Smokers may have more belly fat – particularly visceral fat – than non-smokers, even if they tend to generally have lower body weight than non-smokers, research suggests.
Visceral fat is the fat that surrounds the internal organs in the abdomen and is linked to a higher risk of heart disease, diabetes, stroke and dementia.
However, this can be hard to see, as a person can have a flat stomach yet still carry unhealthy amounts of visceral fat, raising the risk of serious illness.
The study, published in the journal Addiction, found that both starting smoking and lifetime smoking may increase visceral fat.
The Independent reports that the team, at the University of Copenhagen’s NNF Centre for Basic Metabolic Research, looked at data from European ancestry studies involving 1.2m people who started smoking, and more than 450 000 lifetime smokers.
They also looked at data from a body fat distribution study, which included more than 600 000 people, along with information on their waist-to-hip ratio and waist and hip circumference.
They used a form of statistical analysis called Mendelian randomisation to determine whether smoking causes an increase in abdominal fat using genetic information.
Lead author Dr Germán Carrasquilla said: “This study found that starting to smoke and smoking over a lifetime might cause an increase in belly fat, as seen by measurements of waist-to-hip ratio.
“In a further analysis, we also found that the type of fat that increases is more likely the visceral fat, rather than the fat just under the skin.”
He said the influence of smoking on belly fat seems to happen regardless of other factors, like socio-economic status, alcohol use, attention deficit hyperactivity disorder (ADHD) or how much of a risk-taker someone is.
“From a public health point of view, these findings reinforce the importance of large-scale efforts to prevent and reduce smoking in the general population, as this may also help to reduce abdominal visceral fat and all of the chronic diseases linked to it.
“Reducing one major health risk in the population will, indirectly, reduce another major health risk.”
Meanwhile, another study suggests tobacco exposure before birth and beginning smoking during childhood or adolescence is associated with the development of type 2 diabetes later in life.
The preliminary findings, presented at the American Heart Association’s Epidemiology and Prevention: Lifestyle and Cardiometabolic Scientific Sessions 2024 conference, are based on data from almost 476 000 adults in the UK Biobank, which holds medical and lifestyle records of half a million Britons.
Researchers found those who started smoking in childhood had double the risk of type 2 diabetes compared with those who had never smoked, while people who started smoking as adolescents had a 57% higher risk and those who started smoking during adulthood had a 33% increased risk.
Study 1 details
Estimating causality between smoking and abdominal obesity by Mendelian randomisation
Germán Carrasquilla, Mario García-Ureña, María Romero-Lado, Tuomas Kilpeläinen
Published in Addiction on 20 March 2024
Abstract
Smokers tend to have a lower body weight than non-smokers, but also more abdominal fat. It remains unclear whether or not the relationship between smoking and abdominal obesity is causal. Previous Mendelian randomization (MR) studies have investigated this relationship by relying upon a single genetic variant for smoking heaviness. This approach is sensitive to pleiotropic effects and may produce imprecise causal estimates. We aimed to estimate causality between smoking and abdominal obesity using multiple genetic instruments.
Design
MR study using causal analysis using summary effect estimates (CAUSE) and latent heritable confounder MR (LHC-MR) methods that instrument smoking using genome-wide data, and also two-sample MR (2SMR) methods.
Setting
Genome-wide association studies (GWAS) summary statistics from participants of European ancestry, obtained from the GWAS and Sequencing Consortium of Alcohol and Nicotine use (GSCAN), Genetic Investigation of Anthropometric Traits (GIANT) Consortium and the UK Biobank.
Participants
We used GWAS results for smoking initiation (n = 1 232 091), life-time smoking (n = 462 690) and smoking heaviness (n = 337 334) as exposure traits, and waist–hip ratio (WHR) and waist and hip circumferences (WC and HC) (n up to 697 734), with and without adjustment for body mass index (adjBMI), as outcome traits.
Measurements
Smoking initiation, life-time smoking, smoking heaviness, WHR, WC, HC, WHRadjBMI, WCadjBMI and HCadjBMI.
