Her failure: ignoring insulin.

Her blood tests had come back “normal.” She found her problem when she started pricking her finger, testing her morning blood glucose and ketones. After 12 hours of fasting, Michelle’s blood sugar hovered around 100 each morning. Although her doctor said that was normal, she learned that this happens when insulin resistance develops. All of her education, calorie counting, and exercise failed because insulin resistance took over Michelle’s body.

Normal Labs Can Still Hide Insulin Resistance

A big gap exists between “normal blood sugar” and a truly healthy metabolism. For years, your pancreas has overproduced insulin to keep glucose “looking normal.” By the time glucose and A1C come back abnormal enough to show the doctor that you have diabetes, those metabolic problems have been wrecking your body for a long time.

Michelle’s breakthrough happened when she stopped waiting for a diagnosis and started daily at-home testing. Once she realized she was insulin-resistant, she made up her mind to change her life for the better through keto.

Then the question became: What should you eat on Keto?

Keto reverses insulin resistance. Finding the right menu for less insulin production is the first critical step. Many newbies to the ketogenic approach find “Keto Friendly” food filled with fake fiber, sugar replacements, and continue eating several times per day. Success on keto means the food satiates the patient, supports ketone production, and stops the cravings by boosting their natural hormones.

I insist on this list when my patients first start keto.

Eggs

I recommend eggs to everyone, specifically the yolks—one of the best starter keto foods on this list. Many people think egg whites are the healthy part of the egg because of their lean protein content, but people with insulin resistance need the high-fat, nutrient-dense yolks for better satiety. Remember, the albumen (the white part of an egg) mostly contains water and lean protein. Egg yolks contain the majority of fat, vitamins, and minerals needed to make the baby chicken. If you’re only going to eat one part of the egg, eat the yolk.

I like to fry my eggs in butter and sprinkle them with salt, for the extra fat and electrolytes. list

Fatty Meats

With high insulin levels, your body signals hunger more urgently. In a state of high insulin, the body cannot access stored fat, so the brain keeps signaling for more food.

But why fatty meats?

Fatty meats provide the body with a dense, satisfying fuel that does not spike blood glucose and therefore doesn’t spike insulin. Fatty meats on the list below are an excellent source of quick, salty foods that keep blood sugar stable and steadily reduce cravings.

Bacon, sausage, pepperoni, salami, marbled steaks, burger patties, pork belly… The list goes on.

Instinctively, people might ask: aren’t these fatty meats high in calories? Yes. But remember what matters: eating enough fat to curb cravings, correct the hormones of satiety, and lower insulin. Once you fix the chemistry, the rest will get a lot easier.

Butter

Not only does butter make foods more satisfying, but it also adds short-chain fatty acids that support ketone production. For the insulin-resistant beginners, butter can help bridge the gap between burning carbs for energy and accessing fat for energy.

You can fry meat or eggs in it, or add it to your coffee. Trust me, butter in coffee might sound gross, but it tastes just like coffee with heavy cream: delicious! And add some salt to the butter, too, to further curb your cravings.

Let’s be honest, this is an easy one. Who doesn’t like some extra butter in their life?

Canned Fish

I love recommending sardines to patients new to keto. This has granted me the Sardine Queen title. Sardines pack fat, protein, omega-3 fatty acids, and essential minerals into an affordable, practical, single-serving can. No cooking required! Keto rookies and veterans alike can benefit from adding a good can of sardines to their diet.

These nutrient-dense fish also help treat a common problem: addiction to food. Foodies eat, not just to satisfy hunger, but to relieve themselves of boredom. To break this habit, you need to retrain your body to consume food for fuel instead of pleasure. Opening a can of fatty, highly nutritious fish taints the air with a smell that suppresses hunger. This is the goal, but not a great selling point for this gem of a food on our list. Eating small fish delivers a primal response that I cannot explain, but it happens to every person who eats this. Fatty fish allow you to consume less food, stay out of the kitchen, and shift your satiety.

While I espouse the benefits of sardines, they aren’t the only option. Several alternatives exist that also meet this criterion. I recommend: herring, salmon, mackerel, tuna, and anchovies.

If the texture bothers you—or you can’t get past eating a fish that still looks like a fish—buy sardines in brine, add olive oil, mash them into a paste, and add black pepper. This changes the texture, taste, and lets you disassociate eating a fish without adding carbs.

Hard Cheese

Hard cheeses are a staple in my house because they’re high in fat, low in carbs, have decent flavor, and can sit in the fridge for a long time.

Parmesan, for example, has a ton of flavor without much volume; for many insulin-resistant patients, including various flavors makes it easier to stay off sugar. When you remove sugar, the brain still wants stimulation. Salty, fatty, and flavorful foods prevent a carb relapse.

Think of cheese as a tool, not a snack.

Heavy Whipping Cream + BHB (BetaHydroxybutyrate) Powder

I normally don’t recommend anything with artificial sweeteners because many insulin-resistant patients still get a glucose spike from them. But I do have one exception: BHB powder.

For beginners who struggle to produce ketones, BHB powder helps raise circulating ketones quickly! It delivers ketones straight into your body and stimulates your body’s ability to produce its own ketones. BHB powdered supplements need sweeteners to make them taste palatable. This is why I make the exception.

Think of BHB supplements as the metabolic training wheels: eventually, your body will produce its own ketones without needing supplements. But in the beginning, this tool can be the difference between quitting and becoming keto-adapted.

Of course, you can just mix the BHB powders into water, but I prefer to mix them into heavy whipping cream as a treat.

High-Fat Nuts

High-fat nuts provide a great way to diversify the kinds of foods you have access to, but they’re lower on my list because nuts (even the high-fat ones) do contain some carbs. They also taste pretty good, thus making them easy to overeat, kicking you out of ketosis. I don’t allow my husband to buy them because I’ll eat the whole bag. They just taste too good.

If you’re keto-adapted and you want some dietary diversity, I recommend macadamia nuts and pine nuts. They should not be the foundation of your diet, but they make the list.

What is NOT on the list: Sugar Substitutes

Many patients try to keep their old food habits alive by swapping sugar for “sugar-free” sweeteners. They flock to the “health food” aisle and buy every product with the word “KETO” on the packaging. This is a trap!

“Keto” ice cream, candy, drinks… None of it is truly keto— especially for the insulin-resistant patient. Big food producers play games with health-conscious consumers: they market as if sugar substitutes don’t raise blood sugar, they flaunt that fiber doesn’t raise blood sugar, and they round down the carb count wherever possible.​

But in the Dr. Boz camp, we don’t play these games! We do not count net carbs; we only care about Total Carbs. All carbs trigger an insulin response. If you want to take back control and fix your metabolism once and for all, you need to stop cheating.

That means treating every carb, no matter the kind, as a carb. Don’t recreate sugar, recover from it.

Results

Once she accepted that insulin resistance was the real problem, Michelle changed her food choices. She stopped chasing low-fat labels and calorie math and started eating foods on this list that changed her body chemistry to keto.

Four months later, she lost 30 pounds.

If your fasting glucose hovers above 100 after 12 hours without eating, you have an insulin resistance problem. Fix your fridge, recover from your carb addiction, and your weight will come down.

​

If you were here for the past 2 sessions, you know the drill. If you’re new, here’s what I want you to do...

In the comment section below, ask your question. Then read through what everyone else has asked, and press the ‘like’ button on the ones you want answered most. The questions that rise to the top and are more likely to get selected.

Note: I review every question submitted. I cover some of the most important questions during each Office Hours session, and I select others to answer in future sessions or explore in more detail through long-form Substack posts. So if your question isn’t covered live, don’t worry, I will address it.

A word on what makes a question great

The best questions I get all have one thing in common.

They were a story with a twist. “I did X, I expected Y, but Z happened instead. What’s going on?”

They came from a real situation somebody was actually living, and the answer ended up helping far more people than the person who asked it. Those are the ones we can really dig into on the show.

One more thing. My favorite questions are the ones that send me to the latest literature. If your question makes me ask “wait, why does the body do that?” you have my full attention. I want questions that make me study. Bring me one of those, and we will learn it together.

Now… GO!

Reminder: Office Hours is for paid subscribers. If you haven’t upgraded yet, join us to ask your questions, attend live, and get access to the full searchable archive.

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In this Office Hours session, Dr. Boz answers four subscriber questions that show why metabolic advice rarely works as a universal rule.

She covers how much protein to eat when higher protein suppresses ketones, whether exogenous ketones are truly improving metabolism,…

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What does insulin resistance mean? It means your body has grown resistant to the message insulin is sending. You’ve made way too much insulin, for way too long.

Insulin is required for life. Our privileged lives filled with abundant food make it really easy to make too much of it.

When insulin runs high for too long, it stimulates growth. It makes things grow that shouldn’t. That inappropriate growth causes strokes, heart attacks, and kidney failure. It ages the body at hyper speed, driving brain and memory problems like Alzheimer’s, Parkinson’s, and other kinds of dementia. Years of excess insulin feed arthritis and cancer. And most patients have no idea.

The Signs

Lists of criteria help doctors diagnose insulin resistance. After 20 years of seeing these patients, I can spot them from across the room.

Belly Weight

Let’s start with the easiest one. When insulin is high, the body fills its storage cells with fat, and parks that weight right around the belly button. As those cells fill, the weight climbs. Once someone packs on enough fat to push their body mass index over 25, they almost certainly have insulin resistance.

Skin Tags

It’s a dead giveaway when there’s darkened skin on the back of the knees or in the creases of the elbows. If the skin on the back of the neck looks dark, it’s not dirt. It’s extra skin cells piled too high for too long, and they overgrew because of insulin. Let it go long enough and the skin star

ts making appendages, or skin tags. Biopsy that thickened skin, or one of those skin tags, and you’ll find sugar packed in between the cells. Insulin put sugar wherever it can find. And where there’s sugar, yeast grows, right in those dark, moist folds. That’s a yeast infection. From armpits to vaginas, a yeast infection is a dead giveaway of insulin resistance.

Swollen Ankles

Healthy ankles show off with beautiful bony prominences and a slimming, tapering leg. Swollen ankles are a sign of poor health. When health problems leave fluid stuck in the ankle, the shape changes. You can’t see the bones that normally define it, because they’re buried under fluid. Sometimes there’s enough fluid to leave a sock line, or a crease across the front of the ankle. All signs of trouble.

Thumb Shin Print

Check this one on yourself. Find your shin bone, then the spot about three inches north of your ankle. Push down really hard with your thumb and hold it there for 30 seconds. When you take your thumb off, a healthy shin has no impression. If you’ve got early insulin resistance, there’s a thumb print left on your shin.

Slurred Words After a Plate Of Carbs

Some signs don’t show from across the room. Insulin resistance drives blood pressure up, and it leaves people tired after they eat carbohydrates. But there’s one I can hear. About 30 to 40 minutes after someone swallows a plate of carbs, their speech changes. Listen to how they enunciate their words. A slight swelling in the brain sets in, and the cadence slows, almost a slur. It’s a solid clue about the health of their insulin.

The At Home Test

If you’re still not sure, there’s one surefire way to know. It’s a test you do at home, and it’s cheap. Test your Dr. Boz Ratio.

Insulin itself is a messy thing to measure. It’s very volatile. So instead of chasing insulin directly, we measure the Dr. Boz Ratio: Glucose/Ketone. The lower the Dr. Boz Ratio, the lower the insulin.

If your morning Dr. Boz Ratio is under 40, and it’s been at least 12 hours since your last bite, you don’t have insulin resistance. Between 40 and 80, I start to worry. Over 100, you’ve got it.

The best part of this number is that it does more than diagnose you once. It lets me watch your insulin change over time. A single insulin lab cannot do that.

What To Do

Stop counting calories. Start counting insulin.

The diagnosis of insulin resistance means the rules have changed in your body. You gain fat more easily, and the strategies that kept weight off in your younger years may not work the same way anymore. Luckily, the new rules do not require Navy SEAL discipline or an extreme exercise routine.

You may have heard me say that your body does not count calories. That is true. But that does not mean you are unaccountable for what you eat. It means calories are not the signal I want you obsessing over.

I want you watching insulin.

Before your body can efficiently store incoming energy as fat, insulin has to be elevated. Insulin is the hormone that tells your body what to do with the energy you just ate: move glucose into muscle, refill glycogen in the liver, or store excess energy in fat cells.

We can see how powerful that signal is by looking at what happens when insulin is missing.

People with Type 1 diabetes do not make enough insulin on their own. Without adequate insulin, glucose builds up in the bloodstream while the cells struggle to access that fuel. The body responds by breaking down fat at an extreme rate.

There is even a dangerous eating disorder called diabulimia, in which a person with Type 1 diabetes deliberately under-doses insulin to lose weight. Without enough insulin, they can eat enormous amounts of food and still lose weight because their body cannot properly store and use that incoming energy. This is life-threatening. Without enough insulin, ketones can rise uncontrollably and lead to diabetic ketoacidosis.

The problem in insulin resistance is the opposite. Instead of having too little insulin, your body is making far too much of it, too often. That persistent insulin signal keeps directing energy into storage and makes it harder to access the fat already sitting on your body.

For everyone trying to reverse insulin resistance, you need to ask: how much insulin does eating a meal require?

And three things about your food determine that answer: the type of food, the amount of food, and the timing of the food.

No Carbs

Here’s the secret. Every single morsel of food that you swallow stimulates insulin. Yep, that’s a fact. Stop eating food altogether and you produce no insulin. Before you go on a hunger strike, sort your food into three categories: carbohydrates, protein, and fat.

Of the three, carbohydrates squeeze the most insulin out of your pancreas. They cause the fastest, most robust rise there is. Protein comes in second, slower, and it doesn’t peak as high. Swallow fat, and your insulin rise is the slowest and the smallest of all.

So we eat fat first, and a lot of it. Don’t look at the calorie count. Fat has the lowest production of insulin, and it’s the best return on energy per bite. Eat fat while your insulin is low, and it really boosts your metabolism.

I’ve run experiments where I added a quarter cup of MCT oil, medium chain triglycerides, to my day. That’s 500 extra calories, and I still lost weight, because the low insulin let my metabolism run. So eat the fat, and keep those carbs low, under 20 grams per day.

Years of chronically elevated insulin will take years to reverse, so stay focused on the high fat. Oh, that’s the keto diet.

No Powder

The type of food is only part of it. The size of the food matters too, and by size I mean the particle size of what you eat.

