Measure THIS Blood Marker to Predict Heart Damage from Obesity

Obesity is a major risk factor for heart disease. But how? And why? Is it just a correlate? Or is there something about fat tissue that directly damages blood vessels and the heart? Well, breaking new science gives us insight into the biological truth, and it lays the groundwork for innovative solutions. In this video, we're going to review this new science, tell you what specific blood work you can check to gain insights into your metabolic health and vascular function, and reveal nuances about the crosstalk between fat tissue and blood vessels that will have your cardiologist head spinning. Oh, and before we go any further, I'll just tease, yes, the controversial topic of seed oils does make an appearance, but in a rather nuanced and unexpected manner. Canola oil is toxic. Now, let's begin first with the human study. Researchers took patients with obesity and BMIs of at least 37 kilograms per meter squared before and after they underwent weight loss surgery, bariatric surgery, and they compared them to lean people. They were comparing them for blood vessel function and an important biomarker called myeloperoxidase, or MPO for short. Now let's unpack each of these a little bit more— blood vessel function and MPO. There are different ways you can measure how well your blood vessels are functioning. And this is critical to overall heart health and metabolic health. No surprise, right? Blood flow's kind of important. It's the river and the streams that feed your organ with oxygen and nutrients. And one way to measure blood vessel function is with a metric called flow-mediated dilation, or FMD for short. Flow-mediated dilation is a measure of the body's ability to widen blood vessels in response to increased blood flow so you can get nutrients and oxygen where they need to go. The researchers found that people with obesity had worse flow-mediated dilation— they had worse blood vessel function— than lean people. Furthermore, flow-mediated dilation, blood vessel function, improved with weight loss after bariatric surgery, and there was an inverse correlation between body mass index and flow-mediated dilation, suggesting at a high level, worse obesity—excess body fat—contributes to worse blood vessel function and vice versa. But now, what about myeloperoxidase, this NPO biomarker? Well, NPO is a blood marker of oxidative stress and actually itself an enzyme produced by inflammatory immune cells. NPO generates potentially harmful reactive oxygen species and chemicals like hypochlorous acid, or HOCl. These can damage blood vessels, and MPO also leads to the oxidation of LDL particles, contributing to the progression of cardiovascular disease. Interestingly, the researchers found that MPO correlated with body mass index, suggesting Worse obesity, more MPO, which could explain the relationship between excess body fat and worse blood vessel function in poorer cardiovascular health. It certainly seems to be a part of the puzzle. But it gets more complicated and more interesting. You see, MPO floats around inside blood vessels and can hurt them from the inside out, directly damaging blood vessel lining and oxidizing LDL particles, as I mentioned. But there is also fat tissue around blood vessels. This is called perivascular adipose tissue. Peri means around and adipose tissue is fat, so this translates literally to fat around blood vessels. It's named quite logically. And myeloperoxidase, MPO, in the perivascular adipose tissue can also harm blood vessels from the outside in. So inside out and outside in. It's like a metabolic pincer maneuver. And what the researchers show throughout the rest of this paper is that the myeloperoxidase, the MPO, inside the perivascular adipose tissue is a signal that inhibits important beneficial metabolic properties like the browning of fat tissue to burn more energy and the generation of the hormone adiponectin. So, let's dive a little deeper into each of these nuances. There are different types of fat tissue with different metabolic properties. Brown fat in particular generates heat and burns more energy, providing some protection against obesity. White fat, which is more typical in adult humans, can take on brown fat properties in a process called browning, or more technically, beijing.. And myeloperoxidase, MPO, inhibits this process. It inhibits fat browning. This means more myeloperoxidase, higher MPO levels, less browning in Beijing, less energy burning from the fat tissue around blood vessels. And you can see how this sets up a potentially vicious cycle whereby excess fat and less healthy fat tissue leads to the buildup of even more unhealthy fat. And they even showed in this paper that in genetically modified mice, that had MPO eliminated, so the knockdown of myeloperoxidase, so it was super low, this protected against diet-induced weight gain and it improved blood vessel function. I also mentioned the hormone