Medicine is built on population averages. You aren’t average.

A "normal" lab range is just what's typical for a reference population. It may not mean optimal for you.

Meet MayaIllustrative example

Healthy, active, no family history

Maya is 34, a product designer in Brooklyn, and runs three days a week. Her last physical came back with the line most people get: "Cholesterol looks fine, see you next year."

Maya, smiling, seated by a window in a grey sweater.

Maya, 34

  • LDL-C118 mg/dL
  • hsCRP0.6 mg/L
  • HbA1c5.2%

Not on a typical panel

  • ApoB98 mg/dL
  • Lp(a)12 nmol/L
  • FH variantsNone
  • Coronary disease PRS93rd pct
Her genome

Her genome puts her in the top 7% for heart disease risk

Maya's polygenic risk score for coronary disease, a number built from thousands of inherited variants, came back high.

She carries about three times the coronary disease risk of everyone else, the same as if she had familial hypercholesterolemia, a condition that doctors treat early and aggressively.1

93rd

Lower risk

Average

Higher risk

Every year of high LDL adds up

Standard Target< 130

118mg/dL

Lab report flags nothing.

“Cholesterol looks fine”

High genetic risk responds most to lowering LDL

In primary prevention trials, people in the top fifth of coronary polygenic risk score cut their risk 46% on a statin compared to 26% for everyone else.2

According to the American Heart Association, both single-gene conditions and polygenic risk scores predict greater benefit from statins.3

Top 20% polygenic risk46% reduction
3.6 pts
Everyone else26% reduction
1.3 pts
024
Absolute reduction in coronary events from statin therapy, by genetic risk. WOSCOPS, ASCOT and JUPITER trials, 48,421 people.2

Risk tracks the area under the curve

Across 200 studies and 2 million people, LDL causes heart disease in proportion to how high it is and how long it stays there.4 Exposure in your 20s and 30s counts for more than the same exposure later.5

Beyond the guideline. Backed by the evidence

Today's guidelines put a patient in the high-risk category for a single-gene cholesterol condition.6 A high polygenic risk score carries about the same risk,1 but Maya wouldn't qualify.

SONATA categorizes her as high risk. Her target is below 70.

CategoryWho qualifies under the guidelineLDL Goal
NormalA low 10-year risk scoreunder 130a
Borderline / Intermediate riskAn elevated 10-year risk scoreunder 100b
High riskFamilial hypercholesterolemia, a single-gene conditionunder 70b

a The top of a typical lab reference range.b 2026 ACC/AHA dyslipidemia guideline.6

Her plan

Clear next steps

Maya's SONATA doctor walks her through the plan, explains her genetic risk and what her biomarkers mean, and prescribes what she needs.

Priority 1

A daily statin

  • adjustRosuvastatin 10mg1 capsule daily

    Her doctor prescribes Rosuvastatin 10 mg, taken daily. Expected to lower her LDL by about 45%, from 118 to the mid 60s.

Priority 2

A shift in diet

  • continueModified Mediterranean DietNutrition

    A Mediterranean diet is recommended. It's associated with about half the cardiovascular risk over 30 years.7

Ongoing

A care plan that evolves with her

  • At six months, she retests. LDL and ApoB to see whether the statin is working, liver and muscle enzymes to check it isn't causing side effects.
  • If her LDL is still above 70, her doctor adds ezetimibe.
  • If she wants a closer look, her doctor can order a coronary calcium scan earlier than guidelines call for.
The Difference

Found at 34. Half the risk of a heart attack or stroke by 64

With SONATA, Maya avoids about 1,500 mg/dL-years of exposure by age 64. Based on population data, that difference corresponds to roughly half the risk of a heart attack or stroke.5

Maya with her eyes closed, face tilted toward the light.

~50%

lower cardiovascular risk by age 64

Derived from Domanski et al., JACC 20205

Find out what in range means for you

Whole genome, 140+ biomarkers, pace of aging, and a care team that sets your targets from your biology.

Keep reading

See other examples

Sources

  1. Khera AV, et al. Genome-wide polygenic scores for common diseases identify individuals with risk equivalent to monogenic mutations. Nat Genet. 2018;50:1219–1224.
  2. Natarajan P, et al. Polygenic risk score identifies subgroup with higher burden of atherosclerosis and greater benefit from statin therapy in the primary prevention setting. Circulation. 2017;135:2091–2101.
  3. O'Sullivan JW, et al. Polygenic risk scores for cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2022;146:e93–e118.
  4. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. Consensus statement from the European Atherosclerosis Society. Eur Heart J. 2017;38:2459–2472.
  5. Domanski MJ, et al. Time course of LDL cholesterol exposure and cardiovascular disease event risk. J Am Coll Cardiol. 2020;76:1507–1516.
  6. 2026 ACC/AHA/Multisociety Guideline on the Management of Dyslipidemia. Circulation. 2026.
  7. Choi Y, et al. Plant-centered diet and risk of incident cardiovascular disease during young to middle adulthood. J Am Heart Assoc. 2021;10:e020718.

*Maya is an illustrative example, not a real member. Targets and prescriptions on this page show how SONATA physicians may reason; your own targets are set by your doctor from your results, history, and goals. This page is not medical advice.

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