Vegetables,fruit, and cancer. II. Mechanisms

The epidemiologic literature on the relationship between vegetable and fruit consumption and human cancer at a variety of sites was reviewed systematically in Part I.¹ It was concluded that consumption of higher levels of vegetables and fruit is associated consistently, although not universally, with a reduced risk of cancer at most sites, and particularly with epithelial cancers of the alimentary and respiratory tracts. Possible mechanisms by which vegetable and fruit intake might alter risk of cancer are addressed here. A large number of potentially anticarcinogenic agents are found in these food sources, including carotenoids, vitamins C and E, selenium, dietary fiber, dithiolthiones, glucosinolates and indoles, isothiocyanates, flavonoids, phenols, protease inhibitors, plant sterols, allium compounds, and limonene. These agents have both complementary and overlapping mechanisms of action, including the induction of detoxification enzymes, inhibition of nitrosamine formation, provision of substrate for formation of antineoplastic agents, dilution and binding of carcinogens in the digestive tract, alteration of hormone metabolism, antioxidant effects, and others. It appears extremely unlikely that any one substance is responsible for all the associations seen. Possible adverse effects of vegetable and fruit consumption are also examined. One way to consider the relationships reviewed here is to hypothesize that humans are adapted to a high intake of plant foods that supply substances crucial to the maintenance of the organism, but only some of which are currently called essential nutrients. Cancer may be the result of reducing the level of intake of foods that are metabolically necessary—it may be a disease of maladaptation.Authors are with the Division of Epidemiology, School of Public Health, University of Minnesota, 1-210 Moos Tower, 515 Delaware Street SE, Minneapolis, MN 55455, USA. Address correspondence to Dr Potter. This work was supported by NIH Grants CA 50305, CA 46618, and CA 09607.     

Does DeLee suction at the perineum prevent meconium aspiration syndrome?

OBJECTIVE: We attempted to determine the impact of "early" (before delivery of the chest) oronasopharyngeal DeLee suctioning at the perineum in the prevention of meconium aspiration syndrome and to confirm that meconium aspiration syndrome is a postnatal event. STUDY DESIGN: We compared infants with meconium-stained fluid who underwent "early" oronasopharyngeal DeLee suctioning with a similar group of infants whose airways were suctioned "late" (after chest delivery). Practicing obstetricians did not know the study was being conducted by the pediatric staff, and an independent observer documented whether obstetricians performed "early" or "late" oronasopharyngeal DeLee suctioning. Immediate postnatal tracheal suctioning was performed in both groups. The study was conducted in a private tertiary care center averaging 5800 deliveries annually. A consecutive sample of 438 infants with meconium-stained fluid was analyzed. Of these infants, 221 received "early" oronasopharyngeal DeLee suctioning, while 217 infants were suctioned "late". RESULTS: Of the 438 infants with meconium-stained fluid, meconium aspiration syndrome developed in 38 (9%). These infants had higher rates of fetal distress (i.e., abnormal fetal heart rates) and lower Apgar scores (< or = 6) than infants without meconium aspiration syndrome (58% vs 17% and 65% vs 13%, respectively; p < 0.001). Forty-five percent of the infants with meconium aspiration syndrome had renal failure during the first 20 hours of life. In spite of "early" oronasopharyngeal DeLee suctioning, 53% of the infants in this group had meconium below the vocal cords and meconium aspiration syndrome developed in 7%. The time of oronasopharyngeal DeLee suctioning did not affect the rate of meconium aspiration syndrome or the presence of meconium below the vocal cords. CONCLUSIONS: We concluded that "early" oronasopharyngeal DeLee suctioning at the perineum does not affect the rate of meconium aspiration syndrome. We speculate that meconium aspiration syndrome is predominantly an intrauterine event associated with fetal distress and that meconium in the airways is merely a "marker" of previous fetal hypoxia.     

No evidence of an association of JC virus and colon neoplasia.

JC virus (JCV) is an ubiquitous human polyomavirus that frequently resides in the kidneys of healthy individuals and is excreted in the urine of a large proportion of the adult population. Polyomaviruses are associated with disease largely in immunocompromised individuals (progressive multifocal leukoencephalopathy). Colorectal cancers can show chromosome instability and it was hypothesized that JCV may account for some of this instability. We screened urine from 45 healthy donors and 233 colorectal cancer/normal tissue pairs for the presence of JCV sequences using a Taqman assay. This assay could detect 1 virus genome in 10 human genomes. In the urine samples, we found an infection rate of approximately 70%. The JCV isolates in these samples could be categorized into four JCV types (2B, 4, 7, and 8), none of which had a rearranged regulatory region. Among the colon tissues, one normal tissue (<0.5%) and none of the matched tumors tested positive for JCV. There is no evidence in these data to indicate that JCV is the cause of genetic instability in colorectal cancer.