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Background: Nutritional intake after pancreatectomy may be impaired. The
extent of the problem and the effect on intake of specific nutrients is
unknown. Methods: A 1-week weighed dietary food intake (using digital
scales and a food diary) was studied in 15 patients, a median of 4 (range
1-30) months after pancreatectomy. Results were expressed as a percentage
of estimated average requirement (EAR), reference nutrient intake (RNI) or
lower RNI (LRNI) values. Results: The median energy intake was 1914 (range
1154-2804) kcal/day, representing a median of 88 (56-154) per cent of EAR.
Fat intake was low (72 (60-123) g/day); protein intake was adequate (139
(99-219) per cent of RNI). Deficiencies were observed in the intake of
vitamin D (17 (6-56) per cent of LRNI) and, in some patients, selenium (107
(19-203) per cent of LRNI). Conclusion: Nutritional intake in the months
after pancreatectomy could be improved by increasing fat intake (with
enzyme supplements as appropriate). This 7-day study also suggests that
these patients may require vitamin D and possibly selenium supplementation.

Previous studies conducted in Yugoslavia indicated that the concentration
of selenium in soil, food items, and serum of the population is very low.
The aim of the study was to investigate the possible relationship among
environmental, health-related habits, nutrition, and selenium serum levels
in cancer patients and the healthy population. The case-control study
included a group of cancer patients and a matched group of healthy
controls: 57 cancer patients and 41 healthy controls living in Stari Grad
(an urban area of Belgrade), as well as 17 cancer patients and 13 healthy
controls living in Barajevo (a rural community in the vicinity of
Belgrade). The healthy controls were matched to cancer patients in sex and
age; they were not blood related. The selenium serum levels were measured
by atomic absorption spectrophotometry. Health-related habits and relevant
dietary factors ('food frequency' method) that may influence the selenium
serum levels were assessed by questionnaires. The differences in average
values of selenium serum levels between the cancer patients and healthy
controls were not significantly different, but both were below the lowest
recorded in referential studies. A significant difference between the
values obtained from urban and rural subgroups was noted. The most
important factors that influenced the level of selenium included the
residence place in the region with selenium deficiency (Barajevo), age,
associated chronic diseases, and some dietary factors potentially related
to the intake of selenium. The results obtained in this investigation
pointed out that use of selenium supplementation in this area should be
seriously considered.

Although numerous dietary factors influence the fatty acid profile of
human breast milk, little is known about the effect of trace minerals such
as selenium. Consequently, the purpose of this study is to evaluate the
influence of selenium supplementation during pregnancy and lactation on the
concentration of breast milk fatty acids in healthy lactating women from
New Zealand, an area of naturally low selenium status. Milk samples were
obtained at parturition and 3 months postpartum from 22 women supplemented
with either 50 mug selenium daily as selenomethionine or a placebo during
pregnancy and lactation. Selenium concentration of breast milk was
significantly increased by the supplementation (P = 0.0001 and 0.003,
respectively), but glutathione peroxidase activity was unchanged. The
selenium supplement also significantly increased the concentration of
polyunsaturated fatty acids in breast milk (P = 0.02), especially linoleic
acid (P = 0.02), and decreased the concentration of saturated fatty acids
(P = 0.04). These data indicate that selenium plays a unique role in
influencing the lipid content of human breast milk.

The trace element nutrient selenium (Se) has been shown to possess
cancer-preventive activity in both animal models and humans, but the mechanisms by which this occurs remain to be elucidated. Because angiogenesis is obligatory for the genesis and growth of solid cancers, we investigated, in the study presented here, the hypothesis that Se may exert its cancer-preventive activity, at least in part, by inhibiting cancer-associated angiogenesis. The effects of chemopreventive levels of Se on the intra-tumoral microvessel density and the expression of vascular endothelial growth factor in 1-methyl-1-nitrosourea-induced rat mammary carcinomas and on the proliferation and survival and matrix metalloproteinase activity of human umbilical vein endothelial cells in vitro were examined. Increased Se intake as Se-enriched garlic, sodium selenite, or Se-methylselenocysteine led to a significant reduction of intra-tumoral microvessel density in mammary carcinomas, irrespective of the manner by which Se was provided: continuous exposure (7-wk feeding) with a chemoprevention protocol or acute bolus exposure (3 d) after carcinomas had established. Compared with the untreated controls, significantly lower levels of vascular endothelial growth factor expression were observed in a sizeable proportion of the Se-treated carcinomas. In contrast to the mammary carcinomas, the microvessel density of the uninvolved mammary glands was not altered by Se treatment. In cell culture, direct exposure of human umbilical vein endothelial cells to Se induced cell death predominantly through apoptosis, decreased the gelatinolytic activities of matrix metalloproteinase-2, or both. These results indicate a potential for Se metabolites to inhibit key attributes (proliferation, survival, and matrix degradation) of endothelial cells critical for angiogenic sprouting. Therefore, inhibition of angiogenesis associated with cancer may be a novel mechanism for the anticancer activity of Se in vivo, and multiple mechanisms are probably involved in mediating the anti-angiogenic activity. Copyright 1999 Wiley-Liss, Inc.

