China: A new study shows a strong correlation between tobacco exposure early in life, whether in the womb or during childhood and adolescence and type 2 diabetes (T2D) development later in life. The large-scale observational analysis extracted records of about 476,000 adults in the UK Biobank.
Researchers report that people with preexisting genetic factors for T2D face an even higher risk if they smoke. They say that adopting a healthy lifestyle later in life helps reduce the risk.

The data only shows correlation and not causation, however, it adds to the body of evidence that correlates tobacco exposure with poor health – specifically for those who are exposed early in life.
The findings were presented at the annual American Heart Association’s Epidemiology and Prevention/Lifestyle and Cardiometabolic Scientific Sessions in Chicago and have not yet been published in a peer-reviewed journal.
Tobacco exposure in adulthood is a well-established risk factor for type 2 diabetes, but there is no clarity on how early--life tobacco exposure implicates T2D development and whether this association varies by different genetic predispositions to T2D. Addressing these gaps may provide novel insights into early interventions of T2D.
Xuanwei Jiang and Victor W. Zhong from Shanghai Jiao Tong Univ in Shanghai, China, hypothesized that tobacco exposure in utero and utero and childhood/adolescence stages was associated significantly with incident T2D in adulthood and there were significant interactions and joint effects between early-life tobacco exposure and genetic risk for type 2 diabetes about risk of T2D.
In the prospective cohort study, the researchers used data from the UK Biobank. Self-reported questionnaires determined in-utero tobacco exposure and age of smoking initiation [never smoking, childhood (5-14 years), adolescence (15-17 years), and adulthood (≥18 years)]
The associations of tobacco exposure in utero and childhood/adolescence stages with incident T2D were estimated by multivariable Cox proportional hazard models. A polygenic risk score (PRS) for T2D was divided into tertiles, and assessed the interactions and joint effects between early-life tobacco exposure and genetic susceptibility on T2D development. The study included 475,957 participants without T2D at baseline.
The study led to the following findings:
During a median follow-up time of 14.6 years, 23,480 incident T2D events occurred.
Tobacco exposure in utero vs no exposure was significantly associated with incident T2D (hazard ratio [HR], 1.22).
Compared with never smoking, smoking initiation in childhood (HR, 2.19), adolescence (HR, 1.57), and adulthood (HR, 1.33) were significantly associated with incident T2D.
Additive interactions were observed between tobacco exposure in utero or childhood/adolescence stages and PRS for T2D.
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), a 639% higher risk of developing T2D when starting smoking in childhood (HR, 7.39), and a 427% higher risk when starting smoking in adolescence (HR, 5.27).
In conclusion, in utero tobacco exposure was significantly associated with incident type 2 diabetes. Earlier smoking initiation compared to later initiation was more strongly associated with incident T2D.
"The risk of type 2 diabetes was jointly determined by the early-life tobacco exposure and genetic predisposition to T2D," the researchers wrote.
Reference:
https://www.abstractsonline.com/pp8/#!/20343/presentation/114