Nick Norwitz MD PhD

I ate over 100 pounds of meat in 30 days.

And that’s not the craziest part.

But before I tell you what happened we need context.

The carnivore diet has had a fascinating trajectory over the past decade.

It exploded into the mainstream as prominent advocates promoted it as a solution for everything from improving athletic performance and body composition to treating obesity, autoimmune disease, and other chronic illnesses.

Do you get the feeling that your workouts just aren’t working?

You show up day after day, week after week, month after month. You put in the work. And yet, the results don’t match the effort.

You start to wonder: Shouldn’t I be seeing more gains for my effort?

Am I just unlucky?

It feels almost conspiratorial to say out loud. And nobody wants to be a whiner. So, you keep going, and you keep quiet.

*News note: The big news of the last few days was the negative result of the Lp(a) HORIZON trial, a large Phase 3 trial in which an Lp(a)-lowering drug failed to reduce cardiovascular events. The cardiology world is in a little bit of a free fall right now. Whether or not you’re aware of this trial, I’ll provide my commentary in a postscript at the end. All the teachings herein still apply. You just get a little extra nuance.

When I was first diagnosed with elevated Lp(a), I was scared.

I knew what the numbers meant.

Statistically, my lifetime risk of a heart attack was dramatically higher—perhaps by as much as 230%. And because heart disease runs in my family, this wasn’t just an abstract statistic.

I inherited high Lp(a) from my father, who almost died of a heart attack at just 44 years old.

A drug just made old mice live 12% longer.

Not a drug you’ve never heard of, but one that about 15 million Americans are already injecting into their bodies every week: a GLP-1.

Now, the moment anyone tells you something extends lifespan, your skepticism should switch on like a hunger neuron at the sight of pecan pie. And I want you to hold on to that skepticism for this entire letter.

It’s good because longevity claims are notoriously difficult to prove in humans. That’s why we often lean on animal studies. But animal longevity results have a long, humbling history of failing to translate to people.

So, do the results of this new paper, published in Nature, mean you’ll live 12% longer if you start a GLP-1?

For years, my own body tried to eat itself from the inside.

That’s not hyperbole.

That’s roughly what ulcerative colitis is: your immune system turning on your gut. And the standard medicines didn’t work for me. What finally did was an extreme anti-inflammatory diet.

That said, even now, in hard-won remission, my gut keeps a tell: it flares when I’m stressed. International travel. Relationship issues. The usual things all of us deal with as a function of being human.

For a long time I chalked that up to bad luck. Then I read the science, and realized it isn’t luck at all. It might be a nerve.

What’s healthier for your heart and liver: bacon and eggs, or oatmeal and quinoa?

It seems like a bizarre question, and it certainly offends conventional wisdom about what makes up a “healthy diet.”

But a major six-month randomized controlled trial just published in a top science journal put versions of these diets head-to-head.

Researchers compared:

A low-carb, high-fat ketogenic diet (4% Calories from Carbs)

A physician friend recently told me he had just taken a patient off a statin.

Not because the patient’s cholesterol had plummeted. Not because they were experiencing side effects. Not because the patient refused treatment. Quite the opposite.

The patient had become metabolically healthier.

Healthy enough, in fact, that their physician concluded the statin was no longer providing a meaningful net benefit.

If you’ve been told for years that elevated cholesterol automatically means lifelong statin therapy, that decision may sound strange, even reckless.

When I first heard about the peptides “semax” and “selank,” it was from a family friend who simply said:

“Since I started snorting these peptides, my mood has been the best it’s been in decades!”

Naturally, I was a little concerned.

Hearing those words for the first time, they sounded like party drugs.

And when a family friend discloses that they’ve been snorting [insert unknown compound here] and feeling on top of the world, that’s bound to raise a yellow flag.

The biotechnology company Enveda just announced what could be a first-of-its-kind exercise pill.

I say “first-of-its-kind” not just because of its biological effects, but because of how it was discovered.

Enveda, a company with which I have no conflicts of interest, has the motto, “Life is smart, let’s learn from it.”

And they’re now using AI to help sort through the library of natural molecules found in our bodies and those of other organisms to try to develop metabolic medicines.

And they might have just had a major breakthrough, with positive results from a Phase 1 trial for a compound called ENV-308, which is being termed:

If you spend a decent amount of time in the corners of nutrition social media, you’ll hear a multitude of opinions about how to pick your protein.

What’s the real difference between grass-fed and grass-and-grain-fed beef?

