Keto And The High Morning Reading

Rachel 0:00

Imagine this deeply frustrating scenario for a second. You know, you've completely cut out sugar.

Mark 0:05

Oh yeah. A classic setup.

Rachel 0:06

Right. You are strictly following a low carb or ketogenic diet, like carefully tracking every single macro you consume.

Mark 0:14

Absolutely dialing it in.

Rachel 0:16

Exactly. And you monitor your continuous glucose monitor, your CGM, throughout the day, and your glucose curve is just a beautifully flat line. But then you wake up the next morning, check your numbers, and your fasting blood sugar is surprisingly high.

Mark 0:30

It's maddening.

Rachel 0:31

It really is. It feels like a total betrayal by your own metabolic system. I mean, if you aren't eating any carbohydrates, where on earth is this like ghost glucose coming from?

Mark 0:41

It is arguably the single most common and honestly the most maddening metabolic mystery people encounter when they adopt a low carbohydrate lifestyle.

Rachel 0:50

Aaron Powell It just feels wrong.

Mark 0:51

Trevor Burrus It does. It seems to violate the basic laws of thermodynamics. You didn't input glucose, yet your circulating glucose is suddenly elevated.

Rachel 0:58

Aaron Powell And the immediate panic is always my diet is failing.

Mark 1:01

Trevor Burrus Exactly. Or that your insulin resistance is somehow getting worse overnight.

Rachel 1:05

Well, today we are taking a deep dive into this really insightful piece of research and clinical analysis from Quick Lab Mobile. It's titled, Why is Morning Blood Sugar High on a Low Carb or Ketogenic Diet?

Mark 1:17

Aaron Powell It's a great piece.

Rachel 1:18

Yeah. And our mission today is to solve this specific metabolic mystery for you. We're going to isolate where this ghost glucose originates, why your body actually insists on producing it, and you know, how to definitively tell if it's a harmless adaptation or an actual red flag for your health.

Mark 1:34

Aaron Powell Which is such a crucial distinction to make.

Rachel 1:37

Okay, let's unpack this because before we can point fingers at like macronutrient ratios or assume something is pathologically wrong, we have to establish the baseline of what the human

Dawn Phenomenon And Counter Hormones

Rachel 1:47

body does naturally while we sleep.

Mark 1:48

Aaron Powell Right. And the baseline is that sleep is not just this metabolic shutdown. Yeah. It's a highly active, totally orchestrated phase of biological maintenance.

Rachel 1:59

Like a busy workshop.

Mark 2:00

Basically, yeah. Yeah. The main driver behind this morning glucose elevation is your liver. And it's responding to a very specific circadian rhythm.

Rachel 2:08

Okay. So what time are we talking here?

Mark 2:10

Between roughly 3 a.m. and 8 a.m., your endocrine system initiates this cascade of counterregulatory hormones. We are looking at a sequenced release of cortisol, growth hormone, glucagon, and adrenaline.

Rachel 2:25

Wow, that's quite a cocktail. And these hormones are actively antagonizing insulin, right?

Mark 2:29

Exactly.

Rachel 2:30

Because while insulin's primary role is to drive glucose into the tissues and, you know, store energy, this morning cascade is designed to do the opposite. It's mobilizing energy.

Mark 2:39

Yeah, that mobilization is just an evolutionary necessity. Cortisol, for example, it doesn't just wake you up.

Rachel 2:45

It does more than that.

Mark 2:45

Oh, much more. It travels to the liver, enters the cell nucleus, and actively upregulates the transcription of specific enzymes that are responsible for glucose production. Oh wow. This orchestrated release of hormones signals the liver to just dump glucose into the bloodstream. It's fueling your brain and your muscles for the physical demands of waking up and foraging.

Rachel 3:06

So it's preparing you to go hunt for breakfast.

Mark 3:08

Precisely. Clinically, we refer to this widespread physiological process as the dawn phenomena.

Rachel 3:13

The dawn phenomena. Okay.

Mark 3:15

Aaron Ross Powell And the liver accomplishes this through two ways glycogenolysis, which is breaking down whatever stored glycogen remains, and leukoneogenesis, which is the actual synthesis of new glucose. Trevor Burrus, Jr.

Rachel 3:28

You should probably mention this is different from a couple of other morning effects, right?

