Transcription
Welcome back to the centrifuge, where we separate fiction from fact by applying studies to claims made on health shows. In this episode, I'd like to go over some content released by Mr. Thomas Dauer. Thomas Dauer is, according to his website, an expert in nutrition, fitness, and mindset.
In this episode, Mr. Dr. Dauer discusses how mass doses of vitamin D can make unbelievable results on your muscle growth, fat mass and metabolism. So, vitamin D supplementation changes two key hormones related to muscle and metabolism. Vitamin D increases muscle mass and redirects how the body uses calories. And people with more vitamin D related genetics grow more and have an advantage. With that said, let's spin it.
There was a fascinating animal study that recently tested this entire thing in a pretty extreme way. So, researchers raised vitamin D levels in mice far beyond the normal range. Like way beyond what we would normally even look at. They went from about 2,000 IUs per kilogram all the way up to 10,000 IUs per kilogram. We're talking crazy dosages. But what they saw happen inside their fat and muscle was nothing short of amazing.
Now, leptin and myostatin are sort of like opposite ends of a metabolic seesaw. So, leptin is released by fat. It tells your brain, "We have enough stored energy. Feel free to turn down the metabolism or feel free to crank it up." Right? Myostatin comes from the muscle. It's the brake pedal that prevents muscle from growing too much. So when scientists knock out vitamin D receptors in fat cells, meaning they basically made it so that vitamin D couldn't be received by a fat cell, they found that leptin production tanked. So the body couldn't properly sense energy stores anymore. So when they knock out those same vitamin D receptors in muscle, myostatin shot through the roof and muscle growth shut down.
This one is a bit complex, but we can say that the claim is that vitamin D changes two hormones, leptin and myostatin and their impact on our muscle and energy state. So, we're still setting things up here, but I appreciate Thomas's mention that this is a preclinical mouse study, though he ends up discussing some human evidence later, too. Still, this initial idea here is that there's this interplay between vitamin D, leptin, and myostatin. And Mr. Dauer is exactly right that leptin is generally secreted by fat cells in response to energy status in the body. If leptin is high, the brain cells called neurons in control of hunger are bound by leptin and suppressed because it's a feedback for enough energy present in the body. On the other hand, myostatin is a hormone released by our muscle cells and it acts as in what's known as an autocrine fashion, meaning that it is released and then it binds to the receptors on the very same organ, the muscle that it was released or secreted by. When bound, myostatin changes signaling inside the muscle cells to prevent muscle growth.
The first point in relation to these hormones is when vitamin D is knocked out, leptin, this satiety and energy regulation hormone tanks. One correction that I kind of have to throw in here for accuracy, the researchers of the study that Mr. Dau is referencing which he did provide in his linked video did not knock out the vitamin D in fat cells specifically. This is usually done through genetic manipulation and the researchers did not use any direct genetic techniques in this study. What they actually did was give mice a standard amount of vitamin D, a very high vitamin D or none at all. And they do mention that other studies have done these genetic manipulations where they knock out vitamin D and those studies do show that leptin is dropped. This was confirmed in this study that we're going over shown here. So we're measuring leptin concentration and the normal vitamin D consumption had higher leptin levels than both of the no vitamin D condition that we've been focusing on and the high vitamin D.
Thomas then mentions that because of this difference in leptin, the body couldn't sense energy stores anymore. Now, I would not agree. The reason is that the researchers only report the food intake for the normal and high vitamin D groups. This leaves us with incomplete data because we don't know how much the mice with no vitamin D were consuming. Honestly, I find that omission slightly puzzling, but there may yet be an explanation that I'll get into later. In fact, countering that point, body weight was identical for mice with no vitamin D consumed compared to those consuming vitamin D. So, the line of thought doesn't pan out based on closer inspection of the data.
