Oreo Statin Data LEAK!

Okay, so the cat is out of the bag, or at least half the cat. It's the morning of November 27th, 2023, and, um, many of you may have noticed yesterday on X, Dr. Shawn Baker leaked data from, uh, phase 1 of my Oreo versus statin crossover experiment, which was announced a few months back, sharing that in just 16 days, um, I lowered my LDL cholesterol from near 400 mg/dL to 111 mg/dL by eating 12 Oreos per day. About a sleeve of Oreos, about 100 grams of carbs in Oreos. So in this video, I want to cover the who, what, why, how, and where of this Oreo versus statin experiment for those getting up to speed. So, who? Um, for those of you just getting to know me, um, my name is Nick Norwitz. I received my PhD from the University of Oxford in human metabolism. And I'm currently a third-year medical student at Harvard Medical School. I'm a recreational athlete with a rather intense history. I, uh, I think I still hold the Massachusetts state push-up record. In late 2013, I did 427 push-ups in a single set to a 3-second military-style cadence, monitored. And my marathon, um, personal best is 2 hours 40— These are details that I usually don't share in a video. Actually, I don't think I've ever shared them in a video, but you may see why they're somewhat physiologically relevant and informative shortly when we talk about the lipid energy model. I'm also an example of a phenotype called lean mass hyperresponders, or LMHR for short, which is a subject that, um, colleagues and I, including, uh, Dave Feldman and Dr. Adrian Sotomota, have been studying for the past few years. Lean mass hyperresponders are people who, upon commencing a very low carbohydrate, usually ketogenic diet, exhibit changes in their lipid markers such that their LDL cholesterol is above 200, their HDL is above 80, and their triglycerides are below 70. Those cut points were chosen historically and are the topic of, uh, other videos and for further discussion. But typically these people are lean and athletic. In fact, there's actually an inverse association between body mass index, BMI, and LDL cholesterol change on ketogenic diets. Um, in other words, the leaner people tend to have larger LDL cholesterol changes, and I'll get back to why that might be in a moment, but it's something that we've published on in the literature and with confirmatory studies coming. So I'm pretty confident in that inverse association. But again, topic we can discuss in depth in another video. So, um, what? Well, I've buried the lead a little bit, but yes, I'm doing an experiment comparing, um, Oreos as an intervention to statins for LDL cholesterol lowering in a lean mass hyper-responder myself. Of note, I really do wanna highlight I'm doing this with the supervision of my primary care provider, with cardiology input and with appropriate ethics applications. I'm not just going rogue. The protocol was designed a priori and announced and was going to consist of roughly 2 weeks of Oreo cookie addition to my diet to a standardized baseline ketogenic diet, specifically adding 12 Oreos per day, which is 4 servings of Oreos, which is about 100 grams of additional carbs to my diet. Now, of note, this was in addition. I did not swap it out for other foods. Thus, fat, saturated fat, and fiber intake were not decreased, but actually slightly increased overall. Um, after the Oreo intervention, which obviously has completed, I underwent a, uh, sufficient washout period of several months. And have recently started the statin phase. The statin phase was determined to be rosuvastatin for 20, at 20 milligrams for 6 weeks. The statin dose and duration were determined as the maximum starting dose of rosuvastatin that my doctor would actually prescribe me, and the duration as the standard FAIR trial for statin therapy. 6 weeks, as communicated to me by 2 separate cardiologists. I did get cardiologist and lipidologist input while designing this protocol. So my hypothesis was that Oreos will actually lower my— not generalizing here— my LDL cholesterol similar to, or possibly to a greater extent than, the moderate to high dose statin therapy. And my rationale for this is that the Oreo consumption will address the root cause of my elevated cholesterol, my elevated LDL in particular, according to the predictions of the lipid energy model, which I will get to shortly. So, um, but before that, I do want to talk about why I'm doing this experiment, because some people are going to try to tell you that this experiment is trying to make a mockery of statins or show that Oreos are a health food. Neither of those are true. And honestly, if you're an adult human being and someone is able to convince you that Oreos are healthy you probably have other problems. But that aside, my purpose in doing this rather rigorously controlled n=1 experiment is admittedly provocation. I want to provoke discussion, to stimulate thought and force forward a conversation, and following that, research about a phenomenon that needs further study: the LMHR, Lean Mass Hyperresponder phenomenon, and the mechanism behind it, the lipid-energy model, and of course the risk that may or may not be associated with lean mass hyperresponders with respect to cardiovascular disease. So clearly, Harvard medical student massively lowers cholesterol with Oreo cookies is provocative. It's supposed to be. But it's not supposed to end any conversation. It starts— it's supposed to start one. But I'm going to leave that topic and the, you