Mark 3:31

Yeah, good point. It's distinct from the samochi effect, which is a rebound from overnight hypoglycemia. That one is much less common. And it's also different from the feet on the floor effect. That's where simply standing up and anticipating the day spikes your cortisol and releases glucose.

Rachel 3:48

The feet on the floor effect. I love that name. You know, I always think of the liver in this scenario as an overly eager, maybe slightly anxious, breakfast chef.

Mark 3:57

That is a perfect analogy.

Rachel 3:58

Like you are still fast asleep at 4 a.m., but the chef is in the kitchen frantically cooking up a massive carbohydrate feast, throwing it on the counter and declaring you're gonna need this energy for the day even before you've opened your eyes.

Mark 4:12

That's exactly what's happening.

Rachel 4:13

But I have to push back on the mechanics of this for a ketogenic context. If you are

Gluconeogenesis And The Protein Myth

Rachel 4:18

on a strict keto diet, your liver glycogen stores are significantly depleted, right? I mean you've emptied the pantry. Yep. So how does the liver keep dumping glucose morning after morning if the storage tanks are effectively empty?

Mark 4:30

Well, the pantry never stays empty. The body operates on a system of just non-negotiable metabolic demands. Non-negotiable. Right. Even in the deepest state of nutritional ketosis, you cannot run the entire human organism on just fatty acids and beta-hydroxybutyrate alone.

Rachel 4:49

Even though the brain is pretty good at adapting.

Mark 4:51

The brain does an incredible job. It adapts to ketones for up to, say, 70 or 80 percent of its energy needs. But certain tissues have an absolute obligatory requirement for glucose. Red blood cells are the classic example here.

Rachel 5:05

Because red blood cells lack mitochondria.

Mark 5:07

Exactly.

Rachel 5:08

Because they don't have the cellular machinery to perform the Krebs cycle or utilize the electron transport chain, they literally can't oxidize fatty acids or ketones. So they rely 100% on anaerobic glycolysis, which means they must have a continuous supply of glucose just to survive and carry oxygen.

Mark 5:26

Spot on. And beyond erythrocytes, the renal medulla in your kidneys, the lens and cornea of your eyes, and parts of your central nervous system also demand baseline glucose.

Rachel 5:36

So the body has to manufacture it, no matter what.

Mark 5:39

It has to. And that manufacturing process is gluconeogenesis. The liver acts as this incredibly efficient recycling and synthesis plant.

Rachel 5:48

Recycling what, exactly?

Mark 5:49

It takes non-carbohydrate substrates to build new glucose molecules. It utilizes glycerol, which is liberated from the breakdown of triglycerides.

Rachel 5:57

Okay, so fat breakdown.

Mark 5:58

Right. It also uses lactate, which is continuously recycled from those very red blood cells we just talked about, in a process called the Cori cycle. And it utilizes certain glucogenic amino acids too.

Rachel 6:09

Ah, amino acids.

Mark 6:11

Yeah, glucagon and cortisol drive this manufacturing process forward, while your basal insulin, that's the small amount of background insulin your pancreas, constantly secretes that acts as the brake pedal to prevent hyperproduction.

Rachel 6:22

Okay, wait. This brings up a massive debate in the low-carb community regarding protein.

Mark 6:27

Oh, I know exactly where you're going with this.

Rachel 6:28

You hear the rumor constantly, right? If you eat too much protein on keto, the excess amino acids are instantly converted into glucose.

Mark 6:37

It's such a persistent myth.

Rachel 6:38

People treat protein as if it's just, you know, delayed release cake. But based on the hormonal pathways you just described, gluconeogenesis is a demand-driven process, not a supply-driven one.

Mark 6:50

Aaron Powell That distinction is critical. Gluconeogenesis is dictated by the body's physiological requirement for glucose and the corresponding hormonal signals.

Rachel 6:59

Mostly the glucagon to insulin ratio, right?

Mark 7:02

Exactly. It is not an automatic supply-driven reaction triggered simply because you consumed a 20-ounce ribeye.

Rachel 7:08

So the steak doesn't automatically become sugar.

Mark 7:11

No. Consuming protein provides the substrate, the raw building blocks. But the liver doesn't blindly process all available amino acids into a flood of blood sugar.

Rachel 7:20

That makes so much sense.

Mark 7:21

In a healthy ketogenic state, low insulin allows this glucose production to proceed just enough to prevent those glucose-dependent tissues from starving. Just enough. Right. The dysfunction only occurs when the liver's glucose output ignores that basal insulin brake petal and exceeds the body's actual requirements.

