Preeclampsia is a long-term cardiovascular risk factor for the mother and possibly the offspring. Preeclampsia and cardiovascular diseases share common pathophysiological features, including endothelial dysfunction. We explored whether endothelial function, measured noninvasively, as well as circulating biomarkers reflecting lipid metabolism, angiogenesis, and inflammation, differed in paired mothers and offspring 5 to 8 years after delivery. Twenty-six mother and child pairs after pregnancies complicated by preeclampsia were compared with 17 mother and child pairs after uncomplicated pregnancies. In addition, we assessed whether concentrations of maternal circulating biomarkers at delivery predicted findings 5 to 8 years postpartum. We also included an assessment of early onset preeclampsia and specifically addressed the effects of small for gestational age. Endothelial function was significantly reduced in both mothers and children after preeclampsia when combined with a small-for-gestational-age infant compared with mothers and children after pregnancies without a small-for-gestational-age infant (mothers: P<0.001; children: P<0.05). Postpartum maternal soluble fms-like tyrosine kinase 1 (P=0.05) and high-sensitivity C-reactive protein (P=0.02) were elevated in the preeclampsia group compared with controls. High concentrations of these maternal biomarkers both at delivery and 5 to 8 years postpartum were also more frequent in preeclampsia compared with controls (P<0.05). The novelty of our study is the parallel finding of reduced endothelial function in mother and child pairs 5 to 8 years after small-for-gestational-age preeclamptic pregnancies, accompanied by increased inflammatory and antiangiogenic maternal biomarkers. This finding supports the concept of transgenerational risk of cardiovascular disease after preeclampsia.

Preeclampsia is a pregnancy specific disorder and a risk factor for later cardiovascular disease. The cause and detailed pathophysiology remains unknown. G protein signaling is involved in a variety of physiological processes, including blood pressure regulation. We assessed whether distributions of 3 single nucleotide polymorphisms in genes coding for components of G protein signaling pathways that have been associated with hypertension differ between women with preeclampsia and normotensive pregnant women; the G protein β3 subunit gene ( GNB3 ) C825T polymorphism (rs5443), the angiotensin II type 1 receptor gene ( AGTR1 ) 3′UTR A1166C polymorphism (rs5186), and the regulator of G protein signaling 2 gene ( RGS2 ) 3′UTR C1114G polymorphism (rs4606). Two separate Norwegian study populations were used; a large population based study and a smaller, but clinically well-described pregnancy biobank. A descriptive study of 43 women with eclampsia was additionally included. In the population-based study, an increased odds of preeclampsia (odds ratio, 1.21; [95% confidence interval, 1.05–1.40]; P =0.009) and recurrent preeclampsia (odds ratio, 1.43; [95% confidence interval, 1.06–1.92];, P =0.017) was found in women carrying the rs4606 CG or GG genotype. In early-onset preeclamptic patients with decidual spiral artery biopsies available (n=24), the rs4606 CG or GG genotype was more frequent in those with acute atherosis (resembling early stage of atherosclerosis) compared with those without: odds ratio, 15.0; (95% confidence interval, 2.02–111.2); P =0.004. No association was found between preeclampsia and the rs5443 or the rs5186. The genotype distribution in eclamptic women was not different from preeclamptic women. In conclusion, RGS2 rs4606 may affect the risk and progression of preeclampsia.

This clinical study has identified several modifiable risk factors for cardiovascular disease in women and children 5-8 years after pregnancies complicated by preeclampsia or diabetes mellitus. Potential intervention strategies could focus on life style alterations after delivery, with emphasis on weight management.

BackgroundPreeclampsia is associated with an increased risk of hypertension later in life. The regulator of G protein signaling 2 negatively regulates several vasoconstrictors. We recently demonstrated an association between preeclampsia and the CG or GG genotype of the C1114G polymorphism (rs4606) of the regulator of G protein signaling 2 gene. Here, we examined the polymorphism with respect to the development of hypertension after pregnancy.MethodsWe genotyped 934 women on average 15.1 years after preeclampsia and 2011 age matched women with previous normotensive pregnancy. All women in this study were retrospectively recruited from the Nord-Trøndelag Health Study (HUNT2). Information from HUNT2 was linked to the Medical Birth Registry of Norway to identify women with a history of preeclampsia and women without a history of preeclampsia.ResultsNo significant association was found between hypertension (blood pressure ≥140/90 mmHg and/or taking antihypertensive drugs) and the polymorphism in crude analysis (OR (95% CI): CG genotype: 1.07 (0.90-1.27); GG genotype: 1.23 (0.90-1.67)). However, in a minimally adjusted model (age and BMI adjusted), a significant association between the GG genotype and hypertension was found (OR (95% CI): 1.49 (1.05-2.11)). This association remained significant also after adjustment for a history of preeclampsia (OR (95% CI): 1.46 (1.02-2.09)), but not in a model adjusted for multiple other variables (OR (95% CI): 1.26 (0.82-1.94)). In multivariate, but not in crude, analysis, the GG genotype of rs4606 (OR (95% CI): 1.93 (1.05-3.53)) was significantly and independently associated with severe hypertension later in life, defined as systolic blood pressure ≥160 mmHg (stage 2 hypertension) and/or taking antihypertensive drugs. A significant association was also found for the merged CG and GG genotypes (OR (95% CI): 1.43 (1.02-2.00)). Moreover, an interaction with physical activity was found. A history of preeclampsia was a significant and independent predictor of either definition of hypertension, both in crude and adjusted analyses.ConclusionWomen carrying the rs4606 CG or GG genotype are at elevated risk for developing hypertension after delivery. Physical activity may interact with the association. Preeclampsia remains an independent risk factor for subsequent hypertension after adjusting for this polymorphism and classical CVD risk factors.

