APOE4 lab marker · ApoB

What ApoB target should an APOE4 carrier aim for?

Aim for an ApoB under 60 mg/dL (0.60 g/L). That is Phoenix's target for every APOE4 carrier, set on the strictest line in the National Lipid Association's consensus, and at 90 mg/dL or higher it is time to talk to your doctor.

One limit, said once: no ApoB target has ever been tested in APOE4 carriers. Every line below comes from heart guidelines, and the table tells you which line is a guideline and which is a Phoenix choice. This page educates; your doctor decides your treatment. How Phoenix reads the evidence

The ApoB bands

The ApoB bands
ApoB, mg/dL (g/L)BandWhere the line comes from
Under 60 (under 0.60)OptimalPhoenix choice. The National Lipid Association's line for people at very high heart risk, applied to every carrier.
60 to under 90 (0.60 to under 0.90)MonitorPhoenix band. Worth working on.
90 or higher (0.90 or higher)Talk to your doctorGuideline line. The National Lipid Association's line for borderline to intermediate risk. Bring it to your next appointment. It is not an emergency.

The line rule. "Under 60" excludes 60, and "90 or higher" includes 90. So 60 is Monitor and 90 is Talk to your doctor.

Confidence in the optimal line: low to moderate. It is an extrapolation from heart guidelines, chosen on purpose and labelled as a choice.

Why ApoB, and not only LDL-C?

ApoB counts the particles that carry cholesterol and triglycerides through your blood. LDL-C measures how much cholesterol those particles hold. Your arteries respond to the count.

The strongest proof comes from genetics. In a 2019 study of 63 cohorts, gene variants that lower triglycerides and gene variants that lower LDL-C cut coronary heart disease by the same amount for each 10 mg/dL drop in ApoB: 23% lower odds either way (odds ratio 0.77). Once ApoB was accounted for, triglycerides and LDL-C added nothing (Ference, 2019).

The 2026 ACC/AHA guideline still uses LDL-C and non-HDL-C as the main goals, and uses ApoB to find risk that remains once those goals are met. Phoenix prints both. If your LDL-C looks fine and your ApoB does not, believe the ApoB and take the gap to your doctor.

What does APOE4 change about ApoB?

APOE4 pushes LDL cholesterol up, one copy at a time. Across 82 studies of 86,067 healthy people, LDL-C rose in a straight line across the APOE genotypes, and people with ε4/ε4 had LDL-C about 44 mg/dL higher than people with ε2/ε2. Coronary risk rose a little with it (odds ratio 1.06 for ε4 carriers against ε3/ε3) (Bennet, 2007).

The brain data point the same way:

  • In 1.8 million people, each 39 mg/dL higher LDL-C went with a 5% higher dementia rate, and 17% higher when LDL-C was measured before 65 and dementia came more than 10 years later (Iwagami, 2021).
  • In the UK Biobank, the top quarter of ApoB had a 12% higher dementia rate than the bottom quarter (hazard ratio 1.12) (Gong, 2022).

What APOE4 does not come with is its own ApoB number. No study has set one, and none splits 3/4 from 4/4. If someone tells you a 4/4 needs a lower ApoB, ask for the study. There isn't one.

What do the guidelines say?

  • National Lipid Association (2024): ApoB thresholds of 60, 70 and 90 mg/dL for very high, high, and borderline to intermediate heart risk (Soffer, 2024).
  • ACC/AHA (2018): an ApoB of 130 mg/dL or higher is a risk-enhancing factor (Grundy, 2018).
  • ACC/AHA (2026): ApoB is used to assess remaining risk after the LDL-C and non-HDL-C goals are met.

These are heart lines. None came from carrier data.

Why did Phoenix choose under 60?

I chose under 60 for every carrier because it is the lowest line in the National Lipid Association's consensus, and because a carrier's arteries count every year.

Two findings drive it. In the trials, each 39 mg/dL (1 mmol/L) of LDL-C lowering cut major heart and stroke events by about a fifth, with no threshold found (CTT Collaboration, 2010). And Mendelian randomization, which uses the gene variants people are born with, shows that lifelong lower LDL-C brings 54.5% less coronary heart disease per 39 mg/dL, three times the benefit of the same drop started later with a statin (Ference, 2012). Lower, and earlier, wins for the heart.

The brain case is weaker, and I say so plainly: gene studies of the statin, ezetimibe and APOB targets found no effect on Alzheimer's risk (Williams, 2020). The solid reason to keep ApoB low is your heart, and a carrier's heart deserves the strictest line on the table.

Under 70 would pair exactly with the LDL-C goal of under 70. I chose the stricter 60 and Phoenix labels it as a choice everywhere it appears.

