For decades, medical providers misunderstood Type 2 diabetes and treated it just like they treated Type 1. Unfortunately, many still do, and the misunderstanding has contributed to our current public health catastrophe.

Nearly 90% of US adults are metabolically unhealthy, heading down the road to developing type 2 diabetes. And this isn’t just a problem of body weight: roughly 30% of normal-weight adults are metabolically unhealthy too. You might be one of them! Understanding why it happens, and what to do to stop the trajectory, is extremely important to your long-term health.

Here’s what happened and why it matters for your health, even if you DON’T (yet) have type 2 diabetes.

It started with a colossal mistake in the 1990s.

A major study came out showing that keeping blood sugar very tightly controlled helped people with Type 1 diabetes avoid the diabetic complications you have likely heard of: blindness, kidney failure, nerve damage, and over the long run, even heart disease.

All of us in the medical profession at the time assumed that the same tight control would work for Type 2 diabetes, so we started aggressively prescribing more medications to those people, including insulin injections, in an effort to force those high blood sugars down.

But here’s the problem: Type 1 and Type 2 diabetes are actually opposite conditions, and we were making the mistake of treating them as if they were the same.

Type 1 diabetics don’t produce insulin and have none of it in their bloodstream. Type 2 diabetics produce LOTS of insulin and have TOO MUCH of it in their blood stream.

When researchers used medication to raise insulin and tightly control blood sugar in those with Type 2 diabetes, and then looked at the results, they got quite a shock:

• Patients did indeed achieve near-perfect blood sugar control!

• The medications caused them to gain weight

• They had more of the life-threatening low blood sugar episodes

• And MOST importantly: It did NOT protect their health. In fact, more people died, including deaths from heart disease, and the study had to be stopped early!

And it actually makes sense when you look at what those medications were actually doing. The main tools used to force blood sugar down (insulin injections and drugs that squeeze even more insulin out of an already-overworked pancreas) were pouring more insulin into people who already had far too much of it. The lab values looked better, but the underlying problem was still progressively getting worse.

Here’s what researchers now know: lowering blood sugar with medications that raise insulin not only doesn’t help prevent the most serious complications from having type 2 diabetes, in the case of heart disease, it increases the risk!

Luckily, raising insulin isn’t the only way to lower blood sugar. If high insulin increases the risk of heart disease, why not try lowering insulin through dietary change? There is no harm at all in trying, and if it does decrease the risk, then that is fantastic!

Your next logical question is how do you KNOW you are lowering your insulin level without being able to measure it?

Excellent question. It is very true that at the time of this writing you have no way to continuously check insulin levels.

You DO have a way of continuously checking blood sugar, however, and you can use blood sugar as your proxy for what is likely happening with insulin. When blood sugar goes up, insulin goes up in tandem. When blood sugar goes down, so does insulin.

Here’s what to do:

• Get a continuous glucose monitor (such as Stelo by Dexcom – available online without a prescription) so you can see your own glucose response to food.

• Pay attention to what you are seeing on that monitor and make changes as needed. Experiment!

• Avoid the foods that spike blood sugar in 100% of humans (sugars and starches).

• Eat no more than 3 meals a day and avoid snacking between those meals.

• Get your fasting blood sugar to between 70 and 90. (If you carry extra weight, it might take losing some of it to normalize your fasting blood sugar.)

• Avoid meals that raise your blood sugar more than 40 points above your baseline most of the time.

• Avoid meals that cause a prolonged blood sugar elevation. It should return to your normal baseline within 2 hours of starting your meal.

• Seek help from a certified metabolic health practitioner if you need help with any of this!

One important caution: if you take insulin, or a medication that squeezes more insulin out of your pancreas (a sulfonylurea like glipizide, glyburide, or glimepiride, or a meglitinide like repaglinide or nateglinide, for instance), making these effective dietary changes can lower your blood sugar too much! If you take ANY medication for diabetes, but especially those classes, don’t make big changes on your own. Work with your prescriber to adjust your medications as your numbers improve.

The major chronic diseases caused by having Type 2 diabetes aren’t from high blood sugar alone, too much insulin is the bigger problem.

Treating type 2 with more insulin is like trying to fix a flooded basement by adding more water. It’s like trying to get out of debt by maxing out more credit cards. It’s like trying to cure insomnia by drinking more coffee!

You get the picture.

It’s the wrong approach, unless your pancreas has truly run low on insulin. That’s always true in type 1 diabetes. It can happen in long-standing type 2 as well, which is why some people with type 2 do eventually need insulin in spite of making those fantastic lifestyle changes. But for most people with type 2, especially early on, that isn’t the problem.

The real solution is dietary change that addresses the root cause, not medications that make it worse.

The best part? For most people, this is something you can start safely on your own (if you take diabetic medications, see the caution above first), without waiting for more studies to come out, without waiting for the old guard medical providers to die off, and without waiting for public health policy changes. No medications, no side effects - just real food choices guided by real-time data about your body’s response.

Want to work on improving your own metabolic health? Find out exactly how (plus the “why it works”) in my book: Reversible! A Clinician’s Guide to Understanding and Reversing Insulin Resistance, Prediabetes, and Metabolic Disease. It’s available on Amazon and at diabetesgamechanger.com.

Interested in learning more about my online program for reversal of insulin resistance & Prediabetes?

Learn More HERE!

This Week’s Recipe Is, As Usual, AMAZING!

Spaghetti Squash Burrito Bowls

A hearty, plant-forward bowl that trades the rice for roasted spaghetti squash, so you get all the comfort of a burrito bowl without the blood sugar spike.

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Last week I discussed why we will never get blood sugar data that can be applied universally to all humans. This week I want to add a bit more about the science we CAN apply.

In medical training, you learn how to count carbohydrates and then to calculate the correct dose of insulin to control blood sugar. The theoretical idea is simple: if you take your insulin-to-carbohydrate ratio (ICR), such as 1 unit of rapid-acting insulin for every 15 grams of carbs, you can then calculate a dose of insulin that will keep blood sugar from going out of range. Eat 45 grams of carbs, divide by 15, inject 3 units. Done. This is called “precision dosing,” and it has been the backbone of diabetes management for decades.

It rests on one assumption: a carb is a carb. Get the number right, do the math, inject accordingly, and blood sugar falls in line exactly as anticipated.

But in reality, it just about never does. Ask any type 1 diabetic how well it works and they will tell you that when they take that approach, they ride the ups and downs of blood sugar as if on a bucking bronco!

The assumption that we can make this calculation and come out with a reliable formula is wrong, and I think this is at the root of not only our poor management of diabetes, but also of the epidemic of insulin resistance.

Let’s say have type 2 diabetes, and you just ate a meal made up of the foods the diabetic educator taught you to eat: fruits and vegetables, whole grains, nonfat dairy, and lean proteins. You ate nothing that was ultra-processed. A few hours later you’re feeling sluggish, fuzzy-headed and dragging, and you can’t figure out why, because the meal was “healthy.” You also notice that you got a huge blood sugar spike from the food you just ate.

Meanwhile someone else, who ate the exact same thing, feels completely fine and has no spike at all.

If that’s happened to you, you’ve probably assumed something is wrong with you.

It’s not you. And I can show you why.

For most of my career I told patients to eat the categories of foods I mentioned above. I said it so often, the phrase still rolls off my tongue: “eat lots of fruits and vegetables, whole grains, nonfat dairy and lean proteins.”

I was working on two assumptions, assumptions that most providers (and people) believe even today:

1. those categories of foods adequately describe what is “healthy” for everyone, including those with insulin resistance or Type 1 or Type 2 diabetes

2. Every human body will respond the same way to the exact same food, making the blood sugar response predictable.

Pick the right foods, avoid the wrong ones, and blood sugar remains under good control.

Then I started my own journey to reverse my own type 2 diabetes, and I ran headlong into multiple studies that took that assumption apart.

Here’s one from way back in 2015. Researchers put continuous glucose monitors on 800 people for a week and tracked more than 46,000 meals and 1.5 million glucose readings. The participants ate the same 50 gram carbohydrate serving of the exact same bread on two separate mornings.

Looking at each individual uniquely, comparing the person to himself, the blood sugar response was consistently reproducible: a blood sugar spike on day one, and pretty much the same blood sugar spike again on day two. The body was pretty consistent with itself.

But across different people eating that identical serving and type of bread, the top 10% of responders spiked nearly five times higher than the bottom 10%. Five times higher! Eating the exact same bread!

Carbohydrate counting, the method behind the ICR math I was trained to teach patients, turned out to be a terrible predictor of what actually happens to any individual person.

I have since learned, after helping hundreds of patients reverse their prediabetes, that there is much more to blood sugar control than can be applied generically to every person!

Your blood sugar response to a meal isn’t determined by the food alone. It’s determined by the interaction between that food and your particular body. YOUR body. Not mine, not your doctor’s. Yours.

You cannot follow a food guideline that says “eat lots of fruits and vegetables, whole grains, nonfat dairy and lean proteins” and control your blood sugar. It’s much too vague. You also cannot “count the carbohydrates” and anticipate the result based strictly on the math.

In my article last week, I wrote about the variables that make universal food guidelines for control of blood sugar pretty much impossible, so I won’t repeat that here.

