Stress and Recurrent Miscarriage

Our current understanding into the role of stress in unexplained recurrent miscarriages comes from two different research strategies. The majority of research has examined the role of psychological support within this patient population. This support has been provided in a number of ways ranging from weekly interviews with a psychiatrist or gynaecologist and/or visual re-assurance in the form of ultrasound scans. A comparison of psychological support with an absence of such intervention has found differences in successful pregnancy outcome varying from as great as 84 versus 26%, respectively. It has been assumed that psychological support reduces the miscarriage rate by reducing “stress” within this patient population. In addition it provides indirect support for a role of stress in the aetiology of unexplained recurrent miscarriage. Other studies have attempted to directly assess the effect of personality characteristics on miscarriage rate; these studies have yielded conflicting results. The mechanism by which stress may be causal in the aetiology of unexplained recurrent miscarriage has not been examined in humans. Animal studies, however, have found that psychological distress can alter immune parameters that may be intricately involved with implantation. These parameters include an elevation of the “abortive” cytokine TNF-$aL and a reduction in the “anti-abortive” cytokine TGF-β2. Cells that are involved in the release of TNF-$aL at the feto-maternal interface include T cells, macrophages and mast cells. Mechanisms through which stress may act on these cells are explored and an integrated model is postulated.

[1]  L. Regan,et al.  Psychiatric morbidity among patients with recurrent miscarriage , 2002, Journal of psychosomatic obstetrics and gynaecology.

[2]  Toshikazu Nakamura,et al.  a-Adrenergic Regulation of Enzymes of Amino Acid Metabolism in Primary Cultures of Adult Rat Hepatocytes* , 2001 .

[3]  S. Fujii,et al.  Induction of tryptophan 2,3-dioxygenase in the mouse endometrium during implantation. , 2000, Biochemical and biophysical research communications.

[4]  D. Munn,et al.  Prevention of allogeneic fetal rejection by tryptophan catabolism. , 1998, Science.

[5]  T. Li Recurrent miscarriage: principles of management. , 1998, Human reproduction.

[6]  O. Dapunt,et al.  Spontaneous abortion and psychosomatics. A prospective study on the impact of psychological factors as a cause for recurrent spontaneous abortion. , 1997, Human reproduction.

[7]  L. Regan,et al.  Future pregnancy outcome in unexplained recurrent first trimester miscarriage. , 1997, Human reproduction.

[8]  P. Arck,et al.  Regulation of Abortion by γλ T Cells , 1997 .

[9]  Mark M. Davis,et al.  Issues concerning the nature of antigen recognition by αβ and γδ T-cell receptors , 1995 .

[10]  P. Arck,et al.  Stress-triggered abortion: inhibition of protective suppression and promotion of tumor necrosis factor-alpha (TNF-alpha) release as a mechanism triggering resorptions in mice. , 1995, American journal of reproductive immunology.

[11]  J. Brown,et al.  Substance P selectively activates TNF-alpha gene expression in murine mast cells. , 1993, Journal of immunology.

[12]  J. Holoshitz,et al.  Dual antigenic recognition by cloned human gamma delta T cells. , 1992, The Journal of clinical investigation.

[13]  N. Pattison,et al.  Recurrent Miscarriage ‐ Outcome After Supportive Care in Early Pregnancy , 1991, The Australian & New Zealand journal of obstetrics & gynaecology.

[14]  Milton W. Taylor,et al.  Relationship between interferon‐γ, indoleamine 2,3‐dioxygenase, and tryptophan catabolism , 1991, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[15]  S. Tonegawa,et al.  Recognition of MHC TL Gene Products by γδ T Cells , 1991, Immunological reviews.

[16]  G. Chaouat,et al.  Control of fetal survival in CBA x DBA/2 mice by lymphokine therapy. , 1990, Journal of reproduction and fertility.

[17]  R. Smith,et al.  Mood changes, obstetric experience and alterations in plasma cortisol, beta-endorphin and corticotrophin releasing hormone during pregnancy and the puerperium. , 1990, Journal of psychosomatic research.

[18]  J. S. Hunt,et al.  Cytokine networks in the uteroplacental unit: macrophages as pivotal regulatory cells. , 1989, Journal of reproductive immunology.

[19]  P. Braude,et al.  Influence of past reproductive performance on risk of spontaneous abortion. , 1989, BMJ.

[20]  R. Ader Conditioned immune responses: adrenocortical influences. , 1987, Progress in brain research.

[21]  B. Stray-Pedersen,et al.  Etiologic factors and subsequent reproductive performance in 195 couples with a prior history of habitual abortion. , 1984, American journal of obstetrics and gynecology.

[22]  A. Meier,et al.  Tryptophan feeding adversely influences pregnancy. , 1983, Life sciences.

[23]  T. Nakamura,et al.  alpha-Adrenergic regulation of enzymes of amino acid metabolism in primary cultures of adult rat hepatocytes. , 1983, The Journal of biological chemistry.

[24]  E. R. Grimm Psychological Investigation of Habitual Abortion , 1962, Psychosomatic medicine.

[25]  R. Weil,et al.  The problem of spontaneous abortion. IX. The treatment of habitual aborters by psychotherapy. , 1962, American journal of obstetrics and gynecology.

[26]  L. C. Stewart,et al.  The Problem of Spontaneous Abortion , 1957 .

[27]  P. Malpas A Study of Abortion Sequences , 1938 .

[28]  J. Holoshitz,et al.  Rapid Publication Dual Antigenic Recognition by Cloned Human yb T Cells , 2022 .