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High tierMendelian RandomizationCitation verified

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

Brian A Ference, Wonsuk Yoo, Issa Alesh, John M Flack - Journal of the American College of Cardiology, 2012

Using nine genetic variants as a proxy for lifelong lower LDL, the study found that long-term exposure to lower LDL beginning early in life was associated with roughly a 54.5% lower risk of coronary heart disease per 1 mmol/L - about three times the per-unit benefit seen when statins are started later in life.

Key findings

Effect measures

  • Relative Risk Reduction: 54.5% lower CHD risk per 1 mmol/L (38.7 mg/dL) lower LDL-C95% CI 48.8% to 59.5%

Why this evidence tier (High)

Risk of bias:
Mendelian randomization reduces confounding and reverse causation by using randomly-allocated genotypes.
Precision:
Large combined sample (312k) and zero heterogeneity across instruments give high precision.
Directness:
Directly estimates the effect of lifelong lower LDL on CHD - though genetic lifelong exposure differs from a drug started in mid-life (canalization).
Consistency:
Strikingly consistent across nine independent variants.
Funding / COI:
See source disclosures.

High certainty for the causality inference; the main caveat is that lifelong genetic exposure is not the same as later pharmacologic lowering.

Population:
Pooled genetic-association data; primary combined analysis of 312,321 participants across prospective cohort and case-control studies.
Conflicts of interest:
Not reported on the fetched abstract; see full paper for disclosures.
Funding:
Not reported on the fetched abstract.

Limitations

  • MR limitations: potential pleiotropy, weak-instrument bias, predominantly European-ancestry samples.
  • Lifelong genetic exposure (canalization) is not directly comparable to drug therapy started later in life.

How this study is used