🥩 Keto or Carnivore — the Numbers That Move
For everyone · 10 markers · $128.70
with code CAMERON $143.00
Anyone eating ketogenic, carnivore or seriously low-carbohydrate — especially anyone whose LDL cholesterol went up sharply after starting, and anyone who feels cold, flat or is losing training performance months in.
🩸 Order this exact panel — 10% off
All 10 markers load into your cart in one click. No doctor's visit, drawn at any Quest location in the US, results by email in about two weeks. Code CAMERON applies automatically.
Add all 10 markers — $128.70 → Open the full Bloodwork Vault →Why this panel
A low-carbohydrate diet moves a specific and predictable set of markers, and two of them get misread in opposite directions. LDL cholesterol rises in a subset of people — characteristically the lean, insulin-sensitive and athletic — and is usually dismissed or panicked about rather than measured properly. Free T3 falls with carbohydrate restriction and gets read as new hypothyroidism. Uric acid rises through competition for kidney transporters and gets blamed on meat. This panel measures all three together, which is the only way any of them means anything.
What this panel can settle, and by what logic
Ten markers around three numbers that move on carbohydrate restriction and get misread in three different directions.
- ApoB (Apolipoprotein B) rather than LDL-C is the number that survives this diet. LDL-C is usually calculated from total cholesterol, HDL and triglycerides, and the equations lose accuracy at the triglyceride extremes this diet produces Sajja 2021. ApoB counts one particle each and does not depend on the calculation; discordance between ApoB and the cholesterol-based measures is well characterized and is concentrated in exactly this metabolic phenotype Sniderman 2024.
- The lean mass hyper-responder pattern is described, named and under study. Lean, insulin-sensitive people on carbohydrate restriction can raise LDL-C dramatically while triglycerides fall and HDL rises, and the phenotype was argued into the literature as deserving specific attention Norwitz 2022. The dedicated imaging work followed: a trial of carbohydrate-restriction-induced LDL elevation and atherosclerosis Budoff 2024, and its longitudinal follow-up, whose own title states the finding that baseline plaque predicted plaque progression while ApoB did not Soto-Mota 2025.
- Lipoprotein(a) — Lp(a) decides how much any of it matters, once. It is largely genetic, diet does not move it, and a high value alongside a large LDL rise is a materially different risk conversation Kronenberg 2022.
- Free T3 (Triiodothyronine) with TSH (Thyroid-Stimulating Hormone) is the second misreading. Free T3 falls on carbohydrate restriction while TSH and Free T4 (Thyroxine) usually stay normal, and reading free T3 alone produces a thyroid diagnosis that is not there. Thyroid function testing has documented interpretive traps of exactly this kind Van Uytfanghe 2023.
- Uric Acid is the third. Ketones compete with urate for shared proximal tubule transporters, so urate rises for a transport reason rather than a purine one Tatrai 2021.
- Fasting Insulin and HbA1c (Hemoglobin A1c) are where the benefit shows, and the Comprehensive Metabolic Panel (CMP) carries the sodium and potassium this diet depletes first.
What it cannot settle, and what would
It cannot tell you whether you have plaque, and that is the question behind the whole thing. A coronary artery calcium score or a CT angiogram answers it, and in this specific situation the imaging changes decisions in a way the lipids do not: in the longitudinal follow-up, existing plaque predicted progression while the LDL elevation did not Soto-Mota 2025. If you are going to spend money on one thing here, spend it there.
It cannot distinguish a diet-induced rise from familial hypercholesterolemia that was always present. The two can look identical on a single panel. A family history of early heart disease, or an LDL that was already high before the diet, makes that distinction urgent and is a reason to see a lipid clinic Kronenberg 2022.
It cannot settle whether the hyper-responder phenotype is safe. The honest position is that this is an open question under active investigation Norwitz 2022Budoff 2024, and anyone telling you confidently in either direction is ahead of the evidence.
And it cannot measure ketosis. Blood beta-hydroxybutyrate is the test for that and it is not in this catalog; a home meter does it for a few dollars a strip.
Draw conditions that decide whether the money is wasted
Weight stability matters more than the fast does, and almost nobody is told this.
- Do not draw during active weight loss if you want your steady-state lipids. Mobilizing fat transiently raises LDL further, so a draw two weeks into a cut reports the cut. Wait until weight has been stable for 2 to 3 weeks Norwitz 2022.
- Fast 9 to 12 hours. Triglycerides need it, and the LDL calculation depends on the triglycerides Sajja 2021.
- No alcohol for 72 hours and no hard session for 48. Both move triglycerides enough to change the calculated LDL.
- Lipoprotein(a) — Lp(a) needs no fasting and no repeat. One lifetime measurement is the standard and repeating it is the commonest waste on this panel Kronenberg 2022.
How you would know it answered your question, and what each pattern means next
Four patterns, and what each one should prompt.
- ApoB (Apolipoprotein B) high, LDL high, triglycerides low, HDL high: the hyper-responder pattern Norwitz 2022. The decision is about cumulative exposure over decades and it deserves a clinician and an imaging study rather than a forum Soto-Mota 2025.
- ApoB (Apolipoprotein B) normal with a high calculated LDL: the equation is overstating the particle count, which is a known failure mode at these triglyceride levels Sajja 2021Sniderman 2024. Track ApoB from here.
