The Great Cortisol Panic
Why Influencers Are Getting Your Enzymes Spectacularly Wrong
A blood testing deep-dive into 11β-HSD1, enzyme recycling, and why that scary study everyone’s sharing isn’t what you think it is.
Let me set the scene. You’re scrolling through social media at 2 AM (because apparently sleep is optional when you’re carnivore), and you see it: “CARNIVORE DIET RAISES YOUR CORTISOL! Here’s the study that PROVES it!” Cue the dramatic music. Cue the panic buying of adaptogens.
I’ve been testing blood for over a decade. I’ve seen 1,000+ people transform their metabolic health through low-carb and carnivore eating. I’ve watched their cortisol, enzymes, and metabolic markers shift—sometimes dramatically. And I’m here to tell you: that study everyone’s quoting? It’s not nearly as scary or conclusive as influencers want you to believe.
More importantly, they’re misrepresenting how your body actually works. So let’s talk about the real science—the stuff that’s actually happening in your liver, adipose tissue, and bloodstream—without the manufactured hysteria.
First, Let’s Demystify Cortisol Itself
Cortisol gets a terrible reputation online. People talk about it like it’s your metabolic enemy, lurking in the shadows, waiting to destroy your fitness goals and steal your abs.
Here’s the truth: cortisol is a homeostatic hormone. Your body makes it for a reason. It’s not evil. It’s not trying to ruin you. It helps regulate blood glucose, manage inflammation, and respond to ‘stress’, which actually means any ‘threat’ to homeostasis. Without cortisol, you’d literally die. No exaggeration. Death.
The problem isn’t cortisol. The problem is dysregulated cortisol—chronically elevated levels due to persistent hemostatic variation, poor sleep, or metabolic dysfunction. But that’s completely different from your body doing what it’s supposed to do.
Your body is actually quite clever about managing this hormone. Which brings us to...
The Enzyme That Does the Recycling: 11β-HSD1
Here’s where people lose their minds, so pay attention. Your body produces cortisone (the inactive form of cortisol). Then—and this is the genius part—your cells have this enzyme called 11β-HSD1 that converts cortisone back into active cortisol where and when it’s needed.
This is your body recycling hormones. This is evolution being smart.
Think of it this way: Your body isn’t just making cortisol once and hoping it works everywhere. It’s strategically regenerating it in specific tissues—your liver, your fat cells, your immune cells—so it can have localised, targeted effects without bathing your entire system in the hormone. It’s metabolic precision. It’s your body being efficient.
11β-HSD1 activity increases or decreases based on your metabolic needs. When you’re on a low-carb diet, your body needs cortisol to help mobilise glucose and maintain blood sugar stability. More 11β-HSD1 activity isn’t a sign of disease. It’s a sign of metabolic adaptation. It’s your body doing exactly what you hired it to do.
But here’s what influencers won’t tell you: they’re conflating “increased enzyme activity” with “dangerous cortisol elevation.” These are not the same thing. Activity changes don’t automatically mean bad outcomes. Your body upregulates and downregulates enzymes constantly based on what it needs. That’s called homeostasis.
The Exit Strategy: 5α and 5β Reductase (aka “How You Poop Out Cortisol”)
Once your body is done with cortisol, it needs to get rid of it. Enter two enzymes: 5α-reductase and 5β-reductase.
These enzymes do something really simple: they break down cortisol into inactive metabolites that your kidneys and liver can then eliminate. That’s literally it. That’s excretion. That’s basic human physiology.
Here’s the reality check: These reductases aren’t the bad guys. They’re the cleanup crew. Your body upregulates and downregulates them based on the amount of cortisol it needs to process. If you’re eating high-carb, you might have less need for cortisol regeneration, so these reductases work overtime. If you’re eating low-carb, the balance shifts. Your body becomes more efficient at regenerating cortisol where needed and excreting it where it’s not.
When I’m looking at cortisol metabolites in a 24-hour urine test, I’m not seeing a catastrophe. I’m seeing your liver and kidneys doing exactly what they evolved to do. Sometimes people on carnivore have slightly different cortisol excretion patterns—but this is often a sign of improved metabolic flexibility, not metabolic disaster.
The Methylglyoxal Problem (And Why Low-Carb Actually Helps)
Now let’s talk about something that actually deserves the panic: methylglyoxal.
When your cells break down glucose for energy, they don’t always do it cleanly. Methylglyoxal is a toxic byproduct—essentially metabolic exhaust fumes. Unlike cortisol, methylglyoxal is actually dangerous. It’s highly reactive and can bind to proteins, damaging them through a process called glycation. This is the real problem with high blood glucose.
Methylglyoxal accumulates when you’re chronically consuming high amounts of carbohydrates or when your glucose metabolism is dysfunctional. And here’s the part that matters: reducing carbohydrate intake dramatically reduces methylglyoxal production.
