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Continued research and development in the field of wound healing holds the potential to affect both quality of life and incidence of mortality. For the health care provider to promote successful wound healing, an understanding of the function of nutrients in inflammation and tissue growth is helpful. The intent of this paper is to discuss the metabolic and cellular pathways crucial to wound healing and identify appropriate nutritional interventions and clinical applications.

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We previously showed that moderate iron deficiency is associated with increased susceptibility to chemically induced breast carcinogenesis. Epidemiological and experimental data suggest that breast cancer risk may be modulated by the developmental and proliferative state of the mammary epithelium. The adverse effects of iron deficiency on organ growth are well documented. However, the role of iron in mammary gland development has not been examined. Therefore, we studied the effect of iron deficiency on mammary gland development and epithelial cell kinetics in female Sprague-Dawley rats. Weanling rats were fed experimental diets that provide 6 (severe), 12 (moderate) or 35 (control) mg Fe/kg diet. After 6 wk of treatment, hematocrit and blood hemoglobin were lower in iron-restricted rats than in controls, with significant differences from controls observed in rats receiving 6 mg Fe/kg diet (P < 0.05). Liver iron was reduced 90 and 80% in severe and moderate groups, respectively, compared with controls. Puberty onset and 17-beta-estradiol levels were unaltered by iron status, but plasma progesterone was significantly lower in iron-restricted groups (P < 0.05). Microscopic examination of mammary gland whole mounts revealed an increased density of terminal end buds in thoracic glands from iron-restricted rats, indicative of decreased differentiation, although the differences were not statistically significant compared with controls (P = 0.21). Mammary epithelial cell proliferation, determined in contralateral glands by measuring 5-bromo-2'-deoxyuridine incorporation, did not differ between rats receiving 12 and 35 mg Fe/kg diet. In conclusion, these results suggest that alveolar development of the mammary gland and the proliferative capacity of the mammary epithelium are refractory to iron deficiency during early postpubertal growth of the rat.

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In order to establish a research agenda for nutrition and food concerns associated with long-duration space travel, a conference was sponsored by the New Jersey-NASA Specialized Center of Research & Training (NJ-NSCORT), NASA, and the University of Houston Conrad N. Hilton College of Hotel & Restaurant Management. Invited papers were presented and are published in this special issue. Following intensive panel discussions and workshops the participants developed recommendations for a research agenda. The recommendations are listed in this introductory article.

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Asthma is a syndrome that may have many causes resulting in airway inflammation and hyperresponsiveness. The search for the causes of asthma has led to the investigation of genetic, atopic, viral, and nutritional factors. For the last 2 decades, a number of studies have linked particular nutrients to asthma. The studies have examined both the suboptimal status of particular nutrients as causes of asthma and supplements of specific nutrients as therapy for asthma. We reviewed and analyzed data from these studies to determine the role of nutritional therapy in the management of asthma. The studies on food allergies reveal that IgE-mediated reactions to food are a minor cause of respiratory symptoms, affecting more children than adults. Currently, there are no available data to support the use of nutritional supplements in the treatment of chronic asthma.

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The effect of Fe status on murine systemic lupus erythematosus was investigated. Weanling female MRL/MPJ-lpr/lpr mice (systemic lupus erythematosus strain) were fed diets with the following levels (mg Fe/kg diet): 3 (severely deficient), 10 (moderately deficient), 35 (control) and 250 (supplemented). A fifth group was pair fed the control diet in the amounts consumed by the severely deficient group. C3H/Hej mice fed the same diets were used as non-lupus controls. Anemia was more severe in severely deficient mice than in all other MRL groups and C3H severely deficient mice. Incidence of skin lesions was highest in MRL severely and moderately deficient mice compared with pair-fed, control and supplemented mice. By 22 wk of age, mortality was higher in supplemented and severely deficient mice than in moderately deficient, pair-fed and control MRL mice. Anti-dsDNA activity in serum was not altered by Fe. In a second experiment, kidney function was examined in mice fed severely deficient, control, supplemented and pair-fed diets. Urine protein concentration was highest in supplemented mice at 14 wk of age. Serum urea nitrogen was significantly higher in MRL severely deficient mice than in pair-fed and control mice at 18 wk of age. Glomerular filtration rate, measured by creatinine clearance, was significantly lower in MRL severely deficient mice than in pair-fed and Fe supplemented mice at 16 wk of age and pair-fed and control mice at 18 wk of age. Renal histopathology was more severe in Fe supplemented mice than in pair-fed and control mice, and more severe in severely deficient and pair-fed mice than in control mice. Fluorescent staining of kidneys with anti-Ig G and anti-C3 fluorescein-conjugated antibodies was most intense in severely deficient mice, and the concentration of circulating immune complexes in serum was significantly higher in severely deficient mice than in all other groups. These data demonstrate that systemic lupus erythematosus in MRL/MPJ-lpr/lpr mice is altered by dietary iron.