Mr. Dauer makes the same mistake when discussing the vitamin D receptors in the muscle and the relationship to myostatin. It's true here that when mice were not fed vitamin D, they had an increase in this muscle inhibiting hormone. But again, this was not a genetic knockout. Unfortunately, again, when lean mass was measured, which is a general proxy for muscle, though it is imperfect, there were no differences between normal vitamin D consumption and no vitamin D consumed. In fewer words, the correct interpretation here to set up for future looks at vitamin D is that consuming no vitamin D leads to a drop in leptin and an increase in myostatin, which would suggest a change in food intake and a reduction in muscle mass. However, upon further inspection, those suggestions appear not to be accurate. So, all we truly have is a change in the hormonal profile so far. Let's continue and see what happens next.
>> Remember, myostatin is the brakes. So, this posed the million-dollar question. What if we increase vitamin D above normal levels? Can we actually tune both systems at once? So, here's what they found. The mice that were on high dose vitamin D didn't just get stronger, they changed how they got stronger. Their grip strength increased significantly more than the normal vitamin D group. Their lean mass went up, but their total weight didn't budge. What that translates to is that the body redirected calories from fat storage over towards muscle construction. So, think about that. Without changing total food intake or activity, the energy economy of the body just got rewritten and it completely changed where we put calories.
But that's just the surface. Since we initially looked at a lack of vitamin D, we're now shifting our focus to raising vitamin D. The claim being that raising vitamin D improves lean mass and muscle function by redirecting calories to muscle. Unlike the previous section, Mr. Dauer gets a lot right here. For example, we saw that the the data on screen for a moment, but without explanation, it usually just leaves people without a clue on what's happening. So, breaking this up, we can look at lean mass again. Same exact thing that I showed you a few minutes ago. And while yes, there were no differences in the comparison that we discussed before, there were differences between the high vitamin D and normal vitamin D, as in higher vitamin D intake yielded more lean mass. Can we necessarily jump to the muscle mass? Not necessarily because lean mass is a bit of a dirty marker when it comes to qualifying muscle as lean mass consists of water, cartilage, bone, and other lean tissue, not just muscle. But if we pair that with significant improvements in muscle function shown here, pretty remarkable increases in the high vitamin D group. As for the argument that calories are being rerouted to muscle, more specifically nutrients, that's certainly a possibility considering that the lean mass was increased and grip strength was increased and fat mass is reduced. So the takeaway here being that I think that the claim is fair. Increased vitamin D consumption raises relative lean mass and improves physical performance in this preclinical study.
When the researchers looked at myostatin, which is again the muscle growth brakes, the muscle growth inhibitor, they found something subtle but powerful. Normal vitamin D dropped myostatin levels, which made sense. But high-dose vitamin D took it further by decreasing the average amount of myostatin produced per unit of muscle. So as muscles grew, they became even more resistant to the the break. So the stop growing signal. And on the fat tissue side, leptin behaved almost in reverse. So, normally more fat equals more leptin. That's kind of like why leptin resistance happens when people gain a lot of fat. But with high vitamin D, fat tissue started producing more leptin per gram. This means that the brain got a stronger signal like that energy is good. We're fine without adding fat mass. So, the metabolism increased without gaining fat. Right?
But here's where the plot kind of thickens and it gets a little twisted. The mice in this study didn't eat more. They did not move more, but they magically burned more energy even after they adjusted for body composition. In other words, vitamin D didn't just boost motivation or movement, it boosted metabolic activity itself. So, if we take a step back and we kind of reel all this back and we look at what this means mechanistically, raising vitamin D from low to normal increases leptin production. So, that's your first step towards balanced energy. But raising it from normal to high increases leptin sensitivity and simultaneously suppresses myostatin signaling. It's almost as if the body moves from this stored preserve mode into build and repair mode. So calories stop stacking up in fat cells and they start heading towards muscle growth and potentially even linear growth. So meaning tissue expansion, meaning more repair, more vitality, literally signaling life like repair, grow, proliferate. Don't just break down and store fat.
