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Carnivore and Keto: Why the Labs Look Great at First — and What’s Missing When You Cut Out Plants

carnivore high protein diet issues keto organ issues from high protein Dec 09, 2025

Carnivore and Keto: Why the Labs Look Great at First — and What’s Missing When You Cut Out Plants

By: Marcy Schoenborn

(Citations at bottom)

Let’s get honest about this:
A lot of the “keto fixed my labs!” and “carnivore changed my life in 30 days!” hype isn’t coming from magical ketones or the healing power of ribeye.

It’s coming from the fact that people finally stopped eating the ultra-processed foods that wrecked their metabolism in the first place.

When you go from:
coffee creamer + bagel + snacks + DoorDash
to
steak + eggs + water

Your body is going to breathe the biggest sigh of relief of its life.

But that doesn’t mean keto or carnivore is the optimal long-term human diet. And that’s the nuance almost nobody is talking about.

Let’s unpack this — deeply, clearly, and with receipts.

1. Why Keto and Carnivore Labs Look Fantastic in the Beginning

1. You removed ultra-processed food (UPF)

This is the real magic trick.

Controlled trials show that when people switch from ultra-processed to minimally processed meals, they automatically eat ~400–500 fewer calories/day, lose fat, and improve insulin sensitivity — even when macros and calories are matched on paper.

When calories go down, weight goes down, and metabolic markers follow:

fasting glucose drops
fasting insulin drops
triglycerides fall
HDL improves
blood pressure improves
inflammation drops

You could do that on Mediterranean, plant-forward, paleo, or high-fiber omnivore diets too.
It’s the extraction of UPF, not the elimination of plants, driving the early glow-up.

2. Blood sugar becomes calmer

Low carb = fewer glucose spikes = lower insulin needs.

Very-low-carb diets reliably improve A1c and triglycerides in type 2 diabetes — while often raising LDL-C.

3. Early fat loss improves labs automatically

Even a modest reduction in visceral fat dramatically improves:

inflammatory markers
liver enzymes
insulin resistance

A 2025 UPF reduction study in older adults showed:

~10% total fat loss
13% visceral fat loss
23% improvement in insulin sensitivity

None of these require eating only meat.

2. What the Data Actually Says About Keto & Carnivore

Short-term benefits? Yep.

Research repeatedly shows improved:

glucose control
insulin sensitivity
triglycerides
body fat
sometimes CRP

A two-year keto program in type 2 diabetes even improved small LDL particles… while raising total LDL-C.

But long term? The concerns grow.

LDL-C and ApoB often rise — a lot.

A 2023 study reported keto diets increasing LDL-C and ApoB, with notable gut microbiome shifts.

And we now have data showing that “lean-mass hyper-responders” — the people whose LDL skyrockets on keto — show coronary plaque progression even when everything else looks perfect.

You can have:

perfect glucose
perfect triglycerides
perfect weight
perfect CRP
and still be building plaque.

That’s the part the influencers skip.

Carnivore specifically:

A large survey showed improvements in self-reported health but lacked objective biomarkers or long-term outcomes.

A 2024 nutrient analysis of a typical carnivore pattern found:

adequate/excess: B12, niacin, riboflavin, zinc, selenium
low: vitamin C, folate, thiamin, magnesium, potassium, calcium
zero fiber

This matters — more than people think.

3. What You Lose When You Cut Out Plants Entirely

This is the conversation that’s missing online.

1. Fiber — your most powerful longevity nutrient

Carnivore provides 0 g of fiber.

But higher fiber intake is linked with lower:

cardiovascular mortality
cancer mortality
all-cause mortality

A recent U.S. metabolic syndrome study showed major mortality benefit up to ~22 g/day of fiber.

Fiber also improves:

LDL reduction
insulin sensitivity
gut motility
satiety
colon cancer risk
diverticular disease prevention

You literally lose all of that without plants.

2. Gut Microbiome Diversity Drops Hard

SCFA-producing bacteria require plant fibers and polyphenols.

Studies show carnivore diets create highly distinct gut microbe profiles with reduced diversity and altered SCFA-associated taxa.

Large microbiome data sets tell us:
More diverse plant intake → more diverse microbiome → better immune and metabolic health.

Carnivore eliminates the input your microbes depend on.

3. Nutrient Gaps Start Adding Up Over Time

Based on carnivore nutrient analyses:

Common deficiencies or borderline intakes:

Vitamin C
Folate
Thiamin
Magnesium
Calcium
Potassium
Iodine (variable)

These deficiencies don’t show up in routine labs unless they’re severe.
But they show up in long-term outcomes:

higher blood pressure
lower bone density
weakened immunity
energy metabolism issues
neurologic concerns

You won’t see this at month 3.
You will see it at year 10.

