Your coronary artery calcium (CAC) score measures the calcified plaque in your arteries. A CT scan assigns a number to the buildup. A score above zero means you have plaque. Scores between 100 and 400 mean you have moderate plaque burden and higher cardiovascular risk. In many people, CAC scores rise over time, especially when you have metabolic dysfunction.

A 2026 randomized controlled trial in JAMA Cardiology tested whether 360 mcg per day of menaquinone-7 (MK-7, a form of vitamin K2) slows progression. After two years, the K2 group accumulated significantly less new calcification than the placebo group.

In the full version:

• Why calcium ends up in arteries instead of bones

• About the trial

• What to pair with K2

• How to get a CAC scan and what your number means

• What I take and why

[Subscribe to unlock the full article]

Read more

I do about 20.

Before you tell me I’m wrong, read the data more carefully. Because buried inside this research is something the headlines are missing: above 120 minutes per week, all-cause mortality risk stops declining meaningfully, with little additional reduction at higher volumes.

That plateau suggests there may be a threshold beyond which additional training delivers diminishing returns for longevity.

In observational data, 90 to 120 minutes per week associates with roughly 10 to 25% lower all-cause mortality risk, with cardiovascular outcomes and some neurological outcomes showing similar benefits. Those are significant numbers. What the research also found is that people doing two or three times that amount saw little additional longevity benefit.

So the real question is not how much you should train. It is how efficiently you can reach the range that actually gives you results.

In the full version:

• Why the studies are measuring the wrong variable

• What stimulus quality actually means and why it determines your results more than time does

• My actual 20-minute protocol and the science behind why it works

• What to track instead of minutes

[Subscribe to unlock the full protocol]

Read more

That’s not a reason to stop using these drugs if you need them. But it’s a good idea to understand what’s happening in your body, and to know that a different class of compounds is emerging that appears to address the problem.

The compound is eloralintide. It’s a selective amylin receptor agonist developed by Eli Lilly. Eloralintide doesn’t work on the GLP-1 receptor at all. It works through amylin receptors, a pathway that traditional GLP-1 drugs do not directly target. Phase 2 data published in The Lancet in 2025 showed up to 20% body weight loss, comparable to tirzepatide. Preclinical findings suggest eloralintide may preserve lean mass more favorably during weight loss.

In the full version you’ll get:

• The breakdown of every GLP-1 generation and the muscle preservation issue

• The amylin signaling pathway, how it differs from GLP-1, and why those differences change the longevity calculation

• The combination potential with existing GLP-1 protocols and what Lilly’s trial data suggests

• Why eloralintide might be the next best thing

[Subscribe to unlock the full article]

Read more

Here are the details:

All take place on Tuesday, June 23rd 2026

Ditte Youn…

Read more

Bromantane is one of those compounds. Five athletes tested positive for it at the 1996 Atlanta Olympics and got banned. Russia approved it as a prescription drug the following year. Here’s what it does and why the mechanism is unlike anything else in the dopamine space.

In the full version you’ll get:

• Why and how Bromantane works

• The stacking protocol and dosing

• Where to source it and what to look for in quality

[Subscribe to unlock the full protocol]

Read more

Commercial green tea is high in oxalates, which bind to minerals and contribute to kidney stones and systemic issues. It’s also a significant source of fluoride, which accumulates in the pineal gland and disrupts sleep and hormonal signaling. A standardized extract gives you what you want without the baggage.

EGCG is one of the few compounds with research spanning mitochondrial function, cellular stress responses, inflammation, glycation, and brain health. A new study on its protective effects against severe cellular stress gave me another reason to keep it in my daily stack.

In the full version you’ll get:

• The longevity pathways EGCG influences and the science behind them

• What to stack it with and the synergies the research supports

• How to find a quality product

• The full dosing and timing protocol

[Subscribe to unlock the full protocol]

Read more

In the full version you’ll get:

• What deuterium is and why your mitochondria care about it

• The research on DDW and cancer, what it shows and where it falls short

• What you can do instead

• When buying DDW makes sense and when it doesn’t

[Subscribe to unlock the full breakdown]

Read more

In the full version you’ll learn:

• The master longevity switch nicotine shares with exercise and fasting, what it is, and why it’s significant.

• The dose and timing that activates this pathway without burning it out

• Why this mechanism extends well beyond cognitive performance into recovery, aging, and long-term brain health

• What the research says about cumulative effects with consistent use

[Subscribe to unlock the full protocol]

Read more

Your body contains cells that should be dead but refuse to die. Scientists call them senescent cells. You might have also heard them referred to as zombie cells because that is exactly what they are: cells that stopped dividing, stopped functioning, but keep hanging around and causing damage. They pump out inflammatory signals that poison the tissue around them. They accelerate aging in every organ they accumulate in. They show up in your joints, your brain, your heart, your lungs, your skin. The older you get, the more of them you have.

The problem has been finding them precisely. Scientists have markers they use to identify senescent cells in lab settings: proteins like p16 and p21, enzyme activity patterns, inflammatory secretions. But none of them provide a single universal, highly specific surface marker suitable for targeting all senescent cells in living tissue. A new Mayo Clinic study may have just changed that.