If you grind up your carbohydrates, protein, or fat, all of them stimulate insulin. Pulverize a carb and you get the biggest insulin spike of all. What’s a pulverized carb? Flour, cornbread, sugar.

If you’re insulin resistant, you’re already overproducing this hormone, and those protein shakes aren’t doing you any favors. Grind your protein into a powder, blend it into a shake, and you’ll spike your insulin as much as a handful of carbs.

Even fat does it. Anything made from coconut or almond flour will spike insulin. The label says low carb, high fat, high protein. Your body makes the insulin anyway, and if you’re insulin resistant, it stays high for hours.

Remove processed carbs from your menu. Chew your protein, and chew your fat. You can’t chew your food into the tiny particles found in that processed food.

Eat Before Dark

Your pineal gland senses the sun coming up. It’s hardwired into us. That sunrise sets off a rise in cortisol, your brain reading the light, and cortisol tells your liver to release stored glucose into your blood. It’s a bump of fuel every morning, running on your circadian rhythm, meant for the first moments of the day.

If you’re insulin resistant, you top the charts. You and the diabetics put out the highest morning blood sugars of anyone. That high blood sugar squeezes your pancreas for insulin, and you never even swallowed a bite. That’s a dirty trick when you’re trying to reverse things.

You can’t get away from that rise in insulin. It’s linked to the rise in the sun. But you do control one thing: when you eat.

My insulin resistant patients do great when they only eat in the mornings. I know that’s a hard sell, so I start them with one rule.

Eat when the sun is up. If you get home at night and the sun’s already down, it’s too late to eat. Eat at that hour and you keep insulin and glucose high all night, which makes the next day even harder. That’s how the cycle feeds itself, and the whole thing turns into a nightmare.

Protect the dark hours from food. Leave time for your body to recover. Your timer restarts at sunrise. The more empty hours between your last bite and sunrise, the better you’ll do.

In Short

If you’re trying to reverse insulin resistance, stop making insulin. Eat mostly fat with a sprinkle of protein. Eat whole foods, not processed foods. And slide those calories as close to sunrise as possible.

Then keep checking that morning Dr. Boz Ratio, and watch the number fall as your insulin comes down.

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“Eat more fat. Fat makes ketones and keeps you full.”

“Eat more protein. You’re getting older, and if you don’t, your body will lose muscle.”

“Don’t eat too much protein. It’ll turn into glucose and kick you out of ketosis.”

None of those statements are wrong. The mistake is assuming they all apply to everyone, all the time.

After treating hundreds of patients with obesity, autoimmune disease, cancer, epilepsy, and severe insulin resistance, I’ve learned that keto isn’t the same diet for everyone. It’s a progression. As your body chemistry changes, your healing plan should change accordingly.

The advice that gets someone through their first month isn’t necessarily the advice that helps them reverse twenty years of chronic disease. Likewise, what works for someone who’s metabolically healthy is not enough for someone trying to repair decades of damage.

First, Teach Your Body to Burn Fat

There are a lot of highly motivated members in our community who make this mistake: they start keto, cut carbohydrates aggressively, and immediately add fasting without first teaching their body how to use fat for fuel. Incredible willpower, but this is the wrong approach.

During the early stages of keto, eating enough healthy fat gives your body energy while insulin falls and ketone production begins. Fat also provides the raw materials your body uses to make hormones such as cortisol, testosterone, and estrogen. Before your metabolism can efficiently burn the fat stored in your body, it has to learn to burn fat in the first place. This sounds simple: just eat a bunch of fat - indeed, it gets almost all of you into ketone production. However, the ability to burn fat for fuel depends on how excessive your insulin production was before you started Keto. Most of you in your 50s have been advancing your insulin resistance since your late teenage years. To reverse 30 years of this production surplus, you will need to keep the high-fat menu longer.

As your body becomes fat-adapted, important changes begin to occur.

Stored fat becomes available for energy.

Ketones start to fuel the body and calm inflammation.

Hormone production improves.

This is why the ketogenic diet can influence so many different symptoms at the same time. This stable energy production and rise in vital hormones affect every cell.

When fat intake is too low amid this transition, the warning signs appear quickly. Hair loss, dry skin, brittle nails, sluggish energy, depressed mood. These signs mean that the body is trying to adapt without enough fuel.

This stage of eating high fat triggered the first batch of cells in your body to begin burning it. Eating high fat to burn fat opened up the next stage of healing: using your own fat as fuel. The goal is to supply this powerful, superior fuel to all of your cells using your stored resources. Let’s move to the next stage of your Keto journey.

As You Heal, Nutrition Priorities Change

This is a common point of confusion: Will eating too much protein cause the body to convert it into glucose?

That process, called gluconeogenesis, is real. If you eat more protein than your metabolism can currently handle, your body can convert those amino acids into glucose, raise insulin, and lower ketone production. This is especially common in the carnivore world, where someone may eat only animal products yet still consume enough protein to interfere with ketosis.

The right amount of protein depends on your current metabolism and your goal. Someone trying to reverse insulin resistance, autoimmune disease, or obesity may need to restrict their protein intake more than someone who is already metabolically healthy.

However, before I tell a patient to eat less whole-food protein, I like to get an overview of their current lifestyle.

• Are they eating late into the evening?

• Is their eating window too long?

• Are they eating too often?

All three of these factors contribute to one big problem: they eat too much.

This problem prevents morning ketone production even when eating perfectly Keto food.

If morning fasting ketones remain low, excess food(including protein) is the problem.

Speaking of protein, we have to talk about protein powders. Just because the packaging says zero grams of carbohydrates does not mean the powder will have no insulin response. Powdered protein signals receptors in the upper digestive tract quickly and messages the endocrine system that food has arrived. These small, delicate particles of protein are unnatural. When nearly all of the receptors are saturated with powdered protein, this translates to a massive consumption of whole food protein.

1 scoop of powdered protein = 100% of the receptors filled → body converts excess amino acids into glucose (moderate to high insulin production)

20 oz of steak = 30% of the receptors filled → minimal insulin produced

If extra insulin still burns through your veins, you triggered massive disruption with that scoop of protein powder. Save your money. Don’t buy powdered protein.

As you get older, the quality of your protein becomes just as important as the quantity. Sarcopenia, the gradual loss of muscle mass and strength, threatens every aging person. Preserving muscle requires enough leucine, the amino acid that signals your muscles to repair and rebuild. Whole animal proteins, especially beef and other ruminant meats, provide abundant leucine, while collagen powders provide very little.

Your protein target is not the final authority. Your morning fasting glucose and ketones help determine whether your current intake supports healing or quietly sabotages your progress.

Let’s teach you how to eat enough protein to preserve muscles. This means you must produce ketones while you sleep.

Stop Obsessing, and Start Studying

Eventually, something interesting happens.

The food rules that helped you begin keto become less useful. That first crop of cells can no longer carry your body alone. You need more cells on the fat-burning side of the equation. Stop asking how many grams of fat or protein you ate. Start studying your metabolism first thing in the morning. This will predict what your body did while sleeping.

People make fun of me and call me a “number chaser,” but morning fasting glucose and ketone numbers matter.

Ketones measured later in the day mislead you. Once you start moving, exercising, or going several hours without eating, ketone levels fluctuate. Someone can also raise an afternoon reading by taking exogenous ketones or timing the test carefully. A good afternoon number does not necessarily tell me what the metabolism did overnight.

The morning fasting number tattletales on you. It reflects what happened during the hours you slept. In a healthy metabolism, glucose gradually settles overnight while ketones rise to cover the fuel gap. In a metabolically sick person, the decline in their glucose extends hours beyond a normal person. Some patients who eat at noon finally achieve their baseline blood sugar 7 hours later. This extended elevated glucose also kept their insulin high. Only when insulin returned to single digits could they make ketones.

Burning fat for fuel and recycling damaged proteins while you sleep is the holy grail to reverse chronic problems. We cannot directly measure autophagy at home, but morning fasting glucose and ketones provide the math to best estimate.

For people reaching for complete metabolic recovery, the morning numbers are essential. Losing the first twenty, fifty, or even one hundred pounds may happen quickly because carbohydrate intake drops and insulin improves. But reversing chronic metabolic problems requires more than the first easy win. The body needs enough time in ketosis to repair what took years to damage.

A morning ketone level of 0.7 or above indicates you were making ketones while you slept. Repeated morning readings of 0.2, 0.3, or 0.4 suggest the body fails to reach adequate ketosis consistently.

Press Pulse Strategy

You don’t need to chase the highest possible ketone number every morning, but the morning numbers tell the truth about your metabolism. Just because you stick to keto doesn’t mean your body heals the way you’d like it to. Travel, poor sleep, late-night eating, frequent meals, and long stretches without metabolic stress can gradually reduce ketone production.

I use a press-pulse strategy. Most of the time, I maintain a sustainable ketogenic rhythm. Periodically, I press the metabolism harder. I pull a lever to stress my mitochondria. I fast longer, use a sauna, or exercise to use circulating ketones and move glucose. Then I return to my normal routine.

These periodic stressors remind the mitochondria how to produce ketones so the metabolism does not slowly slide backward.

For a metabolically healthy person, checking morning fasting glucose and ketones once weekly confirms your strong motors inside your cells. For someone treating cancer, seizures, autoimmune disease, or severe insulin resistance, you must study more closely.

I eventually tell patients to stop letting macro calculators make every decision. Two people can eat the same amount of fat and protein and produce completely different morning numbers. Check numbers every morning until you restore health.

Important takeaways

• Eating enough fat is important at the beginning of your Keto journey, but this stage should not last forever.

• There is no single correct Fat-Protein intake ratio; it depends on how metabolically healthy you are. Check your numbers, then decide if you can have more protein.

• Stay away from protein powders if you are metabolically sick - it will raise your insulin.

• Morning numbers are the most important metric. Make sure your body makes Ketones while you sleep.

• Create metabolic stressors on top of the usual Keto diet: fast, exercise, sauna.

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Today, I’m answering the most common questions about peptides and listing some of the more common.

Common Questions:

What Are Peptides?

A peptide is a string of amino acids that acts like a signaling agent inside your body. Think of amino acids as the letters of an alphabet and mix those letters together, you get a peptide that delivers a highly specific message to the cell.

That message signals the cell to do something. After the delivery, the peptide quickly breaks down back into the individual letters, harmless amino acids.

What Do Peptides Do?

Well, almost anything.

Different peptides target different systems through the cells they signal. Some signal your body to release more growth hormone, others accelerate tissue repair, some regulate your immune system, improve your sleep, or even change how your body handles sugar. Some peptides break down before they ever get to their targeted cell, so those do nothing.

Do You Have To Inject Peptides?

For the most part, yes. Your stomach recognizes peptides as food and breaks apart those amino acids before they ever reach your bloodstream.

Oral or nasal peptides absorb through the mucosal layer and access your circulation, but injection remains the most reliable delivery system for peptides to reach their intended tissue.

Are Peptides Steroids?

Put simply, no.

Peptides are tiny water-soluble particles that bind to cell membranes. Steroids are large, fat-soluble structures built from cholesterol that pass through the cell membrane and affect gene expression within the cell nucleus.

So, when people inject steroids, they’re replacing or mimicking hormones like testosterone or growth hormone. When people inject peptides, they signal cells to either increase or decrease the function of that cell by kind of knocking on the outside of the cell.

Testosterone-steroids supply testosterone hormone directly, whereas the peptide might increase the production of testosterone by telling the cell what to do. With peptides, your body still controls the output.

Are Peptides Safe?

That depends on several different factors.

An FDA-approved peptide has gone through clinical trials with years of safety data behind it, making them pretty safe. We know the risks going in. Most peptides being discussed today have not gone through that process.

They’re sold as research chemicals, technically not for human use. But millions of people are using them. That doesn’t automatically make them dangerous, it makes it unknown.

Instead of the rigor of fact-check clinical trials, you’re relying on anecdotal experience by folks who might have ulterior motives.

Are Peptides Legal?

That’s more complicated than a simple yes or no. Peptides sit in a gray area.

While most peptides can be purchased, the FDA forbids selling them for human use without approval. So, they get listed as “research chemicals” and sold in that legal gray zone.

Popular Peptides

Let’s run through the most popular peptides people are taking now and what they do.

BPC-157

BPC stands for body protection compound. It was discovered in and isolated from the human gastric juices. Kind of gross, but true.

Patients use this to accelerate the tissue repair of the slow-growing tissues like tendons or ligaments, deep muscle injuries, and have remarkable testimonies. Other folks with chronic gastrointestinal issues have found the reversal of these issues after several weeks of therapy.

They inject the peptide subcutaneously in the fat layer under the skin causing a systemic effect. People typically inject it at the site of their injury hoping for the blood to flood the area with healing cells linked to growth factor and the new blood vessels for these types of tissues.

TB-500

TB-500 perfectly partners with BPC-157. While the BPC-157 is touted as targeting those localized healing for connective tissue, it’s TB-500 that links to muscle cells.

It promotes cell migration to damaged muscle cells, reduces the inflammation in that area, and improves the flexibility of the tissue. If you have a major injury, stacking these two together is widely considered the holy grail of recovery.

Retatrutide

I’m most excited about this one. This peptide lingers just outside my reach in the late-stage clinical trials. It’s the most powerful weight loss drug I’ve ever seen.

Retatrutide hits GLP-1, GIP, and glucagon receptors simultaneously. The human trials have shown that the participants lose more weight with retatrutide and also catabolize less muscle mass.

It swiftly shifts their body into the maximum autophagy while increasing fuel to their brain.

My attraction to this research comes from what it seems to do in brains suffering from chronic metabolic diseases like Parkinson’s or Alzheimer’s disease. I can hardly wait to see what this does to my patients who are teetering on the edge of this problem.

Epitalon and Pinealon

Epitalon and Pinealon stacks together for anti-aging and brain health.

Epitalon regulates the pineal gland, it boosts some natural melatonin, and theoretically lengthens telomeres. Those caps on your DNA linked to biological aging.

Pinealon acts as a biological regulator that apparently protects the brain. It improves cognition, and together it’s claimed that they reset the circadian rhythm, improve deep sleep, and fight that cellular aging.

GHK-Cu

GHK-Cu, known as the beauty peptide. It’s a naturally occurring copper peptide famous for skin remodeling, collagen production, and even wound healing. It also tends to help hair grow. You’ll often see this one included in those high-end creams.

But, people also do inject it for a systemic full body anti-aging effect. Just know that injecting this one is notorious for feeling like a sting of a wasp.

