Effects of postoperative enteral nutrition combined with adjuvant radiotherapy on inflammatory response, nutrition, healing and prognosis in patients receiving radical surgery for esophageal carcinoma.

PURPOSE: To explore the influence of postoperative enteral nutrition combined with adjuvant radiotherapy on inflammatory response, nutrition, healing and prognosis in patients undergoing radical surgery for esophageal carcinoma. METHODS: A total of 114 patients with esophageal carcinoma receiving radical surgery from January 2016 to July 2017 composed the observation group and randomly divided into control group (n=57) and study group (n=57). Patients in the control group were given routine nutritional support after surgery, while those in the study group received enteral nutrition after surgery. The changes in inflammatory response and nutritional level, healing and prognosis in the two groups of patients before and after treatment were compared and analyzed. RESULTS: After treatment, the levels of serum hypersensitive C-reactive protein (hs-CRP) and prostaglandin E (PGE) of patients were decreased in both the control group and study group, and they were lower in the study group than those in the control group, while the levels of serum pro-albumin (PA) and albumin (ALB) of patients in the study group were higher than those in the control group (p<0.05). The postoperative wound healing time, total length of hospital stay, postoperative first exhaust time and defecation time in the study group were shorter than those in the control group (p<0.05). The total incidence rate of postoperative complications of patients in the study group was lower than that in the control group (p<0.05). CONCLUSION: The application of postoperative enteral nutrition combined with adjuvant radiotherapy in patients subjected to radical surgery for esophageal carcinoma can suppress systemic inflammatory response, improve the nutritional condition, promote postoperative wound healing and improve prognosis and therefore it is worthy of promotion in clinical practice.

Combined treatment with vitamin C and sulindac synergistically induces p53- and ROS-dependent apoptosis in human colon cancer cells.

Sulindac has anti-neoplastic properties against colorectal cancers; however, its use as a chemopreventive agent has been limited due to toxicity and efficacy concerns. Combinatorial treatment of colorectal cancers has been attempted to maximize anti-cancer efficacy with minimal side effects by administrating NSAIDs in combination with other inhibitory compounds or drugs such as l-ascorbic acid (vitamin C), which is known to exhibit cytotoxicity towards various cancer cells at high concentrations. In this study, we evaluated a combinatorial strategy utilizing sulindac and vitamin C. The death of HCT116 cells upon combination therapy occurred via a p53-mediated mechanism. The combination therapeutic resistance developed in isogenic p53 null HCT116 cells and siRNA-mediated p53 knockdown HCT116 cells, but the exogenous expression of p53 in p53 null isogenic cells resulted in the induction of cell death. In addition, we investigated an increased level of intracellular ROS (reactive oxygen species), which was preceded by p53 activation. The expression level of PUMA (p53-upregulated modulator of apoptosis), but not Bim, was significantly increased in HCT116 cells in response to the combination treatment. Taken together, our results demonstrate that combination therapy with sulindac and vitamin C could be a novel anti-cancer therapeutic strategy for p53 wild type colon cancers.

Dietary administration of δ- and γ-tocopherol inhibits tumorigenesis in the animal model of estrogen receptor-positive, but not HER-2 breast cancer.

