How to Slow Aging for $0.06 a Day

Scientists just found a way to slow a specific form of biological aging for 6.2 cents per day. Not in mice, in primates, monkeys. And when I tell you what molecule did it, you're gonna wanna click off this video, which is exactly why you shouldn't. What's this, what's this? Vitamin C. Vitamin C, yes. But don't be fooled by the apparent mundaneness of this molecule, because how it works and why it works is where I'll really blow your mind, where my mind was blown. When you realize something you thought was one thing is actually another. When what seemed like overhyped influencer claims meets rigorous science, and when a YouTube video teaches you something cooler and higher yield than you probably get from an entire nutrition degree. Let me prove it to you so you can see what I see. You can optimize metabolic processes to reduce the damage. Biological aging is not a metronome. Your cells are hoarding iron like they're some Iron Golem. The researchers screened a range compounds, 100 molecules, the humble vitamin C prevented brain shrinkage. Now, real quick before we begin, if you want much more deep dives into metabolism, to come down the rabbit hole with me, you should really check out our best-selling science newsletter, Stay Curious Metabolism. This is where you're always going to get first access to breakdowns like this one, extra nuances, and oceans of information that don't even make it to video. Find out why it's the fastest growing premium letter on the Substack platform. But with that, let's get to our nutritional longevity quest. Here's our map. Part 1, we're going to talk about a new cause, a new type of aging. Part 2, I'm going to give you proof that it's happening in me and you right now. Part 3, we're going to investigate how to slow this form of cellular aging. And then Part 4, we're going to go over that 6.2 cents longevity hack protocol. Alright, so part 1: a new cause of aging. Let me introduce you to the high-level biological premise that biological aging is not a metronome just ticking away at a standard pace. It is modifiable. Aging is effectively a process of accumulating cellular damage, which can come from different forms, and one form is called oxidative stress. You can think about it like cellular rusting. Specifically, what's happening is that as a byproduct of metabolism, your body generates different free radicals, harmful compounds. Some are called reactive oxygen species, or ROS for short. And these bounce around inside a cell, damaging cellular components. I think about it like tiny little bowls in a molecular china shop. This includes damaging fragile fats, fragile lipids inside your cells and cell membrane. And over time, this accumulated damage leads to aging, this cellular biological rusting. However, and this is the important point, you can optimize metabolic processes to reduce the damage, prevent the biological rusting from setting in to protect your cellular machinery. Now, let me introduce you specifically to a new cause of aging called ferroaging. Ferro refers to iron, and iron as an element, although it's very important for various metabolic processes, can be highly reactive. Leading to the generation of these free radicals that drive this ferroaging, biological rusting process. Okay, now let's go one level deeper, and please, please, please hang in there with me because it's essential for you to understand this biological background so you can understand how vitamin C really works. Effectively, what happens is iron can accumulate in tissues with age. This happens naturally with age, like your cells are hoarding iron like they're some iron golem. You can actually see that right here. This red is staining for intracellular, within the cell, iron. And look, the old cells are hoarding the iron. But what happens next? Then, through a series of reactions, this leads to the generation of these free radicals, these reactive oxygen species. In particular, fragile fats called polyunsaturated fats in membranes can be attacked by these free radicals, these reactive oxygen species, leading to damaging harmful byproducts of aging, things like 4-HNE and MDA. Those abbreviations aren't important, but I want to draw your particular attention to an enzyme named ACSL4. This plays a pivotal role in this biological aging process. Quoting from the paper, "ACSL4 acts as a central switch in this aging process." I remember it as aging catalyst switch for ACS. A-C-S-L-4. That's not actually what it stands for, but When you go through medical school and a PhD, you kind of get accustomed to making mnemonics so you can remember these ridiculous names. Anyway, in aging, there's more ACSL4 activation in parallel to what we saw with the iron. You can see that here. Look, the old cells have much more aging catalyst switch activity. This is what you're looking at. But that brings us to chapter 2. Let's look at proof it's happening in me and you right now, not just in cells. I'm going to show you something that's going to scare you a little bit, but I promise I'm going to turn that fear into excitement in a moment. Here are human data. I know it looks overwhelming, there are a lot of panels, but it's actually really simple. It compares humans across the age spectrum—young versus old—across different organs—liver, lung, heart, and muscle—and what you see is an accumulation of iron inside cells—remember Iron Golem?—with age, alongside activation of this aging catalyst switch, ACSL4, and the downstream products of this aging process. Basically, over time, there's a buildup of iron in organs along with activation of this aging catalyst switch, and that leads to biological aging. And as a quick aside, if you zoom in at the cellular level, you see hallmarks and features of aging jump up left and right, like SA-beta-gal, a marker of cellular senescence, even amyloid beta, which is involved in Alzheimer's disease. The laundry list of stains and jargony terms from the paper is long, and if you want to nerd out with the paper itself, please have at it. But long story short, With age, iron accumulates in organs, driving a process that eventuates cellular aging, cellular rusting, and decline. And at the heart of this process, this is what's key for you to understand, is ACS L4. Pause. I want to caution against a potential misinterpretation of these data. I am not saying don't eat iron or don't eat steak. You might be thinking, oh, you know, if iron causes cellular aging, I should decrease its intake in my diet. But it doesn't work like that. You need iron for metabolic processes. What you don't want is your cells hoarding iron, leading to this pharaoh aging. What vitamin C does is it deactivates the enzyme that is at the heart of this