- High Lipoprotein(a) — Lp(a) alongside either: the residual risk is genetic and the threshold for treating everything else moves down Kronenberg 2022. This also becomes a family screening conversation.
- Low Free T3 (Triiodothyronine) with normal TSH (Thyroid-Stimulating Hormone) and Free T4 (Thyroxine): the expected adaptation, not a disease. If it arrives with cold hands, a falling resting heart rate and stalled training, raising carbohydrate is the intervention that would reverse it, and free T3 rising on unchanged thyroid medication is how you would know Van Uytfanghe 2023.
Sources read for these sections
- Norwitz NG, et al. Elevated LDL-cholesterol levels among lean mass hyper-responders on low-carbohydrate ketogenic diets deserve urgent clinical attention and further research. Journal of Clinical Lipidology 2022 · PMID 36351849
- Budoff M, et al. Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial. JACC Advances 2024 · PMID 39372369
- Soto-Mota A, et al. Plaque Begets Plaque, ApoB Does Not: Longitudinal Data From the KETO-CTA Trial. JACC Advances 2025 · PMID 40192608
- Sniderman AD, et al. Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention. European Heart Journal 2024 · PMID 38700053
- Sajja A, et al. Comparison of Methods to Estimate Low-Density Lipoprotein Cholesterol in Patients With High Triglyceride Levels. JAMA Network Open 2021 · PMID 34709388
- Kronenberg F, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis. European Heart Journal 2022 · PMID 36036785
- Tatrai P, et al. Modulation of Urate Transport by Drugs. Pharmaceutics 2021 · PMID 34204277
- Van Uytfanghe K, et al. Thyroid Stimulating Hormone and Thyroid Hormones (Triiodothyronine and Thyroxine): An American Thyroid Association-Commissioned Review of Current Clinical and Laboratory Status. Thyroid 2023 · PMID 37655789
The 10 markers — and why each one is here
Counts the atherogenic particles instead of calculating their contents. The number that survives this diet's effect on the equation
Genetic, diet-proof, measured once. Decides how much the LDL rise actually matters
Falls with carbohydrate restriction as an adaptation. Read alone it looks like new hypothyroidism
Stays normal in the adaptation and rises in real hypothyroidism. That contrast is the whole point of measuring both
Ketones compete with urate for the same kidney transporter, so it rises for a reason that is not the meat
Electrolytes, kidney and liver — and the sodium and potassium that low-carbohydrate diets deplete first
The glycemic half. Read knowing that a longer red cell lifespan on this diet can nudge it up without glucose rising
Fasting insulin is where the benefit of the diet shows most clearly and most quickly
Inflammatory status, and the context the lipids are read in
What this panel is ordered to decide
A panel is a set of numbers until it settles something. These are the decisions this one feeds — each links the pathway it belongs to, what that pathway claims, and what its test list is read for.
ApoB counts atherogenic particles; LDL-C estimates the cholesterol inside them. When the two disagree — common in insulin resistance — ApoB is right and LDL-C is falsely reassuring.
This is the pathway with the clearest test. Fasting insulin above roughly 8 µIU/mL, triglyceride:HDL above 2, or raised uric acid all point at insulin resistance — and if that's your picture, this pathway outranks every other one on the page for you specifically.
Related panels
A panel gives you numbers. Skool is where they get read — 103 marker breakdowns with the optimal range rather than just the lab range, 42 evidence-graded protocols, and me answering questions daily. $10/mo, cancel anytime.
Join Skool — $10/mo →Frequently asked questions
10 markers: ApoB (Apolipoprotein B), Lipid Panel, Lipoprotein(a) — Lp(a), Free T3 (Free Triiodothyronine), TSH (Thyroid-Stimulating Hormone), Uric Acid, Comprehensive Metabolic Panel (CMP), HbA1c (Hemoglobin A1c), Insulin (Fasting), hs-CRP (C-Reactive Protein, High Sensitivity).
$143.00 before discount, $128.70 with code CAMERON applied automatically. Individual markers add a one-time $10 draw fee. Ordered through Marek Diagnostics and drawn at any Quest Diagnostics location in the US.
No. These are ordered direct-to-consumer through Marek Diagnostics — you order online, walk into a Quest location, and results are emailed to you in about two weeks. No physician visit or insurance required. Not available in NY, NJ or RI.
Fast 9-12 hours — triglycerides need it and the LDL calculation depends on them. Do not draw during an active weight-loss phase if you want your steady-state lipids: mobilizing fat transiently raises LDL further, and a draw taken two weeks into a cut reports the cut. Wait until weight has been stable for 2-3 weeks. Avoid alcohol for 72 hours and a hard session for 48. Lp(a) needs no fasting and no repeat — one lifetime measurement is the standard.
ApoB high with LDL high, triglycerides low and HDL high is the hyper-responder pattern; the decision is about total exposure over decades and it deserves a clinician rather than a forum. ApoB normal with a high LDL-C means the calculation is overstating the particle count. A high Lp(a) alongside either changes the answer toward treating. A low free T3 with a normal TSH and free T4 is the expected adaptation, not a thyroid disease — if it comes with cold hands, a falling resting heart rate and stalled training, it is a reason to raise carbohydrate rather than to take thyroid hormone. A rising uric acid usually settles as the diet stabilizes.
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.