Tocopherol, a member of the vitamin E family, consists of four forms designated as α, ß, γ, and δ. Several large cancer prevention studies with α-tocopherol have reported no beneficial results, but recent laboratory studies have suggested that δ- and γ-tocopherol may be more effective. In two different animal models of breast cancer, the chemopreventive activities of individual tocopherols were assessed using diets containing 0.3% of tocopherol (α-, δ-, or γ-) or 0.3% of a γ-tocopherol rich mixture (γ-TmT). Although administration of tocopherols did not prevent human epidermal growth factor receptor 2 (HER2/neu)-driven tumorigenesis, δ- and γ-tocopherols inhibited hormone-dependent mammary tumorigenesis in N-methyl-N-nitrosourea (NMU)-treated female Sprague-Dawley rats. NMU-treated rats showed an average tumor burden of 10.6 ± 0.8 g in the control group at 11 weeks, whereas dietary administration of δ- and γ-tocopherols significantly decreased tumor burden to 7.2 ± 0.8 g (P < 0.01) and 7.1 ± 0.7 g (P < 0.01), respectively. Tumor multiplicity was also reduced in δ- and γ-tocopherol treatment groups by 42% (P < 0.001) and 32% (P < 0.01), respectively. In contrast, α-tocopherol did not decrease tumor burden or multiplicity. In mammary tumors, the protein levels of proapoptotic markers (BAX, cleaved caspase-9, cleaved caspase-3, cleaved PARP) were increased, whereas antiapoptotic markers (Bcl-2, XIAP) were inhibited by δ-tocopherol, γ-tocopherol, and γ-TmT. Furthermore, markers of cell proliferation (PCNA, PKCα), survival (PPAR-γ, PTEN, phospho-Akt), and cell cycle (p53, p21) were affected by δ- and γ-tocopherols. Both δ- and γ-tocopherols, but not α-tocopherol, seem to be promising agents for the prevention of hormone-dependent breast cancer.

Vitamin D3 supplementation at 4000 international units per day for one year results in a decrease of positive cores at repeat biopsy in subjects with low-risk prostate cancer under active surveillance.

CONTEXT: We wanted to investigate vitamin D in low-risk prostate cancer. OBJECTIVES: The objective of the study was to determine whether vitamin D(3) supplementation at 4000 IU/d for 1 yr is safe and would result in a decrease in serum levels of prostate-specific antigen (PSA) or in the rate of progression. DESIGN: In this open-label clinical trial (Investigational New Drug 77,839), subjects were followed up until repeat biopsy. SETTING: All subjects were enrolled through the Medical University of South Carolina and the Ralph H. Johnson Veterans Affairs Medical Center, both in Charleston, SC. PATIENTS AND OTHER PARTICIPANTS: All subjects had a diagnosis of low-risk prostate cancer. Fifty-two subjects were enrolled in the study, 48 completed 1 yr of supplementation, and 44 could be analyzed for both safety and efficacy objectives. INTERVENTION: The intervention included vitamin D(3) soft gels (4000 IU). MAIN OUTCOME MEASURES: Adverse events were monitored throughout the study. PSA serum levels were measured at entry and every 2 months for 1 yr. Biopsy procedures were performed before enrollment (for eligibility) and after 1 yr of supplementation. RESULTS: No adverse events associated with vitamin D(3) supplementation were observed. No significant changes in PSA levels were observed. However, 24 of 44 subjects (55%) showed a decrease in the number of positive cores or decrease in Gleason score; five subjects (11%) showed no change; 15 subjects (34%) showed an increase in the number of positive cores or Gleason score. CONCLUSION: Patients with low-risk prostate cancer under active surveillance may benefit from vitamin D(3) supplementation at 4000 IU/d.

Selectively hydrogenated soybean oil exerts strong anti-prostate cancer activities.

Prostate cancer is the second leading cause of male deaths due to cancer in the United States. Hydrogenated vegetable oils have been suspected of inducing adverse health effects, including atherosclerosis and cancer. Here we report that a selectively hydrogenated soybean oil (SHSO) containing a high quantity of conjugated linoleic acids showed remarkably strong anticarcinogenic activity against prostate cancer in the rat model (Copenhagen rats with MAT-LyLu syngeneic rat prostate cancer cells) study in vivo and human prostate carcinoma cell lines studies in vitro, as compared with native soybean oil. A 5% dietary supplementation with SHSO inhibited the growth of prostate cancer by 80% in vivo. The TUNEL method and immunohistochemical staining assays of bax, bcl-2, and survivin clearly showed that SHSO induced prostate cancer cell apoptosis in the tested rats. DNA fragmentation analysis in vitro further confirmed the apoptotic activity of SHSO on the MAT-LyLu prostate cancer cells. The SHSO also showed strong cytotoxicity on human prostate cancer cells (DU145 and PC3). This represents the first report demonstrating the significant anticancer activities of hydrogenated vegetable oils at low levels of dietary supplementation.

