Life-Course Influence of Adolescent Behaviour Problems on Type 2 Diabetes in Midlife: Results from 1958 British Birth Cohort Study

Abstract

Purpose

To assess whether there is a long-term relationship between childhood behaviour problems and type 2 diabetes in midlife. The study will also investigate whether any of such relationship is independent of other factors which may be associated with type 2 diabetes.

Design

Cohort study.

Participants

A total of 9377 members of the 1958 British birth cohort participated in the biomedical survey at age 45 years. The cohort has been followed up at regular intervals in childhood (age 7, 11 and 16 years) and adulthood (23, 33, 42 and 45 years).

Predictor Variables

Information regarding childhood behaviour collected during follow-ups at ages 7, 11 and 16 years.

Main Outcome Variables

Type 2 diabetes assessed using HbA1c at age 45 years.

Results

Unadjusted estimates show that teachers reported adolescent behaviour problems at age of 16 are associated with increased risk of type 2 diabetes in midlife. After adjustment for potential confounders and mediators in childhood and adulthood, a relationship was observed between the severity of adolescent behaviour problems and type 2 diabetes risk in midlife (mild behaviour problems: OR 2.17, 95% CI 1.11–4.23; severe behaviour problems: OR 4.40, 95% CI 1.14–16.99). However, no such relationship was observed between behaviour problems at 7 and 11 years and type 2 diabetes in midlife.

Conclusion

There is an association between adolescent behaviour problems and an increased risk of type 2 diabetes in midlife. Further molecular/genetic studies are required to understand the biological basis for this observed association.

Keywords:

• type 2 diabetes
• adolescent behaviour problems
• 1958 British birth cohort
• National Child Development Study
• HbA1c

Highlights

• This study demonstrated that childhood behaviour problems are associated with an increased risk of type 2 diabetes in midlife.

• Further molecular/genetic studies are required to understand the biological basis for this observed association.

Acknowledgments

No funding received. The abstract of this paper was presented at the ‘27th European Diabetes Congress, June 20-21, 2018 Rome, Italy’ as a poster presentation with interim findings. The poster’s abstract was published in “Poster Abstracts” in J Diabetes Metabolism: https://eur03.safelinks.protection.outlook.com/?url=https%3A%2F%2Fwww.omicsonline.org%2Fconference-proceedings%2Feuro-diabetes-2018-posters-accepted-abstracts.digital%2Findex.html%2310&data=04%7C01%7CMusa.Ibrahim%40study.beds.ac.uk%7C8d433b63c20146857a2908d8e0d9301c%7C3133dbdc3c644bdaa66a751445a19275%7C1%7C0%7C637506570702041461%7CUnknown%7CTWFpbGZsb3d8eyJWIjoiMC4wLjAwMDAiLCJQIjoiV2luMzIiLCJBTiI6Ik1haWwiLCJXVCI6Mn0%3D%7C1000&sdata=9WbpH3GT0Vsbi06XQqTfL%2FFfJAmSIHWkX%2Be597hFAWQ%3D&reserved=0

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that they have no competing interests.