Findings
Both CAUSE and LHC-MR indicated a positive causal effect of smoking initiation on WHR (0.13 [95% confidence interval (CI) = 0.10, 0.16 and 0.49 (0.41, 0.57), respectively] and WHRadjBMI (0.07 (0.03, 0.10) and 0.31 (0.26, 0.37). Similarly, they indicated a positive causal effect of life-time smoking on WHR [0.35 (0.29, 0.41) and 0.44 (0.38, 0.51)] and WHRadjBMI [0.18 (0.13, 0.24) and 0.26 (0.20, 0.31)]. In follow-up analyses, smoking particularly increased visceral fat. There was no evidence of a mediating role by cortisol or sex hormones.
Conclusions
Smoking initiation and higher life-time smoking may lead to increased abdominal fat distribution. The increase in abdominal fat due to smoking is characterized by an increase in visceral fat. Thus, efforts to prevent and cease smoking can have the added benefit of reducing abdominal fat.
Study 2 details
Early-Life Tobacco Exposure, Genetic Risk, and Incident Type 2 Diabetes
Xuanwei Jiang, Victor W. Zhong, Shanghai Jiao Tong Univ, Shanghai, China
Presented at AHA EPI 2024 on 20 March 2024
Abstract
Introduction
Tobacco exposure in adulthood is a well-established risk factor for type 2 diabetes (T2D), but how early-life tobacco exposure implicates in the development of T2D as well as whether this association varies by different genetic predisposition to T2D are unclear. Addressing these gaps may provide novel insights into early interventions of T2D.
Hypothesis
We hypothesised that tobacco exposure in utero and childhood/adolescence stages was significantly associated with incident T2D in adulthood and there were significant interactions and joint effects between early-life tobacco exposure and genetic risk for T2D in relation to risk of T2D.
Methods
This prospective cohort study used data from the UK Biobank. In utero tobacco exposure and age of smoking initiation [never smoking, childhood (5-14 years), adolescence (15-17 years), and adulthood (≥18 years)] were assessed through self-reported questionnaires. Multivariable Cox proportional hazard models, adjusted for demographics and early-life factors, were used to estimate the associations of tobacco exposure in utero and childhood/adolescence stages with incident T2D. A polygenic risk score (PRS) for T2D divided into tertiles was used to assess the interactions and joint effects between early-life tobacco exposure and genetic susceptibility on the development of T2D.
Results
A total of 475,957 participants without T2D at baseline were included. During a median follow-up time of 14.6 years (IQR, 13.7-15.3), 23,480 incident T2D events occurred. Tobacco exposure in utero vs no exposure was significantly associated with incident T2D (hazard ratio [HR], 1.22 [95% CI, 1.18-1.26]). Compared with never smoking, smoking initiation in childhood (HR, 2.19 [95% CI, 2.08-2.29]), adolescence (HR, 1.57 [95% CI, 1.51-1.62]), and adulthood (HR, 1.33 [95% CI, 1.28-1.38]) were significantly associated with incident T2D (P for trend <0.001). Additive interactions were observed between tobacco exposure in utero or childhood/adolescence stages and PRS for T2D (relative excess risk due to interaction >0, P interaction <0.001). Compared with participants having no early-life tobacco exposure and a low PRS, those with a high PRS had a 330% higher risk of developing T2D when exposed to tobacco in utero (HR, 4.30 [95% CI, 4.07-4.54]), a 639% higher risk of developing T2D when starting smoking in childhood (HR, 7.39 [95% CI, 6.84-7.99]), and a 427% higher risk when starting smoking in adolescence (HR, 5.27 [95% CI, 4.95-5.62]).
Conclusions
In utero tobacco exposure was significantly associated with incident T2D. Earlier smoking initiation was more strongly associated with incident T2D than later initiation. Early-life tobacco exposure and genetic predisposition to T2D interacted and jointly determined risk of T2D.
The Independent article – Study finds another surprise consequence of smoking (Open access)
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