Melanotan II

Melanotan II. Often called the Barbie drug, Melanotan II mimics the hormone that stimulates melanin production. So, people use it to get a deep, dark tan without spending hours in the sun.

I would avoid this one. While you do get a good tan it stimulates melanocytes across your entire body, including the ones existing in your moles. With some case reports even progressing that mole into a melanoma, a serious form of skin cancer.

It also has the unfortunate side effect of causing spontaneous erections. This happens because Melanotan II binds to the central nervous system and inadvertently signals the lumbosacral spinal cord and brain centers responsible for erectile function.

In short this peptide activates a receptor system that affects multiple processes across the body. This undirected activation can cause problems from inappropriate erections to skin cancer.

Now, I obviously don’t recommend that you go out and inject peptides that you learn about on the internet. It’s easy to do damage if you don’t know what you're doing. If you're looking to improve your health try keto first.

So what’s the problem?

What happens when you try to stop.

Study after study shows the same pattern: within a year of stopping a GLP-1 medication, the majority of the weight returns and the improvements reverse. Why? Because the drug was doing the work the whole time, while the metabolism underneath never changed.

And it’s not just in the medical literature. I see this with my patients all the time.

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Let me tell you about a patient I’ll call The Trader.

In 2022, his blood sugar had climbed into diabetic territory. His doctors did what they were trained to do and pulled out the best tool in the modern diabetes arsenal: tirzepatide. They prescribed the highest dose available, 15 mg injected weekly.

But two years later, his blood sugar had not improved. It had actually gotten much worse. His average glucose climbed to 266. He didn’t lose any weight or experience a loss of appetite.

The strongest metabolic drug on the market, at the highest possible dose, made him measurably worse.

What They Do

GLP-1 medications work by mimicking a hormone your gut is supposed to release after a meal. That hormone tells your pancreas to secrete insulin, tells your liver to stop dumping glucose, and most importantly, tells your brain that you are full. These medications slow stomach emptying so meals satisfy you longer. They also dampen the food noise, that background static in your mind that is always thinking about the next meal.

That last part is real. I’ve had patients tell me it is the first time in their adult lives they have eaten a meal and simply stopped eating without forcing themselves to stop.

But here’s what the drug is not doing: it is not fixing your mitochondria, it is not reversing the cellular damage that made your metabolism break down in the first place, and it is not teaching you the skill of being hungry but choosing not to eat.

It quiets the symptoms, but I contend that it does not heal your metabolism.

His Real Problem

Back to The Trader.

His problems didn’t start in 2022, they started eight years ago with a diagnosis of colorectal cancer. After the following decade of chemotherapy, surgical bowel resection, and then a catastrophic fall that left him immobile for eight months, after all this his mitochondria were barely functioning.

Healthy mitochondria inside your liver produce ketones. The mitochondria inside your muscle cells burn ketones and fat for fuel. When damaged, whether by chemo, trauma, or years of sugar toxicity, fat stays locked inside fat cells. Your body cannot access its own stored energy.

The Trader’s damaged mitochondria sabotaged the power of Tirzepatide. The drug attempted to optimize his crippled system, but it required significant repair before it could respond. He did not know that. So in a final attempt to fix his metabolism he gave up on the drug and water-fasted for 21 straight days. He tried as hard as anyone I’ve ever met. But his metabolism failed him. After 21 days of fasting, his glucose still smoldered at 108, and his ketones limped along at 0.7. Healthy patients achieve better results simply by skipping breakfast.

His cells could not access fat, so they consumed muscle instead. In my book, we call that starving. Fasting without a functional metabolism is just suffering. Stop that. Learn what The Trader did wrong.

Repair First

When The Trader came to me, I did not impose a stricter protocol on him. I told him to eat.

Specifically, I told him to use a high-fat, low-carbohydrate ketogenic diet designed to trigger mitophagy, the cellular recycling process that clears out damaged mitochondria and builds new ones. If he wanted to get any results out of tirzepatide we had to get the basics working first.

Over the next three weeks, we tracked his glucose and ketones daily.

During week one his glucose dropped from 208 to 160, and he produced measurable ketones for the first time in years.

In week two, after three days of sardine fasting, his glucose dropped to 140 and his ketones rose to 2.0.

Think about that. One week of keto and three days of eating sardines produced three times the ketones that 21 days of water fasting had produced, because now the machinery could actually do its job.

In week three, after a 72-hour water fast his glucose dropped to 118 and his ketones surged to 4.7.

His mitochondria had been rebuilt. Now, when we applied the stress of fasting, it served as a stimulus rather than a trauma.

Then The Drug

After three weeks of repairing his metabolism, I offered The Trader a 12-week extension with the same strict ketogenic diet, the same daily tracking, and one addition: tirzepatide.

At 0.6 mg per week, that was 4% of the dose that had done nothing for 2 years.

Over the next twelve weeks, The Trader lost 44 pounds. His food noise vanished. His ketones continued climbing. In December, his blood glucose dropped below 100 for the first time in years. His A1c went from diabetic to 6.0.

The drug did not change. His metabolism changed. Once the foundation was repaired, a microdose of the same medication that had completely failed him produced a transformation.

What This Means For You

If you are currently on a GLP-1 medication: are you supporting the drug with an already heathy metabolism? Or are you riding the drug and waiting?

If it is the second one, I already know how your story ends. The drug stops, the weight returns, and you are right back where you started with a more expensive medical history.

The exit strategy from Ozempic is not a taper schedule. It is not a meal plan. It is not another medication.

Build a metabolism that no longer needs the drug.

That means building a bed of ketones and repairing your mitochondria before you stress them. The drug is a powerful tool. The Trader is proof of what is possible when it is used at the right moment in the right metabolic state. But that same tool, when used on a broken metabolism, does not fix it.

If you were here for the first one, you know the drill. If you're new, here's what I want you to do...

In the comment section below, ask your question. Then read through what everyone else has asked, and press the ‘like’ button on the ones you want answered most. The questions that rise to the top and are more likely to get selected.

A word on what makes a question great

The best questions I get all have one thing in common.

They were a story with a twist. “I did X, I expected Y, but Z happened instead. What’s going on?”

They came from a real situation somebody was actually living, and the answer ended up helping far more people than the person who asked it. Those are the ones we can really dig into on the show.

One more thing. My favorite questions are the ones that send me to the latest literature. If your question makes me ask "wait, why does the body do that?" you have my full attention. I want questions that make me study. Bring me one of those, and we will learn it together.

Now… GO!

Reminder: Office Hours is for paid subscribers. If you haven’t upgraded yet, join us to ask your questions, attend live, and get access to the full searchable archive.

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My son tore a muscle deep in his back during wrestling season and regionals were three weeks out. Rest was not an option.

I told him the fastest way to repair the injury was to take MCT oil.

I’ve been selling C8:C10 since 2018, so I had a lot on hand, and personally I’d been in a season of low ketones. So, the best way to help somebody with their health journey is to join them, and we did an MCT sprint.

Why MCT Oil?

Medium Chain Triglycerides are a type of fat that bypasses digestion. They are a string of 8-10 carbon molecules linked together in a chain. Thats why you see C8 or C10 everywhere. At this size, they are able to slip through the stomach lining and immediately enter your bloodstream. They then zip over to the liver, and out come a bunch of ketones. If you go to C12 and above, these are considered large-chain triglycerides. They are a bit cheaper to produce but do not help you generate ketones; they're too large to slip through the stomach lining, and they must be digested normally before they can be made into ketones.

Medium Chain Triglycerides are typically what you find in olive oil or lard, and that’s the whole trick. It’s short enough that your body can pull it straight into the blood and send it over to the liver instead of having to break it down first.

These ketones made in your body last from 6 to 8 hours, all while delivering strings of healthy fat to places like the brain and other parts of the body.

So what does it mean to skip the digestion? If you swallow lard or olive oil, the length of that fat requires your body to digest it and sift it through a safety protocol inside your system.

MCTs are so nutrient dense and really have a superpower for turning into ketones, and the body has figured out a way to bypass the safety check. Although this sounds dangerous, it really is a rapid way to enhance ketosis when swallowing them.

So that’s the fuel. Now back to my son’s back.

Why This Helps

But how are ketones supposed to help with back pain? Well, ketones create a very anti-inflammatory setting. My son’s back pain was caused by an overworked and torn muscle.

And this inflammation was a signal sent by the body for the immune system to come repair it. Thanks to the sport’s intensity, the downtime between these extended practices did not allow him to fully shut off that signal. So it was turning into a chronic inflammatory process, much like arthritis.

I told my son that if we could bathe that injured muscle in a generous amount of ketones for an extended period, we would not only reduce inflammation but also accelerate repair, and hopefully have him ready for that regional tournament.

Knowing all of that, the only real question left was how much to take.

What We Did

Instead of titrating the dose like I would with patients, my son started out with a fistful of MCT capsules on day one. I usually start patients out with one pill per day and titrate up over the next couple of weeks to about a dozen pills twice a day.

Is that large of a dose safe? Well, the studies done for mild dementia took patients who started out with 30 pills a day and compared them to the ones who took 45 pills a day, and they started right out at that dose. Needless to say, they lost a few patients in that study because of diarrhea.

In my practice, we back off once they get gut symptoms. But if you have a healthy teenage boy who’s been living in a ketogenic home for a lifetime, he was able to handle two fistfuls a day of MCT and rapidly advanced to three fistfuls per day. Personally, I got to two fistfuls a day and had a tummy ache, so I was able to persist at that dose but not advance.

So what happened to our bodies?

What Happened?

First thing, it suppressed our appetite. Both my son and I forgot to eat.

I don’t forget to eat. My fasting is very intentional. But forgetting to eat is an excellent sign that the fat-based hormones that surge during a ketogenic state are in good health.

The second thing is the blood sugar. That week, I had morning fasting blood sugar levels in the 50s to 60s, and one morning it even dipped to 39. That’s pretty low.

I tell patients to gauge how they feel if this ever happens, and to make sure they’re taking salt. I felt sharp, had strong energy, and I was bridging that energy deficit with a bunch of ketones.

Personally, I love seeing my morning fasting blood sugars drop into the 60s because, after years of insulin resistance, I know that’s a moment when the glycogen stores in my liver are almost gone.

The Results

So what happened to my ketones? Well, they had been wimpy prior to this. My years of doing keto led me to a ketone range of 0.5 to 0.9, and I was stuck.

This graph shows different ranges of my ketones at different times. I lead a course in February and had done some challenges like a 3-day sardine challenge and then a 72-hour fast and had some really awesome results. However, afterward, I didn’t do so well for a while.

Adding those MCT took my ketones from that 0.5, and by the end of the week I’m over 2. Those are morning fasting ketones too, something that’s very difficult for my body to do in the morning.

My most surprising result was the 6-pound weight loss in one week. That was not my goal, but the boost of ketones revved my metabolism and suppressed my appetite, and that effect didn’t just go away at the end of the week.

It carried me for several weeks to come. I was very impressed by how well this worked.

For my son, this little experiment worked wonders. The higher ketone levels reduced inflammation in his back, allowing the torn muscle to heal. If you’re looking for a good way to increase ketones, consider checking out our product.

• A perimenopausal woman who reintroduced carbs and watched her metabolism break…

• A carnivore stalled with low ketones despite initial success losing 100 pounds…

• A listener who fears keto triggered a thyroid storm…

• A woman trying to quit tirzepatide after a brutal rebound…

• And an otherwise lean, healthy woman wondering if her morning blood sugar signals insulin resistance.

In each case, Dr. Boz works from her proven frameworks to give her best answers. The result is a working map of how she thinks when a patient who did everything right hits a wall.

This is a preview. Paid subscribers get the full session, the archive of every Office Hours going forward, and the written letters the team is publishing from the questions we didn’t get to in this session. Subscribe to unlock the full session immediately.

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We discuss:

• Welcome, opening prayer, and why this format exists [0:00]

• What Office Hours is for, and how it differs from YouTube and the 21-Day Metabolic Kick [2:22]

• Question 1 - Siouxie: “Carb cycling broke my metabolism. Now what?” [5:57]

• Perimenopause, estradiol volatility, and how high insulin suppresses fat-based hormones [9:57]

• Is carb cycling is beneficial for hormones? [18:25]

• Question 2 - Dania: Lost 100 lbs on carnivore, but ketones won’t rise [19:52]

• The Keto Continuum, the 72-hour fast, and sliding meals toward morning [20:32]

• The sardine “second meal” strategy [32:37]

• Question 3 - Jackie: Can keto trigger a thyroid storm? [34:49]

• What a thyroid storm actually is, and why thyroid is downstream of insulin [35:56]

• Question 4 - Mrs. Perl: Tirzepatide dependence and how to taper off [42:37]

• Food noise, fear, EMDR, and stretching the dosing interval [46:31]

• GLP-1s and bone density [50:34]

• Question 5 - Cari Ann: Lean, fasting, and is this insulin resistance? [53:05]

• The Kraft insulin patterns and beta-cell burnout [56:06]

• Using uric acid and beta-cell antibodies to make the diagnosis [59:39]

• Closing thoughts on the Substack platform and writing [1:02:06]

Welcome, the opening prayer, and why this format exists [0:00]

• This is the first “Office Hours” session, and the setup is new — we were 15 minutes delayed due to technical problems

• Jack is our co-host handling “all things technical”

• Dr. Boz opens with a prayer, framing teaching as her calling and asking for the session to serve the people listening

• The goal of the format: answer the harder, more specific questions that don’t fit a broad YouTube audience and that carry too much clinical liability to answer casually there

What Office Hours is for, and how it differs from YouTube and the class [2:22]

• The easy questions are already answered elsewhere; this is meant to be a resource for people more committed than a casual understanding of the ketogenic diet

• The way Dr. Boz teaches keto is specifically as a tool to reverse medical problems and deprescribe medications — not as a way for her to take on new patients

• Many listeners end up more educated about the next step than their own provider

• The 21-Day Metabolic Kick only runs twice a year, takes 200 students, and has a $2,500 entry fee, so it doesn’t fit everyone

• The hope is that answering real, vulnerable, story-driven questions multiplies the teaching to a much larger audience

• Questions that aren’t answered live will get researched by the team and published here on Substack

Question 1 - Siouxie: “Carb cycling broke my metabolism. Now what?” [5:57]

Siouxie’s background

• Perimenopausal woman Dr. Boz knows from the keto space

• Followed the ketoCONTINUUM for a couple of years with real success:

