Harvard Med Student & Scientist Lowers Cholesterol with Oreos - with Nick Norwitz

Harvard medical student Nick Norwitz added 100 grams of Oreos daily to his ketogenic diet for two weeks and saw his LDL cholesterol drop 71 percent in 16 days, from 384 to 111 mg/dL. This outpaced a six-week course of the statin rosuvastatin, which lowered it only 32.5 percent. He emphasizes this is a metabolic demonstration under medical oversight, not a health recommendation.
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Yeah, the headlines I hope do read, "Harvard med student and scientist lowers his cholesterol with Oreo cookies," because this is something that I want everybody to turn their heads and go, "Wait, what?" And then actually kind of, you know, go down the rabbit hole. I'm not trying to trick anybody into Oreo cookies being healthy. I mean, that should be kind of obvious that it's not.
A Harvard medical student following a ketogenic diet suddenly starts eating a ton of Oreos simply to see what happens to his LDL and has some pretty surprising findings. Why would he do this and what does he want us to get from it? Well, that's what we're going to talk about today with Dr. Nick Norwitz. Welcome back to Metabolic Mind. I'm Dr. Brett Scher. Metabolic Mind is a nonprofit initiative of Bazooki Group where we share education and resources at the intersection of metabolic health and mental health. And metabolic therapy is like ketogenic therapies as treatment for brain-based disorders. So today we're joined by Nick Norwitz, who's a PhD, but also a medical student at Harvard Medical School. And you can find him on Twitter or X @NickNorwitz and also on his YouTube page. But he wants to call attention to the lean mass hyper-responder and the lipid energy model and what that means for our interpretation of cholesterol and LDL, and he did so in a dramatic fashion. And that's what this interview is about. But before the interview, so lean mass hyper-responder, for those who don't know, it is a description of what we call a phenotype. So an individual who is following a ketogenic diet and is by definition lean from a body mass standpoint and has very high LDL above 200, along with good metabolic health and high HDL and low triglycerides, sort of mirroring that good metabolic health. And the lipid energy model, as proposed by Dave Feldman and others, and now in some published papers, is a hypothesis of the mechanism of why LDL would be so dramatically elevated in this population, basically saying that the body needs LDL, it needs VLDL to traffic triglycerides for energy, which eventually leads to LDL. So those are the basic Explanations of Lean Mass Hyperresponder and Lipid Energy Model, which Nick refers to. Now again, before the interview, please remember our channel is for informational purposes only. We're not providing individual or group medical or healthcare advice or establishing a provider-patient relationship. Many of the things we talk about can be dangerous if done without proper supervision, and as Nick says in this, his experiment is— do not do this at home, it was an N-of-1 experiment. So please, before you consider making any significant changes, always consult with your healthcare team. But with that, let's get on with this interview and find out what all this commotion and excitement about Oreos and LDL is all about. All right, Nick Norwitz, I'm not going to bury the lead. You lowered your LDL cholesterol significantly more with Oreo cookies than you did with a statin medication. So tell us what happened.
Yes. So, um, I'll tell you what happened, then we'll go back and say why I did this. But about 5 months ago, I embarked on a study, a crossover trial in myself, an n 1, to test our model about high LDL and people that are keto, the lipid energy model. And a really bold prediction of this model would be that if you add back carbs in any form, you can lower the LDL. So let's take that to the extreme. Let's make it the most legit baity we could. Let's use Oreo cookies, was my thought. And we want a comparison. Let's compare it to standard of care, high-dose statin therapy. So what I did was a crossover trial where I had Oreo cookies on top of my standard ketogenic diet for about 2 weeks, did a washout period for 3 months, and then did 6 weeks of high-intensity statin therapy, which was 20 mg rosuvastatin. I'll add before we get to the results that I did this with appropriate, you know, IRB ethics. My PCP was on board, and I had a consultant cardiologist, Dr.— Professor William Cromwell, who's the senior author and who was, was very supportive throughout the journey. But yeah, not to bury the lead, it turns out that at least in this n 1, in a lean mass hyper-responder on a ketogenic diet, Oreo cookies were 2 times as potent as high-intensity statin therapy for lowering my cholesterol. The exact numbers were in 16 days on Oreos, my LDL went from $384 to $111. So that was a 71% drop, absolutely massive. In fact, the reason it was a 16-day, uh, protocol rather than 14 days, which is 2 weeks, is because at 14 days the drop was so massive and it was only the, you know, second, you know, time point in the intervention that my PCP and I were like, we have to get this in triplicate just to make sure it's legit. We got days 15 and 16 and it was still dropping at that point in time. Absolutely stunning. So then we did the washout and then did the statin therapy, and the nadir, the lowest point the statin dropped my LDL, was 284, from 421 to 284. So that was a 32.5% drop max. So the Oreo cookies were 2 times as potent as the statin in about, um, 1/3 or 1/2 the time frame. So, all right, it was—
that's the dramatic finding.