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Mammary tumor incidence, natural killer (NK) cell activity, and tumor necrosis factor-alpha (TNF-alpha) activity were measured in iron (Fe)-deficient and iron-replete rats treated with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed AIN-76 diets: the iron-deficient group was fed 5 mg Fe/kg diet; the control group was fed 50 mg Fe/kg diet; the food-restricted group was fed 50 mg Fe/kg diet in the amount consumed by the iron-deficient group; and the replete group was fed 5 mg Fe/kg diet for 45 days and then 50 mg Fe/kg diet. After six weeks of feeding, the rats were given a single intragastric dose of DMBA. Feeding the iron-deficient diet for 20 weeks reduced hematocrit, hemoglobin, liver iron, and tumor iron values and increased spleen weight. Dietary iron repletion for 14 weeks reversed these effects of iron deficiency. Splenic NK cell cytotoxicity against YAC-1 cells was highest in the control group. Repleting rats with 50 mg Fe/kg diet corrected iron deficiency but did not restore NK cell cytotoxicity. No significant differences in macrophage TNF-alpha bioactivity were found among groups. Cumulative tumor incidence over all weeks was lowest in the iron-deficient rats. Iron repletion during the promotion phase of tumorigenesis attenuates the protective effects of iron deficiency. Food restriction to the extent present in the iron-deficient group did not protect against tumorigenesis. The iron-deficient group had the lowest tumor burden and delayed onset of tumors. Iron deficiency significantly reduces tumor incidence in DMBA-treated rats by mechanisms other than NK cell cytotoxicity, TNF-alpha activity, and food restriction.

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OBJECTIVE: Compare milk-based, iron-fortified formulas containing 7.4 and 12.7 mg/L iron and breast-feeding during the first year of life. DESIGN: Partially randomized, double-blind trial: non-breast-fed infants randomly assigned to receive one of two coded formulas, identical except for iron content; infants discontinuing breast-feeding between 1 and 8 weeks of age randomly assigned to a formula late-start group. SETTING: Five general community pediatric practices in Missouri, Indiana, Illinois, and Pennsylvania. PARTICIPANTS: Sample of 347 healthy, term infants, enrolled within 1 week after birth; 172 included in statistical analyses. OUTCOME MEASURES: Length, weight, and indicators of formula intolerance recorded at clinic visits; formula consumption, bowel movements, stool consistency, and other tolerance indicators recorded by parents on daily and weekly report forms; hemoglobin, hematocrit, and serum ferritin, iron zinc, and copper measured at 6 and 12 months. RESULTS: No significant differences between formula-fed groups in growth, attrition, formula consumption, bowel movements, hematocrit, hemoglobin level, and serum iron, zinc, and copper levels (P > .05); first 6-month weight and length changes of the breast-fed group significantly less than in both formula-fed groups (P < .008); serum ferritin level of the formula-fed, high-iron group significantly higher than that of the low-iron and breast-fed groups (P < .008), although all groups' values were normal; no apparent differences between formula groups in formula tolerance and stool characteristics but data were not analyzed statistically. CONCLUSIONS: Milk-based formulas containing either 7.4 or 12.7 mg/L iron support normal growth and iron status of healthy, term, normally fed infants during the first year and both are well tolerated and accepted.

