Studies have indicated that prenatal caffeine intake of 300mg/day or more in women, which is approximately 2 to 3 cups of coffee per day, can result in lower birth weights of their children.
Animal studies have further suggested that prenatal caffeine consumption may have more detrimental long-term effects on liver development with an increased susceptibility to non-alcoholic fatty liver disease, a debilitating condition normally associated with obesity and diabetes. However, the underlying link between prenatal caffeine exposure and impaired liver development remains poorly understood. A good understanding of how caffeine mediates these effects can help to prevent health issues in people in the future.
Prof Hui Wang and colleagues at Wuhan University in China, investigated the effects of low (equivalent to 2-3 cups of coffee) and high doses (equivalent of 6-9 cups of coffee) caffeine, given to pregnant rats, on liver function and hormone levels of their offspring. Offspring exposed to prenatal caffeine had lower levels of the liver hormone, insulin like growth factor (IGF-1), and higher levels of the stress hormone, corticosteroid at birth.
However, liver development after birth showed a compensatory 'catch up' phase, characterized by increased levels of IGF-1, which is important for growth.
Results indicates that prenatal caffeine causes an excess of stress hormone activity in the mother, which inhibits IGF-1 activity for liver development before birth. However, compensatory mechanisms do occur after birth to accelerate growth and restore normal liver function, as IGF-1 activity increases and stress hormone signalling decreases. The increased risk of fatty liver disease caused by prenatal caffeine exposure is most likely a consequence of this enhanced, compensatory postnatal IGF-1 activity.
Findings confirms that prenatal caffeine exposure leads to a lower birth weight and impaired liver development before birth but also expand the current understanding of the hormonal changes underlying these changes and suggest potential mechanism for increased risk of liver disease in the future.
Category(s):Child Development
Source material from Science Daily
