Objective
Recent reports from our laboratory and others suggest that the menopausal transition may represent a window of vulnerability for eating disorders in women. Here, we present new findings ...regarding this issue.
Methods
We surveyed 230 women aged 40–60 years using an anonymous questionnaire focused on eating-disorder and body-image symptomatology. We then compared groups of respondents based on (a) menopausal stage as assessed by World Health Organization (WHO) criteria and (b) menopausal symptomatology as assessed by the Menopause Rating Scale (MRS).
Results
WHO-defined menopausal stage (premenopausal, perimenopausal, and postmenopausal) showed no significant associations with eating and body-image measures. However, MRS scores showed strong associations with most measures of the Eating Disorder Examination Questionnaire, as well as with questions regarding satisfaction with body image. These associations remained little changed even when removing the four psychological items from the MRS score and examining only the association of the MRS somato-vegetative and urogenital items with these outcome variables.
Discussion
Our data augment existing evidence that the menopausal transition may be associated with eating and body-image disturbances. However, reported menopausal
stage
, which is difficult to define reliably, may be less informative than menopausal
symptoms
as a predictor of disordered eating and associated symptoms.
Level of evidence
V—descriptive survey study.
A high prevalence of mental disorders following COVID-19 has been described. It is therefore essential to elucidate underlying biological mechanisms linking SARS-CoV-2 infection and mental health. ...The kynurenine and catecholamine metabolic pathways are modulated by inflammation and can affect systemic levels of serotonin and dopamine. Their activity may hence link physical disorders with mental health. We investigated factors that affect kynurenine and catecholamine pathway activity in SARS-CoV-2 infection and recovery.
The cross-sectional SIMMUN (n = 165) and longitudinal INCOV cohort (n = 167, Su et al. 2022) were analyzed. Demographic and clinical characteristic, inflammatory markers, SARS-CoV-2 infection, symptoms of depression and anxiety (HADS), and mental stress (PSS-4) served as explanatory variables. Blood serotonin and markers of kynurenine (kynurenine/tryptophan ratio), and catecholamine pathway activity (dopamine 3-O-sulfate, phenylalanine/tyrosine ratio) were modeled by multi-parameter linear regression.
In the SIMMUN cohort, the inflammatory marker neopterin (β = 0.47 95% CI: 0.34–0.61), SARS-CoV-2-positivity (0.42 0.16–0.68), mental stress (0.18 0.055–0.31), and age (0.26 0.12-0.39) were positively associated with the kynurenine/tryptophan ratio. The phenylalanine/tyrosine ratio was lower in SARS-CoV-2-positive than uninfected participants (−0.38 −0.68 to −0.08). In the INCOV cohort, markers of inflammation were associated with lower serotonin (IL6: −0.22 −0.38 to −0.053) and dopamine 3-O-sulfate levels (interferon-gamma: −0.15 −0.26 to −0.036). Serotonin (0.76 0.34–1.2) and dopamine 3-O-sulfate levels (0.63 0.28–0.99) were higher during recovery than in acute SARS-CoV-2 infection.
SARS-CoV-2 infection, inflammation, age and mental stress are key independent predictors of kynurenine pathway activity, which may influence serotonin availability. The catecholamine pathway was also affected in SARS-CoV-2 infection. Altered activity of these pathways may contribute to impaired mental health following COVID-19.
•Mental health impairment is common following COVID-19.•Kynurenine and catecholamine pathway activity might be the pathophysiological link.•Data from two cohorts were analyzed using multi-parameter linear modeling.•Inflammation, SARS-CoV-2 infection, mental stress, age influence kynurenine/tryptophan.•Inflammation was associated with lower systemic serotonin and dopamine availability.
The first sentence of the results in the abstract section had been incorrectly published in the original publication. The complete correct result section is given below.
•A decrease in basal velocity was found at 0.4 mGy/h in 96hpf larvae.•The 0.4 mGy/h dose led to a decrease in the response to a tactile stimulus in larvae.•Embryos spontaneous movement and larvae ...heart rate were not affected by 3H exposure.•3H did not induce cataract phenotype nor DNA double-strand break in 24 hpf embryos.
Tritium (3H), a radioactive isotope of hydrogen, is ubiquitously present in the environment. In a previous study, we highlighted a mis-regulation of genes involved in muscle contraction, eye transparency and response to DNA damages after exposure of zebrafish embryo-larvae from 3 hpf to 96 hpf at 0.4 and 4 mGy/h of tritiated water (HTO). The present study aimed to link this gene mis-regulation to responses observed at higher biological levels. Analyses on spontaneous tail movement, locomotor activity and heart rate were performed. Histological sections of eyes were made to evaluate the impact of HTO on eye transparency and whole embryo immunostainings were realized to assess DNA double strand breaks repair using gamma-H2AX foci. We found a decrease of basal velocity as well as a decrease of response in 96 hpf larvae exposed at 0.4 mGy/h after a tactile stimulus as compared to controls. Histological sections of larvae eyes performed after the exposure to 4 mGy/h did not show obvious differences in lens transparency or retinal development between contaminated and control organisms. Gamma-H2AX foci detection revealed no differences in the number of foci between contaminated organisms and controls, for both dose rates. Overall, results highlighted more detrimental effects of HTO exposure on locomotor behavior in 96 hpf larvae exposed at the lowest dose rate. Those results could be linked to mis-regulation of genes involved in muscle contraction found in a previous study at the same dose rate. It appears that not all effects found at the molecular scale were confirmed using higher biological scales. These results could be due to a delay between gene expression modulation and the onset of physiological disruption or homeostatic mechanisms to deal with tritium effects. However, crossing data from different scales highlighted new pathways to explore, i.e. neurotoxic pathways, for better understanding HTO effects on organisms.
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