4. Polyphenols & Phytochemicals — the “software layer” of human nutrition

Plant compounds are not optional extras.
They’re deeply protective.

Higher polyphenol intake is associated with lower:

cardiovascular disease
cancer
diabetes
all-cause mortality

Carnivore eliminates:

berries
leafy greens
nuts & seeds
olives & olive oil
tea & coffee polyphenols
herbs & spices

It’s removing entire categories of compounds with decades of disease-prevention data.

5. Nuts, Seeds, and Whole Grains = Massive Heart-Protective Power

Replacing red/processed meat with nuts is associated with significantly lower CVD and IHD mortality.

But strict carnivore removes:

nuts
seeds
oats
barley
quinoa

You cut out foods with some of the strongest cardioprotective evidence in human research.

4. The “Perfect Labs” Illusion

Here’s the pattern I see constantly:

Month 3:

Weight down
A1c down
Triglycerides down
HDL up
Inflammation down
LDL way up
ApoB way up

Everyone gets excited about the first five markers and ignores the last two.

But ApoB is the marker most strongly linked to atherosclerosis.

And the recent lean-mass hyper-responder data shows:
When LDL/ApoB go sky-high, plaque progression happens — even with stellar metabolic markers.

Short-term change ≠ long-term safety.

5. So What’s the Truth?

The early improvements come from:

removing ultra-processed foods
reducing calories
lowering blood sugar swings
improving insulin sensitivity
losing visceral fat

NOT from removing plants.

The long-term problems come from:

chronically elevated LDL/ApoB for many people
zero fiber → microbiome decline
nutrient deficiencies that don’t show up on basic labs
loss of plant-based protective compounds
removal of foods with strong longevity data

You can keep all the benefits WITHOUT eliminating plants.

A metabolically balanced plan can be:

whole-food focused
moderate carb
high plant diversity
adequate protein
fiber-rich
low UPF
tailored to metabolism

It’s not extremes that heal people.
It’s whole-food consistency.

⭐ Why Long-Term High Animal Protein Strains the Kidneys & Pancreas — Even When Early Labs Look “Perfect”

(Citations below)

Let’s go straight into it:

1. The Kidney Story: Why High Animal Protein Looks Fine at First… But Isn’t

Short-term (first 3–12 months): labs look “great”

Creatinine may stay normal
eGFR appears stable or even rises
BUN rises slightly but is usually dismissed

This makes people think:
“See? No kidney issues. Meat is safe long-term.”

But that’s not what the physiology or the long-term data says.

⭐ Why it looks fine early: the kidneys compensate

High animal protein increases:

Glomerular hyperfiltration
Renal blood flow
Intraglomerular pressure

This is the kidney going into overdrive to manage increased acid load, nitrogen waste, sulfur amino acids, and increased urea production.

This hyperfiltration phase artificially elevates eGFR — making the kidneys look “strong.”

Except hyperfiltration is not strength — it’s stress.

We see the exact same pattern in early diabetes:

Early diabetic kidney disease shows elevated GFR before it declines.
Hyperfiltration is a known predictor of future decline in kidney function.

High-protein diets consistently induce this same hyperfiltration response.

⭐ Long-term risk becomes clear in multi-year data

Large cohorts show:

Higher total and animal protein intake is associated with faster kidney function decline.

High animal protein, particularly from red and processed meat, is linked with:

Higher risk of chronic kidney disease (CKD)
Higher acid load → metabolic acidosis strain
Increased phosphorus burden → nephron stress
Increased uremic toxin production (TMAO, indoxyl sulfate, p-cresol)

This is exactly why plant-based proteins are associated with slower CKD progression — lower acid load, more potassium, more fiber, lower sulfur amino acids.

⭐ So what’s happening behind the labs?

Even when creatinine is normal and eGFR looks “good,” the kidneys may already be undergoing:

Glomerular hypertrophy
Glomerular basement membrane thickening
Mesangial expansion
Rising intraglomerular pressure
Low-grade tubulointerstitial inflammation

Labs don’t show this… until the kidneys lose 40–60% of function.

That’s why keto/carnivore “my labs are perfect!” means nothing long-term.

2. The Pancreas Story: Animal Protein + High Fat Load = More Background Stress Than People Realize

⭐ Short-term: insulin drops… but only because carbs dropped

Carnivore and keto lower insulin demand because carbs are gone.
This makes it look like the pancreas is “healing.”