Effect of intermittent fasting on prostate cancer tumor growth in a mouse model.

Caloric restriction (CR) has been shown to have anti-cancer properties. However, CR may be difficult to apply in humans secondary to compliance and potentially deleterious effects. An alternative is intermittent CR, or in the extreme case intermittent fasting (IF). In a previous small pilot study, we found 2 days per week of IF with ad libitum feeding on the other days resulted in trends toward prolonged survival of mice bearing prostate cancer xenografts. We sought to confirm these findings in a larger study. A total of 100 (7- to 8-week-old) male severe combined immunodeficiency mice were injected subcutaneously with 1 × 10(5) LAPC-4 prostate cancer cells. Mice were randomized to either ad libitum Western Diet (44% carbohydrates, 40% fat and 16% protein) or ad libitum Western Diet with twice-weekly 24 h fasts (IF). Tumor volumes and mouse bodyweights were measured twice weekly. Mice were killed when tumor volumes reached 1000 mm(3). Serum and tumor were collected for analysis of the insulin/insulin-like growth factor 1 (IGF-1) hormonal axis. Overall, there was no difference in mouse survival (P=0.37) or tumor volumes (P ≥ 0.10) between groups. Mouse body weights were similar between arms (P=0.84). IF mice had significantly higher serum IGF-1 levels and IGF-1/IGFBP-3 ratios at killing (P<0.001). However, no difference was observed in serum insulin, IGFBP-3 or tumor phospho-Akt levels (P ≥ 0.39). IF did not improve mouse survival nor did it delay prostate tumor growth. This may be secondary to metabolic adaptations to the 24 h fasting periods. Future studies are required to optimize CR for application in humans.

Early supplementation of parenteral nutrition is capable of improving quality of life, chemotherapy-related toxicity and body composition in patients with advanced colorectal carcinoma undergoing palliative treatment: results from a prospective, randomized clinical trial.

AIM: Patients suffering from advanced colorectal cancer can experience unintended weight loss and/or treatment-induced gastrointestinal toxicity. Based on current evidence, the routine use of parenteral nutrition (PN) for patients with colorectal cancer is not recommended. This study evaluates the effect of PN supplementation on body composition, quality of life (QoL), chemotherapy-associated side effects and survival in patients with advanced colorectal cancer. METHOD: Eighty-two patients with advanced colorectal cancer receiving a palliative chemotherapy were prospectively randomized to either oral enteral nutrition supplement (PN-) or oral enteral nutrition supplement plus supplemental PN (PN+). Every 6 weeks body weight, body mass index (BMI), chemotherapy-associated side effects and caloric intake were assessed, haemoglobin and serum albumin were measured. Body composition was assessed by body impedance analysis, and QoL was evaluated by European Organization for Research and Treatment of Cancer (EORTC) QLQC30 questionnaire. RESULTS: No differences were evident at baseline between the groups for age, sex, diagnosis, weight, BMI or QoL. A difference in BMI was observed by week 36, whereas differences of the mean body cell mass could be observed from week 6, albumin dropped significantly in the PN- group in week 36 and QoL showed significant differences from week 18. Chemotherapy-associated side effects were higher in PN-. The survival rate was significantly greater in the PN+ group. CONCLUSION: A supplementation with PN slows weight loss, stabilizes body-composition and improves QoL in patients with advanced colorectal cancer. Furthermore, it can reduce chemotherapy-related side effects.

Serum insulin-like growth factor-I and mammary tumor development in ad libitum-fed, chronic calorie-restricted, and intermittent calorie-restricted MMTV-TGF-alpha mice.

