Endocrine Abstracts

Background: Consumption of a high-meat, low carbohydrate diet in late pregnancy is associated with fetal growth restriction, and raised blood pressure and glucose intolerance in the offspring. In a recent study in Motherwell, Scotland, where pregnant women had been advised to eat one pound (0.45 kg) of red meat per day during pregnancy and to avoid carbohydrate-rich foods, we found elevated fasting plasma cortisol levels in men and women whose mothers reported higher protein consumption in pregnancy. We aimed to test whether this form of abnormal maternal nutrition (increasingly observed because of the popularity of the Atkins diet) reflects an enhanced stress response by measuring the response to a psychological stress test (The Trier Social Stress Test (TSST)).

Methods: We carried out the TSST (3 min mental arithmetic test and 5 min public speaking test) on 86 men and women born in Motherwell during 1967–68. Ethical approval and written informed consent were obtained. Blood pressure was recorded, and saliva and venous blood sampled for cortisol measurement before and after each stressor.

Results: BP and heart rate rose in response to stress (BP by 14 mmHg, t=−4.5, P<0.0001; HR by 6 bpm, t=−2.35, P=0.02) and fell to baseline values by the end of the recovery period. Plasma cortisol also rose in response to stress (men 371 to 478 nmol/l, t=-5.1, P=0.00002; women 348 to 380 nmol/l, t=−2.2, P=0.03). Between early and late pregnancy, meat consumption almost doubled while carbohydrate intake fell to a third. Offspring of mothers who reported greater meat intake during late pregnancy had greatest cortisol response to stress (P=0.03).

Conclusions: The TSST is a robust method in our hands demonstrating significant changes in BP, heart rate and cortisol in response to stress. Although the specific advice given to mothers in this study precludes direct application to other populations this is the first evidence that an unbalanced maternal diet during late pregnancy influences stress responsiveness in the offspring. These findings add to increasing evidence that adverse maternal factors program lifelong effects in the offspring.