That's the dream.
And as And as you've mentioned, it was specifically designed to be attention-getting or clickbaity, as you've— as you use the term, but done in a way to demonstrate a point. So what is the point you're hoping to demonstrate?
Right, I think I can take this from two angles. I'll talk about, you know, the lean mass hyper-responder and lipid energy model angle first, which is, you know, any model should make bold predictions that you can test. This was a bold prediction of lipid energy model. We've seen in other contexts, at least with carb swapping in a case series, this was from Dr. Tro's patients of 5 patients where they added back carbs, saw LDL drops. And then most recently in Dr. Cooper's interventional trial, we saw the same thing. This was just a more provocative version of that where rather than doing healthy carb in a carb swap, I'm just like, let's just add Oreo cookies and have the comparison of having it be a statin and have it in a subject with very, very high cholesterol who also happens to be a Harvard scientist and med student. So a lot of viral aspects there. The, the purpose was really to force conversation about lean mass hyperresponders. We have a waterfall of data coming out. In fact, by the time this episode drops, we'll probably already have a meta-analysis of randomized controlled trials published in the top nutrition journal in the country, the American Journal of Clinical Nutrition. So that was a new development even as of today. So there's a waterfall of literature coming out, but it's still a conversation that I think a lot of people are reluctant to have. And me being an impatient 28-year-old, I decided to lace up my steel-toe boot and kind of, you know, kick convention in the shin a little bit with this dramatic n 1. So it was It was, it was a metabolic demonstration testing the lipid energy model. And I mean, even I was surprised that it worked. It was one of these things where you have the model or you do the math and you're like, we should, this should work in theory. It's like how I imagine, maybe this is a grandiose comparison, but the moon landing, right? You design it, you do the math, you shoot the rocket up with people inside and you're like, this should work. We've done the model. You land there and you like step out. You're like, oh crap. This actually worked. When I got the week 2 data and saw it, and I was like, I, I, it was, it was a moment for me. I was running downstairs and all around the house all excited with my, my, my Eureka Oreo data. And then even more so when the statin data finally came in. So in part, this was a demonstration of, um, the lipid energy model with respect to lean mass hyperresponders to force a conversation, um, about LIMAS hyperresponders, which absolutely needs to happen. So it's intentionally provocative, it's intentionally clickbait. Yeah, the headlines I hope do read, Harvard med student and scientist lowers his cholesterol with Oreo cookies, because this is something that I want everybody to turn their heads and go, wait, what? And then actually kind of, you know, go down the rabbit hole. I'm not trying to trick anybody into Oreo cookies being healthy. I mean, that should be kind of obvious that it's not. But I have so much awe and scientific curiosity for this topic. This was a way for me to translate it into, you know, to translate that emotion with respect to the science to a general public person, for them to go, "Whoa, what's going on? I want to learn more." So to bring people on our scientific journey.
I love that you compared it to landing on the moon. So we'll see if those headlines now say, "Just like landing on the moon, Harvard med student lowers LDL." Maybe not. But so what you said though, You want someone to say, "Whoa," and like take a breath and look at this and think about it. But you don't want it to be like, "Okay, Oreos are healthy because they lower LDL," or "LDL doesn't matter in vascular disease and has no impact, so ignore it," right? So findings like this can often get sort of misinterpreted and blown out of proportion. So tell us what it's not, and then we'll dig a little more into what it is.
