Shorter Telomeres & Obesity Association Found in Children
A study published in Scientific Reports examined nearly 1,400 mother-child pairs from a multi-centre European birth cohort and found that childhood obesity was associated with shorter telomeres. Telomere length is a useful biomarker of biological ageing, as shorter telomeres are associated with a wide range of diseases. These encompass cancer, premature ageing, and obesity.
Obesity in England affects 16% of 2-15 year olds, whereas adult obesity climbs to 28.7% of the population. Obesity classes as having a Body Mass Index (BMI) of 30 or above and is associated with an average 3-year reduction in life span, along with increased risk of cancer, heart disease and type 2 diabetes.
The study examined the link between obesity and leukocyte telomer length (LTL) in childhood. Using the HELIX European birth cohort study 1,396 mother-child pairs were recruited. Pre-pregnancy BMI of the mothers was recorded along with the BMI, fat mass, waist circumference, and skinfold thickness of the children (aged between 6-11). The associations between these parameters – termed adiposity markers – and telomere length was then examined.
Examining telomere length in childhood can be predictive of life expectancy. The rate of loss can help determine the telomere length in adults and the risk of developing certain diseases that are associated with this.
Shorter telomere length in children was associated with all the adiposity markers. The researchers estimate that with each increase in their scale of obesity markers corresponds to a loss of 2-3 years of life in children. Maternal BMI also had an affect on child telomere length, but not as strongly.
Telomeres are repeated sequences at the end of chromosomes that protect the ends during cell replication – a cap to prevent unravelling. However, during cell replication an end bit of DNA is lost, around 20 bp each time. The repeated sequences that make up telomeres mean no useful information is degraded – at least for some time. It also serves as a ‘stop’ signal, once a critical length is reached it signals that the cell should stop replicating or it will die.
The idea of lengthening telomeres to prevent ageing and disease is a promising one. However, most of our cells are not actively replicating and are in standby. The restarting of active division and avoidance of ageing is a characteristic of cancer cells. Many cancers have high levels of a telomere lengthening enzyme called telomerase. High activity of telomerase leads to functional immortality for these cells and research is in fact aimed at switching this enzyme off, rather than restoring it to the rest of our cells.
Although no mechanistic link between obesity and shorter telomeres was found, the fact that shorter telomeres are associated with an increased risk of developing chronic diseases in adulthood must be considered. Also, which factor influences the other needs to be discovered as this provides a target and direction for further research.