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Experimental Biology and Medicine

Genetic analysis links hip and thigh fat to lower liver cancer odds

In FinnGen, genetically predicted hip and thigh fat, adjusted for body size, was associated with lower liver cancer odds, with an odds ratio of 0.444.

Paper by Hang Liu, Fuming Wang, Jinming Tian, +3 more authorsJijin Yang · Changhai Hospital
Figure 1 from Experimental Biology and Medicine
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Figure 1. Liu et al., CC BY

Our read

Mechanisms
Studied:
Mendelian randomization in individuals of European ancestry (Independent replication)
What changed:
Genetically predicted gluteofemoral adipose tissue was associated with lower hepatocellular carcinoma risk (OR = 0.444)
The catch:
Only 500 hepatocellular carcinoma cases were analyzed in the discovery dataset
Why it’s aging research:
A leading disease of aging, its risks or menopause.

Editor of record: Boris Djordjevic · AgingResearch.News

Paper
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The analysis used human genetic data from UK Biobank, FinnGen and the Million Veteran Program. Researchers used Mendelian randomization, a method that uses genetic differences to examine links between traits and disease. They studied scan-measured hip and thigh fat adjusted for height and body mass index, a measure of weight relative to height.

Genetically predicted fat in this region was linked to lower odds of hepatocellular carcinoma, a type of liver cancer. The association remained after accounting for other risk factors. It also appeared in the Million Veteran Program, with an odds ratio of 0.766; values below 1 indicate lower odds. The authors identified six blood fats as potential partial mediators, each estimated to account for 7.0%–15.4% of the association.

Why it matters

For research on metabolic health during aging, the study raises questions about how fat storage and blood fats may contribute to liver cancer beyond overall body size.

Caveats

This genetic analysis did not test whether deliberately changing fat distribution changes cancer risk. The abstract does not specify the fat increase represented by the odds ratios, and evidence for shared underlying genetic changes was limited.

From the paper

Result

In UVMR, genetically predicted GFATadj was inversely associated with HCC risk (IVW-OR = 0.444, 95% CI 0.294–0.669, P = 1.00 × 10, FDR-adjusted q = 3.00 × 10 ), whereas VATadj and ASATadj showed no significant associations ( Figure 2 ).

Primary MR analysis results

Limitation

While the Mendelian randomization framework strengthens causal inference compared to observational designs, it does not elucidate precise molecular mechanisms.

Discussion

Quoted word for word from the full text on ebm-journal.org.

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