Rachel 7:40

Okay, so we have established the liver is manufacturing this glucose. And we know exactly why the red blood cells and kidneys demand it. Yep. But if the liver is producing just enough to meet those specific needs, why do we see it lingering in the bloodstream and registering as high on a morning CGM reading? Why aren't the muscles pulling it out of circulation?

Mark 7:59

Aaron Powell For that, we have to look at how skeletal muscle adapts to a prolonged low carbohydrate environment.

Adaptive Glucose Sparing In Muscle

Rachel 8:06

Okay.

Mark 8:06

This introduces a metabolic state known as adaptive glucose sparing. You will frequently see it labeled as physiological insulin resistance, though from a clinical communication standpoint, that term causes unnecessary panic.

Rachel 8:19

Oh, for sure. Nobody wants to hear they have insulin resistance.

Mark 8:22

Exactly. But here's what happens. When you restrict carbohydrates for an extended period, your skeletal muscles upregulate the enzymes necessary for lipid metabolism. They become highly specialized in oxidizing fatty acids and ketones.

Rachel 8:37

They get really good at burning fat.

Mark 8:38

Very good. And because their energy needs are being fully met by fat, they essentially downregulate their glucose transporters.

Rachel 8:45

So rather than polite dinner guests refusing a meal, I think of the skeletal muscles in a keto adapted body like a hospital triage system.

Mark 8:54

Triage, I like that.

Rachel 8:55

Yeah. The liver is the supply room handing out glucose. The muscles acting as the triage nurses look at their own abundant supply of fatty acids and say, we are perfectly fine. Redirect these critical glucose supplies to the red blood cells in the brain because they are the critical patients who actually need it.

Mark 9:12

That's a great way to visualize it.

Rachel 9:14

They spare the glucose for the tissues that can't survive without it.

Mark 9:17

The triage analogy perfectly captures the mechanism. The muscles refuse the glucose to prioritize systemic survival. And under optimal conditions, this adaptive glucose sparing coincides with low fasting insulin, high rates of fat oxidation, and pristine metabolic biomarkers.

Rachel 9:34

The key word being optimal.

Mark 9:36

Right. Because this raises an important question. Does a high morning glucose reading always guarantee we are looking at a harmless, healthy adaptation?

Rachel 9:46

I'm guessing the answer is no.

Mark 9:48

The research indicates we cannot be complacent. The Quick Lab mobile analysis heavily highlights a 2024 randomized controlled feeding study that really demands

Study Findings On Glucose Tolerance

Mark 9:58

our attention.

Rachel 9:59

Yeah, I looked at the methodology of that study and it's fascinating. They put participants on a strict ketogenic diet for just four weeks.

Mark 10:06

A very short time frame.

Rachel 10:07

Exactly. It wasn't a multi-year observational study. It was highly controlled. And while the participants saw favorable changes in body weight and fat mass, their actual glucose handling machinery changed drastically.

Mark 10:18

It did. The researchers found that after four weeks, the participants exhibited significantly reduced glucose tolerance. Through skeletal muscle biopsies, they observed alterations in the specific proteins and molecular pathways involved in glucose uptake and oxidation. The skeletal muscle's ability to clear glucose from the blood was fundamentally impaired, at least in the context of an oral glucose tolerance test.

Rachel 10:42

Which means we cannot blindly rubber stamp every high fasting glucose number as just a neat evolutionary trick.

Mark 10:49

Definitely not.

Rachel 10:50

It is dangerously easy to use the phrase adaptive glucose sparing as a psychological shield, you know, to ignore a genuine deterioration in your metabolic health.

Mark 11:00

Labeling your elevated glucose as adaptive is a hypothesis, not a clinical diagnosis.

Rachel 11:04

Hypothesis, right.

Mark 11:05

It requires verification. If you're staring at a fasting glucose of 115 milligrams per deciliter, you have to determine if your muscles are simply triaging glucose to your brain, or if your liver is entirely deaf to the signals of your pancreas.

Rachel 11:20

Which would indicate pathological insulin resistance.

Mark 11:22

Exactly.

Rachel 11:23

Here's where it gets really interesting for me. The only way to solve that mystery is through proper context and the right biomarkers.

Mark 11:30

Context is everything here.

