Rogan Experience
Pharma: Not Their First Rodeo – Umberto Meduri & Paul Marik on DarkHorse
Questions:
Death by lab work
Olivia writes:
Hey Robb and Nicki! Long time listener and strong endorser of the work y’all are doing. I wish more people and healthcare providers were on the same page, or hell even in the same book as this community! ANYWAY….I recently got my labs done and I have some concerns on the results I received. For context: I am a 30 y/o female, no kids, work out 3-4 x week (mostly weight training and average 8-10K steps per day) I work as a nurse, tend to focus my meals around 30g or more of protein (red meat, chicken, dairy, eggs, I eat it all), and drink plenty of water and LMNT :), avoid seed oils and other ultra processed garbage. I went through some hormone issues for 5-7 years (i.e very infrequent cycle due to too much exercising and under fueling). Since then, I have become so much more educated and I have recovered my cycle *naturally*; gaining probably 30-40 ish pounds from my low; currently sitting at 155 5’6. I feel great, but these lab results got me shook! Any and all advice welcome.
Total Cholesterol- 282
Triglycerides- 43
Non HDL- 169
HDL- 113
ApoA to ApoB- 0.41
ApoB- 113
Liver enzymes AST and ALT- slightly elevated
Total T3 – 68 all other thyroid values “normal”
Fasting BGL- 95
A1C- 5.0
Am I destined for an early death related to heart disease?? I’ve listened to Huberman on blood glucose control and will implement his ideas to lower my fasting number, but it’s hard to eat my last meal 2-3 hours before bed on days I work since I get home at 8. I hope this isn’t too long of question, feel free to cut out anything you’d rather not discuss and just give general guidelines. THANK YOU!!!
Stay salty,
Olivia
ApoB confusion
Marit writes:
Hi Robb and Nicki,
I’ve been listening to your podcast and following your work for many years and I’ve thrown some similar hard questions at you, which you were kind enough to try to answer (thanks!). I’m so frustrated that I can’t understand statistics enough to draw my own conclusion based on the literature on ApoB and statins. I listened to a Peter Attia’s podcast and he said (I heard it twice to confirm) that if ApoB were low in the population he “thinks” AS CVD would be dramatically reduced. His pushes alot for statin use. On the flip side, reading the breakdown of studies on statins on Chris Kresser’s website, I just can’t understand why Peter Attia takes this stance. It doesn’t add up! My gut feeling is risk for any chronic disease is never calculated on just one lab value (that’s just logical). but even if it was, why does Attia use statins when they don’t seem to reduce deaths, strokes or heart attacks by very much, in people without CVD? Don’t statins obliterate ApoB?
You’re the absolute best if you answer this question for me. I’d be forever greatful!
Thanks guys for all the work you do. It’s appreciated!
Cholesterol and Diet
Jay writes:
Hi Robb and Nicki,
One of your original six listeners here. (Can’t be wrong!) Thanks for all the good work.
Recent bloodwork revealed high cholesterol and LDL numbers (216 and 123, respectively), as well as non-HDL cholesterol (137) and apolipoprotein B (94). (HDL is 79 and triglycerides are 50.) For what it’s worth, my glucose is in the normal range, though slightly high considering my otherwise overall health, activity level, and diet.
My functional med practitioner has suggested the “Cardiometabolic Food Plan.” (for reference: https://www.allinahealth.org/-/media/allina-health/files/business-units/penny-george-institute-of-health-and-healing/2_ifm_cardiometabolicfoodplan_comprehensiveguide.pdf)
I’m reticent, considering the plan’s emphasis on soy protein, legumes generally, grains, and limiting saturated fat. I could modify it to eliminate those things, but then I’m back to basically what I do already.
Quick background: male, 38, active (commute on a bike, strength train, chase kids), small business owner with two young kids (i.e., non-zero amount of stress, less-than-perfect sleep). I have a pretty good gluten intolerance (which is how I found your work right around when you published The Paleo Solution — thanks again!) and generally follow a paleo-primal-ish template, with some full-fat dairy and rice/corn, occasionally, mostly to coexist with my family without being a *complete* pain in the ass.
So: Would those lab numbers concern you? What do you think about the Cardiometabolic Food Plan, specifically? And generally, what would you suggest for diet or any other interventions to right the ship?
Thanks tons and keep up the good work!
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Transcript:
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Nicki: It’s time to make your health an act of rebellion. We’re tackling personalized nutrition, metabolic flexibility, resilient aging, and answering your diet and lifestyle questions. This is the only show with the bold aim to help 1 million people liberate themselves from the sick care system. You’re listening to the Healthy Rebellion Radio. The contents of this show are for entertainment and educational purposes only. Nothing in this podcast should be considered medical advice. Please consult your licensed and credentialed functional medicine practitioner before embarking on any health, dietary or fitness change. Warning, when Robb gets passionate, he’s been known to use the occasional expletive. If foul language is not your thing, if it gets your britches in a bunch, well, there’s always Disney Plus.
Robb: Welcome back, friends, neighbors, loved ones.
Nicki: Hello, this is episode 164 of the Healthy Rebellion Radio. How’s it going, hubs?
Robb: Good.
Nicki: Good. I’m good too. I just have this persistent stitch in my left peck, anterior delt situation from Jujitsu I think
Robb: I was trying to do some unlicensed ART on you, and Nicki was howling like she was being put to the question.
Nicki: I do need some ART. I do need some ART. And your version that you provide was excruciating.
Robb: I’m gentle with you.
Nicki: No, you’re not. No, you’re not. Let’s see here. Where are we at? As you all know, in the middle of a move, this episode will go up and then we’ll probably have about two weeks where we don’t have one, so apologies for that. But just in the middle of getting internet set up and all the things.
Robb: Regretting all of her life’s decisions.