There are, though, what I call “universal truths” about food. What I mean by that phrase is that there is a category of food where nobody’s blood sugar will rise and if you stick to that category, you will keep blood sugar low and steady. If the diabetic on insulin ate from only this category, his insulin needs would be both low and quite predictable.

There is another category where 100% of people will get a blood sugar spike, although I could not tell you how high or for how long because of that individual variability we are talking about here.

And then there is a last category where some will get a spike, and others will get none, and I could not possibly tell you in advance what your blood sugar would do. It is entirely unique to you.

So how do you find your own unique pattern?

You can’t think your way to this answer, you can’t find it on some universal table, you can’t outsource it to a carb-counting chart or figure it out using the glycemic index. Those tools were built from population averages, and I just described how those averages fall apart at the individual level.

You have to measure it. In you. This is what I mean when I talk about “sciencing yourself.”

A continuous glucose monitor is a small sensor, worn on the arm and transferring data to your phone, that shows your glucose pattern in real time. It’s the same technology used in the research referenced above. It turns your body from a black box into personal science. You stop guessing whether the rice or the potatoes are “your” trigger food and your start seeing it, meal by meal, with your own eyes.

Here’s how that might look like in practice:

Eat the same breakfast two mornings in a row and notice your blood sugar response. It won’t be precisely the same, but it will be pretty much the same. If you get a spike, drill down to figure out which food caused it with some further personal research using additional meals to gather data. Some of your “healthy” habits may turn out to be your biggest spikers. Some may be completely fine. You won’t know until you test it out.

Test food order and food pairing. Does protein or fiber before a starch blunt your spike? For some people it does dramatically. For others, barely at all.

Watch what happens after the spike, not just the spike itself. Note your energy, your focus, and your hunger two hours later. Your blood sugar and how you actually feel often tell the very same story.

You don’t need a research study to do this. You need a blood sugar monitor (which you can now get without a prescription), a bit of curiosity and scientific interest, and a week or two of paying close attention to the data.

The research did make one thing very clear: your own unique pattern is pretty consistent and personal, and once you can see it, you can work with it. This is so much more useful than following someone else’s advice on what and what not to eat!

You are not a population average. You are an experiment of one, and for the first time, you actually have the tool to run that experiment! Go ahead, try it!

Want to work on improving your own metabolic health? Find out exactly how (plus the “why it works”) in my book: Reversible! A Clinician’s Guide to Understanding and Reversing Insulin Resistance, Prediabetes, and Metabolic Disease. It’s available on Amazon and at diabetesgamechanger.com.

Interested in learning more about my online program for reversal of insulin resistance & Prediabetes?

Learn More HERE!

This Week’s Recipe Is, As Usual, AMAZING!

“Not Your Mama’s Potato Salad”

This is one of my own recipes, and I’ve made it often this summer! It’s a crowd-pleasure at potlucks - nobody else needs to know it is perfect for blood sugar control!

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I had a conversation recently with a friend who wanted to know what would happen to his blood sugar if he ate a serving of rice.

And until someone could tell him that, he wasn’t prepared to believe that there was real science underneath any of this “metabolic health” stuff. The whole field, as far as he was concerned, was quite possibly simply people with opinions until he could see that data.

I’ve thought about that conversation more than I expected to, because he wasn’t being unreasonable. He was applying a standard. He just happened to be applying a standard that almost nothing in medicine, and in fact almost nothing in biology, can meet. And the reasons why are, I’d argue, more interesting than the answer he was seeking!

First of all, we can’t really study much of nutrition science with any kind of accuracy.

There are too many variables, too many stakeholders in the outcomes, no money for studies when there is no drug or procedure at the end, and no way to do it without locking up thousands of study subjects for many years of data tracking.

Set that aside for a moment, though, because there’s a second, deeper problem — one that would remain even if we somehow solved the funding and the study design.

Here is a brief reminder of what’s actually going on when you eat a bowl of rice.

First, of course, is the basic physiology described in any physiology textbook. There’s nothing to quibble about there.

Starch is a chain of glucose molecules stuck together and given a new name. It’s called starch, but it’s still glucose. We cannot go out into a rice paddy and eat raw rice. We need to process it first to make it edible. Milling strips away the hull, and cooking gelatinizes the starch granules, loosening their tight crystalline structure so that our digestive enzymes can reach the glucose chains inside.

When you eat a digestible carbohydrate (starch or sugar, but not fiber, which passes through largely untouched), glucose is released and circulates in the bloodstream, raising blood sugar.

As blood sugar rises, insulin rises roughly in tandem. It binds to receptors on your cells, which triggers a signaling cascade that moves glucose transporters, called GLUT4, to the surface of the cell, opening a door for glucose to enter that cell.

Once the cell has all the glucose it needs, those transporters are pulled back from the surface and insulin signaling winds down. The cell is essentially saying “I’m full, stop sending more.” Mild, transient, physiological insulin resistance sets in within that cell.

Since rice is a high starch food, when you eat it, a large amount of glucose will enter the bloodstream.

At this point, though, you are simply describing what happens when you eat rice, not what happens to your blood sugar when you eat that rice.

The serving of rice contains a fixed amount of starch, and it hands that same fixed amount to every single person who eats it. What varies is how much of that starch actually becomes the elevated blood sugar you would see on your glucose monitor.

But here’s the thing that complicates the picture when we are trying to predict a blood sugar response in a human body: we are not measuring the food. We are measuring what happens inside your body when you eat that food.

When you look at a glucose monitor blood sugar reading, it feels like you’re watching the food. You ate something, the line went up, the line came down. Input, output.

You’re not watching the food. You’re watching what leaked past your body’s defenses.

Blood glucose is a defended variable.

Your body is not passively reporting the sugar content of your meal; it is actively, aggressively, and continuously trying to erase any change to your blood sugar at all. Insulin, glucagon, the incretin hormones, your liver deciding whether to release stored glucose or take some off the market, your muscles opening or closing their doors, your kidneys reabsorbing or spilling.

All of it is running at once, all of it is responding to the meal within seconds of you taking your first bite.

The blood sugar rise you see is not the size of the glucose load. It’s the error signal. It’s the part your control system couldn’t handle in time.

Think of a thermostat in two different houses on a cold day. If I open the front door in each house and watch the thermometer, I’m not measuring how cold it is outside. I’m measuring the gap between how cold it is outside and how good the furnace is in that particular house. Two identical doors, two identical winter days, but in two different houses. One thermometer barely twitches while the other drops ten degrees.

That’s why the same bowl of rice is a small hill for one person and a mountain peak for another. The rice didn’t change. The furnace did.

And this is exactly why the question can’t be answered the way my friend wanted it answered. To predict the number, even to get a useful range of numbers, we would need to know the moment-to-moment capacity of your particular control system: how much insulin your beta cells release in the first ten minutes, how loudly your muscle and liver tissue are listening. Those aren’t printed on the package.

The food is not a fixed thing either!

Before we even get to your body, the input itself is unstable. Rice is not rice. The ratio of amylose to amylopectin differs by variety. How thoroughly the starch gelatinized during cooking changes how fast enzymes can attack it. Rice that was cooked, refrigerated overnight, and reheated is chemically different from rice served straight out of the pot. Some of the starch retrogrades into a form your small intestine can’t easily break down. Particle size matters. A whole intact grain and a finely milled flour made of that identical grain behave like two entirely different foods.

Same for fruit: ripeness alone can move the needle substantially. Same for potatoes, oats, pasta, bread, and a whole lot of other things.

Those published glycemic index tables people quote so confidently? Those are population averages with error bars wide enough to swallow most of the distinctions anyone actually cares about.

In my experience, watching hundreds of blood sugar readings from hundreds of clients over the years, they are pretty much garbage for the distinctions people actually want them for.

The glycemic index only tells you how FAST the carbohydrates turn into glucose, not what happens next inside your body. A slightly better tool might be to calculate the Glycemic Load, which accounts for how much carbohydrate is in a normal portion, but both tools lack the ability to predict how that food will interact with YOU.

And YOU are not a fixed thing!

The actual form of the equation isn’t food → glucose excursion. It’s food + your current state + your recent history → glucose excursion.

Your current state includes: how full your glycogen tank is, how much fat is circulating in your bloodstream right now, the makeup of your gut microbiome, whether you are chronically insulin resistant, whether you drank alcohol with that meal, how well you slept, whether you’re stressed, what time of day it is, when your last meal was in relation to this one, where you are in your menstrual cycle if you have one, whether you’re fighting a virus, and what your legs did in the hour before the meal, plus what they’re going to do in the hour after. There’s more, but you get the picture. There are a LOT of variables!

When someone asks “what will this food do to me,” embedded in the question is an assumption that there’s a stable me for the food to act upon.

There isn’t. There’s a you-on-Tuesday-morning-after-six-hours-of-sleep-and-a-fight-with-your-brother, and that’s a different metabolic organism than you-on-Saturday.

So no, I cannot tell this person exactly what will happen when he eats that bowl of rice. I can’t give him a number, and any range honest enough to be true would be too wide to be much use to him.

But what we CAN do, since general prediction is not possible, is to experiment on ourselves to learn OUR OWN response to food. We can learn our patterns, our tendencies, our typical responses on a typical day and with that, we can make informed decisions about what to eat.

And even then, there are some pitfalls!