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BackgroundBaker’s/brewer’s yeast, Saccharomyces cerevisiae, has been used as an alternative to antibiotic growth promoters to improve growth performance in animals. In humans, Saccharomyces cerevisiae is among the most commonly detected fungi in fecal samples and likely originates from food. Recently, an association between anti-Saccharomyces cerevisiae antibodies (ASCA) and obesity in humans was suggested, but the cause of the elevated ASCA levels is not clear. Our aim was to study ASCA in morbidly obese subjects and explore potential associations with anthropometrics, diet, co-morbidities and biomarkers of inflammation and gut permeability.MethodsSubjects with morbid obesity referred to a specialized hospital unit were included. Diet and clinical data were recorded with self-administered questionnaires. Main dietary sources of baker’s/brewer’s yeast (e.g. bread and beer) were used as a proxy for the intake of yeast. Laboratory analyses included ASCA, serum zonulin (reflecting gut permeability), C-reactive protein and a routine haematological and biochemical screening.ResultsOne-hundred-and-forty subjects; 109 (78%) female, 98 with dietary records, mean age 43 years and BMI 42 kg/m2 were included. The number of ASCA positive subjects was 31 (22%) for IgG, 4 (2.9%) for IgA and 3 (2.1%) for IgM. Age, body fat mass and C-reactive protein were significantly higher in IgG-positive compared to IgG-negative subjects (P < 0.05). A borderline significant association was found between elevated zonulin and ASCA IgG-positivity (P = 0.06). No association was found between yeast-containing food and ASCA IgG-positivity, or between yeast-containing food and fat mass.ConclusionsThe findings indicate that ASCA IgG-positivity may be linked to the generalized inflammation commonly seen with increased adiposity, but not to dietary yeast intake. Other potential causes for the raised ASCA IgG concentrations, such as genetic predisposition, deviations in the gut microbiota and cross-reactivity of ASCA with other antigens, were not explored.

BackgroundGastrointestinal (GI) co-morbidity is common in obese patients, but the effect of weight loss surgery on GI symptoms is incompletely elucidated. The aims of the present study were to explore changes in GI symptoms and food tolerance following weight loss surgery and to study whether such changes were associated with dietary modifications and/or the type of surgical procedure [Roux-en-Y Gastric Bypass (RYGB) versus Vertical Sleeve Gastrectomy (VSG)].MethodsParticipants: Patients with morbid obesity scheduled for weight loss surgery.The patients filled in paper-based questionnaires addressing diet, GI symptoms (bloating, pain, satiety, constipation and diarrhea) and food tolerance/quality of alimentation (satisfaction about current food intake, tolerance to specific foods and frequency of vomiting/regurgitation/reflux) 6 months prior to and 6 months after the surgery. Patients with pre-existing major GI co-morbidity or previous major GI surgery were excluded.ResultsFifty-four patients (RYGB/VSG: 43/11) were included. Constipation and satiety increased and food tolerance decreased significantly after the surgery (all p-values < 0.05). The increase in satiety was significantly more notable after VSG than after RYGB (p < 0.05).The increase in satiety also correlated with an overall reduction in food tolerance (rho: -0.488, p < 0.01). Divergent changes were seen in the frequency of vomiting/regurgitation/reflux, with a decline after RYGB (p = 0.01) and an increase after VSG (p = 0.06). Intakes of energy, macronutrients, fiber and fluid decreased significantly after the surgery (all p-values < 0.05), but did not correlate with the changes in constipation, satiety or food tolerance (all p-values > 0.05). Pre-operatively, total energy intake correlated with bloating and abdominal pain (rho = 0.343 and 0.310 respectively, p < 0.05 for both), but these correlations did not persist 6 months after the surgery (rho = 0.065 and 0.054 respectively, p > 0.05 for both).ConclusionA high caloric intake may explain some of the GI symptoms experienced by non-operated obese patients. The worsening or new-onset of symptoms post-surgery is likely due to anatomical or physiological alterations following surgery. The increase in satiety and the decrease in food tolerance are likely explained by the restrictive nature of the surgeries, as satiety increased more after VSG than after RYGB and correlated with an overall reduction in food tolerance.

Women with a history of diabetes mellitus (DM) or preeclampsia (PE) in pregnancy run an increased risk of future cardiovascular associated diseases. Offspring of such pregnancies may possibly also have an altered risk in health status. Descriptive studies of dietary intake and physical activity in mother and children several years after pregnancies complicated by PE or DM are lacking. By the use of a simple questionnaire survey, we aimed at exploring whether there are any differences in these lifestyle factors between women and between offspring 5-8 years after PE (23 women-child pairs) or DM (23 women-child pairs) in pregnancy, compared to uncomplicated pregnancies (controls, 17 women-child pairs). Our data showed that women in the DM- and PE-group were less physically active compared to controls (p < 0.01 and p < 0.05, respectively), and more children in the control-group followed the Norwegian fruit recommendations compared to children in the DM-group (p < 0.01).