Evidence map›Paper›PMID 30445611›Full record

ArticleHuman molecular genetics2019

Causal effects of blood lipids on amyotrophic lateral sclerosis: a Mendelian randomization study.

Ping Zeng, Xiang Zhou

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 6 pooled it
9.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 6 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Two-step Mendelian randomization reveals a lipid-driven protective effect of type 2 diabetes on ALS.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Ping ZengDepartment of Epidemiology and Biostatistics, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Xiang ZhouDepartment of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · USXuzhou Medical College · CN

Funding

Statistical Methods for Modeling Polygenic Architecture in Association and Re-sequencing StudiesR01HG009124 · NHGRI · YALE UNIVERSITY · PI Xiang Zhou · 2017 to 2026
$3.0M
NHGRI NIH HHS R01 HG009124
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a late-onset fatal neurodegenerative disorder that is predicted to increase across the globe by ~70% in the following decades. Understanding the disease causal mechanism underlying ALS and identifying modifiable risks factors for ALS hold the key for the development of effective preventative and treatment strategies. Here, we investigate the causal effects of four blood lipid traits that include high-density lipoprotein, low-density lipoprotein (LDL), total cholesterol and triglycerides on the risk of ALS. By leveraging instrument variables from multiple large-scale genome-wide association studies in both European and East Asian populations, we carry out one of the largest and most comprehensive Mendelian randomization analyses performed to date on the causal relationship between lipids and ALS. Among the four lipids, we found that only LDL is causally associated with ALS and that higher LDL level increases the risk of ALS in both the European and East Asian populations. Specifically, the odds ratio of ALS per 1 standard deviation (i.e. 39.0 mg/dL) increase of LDL is estimated to be 1.14 [95% confidence interval (CI), 1.05-1.24; P = 1.38E-3] in the European population and 1.06 (95% CI, 1.00-1.12; P = 0.044) in the East Asian population. The identified causal relationship between LDL and ALS is robust with respect to the choice of statistical methods and is validated through extensive sensitivity analyses that guard against various model assumption violations. Our study provides important evidence supporting the causal role of higher LDL on increasing the risk of ALS, paving ways for the development of preventative strategies for reducing the disease burden of ALS across multiple nations.

Indexed as

Amyotrophic Lateral SclerosisCholesterolFemaleHumansLipidsLipoproteins, HDLLipoproteins, LDLMaleMendelian Randomization AnalysisPolymorphism, Single NucleotideTriglyceridesCholesterolLipidsLipoproteins, HDLLipoproteins, LDLTriglycerides

Identifiers

PMID30445611
PMCPMC6360326
OpenAlexW2952420414

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.