Nicki: There’ll be a little bit of a pause. But anyway, all that said, this episode is going to be a little bit blood work heavy because we’ve had several questions pertaining to blood work and labs, and so we’re just going to tackle those three together. But before we jump into that, I just wanted to share an episode that I’m listening to currently. I’m about halfway done. It’s a two and a half hour episode from Brett Weinstein, the Dark Horse Podcast. Super interesting. He has a couple on some friends of his that he’s known for a long time who are part of something called the Web3 Working Group, and I just feel like they’re doing a great job of explaining blockchain, Web3, many of the things that it solves for in a way that most people, like everyday people can understand.
If folks are really nerdy and into blockchain technology, nothing that they discuss will be overly earth shattering. But they do a great job of just breaking it down for the average person, and Brett really kind of does his nerd to English translation for some of these concepts. So one thing that I think a lot of people struggle with is when they hear crypto and they hear blockchain, they instantly think crypto and Bitcoin, whereas there’s lots of use cases for the blockchain that has nothing to do with cryptocurrency.
Robb: There’s so many different situations that we could imagine a untamperable ledger that helps to ensure authenticity. And it’s worth noting that the original blockchain was developed when some folks observed that there had been fraud in some biology papers.
Nicki: Are you listening to this episode too?
Robb: I am too.
Nicki: Oh, good job, hubs. We’ve had so many different errands to run. Often when we go to Jujitsu, we are in the same vehicle and we listen to the same thing. But we’ve been kind of each in our own-
Robb: World while driving.
Nicki: … world while driving. So I mentioned that I was listening and he-
Robb: So yeah. So how many of the situations say involving Covid could we have addressed? And really some sort of methodology like this could be applied to all of pharmaceutical development, all of vaccine development such that there is legit fucking transparency. And, “Oh, you started with 2000 people and whittled it down to 600 and you jettisoned 1400 people?” That all gets documented in there. None of that should be round filed. All of that should be transparent, particularly if any type of pharmaceutical development is being publicly funded. That should be absolutely transparent and it should be untamperable. And anybody who has pushback against that, they better have a good god-damn explanation for it. And that is just one of many use cases. Foodborne illness tracking is another use case. There’s so many.
Nicki: Just also just verifying the authenticity of somebody’s posts, like they talk about that image that went around of the Pentagon being bombed that had been AI generated. But before it became known that it was a fake, it impacted the markets significantly. So going forward, how can we trust that the things that we’re seeing are actually real and haven’t been manipulated anyway? It’s a great conversation and it’s I think very, very accessible. I’ll post a link to that in the show notes. And it’s just cool because there’s a lot of people doing a lot of great work in the background to help make this decentralized future, get us away from these big centralized players, this big tech world that we’re in, and hopefully guide us into this next phase which ideally is more decentralized and more trustless. We don’t have to trust a company to do what’s in our best interest. It just is because the protocol and the code underlying the thing makes it so. Anyway, again, I’m only halfway through. I don’t know. How far along are you, babe?
Robb: Maybe 40 minutes, 45 minutes.
Nicki: 40 minutes?
Robb: Yeah. Yeah.
Nicki: Anyway, I’ll post that in the show notes. And if you’re at all interested in that or maybe you’re like, “I have no idea about blockchain or any of this stuff,” but if you’re even the littlest bit curious, definitely give that a listen. Okay. News topic. What do you have for us?
Robb: I’ll be brief on the news topic because you snuck in another news topic. But it’s more of a newsy piece on POTS, postural orthostatic tachycardia syndrome and Covid. This is something that I’ve got to say on the back end of our LMNT team discussions, we’ve seen just massive adoption of folks using LMNT and just recognizing that this condition, POTS, which is an autoimmune condition, historically it’s been more in children than in adults, but Covid has kind of shuffled that around a little bit. But it’s a condition where you go from seated to standing and you can lose blood pressure such that you pass out and you could bonk your head, you could die. All kinds of bad consequences come from it. Within the POTS community, it’s understood that adequate sodium intake is really critical to properly manage the condition.
Within our paleo keto low-carb space, I think it’s pretty obvious that anything that has an autoimmune piece to it, we are probably uniquely positioned to provide some valuable insight there: gut health, vitamin D, photo period, immunogenic foods, on and on and on. But the news piece goes out of its way to make the case that both COVID, the viral exposure and the vaccine can produce this situation although they say that the vaccine is far, far, far less. And if you really dig in and look at the way that they’re categorizing that, I don’t know that it’s exactly true, it doesn’t really matter, either way it’s affecting millions and millions of people. And I think lots and lots of people are walking around with some of this kind of long haul feel and just feeling like garbage in some of this hypovolemic response from seated to standing while they’re driving. Different things like that. And although addressing the longer ranging autoimmune conditions may be a little bit more challenging, simply addressing electrolytes will absolutely deal with symptomatology and at least keep you from passing out.
Nicki: Cool. So that will be also linked to in the show notes so folks can check that out in further detail. The Healthy Rebellion Radio is sponsored by our Salty AF electrolyte company, LMNT. Summer temps are high, especially if you happen to live in Texas as many of our friends do. But even if you aren’t in the south, if you’re hiking or working in the summer heat, if it’s humid where you are, make sure you’re staying salty and getting the electrolytes you need. Same goes for if you eat a low carb or ketogenic diet, if you’re an athlete, if you have muscle cramps, if you’re a breastfeeding mom, if you have POTS like what Robb was just talking about, or even if you’re just feeling a little tired and need a natural energy boost without the caffeine, element is a game changer. And if you buy three boxes, you get the fourth box free at drinklmnt.com/robb. That’s drink L-M-N-T .com/ R-O-B-B. Okay. We have three questions today. As I mentioned up front, they’re all blood work lab work related. This first one is from Olivia, and her title is Death by Lab Work, which-
Robb: We may adopt as a podcast.
Nicki: … I really like that podcast title. “Hey, Robb and Nicki, longtime listener, and strong endorser of the work y’all are doing. I wish more people and healthcare providers we’re on the same page or hell, even in the same book as this community. Anyway, I recently got my labs done and I have some concerns on the results I received. For context, I’m a 30-year-old female, no kids. I work out three to four times a week, mostly weight training, and I average eight to 10,000 steps per day. I work as a nurse, tend to focus my meals around 30 grams or more of protein, red meat, chicken, dairy, eggs. I eat it all and drink plenty of water and LMNT. I avoid seed oils and other ultra processed garbage.
