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

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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

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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

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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

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All take place on Thursday, May 7th 2026

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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

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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

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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

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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

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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

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Standard medical training rarely covers it, and most cardiologists learned almost nothing about it in school.

That is changing. Research published in the Annual Review of Biochemistry in 2025 describes it as central to keeping blood vessels healthy, flexible, and resistant to disease. A 2025 study in Nature found that when this gel thins and breaks down in the brain’s blood vessels, the barrier protecting the brain weakens, harmful molecules enter brain tissue, inflammation rises, and cognitive function declines (in animal models). Cardiologists at the leading edge of prevention now describe this as one of the most important targets in cardiovascular medicine.

In the paid section you’ll learn:

• What the glycocalyx does and why losing it contributes to heart attack and stroke

• What degrades it, including things happening inside your body right now

• What the research shows about protecting and restoring it

• The protocol I use and why

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It is called sulforaphane. And the vast majority of people trying to supplement it are not actually getting it.

In the paid section you’ll learn:

• Why sulforaphane does not exist in broccoli the way people assume

• Why the difference in absorption can be 3 to 4 times depending on the form you take

• What the human research actually shows across detoxification, brain health, blood sugar, and aging

• The one product that solves the stabilization problem and how to use it

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There is a hidden switch inside your immune cells that researchers are calling one of the most important therapeutic targets in the history of medicine. The research keeps finding it at the center of chronic diseases including Alzheimer’s, heart disease, type 2 diabetes, and accelerated biological aging. Pharmaceutical companies have dozens of drugs in clinical trials right now targeting this one pathway.

It is called the NLRP3 inflammasome.

In the paid section you’ll learn:

• What the NLRP3 inflammasome is and why it gets stuck in the “on” position as you age

• The specific diseases it drives and why they all share a common root

• What triggers it, including things in your daily environment you can control

• What the research actually shows turns it off

• The protocol for addressing this and why the compounds in it matter

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In May 2025, researchers at Harvard-affiliated Brigham and Women’s Hospital and the Medical College of Georgia published results from the VITAL trial, one of the largest and longest vitamin D studies ever run. They followed over 1,000 people for four years and measured something specific: telomere length. Telomeres are the protective caps at the ends of your chromosomes. Every time a cell divides, they get a little shorter. Shorter telomeres mean faster biological aging. Longer telomeres mean the opposite.

People taking vitamin D3 daily preserved significantly more telomere length than the placebo group. The researchers calculated the difference: people taking D3 aged roughly three years slower than the placebo group over the course of the trial.

In the paid section you’ll learn:

• Why your doctor’s “normal” vitamin D range is not the longevity target, and what level to actually aim for

• How vitamin D controls over 200 genes and what happens to them when you are deficient

• What you absolutely must stack vitamin D3 with

• The full protocol: what form to take, how much, what to pair it with, and how to test your levels

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What they almost certainly did not check is the number that fifty years of data have linked to cardiovascular disease, stroke, and accelerated brain aging. When elevated, it quietly damages the lining of your arteries. It drives oxidative stress that makes your LDL cholesterol more likely to become the dangerous kind. It has been linked to faster biological aging in the brain. And it builds the conditions for serious cardiovascular events, often for years before anything shows up on a standard panel.

The number is homocysteine. It is a byproduct your body makes during normal protein metabolism. Your body is supposed to clear it continuously using a process called methylation, a set of biochemical reactions that also drive DNA repair, neurotransmitter production, and detoxification. When methylation is running well, your body clears homocysteine quickly and it causes no harm. When it is not, whether because of a genetic variant, a B vitamin deficiency, or both, it builds up and starts doing damage throughout your body.

The reason cardiologists largely ignore it is because of a legitimate controversy in the research: B vitamin supplementation reliably lowers homocysteine, but not all trials show this reduces cardiovascular events. Some doctors took that as proof it does not count. But this isn’t the full picture.

Everyone should know their number on this, especially if you’re over 40. You can test it through axo.health for $25 ($21.25 if you’re a member), no doctor required. And what it is really measuring is whether your methylation system is functioning. That system is also responsible for DNA repair, neurotransmitter production, detoxification, and cellular energy production. When homocysteine builds up, all of it is under strain.

In the paid section you’ll learn:

• Why your lab’s “normal” range is not the target, and what the optimal number actually is

• How homocysteine damages your arteries, oxidizes your LDL, and accelerates brain aging

• Why 40% of people have a gene variant that makes this worse, and what to do about it

• The trial that cut brain shrinkage by 53% just by fixing this one number

• The full protocol: what to take and what to avoid

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DHM comes from the Japanese raisin tree and Chinese vine tea, plants that have been used in traditional Asian medicine for over a thousand years. Researchers have been studying it seriously for about a decade. What they have found goes well beyond liver enzymes and alcohol metabolism.

In the full version of this article you will get:

• What senescent cells are, why they accumulate in your brain specifically

• How DHM selectively clears out the most dangerous type of aging brain cell while leaving healthy ones alone

• The epigenetic angle: how DHM essentially turns back a biological clock

• The protocol I use, including dose, timing, form, and what to stack it with

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The problem is that glutathione levels decline 30 to 50 percent between young adulthood and old age. That decline accelerates with stress, alcohol, poor diet, toxin exposure, and illness. By the time most people notice the effects like fatigue, slower recovery, brain fog, and getting sick more often, the depletion has been building for years.

I have been focused on glutathione for over 25 years. It has been a foundational part of my biohacking stack since the early days. And the biggest mistake I see people make is trying to fix a glutathione problem the wrong way.

In the full version of this article you will get:

• Why oral glutathione supplements almost never work and what the research actually shows

• The precursor strategy that a clinical trial used to reverse seven aging biomarkers simultaneously

• The delivery breakthrough that bypasses the absorption problem entirely

• The specific protocol, doses, and products that work best

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For decades, researchers have been trying to explain why people who eat a Mediterranean diet live longer. The answer they kept landing on was olive oil. Olive oil is mostly fat, and the fat alone does not explain the longevity data. One compound getting serious scientific attention right now is called hydroxytyrosol (pronounced hy-drox-ee-TY-roh-sol). The way most people consume olive oil delivers almost none of it.

A 2025 study in GeroScience, one of the top peer-reviewed journals on aging, identified hydroxytyrosol as a potential geroprotective compound. That means it may target the underlying mechanisms of aging directly, not just the symptoms. Researchers examined how it interacts with several processes that drive biological aging: damaged DNA, failing mitochondria, senescent cells, and the chronic low-grade inflammation that quietly accelerates aging across every system in your body. Senescent cells are sometimes called zombie cells. They stop functioning but refuse to die, and they poison the tissue around them.

Most longevity compounds interact with one or two of these processes. Hydroxytyrosol appears to interact with several.

In the full version of this article you’ll get:

• Exactly how much hydroxytyrosol you need per day to move the needle

• Why olive oil, even good olive oil, almost never delivers a meaningful dose

• The supplement form I use and how I stack it

• How it may help protect your NAD, and why that matters if you’re over 35

• What to look for on a label so you don’t waste your money

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