Researchers at Mayo Clinic published a paper in the journal Aging Cell describing a new approach. A team of graduate students, working across two separate labs, discovered that synthetic DNA molecules called aptamers can selectively attach to proteins on the surface of senescent cells and flag them for identification. They screened more than 100 trillion DNA sequences (the standard library size for this type of screening) to find the rare ones that worked.

One major bottleneck holding back the senolytic field has been the lack of precise ways to identify senescent cells in living tissue. Cracking that opens the door to what comes next.

In the full version you’ll get:

• What zombie cells actually do to your biology and why your senescent cell load is probably higher than you think

• What the Mayo breakthrough means for the future of targeted senolytic therapy

• What you can do right now, today, to start reducing your senescent cell burden before precision targeting arrives

[Subscribe to unlock the full protocol]

Read more

About fourteen years ago, I put modafinil on the map. ABC Nightline came to my house and filmed for two days because I was the only executive in Silicon Valley willing to talk about using a cognitive enhancer without a bag over my head. Watch it here. The drug was called Provigil. It had been FDA-approved for narcolepsy since 1998, but nobody outside of a small circle was talking about using it as a performance tool. They had to invent a brand new category of medication to describe what it does, a “wakefulness-promoting agent,” because it wasn’t a stimulant. It doesn’t raise your heart rate. It doesn’t make you jittery. The lights simply turn on.

Modafinil increases orexin signaling in your hypothalamus, one reason it produces clean wakefulness without the jittery profile of traditional stimulants. Orexin is a neuropeptide, a signaling molecule your brain produces to regulate alertness and the sleep-wake cycle.

I wrote about the full science of modafinil, how to dose it, and how I stack it at daveasprey.com/modafinil-benefits.

The same orexin system that modafinil ramps up to keep you awake is the system that, when it fires too hot at night, costs you sleep quality. There is now a class of drugs that works on the exact opposite end of that same system. Instead of increasing orexin signaling to promote wakefulness, they block orexin receptors to let sleep happen.

They’re called DORA drugs. Dual orexin receptor antagonists. A new drug category. Most primary care doctors have never prescribed one.

In the full version you’ll get:

• Why the orexin system is the missing variable in most people’s sleep, even people who think they sleep fine

• A breakdown of all three FDA-approved DORA drugs, how they differ, and which one the evidence currently favors

• How to have a productive conversation with your doctor about getting access

[Subscribe to unlock the full protocol]

Read more

The standard dose of creatine is 3 to 5 grams a day. That dose is well-researched and effective for muscle performance. The research on what your brain actually needs tells a different story. And recently, the world’s most-cited creatine researcher made it official.

In the paid section you’ll learn:

• Why 5 grams is insufficient for cognitive benefit

• What dose the research actually supports for brain health

• The specific populations who need creatine most urgently

• How to time it, what to take it with, and what works against it

[Subscribe for the full article]

Read more

The anti-smoking movement buried the science on nicotine. The tobacco industry spent decades fusing nicotine and smoking into a single idea, and public health spent the next few decades hammering that association home. What nobody talked about was the actual research on what nicotine does to your brain when you pull it away from combustion, from tobacco, from the 7,000+ other compounds in cigarette smoke.

I’ve been using nicotine as a cognitive tool for years. Not cigarettes. Not vaping. Low-dose, clean delivery, used strategically.

A 2010 meta-analysis in Psychopharmacology reviewed 41 double-blind, placebo-controlled studies on nicotine and human cognitive performance. Researchers repeatedly saw improvements in attention, memory, and motor performance across multiple task types. These effects showed up in non-smokers who had no tobacco deprivation, meaning the results had nothing to do with reversing withdrawal. Multiple studies since then confirm improvements in working memory, visual memory, and information processing speed in healthy non-smoking adults.

The research consistently shows measurable improvements in attention and processing speed under specific conditions. Thirty-plus years of controlled studies establish that. The question is why, and how to use it without creating a dependency you never intended to build.

In the full version you’ll get:

• Why your brain already runs on the same receptors nicotine activates, and what happens to them as you age

• The exact protocol: form, dose, timing, and how to use it without wrecking your sleep or building dependence

[Subscribe to unlock the full protocol]

Read more

There’s a number that predicts how long you live better than your cholesterol, your blood pressure, or your weight. Researchers call it VO2 max. It measures how much oxygen your body can use during exercise, and it’s essentially a direct readout of how well your cardiovascular system is functioning. Think of it as your engine size. A bigger engine means your heart, lungs, and muscles can deliver and use more oxygen, which means your whole body handles stress, disease, and aging more effectively.

A 2024 meta-analysis covering 20.9 million observations across 199 cohort studies found that cardiorespiratory fitness rivals and in many analyses exceeds traditional risk factors like blood pressure and BMI in predicting whether you'll die early. People with high cardiorespiratory fitness have a 53 percent lower risk of all-cause mortality compared to people with low fitness. That association holds across age groups, sexes, and health conditions.