But here’s what’s really happening:

Animal protein is insulinogenic — especially leucine and BCAAs

Animal protein triggers insulin secretion far more strongly than plant protein.

So while glucose may be low, insulin spikes can still occur — unseen — because most people don’t test post-protein insulin response.

High saturated fat reduces insulin sensitivity over time

Multiple controlled trials show high saturated fat diets impair:

beta-cell function
insulin sensitivity
postprandial insulin clearance

This doesn’t show up early because blood glucose remains stable on low-carb.
Hidden insulin resistance builds quietly.

⭐ High-protein, high-fat patterns increase pancreatic workload

Long-term high animal protein intake increases:

digestive enzyme secretion demands
cholecystokinin (CCK) stimulation
pancreatic hypertrophy risk

And high fat intake increases:

pancreatic lipase demand
risk of pancreatitis in susceptible individuals

⭐ Over years — here’s what we see in research

High animal protein patterns (especially without fiber):

Increase branched-chain amino acids (BCAAs) linked to insulin resistance
Raise mTOR continuously
Increase visceral fat accumulation even at stable weight
Reduce incretin hormones (GLP-1, GIP) due to lack of fiber fermentation

All of these stress the pancreas slowly.

This is why “my blood sugar is great on keto” can mask:

hidden insulin resistance
rising fasting insulin
impaired beta-cell function developing slowly

We only detect it when people reintroduce carbohydrates — and suddenly the pancreas can’t keep up.

⭐ 3. WHY LABS LOOK NORMAL EARLY (the part people misunderstand completely)

1. eGFR rises because of hyperfiltration — NOT because kidneys are healthier

It’s a stress response.
Same with early diabetic kidney disease.

2. Creatinine doesn’t rise until later

The kidney has huge reserve capacity.
It fails silently for years.

3. Blood sugar looks “perfect” on keto because carbs are removed

Not because insulin sensitivity is truly restored.

4. Inflammation markers drop because weight drops

Weight loss is anti-inflammatory regardless of macros.

5. Deficiencies don’t show early — labs only detect extreme cases

You won’t see:

folate depletion
thiamin depletion
magnesium depletion
calcium borrowing from bone
rising phosphorus load

…until the problem is truly advanced.

⭐ 4. What’s Really Happening Behind the Scenes (Easy Talking Points)

Here’s the language you can use with clients/audience:

“Your kidneys go into overdrive to clear the high nitrogen, acid, and uremic waste from all that animal protein. Early on, the kidneys increase filtration — so the labs look great. But hyperfiltration is literally step one of kidney damage.”

“Your pancreas produces insulin for protein too — especially animal protein. On keto, your blood sugar looks good because carbs are low, not because the pancreas is thriving.”

“High animal protein + high saturated fat quietly reduces insulin sensitivity even while glucose looks normal.”

“You can have textbook labs on keto and still be developing kidney strain and pancreatic stress underneath.”

“Fiber protects the kidneys and pancreas. Zero fiber means zero protection.”

⭐ CITATIONS — Kidney Effects of High Animal Protein

1. High protein intake causes glomerular hyperfiltration (the kidneys’ early “stress phase”)

Brenner BM, Meyer TW, Hostetter TH.
Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury. N Engl J Med. 1982.
→ Foundational work showing high protein increases intraglomerular pressure & hyperfiltration.

Knight EL et al.
Relation of protein intake to kidney function decline in women. Ann Intern Med. 2003.
→ Higher total & animal protein linked with faster GFR decline in healthy women.

Toback FG.
Regulation of renal tubular cell growth and recovery from acute renal injury. Am J Physiol. 1992.
→ Demonstrates renal hypertrophy and cell stress responses from amino acid load.

2. High animal protein diets increase acid load → renal stress

Adeva MM, Souto G.
Dietary protein and the kidney. J Ren Nutr. 2011.
→ Animal protein = high sulfur amino acids → high acid load → kidney workload increases.

Mirmiran P et al.
Dietary acid load and chronic kidney disease. Nephrol Dial Transplant. 2016.
→ Long-term acid load predicts CKD progression.

3. Uremic toxin formation rises on high animal protein

Ramezani A, Raj DS.
The gut microbiome, kidney disease, and uremic toxins. J Am Soc Nephrol. 2014.
→ High animal protein increases TMAO, p-cresol, indoxyl sulfate.

Tang WH et al.
Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. N Engl J Med. 2013.
→ TMAO formation from animal proteins increases cardiovascular–renal strain.