The effect of chronic (CCR) and intermittent (ICR) caloric restriction on serum insulin-like growth factor (IGF)-I levels and mammary tumor (MT) development was investigated. Ten-week-old MMTV-TGF-alpha female mice were assigned to ad libitum-fed (AL; AIN-93M diet), ICR [3-week 50% caloric restriction using AIN-93M-mod diet, 2x protein, fat, vitamins, and minerals followed by 3 weeks of daily 100% AL consumption of AIN-93M ( approximately 75% of AL for each 6-week cycle)], and CCR (calorie and nutrient intake matched for each 6-week ICR cycle) groups. Half of the mice from each group were sacrificed at 79 (end of restriction) or 82 (end of refeeding) weeks of age. Serum was obtained at euthanasia and in cycles 1, 3, 5, 8, and 11. MT incidence was 71.0%, 35.4%, and 9.1% for AL, CCR, and ICR mice. ICR-Restricted mice had significantly lower terminal serum IGF-I and IGF-I/IGF binding protein-3 (IGFBP-3) ratio than CCR, ICR-Refed, and AL mice. There were no differences in terminal IGFBP-3. Final body, internal, and mammary fat pad weights correlated positively with IGF-I and negatively with IGFBP-3. Few changes were found for protein expression of IGF-IRalpha and IGFBP-3 in mammary tissue and MTs. During the study, IGF-I levels of ICR-Restricted mice were reduced, whereas refeeding allowed partial recovery. For all groups, elevated IGF-I levels preceded MT detection, although not all values were significant versus mice without MTs. However, the specific role of IGF-I in the protective effect of calorie restriction remains to be determined. These results confirm that ICR prevents MT development to a greater extent than CCR.

Dietary intervention in the management of prostate cancer.

PURPOSE OF REVIEW: This review integrates recent reports related to the dietary management of prostate cancer with the existing body of science in an effort to best inform practicing clinicians. RECENT FINDINGS: Dietary factors are hypothesized to play a significant role in prostate cancer, and have proven to be important in managing prevalent comorbidities in this patient population (cardiovascular disease, diabetes, and osteoporosis). Data regarding diet and prostate cancer are accumulating and randomized controlled trials are underway which will ultimately yield evidence on which to base recommendations regarding dietary regimens, functional foods, and supplement use. Until that time, most data derive from epidemiologic studies that have limitations in showing cause and effect. During the past year, the greatest and most consistent strides have been made in the area of energy balance, with data consistently showing that overweight and obesity are associated with progressive disease and increased overall mortality. SUMMARY: To date, the strongest evidence regarding diet and prostate cancer relates to energy balance. Urologists aspiring to best clinical practice should encourage their patients to achieve a healthful body weight through regular exercise and a healthful plant-based diet rich in fruits, vegetables, and whole grains. Advocating functional foods or supplements explicitly for cancer control purposes would currently be premature.

Do the dietary supplements epigallocatechin gallate or vitamin e cause a radiomodifying response on tumors in vivo? A pilot study with murine breast carcinoma.

The primary aim of this study was to evaluate a systematic and reproducible assay to examine the potential radiomodifying effects of vitamin E (VE) or epigallocatechin gallate (EGCG), antioxidants commonly consumed by cancer patients as dietary supplements, on tumor control. C3H mice were randomized to a control diet or to the control diet supplemented with VE or EGCG. A tumor control dose 50% (TCD(50)) assay was used to evaluate for a radiomodifying response in stage IV murine cancer (MCa-IV) tumors, implanted in the hindleg of mice, and allowed to grow to 8 mm before receiving a single dose of radiation. The effects of VE and EGCG on intratumoral angiogenesis and apoptosis were evaluated in a group of nonirradiated mice using immunohistochemical staining. Cell proliferation assays were conducted on MCa-IV tumors in vitro. EGCG slowed tumor growth rate by 10%. EGCG and VE slowed tumor regrowth by 24 to 25%. There were no significant differences in TCD(50) values between the groups (control = 73.9 Gy, VE = 77.2 Gy, EGCG = 76.4 Gy); however, normal tissues were protected from late radiation effects (autoamputations) in the VE group. VE and EGCG increased tumor cell apoptosis and decreased tumor cell proliferation but had no effect on microvessel density. In this pilot study, neither VE nor EGCG exerted a significant radiomodifying effect on the MCa-IV tumor. Nonetheless, the suggestion of a small degree of tumor radioprotection by these antioxidant compounds warrants further research. As supplementation with VE radioprotected normal tissue, additional studies on this putative benefit are recommended.