pharaoh aging process. But ironically, vitamin C increases the absorption of iron, more particularly non-heme iron, like from spinach and green things, more than from, say, steak. But the same applies. You can actually think of vitamin C as an iron optimizer. It gets it into your body, which you do want. You don't want to become anemic, but then it prevents it inside cells from accelerating cellular aging. Let me know if that makes sense. It's not a paradox, it's metabolic optimization. The body is wise. Are you still with me? Good. That means your brain is working. So let's keep going because I'm going to show you how to keep it that way with brain MRI images in a moment. Part 3: Slowing Cellular Aging. The next major step for the researchers was to determine whether they could slow cellular aging by blocking this keystone enzyme, this aging catalyst switch, ACSL4. Now, in animal models, this is kind of easy because you can do genetic modifications and genetic knockout. You modify them so they don't produce the active enzyme and observe what happens. Indeed, knocking out the ACSL4 aging catalyst switch prevented pharaoh aging, this biological aging process. Okay, but now you're probably wondering, like I was, what good does this do us? Because we're not going to genetically modify humans, at least not today. There are a few exceptions, but we'll put those aside for another time. So then the researchers screened a range of compounds, 100 molecules that might mitigate this aging process, this pharaoh aging biological process. And the one that popped out was the mundane, the humble vitamin C. Vitamin C clearly stands out as the winner. But here's the question that actually matters. Does any of this hold up in a living organism? Primates? Humans? Or is it just another promising mechanism that falls apart in the real world? We're gonna get to that, I promise. But the researchers then showed that vitamin C does in fact directly bind to the ACSL4 aging catalyst switch, blocking it and blocking this entire ferroaging process. But that's not all. Vitamin C was also found to activate antioxidant defenses. So in effect, vitamin C is responsible for like a pincer maneuver on biological aging, this form biological aging. It shuts down the aging catalyst switch, ACSL4, and it amplifies antioxidant defenses to protect against any damage that leaks through. But now, you ready? For the real moment of truth: does any of this actually prevent aging in living organisms? So what the researchers did is they conducted a 40-month, 3.33-year interventional trial in middle-aged monkeys. Starting at monkey age 12 to 16 years old, which is roughly the equivalent of 40 to 50 years in human years, the monkeys were dosed— at 30 mg/kg of vitamin C or given a control treatment under tightly controlled conditions, and the results were really impressive. There was a widespread reduction in pharaoh aging markers, lower expression of this ACSL4 aging catalyst switch, and overall decrease in just biological aging. I break down the biomarker data more in the letter associated with this video, but I wanted to respect your time, so let me hit you with something that should make a real impression. The researchers conducted MRI brain scans on the monkeys and showed that vitamin C counteracted—slowed—age-related brain shrinkage. The humble vitamin C prevented brain shrinkage. That's amazing! So if we zoom out, we see a surprisingly coherent and well-supported story. With age, iron becomes trapped in organs. This sets off a cascade of events orchestrated by this aging catalyst switch ACSL4 that leads tissue damage of biological aging. But vitamin C, that simple compound you can get at the grocery store or any supplement store, interrupts this process and binds to ACSL4, inhibits it, and boosts antioxidant defenses. That brings us to the chapter I know you've been waiting for: the Six Cents Protocol. Let's come back to the claim I made at the beginning: 6.2 cents per day is a longevity hack. You can buy vitamin C cheaply, For example, if I go on Amazon, I can get a 2-pound bag, 907 grams, for about $27. In the animal studies, the dose was 30 milligrams per kilogram. So for a 70-kilogram human, that's 2.1 grams per day. If you do out the math, you actually find that that dose costs about 6.2 cents. Now, you might be wondering how many oranges you'd have to eat to get that dose. About 21 oranges. So feel free to eat whole foods rich in vitamin C. I encourage that. That's fine. Although supplementation in this particular case to get the longevity effects might be a little bit more reasonable and totally economical. And now I actually want to get a little bit more specific with protocols. Because while you can simply take 2.1 grams per day, split dosing, where you have multiple doses per day that are smaller, might be better for a couple key reasons. First, absorption improves if you split up the doses. Vitamin C can get absorbed at higher doses, but it's just less efficient. Second, taking 2.1 grams of just plain vitamin C at once can cause gastrointestinal distress. It's not dangerous, it's just an osmotic, it draws in water, so you can get bloating and a little diarrhea. I would suggest splitting that 2.1 gram dose into 3 or 4 doses per day. Additionally, taking these split doses with food can help minimize GI distress. And another way to minimize GI distress and potentially increase bioavailability of the vitamin C is to use a form of vitamin C called liposomal vitamin C. The drawback here is just cost. Liposomal vitamin C is significantly more expensive. And while there's no exact conversion, a reasonable rule of thumb is that liposomal vitamin C is about 3 times more bioavailable. That means you're you could achieve a similar effect with something like 700mg of liposomal vitamin C taken once per day. And something else really important to keep in mind is how vitamin C is actually used in your body once it's in your body. It can be burned through rapidly or can actually be recycled. And the degree to which your body uses vitamin C efficiently depends heavily on your overall metabolic health and antioxidant status. I put more specifics in the letter on NADPH and glutathione, but to keep it very simple, A very healthy person can get more anti-aging benefits, or likely get more anti-aging benefits of vitamin C at lower doses, say 1 gram per day, versus a really unhealthy person might need 3 grams per day to get the same effect. Metabolic context matters. It always matters. It's not just about the dose, but how that dose is used by your body. And that extends far beyond vitamin C. I think this is all very exciting and super high yield. 6.2 cents per day to extend healthspan, if not lifespan. That is awesome.