Wild salmon versus farmed salmon? What about pollutants?

Pasture-raised eggs versus free-range eggs versus organic eggs?

And are sardines really loaded with heavy metals?

If I gave you 100 mg of caffeine… and then I gave you another 100 mg of caffeine, and then another... you’d think they’d feel the same, right?

But they don’t.

Coffee can make some people laser-focused and productive.

Green tea can feel calm and almost meditative.

Yerba mate has developed a cult following among entrepreneurs who swear it gives them energy without the crash.

Just as my life was beginning to show promise on paper, I hit my lowest point.

I was 22 years old, living in a new country for the first time, and sicker than I’d ever been. I spent days in the hospital, in intensive care and even palliative care, while my peers at Oxford were in the lab or at social gatherings.

What put me in that hospital bed was a case of inflammatory bowel disease that a laundry list of medications had been unable to keep at bay.

As a result, the promise my life seemed to hold on paper, including my scholarship to Oxford for my PhD and a position at Harvard Medical School thereafter, felt like empty promises. They were opportunities I wanted to pursue, but my health was standing in the way.

It’s ironic, that tension. Maybe you see it.

When I was 23 years old, I developed extraordinarily high cholesterol.

I was told repeatedly that my cholesterol was so high that I would be developing cardiovascular plaque within years and probably have my first heart attack by age 30.

I never did.

My arteries are perfectly clean, even on the most sensitive imaging.

The reason why has been a source of debate. Special genetics? I don’t think so. A fluke of fate? That’s not scientific. Just not enough time? Maybe, but it actually skirts around the question.

In a new study published in Cell Host & Microbe, researchers went looking in the guts of people with irritable bowel syndrome (IBS) and people with insulin resistance.

They found that both groups were missing the same ingredient.

Not a vitamin. Not a mineral.

A gut-derived molecule that can be produced from a common dietary fat.

I promise we’re going to get into the specifics, and the solutions. But before we do, I need to provide a little more framework.

A couple of months ago, I started injecting myself with a strange little blue peptide formulation called the KLOW Stack.

Technically, it’s not one peptide but four, each targeting different aspects of healing and recovery. Together, they’re designed to work synergistically and, at least in theory, accelerate the body’s ability to repair itself.

I’ve already noticed some encouraging changes.

In particular, one involves an injury I’ve been dealing with for more than a decade: damage to my right knee sustained after a series of fractures and surgeries. Ever since, running has been difficult. Even short jogs often leave the knee swollen and the surrounding scar tissue inflamed.

But recently, for the first time in years, I’ve been able to run without the usual aftermath.

A new study of more than 1 million people, just published in Nature, has uncovered a rare genetic variant linked to: lower body fat, greater lean mass, better blood sugar control, healthier triglycerides, and a remarkable 60% lower risk of cardiometabolic disease.

But this isn’t just an interesting genetic fluke — or a reason to envy the lucky few who won the DNA lottery.

The real story is that discoveries like this are becoming blueprints for tomorrow’s medicines.

Thanks to advances in genetics and biotechnology, we’re increasingly able to turn nature’s experiments into therapies that could benefit everyone. In fact, the researchers found that of the dozens of genes they flagged, nearly 40% already encode approved or clinical-stage drug targets.

This isn’t a curiosity cabinet. It’s a pipeline.

Imagine two 80-year-olds.

One struggles to climb a single flight of stairs. They move cautiously, spend most of the day sitting, and increasingly lose pieces of the mind they once had.

The other seems to have ignored the calendar entirely. They still go for morning jogs, can still spend all day walking Disneyland with their grandchildren, and remain as mentally sharp as they were decades earlier.

What separates these two people?

Is it simply genetics? Luck? How much of how we age is under our control?

The field of cardiology is in mourning.

A drug that much of the cardiovascular world expected to become a blockbuster just failed in a huge trial.

The past president of the American Society for Preventive Cardiology said, “I think we’re all in a state of shock.” And the story the headlines are telling is already hardening into a conclusion:

Targeting inflammation doesn’t help the heart. The inflammatory hypothesis of atherosclerosis is dead.

That conclusion is wrong. I want to show you why. I want to show you what we really learned from this “failed trial.” And I want to show you several more natural ways to lower inflammation that actually improve your health.

For a neuroscientist, I suck at sleep.

It’s been a lifelong struggle, and it’s caused me a lot of anxiety.

When I sleep poorly, not only do I not function as well the next day, but I worry about my long-term brain health.

