Ancestral Secondary Cases on Paternal and Maternal Sides in Bipolar Affective Illness

1978 ◽  
Vol 133 (1) ◽  
pp. 68-72 ◽  
Author(s):  
G. F. S. Johnson ◽  
M. M. Leeman

SummaryAn analysis of the distribution of ancestral secondary cases of affective illness in families of patients with bipolar manic-depressive disorder was undertaken. Twenty probands with at least two affectively ill second degree relatives were available for study. Probands with both parents affected were excluded. The distribution of unilateral to bilateral pairs of all affected relatives, both excluding and including parents, of probands showed no significant differences from that expected in polygenic inheritance. However, separation into bipolar family history, positive or negative, showed significant differences from the expected ratio of unilateral to bilateral pairs in a bipolar family history positive group consistent with a single dominant gene inheritance.

1970 ◽  
Vol 116 (535) ◽  
pp. 625-635 ◽  
Author(s):  
Remi J. Cadoret ◽  
George Winokur ◽  
Paula J. Clayton

During the past twenty years, the unity of manic-depressive disease as defined by Kraepelin (1913) has been questioned by investigators who have presented clinical and genetic evidence that the disease is heterogeneous and contains at least two discrete groups (Leonhard, 1957; Perris, 1966). In one of these groups mania occurs and patients exhibit both manic and depressive phases during the course of their illness. This group has been designated bipolar by most investigators (Leonhard, 1957; Perris, 1966). In the other group there are only episodes of depression, and this has been designated the unipolar group by some (Perris, 1966) and corresponds largely to the ‘monopolar’ group of Leonhard (1957). In this paper we shall use the term unipolar throughout to designate an affective illness in which only depression occurs.


1973 ◽  
Vol 122 (566) ◽  
pp. 31-34 ◽  
Author(s):  
Julien Mendlewicz ◽  
Ronald R. Fieve ◽  
John D. Rainer ◽  
Mima Cataldo

Recent family studies of manic-depressive psychosis have emphasized the role of genetics in the aetiology of this bipolar illness (3, 8). However, the mode of genetic transmission is still unknown, the main controversy being between major gene and polygenic inheritance. Furthermore, it is not yet evident whether bipolar illness constitutes a homogeneous entity or whether it may be subdivided into different genetic subgroups. Mendlewicz, Fieve, Rainer, and Fleiss (1) recently produced some evidence that bipolar psychosis can be differentiated into two subgroups on the basis of family history data. Two matched samples of 30 patients each were studied, distinguished by the presence or absence of bipolar illness in their first degree relatives. The patients with a positive family history (FH+) in first degree relatives showed earlier onset of illness and more psychotic symptoms occurring in the manic phase. Alcoholism, if present, was of an episodic pattern. In patients with a negative family history (FH—), there was a later onset of illness; psychotic symptoms occurred usually in the depressive phase; and alcoholism, when present, tended to be chronic.


1977 ◽  
Vol 131 (5) ◽  
pp. 478-485 ◽  
Author(s):  
Olga Trzebiatowska-Trzeciak

The mode of inheritance of affective psychoses was studied in 800 first degree and 582 second degree relatives of 122 probands. Morbidity risk for unipolar depression was 12·0±3·2 and 11·4±2·7 per cent respectively for parents and siblings of probands suffering from unipolar depression. Morbidity risk for manic-depressive psychosis for the respective groups of first degree relatives of manic-depressive probands was 15·1±3·2 and 16·9±3·2 per cent. In second degree relatives the morbidity risk was 3·4±1·0 and 5·3±1·4 per cent for unipolar depression and manic-depressive psychosis respectively.The results indicate the role of genetical factors in the etiology of both types of affective disorder and show that unipolar depression and manic-depressive psychosis are distinct entities. The hypothesis of X-linked dominant transmission was not confirmed in either of these affective disorders. By means of the computational model of Slater, no results compatible with a polygenic inheritance of unipolar depression or manic-depressive psychosis were found.