  • Lost about 45 lbs

  • C-reactive protein down to 0.2 (a very good sign)

  • Blood sugars in the 80s, ketones north of 1.0 and sometimes near 2.0

• She was winning. If she ate some carbs, she was back in ketosis within 24 hours

What went wrong

• In December, she assumed the success meant she had reversed her insulin resistance and could return to “life before keto”

• She added sweet potato and rice and stopped checking her numbers daily

• Over the next three months: ~30 lb weight gain, 5 inches added at the waist

• Even back on strict keto, her fasting glucose crept from 85 up to ~100; she could get glucose back down but her ketones never recovered, staying stuck at 0.3–0.5

Siouxie’s own theory vs. Dr. Boz’s

• Siouxie blames “bad luck” that menopause hit at the same time

• Dr. Boz’s counter-argument: Siouxie induced menopause by carb cycling while her hormones were still fragile

Perimenopause, estradiol, and hormones as fat-based [9:57]

• In perimenopause, estradiol (from the ovaries) is extremely volatile — bouncing up and down before finally dropping to the floor

• Estradiol slams down within a few months while brain hormones (FSH, LH) climb, “hollering” for a hormone the ovaries can no longer make

• Hormone replacement essentially restores both the estradiol and progesterone lines

• Key mechanism Dr. Boz emphasizes:

  • The sex hormones (estradiol, progesterone) are fat-based hormones, made from cholesterol

  • As Siouxie lost stored fat over two years, she released fat-based hormones into circulation

  • When insulin went back up, those hormones were suppressed and kept in dormant/cholesterol form

• Sardines brought her glucose down, but did not bring her ketones up — glucose control alone is misleading because it doesn’t reveal the still-high insulin state

• These hormones aren’t just about hair and skin — they affect brain function, sleep, and immune function

The fix

• Once insulin is being produced at that level, it stays there until you do something pretty extreme, and you’ll know you’ve succeeded when ketones rise

• 16:8 is not a strong enough stimulus for where she is now

• She needs to advance along the ketoCONTINUUM: shorten the eating window further and add fasting (e.g., a 72-hour fast)

• A single can of sardines “tickles” the metabolism; real progress requires the “nothing burger” (fasting) done more than once to repair fat cells and fat-based hormones

Is carb cycling beneficial for hormones? [18:25]

• Jack asks: Siouxie tried carb cycling because she’d heard it was good for hormones — is there any benefit at all?

• Dr. Boz: no. She gets many questions about eating sweet potato during the luteal phase

• Good research teams are showing this claim isn’t true, and in practice she sees carb cycling repeatedly harm fragile patients

• Siouxie had barely stepped over the line of reversing insulin resistance, and sprinkling carbs back in pushed her into menopause — creating a bigger puzzle to solve

Question 2 - Dania: Why must I fast to make ketones after losing 100 lbs? [19:52]

• Dania is 63 years old, 5’6”, currently 200 lbs; lost 100 lbs on carnivore over 20 months

• Once she started testing ketones, she rarely saw above 0.5, mostly 0.3

• Wants to know why she has to keep fasting to make morning ketones if she’s already zero-carb and eating only twice a day. She also wonders whether she’s eating too much protein (macros 65–75% fat)

That’s the question, and the answer is not what Dania expected.

In the rest of the show, for Dr. Boz Office Hours members, we cover:

• Why zero-carb and two meals a day stopped working, and what has to replace it

• The 72 hour fast plotted hour by hour, and what only happens at hour 72

• The one change that drops the overnight Dr. Boz Ratio into the 60s, which most carnivores never try

• Whether keto can trigger a thyroid storm, and why the thyroid is downstream of insulin

• How to taper off tirzepatide without the rebound that sent Mrs. Perl back on it

• The Kraft insulin pattern that hides behind a normal fasting test, and the lab that catches it early

If you want to understand your own metabolism instead of following someone else’s rules, come inside.

The weight loss is the smallest thing that happens here. Members learn to read glucose, ketones, and the Dr. Boz ratio well enough to know what their own body is doing on any given morning, which is the skill that outlasts every plan.

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Many of my patients have wasted their time and money without thinking through this first. If you’re planning to do keto for more than just a flash in the frying pan, don’t run to the grocery store. I insist that my patients push reset inside their home and remove food before going out and buying some.

Clean your cupboards

I mean it. Carbs are addicting, throw any out before you start. You need your house to be a sanctuary without temptation. On the diet, you’re limited to 20 carbohydrates a day. Many of my old favorite snacks took up most, if not all, of that, so out they went. If it helps, think of this as some spring cleaning. Don’t skip this, it makes everything easier.

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Before you listen to any more of my advice, you should know two things about me. Number one, I was raised by a beef and pork farmer from the Midwest. Everyone in the county had a deep freeze filled with quality meats from the neighbors in the county who raised them, so having good meat seems like an obvious part of the ketogenic diet.

Number two, I’m super stingy. I hate throwing away food, and I really hate it when it goes bad, so this list will reflect that. But I still insist that you empty your cupboards, freezer, and fridge before you start.

Salt

First on the list: salt. One of the key issues with starting the ketogenic diet is the dramatic shift in fluids during the first week. This fluid shifts occurs because of the drop in glycogen, this causes you to flush out several salts and minerals. Before you start keto, you should stock up on some good quality salt to replace what you’ll lose in the first week.

The key is to start with high-quality salts and then add the flavors you like. For high-quality salts I like Redmond Salts. When you’re ready to add some flavors onion and garlic salt are some good alternatives. Other seasonings I would recommend include dried onions, black pepper, and some oregano.

I’m kind of a nut about basil. I love the flavor, but I think it tastes disgusting when it’s been dried out, so I buy the plant. It’s the only plant you’ll find in my house. The final two seasonings I’d throw in are some ginger paste and one of those plastic limes or lemons for the juice.

Vegetables

Before we take on vegetables do not go to the produce aisle. It’s filled with a landmine of temptation called fruit! Stay away from that! Head over to the freezer section, and while you’re walking there, honestly ask yourself this question: Do you like vegetables? Actually, like them? If so, great! Pick the green ones.

The purpose of vegetables on the keto diet is to add fat to your gut. It’ll be the carrying agent for fats to your gut without adding too many carbs. Remember, this diet is restricted to 20 carbs per day.

My favorite frozen keto vegetables are Brussels sprouts and spinach. If you wrinkle your nose at that, follow my lead by ordering the spinach dip off the appetizer menu the next time you eat out. I ask for celery instead of bread. It’s great. I soak Brussels sprouts in butter or bacon grease, and then I broil them to a crisp. They’re great. Remember, vegetables are here to help transport fat to your gut.

If you sneak over to the produce aisle, grab a head of cabbage. It lasts for months and doesn’t go bad, but when you don’t know what to cook and you’re tired of frozen vegetables, it’s a great way to get something fresh. I also like to crisp it up, like with the brussels sprouts under the broiler.

The great thing is, if you don’t like vegetables, this diet has all the yummy additions that make them taste wonderful, like butter, salt, cream cheese, and bacon.

If you are in the habit of eating vegetables, buy the vegetables you like, but be careful to look at the carb count. Remember: you’re limited to 20 carbohydrates a day. I don’t eat that many vegetables on the keto diet now, but when I started, I had frozen broccoli, cauliflower, onions, peppers, and kale. The latter is an acquired taste, but you get used to it.

Don’t waste your money on vegetables if you didn’t like them before going keto. You’ve already thrown away a bunch of food. Don’t waste your money on vegetables you don’t like. Start with one vegetable and spend your money on the salt and fat to make it taste good.

Saturated Fat

I want to remind you that this is a high-fat diet, so everything we’re talking about is filled with fat. You need to eat fat. It’s what makes us feel full and acts as an anti-inflammatory. It’s also the source of the missing endocrine and hormonal messes that most of my patients are suffering from. They are chronically inflamed, and fat is the antidote.

I know it goes against what you’ve all grown up believing, but saturated fat is actually an anti-inflammatory, not a villain. Saturated fats are those fats that are hard at room temperature, like butter, coconut oil, and lard. These are great to cook with, an old stand by I’ve already mentioned is bacon grease. If you love the taste of bacon save the grease after you’re done and use it to cook your eggs. They taste great!

Add salt to the fat. Even if you add it to water, swish it around your mouth, and swallow it, the salt will cut through that fatty lining and stimulate your parotid gland to wake up and do its job. That gland, along with several others, are supposed to help your body emulsify the fats and get them into circulation, and if you’ve been on a low-fat diet, it’s going to take a week or two to wake up those organs and let them do their job. Keep eating fat and use salt.

Eggs, Cream and Cheese

Next, buy lots of eggs, but every keto list tells you that. My favorite way of eating eggs after years of this diet is actually to pickle them. You take a boiled egg and you soak it in brine for four to six weeks. It is delicious.

Butter and heavy whipping cream are the staples of this diet. For those of you who are lactose intolerant, remember that lactose is a sugar, and when you buy the fattiest cream, there should be no sugar or lactose in it. Add some full-fat cream cheese, full-fat sour cream, and some mayonnaise. I like the mayonnaise made out of avocado oil.

Grab some block cheese. I recommend the harder ones, and I tell folks to stay away from the shredded cheese. There’s a fine dusting of powder on each shred of cheese that keeps it from clumping, and that powder is often flour or starch, both carbs.

Meats

And then there’s the meat, which seems like the easiest one, but maybe it’s because of where I grew up. You can add bacon, brisket, ribs, salmon, pepperoni, hard salami, and poultry, then cook it in fat. The best advice I can give is to keep it simple. Keto can be a hard transition, so don’t complicate it any more than it is.

Fish

Canned fish can be an exalt source of fat and other nutrients you need on the keto diet. My go to are Sardines in olive oil. They're great because a single can is usually enough to fill me so it stops me from over eating. They're also packed with various nutrients. If you don’t like the taste of sardines try mackerel.

Keto Comfort Food

Carbs are addictive, and they’re addictive for a reason. They comfort us. As I’ve said, I grew up on a farm, and for my whole childhood, we ate ice cream every night, delivered to the farm by the Schwan’s man. It took me over a year and a half to break that habit.

Something that really helped me was freezing avocados that were starting to go bad, since I didn’t want to throw them away, and then mixing those frozen avocados with stevia, cacao powder, and either heavy whipping cream or cream of coconut milk. It was a lifesaver when I was stressed out. It brought me back to my childhood and gave me some easy comfort and a feeling of safety.

Another staple: small bite-sized bits of pork belly. I usually get my pork belly from Costco and cook it all in one go. This would leave me with a big bag of salted pork belly that I could easily snack on for weeks.

Let’s help each other out by sharing some of your comfort foods in the comments below. Share some keto recipes you use to comfort yourself.

She was fighting her third battle with cancer. We stood together in the hospital lobby, trying to absorb the news that it was back. She had refused chemotherapy after the devastation the last round caused, and she looked at me and asked, “If it was you, what would you do?”

I told her, “Go home and throw out the carbs.” And I did it right alongside her.

Six weeks later, her cancer was down by 70%, and I had lost 10 pounds.

But we made a ton of mistakes in the beginning. Our resolve to fight back against cancer kept us going through the long stalls, but if I could do it all again, these are the mistakes I wish I hadn’t made.

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Mistake #1: Gluttony

I was gluttonous about fat, and I stayed that way for too long.

When you transition to a high-fat metabolism, you have to nourish your fat-based hormones. Every one of them starts with cholesterol, which is itself a form of fat. In those first weeks it’s crucial to restore the cholesterol your body keeps in motion, because that cholesterol is the raw material your body uses to build all of those hormones.

This is why the first few weeks of keto feel so good. Your energy climbs, your immune system gets stronger, your metabolism comes alive.

When I started, I was like you. All of those fat-based hormones were locked inside my fat cells. When I changed my chemistry, they replenished. Then they activated. They left my fat cells and moved back into my lean tissue, where they went to work on my immune system and my energy.

I never felt hungry eating so much fat. I loved it. It tasted great and it kept me full.

But on the ketogenic diet, everything stabilizes eventually. To keep getting the benefits, I had to move on and put my metabolism under new stress.

Before keto, my blood sugar told the whole story. Three meals a day, every one of them processed, and my food sent my blood sugar way up.

When I started keto and held myself to 20 total carbs, that blood sugar dropped. At the same time, a wave of ketones rolled in, and that’s the moment I started feeling so well. My whole metabolism changed.

Then my body did what it was supposed to. It adapted. Those ketones settled back down to only the ones I was actually using.

That is when my results stalled, and the clue was right in front of me. I accidentally skipped a meal one day and barely noticed, because the chemistry was carrying me. I was doing great, so I never took the next step. I never dropped down to two meals a day.

This high-fat, three-meal stretch, the gluttony phase, should have lasted four to six weeks. I stayed in it for months.

Mistake #2: Keto Desserts

In my high-carb life, I used food for comfort. On keto, I tried to do the exact same thing, reaching for sugar substitutes and rebuilding the foods I missed without the carbs.

Just don’t.

Stay away from the fat bombs and the keto desserts. It is not a good plan. You would never tell an alcoholic to replace whiskey with wine. Don’t replace dessert with keto dessert. Replace it with community.

If you’re used to something sweet after a meal, build a different ritual in its place. A board game. A card game. Anything that raises your oxytocin and stirs up that loving hormone inside you. That will serve you far better than a fat bomb ever could.

Here is how I mine my own oxytocin. I pray. I write a gratitude list. I play with the dog. I love a good puzzle. When I need a distraction, my husband and I find a show to watch. We play games together. We do whatever it takes to keep our focus off food as we wind down at the end of the day.

Mistake #3: Measuring

This brings me to my biggest mistake of all. Measuring.

Through everything I just described, I wasn’t really testing. I was enjoying my improved metabolism so much that the stall slipped right past me. I had forgotten the most basic rule of all: you are not on the ketogenic diet if you are not circulating ketones.

The urine strips are great. I tell my patients to pee on one first thing every morning, because it’s wonderful affirmation that you’re making ketones and putting them into circulation. But I waited a full year before I pricked my finger to prove I was still circulating them once I was keto-adapted. That is exactly when blood ketones start to fall, and exactly when you need a better measurement to know what is really going on.

Once I finally started measuring, the numbers told me precisely when to move.

Here is what happened when I dropped to two meals a day:

At first it put a real stress on my metabolism, and it produced a fresh wave of ketones. But before long, my circulating ketones fell below 0.5. That was my signal to push my metabolism again.