Sleep is foundational for learning and memory.

When sleep is impaired or insufficient, metabolic waste can accumulate in the brain, contributing to cognitive decline, and even Alzheimer’s disease.

Nutrition—especially as it relates to cardiovascular health—is probably the most confused, conflicted, and muddled topic in all of science.

Some people believe saturated fat increases the risk of heart disease.

Others believe seed oils are the bane of human existence and should be completely eliminated.

Then there’s fiber, animal versus plant protein, omega-6 versus omega-3, intermittent fasting—the list goes on.

While I understand that the conflicting information is frustrating, what’s equally frustrating for me is how the underlying complexities are ignored or oversimplified.

As a neuroscientist who wants to protect his brain for life, I never skip leg day.

And here’s why. Research shows that leg power predicts cognitive decline over a 10-year interval.

But that’s not all.

In a study of human twins, differences in leg power predicted not just long-term cognition, but actual brain volume measured by MRI.

What these findings strongly suggest is that your musculature, and particularly your leg muscles, are actively doing something to protect the brain.

Imagine you could know only 7 measures about your health.

No full-body MRI. No 200-page blood panel.

Just 7 measurements that, together, tell you as much information as possible about your overall health.

Which 7 would you choose?

I was recently asked this question, and I loved it because it’s both intellectually difficult and incredibly practical. It forces you to separate signal from noise—to ask what actually matters. What can you use?

In the storm of the peptide craze, it’s sometimes difficult to separate fact from fiction.

But over the past several years, one thing I’ve learned is that even the most fantastical claims occasionally contain a kernel of valuable truth.

So, when I hear people talking about the “Wolverine Stack,” named after the Marvel superhero famous for being nearly impossible to kill because he can regenerate damaged tissues and regrow parts of his body—my skepticism alarm goes off, just like yours probably does.

Honestly, fair enough.

After all, that kind of regeneration belongs in comic books. (Or perhaps in an axolotl).

When it comes to protecting your long-term brain health, you need to think about fat—specifically visceral fat, the inflammatory fat that accumulates deep within the abdominal cavity, wraps around your organs, infiltrates the liver, surrounds the intestines, and contributes to metabolic dysfunction.

But the story of visceral fat just took a fascinating turn.

A new 2026 study from an international team of researchers spanning Harvard, Israel, and Germany suggests that the more exposure you have to visceral fat over the course of your life, the faster your brain shrinks.

What makes this study particularly compelling is the methodology.

The researchers drew from four previous lifestyle randomized controlled trials in which participants underwent:

When I was 21, my body started attacking itself.

Ulcers opened in my intestines.

Food became dangerous.

There was a real chance I could lose my colon entirely. I was diagnosed with inflammatory bowel disease.

And for years, my life revolved around pain, bathrooms, medications, fear, and this constant question: Why was my gut on fire?

Maybe you’ve heard of brain-derived neurotrophic factor (BDNF).

It’s often called “Miracle-Grow for neurons” and frequently comes up in discussions about enhancing cognitive performance and protecting against dementia.

But what if I told you there’s a compound rumored to be 10 million times more powerful than BDNF?

That’s the buzz around Dihexa.

When I first heard these claims, I had my usual two-pronged reaction:

I once almost burned my house down… with a fish.

I know that’s a strange place to start but bear with me.

My mom makes the most incredible Chilean sea bass. It’s one of my favorite meals. The skin is thick, fatty, and perfectly crisped in a cast-iron skillet with ginger butter.

One day, craving that exact dish, I decided to make it myself.

Mistake.

I need to admit something:

When GLP-1s for weight loss started becoming big and everyone was talking about how they would change obesity medicine, I was a strong skeptic.

This has happened before: medicine and big pharma tell a compelling story about a miracle drug — then years later we find out we didn’t have the whole story, and people ended up harmed, sometimes critically.

However, the more I read about GLP-1s and their newer evolutions, the more my opinion shifted.

In fact, my perspective has even leapfrogged from “these are being overhyped” to “maybe they’re not being hyped enough.”

“This work establishes that damage to aging proteins previously thought to be irreversible can be repaired.”

That’s the line from a new paper published 3 days ago in Nature Communications.

Bold words.

But they’re backed by data showing—for the first time ever—that age-related protein damage can be reversed.

Now, there are caveats. We haven’t found the Fountain of Youth just yet. But I’d be lying if I said this paper didn’t bring us one jump closer.

What if you didn’t need to sleep?

No, seriously!