[Proliferation and apoptosis in tongue epithelium of mice bearing salivary tumors induced by dimetilbenzantraceno (DMBA) and modulated by dietary lipids]. / Proliferación y apoptosis en epitelio lingual de ratones con tumores salivales inducidos por dimetilbenzantraceno (DMBA) y modulados por lípidos dietarios.

INTRODUCTION: According to the concept of field defects during the carcinogenesis process, excessive epithelial proliferation/apoptosis may exist in areas near tumors. Proliferation or apoptosis could be modified by dietary lipids. PURPOSE: The present study was designed to analyze proliferation and apoptosis in tongue epithelium of mice fed diets based on different lipids followed by induction of salivary tumors with DMBA. MATERIALS AND METHODS: Forty-five days after weaning, ten BALB/c mice were assigned to two diets: corn oil (CO) and fish oil (cod liver, FO). Two weeks later, DMBA was injected in the submandibular area. Animals were sacrificed at the 13th post-injection week. Samples of tongue were fixed in formalin-ethanol and immunohistochemically stained for proliferation (Ki-67) and apoptosis (Bax). By light microscopy, the number of nuclei positive for these markers were counted out of three-hundred total interphase cells both in dorsal and in ventral tongue surfaces. Results were analyzed through Analysis of Variance and t Test. RESULTS: Cell proliferation was greater in dorsal than in ventral tongue surfaces (p < 0.0001) with no diet difference. Apoptosis was significantly greater in mice fed FO than CO, particularly in tongue dorsal epithelia (p < 0.018). CONCLUSIONS: This study shows that FO diet induces higher levels of apoptosis in tongue epithelia suggesting a tissue defensive mechanism when exposed to a carcinogenic-tumoral agent.

Proliferación y apoptosis en epitelio lingual de ratones con tumores salivales inducidos por dimetilbenzantraceno (DMBA) y modulados por lípidos dietarios / Proliferation and apoptosis in tongue epithelium of mice bearing salivary tumors induced by dimetilbenzantraceno (DMBA) and modulated by dietary lipids

INTRODUCTION: According to the concept of field defects during the carcinogenesis process, excessive epithelial proliferation/apoptosis may exist in areas near tumors. Proliferation or apoptosis could be modified by dietary lipids. PURPOSE: The present study was designed to analyze proliferation and apoptosis in tongue epithelium of mice fed diets based on different lipids followed by induction of salivary tumors with DMBA. MATERIALS AND METHODS: Forty-five days after weaning, ten BALB/c mice were assigned to two diets: corn oil (CO) and fish oil (cod liver, FO). Two weeks later, DMBA was injected in the submandibular area. Animals were sacrificed at the 13th post-injection week. Samples of tongue were fixed in formalin-ethanol and immunohistochemically stained for proliferation (Ki-67) and apoptosis (Bax). By light microscopy, the number of nuclei positive for these markers were counted out of three-hundred total interphase cells both in dorsal and in ventral tongue surfaces. Results were analyzed through Analysis of Variance and t Test. RESULTS: Cell proliferation was greater in dorsal than in ventral tongue surfaces (p < 0.0001) with no diet difference. Apoptosis was significantly greater in mice fed FO than CO, particularly in tongue dorsal epithelia (p < 0.018). CONCLUSIONS: This study shows that FO diet induces higher levels of apoptosis in tongue epithelia suggesting a tissue defensive mechanism when exposed to a carcinogenic-tumoral agent.