I went through some hormone issues for five to seven years, i.e. a very infrequent cycle due to too much exercising and under fueling. Since then, I’ve become so much more educated and I have recovered my cycle naturally, gaining probably 30 to 40 ish pounds from my low. I’m currently sitting at 155 pounds at five foot six. I feel great, but these lab results got me shook. Any and all advice welcome.” So her total cholesterol is 282, triglycerides of 43, non HDL 169, HDL 113, apo A to apo B, 0.41. Apo B, 113. Liver enzymes, AST and ALT slightly elevated. Total T3, 68, and all other thyroid values are normal. Fasting blood glucose 95, A1C 5.0. And she asks, “Am I destined for an early death related to heart disease? I’ve listened to Huberman on blood glucose control and will implement his ideas to lower my fasting number. But it’s hard to eat my last meal two to three hours before bed on days I work since I get home at 8:00 PM. I hope this isn’t too long of a question. Thank you so much. Stay salty, Olivia.”
Robb: Man, there’s a lot to unpack with this and because all three questions are kind of apo B cholesterol related, I may end up being a little bit redundant on this. And the other questions actually get into asking about statins and stuff like that. So I’ll try to maybe stage this stuff out. Olivia, from what I’m looking at here, the apo B is maybe a little higher than what we would want. It’s higher than what Peter Attia would want. There’s so many moving parts with this stuff. And I think I’ve said this before, and maybe this is just like the classic Dunning Krueger admission on my part. I feel like 15 or 20 years ago, I had the cholesterol heart disease thing figured out, which was so long as you keep insulin low, then everything is good. And then it looks like it’s a little more complex than that.
It’s interesting. Folks like Peter, who I think is quite smart on this, and he’s very, very smart, great at analysis, and he also has a really vested interest in getting this right because he doesn’t want to die. He wants to live as long and effectively as possible. And so I put some pretty good truck in that. I think that we all want this. But I think Peter, I had a conversation with him a few days ago about some of this stuff, and he’s highly motivated on this, possibly to the point of neurosis. And I think that he would fully admit that. He will also admit, because this is what the literature really tells us, that apo B or the LDL portion mainly of what we’re talking about in this potential atherosclerotic story and heart disease story, it’s necessary for cardiovascular disease, but not the whole piece.
And this gets kind of weird because at the margins, at the edges of the cholesterol apo B story, we see some things that I think in some ways do kind of point a finger in a particular direction. One is that people with a type of inherited trait that results in very, very low cholesterol and lipoproteins, these people effectively get no cardiovascular disease. They smoke, they drink, they can do damn near whatever they want to do, and they die from something. And one of some things that they die from not infrequently is sepsis. So the trade-off with very low lipoproteins is that if you have a septic event, if you end up with a nicked bowel or a surgery that goes weird or something like that, the likelihood of you dying because the lipoproteins have a molecule on them that help to clear lipopolysaccharide, and lipopolysaccharide is this incredibly inflammatory agent that’s found in the cell membranes of gram-negative bacteria, that shit will kill you.
So there’s trade-off there. These people appear to punt on developing cardiovascular disease potentially because their lipoproteins are so incredibly low, but it also ends up manifesting in other disease susceptibilities. And sometimes you see some signal around elevated cancer rates and some things like that. So that’s a piece of this thing. Another piece to the story is the endothelial damage model, which Malcolm Kendrick has really championed. And there’s some interesting pieces to that.
So he points out that children who typically have very, very low lipoproteins and should see virtually no atherosclerotic plaquing or disease development, although that’s starting to change because kids are starting to develop worse and worse lipoprotein profiles earlier and earlier. But he has pointed out that children with really low lipoproteins, really low apo B end up dying from effectively occlusive cardiovascular events because they are sickle cell anemia carriers genetically, and they end up with the sickle cell anemia phenotype, which is these red blood cells that are oddly shaped. It buys you some buffer against bloodborne parasites like malaria. But the downside is that because of the odd shape of these red blood cells, they don’t move through the tiny little vascular beds the way that they should. And they’re in fact pointy and kind of jagged, and they end up damaging the vascular endothelium. And these children can die at age 10, 12. And putting them on statins or other lipid lowering drugs doesn’t change that. There is so much vascular endothelial damage occurring that they end up succumbing to the disease from basically cardiovascular disease.
And then the other side of the spectrum is familial hypercholesterolemia, which shows people who phenotypically end up having very, very high lipoprotein and cholesterol levels, they end up with really early, pretty severe atherosclerotic plaquing and they usually end up having a pretty rough go of living into their thirties. It’s fairly clear that lipid lowering drugs end up extending the lifespan of people in these scenarios, but it’s a lot of moving parts. And again, I know we have some other questions, and so I’m thinking about stuff that I’ll probably say in some of these other things. You could look at some lipid lowering approaches. You could look at a really thorough investigation into your thyroid.
Although that T3 looks okay, within the Bernstein diabetes community, they really go after elevated lipoproteins, elevated cholesterol as a thyroid dysregulation issue. Most of those folks look at the lean mass hyper responder population as people who basically have subclinical hypothyroid. And if you address the thyroid insufficiency, it’s going to address the elevated lipoproteins. And before we had statins in some of these other things, one of the treatment methods that was tried and didn’t really work that well was putting people on thyroid because elevated thyroid… or saying it the other way, low thyroid will definitely lead to elevated lipoprotein, specifically LDL.
So Olivia, you’re in a similar boat as I am where I have to eat the way that I eat to address a host of different things going on. I have some gut issues. I have some blood sugar dysregulation that makes things kind of dodgy. I have some autoimmune conditions that I need to eat in some specific ways. And it makes it kind of tough to navigate all that stuff. Where else do I want to go with this? Maybe we’ll leave this one here for now. And Olivia-
Nicki: We can circle back.
