The keto world keeps forgetting one thing: NADPH.
Ketones don’t make it.
Fat doesn’t make it.
Fasting doesn’t make it.
The only way to generate NADPH at scale — in a real, depleted, post-industrial body — is through the oxidative branch of the pentose phosphate pathway.
And that requires glucose.
Not gluconeogenesis. Not glycerol. Not amino acid conversions.
Glucose.
This is the part no one’s tracking.
Everyone’s arguing about ketones, carbs, blood sugar, insulin load — and missing the fact that NADPH is the thing that collapses first in terrain failure.
If you’re not making NADPH, you can’t:
– recycle glutathione
– neutralize oxidative stress
– support steroid hormone synthesis
– stabilize mast cells
– tolerate histamine
– or maintain redox margin
And here’s the deeper terrain profile the keto–carnivore–low-carb crowd keeps ignoring:
Yes, there are other biochemical pathways that can produce NADPH:
– the malic enzyme,
– isocitrate dehydrogenase (IDH1/2),
– and folate-driven reactions via methylene-THF dehydrogenase.
But in a terrain that’s already running on low ATP, unstable voltage, collapsed mitochondrial coupling, low magnesium, low niacin, and stress-induced catabolism, those secondary NADPH sources are either downregulated, cofactor-starved, or too slow to meet demand.
Malic enzyme requires adequate mitochondrial flux, intact malate–aspartate shuttling, and stable oxaloacetate availability — all of which are disrupted in energy-deficient states.
Isocitrate dehydrogenase is tightly coupled to TCA cycle function and intracellular pH — and when mitochondrial throughput is compromised, that enzyme barely moves.
And folate-linked NADPH generation is highly dependent on methylation cofactors (B2, B6, B12, zinc), adequate glutamine, and clean ammonia clearance — none of which are reliable in a terrain marked by catabolic metabolism, low nutrient intake, and impaired urea cycle activity.
And even if the cofactors are present, genetic and epigenetic blocks can still disrupt the pathway.
Variants in the MTHFR gene — especially C677T and A1298C — can impair conversion of folate into 5-MTHF, slowing the folate cycle and NADPH output.
And chronic stress, inflammation, or toxin exposure can epigenetically downregulate key enzymes, even in people without mutations.
So the folate-linked pathway is genetically fragile, environmentally sensitive, and too easily impaired to serve as a reliable NADPH source under stress.
Those alternate NADPH routes only work in well-resourced systems — with steady ATP production, strong mitochondrial throughput, stable pH, and full micronutrient availability.
But in a body that’s been pushed into sympathetic dominance, burned through its reserves, and stuck in a long-term catabolic state — they don’t keep up.
This is what happens when someone’s been fasting too long, cutting carbs, overtraining, overusing stimulants, or living in chronic fight-or-flight:
The system can no longer meet the energy and cofactor demands to run those slower, auxiliary NADPH sources.
Only glucose — via direct entry into the PPP — can reliably and rapidly generate the NADPH needed to reverse terrain breakdown, restore glutathione recycling, stabilize inflammatory load, and restart steroid hormone production.
That’s not preference.
That’s bioenergetic triage.
This is why “keto clarity” doesn’t last.
This is why fasting works until it doesn’t.
This is why carnivore collapses into hormone loss, emotional flatness, and fatigue no one can explain.
Because when you’re running a body that’s already in collapse, and you pull out the one substrate that drives NADPH, you don’t get metabolic flexibility.
You get terrain failure.
I don’t care how well your body makes ketones.
If you’re not running the PPP, you’re not repairing.
You’re bypassing.
And the longer you bypass, the more the system breaks down — electrically, hormonally, neurologically.
That’s what I track.
Not ketone levels.
Not macros.
Not weight loss.
NADPH.
That’s the first collapse.
And if no one’s talking about it, they’re not reading the terrain.
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And yes — I know the pushback that’s coming.
You’re going to say:
“But the malic enzyme makes NADPH.”
“But IDH makes NADPH.”
“But the folate cycle makes NADPH.”
You’re right — but only in a body that’s already stable.
Those auxiliary systems do work — when terrain is intact. When mitochondria are firing. When the urea cycle is clear. When voltage is steady. When the body has enough magnesium, B2, B3, B6, B12, and zinc to push those reactions forward.
But most people are not running that body.
Less than 1% of the adult population in industrialized nations has an optimized terrain.
Even among the biohacking elite, most are secretly compensating — with caffeine, with supplements, with dopamine hits, or fasting cycles that mask the underlying instability.
And of the people who do still have high-functioning terrain?
Most of them are men.
Why?
Because testosterone protects muscle, mitochondrial density, and insulin sensitivity.
Because women are cyclically more vulnerable to progesterone collapse, cortisol dysregulation, and underfueling.
Because the wellness industry pushes women into fasting, carb fear, and endless detox loops that shred NADPH production without anyone realizing what’s happening.
This post isn’t about carbs versus keto.
I’m not here to argue macros.
I’m not here to debate you on the public timeline.
If you comment something dismissive, combative, or totally off-topic, I’m not going to respond.
This post is for the people who already know something deeper is broken.
And they’ve tried everything.
Except repairing the actual terrain.
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Let’s be real:
It’s a lot more complicated than people in the comment section make it sound.
This isn’t just about which molecule can make NADPH.
It’s about which systems actually function under stress, collapse, and depletion.
And most people arguing in favor of “alternate pathways” have never rebuilt a terrain from the ground up.
I have.
That’s why I don’t debate biochemistry in isolation.
I read it in context — inside a real, electrical, collapsing human body.
That’s the difference.
That’s terrain medicine.