Here’s one: there’s a “rate-limiting” step for the blood sugar rise that hinges on how fast your stomach passes the food down to your small intestine.

Gastric emptying is the trap door, and it’s somewhat throttled by fat, protein, acidity, the sheer volume of the meal, and even the order in which you ate your food. If you eat your vegetables and protein first, and your rice last, you’ve changed the blood sugar excursion without changing a single ingredient.

And that emptying rate isn’t fixed within a person either. It varies day to day for a variety of reasons.

Here’s another: unless you are willing to really work at perfecting the science for yourself, you only get one shot at each meal.

You can’t run the same meal twice and get perfectly predictable results. The moment you eat something, you’ve changed the initial conditions for every subsequent meal. There’s no counterfactual, no parallel version of you who skipped the rice at that meal, so that we could compare. Every meal is a single draw from a distribution, observed once, never exactly and precisely repeatable.

So even a perfect prediction couldn’t be verified at the level of one meal on one day.

That’s not a failure of the science. That’s the structure of the situation.

Even the ruler wobbles! The CGM itself. It doesn’t measure blood. It measures interstitial fluid, which lags behind blood by several minutes. It applies a smoothing algorithm, and it has a margin of error. Put two sensors on the same arm and they will not agree precisely about your blood sugar peak.

So, is there no science here?

We predict tendency very well. We predict the instance poorly.

Physics does this constantly and nobody calls it unscientific. Nobody demands to know exactly which route a particular hurricane will take before accepting that hurricanes exist and can be dangerous. Nobody refuses to believe in smoking’s harms because we can’t say which cigarette causes the tumor. Population-level certainty plus individual-level uncertainty is the normal condition of nearly all useful biological knowledge.

The demand for an exact number isn’t a higher standard of evidence. It’s a different question wearing the costume of a higher standard.

Here’s the good news. You may not be able to get the population answer, but you sure can get your answer. You can even get a pretty specific answer, if you are willing to really science yourself!

Hold the confounders still, same time of day, same previous meal, similar sleep, similar activity before and after, and you repeat a meal several times, the noise starts to cancel and your personal signal comes through. It’s still not a precise prediction, but it is a pattern. And a pattern is plenty good enough to make decisions with.

Stop asking science to hand you a universal number, and start running a small, careful experiment on the only subject whose answer you needed in the first place.

Which, I’d gently point out, is a considerably more scientific posture than waiting on the sidelines for a certainty that no one was ever going to be able to give you.

Want to work on improving your own metabolic health? Find out exactly how (plus the “why it works”) in my book: Reversible! A Clinician’s Guide to Understanding and Reversing Insulin Resistance, Prediabetes, and Metabolic Disease. It’s available on Amazon and at diabetesgamechanger.com.

Interested in learning more about my online program for reversal of insulin resistance & Prediabetes?

Learn More HERE!

This Week’s Recipe Is, As Usual, AMAZING!

Grilled Pork Loin Chops

Quick, easy and delicious!

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A family member just had his yearly blood tests done, including an HbA1c, a test that shows how much sugar has stuck to the hemoglobin inside his red blood cells over the past three months.

The result came back at 5.9%.

His doctor told him everything looks fine, and that he’d see him again next year. You can see his lab result was in the “green zone” of normal.

Everything is NOT fine.

By the American Diabetes Association’s own criteria, an HbA1c between 5.7% and 6.4% is prediabetes. At 5.9%, my family member is not in the normal range. He is not borderline. He meets the standard, published, widely accepted definition of prediabetes, and yet nothing was said of this and he was told to come back in a year.

That is the problem in a single sentence. We have a diagnostic threshold that nearly everyone agrees on, and yet it still gets waved right on through as if nothing is wrong.

Before that HbA1C begins to rise, something is happening with insulin. It is working overtime to keep that blood sugar normal. It spikes higher and higher in an effort to do the job, and eventually it is high just about all the time.

Insulin can be measured in a lab long before blood sugar begins to rise.

As insulin begins to fail to keep up with demand, blood sugar begins to climb. A fasting blood sugar of 100 or above (the ADA’s impaired fasting glucose range is 100 to 125) means blood sugar is no longer being kept in good control.

Type 2 diabetes is diagnosed when fasting blood sugar reaches 126 or above, or HbA1c reaches 6.5% or above. Unfortunately, that is typically the first time the patient hears there is any kind of problem, even though the clues were there for years prior.

The scale of this problem is hard to overstate.

• In a NHANES analysis, way back in 2016, only 12.2% of American adults met the criteria for optimal metabolic health. A more recent analysis of NHANES data through 2018 put the figure at a mere 6.8%. It is surely even worse today.

• In 2023, the CDC estimated that 32.7% of adolescents aged 12 to 17 had overt prediabetes. Not just early insulin resistance, but actual prediabetes.

And, contrary to popular belief, you do not have to be overweight to have a metabolic problem.

Metabolic dysfunction is common even among people at a perfectly normal weight. In the NHANES analysis above, only about one third of normal-weight adults were metabolically healthy. Thin is not the same as metabolically well. What matters is where the fat is located along with what your insulin is doing, not what the scale says.

Which means the burden falls on YOU to ask for testing, to understand the results, and to then take action where needed.

First, get your HbA1c tested.

If it is 5.6% or above, it is time to make some changes so you can reverse the trajectory. You are losing control of blood sugar.

If your HbA1c is 5.5% or below, get a fasting insulin.

Insulin is the earlier signal. It rises to compensate long before loss of blood sugar control. Most labs will call consider a fasting insulin of around 25 µU/mL normal. Those of us working in the field of metabolic health use a much tighter target — under 6 — because that is where it is in a metabolically healthy human, not merely where the population average happens to be. Expect your lab to flag your result as normal even when I would not.

What causes insulin resistance?

Here are the usual triggers, the ones we know about, ordered roughly from the most common to the least. There may well be more:

• Frequent blood sugar spikes from foods high in available glucose. You would not know you are having them without measuring blood sugar. Continuous glucose monitors are now available over the counter, and wearing one for a few weeks will show you exactly which foods spike you. The common offenders:

• Added sweeteners

• High Starch Foods: grains, potatoes and other starchy root vegetables, plus corn

• Fruit, especially juice and dried fruit

• Milk. Its glycemic load is modest, but milk provokes a disproportionately large insulin response.

• Fat accumulation in the liver (“fatty liver”), which drives hepatic insulin resistance and excess glucose output.

• Visceral fat, the fat packed inside your abdomen and in and around your organs, even if you are not overweight. The amount it takes to cause trouble is small, often just a pound or two.

• Too much subcutaneous fat (the jiggly kind of fat). “Too much” is unique to each person, but everyone has a unique threshold above which the extra fat causes insulin resistance.

• Chronically high blood sugar. This is both a consequence of insulin resistance and a trigger for more of it in a dangerous feedback loop.

• Chronic inflammation, which can be caused by visceral fat, too much subcutaneous fat, blood sugar spikes, fatty liver, chronic illness, and more.

• Mitochondrial dysfunction, which can arise from the all of the same sources.

• Eating too much fat when your fat cells are already full of fat.

• Stress hormone elevation. Cortisol and adrenaline are both released during stress, and both raise blood sugar and contribute to insulin resistance.

• Sleep deprivation.

• Fat accumulation in muscle, along with underlying muscle insulin resistance from lack of movement.

• An altered gut microbiome, which increases intestinal permeability, allowing bacterial endotoxins to seep into the bloodstream and trigger inflammation and insulin resistance.

• Dehydration.

• Genetic predisposition. Variations in genes can affect insulin signaling, glucose metabolism, and fat distribution. Notice this one is last in the list of potential triggers – the LEAST powerful one.

None of these triggers act in isolation. They create reinforcing feedback loops in which insulin resistance begets more insulin resistance, eventually overwhelming the pancreatic beta cells’ capacity to make enough insulin. That is type 2 diabetes.

So don’t wait.

I hate to say it, being a provider myself, but don’t wait for your own provider to tell you there is a metabolic problem. Ask for the right tests. Learn to interpret them yourself. Then act on the data you obtain.

Type 2 diabetes is just about 100% preventable, and if not prevented, it is often completely reversible.

The earlier you catch the problem, the better the odds that you can return your body to its original “factory settings.” A 5.9% deserves a thorough and urgent conversation, not a “see you next year.”

What you have just read is meant to be educational content, not medical advice. Any testing, treatment or lifestyle decisions should be made in consultation with your own medical provider. And, as always, all references can be found on my website at diabetesgamechanger.com.

Interested in learning more about my online program for reversal of insulin resistance & Prediabetes?

Learn More HERE!

This Week’s Recipe Is, As Usual, AMAZING!

Tzaziki!

This recipe is perfect for those hot summer days, when cucumbers are at their best! The Greek yogurt provides a little protein, giving you a winner of an appetizer, or even an entire lunch!

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My uncle just read my book about reversing insulin resistance, and I have a feeling he’s going to have some questions!

In my experience, where a physicist’s understanding of weight loss and weight gain begins and ends is with calories. If you “eat too much” you gain weight, and thus you need to “eat less” to lose weight. It doesn’t matter what food you choose, it’s just that simple.

Where that idea comes from is something called the “first law of thermodynamics:” energy cannot be created or destroyed, only transformed from one form to another.