The best way to do that is to shrink the number of hours you allow yourself to eat. It’s called closing your eating window, or time-restricted eating. I did what most people do. I skipped the morning, ate around noon, and ate again in the evening. It worked fine at first. Then those ketones sank right back down. Even on a morning when I ate nothing, my blood sugar still ran high. It was like half a meal showing up in my bloodstream out of nowhere.

The fix is to move both meals earlier in the day. That gives you a higher wave of ketones that lasts longer. When your first meal overlaps with that natural morning rise in glucose, you cut down the number of times insulin has to surge.

If pricking your finger scares you, here’s a pro tip. Use the side of your finger, and use a spring-loaded lancet. You barely feel it, and if you do, it’s so small it isn’t worth a complaint.

WARNING: The steps I’m about to share with you will lower your blood pressure extremely fast. If you are currently taking blood pressure medications, you cannot just try this without talking to your doctor.

Why? Because this works so quickly that if you don’t titrate your prescription, your blood pressure could actually drop too low. Talk to your doctor.

Your Blood Pressure Medication Isn’t Treating the Root Cause

High blood pressure is called the silent killer — but what if I told you most people have it for a completely fixable reason that has nothing to do with salt or genetics?

And while the blood pressure medications your doctor prescribes are perfectly good drugs… they have a problem: those pills will never treat the root cause of your high blood pressure.

I don’t want to subject my patients to a lifetime of medication if we could just treat their problem in the first place, so let’s break this down once and for all… starting with the #1 culprit of high blood pressure.

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Salt Isn’t the Root Cause of High Blood Pressure

For decades, we’ve been told that salt is the ultimate enemy of blood pressure. But the truth is, salt was just the scapegoat. The real driver, the root cause for the vast majority of people, is insulin resistance.

The Three Ways Insulin Raises Your Blood Pressure

Most people think of insulin as just a diabetes thing. It’s not. It’s a blood pressure thing too.

Insulin tells your kidneys to hold onto sodium. Water then follows that sodium and the total volume of blood in the system expands… therefore the pressure goes up. That’s pathway one.

Insulin also activates your sympathetic nervous system, your fight-or-flight system. Your vessels constrict. Pressure goes up again. That’s pathway two.

And over time, chronically elevated insulin causes your arterial walls to thicken and stiffen. Your vessels can’t expand the way they should. Pressure goes up a third time.

Three separate pathways driven by one hormone. And it’s all reversible.

How to Know If Insulin Resistance Is Your Problem

You do not need any fancy labs. In my clinic, spotting insulin resistance is simple: If you carry weight around your midsection, crash after meals, crave carbs, or you’ve been told your fasting glucose is “borderline”… your insulin is almost certainly elevated.

To fix this, the ketogenic approach wins… every time. Cut the grains, the sugars, and the carbohydrates entirely. The goal is to stop spiking insulin repeatedly throughout the day.

Every spike tells your kidneys to hold fluid, tells your nervous system to squeeze your vessels, tells your arteries to stiffen up. Stop the spikes, and all three of those pathways start unwinding.

I know what you’re thinking. “But I already eat healthy.” Define healthy. Whole wheat bread still spikes insulin. Low-fat yogurt with fruit is loaded with sugar. The cereals that say “heart healthy” on the box are some of the worst offenders.

Track what you eat for three days and tally up the total carbohydrates. Most people are surprised by what they find.

If that number is over 20 grams per day… insulin will keep your blood pressure high.

When You Eat Matters As Much As What You Eat

On top of what you eat, I also want you thinking about when you eat. Compress your eating into a defined window of 8 to 10 hours and you’ll lower your insulin exposure without changing a single food choice.

And here’s the part that shocks most patients when they fix their insulin…

Some people lose 5 to 10 pounds in the first week. But it’s not fat.

Within days of lowering insulin, your kidneys start releasing the sodium and water they’ve been holding onto. It’s the fluid that’s been piling up because insulin told the kidneys to hold it there.

That excess fluid drains and your blood pressure rapidly drops.

Exercise

Exercise works on blood pressure through mechanisms most people don’t appreciate.

It increases nitric oxide production, which tells your vessels to dilate.

It improves vascular compliance; your arteries literally become better at expanding and contracting. It lowers your resting sympathetic tone, so your nervous system isn’t running at a low hum of tension all day.

Specifically, Zone 2 cardio that’s the kind of activity where you can still hold a conversation, but you’re working. Think brisk walking, cycling, swimming.

I’m a big believer in saunas as well, and the evidence supporting them keeps growing. The most important part: work to increase your endurance and make sure it’s hard enough to make you sweat.

Visceral Fat

Visceral fat is the deep abdominal fat wrapped around your organs, and it’s metabolically active. It pumps out inflammatory compounds and worsens insulin resistance. It physically compresses the blood supply to your kidneys and produces its own hormones that affect vascular tone.

The subcutaneous fat you can pinch? Far less dangerous. The fat you can’t see is the one doing damage.

Here’s why: visceral fat accumulates because of chronic insulin elevation. Lower insulin, and visceral fat is preferentially released first.

Managing Stress and Sleep to Protect Your Blood Pressure

And sleep matters here too. Inadequate sleep specifically increases visceral fat accumulation through cortisol and hunger hormone dysregulation.

Cortisol activates your sympathetic nervous system, causing vasoconstriction, increased heart rate, and blood pressure spikes. That acute response is normal and healthy. Chronic stress is the problem.

Chronically elevated cortisol is like having your foot slightly on the gas pedal all day, every day. Your vessels never fully relax.

And on top of that, chronic cortisol promotes visceral fat accumulation, impairs sleep, and worsens insulin resistance.

What actually helps? The goal is to deliberately activate your parasympathetic nervous system. For that, exercise is one of the most powerful interventions that exists.

Deep Sleep Naturally Lowers Blood Pressure by 10 to 20 Percent

Then there’s sleep.

During normal deep sleep, your blood pressure naturally drops 10 to 20%. We call this nocturnal dipping; your cardiovascular system gets a recovery window every single night.

But poor sleep eliminates that window. Your blood pressure never gets its nightly break. Over time, baseline pressure rises.

Five Sleep Habits That Actually Move the Needle

For sleep hygiene that actually makes a difference: lock in a consistent wake time first. That is your anchor.

Get morning light within 30 to 60 minutes of waking. Avoid bright light and screens one to two hours before bed.

Keep the room cool. And stop eating two to three hours before bed.

Salt

Doesn’t everyone know salt causes high blood pressure? It’s not true.

The reason you have high blood pressure isn’t because you’re eating too much salt. It’s because your body has been overproducing aldosterone—the hormone that tells your kidneys to hang on to extra salt and fluid.

Stopping salt intake is a fool’s game. It makes a tiny change that lasts short term. Lowering salt just makes your kidneys hold onto salt even more aggressively. You have to lower your insulin, since insulin is the driving hormone behind aldosterone.

Once you fix the insulin resistance, your kidneys regain the ability to excrete sodium properly. This is why people who fix their metabolism can enjoy salt without their blood pressure skyrocketing.

Key Takeaways

• Salt was never the villain. The root cause of high blood pressure for most people is insulin resistance, not the shaker on your table.

• One hormone, three pathways. Insulin raises your pressure by telling your kidneys to hold sodium, firing up your fight-or-flight system, and stiffening your arterial walls over time. All three are reversible.

• You don’t need fancy labs to spot the problem. Weight around your midsection, crashing after meals, carb cravings, or “borderline” fasting glucose all point to elevated insulin.

• Get under 20 grams of carbs a day. Track what you eat for three days and tally the total. “Healthy” whole wheat, low-fat yogurt, and heart-healthy cereal all spike insulin.

• Exercise does more than burn calories. Zone 2 cardio boosts nitric oxide, improves how your arteries expand, and dials down the constant low hum of nervous system tension. Work hard enough to sweat.

• Visceral fat is the dangerous fat. The deep fat around your organs worsens insulin resistance and compresses your kidneys. Lower insulin and it’s the first fat to go.

• Sleep is blood pressure medicine. Deep sleep drops your pressure 10 to 20% every night. Poor sleep steals that recovery window and raises your baseline over time.

• Chronic stress keeps your foot on the gas. Elevated cortisol constricts your vessels, drives visceral fat, and worsens insulin resistance. Deliberately activate your parasympathetic system.

• Fix the insulin, and you can enjoy salt again. Once your metabolism heals, your kidneys excrete sodium properly and salt stops being a threat.

It’s the story of a 68-year-old man named Doug. For 14 years, Doug was the perfect patient. He saw the best cardiologists and was on the best medications, including top-of-the-line statins.

On paper, he was a massive success. His numbers looked incredible. His LDL cholesterol (what his doctors called “bad” cholesterol) was as low as 7 mg/dl. For reference, Doug’s expert team of cardiologists were happy as long as that number was under 100.

But while his cholesterol numbers looked perfect, a different, more dangerous process was happening inside his arteries. Over that same 14-year period, his Coronary Artery Calcium (CAC) score, a direct measure of plaque buildup in his heart, grew from 603 to over 2,000, putting him at severe risk for a heart attack.

We also saw signs of danger in his ejection fraction; the powerhouse of his heart was beginning to fail. Doug was on a path to a major cardiac event, despite having the “best” cholesterol numbers I’ve ever seen.

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The Real Villain

How is this possible? How can you have perfect cholesterol but still be actively calcifying your arteries?

The answer is that his team, despite their incredible diligence, was focused on the wrong metric.

There was another number, one that wasn’t being tracked as closely, that was driving his disease all along: his morning blood sugar.

Doug had triple-digit fasting glucose numbers, which is a screaming red flag for high insulin. That high insulin told me his liver was “full”—it was already packed with fat, a sign of fatty liver.

When your liver is full, it doesn’t want to recycle any more particles. This high-insulin state was preventing his body from properly recycling those lipoprotein particles, letting them hang around in his circulation for way too long. It’s this long residency time—not the number of particles—that was allowing them to become damaged, oxidized, and stick to his artery walls, no matter how low his LDL number was.

The fix wasn’t about lowering his cholesterol even further. It was about lowering his insulin.

Doug’s case is the perfect example of a new and critical understanding in heart disease: Insulin resistance is a much stronger risk factor for cardiovascular disease than LDL cholesterol.

Your doctor can’t see this by just looking at your A1c. Your A1c is a measure of long-term blood sugar, but you can have normal blood sugar and still have dangerously high insulin. This is the stage where the damage starts.

The Right Test

So, how do we measure this? We use a test called a lipoprotein insulin resistance (LP-IR) score, which you get from an advanced blood test called an NMR LipoProfile. This score directly measures the lipoprotein abnormalities caused by insulin resistance. It gives you a score from 0 (very sensitive to insulin) to 100 (extremely resistant to insulin).

An LP-IR test will detect insulin resistance before a hemoglobin A1c test.

This isn’t just a theory. A major 2021 study from Mayo Clinic and Harvard looked at 28,000 women over 21 years. They compared more than 50 risk factors for heart disease before age 55. The LP-IR score beat every single one of them.

Look at where LDL cholesterol landed. The number your cardiologist has been chasing for years sits near the bottom of the list. A typical rise in LDL raised the risk of early heart disease by 38 percent. The same kind of rise in your LP-IR score raised it by 540 percent.

From “Pattern B” to “Pattern A”

Let’s look at Doug’s actual lab reports.

His advanced NMR test showed a “Pattern B”. That is the lab’s bright red flag for high insulin resistance. It means his particles were small and dense, precisely because they were hanging out in his bloodstream for too long. His “perfect” LDL number was a complete illusion; his metabolism was broken.

So, what happened when he finally started focusing on the right metric?

Doug’s wife enrolled him into the 21-Day Metabolic Kick. We didn’t focus on his cholesterol. We focused on one thing: getting his morning blood sugar out of the triple digits.

He learned to measure his glucose and ketones. He learned how to use fasting. Within just a few days of the class, he had a morning glucose of 96 and ketones of 1.2. He was finally lowering his insulin.

The best part? He repeated his advanced labs and his numbers showed a profound change. He had shifted from the dangerous “Pattern B” to a healthy “Pattern A”. For the first time in decades, he was actually reversing the root cause of his disease.

If you are just chasing a lower LDL number, you could be missing the fire that’s burning right behind it. Your fasting glucose and, more importantly, your LP-IR score, are the numbers that will actually tell you if you are at risk.

What is the truth? Can a pill really trigger autophagy, replacing the need for fasting? Or is it another fad that is not backed by science?

Today, we are going to examine three medications that are rumored to trigger autophagy: Metformin, Spermidine, and Rapamycin.

Key concepts

Before we dive in, we fist need to introduce some key terminologies and concepts.

Autophagy

Think of autophagy as your body’s internal waste-removal system. It clears out the junk before that junk creates more inflammation.

Autophagy tends to increase when your metabolism gets challenged. Fasting is one of the most powerful ways to send that signal. In that state, the body is no longer being told to constantly build and store. Instead, it finally gets the repair message.

That is why the longevity community chases autophagy as if it were the fountain of youth. In a way, they are chasing the right thing. Autophagy is one of the body’s built-in defenses against the cellular damage that accumulates with age.

Many of the diseases we associate with aging are diseases of a struggling metabolism. Type 2 diabetes is the obvious one, often built on years of too much insulin. Chronically high insulin levels and insulin resistance are also linked to heart disease, fatty liver, cognitive decline, increased cancer risk, and reduced immune resilience.

The antidote is to retrain the metabolism: you have to stress it enough for the body to remember how to repair. That is the promise of autophagy.

Metformin

Let’s start with the most familiar drug in this conversation: metformin.

I used to prescribe metformin for diabetic patients who need help controlling blood sugar. If a patient’s fasting glucose keeps climbing above 100 and diet alone is not enough to bring it down, metformin can be a very useful tool. It is cheap, widely available, and has been used by millions of people for decades.

Its main job is to reduce the amount of glucose the liver releases into the bloodstream. In a person with type 2 diabetes, that is extremely effective. One problem with diabetes is that the liver keeps releasing sugar into the blood, even when the body already has too much circulating. Metformin helps quiet that signal, and the whole system gets a little less overloaded.

Inside the cell, metformin changes how the mitochondria handle energy. Mitochondria are the little powerhouses that convert fuel into usable energy, and metformin slightly reduces their output. The cell senses that drop in available energy and activates AMPK.

