Is smoking linked to abdominal obesity?

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Previously, Mendelian randomization (MR) studies person explored nan causal narration betwixt smoking and abdominal obesity utilizing a azygous familial version for smoking heaviness. Similarly, a recent Addiction study uses aggregate familial instruments to estimate nan causal narration betwixt smoking and abdominal obesity.

Study: Estimating causality betwixt smoking and abdominal obesity by Mendelian randomization. Image Credit: kong-photo / Shutterstock.com

How does smoking impact obesity?

Smoking leads to respective chronic disorders, peculiarly cardiovascular and respiratory diseases. In fact, smokers often person much abdominal fat arsenic compared to non-smokers, which further increases their consequence of cardiometabolic diseases.

It remains unclear whether nan relation betwixt assemblage fat distribution and smoking is causal. Genetic variants associated pinch vulnerability traits person been utilized arsenic instrumental variables by MR studies to measure this perchance causal relationship. MR is akin to a people randomized controlled proceedings as, during conception, paternal and maternal alleles are randomly allocated.

Previously, MR studies person explored nan causal narration betwixt nan heaviness of smoking and abdominal obesity utilizing a azygous familial variant. Two studies noted nary causal relationship, whereas a 3rd suggested a causal nexus betwixt nan number of cigarettes smoked each time and nan waist-hip ratio (WHR), moreover aft controlling for nan assemblage wide scale (BMI). 

About nan study

The existent causal study utilizing summary effect estimates (CAUSE) study progressive two-sample MR analyses to quantify nan effect of smoking initiation, heaviness, and life-time smoking connected abdominal adiposity. To this end, genome-wide relation studies (GWAS) summary statistic were obtained from nan GWAS and Sequencing Consortium of Alcohol and Nicotine Use (GSCAN), United Kingdom Biobank, and Genetic Investigation of Anthropometric Traits (GIANT) Consortium.

All study participants were of European ancestry. Exposure traits included smoking initiation, heaviness, and life smoking were used, whereas result traits including WHR, arsenic good arsenic waist and hep circumferences (WC and HC) were used. The result traits were considered pinch and without accommodation for BMI.

Study findings

Lifetime smoking and smoking initiation causally accrued abdominal adiposity, independent of socio-economic status, intoxicant consumption, and different factors. Visceral fat aliases visceral adipose insubstantial (VAT) accrued much than abdominal subcutaneous fat (ASAT).

The causal narration betwixt abdominal fat and smoking heaviness could not beryllium established. However, reverse causality analyses indicated that smoking heaviness could beryllium accrued causally by abdominal adiposity.

Previous studies person utilized a azygous familial version successful nan CHRNA3/5 locus to found causality betwixt abdominal adiposity and smoking heaviness, some of which did not place a causal narration betwixt these 2 factors. The Wald ratio estimates for nan CHRNA3/5 locus successful nan existent study observed causal effects; however, upon instrumenting smoking heaviness pinch each known familial loci, this effect was not present. 

Consistent pinch erstwhile studies, two-sample MR analyses pinch 13 smoking heaviness variants showed antagonistic causality betwixt BMI and smoking heaviness owed to nan CHRNA3/5 locus. Moreover, LHC-MR and CAUSE study grounded to found causality betwixt little BMI and smoking heaviness, frankincense suggesting a pleiotropic effect of nan CHRNA3/5 locus connected BMI and smoking heaviness, alternatively than a causal effect.

Smoking could lead to higher abdominal fat by expanding ASAT aliases visceral fat. The results for magnetic resonance imaging (MRI)-based adipose depot volumes suggested accrued VAT to beryllium chiefly responsible for higher abdominal adiposity, alternatively than ASAT, which is accordant pinch nan findings successful existing research.

Conclusions

Lifetime smoking and smoking initiation whitethorn causally lead to higher abdominal and peculiarly visceral fat. Thus, nationalist wellness efforts to trim and forestall smoking could assistance successful lowering abdominal fat and nan associated consequence of chronic illnesses.

The strengths of nan existent study see nan exertion of different complementary MR methods and sensitivity analyses, arsenic good arsenic nan usage of large-scale GWAS summary-level information to trim reverse causality, sample overlap, and pleiotropic effects.

The main limitation of nan coming study involves nan beingness of residual pleiotropic effects and their power connected causal estimates. These effects could not beryllium wholly removed, contempt performing aggregate sensitivity analyses.

Additionally, successful nan sub-sample of existent smokers, nan sample size for assemblage fat distribution was small. This restricted nan statistical powerfulness of nan study of smoking heaviness. Another limitation progressive nan inability to measure nan effect of smoking cessation connected assemblage fat distribution.

Importantly, cigarettes picture unstandardized baccy doses, which could person had a non-negligible effect connected nan accuracy of nan estimates for smoking heaviness. Furthermore, nan study population, which was restricted to individuals of European familial ancestry, limits nan generalizability of nan study findings to different divers populations.

Journal reference:

  • Carrasquilla, G. D., Garcia-Urena, M., Romero-Lado, M. J., & Kilpelainen, T. O. (2024). Estimating causality betwixt smoking and abdominal obesity by Mendelian randomization. Addiction. doi:10.1111/add.16454