This is one of the genuine metabolic wins of low-carb and carnivore eating. Less glucose processing = less toxic byproducts = less damage to your proteins and tissues. This is actually something worth getting excited about.
So here’s the irony: influencers are panicking about enzyme recycling (which is normal), while ignoring the real glycation damage happening from excess carbs. They’ve got the priorities completely backwards.
Now, About That Study Everyone’s Citing...
Let’s talk about the Stimson et al 2007 study, because this is where the real problems begin.
Study Title: “Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight Changes in Obese Men”
Published: Journal of Clinical Endocrinology & Metabolism, November 2007
Here’s what happened: Researchers took 17 obese men (just 17!), put them on different diets for 4 weeks, and then—and this is the critical part—they infused radioactively labelled cortisol directly into their bloodstream to measure how their bodies metabolised it.
The diets compared were a high-fat-low-carbohydrate diet (66% fat, 4% carbohydrate) versus a moderate-fat-moderate-carbohydrate diet (35% fat, 35% carbohydrate).
Let me unpack why this is problematic:
Sample size: 17 participants. That’s not a study. That’s a preliminary observation. This has absolutely no power to make broad claims about the general population.
Duration: 4 weeks. Your body’s metabolic machinery needs time to adapt. Four weeks is barely long enough to know what you’re doing for dinner, let alone draw conclusions about enzyme adaptation.
The infusion issue: They didn’t measure how your body naturally handles cortisol. They artificially injected labelled cortisol (9,11,12,12-[2H]4-cortisol) and watched what happened. This is not how cortisol metabolism works in real life. When you’re living your actual life—working, sleeping, eating, existing—your cortisol production and metabolism are dynamic, integrated processes. You can’t replicate that by infusing a tracer and measuring its clearance.
Real-world applicability: None. Zero. This is a mechanistic study conducted in a highly controlled setting with a small number of participants over a short period. It tells us something about cortisol kinetics under artificial conditions. It does not tell us whether low-carb eating actually causes health problems.
I’ve been testing cortisol levels in real people for over a decade. I’ve seen thousands of people—people actually living their lives, not lying in a research lab with radioactive cortisol in their veins—do incredibly well on carnivore and keto diets. Their cortisol levels stabilise. Their metabolic markers improve. Their symptoms resolve.
One small, short-term mechanistic study with artificial conditions doesn’t outweigh real-world observation of thousands of people getting healthier.
The Bottom Line
Your body is not your enemy. Your enzymes are not your enemy. Your cortisol is not your enemy.
What is a problem: chronically high intake of dietary carbohydrates, constant inflammation, and the toxic byproducts like methylglyoxal that come from metabolic dysfunction. Low-carb and carnivore eating address these problems directly.
Are your enzyme activity patterns different on a carnivore diet? Probably yes. That’s metabolic adaptation. That’s your body doing what it evolved to do. And unlike methylglyoxal accumulation from high-carb eating, enzyme recycling isn’t something that requires panic.
The enzymes 11β-HSD1, 5α-reductase, and 5β-reductase aren’t villains in some metabolic thriller. They’re doing their job. Your body is doing its job. And if you’ve seen your health improve on this way of eating—better energy, clearer thinking, stable blood sugar, reversal of Type 2 diabetes, loss of stubborn fat—that’s not because you’ve somehow tricked your body into self-destruction. That’s because you’ve given it the metabolic environment it actually needs.
Stop listening to influencers who cherry-pick small studies and misrepresent enzyme activity. Start trusting what you observe in your own body and in the thousands of people around you who are genuinely getting healthier on low-carb and carnivore approaches.
Your enzymes know what they’re doing. Your body knows what it’s doing. The real issue is never cortisol or enzyme recycling. The real issue is always going to be metabolic dysfunction and poor metabolic flexibility—and that’s exactly what you fix by eating this way.
Now go get your bloodwork done. Preferably with someone who actually understands what the numbers mean.
About the author: I’m a consultant with an honours degree in physiology and health sciences, over a decade of private blood testing experience, and a qualified phlebotomist. I’ve worked with 1,000+ people who’ve seen reversal of Type 2 diabetes and metabolic transformation through low-carb and carnivore eating. I’ve written six books on blood testing in the context of keto and carnivore nutrition. When I look at bloodwork, I’m not seeing panic. I’m seeing physiology.
Study (1): Beisswenger BG, Delucia EM, Lapoint N, Sanford RJ, Beisswenger PJ. Ketosis leads to increased methylglyoxal production on the Atkins diet. Ann N Y Acad Sci. 2005 Jun;1043:201-10. doi: 10.1196/annals.1333.025. PMID: 16037240.