BACKGROUND: Studies on potential benefits of selenite in cancers of the female genital tract and breast cancer have concentrated on 2 fields: prevention on one side, complementary oncological therapy on the other side. Big studies have been realized in the past which have shown no clear effect of selenium
supplementation in prevention of female cancers and breast cancer in the
industrialized nations of Europe and Northern America. Few investigations exist
on the therapeutic effects of selenium therapy in the clinical field of
gyneco-oncology. EXPERIENCES: Many patients with malignant disease of the female breast and genital tract are strongly demanding additional therapeutical
concepts in natural medicine in addition to adjuvant or palliative chemo- or
hormonal therapy and supportive medication. In pilot studies with low-dose
natrium selenite (up to 300 micrograms/day) they report a better quality of
life. Side effects were not reported. Analysis of the immune system reveal a
stimulation of B19 lymphocytes and natural killer cells. CONCLUSION: In Germany, a country with selenium deficiency, clinical studies are now carried out on the effects of selenium as a drug to reduce side effects of chemo- and radiotherapy, enhance quality of life by reducing toxic side effects and help to restore immune function.

BACKGROUND: In various epidemiologic studies an association of low selenium blood levels and reduced glutathione peroxidase with an increased risk of cancer incidence was described. The antitumoral therapy and a suboptimal nutrition could intensify this deficiency. Every reduction of disease related and therapeutic caused symptoms may improve life quality. APPLICATION: We report our preliminary experiences in the adjuvant radiochemotherapy of advanced rectal cancer (UICC II/III) corresponding to the NCl recommendation. An oral selenium supplementation was carried out with 2000 micrograms Na2SeO3 after every course of fluorouracil chemotherapy and daily 400 micrograms Na2SeO3 after irradiation of tumor region and lymph nodes. A weekly life quality assessment was explored with special interest in diarrhea, dysurie, pain, appetite, nausea and emesis. CONCLUSION: Damages to normal tissue specially to DNA enzymes and membranes caused by free radicals is one mechanism in tumorgenesis, tumor progression and therapeutic consequence. A radioprotective effect of selenium is verified by in vitro and in vivo data. Our data show that oral selenium intake in rectal cancer patients is easily tolerated with no side effects. Improving life quality and secondary cancer prevention with supplementation of selenium has to be proven in prospective randomized studies.

PURPOSE: It is still controversial whether a low selenium level and a reduced activity of the selenium-dependent enzyme, glutathione peroxidase, in blood are associated with an increased risk and poor prognosis of cancer in humans. This study evaluates whether colorectal cancer patients have lower serum selenium and glutathione peroxidase levels than a gender-matched and age-matched control group and whether there is a correlation to clinical data and prognosis. METHODS: In a retrospective study, serum selenium and glutathione peroxidase activity of 106 patients with colorectal cancer were determined. Clinical data were provided by our long-term follow-up program for colorectal cancer patients. RESULTS: Patients with a selenium level <70 microg/l had a significantly lower mean survival time and a lower cumulative cancer-related survival rate than patients with a selenium level >70 microg/l (P = 0.0009). When considering the different tumor stages, a decline of the mean selenium level in the T4 carcinoma group was found in the analysis of variance (P < 0.05). The lowest selenium level was found for patients with advanced tumor disease and in a preoperative situation, ie., high tumor burden. In comparison with the control group, the cancer group showed a significant reduction of serum glutathione peroxidase activity (P < 0.01) but no significant difference in selenium level. CONCLUSIONS: These results support the hypothesis of an association between low selenium level and advanced tumor disease. From our data, it cannot be decided whether this phenomenon is more likely to be a consequence or a causative factor for development and course of the disease.

Serum selenium concentration (scSe) (microgram/l) was comparatively measured in healthy persons (n = 202), patients with colorectal adenoma(s) (n = 44) and colorectal carcinoma (n = 48). In patients with adenoma(s) scSe (59.05 15) was significantly lower (p < 0.001) compared with scSe in the control group
(66.8 14.43). Hyposelenemia was more pronounced in patients with multiple
polyps (n = 11) than in patients with single adenoma (n = 33) (p < 0.05).
Patients with colorectal carcinoma had also significant decrease in scSe (50.93
13.81) compared with the control group (p < 0.001 and with the adenoma
patients (p < 0.001). According to the analysis of variance, highly significant
differences were found among the cancer patients stratified in Dukes' stages A
to D (p < 0.001), indicating a strong negative correlation between extension of
cancer and hyposelenemia. Furthermore, hyposelenemia seemed to be more
pronounced in the mucinous type of carcinoma than in adenocarcinoma (p = 0.056). This results indicate that hyposelenemia is strongly associated with colorectal neoplasia (including extension and severity of the disease) and that it may not only be a result but also one of tumorogenic factors. That means that selenium supplementation could be important in prevention or even adjuvant therapy of colorectal cancer.

The element selenium (Se) was recognized only 40 years ago as being essential in the nutrition of animals and humans. It is recognized as being an essential component of a number of enzymes in which it is present as the amino acid selenocysteine (SeCys). Selenium compounds have also been found to inhibit tumorigenesis in a variety of animal models and recent studies indicate that supplemental Se in human diets may reduce cancer risk. Anti-tumorigenic
activities have been associated with Se intakes that are more than sufficient to
correct nutritionally deficient status; that is, Se appears to be
anti-tumorigenic at intakes that are substantially greater than those associated
with maximal expression of the known SeCys-containing enzymes. Therefore, while some cancer protection may involve one or more Se-enzymes, it is probable that anti-tumorigenic functions of Se are discharged by certain Se-metabolites produced in significant amounts at relatively high Se intakes. Thus, Se supplementation of individuals with relatively low or frankly deficient natural
intakes of the element can be expected to support enhanced anti-oxidant
protection due to increased expression of the Se-dependent glutathione
peroxidases and thioredoxin reductase. Higher levels of Se-supplementation can be expected to affect other functions related to tumorigenesis: carcinogen
metabolism, immune function, cell cycle regulation and apoptosis. Thus,
according to this 2-stage model of the roles of Se in cancer prevention, even
individuals with nutritionally adequate Se intakes may benefit from
Se-supplementation.