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Cytotoxicity of peritoneal macrophages (pMs) and peritoneal natural killer (pNK) cells toward xenogenic tumor cells was studied in anemic, suckling rats. Dams were fed 6, 12, or 250 mg Fe/kg diet ad libitum throughout gestation and lactation. Pups were injected intraperitoneally with 10(5) plaque-forming units of virus. Four days later cytotoxicity of pMs and pNK cells against YAC-1 mouse lymphoma cells was measured. Body weight, hemoglobin, hematocrit, and viable cell yield of pups were significantly decreased with decreasing dietary iron. pM cytotoxicity was significantly impaired in anemic pups at pM-target-cell ratios of 10:1 and 30:1 at 4 and 16 h (P less than or equal to 0.03). pNK-cell cytotoxicity was significantly impaired in anemic pups at pNK-target-cell ratios of 10:1 and 50:1 at 16 h. Iron-deficient diet consumed by dams throughout gestation and lactation resulted in anemic offspring whose immunologic defense by pMs and pNK cells against xenogenic tumor cells was significantly reduced.

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Inadequate nutriture of zinc, copper and iron alter immunocompetence in humans and experimental animals. For each of these minerals deficient status leads to increased susceptibility to infectious illnesses. Specific components of the immune response may be altered in a variety of patients and models. Although many generalized functions for these nutrients could lead to altered immune function, specific functions for these minerals in immunity have not yet been identified. For zinc, copper and iron the importance of adequate nutrition in maintaining immunocompetency cannot be understated.

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Natural killer (NK) cell activity is impaired in iron-deficient rats. Natural killer cells destroy tumor cells; therefore, iron-deficient rats may be less able to combat cancer growth. Natural killer cell cytotoxicity, both basal and interferon gamma (IFN gamma)-stimulated, was studied in moderately and severely iron-deficient rats challenged with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed ad libitum semipurified diets containing 8, 13 or 42 mg Fe/kg. A pair-fed group was fed the 42 mg Fe/kg diet at the level consumed by the 8 mg Fe/kg group. Following 6 wk of dietary treatment, DMBA-treated rats received a single intragastric dose of DMBA. Dietary treatment was continued. Rats were killed at 1, 4, 8, 14 and 20 wk post-DMBA treatment. Natural killer cell cytotoxicity (both basal and IFN gamma-stimulated) was analyzed. Feeding the 13 mg Fe/kg diet resulted in lower NK cell activity (P = 0.006) and greater tumor burden (P = 0.045) and tumor incidence. Interferon gamma treatment relieved the lower NK cell cytotoxicity observed in moderate iron deficiency. Feeding the 8 mg Fe/kg diet impaired NK cell activity (P = 0.006), but tumor burden and incidence were less than in moderate iron deficiency. In this model, iron deficiency, particularly moderate iron deficiency, contributed to cancer development and compromised NK cell cytotoxicity.

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The effect of tannin content on iron (Fe) bioavailability from several legumes was evaluated. Absorption of Fe from a casein (C), isolated soy protein (ISP), chickpea (CP) or red kidney bean (RKB) test meal was tested in marginally Fe-deficient rats [9.9 +/- 0.2 g Hb/100 mL (mean +/- SD)] using the extrinsic tag technique. Also, the effects of a casein habitual diet or of one of three casein-legume habitual diets fed before and after the test meal were investigated. Weanling male rats were fed the habitual diets containing 23 +/- 4 mg Fe/kg of diet (range 17-28) for 13 d. On d 14, after an overnight fast, rats were fed the test meal (1.5 g + 0.1 microCi 59Fe), and whole-body radioactivity was determined. The same habitual diet was refed for seven additional days, and whole-body radioactivity was determined again. Rats retained more iron from C (86%) than from ISP, CP or RKB test meals (73%, 75% and 67%, respectively) when the respective casein-legume habitual diets were fed before and after the test meals. With the casein habitual diet, there was no difference in retained iron from C, ISP, CP or RKB test meals (86%, 87%, 83% and 82%, respectively). Retention of iron from an RKB test meal was increased from 69.6 to 73% when about 90% of the extractable tannins were removed, but the difference was not statistically significant. Thus, feeding a casein-legume diet but not a casein diet prior to a test meal apparently predisposes the rat to lower iron absorption. However, in these studies, tannins per se did not significantly depress iron bioavailability.

