Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The overall importance of nutrition to favorable perinatal outcome is only beginning to be fully appreciated. Although nutritional status can be linked to such things as socioeconomic class and education, it is nutrition directly that exerts a biologic effect. This review has attempted to look at three elements and their relationship to maternal and fetal outcome. At the present time, there does not seem to be a role for routine magnesium supplementation during pregnancy. Magnesium deficiency, as an isolated nutritional deficiency, is rare, and the evidence is, at best, weak that magnesium supplementation reduces the risk of poor perinatal outcome. Zinc deficiency is also a very rare isolated nutritional finding. Our ability to measure zinc accurately, be it in leukocytes or serum, is improving, but the routine use of zinc supplements during pregnancy cannot be recommended at this time. It may be that zinc will be a useful diagnostic marker, rather than a therapeutic intervention. There is substantial evidence that the average American diet does not contain sufficient calcium. An expansive literature continues to grow in the areas of calcium and colon cancer, calcium and breast cancer, calcium and hypertension, and calcium and osteoporosis. Is it possible that our susceptibilities to these problems begin in utero? Obviously, the answer is unknown. What is known is that supplemental calcium to some degree is needed in the diets of most Americans and in about two thirds of pregnant women. Calcium supplementation seems to affect blood pressure favorably and, pending confirmation with larger trials, may significantly reduce prematurity and preeclampsia risk, thus improving perinatal outcome for a large number of our high-risk patients.
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PMID:Calcium, magnesium, and zinc supplementation and perinatal outcome. 186 34

As zinc status may influence susceptibility to colon cancer, we examined the effect of dietary zinc deficiency on the proliferation of epithelial cells (colonocytes) in the large bowel of rats. When compared to feed-restricted rats, those with zinc deficiency showed a significant reduction in proliferation in the distal colon as assessed by accumulated metaphase arrest and crypt cell production rates in vivo. Zinc deficiency had no apparent effect on thymidine kinase activity in colonocytes but was accompanied by minor changes in fecal mass and fecal pH. In rats, zinc deficiency is associated with a reduction in the rate of proliferation of colonocytes in the distal colon.
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PMID:Zinc deficiency is associated with suppression of colonocyte proliferation in the distal large bowel of rats. 248 56