I carry APOE4/4, and under 60 is my own goal too. I am not there yet (my numbers are below).

How do you get ApoB tested?

Ask for "apolipoprotein B" (apoB) by name. Many standard lipid panels leave it out.

You do not need to fast. In 33,391 people, ApoB did not change after normal meals (Langsted, 2008).

Labs report ApoB in mg/dL or g/L. Divide mg/dL by 100 to get g/L: 60 mg/dL is 0.60 g/L. Check the unit beside your result before you compare it with the table.

What moves ApoB?

Medicines move ApoB the most. Food and weight move it by single digits to the low teens. Most trials report LDL-C rather than ApoB, so the numbers below are LDL-C unless marked ApoB. Ranked by size of effect:

  1. PCSK9 inhibitors: about 50 to 60% lower. Evolocumab on top of a statin cut LDL-C by 59%, from 92 to 30 mg/dL (Sabatine, 2017). Inclisiran, injected twice a year after two starting doses, cut it by about 50% (Ray, 2020).
  2. Statins: 30 to 50% or more. High-intensity statins lower LDL-C by 50% or more, moderate-intensity by 30 to 49% (Grundy, 2018). They work just as well in carriers (Zintzaras, 2009).
  3. Ezetimibe: about 23% lower on top of a statin. In 18,144 patients, adding it brought LDL-C to 54 mg/dL against 70 with the statin alone (Cannon, 2015).
  4. Bempedoic acid: about 21 percentage points lower. In people who could not take statins, LDL-C fell 21 percentage points more than with placebo (Nissen, 2023).
  5. Psyllium fiber: ApoB down about 5 mg/dL. About 10 g a day lowered ApoB by 0.05 g/L and LDL-C by 13 mg/dL (Jovanovski, 2018).
  6. Plant sterols and stanols: 6 to 12% lower. The effect grows with dose up to about 3 g a day (Ras, 2014).
  7. Less saturated fat. A small LDL-C drop, and 21% fewer cardiovascular events in trials of two years or more (Hooper, 2020).
  8. Weight loss: about 1.3 mg/dL per kg. With diet and exercise, each kilogram lost lowered LDL-C by 1.28 mg/dL at 12 months (Hasan, 2020).
  9. Exercise on its own: mainly triglycerides. Aerobic exercise alone lowered triglycerides but not LDL-C; adding diet lowered both (Kelley, 2012).

One lever runs the wrong way for some carriers: low-carbohydrate diets raised LDL-C by about 6 mg/dL on average against low-fat diets (Mansoor, 2016), and far more in some people (see the keto question below).

What Phoenix members use, as logged in the app (as of 2 October 2026): statins (80 members), ezetimibe (65), berberine (38), psyllium (34) and PCSK9 inhibitors or similar injections (14). Among members who uploaded two or more ApoB results, those who have logged a lipid drug saw their ApoB fall by a median 10.5% between their first and latest test (36 members), against 4.0% for those who logged none (34 members). That comparison counts anyone who ever logged a drug, without checking that it started between the two tests.

How often should you retest?

Retest 4 to 12 weeks after any change, then every 3 to 12 months. That is the ACC/AHA schedule for lipid tests after starting or adjusting a lipid medicine or a lifestyle change (Grundy, 2018). Phoenix applies that lipid-panel schedule to ApoB.

What Phoenix members actually do: 152 of the 212 Phoenix members who uploaded blood work (72%, as of 2 October 2026) have tested more than once. For ApoB, the median span from first to latest test is 216 days, about seven months.

My numbers

I carry APOE4/4. Here is where my ApoB started and where it is now:

My numbers
WhenApoBBand
When I started115 mg/dLTalk to your doctor
8 June 202671 mg/dLMonitor

That is about 38% lower, out of the talk band and into Monitor. I made three changes close together: I moved to a Mediterranean-leaning diet with some keto experiments, took about 10 g of psyllium before meals, and added ezetimibe 10 mg, which was my single best lever. I added ezetimibe in spring 2025 and still take it. Because the changes overlapped, I cannot split the credit between them.

I am not under 60 yet. It is my goal, and I am still working on it. This is one carrier's result, not a promise of yours.

What Phoenix members' results show

Most carriers are not at target yet, and that includes me. Of 166 Phoenix members who uploaded an ApoB result (as of 2 October 2026), 17 (10%) have a latest value under 60, 79 (48%) sit between 60 and under 90, and 70 (42%) are at 90 or higher. The median is 85 mg/dL. Members with two copies of APOE4 look the same: 10% under 60 and 45% at 90 or higher (101 members).