AMPK is one of the body’s metabolic alarm systems. It turns on when the cell thinks fuel is scarce or energy production is strained. Once AMPK wakes up, it nudges the body away from constant building and toward conserving, recycling, and repairing. It can also inhibit mTOR, a growth pathway.

Sound familiar?

Fasting and exercise also reduce energy availability and activate AMPK. All three create an energy drain, and when AMPK senses low energy, it signals the cell to recycle. That means autophagy.

When energy is abundant, the body hears a different command. It signals growth through mTOR. mTOR tells the cell to divide, build, and grow. That is exactly what your teenager needs during a growth spurt. But in adults living in constant nutrient abundance, too much growth signaling is not always a gift. It can help us store more fat and cause inflammation in our tissues.

Your body is always teetering between growth and repair. When resources are plentiful, mTOR activity increases, and autophagy is suppressed. When growth signaling quiets, autophagy can turn on.

When I prescribe metformin for a patient with high blood sugar, it helps correct a dangerous metabolic situation. Their liver is releasing too much glucose, their insulin demand is too high, and their cells are already struggling under metabolic overload. In that setting, metformin makes sense.

Let’s hope that is not you.

The real question is whether metformin creates the same benefit in someone whose blood sugar is not elevated.

Our current understanding says metformin can trick the cell into sensing low energy, which may activate AMPK and autophagy-related pathways. But tricking the body into thinking resources are scarce is not automatically the same as building a healthier metabolism. If your system is not overloaded to begin with, forcing that signal may not give you the same benefit.

The lack of definitive human studies showing that metformin boosts longevity has us all guessing.

But I vote no.

People like billionaire Bryan Johnson have taken metformin in hopes of living longer. But my brain says danger.

Metformin is helpful when blood sugar is too high, but in a healthy person, I am not convinced that nudging mitochondria into a lower-power state is the path to a longer life. We need the next round of human trials before anyone can honestly say metformin extends life in healthy, non-diabetic humans.

In the meantime, I do not prescribe metformin for longevity. I respect a patient’s choice to try it with proper supervision, but I do not treat it like a daily anti-aging vitamin.

Berberine

I know some of you have heard that Berberine is the “Natural Metformin” and are curious about that. Think of Berberine as the over-the-counter, wimpier cousin of metformin. It works in a similar direction by nudging glucose metabolism and AMPK-related pathways, but with less strength, less consistency, and far less long-term human data behind it. So the answer will be the same as with metformin, only weaker. If metformin still has not proven itself as a true longevity drug in healthy people, then berberine certainly has not earned that title either. It may help some people with blood sugar problems, but I would not call it an autophagy shortcut or an anti-aging plan.

Spermidine

Spermidine appears to slightly activate AMPK, but its primary mechanism of action in autophagy differs from metformin’s. Metformin elicits a mild energy-stress signal, whereas spermidine appears to act more directly on the cellular machinery that regulates autophagy. One proposed mechanism is that spermidine inhibits EP300, an enzyme that normally acetylates proteins involved in autophagy and helps keep the cleanup process turned down. By inhibiting that “off switch,” spermidine may keep autophagy-related proteins more active, giving the cell a stronger signal to recycle damaged components.

That is why the research world is interested. Animal and cell studies look promising, with findings suggesting improved mitochondrial function, cardiac protection, and reversal of some markers of cellular aging.

However, the human data is much thinner. A few human studies have suggested potential cardiovascular or cognitive benefits, but the evidence is insufficient to establish spermidine as a proven longevity supplement. The SmartAge trial, a randomized clinical trial in older adults with subjective cognitive decline, found that 12 months of spermidine supplementation did not significantly improve the primary memory outcome compared with placebo.

Sadly, most human studies do not directly measure autophagy markers such as LC3, p62, or autophagic flux, so we cannot honestly say, “This supplement caused autophagy in humans.” In cell and animal studies, researchers can examine those markers more directly, but that is not the same as demonstrating the same effect in a living human taking a capsule.

The good news is that, based on available human data, spermidine appears to be fairly safe, with minimal side effects for most people. As with metformin, some patients report GI bloating or discomfort. It will also not cost as little as metformin, but it is still relatively affordable, usually around $15 to $40 per bottle.

The problem is that research on spermidine lags far behind that on metformin. So, like metformin, this doesn’t interest me much as a longevity gamble. If a patient wanted to take it, I probably wouldn’t object, but I also wouldn’t push people to take it.

Rapamycin

Rapamycin is where this conversation gets more dangerous.

Originally discovered in Easter Island soil as an anti-fungal, Rapamycin is now a powerful immunosuppressant used to prevent organ transplant rejection and, in some cases, to treat cancer. Its reputation in the longevity world stems from its ability to inhibit mTOR.

But it is important to remember that mTOR is crucial for normal body functions: it supports immune defense, tissue repair, protein synthesis, wound healing, and muscle maintenance. Suppressing mTOR too much disrupts these essential processes. For example, mouth sores are a common side effect in patients taking mTOR inhibitors, showing how quickly tissue health can be compromised when growth signals are dampened.

Rapamycin can encourage cellular cleanup by tilting the balance toward repair, but the body still requires ongoing growth for everyday maintenance. Over-suppression can impair the very tissues that keep us healthy.

Animal studies of rapamycin show potential for lifespan extension, but there’s no definitive evidence it works the same in healthy humans. Are the potential side effects of rapamycin worth it, and could efforts to extend life inadvertently cause harm?

Bryan Johnson (the billionaire biohacker), even with extensive monitoring and experimentation, stopped taking rapamycin after experiencing concerning side effects such as infections, changes in lipid and glucose levels, and a higher resting heart rate. His careful self-tracking makes this decision especially noteworthy; when someone with such rigorous oversight decides to stop, it’s a signal for others to be cautious about using rapamycin casually. Of course, Johnson’s case is just one example. His protocol was complex, and these side effects may have been from the drug’s interaction with the other drugs he was taking. Nevertheless, his experience demonstrates how unpredictable the outcomes can be when using rapamycin for longevity.

Prominent voices like Peter Attia acknowledge rapamycin’s potential, but also the many unknowns: optimal dose, timing, long-term effects, and safety in healthy people. Most side effect data come from transplant and cancer patients, very different from healthy individuals taking low, intermittent doses for longevity. We can’t simply extrapolate those risks.

To put it simply, we lack sufficient long-term human data on rapamycin’s longevity effects. Preliminary studies show some promise, but questions remain about safety, patient selection, immune effects, and whether rapamycin genuinely slows aging.

Rapamycin is harder to access: it’s a prescription drug with widely variable costs and limited medical support for longevity use.

Ultimately, there’s no solid proof that rapamycin extends human lifespan. Animal results are interesting, but don’t always translate to people. Rapamycin is a potent drug that warrants caution, not a shortcut to autophagy or longevity.

My Take on Pills for Autophagy

Pills for autophagy may appeal to biohackers willing to experiment and accept risks, but their protocols, resources, and risk tolerance are on another level.

Remember, always evaluate the evidence: look for human studies and understand whether claims are based on cell, animal, or patient data. The reality is, pills that claim to boost autophagy remain largely unproven guesses.

Now let’s return to the tried and true method: Fasting. Fasting reliably shifts metabolism, lowering glucose and insulin, raising ketones, and promoting the transition from storing to burning fuel. It’s a comprehensive metabolic reset, not a single targeted pathway. While medications can rapidly trigger autophagy markers, fasting trains the body over weeks or months for lasting adaptation. Fasting also activates not just one, but a suite of repair pathways: AMPK, mTOR inhibition, and sirtuins.

Autophagy markers aren’t measurable at home, but you can track indirect clues: glucose, ketones, duration of fasting, hunger, and energy. These practical signals reveal whether your metabolism can switch between fed and fasted states.

If you’re serious about autophagy, fasting is always a better answer than pills.

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​Sources

1. Johnson, Bryan. “I stopped taking rapamycin.” Blueprint, January 25, 2025.
   https://blueprint.bryanjohnson.com/blogs/news/i-stopped-taking-rapamycin

2. U.S. Food and Drug Administration. “Metformin Hydrochloride Tablets: Prescribing Information.”
   https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/020357s037s039%2C021202s021s023lbl.pdf

3. Barzilai, N., et al. “Metformin as a Tool to Target Aging.” Cell Metabolism, 2016.
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4. American Federation for Aging Research. “TAME Trial: Targeting Aging with Metformin.”
   https://www.afar.org/tame-trial

5. Pietrocola, F., et al. “Spermidine induces autophagy by inhibiting the acetyltransferase EP300.” Cell Death & Differentiation, 2015.
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6. Schwarz, C., et al. “Effects of Spermidine Supplementation on Cognition and Biomarkers in Older Adults With Subjective Cognitive Decline: A Randomized Clinical Trial.” JAMA Network Open, 2022.
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7. U.S. Food and Drug Administration. “Rapamune / Sirolimus: Prescribing Information.”
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8. Vézina, C., Kudelski, A., and Sehgal, S. N. “Rapamycin (AY-22,989), a new antifungal antibiotic.” The Journal of Antibiotics, 1975.
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9. Ferron, G. M., et al. “The Long Scientific Journey of Sirolimus (Rapamycin): From the Soil of Easter Island to a Bright Future.” Biology, 2023.
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10. Kraig, E., et al. “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.” Aging, 2025.
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11. ClinicalTrials.gov. “Participatory Evaluation of Aging with Rapamycin for Longevity Study — PEARL.”
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12. Freitas, A. E., et al. “A Narrative Review about Metabolic Pathways, Molecular Mechanisms and Therapeutic Potential of Intermittent Fasting-Induced Autophagy.” Current Nutrition Reports, 2025.
    https://link.springer.com/article/10.1007/s13668-025-00666-9

I have guided thousands through this transition. In 25 years of practicing medicine, I have not seen a process more predictable and misunderstood than the first month of keto.

This is the guide I wish every one of my patients had before they started.

Before Day One: The only number that matters

Before we talk about what happens to your body, I need to give you the only number we care about during the first 30 days of keto: twenty.

Twenty grams of total carbohydrates per day.

Not net carbs. Not calories. Not macros. Not fiber. Total carbohydrates. Eat no more than twenty grams in a day.

That number is absolute in the first 30 days. Every symptom, timeline, and milestone depends on it. Go above it, and the clock resets. The chemistry doesn’t care how close you were.

Write it on a sticky note and put it on your refrigerator. Twenty grams. That is your only job.

Now let’s talk about what is coming.

Days 1–3: The last gasp of your old metabolism

The first three days feel deceptively easy for most people.

You cut carbs: eat bacon, eggs, butter, and ground beef. You feel mostly normal, maybe a little tired or foggy, but it’s manageable.

Your body uses stored glucose—glycogen in your liver and muscles—to fuel a day or two of activity. You’re living off that reserve while your body adjusts.

This is why days one through three feel okay. You have not changed the fuel yet; you are just burning down the tank.

Enjoy it, because day three is usually when things change.

Days 3–7: The crash

This week ends most keto journeys before they truly start.

Somewhere around day three or four, the glycogen runs out. Your body has been running on glucose for decades, and it does not smoothly switch to fat when glucose is depleted. There is a gap, and we call that gap the keto flu.

It feels like crushing fatigue, a headache that does not go away, muscle cramps, and a foggy brain. These occur because as your body loses glucose, it also loses vital minerals, leading to what we call keto flu. This is the time when almost every patient concludes that this keto experiment was a mistake. Arm yourself with the knowledge of why this happens.

When you cut carbs, insulin drops, and the kidneys stop holding onto as much sodium. Sodium leaves first, water follows, and that rapid fluid shift explains much of the dramatic weight loss people see in the first few days of keto. Sodium loss triggers the loss of potassium and magnesium, leaving your body short of essential minerals for your muscles, heart, and brain.

Every single keto flu symptom stems directly from the loss of sodium, magnesium, and potassium. When these are low, your muscles, brain, and heart lose the minerals needed to function well, leading to fatigue and cramps typical of the keto flu.

The fix is simple and quick: salt your food, add electrolyte to water, or even add table salt to coffee. Supplement 300–400 mg of magnesium glycinate, or try a magnesium float tank.

Days 4–7: Your first ketones

Between days four and seven, most experience a shift.

Your liver, deprived of glucose, starts burning fat. It pulls fatty acids, processes them in mitochondria, and makes ketones.

This is the moment you have been working toward, and now you can measure it.

Get urine ketone strips from the pharmacy. Keep them in the bathroom. When the strip turns pink, you have made your first ketones.

Some patients hit this on day four. Some take until day ten. If you are past day ten and the strip is still white, there are three likely reasons.

First, your strips may be old. Ketone strips expire faster than most people realize. If the canister has been open for more than a month, buy a new one and test again.

Second, you may be drinking alcohol. Alcohol is a fuel just like glucose and ketones. Your mitochondria will burn it first every time. When there is alcohol in your system, ketone production pauses. If you are serious about getting through this transition, abstain completely for the first six weeks.

Third, you may be sicker than you realized. Severe insulin resistance and metabolic dysfunction can slow progress. Years of glucose can weaken fat-processing machinery. This doesn’t mean keto won’t work—it just takes more time and patience. Keep going; ketones will come.

Days 7–14: The ugly middle

Nobody talks about the middle part.

Keto flu has passed. Your electrolytes are fixed. The strip turns pink. You feel better than on day five, but not yet good. You eat fat and protein, which is fine, but you’re still hungry and still miss old foods.

This means you are normal. This is the week that requires the most deliberate commitment.

Your brain adapted to glucose for decades, forming habits around food, reward, and rituals. That doesn’t change in a week. What you feel isn’t true hunger—it’s habit seeking routine. The most important thing I can tell you about this week is this: you must eat the fat. Do not fast, and do not add any additional complexity to this. Many make the mistake of adding fasting after seeing early results, then get discouraged when progress slows in week two and think keto has stopped working.

Your only job in week two is the same as week one. Keep carbohydrates at twenty grams. Eat enough fat. Do not cheat. Let the chemistry do the work.

Days 14–21: The shift

Patients describe this phase differently: clearer thinking, no more preoccupation with food, or looser clothes—sometimes before the scale moves.

This is fat adaptation: the body gradually learns to run on fat more efficiently. Cells build more of the enzymes needed to use ketones, mitochondria become better at turning fat into fuel, and hunger signals begin to steady instead of swinging with every carb crash.

Most patients are surprised: they leave food uneaten or handle social events without slipping. These are big hormonal milestones.