Rachel 11:31

For someone who tracks their own numbers closely, the good pattern usually looks like a modest glucose rise before waking, say, hovering around 105, that quickly normalizes after you start moving around or have your first meal. Yes. But the crucial part is that this glucose number is accompanied by rock bottom fasting insulin, an A1C that remains stable in the low fives, triglycerides well under 100, and robust blood ketones.

Mark 11:58

That's the perfect picture of adaptation.

Rachel 12:00

Right. If you have that specific constellation of labs, your liver is just executing the dawn phenomenon.

Mark 12:05

But the alternative, the pathological pattern, presents a very different metabolic picture.

Rachel 12:10

What does that look like?

Mark 12:11

You will see that high morning glucose paired with steadily rising fasting insulin. The pancreas is being forced to hypersecrete insulin because the liver is resisting the signal to stop glucomeogenesis.

Rachel 12:21

The brake pedal is broken.

Mark 12:23

Essentially, yes. In this scenario, you will track an upward creeping A1C, elevated triglycerides, creeping liver enzymes indicating non-alcoholic fatty liver development, and paradoxically, suppressed ketone production.

Rachel 12:35

Because high insulin halts ketogenesis.

Mark 12:37

You've got it.

Rachel 12:38

So the relationship between fasting glucose and fasting insulin

The Lab Pattern That Matters

Rachel 12:42

is really the entire linchpin.

Mark 12:43

Without a doubt.

Rachel 12:44

The Quick Lab Mobile article points to the HOMA IR calculation, which I think everyone tracking their metabolic health should know. It stands for homeostatic model assessment for insulin resistance.

Mark 12:55

It's a fantastic tool.

Rachel 12:56

You take your fasting glucose, multiply it by your fasting insulin, and divide by 405. It mathematically proves that a fasting glucose of 105 means something entirely different if your fasting insulin is a highly sensitive three microinternational units per milliliter compared to an insulin resistant 15.

Mark 13:15

That's exactly why HOMA IR provides a highly accurate estimation of your baseline hepatic or liver insulin resistance. Right. The greater the volume of insulin required to hold your circulating glucose at 105, the more resistant your system is become. But deriving that calculation requires rigorous laboratory testing, which introduces another variable.

Rachel 13:34

Oh, because beyond just glucose and insulin, a comprehensive evaluation should really include C peptide.

Mark 13:40

Yes, C peptide is crucial.

Rachel 13:41

Let's break down C peptide, because it is rarely included in a standard physical. Why is it a more reliable marker for what the pancreas is actually doing than just testing insulin alone?

Mark 13:53

Well, when your pancreatic beta cells manufacture insulin, they initially create a larger precursor molecule called pro insulin.

Rachel 14:00

Okay.

Mark 14:01

Before releasing it into the bloodstream, the beta cell cleaves pro insulin into two pieces, one molecule of active insulin and one molecule of C peptide.

Rachel 14:09

So they come out together.

Mark 14:10

Exactly. They are released in a one-to-one ratio. The challenge with measuring peripheral insulin is that its half-life is incredibly short, around four to six minutes.

Rachel 14:19

That fast.

Mark 14:20

Yeah. And a massive percentage of it is immediately extracted and cleared by the liver on its first pass.

Rachel 14:26

Oh, I see. So the insulin level measured in your arm vein doesn't necessarily reflect the total amount the pancreas just pumped out.

Mark 14:32

Correct. It's just what's left over. C peptide, however, is not heavily extracted by the liver and has a much longer half-life of about 30 minutes.

Rachel 14:40

That makes it a much better measuring stick.

Mark 14:42

It does. By measuring C peptide, we get a much clearer, more stable window into your total endogenous insulin production.

Rachel 14:50

But getting these exact numbers requires a true, undisturbed baseline, right? The article notes that Quick Lab Mobile actually facilitates at-home blood collection in the Miami area for this exact reason. They draw true fasting samples for C peptide, A1C, fasting insulin, and a comprehensive metabolic panel directly in your home environment.

Mark 15:11

Which is brilliant, clinically speaking.

Rachel 15:13

Because the at-home aspect isn't just a luxury, it removes a massive confounding variable.

Mark 15:18

Oh, a huge one.

Rachel 15:19

If you wake up, realize you're running late, fight through Miami morning traffic, and then sit under fluorescent lights in a crowded waiting room for 40 minutes, your adrenal glands are just dumping cortisol and adrenaline.