A new article published in Nature Neuroscience explores a provocative possibility: what if we could replicate the restorative benefits of sleep without ever fully shutting down the brain?

Imagine staying awake for 24 hours a day without compromising memory, cognitive performance, or neurological health.

The trick would be to stop thinking about sleep as an all-or-nothing phenomenon.

I don’t say this lightly: this may be one of the most interesting metabolic drugs I’ve ever reviewed.

Officially, it’s in clinical trials for diabetes.

Unofficially, it may represent something much bigger—a compound that reproduces some of the core metabolic effects of exercise itself.

If the early data continue to hold up, this could reshape how we think about treating insulin resistance, fatty liver, obesity, GLP-1s, and even exercise mimetics.

But before we get to the preclinical data and the human trials, I need to build a bit of biological foundation first.

In the universe of peptides, none is more mysterious — and more misunderstood — than the copper peptide, GHK-Cu.

Legends surround it: that it can:

Reverse wrinkles

Accelerate healing

Even protect against cancer

Mitochondria are often referred to as the “powerhouse of the cell,” as if they’re little batteries.

But they’re so much more than that.

They’re living, breathing, fluctuating, even dancing signaling networks that determine how your body generates energy at the most fundamental level, and even how you age.

In fact, if you look for the signature that distinguishes the longest-lived people — including a recent report on a woman who lived to 117 — what stands out in healthy aging is healthy mitochondria.

But the amazing thing about mitochondria is that, unlike a battery or an engine in a car, they can recover, heal, and renew themselves. And you can make them do this, starting today with free tools – but also, cutting-edge tools like performance enhancing mitochondrial peptides and hormones.

There is a common medication that costs as little as $1 a day that has recently begun attracting attention for its potential effects on cardiovascular disease, dementia risk, metabolic health, and even overall longevity.

It’s called tadalafil.

Most people know tadalafil as a treatment for erectile dysfunction, though it also carries FDA approval for conditions like benign prostatic hyperplasia and pulmonary arterial hypertension.

But a growing number of clinicians and researchers are now asking a much broader question:

What if tadalafil has meaningful effects on the heart, brain, blood vessels, exercise performance, and perhaps even mortality?

There’s a simple little peptide that’s becoming increasingly popular for the treatment of gut inflammation.

It’s called KPV.

And it’s something I wish I’d had access to eight years ago.

Let me start by telling you something personal, and then we’ll get into the science.

I want to rewind about eight years, to the day of my college graduation.

What do you do if your GLP-1 stops working?

Or maybe it never worked all that well in the first place?

Those are not a hypothetical questions.

While GLP-1 drugs have helped millions of people lose weight, some people barely respond, some experience debilitating side effects, and many wonder whether the benefits will eventually fade.

So today we’re going to tackle the difficult questions:

I saw something the other day that genuinely pissed me off.

I thought it was just an internet joke, but when I saw it in real life, the anger center of my brain lit up like a candle.

It was a plaque that said, “Don’t confuse your Google search with my medical degree.”

Now, before we go any further in this letter, which is going to be about why smart people believe dumb health ideas, I want to give you organically what rolled off my metaphorical tongue into a post I made after encountering that disturbing plaque:

I’m about to say what a lot of people and patients want to say, but might not have the words for.

Surviving long periods without food has shaped human evolution.

In both ancient and modern societies, fasting has been practiced by billions of people and been used to treat diseases ranging from autoimmune and inflammatory disorders to neurological disorders, such as epilepsy.

But we still have a limited understanding of the adaptations humans undergo during a prolonged fast, and how these relate to chronic disease.

So, what happens when you fast for one day, two days, three days, or even a full week?

What changes occur across your metabolism, and different organ systems?

Can statins cause Alzheimer’s disease and dementia?

The answer is uncomfortably complex.

And in my experience, almost no one will give it to you straight.

Let me back up and provide some personal context.

Friends and family come to me all the time asking for a second opinion on whether they should start a statin.

I spent a month obsessed with cottage cheese.

I ate ~36 pounds of the stuff over the course of April.

But I should back up.

I recently released an article about my personal experience taking the new GLP-1 receptor agonist, retatrutide.

I wasn’t trying to lose weight. But I did want to explore what happened under my metabolic hood, so to speak.

A new study in Cell Metabolism has me scratching my chin and rethinking my recipe book.

The paper reports that a compound found in aged garlic may protect both the brain and skeletal muscle from age-related decline.

As far-fetched as that sounds, the data are surprisingly strong.