So very clearly, this is a metabolic demonstration. Even in the graphical abstract, we have that with little caution signs. This is a metabolic demonstration. I say in the video abstract, do not do this at home. And clarifying the paper in case it's not clear, eating excess refined carbohydrates and junk food is not healthy. That's something I would hope I could rely on just basic human common sense to carry forward, but If you want me to be 100% clear, this is not a health intervention. This is a metabolic demonstration. And it brings to the fore an uncomfortable question which you alluded to, which is, yeah, this is something that we probably can agree is not a healthy intervention. And nevertheless, at least in me, whether or not it's generalizable, but even if it's just the one patient, you have this response where a bad marker, quote unquote, goes down massively. And so you have to grapple with these two things. This is what happened. This is what exists. You had an unhealthy intervention, or what was perceived as unhealthy, and you had a, quote, healthy response. So the point is to draw this uncomfortable tension, because that's what science is about. I mean, the best science is dealing with things that defy our expectations and trying to figure out why they exist. So there isn't an obvious 'this is good and this is bad.' That's the whole point. It's to provoke a cognitive dissonance that makes people a little bit uncomfortable so that they want to learn more.
Yeah, and that makes a lot of sense because so much of the discussion around LDL is black and white in contemporary medicine and doesn't talk about mechanisms or doesn't talk about the process of what is causing or leading to the rise or fall in LDL, which— to be honest, really hasn't been addressed hardly at all until this lean mass hyper-responder sort of wave of discussions have come about. Because now it's like, well, why is LDL elevated? Because in order for it to be this elevated, it was a genetic mutation, it was familial hypercholesterolemia. But now we're seeing similar numbers without that. So the whole point is that we can see rises and falls for mechanistic reasons that don't necessarily translate to healthy or unhealthy. But that's a mouthful, right? That's a lot to say. Say and a lot to process for the average person. So do you think people are going to get it?
I have a lot of confidence in the average person's ability to process data if given the chance. What I'm most concerned about, to be honest, is people intentionally making this into a caricaturization of what it is, because there are people with much bigger megaphones than me, and if they choose to try to steer the narrative in a certain direction it's pretty easy to do so. I've given out a headline that can very easily be manipulated. I realize that. And going to the point of, you know, what you talked about before and this potentially being misunderstood, if you want my honest take, this was something I was actually just yesterday talking with Professor Walter Willett about. We had a lovely interview, um, the host was Chris McCaskill on his Plant Chompers podcast, and I brought up the Oreo topic. And rather than talking just about the data What I was questioning him about was, look, my intention in doing this, as I've expressed to you, is to provoke scientific awe. This is interesting. I don't know how you could look at this and say this is not freaking cool. And I want them— people to engage and ask questions like I know they can. However, when you put something like this out into the public, it— what I'm learning very quickly is you only have so much control. Over how the narrative develops. Now, what do you do with that? What do you do with that if it's me? Do you then say, well, so I'm just not gonna do it? Do you say, I'm gonna do it and, you know, do my best to control the messaging, get on as many channels with as many diverse points of view as possible and talk about it as much as I can to be very clear on my messaging, emphasizing again and again, this is a metabolic demonstration, don't do this at home, this is why I'm doing what I'm doing, Um, you know, and obviously, you know, at this point in time, that's the decision I chose. I don't know, it will be, you know, hindsight 20/20 whether that I'm actually able to control this narrative or it does get away from me.
Yeah.
Are major media outlets going to use this to mislead people and boost Oreo sales? That's a possible outcome. And if that turns out to be the outcome, I would be quite upset. So there's a little bit of a gamble in what I'm doing, and I'm, I'm aware of that, and I'm gonna try to reflect on this process as it evolves because I, I, I don't know if I'm playing with fire that I can control, to be perfectly honest. Um, I hope I can, but we're gonna find out shortly. So, um, I don't know, I'm, I'm, I'm rolling the dice a little bit here. Hopefully I don't blow things up in the wrong direction, but it To this point, this is actually a call to action from me to the, um, not the lay public, but the academic community, including those who, um, well, especially those who want conservative messaging around this topic of lean mass hyperresponders. This is a community responsibility to highlight something that is very interesting, very controversial, and with which I think we need to approach with a lot of interest And we can demonstrate that interest through extreme demonstrations, but also clinical caution in the presence of an unknown. We have an editorial to this effect, which I think you've probably read, saying, look, urgent research needed, clinical caution also needed in the face of unknown. But in order to progress the research and turn the unknown into the known, we need research resources. How do we get those? Well, dramatic demonstrations that attract attention is one way that, you know, 28-year-old med student PhD could maybe attract some resources to do things like crossover trials that I really want to do. So the whole objective here is to provoke interest, to push the research forward, and I hope the net effect is positive. I won't know until this story really develops, so we'll find out together.
