Embryonic caffeine exposure acts via A1 adenosine receptors to alter adult cardiac function and DNA methylation in mice.
Level 5 - mechanism / opinion, no new human data
Animal study evaluating prenatal caffeine exposure in mice
PubMed 24475304 · doi:10.1371/journal.pone.0087547
What was done
Pregnant wild-type (A1AR+/+) and A1AR knockout mice were administered caffeine (20 mg/kg, stated to yield serum levels equivalent to 2-4 cups of coffee in humans) or vehicle (0.09% NaCl) via intraperitoneal injection at embryonic day 8.5. Offspring were assessed at 8-10 weeks of age for body weight, cardiac morphology and function using echocardiography, and cardiac epigenetic modifications using DNA methylation arrays.
What was found
In A1AR+/+ adult offspring exposed in utero to caffeine, body weight was 10% heavier than vehicle controls. Cardiac output decreased by 11% and left ventricular wall thickness during diastole increased by 29%. DNA methylation arrays showed a 26% overall decrease in DNA methylation with 7719 differentially methylated regions, many located in genes associated with cardiac hypertrophy.
Why it matters
This study provides mechanistic evidence that prenatal caffeine exposure can alter adult cardiac structure and function through A1 adenosine receptor-mediated epigenetic modifications in mice.
Limits
The study is limited to a mouse model using a single-dose intraperitoneal administration at one embryonic time point, which may not reflect chronic oral human consumption. The abstract does not report the sample size (n), variance or confidence intervals, p-values, or the specific numerical values for the A1AR knockout offspring.
Cited by
- supports Animal studies show that maternal caffeine consumption during pregnancy causes smaller offspring, altered cardiac development, and delayed fetal brain growth.