Introducción: Según el concepto de cancerización de campo, existría alteración en la proliferación epitelial en áreas cercanas a tumores. Dicha proliferación podría ser modificada por lípidos dietarios. Objetivos: este estudio fue diseñado para analizar proliferación y apoptosis en epitelio lingual de ratones portadores de tumores salivalesinducidos por DMBA y alimentados con dietas a base de diferentes lípidos. Materiales y Métodos: Cuarenta y cinco días posteriores al destete, diez ratones BALB/c fueron asignados a dos dietas: maíz(M) y bacalao (B). Dos semanas después se inyectó DMBA en la zona submandibular. Los animales fueron sacrificados a ala 13º semana post-inyección. Muestras de lengua fueron fijadas en formal-etanl y procesadas inmunohistoquímicamente con marcadores de proliferación (Ki-67) y apoptosis. Mediante microscopia óptica, se efectuó un conteo de núcleos positivos a ambos marcadosres en un total de trecientas células en interfase, tanto en cara dorsal como ventral de lengua. Los resultados fueron analizados mediante Anális de Varianza y Test t. Resultados: La proliferación celular fue mayor en cara dorsal que en ventral (p> 0.001), sin diferencias por dieta. La apoptosis fue significativamentes mayor en ratones alimentados con B que M, en particular en cara dorsal (p<0.018). Conclusiones: Este estudio demuestra que la dieta B induce mayor apoptosis en ela epitelio lingua, sgiriendo un mecanismo defensivo de los tejidos ante el agente cancerígeno-tumoral.

Proliferación y apoptosis en epitelio lingual de ratones con tumores salivales inducidos por dimetilbenzantraceno (DMBA) y modulados por lípidos dietarios / Proliferation and apoptosis in tongue epithelium of mice bearing salivary tumors induced by dimetilbenzantraceno (DMBA) and modulated by dietary lipids

INTRODUCTION: According to the concept of field defects during the carcinogenesis process, excessive epithelial proliferation/apoptosis may exist in areas near tumors. Proliferation or apoptosis could be modified by dietary lipids. PURPOSE: The present study was designed to analyze proliferation and apoptosis in tongue epithelium of mice fed diets based on different lipids followed by induction of salivary tumors with DMBA. MATERIALS AND METHODS: Forty-five days after weaning, ten BALB/c mice were assigned to two diets: corn oil (CO) and fish oil (cod liver, FO). Two weeks later, DMBA was injected in the submandibular area. Animals were sacrificed at the 13th post-injection week. Samples of tongue were fixed in formalin-ethanol and immunohistochemically stained for proliferation (Ki-67) and apoptosis (Bax). By light microscopy, the number of nuclei positive for these markers were counted out of three-hundred total interphase cells both in dorsal and in ventral tongue surfaces. Results were analyzed through Analysis of Variance and t Test. RESULTS: Cell proliferation was greater in dorsal than in ventral tongue surfaces (p < 0.0001) with no diet difference. Apoptosis was significantly greater in mice fed FO than CO, particularly in tongue dorsal epithelia (p < 0.018). CONCLUSIONS: This study shows that FO diet induces higher levels of apoptosis in tongue epithelia suggesting a tissue defensive mechanism when exposed to a carcinogenic-tumoral agent.(AU)

Introducción: Según el concepto de cancerización de campo, existría alteración en la proliferación epitelial en áreas cercanas a tumores. Dicha proliferación podría ser modificada por lípidos dietarios. Objetivos: este estudio fue diseñado para analizar proliferación y apoptosis en epitelio lingual de ratones portadores de tumores salivalesinducidos por DMBA y alimentados con dietas a base de diferentes lípidos. Materiales y Métodos: Cuarenta y cinco días posteriores al destete, diez ratones BALB/c fueron asignados a dos dietas: maíz(M) y bacalao (B). Dos semanas después se inyectó DMBA en la zona submandibular. Los animales fueron sacrificados a ala 13º semana post-inyección. Muestras de lengua fueron fijadas en formal-etanl y procesadas inmunohistoquímicamente con marcadores de proliferación (Ki-67) y apoptosis. Mediante microscopia óptica, se efectuó un conteo de núcleos positivos a ambos marcadosres en un total de trecientas células en interfase, tanto en cara dorsal como ventral de lengua. Los resultados fueron analizados mediante Anális de Varianza y Test t. Resultados: La proliferación celular fue mayor en cara dorsal que en ventral (p> 0.001), sin diferencias por dieta. La apoptosis fue significativamentes mayor en ratones alimentados con B que M, en particular en cara dorsal (p<0.018). Conclusiones: Este estudio demuestra que la dieta B induce mayor apoptosis en ela epitelio lingua, sgiriendo un mecanismo defensivo de los tejidos ante el agente cancerígeno-tumoral. (AU)