Yeah, yeah. And, and I have to go back to one thing that you said, that you hope it's not going to be misused by Oreo company to say, now look at our product, lowers LDL. But that's exactly what happens on so many sugary cereals with whole grains proven to lower cholesterol with the heart mark on it. You can actually say it's sort of the same analogy.
I actually thought about using Cheerios literally to lean into that marketing ploy. Again, I find it because it's such an extreme example, I find it really difficult that you could sell the public on the idea that Oreos are healthy. I know it's a joke that people respond to with respect to this Oreo versus statin study. Oh, he's proving Oreos are healthy.
Hahaha.
I don't know what your take is. My take is no one could really believe that, that it is just—
I sure hope not.
I— that's what I would think. I'm like, I want to have some confidence in the basic common knowledge of the average person. That wouldn't actually be misled to be eating sleeves of Oreo cookies thinking it's healthy, that it is, right, you know, more of a joke comment. I sincerely hope that I'm correct in that interpretation for a couple reasons. One, I would hate to mislead people to actually think Oreo cookies are being— are healthy. And two, if that's the case, I mean, that's a pretty upsetting commentary on the basic intelligence of population, to be perfectly honest.
But yeah, and I mean, your point is this is a very specific situation. You are a lean mass hyper-responder. Your mechanism of LDL increase and decrease is significantly different from a physiologic standpoint than the average American who's not in ketosis. So, and that's another really important point to emphasize.
So, the sort of aspect is, yes. The, the clinical effect of adding Oreo cookies is going to be specific to people like me, which is a small, small population. Where I say sort of is it's in studying these extremes that we learn so much that can be generalizably applicable. It's not always clear what that is, but it's by taking an extreme observation and chasing the physiology behind it, which is how we gain a lot of, um, Uh, we gain knowledge that can then be useful for the broad population. A good example would be the GLP-1 receptor agonists. Do you know where they come from originally?
What do you mean where they come from? Like your gut, or what do you mean?
Um, so, so the class of drugs was derived, I believe, in '95 by Drucker— gila monster venom. So I think scientists are studying gila monster venom. Why does it screw up the metabolism of its prey?. And that was the basis for what became the early GLP-1 receptor agonists. I hope I'm presenting that history correctly, but it was Gila monster venom in some respect that led to, you know, this class of drugs. Now, you know, be a fan or not, they're highly effective and, you know, with clinical utility. And you got that effectively out of just chasing interesting scientific questions. And you see that, you know, motif again and again in science. Somebody makes an observation. It's not immediately obvious how it's applicable to the general population. Even Brown and Goldstein's study of homozygous familial hypercholesterolemia, that's a very rare condition. Nevertheless, you study it and you learn stuff about physiology that then becomes applicable. So that's why I say, because I think the lipid energy model holds keys to understand human physiology that can then be generally applicable.
Yeah, great point.
Yeah, I just want to add is, um, how this is applicable to your average person. A journalist asked this to me the other day. Most people aren't keto. Most people that are keto aren't lean. So why should your average Joe care? And my answer to that was, you know, for me, this is a story about awe, scientific awe and curiosity, which is something that we all, I think, have the potential for. And the really cool thing about being in this day and age and now 2024 is there is so much access to your average person, um, so much access to science via social media and the internet. And that can be used for good or bad, but it really does allow people to engage in the scientific process and studying lean mass hyperresponders. The lipid energy model for me has been so awe-inspiring This is a way that I can share that awe with everybody. You don't have to be keto to see this observation and be like, whoa, this is cool, and feel that awe, feel that scientific curiosity. And what we're inviting you to do is join the research journey. I'm pretty active on social media, put up YouTube videos and Twitter. So like somebody reads a story about this, come engage, come join the research, follow the journey and feel the awe in science, which is one of the greatest pleasures I have in my life and something that in my career I just want to work on spreading because I think that's such a treasured part of the human experience that I just want everybody to be able to enjoy.
Yeah, I love the discussion around awe of science, joy of science, exploration of science, but there are going to be plenty of doctors, scientists, what have you, who see this and completely discount it. That does not matter. High LDL is dangerous. Doesn't matter how you get there. You manipulate it all you want. It doesn't matter, and just ignore it. Like, does that bother you? I mean, it's just the fact, right? People are going to discount it. Does it bother you that people are going to discount it and not share in your awe?