Why This Study Doesn’t Say What People Claim It Says
The Fatal Flaw: Measurement ≠ Damage
The study measured that MG production increased, but—and this is absolutely crucial—they did not measure whether this caused actual harm. They didn’t measure glycation damage, AGEs (advanced glycation end products), or any functional outcome. They just measured a number going up and stopped there.
It’s like measuring that your car’s engine produces more heat at higher RPMs and concluding the engine is being damaged. The heat is a byproduct of the process working, not evidence of damage.
What Happened in Ketosis (The Critical Missing Piece)
Here’s the part influencers gloss over: During ketosis, your body produces acetoacetate (a ketone body). A 2017 study (Poulin et al) in Cell Chemical Biology discovered something remarkable: acetoacetate directly buffers and neutralizes methylglyoxal through a non-enzymatic aldol reaction, converting it to 3-hydroxyhexane-2,5-dione, which is then metabolized to non-glycating species. (2)
In other words, your body produces the antidote at the same time it produces the problem. This isn’t a flaw—this is elegant metabolic design.
A Newer Study That Actually Looked at Real Outcomes
More recent evidence flips this narrative entirely. In a 2010 study of 16,523 Korean adults, people with ketonuria (evidence of active fat oxidation) had:
Lower obesity rates than non-ketone-producing individuals
Better metabolic parameters across the board (glucose, triglycerides, HDL, blood pressure, insulin)
Lower prevalence of metabolic syndrome (odds ratio of 1.356-3.505 in non-ketone producers)
Greater body fat loss and metabolic improvements
These are real people living real lives, not a snapshot of one biochemical measurement. (3)
(2) Trine Salomón, Christian Sibbersen, Jakob Hansen, Dieter Britz, Mads Vandsted Svart, Thomas Schmidt Voss, Niels Møller, Niels Gregersen, Karl Anker Jørgensen, Johan Palmfeldt, Thomas Bjørnskov Poulsen, Mogens Johannsen, Ketone Body Acetoacetate Buffers Methylglyoxal via a Non-enzymatic Conversion during Diabetic and Dietary Ketosis, Cell Chemical Biology, Volume 24, Issue 8, 2017, Pages 935-943.e7, ISSN 2451-9456, https://doi.org/10.1016/j.chembiol.2017.07.012.(https://www.sciencedirect.com/science/article/pii/S2451945617302702)
(3) Joo, N. S., Lee, D. J., Kim, K. M., Kim, B. T., Kim, C. W., Kim, K. N., & Kim, S. M. (2010). Ketonuria after fasting may be related to the metabolic superiority. Journal of Korean medical science, 25(12), 1771–1776. https://doi.org/10.3346/jkms.2010.25.12.1771
(1) Beisswenger BG, Delucia EM, Lapoint N, Sanford RJ, Beisswenger PJ. Ketosis leads to increased methylglyoxal production on the Atkins diet. Ann N Y Acad Sci. 2005 Jun;1043:201-10. doi: 10.1196/annals.1333.025. PMID: 16037240.
Notes regarding study 1. A Flawed Study Undermined by Selective Exclusion and Large Measurement Uncertainty
This study contains critical flaws that render its conclusions unreliable. First, the cherry-picking problem is now evident in the text itself. The study recruited 10 subjects but reports results for only 6 who were “compliant” with the diet.
The excluded four subjects either “did not stay on the diet due to nausea” (subject 9) or did not meet the predetermined criteria for ketosis markers. Critically, subjects 2, 7, and 10 are marked in Table 1 as “nonketotic, deficient as negative acetoacetate (AcAc), β-hydroxybutyrate (BOB), or both”—meaning they were disqualified because they didn’t demonstrate ketosis, not necessarily because they truly responded differently to the diet.
This is selective reporting: only participants who achieved ketosis were included in the final analysis, which artificially homogenizes the sample and masks the true heterogeneity of human responses. Second, and equally damning, the measurement error is enormous and exceeds the treatment effect itself. The intent-to-treat methylglyoxal increase was 113.6 ± 38.6 nM to 189.3 ± 72.7 nM (a difference of ~76 nM), yet the standard deviation of the post-diet measurement (±72.7 nM) is nearly as large as the effect size itself. This means the 95% confidence interval around the increase spans from essentially zero to over 150 nM—so wide that it includes trivial and substantial increases alike.
In the compliant subgroup (n=6), measurements ranged from 97.9 ± 34.7 to 216.5 ± 73.5 nM (P=0.005), but again, these enormous error bars dwarf the biological significance of the finding. With measurement uncertainty this large relative to the effect size, and with only six participants in the final analysis after selective exclusion, the study provides no convincing evidence that ketosis meaningfully increases methylglyoxal or that this translates to increased glycation risk.
Below are my additional thoughts, written up as a thank you for my paid subscribers.