That law is certainly real, but it doesn’t do much to explain why we gain or lose weight.

In this article, I’ll explain why that is. The topic can sometimes be confusing!

Your Body Isn’t a Furnace

Think of a calorie as just a number, like a price tag. It tells you how much energy is in your food. But it doesn’t tell you what your body does with that energy once you eat it.

When you eat, your body has to make a choice: burn that energy right now, or store it as fat for later. That choice isn’t made by counting numbers. It’s made by the hormone insulin.

When insulin is high, your body goes into “fat storage mode.” Your fat cells lock their doors and won’t release fat to be burned. It doesn’t matter how careful you were with your calorie count for the day, if insulin is high, your body fails to harvest your fat stores.

When insulin is low, the opposite happens. Your fat cells open back up, and your body is able to harvest your body fat and burn it for fuel.

This is why two people can eat the exact same 500 calories and end up with totally different results. What matters isn’t just how many calories were in that food, it’s how that food affects insulin. Carbohydrates raise insulin the most, but protein and other things play a role too.

The calorie number tells you the size of what you ate. Insulin tells you whether your body stores it or burns it.

“But Doesn’t the Physics Law Prove Calories Matter Most?”

If energy can’t be created or destroyed, it means weight loss really is just calories in versus calories out, right?

Insulin doesn’t break this law. Insulin is simply the switch that decides what happens to the energy you eat. (It also affects how hungry you feel!).

When insulin is high, you feel hungrier, because your body is stuck in storage mode, unable to harvest body fat for fuel. Your body thinks you are starving to death! Hunger feels urgent.

Saying “a calorie is a calorie because of physics” is a bit like saying “a dollar is a dollar because of math.” That’s technically true, but it doesn’t explain why your paycheck disappears into paying rent instead of going into the savings account.

The law of thermodynamics says the math does have to add up in the end. It doesn’t tell you how the energy coming in was ultimately spent, though. Was it used to pay the rent, or was it put away in the savings account?

And a follow-up question: “If high insulin makes you hungrier, and being hungrier makes you eat more, isn’t that still just calories in, calories out causing the weight gain?”

It’s a fair question, but here’s the difference. The old calories in/calories out model treats how much you eat as something random, just a choice.

The insulin model says something different: insulin itself is steering the ship. It decides both how hungry you feel and whether your fat cells hold on to fat or let go of fat.

Eating more is not the root cause of the weight gain. It’s a symptom of what insulin is already doing to promote that weight gain.

Think of it like a fever: a fever doesn’t cause the flu, it’s a sign your body is fighting an infection. Eating more because hunger is out of control when insulin is high works the same way. It’s a sign of what’s already happening inside you, not the root cause.

“But People DO Lose Weight on Low-Calorie Diets. Explain That.”

That’s a fair observation! If insulin really controls fat storage, why do people who just go on a plain low-calorie diet still lose weight, even without trying to lower insulin on purpose?

The answer is that eating less food just about always also lowers insulin, even if by accident. Less food coming in usually means less carbohydrate and less protein hitting your system at each meal. Less food means less insulin gets released to partition that food. So a low-calorie diet can end up quietly lowering insulin as a side effect, even when that was never the goal.

Fasting is the clearest example of this, since it drops insulin down to its lowest point. That’s a big reason fasting works so well for fat loss. Not because “zero calories” is some magic number, but because zero calories also means very low insulin needs.

This also helps explain why some low-calorie diets are so hard to stick to and so slow to bring about weight loss. If you cut your calories mostly by eating smaller portions of the same foods, keeping the same amount of carbs and snacking just as often, you may barely lower your insulin at all. You’re just fighting hunger with willpower instead of getting help from your hormones. That’s a much harder way to lose weight, and it’s part of why so many low-calorie diets end in a rebound.

There’s one more piece worth mentioning. If you restrict calories for too long, your body pushes back in other ways. Hunger hormones go up, and your metabolism slows down in an attempt to “match” the calorie deficit. Your body thinks there is a famine, and it’s trying to save you. That’s a separate problem from insulin, and it’s part of why “just eat less” tends to stop working over time, even when it does lower insulin somewhat at first.

So the real story isn’t that calories don’t matter at all. It’s that cutting calories only helps when it also lowers insulin. The diets that lower insulin the most, on purpose, tend to not only be easier to stick with because hunger isn’t a problem, but also the low insulin promotes the harvesting of body fat. Win-win!

You Can’t Count Calories Accurately Anyway

Even if calorie counting worked, you couldn’t actually do it with any accuracy. Here’s why:

Digesting food costs energy, and that cost is different for every kind of food. Protein takes a lot of energy to digest. You will burn off 20–30% of its calories just breaking it down. Fat barely costs anything to digest. So 400 calories of eggs and 400 calories of crackers are not the same to your body, even before insulin comes into play.

Everyone digests food a little differently, too. Your gut bacteria, how sensitive you are to insulin, how much muscle you have, and how well you sleep all change how much energy you actually get out of a meal. Two people can eat the exact same meal and absorb different amounts of energy from it.

Even the calorie count on the label can be wrong. The FDA allows food labels to be off by up to 20%. If you tracked every single bite perfectly, the numbers you were tracking were never fully accurate to begin with.

And don’t even get me started on the ridiculous practice of keeping track of how many calories you “burn” in a day with exercise!

Ok, so now I might have you convinced that insulin matters. But now I hear you saying:

“But My CGM Shows I’m Not Spiking, So Why Aren’t I Losing Weight?”

If you wear a continuous glucose monitor (CGM), and you’ve been working on your library of meals that keep blood sugar low and steady, you will see a nice, flat blood sugar line. So why aren’t you losing weight?

Here’s why: a CGM measures your blood sugar, not your insulin, and although they tend to rise and fall in tandem, they are not perfectly aligned.

If your body is insulin resistant, your pancreas has to release more insulin just to keep your blood sugar steady. That means you can have a perfectly flat CGM graph and still have high insulin working overtime behind the scenes to keep it that way. The only way to know for sure is to test your insulin directly, not just your blood sugar. (Someday I hope we have continuous insulin monitors!)

There’s another thing a CGM won’t show you: protein can raise insulin even though it barely raises blood sugar.

So can eating too often throughout the day. If you’re eating “clean,” low-carb meals every few hours, you could be keeping insulin elevated all day long, even with a perfect-looking CGM graph.

Bottom line: a flat CGM tells you your blood sugar is doing fine. It doesn’t tell you your insulin is low.

A Reality Check

I want to be fair here. If someone overeats low-carb food and their blood sugar stays flat, it’s tempting to assume their insulin must be high somewhere else, and most of the time, that is exactly what’s going on.

But I can’t say it is always true.

For those whose fat cells are already overfilled, particularly belly fat, those fat cells can become insulin resistant in an effort to avoid even worse over-filling, a real, documented phenomenon sometimes called adipose tissue “overflow.”

That does NOT mean that a fatty meal makes your pancreas release a burst of insulin in the moment. Dietary fat is actually one of the weakest direct triggers of insulin release of any macronutrient.

What it does mean is a slow but powerful background process. Overfilled fat cells lose some of their ability to hold onto what they’re storing, and they leak free fatty acids into your bloodstream more than they should, even when insulin is telling them to stay closed.

Those free fatty acids don’t just float around harmlessly. Your liver and muscles pick them up, and in tissues that aren’t built to store much fat, that extra fatty acid load starts interfering with how those tissues respond to insulin, a process researchers call “lipotoxicity.” Your liver and muscles become insulin resistant too, not just your fat cells.

Once that happens, your pancreas notices insulin isn’t doing its job as well as it used to, so it compensates by making more of it! Which pushes your baseline insulin level up throughout the day, even between meals and overnight.

Researchers are still working out the exact sequence of this feedback loop and which piece comes first, but the overall pattern is well established: overfilled fat cells → more free fatty acids in the blood → insulin resistance in the liver and muscle → higher baseline insulin to compensate.

And leaking fatty acids isn’t the only path here. Overfilled fat tissue also turns “inflammatory.” It starts pulling in immune cells and releasing signaling molecules that interfere directly with how your cells respond to insulin, separate from anything happening with fatty acids.

At the same time, fat tissue makes less adiponectin, a hormone that normally helps keep you insulin sensitive, so you lose some of your natural protection on top of everything else.

Location matters too: fat carried around your belly is more metabolically active and drains straight into your liver, giving it an outsized effect on liver insulin resistance compared to fat carried elsewhere on the body. Leaking free fatty acids and fatty liver are a big piece of this story.

If your baseline blood sugar is higher than normal, even just a little bit (baseline is what it is between meals and overnight), something is causing chronic insulin resistance. You’re not having spikes in blood sugar because you are managing your carbohydrate intake, but you ARE carrying a higher overall insulin level around the clock.

Where This Leaves Us

None of this means portions don’t matter, or that you can eat unlimited amounts of food with no consequences as long as blood sugar stays low. It means the tool most people have been using, calorie counting, was never the right tool for controlling fat storage.

Insulin is.

And the good news is, you can influence insulin far more reliably through what you eat, how you combine foods, and when you eat, than you can ever count your way to a calorie deficit.

