Low Carb High Fat - Ketogenic

LDL in context

• A red flag next to LDL tells you almost nothing about you. Some people dismiss LDL as unimportant; LDL is not unimportant. LDL and ApoB are part of the atherosclerotic process, but they need context.
• LDL is not the whole story: the standard panel also gives triglycerides, HDL, total cholesterol, and non-HDL cholesterol, and reading LDL in isolation as good or bad captures only a fraction of the picture.
• Potassium and hematocrit have ranges where a sufficiently abnormal value is dangerous largely independent of the individual. LDL is not like that; its meaning depends on the rest of the individual.
• A healthy 32-year-old with no family history and a 72-year-old with two cardiac stents can both have LDL of 130 mg/dL with completely different clinical pictures, so LDL requires a conversation and broader evaluation.
• The 2026 guidelines make LDL above 190 mg/dL an exception: it is high risk regardless of the individual and leads to medication because it is often associated with familial hypercholesterolemia (FH). [1]
• FH is a genetic condition affecting roughly 1 in 250 people and increases cardiovascular risk at a young age. [2]
• Data include people with LDL at that level who do not have heart disease and people who have high LDL without FH.
• Even above 190 mg/dL, high LDL is not automatically high risk in the same way as potassium or hematocrit. The number warrants attention, a thoughtful conversation, further evaluation, and proper FH diagnosis; medication may still be appropriate, but high LDL does not automatically establish a genetic abnormality.

Triglycerides and HDL

• Before LDL targets, triglycerides and HDL deserve attention because many patients have said their doctor never mentioned those numbers and only looked at LDL. Whether that is literally true matters less than the fact that it was the patient's experience, meaning that is mostly where the conversation went or did not go.
• A laboratory may call triglycerides under 150 mg/dL normal, while 150 is normal for a metabolically unhealthy population here and triglycerides under 100 mg/dL are the preferred level; that goal is aggressive and important.
• The triglyceride-to-HDL ratio matters even more, with a preferred level below 1.5. Published insulin-resistance cutoffs are usually around 2 to 3; the aim is optimal metabolic health, while "optimal" is tough to define and kind of squishy, and moving toward below 1.5 remains the goal.
• The ratio does not behave the same for everyone: Black patients tend to have lower triglycerides at the same degree of insulin resistance, so the cutoff may need different interpretation and requires context, not an absolute threshold. [3]
• Multiple trials of drugs that raised HDL failed to prevent heart attacks, but interpreting that as HDL not mattering is a misreading of the data. Failure of a drug to prevent heart attacks is not the same as HDL completely not mattering. [4]
• Low HDL is a very reliable marker of metabolic dysfunction and still tracks with higher cardiovascular risk.
• In the early cohort data, HDL was a better predictor of heart disease than elevated LDL. [5]
• General HDL cutoffs are not below 40 mg/dL for men or 50 mg/dL for women.
• Raising HDL with a drug that does nothing about the underlying metabolic dysfunction is very different from HDL rising because diet changed, exercise started, and visceral fat was lost. In the latter case, the rise signals that the underlying problem is getting better and will absolutely reduce cardiac risk.
• Genetically very high HDL, around 90 mg/dL or higher for an entire life, is not necessarily beneficial; some people in that range have genetically high HDL that is actually dysfunctional. The number matters less than why the number is what it is. [6]

Lp(a), ApoB, and risk estimation

• Lp(a) is not on the standard lipid panel, but the 2026 guidelines recommend that every adult have it measured at least once in a lifetime because it is a separate genetic risk factor that can refine overall cardiovascular risk. Even with its inclusion in the guidelines, patients may still need to ask their doctor specifically for it. [1]
• In reality, the focus should be ApoB, not LDL. ApoB is still underused, while LDL is the most common lipid test on the standard lipid profile, so patients can ask their provider for ApoB.
• The LDL number means almost nothing on its own.
• The 2026 guidelines use the PREVENT risk calculator. [1][7]
• The older Pooled Cohort Equations overestimated risk, so people were being told they were at higher risk than they actually were. [8]
• There is a legitimate concern that medicine keeps moving the goalposts with lower thresholds to put more people on more medications, but PREVENT went in the opposite direction: its risk estimates came down, even though the targets continue to get lower. [8]
• Risk calculators are evidence-informed estimates, not absolutes, and should spark a conversation without dictating care. Medical practice often breaks down at the last stage of translating a population-based estimate to the individual.
• PREVENT uses age, blood pressure, BMI, kidney function, smoking, diabetes status, and the lipid profile; places the individual into low, borderline, intermediate, or high risk; adjusts for risk enhancers such as family history, obesity, lupus, rheumatoid arthritis, and other inflammatory conditions; and then gives a recommendation about whether LDL-lowering medication is used and how intensive it is. [1]