I think that's an inevitability that I've just come to terms with. I think they're doing themselves a disservice. I understand the response, um, because the conservative stance is to always, you know, lower the ApoB in your patients, because all things being equal, with respect to heart disease as an isolated entity, quote, lower is better. There's a lot of qualifications there, but with that, generally people feel more comfortable lowering patients' LDL levels and so don't want to give any inch to the idea that this could be a physiologic response. And possibly this is a, you know, a distinction— mechanism doesn't necessarily imply risk— but that it might be a unique case where the risk isn't as elevated as we would otherwise think. And we're doing studies currently to assess that possibility. What I would say is it's really important to distinguish between the claim high LDL isn't risky in lean mass hyperresponders and the question, do we know it is risky? Those are two hugely different things. So we're not making the former claim, we're asking the latter question, which is a legitimate scientific question. And what I see from— and hear from lean mass hyper-responder patients in talking to their doctors is they understand that distinction. They realize it's a legitimate question to be asked, and they get really frustrated when the, the question is discounted by their physicians. And that actually can create a rift in the patient-physician relationship and create some pushback and then even more tension. So I think— and apologies to physicians listening if they feel a medical student saying this seems grandiose, um, or out of place— but I, I do think I guess speaking from the position of a patient, let me put it that way, because I'm a lean mass hyper-responder patient, it would be better for me, let's say, lubricate the conversation if we said, look, this is a legitimate question to ask. Here are the data we have now. How are we going to handle your clinical situation with the data we have now? And not discount the observation. Now, if a patient goes forward to their doctor and said, oh, look at this, n 1, Nick Norwitz lowered his cholesterol with Oreo cookies, let's try that. And the doctor says, No, I'm good with that. Very appropriate response, um, to be clear. But, um, I, I would hope that those who are curious in this topic would at least privately see this and go, wow, this is cool. And I can tell you the response from within Harvard, from attendings and resident doctors, like, this is something that I literally talked about while I was ongoing on surgery with like a patient under anesthesia, talking with my resident, and she's like, Oh my God, I'm a lean mass hyper-responder. This is so cool. Like, tell me like how this is going to turn out. So behind the scenes, this is something that I think academics can be very excited about, but want to reserve that enthusiasm in a clinical setting. And I get that. Um, but point being, I think we can try to separate the scientific awe from clinical caution in dealing with individuals. Pushing back on this as just nothing, I don't think is going to be the most effective way to promote thoughtfulness and receptivity by lean mass hyper-responder patients. That's my impression. Sorry, there's a long answer. Yeah, it's kind of why I am.
Yeah, but then, but pushback saying like, this tells us nothing about if it's healthy or not healthy, we can't use this as anything, and more information is needed, you would kind of say, "Yes, that's exactly what I'm saying, and that's why we should look into it." It's the uncomfortable question.
It's the uncomfortable question that constantly arises. Is this good or bad? And the answer is, obviously, we don't know because nobody's going to say eating lots of Oreos for a long period of time is good for you. That's obviously not true. And yet, if it lowers my LDL and that's supposedly good, then how do you weigh those things? Yeah. The point is the answer isn't clear. It makes you a little bit uncomfortable to even hear it as a clinician. That's the point. This is supposed to be provocative and turn heads and get people to ask questions. It's not supposed to be definitive. Obviously not. The more definitive stuff is, you know, the meta-analysis of RCTs. However, that doesn't necessarily translate to public enthusiasm in the headlines that maybe we need to push the discussion in the direction I want to push it. So—
Well, and the other thing that comes up, that frequently comes up whenever you sort of contradict what is thought to be common knowledge is, look at the totality of evidence in the literature that lower LDL is better, that in the general population, lower LDL is associated with fewer heart attacks, whether it's inborn genetic mutations, whether it's medication therapy, for the totality of evidence, people will say that is what is shown. This does nothing to refute that. And you're not trying to refute that, I would say.
I mean, there's two things to that. One, again, think about the— please assess the claims I'm making, not the claims Joe Schmo is making based on my experiment. What am I saying? Yeah, I'm saying this is interesting and we need to do more research. I am not saying this tells us anything about clinical management whatsoever. Maybe beyond myself as an n 1. I can have this discussion with my doctor. But no, I'm not making any claims about clinical management. I'm saying this is interesting and that we need to study it more. As for the whole totality of evidence, often the term is used as preponderance of evidence. There's a catch there, which is that you can talk about the preponderance of evidence all day, but if the preponderance of evidence is drawn from a population that's distinct from the population you're treating, then what value really is the preponderance of evidence? And the whole thing is that lean mass hyperresponders are an independent group with independent etiology. Now, is the clinical risk different? The answer is we don't know. And you can go off the preponderance of evidence to take a conservative clinical stance, but that comes, man, again, back to the question: do we know they're at increased risk? The answer is no. And what we need is more of a preponderance of evidence on the population in question, not a preponderance of evidence just on everybody pooled.