I’ll say this too: the calorie model still dominates mainstream nutrition guidance, and there are researchers who’d push back hard on what I’ve written here, pointing to controlled feeding studies where calorie-matched diets produced similar fat loss regardless of carbohydrate content. That debate is real, and it’s not fully settled in the research literature. What I can tell you from the clinical and physiological side is that when you shift the focus from counting calories to lowering insulin, thereby lowering the hormonal signal that tells your body to store rather than burn, the results tend to speak for themselves in a way that spreadsheets never can.

If you’re tired of tracking every bite and still not seeing results, maybe it’s time to stop asking “how many calories is this?” and start asking “what is this doing to my insulin?”

Want to work on improving your own metabolic health? Find out exactly how (plus the “why it works”) in my book: Reversible! A Clinician’s Guide to Understanding and Reversing Insulin Resistance, Prediabetes, and Metabolic Disease. It’s available on Amazon and at diabetesgamechanger.com.

This Week’s Recipe Is, As Usual, AMAZING!

Cabbage Slaw With Nut & Seeds

So delicious even the “naysayers” in the room will love it!

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My discouragement stems from a conversation I had with a concerned grandmother about her 8 year old grandchild with Type 1 diabetes, diagnosed two years ago. She’s on insulin, of course, since someone with Type 1 does not make any of their own.

Her mother was apparently told to “give her a healthy diet” but not given specific information on how to evaluate food for its effect on blood sugar.

She was told to offer “normal” food and that the insulin would “fix” the blood sugar. Her daughter rides a roller coaster of blood sugars up and down, with the alarms on her glucose monitor going off multiple times a day for both blood sugar highs and lows.

She was never told that when insulin is frequently high, as it would be if a person were eating in a way that provoked blood sugar spikes, that high use of insulin over time would increase the odds that insulin resistance would eventually set in. She can easily develop Type 2 diabetes on top of the existing type 1, compounding and exaggerating a very serious problem over time. This is called “double diabetes,” and is an increasing problem now, where it was unheard of years ago prior to our epidemic of type 2.

She was never told that her daughter’s total daily insulin dose is itself something extremely important, separate from the blood sugar and the overall HbA1c. A1c can look perfectly acceptable while the dose required to get there quietly climbs, month after month. That climb is the early warning sign of insulin resistance creeping in, often long before anything shows up on a lab report.

She was never told that it is not just blood sugar, but it is also insulin that contributes to the terrible down-stream consequences of having either type 1 or type 2 diabetes. The loss of limbs. The Alzheimer’s. The heart attacks and strokes. The cancers. There is so much more I could say....but I’m already feeling down so I’ll stop there.

She was never told that both the highs and the lows affect both her behavior and her brain’s ability to function well, which will impact her progression through school and through her various phases of life. And she was never told that this matters most of all right now, at 8 years old. A young child’s brain is especially vulnerable to the effects of repeated high and low blood sugars, and those effects can show up later as subtle struggles with attention, memory, and problem-solving, long after anyone remembers to connect the dots back to the highs and lows she had in elementary school.

She was never told that insulin is a powerful gonadotrophic hormone that acts directly on the reproductive organs. While insulin secreted by the pancreas goes through the portal vein to the liver, which clears out about half of it before it ever reaches the rest of the body, injected insulin (or from an insulin pump) goes into the fat tissue and then directly into circulation in the blood stream, bathing ovaries (as well as all the other cells in the body) in higher concentrations of insulin than anything mother nature could ever achieve.

She was never told that if she wants to have children someday, requiring less insulin now, as a child, will help her achieve that.

She was never told that the roller coaster of ups and downs, rather than a steady glucose pattern, will contribute to oxidative stress and inflammation, both of which contribute to chronic disease later in life.

She was never told that high insulin, required when a person is eating in such a way that blood sugar spikes, directly affects blood vessels, accelerating heart disease independently from the damage done by high blood sugar alone.

But here’s the thing that makes me feel the saddest of all: she was never told that she could feed her child in such a way that she could keep blood sugars from spiking high and that would keep her insulin needs steady, predictable, and minimal.

And she could do it deliciously! There are SOOOOO many fantastic recipes and ideas out there now!

She was never told that it isn’t just sugar that raises blood sugar, it is also starches. She was never told that eating a piece of toast for breakfast is not much different than eating a candy bar. Glucose is glucose no matter where it comes from.

She was never taught how to read a food label, to notice that the bottle of special sauce has 10 grams of carbohydrate per serving, giving her 3 times the amount of glucose her body wants to have circulating in the blood stream.

Her doctor said “you’re doing a great job.”

And she is -- she really is. She is following ADA guidelines and the advice given by doctors.

What is in her daughter’s future is not her fault. Not at all.

It’s OUR fault as humans for not teaching basic physiology to every person. For allowing food companies to produce food that addicts us and makes us sick.

For thinking we can only get our children to eat if we put sugar on the food, and that otherwise they will starve to death.

For failing to help people understand how food interacts with the human body.

For not defining what “healthy” food is when it comes to blood sugar control.

I hope in my lifetime we can somehow spread the word that none of this needs to happen. That there is a different way.

So, if you’re a grandmother, a mother, a father or a grandfather and you are reading this and feeling that same lump in your throat about the future of your precious loved ones, here is one small step you could take.

Check out the resources available by the American Diabetes Society (Society, not Association!) and see what they have to offer for Type 1, particularly for children.

The difference between type 1 and type 2 is in where the insulin comes from, and whether the situation can be reversed, as it often can be with Type 2. The dangers, the chronic diseases, the eating strategy that helps with all of it…..it’s all exactly the same.

So, if you happen to be one of the 89% of US adults who have insulin resistance, prediabetes or type 2, I’ve got great news for you!

(Check your HbA1C and make sure it is below 5.6%, and make sure your fasting insulin is below 6!)

You can reverse it!

And in the process of learning a bit about your physiology, you can help your daughter, your granddaughter, your sisters and your brothers.

You can even make a difference in the health of those around you by simply talking about what you’ve learned. They’ll go home and think about it. You don’t need to tell anyone what they “should” or “should not” do. You can just share what you’ve learned about yourself, and maybe spark a bit of curiosity in those around you. That WILL make a difference!

And, of course, you can serve metabolically healthy (and DELICIOUS!) food to your grandchildren when they come over for a visit!

Want to work on improving your own metabolic health? Find out exactly how (plus the “why it works”) in my book: Reversible! A Clinician’s Guide to Understanding and Reversing Insulin Resistance, Prediabetes, and Metabolic Disease. It’s available on Amazon and at diabetesgamechanger.com.

Interested in learning more about my online program for reversal of insulin resistance & Prediabetes?

Learn More HERE!

This Week’s Recipe Is, As Usual, AMAZING!

Blueberry Muffins!

So good, even the grandchildren will love them!

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Last week I wrote about alcohol and its effect on metabolic health, and I mentioned something called “oxidative priority.” I want to expand on that today, because once you understand this concept, a lot of things about weight, fat burning, and food choices start to make a lot more sense.

I’ll also introduce its close companion: the thermic effect of food. Together, these two principles give you a powerful framework for understanding how your body actually processes what you eat, and how to work with that rather than against it.

Your metabolism has a VIP list – I wrote about that last week because alcohol is at the very top of that list!

There is a non-negotiable priority list, and no one cuts in front of it. Every fuel you consume is processed according to strict metabolic rules that determine what gets burned for energy and what gets stored as fat.

The hierarchy is governed by two key factors: how harmful each fuel would be if left circulating in your bloodstream, and how easily it can be stored.

Your body burns the nutrients you ingest in the following order, every single time: alcohol, protein, carbohydrates and then finally fats.

First: Alcohol

Since I wrote about that last week I won’t go into why it’s first again here. If you missed it, check that article out!

Second: Protein

Protein sits in second place, but its position on the list is somewhat misleading — because protein isn’t really a fuel at all. Your body doesn’t want to burn protein for energy any more than you’d want to burn your furniture to heat the house. Protein is needed for building and repairing muscle, producing enzymes and hormones, supporting immune function, and running virtually every cellular process in your body.

So when you eat protein, your body immediately puts it to work for all those important structural and functional purposes. It does this so efficiently and completely that relatively little is left over to contribute to fat storage.

Can the body burn protein for fuel? Yes, if it absolutely has to. But it’s a less efficient and more metabolically costly process. It certainly works in a pinch, but it’s not the intended use, and your body will always look for a better option first.

Third: Carbohydrates

Carbohydrates move up the priority list quickly because of what happens when the glucose harvested from those carbs sits in your bloodstream: your blood sugar rises, and elevated blood sugar is damaging to tissues. Your body wants to clear it out as fast as possible.

Here’s how that process works:

• First, circulating glucose is used to fuel any cells that need energy right now

• Any remaining glucose gets stored as glycogen in your muscles and liver. You can hold roughly 400–500 grams this way

• Once glycogen stores are full, the rest gets converted to triglycerides and stored as body fat

Carbohydrates also create a second problem that the other macronutrients don’t: they raise insulin. And insulin is your primary fat-storage hormone. When insulin is elevated, your body is in a physiological mode that actively prioritizes fat storage over fat burning. The more refined and rapidly digested the carbohydrate, the sharper the insulin spike, and the more pronounced this effect becomes.

This is why the type of carbohydrate matters enormously. Whole, fiber-rich carbohydrates from non-starchy vegetables and legumes, for instance, digest slowly, produce a modest and gradual glucose rise, and trigger far less insulin than their starchy, sugary or processed counterparts.