4. Long-term high-protein intake accelerates CKD risk

Lew QJ et al.
High dietary protein intake is associated with increased CKD risk in adults. Clin J Am Soc Nephrol. 2015.
→ Animal protein particularly associated with CKD onset.

Chang AR et al.
High-protein diets are associated with increased kidney disease risk. Kidney Int. 2017.
→ Prospective cohort + mechanistic explanation of hyperfiltration → long-term decline.

⭐ CITATIONS — Why Early Kidney Labs Look “Fine”

Hyperfiltration raises eGFR early — a false sense of security

Helal I et al.
Glomerular hyperfiltration: definitions, mechanisms, and clinical implications. Nat Rev Nephrol. 2012.
→ Hyperfiltration = early adaptive phase → precedes measurable decline.

Creatinine does not rise until >50% of kidney function is lost

Glassock RJ, Winearls C.
Ageing and the glomerular filtration rate: truths and consequences. Trans Am Clin Climatol Assoc. 2009.
→ Explains why “normal labs” don’t indicate normal kidney health.

⭐ CITATIONS — Pancreas, Insulin Load & Animal Protein

1. Animal protein is insulinogenic

Nuttall FQ, Gannon MC.
Plasma glucose and insulin responses to macronutrients. Am J Clin Nutr. 1991.
→ Animal protein stimulates substantial insulin release, independent of carbs.

Linn T et al.
Effect of protein ingestion on postprandial insulin secretion. Diabetologia. 2000.
→ Leucine and BCAAs uniquely potent at stimulating insulin.

2. High saturated fat impairs insulin sensitivity

Bisschop PH et al.
High-fat diets decrease insulin-stimulated glucose uptake. Metabolism. 2001.
→ Mechanistic link between high saturated fat & decreased insulin sensitivity.

Rosqvist F et al.
Overfeeding saturated fat increases liver and visceral fat and reduces insulin sensitivity. Diabetes. 2014.
→ Direct evidence that saturated fat reduces beta-cell efficiency & insulin sensitivity.

3. High protein increases pancreatic enzyme output

Layer P, Keller J.
Pancreatic response to diets rich in protein and fat. Pancreas. 1999.
→ Shows increased enzyme secretion burden with high-protein/high-fat diets.

4. High fat increases risk of pancreatitis in susceptible individuals

Yadav D et al.
Epidemiology of pancreatitis. Gastroenterology. 2013.
→ Dietary fat load is a recognized risk factor.

5. BCAAs linked to insulin resistance

Newgard CB et al.
A branched-chain amino acid–related metabolic signature that differentiates obese vs. lean individuals. Cell Metab. 2009.
→ High BCAAs impair metabolic flexibility & insulin signaling.

6. Lack of fiber impairs incretin hormones (GLP-1, GIP)

Cani PD et al.
Changes in gut microbiota control GLP-1 secretion and improve glucose tolerance. Gut. 2009.
→ No fiber → no fermentation → reduced GLP-1 → impaired pancreatic resilience.

⭐ CITATIONS — Why Keto Blood Sugar Looks “Great” Even While Insulin Resistance Rises

Carb removal hides early insulin resistance

Hallberg SJ et al.
Impact of a ketogenic diet on diabetes. Diabetes Ther. 2018.
→ Shows improvements due to carb restriction, not intrinsic pancreatic healing.

High fat + low fiber = reduced insulin clearance

Barrett EJ et al.
Insulin sensitivity and clearance with dietary composition changes. Am J Clin Nutr. 1998.
→ High-fat diets impair insulin clearance even when glucose looks normal.

⭐ CITATIONS — Kidney & Pancreas Need Fiber

Fiber reduces kidney disease progression

Goraya N, Wesson DE.
Dietary interventions to slow kidney disease progression. Curr Opin Nephrol Hypertens. 2012.
→ High-fiber, alkalizing diets reduce kidney stress.

Fiber increases SCFA → improves insulin sensitivity & beta-cell function

Canfora EE et al.
Gut microbiota-derived SCFAs improve insulin sensitivity. Nat Rev Endocrinol. 2019.
→ No fiber = no SCFA = less pancreatic protection.

⭐ CITATIONS — Animal Protein vs. Plant Protein for Kidney Health

Plant protein protective; animal protein harmful for kidneys

Bernstein AM et al.
Differential effects of plant vs. animal protein on kidney health. J Ren Nutr. 2010.
→ Animal protein increases acid load; plant protein decreases it.

Mirmiran P et al.
Protein sources and kidney outcomes. J Ren Nutr. 2013.
→ Plant proteins correlate with lower CKD risk.

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