Robb: … some of the other questions that we have asked specifically about statins and stuff like that. And she didn’t ask specifically about that. But I think what you’re doing is great without a doubt.
Nicki: Definitely working on the fasting blood glucose levels.
Robb: Yeah. An A1C of five is not terrible, but you could maybe budge that down just a little bit, make sure your vitamin D levels are good. As you get older and you head towards perimenopause and menopause, then you’re probably going to want to look at donating blood so that you don’t end up with iron overload, which is when these oxidative stress inducing scenarios that can worsen all of these types of conditions. But I think when we look at the risk profiles, you’re not a smoker, you’re not diabetic even if your blood sugar is just a hair-
Nicki: Her triglycerides are great.
Robb: Yeah. Her triglycerides are great. Bill Cromwell makes the case, he has a really interesting study where he makes the case that absolutely diabetes is this major risk factor for cardiovascular disease, stroke and heart attack. But he also, he’s kind of convinced me that there’s a bifurcation there where at some point you can be quite insulin sensitive, but still at a risk for cardiovascular disease because of these lipoproteins and whatnot. And I know there are a lot of people that don’t want to hear… I don’t want to hear that. I’d like to just hear, “Keep your insulin low, keep your inflammation low when it all is good.”
I forget who it was. There’s this refrain that goes around if you buy into the vascular endothelial damage model, which I think it has a lot of laudable characteristics to it. Some people will say, “Just keep your inflammation low and everything’s good.” That’s fine. But our endothelial lining gets some amount of damage all the time no matter what. Our skin gets some amount of damage all the time no matter what. And it’s got to replace itself. And there’s perfect and imperfect features of all that stuff.
But the theory is that the higher the lipoproteins amidst some amount of vascular endothelial damage, you just have a higher likelihood of something going sideways and then developing that atherosclerotic plaque, which can then progress into an unstable plaque, and that thing can pop. And then you release this pro-inflammatory cytokine storm into circulation and you get a clotting cascade. And that’s where you can end up going from a mildly occluded cardiovascular system to where you throw a huge clot and and either plug something in the brain or in the heart or even in the lungs. So let’s leave that at that one for now. And then Olivia, listen to these other questions because we’re going to end up talking more about treatment and trade-offs and all that type of stuff.
Nicki: Okay. So our next one is from Merit on apo B confusion. “Hi, Robb and Nicki. I’ve been listening to your podcast and following your work for many years, and I’ve thrown some similar hard questions at you, which you were kind enough to try to answer.” Thanks. “I’m so frustrated that I can’t understand statistics enough to draw my own conclusion based on the literature on apo B and statins. I listened to a Peter Attia podcast and he said, I heard it twice to confirm, that if apo B were low in the population, he thinks-“
Robb: Atherosclerotic cardiovascular disease
Nicki: … yeah, “ASCVD would be dramatically reduced. He pushes a lot for statin use. On the flip side, reading the breakdown of studies on statins on Chris Kresser’s website, I just can’t understand why Peter Attia takes this stance. It doesn’t add up. My gut feeling is risk for any chronic disease is never calculated on just one lab value. That’s just logical. But even if it was, why does Attia use statins when they don’t seem to reduce deaths, strokes, or heart attacks by very much in people without CVD? Don’t statins obliterate apo B? You’re the absolute best. If you answer this question for me, I’d be forever grateful. Thanks for all you do.”
Robb: Well, Jay, I will take-
Nicki: This is Merit.
Robb: This is Merit, Merit. I’ll take a stab at this. But again, this stuff is… I don’t know, maybe it’s straightforward for other people. But it makes my head spin. I devote a fair amount of time to staying up on this, and it still just kind of makes my head swim a little bit. One thing that I think is valuable to dig into all this is the number needed to treat for a given… How do I want to say this? There’s a risk reward with anything. And when we’re talking about statins specifically, they have a non-trivial risk profile. There is some neurodegenerative disease that’s associated with them. There’s muscle damage that’s associated with them. It is crystal clear that they worsen your likelihood of type two diabetes, basically insulin resistance. So it’s not like there’s a free lunch. Again in this story, we are wanting to hopefully not die from cardiovascular disease. But what are we trading in the process of hopefully mitigating that?
And something that’s interesting to me in all this story is the generally accepted number needed to treat with statins, and this depends on the person and the drug and a bunch of different factors. But the more mainstream accepted number is that you need to treat about 150, 130 to 150 people for five years to prevent one death from cardiovascular disease. So you’ve got a group of people, and this usually is within people that already have a cardiovascular disease. But what Peter’s point is, this medicine 3.0 position that he’s taking, and I don’t think he’s wrong in this regard, is what if we got out earlier and did more sooner so that we flattened that disease vector, we flattened the curve? God, it just gives me heebie-jeebies even saying that. But it makes sense. Why wait until there’s something already brewing when we could maybe modify the disease burden?
Well, one of the challenges there is that let’s say, I don’t know what this number is, but let’s say most people go on a statin in their fifties. Let’s say then that most people live till they’re 80, we’ll be generous on that. That’s 30 years of statin use. What we’re suggesting is that potentially people go on a statin in their twenties. So now we’re talking about 60 years of statin use. What risks does that present with regards to neurodegenerative issues, muscle damage, recovery, neurodegenerative issues? And it’s kind of murky getting in and figuring all this stuff out. And when we look at the efficacy of these things, and I got to pull this up on my phone because I-
Nicki: It’s been a long time since I listened to it. It was probably two or three months ago. But when Dr. Aseem Malhotra was on Joe Rogan, he talked a lot about statins and his conclusion was there was no-
Robb: Net benefit.
Nicki: … net benefit to using them.
Robb: Absolutely.
Nicki: So that’s another variable to kind of weigh. Peter has his view, and then there are other cardiologists that have an opposing viewpoint.
