Anti-Saccharomyces cerevisiae antibodies (ASCA) are associated with body fat mass and systemic inflammation, but not with dietary yeast consumption: a cross-sectional study

Abstract

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.

Uric acid levels are independent of anti-Saccharomyces cerevisiae antibodies (ASCA) in Crohn’s disease: A reappraisal of the role of S. cerevisiae in this setting

“…[6] included subjects with excess of weight it is possible that this could be the origin of the correlations they observed. By contrast in a recent study investigating ASCA and the presence of S. cerevisiae in the diet, no association was found between yeast-containing foods and ASCA IgG-positivity, or between yeast-containing foods and fat mass [15]. Thus, our study does not support the ASCA-based hypothesis derived from studies in mice that S. cerevisiae could worsen colitis by affecting host purine metabolism leading to increased UA production.…”

“…Interestingly, it has recently been shown that, besides CD, ASCA may also be associated with other diseases such as autoimmune diseases, including celiac disease [14] or physiological disorders[15] . Regarding UA, the levels encountered in our cohorts were well within the normal range for males and females, and no differences were found between IBD patients and controls.…”

Risk factors associated with intestinal permeability in an adult population: A systematic review

“…High‐sensitivity C‐Reactive protein (hsCRP) was reported to have a weak positive correlation IP (Table ) with two studies also reporting that hsCRP correlates with IP as measured by zonulin ( β = 0.013; 95% CI: 0.003, 0.023; P = 0.015, β = 0.075; 95% CI: 0.008, 0.158; P = 0.046) (Table ). In contrast, another study reported CRP to be an independent risk factor for IP ( β = 3.28; 95% CI: 1.28, 5.46; P < 0.01) . Circulating interleukin‐6 (IL‐6) was reported to have a weak to moderate positive correlation with IP according to four studies ( r = 0.542; P < 0.001) .…”

“…Twenty‐four studies reported on 29 statistically significant biomarkers and association with altered IP . Two studies reported that fasting glucose had a weak positive correlation with IP (Table ).…”

“…Twenty-four studies reported on 29 statistically significant biomarkers and association with altered IP. 10,23,25,32,35,[40][41][42][43][44][50][51][52][53][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72] Two studies reported that fasting glucose had a weak positive correlation with IP 44,53 (Table 5). Moreover, an additional study reported that a plasma glucose level >5.7 nmol/L is associated with a greater odds of having altered IP (OR = 2.09; 95% CI: 2.09, 4.18; P = 0.036) in the general population 23 (Table 3).…”