Imaging vascular disease

• High LDL by itself does not cause heart attacks or strokes; arterial plaque causes heart attacks and strokes. LDL is not the disease; vascular disease is the disease.
• For borderline and intermediate risk, the guidelines include coronary artery calcium (CAC) testing. A CAC score is a quick non-contrast CT that looks at calcium in the actual arteries and screens the individual for vascular disease beyond reliance on a population formula. [1]
• CAC scans are not perfect, but for men over 40 and women over 45 they are a good test to refine cardiac risk. Coronary CT angiography is even better, although it is harder to obtain and is not included in the guidelines. [1]

LDL goals and medication decisions

• The repeated focus on factors beyond LDL reflects that LDL is only a small part of the picture. LDL targets are more controversial because the goalposts have moved the most over the past few decades.
• The 2026 guidelines set LDL under 100 mg/dL for borderline or intermediate risk, under 70 mg/dL for high risk or established heart disease, and under 55 mg/dL for very high risk; in reality, most patients with established heart disease end up with the under-55 target. High-risk patients also need at least a 50% reduction from baseline on top of hitting the goal. [1]
• Those targets have continued to get lower and lower, but they are not completely made up: they come from studies showing fewer cardiovascular events at those levels.
• Evidence-based targets still leave questions about absolute benefit at lower targets, diminishing returns, cardiac events versus all-cause mortality, which people benefit most, and whether higher drug doses produce more side effects.
• Borderline risk with LDL 120 mg/dL but no plaque is a case for conversation, not a reflex prescription by any means.
• Not everyone wants medication, and that is their right to choose. Some people value agency and bodily autonomy more, value current certainty over a future possibility, and for some the psychological burden of giving that up degrades quality of life; clinicians and guideline writers need to respect that because numerical guidelines do not capture it.
• Coronary disease with LDL 65 mg/dL and multiple medications raises another important conversation about adding to growing polypharmacy for a small absolute event reduction to get below 55, not a reflex prescription.

Metabolic health and practical use

• LDL by itself means nothing and needs context, and all of this takes a backseat to making sure metabolic health is being addressed.
• Lowering LDL as far as possible while not aggressively addressing insulin resistance is like using scotch tape to plug a leaky dam: it may make someone feel better briefly, but it will not solve the problem.
• Even the best LDL-lowering trials reduce cardiac events by only a small absolute amount and do not eliminate them, not even close, so other issues still need attention and metabolic health rises near the top.
• This complexity is appropriate. Simplifying LDL to one number or equation that is simply good or bad does everyone a disservice; LDL is not a clear universal normal-or-abnormal value like potassium.
• When a lab comes back flagged, do not panic and do not ignore it: look at the whole panel; ask about triglycerides, HDL, the triglyceride-to-HDL ratio, Lp(a), and ApoB; ask for the PREVENT score; and ask whether CAC or possibly coronary CT angiography makes sense.
• People have more agency over their health than most realize, and access to more information can help them make better decisions than any one single number on a lab sheet can.

References

1. [00:39] 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines — https://doi.org/10.1161/CIR.0000000000001423
2. [02:43] Estimating the prevalence of heterozygous familial hypercholesterolaemia: a systematic review and meta-analysis — https://doi.org/10.1136/bmjopen-2017-016461
3. [04:39] Should triglycerides and the triglycerides to high-density lipoprotein cholesterol ratio be used as surrogates for insulin resistance? — https://doi.org/10.1016/j.metabol.2009.07.027
4. [04:56] Effect of HDL-Raising Drugs on Cardiovascular Outcomes: A Systematic Review and Meta-Regression — https://doi.org/10.1371/journal.pone.0094585
5. [05:17] High density lipoprotein as a protective factor against coronary heart disease: The Framingham Study — https://doi.org/10.1016/0002-9343(77)90874-9
6. [05:57] Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease — https://doi.org/10.1126/science.aad3517
7. [07:08] Development and Validation of the American Heart Association's PREVENT Equations — https://doi.org/10.1161/CIRCULATIONAHA.123.067626
8. [07:15] Evaluation and Comparison of the PREVENT and Pooled Cohort Equations for 10-Year Atherosclerotic Cardiovascular Risk Prediction — https://doi.org/10.1161/JAHA.124.039454