Robb: Malcolm Kendrick, Mike and Mary Eades, Aseem, yeah. Yeah. So I’ll ping this to Nicki so that this gets into the show notes, association of lowering apo B with various pharmaceuticals. And the weighted meaning absolute reduction in apo B across all the interventions was 21.1 milligrams per deciliter for statins. Non-statin therapies, PCSK-9 inhibitors was a 45 milligram per deciliter reduction. And then there are some of these other things like binding cholesterol in the feces and some things like that that are really fib rates, niacin. They’ll move it five milligrams per deciliter, six milligrams on average. But it’s really modest moves. So with Olivia, she had 113 apo B. Peter doesn’t want to see it over 60. And I think that 60 was like the 50th percentile. He would like to see it in the fifth percentile, which is getting it down around 20 or something like that. Maybe even a little bit lower.
You’ve got to be a shockingly good responder to the pharmaceuticals to get it there. So the PCSK-9 inhibitors, which are really cool, what they end up doing is blocking the expression of the PCSK-9 protein, which tends to bind to the LDL receptors on the liver, and it prevents the LDL cholesterol being cleared. So the PCSK-9 inhibitor basically keeps the LDL receptors on the liver active so that it pulls LDL out of circulation and it gets reprocessed. And the PCSK-9 inhibitors are really cool. I got to say, when I poke around and look at the side effects, they don’t have any of the risk profile of statins. The thing is is that you can get a generic-
Nicki: Statins are cheap and PCSK-9 inhibitors are not.
Robb: Oh dude, a generic statin, you could probably do five bucks a month or something like that. It might be a little bit more than that. PCSK-9 inhibitors have come down in price. They’re only injectable. They are close to getting an oral PCSK-9 inhibitor. At least it’s in research right now. But these things are about $6,000 a year and generally insurance won’t pick them up. Sometimes they do. You’ve got to get pre-authorization on them and stuff like that. The insurance company would rather you just die than maybe address this stuff.
Nicki: Not the life insurance company.
Robb: Not the life insurance company. Which side of the insurance story are you trying to play? So let’s just look back at Olivia really quickly. She had a 113. If we put her on a PCSK-9 inhibitor, let’s say she responds beautifully to this, she can shave 45 points off that. So what are we at? Like 65-ish then. If she does well on a statin, then we can get another 25 points off of that. So we’re down in the forties. So you can get some non-trivial lipid lowering. But that’s if everything works well the first time. And not everybody responds the same way as far as lipid lowering, particularly as it relates to statins.
And this is one of these interesting things too, is that although some people will claim that… Let’s say Aseem is on one side of the aisle saying that statins do not overall provide a net benefit, we’ll say that that’s there. Then there are other people who say that it does provide a net benefit. But to get to that net benefit, you need to get an efficacious dose. And what we know is that a lot of people get a really modest reduction. Some people get a great reduction in apo B and lipoprotein. Some people get a really piss poor reduction.
And there’s this thing called the law of sixes with statins. You get whatever you get out of the first dose, the first therapeutic dose. Let’s say it drops you by 20 points, which would be a pretty, pretty good response. You have to double the statin dose to get an additional six points reduction in the lipoprotein. So it really bogs down. And not surprisingly, when you double the statin dose, you really worsen the risk profile of side effects. So you start getting into a little bit of a weird scenario in which, depending on what your lipoproteins are, you could throw the fucking kitchen sink at this stuff and you’re really not going to be budging these things all that much.
And so this is in my mind… I had a chat with Peter the other day. And again, he understands this stuff far better than I do, at least I think he does. So I tip my hat to him in many regards. And he made this case that if you’ve got the means, use a PCSK-9 inhibitor because the risk profile seems to be really, really non-existent. In the drug trials, there appeared to be more side effects within the placebo group than the main testing group. And I say that with a big shit eating grin on my face because as time has gone on, I trust these results less and less and less. When I look at what has come out of the testing around the Covid scenario, around vaccines in general, the fact that they don’t use controls with a bunch of this stuff, the fact that they cherry pick people-
Nicki: The people that are participating in the trials get omitted if they have an unfavorable response.
Robb: … if they do have an unfavorable response.
Nicki: Which circles back to our original point about the whole future of-
Robb: If we had a hundred percent transparency in this, science is still tough to do, but… And it’s so funny. This guy from high school was giving me hell on Instagram because, “Oh, you’re a conspiracy theorist,” and everything. I’m like, “Tell me what I’ve got wrong.” And he wouldn’t do it. He just wouldn’t do it. His politics are different than mine and they clearly are, and he just… This is kind of a side diversion. But the last thing that I said to him was, “You live a bitter life. And because I’m a white male who’s at a modicum of success, you feel entitled to jump on me with both feet without justifying your position at all.” And that was kind of the last interaction that we had. But I kept asking him, “Tell me one thing that I’ve gotten wrong here.” And I say this because I am feeling more and more just a complete conspiracy theorist. You just can’t trust anything.
Nicki: It’s like Brett can’t mentioned at anything the beginning of his thing. If we don’t find a solution, you either end up with people who are completely bitter and cynical and don’t trust anything, or you get the opposite of the people that believe everything that’s coming down their feed that is manipulated and it’s like, “Squirrel, squirrel.” You’re constantly embroiled in the latest thing. And so we don’t want either of those scenarios. We definitely don’t want people to be so cynical that they can’t trust-
Robb: Anything.
Nicki: … anything. I’ve been seeing in my Twitter feed a little more this term, there’s defi, decentralized finance. And I’m now seeing desci, S-C-I like decentralized science.
Robb: Decentralized science.
Nicki: And I haven’t dug into it. But I feel like people recognize this need. People recognize that there’s this massive distrust for all of our major institutions, particularly our health institutions after the past three years.
Robb: And I know we’ve kind of diverted a little bit, but here’s the opportunity there. If you’ve got people who, because of captured financial interests, want to control the narrative, it’s like, “Okay, I got that. That’s fine.” But if they’re lying about the nature of reality and then people are able to squeeze through the cracks and do science that ferrets out the real answer, the only thing that they’ve got is censorship. And that is in part I think why the censorship piece of all this is so hot and so heavy because, and this circles back around to another Dark Horse podcast recently with Umberto and-
Nicki: Paul Marik.