adiponectin. Adiponectin improves blood vessel function, making blood vessels less stiff. You can kind of think about it, if you want a goofy analogy, as adiponectin is basically yoga for your arteries. Make sense? So more myeloperoxidase means less adiponectin. MPO inhibits adiponectin production, and this means stiffer, worse functioning blood vessels. And what's more, adiponectin itself inhibits myeloperoxidase. So reduction in adiponectin leads to the generation of more myeloperoxidase, which further reduces adiponectin. Setting up yet another vicious cycle. That's concerning to say the very least. But I don't mean for this video to be just doom and gloom. I mean for it to be empowering because you can measure and modify your myeloperoxidase levels to improve your blood vessel function and overall metabolic health. MPO is in fact a blood marker you can get ordered at many labs. And now you understand what it means. I wonder if your doctor does. Now, it's true, I'll call out, that when you're getting the blood test, you're not directly measuring MPO in your perivascular adipose tissue, but the two are thought to correlate pretty closely. Plus, and this is the important thing, there are many things you can do to potentially modify and track your MPO levels over time. For example, there are early data showing that the mineral zinc and the amino acid taurine, which is being studied a lot in the longevity space, can help reduce myeloperoxidase levels. Granted, supplementations with nutrients, like zinc, tend to be most beneficial in those who have a deficiency, so I'm not going to say it's going to benefit everyone. There's also data suggesting that statin drugs also decrease MPO. I know that might be controversial, it's a controversial topic, but there's little doubt that the pharmacological effects of statins are multifactorial. In other words, the The benefits in some patients due to statins are not simply due to LDL and ApoB lowering effects. One drug can have multiple effects, and the decrease or inhibition of myeloperoxidase by statins may be a mechanism by which some patients derive protective benefits. That's not medical advice, but I invite you sincerely to contemplate this possibility with an open mind. It's always a good exercise to play devil's advocate. For both sides. Additionally, and even more interesting to me, the sleep hormone melatonin at both physiologic and supplemental doses can inhibit MPO via multiple pathways. Personally, I'll just be honest, I do supplement with melatonin, but the point I actually want to leave you with is that this could be a way by which proper sleep hygiene could directly impact your blood vessels and cardiovascular health. The cascade of events I'd like you to imagine is that sleep and better melatonin levels leads to the inhibition of MPO and, at least theoretically, improved perivascular adipocyte browning and increased adiponectin to make your blood vessels more flexible and blood flow better. The point is, the big point is, there are many steps you can take to modify your myeloperoxidase levels, lower them, and improve your health. All that said, generally the most important and impactful intervention is to reduce excess body fat and improve your metabolic health. I know that's not satisfying or directly helpful, but it's the truth. So the fundamentals remain key: reduce your sugar intake as best you can, get exercise, get sleep, and so on. And I wanna just name, this is not fat shaming, it's fat explaining. I know these metabolic discussions can become entangled with obesity bias, weight stigma, and important psychosocial complexities. But biology remains biology, no matter what is PC and what's not. And metabolism deserves to be acknowledged and explained. That's at least how I feel. And because I clearly seem to gravitate towards controversy, I'll just add this little tidbit: that the omega-6 fat linoleic acid, which is at the heart of the seed oil debate, if you follow that, can and is oxidized by MPO to form various oxidized products like hydroxyoctadecadinoic acids. And in theory, this could provide a biological link whereby excess linoleic acid, including excess dietary linoleic acid, can exacerbate oxidative stress and inflammation in those with obesity. To be clear, I'm not saying don't eat nuts, or that butter beats tahini, or any of that. I'm just planting a seed, hehe, punny, for curiosity and food for thought. There are many hard and controversial questions still to unpack about obesity, and that's the fun part. Now, tell me in the comments, have you ever measured your MPO levels? And if not, Will you? Finally, my only ask to you is, if you found this video helpful, informative, or just a good excuse to nerd out on blood vessels and biochemistry, please hit that like and subscribe button. Because let's face it, if your fat's talking behind your back to your blood vessels, the least you can do is eavesdrop. Stay curious. I hope you found this useful.