1972 ◽  
Vol 120 (554) ◽  
pp. 91-94 ◽  
Author(s):  
Michael S. Mccabe ◽  
Richard C. Fowler ◽  
Remi J. Cadoret ◽  
George Winokur

In 1966 Slater proposed a computational model for distinguishing polygenic inheritance and the effects of a single dominant gene. For a single dominant gene with diminished penetrance, affected relatives should be found predominantly on either maternal or paternal sides. He further proposed that to support a dominant gene hypothesis the ratio of unilaterally ill pairs to bilaterally ill pairs of relatives should exceed 2:1. ‘Unilateral pairs' means that there have been two or more ill relatives on either paternal or maternal sides; ‘bilateral pairs' that there has been at least one ill relative on each side.


1980 ◽  
Vol 137 (4) ◽  
pp. 337-342 ◽  
Author(s):  
J. Mendlewicz ◽  
P. Linkowski ◽  
J. Wilmotte

SummaryHeredity has been shown to be an important factor in the aetiology of manic-depressive psychosis. Recent linkage studies with colour blindness have suggested the presence of an X-linked dominant gene in the transmission of manic-depressive psychosis. We report here positive evidence of a linkage between manic-depressive psychosis and glucose-6-phosphate dehydrogenase deficiency in an informative family assorting for both traits. These results strengthen previous linkage studies in affective illness and support the hypothesis of X-linkage in a subgroup of manic-depressive psychosis.


HortScience ◽  
1998 ◽  
Vol 33 (3) ◽  
pp. 534b-534
Author(s):  
James D. McCreight

Yellowing of melon (Cucumis melo L.) incited by lettuce infectious yellows virus (LIYV) reduces yield and fruit quality of infected plants. LIYV is transmitted only by the sweetpotato whitefly (Bemisia tabaci Genn.). Two naturally infected field tests indicated several potential sources of resistance to LIYV. PI 124112 and `Snake Melon' had mild symptoms in both field tests whereas PI 313970 was asymptomatic in the test in which it was included. In greenhouse tests using controlled inoculation, PI 313970 was asymptomatic, had negative ELISA assays for LIYV, and was negative for LIYV in serial transfers to Chenopodium. `Top Mark' and `PMR 5' were symptomatic, had positive ELISA assays for LIYV, and were positive for LIYV in serial transfers to Chenopodium in these greenhouse tests. Limited data indicate that resistance in PI 313970 is conditioned by a single, dominant gene.


1986 ◽  
Vol 149 (2) ◽  
pp. 191-201 ◽  
Author(s):  
Robert M. Post ◽  
David R. Rubinow ◽  
James C. Ballenger

Few biological theories of manic-depressive illness have focused on the longitudinal course of affective dysfunction and the mechanisms underlying its often recurrent and progressive course. The authors discuss two models for the development of progressive behavioural dysfunction—behavioural sensitisation and electrophysiological kindling—as they provide clues to important clinical and biological variables relevant to sensitisation in affective illness. The role of environmental context and conditioning in mediating behavioural and biochemical aspects of this sensitisation is emphasised. The sensitisation models provide a conceptual approach to previously inexplicable clinical phenomena in the longitudinal course of affective illness and may provide a bridge between psychoanalytic/psychosocial and neurobiological formulations of manic-depressive illness.


2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110166
Author(s):  
Yuan Wang ◽  
Hua Gao ◽  
Wen Di ◽  
Zhuowei Gu

Objective We aimed to investigate whether patients with polycystic ovary syndrome (PCOS) and a family history (FH) of type 2 diabetes mellitus (T2DM) are at increased risk of endocrinological and metabolic abnormalities, and whether this risk differs between first-degree and second-degree relatives, and between maternal and paternal transmission. Methods A total of 680 patients with PCOS were enrolled in this retrospective, single-center study. Endocrine and glycolipid metabolism parameters were compared. Results The free androgen index (FAI), and levels of fasting blood glucose (FBG), fasting insulin (FINS), homeostatic model assessment-insulin resistance (HOMA-IR), total cholesterol (TC), and low-density lipoprotein cholesterol were significantly higher, whereas sex hormone binding globulin (SHBG) levels were significantly lower in patients with PCOS and a FH of T2DM. In patients with PCOS with a FH of T2DM in first-degree relatives, age and levels of FBG, FINS, and HOMA-IR were significantly higher than those who had a FH of T2DM in second-degree relatives. A maternal history of T2DM was associated with a higher body mass index, FAI, and TG levels, and lower SHBG levels. Conclusions Patients with PCOS and a FH of T2DM have more severe hyperandrogenism and metabolic disorders, especially in those with maternal transmission.


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