Robb: … Paul Marik. The use of corticosteroids for ARDS, acute respiratory distress syndrome, looks like it would’ve potentially reduced like 50% of the fatalities, would’ve kept people off ventilators and all this other type of stuff. And Umberto just in passing threw this one out there. And I was like, “Oh, shit.” But he was like, “All those statins, do you know what statins work on? They work on the glucocorticoid receptor and the macrophages. And that to the degree that they have efficacy is what’s doing it. It’s not lowering lipids.” And he also said, “But we can’t study that because this is being blocked at every level because glucocorticoids are off-label and they’re generic-“
Nicki: Not patented.
Robb: … “and not patented,” and all that type of stuff patented. And this again circles back around to this, how are we 60 years, 80 years into this discussion around lipids and we don’t have a real firm handle on it? How is this possible? How many fucking papers have been done on this stuff? And granted, biology is complex and all that. But even on let’s say the type one and the type two diabetes management story, it is crystal fucking clear that if you have a condition in which glucose management is challenged either from insulin resistance or because of the loss of the ability to produce insulin because of damage to the beta cells or the pancreas, if you reduce carbohydrate load, that dramatically simplifies the process of dealing with that.
Now, there may be other side effects, including elevated lipoproteins because you’re eating a higher fat diet and some things like that. But it’s interesting that there is still this… Let’s say Aseem is nuts. Let’s say that Malcolm Hendrick is nuts.
Nicki: Kendrick.
Robb: Malcolm Kendrick. How are they that nuts? How do these smart people get it that wrong? And I know smart people can get wrong, but it’s like how do you get it that wrong? And the more that I nose around this stuff, it just feels like we don’t want the right answer. We want treatments. And we want treatments that are marketable and patentable and all the rest of that shit. And I know that this is kind of spinning out off of what our main thing was. So this is-
Nicki: This is Merit.
Robb: … Merit. Merit, we may end up punting on this one a little bit.
Nicki: All three questions kind of layer-
Robb: They all layer together.
Nicki: … and that’s why we decided to do them together.
Robb: And so Merit, I know I’ve covered a lot of stuff. At the end of the day, I think there are pluses and minuses to the treatment story. I too am perplexed by the use of statins because we generally see a very modest improvement in lipoproteins. You have to really kind of divine the tea leaves to see where a net benefit is had. The industry accepted numbers is this like 130, 150 people treated for five years to get one life saved from cardiovascular death. That’s a lot. That’s a lot of involvement and there’s some type of risk profile there. The PCSK-9 inhibitors seem to work far better at lowering-
Nicki: And what’s the situation with the cost on them? They’re just still under patent?
Robb: They’re injectable and they’re patented. Yeah. But they are definitely still under patent.
Nicki: And what’s the timeline for something to come out?
Robb: Seven years I believe.
Nicki: So seven years. So these are relatively new.
Robb: Pretty new.
Nicki: Okay.
Robb: Yeah, yeah. Seven years, 10 years. I think it’s seven years though. But yeah, yeah.
Nicki: Okay. And then so theoretically after that seven year mark elapses, they’re still injectable so they might be more expensive than your average-
Robb: Yeah. But any pharmaceutical company could spin up their version of it and then you have some price competition.
Nicki: But you could potentially get a generic one for 20 bucks a month or 50 bucks a month instead of 600.
Robb: Absolutely.
Nicki: Okay.
Robb: Yeah.
Nicki: All right. Let’s move on to our last question and then maybe you’ll have some overarching thoughts on-
Robb: Yeah, we tie it all together. Yeah.
Nicki: … all of it. This one just came in yesterday from Jay on cholesterol and diet. And again, because it all tied in, it made sense to put them all together. “Hi, Robb and Nicki. I’m one of your original six listeners. Can’t be wrong. Thanks for all the good work. Recent blood work revealed high cholesterol and LDL numbers 216 and 123 respectively, as well as non HDL cholesterol of 137 and apo lipoprotein B of 94. HDL is 79 and triglycerides are 50. For what it’s worth, my glucose is in the normal range though slightly high considering my otherwise overall health, activity level and diet. My functional medicine practitioner has suggested the cardiometabolic food plan,” and he includes a link to that.
“I’m reticent considering the plan’s emphasis on soy protein, legumes generally, grains and limiting saturated fat. I could modify it to eliminate those things, but then I’m back to basically what I do already. Quick background: I’m male, 38 years old, active, commute on a bike, strength train, chase kids, have a small business. Small business owner with two young kids, i.e. non-zero amount of stress and less than perfect sleep. I have a pretty good gluten intolerance, which is how I found your work right around when you publish The Paleo Solution. Thanks again. And I generally follow a Paleo primal-ish template with some full fat dairy and rice/corn occasionally, mostly to coexist with my family without being a complete pain in the ass. So would those lab numbers concern you? What do you think about the cardiometabolic food plan specifically? And generally what would you suggest for diet or any other interventions to right the ship? Thanks tons and keep up the great work.”
Robb: Good questions. And some of the stuff that we at least have something of a grasp on is very low carb can elevate lipoproteins in people. When you look at the enzyme pathway in which cholesterol is synthesized, ketosis has kind of a back feed mechanism in which in some susceptible people, it just drives up lipoproteins like crazy. Just the state of ketosis drives up lipoproteins. Some people, just simply consuming saturated fat of any variety will drive up lipoproteins and there’s certain types of saturated fats which tend to elevate lipoproteins more. Palm oil, palmitate, some of the longer chain fats found in coconut. Stearate, which is in beef and also in chocolate, seems to be kind of cardio neutral. It might bump up LDL a little bit, but it elevates HDL and it seems to have some other benefits. So it tends to be kind of cardio neutral.