know, associated topic of science politics for for a longer-form conversation for later, which will come in one form, one platform or another. But now, the how. How did this work? How did I predict it would work? How did Oreo cookies lower my cholesterol, my LDL cholesterol specifically, from near 400 to 111 milligrams per deciliter, as revealed by Dr. Shawn Baker, Yesterday. The answer is the lipid energy model, the skeleton of which I have to afford credit to Dave Feldman, who over the past couple years together we've kind of fleshed out with the help of many others. So thank you to the scientific community who has contributed. The model works briefly as follows. In lean people, who go on very low carbohydrate diets, liver glycogen gets depleted and there is a demand from fat, or demand for fuel specifically from fat as compared to glucose, again, because liver glycogen is depleted. So circulating fatty acids that have been released from fat cells go up to feed local oxidative tissue like muscle tissue, but they also circulate around in the blood, and are taken up by liver cells and resynthesized in the liver into the storage form of fat, triglycerides. So you put the fatty acids, 3 fatty acids on a glycerol backbone, you get a triglyceride. And the triglycerides are shipped out of the liver on these very low-density lipoprotein particles, these VLDL particles, as part of a systemic fuel trafficking system to get energy back to muscle and depleted fat cells. So in the periphery, um, muscles and fat cells, an enzyme called lipoprotein lipase quickly turns over these VLDL particles, these very low density lipoprotein particles, depleting them of triglycerides. So there's spheres, and in the middle are packed triglycerides, and those triglycerides are harvested to fuel hungry muscles and replenish the small fat cells. And this turnover process actually shrinks the large VLDL spheres into their descendants, you could call them LDL particles, thus increasing LDL cholesterol, and also increases HDL cholesterol as the surface of the VLDL shrinks down and is picked up by HDL cholesterol. So LDL cholesterol increases as the VLDL actually turn into LDL and HDL cholesterol increases because the shrinking of the sphere requires that there is decreased surface area, and cholesterol from the surface then gets picked up by the HDL lineage of particles, resulting in decreased triglycerides from the depletion of the VLDL, and then increased LDL and increased HDL from the turnover process mediated by lipoprotein lipase. And so you can see how this results in the metabolic triad of high LDL, high HDL, and low triglycerides that typifies lean mass hyperresponders. Now, I didn't explain here in this brief review why it's particular to lean people, which has to do with hormones like insulin and leptin, and why there's an inverse association between BMI and LDL change, but you can find explanations for that in the link below the video to our published peer-reviewed paper on the lipid-energy model complete with references. So, um, at this point it's also probably worth sharing that lean mass hyperresponders like me typically have normal LDL when they're not on a ketogenic diet. So adding back the Oreos and making my diet, quote, mixed, repleting my hepatic glycogen stores, basically started to bring my LDL back to what it would normally be on a mixed diet. My LDL on a standard American diet prior to going keto was 95 milligrams per per deciliter, and the addition of Oreos was trending me back in that direction. We also tend to test negative— we being lean mass hyperresponders— for genetic mutations that could explain the phenomenon, the lean mass hyperresponder phenomenon, the inverse association between BMI and LDL that I've described. And indeed, I've had a whole exome sequence by Veritas with no clearly informative polymorphisms. And quite honestly, if you want me to look at my own exome for SNPs, just let me know the RS code below in the comments. I will check and I will report back to you. Happy to do it. I am also negative for phytosterols in the blood. I don't have cysteineemia, and my LDL does in myself run inversely to BMI over time, an effect that definitely dominates over my saturated fat dietary content. In fact, my LDL cholesterol peak, which was 545, mg/dL occurred on a pretty low saturated fat diet, which I've published about before. Low saturated fat relative to MUFA/PUFA. Um, my MUFA/PUFA intake was like 80%, uh, above 80% actually of my total fat intake, with less than 20% saturated fat. Um, other little details are that on a ketogenic diet, my HDL does tend to run between 90 and 125. 5. It's more normal on a mixed diet, again closer to 50-60. And my triglycerides, um, run quite low between 30 and 65, which is pretty typical of a lean mass hyper-responder. So now the where. Where are we now? I've, um, recently commenced the statin arm of this study, and I hope to have the results ready to share early in the new year. And finally, I do want to impress that this n 1 is not the bomb drop. It's only a head-turner to get you to look this way for the bomb drops, plural, to come. We have other big projects, colleagues and I, with more robust, um, data regarding lean mass hyperresponders in the lipid energy model to come, um, probably in 2024. Several papers that we're really excited about. So I want you to watch this space. Again, this Oreo experiment was a provocation, a provocation for a discussion that really needs to happen. Have a good day.