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Depression, Bipolar (manic-depressive disorder)


Description:There is a strong association between Blood Type O and bipolar disease, verified by several independent research studies. Family studies have also demonstrated a higher incidence of genetically-transmitted bipolar disease. Research has also shown a strong association between Type O and unipolar disease, characterized by deep depression without mania.

Most investigators emphasize the importance of neurotransmitter substances such as the catecholamines, noradrenaline and adrenaline, in the pathogenesis of unipolar and bipolar depressive states. According to this hypothesis, depression is associated with a deficit in brain catecholamines, while mania may be due to an excess of catecholamines. High catecholamines in the manic state are in large part the result of high levels of activity of the dopamine beta hydroxylase. Conversely, the low levels of catecholamines in the depressed state are the result of lower levels of dopamine beta hydroxylase activity.

One other important aspect of the action of catecholamines in Type O is the role of the enzyme monoamine oxidase, or MAO. MAO is very important when it comes to emotions. Indeed, until the newer class of seritonin uptake modifers like Prozac came along, the most common kind of anti-depressants prescribed by conventional medicine were a class of drugs called MAO-inhibitors (Iprozid, Neuralex).

MAO comes in two forms-- MAO-A and MAO-B. MAO-A is found throughout the body, but especially in the GI tract, while MAO-B is found primarily in the brain. Both MAO-A and MAO-B metabolize dopamine into a variety of other compounds, and so blocking this enzyme has the effect of increasing dopamine concentrations. Platelet MAO is believed to be the peripheral marker for the central seritonin system. Low concentrations of this genetically determined marker may indicate vulnerability to psychopathology and certain behavioral disorders. Variations in both platelet MAO and dopamine beta hydroxylase have been associated with bi-polar illness.

Genetic transmission in manic depressive illness (MDI) has been explored in twins, adoption, association, and linkage studies. The X-linked transmission hypothesis has been tested by using several markers on chromosome X: Xg blood group, colour blindness, glucose-6-phosphate dehydrogenase (G6PD), factor IX (haemophilia B), and DNA probes such as DXS15, DXS52, F8C, ST14. The hypothesis of autosomal transmission has been tested by association studies with the O blood group located on chromosome 9, as well as linkage studies on chromosome 6 with the Human Leucocyte Antigens (HLA) haplotypes and on Chromosome 11 with DNA markers for the following genes: D2 dopamine receptor, tyrosinase, C-Harvey-Ras-A (HRAS) oncogene, insuline (ins), and tyrosine hydroxylase (TH). (1)

Results of the present study provide evidence of: 1) a positive association between bipolar affective disorder and blood type O and a corresponding negative association between the former and blood type A, 2) a positive association between unipolar affective disorder and blood type O, and 3) a positive association between involutional depression and blood type A and a corresponding negative association between the former and blood types B and O. Sex does not appear to modify the ABO blood types' distribution in patients with bipolar, unipolar affective disorder, or involutional depression, and the same holds for early- or late-onset of the illness in patients with bipolar or unipolar affective disorders. Findings in the present study do not support the validity of the bipolar-unipolar distinction of affective disorders, and provide evidence in favour of the view that involutional depression is a genetically distinct nosological entity.(2)

Distributions of seven blood groups (ABO, MNSs, P, Rh, Duffy, Kidd and Xg) were studied in a total of 118 Japanese patients with affective disorders. The patients were diagnosed according to the DSM-III: (1) Major Depression (= Unipolar Disorder, UP) (2) Bipolar Disorder (BP) and (3) Other Affective Disorders. The following results were found: (1) a high frequency of the B blood group in all patients with affective disorders compared with controls; (2) a high frequency of the Fy(a+b+) and a low frequency of the Fy(a+b-) in all patients with affective disorders, UP and BP compared with controls; (3) a low frequency of the Jk(a+b+) and a high frequency of the Jk(a+b-) in BP compared with controls and with UP. (3)

As a prerequisite for psychopharmacological studies in subgroups of psychiatric patients two approaches will be described: a. A multiaxial classification system for affective disorders (MULTI-CLAD). b. Studies of ABO- and HLA-systems in patients with affective disorders. In sixty-six manic-melancholic patients selected with this criteria, the differences between all patients combined versus controls were not significant, but a significantly higher percentage of bipolar patients (70%) than of unipolar patients (22%) had blood group O, while a significantly higher percentage of unipolar patients (65%) than of bipolar patients (23%) had blood group A. 2. The findings are in the process of further study involving some 300 patients from the Psychochemistry out-patient-clinic. The purpose is to see whether less selected groups of patients with affective disorders show less marked profiles for ABO and HLA, as this will have importance for the selection of subgroups of patients for psychopharmacological studies.(4)

The authors compared the ABO blood type distribution pattern of 246 manic-depressive patients to that of 6000 controls. The blood type distribution of all patients did not differ from that of the controls. After subdivision of the patients into subgroups Bipolar I (n = 151) and Bipolar II (n = 95) significant differences were found for blood types O and A between the 2 subgroups, and between the Bipolar II patients and controls. After division of the patients into 3 diagnostic subgroups (Bipolar-A, n = 30; Bipolar-B, n = 121; Bipolar-C, n = 95) significant differences were found in the distribution of blood groups O and A among the 3 subgroups, and Bipolar-A and Bipolar-C patients also differed from the controls. The results may provide additional support for the subclassification of bipolar major affective disorders into 3 subgroups. (5)
ABH non-secretors have a higher incidence of psychiatric disorders in general.
References:1.Life Sci 1993;52(3):231-242 Minireview: Molecular genetics in affective illness. Mendlewicz J, Sevy S, Mendelbaum K

2.Acta Psychiatr Scand 1979 Sep;60(3):272-278 Affective disorders and ABO blood types. Rinieris PM, Stefanis CN, Lykouras EP, Varsou EK

3.Jpn J Psychiatry Neurol 1988 Dec;42(4):753-758 Blood groups and affective disorders. Takazawa N, Kimura T, Nanko S

4.Prog Neuropsychopharmacol 1979;3(1-3):147-154Psychopharmacological studies in genetically determined subgroups of psychiatric patients. Rafaelsen OJ, Shapiro RW

5.J Affect Disord 1981 Mar;3(1):1-7 ABO blood groups in manic-depressive patients. Rihmer Z, Arato M





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2014-12-21: Current Date 13:39:1 GMT: Current Time


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