The movement is real. Of 70 members who tested ApoB more than once, the median result fell from 91.9 to 82 mg/dL over a median of 216 days, and 19 (27%) moved to a better band. In the 476-member Phoenix Research Release 001, 28 of 59 repeat testers lowered their ApoB by 5% or more.

Two members from Release 001 show what a big move looks like:

  • Statins. An APOE3/4 woman in her 60s took her ApoB from 98 to 59 mg/dL (40% lower), on a stack built around a statin.
  • Ezetimibe plus psyllium. An APOE4/4 woman in her 60s went from 131 to 90 mg/dL (31% lower) in 133 days.

Both started other things in the same window, and the report lists every item in their stacks.

When should you talk to your doctor?

Talk to your doctor if your ApoB is 90 mg/dL (0.90 g/L) or higher. That is the National Lipid Association's line for borderline to intermediate risk. At 130 mg/dL or higher, the ACC/AHA guideline counts ApoB as a risk-enhancing factor, which strengthens the case for treatment (Grundy, 2018).

Between 60 and under 90, the result is worth working on. Bring it to your next appointment with your LDL-C, your family history and your other results, and ask when to repeat it.

If you already take a lipid-lowering medicine, keep it exactly as prescribed and bring any change to your doctor.

Questions carriers ask

Frequently asked questions.

What is a good ApoB for someone with APOE4?

Under 60 mg/dL (0.60 g/L) is Phoenix's target for every APOE4 carrier: the National Lipid Association's strictest line, applied to carriers as a deliberate choice (Soffer, 2024). Between 60 and under 90 is worth working on. At 90 mg/dL or higher, talk to your doctor at your next appointment.

Is ApoB under 60 a medical guideline?

It is a guideline line used as a Phoenix choice. The National Lipid Association sets 60 mg/dL for people at very high heart risk (Soffer, 2024). APOE4 carriers are not a guideline risk group, so applying it to every carrier is Phoenix's decision. The guideline line for talking to your doctor is 90 mg/dL or higher. If your doctor sets a different goal, follow your doctor.

Do APOE4 carriers with two copies need a lower ApoB?

No study shows that. APOE4 raises LDL cholesterol one copy at a time, and ε4/ε4 runs about 44 mg/dL higher LDL-C than ε2/ε2 (Bennet, 2007). But no study has set an ApoB target by genotype, so "under 70 for 3/4, under 60 for 4/4" has no evidence behind it. Phoenix uses one number for every carrier: under 60 mg/dL.

Should I test ApoB or LDL-C?

Test both. LDL-C is the main goal in the 2026 ACC/AHA guideline, and ApoB counts the particles that damage arteries: heart risk falls in step with ApoB, whatever lowers it (Ference, 2019). If your LDL-C looks fine and your ApoB is high, take that gap to your doctor. Phoenix's optimal lines are ApoB under 60 and LDL-C under 70.

Does lowering ApoB lower Alzheimer's risk?

For your heart, yes, and that is proven. For your brain, the data split. Higher ApoB and LDL-C go with more dementia in large cohorts (Gong, 2022; Iwagami, 2021), but gene studies of statin and ezetimibe targets found no effect on Alzheimer's risk (Williams, 2020). Phoenix keeps ApoB low for the heart, which is reason enough, and treats any brain benefit as a bonus still to be proven.

Do statins work for APOE4 carriers?

Yes. In a meta-analysis by APOE genotype, statins lowered total cholesterol by 25.1% in ε4 carriers and 25.3% in ε3/ε3, with no difference in LDL-C response (Zintzaras, 2009). On the brain side, a 2025 meta-analysis of 170 studies found statins were one of four factors whose link with dementia was stronger in carriers than in non-carriers (Huang, 2025). Whether a statin fits you is a decision for you and your doctor, based on your overall risk.

Is ApoB under 60 too low for the brain?

The trial data say no. Your brain makes its own cholesterol: it holds about 23% of the body's cholesterol and builds it locally (Dietschy, 2004). In a trial that took LDL-C to a median of 30 mg/dL, thinking and memory did not differ from placebo over 19 months (Giugliano, 2017), and executive function held steady over a further 5 years on the drug at a median LDL-C of 35 mg/dL (Zimerman, 2025). In 13,481 genotyped patients, 28% of them ε4 carriers, the drug did not harm cognition in carriers (Korthauer, 2022).

Does keto raise ApoB?

It can. On average, low-carbohydrate diets raised LDL-C by about 6 mg/dL compared with low-fat diets (Mansoor, 2016). Some people see far bigger jumps: one 2026 report describes three people whose LDL-C reached 364 to 682 mg/dL on a ketogenic diet and fell substantially when they added back some carbohydrate (Lechner, 2026). If you start keto, retest ApoB 4 to 12 weeks later and judge the diet by your own number.