Days 21–30: The moment that changes everything

There is a moment I look for in every new keto patient. I have watched it happen hundreds of times, and it still moves me.

They check in and say, “Something strange happened: I forgot to eat lunch. I wasn’t even hungry. That’s never happened before.”

That is the moment that changes everything: the first true sign of keto adaptation!

Your metabolism has found another fuel source and no longer needs to be refueled every three hours. Your fat-based satiety hormones, suppressed for years by carbohydrate intake, are finally strong enough to do their job.

By day thirty, most patients are firmly in this new territory. The cravings that dominated week two have largely quieted. Energy is stable, with no more afternoon crashes, no more blood sugar rollercoasters, and no more desperate need for coffee at two o’clock. The hunger that used to appear every two to three hours has stretched to every five or six.

Your body has learned to run on fat. Only now are you ready for the next stage of what this diet can actually do.​

If you know anyone new to Keto, be sure to send them this post!

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Her scale barely moved, but her waist had grown fourteen inches. A patient of mine did everything right for fifteen years. She ran the miles, cut the calories, and recently added the ab work, yet she grew the most dangerous fat: Belly Fat. It snaked around her organs, slowly increasing the pollutants responsible for more of the added mass. Her doctor called her labs normal. They weren’t.

Neither you nor Brenda can outrun, out-diet, or out-crunch a bulging waistline. It’s chemistry that promoted the growth of that deadly centralized fat, and only when you reverse two hormones while sweeping away a specific, weaselly sugar, will it go away.

14”

Fourteen inches.

Brenda’s waist had grown 14 inches, while her scale weighed nearly the same. Her waist had grown from twenty-six inches to almost forty. Not pregnant. Still running miles every week. Why?

Standing in her closet, she exhaled with a groan, sorting what to wear to the kids’ soccer tournament. Her eyes rest on her favorite size-six jeans, but those no longer fasten around the middle. She reached past them for yoga pants and a long t-shirt. Not because it’s cute. Because it covered the belly that didn’t used to be there.

She’d run for fifteen years. Three miles three times a week, most weeks. This bulge across her middle coaxed her to cut calories and add ab workouts. And her belly grew anyway.

Brenda was told the wrong answer: try harder.

For over twenty years, I told women exactly what Brenda’s doctor told her: eat less, never drink your calories, move more. Watching every middle-aged woman fail scored me as an incapable doctor. Did I not understand hormones well enough? Could metabolism just flip and add centralized fat?

Let me teach you what all those women should have learned from me a decade ago.

Physicians walked past Brenda’s normal BMI. Twenty-four point eight (24.8) measured textbook. Her doctor looked at that number and told her she was fine. She was not fine.

I use BMI in my practice for every single patient. Like most doctors, they trained that habit into my workflow on week one of clinical practice. The tool works well for many, but it will not catch Brenda’s problem. BMI cannot tell the difference between the soft, harmless fat resting underneath the skin around your hips, and the angry, deadly fat slithering inside you, around your liver, guts, and heart. There’s a clinical name for Brenda’s body type, TOFI, thin-outside-fat-inside, and you may know it by its street name: “skinny fat,” or normal-weight obesity. The scale says one thing. The tape measure tells the truth.

Brenda’s slimy, visceral fat lives deep inside her belly and wraps around internal organs. It does not just sit there. It behaves like an active, inflammatory organ spewing out the message, “Grow more of this type of tissue.” Your liver, pancreas, kidneys, and heart get swaddled by this oily monster running a chemistry experiment deep within your body.

Brenda’s normal labs teach you how sneaky this fat is.

Brenda’s labs, decoded

Compare Brenda’s results to her doctor’s recommendations versus mine.

Average blood sugar (eAG): ~105. A1c: 5.3%.

Pre-diabetes starts at 5.7% or an average blood sugar of 115. Her doctor blinked right past this A1c.

Her pancreas had been making extra insulin for years to keep that blood sugar down. Brenda’s normal blood sugar in the setting of extra insulin grew belly fat. Stopping the growth of her belly fat meant lowering insulin production. She needed to lower her blood sugar further to turn off the spigot of insulin.

Offering reassurance to Brenda that this blood sugar was fine trapped her in the cycle of growing belly fat. I like patients’ average blood sugar to be less than 100, which means their A1C is 5.1% or less. This is my rule with or withOUT belly fat. Keep reading and learn why we want blood sugars to never spike over 110.

Triglycerides: 170.

Her doctor agreed that these triglycerides are too high. When triglycerides circulate at 100 mg in a deciliter of blood, it marks the fingerprint of too much sugar and insulin. By the time 150 mg/dL, triglycerides act like the smoke signal of cells burning too much glucose, not enough fat. I rest easily when their triglycerides hang out in the 60-70s.

Uric acid: 7.0.

We slap the diagnosis of gout onto your chart when uric acid comes back at 7.0 mg/dL. This waste product builds up inside bodies suffering from metabolic disease. Just like Brenda, it causes no gout-like symptoms of red, swollen joints for the first decade of abnormal labs. Healthy people keep this waste product under 5.1. As these numbers slide into the 6’s (like Brenda’s), it reflects a specific sugar most people never suspect. If Brenda never removes this sugar, her uric acid will continue to rise and fuel her belly-fat growth. I’ll explain that. It’s my favorite part of this article.

Every lab result sat inside the “normal” column. Together, they told the story of three “hormones” quietly growing her dangerous belly. Technically, it’s two hormones and a sugar, but that sugar is gnarly enough to be called a hormone. Hormone means the molecule circulates as a messenger delivering strict orders to other cells. As long as this hormone signals within the body, nothing else can overrule that command.

Hormone #1: Insulin, the King ​​

When you eat, and your blood sugar climbs more than just a little, your body hits a panic button to shove extra sugar out of the blood and into storage. That panic button is the hormone insulin. Our bodies press the panic button when we consume more than a teaspoon of glucose.

Insulin is king of metabolism. Just like a narcissistic, overpowering ruler, it becomes a monster when you give it too much power. Elevated insulin dictates the removal of extra fuel from circulation. That teaspoonful of fuel sparks insulin production, shuffling glucose out of your blood and into cells. Insulin also locks fat into your fat cells and bolts the doors shut. When you loft the insulin up a couple of times a day for a few minutes, it serves you well. When you live like Brenda, insulin stays elevated the whole day. This is where the narcissistic dictator is born. With King Insulin on the throne, fuel gets stored, not released. Both fat and sugar are abundantly stored inside Brenda. Her growing belly fat is all the proof I need to know the culprit for this problem is King Insulin.

Brenda’s insulin had steadily risen for a decade. All those years of running couldn’t overpower her extra insulin. The hormone overpowered the current scene. In her twenties, a meal might have called for a teaspoon of insulin. Two kids and fifteen years later, that same meal called for 50 times that amount of insulin. Brenda’s storage cells wilted over the years as the tyrant grew more powerful. Over time, some of her cells stopped listening to that dictator. Tit-for-tat, her pancreas made more insulin. The ratcheting upward production of insulin won. It produced enough insulin to keep the glucose down around 100.

Rule #1: You cannot empty a belly-fat cell while insulin is rising. Bring the king down first.

Hormone #2: Cortisol targets the fat at your belly

Now add stress. When you’re under pressure, a hard run on no sleep, a toddler at 5 a.m., a job, a girl-boss-life, your body releases cortisol. Cortisol is your stress hormone. Sure. We’ve all learned that. A better descriptor of it is a master conductor of the long-game for fuel storage. Cortisol’s signature move is to instruct fat to park specifically around the organs in your belly. When stress reigns over our schedules, cortisol adds to the fatty padding around our hearts and kidneys. Sadly, the churning production of cortisol is based on the numbers from the past weeks to months. Changing how much cortisol you produce takes time.

When I teach ladies about cortisol, I use this study from 2000, where researchers at UC San Francisco put women through psychological stress and watched their cortisol. The women carrying more belly fat made way more cortisol during this stress test. To compound that problem, the belly-fat women didn’t switch cortisol off the way they should. It just kept running. Belly fat triggers cortisol, and cortisol makes more belly fat. It’s a loop that feeds itself, especially if you punish it with 5 a.m. runs on no sleep.

You don’t need a lab test to find your cortisol.

Your waistline is the readout.

Rule #2: Blame cortisol if this equation is true: 2 x fattest waste measurement > height.

My height is 5’3” (63”), and my waist is 28”. [2 x 28= 56”].

56” is less than my height of 63”. This means my belly fat is likely healthy.

Brenda’s waste measured 37”. [2 x 37 = 74”]

Brenda stood 5’6” (66”) tall. 74 is greater than 66, confirming the abundance of her belly fat.

Use this formula instead of the scale to know if you have belly fat under construction.

Hormone #3: The silent one that you make yourself.

Nobody checks this one, not even me. And Brenda was sure it didn’t apply to her. The “hormone” is fructose.

I know. Fructose isn’t technically a hormone. It’s a sugar. Insulin and cortisol are the real hormones. I put fructose in the lineup because it hijacks those two hormones and drives belly-fat storage.

Brenda knew that High-Fructose Corn Syrup (HFCS) was evil. She knew that fructose makes us fat. Specifically, the more fructose you swallow, the bigger your belly fat grows. Brenda knew not to drink or eat foods with that in it. Her kids didn’t get HFCS. Heck, she’s ahead of most and doesn’t use white table sugar (50% fructose) or honey ~40% fructose). So in her head, she’d already filed fructose under doesn’t apply to me. But she was wrong, and so was I, for years.

Your body has a hidden assembly line to make fructose called the polyol pathway. It takes the ordinary blood sugar (glucose) already in your veins and converts it into fructose. Inside you. No HFCS required. Your body just starts making fructose without your permission.

The way Brenda fattens up her belly-fat is to shuffle fructose through her liver’s mitochondria, where it produces uric acid. Yes. Uric acid—that waste product found in my gout patient—stimulates the production of fat. Especially visceral fat! Unlike glucose, which shuffles through the Krebs Cycle to produce ATP energy, fructose gets metabolized so fast that it produces less energy. ADP and AMP are shunted out of the mitochondria instead of ATP. The resulting depleted energy pathway ultimately produces uric acid.

Unlike monkeys, humans do not have the uricase enzyme. Uricase breaks down uric acid. This cartoon helps teach how powerful uric acid is at making belly fat. Monkeys have no belly fat, in part, because their uricase enzyme gobbles up uric acid quickly, keeping their blood levels very low. Humans lack this enzyme, and their uric acid levels rise when we consume sugar, alcohol, and tons of processed carbs. The presence of uric acid sparks the vicious cycle of converting glucose into fructose, and then wildly spinning that into more uric acid. Uric acid makes more uric acid in us.

When I measure uric acid in Brenda’s blood, it approximates how much fructose she metabolizes. Elevated uric acid means the chemistry set spews out this toxic message to make visceral fat.

You make the poison yourself.

What opens the door to this hidden assembly called the polyol pathway? We know that uric acid activates the polyol pathway, making fructose from glucose, but how did Brenda get the uric acid in the first place? The answer hid in her blood sugar.

Dr. Richard Johnson, the nephrologist who wrote the book on this, is clear about the mechanism that triggers this polyol pathway: it’s high blood sugar. Elevated glucose pries that pathway open. The higher and longer your blood sugar stays up, the more fructose your body brews. More fructose means more uric acid means more fructose means more uric acid … and the runaway train escapes.

When I first read his work, I figured “high” blood sugars meant diabetic numbers — 150, 160. That answer was not obvious, and Dr Johnson would not slip me the Cliff Notes from his unpublished research. I wanted an answer: “What do I tell patients to keep their blood sugars below to stop the production of fructose and therefore uric acid?” How low do I have to keep my blood sugar to keep this polyol pathway turned off?

110

the line to hold

One hundred and ten. That’s barely above where a healthy person sits. It’s a number a normal person blows right past after a bowl of oatmeal. And every time you cross it, you flip on the factory that manufactures the most belly-fat-growing fuel there is: Fructose.

Fructose, in a bath of extra insulin, triggers you to fatten up as your body stores fat and blocks fat-burning at the same time. Fructose to uric acid shows up in Brenda’s labs with a lab value of 6.5. These “normal” labs left fingerprints all over the crime scene.

Rule #3: Keep uric acid under 5.1 by keeping blood sugars under 110.

Advice for Brenda’s endocrine system

The three “hormones” ruining Brenda’s efforts were

1. Excess insulin, bolting the fat in.

2. Excess cortisol, aiming it at her belly.

3. Fructose quickly zipped into uric acid every time her blood sugar slipped over 110.

First: you cannot out-train a hormone problem.

When insulin is high and the fructose factory is running, the chemistry storing belly fat will overpower your exercise. The research backs this up. Put people on an exercise program but leave the diet and the insulin untouched, and the deep fat barely budges. Bring the hormones down first; then exercise pays off.

Second: chronic cardio on too little sleep keeps cortisol high.

Cortisol aims fat straight at your belly. So a 5 a.m. run on five hours of sleep pours fuel on the exact fire you’re trying to put out. Both high insulin and high cortisol cost you the wrong kind of mass: muscle loss. Brenda trains harder, sleeps less, stresses more, and the scale holds steady while the belly keeps winning, and her muscle mass shrinks. The scale hides it. Your waist doesn’t. Use the formula that 2 times your waste-circumference should be less than your height.

Antidote #1 — Empty the liver (bring the king down).

No sugar. No starch. High fat. Under 20 grams of total carbohydrate a day. And close the kitchen at sunset, stop eating early so your insulin has hours every night to fall all the way back down. Low insulin is the only condition under which a fat cell will open its doors. This is step 1. You will know your chemistry shifts by the presence of ketones in your urine.

Antidote #2 — Reset the dark (starve the cortisol).

The biggest driver of Brenda’s runaway cortisol happened while she slept. New bedtime: 9:30. House rule: no screens after 7 p.m. and not just for her. For the whole family. Then, in the morning, get bright light in your eyes early; that’s the good cortisol pulse that sets your rhythm so the stress version can switch off at night. And move your body, but you don’t need to punish it. For my 40-and-over moms, skip the long cardio workouts. Instead, march, carry something heavy, do step-ups, and squat to a sweat. Same chemistry.

Antidote #3 — Shut down the factory (the fructose move).

Fructose made from your elevated sugars sparks visceral fat to grow. Keep your blood sugar low enough that the factory stays dark. For Brenda, that meant going strict keto, mostly carnivore, for six weeks to get her sugars reliably into the 80s and 90s under 110, around the clock.

