Extensive tests on animals and tests on human beings have established that the storage capacity of the organism for zinc (Zn) is very limited and that there exists no proper storage organ for this trace element. Particularly during pregnancy a nutritional zinc deficiency therefore quickly brings about a general zinc deficiency Situation. Up to now however it has not been possible to recognize these deficiencies in time, let alone to treat them. In this investigation we tested to what extent there exists a correlation between fetal malnutrition and the zinc content or total protein content in the amniotic fluid (AF). For this purpose we used methods described in Part I of this publication [10]. These were atomic absorption spectrophotometry for the zinc measurement and a Biuret method adapted for the amniotic fluid for the total protein measurement. Various risk-collectives were examined and the results were compared with 230 cases of a control group. The results show, that the significant increase in the zinc content of the amniotic fluid in the control group from the 38 th week of gestation (WG) onwards to about three times äs much äs the initial level, occurred only in weak form in 123 cases of mild or severe hypotrophy. So ‘the amniotic fluid zinc levels (AFZL) lie clearly lower towards the end of the third trimenon than in the control group. The difference according to the U-test at p < 0,01 is significant. The concentration difference from the 38th WG onwards lies at about 0,05 μg Zn/ml AF. The calculation of the total proteincontentof the amniotic fluid does not appear tobe a suitable method of recognizing a hypotrophy, since it doesnot show a significant difference from the control collective. However, towards the end of the pregnancy zinc and protein content show the same tendency. 36 cases with EPH-gestosis showed — in comparison with the control group - around the 32nd to 33rd WG significantly higher, and around the 40 th to 41 st WG significantly lower levels of zinc (p < 0,05). The explanation for this is in our opinion due to the increased protein mobilisation following the protein loss, which, on account of the high albumin linking of zinc, is combined with a zinc loss. However tests on the amniotic fluid of 61 patients with diabetic metabolism conditions brought another result. Here zinc levels lie below those of the control group during the complete pregnancy period tested. After the 39th WG the difference is significant (p < 0,05). The lOth percentile of the control group goes up to 0.04 μg Zn/ml AF in the 37 th WG and reaches the level of 0,14 μg Zn/ml AF in the 42nd week. Levels lying below this line can be regarded äs suspect due to negative influences through hypotrophy, diabetis mell. or gestosis. Increased AFZL occur after the 34 th WG only in cases of intrauterine fetal death or green amniotic fluid. Furthermore zinc has an important function for the antibacterial activity of the amniotic fluid. For example, the zinc levels of the amniotic fluid are reduced in the amnionic infection syndrome. Therefore the calculation of the AFZL could be of importance to the early diagnosis of such infections. The longheld viewthat zinc deficiency in human nutrition is not to be expected through the widespreading of this trace element, must be revised today. Insufficient zinc supply to the organism clearly leads - among other disturbances - to a diminished growth, which according to the foregone investigations also appears to have a great importance on pregnancy. Experiments on animals and therapy tests on groups of people with zinc deficiency supply have shown that the alimentary zinc deficiencies and even some medicinal or disease disturbances do respond quickly and successfully to an oral or parental zinc therapy. An early detection of zinc deficiency during pregnancy could therefore open new possibilities of treatment. © 1979, Walter de Gruyter. All rights reserved.