I'm gonna pause here and instead of covering the myostatin and leptin angle again, which is what was discussed at the beginning, I'm going to skip it. One, because we've already covered it. And two, because the data that the researchers are basing these claims of myostatin per muscle mass and leptin per gram of fat are based on some correlations and definitely some assumptions like the idea of increased leptin sensitivity is raised in the brain. Yet, no measures were actually made. The novel introduction is the inclusion of the metabolism aspect, as in the claim being that the mice didn't move more. They didn't eat more and yet somehow burned more energy when consuming high vitamin D. That's all true. Although, as a quick point, physical activity, while measured, was never shown. So, we're basing that on faith. I think that the bigger point is that we're looking at a mix of decent and low-quality evidence, and we're extending the conclusions further than they probably should be extended. Not necessarily because this is an animal study, but because we're discussing speculations, correlations, direct intervention data, and omitted data together into a confusing mess where everything is considered the same playing field.
So, here's what the data says, and then I'll return to something that's going to be pretty telling. I think this pre-clinical study clearly indicates that normalizing vitamin D intake can raise leptin and reduce myostatin. It also indicates that physical function improves and even more so at higher doses of vitamin D, including increases in lean mass at higher doses of vitamin D. And finally, it tells us that very high vitamin D intake raises metabolism independent of increased physical activity.
Now, I've mentioned a few times now where I'm unimpressed with this study, and some of the more science-minded of you might think, well, how did this pass peer review? For example, omitting the intake of food for the no vitamin D condition. Well, the reality is it hasn't passed peer review. This paper has been in preprint, as in not published, in a peer-reviewed journal for almost two years now, but it keeps being picked up and hailed as the savior of vitamin D. This isn't actually the first time that I've seen it, and I was excited to cover it until I realized how speculative everything was. My guess is that when it does get published, assuming that it does, though I think that it will, the reviewers may ask for more work and more data to be presented. In fact, that may be exactly why the study is still locked in preprint because the peer reviewers can ask for a lot if they feel that it's necessary. Now I don't know the story but the point that you should know which wasn't mentioned is that this study remains unpublished at the time of this recording and has been for 2 years now.
But let's move on from the animal data. Let's get into the human research related to this topic. Before we get to that human research which I have some opinions to share. If you're looking for more on the research within this study that we've been going over or how supplementing vitamin D might affect muscle growth, I cover a few more studies for the Physionic Insiders in my full analysis, including an extended breakdown of everything that we've been over. Or if you prefer to read it all, it all comes in a written article as well and a podcast and more like these perks right here. If you're a game, then you can join the Physionic Insiders using the link in the description. Hope to see you there.
So yeah, I've talked a lot of animal data. What about the human stuff? Let's take a look there because this is where it gets interesting. If this energy allocation mechanism really exists, we should see traces of it in our own genetics, right? And that's exactly what the researchers have been looking for. They analyzed massive genome-wide association studies. So one for vitamin D levels and another for height. And they found that there was a consistent pattern. So genetic variants that increase serum vitamin D also tend to increase height. Now that doesn't mean that taking mega doses of vitamin D is going to make you taller. But what it suggests is that people genetically wired for higher vitamin D operate with a metabolism that is more growth oriented where energy gets used for building not for hoarding. So this manifests in more height as you're growing or possibly more muscle as you're older. So when we see people with naturally higher vitamin D levels having better muscle quality, having leaner body composition, better insulin sensitivity, that's not necessarily coincidence. It's part of the same signal.
Yeah. The claim here is that there is a genetic translation to humans in that people with elevated vitamin D will grow to be taller and possibly more muscular due to this nutrient partitioning that happens with elevated vitamin D. There's definitely some truth to that as researchers included a Mendelian randomization study inside of this mouse study that we've been going over. Essentially, they look at thousands, if not millions of people with specific gene mutations that cause them to have lifelong elevated vitamin D and then measure their growth and plot that data, creating a link between the two. To Mr. Dau's point, the researchers show that there is a relationship between those with genetically elevated vitamin D and growing taller. I also really like that he mentions that doesn't mean that supplementing with vitamin D is suddenly going to make you taller. He's spot on there. I take it a step further, though. I think that the inclusion of the Mendelian randomization data is a nice touch and it speaks to the general relationship between higher vitamin D and the partitioning toward growth. But it's definitely stretching in this context because growth for height occurs in childhood and a bit in in adulthood and does not occur later. The researchers are trying to point to this as further evidence that vitamin D can promote growth in the right i.e lean tissues. But we're still making a huge leap to go from data in primarily young growing humans to what we're looking at here in adult mice. Aside from the different species, we're talking about two different periods of life, childhood versus adulthood, and two different measures, height versus muscle and physical function. So, it makes me wonder, why not use similar vitamin D genes and relate it to muscle size in adults or physical function? It's possible that the researchers didn't have the access to that data, but if it were possible, that would be far more telling than what we're examining here. The point here being that I love Mendelian randomization studies, but in this context, it misses the mark on multiple fronts. I don't find this altogether compelling evidence.