Right, right, very good distinction. And I guess what's lost here is that so many of these individuals who are lean mass hyperresponders are following a ketogenic diet for a reason, whether they're treating, you know, ulcerative colitis, whether they're treating a mental health disorder, bipolar disorder, schizophrenia, whether they're reversing their type 2 diabetes or whatever the case may be, treating their epilepsy. It's not that they're on keto just to see what happens to their LDL. The majority of people are using it as a medical intervention with benefits, and that's when it comes down to someone saying, "Well, the risks clearly outweigh the benefits." Well, how can you say that if you don't know what the benefits are? So when the benefits are so high, that's when you really have to dig down to say, "Well, let's learn more about the risks." So I assume that's also a message you want people to understand about that risk-benefit ratio.
Obviously, yeah, it's— I said this earlier, the whole ApoB is lower specifically for cardiovascular disease, all things being equal. And it's that all things being equal clause that is so critical because all things are never equal in the clinical management of an individual. There's so many things to, you know, factor in, including comorbidities, medication side effects, costs. Um, and, and, um, again, just patient preferences. So one major thing is, yeah, complicating comorbidities and things people are dealing with. Um, so it's not for me or anybody else on social media, including licensed doctors, to say what's best for an individual. That's a conversation between patient and physician.
But to—
in order to make that best decision, you need to really understand risks and benefits. And to understand the risks, you need data on this population, which we don't have, which we want to collect, and to understand the physiology again. So this is all about pushing knowledge forward, which, you know, does not necessarily come through an Oreo versus statin experiment, but that can be a lever that people like me can pull in order to get the resources to do the studies we really want to do. You kind of have to you know, direct the conversation and public opinion a little bit when you, you aren't a senior scientist with multi-million dollar grants, which hopefully one day will happen for me. But I'm, I'm not waiting for that moment to, um, to engage with this topic.
All right, well, we've talked a lot about your motivation, what you hope to get out of this, what the study was, what it wasn't. But I gotta ask you, as a guy who's been following a ketogenic diet for so long, probably haven't had sugar or junk food in so long. How'd you feel? Like, how'd you feel for those 2 weeks eating all those Oreos?
I sincerely hope I don't offend anybody when I say this, but this is just the way I was describing it, the only way I can describe it. It's— I felt like I was on my male period. That's what people are telling me. My emotions were up and down and up and down. I'm probably going to get canceled for saying that or something, but it was true. I was, I was so emotionally, like, liable. Like, I'd be like furious in one moment and ecstatic the next. You can actually even see it a little bit when, if you watch the Plant Chompers episode, when I announce it, I'm a little bit manic because I had just started it. And you can ask Dave— when people are watching this, tag Dave Feldman and ask him how I was on the Oreo cookie phase. I was nutty. I'm actually thinking about going back to the Y where I was working out at the— at that point in time, because even the trainers were like, what's up with this? What's up with Nick now? Is he like on pain or something? And I was up and down and all over the place. It really— it, it, it threw me off pretty hard. And I kind of knew that was a possibility just jumping into it, going from 0 to 100 with the protocol. But yeah, I just committed to it and went for it. So the Oreos were—
did it track with your blood sugar? Did it track with your blood sugar at all? Do you know?
I wasn't wearing a CGM. I didn't have one at the time. I was finger sticking and, you know, I would have a bump postprandially and then it would come down. So it wasn't like I was shooting up to crazy high blood sugars or crazy low, but I didn't sleep super well. I had obviously stomachaches for that period of time. No, it was not fun. How about you? Any means.
How about your first Oreo though? Like, you know, did you go back to the time where you were a kid and ate Oreos and was it like, oh, this is great? And then— or was it just bad from the beginning?