Last: Dietary Fat

Fat sits at the bottom of the oxidative priority list, not because it’s unimportant, but because it’s so easily stored and because your body can hold virtually unlimited amounts of it. There’s no metabolic emergency associated with dietary fat the way there is with alcohol or glucose, so fat can wait.

The practical consequence of this is significant: dietary fat gets burned for energy only when the higher-priority fuels have been dealt with. When you eat a meal high in both carbohydrates and fat — pasta with cream sauce, chips, buttered bread, most fast food — your body burns the carbohydrates and stores the fat. The fat waits in line, and never gets called.

This is one of the key reasons why the combination of high carbohydrate and high fat is so metabolically problematic: you’re eating two fuels, but your body can only efficiently burn one at a time. The other one gets stored.

What About Body Fat?

Here’s something important to understand: oxidative priority doesn’t just apply to the food on your plate! It applies to your body’s stored fat reserves too.

Whenever you eat, regardless of what you eat, your body pauses the burning of stored body fat until the meal is fully processed. It’s focused on dealing with the incoming fuel, not raiding the reserves. For a large mixed meal, that processing window can extend 4–6 hours or even longer. This is one of the physiological reasons that eating frequency matters: the more often you eat, the less time your body spends in the metabolic state where it can access stored fat for fuel.

This is also the mechanism behind why intermittent fasting is so effective for both fat loss and for blood sugar control. In a fasted state, once glycogen stores drop below a certain threshold, your body turns to stored body fat as its primary fuel. The longer the fast, the more time your metabolism spends in fat-burning mode. (This is also why exercise in a fasted state tends to accelerate fat oxidation — glycogen is already partially depleted, so fat burning kicks in sooner.)

The Thermic Effect of Food: Your Metabolism’s Hidden Calorie Burn

Oxidative priority tells us what gets burned first. The thermic effect of food tells us how much energy your body spends in the process of burning it.

Every time you eat, your metabolism ramps up to digest, absorb, transport, and process what you just consumed. This increase in energy expenditure after eating is called diet-induced thermogenesis (DIT), and it’s also commonly referred to as the thermic effect of food (TEF). Across a full day, it accounts for about 10% of your total energy expenditure. That can be an important component of your metabolic rate.

Not all foods “cost” the same amount of energy to process. The thermic effect varies considerably by macronutrient:

Protein: 20–30% thermic effect. If you eat 100 calories of protein, your body burns 20–30 of those calories just in the process of digesting and metabolizing it. This is the highest thermic effect of any macronutrient, and it’s one of the primary reasons high-protein diets are so effective for weight management.

Alcohol: approximately 10–30% thermic effect. In research settings, the thermic effect of alcohol is actually comparable to protein, and is considerably higher than the commonly cited generic “15%” figure, with some studies finding it even higher when alcohol comprises a significant portion of the meal. This surprises a lot of people, because it might sound like alcohol is therefore “good” for metabolism. It is not. The thermic cost of processing alcohol does nothing to offset its other metabolic harms: halted fat burning, hormonal disruption, insulin effects, and sleep damage.

Carbohydrates: 5–10% thermic effect. The number is very heavily influenced by the fiber content of the carbohydrate, which can vary enormously. High fiber vegetables that generally grow above the ground, for instance, take much more energy to break down than either the high starch vegetables, such as potatoes, or the refined ones, such as rice.

Fat: 0–3% thermic effect. Dietary fat requires almost no energy to process , it’s metabolically “cheap,” which partly explains why it sits at the bottom of the oxidative priority list.

Ultra-processed foods: effectively 0%. Pre-digested, chemically broken down food requires almost nothing from your metabolism to process. Your body barely has to work at all, which means virtually all of that fuel is available for storage.

There’s another important variable here: research has found that the thermic effect of food is meaningfully blunted in people with obesity and insulin resistance. In other words, if you already have metabolic dysfunction, your body is less efficient at generating heat from food. That means fewer calories are burned in processing, and more are available for storage. This is one of the ways that metabolic disease creates a self-reinforcing cycle that makes fat loss ever harder.

Time of day also appears to matter. Multiple studies have found that the thermic effect of a meal is higher in the morning than in the evening for the identical meal. Eating earlier in the day squeezes more calorie burn from your food than eating the same meal at night, another finding that supports the metabolic value of front-loading calories earlier in the day when it works with your schedule.

How to Work With These Principles

Understanding oxidative priority and the thermic effect of food gives you a practical metabolic framework. Not a set of rigid rules, but a set of principles you can apply strategically when it works in your day.

Prioritize protein at every meal. It gets preferential oxidation, has the highest thermic effect, preserves muscle mass during weight loss, and is the most satiating macronutrient. Getting protein at every meal is one of the highest-leverage dietary strategies you can implement.

Be strategic about carbohydrates. Reducing refined carbohydrates removes a higher-priority fuel from the queue and gives your body more opportunity to burn stored fat. When you do eat carbohydrates, choose high-fiber, minimally processed sources, which will produce a smaller insulin response and come with a higher thermic cost. And if you’re going to eat carbohydrates, timing them around exercise is smart: glucose taken in around a workout gets used to refuel glycogen rather than stored as fat.

Minimize or eliminate alcohol. Nothing else jumps the oxidative queue the way alcohol does, and nothing else creates such a comprehensive metabolic disruption. Even modest amounts meaningfully impair fat oxidation for hours.

Reduce meal frequency if fat loss is your goal. Every time you eat, stored fat burning pauses. Two or three meals per day, with no snacking in between, creates longer windows in which your body will need to access stored fat. This is the metabolic principle behind both intermittent fasting and the advice to stop eating between meals.

Don’t underestimate fat-carbohydrate combinations. High-fat, high-carb meals, the combination that dominates most ultra-processed food, are metabolically the worst of both worlds: the carbs get burned while the fat gets stored. Separating fat from refined carbohydrates, or choosing whole food sources where the two occur together naturally (avocado, nuts, eggs), produces very different metabolic outcomes.

Your metabolism follows strict rules about what gets burned, in what order, at what cost. You can’t change the rules. But understanding them puts you in a much better position to make choices that work with your biology rather than against it.

Educational content, not personal medical advice. Any testing or treatment decisions should be made with your own clinician. As always, all references can be found on my website at diabetesgamechanger.com.

Want to know more about my online program for reversal of Insulin Resistance?

Find Out More RIGHT HERE!

This Week’s Recipe Is, As Usual, AMAZING!

PIZZA!

Metabolically friendly, TONS of protein, even in the crust, hearty enough to pick up the slice, quick and easy to make!

Get the Recipe RIGHT HERE!

Most of my weekly highlighted recipes are created by my sister, Katherine Aitken-Young, nutritionist, nurse and IBS specialist. “But I don’t have IBS”! Well neither do I! But there is a close relationship between IBS and Insulin Resistance, so many of her recipes work perfectly for my clients as well as for hers!

The recipes are quick and easy to make, are never fussy, they taste amazing, and they make up the majority of meals I cook and eat myself every day. The recipes simply avoid those ingredients that are common IBS triggers. Because I don’t have IBS, I often make certain substitutions. Some examples:

• Oyster mushrooms – I use any type of mushroom

• Garlic infused olive oil – I use olive oil and some crushed garlic

• Gluten free items – I use the regular item

• Smoke insanity spice mixes – I use regular spices

• When amounts are limited (such as “no more than 40 cashews”) I use however many I want to use

• When it calls for lactose free, I use the regular version

And since I want to eat a very low starch diet for best metabolic health, if the recipe calls for any kind of sugar, I substitute Allulose. If it says “serve over a bed of rice,” I don’t! You get the picture.

If you would like access to ALL of her recipes, you can find her

RIGHT HERE!

Ever wonder why that glass of wine with dinner seems to sabotage your weight loss goals? Or why you wake up after an evening out that involved a couple of glasses of wine feeling puffy, tired, and craving carbs? The answer isn’t the calories, it’s a fascinating (and frustrating) aspect of human metabolism called oxidative priority.

I think it’s helpful to understand the concept so that you can make more strategic decisions about when and how often you enjoy alcohol!

Your Metabolism Has a VIP List

Your body is a control freak when it comes to fuel, worse than a bouncer at an exclusive club. Every nutrient you consume is treated according to strict metabolic rules that determine what gets burned for energy and what gets stored as fat. The hierarchy is based on two key factors: how easily each fuel can be stored as fat, and how harmful it would be to your health if it were left to circulate in your bloodstream.

Here’s the exact order your body burns nutrients, every single time:

• Alcohol: first, always, because it’s a toxin your body can’t store

• Protein: used immediately for muscle repair, enzymes, and cellular functions

• Carbohydrates: used for immediate fuel if needed, then the extra is stored as glycogen or as fat

• Fat: the last in line, because it’s so easily stored and so essential for survival

When alcohol enters your system, it immediately jumps to the front of this line. This is not because your body likes it, but because it has absolutely zero capacity to store it. Your body treats alcohol as a toxin (because it is) and works urgently to clear it from your bloodstream. Everything else gets put on hold until every last drop of alcohol is processed.

The Wine with Dinner Scenario

Picture this: you sit down with your glass of wine to eat a nice dinner of chicken, new potatoes and salad with vinegar and oil dressing.

