According to the Journal of the American Heart Association research online publication on June 15, inhibiting the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) gene directly, as opposed to via a transgenic animal model and comparing it to placebo treatment, heightened the risk of cataract.

A team of researchers led by Copenhagen University Hospital’s Jonas Ghouse, M.D., Ph.D., assessed the link between genetically controlled inhibition of HMGCR and cataract development.

A weighted genetic score was determined based on the five most prevalent variants in the HMGCR gene and their relationship to low-density lipoprotein (LDL) cholesterol.

Investigation of genome sequencing data and the link between cataract surgery and cataract were used to identify carriers of anticipated loss-of-function transformations in HMGCR.

In a study of more than 402,000 people, the researchers realized that a 38.7 mg/dL decline in LDL cholesterol by the genome score of HMGCR was linked to a heightened risk of cataract surgery and cataract.

An infrequent HMGCR predicted loss-of-function variation was found in 32 out of the total 169,172 people (0.02%). Heterozygous couriers of HMGCR foresaw loss-of-function variations had an elevated cataract development risk and subsequent cataract surgery when compared to noncarriers of developing cataract and undergoing cataract surgery than noncarriers.

“We established a relationship between genetic variations that imitate HMGCR inhibition and cataracts development,” Ghouse stated. “We were unable to establish any relationship between non-statin, fat-reducing drugs, and cataract risk, so this outcome seems to be unique to statins.”

One writer had a monetary connection to the pharmaceutical sector.

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