There are even human clinical evidence supporting the idea that this compound could has anti-aging potential.

Quoting the researchers: [our] findings raise “an interesting possibility of S1PC as a nutraceutical anti-aging compound.”

Yesterday, I ‘accidentally’ got 29,000 steps.

Last week, I hit a bench press personal best.

And this month, my focus and productivity have been at their peak.

Why?

I tried something recently that really kicked me into a new gear.

As a metabolism scientist, I spend my days obsessed with the intricate inner workings of the human body and how they relate to lifestyle interventions, including diet, exercise, supplements, peptides, and many of the other topics we routinely discuss here at StayCurious Metabolism.

But there is a curious observation that, honestly, humbles my entire field.

When you look at some of the longest-lived and healthiest people in the world, they typically aren’t united by any one diet, supplement regimen, or rigorous daily exercise routine.

(Sorry. I know you’re disappointed to know treadmills aren’t the secret to living to 120.)

Instead, what unites the people with the longest lifespans and health spans are strong social connections and a deep sense of purpose.

Muscle & peptides.

If I had to pick the top buzzwords in health and medicine right now, those might be it.

And where they overlap—muscle-building peptides—you run into a dense thicket of multisyllabic names and acronyms that can make even a literary PhD’s head spin: CJC-1295, Ipamorelin, Sermorelin, Tesamorelin, MK-677, Follistatin-344, ACE-031, IGF-1, hGH, and on and on.

So today, the objective is simple: demystify the space.

Author’s Note: The structure of this letter is going to be a bit different from our usual, more narrative style at StayCurious Metabolism.

A new paper came out on a curious driver of Alzheimer’s disease, and as soon as I read it, I texted my mom:

Nick: “[Mom], are you take glucosamine [for your joints]? If so, stop…”

Mom: “Yes, I am. Will Stop.”

You’ll notice the introduction to this letter is different.

I’m not burying the lede, and the tone is one of caution and a bit of negativity.

What causes bloating?

It’s a deceptively complicated question.

And whether you have IBS, IBD, celiac disease, or another functional gastrointestinal disorder, chances are you’ve experienced bloating once or twice… or more.

But again, I ask: what causes it?

There isn’t a single straightforward answer, but one contributing factor is something called leaky gut.

As many of you know by now, I’m a neuroscientist who is himself at high risk for Alzheimer’s disease.

This is due to the fact that I carry two copies of the Alzheimer’s risk variant ApoE4, which is thought to increase my risk of developing Alzheimer’s disease by roughly 10- to 15-fold.

As a result, I leave no stone unturned when evaluating interventions that might help prevent it.

And one of the most interesting, provocative, and promising possibilities to cross my radar recently has been GLP-1 drugs.

Yes, the same blockbuster weight-loss medications you hear about in the news practically every day.

There’s a new weight loss drug that people think could become the biggest drug in history.

It’s called retatrutide.

We’ve discussed it before.

Briefly, in the published trials people are losing a quarter of their body weight, like a snake shedding its skin, or like they just flew through a 20 second body recomposition movie montage.

The power of this compound is insane, outperforming all other weight loss drugs, by a wide margin.

Most organs in our body have a nutrient delivery system, blood vessels, and a waste removal system, called lymphatic vessels.

But my brain is apparently missing the waste disposal part!

(Maybe that’s why it’s packed with completely random animal facts.)

Jokes aside, all of our brains are, for the most part, missing the conventional lymphatic system.

The brain is so densely packed with blood vessels, neurons, and support cells that there simply isn’t room for the lymphatic vessels found throughout the rest of the body.

It’s just about Pet Appreciation Week (often called PAW), which takes place from June 7–13, 2026.

As far as esoteric holidays go, I think this is a great one to acknowledge.

And, on a personal note, now that I am finally settling down in a place where I can have a pet, I’m actually looking to adopt a dog myself.

So, in celebration, I thought I’d blend dogs with health—specifically heart health—in a way that’s hopefully both informative and entertaining.

Let’s talk DOGMATIC: a hypothetical randomized controlled trial.

We might be extremely close to developing treatments that simultaneously blast away fat and build muscle.

Now, I understand why you might be skeptical, or even afraid to hope that something like this is possible.

But the data from both humans and monkeys suggests that it very much is possible… and maybe even around the corner.

But that may provoke a second layer of skepticism: even if it’s possible, is it actually desirable?

After all, in nature and medicine, there’s rarely a free lunch. I’ll absolutely address that concern, along with the limitations of the data, as we move through this scientific story together.