Your body immediately prioritizes the alcohol, putting the protein from the chicken and the fat and carbs from the potatoes and the salad on standby. While the alcohol in the wine is being processed, the fat from the meal gets shuttled directly into fat storage, because at the moment, there’s no room in the metabolic queue to deal with it. The alcohol has essentially hijacked your entire energy system.

And if you’re someone working on metabolic health, losing weight, or reversing insulin resistance, that number matters! Fat burning doesn’t just pause; it stops completely while alcohol is on board. Depending on how much you drink, that shutdown can last for hours.

What About Drinking on an Empty Stomach?

Drinking with food and drinking without food create two different metabolic problems, and neither one is ideal.

With food: Alcohol gets dealt with while the meal’s fuel gets stored.

On an empty stomach: Your liver normally keeps your blood sugar from dipping too low by releasing stored glycogen when needed. But when your liver is busy processing alcohol, it won’t do that. The result? Dramatic, and sometimes dangerous, blood sugar lows. Those lows then trigger food cravings and poor food choices, which are followed by even more dramatic fat storage once you eat.

This is the lesser-known connection between alcohol and blood sugar: alcohol can cause hypoglycemia, particularly in people who are fasting, following a low-carb diet, or already working to lower their blood sugar levels. The liver’s role in glucose regulation is completely overridden when it’s dealing with the detox priority of alcohol.

Alcohol and Insulin Resistance

Beyond a single evening, regular alcohol consumption effects insulin sensitivity, which has a profound effect on overall metabolic health.

Research on binge drinking (defined as 4–5 drinks within two hours, even just once a month) shows it promotes inflammation and insulin resistance that can persist well after the alcohol is fully metabolized. A study in rats found that a binge-drinking equivalent for three consecutive days produced a state of rapid insulin resistance lasting more than two days after the last drink.

And here’s a shocker: chronic high-dose alcohol consumption has been shown to produce a reversible form of insulin resistance on its own, independent of diet!

Side note: how is “chronic high dose” defined? More than 4 drinks per day or 14 drinks per week for men, and more than 3 drinks per day or 7 drinks per week for women. A standard drink is 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80 proof distilled spirits.

It can damage the pancreatic beta cells that produce insulin, impair insulin receptor signaling, and interfere with the body’s ability to store glucose as glycogen, all of which creates the cellular conditions for insulin resistance and, over time, significantly elevated risk for type 2 diabetes.

The liver sits at the center of all of this. Any chronic strain on the liver from alcohol directly undermines its ability to do its job.

And There’s More!

Alcohol doesn’t just affect your macronutrient metabolism or the liver’s ability to regulate blood sugar. It triggers a hormonal cascade that compounds the metabolic damage.

Testosterone and estrogen: Alcohol decreases testosterone for up to 24 hours after drinking while measurably increasing estrogen levels by inhibiting its breakdown in the liver. This hormonal shift actively promotes fat storage, particularly the visceral fat that accumulates around the midsection, the metabolically dangerous kind that surrounds your organs and drives systemic inflammation. Yes, that’s the biological explanation for the “beer belly.”

Cortisol: Alcohol also raises cortisol, your body’s primary stress hormone. Cortisol signals the liver to produce more glucose (raising blood sugar), makes cells less responsive to insulin, and preferentially deposits fat in the abdomen, where glucocorticoid receptors are densely concentrated. Research suggests alcohol also upregulates an enzyme (11β-HSD1) that increases localized cortisol availability in liver and fat tissue, amplifying these effects.

The result is a perfect hormonal storm for fat storage: suppressed fat burning, elevated insulin-disrupting hormones, and a cortisol-driven metabolic shift toward abdominal fat accumulation.

Yup, There’s More!

One of the most underappreciated ways alcohol damages metabolic health is through its impact on sleep. Alcohol may help you fall asleep, but it profoundly disrupts normal sleep architecture, particularly deep sleep and REM sleep.

Here’s what’s happening:

• If you drank your alcohol later in the day, then while you sleep, your body metabolizes that alcohol. That will keep cortisol elevated throughout the night

• Alcohol suppresses melatonin production, disrupting your circadian rhythm

• Poor sleep raises ghrelin (the hunger hormone) and lowers leptin (the satiety hormone) the next day

• Even one night of disrupted sleep can increase hunger, reduce fat oxidation, and impair glucose control, all of which creates a hormonal environment that favors fat gain

Chronic alcohol consumption can dysregulate the entire stress response system (the HPA axis), leading to persistently elevated cortisol even when you’re not drinking.

There is One Small Silver Lining…. But it’s VERY Small…..

All food requires energy to metabolize. This is called the “thermic effect” of food. Alcohol does have a thermic effect — it uses about 15% of its own calories for processing. That’s more than carbohydrates (5–10%) or fat (0–3%), though less than protein (20–30%). But this small energy cost does nothing to offset the much larger metabolic costs: the halted fat burning, the hormonal disruption, the insulin resistance, and the sleep damage.

The Bottom Line for Metabolic Health

If you’re working to reverse insulin resistance, lower your blood sugar, lose weight, or simply protect your metabolic health, the effect of alcohol is worth understanding clearly so that you can make informed decisions about where it fits for you:

• Every time you drink, fat burning stops completely until the alcohol is cleared

• Alcohol suppresses your liver’s ability to regulate blood sugar, creating risk for dangerous lows, plus the rebound highs from cravings and poor food choices that typically follow

• Regular drinking drives hormonal shifts that actively promote visceral fat storage

• Even moderate drinking disrupts sleep in ways that cascade into impaired insulin sensitivity, hunger, and fat metabolism the next day

• Chronic heavy drinking can cause insulin resistance independently of diet and body weight

None of this means you need to be perfect, or that an occasional drink will undo your progress. But it does mean that if you’ve been doing everything “right” with your eating, exercise, and supplements, and the scale isn’t moving or your blood sugar numbers aren’t improving, alcohol may be the variable you haven’t fully accounted for.

Your metabolism follows rules. Alcohol breaks every one of them, temporarily but reliably, every single time.

Understanding that is the first step to making truly informed choices about when, whether, and how much you drink.

Want to learn more about my online program for reversing insulin resistance?

Find Out More RIGHT HERE!

This Week, I’m Sharing My Own Collection of Fantastic Salad Dressings.

I have found that salad dressing is REALLY hard to find without added sugars, starches or the high-heat “seed oils,” none of which I want to eat. So I ALWAYS make my own! It’s fast and simple to do, and then I get something delicious, metabolically friendly, and FAST. Some were originally from my sister’s collection, and some are my own creations.

Find My Collection RIGHT HERE!

Food companies know how our primitive brain is wired, and they capitalize on that knowledge. All those coffee shops know it too!

When we get a reward in the form of feel-good brain chemicals, our primitive brain connects that “something” with survival. The brain literally thinks we need to seek it out again to help us survive. Food companies know this, even if we don’t.

It’s easy to say, “I need some caffeine; I’m going to stop and get a coffee.”

And do you order it black? Probably not. Because what you’re seeking is not the coffee or the caffeine (although you may be telling yourself it is, as I used to). It’s the “hit.”

You’re seeking a hit of dopamine that makes your brain feel good. But you’re getting a front-end pleasure that comes with a back-end consequence, because all that sugar is contributing to your current ill health, your future disease, your fatigue, your inflammation, and your fuzzy thinking. Not to mention your weight, your insulin resistance, and your blood sugar.

Yes, even that innocent “nonfat latte” I used to order every single day was giving me a hit!

In my daily grande nonfat latte, I was getting about 20 grams of glucose, all of it from lactose, the sugar in milk. But your blood sugar doesn’t care where that glucose comes from. It’s all the same. 20 grams of glucose is about 5 teaspoons of sugar. My insulin and blood sugar responded accordingly, and so did my brain. (Dairy is especially good at this: milk can trigger a bigger insulin response than its blood-sugar bump alone would predict.)

And here’s the thing: when I switched to black coffee, I stopped buying coffee. The only thing that disappeared was the sugar from the milk, and with it, the pull. Suddenly I wasn’t so interested in going to Starbucks anymore. The appeal was gone without the hit.

Ahhh, yes. I was NOT seeking the caffeine. I was seeking the hit. I’m on to myself now….

How about you? Do you drink coffee? Tea? Do you drink it black, or with something in it? Have you done the math on your glucose load with that “coffee”? Your entire body wants about 5 grams of glucose circulating in it at any given time. How much are you adding with your coffee drink?

Or, better yet, slap on a continuous glucose monitor and see exactly what is happening when you enjoy that “coffee.”

I love coffee. I now love black coffee, which I drink every morning at home. But the urge to buy some at the coffee shop? Gone.

Want to learn more about my online program for reversing insulin resistance?

Learn More RIGHT HERE!

This Week’s Recipe Is, As Usual, AMAZING!

Creamy Gorgonzola Chicken

Get the Recipe RIGHT HERE!

Most of my weekly highlighted recipes are created by my sister, Katherine Aitken-Young, nutritionist, nurse and IBS specialist. “But I don’t have IBS”! Well neither do I! But there is a close relationship between IBS and Insulin Resistance, so many of her recipes work perfectly for my clients as well as for hers!