The conventional approach to raising VO2 max calls for hours of moderate cardio each week. There’s a faster and more effective approach.

In the paid section you’ll learn:

• Why VO2 max is one of the strongest longevity predictors in the research literature

• The exact protocol that raises VO2 max 12% in 8 weeks with three sessions per week

[Subscribe for the full article]

Read more

I spent six weeks in Hawaii with zero sunscreen, intentionally trying to raise my vitamin D levels naturally. It was a disaster. I got sun damage on my arms and face, and my vitamin D only hit 30 ng/mL when my personal target is around 60 to 90. What I learned from that experiment changed how I think about sun protection. It had nothing to do with what I was putting on my skin.

In the paid section you’ll learn:

• Why the fat in your cells determines how badly UV light damages your skin

• The supplement stack that provides real sun protection from the inside out

• The truth about chemical sunscreen

• How to be smart about sun exposure

[Subscribe for the full article]

Read more

Here are the details:

All take place on Thursday, May 7th 2026

Dr. Elie Ab…

Read more

A few years ago I took one low dose injection of Ozempic so I could record an episode with Dr. Robert Kushner, one of the researchers behind the original semaglutide trials. I felt nauseous the entire time and didn’t want to eat. One injection, and I was done with it.

After that I started paying close attention to what these drugs actually do to your body. Weight loss numbers get all the headlines. What’s happening to your muscle gets almost none.

Millions of people are taking semaglutide and tirzepatide right now, and retatrutide is one to watch. It’s a triple agonist hitting GLP-1, GIP, and glucagon receptors simultaneously, and early Phase 2 data showed weight loss approaching 24%.

If you’re on one of these drugs you’re probably losing weight. What you may not know is how much of that weight is muscle.

Losing fat is good. Losing muscle in the process is one of the worst things you can do for your long-term health.

In the paid section you’ll learn:

• Why muscle loss on GLP-1 drugs is a bigger problem than the industry admits

• What happens to your metabolism when lean mass drops fast

• The exact protocol I use to protect muscle while losing fat

• Why people who stop these drugs gain all the weight back

[Subscribe for the full article]

Read more

The test that helps identify whether you’re in a high-risk inflammatory state, one that makes plaques more likely to rupture, is called high-sensitivity C-reactive protein, or hsCRP. It measures chronic inflammation. A standard cholesterol panel doesn’t measure inflammation at all. Your LDL could look perfect while your arteries are quietly on fire.

A 2025 study published in JACC: Cardiovascular Interventions, the PROSPECT II trial, used advanced imaging inside the coronary arteries of 501 heart attack patients and found that higher hsCRP levels were associated with lipid-rich, higher-risk plaques more likely to cause future events.

Inflammation is now front and center in cardiology. The American College of Cardiology now treats hsCRP as a key part of cardiovascular risk assessment, especially when traditional markers don’t tell the full story. And it’s still underused.

In the paid section you’ll learn:

• What hsCRP actually measures and why standard CRP is the wrong test

• What your number means and what longevity-focused clinicians actually target

• The interventions with the strongest evidence for lowering it

• What to do to keep inflammation low

[Subscribe for the full article]

Read more

A gene therapy that aims to reset epigenetic markers associated with aging just entered human trials. This is one of the most important stories in longevity science right now.

In the paid section you’ll learn:

• What epigenetic reprogramming is and why it changes everything we thought about aging

• What the science actually shows in animals and human cells in the lab

• What the FDA trial means and what happens next

• What you can do right now to slow epigenetic aging while this technology develops

[Subscribe for the full article]

Read more

Bartonella is one of those blind spots.

It’s a bacterial infection transmitted by cat scratches, flea bites, ticks, and lice. Doctors know it as the organism behind cat scratch disease, a short-lived illness that resolves on its own. What they are not telling you, because most of them don’t know, is that there is growing evidence Bartonella can persist in your body far longer than previously believed, interfere with your brain’s immune system, and produce symptoms that overlap with anxiety, depression, chronic fatigue, and even psychosis, while every standard blood test comes back negative.

I’ve spent decades tracking down the hidden biological factors that wrecked my performance. Mold was a major one. Infections that nobody tested for were another.

In the paid section you’ll learn:

• What Bartonella actually does inside your body and brain

• The studies linking it to brain fog, fatigue, psychiatric symptoms, and neurological disease

• Why standard testing often misses it, and what to ask for instead

• What to do if you think this could be relevant to you

[Subscribe for the full article]

Read more

A study published in The American Journal of Medicine in early 2025 analyzed outcomes in over 1.6 million men and found that tadalafil use was associated with roughly a 30–40% lower rate of all-cause mortality, along with 20–35% lower rates of heart attack, stroke, and dementia compared to men who did not take it. A separate 2024 analysis of more than 200,000 patients, looking across 407 different prescription drugs, found that tadalafil and its drug class were among the compounds most consistently associated with lower mortality in men.

In the paid section you’ll learn:

• How tadalafil works and what it has to do with aging

• The data on heart disease, dementia, and all-cause mortality

• Why taking it daily is different from taking it on demand

• How I use it

[Subscribe for the full article]

Read more