A massive study was just published in Nature, one of the world’s top scientific journals, and when I finished reading it, I was left a bit stunned.

It felt like the paper itself had just walked out of the room after dropping an intellectual mic.

Here’s the punchline:

The thymus—a largely overlooked organ that sits behind your breastbone, just above your heart—may be one of the most important organs for human longevity. In fact, individuals with healthier thymic function had roughly a 50% lower risk of death.

You read that right: a 50% lower risk of death.

In the world of peptides, few compounds are as hyped or as controversial as BPC-157.

It’s become almost mythical for its supposed ability to accelerate healing across the body: from gastrointestinal disorders like inflammatory bowel disease—which is personally relevant to me—to tendon, ligament, and muscle injuries.

But there’s tension here, both scientifically and culturally.

On one side, you have people actually using this compound and reporting remarkable recoveries. Perhaps the most famous example is podcaster Joe Rogan, who has spoken emphatically about how BPC-157 helped him recover from injuries that should have sidelined him.

On the other side, there’s significant pushback from the scientific establishment. In an interview for STAT News, Dr. Flynn McGuire at the University of Utah, for example, said: “The amount of hype to evidence is so skewed, it’s crazy,” and that BPC-157 “Should not be used by humans.”

You can increase your attractiveness to the opposite sex with light.

I know that sounds insane.

It sounds far-fetched. Honestly, that was my reaction too — until I started digging into the data we’re about to break down today.

I’m going to walk you through something that is both deeply surprising and surprisingly well-supported—how exposure to specific wavelengths of light can:

Increase testosterone in men

A massive new paper just dropped in the New England Journal of Medicine days ago on gene therapy for lowering LDL cholesterol.

And it’s breaking headlines.

Now, I realize that sentence, and the associated headlines, are going to provoke two polar-opposite reactions.

On one hand, we have those pronouncing: “We are curing heart disease with one shot!”

On the other, we have those warning: “This is ridiculous. Why would you lower LDL cholesterol with gene therapy? This is pure idiocy.”

As an MD PhD who literally wrote his thesis on neurodegenerative disease—and as someone who carries not one but two copies of the major risk gene variant for Alzheimer’s (ApoE4/4)—you can imagine I’m highly motivated to build a routine that protects my brain until the day I die.

Now, forgive the authoritative opening tone, but I want to get you laser focused on what this letter is going to be about: This is a high-yield synthesis of my supplement and medication protocol for Alzheimer’s prevention.

Summarize what I do to protect my brain and why in a manner that is as concise as possibly while maintaining nuance.

Throughout, I’ll back every statement with links out to deep dives from our archives for those who want to scrutinize the mechanisms and evidence behind each decision.

No fluff. No hedging. Let’s get straight to it.

The FDA recently approved a peptide for a rare mitochondrial disease.

But that’s not the interesting part.

What is interesting is that this same molecule might have implications for some of the most common and burdensome chronic diseases on the planet, from heart disease to diabetes and even to Alzheimer’s and Parkinson’s disease.

This is certainly a peptide I might consider including in my health routine.

But not before first diving into the scientific literature. And when I did, I was struck by genuine optimism.

Last year, I read a paper last year and immediately thought, “this can’t be right.”

It was a human controlled study published in Nature Metabolism that found people who ate less protein burned dramatically more calories—without any meaningful muscle loss.

So, I return to, “this has to be wrong. I just has to be wrong!”

But, I was curious. So, I decided to test it on myself.

And it wasn’t wrong. I was.

I’ve always been fascinated by superheroes—especially the transformations where ordinary people become extraordinary in an instant.

Think Spider-Man bitten by a radioactive spider, or Captain America infused with the super-soldier serum.

Of course, these stories are fantasy.

But they capture something deeper in the human imagination than simple childhood wonder. They tap into a timeless desire: the urge to engineer ourselves into something greater. Stronger. Smarter. Healthier. Maybe even morally better.

Some people wrinkle their noses at that idea. They say it’s “playing God.”

My heart should be riddled with cardiovascular plaque.

I should be having heart attacks like rabbits have babies.

For most of the last seven years, my total cholesterol has hovered around 700 mg/dL. I also have a history of inflammatory disease (ulcerative colitis), my Lp(a) is 194 nmol/L, and my father had a cardiovascular event in his 40s.

In other words, things should not be looking great for me.

And yet, what I’ve found is the opposite: my heart is perfectly clean.