And then for whatever reason, dairy proteins do in at least some people seem to dramatically elevate lipoproteins. Like again mentioning Peter Attia, when I was chatting with him when he was on that really like a three to one, four to one ketogenic diet, like pretty low protein, very high fat, he said that fully 25% of his calories came from dairy in one form or another. He really leaned on full fat Greek yogurt, butter, cream. It was just impossible to get 4,000 calories a day to maintain his activity level through 3,500-4,000 calories without the dairy inputs. And that’s a lot of what I find myself out because the solution for some of this on the lipoprotein front is putting in a little bit of carbs, which it sounds like he’s doing some of that with the rice and corn and whatnot, avoiding dairy, and just checking to see if we get a benefit there.
Nicki: It seems like instead of jumping onto the soy protein legume ship, maybe sticking with your paleo template, but just dropping the full fat dairy, just dropping the dairy and just running with that for a few months and then retesting and seeing if that moves the needle enough.
Robb: And one can find 90 and 95% lean beef. You can find very lean cuts of pork, poultry. Which I’ll eat poultry, but it’s-
Nicki: Shrimp.
Robb: I like shrimp if you can get some wild caught shrimp and some fish. But you can really do kind of a, “Paleo Mediterranean,” version of this thing. I wish I could just crush nuts and seeds all day. I do okay with macadamias. But if I get too high a percentage of my calories from nuts, it just kind of blows me out. I don’t digest it well. The funny thing is that digestively at the gut interface, I do great on dairy. I feel good with butter and cream, but my lipoproteins go up. And this is one of these things where I’m like, “Fuck. Okay. Do I manage all this other shit?”
Nicki: You plug one hole in the dyke and then another one sprouts open and then you’ve got-
Robb: Then like six other ones open.
Nicki: … all your fingers plugging the holes.
Robb: But many people have found that if they put a little bit of diligence, so you could emulate some of what they’re trying to do with this cardiometabolic food plan without soy protein and a bunch of legumes and stuff like that. I think that you can very easily have a low glycemic load involved with that. And if you want to do a little bit of beans and everything, if you digest them fine, go for it. I would soak them, sprout them, do the traditional methods like the Weston A Price type stuff to improve the digestibility on those things. But I think it’s relatively easy to turn this thing into a little bit more of a Mediterranean flare, reduce the total saturated fat, and I would just test. And I would see how you look, how you feel, how you perform and then track those biomarkers of health and disease. Does it even move the needle? Do we see improvements in the lipoproteins? I would get apo B checked, either apo B or LDLP.
Nicki: He got the apo B.
Robb: He got the apo B before, so I would just keep doing that-
Nicki: 94.
Robb: … that apo B and just kind of track that. It’s so cheap compared to the LDLP and it is very easy to get and whatnot. So that’s a way to tackle this. And again, when I had a conversation with Peter, just trying to wrap all of this stuff. So for his questions specifically for Jay, I think that it would be easy to make this more of a paleo med approach, Mediterranean approach. Do more nuts and seeds, do more olive oil, try to reduce the saturated fat.
Nicki: Ditch the dairy.
Robb: Ditch the dairy for the most part and just see. If it takes it from an apo B of 94 to 89 and it’s a complete pain in the balls, I don’t know if I would continue doing that. And then wrapping this whole thing back around, one thing that is fairly clear, unless you’re a smoker, unless you’re diabetic, in general the cardiovascular disease process takes a long time. And I do really Peter’s idea around Medicine 3.0 where we get out in front of this stuff and try to do something to really prevent things.
And he’s really of the opinion that if you can get your lipoproteins, that apo B down into the range that you had when you were 10, that you’re going to probably be golden. And he had tracked his CT angiogram 15 years ago and he had some calcification, some plaquing. And he has tracked that I think bi-annually ever since then because again, he’s kind of neurotic about that stuff. He has done a variety of different interventions, mainly pharmaceutical and I believe including a little bit of a statin and then using the PCSK-9 inhibitor. And he’s seen no worsening of the CT angiogram since he did it. So it seems to be doing something.
It’s interesting, you look at some folks like Sean Baker who eats a carnivore diet, but he has wonderful lipoproteins eating a high protein, zero carb, high saturated fat diet. McKayla Peterson had wonderful lipoproteins doing it. Not everybody does. It fucking sucks. It’s like some people do great on that type of thing. And here’s the thing, we still don’t really know what the full story is. Maybe they look great, but there’s some other fucked up thing that’s brewing and you’re going to die from that. You just don’t know about it. But I think for a little bit of peace of mind, if my lipoproteins looked a little bit better just naturally, I’d be probably happy with that. It’s just one less thing to worry about. Maybe there’s something lurking below the waters, but at least you can kind of accept that.
But I’m still perplexed about statins. PCSK-9 inhibitors. When I first heard about them, I’m like, “Why would anybody use statins?” It’s like, well, when they first came out, they were $18,000 a year. That’s why not everybody uses them. They’ve come down in price. They will continue to come down in price. They will go off patent at some point, in which case the price should really drop. There might be an oral administered option sooner as opposed to later. And I think that that would come at a markedly reduced price.
And I think that so long as one looks at this stuff through the lens of understanding that there’s a risk to just about anything that we do, and this would be an interesting thing to run by Peter, it’s like, “Okay. So you’ve knocked your lipoproteins down really low. Are you concerned about sepsis? Are you concerned about an infection that could kill you because your lipoproteins are so low?” And I would suspect he would say no, because modern medicine being what it is. And he lives in the Austin area with great hospital care and everything. The likelihood of him ending up in a scenario where he goes septic and doesn’t get immediate medical care is probably pretty low. So that’s a thing. But I think that all of this needs to be looked at through the lens of a risk reward story. And the statins are still really perplexing to me.
You look at, again, the industry accepted numbers of 150 people, five years to reduce one death. It’s kind of like, “Well, okay.” And it’s also pretty obvious. So something that I didn’t mention around the statins, used to doctors administered statins and would keep doubling down on the dose, doubling down on the dose to hit lipid targets. They don’t have lipid targets anymore. This is what’s interesting. To the degree that statins work… And Aseem would say that they don’t work at all, Malcolm Kendrick would probably say that they don’t work at all. But let’s say that they do. To the degree that they do, it’s via a mechanism not actually most likely related to lipoprotein count. It’s due to modifying some other inflammatory process or some other immunological process that’s going on. So what else could we do that might be modifying that other parameter and whatnot?
