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Susanne M. Clee (ORCID 0000-0001-7946-688X, University of British Columbia) has a bibliometric profile indicating substantial, sustained scientific impact: 79 indexed works, ~6,869 cumulative citations, and an h-index of 36 (OpenAlex, as of October 2026). Her citation record is dominated by two landmark findings, both with her listed at University of British Columbia.

Landmark contributions

Her most-cited work is the 1999 Nature Genetics paper identifying mutations in ABC1 (ABCA1) as the cause of Tangier disease and familial HDL deficiency (1,706 citations) Nature Genetics ABCA1 discovery. A companion Lancet paper on ABCA1 mutations in familial HDL deficiency with defective cholesterol efflux adds 352 citations Lancet familial HDL deficiency paper. She then translated this into human genetics: as first author she characterized ABCA1 heterozygotes in JCI (314 citations) and tested common ABCA1 variation against CAD risk in Circulation (291 citations) ABCA1 heterozygote JCI studyABCA1 common-variant CAD study. Transgenic mouse work showing increased ABCA1 activity protects against atherosclerosis (JCI, ~250–470 combined citations across duplicate records) ABCA1 transgenic atherosclerosis study and an observational Lancet study linking impaired ABCA1 efflux to arterial-wall thickening round out the ABCA1 program Arterial wall thickness and ABCA1 efflux.

Second career phase: metabolic genetics and neuroscience

A first-author review, The Genetic Landscape of Type 2 Diabetes in Mice (Endocrine Reviews, 220 citations), signals deep expertise in mouse diabetes genetics Mouse T2D genetics review. As senior-group collaborator she contributed to the influential Cell Metabolism study showing hyperinsulinemia drives diet-induced obesity (498 citations) Hyperinsulinemia-obesity Cell Metabolism paper and a Nature Neuroscience paper on insulin-induced synaptic plasticity in VTA dopamine neurons (240 citations) Insulin endocannabinoid VTA study.

Citation trajectory

The spike in 1999 reflects the ABCA1 discovery era; sustained citations through 2012–2015 reflect the diabetes/metabolism work. Output has been sparse since 2019 (1–2 works), so current productivity cannot be verified from these data.

Blind spots and limitations

• OpenAlex counts may double-count duplicate records (e.g., the 2002 JCI paper appears twice), inflating totals modestly.
• Most landmark work is middle-author; independent scientific leadership is clearest in the 2000–2007 first-author and review papers.
• Human ABCA1 common-variant associations from 2001 predate GWAS; effect sizes from candidate-gene era studies often shrink in larger meta-analyses — a caveat the field recognizes.
• Key mechanistic claims (hyperinsulinemia-obesity causality) rest on mouse models; species translation to humans remains contested.

Bottom line: Clee's record shows a genuine, field-defining discovery contribution (ABCA1), strong first-author follow-through in human genetics, and a successful pivot to metabolic physiology — a high-impact, verifiable career. Confidence: moderate-to-high; based solely on OpenAlex metadata, not full-text review of all 79 works.

 BGPT Author Review

Scientific Quality

Clee co-authored the ABCA1/Tangier disease discovery—one of the defining gene identifications in lipid biology—and followed through with first-author human genetics and a comprehensive mouse T2D genetics review. h-index 36 and ~6,900 citations confirm durable impact. Points off: landmark work was collaborative (middle author), recent output is thin, and era-specific candidate-gene associations carry replication risk.

Communication Quality

Her Endocrine Reviews synthesis (381 references) demonstrates strong ability to organize a complex field. High-profile journal publications suggest clear writing, but no direct full-text assessment of her prose was possible from available metadata, so this estimate carries uncertainty.

Author Novelty

Identifying ABCA1 as the Tangier disease gene was genuinely groundbreaking, opening the reverse cholesterol transport field. The later diabetes genetics and hyperinsulinemia work is novel but builds on existing frameworks rather than opening new fields.

Scientific Rigor

Genetic evidence spans human pedigrees, association studies, and transgenic mouse causality—a strong triangulation strategy. Deductions for candidate-gene era methodology predating GWAS standards, observational (non-causal) IMT findings, and mouse-model translational limits in the hyperinsulinemia work.