Sickness in pregnancy and sex of child [Letter]

Karolinska Institutet, Сольна, Stockholm, Sweden
The Lancet (Impact Factor: 45.22). 01/2000; 354(9195):2053. DOI: 10.1016/S0140-6736(99)04239-7
Source: PubMed


We report a female predominance among the offspring of mothers with hyperemesis gravidarum.

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    • "However, it would not explain the fetal sex impact on maternal disgust sensitivity during pregnancy. The DS-R [29] has been criticized in previous research, mainly due to the overlap between core disgust and contamination disgust, and also due to exclusion of sexual and moral disgust [32] [44]. Sexual disgust evolved to avoid sexual partners and behaviors that would reduce one's long-term reproductive success [2], and moral disgust serve to avoid individuals who inflict social costs on oneself or members of one's social network [32]. "
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    ABSTRACT: Disgust, an emotion triggering behavioral avoidance of pathogens, serves as a first line of defense against infections. Since behavior related to disgust involves some cost, the aversive reaction should be adjusted to the level of an individual's immunocompetence, and raise only when immunological function is lower (e.g. during pregnancy). We studied changes in disgust sensitivity in pregnant women, and tested if disgust sensitivity is related to a fetus's sex. 92 women participated in a three-stage research, answering the Disgust Scale-Revised questionnaire at each trimester of pregnancy. The result showed that total disgust and disgust sensitivity in the Core Domain were the highest in the first trimester (when maternal immunosuppression is also the highest), and decreased during pregnancy in women bearing daughters. Women bearing sons had relatively high disgust sensitivity persisting in the first and in the second trimester. The elevation in disgust sensitivity during the second trimester for mothers bearing male fetus can be explained by the necessity to protect for a longer time, a more ecologically sensitive fetus, and also herself when bearing a more energetically costly sex. The proximate mechanism may involve the differences in maternal testosterone and cortisol concentrations in the second trimester of pregnancy.
    Physiology & Behavior 11/2014; 139. DOI:10.1016/j.physbeh.2014.11.032 · 2.98 Impact Factor
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    • "HCG HCG is often stated as the most likely cause of HG. This is because the highest incidences of HG occur at the time HCG has its peak level and because HG has a higher incidence in conditions said to be associated with elevated HCG levels, namely twin and molar pregnancies, pregnancies of female foetuses and those with down syndrome (Danzer et al., 1980; Goodwin et al., 1994; Askling et al., 1999; del Mar Melero-Montes and Jick, 2000; Basso and Olsen, 2001; Furneaux et al., 2001; James, 2001; Steier et al., 2004). How HCG could cause HG remains unclear, but proposed mechanisms include a stimulating effect on the secretory processes in the upper gastrointestinal tract (GIT) or by stimulation of thyroid function because of its structural similarity to thyroidstimulating hormone (TSH), as will be discussed below (Panesar, 1999; Hershman, 2004). "
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    ABSTRACT: Hyperemesis gravidarum (HG) is a condition causing severe nausea and vomiting in early pregnancy often resulting in hospital admission. The incidence of HG is approximately 0.5% of live births, said to be higher in multiple pregnancies, hydatidiform mole and other conditions associated with increased pregnancy hormone levels. Both the aetiology and pathogenesis of HG remain unknown. We conducted a literature review (1966-now) to summarize the current evidence on the aetiology and pathogenesis of HG. The potential role of pregnancy-related hormones such as progesterone, estrogen and HCG has been widely studied; however, various other hormones such as leptin, placental growth hormone, prolactin, thyroid and adrenal cortical hormones have been implicated in the aetiology of HG. In addition to endocrinological hypotheses, the rationale and evidence considering infectious, immunological, psychological, metabolic and anatomical causes for HG have been analysed here. Many studies suffer from the low number of patients included, the variable definition used for HG and varying assay methodology used in studies of hormone measurement. This review highlights the need for more extensive studies addressing the pathogenesis and aetiology of HG.
    Human Reproduction Update 09/2005; 11(5):527-39. DOI:10.1093/humupd/dmi021 · 10.17 Impact Factor
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    • "Thus, opposing effects on breast cancer risk by the different hormones seem unlikely. Hyperemesis has also been linked to reproductive history, twinning and to an altered sex ratio of the offspring (Askling et al, 1999; Eliakim et al, 2000), all of which could possibly affect breast cancer risk (Kelsey et al, 1993; Hsieh et al, 1999). All these factors were accounted for in our study, and adjustments had no marked impact on the estimates. "
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    ABSTRACT: Both parity and a young age at first pregnancy are associated with a reduction in breast cancer risk. The hormones involved in this process are not fully investigated. Human chorionic gonadotropin is a placental hormone, which in rats and in human breast cells in vitro has been shown to prevent against breast cancer. Hyperemesis, a severe nausea combined with vomiting during pregnancy, is associated with increased levels of human chorionic gonadotropin. We investigated the possible relationship between hyperemesis and subsequent breast cancer risk in a case–control study based on registry data. Among 13 079 breast cancer cases and 34 348 individually matched controls we found 148 cases and 405 controls who had been hospitalised for hyperemesis. Hyperemesis was not associated with breast cancer risk (adjusted odds ratio 1.05, 95% confidence interval 0.86–1.27), and similar risks were observed regardless of age at diagnosis, number of hospitalisations for hyperemesis or time of follow-up. Our results do not support the hypothesis that human chorionic gonadotropin is responsible for the protective effect of pregnancies upon breast cancer risk. British Journal of Cancer (2002) 87, 974–976. doi:10.1038/sj.bjc.6600605 © 2002 Cancer Research UK
    British Journal of Cancer 11/2002; 87(9):974-6. DOI:10.1038/sj.bjc.6600605 · 4.84 Impact Factor
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