Mark 15:30

Your stress hormones are through the roof.

Rachel 15:32

You are artificially supercharging the dawn phenomenon and the feet on the floor effect before the phlebotomist even preps your arm. Your glucose and insulin are reacting to the stress of the commute, not your baseline metabolic state.

Mark 15:44

That is so true. Securing an unstressed physiological baseline is imperative.

C Peptide And Clean Testing

Mark 15:50

Continuous glucose monitors provide immense data, but they measure interstitial fluid, which carries a time lag.

Rachel 15:56

Right, it's not blood plasma.

Mark 15:58

Exactly. And it's easily influenced by sensor pressure during sleep or even mild dehydration.

Rachel 16:03

I really want to focus on that day-to-day CGM panic. It is incredibly easy to obsess over a single data point.

Mark 16:11

We see it all the time.

Rachel 16:12

Someone might have a terrible night of sleep, toss and turn, wake up, and their CGM reads 118. The immediate reaction is my keto diet is completely failing. I'm pre-diabetic.

Mark 16:23

It's a natural fear.

Rachel 16:24

We need to delineate an isolated stress response from a genuine metabolic trend.

Mark 16:28

It requires separating the environmental noise from the biological signal.

Rachel 16:32

How do you do that?

Mark 16:33

Well, a fasting glucose that bounces between 90 and 115, depending on whether you slept four hours or eight hours, is demonstrating your nervous system's immediate stress response.

Rachel 16:42

Just a bad night.

Mark 16:43

Right. That is entirely different from a relentless multi-month progression where your baseline floor moves from 85 to 98 to 110, regardless of how perfectly you slept.

Rachel 16:54

So you have to look at the big picture.

Mark 16:56

The trajectory of the trend line over a quarter is vastly more diagnostic than an anomalous reading on a random Tuesday.

Rachel 17:03

Let's apply this to a real scenario for you. Say a listener gets their full panel done, the home AIR is creeping up, the C peptide is elevated.

Mark 17:11

Not what you want to see.

Rachel 17:12

Right. The trend clearly indicates this is not just harmless adaptive glucose sparing, but they track their macros religiously. They are eating a perfectly clean ketogenic diet with zero hidden carbohydrates.

Mark 17:24

They're doing everything right nutritionally.

Rachel 17:26

Exactly. What are the hidden culprits driving the liver to overproduce

Hidden Stressors Behind Morning Spikes

Rachel 17:30

glucose?

Mark 17:30

When the nutritional variables are locked down, the investigation must pivot to lifestyle stressors. Obstructive sleep apnea is a primary hidden driver.

Rachel 17:39

Sleep apnea. Wow.

Mark 17:40

Yeah. If the airway collapses during sleep, blood oxygen plummets. The state of hypoxia triggers an intense survival reflex in the sympathetic nervous system.

Rachel 17:49

It's a panic button.

Mark 17:50

The body releases a massive surge of adrenaline and cortisol to shock you into breathing, which simultaneously commands the liver to dump glycogen.

Rachel 17:59

The body literally thinks it is suffocating. Of course, it is going to flood the bloodstream with emergency fuel to escape the threat.

Mark 18:06

Exactly. The metabolic fallout of sleep apnea is profound. But beyond respiration, short sleep duration itself degrades insulin sensitivity.

Rachel 18:16

Just not sleeping enough.

Mark 18:17

Yeah. And intense evening workouts, particularly heavy resistance training or high-intensity interval training, elevate circulating catecholamines.

Rachel 18:26

Like adrenaline and noradrenaline.

Mark 18:28

Yes. And those can remain high throughout the night, sustaining elevated hepatic glucose output well into the morning.

Rachel 18:34

I've also noticed that meal timing plays a huge role. Even if a late night snack is perfectly low carb, say a massive handful of macadamia nuts or a piece of cheese at 10 p.m., it seems to push the morning numbers higher.

Mark 18:46

Because late consumption extends the Fed state. Processing a calorie-dense meal requires digestion and hormonal shifting.

Rachel 18:52

Even if it's just fat and protein.

Mark 18:54

Absolutely. Furthermore, the glycerol from the fats and the amino acids from the protein provide the exact substrates the liver uses for gluconeogenesis.

Rachel 19:04

Oh wow.

Mark 19:04

You are fully restocking the liver's inventory just hours before the dawn hormone surge arrives to empty it.

Rachel 19:10

That makes total sense.