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The effect of in vitro interferon stimulation on nonimmune- and immune-spleen natural killer cell activity was studied in iron-deficient rat pups. Dams were fed 6, 12 or 250 mg Fe/kg diet during gestation and lactation. Approximately one-half of the 17-d-old pups were injected intraperitoneally with 10(5) plaque-forming units of vaccinia virus. Four d later, nonimmune and vaccinia-immune pups were killed. Spleen lymphocyte suspensions were prepared and plated with or without rat alpha/beta interferon for 2 h at 37 degrees C. Washed lymphocytes were combined with 51chromium-labeled YAC-1 target cells and co-cultured for 4 and 16 h at 10 and 50:1 effector-to-target ratios. Hemoglobin concentration, hematocrit, body weight, spleen weight and lymphocyte numbers per spleen were lower in iron-deficient pups than in controls. In general, interferon stimulation increased natural killer cell activity above baseline. Analysis of variance comparison among groups showed that interferon was incapable of restoring natural killer cell activity of iron-deficient pups to the levels observed in control pups. Impaired spleen natural killer cell activity in iron-deficient neonates may be due to a limited capacity for stimulation by interferon.

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1. The effect of maternal iron deficiency on milk composition and consumption by sucking rats was investigated. 2. Dams (n 42) were fed on semi-purified diets with either 8 (Fe-) or 250 (Fe+) mg Fe as ferrous sulphate/kg throughout gestation and lactation. Total milk intake was determined at days 7, 12 and 17 of lactation from the rate of disappearance of 3H2O from the total body water pool of pups. Measurements of milk constituents and Fe status of animals also were made. 3. Feeding the Fe- diet led to the development of anaemia in dams and pups and to growth retardation of sucking pups. 4. Concentrations of total lipid and Fe in milk from Fe- dams were significantly lower than those from Fe+ dams. Mean milk intakes (ml/d) of Fe-deficient pups were 21 and 28% less than intakes of Fe-sufficient pups on days 12 and 17 respectively. However, when expressed per kg body-weight, mean milk intakes were similar between groups on days 17 and 12 and increased by 47% in the Fe-deficient group on day 17 of lactation. 5. It is concluded that maternal Fe deficiency affects the quality of milk ingested by neonatal rats. However, Fe-deficient pups are at least partially able to compensate for reduced milk energy and nutrient contents by increasing intake in late lactation.

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Some employers spend half their health benefits dollars on outpatient care. Utilization of ambulatory services is up, costs-per-case are escalating fast--with some procedures demonstrably costing 85%-95% of inpatient charges--and providers' profits are increasing. Executives of the Health Data Institute and The Associated Group describe a multi-pronged approached to managing the burgeoning costs of a health care delivery alternative that was supposed to save employers money.

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The present study was designed to determine whether reduced folate incorporation into milk can account for folate depletion of iron-deficient suckling rats. Dams were fed diets containing 2 mg/kg folate and either 8, 12 or 250 mg/kg iron throughout gestation and lactation to produce severely iron-deficient, moderately iron-depleted and iron-sufficient states in 17-d-old pups (n = 15 litters/group). On d 17 of lactation, dams were separated from litters and given intraperitoneal injections of [3',5',7,9-3H]pteroylmonoglutamic acid ([3H]PteGlu) or physiological saline. Mean [3H]PteGlu incorporation into milk of severely iron-deficient dams was 67% of that in iron-sufficient controls, while "total" and "free" milk folate activities were 54 and 61%, respectively. Values for milk [3H]PteGlu incorporation and folate activities were intermediate in moderately iron-depleted dams. Pup red blood cell folate activity was positively correlated with both free (r = 0.43, P = 0.004) and total (r = 0.37, P = 0.015) milk folate activities. Mean plasma folate activities of severely and moderately iron-deficient pups were 68 and 86% of control values, respectively. Results show that in both mild and severe iron deficiency, reduced folate secretion into milk is at least partially responsible for impaired folate status of suckling pups.

