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Overview: What Keto and Atkins Diets Do

Posted on Monday November 10, 2025 in Metabolic Health

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1. Overview: What Keto and Atkins Diets Do

Both ketogenic and Atkins-type diets are low-carbohydrate, high-fat regimens.
They share several features:

Carbohydrate intake is markedly restricted (< 50 g/day in keto).
Fat becomes the dominant energy source.
The liver increases fatty acid oxidation and produces ketone bodies (β-hydroxybutyrate, acetoacetate) as an alternative fuel for muscle and brain.
Insulin levels fall; glucagon rises.

While these shifts improve insulin sensitivity and triglyceride metabolism, they also modify hepatic cholesterol synthesis, VLDL secretion, and LDL receptor activity.

2. Hepatic Effects: The Acetyl-CoA Overflow

When carbohydrate intake is low, acetyl-CoA — the central carbon substrate — is no longer channelled toward fatty acid synthesis but toward ketogenesis and cholesterol synthesis:

The liver oxidises large amounts of fatty acids, producing acetyl-CoA.
Some of this acetyl-CoA is diverted to HMG-CoA reductase, driving cholesterol synthesis.
However, reduced insulin signalling also downregulates SREBP-2, partially offsetting this effect¹. Thus, keto diets can increase intrahepatic cholesterol turnover, but whether that translates into higher LDL in plasma depends on receptor activity and VLDL export.

3. VLDL and LDL Dynamics

On keto or Atkins diets:

Triglycerides usually fall sharply because carbohydrate restriction suppresses hepatic triglyceride synthesis and VLDL output².
However, in some individuals, VLDL particle size decreases while LDL particle number rises, leading to higher measured LDL-C despite lower TG.
This “lean mass hyper-responder” phenotype is often seen in people who are slim, insulin-sensitive, and highly fat-adapted³.

Mechanistically:

Greater hepatic fat oxidation → increased acetyl-CoA → increased cholesterol availability for VLDL assembly.
Low insulin → reduced LDL receptor expression and activity → slower LDL clearance.
The net effect can be a rise in circulating LDL-C, though HDL rises and TG fall.

4. LDL Particle Quality: Not All LDL Is Equal

Multiple studies show that low-carb, high-fat diets tend to shift LDL particles toward larger, more buoyant LDL (pattern A).
These particles are considered less atherogenic than small, dense LDL (pattern B), typical of insulin resistance.

Therefore, while LDL-C concentration may rise, LDL particle number (apoB) or non-HDL cholesterol may not rise proportionally — and inflammation markers (hs-CRP, TG/HDL ratio) often fall⁵.

However, in genetically susceptible individuals (e.g. with familial hypercholesterolaemia or low baseline LDL receptor activity), this LDL-C rise can be substantial and clinically relevant.

5. LDL Receptor and Clearance Effects

Low insulin and low carbohydrate intake reduce hepatic SREBP-2 activation and LDL receptor transcription⁶.
This downregulation slows LDL clearance.

Saturated fats — common in some keto diets (butter, coconut oil, red meat) — can further reduce LDL receptor activity by:

Increasing hepatic free cholesterol.
Inhibiting LDL receptor recycling.

Hence, the composition of fats matters greatly:

Diets high in unsaturated fats (olive oil, nuts, fish) maintain LDL receptor activity and improve clearance.
Diets high in saturated fats tend to increase LDL-C through receptor downregulation.

6. Clinical Summary: Mixed Effects

Effect	Keto/Atkins Diet	Mechanism
↓ Triglycerides	Strong	↓ hepatic de novo lipogenesis
↑ HDL cholesterol	Moderate	↓ TG exchange with HDL
↑ LDL cholesterol	Variable (10–30% in some)	↓ LDL receptor activity, ↑ VLDL cholesterol
LDL particle size	↑ (larger, less dense)	Shift from pattern B → pattern A
Inflammation markers	↓	↓ insulin, ↓ CRP
ApoB (LDL particle number)	Usually stable, occasionally ↑	Individual variation

7. Practical Guidance

Monitor lipids carefully: Some keto dieters develop marked LDL-C elevation despite excellent metabolic improvement.
Check Apo B levels and LDL: Apo B ratio – should ideally be >1.3
Fat source matters: Prefer monounsaturated and polyunsaturated fats over saturated fats.
Moderate-carb Mediterranean variants of low-carb diets (rich in olive oil, fish, fibre, nuts) achieve similar metabolic benefits with smaller LDL rises⁷.
Individualise: In those with existing coronary disease, familial hypercholesterolaemia, or high apoB, persistent LDL elevation warrants intervention (diet modification, statins, or ezetimibe).

In summary

Keto and Atkins diets lower triglycerides and improve HDL, but may raise LDL cholesterol in certain individuals by reducing LDL receptor activity and increasing hepatic cholesterol export.
The effect is highly individual and fat-source dependent.
LDL quality often improves, but in patients with pre-existing vascular disease, sustained LDL elevation remains undesirable.

References (with links)

Goldstein JL, Brown MS. The SREBP pathway: regulation of cholesterol metabolism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC150968/
Volek JS et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low-fat diet. Lipids 2009;44:297–309. https://pubmed.ncbi.nlm.nih.gov/19082851/
Norwitz NG, Feldman DI. Understanding the lean mass hyper-responder phenotype. Curr Opin Endocrinol Diabetes Obes 2021;28(5):404-412. https://pubmed.ncbi.nlm.nih.gov/34397713/
Krauss RM et al. Effects of low-carbohydrate diet on LDL subclasses in healthy men and women. Atherosclerosis 2006;185(2):420-431. https://pubmed.ncbi.nlm.nih.gov/16257405/
Bhanpuri NH et al. Cardiovascular disease risk factor responses to a carbohydrate-restricted diet in overweight adults. Diabetol Metab Syndr 2018;10:8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5800510/
Mensink RP. Effects of saturated fatty acids on LDL receptor activity and plasma lipids. Am J Clin Nutr 2016;103:465–473. https://pubmed.ncbi.nlm.nih.gov/26733637/
Esposito K et al. Mediterranean diet improves lipid profile and endothelial function compared with a low-fat diet. Ann Intern Med 2004;141:1-11. https://pubmed.ncbi.nlm.nih.gov/15238367/

Technical papers: located in Dr Leatham’s “VAT Trap” Digital Companion and Resources

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