Very disappointing actually. I loved Oreos. Yeah. And I thought I'd have it and be like, all right, this is gonna like be unpleasant in terms of my GI side effects, but it's gonna taste good. It did not taste good. Yeah. Because— and I'm not sure why this is. I think part of it is I've habituated to keto, so I'm, I'm used to super rich foods. So the cream didn't even hit it. It wasn't like at the threshold I need for richness. And then the biscuit felt a little bit dry. So I remember Oreos being so hedonically pleasurable as a kid, and I didn't even get that, which was disappointing. And people asked me, actually, like Sean Baker asked me, are you gonna add a supplement where you compare Oreo flavors? I literally thought of that, but different Oreo flavors have different macros. So I couldn't, so I had to stick to my variables. Um, but I did learn a lot about Oreos during that point in time. Oreo history. The fact that a Double Stuffed is apparently only 1.86 times stuffed, et cetera, et cetera. It was, it was an experience. The statin had some side effects, but they were pretty mild. I had myalgias and an elevated creatine kinase at 3 weeks, mildly elevated.
So myalgias meaning muscle aches and then elevated—
My calves mostly. It was pretty mild. My PCP wanted me to actually stop at that point because I had an elevated marker of muscle damage, the CPK, and myalgias, but it wasn't that elevated. So it was more just unpleasant, not unsafe. So we decided to stick it through. But even my consultant cardiologist said, yeah, with these symptoms and this, this CPK, we probably would stop you eventually. But for 3 extra weeks, because it started at week 3, it wasn't unsafe. So, um, neither were ideal. I will say for side effects alone, I would preference the statin because the Oreos were not pleasant on my, uh, sensitive, my sensitive tummy. Although I used to love them. We used to eat them by the sleeve when I was a kid. In fact, I think my brother blames me for his kind of chunky phase when he was little. We would just sit there and just eat, like, you know, the 3-sleeve packs, the really big ones. I mean, split that. We were both tiny, but he was more prone to putting on weight. So then—
Yeah, but it is, it is such a great lesson about what happens when you eat real foods and you cut out the processed, you know, junk food. And then what used to be so pleasurable is no longer. And that's just such a testament of how we're— we don't have to be slaves to the processed food industry, that we can change our taste, we can change our taste buds, we can change our perception. And I think that's another really important part out of this.
It's really an interesting conversation to have. Now going on a tangent, because there's the personal response, which is so shocking that people who haven't gone through it can't empathize with it, can't really like appreciate the fact that you're being genuine when I say, honestly, I don't want the cake. Like, I can get more pleasure out of like a few frozen cherries. And I'm perfectly happy with just like some eggs and salmon. And I don't know how you are. Me, as quite, you know, a 28-year-old guy who, you know, tries to be at some level social, it's a difficult thing to communicate. And sometimes you find yourself just eating food just because you— just for social reasons, because people won't believe the, the, the taste recalibration you'll have. I was trying to explain this to my Um, actually, I'm not going to go there.
We're—
I'll put the conversation there. I was going to go on my tangent, but yeah, I get what you're saying.
Yeah. Yeah. Well, I mean, look, it— I think this is accomplishing exactly what you want it to accomplish. It's outrageous. It is click-worthy and it raises the question and is going to drum up a lot of discussion. Um, so what's next?
You're—
it seems like you're always doing something. You've already got— always got a bunch of irons in the fire. So what's next?
Yeah, I can't talk about everything that's next, but I will say we're trying to get a lot going with Lean Mass Hyperresponders. 2024 is going to be a huge year. And, um, this whole journey for me is about engaging as many people as possible along the way, um, and also leveraging that engagement to push the research forward. So this is the kind of thing that I think you know, everybody listening can, could actually make a material contribution to, not only, you know, just, just through engaging and providing the morale boost that we really appreciate from the nice comments, but, um, as we mentioned, the discussion and the science is driven, um, by engagement metrics. So doing things— and this is me just being perfectly transparent— doing things like if you share the, the paper link in this video, if somebody takes the paper link it puts it in an original tweet on Twitter. Those kind of metrics get tracked for, you know, how many people are engaging with it, how many people are posting the video, sharing, or posting the link to the paper, sharing the video. So the best thing people can do is watch the video abstract and, you know, click on the paper link, share the link in an original tweet. Those kind of things really actually help boost engagement, we're finding, and push the conversation forward. So again, the purpose of this was to provoke, and we can, you know, track those engagement and provocation metrics, and people can help demonstrate that, you know, what we're doing is interesting by doing what I just said— share the paper link on Twitter with your comment. We'll definitely be reading and replying to them. So if people could do that, that's my call to action, and I'd appreciate it greatly.