Now, for the rest of the evidence, Mr. Dauer goes into a cell study using human cells and another animal study. Now, I can tell you right now that considering that there's no additional human research presented, these studies could claim to eliminate all disease and it wouldn't make a difference on the conclusions. So, let's discuss what we can and can't take away from all this. Uncross your eyes. I'd like to also acknowledge that Mr. Dauer does also mention, but here's the part that people kind of get hung up on when they take vitamin D. They they don't really necessarily do it right. They skip this part, which is how to actually keep that vitamin D machinery going all day long because supplements work when you're deficient, and they definitely have a place just to take a regular vitamin D supplement. But I think we need to understand a bigger like playbook here.
>> He's right that the biggest bang for your buck is when dealing with deficiency in vitamin D. I think that's an important point that he brings up. And beyond that though, he later gets into different foods that raise vitamin D and begins discussing some of what we've uh been over as if it applies to humans. What have we kind of recapped and learned in this video? We learned that it tunes leptin and myostatin. So you're balancing energy between fat and muscle. Okay. Then we saw that high vitamin D reallocates calories, right? So it's burning more energy at rest. It's influencing growth patterns in the muscle in humans literally. And finally, we saw that vitamin D directly amplifies the literal molecular machinery that builds muscle. So it's that simple.
Now, if you wanted to take a straight up vitamin D supplement, you could absolutely take higher dosages. Okay? You can reach a level of vitamin D toxicity if you're not careful. So, what you want to do is if you're going to titrate your dose up, A, make sure you have enough magnesium on hand, okay? B, add glycine into the mix. Glycine is going to help kind of give the liver a little bit of help with potential detoxification, which allows for better synthesis of vitamin D in the first place. Okay? So, take three to five grams of glycine or good collagen supplements, right? But then what you want to do is you want to get your blood work done. Vitamin D tests are cheap. They're inexpensive. And if you start increasing that dose, do a quick vitamin D test every two to four weeks and make sure you're not getting yourself into an upper level that's too high. Okay? You do want to be on the high end of normal, but you can get more done with the sun if your nutrition is in line. Okay? There's a lot more going on than just pure simple vitamin D. That's like saying, "My testosterone is low." Why is your testosterone low? I don't know. Just give me testosterone supplement. But what's going on, right? Same with vitamin D. It is a hormone and there's a lot of different things feeding into it.
>> I want to be clear here. The evidence that Mr. Dawer presented is weak and does not apply to humans. Suddenly presenting this as if we can raise our vitamin D and potentially get these effects based on the data presented is not giving enough weight to the fact that these studies are not translational. I'm also baffled as to how we went off the rails and started throwing magnesium and glycine into the mix for these mechanisms considering that we didn't cover any data on that adventure. That's complete speculation. Even if there could be data on the benefits of magnesium and glycine, they just don't necessarily apply to this context. Okay, enough babbling on my part. Mr. Dau goes over some fascinating mechanistic research and it's certainly an exciting possibility, but that's where it should remain. Early incomplete research presented here indicates that vitamin D supplementation raises the energy status and the hunger hormone leptin and reduces the muscle inhibition hormone myostatin. This same research indicates that high-dose vitamin D raises metabolism independent of physical activity and improves physical function and increases lean mass. None of the research in isolation or combined as presented offer compelling evidence that vitamin D does these things in humans. So supplementation or optimization for that end goal is premature. Though I do recognize that vitamin D is important for general health.
But hey, the fun doesn't need to end there. There's more centrifuge episodes right here. Happy to nerd out further with you if you're up for it. Anyway, I'll see you in the next one. Thanks for tuning in. Bye.