What if my result is exactly 60 or exactly 90?

The line belongs to the higher band. 60 mg/dL is Monitor, because "under 60" excludes 60. 90 mg/dL is Talk to your doctor, because "90 or higher" includes 90. The same applies in g/L: 0.60 is Monitor and 0.90 is Talk to your doctor. Phoenix uses this rule for every marker, and exact-line results are common because many labs report ApoB as a whole number.

Sources

  1. Soffer, National Lipid Association apoB consensus, J Clin Lipidol 2024. Role of apolipoprotein B in the clinical management of cardiovascular risk in adults: An Expert Clinical Consensus from the National Lipid Association.
  2. 2026 ACC/AHA dyslipidemia guideline, JACC (Circulation). 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.
  3. Grundy, 2018 ACC/AHA cholesterol guideline, Circulation. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.
  4. Bennet, JAMA 2007. Association of apolipoprotein E genotypes with lipid levels and coronary risk.
  5. Iwagami, Lancet Healthy Longev 2021. Blood cholesterol and risk of dementia in more than 1·8 million people over two decades: a retrospective cohort study.
  6. Gong, EClinicalMedicine 2022. Serum lipid traits and the risk of dementia: A cohort study of 254,575 women and 214,891 men in the UK Biobank.
  7. Williams, Ann Neurol 2020. Lipid lowering and Alzheimer disease risk: A mendelian randomization study.
  8. Huang, J Neurol 2025. The role of APOE ε4 in modulating the relationship between non-genetic risk factors and dementia: a system review and meta-analysis.
  9. Ference, JAMA 2019. Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease.
  10. Ference, J Am Coll Cardiol 2012. Effect of long-term exposure to lower low-density lipoprotein cholesterol beginning early in life on the risk of coronary heart disease: a Mendelian randomization analysis.
  11. Cholesterol Treatment Trialists' (CTT) Collaboration, Lancet 2010. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials.
  12. Langsted, Circulation 2008. Fasting and nonfasting lipid levels: influence of normal food intake on lipids, lipoproteins, apolipoproteins, and cardiovascular risk prediction.
  13. Sabatine, N Engl J Med 2017 (FOURIER). Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease.
  14. Ray, N Engl J Med 2020 (ORION-10 and -11). Two Phase 3 Trials of Inclisiran in Patients with Elevated LDL Cholesterol.
  15. Zintzaras, Pharmacogenomics J 2009. APOE gene polymorphisms and response to statin therapy.
  16. Cannon, N Engl J Med 2015 (IMPROVE-IT). Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes.
  17. Nissen, N Engl J Med 2023 (CLEAR Outcomes). Bempedoic Acid and Cardiovascular Outcomes in Statin-Intolerant Patients.
  18. Jovanovski, Am J Clin Nutr 2018. Effect of psyllium (Plantago ovata) fiber on LDL cholesterol and alternative lipid targets, non-HDL cholesterol and apolipoprotein B: a systematic review and meta-analysis of randomized controlled trials.
  19. Ras, Br J Nutr 2014. LDL-cholesterol-lowering effect of plant sterols and stanols across different dose ranges: a meta-analysis of randomised controlled studies.
  20. Hooper, Cochrane Database Syst Rev 2020. Reduction in saturated fat intake for cardiovascular disease.
  21. Hasan, J Clin Endocrinol Metab 2020. Weight Loss and Serum Lipids in Overweight and Obese Adults: A Systematic Review and Meta-Analysis.
  22. Kelley, Clin Nutr 2012. Comparison of aerobic exercise, diet or both on lipids and lipoproteins in adults: a meta-analysis of randomized controlled trials.
  23. Mansoor, Br J Nutr 2016. Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials.
  24. Lechner, J Clin Lipidol 2026. Severe diet-induced hypercholesterolemia mimicking familial hypercholesterolemia in atypical lean mass hyper-responders on ketogenic diets: A case series.
  25. Dietschy, J Lipid Res 2004. Thematic review series: brain Lipids. Cholesterol metabolism in the central nervous system during early development and in the mature animal.
  26. Giugliano, N Engl J Med 2017 (EBBINGHAUS). Cognitive Function in a Randomized Trial of Evolocumab.
  27. Zimerman, NEJM Evid 2025. Long-Term Cognitive Safety of Achieving Very Low LDL Cholesterol with Evolocumab.
  28. Korthauer, PLoS One 2022. No association between APOE genotype and lipid lowering with cognitive function in a randomized controlled trial of evolocumab.