The recipes are quick and easy to make, are never fussy, they taste amazing, and they make up the majority of meals I cook and eat myself every day. The recipes simply avoid those ingredients that are common IBS triggers. Because I don’t have IBS, I often make certain substitutions. Some examples:

• Oyster mushrooms – I use any type of mushroom

• Garlic infused olive oil – I use olive oil and some crushed garlic

• Gluten free items – I use the regular item

• Smoke insanity spice mixes – I use regular spices

• When amounts are limited (such as “no more than 40 cashews”) I use however many I want to use

• When it calls for lactose free, I use the regular version

And since I want to eat a very low starch diet for best metabolic health, if the recipe calls for any kind of sugar, I substitute Allulose. If it says “serve over a bed of rice,” I don’t! You get the picture.

If you would like access to ALL of her recipes, you can find her

RIGHT HERE!

I’ve spent 35 years talking with people about blood sugar, and I still sometimes feel surprised by how far the ripples of the problem reach. Recently, a client asked me about macular degeneration, and of course that sent me down a rabbit hole finding out what the research has to say about it! The more I dug, the clearer it became that macular degeneration is just one more problem related to insulin resistance!

I knew about diabetic retinopathy, of course. You’ve probably heard of that one too! About one in four people with type 2 diabetes develop diabetic retinopathy, and for many it progresses to some level of vision loss, including blindness. But to my surprise, there is a lot more to the story. Your eyes, all the working parts of them, are quietly suffering in quite a few ways when insulin resistance is present.

I’ve written before about how insulin resistance develops. It starts with insulin going up, long before blood sugar begins to rise, and it is at this early stage that eyes begin to suffer. (They suffer even more when blood sugars begin to rise, but it starts with insulin.)

That makes the eye one of the earliest windows into metabolic trouble, and yet another imperative reason to take action while everything is still reversible.

First, why is the eye so vulnerable?

The retina, with the macula at its center, is one of the most metabolically active tissues in your entire body. Gram for gram, it burns through oxygen and nutrients at an incredibly fast rate, and it never really gets time to rest. Tissue that demanding is extremely sensitive to anything that disrupts the energy supply, and insulin is a disruptor!

• Chronic low-grade inflammation. High insulin levels, which of course happen with insulin resistance, keep the body in a chronic low-grade inflammatory state. Inflammation wreaks havoc pretty much everywhere in the body, but the eyes are particularly sensitive. “Drusen” are tiny yellow or white deposits of cellular debris, lipids, and proteins that can build up underneath the retina. They form specifically underneath the Retinal Pigment Epithelium, a crucial cell layer that supports central vision, and this is the hallmark of macular degeneration. Inflammation promotes the formation of drusen.

• Oxidative stress and exhausted mitochondria. Insulin resistance ramps up free-radical production and impairs the cell’s power plants – the mitochondria. The retina consumes enormous amounts of oxygen, which makes it especially vulnerable to that kind of damage.

• Damaged small blood vessels. Insulin resistance impairs the delicate lining of blood vessels called the “endothelium,” reducing blood flow, which starves the retina of the nutrients it depends on to function.

• Impaired insulin signaling in the retina itself. As with just about every part of the body, the retina has insulin receptors and is therefore an insulin-sensitive tissue. When its cells become resistant, energy production falls and repair mechanisms weaken. Because the retina is technically neural tissue, some researchers describe this as a form of “brain insulin resistance,” much like the brain insulin resistance now implicated in Alzheimer’s disease.

• Advanced glycation end products (AGEs). Too much glucose and too much insulin accelerate the formation of these sticky, damaging compounds. They accumulate in retinal tissue, they fuel inflammation, they damage proteins, and—what do you know—they’ve been found right inside the drusen deposits of macular degeneration.

Different conditions, one common through-line

Not every eye condition tied to metabolic health is equally proven, so let me be clear about where each one currently sits. The diabetes complications are direct and way beyond dispute at this point. The others range from “clearly higher risk” to “growing, suggestive evidence.” Here’s what we currently understand:

• Diabetic retinopathy. This is the classic one. Chronically high blood sugar damages retinal vessels, producing microaneurysms, bleeding, and swelling. Notably, early changes can show up way before diabetes is ever diagnosed.

• Diabetic macular edema. Fluid leaks into the macula, blurring and distorting central vision. It’s one of the leading causes of vision loss in diabetes.

• Age-related macular degeneration. The evidence here is growing rather than settled, but insulin resistance appears to raise risk and may speed progression through the same inflammation, oxidative stress, mitochondrial, and vascular pathways outlined above. (More on the most striking finding in a moment.)

• Cataracts. People with insulin resistance and diabetes develop cataracts more often, and often younger. Blame glycation of the lens proteins, oxidative damage, and sorbitol (a by-product of high blood sugar) building up inside the lens.

• Glaucoma. Type 2 diabetes raises glaucoma risk, likely through impaired blood flow to the optic nerve, oxidative stress, and nerve cells that are simply more vulnerable to injury.

• Retinal vein occlusion. Sometimes called a “stroke of the eye.” Insulin resistance contributes to abnormal clotting, endothelial dysfunction, and vascular inflammation — the exact ingredients for a blockage.

• Dry eye disease. Common and frequently overlooked. Insulin resistance can alter tear production, inflame the ocular surface, and damage the nerves involved in blinking and tear secretion.

• Cranial nerve palsies. Diabetes can injure the nerves that move the eyes, causing double vision, misalignment, or trouble focusing.

The macular degeneration story

In the Age-Related Eye Disease Study (AREDS) — over 4,000 older adults — people eating a higher-glycemic-index diet had significantly more AMD, and worse AMD. In fact, eating below the median glycemic index was linked to a roughly 49% lower risk of advanced disease. The researchers estimated that about 20% of the advanced AMD in that population could have been avoided with below-median-glycemic-index eating. And it held in people without diabetes, so it’s the glycemic index itself, not hyperglycemia sneaking in the back door.

White bread and the back of your eye, it turns out, are on speaking terms.

Why this matters before you ever hear the word “diabetes”

This is the point I most want to drive home. Many of these eye changes begin during insulin elevation, which happens long before you lose control of blood sugar.

In other words, your eyes may be showing signs of metabolic dysfunction years before a lab ever flags it. Which leads to a useful and I think practical takeaway: a dilated eye exam is, in a real sense, a metabolic checkup. Eye doctors sometimes spot the first hint of metabolic disease before anyone else does.

If it’s been a while, get those peepers checked out! That appointment is doing double duty.

The good news (same as it ever was)

I’m not saying all this to add eight new things to your worry list. I’m saying it because of the good news hiding inside it: these conditions share a root, which means the work that protects one tends to protect all of them. And that work is the same insulin-sensitizing approach I teach for reversing prediabetes.

• Get some lab tests to check up on yourself. Fasting insulin should be less than 5. HbA1C should be 5.5% or less. If it’s out of this range, you’ve got a problem! Work on reversal!

• Keep blood sugar low and steady most of the time

• Move your body; exercise is one of the best blood sugar “sinks” there is

• Eat food as close to the way mother nature made it as possible most of the time

• Keep blood pressure in the normal range

• Don’t smoke

That’s the thing about metabolic health I keep circling back to: it’s almost never about one number or one organ. Fix the soil, and a lot of different plants do better — including the two doing all your seeing.

This is educational, not medical advice. If you have vision changes or any of the conditions above, please see your eye doctor! The metabolic reversal work runs alongside standard care, not instead of it. All references used can be found on my website at diabetesgamechanger.com

This Week’s Recipe Is, As Usual, AMAZING!

Kalamata Olive Parmesan Salad Dressing!

Get the Recipe RIGHT HERE!

Most of my weekly highlighted recipes are created by my sister, Katherine Aitken-Young, nutritionist, nurse and IBS specialist.

“But I don’t have IBS”!

Well neither do I! But there is a close relationship between IBS and Insulin Resistance, so many of her recipes work perfectly for my clients as well as for hers!

The recipes are quick and easy to make, are never fussy, they taste amazing, and they make up the majority of meals I cook and eat myself every day. The recipes simply avoid those ingredients that are common IBS triggers. Because I don’t have IBS, I often make certain substitutions. Some examples:

• Oyster mushrooms – I use any type of mushroom

• Garlic infused olive oil – I use olive oil and some crushed garlic

• Gluten free items – I use the regular item

• Smoke insanity spice mixes – I use regular spices

• When amounts are limited (such as “no more than 40 cashews”) I use however many I want to use

• When it calls for lactose free, I use the regular version

And since I want to eat a very low starch diet for best metabolic health, if the recipe calls for any kind of sugar, I substitute Allulose. If it says “serve over a bed of rice,” I don’t! You get the picture.

If you would like access to ALL of her recipes, you can

find her

ON PATREON RIGHT HERE!

I’ve always loved being able to listen and read when I’m trying to truly understand something, so here’s the heart of the book, read aloud, for your commute, your morning walk, or wherever you do your best thinking.

A quick word on order: I sequenced these sections on purpose. We start with the tool that lets you see what’s happening inside your own body…

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There’s something powerful about being able to both listen and read when you’re trying to truly understand a topic. This audio collection brings you sections 1 through 12 of my book, Reversible! A Clinician’s Guide to Understanding and Reversing Insulin Resistance, Prediabetes, and Metabolic Disease — ready for your commute, your morning walk, or wherev…

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