Can a soft diet prevent bowel obstruction in advanced pancreatic cancer?

Although many patients are advised to follow a high-fiber diet to avoid constipation, it seems that a soft diet such as that recommended after bowel surgery may well be more helpful in avoidance of intestinal obstruction.

Reevaluation of the impact of a stringent low-iodine diet on ablation rates in radioiodine treatment of thyroid carcinoma.

Prior analyses of the impact of stringent, preablative low-iodine diets (LIDs) on ablation in patients with differentiated thyroid cancer postthyroidectomy are dated. We retrospectively reviewed first-time, short-term ablation rates for 44 LID patients and 50 patients following a regular diet (RD) who were verbally instructed to avoid salt, seafood, and multivitamins containing iodine. Patients who had undergone ablation were given between 100 and 200 mCi of 131I, depending on the presence of metastases. We found a 68.2% ablation rate for LID patients, compared to a 62.0% rate for RD patients, a nonsignificant difference (p = 0.53). We observed a dose-response relationship for both patient groups, with higher ablation rates corresponding to higher doses of radioiodine administered. We also measured iodine levels in spot urine samples from 7 matched LID patients and 7 matched RD adherents (healthy volunteers) prediet and postdiet as well as 39 healthy volunteers. LID patients had a lower mean urinary iodine level postdiet (173.9 microg/L; range, 45-1,217 microg/L; standard deviation [SD] = 127.7) than the RD patients (mean, 381.4 microg/L; range, 140-630 microg/L; SD = 196.3) or the 39 normal controls (444.0 microg/L; range, 50-1,690 microg/L; SD = 413.4). Whereas the LID lowered urinary iodine levels by 69.4% from prediet values, the RD reduced urinary iodine by 23.6%. Although differences in the reduction of urinary iodine levels between the LID and the RD were substantial, both groups experienced equivalent outcomes. The level of iodine in the American diet has progressively decreased, and may be much lower now than when prior LID studies were conducted. We suggest that prescribing a refined, less stringent diet that avoids high-iodine-containing foods would offer equivalent outcomes with increased patient convenience.

Inhibition of experimental colorectal carcinogenesis by dietary N-6 polyunsaturated fats.

The influence of dietary fats on azoxymethane-induced colorectal carcinogenesis and erythrocyte, adipose, colon mucosa and tumour tissue fatty acids was investigated in 228 Wistar rats. The two main diets compared were beef suet rich in saturated fatty acids and corn oil rich in a linoleic acid, an N-6 polyunsaturated fatty acid. The animals were placed in one of four dietary groups: A = 5% saturated fat, B = 20% saturated fat, C = 5% N-6 fat and D = 20% N-6 fat. There was no difference in the number of adenomas between any of the dietary groups. The mean (+/- SEM) carcinoma yield per rat was A = 0.93 +/- 0.28, B = 1.93 +/- 0.50, C = 0.70 +/- 0.07, D = 0.13 +/- 0.04; the tumour yields in rats fed the saturated fat diets were significantly different from each other and from those fed the N-6 fat diets. The fatty acid profiles in all tissues were dependent upon the type and level of dietary fat and the tissue type. Arachidonate was higher in tumours compared to normal mucosa. Significant correlations were found between adipose linoleate (reflecting dietary intake) and tumour oleate and tumour arachidonate but not with the colorectal mucosa of control animals. This is the first in vivo study to show reduced colorectal carcinogenesis by N-6 polyunsaturated fatty acids.