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The production of the immunotransmitter, interleukin 1 (IL-1), by peritoneal exudate cells (PEC) was examined in iron-deficient and control rats. Three groups of weanling male Sprague-Dawley rats were fed a purified diet containing 6, 12, or 35 ppm iron for 6 wk to produce severe iron deficiency, moderate iron deficiency, or adequate iron status. Crude IL-1 samples were prepared from acute PEC and assayed for activity. IL-1 preparations from severely and moderately iron-deficient rats enhanced mouse thymocyte proliferation in vitro less than half as much as IL-1 preparations from control rats. In a rabbit bioassay, injection of IL-1 prepared with PEC from either group of iron-deficient rats had little effect on body temperature or plasma minerals, while IL-1 from iron-adequate source PEC produced a febrile response and markedly lowered plasma iron and zinc in recipient rabbits. Severe or moderate iron deficiency, then, clearly impairs IL-1 production by rat PEC.

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To determine if decreased protein synthesis is a factor in reduced immunocompetence of iron deficiency, RNA, DNA and in vitro protein synthesis were measured. Rats were fed diets containing 6 (severe anemia), 11 (moderate anemia) or 250 (iron sufficient) mg iron/kg diet throughout gestation and lactation. On d 2 of lactation, litters were adjusted to contain six pups. On d 12 of lactation, two pups from each litter were immunized with sheep red blood cells (SRBC) and on d 17, tissues were removed for the determination of protein synthesis and evaluation of RNA and DNA contents. In the moderately iron-deficient pups, protein synthesis was lower (30%) in spleen than that in iron-sufficient pups. Protein synthesis in liver and thymus was not changed by moderate iron deficiency. In spleen, liver and thymus, protein synthesis in severely iron-deficient pups was less than half that of iron-sufficient pups. Protein synthesis in the spleen of the moderately iron-deficient group was higher after immunization with SRBC than in iron-sufficient controls, whereas the severely iron-deficient pups failed to respond. Impaired protein synthesis may be the mechanism responsible for compromised ability to produce antibody in iron deficiency.

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Natural killer (NK) cell activity was studied in iron-deficient rat pups. Pregnant dams were fed diets containing 6, 10 or 250 ppm Fe ad libitum from d 1 of gestation through d 21 of lactation. Two days post parturition litters were adjusted to seven pups each, and on d 17 the pups were injected intraperitoneally with 5 X 10(5) plaque-forming units of vaccinia virus. Following a 4-d incubation period, spleens were removed and the cell suspensions combined with YAC-1 target cells to measure cytolysis in a 4- and 16-h chromium release assay. Hematocrit levels of severe (6 ppm) and moderately (10 ppm) iron-deficient rat pups were significantly lower than that of controls. Similarly, body weight and spleen weights were significantly lower in iron-deficient pups than in control pups. Iron deficiency significantly impaired spleen NK cell activity when measured by two different effector:target ratios and assay time periods.

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Livers of Fe-deficient rat pups contain significantly less carnitine and more triacylglycerol (TG) than livers of control pups. Carnitine affects ketogenesis (KG), which is a vital adaptation in the neonate. To determine if KG is impaired by low carnitine in Fe-deficient pup liver, ketone body synthesis was measured in liver mitochondria from 15-d-old pups. Litters from Fe-deficient (-Fe) and Fe-adequate (+Fe) dams were orally supplemented with water (W) as a control, 18 mM ferrous sulfate, or 10 mM L-carnitine from d 8 through d 15 of lactation. The amount of ketone bodies (beta-hydroxybutyrate + acetoacetate) synthesized was 68% less (P less than 0.05) in -FeW pups than in +FeW pups. Iron or carnitine supplementation increased KG in -Fe pups to +Fe KG levels, but carnitine did not affect KG in +Fe pups. Liver TG in +Fe pups was not altered by supplementation, but liver TG was -FeW pups. The data support the hypothesis that in the Fe-deficient suckling rat -FeW pups. The data support the hypothesis that in the Fe-deficient suckling rat, low carnitine levels may contribute to impaired ketogenesis and increased lipids in liver.

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