Volume 158 Number I newborn care. I. Secular trends in cerebral palsy. Devel Med Child Neurol 1981 ;23:533-8. 12. Stanley FJ, Watson L. Methodology of a cerebral palsy register: the Western Australian experience. Neuro- epidemiology 1985;4:146-60. 13. Moore DJ. Perinatal statistics in Western Australia. 2nd annual report of the WA midwives' notification system for 1984. Perth: WA Health Department, 1986. 14. Stanley FJ, Waddell VP. Changing patterns of perinatal and infant mortality in Western Australia: implications for prevention. Med J Aust 1986; 143:379-81. Cerebral palsy trends in Western Australia 15. Nelson KB, Ellenberg JH. Antecedents of CP: multivar- iate analysis of risk. New Engl J Med l 986;315:81-6. 16. Paneth N, Stark RI. Cerebral palsy and mental retardation in relation to indicators of perinatal asphyxia: an epide- miological overview. At-t J OBSTET GYNECOL 1983;147: 960-6. . 17. Stanley FJ. The changing face of cerebral palsy? Dev Med Child Neurol 1987;29:258-70. Dietary factors and risk of trophoblastic disease Fabio Parazzini, MD, Carlo La Vecchia, MD, Giorgia Mangili, MD, Caterina Caminiti, ScD, Eva Negri, ScD, Gabriela Cecchetti, MD, and Monica Fasoli, MD Milan, Italy The risk of gestational trophoblastic disease in relation to frequency of consumption of selected dietary items was evaluated with data from a case-control study conducted in Northern Italy on 148 women with histologically confirmed gestational trophoblastic disease and two control groups, one consisting of 372 obstetric control subjects and one consisting of 406 patients in the hospital for acute, nonobstetric, nongynecologic conditions. Patients with gestational trophoblastic disease tended to consume several foods less frequently, including the major sources of vitamin A and animal protein in the Italian diet. Relative risk estimates were significantly below unity in both control groups for green vegetable, carrot, liver, and cheese consumption and in the obstetric control group only for milk, meat, eggs, fresh fruit, and fish. Inverse relationships emerged between the risk of gestational trophoblastic disease and j.3-carotene or retinal intake index. The trend of decreasing risk with increasing intake was significant for j.3-carotene consumption. The present findings confirm that various aspects of diet may influence the risk of gestational trophoblastic disease. However, the limitation of available evidence still introduces serious uncertainties in the interpretation of these findings and suggests the potential importance of further epidemiologic and biochemical research to obtain more precise definition of specific dietary correlates of gestational trophoblastic disease. (AM J OBSTET GYNECOL 1988;158:93-100.) Key words: Dietary factors, gestational trophoblastic disease The role of dietary factors in the etiology of gesta- tional trophoblastic disease has been repeatedly con- sidered. Early descriptive studies conducted in the 1960s in Mexico' and the Philippines 2 suggested that the higher frequency of gestational trophoblastic dis- From the Mario Negri Institute for Pharmacological Research, the First and Third Obstetric and Gynecology Clinics and the Institute of Biometry and Medical Statistics, University of Milan, and the Inter-University Consortium of Lombardy for Automatic Data Pro- cessing. This study was conducted within the framework of the CNR (Italian National Research Council) applied projects "Preventive and Re- habilitative Medicine" (contract No. 85.00549.56) and Oncology (contract No. 85.02209.44). Data processing and analysis were conducted fry the computing facilities of the Inter-University Con- sortium of Lombardy for Automatic Data Processing (CILEA). Received for publication N ovemb.er 24, 1986; revised May 14, 1987; accepted August 30, 1987. Reprint requests: Fabio Parazzini, MD, Mario Negri Institute for Pharmacological Research, Via Eritrea, 62-20157 Milan, Italy. ease among low social classes in developing countries could be explained by malnutrition and in particular by a low intake of proteins. Subsequent studies, how- ever, reported conflicting results: For instance, the fre- quency of hydatidiform mole is high in native Alas- kans,' who consume a high-protein diet. Furthermore, in Hawaii,• Malaysia,' China,6 or the United States,' no relation was found between indicators of adequate pro- tein diet (mostly based on measures of socioeconomic status) and gestational trophoblastic disease. These discrepancies can be explained by limitations on available data and methodologic problems: Gener- ally those studies were based on descriptive uncon- trolled designs, diet was only indirectly examined, and the role of potential confounding factors could not be adequately assessed. Recently, a case-control study conducted in the United States" showed about a 50% decrease in the risk 93