You can’t feel your blood sugar. It’s invisible. You certainly can’t feel a mild shift in blood sugar to 110. So I put a monitor on Brenda. (Continuous Glucose Monitor)

The first time Brenda watched her continuous glucose monitor stay parked over 110 all night long while she slept, she dialed in. This was not a number I told her at an office visit. Her CGM showed her the problem happening all throughout the night. Brenda committed the day the data stopped being my opinion and started being her own.

Brenda put on the monitor. She did the six weeks. Her morning numbers corrected. The belly faded slowly, then steadily, and she stopped reaching past the size-six jeans.

What to measure THIS week (start tonight)

You don’t need a prescription or a doctor’s permission to start measuring. Knowledge is free. Pick up the tape measure and start here:

1. Your waist — not your weight.

   Measure around your belly button, first thing in the morning. Then measure your height. Goal: waist under half your height. Write both numbers down.

2. Your morning blood sugar, if you can. A cheap drugstore meter works. You’re looking to keep it under 110, especially overnight and after meals.

3. Your PeeTones or a ketone reading. Are you actually in fat-burning, or do you just think you are? Measure. Don’t guess.

4. Sunset and 9:30. Close the kitchen at sundown. Lights-down and screens-off so you’re asleep by 9:30. Watch what one week does to your morning.

That’s it. Four numbers. Free. The people who win are the ones who measure, not the ones who believe.

Everything Brenda did, she did without a prescription: a sunset, a light switch, a monitor, and the guts to look at her own numbers.

It was never the jeans.

Maybe you’re Brenda. Maybe you’ve run the miles, cut the calories, done the crunches and the middle keeps winning, and you’ve been blaming yourself.

Stop blaming yourself.

It was never willpower. It’s a three-hormone problem. Insulin. Cortisol. Fructose. And every one of them is fixable without a prescription, starting tonight, for the price of a tape measure.

It was never the jeans. It was three hormones nobody told her to check.

Now you know all three.

Drop a comment and tell me why you picked it I read these, and your answer helps me write the next one.

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For years, we’ve put creatine in a box labeled “sports performance.” But the science is clear: this molecule is a critical tool for anyone interested in cognitive function, fighting brain fog, and protecting their brain at any age.

Your brain and your muscles are the most energy-demanding tissues in your body. So, keeping them saturated with creatine is one of the best things you can do for your physical and mental performance. But I see so many people taking it the wrong way, wasting their money, and complaining about side effects.

So what is it?

Creatine is a naturally occurring organic compound that you typically get from your diet, specifically, red meat, seafood, or milk. Your liver and your pancreas also synthesize it from the amino acids arginine, methionine, and glycine. Altogether, that usually totals to about 1-2 grams per day. Of that 1-2 grams, the vast majority, around 95%, is used in skeletal muscle. These are the muscles responsible for voluntary movement, such as running and lifting weights. Only 5% reaches the brain, heart, and other organs. If we want the mental benefits, we need to supplement.

What does it do?

The primary benefit from creatine comes from its ability to renergize ADP into ATP. Think of creatine as a recharger for your cellular batteries. Every cell in your body runs on ATP, a molecule of energy. When you use ATP, it becomes a drained battery called ADP. Creatine’s job is to swoop in and rapidly slap a new energy unit onto that ADP, turning it back into a fully charged ATP battery. This noticeably improves energy levels both physically and mentally.

The obvious question, does this improved energy actually improve performance?

To answer this question in 2006, McMorris and colleagues conducted a study to determine the effect of creatine on sleep deprivation. They tested two groups, each prevented from sleeping for 24 hours, on a wide array of mental exams. In one group, they provided a large dose of creatine (25 grams), and in the other, they fed a placebo. McMorris and colleagues found that creatine mitigated the effects of sleep deprivation, allowing subjects to maintain peak performance. For moments of extreme mental stress, such as after a night of no sleep, researchers have found that a single high dose of ~25 grams can significantly improve memory and cognition.

How to take it right.

I see people mess up taking creatine in two ways. First, they buy the wrong kind. Second, they take it the wrong way.

Let’s start with buying the wrong kind. You walk into a supplement store and see a dozen different forms— all claiming unique benefits with huge price tags. Watch out. The most studied, most proven, and cheapest form is simple pure creatine monohydrate. No flavoring or anything else added. It’s the cheapest and best bang for your buck.

Now, let’s talk about how to avoid wasting the creatine you just bought.

First, let’s talk about the dose. If you only care about your muscles, a daily dose of about 5 grams will work. But if you’re like me, you care about what’s happening from the neck up.

Our brain is very stubborn about letting things in. To get creatine past the blood-brain barrier and see real cognitive benefits, the best studies use a “loading phase” of 20 grams per day for at least a week.

Now, that sounds like a lot, and it is. That’s why you have to titrate up. Don’t jump straight to 20 grams on day one. Start with 5 grams a day, see how you feel, then go to 10, and work your way up. This gives your gut and brain time to adjust.

After you’ve loaded for a week, you can drop to a maintenance dose. I take 10 grams a day. This brings me to the most common complaint I hear: “Dr. Boz, creatine gives me an upset stomach.” Aka diarrhea.

If you’re getting diarrhea, there are two possible causes: either you increased the dose too quickly and should work your way back down, or you took the dose too fast. Creatine is osmotic, which means it pulls water into your intestines. If you chug it, the sudden rush into your gut can send you trotting to the toilet. Sip on it over 10-15 minutes. Taking it with a meal helps buffer the osmotic effect and slow absorption, allowing you to benefit from the effects without triggering diarrhea.

Lastly, I see people mix their creatine with their coffee at the start of the day. While this is convenient, it’s not the most effective. You’ve probably heard people argue not to mix them before, saying you can’t mix creatine in coffee or sour sports drinks because the acid will break it down into useless creatinine. This is technically true, but practically false. Yes, creatine will eventually break down in a strong acid, but this process takes days. The few minutes your creatine sits in your coffee before you drink it? It’s not going to do a thing. Your stomach acid is far stronger, and your body has no problem absorbing the creatine before it has any chance to degrade.

The reason I don’t drink coffee with my creatine: there’s evidence that dosing creatine and caffeine at the same time can hinder performance. They have opposing actions on how your muscles handle calcium. This conflict really only seems to matter at high caffeine doses—over 250 milligrams. To be safe, I don’t mix them. I have my coffee in the morning and wait at least 2 hours before taking my creatine. This also catches me when the caffeine boost starts to fade, perfect timing for the energy boost from the creatine.

Myth Busting

Now, let’s bust a few myths that scare people away from one of the safest supplements on the planet.

Myth #1: Creatine will make you fat.

This is false. Creatine pulls water into your muscles, not your fat cells. You might see the number on the scale go up by a few pounds in the first week, but that’s water weight inside the muscle. It’s a sign that it’s working! It is not fat.

Myth #2: Creatine causes hair loss.

This myth comes from a single small study from van der Merwe et al years ago that found creatine might slightly increase a hormone called DHT. DHT is linked to hair loss, but the subjects’ DHT levels remained within the normal, healthy range. In addition, that study never even measured hair loss.

Is creatine a Steroid?

Bluntly, creatine is not a steroid.

Anabolic steroids are typically synthetic versions of testosterone. This increases muscle mass when combined with resistance training, as testosterone enters muscle cells and increases the expression of various muscle-specific genes.

In contrast, the primary benefit of creatine is the increased energy it provides by helping convert ADP back into ATP. This maintains ATP supply to your muscles during a workout. Thus keeping energy up. This lets you perform more intense exercise and thus get more out of each workout.

The secondary benefit of creatine for muscle growth comes from its osmotic effect: it pulls water into the muscles. This improves muscle Hydration and swells the cells. This enhances the muscle repair response, augmenting the proliferation and activation of satellite cells. Satellite cells are specialized stem cells located near but apart from your skeletal muscles, hence the name, that operate muscle cell repair to instigate muscle repair and growth.

Anabolic steroids artificially increase protein synthesis, while creatine enhances workout intensity and triggers an improved repair response.

Myth #3: Creatine is bad for your kidneys.

This is the most persistent and dangerous myth. In dozens of human studies on people with healthy kidneys, creatine has been proven to be completely safe. In fact, this safety profile extends even to populations where organs might be under more stress, like postmenopausal women or those with type 2 diabetes; studies have consistently shown no evidence of creatine causing kidney damage.

The confusion comes from a lab test. Creatine supplementation will increase the waste product creatinine in your blood. An uninformed doctor might see that number and think your kidneys are failing, but it does not mean your kidney function is actually declining.

The standard test to check your kidneys, called an eGFR, uses your blood creatinine level in its formula. Because your creatine supplement directly and harmlessly increases your creatinine, it artificially inflates one of the key variables in the equation. This can make the final eGFR result look falsely low, creating a false alarm that your healthy kidneys are damaged. If you’re worried about this, you need a better test. Insist that your doctor order a cystatin C test.

Cystatin C is a protein produced by almost all cells in your body at a very constant rate. Critically, its production is not affected by factors like your muscle mass, a high-protein diet, or creatine supplementation.

My Takeaway

Ultimately, creatine stands apart as the king of supplements. Both safe, extensively researched, and uniquely effective at optimizing energy metabolism. It is a simple, evidence-backed tool that offers significant, long-term benefits for your overall well-being.

If this interests you and you would like to try Dr. Boz’s favorite, check it out here: Link

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Sources

Antonio, J., Candow, D. G., Forbes, S. C., Gualano, B., Jagim, A. R., Kreider, R. B., Rawson, E. S., Smith-Ryan, A. E., VanDusseldorp, T. A., Willoughby, D. S., & Ziegenfuss, T. N. (2021). Common questions and misconceptions about creatine supplementation: what does the scientific evidence really show? Journal of the International Society of Sports Nutrition, 18(1), 13. https://doi.org/10.1186/s12970-021-00412-w
https://pmc.ncbi.nlm.nih.gov/articles/PMC7871530/

Shenkman, B. S., Turtikova, O. V., Nemirovskaya, T. L., & Grigoriev, A. I. (2010). Skeletal muscle activity and the fate of myonuclei. Acta Naturae, 2(2), 59–66.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3347558/

Bazgir, B., Fathi, R., Rezazadeh Valojerdi, M., Mozdziak, P., & Asgari, A. (2017). Satellite cells contribution to exercise-mediated muscle hypertrophy and repair. Cell Journal, 18(4), 473–484. https://doi.org/10.22074/cellj.2016.4714
https://pmc.ncbi.nlm.nih.gov/articles/PMC5086326/

Olsen, S., Aagaard, P., Kadi, F., Tufekovic, G., Verney, J., Olesen, J. L., Suetta, C., & Kjaer, M. (2006). Creatine supplementation augments the increase in satellite cell and myonuclei number in human skeletal muscle induced by strength training. The Journal of Physiology, 573(2), 525–534. https://doi.org/10.1113/jphysiol.2006.107359
https://pmc.ncbi.nlm.nih.gov/articles/PMC1779717/

Luu, B. (2024). Creatine for the Sleep-Deprived Brain. Brandon Luu, MD.
[Substack article]

McMorris, T., Harris, R. C., Swain, J., Corbett, J., Collard, K., Dyson, R. J., Dye, L., Hodgson, C., & Draper, N. (2006). Effect of creatine supplementation and sleep deprivation, with mild exercise, on cognitive and psychomotor performance, mood state, and plasma concentrations of catecholamines and cortisol. Psychopharmacology, 185(1), 93–103. https://doi.org/10.1007/s00213-005-0269-z
https://pubmed.ncbi.nlm.nih.gov/16416332/

Cleveland Clinic. (n.d.). Creatine.
https://my.clevelandclinic.org/health/treatments/17674-creatine

[PubMed source].
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Turner, C. E., Byblow, W. D., & Gant, N. (2015). Creatine supplementation enhances corticomotor excitability and cognitive performance during oxygen deprivation. Journal of Neuroscience, 35(4), 1773–1780. https://doi.org/10.1523/JNEUROSCI.3113-14.2015
https://pubmed.ncbi.nlm.nih.gov/25632150/

Here’s what I want you to do…

In the comment section below, ask your question. Then read through what everyone else has asked, and press the ‘like’ button on the ones you want answered most. The questions that rise to the top and are more likely to get selected.

A word on what makes a question great

The best questions I get all have one thing in common.

They were a story with a twist. “I did X, I expected Y, but Z happened instead. What’s going on?”

They came from a real situation somebody was actually living, and the answer ended up helping far more people than the person who asked it. Those are the ones we can really dig into on the show.

Now… GO!

Reminder: If you haven’t become a paid subscriber yet, upgrade before July 14th to lock in the lowest price for life.

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But the questions I couldn’t answer were actually my favorite. I’d fly back to residency, ask the senior doctors about it and they’d refer me to a study that they’ve read. I hit the library, do a bunch of reading and come back next month with a deep, researched answer.

Those were the questions I loved. The ones that forced me to do the work and become a better doctor.

That’s why I’m starting Dr. Boz Office Hours. You have questions, and I want to be the one who’s done the homework.

What is Dr. Boz Office Hours?

It’s an exclusive, members-only Q&A, hosted live once a month here on Substack.

Here’s how it works. Ahead of each session, paid subscribers post their questions, and fellow subscribers vote on the ones you most want me to dig into. I take the questions that rise to the top, I do the homework on each one, the mechanism and the studies and the numbers behind it, and then I sit down live for one hour and give you the real answer. The way I’d want it explained if it were my own family asking.

The session is live, and the recording goes into the archive afterward, so members can watch it again or read the detailed show notes. Each session adds to a searchable library of content for Substack subscribers.

The first session is Monday, July 20. The first question thread is open now, and only paid subscribers will be able to put questions in.

Why members only?

Dr. Boz Office Hours is the next step for the people who want to go deeper. For those who have the complicated, specific question that deserves a researched answer rather than a quick one.

I answer questions for free every week on my Tuesday night live shows on YouTube, and I’m not stopping. If you’re new, keep showing up to those.

I want to reward the members of my community that have been with me the longest and have mature questions.

Lock in your price before July 14

The current subscription price of $20/mo or $100/yr goes up to $40/mo or $200/yr on July 14. Anyone who joins before then locks in their price for life.

My mission is to reverse medical problems with healthy keto living. Office Hours offers the most people the best access to my brain. I’ll see you on July 20th.

The first question thread is open now!

— Dr. Boz

Annette Bosworth, MD