Mark 19:12

Simply shifting the feeding window to conclude earlier in the evening can dramatically lower morning glucose without altering a single macronutrient. We also must consider caffeine.

Rachel 19:22

Ah. The most controversial biohacking variable.

Mark 19:26

It always is. Caffeine's impact on glucose metabolism is highly individualized. In some people, ingesting a large dose of caffeine immediately upon waking, particularly deep into a fast, amplifies the release of epinephrine.

Rachel 19:39

Which raises blood sugar.

Mark 19:40

It transiently reduces insulin sensitivity and exacerbates the Dawn phenomenon spike. The most effective way to identify this is by running an N of 1 trial using a CGM.

Rachel 19:49

Like testing it on yourself.

Mark 19:51

Exactly. Alternating mornings with and without caffeine to observe the distinct glycemic curves.

Rachel 19:56

Identifying these triggers points us toward the actual solutions. Because often when someone sees a high morning reading on keto, their first instinct is to punish themselves.

Mark 20:05

By cutting more carbs.

Rachel 20:07

Right. Aggressively cutting their carbohydrates from 20 grams down to zero, or initiating a grueling 48-hour fast to force the glucose down. But if sleep apnea or chronic stress is driving the liver's overproduction, restricting an already strict diet is targeting the wrong pathway.

Mark 20:25

It's totally misguided.

Rachel 20:26

It's like changing your car's oil because you have a flat tire. You have to address the actual stressor.

Mark 20:31

That's it, exactly. Adjusting

Practical Fixes And A Circadian Riddle

Mark 20:33

macronutrients to solve a stress-induced hormonal imbalance is an exercise in futility.

Rachel 20:39

So what should they do instead?

Mark 20:40

If your daytime insulin and post-cranial glucose are excellent, the interventions must be lifestyle-centric. Shift the final meal to earlier in the afternoon. Incorporate a light 10-minute walk after dinner.

Rachel 20:52

Just a walk.

Mark 20:53

Yeah. Muscle contraction independently activates GLUT4 transporters to clear glucose from the blood without requiring insulin.

Rachel 21:00

That's a great tip.

Mark 21:01

Prioritize sleep architecture and seek a clinical evaluation for apnea if you wake up unrefreshed. If APM CrossFit is keeping your sympathetic nervous system locked in overdrive all night, transition that training to the morning. Address the specific physiological stressor.

Rachel 21:16

To bring all of this together for you, elevated morning glucose on a ketogenic diet is fundamentally an evolutionary survival mechanism. Your liver is responding to an ancient hormonal alarm clock, utilizing gluconeogenesis to ensure your obligate tissues have the energy required to function.

Mark 21:35

Beautifully summarized.

Rachel 21:36

Thank you. And if you are deeply fat adapted, your muscles will triage that glucose, allowing it to pool in the blood, but you cannot simply assume this mechanism is harmless.

Mark 21:45

You really can't.

Rachel 21:46

You must verify it by checking your fasting insulin, C peptide, and triglycerides to ensure you aren't masking developing insulin resistance.

Mark 21:53

If we connect this to the bigger picture, assessing metabolic health demands, looking at the entire physiological landscape. A single isolated glucose reading on a Tuesday morning is merely one pixel in an extraordinarily complex, dynamic image. You must evaluate the full biochemical context.

Rachel 22:12

That context is everything. And as we wrap up this deep dive, I want to leave you with a completely different angle to ponder.

Mark 22:19

Oh, I like where this is going.

Rachel 22:20

We've established that the Dawn phenomenon is an ancient circadian-driven hormonal cascade. But consider the environment we live in today. From the moment the sun goes down, we are staring into the bright blue light emitting screens of our phones, tablets, and televisions, often until the minute we close our eyes.

Mark 22:37

Guilties is charged.

Rachel 22:38

Most of us are. Light is the primary sightgebber, the external cue that sets our internal biological clocks. If our modern artificial lighting environment is chronically suppressing melatonin and altering our deep sleep architecture, we have to wonder. Are we artificially hacking the timing and the intensity of our own dawn phenomenon? Are these abnormal morning glucose spikes not just a byproduct of our diets, but a direct consequence of a circadian rhythm that has been completely fractured by modern technology?

Mark 23:08

That is a profound thought.

Rachel 23:09

It is a fascinating biological puzzle to consider the next time you find yourself doom scrolling in bed at midnight.