But Peter, it was interesting, when I was chatting with him, he was just like, “If you can afford it,” I don’t know why, “don’t use nutrition to modify your lipid risk. Use nutrition to modify gut health, autoimmune disease, neurodegenerative disease.” We have shit options for managing that. But if you can afford a PCSK-9 inhibitor and you get that 40 point drop on it, use that. And I think it’s compelling. It’s an interesting angle. It’s an expensive angle. If I went on that right now at 51, let’s say I live to be 81-
Nicki: 30 years of-
Robb: It’s going to be 100-
Nicki: Well, but it’s not going to be $6,000 a year forever.
Robb: It’s not going to be $6,000 a year forever. That’s a good point. That’s a good point. It will come down. So who knows? And I might end up doing some tinkering with that stuff. I have not done the CT angiogram and really mapped, where am I at? Do I have any cardiovascular disease progression right now? Hopefully not. But if I do, it’d be interesting to see where that’s at. And then maybe I do some more aggressive interventions to try to put a halt on it and then monitor it from there. But I appreciate everybody’s questions and hopefully this was helpful. I know that it was all over the place and I really wish I was more like either Aseem or Malcolm or Peter in that these people seem to have some crystal clarity on some things.
But for me, all that I see are kind of risk reward profiles in this and options. And I think that there’s a lot to be said about individual risk appetite and tolerance and what you’re trading, the devil you know for the devil you don’t know. I do think that it’s worth doing some advanced testing. I think it’s worth maybe getting in and doing some of the CT scan, coronary calcium. Get some benchmarks on that, especially if you’ve got a little bit of means, you’ve got some resources. You’re 40 plus years old. Go in and get a benchmark on that stuff. Get your full hormonal profile done.
And the hormonal profile, I would love it if people would do that in their twenties, both males and females, so that as you enter into later age and maybe we have to do some augmentation of our hormonal profile, we actually know what we’re shooting for. What does youth look like for you? Because once you start down that path, and you know we’ve talked about this in other shows, you put somebody on testosterone and their DHT looks like it’s really high. But is that where their DHT was all the time before and it’s fine or no, it’s three times higher than what we would want and we want to do things to modify that? But anyway, I think investing some time in that to assess it is worthwhile. And yeah.
Nicki: Just before we close here, I want to make a comment. This is separate from blood work. This is related to your essential tremor. You’ve been saying that you feel like you’ve been doing more thiamine and you’ve been feeling like it’s less. And I just want to comment because it’s only been like a week since you’ve really upped your dose. And normally when we record, when Robb’s answering the question, it’s slight, but I can see it in his face-
Robb: Just my face.
Nicki: … in your head. And I’ve been kind of scrutinizing you this whole time and I haven’t noticed it at all.
Robb: Yeah. And I will do an update on that. I know this thing has run long. But I think it was Amy Peikoff pinged me something about the high dose thiamine.
Nicki: I think it was Jack Reston.
Robb: Or maybe it was Jack first.
Nicki: It was Jack.
Robb: It was Jack. But both of them I think jumped in and mentioned it because there was a paper that had mentioned injectable thiamine and it dramatically improving essential tremor. And then there was a YouTube guy, and I’m blanking on his name, but he seems really credible and he does a really nice balance of, “Here’s some paid stuff,” but all this information is available for free. You just kind of piece it together. So he seems like a pretty credible dude. I watched this thing. I got a bunch of different thiamines because there’s the thiamine hydrochloride and the thymine nitrate, and then there’s benfotiamine and some other varieties, like four or five main varieties titrated up. Did it for a good month, maybe longer, maybe three months.
Nicki: You didn’t really notice anything at all.
Robb: I didn’t notice anything with it to be honest. I just didn’t notice anything with it. And I haven’t taken any phenibut today. I’ve been using phenibut. If I do anything out in public, including going to jujitsu, it’ll take generally the worst kind of gnarliness off the edge of the essential tremor. Haven’t had any of that today. But I kept just taking some of the benfotiamine timing every other day, something like that. And then I watched another piece on this and it was really dramatic improvements in Parkinson’s and a bunch of these different things. I’m like, “Fuck, man.”
Nicki: So you just weren’t taking enough?
Robb: I just upped it again. And I’m not even taking that much relative to what a lot of people take. And so what I should do is reach out to this guy and do a consult and be like, “Tell me exactly what to do,” and then do it. But I got to say, shockingly improved. Just even things like shaving, brushing my teeth. It’s awesome when you’ve got a nose hair trimmer and you’re like, “Am I going to slice my nose off?” because your hands are shaky. And I don’t know if we mentioned it on here, but we were at the LMNT event at the PBR and I stood up and was introducing one of our folks and doing kind of a short presentation and I had to sit down and stop because my tremor got so bad I couldn’t talk. I was rattling around. It was I can’t even describe how frustrating.
So anything that can move that thing forward and improve it was pretty amazing. And this is another one of these things. What other health issues were percolating because the essential tremor was happening because of some sort of neuroinflammation. There’s damage happening to certain GABA related neurons. And if I’m addressing that, what else is working? Is my gut improving? What other things are theoretically improving? Because this high dose thiamine protocol seems to help type two diabetes dramatically, peripheral neuropathy. There’s a bunch of different things. So that’ll definitely be something that we’ll circle back on. And maybe we just do a show where you maybe Q&A me about it and we go through it.
Nicki: Cool. Sounds good. All right, everybody. Thank you for joining us. Be sure to check out our show sponsor LMNT for all your electrolyte needs. You can grab your LMNT at drinklmnt.com/ R-O-B-B. Wishing you all a wonderful couple of weeks.
Robb: Wish us an easy move, please.
Nicki: Easy move and we’ll catch you in a couple of weeks.
Robb: Bye, everybody.
Nicki: Take care.
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